!'■!■■' ' . • ' , ■ ■.
A CONCISE
TEXTBOOK
OF
SURGERY
A CONCISE
Somen Das
M.B.B.S. (Cal.), ER.C.S. (Eng. & Edin.)
Senior Consnltant Surgeon
AUTHOR OF
A MANUAL ON CLINICAL SURGERY,
A CONCISE TEXTBOOK OF SURGERY,
A TEXTBOOK ON SURGICAL SHORT CASES,
A PRACTICAL GUIDE TO OPERATIVE SURGERY
&
UNDERGRADUATE FRACTURES & ORTHOPAEDICS.
SIXTH EDITION
KOLKATA
2010
All Rights Reserved
This book or any part thereof must not be reproduced in any form
without the written permission of the author, DR. S. DAS.
Copyright © DR. S. DAS.
First Edition ......................................... June, 1994
Second Edition ............................ September, 1999
Reprinted - August, 2000
Third Edition ........................................ June, 2001
Reprinted
Reprinted
Reprinted
Reprinted
- September, 2002
- August,
2003
April, 2004
May, 2005
Fourth Edition ................................February, 2006
Reprinted July, 2006
Reprinted - January, 2007
Reprinted July, 2007
Fifth Edition .......................................March, 2008
Reprinted - October, 2008
Reprinted - March, 2009
Sixth Edition .......................................... July, 2010
US $ 27.00 Rs. 778.00
ISBN-978-81-905681-2-8
Published by
Dr. S. Das.
13, Old Mayors' Court,
Kolkata - 700005.
INDIA
Email - drsdaslOO@rediffmail.com
Website : http://www.surgerybooksbydrsdas.com
in this profession and I have consulted many books and various established global journals.
I must acknowledge with thanks the masters of Surgery including my late father from whom I have
learnt this subject and technique of writing a textbook, all my patients who have offered themselves to be
photographed and repeated examinations, all my students whose questions made me think and showed me
the way to write this book and lastly my colleagues who have encouraged me in this work. I owe a deep
debt of gratitude to vast number of students and young teachers from all comers of Indian subcontinent
who had requested me and even pressed me to write a comprehensive textbook which they felt absence
of. In fact it is only for them I could venture and complete this task. If this book helps the great mass of
medical students to learn the basis of Surgery, I shall consider that it has done its job.
This book is fully dedicated to the memory of my late father Dr. K. Das, FRCS (Eng. & Edin.).
He, I believe, does not require any introduction. He was a doyen among surgeons with towering stature,
professional excellence and academic brilliance. His legendary personality will always be remembered by
the future generation. He also cherished the desire to write a Textbook of Surgery. But his health did not
permit. How better can one pay tribute to this great teacher of Surgery than to dedicate this Textbook
to his memory by fulfilling his ambition. This book is dedicated to commemorate his 25th death anniversary
(12th January, 1993). I tried my best to bring out this book in 1993, but the Type Setters, Processors and
Printers did not lend their support, so I was late in publishing this book.
June, 1994.
13, Old Mayors’ Court,
Calcutta - 700 005.
S. DAS.
Preface To The Sixth Edition
It is a pleasure to acknowledge my sense of gratitude to the teaching faculty and the students
of the Indian Subcontinent, who have widely accepted, appreciated and recommended this book.
This book is now an accepted Textbook in major teaching institutions of this country. It has
transcended other Foreign Textbooks in terms of sales and popularity. This has definitely encouraged
me to bring out this edition.
Surgery is advancing very fast. This edition mirrors the important changes which have taken
place recently. This book provides an update for the students both the undergraduate and the
postgraduate. The trend is now towards minimal access surgery, it has gone upto needlescopic
laparoscopy and the scope and application of these are discussed in almost all the chapters. I have
always averted altercations and only accepted facts have been enumerated. I have not shown any
interest to embellish this edition with coloured photographs as these are more ornamental and do
not always help the students to understand their implications.
The success of this book reflects the wide appeal of its presentation of the fundamentals of
surgical practice in a direct and concise way. Editing a warmly accepted book is more of a challenge
which I am well aware of and it may be assured that an honest attempt has been made. All the
chapters have been updated and recent advances are included. What I have not changed is the basic
idea — that one should have a clear conception of this subject based on Anatomy, Physiology and
Pathology to know the symptoms and signs of surgical diseases and their respective treatment in the
present scenerio. To let the readers know about the primary intention of this book, I have not
reprieved preface to the first edition.
Now standard radiology has largely been replaced by Ultrasound Scanning, Computerised
Axial Tomography and Radioisotope Scanning. Nuclear Magnetic Resonance is now increasingly
used to get improved quality of imaging. So more space has been provided for these investigations
in this edition. Without surgical anatomy and physiology no chapter of a Surgical Text can be
complete and I have provided adequate emphasis on these sections.
I
again thankfully acknowledge the inspiration received from my colleagues and the students
to bring out this edition. I am grateful to the patients who voluntarily submitted themselves to the
trouble of being photographed. I am obliged to the great mass of students who made me feel the
dearth of a proper book on this subject and their difficulties to understand this subject. My sincere
thanks to the DTP composer, processor and printer on whom depend the quality of production of
this treatise.
My obeisance to the stalwarts of this field without whose contributions surgery would not have
progressed to this level.
13, Old Mayors’Court,
Kolkata - 700 005.
July, 2010.
S. DAS.
A CONCISE
TEXTBOOK OF SURGERY
DEDICATED
TO THE MEMORY OF MY FATHER
Late Dr. K. Das, F.R.C.S. (Eng. & Edin.)
Whose blessings have only made thtis venture possible
&
TO THE MEMORY OF MY MOTHER
Late Mrs. Gitanjali Das
Who had always inspired me during my father’s absence to achieve this goal.
Preface To The First Edition
While I was a medical student, I felt dearth of a
single comprehensive textbook in Surgery which could
provide all the informations an undergraduate should know
to become a full-fledged doctor. My friends also shared
the same idea. Most textbooks of Surgery originate from
the West and present whimsical and often desultory
approach to the subject. These authors deal with certain
topics of their interests in great depth while leave other
topics which are not of their interest though of similar
importance, if not more, to the students. So being
constantly insisted and hard pressed by my beloved
colleagues and students, I ultimately ventured to write a
Textbook on Surgery, which should be complete,
comprehensive and exam-oriented. My intention has been
to write in a clear, concise and easily understandable way,
in my own style keeping always a vigilant watch to the
students’ interest. I was never keen in providing numerous
illustrations in this treatise, as I had already submitted a
total of more than 1,500 illustrations in my other three well-established books —- ‘A Manual On Clinical
Surgery’, ‘A Practical Guide To Operative Surgery’ and ‘A Textbook On Surgical Short Cases’. I did not
want to repeat my illustrations from these books. In this text I have included more than 400 illustrations,
which I think will help the students in understanding the subject.
This book is primarily intended for the undergraduate, though I believe it should prove useful to
those aspiring for diploma and postgraduate degrees in Surgery. In each chapter I have included a section
of Embryology and Surgical Anatomy to help the students to understand Surgery. Reasoned explanation
based on Physiology and Pathology has been included in each chapter to explain the symptoms, signs and
treatment.
Surgery has been full of exciting developments in last few decades. I have tried to include these
developments without increasing the bulk of the book. I have tried to cover all aspects of Surgery with
same depth. The various sophisticated investigations which are now available in developing countries like
ours have made the diagnosis simpler and faster, though these investigations are more expensive and often
inaccessible to the remote health centres. These investigations like Ultrasound, Computed Tomography
(CT), Magnetic Resonance Imaging (MRI), Radionuclides are all discussed with reasonable depth and
illustrations but without unnecessary details to increase the bulk of the book. Thus all relevant and upto-date materials have been included in a pertinent and precise manner emphasizing the common surgical
problems which a student must know to become graduate and ultimately a successful clinician. Covering
the whole field of Surgery has been my intention with particular emphasis on those which are required for
examinations both undergraduate and postgraduate. In treatment my approach has been rational and I have
mentioned only those which are accepted and left those which are still in the experimental stage. I could
not resist myself in including a few very update topics like Laparoscopic Cholecystectomy, Extracorporeal
Shock Wave Lithotripsy (ESWL) etc. though these seem to be less important from undergraduate examinatio
point of view, yet it may quench the thirst of a few inquisitive students. Although surgery is becoming
increasingly specialised and fragmented, yet all surgeons must be exposed in the beginning to the widest
possible spectrum of surgical practice, and here lies the importance of this type of text which cannot be
ignored in years to come.
In preparing a textbook like this, I have freely utilised the knowledge and experience of the stalwarts
Contents
CHAPTER_______________________________________________________________________PAGE
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
WOUND HEALING
SHOCK
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
NUTRITION (INCLUDING PARENTERAL NUTRITION)
BURNS
BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS
SPECIAL INFECTIONS
CYSTS
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
ULCERS, SINUS AND FISTULA
.....
.....
.....
.....
....
.....
.....
.....
.....
.....
.....
1
11
24
42
56
61
77
86
94
102
156
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
TETANUS
GAS GANGRENE
SKIN GRAFTING
DISEASES OF ARTERIES
DISEASES OF VEINS
DISEASES OF THE LYMPHATIC SYSTEM
THE PERIPHERAL NERVES
AMPUTATION
THE HAND
THE FOOT
THE SPINE AND PELVIS
THE HEAD
SWELLINGS OF THE JAW
MOUTH, TONGUE AND LIPS
CLEFT LIP AND CLEFT PALATE
SALIVARY GLANDS
THE NECK
THE THYROID AND PARATHYROIDS
THE ADRENAL GLANDS
THE BREAST
INJURIES OF THE CHEST
DISEASES OF THE CHEST (INCLUDING THE MEDIASTINUM AND
THE DIAPHRAGM)
THE HEART AND PERICARDIUM
THE OESOPHAGUS
THE STOMACH AND DUODENUM
THE LIVER AND PORTAL HYPERTENSION
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
.....
169
174
178
187
256
286
312
337
349
371
387
420
448
461
479
485
501
526
561
573
621
....
....
.....
.....
....
632
657
676
708
758
34.
35.
36.
37.
CHAPTER
PAGE
38.
THE BILIARY SYSTEM
786
39.
THE SPLEEN
821
40.
THE PANCREAS
836
41.
THE SMAL^ INTESTINE
869
42.
INTESTINAL OBSTRUCTION
880
43.
THE PERITONEUM, OMENTUM AND MESENTERY
893
44.
THE VERMIFORM APPENDIX
904
45.
THE COLON
917
46.
THE RECTUM AND ANAL CANAL
949
47.
UMBILICUS AND ABDOMINAL WALL
988
48.
HERNIAS
995
49.
THE KIDNEY AND URETER
1031
50.
THE URINARY BLADDER
1105
51.
THE PROSTATE AND URETHRA
1137
52.
TESTIS, EPIDIDYMIS AND SCROTUM
1173
53.
THE PENIS
1204
INDEX
1217
WOUND HEALING
The word 'healing' means replacement of destroyed tissue by living tissue.
Wounds may be caused by —
(i) Trauma — either accidental or surgical.
(ii) Physical, chemical and microbial agents, which give rise to inflammation and may
lead to necrosis or destruction of living tissue.
(iii) Ischaemia, which leads to infarction.
In the context of wound healing two terms should be understood —
1. Regeneration, which means replacement of lost tissue by tissue similar in type.
This occurs due to proliferation of surrounding undamaged specialized cells. The term
regeneration should not be confused with the term 'reconstitution', which means coordinated
regeneration of several types of lost tissue resulting in reformation of whole organ or limb.
This is not possible in human beings, though this is found in lower animals like amphibians,
crustaceans etc. Reformation of pancreas following partial pancreatectomy is the nearest
approach to reconstitution seen in man.
2. Repair, which means replacement of lost tissue by granulation tissue, followed by
fibrosis and scar tissue formation. This occurs when the surrounding specialized cells do not
possess the capacity to proliferate e.g. neurons and muscle or destruction of tissue to such
an extent that proliferation of the surrounding undamaged cells cannot make good the loss.
TYPES OF WOUNDS.—
1. Incised wounds.— These are usually caused by a sharp knife or glass. These
wounds are relatively clean. After suitable exploration, in which the underlying structures
are repaired, these wounds may be closed by primary suture if the wound is explored
within 6 hours of its occurrence. Within this period all damaged tendons, nerves and major
blood vessels should be repaired.
2. Lacerated wounds.— These wounds are commonly occurred following road traffic
accidents. The wounds usually have jagged edges with certain lacerated and devitalized
structures inside the wound. Thorough debridement of these wounds is required if received
within 6 hours of injury. The object is to convert the lacerated wound into an almost incised
wound. Repair of tendons and nerves is not recommended at the time of initial surgery
due to risk of infection and should wait for 4 to 6 weeks for complete healing of the
wound and these repairs are done as a secondary procedure after healing.
3. Penetrating wounds are almost similar to incised wounds, except that its depth
is more. The wound should be explored layer by layer, followed by primary suturing if it
has come within 6 hours of injury.
4. Crushed wounds.— These occur due to industrial, road traffic and war injuries.
These wounds are managed by debridement and removal of all necrotic tissues. Often there
1
2
A CONCISE TEXTBOOK OF SURGERY
is great tension deep to the deep fascia and that is why these wounds should be left open
and dressed. When the oedema and tension have subsided and the tissues within the wounds
are viable, delayed primary suture should be performed. An old adage in this context
should be remembered — 'when there is difficulty in bringing the skin together or there is
doubt about viability of tissues within the wound, it is better not to close the wound'.
Healing by first intention.— When a wound is sutured primarily with clips, sutures
or adhesive materials, the wound healing occurs with minimum scarring and it is known
as healing by first intention.
Healing by second intention.— When there is irrepairable skin loss or the wound
becomes infected and breaks open, primary suturing is not possible. So the wound heals
with more scar tissue and takes longer time to heal. This is known as healing by secondary
intention. An ulcer also heals in the same way.
The four basic processes which take place in wound healing are :—
A. Inflammation.
B. Wound contraction.
C. Epithelialization.
D. Granulation tissue formation.
E. Scar remodelling.
Although all wounds heal by the same basic processes, yet their application is different
in closed wounds and open wounds.
A.
Inflammation.— Immediately after disruption of tissue integrity either by
accidental trauma or by surgeon's knife, inflammation starts. Platelets become adherent
and with clotting factors form a haemostatic plug to stop bleeding from the small vessels.
The blood vessels undergo transient vasoconstriction followed by vasodilatation. Histamine
is considered to be the primary mediator of inflammatory vascular responses. This is
liberated by platelets, mast cells and granulocytes. Histamine produces local vasodilatation
and increases permeability of small vessels. With increase of permeability, proteins and
plasma leak out of the vessels. However the action of histamine is short lasting and local
sources are depleted rapidly. Soon the kinins, a series of biologically active peptides and
the prostaglandins, principally PEGi and PEG2 take over the job of implicating local
inflammatory vascular responses from histamine. Kallikrein, an enzyme found in plasma
and in granulocytes, releases bradykinin and kallidin. In the presence of kinins, the local
cells produce a variety of prostaglandins. These prostaglandins seem to be the final
mediators of acute inflammation and may play a chemotactic role for white cells and
fibroblasts. Aspirin and indomethacin are potent inhibitors of prostaglandin biosynthesis
and the antiinflammatory action of these drugs actually result from their effects on
prostaglandin metabolism.
In the early stages of inflammation, actively motile white cells migrate into the wound
and start engulfing and removing cellular debris and injured tissue fragments. At first,
polymorphonuclear leucocytes dominate. This stage has also chemical mediators.
Leukotaxine, a peptide formed in damaged tissues by the enzymatic destruction of albumin,
is thought to be the chemotactic agent — attracting leucocytes into the wound.
As the transient phase of white cell migration ends, the granulocytes with shorter life
die and release acid hydrolases into the local environment. Previously the proportion of
granulocytes and monocytes in the wound area were in the same ratio as they are in the
WOUND HEALING
3
blood. As the granulocytes are dying, the proportion of monocytes increases significantly
and these monocytes continue their scavenging activity for weeks. Monocytes become the
dominant cell type by the 5th day. They are phagocytic and ingest cellular debris. It has
been found out experimentally that wound healing may proceed normally in the absence
of granulocytes and lymphocytes, but monocyte must be present to create normal fibroblasts
production. Depression of monocytes will delay wound healing.
'
<
Clinically, inflammation is presented by redness, tenderness, heat, swelling and loss of
function.
B.
Wound contraction.— Wound contraction has been noticed in open wounds with
tissue loss for centuries. Only recently however, the mechanisms responsible for K)ound
contraction have been investigated extensively.
This wound contraction does not begin immediately and that about 3 to 4 days elapse
before movement of the edges become measurable. This period, when no wound contraction
is noticed, is called the initial 'lag period'. After this period, there is a period of rapid
contraction, which is completed by the 14th day. At this time the wound is reduced to
approximately 80% of its original size. The magnitude of contraction varies with the species
of animal and with the shape, size and site of the wound. In the rabbit the wound is
reduced to approximately 20%.
i-*;
The amount of contraction depends on the amount of skin available surrounding the
wound to be stretched over the wound. Hands and face of a young person do not contain
excess skin. So wound contraction is limited in these places, whereas in cervical region or
face of old people wound contraction may be more and effective due to lax skin around.
When loss of skin occurs over an area such as the malleolar surface of the lower leg and
ankle, wound contraction simply cannot occur because there is not enough extra skin around
the defect.
The first step in studying the mechanism of wound contraction is to try to define
precisely where the fundamental process is located. It should be determined whether a
centripetal movement occurs because an energy or power source located outside the defect
is pushing the skin edges inwards or whether a centrally located power source is pulling
the skin edges to the centre of the defect.
CAUSES OF WOUND CONTRACTION.—
Over the years a great deal of research work has been performed to know the
mechanism of wound contraction, but yet it is not known with certainty.
1. Removal of fluid by drying has been suggested as a cause of diminution in the size
of wound. But this has not been substantiated, as water content of central wound tissue at
the beginning of wound contraction has not changed significantly as at the end of
contraction.
2. Contraction of collagen has also been incriminated as the cause of wound contraction.
Although collagen increases markedly between the 5th and 8th day of healing, yet the total
collagen in the wound falls significantly after this period, so it does not correlate with the
period of wound contraction. Moreover the rate of wound contraction is not affected by
suppressing collagen synthesis. In scorbutic animals, although granulation tissue is formed,
collagen production is inhibited and yet wound contraction proceeds normally.
3. Contraction of granulation tissue.— That contraction occurs at a time when granulation
tissue is actively being formed has laid many workers to regard the granulation tissue as forming
4
A CONCISE TEXTBOOK OF SURGERY
an organ of contraction. But curiously excision of central granulation tissue did not affect the
rate of wound contraction. It was further noticed that although wound contraction was not
inhibited by excising the central mass of granulation tissue, it could be stopped decisively by
excising a very limited zone of tissue just beneath the advancing dermal edge. So this indicated
that the contracting mechanism is located in the margins of the wound, the so called ‘pictureframe area'. This area is the strategic location of cells which appear to constitute the machinery
for wound contraction. The histologic area of this 'picture-frame area' reveals a collection of
large, stellate, pale staining cells which have been thought to be the cells responsible for moving
the overlying dermis. These are myofibroblasts. These cells show characteristics of fibroblasts
and smooth muscle cells including a rough endoplasmic reticulum and microfilament bundles
similar to smooth muscles.
FACTORS INHIBITING WOUND CONTFtACTION.—
(i) Corticosteroid administration has inhibitory effect on wound contraction.
(ii) Contraction does not occur normally in burns.
(iii) Immediate skin grafting prevents wound contraction.
(iv) X-irradiation, if applied on the wound, causes delay in wound contraction.
(v) Trocinate, which is a smooth muscle inhibitor, acts on actin which is the contractile
protein in myofibroblasts, also inhibits wound contraction.
(vi) Colchicine and vinblastin also inhibit wound contraction, as they are inhibitors of
microtubule formation in the myofibroblasts. In fact colchicine is presently used in the
control of fibrous contractures in human beings. '
(vii) Cytotoxic agents particularly the cytochrome poisons in non-lethal doses inhibit
wound contraction.
C. Epithelialisation.— In skin wounds, the epidermis immediately adjacent to the
wound edge begins thickening on the first day. Marginal basal cells lose their firm attachment
to the underlying dermis, enlarge and begin to migrate into the wound. The fixed basal
cells in a zone near the wound edge undergo rapid mitotic divisions (proliferate) and the
daughter cells migrate. Within 48 hours, the entire wound surface is re-epithelialized. After
bridging the wound defect, the migrating epithelial cells lose their flattened appearance
and become more columnar in shape. Layering of the epithelium starts and surface cells
keratinize. The epithelial cells also migrate down the suture tracts. Subsequent epithelial
thickening and keratinization may produce marked foreign body reaction and formation of
sterile abscess. So non-absorbable skin sutures should be removed in right time.
In one sentence epithelialization of the wound mainly occurs by proliferation and
migration of the marginal basal cells lying close to the wound margin.
When there is skin loss, dermal pits which are left behind act as islands for regenerating
epithelium. But there is no regeneration of hair follicles, sweat and sebaceous glands in the
new epidermis.
D. Granulation tissue formation.— The haematoma within the wound is soon
replaced by granulation tissue, which consists of new capillaries and fibroblasts. This
formation of granulation is preceded by two phases — (i) phase of traumatic inflammation
and (ii) phase of demolition.
1. PHASE OF TRAUMATIC INFLAMMATION.— The details of this traumatic
inflammation has been discussed earlier in this section (Page 2).
2. PHASE OF DEMOLITION.— The dead tissue cells liberate their autolytic enzymes.
WOUND HEALING
5
Similarly disintegrating polymorphs liberate proteolytic enzymes. The mononuclear cells
alongwith large phagocytic macrophages infiltrate and ingest particulate matters. They either
digest or remove them. Fusion of these macrophages results in the formation of foreign
body giant cells.
3.
GRANULATION TISSUE FORMATION.— The granulation tissue is mainly formed
by proliferation and migration of the surrounding connective tissue elements. It is in fact
composed of in the first instance by capillary loops and fibroblasts with a variable number
of inflammatory cells. So initially it is a highly vascular tissue, which gradually turns into
an avascular scar tissue. The two stages are considered in this process — (a) stage of
vascularization and (b) stage of devascularization.
(a) Stage of vascularization.— As mentioned above the wound clot is invaded by
macrophages, which with their phagocytic activities remove the particulate matters and
move towards the centre of the wound. This process is followed by capillary loops and
fibroblasts. The ingrowth of capillary loops and fibroblasts which help to form living
granulation tissue is known as organization.
Solid buds of endothelial cells grow out of the existing damaged blood vessels at the
surface of the wound. These undergo canalization and by anastomosis with their neighbours
form a series of vascular arcades. Under the electron microscope gaps are seen between
the endothelial cells and the basement membrane is poorly formed. These newly formed
capillary loops leak protein and thus the tissue fluid which is formed is a very suitable
medium for fibroblastic growth.
Gradually these capillary loops differentiate, a few acquire muscle coat and become
arterioles, whereas others enlarge to form thin walled venules. A few disappear or persist
as part of the capillary bed. The source of smooth muscle fibres to form arterioles is either
cell migration or differentiation of existing primitive mesenchymal cells. Direct arteriovenous
shunts are also formed.
The fibroblasts, which accompany the capillary loop, gradually become larger to become
elongated fibrocytes. During this process of fibrogenesis, pH becomes alkaline. From these
fibroblasts ultimately collagen is formed. Collagen is an extracellular secretion from specialized
fibroblasts and the basic molecules which fibroblasts synthesise are frequently called
tropocollagen. This tropocollagen condenses in the mucopolysaccharide extracellular space to
form fibrils. These fibrils are grouped together to form the reticulin fibres. These fibrils when
condensed together form the collagen fibres. This collagen is not inert and it undergoes constant
turnover under the influence of tissue collagenase. More thicker collagen fibres are laid down
haphazardly.
There are several types of collagen which differ in the aminoacid sequence of the
constituent chains, though hydroxyproline, proline and glycin dominate. Type I collagen is
found in the tendon, ligament, skin and bone. Type II collagen is found in cartilage, mainly
in articular and costal cartilages. Type III collagen is found in foetal dermis and later on is
replaced by type I collagen at birth. Type III collagen appears to be an important component
of tissues with unusual degree of elasticity such as aorta, oesophagus and uterus. The
aminoacids found in collagen are hydroxyproline and hydroxy lysine. Other fibrous tissues
such as elastin do not contain significant amount of hydroxyproline.
Fibroblasts are also thought to be responsible for the production of mucopolysaccharide
ground substance.
(b) Stage of devascularization.— In this stage fibroplasia proceeds and some vessels
6
A CONCISE TEXTBOOK OF SURGERY
undergo atrophy, whereas others show endarteritis obliterans, that means their lumens
become obliterated due to intimal proliferation. So the granulation tissue looks pale at this
stage, which is known as devascularization.
At the beginning of this stage, nerve fibres and lymphatics form. With the ingrowth of
nerve fibres, the arterioles exhibits rhythmic contraction. The new lymphatics develop from
existing lymphatics in the same way as do the capillary loops. Mast cells also make their
appearance and their granules are derived from the ground substance. At later stage these
mast cells disappear and hyalinization occurs. There is also formation of scar tissue. This
process is known as cicatrization. Collagen turn over and remodelling in the scar never stops.
In fact the turn over of collagen in scar tissue is faster than in other tissues. The phenomenon
of scar remodelling is the basic function of injured tissues. The gross appearance of remodelling
scars suggests that collagen fibres are altered and rewoven into different architectural patterns
with time.
E. Scar remodelling.—
This is the last stage of wound healing. Approximately 12 hours after injury has
occurred and when inflammation is established, epithelial migration, which is the first
clear cut signs of rebuilding occurs. In a primary wound epithelialization is complete in
a few hours. In a secondary healing wound migration of cells is rapid, as the line of
cells from the wound margin become extended, but progress becomes slower, so that
days or even weeks may elapse before epithelialization is complete. After 4 or 5 days,
epithelialization is assisted by wound contraction. Later on granulation tissue appears as
mentioned earlier but collagen synthesis which is the main feature of scar remodelling
cannot be found before 4th to 6th day. On or about the 7th day wounds will show a
delicate fine reticulum of young collagen fibres. The physical properties of scars depend
on the collagen fibres they contain. Scar strength increases progressively with time. In
fact scar maturation takes a period of many months. All scars slowly and progressively
chcinge in bulk and form. During later stage of wound healing, scars change their
anatomic arrangement. As fibrogenesis proceeds, purposefully oriented fibres seem to
become thicker presumably because there occurring more collagen particles. Non-oriented
fibres seem to disappear. The overall effect appears to be one of lacing the wound edges
together by a 3-dimensional weave. There is one of replacing granulation tissue, allowing
the surface to become covered with epithelium and filling the remaining skin defect with
scar tissue after contraction is complete. This is the picture of secondary healing. As far
as the filling of the defect is concerned, contraction is the major influence. It exerts full
potential before scar tissue synthesis is complete. The central scar seems to remodel itself
to fill the defect after contraction is over. Development of tensile strength (strength of
per unit of scar tissue) and burst strength (strength of the entire wound) is the result
initially of blood vessels growing across the wound, epithelialization and aggregation of
globular protein. Later collagen synthesis is important. The really significant gain in
tensile strength begins about the 5th day. Increasing strength is rapid for 17 days and
slow for additional 10 days. There is an almost imperceptable gain in tensile strength for
2 years subsequent to that. Collagen content of the wound tissue rises rapidly between
the 6th and 17th days, but increases very little after 17 days. So gain in strength after
17 days is primarily due to remodelling of collagen. It must be remembered that
secondary wounds contain slightly less collagen than primary wound of the same age.
WOUND HEALING
7
Due to thermal shrinkage temperature of secondary wound collagen is significantly higher
than that of the primary wounds of the same age. More effective cross-linking of better
physical weave of collagen subunits is responsible for rapid gain in strength for secondary
wounds.
TENSILE STRENGTH.— The strength of a healing wound is of great practical
importance to the surgeon. It acts as the main safeguard against wound dehiscence.
Experimentally it may be estimated by measuring the force necessary to disrupt the wound.
In the first few days the strength of a wound is only that of the clot which cements
the cut surfaces together. Later on various changes take place in the wound healing process
as mentioned above and at the end the tensile strength of the wound corresponds to the
increase in amount of collagen present.
Many factors influence the tensile strength of the wound. These are :—
(i) Direction of the wound.— Skin wounds parallel to the lines of Langer heal faster.
Skin incisions made across Langer's lines tend to gape and their healing is delayed. Tensile
strength of the wound becomes more when this is parallel to the lines of Langer. That is
why the transverse abdominal incisions produce stronger scar than the longitudinal ones.
(ii) Pull of underlying muscles.— The wounds which are parallel to the pull of the
underlying muscles constitute stronger scar.
(iii) Previous wound.— Resutured wounds heal faster than those sutured primarily, as
the repairative process has already commenced.
(iv) Abdominal binders — reduce the rate of gain in strength.
Factors affecting granulation tissue formation.—
(i) Cortisone administration.— Excess corticosteroid administration inhibits granulation
tissue formation. Fibroblasts remain small with little collagen formation. This effect is well
accepted in the experimental animals, but corticosteroid in normal dosage may not influence
wound healing in human beings.
(ii) Scurvy.— In this condition though vascular granulation tissue is formed, yet there
is failure of collagen formation. Instead there are thick reticulin fibres. Maturation to collagen
does not occur in the absence of vitamin C.
(iii) Protein starvation — also causes delayed formation of collagen. There remains
excessive accumulation of poorly-sulphated ground substance.
HEALING OF SKIN WOUNDS
I. Healing of a clean incised wound, the edges of which are closed (closed wound)
— takes place by a process known as healing by first intention. The following changes
take place — (i) initial haemorrhage results in the formation of a fibrin-rich haematoma.
(ii)
Acute inflammatory process occurs and the fibrinous exudate helps to cement the
cut margins of the wound together.
(iii) Minimum granulation tissue is formed, which can be called organization.
(iv) Regeneration of epithelium.— The process of epithelialization has been discussed
above. In the first 24 hours basal cells mobilise from the undersurface of the epidermis. By
48 hours the advancing epithelial edge undergoes cellular hypertrophy and mitosis. Epithelial
cells gradually line the wound deep to the fibrin clot and it also lines the suture tracks.
Implantation epidermoid cyst may develop from epithelial remnants. There may be formation
8
A CONCISE TEXTBOOK OF SURGERY
of ugly punctate scars from sutures which are left in position for longer period. The use of
adhesive tapes instead of sutures for closing wounds avoids these marks and gives better
cosmetic result.
II.
Healing of open wounds.— If delayed closure is not performed and if there is
skin loss, a remarkable change in the physical dimension of the wound occurs. Healing of
such wound is known as healing by secondary intention. The main bulk of tissue which
performs the healing process is the granulation tissue and that is why this type of healing
is also called healing by granulation. But this does not mean that granulations are not
formed in the simple incised wounds. The difference is quantitative and not qualitative.
The followings are the various important processes of this type of wound healing :—
(i) Initial inflammatory phase affects the surrounding tissues and the wound is filled
with coagulum. This coagulum dries and forms a scab.
(ii) The most important feature of healing of this type of wound is wound contraction.
It must be remembered that the skin wound contracts by stretching the surrounding skin
to close the defect and not by the production of new skin. After a delay of 'lag period' of
2. or 3 days, the dermal edges begin moving towards each other. Between 5 and 10 days,
the wound edges move rapidly and after 2 weeks it becomes slowed down again. The
process of wound contraction has been elaborately described above.
(iii) The exposed wound gradually becomes completely covered with granulation tissue.
In fact this granulation tissue forms a temporary protective layer against infection until the
surface is covered by epithelium.
(iv) The epithelium gradually grows over the granulation tissue, but beneath the scab
to complete the healing process. It must be remembered that specialised epithelial structures
like interpapillary processes, hair follicles and sebaceous glands are not reformed.
The epithelial cells in fact slide into the wound forming a thin tongue of cells between
the granulation tissue and the clot. Gradually as the epithelialization continues, there is also
remodelling of the granulation tissue and scar, so that the wounded area which was at first
depressed, ultimately forms a flat scar.
Complications of wound healing,—
(i) Implantation cysts.
(ii) Painful scars.
(iii) Cicatrization.— It often produces various deformities.
(iv) Keloid formation.
(v) Neoplasia.— Squamous cell carcinoma has been seen to develop from the edges
of healing wounds. This may be due to uncontrolled growth with invasive potentiality of
the surrounding epithelial cells which are concerned with epithelialization. In these cases
there is not only mitosis, but there is pleomorphism, disorganization and loss of polarity.
lectors Influencing wound healing.— The various factors which influence wound
healing can be divided into two groups — general factors and local factors.
General factors.—
1. AGE.— Wound healing is fast in the young, but it is normal in old age unless
associated with debilitating diseases or ischaemia or diabetes etc.
2. NUTRITION.— (i) Protein deficiency.— As mentioned above, protein depletion
causes impairment of granulation tissue and collagen formation. It should be noted that it is
not always due to inadequate intake, but may be due to excessive loss e.g. nephrotic
WOUND HEALING
9
syndrome, cirrhosis, chronic inflammatory conditions etc.
(ii) Vitamin C deficiency.— This is discussed above.
(iii) Vitamin A is required for proper epithelialization, which may be hampered due
to its deficiency.
(iv) Zinc, Calcium, Copper and Manganese deficiency.— Zinc is an essential component
of many enzymes which are involved in protein synthesis. There is some failure of
granulation tissue formation in case of zinc deficiency. Others are essential minerals which
are also required for proper wound healing. These may be depleted in intestinal fistulas
and burns.
3. HORMONES.— (a) Corticosteroids.— The effects of this hormone on granulation
tissue formation and wound contraction have been discussed above. Cortisone and its
derivatives decrease the rate of protein synthesis, stabilize liposomal membranes and inhibit
the normal inflammatory reaction. High doses of corticoids limit capillary budding, inhibit
fibroblast proliferation and decrease the rate of epithelialization.
(b)
Desoxycorticosterone acetate and anabolic steroids like testosterone are also
concerned with increase in the speed of wound healing.
4. CYTOTOXIC DRUGS and RADIATION.— Radiation effects and effects of other
cytotoxic agents also influence healing rate. Most cytotoxic agents show their greatest effects
on dividing cells. Any agent that inhibit the division of local fibroblasts or epithelial cells
should prevent or delay healing. Even chronic local application of 5-fluorouracil can
completely prevent healing. Similarly high doses of radiation especially during first 3 days
delay strength of the wound significantly.
The following conditions delay or hamper the quality of wound healing. These are:—
1. Anaemia.
2. Uraemia.
3. Jaundice.
4. Diabetes.
5. Blood dyscrasias.
6. Malignant disease.
7. Cytotoxic drugs.
Local factors.—
1. Position of skin wound.— As mentioned above when the skin wounds are parallel
to the lines of Langer, they heal faster. These lines of Langer are due to arrangements of
collagen bundles in the dermis. The wounds right angle to these lines tend to gape and the
healing is delayed.
2. Blood supply.— Wounds with poor blood supply heal slowly. That is why wounds
in the pretibial region take much more time to heal than those in the face, which are well
vascularized. Wounds of the leg in patients with varicose veins are slow to heal. Similarly
wounds in the ischaemic limbs also heal slowly.
3. Tension.— If the wound is in tension, its healing will be jeopardized. Haematoma
and infection increase tension.
4. Infection.— Once infection occurs in a wound, healing is always delayed. It may
be considered as the most important factor that delays healing. Due to infection, fibroblasts
face tough time to persist as they have to compete with inflammatory cells and bacteria
for oxygen and nutrients. So proper granulation tissue formation and collagen formation
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A CONCISE TEXTBOOK OF SURGERY
become affected. This has been often the cause of 'burst wound' which requires secondary
sutures.
5. Movement.— Movement itself delays wound healing. So rest is very essential for
wound healing. The delicate capillary loops of the granulation tissue and the delicate
epithelium are damaged due to movement. Frequent change of dressing also has the same
adverse effect and should be avoided. Movement also causes entry of infection.
6. Exposure to ionizing radiation.— Previous X-irradiation may affect vascularity of
the part. It also causes delay in the formation of granulation tissue. But most important is
that it inhibits wound contraction.
7. Foreign bodies.— These include tissue reaction and inflammation. If sutures are
kept for longer period, it may cause aseptic abscess.
8. Adhesions to bony surfaces cause delay in wound healing probably by preventing
proper wound contraction. This is particularly seen in wounds over the tibia.
9. Necrosis.— This obviously retards healing.
10. Lymph drainage.— Impairment of lymph drainage, which causes oedema of the
part, jeopardizes the process of wound healing. Elevation of such limb often facilitates wound
healing.
11. Ultraviolet light is well known clinically to increase the rate of healing. This has
been confirmed experimentally.
12. Faulty technique of wound closure is obviously responsible for delay in wound
healing in many cases.
SHOCK
DEFINITION.—
It is very difficult to define shock in one sentence. Probably the best definition would be that
'shock is a condition in which circulation fails to meet the nutritional needs of the cells and at
the same time fails to remove the metabolic waste products'. It is a peripheral circulatory failure
which results from a discrepancy in the size of the vascular bed and the volume of the intravascular
fluid. It is a clinical condition which is characterized by signs and symptoms arising when the
cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to
provide all the organs and tissues with adequate blood flow. The low blood flow state in vital
organs is the main cause of shock.
TYPES of Shock—
There are various types of shock, of which haematogenic or hypovolaemic shock is the
most common and important. The various types of shock are as follows :—
1. Haematogenic or hypovolaemic shock.— This type of shock is due to loss of
blood, plasma or body water and electrolytes or in one word loss of intravascular volume. It
is often caused by haemorrhage, vomiting, diarrhoea, dehydration etc. The characteristic
features are decreased filling pressure of the heart, decreased systemic arterial pressure,
tachycardia and increased vascular resistance. This is clinically manifested by low cardiac
output, tachycardia, low blood pressure and vasoconstriction revealed by cold clammy
extremities.
2. Traumatic shock.— This type of shock is caused by major fractures, crush injuries,
burns, extensive soft tissue injuries and intra-abdominal injuries. In this type of shock there is
hypovolaemia due to bleeding both externally and internally (intraperitoneal haemorrhage) from
ruptured liver or spleen or from torn vessels of the mesentery alongwith toxic factors resulting
from fragments of tissue entering the blood stream. This activates intravascular inflammatory
response. The vascular permeability also increases resulting in further hypovolaemia. Injury to
the chest may cause damage to the respiratory system resulting in hypoxia and shock. Chest
injury may also lead to contusion of the heart which may cause failure of pump resulting in
shock.
Shock due to bums occurs as a result of rapid plasma loss from damaged tissues. This
causes hypovolaemia. This becomes worse with more than 20% of the whole body surface
bum in which there occurs generalized capillary leakage in the first day leading to gross
hypovolaemia. Toxins liberated from infected burns also aggravates shock. This causes an
intravascular inflammatory response with increase in vascular permeability, which requires
large volumes of colloidal and crystaloid fluids for resuscitation.
3. Xeurogenlc shock.— This is caused by paraplegia, quadriplegia, trauma to the spinal
cord or spinal anaesthesia. Such shock is primarily due to blockade of sympathetic nervous
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A CONCISE TEXTBOOK OF SURGERY
system resulting in loss of arterial and venous tone with pooling of blood in the dilated
peripheral venous system. The heart does not fill normally, so that the cardial output falls. So
there is low blood pressure with a normal cardiac output and normal pulse rate and a warm
dry skin. In case of spinal anaesthesia and trauma to the spinal cord, low blood pressure can
be easily corrected by putting the patient in Trendelenburg position (i.e. head end of the bed is
lowered) and rapid administration of fluids with a vasopressure drug.
Vasovagal or vasogenic shock is also a part of neurogenic shock in which there is pooling
of blood due to dilatation of peripheral vascular system particularly in the limb muscle and
in the splanchnic bed. This causes reduced venous return to the heart leading to low cardiac
output and bradycardia. Blood flow to the brain is reduced causing cerebral hypoxia and
unconsciousness. This condition can also be corrected by Trendelenburg position which
increases cerebral flow and consciousness may be restored.
Psychogenic shock, which may follow sudden fright from unexpected bad news or at the
sight of horrible accident, is also included in this group. Its effect may vary in intensity from
temporary unconsciousness to even sudden death.
4. Cardiogenic shock.— This type of shock is usually caused by injury to the heart,
myocardial infarction, cardiac arrhythmias or congestive cardiac failure. In this condition the
heart fails to pump blood. The left ventricle mainly fails, so that there is over-distension of
the right ventricle and ultimately there is increase of back pressure in the pulmonary capillaries.
This leads to pulmonary oedema and hypoxia. Gradually the vascular volume will increase
as a result of salt and water retention by hypoperfused kidneys.
In case of massive pulmonary embolism, if the embolism obstructs 50% of the pulmonary
artery, it will cause acute right ventricular failure. This will severely reduce venous return to
the left ventricle and thus the cardiac output falls drastically to cause severe cardiogenic
shock and even sudden death.
Cardiac compressive shock is usually caused by pericardial tamponade, tension
pneumothorax or by large diaphragmatic hernia. This is a type of cardiogenic shock, in which
the heart is compressed from outside leading to failure of its pumping mechanism, though
the heart itself is normal.
5. Septic shock.— Such type of shock is most often due to gram negative septicaemia.
Such type of shock may occur in cases of severe septicaemia, cholangitis, peritonitis or
meningitis. In early stages cardiac output increases, but vascular resistance decreases due to
dilated cutaneous arteriovenous shunts. In late cases, vascular permeability increases, so that
the blood volume decreases leading to hypovolaemia. In further advanced cases the cardiac
function is damaged due to toxins liberated by the organisms.
6. Miscellaneous types.— These include unclassified types of shock e.g. anaphylactic
shock, insulin shock etc.
Anaphylactic shock is commonly seen after penicillin administration or administration of
serum, dextrose, anaesthetics etc. Such shock is usually caused by bronchospasm, laryngeal
oedema and respiratory distress which totally lead to hypoxia. This is aggravated by massive
vasodilatation which causes hypotension and ultimately shock. Such type of shock is said to
be due to increased release of histamine and Slow Release Substance (SRS) of anaphylaxis by
combination of antigen with IgE on the mast cells and basophils. This histamine and SRS are
concerned to cause bronchospasm, laryngeal oedema and respiratory distress alongwith massive
vasodilatation.
SHOCK
13
HYPOVOLAEMIC SHOCK
Pathophysiology.— Such shock is usually due to sudden loss of blood volume or loss of
fluid from the vascular space. It is the haemorrhagic shock which is the most common form
in this group and is discussed in details below :—
Haemorrhage mostly occurs from the systemic venules and small veins which usually
contain about 50% of the total blood volume. Loss of blood will cause decreased filling of the
right heart. This causes decrease of filling of the pulmonary vasculature, which in turn
decreases filling of the left atrium and ventricle. So left ventricular stroke volume also decreases
by Frank-Starling mechanism. This causes a drop in arterial blood pressure.
COMPENSATORY MECHANISMS.— The compensatory mechanisms which occur after
haemorrhage include (i) adrenergic discharge, (ii) hyperventilation, (iii) release of vasoactive
hormones, (iv) collapse, (v) resorption of fluid from the interstitial tissue, (vi) resorption of
fluid from the intracellular to the extracellular space and (vii) renal conservation of body water
and electrolytes.
(i) Adrenergic discharge causes constriction of the venules and small veins, increase of
heart rate and also constricts the vascular sphincters in the kidneys, splanchnic viscera and in
the skin. Adrenergic discharge starts within 60 seconds after blood loss. Constriction of venules
and small veins displaces blood to the right atrium and ventricle. This causes increase of the
diastolic pressure of the right ventricle and also its stroke volume. This causes an increase of
blood in the pulmonary vasculature and so into the left atrium and ventricle. Both left atrial
and left ventricular fillings increase and so increases the left ventricular stroke volume.
Adrenergic discharge constricts sphincters in the splanchnic viscera, kidneys and the skin. This
selective vasoconstriction improves filling of the right heart and increases cardiac output. This
also diverts blood to the heart and brain. So adrenergic discharge takes away a portion of the
blood flow from the splanchnic viscera, kidneys and skin and diverts it to the heart and brain.
(ii) Hyperventilation.— This occurs in response to metabolic acidaemia which develops
shortly after haemorrhage. Spontaneous deep breathing sucks blood from extrathoracic sites to
the heart and lungs. This also increases the filling of left ventricle and. also its stroke volume.
It must be remembered that both adrenergic discharge and hyperventilation occur within
one minute of blood loss.
(iii) Release of vasoactive hormones.— Low perfusion of the kidneys leads to release of a
hormone known as Renin from the juxtaglomerular apparatus. Renin liberates angiotensin I
from the liver, which is converted to angiotensin II by the lungs. Angiotensin II is a potent
selective vasoconstrictor. It selectively constricts the vasculature of the splanchnic organs, kidneys
and the skin. So its vasoconstrictive effect is almost similar to that of adrenergic discharge.
After haemorrhage another vasoactive hormone, Vasopressin is released due to stimulus
from the baroreceptors such as those situated in the carotid bodies and aortic arch caused by
hypotension. Vasopressin acts as a systemic vasoconstrictor thus diverting blood to the brain
and heart and increases cardiac output.
Epinephrine is also vasoactive hormone which is released from the adrenal medulla as a
consequence of discharge of the adrenergic nervous system.
Release of vasoactive hormones usually takes place after 1 to 2 minutes of haemorrhage.
(iv) Collapse.— Assumption of the recumbent posture due to collapse automatically
displaces blood from the lower part of the body to the heart and increases cardiac output.
(v) Resorption of fluid from the interstitial tissue.— Due to adrenergic discharge the arterioles,
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A CONCISE TEXTBOOK OF SURGERY
precapillary sphincters, postcapillary sphincters, the venules and the small veins of the skin
and splanchnic organs and skeletal muscles constrict. This leads to decrease of the capillary
intravascular hydrostatic pressure. This leads to influx of water, sodium and chloride from the
interstitial tissue space into the capillaries.
(vi) Resorption of fluid from the intracellular to the extracellular space.— Release of epinephrine
from the adrenal medulla, cortisol from the adrenal cortex and glucagon from the pancreas
and inhibition of release of insulin all lead to high extracellular glucose concentration. Products
of anaerobic metabolism also accumulate in the extracellular space. Both these cause
hyperosmolarity of the extracellular tissue which draws water out of the cells. Interstitial pressure
increases, which forces water, sodium and chloride across the capillary endothelium into the
vascular space.
(vii) Renal conservation of body water and electrolytes.— Adrenocorticotropic hormone is
released by any stress including shock. This hormone and angiotensin II stimulate the synthesis
and release of hormone aldosterone from the adrenal cortex. Aldosterone is concerned with
resorption of sodium from the glomerular ultrafiltrate into the vascular space. Reabsorption of
sodium and water by the kidneys helps to maintain the vascular volume.
Clinical Features.— The clinical features of hypovolaemic shock depend on the degree
of loss of blood volume and on the duration of shock.
I. MILD SHOCK.— Loss of less than 20% of blood volume is included in this category.
The most sensitive clinical findings of shock are those caused by adrenergic constriction of
blood vessels in the skin. The result is collapse of the subcutaneous veins of the extremities,
particularly the feet which become pale and cool. There may be sweat in the forehead, hand
and feet due to adrenergic discharge. Urinary output, pulse rate and blood pressure at this
stage remain normal. The patient feels thirsty and cold.
II. MODERATE SHOCK.— Loss of blood volume from 20 to 40% causes this type of
shock. Alongwith the other findings mentioned above, there will be oliguria. This oliguria is
due to adrenergic discharge alongwith the effects of circulating aldosterone and vasopressin.
The pulse is also increased but usually less than 100 beats per minute. In the initial stage the
blood pressure remains normal but may fall in the later stage in the more severe group. So the
students should remember that pulse rate and blood pressure are never the main signs of shock. Shock
may be present even with normal pulse rate and normal blood pressure.
III.
SEVERE SHOCK.— Loss of blood volume of more than 40% usually causes severe
shock. At this stage there is pallor (skin of the extremities becomes pale), low urinary output,
rapid pulse and low blood pressure.
Clinical Monitoring.— Once shock is diagnosed, constant monitoring of the patient is
required to assess the degree of blood loss and haemodynamic impairment.
(i) BLOOD PRESSURE.— Measurement of blood pressure is very essential in shock,
though it may be normal in mild shock. The diastolic pressure is the main indication of the
degree of vasoconstriction. The systolic pressure indicates vasoconstriction alongwith stroke
volume and rigidity of the main vessels. The pulse pressure, which is systolic pressure minus
diastolic pressure, indicates the stroke volume of the heart and cardiac output.
(ii) RESPIRATION.— Hyperventilation, i.e. increase in the rate and depth of respiration
is an important indicator of shock. Hyperventilation is a normal response of early shock. If the
patient is not hyperventilating in shock, he is probably suffering from central nervous system
or respiratory system damage. Persistent hyperventilation is an ominous sign and indicates
improper treatment of shock.
SHOCK
15
(iii) URINE.— Urine output is a good indication of severity of shock. Urine output is
affected quite early even in moderate shock. It is also a good index of adequacy of replacement
therapy.
(iv) CVP.— Measurement of Central Venous Pressure is quite important in assessing shock.
In hypovolaemic shock, the blood volume is decreased, so is the CVP, whereas in cardiogenic
shock there is no depletion of blood volume and the CVP remains normal.
Technique of measuring CVP.— A standard length of 20 cm of intravenous catheter is passed
into the right internal jugular vein. This is performed with full aseptic precautions with the
patient in head-down position. The head-down position is used to distend the vein and to
prevent air being sucked in. The catheter tip is gradually pushed in to be positioned in the
superior vena cava. The catheter is connected to a saline manometer. By the level of the saline,
one can detect the Central Venous Pressure. If the CVP is low, intravenous infusion is suggested
and if the CVP is high intravenous infusion may not be required.
An alternative route is the insertion of the catheter via the median basilic vein in the
antecubital fossa. The results are less accurate than the above method.
(v) E.C.G.— In severe shock electrocardiogram may show signs of myocardial ischaemia
with depression of ST-T segments.
(vi) SWAN-GANZ CATHETER.— This catheter is used in sophisticated centres to get
valuable information about the precise diagnosis and circulatory derangements of shock. This
catheter provides 3 types of information — (a) flow in the cardiovascular system; (b) sampling
of blood from the pulmonary artery to give accurate measurements of blood gases in mixed
venous blood and (c) filling pressure of both right and left sides of the heart can be measured.
(a) Cardiac output is measured by thermo-dilution technique. A known volume of a cold
crystalloid solution is injected into the right atrium and by measuring the resulting temperature
drop in the pulmonary artery is passed by a thermistor located at the end of the catheter. The
greater the temperature drop, the slower is the flow through the right heart. Computers specially
designed to calculate cardiac output from thermodilution measurements are available.
(b) Mixed venous oxygen levels.— This catheter is used to draw blood from the pulmonary
artery for determination of mixed venous oxygen contents. Normally the PCo2 of mixed venous
blood is approximately 4 mm Hg higher than the PCo2 of the systemic arterial blood.
(c) Vascular pressures.— The right atrial pressure is accurately measured by this catheter.
The pulmonary artery systolic and diastolic pressures can also be measured but with less
accuracy.
The pulmonary artery wedge pressure is a better indicator of circulating blood volume and
left ventricular function. If the catheter is in a portion of the lung where inflation of the lung
occludes the pulmonary capillaries the end of the Swan-Ganz catheter estimates the pressure
in the alveoli rather than the pressure in the left atrium. So the end of the catheter is to be
positioned where it is not compressed by the lungs. This requires a lateral chest X-ray. This
catheter is used to differentiate between left and right ventricular failure, presence of pulmonary
embolism and can also be used as a guide to therapy with fluids.
Method of introducing catheter.— With strict aseptic precaution the Swan-Ganz catheter
is introduced into the central venous system mostly through right internal jugular vein.
Appropriate introducers, cannula and guide wire are used and the catheter is flushed with
heparin saline where it is introduced into the right atrium. The balloon is inflated with 1.5 ml
air and is advanced slowly via the right ventricle into the pulmonary artery. This is checked by
X-ray. The pulmonary artery pressure is measured. Gradually the balloon wedges in a small
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A CONCISE TEXTBOOK OF SURGERY
branch to get the capillary wedge pressure. The normal pulmonary capillary wedge pressure is
between 8 and 12 mm Hg or 11 and 16 cm H20. The normal pulmonary artery pressure is
about 25 mm Hg systolic and 10 mm Hg diastolic.
TREATMENT.— Mainly the treatment of haemorrhagic shock, which is the most common
form of hypovolaemic shock, is discussed below. Though treatment of other types of shock are
also described. The whole treatment can be described adequately under several heads —
1. RESUSCITATION.— This should begin immediately as the patient is admitted with
hypovolaemic shock. This starts with establishment of a clear airway and maintaining adequate
ventilation and oxygenation. Lowering of the head with support of the jaw to prevent airway
obstruction and administration of oxygen are usually all that are needed. Lowering of the head
will improve venous return preventing stasis of blood in the muscles of the leg and preventing
oedema. This also increases cerebral circulation which is quite important at this stage. In those
patients where there is airway obstruction, intratracheal intubation and mechanical ventilation
are required.
Many patients in shock, particularly those who are suffering from traumatic or septic shock
require intubation and positive-pressure ventilation. Positive-pressure ventilation improves the
patient's cardiovascular status. Abrupt increase in airway pressure expands the alveoli and
displaces blood from the pulmonary vasculature into the left atrium and ventricle. So both left
ventricular output and systemic arterial pressure increase. But it must be remembered that
positive-pressure ventilation is only applied when it is necessary otherwise it may compress
the superior and inferior venae cavae and impair right atrial filling causing decrease in the
right atrial stroke volume.
2. IMMEDIATE CONTROL OF BLEEDING is highly important in case of haemorrhagic
shock. This may be achieved by raising the footend of the bed and by compression bandage to
tamponade external haemorrhage. Operation may be required to stop such bleeding as soon as
some resuscitation has been achieved.
3. EXTRACELLULAR FLUID REPLACEMENT is probably the most important point
in the treatment of hypovolaemic shock. When the patients are admitted to the emergency
room, a large-gauze needle or catheter is inserted into an appropriate vein (preferably in the
arm or in the leg) and fluid should be administered immediately. Fluid replacement should be
started immediately followed by the control of bleeding. In sophisticated centres another catheter
is inserted into the subclavian and internal jugular vein to measure the CVP (Central Venous
Pressure). A non-sugar, non-protein crystalloid solution with a sodium concentration
approximately that of plasma is preferable in the initial stage of fluid replacement. That solution
can be Ringer's lactate, Ringer's acetate or normal saline supplemented with 1 or 2 ampules of
sodium bicarbonate. Ringer's lactate or Ringer's acetate solution should not be used in patients
with severe pre-existing liver disease. This solution is run at a rapid speed so that in 45 minutes
between 1000 and 2000 ml solution is given intravenously. It is often observed that blood
pressure will return to normal and become stable after infusion of 1 or 2 litres of such solution.
But it must be remembered that if blood loss has been severe or haemorrhage is continuing the
elevation of blood pressure is usually transient. A sample of blood must be sent during insertion
of the intravenous catheter for grouping and cross matching. Lactate acidosis has been reported
with great concern by a few surgeons with the use of too much Ringer's lactate solution. Further
experiments have suggested that this is more theoretical than practical. Rapid administration
of 5% glucose solution is never recommended, as this may induce osmotic diuresis, which
further depletes patient's vascular volume.
SHOCK
17
Resuscitation should always be started with crystalloid solution even if blood is available.
If resuscitation is started with acidotic cold bank blood with a potassium concentration,
efficiency of myocardium is tremendously jeopardized.
3
litres of fluid given over 45 minutes should resuscitate any patient with arrested
haemorrhage. The need for more fluid indicates continuation of bleeding and such haemorrhage
should be controlled surgically.
It is better to withhold administration of blood until surgical control of bleeding is obtained
or at least until just before induction of anaesthesia. Rapid replacement of fresh blood after
control of haemorrhage will lead to the fewest complications of coagulation and the least risk
of transfusion complications.
At times when bleeding has been severe, blood should be given before surgical control of
haemorrhage.
It must be remembered that blood substitutes like plasma or dextran should only be
used when whole blood is not available. If whole blood is available these substances should
not be infused before transfusing blood, as this may cause difficulty in cross matching and
may inhibit the clotting system and exacerbate bleeding.
A few points to be remembered in case of extracellular fluid replacement —
(a) The I.V. fluid, particularly the crystalloid, which should be given first, is administered
with rapidity, so that replacement is done as quickly as possible without burdening the heart.
(b) To know how much fluid should be given, blood pressure, pulse rate, urine output,
CVP and other laboratory tests should be performed.
(c) If there is blood loss, it is best replaced by blood. Blood substitutes cannot take the
place of blood.
(d) If blood is available, blood substitutes are better avoided.
4.
DRUGS.— A few drugs are sometimes used in different types of shock. These drugs
are as follows :—
(i)
Sedatives.— These drugs are commonly used to alleviate pain in patients with shock.
Some amount of sedation is almost always required in any type of shock. Morphin is quite
good in this respect and should be given intravenously, as subcutaneous injection may not
yield its result due to poor absorption due to peripheral vasoconstriction. However it should
not be administered in children, in head injury patients and in patients with acute abdomen,
whose diagnosis has not been confirmed. For children berbiturates are preferred, whereas in
head injuries largactil is a better choice. It must be remembered that treatment of pain is not
obligatory from the stand point of shock itself. But if the patient is in severe pain as in
fracture, peritonitis etc. control of pain is mandatory. Injection pethidine can also be used
intramuscularly, but it has got slight vasodilator effect.
(ii) Chronotropic agents.— The patients in shock who have slow heart rates may benefit
from administration of chronotropic agents, which primarily increase the heart rate. This drug
should probably be used selectively to patients with bradycardias. Atropine is the most widely
used in this group, followed by isoproterenol. The latter drug has several beneficial effects in
addition to that of increasing heart rate. It is also a vasodilator of the systemic arterial and
capillary sphincters. It must be remembered that the adverse effects of administering these
drugs should be compared with their beneficial effects. Rapid heart rates require increased
myocardial work, which in turn requires increased coronary blood flow.
(iii) Inotropic agents.— These drugs improve the strength of cardiac muscle contraction.
Patients in cardiogenic shock and in severe septic shock may require such drug. The most
2
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A CONCISE TEXTBOOK OF SURGERY
commonly used drugs in this group are dopamine and dobutamine. These drugs in low doses
increase myocardial contractility and selectively increase renal blood flow by dilating the renal
vasculature. These drugs have also vasoconstrictor effect, so they should be used carefully
and in low doses.
(iv) Vasodilators.— Some patients in severe septic, traumatic and in cardiogenic shock
may require these drugs. The most commonly used drugs in this group are nitroprusside and
nitroglycerin, as these are easily reversible and short acting. When the systemic vascular
resistance is too much raised, these drugs may be used. So these drugs are usually used in
patients with high systemic mean arterial pressures. It should be remembered that excessive
dilatation of the venules and small veins may decrease filling of the heart so that the cardiac
output falls. Similarly excessive peripheral vasodilatation may lead to low systemic arterial
pressures and decreased filling of the coronary vasculature which may be evidenced by
electrocardiography. However administration of vasodilators to patients in shock with high
systemic vascular resistances and high filling pressures of the heart seems to be an ideal
therapeutic manoeuvre.
(v) Vasoconstrictors.— These drugs are particularly beneficial in neurogenic shock. The
main role of these drugs in this condition is that they increase blood pressure and increase
perfusion pressure for coronary circulation. These drugs also increase myocardial contractility.
The drugs commonly used are phenylephrine and metaraminol. However these drugs are
seldom used in hypovolaemic or traumatic shock.
(vi) Beta-blockers.— Patients in cardiogenic shock with stiff myocardium and rapid heart
rate will benefit from administration of a beta-blocker. The drug increases efficiency of
ventricular contraction. The drug however should be used with caution as it induces a slower
heart rate. Propranolol is the most widely used drug in this group.
(vii) Diuretics.— These drugs are sometimes used in treating patients with cardiogenic
shock. These drugs reduce the vascular volume and decrease filling pressure. Diuretics should
never be used in the initial treatment of patients with haemorrhagic or traumatic shock. Though
oliguria is one of the main clinical manifestations of hypovolaemic shock, yet diuretics will
not correct the underlying cause of oliguria, but will aggravate the situation by inducing
further hypovolaemia. Diuretics are also not used in septic shock.
TRAUMATIC SHOCK
Pathophysiology-.— The peculiarity of this shock is that traumatized tissues activate the
coagulation system and release microthrombi into the circulation. These may occlude or
constrict parts of pulmonary microvasculature to increase pulmonary vascular resistance. This
increases right ventricular diastolic and right atrial pressures.
Humoral products of these microthrombi induce a generalized increase in capillary
permeability. This leads to loss of plasma into the interstitial tissue throughout the body. This
depletes the vascular volume to a great extent.
Clinical features — of traumatic shock are almost similar to those of hypovolaemic shock.
The two differentiating features are — (i) presence of peripheral and pulmonary oedema in
this type of shock and (ii) infusion of large volumes of fluid which may be adequate for pure
hypovolaemic shock, is usually inadequate for traumatic shock.
Treatment.—
1. Resuscitation.— In this type of shock mechanical ventilatory support is more needed.
SHOCK
19
2. Local treatment of trauma and control of bleeding.— This is almost similar to hypovolaemic
shock. Surgical debridement of ischaemic and dead tissues and immobilization of fractures
may be required.
3. Fluid replacement.— As mentioned earlier more fluids should be required to bring
back the patient to normalcy than hypovolaemic shock. Role of anticoagulation therapy to
prevent disseminated intravascular coagulation has a debateable role. Increased coagulation
consumes clotting factors of the blood leading to more bleeding. Moreover obstruction of
microvasculature with such microthrombi lead to more tissue ischaemia. Anticoagulation with
doses of heparin large enough to fully anticoagulate the patient may reverse this abnormality.
The problem of this therapy is to calculate the dose. One intravenous dose of 10,000 units of
heparin seems to be effective for this purpose.
CARDIOGENIC SHOCK
Pathophysiology.— It is usually due to primary dysfunction of one ventricle or the other
(rarely of both). Such dysfunction may be due to myocardial infarction, chrortic congestive
heart failure, cardiac arrhythmias, pulmonary embolism or systemic arterial hypertension.
In cardiogenic shock caused by dysfunction of the right ventricle, the right heart is unable
to pump blood in adequate amounts to the lungs. Filling of the left heart decreases. So left
ventricular output decreases.
In cardiogenic shock caused by dysfunction of the left ventricle, the left ventricle is unable
to maintain an adequate stroke volume. Left ventricular output and systemic arterial blood
pressure decrease. There is engorgement of the pulmonary vasculature due to normal right
ventricular output, but failure of the left heart.
CARDIAC COMPRESSIVE SHOCK arises when the heart is compressed enough from
outside to decrease cardiac output. The important causes are tension pneumothorax, pericardial
tamponade and diaphragmatic rupture with herniation of the bowel into the chest.
Clinical features.— In the beginning the skin is pale and cool and the urine output is
low. Gradually the pulse becomes rapid and the arterial blood pressure becomes low. In case
of right ventricular dysfunction the neck veins become distended and the liver may also be
enlarged. In left ventricular dysfunction the patient has broncheal rales and a third heart sound
is heard. Gradually the heart becomes enlarged and when the right ventricle also fails distended
neck veins will be visible.
Treatment.— Airway must be clear with adequate oxygenation. In case of right sided
failure caused by a massive pulmonary embolus should be treated with large doses of heparin
intravenously. If pain is complained of in case of left sided failure proper sedative e.g. morphin
should be prescribed. Fulminant pulmonary oedema should be treated with a diuretic. Further
treatment of cardiogenic shock is complex and beyond the scope of this treatise.
NEUROGENIC SHOCK
Pathophysiology.— In this type of shock there is dilatation of the systemic vasculature
which lowers the systemic arterial pressure. Blood pools in the systemic venules and small
veins. The right heart filling and stroke volume decrease. This decreases pulmonary blood
volume and left heart filling so that left ventricular output decreases. Discharge of adrenergic
nervous system to the innervated parts of the body and release of angiotensin and vasopressin
A CONCISE TEXTBOOK OF SURGERY
20
are the compensatory mechanisms which of course fail to restore cardiac output to normal,
though systemic arterial pressure responds in part.
Clinical features.— The peculiar features are that the skin remains warm, pink and well
perfused in contradistinction to the hypovolaemic shock. Urine output may be normal. But the
heart rate is rapid and the blood pressure is low.
Treatment.—
1. Elevation of the legs is effective in treating patients with neurogenic shock.
Assumption of Trendelenburg position displaces blood from the systemic venules and small
veins into the right heart and thus increases cardiac output. Left ventricular emptying is
quite efficient inspite of elevated legs as the systemic vascular resistance is low.
2. Administering fluid is important though not so as in hypovolaemic shock. This
increases filling of the right heart which in its turn increases cardiac output.
3. Neurogenic shock is probably the only form of shock that can be safely treated with
a vasoconstrictor drug. Though there is some risk as the vasculature above the spinal cord lesion
may also be constricted excessively and may develop ischaemic necrosis of the fingers, yet its
action to restore venous tone and thus restoring right heart filling and cardiac output is more
important. Its prompt action saves the patient from sudden low blood pressure and low cardiac
output from imminent damage to the more important organs like brain, heart and kidneys.
SEPTIC SHOCK
,
Pathophysiology.— During the past few years there has been a progressive increase in
the incidence of septic shock. The importance of this shock is that it possesses a high mortality
rate of about 50% or more. Even though this shock is now better understood and there are
more potent antimicrobial agents available in the market, yet its mortality rate is still alarming.
The most frequent causative organisms are gram-positive and gram-negative bacteria,
though any agent capable of producing infection (including viruses, parasites and fungi) may
cause septic shock. Because of effective antibiotic treatment available for most gram-positive
infections, the majority of cases of septic shock are now caused by gram-negative bacteria.
The common organisms which are concerned with septic shock are — (i) E. coli, (ii)
Klebsiella aerobacter, (iii) Proteus, (iv) Pseudomonas and (v) Bacteroids in order of decreasing
frequency. Recently Klebsiella groups are more isolated in cases of septic shock. Bacteroids
which are difficult to culture may account for a far greater number of infections than was
previously reported.
Gram-positive sepsis and shock.— This type of shock is usually caused by dissemination of a
potent exotoxin liberated from gram-positive bacteria without evidence of bacteraemia. This is
noticed more often in Clostridium tetani or Clostridium perfringens infections and fulminating
infections from staphylococcus, streptococcus or pneumococcus organisms. Such shock is
basically caused by massive fluid losses. Arterial resistance falls, but the peculiar feature is
that there is little or no reduction in cardiac output even with progressive hypotension. Urine
output is usually normal.
Gram-negative sepsis and shock.— The most frequent source of gram-negative infections
is the genitourinary system, often the patients had associated operations or instrumentations
of the urinary tract. The second most frequent site is the respiratory system and many patients
have had tracheostomy done. Third in frequency is the G.I. system with diseases such as biliary
tract infections, intra-abdominal abscesses and peritonitis.
SHOCK
21
Gram-negative sepsis as a cause of shock is a difficult problem. The severity of the shock
varies considerably. There may be mild hypotension following instrumentation of the
genitourinary tract. In contrast the patient with multiple intra-abdominal abscesses or necrotising
pneumonia may suffer from fulminating septic shock with poor prognosis. Outlook is more
favourable when the source of infection is accessible to surgical drainage e.g. septic abortions.
Clinical features.— Septic shock is often recognized initially by the development of chills
and elevated temperature above 100°F. Two types are usually clearly defined — early zvarm
shock and late cold shock.
In early warm shock there is cutaneous vasodilatation. The toxins from the infected tissues
increase the body temperature. To bring this temperature down, the vasculature of the skin
dilates. The cutaneous vasodilatation decreases systemic vascular resistance. So the arterial
blood pressure falls, but cardiac output increases because the left ventricle has minimal
resistance to pump against. Adrenergic discharge further increases cardiac output. In this
stage the skin remains warm, pink and well perfused. The cutaneous veins remain full. The
pulse rate becomes high and the systemic arterial pressure low. Diagnosis is not difficult as
this condition is associated with intermittent spikes of fever alternating with bouts of chills.
In late cold shock there is increased vascular permeability due to liberation of toxic
products into the centre circulation. This results in hypovolaemia and right heart filling
decreases. Similarly there is decrease of flow into the pulmonary vasculature, so left heart
filling decreases, so is the cardiac output. Clinically it may be difficult to differentiate this
type of shock from hypovolaemic shock or from traumatic shock, only guide remains is the
knowledge of existence of a septic focus.
Treatment.— The only effective way to reduce mortality in septic shock is by prompt
diagnosis and treatment. Treatment can be broadly divided into two groups — (I) Treatment of
infection by early surgical debridement or drainage and by use of appropriate antibiotics and (II)
Treatment of shock which includes fluid replacement, steroid administration and use of vasoactive
drugs.
(I)
Once a case of septic shock is diagnosed, thorough search for the source of infection
is made while treatment of shock is started with fluid replacement. In sophisticated centres
careful monitoring is started immediately with measure of central venous pressure, pulmonary
wedge pressures by Swan-Ganz catheter, urine output and arterial and venous blood gases.
Debridement operation or drainage of infection should be performed under local or general
anaesthesia as soon as possible after initial stability of the patient's condition. This becomes
easy when the infection is easily accessible. But problem remains when infective site is not so
easily accessible. A patient with ascending cholangitis may respond temporarily to supportive
treatment or shock therapy. This improvement is usually short-lived, unless prompt drainage
of the biliary tract is performed.
The use of specific antibiotics based on appropriate culture and sensitivity test is desirable.
Antibiotics must be chosen on the basis of the suspected organisms prior to the sensitivity
results. Often a combination of antibiotics may be started in the beginning before getting the
sensitivity result. When the report becomes available more specific antibiotic coverage should
be instituted if the infection is not under control. Cephalothin (6 to 8 Gm/day I.V. in 4 to 6
divided doses), gentamicin (5 mg/Kg/day), clindamycin (particularly when infecting organism
is Bacteroides) or chloromycetin (particularly in case of Bacteroides infection) are the antibiotics
which may be started in the beginning.
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A CONCISE TEXTBOOK OF SURGERY
(II)
Fluid Replacement is of great importance in late septic shock. This will provide sufficient
blood volume to the vital organs.
Mechanical ventilation alongwith endotracheal intubation is frequently needed in treating
patients with late septic shock. Inadequate tissue oxygenation is a consistent feature of shock
and attention to all components of the oxygen transport system is essential.
Steroids have been used for quite sometime in the treatment of septic shock, though its
effectivity is still questioned. The serious question which has been asked that whether
administering an agent that impaires the immune response of the body will be beneficial or
not. On the other hand favourable responses with improvement in cardiac, pulmonary and
renal functions and better survival rates have been reported with this therapy. It has been
suggested that steroids protect the body cell and its contents from the effect of endotoxin.
Larger doses of steroids are known to exert inotropic effect on the heart and produce mild
peripheral vasodilatation. Short term, high dose steroid therapy is recommended in most
cases that do not respond to the other methods of treatment. An initial dose of 15 to 30 mg
per Kg body weight of methyl prednisolone or equivalent dose of dexamethasone is given
intravenously in 5 to 10 minutes. The same dose may be repeated within 4 hours if the
beneficial effects have not been achieved. There is hardly a need for more than 2 doses. It has
been shown that this short term high dose steroid therapy has little effect on
immunosuppression, but possesses the other possible benefits to outweigh this bad effect.
Vasoactive drugs.— The vasopressure drugs with prominent alpha-adrenergic effect are of
limited value in treatment of this type of shock. Use of vasoactive drug with mixed alpha- and
beta- adrenergic effects (e.g. metaraminol) may be indicated. Vasodilator drugs such as
phenoxybenzamine are more popular particularly when combined with fluid administration.
Inotropic agents e.g. isoproterenol or dopamine is ideal when simple volume replacement and
other measures have failed to restore adequate circulation. Isoproterenol has inotropic and
chronotropic effects on the heart and produces mild peripheral vasodilatation. This may cause
a slight fall in blood pressure due to vasodilatation which requires additional volume replacement.
CRUSH SYNDROME
It is a symptom complex in which a portion of the body becomes crushed due to a heavy
weight falls on that portion of the body and is kept there for sometime to crush all the
tissues in that portion of the body. This type of injury is come across after earthquakes, mine
injuries, air raids, collapse of a building or use of tourniquet for longer period. In this syndrome
oligaemic shock occurs due to extravasation of blood into the muscles in the affected portion
of the body. But the degree of shock has no relation to the development of the syndrome. The
muscles become crushed and myohaemoglobin enters the circulation and may cause acute
renal tubular necrosis. The crushed muscles swell considerably. As they are confined within a
tough deep fascia in the inferior extremity and superior extremity, tension develops within
the fascia. This endangers circulation and causes ischaemic damage to the limb. At this stage
the limb fills tense and the patient complains of severe pain in the limb. Urine output will be
obviously reduced if uraemia supervenes, the patient may show restlessness, apathy and mild
delirium.
Treatment.— As a first-aid measure application of tourniquet to the affected limb above
the crush injury is a good method to reduce admission of deleterious substances into the general
circulation.
SHOCK
23
Parallel incisions may be applied to relieve tension, through which the crushed swollen
muscles may protrude. Administration of intravenous fluid is required to combat hypovolaemic
shock, but it should be remembered that in this condition kidney function is also jeopardized.
So administration of fluid should be restricted to 500 ml + urinary output. Low molecular
weight dextran (40000) or Rheomacrodex is particularly effective in this condition as it prevents
sludging of red cells in small blood vessels and maintain circulation to the kidneys. Mannitol
is also very effective in this condition. lgm/Kg body weight of mannitol is introduced
intravenously as 20% solution in 12 hours. This approximately corresponds to three infusions
of 100 ml during and after operation. This restores urinary output and prevents acute renal
failure. Catheterization of the bladder should be performed before instituting mannitol.
Tourniquet should be removed, if applied, before schedule period. If the patient has bled
considerable amount, blood transfusion is required after the urinary output has brought to
normal level and chance of renal failure has been minimised.
Haemodialysis should be used as life saving procedure in grave conditions.
FLUID, ELECTROLYTE AND
ACID-BASE BALANCE
ANATOMY OF BODY FLUIDS
TOTAL BODY WATER (TBW).—
The total body water, as measured by deuterium oxide dilution or tritiated water, accounts
for 60 per cent of body weight in young adult male and 50 per cent for young adult females. A
normal variation of ±5 per cent applies to both groups. The total body water is highest in the
new bom infant, which constitutes 77 per cent of its body weight. The water content falls rapidly
during the first 6 months of life to below 65 per cent and more slowly during the next years to
an average of 59 per cent. The ratio of total body water to surface area increases progressively
upto about the age of 12 years, but the absolute volume of body water is highest in males
between the ages of 1 to 40 years. Fat contains little water, so the thin individual has a greater
proportion of water to total body weight than the obese person. The lower percentage of total
body water in females correlates with the relatively large amount of subcutaneous fat and small
muscle mass. An extremely obese individual may have 25 per cent to 30 per cent less body
water than a thin individual of the same weight.
The total body water is divided into two functional compartments — 1. Intracellular fluid,
which constitutes fluid within the body's total cell population and this is about 30 to 40 per
cent of the body weight. 2. The extracellular fluid, which represents 20 per cent of the body
weight, is divided into (i) intravascular fluid (this represents 5 per cent of body weight) and (ii)
interstitial or extracellular fluid (which represents 15 per cent of body weight). It should be
remembered that intracellular fluid is larger subdivision and constitutes 70 per cent of total
body water, whereas the extracellular water amounts to about 30 per cent of total body water
and actually forms the suitable environment for the cells of the body.
Intracellular fluid.—
The intracellular fluid is measured by subtracting the extracellular fluid from the measured
total body water. This water forms part of the protoplasm of the cells and is distributed in
many small compartments or cells separated from each other by two cell membranes and layer
of interstitial fluid. The largest portion of this intracellular water is within the skeletal muscle
mass. As the females possess smaller muscle mass, the percentage of intracellular water is lower
in females than in the males.
If the chemical composition of the intracellular fluid is studied, it will be found that
potassium and magnesium are the principal cations, whereas the phosphates and proteins are
the principal anions. The intracellular concentration of potassium is approximately 125 mEq/L,
magnesium is approximately 40 mEq/L and sodium is about 10 mEq/L. The concentration of
phosphates is about 150 mEq/L in intracellular fluid, whereas protein constitutes 40 mEq/L of
intracellular fluid.
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
25
Extracellular Fluid.—
This constitutes about 30 per cent of total body water. It can be divided into 3 subdivisions
— (i) intravascular fluid (which is situated within the blood vessels) constitutes 7 per cent of
total body water or 4 per cent of the body weight in normal adult; (ii) the interstitial or
extravascular fluid (which lies outside the blood vessels and around the cells of the tissues of
which it forms the immediate environment) constitutes 17 per cent of total body water or 7.5
per cent of total body weight and (iii) transcellular fluid (which includes fluid which is
extravascular but not interstitial, e.g. cerebrospinal and synovial fluids, urine in the collecting
tubules and urinary tract, fluid in the ducts of the glands, in the eyes and ears and in the elementary
tract) accounts for 6 per cent of total body water or about 3.5 per cent of total body weight. Of
these the transcellular fluid is relatively non-functional.
The volume of the extracellular fluid can be measured by the dilution of a substance which
passes freely through the walls of blood capillaries but does not enter into the cells of the body.
The substances which have been used are inulin, thiocyanate, mannitol, thiosulphate, radioactive
chlorine, bromine or sodium etc. Blood volume can be measured directly by dilution principle
using red cells labelled with radioactive chromium (51Cr).
The most important cation of extracellular fluid is sodium (which constitutes 140 mEq/L),
whereas potassium (5 mEq/L), calcium (3 mEq/L) and magnesium (2 mEq/L) are the other cations
available in the interstitial fluid. The principal anions are chloride (114 mEq/L) and bicarbonate
(30 mEq/L). There are minor differences in ionic composition between the plasma and interstitial
fluid due to difference in protein concentration. As the plasma contains higher protein content
(organic anions), the total concentration of cations is higher in plasma than in the interstitial fluid.
NORMAL EXCHANGE OF FLUID AND ELECTROLYTES
Water intake.—
Normal individual consumes an average of 2,000 to 2,500 ml of water per day. This intake is
derived from two sources — (a) exogenous source and (b) endogenous source.
(a) Exogenous water.— This water is either drunk as various drinks or ingested in solid foods.
About 1,200 ml water is drunk everyday from various beverages, whereas about 1,000 ml is
derived from solid foods.
(b) Endogenous water.— This water is released during oxidation of ingested food and the
amount is approximately 300 to 500 ml per day. During starvation this amount is supplemented
by water released from the break down of body tissues.
It must be remembered that water requirements of children are relatively greater than those
of adults as (i) the water content is higher in respect to their total body weight, (ii) the metabolic
activity is greater in children due to growth and (iii) the immature kidneys of the children are
poor in concentrating ability.
Water output.—
Water is mainly excreted by three routes —■
1.
Urine.— The normal urinary output is about 1,500 ml per day. The amount of course
varies with the amount of intake as various drinks. The output of urine is under the control of
secretion of a hormone known as anti-diuretic hormone (ADH) secreted by the posterior lobe of
the pituitary gland. The secretion of this hormone is controlled by tonicity of the body fluids. ADH
stimulates reabsorption of water from the renal tubules thus varying the amounts excreted as urine.
The students must remember that minimum urinary output is about 500 ml per day, inspite of the
26
A CONCISE TEXTBOOK OF SURGERY
individual is deprived from all exogenous intakes. This amount of urine is excreted to get rid of
the products of catabolism and end products of metabolism.
2. Faeces.— Water loss in stool is about 100 ml to 200 ml per day. In diarrhoea this amount
is multiplied by the number of stools as also their fluidity.
3. Insensible loss of water from skin and lungs.— About 900 ml of water is lost from the body
as insensible loss. This loss mainly occurs through the skin (75%) and through lungs (25%). The
insensible water loss through the skin is not from evaporation of water from sweat glands but
from water vapour formed within the body and lost through the skin. The average loss through
the skin is between 500 and 1,000 ml per day. This is less in temperate climate and more in tropic
countries. The loss from the skin varies in accordance with the atmospheric temperature and
humidity, muscular activity and body temperature. In warm weather such loss may go up to
1,500 ml per day. With hypermetabolism and fever insensible loss of water through skin increases.
This loss increases by about 100 ml per degree of fever per day.
About 400 ml of water is lost in expired air everyday. In case of hyperventilation and increased
respiratory rate this loss is increased. In dry atmosphere, this loss is more than in wet atmosphere.
SALT INTAKE AND OUTPUT
In normal individual salt intake in food varies approximately from 80 to 100 mEq (average
5 gm). Output of salt in urine in average normal individual is about 70 to 90 mEq. In faeces excretion
of salt is quite negligible. Salt is also excreted by sweat which represents a hypotonic solution of
salt with an average sodium concentration of 15 mEq/L. The sodium concentration in sweat
however is exceeded to 60 mEq/L in unacclimatized individuals. The insensible fluid lost from
skin and lungs is in fact pure water and does not contain any salt. Various gastrointestinal
secretions contain various amounts of salts which of course are reabsorbed, except a small amount
which is excreted with faeces.
Sweat is a major source of loss of salt in tropical countries and this amount varies considerably
according to the temperature and humidity of the environment. The volume of sweat varies
widely between individuals in the same circumstances. The evaporation of sweat provides an
additional means of dissipating body heat. When the humidity is higher, sweating begins at lower
temperature. Whether sweating is noticeable depends on how rapidly it evaporates, which in turn
is related to the humidity as well as to the temperature of the environment. The secretion of sweat
may be as high as 3 litres per hour or 10 litres in a day. But such high rate of sweating cannot
be maintained for long and the rate falls down even if the individual is exposed to heat for more
time. The sweat glands are partly under the influence of adrenal cortical hormones and the
composition of sweat varies greatly, so much so that average figures cannot be given. Sodium
concentration may vary from 6 to 85 mEq/L but is always lower than the plasma concentration.
But the potassium concentration varies from 5 to 21 mEq/L and is always higher than that of the
plasma. Concentrations of sodium and chloride in sweat are related also to the intake of these
ions and usually decline when their body contents fall. When the salt intake increases, the
concentrations of sodium and chloride in the sweat rise.
Salt loss by kidneys also vary considerably. About 100 mEq of sodium is excreted in the
ur ine in normal individuals in temperate climate. This amount varies considerably according to
the circumstances and normal kidneys have the power to reduce sodium excretion to less than
1 mEq/day. Excretion of urine and of sodium depends on glomerular filtration, which depends
on the renal blood flow. This falls considerably when blood volume is reduced. With the
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
27
administration of intravenous fluid, glomerular filtration increases so is the urinary output. The
control of sodium excretion through the kidneys is not well understood. Desoxycorticosterone
acetate causes sodium retention by the tubules regardless of the sodium concentration in the
plasma. The most powerful conservation of sodium is effected by aldosterone which is about 30
times as effective as desoxycorticosterone acetate. Release of aldosterone depends on dietary
intake of sodium and its secretion falls when sodium intake rises. It probably acts mainly on
the distal tubules, though it may also have effects on the proximal tubules. Other factors e.g.
osmotic pressure in the peritubular space and variation in absorptive capacity of different
nephrons are concerned in the output of sodium in the urine.
WATER DEFICIT AND EXCESS
Water or volume deficit.—
Extracellular fluid volume deficit is a common fluid disorder in surgical patients. The fluid
deficit is not water only, but water and electrolytes in approximately the same proportion as
they exist in normal extracellular fluid. The CAUSES of such deficit are —
(a) Difficulty or inability to swallow may be due to painful conditions of the mouth
and pharynx or obstruction in the oesophagus.
(b) Loss of gastro-intestinal fluid due to vomiting, nasogastric suction, diarrhoea and fistula
drainage.
(c) Sequestration of fluid in soft tissue injuries and infections.
(d) Intra-abdominal and retroperitoneal inflammatory processes and peritonitis.
(e) Intestinal obstruction.
(f) Bums.
(g) Pure water loss may occur from lungs after tracheostomy. This loss is about 500 ml
more than the normal insensible loss.
CLINICAL FEATURES.— The main manifestations of loss of blood volume are reflected
early in the central nervous system and cardiovascular system. The CNS symptoms and signs
are weakness, apathy, sleepiness, anorexia and intense thirst. In more severe conditions the CNS
symptoms and signs become decreased tendon reflexes, stupor and even coma. The
cardiovascular symptoms and signs are mainly due to decrease in plasma volume e.g.
hypotension, collapsed veins, tachycardia, cold extremities, thready pulse and cutaneous lividity.
There are certain other symptoms and signs reflected in the gastrointestinal system and general
tissues. In G. I. system these are nausea, vomiting, refusal to eat, ileus and distension. In tissues,
there is skin turgor, which may be difficult to assess in the elderly patients. The patients may
become hypothermic.
TREATMENT.— Obviously intake of water should be increased. Water, dextrose or saline
should be given hourly or even half-hourly. When the individual is diseased and oral
administration is not possible, intravenous drip should be started with 5% dextrose or dextrose
saline or simple normal saline. Intake output chart should always be maintained to properly
adjust the fluid administration and to prevent water intoxication.
Water or volume excess.—
In contradistinction to volume deficit, volume excess is usually iatrogenic — (i) excessive
amount of intravenous fluid has been administered; (ii) Colorectal wash out with plain water
when used in patients with Hirschsprung's disease may cause water excess or intoxication in
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A CONCISE TEXTBOOK OF SURGERY
children; (iii) When water has been used instead of saline in total bowel wash prior to colonic
surgery; (iv) Excessive irrigation of fluid during transurethral resection of prostate. In two
pathological conditions volume excess may occur — (i) secondary to renal insufficiency and (ii)
ADH secreting tumours e.g. oat-cell carcinoma of bronchus.
CLINICAL FEATURES.— In this condition also mainly the CNS, cardiovascular and
gastrointestinal systems are affected. Drowsiness, weakness, sometimes convulsions and even
coma may be seen. There is increased venous pressure, with increased cardiac output, distension
of peripheral veins, bounding pulse, high pulse pressure and increased pulmonary second sounds
are some of the features noticed in this condition. In chest one may hear basilar rales, similarly
pitting oedema at the ankle or bottom of the back (in recumbent cases) may be elicited. In the
elderly patients congestive cardiac failure with pulmonary oedema may develop quickly.
Laboratory investigations show low haematocrit and a high mean corpuscular volume
(M.C.V.). The serum sodium and other electrolytes also become low.
TREATMENT.— Fluid intake should be stopped, particularly the intravenous fluid. Even
with this the patient still remains stupor, particularly due to renal insufficiency, 200 ml of
hypertonic (5.85 percent) saline solution should be given intravenously. This may be added with
a diuretic.
ELECTROLYTE BALANCE
As mentioned earlier both extracellular and intracellular fluids contain certain cations and
anions. Cations are electropositive and anions are electronegative. These are collectively called
electrolytes. These electrolytes are maintained in certain concentration in both extracellular and
intracellular fluids. In normal individuals the balance is always maintained and this is known
as electrolyte balance. To understand this process, one has to know the various electrolytes of
these fluids, their various concentrations and their exchanges to maintain equilibrium. These
are discussed in detail below.
SODIUM
Sodium ion is mainly responsible for osmolarity of the extracellular fluid. About 44% of the
total body sodium is in the extracellular fluid, 9% is in intracellular fluid and remaining 47% is
in the bone. The peculiarity of the sodium in the bone is that only 45% of it is exchangable and
takes place in the metabolic processes. The total content of sodium in the body is about 90 gm.
Sodium exchanges in sweat, its renal regulation and its normal intake and output have been
discussed earlier. Here we shall discuss about (i) sodium in bone and (ii) sodium conservancy
following trauma.
(i)
Sodium in bone.— The importance of sodium in bone is that about 1/2 of it is osmotically
inactive, does not take part in exchanges and is soluble in acid. Loss of sodium from bone has
been noticed in acute sodium depletion or with adrenal hypofunction. Similar shifts of sodium
may occur in patients particularly after losses by diarrhoea or sweating, in diabetic acidosis or
prolonged restriction of sodium intake.
(ii)
Sodium conservancy following trauma.— Following trauma of any kind there is a time, the
length of which varies directly with the degree of tissue damage, in which there is almost no
excretion of sodium. The output of sodium during this period becomes not more than 10 mEq/L.
The interesting feature is that it cannot be increased by more intake of sodium. After operation this
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
29
period is approximately 48 hours. That the sodium is conserved after trauma is due to increased
adrenocortical activity. Due to this it is not wise to administer large quantities of normal saline
immediately after operation.
Hyponatraemia.—
The causes of hyponatraemia can be divided into 2 categories — (a) real sodium depletion,
in which both sodium and water is lost, (b) apparent sodium depletion, in which there is sodium
dilution or loss of sodium in comparison to the water. The sodium level should be at least less
than 130 mEq/L in extracellular fluid to be called hyponatraemia.
(a) Real sodium depletion — is due to bums, loss of large quantity of sweat which is replaced
by drinking water only, loss of gastrointestinal secretions due to small bowel obstruction or
excessive vomiting or gastrointestinal aspiration or high intestinal fistulae or severe diarrhoea in
cases of dysentery, ulcerative colitis, pseudomembranous colitis or cholera. Such hyponatraemia
may also be seen in cases of secretion of antidiuretic hormone as in bronchial carcinoma.
(b) Apparent sodium depletion — may be caused when the above losses have been
replenished by administration of water or glucose solution. This is also noticed after operation
when excessive quantities of glucose solution is administered.
The students should remember the various electrolyte concentrations of different gastrointestinal
secretions. Saliva contains 15 mEq/L of Na+ and 40 mEq/L of K+ and it is secreted about 1,500
ml/24 hours. Gastric secretion contains 50 mEq/L of Na+, 80 mEq/L of C1-, 10 mEq/L of K+
and it is secreted about 2,500 ml/24 hours. Intestinal secretion contains 140 mEq/L of Na+, 100
mEq/L of C1-, 25 mEq/L of bicarbonate and 10 mEq/L of K+ and its secretion is about 3,000
ml/24 hours. Biliary secretion contains 140 mEq/L of N+, 100 mEq/L of C1-, 30 mEq/L of
bicarbonate and 5 mEq/L of K+. Pancreatic secretion contains 140 mEq/L of Na+, 70 mEq/L of
C1-, 120 mEq/L of bicarbonate and 5 mEq/L of K+. These secretions can be compared with the
electrolyte concentration of plasma which is about 140 mEq/L of Na+, 100 mEq/L of C1-, 25
mEq/L of bicarbonate, 5 mEq/L of K+ and 1.9 mEq/L of mg.++.
CLINICAL FEATURES.— These are almost similar to extracellular dehydration e.g. the eyes
are shrunken and the face is drawn, the expression is anxious. The tongue is dry, hard and
reddish brown in colour, though the patient is usually not thirsty. The skin is dry, wrinkled and
the subcutaneous tissues feel laxed. In one word the patient appears to have aged by many years
in a few hours. The blood pressure reduces and the pulse rate becomes fast. The urine becomes
dark and scanty with high specific gravity. The peripheral veins are constricted and contain dark
blood.
Haemoconcentration may be noticed, but this may be masked by pre-existing anaemia. The
plasma sodium concentration may be normal or slightly reduced. The sodium concentration will
be low only when lost fluid is replaced with solutions containing less concentration of sodium.
TREATMENT.— The first step in the treatment is to administer normal saline (0.9%) through
I.V. drip. In the beginning the infusion rate must be rapid to make good the sodium loss. Ringer's
solution may be administered in case normal saline is not available. Renal function should be
monitored and over infusion should be checked. For this plasma protein levels may be measured
to avoid over dosage. When there is severe loss of plasma volume, infusion of plasma or plasma
substitute should be considered.
Hypernat raemia.—
Hypematraemia or sodium excess can be also from (a) real causes and (b) apparent causes.
(a) Real causes.— Here the sodium content of the body is really increased. The main causes
30
A CONCISE TEXTBOOK OF SURGERY
are iatrogenic i.e. excessive administration of normal saline solution intravenously during early
postoperative period, when sodium retention is to be expected. Even a daily intake of sodium
may increase total sodium content when renal excretion of sodium is delayed due to renal disease
or altered by the administration of adrenal cortical hormones.
The result of hypematraemia is over loading of the circulation, as excess sodium will increase
osmotic pressure within the capillaries and will draw excess water into the circulation from the
interstitial tissue. This may result in oedema of the dependent tissues and also oedema of the
suture lines after abdominal operations. There is also a danger of pulmonary oedema.
(b)
Apparent causes.— Sodium excess may occur in true dehydration when the total body
water content is reduced, but the sodium content remains as normal. This may occur if there is
loss of both water and sodium, but the loss of water is greater.
CLINICAL FEATURES.— Puffiness of the face, pitting oedema in the sacral region or around
ankle are the main features of this condition. Increased weight and polyuria are also noticed. In
infants increased tension in the anterior fontanelle may be noticed.
TREATMENT.— Treatment of real hypematraemia is stoppage of infusion. If there is oedema,
diuretics may be prescribed.
Treatment of apparent hypematraemia should be according to the merit of the individual
cases.
POTASSIUM
This is mainly an intracellular cation. Nearly 98% of the total content of the potassium in
the body (130 gm) is in the cells or intracellular. Only 2% is in the extracellular fluid. Three
quarters of the intracellular potassium is in the skeletal muscle. Potassium is the predominant
cation of intracellular fluid and accounts for 2/3rds of total active intracellular cations, the
remainder being the magnesium.
Normal Intake and output,—
A healthy adult consumes about 2 to 3 gm of potassium each day and almost the same
quantity is excreted in the urine everyday. A very small quantity is excreted in faeces and sweat.
The most striking difference between sodium and potassium is the way in which they are
handled by the kidneys. Sodium is always under careful control and any excess of intake will
be excreted in the urine and any deficiency of sodium will be tackled by renal conservation.
Excess intake of potassium after absorption in the intestine is transported to the cells by the
extracellular fluid. The rapid uptake of this absorbed potassium by the cells prevents any increase
in the concentration of the potassium in the extracellular fluid. When there is excessive
metabolism in the body, endogenous protein is used as source of energy, both potassium and
nitrogen are mobilised. With the shift of potassium into the extracellular fluid, concentration of
potassium rises. But usually this is dealt with by the kidneys which excrete the potassium in
the urine sufficiently fast to maintain the concentration of the potassium in the extracellular
fluid within the normal limits. During starvation and after injury protein is catabolized and
large quantities of potassium are released. Approximately 2.5 mEq of potassium is released with
every gram of nitrogen. In patients with anuria the accumulation of potassium occurs in the
extracellular fluid and raises its concentration to a toxic level. It is probably the commonest
cause of death in this condition. Potassium excretion in the urine is increased by the
administration of ACTH, cortisone, desoxycortisone, aldosterone and other diuretics. The daily
output of potassium in the urine is closely related to the dietary intake.
FLUID, ELlCTROm'E AND AC1D-RASE BALANCE
31
The normal range of potassium concentration in the plasma is from 3.8 to 5.1 mEq/L. Values
of less than 3.5 mEq/L or more than 7 mEq/L are considered to be highly abnormal.
Potassium deficiency or hypokalaemia.—
It must be remembered that when the intake of food is restricted or potassium content of
the food is diminished, continuous urinary loss leads to slow depletion of the body content of
potassium.
CAUSES —
(i) Following trauma (which includes operation) there is increased mobilization of
intracellular potassium to extracellular space and there is also increased excretion of potassium
by the kidneys. This loss is highest during the first day following trauma, but this duration
depends directly with the degree of trauma and tissue damage. The students must remember
that in the immediate postoperative period there is excessive loss of potassium, but the sodium
is conserved. As body's reserve of potassium is quite good, so therapeutic administration of
potassium is not required before the 3rd day of continuous parenteral nutrition.
(ii) In starvation as a result of catabolism of protein tissue, potassium and nitrogen are
excreted in the urine in the same proportions as they are found in the skeletal muscle.
(iii) In loss of gastrointestinal secretions by external fistulae e.g. duodenal fistula, ileostomy
etc. and through diarrhoea caused by ulcerative colitis and villous tumour of the rectum, there
is excessive loss of potassium, as these fluids contain potassium concentration twice as that of
plasma. If nasogastric aspiration is continued for a long time with fluid replacement by
intravenous isotonic saline solution there is chance of potassium depletion.
CLINICAL FEATURES.— The most striking feature of potassium depletion is the gradual
onset of drowsiness. The patient lies in bed with the head drooping down on one shoulder and
the jaw and cheeks hanging slack. He can be roused with difficulty and opens his eyes slowly.
After a short while eyelids close and the patient goes back to sleep. Speech becomes slow and
slurred and he may break off in the middle of a sentence. He also becomes irritable. Muscular
hypotonia and weakness is an outstanding physical sign. The deep reflexes may be absent.
Incontinence of urine is common.
Potassium depletion causes diminished motility of the intestinal musculature, which results
in the accumulation of intestinal secretions. This in turn stimulates further secretion and more
potassium is thereby lost into the lumen of the intestine. This causes ileus and abdominal
distension which are common features of potassium deficiency in the postoperative period.
The peripheral blood pressure is lowered and the pulse rate becomes slow. The skin remains
warm and dry and the superficial veins are well filled. There is reddish flush of the face. It
must be remembered that in sodium depletion also the blood pressure is reduced, but there is
increase in the pulse rate and the peripheral veins are poorly filled.
The electrocardiographic changes are particularly peculiar to potassium deficiency, but they
do not seem to be closely related either to the severity of deficiency or to the serum potassium
concentration. A large number of changes have been described — increased QT interval,
decreased height, inversion or rounding of T wave, there is also prolongation of T wave, there
is depression of ST segment or inversion of P wave. These changes may be produced by alkalosis
as well as by potassium deficiency.
Potassium depleted patients are often very thirsty and may drink large quantity of fluid.
Treatment.— Replacement of a large deficit of potassium involves the administration of
sufficient potassium and its transfer into the depleted cells. Whenever possible potassium salt
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A CONCISE TEXTBOOK OF SURGERY
should be administered by mouth. Potassium chloride in the form of effervescent tablets may
be given by mouth in the doses of 2 gm 6 hourly. Oral administration of potassium is always
chosen first, to avoid the danger of increase of potassium concentration with intravenous
administration of solutions of potassium salts. When the patient is comatose or nauseated and
has difficulty in swallowing, intravenous administration is unavoidable. Infusion of as little as 1
gm of potassium chloride may lead to the recovery of consciousness. One must be careful to
prevent increase of potassium concentration above 7 mEq/L in the extracellular fluid. This is a
toxic level and will cause cardiac arrest. One must ensure adequate flow of urine before
administering potassium intravenously.
When alkalosis is present, which is often an accompaniment of potassium deficiency in
case of excessive vomiting and high small intestinal fistulas, potassium chloride should be
administered. If the urinary volume is adequate, 2 gm of potassium chloride may be administered
intravenously over a period of 4 hours. Alternatively potassium chloride may be administered
dissolved in glucose solution — 20 ml of 10% solution of potassium chloride in 500 ml of 5%
glucose solution.
When there is associated acidosis, which is commonly seen in diarrhoea and low intestinal
fistulas, the intravenous solution should contain sodium acetate in addition to potassium chloride.
If given orally, potassium citrate should be administered by mouth in the dose of 2 gm every 6
hours.
Intravenous administration of potassium salt is dangerous and should not be treated as a
matter of routine. The quantity to be given and the rate of its administration should be carefully
monitored.
Potassium retention or hyperkalaemia.—
In healthy subjects it appears to be impossible to increase the potassium content of the body.
Hyperkalaemia is mainly iatrogenic and is due to excessive intravenous infusion of potassium salts.
This is usually associated with (i) severe oliguria or anuria, and (ii) reduction in the volume of
extracellular fluid may raise the potassium concentration.
CLINICAL FEATURES.— The signs of significant hyperkalaemia are mainly limited to the
gastrointestinal system and cardiovascular system. The gastrointestinal symptoms include nausea,
vomiting, intermittent intestinal colic and diarrhoea. The cardiovascular signs are low heart rate
with irregular beats, low blood pressure, poor peripheral circulation and cyanosed skin.
There may also be some mental confusion, apathy, sensory disturbances and weakness of
limbs.
The electrocardiographic changes are particularly characteristics in hyperkalaemia when the
concentration goes up to 7 mEq/L. The findings are — high peaked T wave, widened QRS complex,
increased PR interval and depressed ST segment. Gradually there will be disappearance of T
waves, heart block and cardiac arrest in diastole.
TREATMENT.— Firstly the exogenous administration of potassium should be stopped. If
the potassium was given orally or intravenously, such administration should be culminated.
Temporary lowering of serum potassium and suppression of myocardial effects of hyperkalaemia
can be accomplished by intravenous administration of 10% solution of calcium gluconate or chloride
10 to 30 ml over 15 to 30 minutes or in 1 litre of intravenous fluid. The urinary volume and
excretion of potassium is promoted by rapid infusion of 5% glucose. Administration of glucose
stimulates insulin release, which augments cellular potassium uptake. Addition of insulin (1 unit/
5 gm of glucose) is often recommended. Alkalanization of the extracellular fluid with either sodium
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
33
lactate or bicarbonate promotes transfer of potassium into cells. This is absolutely necessary when
hyperkalaemia is associated with metabolic acidosis. Calcium ions do not affect serum potassium
concentration but does counteract the effects of hyperkalaemia on cardiac cells.
It cannot be emphasised too hard that the above-mentioned manoeuvres are temporary and
give adequate time of removal of excess potassium by cation-exchange resins, peritoneal dialysis
or haemodialysis.
When associated with oliguria, urinary output may be increased by infusion of hypertonic
saline in the form of 50 gm glucose and 50 units insulin in 1 litre solution. Later on of course cation
exchange resins or dialysis should be called for.
MAGNESIUM
Magnesium is an important ion in the maintenance of normal contractility of muscle and
excitability of neural tissue. Total magnesium content of a typical 70 kg adult man is about
2,000 mEq, compared to 3,400 mEq of potassium and 3,900 mEq of sodium. About half the
magnesium is in the bone and nearly all of the rest is in the cells of the soft tissues, whereas
less than 1% is in the extracellular fluid. The plasma concentration of magnesium in a normal
individual varies between 1.7 and 2.2 mEq/L. The normal dietary intake of magnesium is about 20
to 25 mEq daily, of which only 8 mEq is absorbed and this same quantity is excreted daily in
the urine. The kidneys have reasonable power to conserve magnesium on a magnesium-free diet,
in which case renal excretion of this ion may be less than 1 mEq/day.
Magnesium deficiency.—
The normal daily requirement of magnesium during growth is about 10 mg (0.85 mEq) per
day. Since ordinary food stuffs contain an abundant amount of magnesium, magnesium
deficiency is extremely rare in health.
CAUSES.—
(i) Reduction of intake, particularly in chronic alcoholics, in which excretion of magnesium
in the urine is increased by ingestion of alcohol.
(ii) Starvation.
(iii) Malabsorption syndrome.
(iv) Magnesium depletion is most common in association with prolonged loss of
gastrointestinal secretion due to intestinal fistula and replacement by prolonged parenteral fluid
therapy with magnesium-free solutions.
(v) Acute pancreatitis.
(vi) Diabetic acidosis.
(vii) Primary aldosteronism.
(viii) Cirrhosis of liver.
(ix) Diseases of parathyroids.
CLINICAL FEATURES.— It is difficult to describe the clinical features which are typical of
magnesium depletion alone. In majority of cases it is combined with potassium or calcium
deficiencies. The magnesium is an essential intracellular ion of muscle and neural cells, so its
depletion is usually characterized by neuromuscular and CNS (Central Nervous System)
hyperactivity. These are also similar to those of calcium deficiency. Hyperactive tendon reflexes,
muscle tremors and tetany with a possible Chvostek's sign are characteristically seen in
magnesium deficiency. When tetany is not relieved by the injection of a calcium supplement,
3
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A CONCISE TEXTBOOK OF SURGERY
magnesium deficiency should be the diagnosis. Mental apathy and profound weakness are also
seen in magnesium deficiency. In this condition the patient becomes irritable, aggressive, anxious
and restless with athetoid movements. The patient looks pale and ill.
Diagnosis of magnesium deficiency is mainly made by awareness of this condition. A low
serum magnesium concentration does not always indicate magnesium depletion and conversely
there may be severe magnesium deficiency without any reduction of the serum concentration.
The only possible way to definitely diagnose magnesium depletion is to compare the urinary
magnesium output in two urine collections one before and after giving a loading dose of
intravenous magnesium chloride or sulphate. Normally 90% of the loading dose is promptly
excreted in the urine, whereas in magnesium depletion more than 50% may be retained.
TREATMENT.— Magnesium deficiency is best treated by parenteral administration of
magnesium chloride or sulphate solution. About 2 mEq of magnesium per kg body weight may
be administered daily when the renal function is good. In this condition also one must be
particular to avoid the possibility of acute magnesium toxicity from over dosage. When large
doses are given, the heart rate, blood pressure, respiration and electrocardiogram should be
monitored for signs for magnesium toxicity, which may lead to cardiac arrest. It is wise to keep
calcium chloride or gluconate available in hand to counteract any adverse effect of rapidly rising
plasma magnesium level. Though partial or complete relief of symptoms may follow immediately
after this infusion due to increased concentration of magnesium in the extracellular fluid, yet
continuous replacement over 1 to 3 weeks period is necessary to replenish the intracellular
compartment. For this 10 to 20 mEq of 50% magnesium sulphate solution is given daily by I.M.
or I.V. injection.
Magnesium ion should not be given to the oliguric patient due to chance of magnesium
toxicity.
Magnesium excess.—
Hypermagnecaemia is extremely rare and only seen in severe renal insufficiency. This is
more so when renal dialysis has been carried out with a dialysate containing magnesium sulphate.
So magnesium level should be carefully monitored in patients with acute or chronic renal failure.
It is well established fact that increased serum concentration of magnesium ion does not occur
until the glomerular filtration rate falls below 30 ml per minute with ordinary dietary intake of
magnesium.
There is another possibility of magnesium excess when magnesium-containing antacids or
laxatives are administered while the patient is suffering from impaired renal function.
This condition may also appear in severe acidosis and severe extracellular volume deficit
following bums or massive trauma.
CLINICAL FEATURES include lethergy, weakness and progressive loss of deep tendon
reflexes. With increasing levels of magnesium there is interference with cardiac conduction and
electrocardiographic changes will be reflected in the form of increased P-R interval, widened
QRS complex and elevated T waves. These are almost similar to the findings of hyperkalaemia.
Gradually muscular paralysis will occur followed by coma. Death may occur due to respiratory
or cardiac arrest.
TREATMENT.— This should be to withhold administration of exogenous magnesium and
by correcting any acidosis present. Acute symptoms may be controlled by slow intravenous
administration of 5 to 10 mEq of calcium chloride or gluconate. However for elevated levels
and for persistence of symptoms, peritoneal dialysis or haemodialysis should be called for.
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
35
CALCIUM
Calcium is mainly an extracellular cation and its normal level is between 9 and 11 mg. per
100 ml. The normal daily intake of calcium is between 1 and 3 gm. The total body calcium in an
individual of 70 kg weight is about 1,000 to 1,200 gm. The majority of this is found in the bone
in the form of phosphate and carbonate. The majority of the calcium which is ingested is excreted
via G. I. tract, only 200 mg or less is excreted in the urine daily. Calcium in the serum is available
in three forms — (i) about half is bound to plasma protein; (ii) About 5% of nonionized fraction
is bound to other substances in the plasma and interstitial fluids; (iii) The remaining 45% is in
the ionized form and is responsible for neuromuscular stability. So the ratio of ionized to non­
ionized calcium is related to the plasma protein level as also to the pH (acidosis causes an
increase of ionized fraction, whereas alkalosis causes decrease of this fraction).
Ilypocaleaemi a.—
The common CAUSES include — (i) acute pancreatitis, (ii) acute and chronic renal failure,
(iii) pancreatic and small intestinal fistulae, (iv) hypoparathyroidism, (v) transient hypocalcaemia
may occur following removal of parathyroid adenoma in hyperparathyroid patient.
CLINICAL FEATURES include numbness and tingling sensation in the circumoral region
and the tips of the fingers and toes. There will be hyperactive tendon jerks, muscle cramps with
carpopedal spasms and tetany. The Chvostek's sign will be positive.
TREATMENT is intravenous administration of calcium gluconate or chloride. Calcium lactate
may be given orally with supplement of vitamin D.
At present available data indicate that the majority of patients receiving blood transfusion
do not require calcium supplementation. The binding of ionized calcium by citrate is generally
compensated by mobilization of calcium by body stores. But when blood is given as rapidly as
100 ml/minute, however calcium administration is indicated.
Hypercalcaemia.—
A serum calcium concentration above 15 mg/100 ml is a serious condition and require
immediate treatment. Majority of these patients show vigorous volume depletion due to excessive
vomiting. When the serum calcium level goes above 16 mg, it may cause death.
The main CAUSES of hypercalcaemia are (i) hyperparathyroidism, (ii) cancer with bony
metastasis, (iii) sarcoidosis and (iv) myelomas.
CLINICAL FEATURES.— Symptoms of hypercalcaemia start with vague gastrointestinal,
musculoskeletal and central nervous system symptoms. Anorexia, nausea and vomiting, fatigue,
lassitude and weakness are the main symptoms in the early stage. Gradually headache, pains in
the back and extremities, thirst, polydipsia and polyuria gradually become worse with more
serum calcium levels to lead to stupor and finally coma.
TREATMENT.— Oral or intravenous inorganic phosphates effectively lower serum calcium
level by inhibiting bone resorption and forming calcium-phosphate complexes that are deposited
in soft tissues and bones. Intravenous administration may reduce the calcium level abruptly,
but there is fear of tetany, hypotension and acute renal failure. So intravenous phosphates should
be given slowly over a period of 12 hours once daily for no more than 2 to 3 days. Corticosteroids
decrease resorption of calcium from bone and reduce intestinal absorption of Vitamin D. This is
particularly useful in treating patients with sarcoidosis, myelomas, lymphomas and leukaemia.
Calcitonin also decreases serum calcium level. A cytotoxic agent Mithramycin effectively lowers
serum calcium in one or two days by direct action on bones. Concomitant use of large doses of
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A CONCISE TEXTBOOK OF SURGERY
intravenous frusemide may be recommended to increase urinary calcium excretion, but
replacement of fluid and other electrolytes are required to make good the losses.
The definitive treatment of hypercalcaemia in hyperparathyroidism is immediate surgery.
PARENTERAL FLUID THERAPY
Administration of fluid by any route other than the elementary canal i.e. intravenous,
intramuscular, subcutaneous or into the bone marrow is called parenteral fluid therapy. The Greek
word 'enteron' means intestine. Para 'enteron' means besides the intestine, so parenteral means
by any route except intestinal.
Various solutions have been used to maintain fluid and electrolyte balance in the body.
Majority of these solutions are introduced intravenously, which is by far the most common
method of parenteral administration. A broad gauge needle is introduced in a suitable vein
after it is made engorged by application of a light tourniquet or manual pressure on the limb
proximal to the site of administration. If the vein cannot be made prominent either in obese
individuals or in patients in severe hypovolaemic shock due to venoconstriction, a suitable vein
should be exposed with a small incision on the skin. This is known as venesection. In this case a
slender catheter or a narrow polythene tube is introduced into the vein and is tied against the
vein. This limb is then splinted so that it cannot be moved. This is the best way of giving
continuous intravenous infusion which is known as ‘venoclysis’.
Sites.— Mostly the median cubital vein in the cubital fossa is used for venepuncture. In
obese individuals, in women and children this vein may not be made prominent for
venepuncture. In these cases one may try the long saphenous vein in front of the medial
malleolus. But there is risk of thrombophlebitis and pulmonary embolism. Infants and small
children are relatively immune to thrombophlebitis and this route is probably a good one for
these patients. Scalp vein has also been chosen in case of neonates and small children. Obviously
the best will be the cephalic vein in the deltopectoral groove, subclavian vein, internal jugular
vein and external jugular vein.
It goes without saying that the solutions for parenteral use must be sterile. These should
also be free from dead bacteria and particulate matters.
The various solutions which are commonly available in the market for parenteral fluid
therapy are —
1. 5% DEXTROSE SOLUTION.— It is an isotonic solution, which supplies calories, but
not electrolytes. So this solution can only be used when the patient does not require any
electrolytes, but a solution to replenish his blood volume alongwith some nutrition. This solution
is particularly used in the immediate postoperative period when sodium excretion is considerably
diminished by renal conservation. Prolonged administration of this solution will obviously result
in hyponatraemia. It may cause thrombosis of the vein.
2. ISOTONIC (0.9%) SODIUM CHLORIDE (SALINE) SOLUTION.— This solution is
isotonic and contains sodium and chloride in the concentration almost similar to that in plasma.
In plasma sodium concentration is about 140 mEq/L and chloride concentration about 100
mEq/L, potassium concentration about 5 mEq/L and bicarbonate concentration (HC03) about
24 mEq/L. In extracellular fluid the concentrations are 142 mEq/L of Na, 4 mEq/L of K, 103
mEq/L of Cl, 27 mEq/L of HC03 and 5 mEq/L of Ca. In normal saline or 0.9% sodium chloride
solution the concentrations are 154 mEq/L of Na and 154 mEq/L of Cl. It is a good available
solution for replacing gastrointestinal losses either by vomiting or by nasogastric aspiration or
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
37
through intestinal fistula. It must be remembered that this solution should not be used in first
24 hours after operation due to natural sodium conservation.
One thing to be noticed is that it has a high concentration of chloride more than the plasma
concentration. It imposes an appreciable load of excess chloride on the kidneys that cannot be
readily excreted. Thus a dilutional acidosis may develop. However this solution is ideal to use
in extracellular fluid deficiency in presence of hyponatraemia, hypochloraemia and metabolic
alkalosis.
3. RINGER’S LACTATE SOLUTION.— This solution contains 130 mEq/L of Na,
109 mEq/L of Cl, 28 mEq/L of HC03, 4 mEq/L of potassium, 2.7 mEq/L of Ca and 28 mEq/L
of lactate. The main advantage of this solution is that it has almost similar electrolyte
concentration as extracellular fluid and the pH remains normal even if infused in large quantities.
This solution is the best to be used in hypovolaemic shock while awaiting for blood. The chief
disadvantage is that it has slight hypo-osmolarity with respect to sodium. It is also quite suitable
for replacing gastrointestinal fluid loss.
4. DEXTROSE 4.3% WITH SALINE 0.18% (1/5TH OF NORMAL SALINE).— This is
an isotonic solution in contradistinction to 5% dextrose with isotonic saline solution which is
hypertonic. It can be used in any case of hypovolaemia, where there is not considerable depletion
of sodium and chloride. It has an additional effect of having some calorie value. It may be
infused for prolonged period without any fear of hypematraemia or hyperchloraemia. There
may be a chance of introducing thrombosis.
5. MOLAR (M) SODIUM LACTATE SOLUTION.— This solution has a sodium concen­
tration of 1,000 mEq/L and HC03 concentration of 1,000 mEq/L. This solution is particularly
suitable for symptomatic hyponatraemic states. Its anion is lactate instead of chloride, so it cannot
be used in hypochloraemic conditions. It is also suitable in metabolic acidosis cases.
6. M/6 SODIUM LACTATE SOLUTION.— It contains about 167 mEq/L of Na and
167 mEq/L of HC03. It is particularly useful in cases of moderate metabolic acidosis.
7. DARROW’S SOLUTION.— This is the only solution which contains more potassium
than available in the plasma or extracellular fluid. Its potassium concentration is about
36 mEq/L, sodium 124 mEq/L, Cl 104 mEq/L and lactate 56 mEq/L. Obviously this is the best
solution to combat hypokalaemia. It supplies potassium at a relatively safe rate provided alkalosis
is not present. The rate of infusion should be slower than other solution to avoid hyperkalaemic
state, which is more dangerous and it should not be given more than 60 drops per minute. This
solution should be given when gastrointestinal losses are being replenished with isotonic saline
solution or Ringer's lactate solution for a considerable period. Some potassium loss is always
expected in gastrointestinal fluid losses which will obviously induce hypokalaemia if potassium
cannot be given in some form or the other.
FY»s<joperative fluid regime.—
In the first 24 hours after surgery there is an increased secretion of aldosterone and
antidiuretic hormone. There is conservation of sodium and loss of less water than in normal
individual. 5% dextrose solution is probably the best in this period and 2 litres will suffice in 24
hours. If there is operative loss of blood, this should be replaced. It must be remembered that it
is unwise to administer potassium at this stage unless definite potassium deficiency exists.
During the 2nd or subsequent 24 hour period, it is expected that patient will lose about
900 ml by insensible loss, which may be increased by hyperventilation and fever to a maximum
A CONCISE TEXTBOOK OF SURGERY
38
of approximately 1,500 ml in a day. This loss should be replaced with 5% dextrose solution.
Approximately 1 litre of fluid should be given to replace the volume of urine. This is given
mainly in the form of 5% dextrose, since the kidneys are able to conserve sodium even at this
stage and it is probably unnecessary to stress the kidneys by giving saline solution. If there is
nasogastric aspiration going on, 1 litre of isotonic saline solution should be given to replace
this. So 3 litres in total in the 2nd 24 hours will suffice.
On the third postoperative day it is better to give isotonic solution of 4.3% dextrose and
0.18% saline for 2 litres to combat loss of sodium through urine and sweat. 1 litre of Darrow's
solution should be given to combat potassium loss. This is particularly required when nasogastric
aspiration is being continued, as some loss of potassium is expected through G. I. secretions.
It is always essential to make a fluid intake and output chart. This will figure in intake —
oral intake and through intravenous drip. In output chart — urine output and aspiration
alongwith vomitus are recorded. To this chart about 1,000 ml should be considered for insensible
loss through lungs and skin and another approximately 500 to 1,000 ml for sweating. These
should be made good besides urine output and aspiration losses.
ACID-BASE BALANCE
In health the pH of the body fluid is normally maintained within narrow limits inspite of
large load of acid produced endogenously as a by-product of body metabolism. These acids are
neutralized efficiently by several buffer systems and also excreted by the lungs and kidneys.
There are buffer systems in the blood, which are the proteins and haemoglobin and the latter is
of prime significance as a buffer in the red cell.
There are also important buffers in the body fluids which are mainly weak acids or bases.
Kidneys are also important agents in the regulation of the composition of body fluids. In health
the reaction of blood lies within the range of pH of 7.36 to 7.44.
The details of the various buffers and the mechanism how the acid-base balance is
maintained is beyond the jurisdiction of this treatise and the students are referred to any standard
Text Book of Physiology to learn about this. Here I shall discuss only the various acidotic and
alkalotic states which one may come across in surgical patients.
ACIDOSIS
Metabolic acidosis.—
This is a condition in which there is a gain or retention of fixed acids or loss of base (mainly
bicarbonate). The CAUSES are —
(a) Gain of fixed acids may occur in diabetic acidosis, lactic acidosis, azotaemia, retention
of metabolites in renal insufficiency, rapid increase of lactic and pyruvic acids by anaerobic
tissue metabolism due to shock or cardiac arrest, or due to rapid transfusion of bank blood
which has been preserved with acid citrate dextrose. Such condition may also occur during
cardiac by-pass surgery and it may follow sudden restoration of blood flow to a large mass of
poorly perfused tissue e.g. when an aortic embolus is removed or volvulus of intestine is
untwisted.
(b) Loss of bases may occur in continuous diarrhoea e.g. ulcerative colitis, small bowel fistula
or prolonged intestinal aspiration.
The pH level goes down to even 7.1 in serious cases.
FLUID, ELECTROLYTE AND ACID-BASE BALANCE
39
CLINICAL FEATURES.— The initial compensation of metabolic acidosis is pulmonary with
an increase in the rate and depth of breathing, which depresses the arterial PCCX,. So the most
marked clinical sign in this condition is rapid, deep and noisy respirations which is often called
'air hunger'. The respiratory rate may rise to as fast as 50 per minute. In the midst of this the
patient stops breathing and tries unsuccessfully to moisten his dry lips with his brown parched
tongue. Such hyperpnoea is due to stimulation of the respiratory centre by the lower pH of the
blood. Over breathing eliminates carbonic acid in the form of carbondioxide. Kidneys also try
to combat acidosis by sodium conservation which helps to raise the pH. The urine becomes
strongly acid. The pulse rate and the blood pressure may also be raised.
TREATMENT.— In case of causes (b), administration of Ringer's lactate solution alongwith
sodium bicarbonate infusion easily cure the patient. In dehydrated cases sufficient normal saline
solution or Ringer's lactate solution should be infused. Sodium bicarbonate may be administered
as 4.2% solution which contains 0.5% mEq bicarbonate per ml. This solution is hypertonic and
is usually mixed with other solutions. Repeated use of it may lead to retention of undesirably
large amounts of sodium.
In case of (a) causes, similar solution of sodium bicarbonate should be infused. This should
particularly be used judiciously during cardiac arrest. The initial dose of bicarbonate should not
exceed 50 ml of 7.5% solution and the decision for additional doses should be best judged after
measurement of pH and PC02 when possible. Frequent measurement of electrolytes and blood
pH are the best guide to therapy to estimate the amount of alkali needed.
Respiralorv acidosis.—
This is less common than the metabolic type and is normally caused by interference with
gaseous exchange in the lungs leading to retention of carbondioxide. In one word inadequate
ventilation is the cause of respiratory acidosis.
The CAUSES are — (i) anaesthetized patient with too much relaxants may be unable to
start proper ventilation for quite a long time, (ii) certain lung disorders e.g. emphysema,
bronchopneumonia, chronic bronchitis, pulmonary oedema etc. (iii) Crushing or other injuries
to the chest, (iv) peritonitis, (v) respiratory centre may be depressed by brain injury or by
poisoning with alcohol, barbiturate drugs or morphine and (vi) airway obstruction.
CLINICAL FEATURES.— These depend on the cause and the degree to which compensation
is effective. During anaesthesia there may be slow rise of systolic or diastolic blood pressure. In
most cases respiration is abnormal. Restlessness, hypertension and tachycardia are signs which
indicate inadequate ventilation.
TREATMENT.— Management of respiratory acidosis involves immediate treatment of
pulmonary defect. All measures should be adopted to ensure adequate ventilation. Endotracheal
intubation and mechanical ventilation are sometimes necessary to achieve this goal. Encouragement
of deep breathing, coughing and using humidified air to prevent inspissation of secretions may
be required. Above all over-sedation and over-use of muscle relaxants should be avoided.
ALKALOSIS
Metabolic alkalosis.—
In this condition both pH and plasma bicarbonate concentration are elevated. Metabolic
alkalosis results from loss of fixed acids or gain of base bicarbonate. It must be remembered
that majority of patients with metabolic alkalosis are associated with some degree of
40
A CONCISE TEXTBOOK OF SURGERY
MiMMIMMtMMiiMMIMMIfMdM
hypokalaemia. Depletion of cellular potassium results in entry of hydrogen and sodium ions
into the cells causing lowering of intracellular pH and an extracellular alkalosis. Metabolic
alkalosis, in turn, causes excessive urinary potassium loss in exchange for sodium which further
accentuates alkalosis, so a state of hypokalaemic metabolic alkalosis results.
CAUSES.—
(i) Excessive ingestion of absorbable alkali, which is not uncommon in patients who take
various antacids or indigestion remedies without medical supervision.
(ii) Persistent vomiting in pyloric obstruction or continuous gastric aspiration is quite
common cause. The loss of chloride causes accelerated loss of sodium and bicarbonate in the
urine and partial compensation of alkalosis. The alkalosis itself causes increased renal excretion
of potassium.
(iii) Prolonged administration of cortisone, ACTH or desoxycorticosterone acetate may cause
alkalosis with potassium deficiency.
To compensate for alkalosis there is reduction in respiratory exchange due to inhibition of
respiratory centre by raised pH. This leads to accumulation of carbondioxide and of carbonic
acid to lower the pH. There is also an increase in the excretion of bicarbonate as also sodium in
the urine. There is reduction in the output of hydrogen ions.
CLINICAL FEATURES.— Mild degrees of alkalosis do not cause any particular clinical
feature. This is only recognized by raised plasma bicarbonate concentration. The most striking
feature of alkalosis is the phasic respiration, which is a period of apnoea of 30 seconds or more
followed by onset of respiration which is at first shallow and then increase in depth until the
excursion is normal. After 2 or 3 respirations of normal range it again declines to apnoea. Tetany
may occur in severe alkalosis, which is the cause of an increased irritability of skeletal muscles.
The proportion of free calcium ions depends on the pH and as the pH rises calcium ion tends
to be combined with phosphate to result low free calcium ions which causes tetany. Latent
tetany is more common, which is revealed by Trousseau's sign. About other manifestations
alkalosis and hypokalaemia are so intermixed that it is difficult to distinguish.
TREATMENT.— The main treatment is to remove the cause. Next consideration is to
maintain an adequate volume of blood. Next consideration is to bring down alkalosis by giving
ammonium chloride. It must be remembered that potassium depletion goes hand in hand with
metabolic alkalosis. So intravenous infusion of a solution of potassium chloride is also necessary.
Respiratory alkalosis.—
Respiratory alkalosis is caused by hyperventilation, which reduces the tension of
carbondioxide in the alveolar air and hence in the plasma. So extracellular carbonic acid
concentration falls and the pH rises.
The main CAUSES in surgical practice are (i) during anaesthesia when excessive manual
pulmonary ventilation is executed with the use of muscle-relaxant, (ii) it may also occur due to
apprehension, pain or central nervous system injury, (iii) due to hysteria, (iv) in men at high
altitudes and those working in very dry atmospheres, (v) high fever and (vi) salicylate or carbon
monoxide poisoning. It should be kept in mind that the majority of patients who require
ventilatory support in the postoperative period will develop varying degrees of respiratory
alkalosis. So frequent measurement of blood gases and appropriate corrections of the ventilatory
pattern are required when mechanical ventilators are used. Arterial PC02 should not be allowed
to fall below 30 mm Hg, as complications may occur, particularly in presence of a complicating
hypokalaemia.
FLUID, ELECTROLYTE AND ACID-BASF BALANCE
41
Compensation depends on the increased renal excretion of bicarbonate. The dangers of severe
respiratory alkalosis are those related to potassium depletion and include the development of
ventricular arrhythmia and fibrillation.
CLINICAL FEATURES of this condition are very vague and suspicion is the main criterion
for diagnosis. The patient becomes pallor and the blood pressure falls. In both acidosis and
alkalosis of respiratory origin there is some risk of respiratory arrest when the disturbance is
severe. This is much more common in alkalosis than in acidosis.
TREATMENT.— This is primarily directed towards preventing this condition. That means
frequent blood gases estimation and appropriate corrections of the ventilatory pattern are required
when mechanical respirators are used. Adequate care should be taken to correct potassium deficit,
which is a common accompaniment of this condition. If alkalotic respiratory arrest occurs it
should be immediately corrected by insufflation of carbondioxide.
HAEMORRHAGE, HAEMOSTASIS
AND BLOOD TRANSFUSION
HAEMORRHAGE
According to the SOURCE OF HAEMORRHAGE, haemorrhage can be classified in two
ways —
A. Haemorrhage may be 1. External or 2. Internal.
1. External haemorrhage — is one that is revealed outside or seen externally,
2. Internal haemorrhage — is one that is not seen from outside or it is concealed
haemorrhage. This type of haemorrhage is seen in bleeding peptic ulcer, ruptured ectopic gestation,
fracture of major bones, ruptures of spleen or liver. Sometimes concealed haemorrhage may be
revealed or external haemorrhage. Examples of these are haematemesis or melaena from bleeding
peptic ulcer, haematuria from ruptured kidney etc.
B. Haemorrhage may be 1. Arterial, 2. Venous or 3. Capillary.
1. Arterial haemorrhage.— When haemorrhage comes from an artery, it is called an
arterial haemorrhage. Such haemorrhage is recognized by bright red colour and it is ejected in
spurts with each systole of the heart.
2. Venous haemorrhage is one which comes from a vein. It is characterized by dark
red colour and it flows out steadily instead of spurts. Blood loss is also copious in case of
venous haemorrhage, particularly when large veins are damaged. Venous haemorrhage may
become darker, when the patient is in the state of anoxia, either due to less oxygen given to the
anaesthetized patient or there is airway obstruction or there is sudden cardiac arrest. In case of
the latter the blood becomes even more darker due to excessive desaturation of oxygen in the
blood.
It is not very easy to stop venous haemorrhage. Penetrating wounds involving main veins
iri the thigh may become fatal if t is not controlled properly. Similarly venous haemorrhage
from varicose vein is also difficult to control. As a first aid measure a compression bandage and
elevation of the limb is a good method to control bleeding for the time being. But such
haemorrhage is best controlled by opening the wound and ligating the vein in the operation
theatre.
3. Capillary haemorrhage is one in which haemorrhage comes from capillaries. In such
haemorrhage blood is bright red and oozes rather than flows out.
According to the TIME OF APPEARANCE haemorrhage can be classified into 1. Primary
haemorrhage, 2. Reactionary haemorrhage and 3. Secondary haemorrhage.
1. Primary haemorrhage is one which occurs at the time of injury or operation.
2. Reactionary haemorrhage is one which occurs within 24 hours of injury or operation.
In majority of cases reactionary haemorrhage occurs within 4 to 6 hours. Such haemorrhage
takes place due to dislodgement of blood clots or slipping of ligatures. This mostly occurs due
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
43
to rise of blood pressure when the patient is recovering from anaesthesia or shock. Such bleeding
may also occur due to restlessness, coughing or vomiting which raises the venous pressure.
3.
Secondary haemorrhage.— This occurs usually after 7 to 14 days of injury or
operation. This is usually due to infection and sloughing of part of the arterial wall. Sometimes
it is preceded by warning haemorrhage, which stains the dressings with blood. This is followed
by the actual haemorrhage which is often moderate to severe. Such type of secondary
haemorrhage may occur externally or internally. The examples of latter are haemorrhage from
the anastomotic site following peptic ulcer operation, in which bleeding is revealed in the form
of haematemesis. Similarly secondary haemorrhage may occur at the operation site of
haemorrhoidectomy in the form of anorectal bleeding.
Clinieal features of haemorrhage.— In case of external haemorrhage the bleeding is seen
from outside and the diagnosis of haemorrhage is confirmed. In case of internal haemorrhage
bleeding is concealed and is not seen from outside. A few symptoms and signs usually
accompany heavy blood loss, be it internal or external. In case of internal haemorrhage these
are helpful to come to the diagnosis. Increased pulse rate, low blood pressure, increasing pallor,
restlessness and deep sighing respiration (air hunger) are the typical features of acute blood
loss. Cold and clammy extremities, empty veins are also characteristically seen when the bleeding
is continuing.
Pulse rate and blood pressure should be measured l/4th or 1/2 hourly intervals when the
patient is losing blood during his stay in the emergency department. Though fall of blood
pressure is often noticed in case of haemorrhage, yet a normal blood pressure cannot exclude
the diagnosis of haemorrhage. Often the blood pressure is maintained at normal level by
peripheral vasoconstriction due to adrenergic release when the patient is still bleeding. Suddenly
the blood pressure may fall abruptly with collapse and even death of the patient. Pulse rate is a
better indicator of haemorrhage than blood pressure. Usually with haemorrhage the pulse rate
is increased. When the blood loss has been excessive the pulse becomes of low volume, which
is classically known as 'thready pulse'.
Measuring of urine output is obligatory in patients who is losing blood. Urine output becomes
low in patients suffering from haemorrhage and shock.
Measurement of blood loss.— It is often important to measure how much the patient
has lost blood. This amount should always be replaced. Whatever methods are adopted to
measure blood loss, they do not give the actual figure. The blood loss detected by the methods
is usually less than the actual loss, because a considerable amount of plasma is lost into the
interstitial tissues and a considerable amount of water is lost via lungs, from the wound and by
evaporation of sweat from the skin. This loss of plasma and water constitutes approximately
20% more than the blood loss detected by various methods.
The best method of detecting blood loss is by weighing swabs. The other methods are
measurement of swelling in case of bleeding from fractures and measurement of blood clot in
haemorrhage.
(i)
Weighing of swab.— This of course is the best method of measuring blood loss during
operation. The swabs are weighed before they are used and they are weighed again after they
are soaked with blood and thrown individually into a collecting basket. The difference of weight
is the amount of blood loss. 1 gm = 1 ml of blood loss. As mentioned earlier it cannot give the
actual amount of blood loss and it should be multiplied by a factor of 1 Vi in case of moderate
operations like partial gastrectomy or radical mastectomy. In case of longer operations like
44
A CONCISE TEXTBOOK OF SURGERY
abdominoperineal operations the swab weighing total should be multiplied by a factor of 2.
(ii) Measurement of swelling in closed fractures.— In case of moderate swelling in closed
fractures of the tibia, the blood loss is estimated at 1,000 to 1,500 ml. In moderate swelling in
case of fractured shaft of femur, the estimated blood loss is about 1,000 to 2,000 ml.
(iii) Measurement of blood clot.— When the collected blood clots are kept in a pot and
measured against a clenched fist of the patient, total blood clot of the size of the clenched fist is
equal to 500 ml. of blood.
Blood volume determinations.— Blood volume = red cell volume + plasma volume. The
haematocrit reading gives the ratio of plasma to red cells. Firstly the plasma volume or the red
cells volume is measured and from the haematocrit value the total blood volume can be
determined. The normal blood volume is about 80 ml of whole blood per Kg body weight. That
means in case of an adult of normal structure the normal blood volume is about 5 to 6 litres. In
certain pathological conditions this blood volume is increased e.g. in chronic anaemia and
arteriovenous fistula.
Haemoglobin level is often considered as a good indication of haemorrhage. But it is practically
not so. In the initial stage the haemoglobin level remains normal. It is only lowered after a few
hours by haemodilution caused by movement of extracellular fluid into the vascular space
due to natural attempt to restore blood volume. The normal value of haemoglobin is about
12 to 16 g per 100 ml.
Measurement of C.V.P. or Central Venous Pressure is a good method to detect loss of blood
volume in haemorrhage.
Treatment of haemorrhage.— It consists of two parts —
A. To stop blood loss and B. To restore blood volume by blood transfusion, infusion of
crystalloid solution and infusion of plasma or plasma substitutes.
A.
The blood loss is stopped by mainly 3 methods — 1. Rest, 2. Pressure and packing
from outside and 3. By operative methods.
1.
REST.— Absolute rest is vital so far as the treatment of haemorrhage is concerned.
Restlessness causes more blood loss. Some sedatives and analgesics may be prescribed to provide
rest to the patient. If the patient becomes restless due to pain, haemorrhage will be more.
Morphine is a good sedative and is often used intravenously in the dose of l/4th gr. It is given
intravenously or even intramuscularly but not subcutaneously. Due to vasoconstriction of the
subcutaneous vessels following haemorrhage absorption of the drug will be minimal. As the
effect of the drug is not properly achieved, the surgeon may push some more amount
subcutaneously. When the blood volume is restored and the circulation improves,
vasoconstriction diminishes and excessive amount of morphine will be absorbed. This may induce
disastrous effect. Morphine however is contraindicated when there is respiratory depression in
head injuries, where chloralhydrate is more preferred. It is also avoided in children and in very
old individuals. Inj. pethidine is a better drug than morphine. Some sedative may be prescribed
alongwith morphine to induce sleep. In this respect short acting temazepam or benzodiazepam
may be used.
Position of the patient is sometimes helpful to reduce haemorrhage. In case of haemorrhage
from thyroidectomy wound, the head end of the bed should be raised (anti-Trendelenburg
position). In case of haemorrhage from varicose vein, the footend of the bed is raised
(Trendelenburg position), in this case gravity reduces bleeding. Trendelenburg position is also
helpful as it increases blood supply to the brain and helps to restore blood pressure.
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
45
2. PRESSURE AND PACKING FROM OUTSIDE.— This is mainly a first-aid treatment.
Sterile pieces of gauze and bandage may be used as pressure bandage to reduce bleeding from
external wound. If sterile gauzes and bandages are not available clean linen cloth may be used
as bandage to reduce bleeding from the wound. The gauze pieces are used as package.
Use of tourniquet to stop haemorrhage has been obsolete. This in fact cannot stop arterial
bleeding, on the contrary causes venous congestion and increases venous bleeding.
In modern surgery place of tourniquet is only restricted in the operation theatre for use in
certain operations as prophylactic measure to control haemorrhage. Its uses are —
(i) In amputations except for atherosclerotic gangrene.
(ii) To get a blood-less field for orthopaedic and soft tissue operations (e.g. in menisectomy
operations, to remove ganglion from tendon sheath etc.).
(iii) To control haemorrhage temporarily while exploration and repair are being carried
out.
Method of application.— The limb is elevated and an Esmarch bandage is applied spirally to
the elevated limb from toes towards the thigh. The bandage is wound upto the groin and the
cuff of the tourniquet is inflated. The distal spirals of the Esmarch bandage are now unwound
to expose the site for operation.
Removal of tourniquet.— The time of application of the tourniquet must be written on the
blackboard in the operation theatre. The tourniquet should not be used for more than \Vi hour.
The operation must be finished before that period. Before deflating the cuff a firm bandage is
applied on the operating wound, so that haemorrhage from minute vessels are stopped by the
pressure bandage.
3. BY OPERATIVE METHODS.— During operation haemorrhage is usually stopped by
artery forceps (haemostats) and clips applied to the bleeding vessels. Now the bleeding vessel
is either ligated with catgut or silk according to the size of the vessel. Smaller vessels can be
coagulated with diathermy.
In case of big vessels like renal artery and vein transfixion suture may be used with silk.
When haemorrhage is in the form of oozing, Oxycel or gelatine sponge may be used to
stop such bleeding. This type of material provides a network upon which fibrin and platelets
are deposited to stop bleeding. Such bleeding can also be stopped by gauze soaked in adrenalin
solution (1 : 1000). 'Stypven' or Russell Viper Venom may be applied. In case of oozing from
bone, bone wax may be used.
When the actual bleeding vessel cannot be detected, it is customary to use rolls of gauze
for packing the wound for sometime. After 5 minutes the gauze pack is removed and slight
bleeding from the spurting vessel can be identified. This is held by long curved artery forceps
and then ligated to stop bleeding.
If a solid viscus is ruptured and bleeds heavily, the whole or part of such viscus should be
excised e.g. splenectomy, partial hepatectomy, nephrectomy etc.
Chronic haemorrhage.— Bleeding from haemorrhoids, carcinoma of caecum and peptic
ulcer are examples of chronic haemorrhage. These bleedings are small in quantity and continue
for quite a long time till effective treatment is performed. In these cases the blood volume is
never diminished as plasma replacement occurs as bleeding continues. Red cell replacement
however lags behind, which results in microcytic hypochromic anaemia. The patient becomes
anaemic. As the blood volume is normal or slightly more than normal, these patients often
develop high-output cardiac failure. This high-output is due to increased cardiac output which
A CONCISE TEXTBOOK OF SURGERY
46
is required to reverse the state of anaemic hypoxia. If acute haemorrhage occurs in these cases,
it is more dangerous than normal individuals as oxygen carriage is already depleted due to low
R.B.C. count.
When these cases are treated, packed cells should be used instead of whole blood to reduce
extra burden on the heart. What these patients require is not the plasma but only the red blood
cells.
Natural restoration of blood volume after haemorrhage.— As soon as haemorrhage
or bleeding takes place nature almost immediately starts to replenish the blood volume. This is
required to maintain blood flow to the vital organs. First of all interstitial fluid is absorbed into
the vascular space. This causes haemodilution. Plasma proteins are replaced by the liver in a
short time. However red cell recovery takes more time, about 5 to 6 weeks. Iron absorption
should be sufficient to maintain this period.
B.
As soon as haemorrhage takes place, every effort should be made to restore blood volume
by blood transfusion. Blood sample should be sent for grouping and cross-matching. By the
time the report is received, infusion of crystalloid should be given. Only when blood is not
available for the time being plasma or plasma substitutes may be used.
HAEMOSTASIS
Natural attempt of haemostasis or stoppage of bleeding starts immediately at the site of
bleeding. The first step in achieving haemostasis is due to local release of a humoral agent,
known as thromboxane. This agent is a powerful constrictor of smooth muscle and promotes
aggregation of platelets. This causes constriction of the small arteries and spontaneous sealing
off. It is probably released by the platelets at the site of disruption of the endothelial surface. It
is a product of prostaglandin metabolism. It must be understood that larger vessels and medium­
sized arteries also constrict, after they have been transected in response to direct sympathetic
innervation and to circulating humoral agent like norepinephrine. Only diseased arteries and
atherosclerotic arteries cannot contract. Larger veins are less efficient at spontaneous sealing off.
Incomplete transection of arteries paradoxically contracts less as they are less respondent to
humoral agent.
Platelets are one of the essential components of haemostasis. A contractile protein in platelets,
which is known as thrombosthenin allows the platelet plug to contract, thus reinforces the
contraction of the vessels. Platelet factor III, a thrombogenic phospholipid is also released locally
which promotes coagulation.
The next mechanism in haemostasis is the formation of a fibrin clot, the process of which is
known as coagulation. The coagulation sequence leads to the formation of thrombin, which splits
fibrinogen to form insoluble fibrin which is acted upon by a factor XIII to form a tough clot.
The detail process of coagulation and involvement of various factors is beyond the scope of this
book and the students are instructed to follow any standard TextBook on Physiology for this
purpose.
Another important aspect of coagulation is the fibrinolytic process, which prevents formation
of intravascular fibrin. Formation of such fibrin and excess fibrin in areas where it is not necessary
will be disastrous. For this a strong proteolytic enzyme that breaks down fibrin into much smaller
soluble fragment is formed which is known as plasmin (also called fibrinolysin). This is formed
from plasminogen, a circulating precursor that converts to plasmin by the action of activators
which are found in the blood, many tissues and especially in vascular endothelium. It is not
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
47
clear how the effects of plasmin are limited to the areas of need. Plasminogen and circulating
plasminogen activators are selectively adsorbed on fresh fibrin. By this the beneficial clots are
preserved, whereas harmful clots are lysed.
CONGENITAL ABNORMALITIES OF HAEMOSTASIS
The most common congenital abnormality of haemostasis is haemophilia. Christmas disease
is the next.
Haemophilia (Haemophilia A).— It is a sex linked inherited disorder and is carried by a
recessive gene, so that it manifests only in males and asymptomatically transmitted through
female carriers. It involves an almost total lack of factor VIII activity. The level of coagulation
factor VIII in the blood may be less than 1% of normal individual.
Clinical features.— Clinical manifestations vary considerably. Bleeding after slight trauma is
the main problem. Surgical problems are mainly orthopaedic resulting from repeated
haemorrhages into joints. Spontaneous retroperitoneal bleeding may occur and will be manifested
by severe abdominal pain, tenderness and ileus. Sometimes haematuria is noticed. Death in
haemophiliacs usually results from bleeding into the central nervous system.
Haemophilic joints is an orthopaedic problem. Recurrent haemorrhage with mild trauma
characterizes this condition. Such recurrent haemarthrosis is not only seen in haemophilia but is
also come across in Christmas disease. Such recurrent haemarthrosis may result in permanent
damage to the articular cartilages, articular surfaces and will cause disorganization of the joints.
Treatment.— Cryoprecipitate is a rich source of factor VIII and is discussed under the heading
of 'Blood Substitutes' later in this chapter. Periodic infusions of this cryoprecipitate will increase
the level of factor VIII. Monitoring of factor VIII level should be performed after each infusion.
If any operation has to contemplate, this should be performed only after raising the level of
factor VIII to almost normal level. Alternative forms of therapy include fresh blood or fresh
frozen plasma.
Christmas disease (Haemophilia B).— This is the second most common congenital disorder
of coagulation. In this condition there is a congenital deficiency of factor IX.
The clinical manifestations are milder than haemophilia A and are almost same as those.
Treatment is transfusion of fresh frozen plasma. There is no definite substitue of factor IX
and hence treatment is less effective. Cryoprecipitate may be used in this condition also.
Von Willebrand’s disease.— This is the 3rd most common inherited disorder of
coagulation.
Clinical manifestations vary in severity, but the bleeding tends to be more from mucous
membrane than from the musculo-skeletal system. In this peculiar condition there are low plasma
levels of factor VIII complement and factor VIII related antigen. There is also some platelet
abnormalities.
All these combine to give rise to bizarre episodic bleeding manifestations.
BLOOD TRANSFUSION
Indications.—
1. The commonest indication of blood transfusion is during acute haemorrhage be it
external or internal.
2. It is indicated during certain major operations, where a good amount of blood loss is
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A CONCISE TEXTBOOK OF SURGERY
inevitable e.g. radical mastectomy, abdominoperineal resection etc.
3. In case of deep bums blood transfusion is indicated besides initial fluid and plasma
administration, as there is considerable haemolysis and destruction of RBCs.
4. Preoperatively blood transfusion is required when the patient is already anaemic and
there is no adequate time for iron replacement therapy before operation. This is particularly
needed before operations for malignant diseases.
5. In postoperative cases blood transfusion is required when the patient has become
considerable anaemic and debilitated, either due to excessive bleeding during operation, or as a
result of infection or septicaemia.
6. In anaemic patients, particularly when the haemoglobin level is below 10 g/100 ml,
blood transfusion is often indicated to treat anaemia. It must be remembered that in chronic
anaemia, it is better to transfuse packed cells rather than whole blood to reduce more burden to
the already burdened heart due to hypervolaemia.
7. In severe malnutrition and hypoproteinaemia, blood transfusion is indicated before
any type of surgery.
8. In certain coagulation disorders like haemophilia, Christmas disease, thrombocytopenic
purpura etc., blood transfusions or blood fraction transfusions are required. In a few blood
diseases e.g. Hodgkin's disease, leukaemia, aplastic anaemia whole blood transfusion is required.
9. In treating cases of erythroblastosis foetalis due to Rh incompatability, exchange
transfusion is often performed through umbilical vein of the new bom baby.
10.
During chemotherapy for malignant diseases blood transfusion is often indicated if
the routine blood examination shows considerable diminution of RBC level.
Collection of blood for blood transfusion.— Before collecting blood from an individual
or donor, one has to make sure that the donor is not suffering from any disease which may be
transmitted through the blood. Particular attention is made that the donor is not suffering from
hepatitis or AIDS (which is transmitted by HIV I and II viruses).
The donor lies down on a bed. A sphygmomanometer cuff is applied to the upper arm and
is inflated to a pressure of 80 mm Hg. 0.5 ml local anaesthetic solution is injected subcutaneously
in the antecubital fossa through which 15 gauge needle is introduced into the median cubital
vein. The needle is connected to a plastic tube which is attached to a plastic bag which form a
close sterile unit. Blood from the donor is allowed to come out and run into the sterile bag
which already contains 75 ml of anticoagulant solution. During collection, blood is constantly
mixed with the anticoagulant solution to prevent clotting. A specimen of blood is sent for
grouping and cross-matching. About 410 ml of blood is taken in a single bag.
Two types of anticoagulant solutions are usually used to mix with the donor blood, (i) CPD
solution contains trisodium citrate (dihydrate), citric acid (monohydrate), sodium dihydrogen
phosphate (monohydrate) and dextrose mixed with water to make the solution, (ii) With the
above-mentioned solution adenosine is added (CPDA-I) to increase the storage life of the blood.
Blood storage.— All bloods that are collected from donor are stored in blood bank in
special refrigerator at controlled temperature of 4°C (ranging from 6°C to 2°C). If blood is allowed
to come in contact with higher temperature, there is danger of transmitting infection.
During storage of blood, the red blood cells or erythrocytes, which constitute the major
component, lose their ability to release oxygen to the tissues of the recepient within 7 days. So
when a patient requires massive transfusion, it is advisable to use at least 1 or 2 units of blood
which are less than 7 days old.
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
49
White blood cells or WBC are rapidly destroyed in the stored blood.
Platelets are also destroyed considerably at 4°C. But a few are still functionally useful after
24 hours. Clotting factors e.g. factor V, VIII and platelets are also destroyed quickly.
Shelf-life of stored blood in CPD solution is about 3 weeks. When blood is stored in CPDAI solution, the storage life is increased to 5 weeks.
Types of blood transfusion.—
Five types of whole blood transfusion may be used —
(i) The typical stored CPD blood from blood bank is most commonly used.
(ii) Warm blood.— During cardiopulmonary operations the blood may be warmed by
passing the stored blood through a blood warming unit to reduce the risk of cardiac arrest
which may be caused by transfusion of large volume of cold blood direct from blood bank.
(iii) Filtered blood is sometimes used by filtering blood through a membrane with 40pm
pores to filter off platelet aggregates and leucocytes in stored blood.
(iv) Autotransfusion is an old method of restoring the patient's blood volume by
transfusing his or her own blood who is excessively losing blood by injury such as ruptured
spleen or ruptured liver or in ruptured ectopic gestation. The blood is collected from the
peritoneal cavity and put into a sterile container. This blood is now filtrated through a few
layers of sterile gauge into a container which already contained anticoagulant CPD solution.
This blood is now immediately transfused into the patient. This method is particularly used
when stored blood is not available.
•
(v) Exchange or replacement transfusion is indicated in new bom infants suffering from
erythroblastosis foetalis. The transfusion is given through the umbilical vein of the infant with a
syringe with four way adaptor — one to the infant's body, one to the donor, one to the citrated
saline and the other to the waste. Rh negative blood is exchanged with the infant's blood 5 to 10
ml at a time.
Such transfusion is also indicated in carbon monoxide poisoning to remove
carboxyhaemoglobin in exchange of fresh oxyhaemoglobin.
Besides whole blood, packed red cells are also transfused in certain conditions.
Packed red cells.— This is specially transfused to patients with chronic anaemia, in elderly
individuals, in children and in those patients whose cardiac reserve is low and may suffer from
cardiac failure if whole blood is transfused. If the whole blood is centrifuged at 2,000 to 2,500 g
for 15 to 20 minutes or if the stored blood is allowed to stay idle so that the supernatant plasma
is taken off and the blood sediment is used for packed cells.
Certain other fractions of blood e.g. plasma, platelet rich plasma etc. are also transfused
in various conditions. These are discussed in details in the section of blood substitutes later in this
chapter.
Amount of blood transfusion.— It should be kept in mind that approximately 70% of
the amount of blood loss should be replaced by transfusion of blood. 500 ml of CPD stored
blood will generally raise the haemoglobin by 10%.
How to measure the amount of blood loss in haemorrhage has been discussed in the section
of 'haemorrhage' earlier in this chapter.
Blood groups and compatibility.—
BLOOD GROUPS.— The red cells contain agglutinogens named A and B and the serum
contains agglutinins named anti-A and anti-B. For transfusion, the red cells of the donor are
matched against the serum of the recipient. As agglutinins, present in the recipient, are in high-
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A CONCISE TEXTBOOK OF SURGERY
titre, can act on the agglutinogens in the red cells of the donor's blood to produce agglutination
and haemolysis. To the contrary, the small amount of agglutinins, present in donor's serum, is
not sufficient to cause agglutination of the recipient's cells as its titre falls on being diluted in
the huge blood volume of the recipient. According to the presence or absence of the two
agglutinogens A and B, there are 4 blood groups : (i) Group A is one, whose red cells contain
A agglutinogen and the serum contains anti-B agglutinin; (ii) Group B is one, whose red cells
contain B agglutinogen and the serum contains anti-A agglutinin; (iii) Group AB is one, whose
red cells contain both A and B agglutinogens and the serum contains neither anti-A nor anti-B
agglutinin; (iv) Group O is one, whose red cells contain neither A nor B agglutinogen and the
serum contains both anti-A and anti-B agglutinins. The persons with group AB can receive blood
from any group (universal recipient). The persons with group O blood can give blood to
anybody as it has got no agglutinogen in the red cells (universal donor). So in emergency, one
can use group O blood if the time does not permit to do proper grouping and cross-matching
or to wait for the availability of the proper cross-matched blood. Before transfusion, the donor
and the recipient must be grouped and cross-matched. For transfusion, the red cells of the donor
are matched against the serum of the recipient. There is another factor known as Rhesus (Rh)
factor, which is very important to be considered during cross-matching.
RH FACTOR.— This is an antigen found in the red cells. Human beings can be divided
into Rh positive and Rh negative groups accordingly whether the red cells contain Rh factor or
not. Obviously persons with Rh positive blood do not posses Rh anti-body in the serum. When ,
Rh positive cells are injected into Rh-negative persons, the anti-body Rh develops. The first
transfusion may escape to produce any symptom but further transfusion will definitely produce
serious reactions. A similar condition happens when a Rh-negative woman carries Rh-positive
foetus. The red cells of the foetus when come in contact with the mother's serum, will form
anti-Rh. The anti-Rh will pass into foetal circulation and destroy the red cells of the foetus,
producing haemolytic reaction.
Approximately 85% of population are Rh positive and 15% are Rh negative.
Technique of blood grouping.— On a glass slide, one drop of stock serum from group A
and one from group B, are placed side by side. The person, who is to be grouped, is pricked in
his finger tip and a drop of blood is added to each of these drops of serum placed on the slide.
After 5 minutes, the slide is examined under the microscope. If agglutination is observed in
serum of group A, the person belongs to group B. If agglutination occurs in the serum of group
I>, the person belongs to group A. If agglutination is seen in both, the person belongs to group
AB and if agglutination is not seen in either of the two, the person belongs to group O.
Before the blood is sent for transfusion, direct cross-matching is carried out. One drop of
the patient's serum is mixed with one drop of donor's blood (diluted 1:20 in saline). The slide is
examined under microscope after 5 minutes. If agglutination does not occur, the blood is
compatible. If agglutination occurs the blood is incompatible.
Incompatibility.— If incompatible blood has been transfused, agglutination and then
haemolysis of transfused RBCs occur. If haemolysis is severe, it may cause acute renal tubular
necrosis, renal failure and death of the individual. So it is extremely essential that compatibility
of the donor's blood is checked. This is done by —
(i)
Transfusion of blood of same group as the recipient should be given, (ii) Rh. compatibility
should also be checked that means Rh. status of the transfused blood should be similar to the
Rh. status of the recipient, (iii) Direct cross-matching of the donor's red cells against recipient's
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
51
serum should be performed before transfusion.
COMPLICATIONS OF BLOOD TRANSFUSION.— There are various complications of
blood transfusion, though attempt should be made that blood transfusion, given to the patient,
should be free of complications. Of the complications of blood transfusion, two groups are very
important. These are — A. Transfusion reactions and B. Transmission of diseases. Other complications
are not insignificant. The various complications are follows :—
A.
Transfusion reactions.— The followings are the various transfusion reactions which
may be seen as complications of blood transfusion. Of these incompatibility is probably most
important and should be avoided at all costs.
1. INCOMPATIBILITY.— There are three causes of incompatibility —
(i) Incompatible transfusion.
(ii) Transfusion of blood which is already haemolyzed by heating or over freezing or shaking.
(iii) Transfusion of blood after expiry date.
From the above causes it is clear that incompatibility is mainly due to human error —
negligence in looking at the label of the bottle of blood and imperfect grouping and cross-matching.
Clinical features.— Once the incompatible blood has been transfused, the patient first develops
rigor and fever. If he is not anaesthetized, he will complain of headache, nausea and vomiting,
pain in the loins and tingling sensation in the extremities. Pain in the loin is a very characteristic
feature and it indicates blockage of renal tubules, which means grave consequences.
Pain in the loin may be preceded by a filling of tightness in the chest and dyspnoea.
If the patient is already in shock, it becomes pronounced instead of curing it. The patient
may gradually lose consciousness.
Urine output is gradually diminished and haemoglobinuria occurs within 2 or 3 hours.
Appearance of jaundice is a definite sign of incompatible transfusion and it usually appears
within 24 to 36 hours.
Ultimately renal failure sets in due to blockage of renal tubules with haematin pigment.
Treatment.— The transfusion should be stopped immediately. A fresh specimen of venous
blood and urine from the patient are sent to the laboratory for checking alongwith the rejected
bottle of blood.
Administration of fluids intravenously should be started instead of blood. Haematin
pigments tend to be precipitated in acid medium, so alkalization of blood should be done with
10 ml of isotonic solution of sodium lactate and simultaneously 10 ml of saturated solution of
sodium bicarbonate are injected intravenously. Frusemide 80 to 120 mg intravenously is given
to provoke diuresis. This may be repeated if urine output is not increased upto 30 ml/hour.
Antihistamine and hydrocortisone may be prescribed.
Haemodialysis with artificial kidney may be used in extreme cases.
2. PYREXIAL REACTIONS.— Sometimes blood transfusion is accompanied by pyrexia,
chill, rigor, restlessness, headache, increased pulse rate, nausea and vomiting.
The causes of such pyrexial reactions are as follows —
(i) Improperly sterilized transfusion sets.
(ii) Presence of 'pyrogens' in the donor apparatus.
(iii) Transfusion of infected blood.
(iv) Presence of sulphur compounds in the rubber tubing (this is not used nowadays due
to availability of plastic disposable sets).
(v) Very rapid transfusion of blood.
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Prevention.— These pyrexial reactions can be largely prevented by the use of plastic
disposable transfusion sets now available in the market.
Treatment.— The transfusion is immediately stopped temporarily. The patient is covered
with blankets.
Antipyretic and antihistaminic drugs are injected. If the temperature has come down and
the patient is feeling comfortable, transfusion is again started with a fresh plastic disposable set
at a slow rate.
3. ALLERGIC REACTIONS.— Sometimes after blood transfusion (usually within a few
hours) the patient develops mild tachycardia, urticarial rash, fever and dyspnoea. In acute cases
there may be circulatory collapse, which is known as acute anaphylactic shock.
The cause is the allergic reaction to plasma product in the donor's blood.
Treatment.— The transfusion is immediately stopped. Antihistaminic drugs e.g.
chlorpheniramine 10 mg or diphenhydrazine 25 mg should be administered. Sometimes
hydrocortisone and calcium may be administered in acute anaphylactic reactions.
4. SENSITISATION TO LEUCOCYTES AND PLATELETS.— This is occasionally seen
where many blood transfusions have been given in the recent past. The patient develops
antibodies against the white cells or platelets of the donated blood. This causes reactions.
Prevention.— Such unusual reaction can be avoided by giving packed red cells, whenever
many blood transfusions are required.
Treatment.— Antipyretics, antihistamines and steroids may be given to combat reactions.
B. Transmission of diseases.— The most common serious complication directly
attributable to transfusion is the transmission of diseases.
■ 1. SERUM HEPATITIS.— While many diseases have been transmitted by transfusion,
the most important is by far the serum hepatitis. It is usually called non-A, non-B hepatitis
which is the most common form of transfusion related hepatitis in developed countries, where
immunologic markers for different types of hepatitis have been used. In Indian subcontinent it
is mainly the hepatitis B, the virus of which is transmitted from the donor to the recipient. So
all blood donors should be carefully tested for presence of hepatitis B virus associated antigen
in the blood prior to transfusion. But the method of testing is not sensitive enough to eliminate
all cases bearing that virus. About 1% of cases pass undetected. The symptoms and signs of
serum hepatitis is usually revealed within 3 months after transfusion.
2. It is now clear that ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS) can be
transmitted by transfusion. HIV virus is transmitted from the donor's blood to the recipient.
Although AIDS has received considerable attention it ranks far behind hepatitis as a cause of
death resulting from transfusion.
3. BACTERIAL INFECTIONS.— This is not common and occurs due to faulty storage
technique. The donor's blood when left in a warm room for some hours before transfusion,
bacterial infection to the recipient may occur. In fact in this warm room temperature proliferation
of any bacteria may take place. Such bacterial infection is revealed by septicaemia in the recipient.
C. Reactions caused by massive transfusion.— There are quite a few hazards of
massive transfusion, which should be kept in mind. These are discussed in details below :—
1.
ACID-BASE IMBALANCE — is reasonably expected in massive transfusion. Extensive
transfusion usually results in significant metabolic alkalosis. This is because most of the citrate
in the anticoagulant solution is present as sodium citrate, which becomes sodium bicarbonate
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
53
as the citrate is consumed. This alkaline nature of the blood may help the patient who is already
acidotic.
2. HYPERKALAEMIA — is also a theoretical possibility as the potassium level of the
stored blood may reach up to 30 mEq/L. This is due to shift of potassium out of the red cells
due to low temperature of storage. But after transfusion, the transfused red cells take back as
much potassium as they had released during storage. So at the end there should not be
hyperkalaemia at the end of transfusion. But all studies show that patients at the end of massive
transfusion are hypokalaemic. This is probably due to alkalosis induced by massive transfusion.
3. CITRATE TOXICITY — is mainly a theoretical problem rather than practical. Its main
effect is to consume ionized calcium from the patient's body. But the body mobilizes calcium
rapidly from skeletal stores. So supplemental calcium is not required. Only in rare cases when
report of hypocalcium is received, one may consider of infusing calcium, which is also not
absolutely harmless.
4. HYPOTHERMIA.— Since massive transfusion usually occurs under most urgent
circumstances, blood is usually rushed directly from the refrigerator to the patient. If the patient
is in the operation theatre, he is paralyzed and unable to shiver, consequently these patients
almost always experience a drop in body temperature of at least 3 to 4 degrees.
5. FAILURE OF COAGULATION.— Probably the most important danger of massive
transfusion is the failure of natural process of coagulation. This is mainly caused by two factors—
(a) Dilution of platelets and various clotting factors due to transfusion of large volume
of stored blood, as stored blood has low content of platelets, fibrinogen and various coagulating
factors — factor V, VIII etc.
(b) Disseminated intravascular coagulation (DIC) has been the complication of massive
transfusion. This of course follows obviously an incompatible blood transfusion, but this may
be noticed in certain cases of massive blood transfusion.
Treatment.— Coagulation failure is mainly treated by transfusion with fresh frozen plasma,
platelet concentrate or cryoprecipitate: If DIC is considered to be the cause heparin may be
used.
D. Complications of over-transfusion.— This complication is particularly noticed in
cases of chronic anaemia, in children and in elderly individuals. These cases should be transfused
with packed red cells rather than whole blood. Congestive cardiac failure is particularly seen if
whole blood transfusion is given to chronic anaemic patients and elderly individuals.
In cases of chronic anaemia packed red cells should be transfused and diuretics should be
prescribed. Transfusion should be given slowly at the rate of 1 unit in 4 to 6 hours. Transfusion
should not be continuous, instead it should be given on separate occasions giving intervals
between consecutive transfusions.
Patients over 60 years of age should also be given packed red cells with diuretics. They
should not be transfused more than 300 ml at a time.
E. Complication of general intravenous fluid administration,— A few complications
are common to any intravenous infusion. These complications may also occur after blood
transfusion. These are (a) thrombophlebitis, (b) air embolism etc.
Considering the complications and dangers of blood transfusion, it should be concluded by
saying 'the best amount of blood to give is the least amount that is needed'.
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BLOOD SUBSTITUTES
Various blood substitutes may be used to replenish blood loss. But the blood is the best
replacement for blood loss due to its oxygen carrying ability, which is missing in the blood
substitutes. Normal arterial oxygen content is 20 ml/dl and normal venous oxygen content is
15 ml/dl. This oxygen content is dependent on haemoglobin concentration and if Hb
concentration goes down by 50%, arterial oxygen content will also be reduced to 50%.
The blood substitutes can be basically divided into 2 groups — A. Plasma and its derivatives
and B. Synthetically prepared various solutions.
A. PLASMA AND ITS DERIVATIVES.—
1. Plasma.— If the whole blood is kept for sometime, a sediment will form at the bottom
of the container. The upper clear portion is the plasma and the blood sediment is the packed
red cells. If the whole blood is centrifuged at the rate of 2000 to 2500 g for 15 to 20 minutes, the
whole blood will be divided into 2 groups — plasma and packed red cells. The plasma can
thus be separated from the blood.
Fresh frozen plasma.— Plasma removed from fresh blood, which is obtained within 4 hours,
is rapidly frozen by immersing solid carbondioxide and ethyl alcohol mixture. Such plasma is
stored at -20°C. This process preserves all the coagulation factors, particularly factors V and
VIII. Such plasma is very useful in the treatment of coagulation deficiencies, in liver disease, in
haemophilia (factor VIII deficiency), in Christmas disease (factor IX deficiency) and in
defibrination cases. It is also useful in cases of vitamin K deficiency.
2. Platelet rich plasma.— This is suitable for transfusion to patients who are suffering
from thrombocytopenic purpura. This is prepared by slow centrifugation of fresh whole blood
(at the rate of 150 to 200 g for 15 to 20 minutes).
PLATELET CONCENTRATE.— Platelet concentrate is prepared from platelet rich plasma
by centrifugation at the rate of 1500 g for 20 minutes. This is further acidified to a pH of 6.5.
The platelet remains active in vitro for 48 hours. If the platelet concentrate is stored frozen, its
effectiveness may be extended to many months of storage.
Both platelet rich plasma and platelet concentrate are used in cases suffering from
thrombocytopenic purpura. This condition is characterized by prolonged bleeding time. Normal
bleeding time is 5 minutes or less and a bleeding time more than 8 minutes is pathognomonic
of impairment of platelet function. It must be remembered that platelet count of 50,000 per
cubic mm is rarely associated with significant bleeding. So in thrombocytopenic purpura, the
platelet count is usually below that.
3. Fibrinogen.— It is prepared by organic liquid fractionation of plasma. It is stored in
the dried form and before using it is made soluble with distilled water. Such solution is required
in cases of severe depletion of fibrinogen e.g. congenital afibrinogenaemia and in disseminated
intravascular coagulation (DIC).
It should be kept in mind that such fibrinogen solution carries the risk of transmitting hepatitis.
4. Albumin.— Albumin is prepared by repeated fractionation of plasma by organic liquids
and then followed by heat treatment. It may be stored for several months in liquid form at 4°C.
The main advantage of this is that it is free from the danger of transmission of serum hepatitis.
It is particularly useful as a volume expander in patients who cannot tolerate a sodium
load (cirrhotic patients) and in patients with severe albumin loss e.g. following severe bum and
in nephrotic syndrome. The main disadvantage of it is that it is very costly.
HAEMORRHAGE, HAEMOSTASIS AND BLOOD TRANSFUSION
55
5.
Cryoprecipitate.— If the frozen plasma is allowed to bring at a temperature of 4°C,
it will be divided into a white glutinous precipitate and a supernatant plasma. The glutinous
precipitate is known as cryoprecipitate. It is usually stored at -40°C. It is very rich source of
factor VIII. So it is the best treatment of patients with haemophilia (factor VIII deficiency).
When this is injected intravenously, a large quantity of factor VIII can be administered in
relatively small volume. It also contains a good amount of fibrinogen and may be used in
conditions of hypofibrinogenaemia.
B. SYNTHETICALLY PREPARED VARIOUS SOLUTIONS.
1. Dextran.— It is polysaccharide polymer with varying molecular weights. The bacterium
Leuconostoc Mesenteroides produces this polysaccharide compound to which a yeast extraction
is added. The molecular weight of such dextran may vary from 40,000 to 1,50,000.
This solution induces rouleaux formation of red cells. It also interferes with the platelet
function, so that it may induce abnormal bleeding. So this solution should not be used more
than 1,000 ml. It also interferes with blood grouping and cross-matching, so blood sample for
grouping and cross-matching should be drawn before introducing this solution. Two types of
dextrans are usually used —
(a) LOW MOLECULAR WEIGHT DEXTRAN (MOLECULAR WEIGHT — 40,000).— This
is also known as rheomacrodex or dextran 40. Dextrans are usually used to restore plasma volume
and this type of dextran is also used for this purpose. But it has transitory effect of restoring
plasma as small molecules are readily excreted by the kidneys. It is more often used to prevent
sludging of red cells in small vessels. It is also used in cases of disseminated intravascular
coagulation (DIC) due to this action.
(b) HIGH MOLECULAR WEIGHT DEXTRAN (MOLECULAR WEIGHT — 70,000).—
This is also known as dextran 70. Its main use is to restore plasma volume for a longer time, as
the large molecules are not excreted by the kidneys and are retained in the circulation for longer
period. About each gram of this dextran binds approximately 20 ml of water, whereas each
gram of albumin binds approximately 14 ml of water. This results in a significance increase in
plasma volume when this dextran is infused.
2. Gelatine.— Gelatine solutions are among the first used as blood substitutes. This
solution has molecular weights varying between 20,000 to 40,000. This is less effective than
dextran as plasma volume expander. Only 30% of this solution remains in the intravascular
compartment after 4 hours of infusion.
3. Hydroxvethylstarch (HES).— It is made by treating starch with sodium hydroxide
and ethylene oxide. Its molecular weights vary from 60,000 to 4,50,000. It is second to dextran
in its efficiency as a plasma volume expander. Its duration of activity is unfortunately not more
than 6 hours.
4. Fluorocarbons.— These are hydrocarbons in which the hydrogen atoms have been
replaced by fluorine. This is a colourless, odourless dense liquid, that is chemically inert and
poorly soluble. This should be emulsified with albumin of fats for better tolerance. Emulsions
of fluorocarbons, if injected alone, may cause pulmonary embolism, asphyxia and death. Its
half-life varies from 2 to 7 days.
Its main efficacy is that it can bind and release oxygen rather than merely passively
transporting dissolved oxygen. It is considered to be a red cell substitute. But the main difficulty is
that there is considerable fall in partial pressure of oxygen very quickly. This means that in order
to maintain adequate arterial oxygen content the patient should be kept in hyperbaric environment.
NUTRITION (INCLUDING
PARENTERAL NUTRITION)
Nutrition requirements.— In day to day normal life nutritional requirement is much
lower than in postoperative cases and hypercatabolic states. A healthy adult usually requires
1500 to 2000 non-protein calories per day for energy. The carbohydrate provides a 4 kcal/gm,
whereas fat provides 9 kcal/gm. A healthy adult in normal state requires about 40 gm of protein
or 6 gm of nitrogen per day. In hypercatabolic state patients need 3 to 4 times this amount of
protein. A negative balance of 10 gm nitrogen in a day is equivalent to a loss of 63 gm of
protein.
Vitamins are necessary as supplements, whatever may be the method of feeding. Vitamins
are essential for maintenance of normal metabolic functions and these are not synthesized by
the body. The water-soluble vitamins B and C help in collagen formation and wound healing,
hi the postoperative period the vitamin C requirement increases to 60 to 80 mg per day. Vitamin
C is more depleted preoperatively if the patient was on aspirin or barbiturates therapy or if he
was suffering from anorexia or in the habit of excessive smoking. In these cases requirement of
vitamin C is more. Vitamin Bu is depleted in Crohn's disease, ileal resection or bypass, blind
loop syndrome, reduced pancreatic secretion, excess alcohol intake, anti-convulsant therapy and
after gastric surgery. Vitamin B12 is usually given in the dose of 500 jag i.m. weekly.
Fat-soluble vitamins e.g. A, D, E, K are depleted in steatorrhoea and absence of bile. Vitamin
A may be given after surgery in the dose of 5000 units per week. Vitamin K is particularly
given in case obstructive jaundice, where bile is not available for its absorption from the ileum
and when there is bleeding tendency. This is given in the dose of 5 to 10 mg i.m. weekly.
Malnutrition.— Malnutrition is not a common occurrence in surgery, though a few
patients are seen to be suffering from malnutrition, either being present preoperatively or
postoperatively or in certain hypercatabolic states.
Preoperative malnutrition is often due to starvation or failure of digestion of food before
operation. Such malnutrition may develop in (a) cases of poverty, (b) cases of dysphagia, (c)
cases of excessive vomiting, (d) cases of carcinoma of the stomach, pancreas, liver or biliary
tracts giving rise to failure of proper digestion and jaundice, (e) cases of blind loop syndrome
and intestinal fistulas and (f) the elderly and alcoholics who do not care to take proper food.
Postoperative malnutrition is quite common and occurs in almost all cases in transient form. As
soon as the patient recovers from postoperative period and starts taking normal diet, such
malnutrition disappears. Any delay to the normal diet e.g. following complications like paralytic
ileus and postoperative peritonitis or following such operations like oesophagectomy, severe
malnutrition may occur.
Hypercatabolic states.— After severe trauma, extensive surgery, bums, severe sepsis, high
fever and hypercatabolic renal failure there is excessive calorie utilization and unless generous
calorie intake is given, the body proceeds quickly to breakdown fat and muscle protein in
NUTRITION
57
approximately equal proportion to provide the necessary calories for survival. Total carbohydrate
stores in healthy adult do not exceed 100 to 200 gm and this will provide only 400 to 800
calories. So that in serious illness protein destruction will occur rapidly. As every gram of negative
nitrogen balance represents the loss of approximately 30 gm of the lean muscle mass, it can be
seen that for a daily negative nitrogen balance of 10 gm per day, about \Vi kg. of lean muscle
mass will be lost over a 5 day period. In many situations nitrogen losses may greatly exceed
this. After herniotomy operation the usual daily nitrogen loss is about 3 gm, which approximates
90 gm of muscle loss. In appendicectomy operation daily nitrogen loss is approximately 6 gm
which approximates to 180 gm of muscle loss. In cholecystectomy daily nitrogen loss is about
12 gm, which approximates to 360 gm of muscle loss and in oesophagectomy daily nitrogen
loss is approximately 90 gm which approximates to about 2700 gm of muscle loss. In peritonitis
and in sepsis the daily nitrogen losses are approximately 18 and 24 gm. When lean body mass
protein catabolism is accentuated and energy supplies are derived from the body fat stores
which may contribute 30 to 50 per cent of the calories required. While glycolysis soon stops,
lipolysis continues and aminoacids are further degraded through gluconeogenesis to provide
energy. Accompanying the negative nitrogen balance is a negative potassium balance.
EFFECTS OF MALNUTRITION — are many of which defective wound healing (which
may lead to wound dehiscence) and leaking anastomosis of bowel are the main. There may be
increased susceptibility to infection, there may be reduced enzyme synthesis, defect in
coagulation, decreased tolerance to radiotherapy, delayed callus formation in fracture and
decreased tolerance to cytotoxic chemotherapy.
ASSESSMENT OF MALNUTRITION.— Though approximate assessment of the amount
of deficient nutrition can be assessed and nutrition can be provided accordingly, yet a definite
method of assessment of malnutrition may help the clinician to estimate how much nutrition
has to be given.
1. Body weight.— There is a list of ideal body weight according to height of the patient.
weight (kg)
By applying the body mass index (B. M. I.) which is equal to--------------------. A man should have
height2 (m)
B. M. I. ranging from 20 to 24 according to structure. Whereas a woman should have an index
of 19 to 23 according to structure.
2. Upper arm circumference before and after operation is a good indication of the amount
of malnutrition or the negative nitrogen balance the patient is having.
3. Serum albumin estimation should not be less than 33 g per litre.
4. Nitrogen balance studies.— Total nitrogen intake is compared with loss from all sources
e.g. nasogastric aspiration, fistula drainage, urine etc. Greater loss than intake indicates a negative
balance and tissue breakdown. More intake than the loss means positive balance which means
anabolism or tissue synthesis.
METHODS OF FEEDING. A. ENTERAL NUTRITION.—
1. BY MOUTH.— This is obviously the most convenient and effective route to provide
nutrition. This being the physiological route, where ever possible, this route should be chosen to
provide nutrition.
2. BY TUBE.— If mouth feeding is not possible, a nasogastric tube is passed and nutrition
is provided in liquid form through this tube. In case of oesophageal carcinoma a special tube in
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the form of Souttar's tube or Celestin tube should be passed by endoscopy to provide nutrition
through this tube.
3. GASTROSTOMY.— This is performed when feeding cannot be provided by mouth as
well as by nasogastric tube. This is particularly required in cases of oesophageal carcinoma or
high gastric carcinoma. A plastic tube of about 8 to 10 mm in diameter is passed through a
separate 'stab' incision through the upper left rectus muscle or through a short muscle splitting
incision. The tube is passed through a small incision in the anterior wall of the stomach using
two rows of purse-string sutures around the tube on the stomach wall. The tube should be
directed towards the fundus of the stomach. The tube is secured to the skin with adhesive
strapping or a silk suture.
4. JEJUNOSTOMY.— When gastrostomy is not possible either due to earlier gastrectomy
or due to carcinoma involving the stomach, tube jejunostomy is performed for feeding.
Jejunostomy seems to be a more successful method of feeding than gastrostomy, even when the
stomach is available e.g. oesophageal carcinoma.
B. PARENTERAL NUTRITION.—
Indications.— (i) When enteral feeding is contraindicated, intravenous feedings become
mandatory, (ii) The aim should be to provide a generous calorie intake intravenously, of which
about 40% should be from carbohydrate source. In addition, a utilizable source of nitrogen is
required if parenteral nutrition is indicated for more than a day or two. (iii) In fact when a
severely ill patient is unable to take adequate oral nutrition either voluntarily or through a
nasogastric tube, after 3 days intravenous nutrition must be considered, (iv) The aim of such
treatment is partly to restore losses that have already occurred and to arrest catabolism, but
preferably to prevent large losses by beginning treatment early enough and thereby restoring
the internal environment towards normalcy as soon as possible, (v) Intravenous nutrition therefore
is not only concerned with the supply of calories or nitrogen but also it provides with electrolyte
equilibrium and maintenance of serum oncotic pressure, (vi) When there is severe extra-renal
loss of protein e.g. ulcerative colitis or intestinal fistulae. (vii) It is particularly indicated in marked
catabolic response of severe injuries such as severe bums, prolonged coma or hypercatabolic
renal failure.
Contraindications.— There are however certain contraindications to intravenous or parenteral
nutrition. These are severe hepatocellular damage, renal damage, congestive cardiac failure,
uncontrolled diabetes and severe blood dyscrasias.
CARBOHYDRATE.— The need for carbohydrate in parenteral nutrition is too well known
to require emphasis. Carbohydrates are the most readily available source from which necessary
calories are derived. Because carbohydrate stores in the liver are rapidly utilized, calorie
deprivation for more than several hours leads invariably to the breakdown of muscle protein
unless carbohydrate calories are replaced.
There can be little doubt that glucose is the carbohydrate of choice, being the normal
physiological substrate and essential for cerebral metabolism. It is used usually as a 5% or 4.3%
solution. But glucose has the disadvantage that it supplies only a very few calories in a large
fluid load, and concentration above 10% causes thrombophlebitis. Hypertonic solutions of upto
30% can be given slowly into the inferior vena cava, but the use of caval catheters for the routine
intravenous feeding of all patients is inconvenient and not without risk.
Fructose is a better alternative, since concentration upto 20% does not cause significant
phlebitis so a greater calorie intake can be obtained from the same fluid load. It is more rapidly
NUTRITION
59
metabolized in the liver than glucose and is less dependent on insulin for its early metabolism.
A further advantage of fructose is that when used in combination with aminoacids, the urinary
losses of peptides are less than when glucose is used. The anabolic properties of fructose may
be greater than that of glucose in equal concentrations.
Comparatively recently sorbitol has received some interest as an intravenous carbohydrate
source. However it appears in the urine at comparatively low infusion rates, probably because
it is not appreciably reabsorbed by the renal tubules. So the urinary loss of calories and the
osmotic diuresis are greater than for fructose or glucose. At present the choice of intravenous
carbohydrate favours fructose.
Alcohol.— The nitrogen-sparing effect of ethanol has been long known. In even low
concentration ethanol increases tissue oxygen uptake. Carbohydrate increases the oxydation rate
of alcohol as also do aminoacids. Ethanol is a useful calorie source providing 7.1 cal/gm. It is
not associated with urinary losses. It can be conveniently combined with aminoacid and fructose
in nutrient solutions. Concentrations of alcohol above 3% are irritant to veins and it can therefore
only constitute a supplementary source of intravenous calories. Alcohol however cannot replace
carbohydrate as an energy source, since nitrogen balance is not secured unless carbohydrate is
also present.
FAT EMULSIONS.— Since fat has a calorie ratio twice that of carbohydrate or protein, it is
theoretically a valuable source of compact calories. It has taken many years to produce reasonably
safe fat emulsion suitable for intravenous use. These can be produced either from soya bean oil
or cotton seed oil with phosphatids, lecithine or other chemicals as emulsifying and preserving
agent. It has been confirmed that as a calorie source it has a potential value with protein sparing
properties. Extensive application confirms that substantial reduction can be made in nitrogen
loss, although the deficit is rarely abolished completely or converted to positive balance. Toxic
reactions to intravenous fat emulsions are quite well known. The immediate reactions are pyrexia,
chills and nausea. The late reactions are anaemia, gastrointestinal bleeding, impaired liver function
and persistent lipaemia. Fortunately the need for fat emulsions rarely lasts for more than 7 to 10
days. The only reaction, which is frequent, is pyrexia, which is a reflexion of rapid peripheral
metabolism. It has been shown that extensive use of soya bean oil emulsion has been made in
parenteral nutrition in intensive care units without any serious complications.
AMINOACID SOLUTIONS.— Although carbohydrates exhibit a protein-sparing action, this
is only partial in degree and fails to avoid the extensive loss of the lean muscles mass that may
follow trauma, surgery, sepsis, bums or other serious illnesses. Since the minimum urinary nitrogen
excretion is between 2 and 2.5 gm/day and faecal nitrogen excretion varies little with the dietary
nitrogen content between 3.5 and 4 gm of nitrogen daily even if nitrogen intake is nil, it is
therefore essential in parenteral nutrition to provide a nitrogen source in the form of aminoacids
in physiologically balanced proportion. These are available either as hydrolyzed aminoacids
derived from casein or as pure synthesized ^/-aminoacids. Normally only L-aminoacids are
metabolized effectively for the maintenance of nitrogen balance. Although the clinical use of dlaminoacids has been held to be as satisfactory as that of hydrolyzed aminoacids, comparative
studies confirm that nitrogen balance is not as satisfactory with synthesized dl-aminoacids as
with hydrolyzed preparations. Numerous studies have confirmed that the concomitant use of
hydrolyzed aminoacids with carbohydrates or fat emulsions provides a utilizable anabolic protein
source. Optimum metabolic usage requires simultaneous or prior administration of the
carbohydrates and of potassium in the dosage of 5 mEq for every gm of aminoacid nitrogen
infused. So the choice of preparation favours the hydrolyzed aminoacids.
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PLANNING OF INTRAVENOUS REGIMEN.— It should be remembered that energy from
carbohydrate sources should provide not less than 30% of the total calories to ensure that there
is sufficient generation of oxaloacetate for cycling in Krebs' tricarboxylic acid cycle. The conversion
of pyruvate to acetate is irreversible and oxaloacetate has to be produced from sources other
than fat. It has been shown that a regimen that does not supply any carbohydrate calories will
not arrest loss of body weight. In cases with very high metabolic demands, insulin/glucose
regimen provides a valuable additional approach to the problem. If a patient already has
hypoproteinaemic oedema at the start of an intravenous nutrition regimen, it is best corrected
by giving plasma or human plasma protein fraction, as it will take some days for new albumin
synthesis from intravenous aminoacids. In long term intravenous nutrition regimen, one unit of
plasma per week is essential. Magnesium, potassium and vitamins will have to be added in
case of long intravenous regimen.
Composition of intravenous nutrition to be given per 24 hours. In first 8 hours — Vi litre
Aminosol 3.3%, Fructose 15%, Ethanol 2.5% plus 26 mEq. Kcl (2 g.); Vi litre 20% intralipid and
5000 units Heparin.
In second 8 hours — Vi litre 3.3% Aminosol, Fructose 15%, Ethanol 2.5% plus 26 mEq. Kcl
and ]/2 litre 10% Aminosol.
In third 8 hours — Vi litre 3.3% Aminosol, Fructose 15%, Ethanol 2.5% plus 26 mEq. Kcl and
lA litre 20% intralipid + 5000 units Heparin.
BURNS
A bum is a wound in which there is coagulative necrosis of the tissue. The various types of
bums are as follows :—
1. ORDINARY BURNS are usually caused by dry heat with fire, open flame, hot metal
or aeroplane crash in civil life and bomb injuries in war time.
2. SCALDS are caused by moist heat e.g. hot liquid or steam.
3. ELECTRIC BURNS.— Low-voltage electrical sources produce direct injury at the point
of contact. Skin and subcutaneous tissue are involved most commonly, although muscle and
bone beneath the cutaneous bum may be damaged. High-voltage current not only causes direct
injury at the point of contact but also damages tissues that conduct the electricity through the
body. Tissue damage associated with electrical injury occurs when electrical energy is converted
to thermal energy. The resulting injury is a thermal bum. Skin represents the initial barrier to
current flow and is an effective insulator to deeper tissues. The skin gradually undergoes
coagulation necrosis. At high voltages, skin resistance is initially overcome and the current flows
through deep tissues in the body unimpeded. Except bone, these internal tissues act as a volume
conductor offering little resistance to electrical flow.
Majority of electric bums are caused by high-voltage electric current. The peculiarity of
electrical burns is that it causes minimal destruction of the skin. The skin is involved at 2 points
— at the point of contact with the electrical source and at the site of exit at which the patient is
grounded. The magnitude of injury of the tissues between the point of entry and the point of
exit of the electric current is directly related to the amount of electric current passing through.
The amount of damage also depends on the resistance of the tissues. The muscle, the nerve and
blood vessels offer least resistance to the electric current and so sustain maximum amount of
tissue damage. But the skin offers considerable resistance and that is why cutaneous injury may
be apparently small, although there may be considerable deep tissue destruction involving the
upper and lower extremity musculatures. However it should be remembered that electrical
resistance of skin is markedly reduced by moisture, so ulcers are more often seen in the axilla
and antecubital fossa in case of electrical bum of the upper extremity. Electrical injury to the
musculature is often associated with release of haemochromogens into the blood stream which
are ultimately excreted through urine. So 'port-wine' coloured urine is not unusual following
major electrical injury.
4. CHEMICAL BURN is caused by strong acid or base which comes in contact with skin
or any other tissue. The severity of the damage is directly related to the concentration of the
chemical agent, the amount of agent and the duration of contact. Such bum injury tends to be
deeper than it is assessed from outside. If the superficial slough is removed, the depth of the
injury can be assessed.
5. RADIATION BURNS are usually caused by X-rays or radium. This is in fact a type of
inflammation of the skin which can be regarded as bum. This only occurs when the tissue has
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been irradiated beyond its tolerance limit. Two types of radiodermatitis are usually seen — (i)
acute radiodermatitis which presents the usual changes of acute inflammation with erythema,
varying degrees of oedema and exfoliation. These usually develop on or about the 5th day. If
the exposure dose is highly excessive, it may cause necrosis in both epidermis and dermis. In
such cases a slough is formed, which on separation leaves a deep indolent ulcer, (ii) Chronic
radiodermatitis may occur if small doses of irradiation are given for too long a time or if acute
radiodermatitis has occurred a few years ago which may leave chronic radiodermatitis as legacy.
In this condition the skin shows irregular pigmentation or depigmentation in certain areas,
telangieactases and small indolent ulcers. Microscopically there may be atrophy and flattening
of the epidermis, but the dermis becomes dense and sclerotic. Skin appendages may disappear
and the small cutaneous vessels may become dilated. The most important feature of this chronic
radiodermatitis is its liability to grow into cancers.
6.
COLD BURNS are caused by exposure to cold which include freezing injuries (frostbite)
or non-freezing cold injuries e.g. chilblain (localized painful erythema in the fingers, toes or ears
produced by cold damp weather), trench foot (seen in soldiers due to prolonged exposure to
extreme cold water combined with circulatory disturbances predisposed by tight clothing, garters
or ill-fitting shoes) and immersion foot (a condition resembling trench foot occurring in
shipwrecked persons who have spent protracted periods in waterlogged boats). It is usually a
concern in military populations, though it is being encountered increasingly in the civilian
population with the rise in popularity of winter sports. Cold bums also cause coagulative necrosis
of the tissue.
FROSTBITE results in actual freezing of tissues with the formation of ice crystals. Mostly
the skin and subcutaneous tissue of the hands, feet, ears and nose are affected. When these
parts are exposed to low temperatures for prolonged period of time such injury may occur.
Tissue necrosis following frostbite is related primarily to the mechanical effects of ice crystals,
cellular dehydration and microvascular occlusion. Crystals of ice appear both intracellularly and
extracellularly in any tissue. As freezing progresses intracellular water shifts to the extracellular
space and leads to intracellular dehydration with increase in intracellular concentrations of
electrolytes, proteins and sugar. The resulting hyperosmolarity leads to denaturation of
intracellular proteins. The skin is relatively resistant to these damaging effects, though other
tissues like nerves, muscles and blood vessels are quite sensitive. Clinical features of frostbite
are described by various degrees. First-degree frostbite is hyperaemia and oedema of the skin
without necrosis. Second-degree frostbite causes hyperaemia, vesicle formation and partial thickness
necrosis of the skin. Third-degree frostbite causes necrosis of the entire skin thickness and may
extend to a variable degree into the underlying subcutaneous tissue. Fourth-degree frostbite means
necrosis of full thickness of the skin including subcutaneous tissue and all underlying structures
including muscle and bone. This leads to gangrene of the affected part.
PATHOLOGY of bums.— For advantage of description, pathological changes of bums
are divided into 2 heads — I. Local changes and II. Systemic changes.
I.
Local changes.— These can be described under 4 heads — 1. Severity of bum, 2. The
extent of bum, 3. Vascular changes and 4. Infection.
1.
SEVERITY OF BURN.— Bums are classified into 3 grades or degrees according to
the depth of necrosis. In first-degree bum there is simply hyperaemia of the skin with slight
oedema of the epidermis. There is only microscopic destruction of the superficial layers of the
epidermis, which are desquamated within a few days. It is of little clinical significance as the
BURNS
63
superficial layers of epithelium are soon replaced from the basal layers, so that there is no
scarring. First-degree bums rapidly heal if the patient avoids further exposure to source of heat.
First-degree bums are not considered while estimating the magnitude of bum for purposes of
planning intravenous fluid replacement. In second-degree burns the entire thickness of the
epidermis is destroyed. Blebs or vesicles are formed between the separating epidermis and
dermis. Vesiculation is the hall mark of the second-degree bum. Second-degree bum is further
subdivided into (a) mild and (b) severe varieties. In mild cases enough epithelium is left in the
hair follicles and dermal glands to provide new cells for resurfacing the burned area. In severe
cases, there is not enough epithelium left, so that resurfacing of the burned area is not possible
and skin grafting becomes necessary. In third-degree bum there is complete destruction of the
epidermis and dermis with irreversible destruction of dermal appendages and epithelial elements
including the sensory nerves. Skin grafting becomes obligatory to cover the area.
Another type of classification is in vogue to describe severity of bum. In this classification
two degrees are considered — (a) partial thickness bum and (b) full thickness bum.
(a) Partial thickness bum is that type of bum in which the superficial layers of the skin e.g.
the whole of epidermis and sometimes the superficial part of the dermis become destroyed. But
there are enough epithelial cells surrounding the hair follicles or sweat glands from which
regeneration may take place. So in partial-thickness bum, spontaneous regeneration of epithelium
is expected and skin grafting is not necessary.
(b) Full thickness burn.— In this condition the whole thickness of the skin including the
epidermis and the total depth of the dermis is destroyed. Spontaneous regeneration of epithelium
is not possible, so development of scar tissue and contractures are inevitable unless skin grafting
is performed in right time. As sensory nerves are also destroyed in full thickness bum, sensation
is lost in full thickness bum and pin prick test (by firmly pressing a needle over the burned
area) will be negative. To the contrary sensation of the skin remains and pin prick test will be
positive in partial thickness bum. It must be remembered that since skin varies in thickness in
different parts of the body, application of the same intensity of heat for a given period of time
will result in a bum which will vary in depth depending on the thickness of the skin in the
local area and on the degree of development of the dermal appendages (sweat glands and hair
follicles) and dermal papillae.
2.
EXTENT OF BURN.— The length and width of the bum wound is expressed as a
percentage of the total surface area displaying either second or third-degree bum. The extent of
bum is most commonly estimated by the 'rule of nines'.
'Rule of nines' for estimating percentage of body surface involved in bums are as follows:—
Anatomic area
Percentage of body surface
Head, face and neck
9%
Right upper extremity
9%
Left upper extremity
9%
Right lower extremity (thigh - 9%, leg and foot - 9%)
18%
Left lower extremity
18%
Anterior trunk ( chest - 9%, abdomen - 9% )
18%
Posterior trunk ( upper half - 9%, lower half - 9% )
18%
External genitalia
1%
Of course the above-mentioned 'rule of nines' is applicable only to the adults. This rule
does not apply strictly to infants and children as the surface area of the head and neck of children
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is significantly larger than 9%. For example in one year old child the surface area associated
with head is about 19% as compared to only 7% in adults. In contrast, each lower extremity
represents only 13% of the total body surface area in these patients.
3.
VASCULAR CHANGES.— It is of great
importance in the burnt area. Two main changes are
noticed —
There is dilatation of small vessels due to direct injury
to the vessel walls and to local liberation of histamine.
This increases blood flow to the injured part as seen in
case of inflammation. This increased blood flow is not
followed by stasis as happens in inflammation.
Capillary permeability is greatly increased. Due to this,
plasma rich in protein pours out continuously in large
amount. This exudate collects in blisters or begins to dry
to form a dry brown crust which protects the wound.
This crust separates in one or two weeks in case of
superficial bums, but it takes longer times in case of deep
bums.
4.
INFECTION.—
skin is sterilized. In case of first-degree bums the intact
epidermis will act as barrier against infection. But in case
of deep bums, if the crust which protects the raw wound
is broken virulent organisms may enter the bum wound
to cause severe infection. It is a very suitable nidus for
flourishing organisms in the raw wounds. Moreover
general malnutrition, loss of plasma and blood volume
Pig. 6.1.— A diagrammatic representation and anaemia in extensive bums severely handicap the
to show how to apply Rule of Nines’. defence mechanism against infection. It is in fact the
See the text for details.
challenging task in front of the surgeons to fight against
this infection. Bacteriaemia and bacteriaemic shock are
the second commonest cause of death in bum following oligaemic shock. This usually occurs
between the second and third weeks.
n. Systemic changes.— These can be conveniently described under four heads — 1.
Shock, 2. Biochemical changes, 3. Changes in blood and 4. Systemic lesions.
1.
SHOCK.— This is the most important effect of bums. Various types of shock are come
across in burns, but by far it is the oligaemic shock which is the most important and claims
majority of lives following bums.
(a)
Oligaemic shock.— The direct effect of heat as well as liberation of vasoactive materials
from the area of injury increases capillary permeability, which permits loss of fluid and protein
from the intravascular compartment into the extravascular tissue. These volume shifts occur in
direct proportion to the extent of bum and are clinically apparent as oedema and blebs. Owing
to the outpouring of fluid there is remarkable concentration of blood as shown by haemoglobin
concentration. This leads to olegaemic shock and oxygen starvation of the tissues. There is an
immediate apparent increase in the number of red cells and the haemoglobin level. Protein loss
and electrolyte imbalance soon become apparent. Sludging of the blood may occur with
BURNS
65
intravascular agglutination of red blood cells into smooth firm clumps. This may reduce the red
cell volume and thus aggravates the state of shock. Though there is haemoconcentration, yet the
sodium chloride content of the blood tends to fall owing to great losses in the exudate. The
potassium level usually increases, probably due to massive cell destruction and release of
intracellular fluid. The result of these changes is bum shock. The intense heat destroys the red
blood cells and causes haemolysis which may be massive and accompanied by haemoglobinuria.
These factors may result in ischaemia of important organs particularly the liver and kidney, so
that acidosis and uraemia may develop. This leads to stimulation of adrenal cortex with immediate
rise in urinary excretion of 17-Ketosteroids.
Besides oligaemic shock, other varieties of shock are also come across in burns. These are —
(b) Neurogenic shock, due to severe pain and apprehension.
(c) Cardiogenic shock.— Cardiac output falls in the early postbum period initially as a result
of marked increase in peripheral resistance and later on as a result of decreased blood volume
and also increased viscosity. The increase in blood viscosity results from the combined effect of
increased haematocrit and aggregation of red cells, white cells and platelets. Depression of
myocardial function by a humoral factor has been incriminated as a cause of impaired cardiac
output in patients with extensive bums. However hypovolaemia causing impaired venous return
is an obvious cause of diminished cardiac output. Hypovolaemia and diminished cardiac output
cause decreased renal blood flow and oliguria which may culminate in acute renal failure. The
same causes may also impair blood flow to other organs.
(d) Bacteriaemic shock is mainly due to infection and release of toxic material absorbed
from the burnt area. The toxic symptoms of bums e.g. fever, delerium, vomiting and bloody
diarrhoea are usually caused by both infection and absorption of toxic material.
2. BIOCHEMICAL CHANGES.— These have already been described to certain extent in
the above section.
(i) Electrolyte imbalance — becomes obvious in the form of low sodium and chloride
concentration and high potassium level in the blood.
(ii) Hypoproteinaemia is obvious due to excessive loss of plasma protein as a result of
increase in the capillary permeability and infection.
(iii) Hyperglycemia may often develop in bums.
(iv) There will be rise in blood urea, N.P.N. and creatinine levels due to kidney damage in
extensive bums.
3. CHANGES IN BLOOD.— These have also been described above in the section of
'shock'.
(i) Haemoconcentration is due to outpouring of serum. Haemoglobin level may rise to 150%
in severe bums.
(ii) Apparent increase in the number of red cell is also due to outpouring of plasma.
(iii) Sludging of blood may occur due to intravascular agglutination of R.B.Cs.
(iv) An abrupt fall in the eosinophil count during the first 12 hours is very characteristic of
bums. The level of fall has no relation to the extent of bum. In the course of 24 hours the count
should begin to rise. Eosinophil count may give an indication to the prognosis of the case. A
persistent eosinopenia, failure in the early rise after the initial drop and lack of late rise in the
eosinophil count indicate bad prognosis.
(v) Aggregation of red cells, white cells and platelets is a common finding in bums. This
increases blood viscosity.
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(vi)
Anaemia.— There is immediate red cell destruction in the early postbum period. The
amount of destruction is in direct proportion to the extent of third-degree bum. There is also
continuous red cell loss of variable extent during the first 5 to 7 postbum days. 8 to 12% loss of
red cell mass per day is the general measurement, although some investigators measure higher
loss rates.
(vii)
A biphasic alteration of the coagulation system is also seen in bums. There is an early
marked depletion of platelets and depression of fibrinogen level. This is accompanied by a parallel
increase in fibrin split-product level. There is also an increase in factors V and VIII. Particularly
when infection ensues, intravascular coagulation may be seen.
4. SYSTEMIC LESIONS.— Various organs in the body are involved in bums.
(i) The liver may show numerous areas of focal necrosis. In the necrotic areas the cells
may contain intranuclear inclusions and Councilman bodies similar to those found in yellow
fever. In fact in majority of cases of bums, liver necrosis can be detected.
(ii) Kidney is often involved due to low blood perfusion. Moreover large amount of blood
pigment may be deposited in the collecting tubules of the kidney as a result of haemolysis. In
severe cases there may be haemoglobinuria. Gradually oliguria and anuria may develop and
the patient may die of uraemia.
(iii) Adrenals become slightly enlarged and deeply congested. Chemically one may find
decrease in cholesterol and lipid content of the gland. In severe bums there may be petechial
haemorrhages and small areas of focal necrosis. Due to thrombosis bilateral necrosis of adrenal
cortex may take place in severe cases. In post-mortem examination after majority of deaths
following bums one may find shrunken glands with necrosis and haemorrhage.
(iv) The gastrointestinal tract also responds to bum injury, which of course is related to the
extent of bum. Gastric and duodenal mucosal changes indicative of focal ischaemia can be
observed as early as 3 to 5 hours after bums. This is due to diminished mucosal blood flow.
Acute ulceration of the stomach and duodenum has been noticed as a common complication
of major thermal injury. These ulcers were first described by Curling in 1842 and is reported to
occur in 25% of hospitalised burn cases. Such ulcers are prone to cause gastrointestinal bleeding.
But it must be remembered that 85% of such haemorrhage is due to bacteraemia. The decreased
incidence of Curling's ulcer is due to reduced frequency of major septic complications,
prophylactic introduction of antacids or H2 receptor antagonists therapy into the stomach via
nasogastric tube and the improved provision of nutritional supplements allowing more rapid
healing of these acute mucosal erosions. Ulcers ultimately may develop in the duodenum and
upper jejunum.
Acute ulceration of the colon has been recognized in severe bum patients. A few of these
lesions may penetrate the full thickness of the colonic wall upto the serosa. Perforation has not
yet been reported.
(v) Alterations of pulmonary function vary according to the extent and location of the bum
and the presence or absence of inhalation injury. Pulmonary vascular resistance increases in the
immediate postbum period. So pulmonary oedema usually does not occur even when large
volumes of fluid are infused. The actual changes in pulmonary function following bums are
hyperventilation and pulmonary insufficiency which may be of such magnitude as to require
mechanical ventilatory support.
(vi) A change in the endocrine pattern is seen in bum patients. There is elevated glucagon,
cortisol and catechplamine levels. Insulin and triiodothyronin levels are depressed. These cause
BURNS
67
a change in the metabolic rate, glucose flow and negative nitrogen balance. Endocrine function
can be further influenced by sepsis and other complications in which there may be exaggeration
of the changes.
(vii) Neurogenic changes are not commonly seen in burn injuries. There may be some delirium,
disorientation due to less blood flow to the brain and electrolyte imbalance. However specific
neurologic changes are most commonly seen in patients with high voltage electrical bums.
(viii) Immunologic impairment is often seen in patients with bums over 50% of total body
surface. This predisposes the burn patient to a high incidence of infection, which may in turn
further impair the patient's ability to defend against invasion by organisms. There is depression
of the immunoglobulin level in the early postbum period. Lymphocyte level is also depressed,
with a relative decrease in T cells and a relative increase in B cells. Impairment of neutrophil
function also occurs.
TREATMENT
This is conveniently described under three headings — I. Treatment of shock, II. General
treatment and III. Local treatment of bum wound.
I. TREATMENT OF SHOCK.—
1. Sedation.— Sedative and analgesic medications are almost always required in bum
patients. Bum is a very painful condition and moreover sedation is also valuable in shock. As
the patients are almost always in shock, sedatives should be given by intravenous route and at
an absolute minimum dosage. This should be administered during the first 4 to 5 days.
Administration by intravenous route ensures rapid and predictable concentration of the drug in
the central nervous system. The dosage should be minimum to prevent depression of
cardiopulmonary function and to allow evaluation of the sense of the patient, which is an
important indicator of adequacy of fluid replacement. The dosage can be reduced markedly
after 48 hours. Usually injection morphin l/4th gr or less is administered intravenously. In case
of children barbiturates are preferred.
2. Fluid resuscitation.— This should be started as soon as possible in all adults with
bums of 15% or more of the total body surface. In case of children bums above 10% should be
given fluid resuscitation. As the patient is in shock, the veins are usually collapsed and
venesection is often required. A large-calibre cannula is pushed into a vein (which lies beneath
unbumed skin) of sufficient size to permit fluid flow unimpeded.
Blood transfusion is required when bums involve more than 20% of full thickness or 40%
of partial thickness of total body surface. This is due to replace the destroyed R. B. Cs. Studies
by several investigators have indicated that during the first 24 hours of postbum period colloidcontaining fluids are not essential for resuscitation as it is not retained within the circulation or
exerts greater restorative effect on cardiac output than an equal volume of colloid-free electrolyte
containing fluid such as Ringer's lactate solution. But subsequent studies have shown that the
colloid solutions not only restore cardiac output more rapidly but also is more efficient in
adequate organ perfusion. This is due to more rapid replacement of plasma volume deficits
during this time. However on the 2nd day both crystalloid and colloid solutions are equally
effective in restoring cardiac output and intravascular volume.
The goal of bum patient resuscitation is the maintenance of vital organ function as soon as
possible. Several formulas have been proposed for estimating the patient's fluid needs and these
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are based on the weight of the patient and the extent of bum. The formula advocated by Moore
is that in 1st 24 hours in adult patients Ringer's lactate solution is given 1000 to 4000 ml and
normal saline 1000 ml, 5% dextrose solution 1500 to 5000 ml and colloid containing fluid in the
form of plasma or plasma substitutes 7.5% of body weight; In 2nd 24 hours same amount of
Ringer's lactate solution, normal saline and dextrose solution are given whereas colloid-containing
fluid is reduced to 2.5% of body weight. Evans' formula is that in 1st 24 hours normal saline is
given 1 ml/kg/% bum, 2000 ml of 5% dextrose and colloid-containing fluid 1 ml/kg/% bum; In
2nd 24 hours normal saline is given Vi the amount of 1st 24 hours requirement, colloid-containing
fluid is also given the Vi the requirement of 1st 24 hours, whereas 5% dextrose is given 2000 ml.
In Brooke's formula in 1st 24 hours Ringer's lactate solution is given 1.5 ml/kg/% bum, colloidcontaining fluid 0.5 ml/kg/% bum and 2000 ml of 5% dextrose solution. In 2nd 24 hours Vz to
%th of 1st 24 hours requirement of Ringer's lactate and colloid-containing fluid, whereas same
2000 ml of dextrose saline are given.
The rate and amount of transfusion as well as efficacy of intravenous resuscitation are
assessed by repeated red cell volume and haematocrit estimations and at the same time by
hourly monitoring of vital signs, general condition and urinary output. Urinary output is a good
reflection of adequacy of resuscitation. Oliguria should always be treated by increased fluid
administration. These patients usually do not require any diuretic except in 4 categories — (i)
those with high voltage electrical bum, (ii) those with associated mechanical soft tissue injury,
(iii) those with particularly deep bums involving muscles and (iv) those with extensive bums
and who remain oliguric inspite of giving excess fluid volumes than estimated needs. In first 3
categories there is chance of heavy loads of haemochromogens in their urine and are prone to
develop acute renal failure unless the urine output is maintained with diuretic. Fluid should be
infused at the rate needed to achieve an hourly urinary output of 75 ml to 100 ml. The diuretic
which is commonly used is mannitol of 1 ampule (12.5gm) added to each litre of intravenous
fluid until the desired level of urinary output is achieved. There is usually limitation of
measurements of central venous pressure. However chest X-rays should be obtained at least
daily during resuscitation to exclude pneumonia or other pulmonary complications. Serum
electrolytes, blood gases and other base line blood studies should be performed at frequent
intervals.
For bums involving more than 20% of full thickness or 40% of partial thickness of total
body area, whole blood transfusion should be given and this whole blood is considered as part
of colloid-containing fluid and may be given upto 50% of total.
3.
Maintenance of airway.— Patients with bums often exihibit signs and symptoms of
hypoxia which may range from pronounce tachypnoea to respiratory arrest and coma. The
diagnosis is confirmed by analyzing the concentration of carbondioxide in the blood. Treatment
includes administration of 100% oxygen with ventilatory support.
Upper airway obstruction may occur in patients with bums of head and neck during first
48 hours. Such obstruction is due to soft tissue oedema of oral pharynx and vocal cords due to
exposure to hot fumes. Direct thermal injury to the lower respiratory tract is very uncommon,
as nose and oral pharynx are quite efficient heat exchangers allowing cooling of inhaled hot gas
prior to its entrance into the trachea. Though lower respiratory tract injury does occur when the
patients are injured by superheated steam as it is difficult to extract heat from liquid.
Impending upper airway obstruction is treated by immediate insertion of endotracheal tube.
Tracheostomy may be needed when endotracheal intubation becomes impossible or
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contraindicated. Once introduced endotracheal tube is not removed until 3rd postbum day, since
reintubation becomes technically difficult.
II.
GENERAL TREATMENT.— These include — 1. Escharotomy and fasciotomy, 2. Tetanus
prophylaxis, 3. Antibiotics, 4. Nutritional support, 5. Gastric decompression and 6. Treatment of
G.I. complications.
1. Escharotomy and fasciotomy.— Circumferencial third-degree or full thickness bums
of the extremities or thoracic wall may form an unyielding crust (known as eschar) which exerts
pressure on the blood vessels causing diminished peripheral pulses and decreased skin
temperature with oedema (due to venous obstruction). The clinical signs of such diminished
distal flow include cyanosis, impaired capillary refilling and progressive neurologic signs
particularly paresthesia. Restriction of chest wall motion to the point at which ventilatory
exchange is impaired is an indication of the need for a chest wall escharotomy.
Escharotomy is performed as a ward procedure and neither general nor local anaesthesia is
required. The eschar, which is insensitive, is incised on either midlateral or midmedial line. The
incision should extend along the entire length of the burned area and carried down deep through
the eschar and the superficial fascia to a depth sufficient to allow the cut edges of the eschar to
separate. The bleeding is usually minimal and can be controlled by electrocoagulation. Chest
wall escharotomies are made on the anterior axillary line bilaterally extending from the clavicle
to the costal margin. The need for limb escharotomies may be reduced by continuous elevation
of the burned extremity and active motion of it for 5 minutes every hour. If escharotomy has
been performed, constant coverage of the escharotomy wound with a topical antimicrobial agent
is essential.
Sometimes escharotomy may not result in improvement of blood flow to the peripheral
part. In these cases fasciotomy is required. When oedema occurs beneath the investing fascia
such fasciotomy may be required. Fasciotomy should be performed under general anaesthesia
and the fascia of all involved compartments should be adequately released. Such fasciotomy is
usually required in severe bums with extensive damage to the underlying fat and muscles.
Fasciotomy is also required in the treatment of electrical bums where there is extensive muscle
injury. Fasciotomy incisions, like escharotomy incisions, should be protected with bandage soaked
in topical antimicrobial agent.
2. Tetanus prophylaxis.— All bum injuries should be considered contaminated and
tetanus prophylaxis is obligatory. Intramuscular administration of tetanus toxoid in the dose of
0.5 ml usually provides adequate prophylaxis. But this is effective only if the patient receives a
booster dose within the preceding 10 years. In case of absence of active immunisation within 10
years prior to bum injury 250 to 500 units of tetanus immunoglobulin (human) should be
simultaneously administered at another site using different syringe and needle.
3. Antibiotics.— In bums, microorganisms contaminate the wound. These organisms
will proliferate if topical chemotherapeutic agents are not applied. Usually gram-positive
organisms colonize in the burn wounds. That is why there is a place of prophylactic
administration of penicillin to patients with bums. But such systemic administration of antibiotics
should be given on 1st or 2nd day, as the full thickness bum becomes relatively avascular after
48 hours. Subsequently gram-negative bacteria may also colonize. Once necrosis occurs, the
wound is essentially avascular, which prevents effective delivery of systemic antibiotics if
infection occurs. The pattern of bum wound infection has changed over the past several decades.
Before the availability of penicillin, streptococci and staphylococci were the predominent
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organism. By the late 1960s, gram-negative bacteria, primarily pseudomonas species emerge as
the dominant organism. Microbial species colonise the surface of the wound and may penetrate
the avascular eschar. Bacterial proliferation may occur beneath the eschar at the viable-nonviable interface, leading to subeschar suppuration and seperation of the eschar. In a few patients
micro-organisms invade the underlying viable tissue producing systemic sepsis. The bum wound
is a potential portal for bacterial entry into the blood. P. aeruginosa produces the protrotypical
lesion of invasive bum wound sepsis. Topical antibiotic has a significant role to play in bum
infection, though systemic infections are not uncommon and such infections have actually
increased as principal causes of death.
The most common site of involvement in the bum patient is the lungs. Bronchopneumonia
in burn patients is commonly caused by opportunistic organisms especially gram-negative
bacteria. Haematogenous pneumonia may also begin relatively late in burn patients due to
haematogenous spread of microorganisms from a remote septic focus. Bronchial secretions should
be cultured and antibiotic treatment is begun on the basis of the sensitivity test. Usually an
aminoglycoside and a semisynthetic penicillin are administered as the common causative
organism is often a strain of Pseudomonas. It must be remembered that prophylactic antibiotics
are to be avoided and antibiotics should be administered only on the basis of a clinical or
laboratory diagnosis of infection. Indiscriminate use of antibiotics will develop antibiotic
resistance in the bacteria present in the burn wound and elsewhere. From burn wound
haematogenous dissemination of microorganisms may occur. To minimise such dissemination
of organisms and development of bacteremias, antibiotics active against both gram-positive and
gram-negative organisms should be administered to patients undergoing surgical debridement
of the bum wound or bum wound excision. In bum patients with sepsis, blood cultures should
be obtained and proper antibiotic should be administered.
4.
Nutritional support.— In case of all major injuries increased metabolism or
hypermetabolism takes place. Resting metabolic rate approaches approximately twice normal in
patients with burns of more than 50% of total body surface. Such hypermetabolism is also
manifested by increased oxygen consumption, elevated cardiac output, increased core
temperature, wasting of body mass and increased urinary nitrogen excretion. The metabolic
needs of the bum patients can be measured by indirect calorimetry. Adult patients with bums
of over 40% of the total body surface such measurement estimates about 2000 calories per square
meter of body surface per day.
So one must be careful in providing adequate exogenous calorie and nitrogen to prevent
excessive catabolism in bum patients. Wherever possible tube feeding should be utilised to
provide nutritional needs of the patients. Feedings may be accomplished by insertion of a small
silastic nasogastric feeding tube through which nutrients are delivered 24 hours a day with a
constant delivery pump. If diarrhoea or ileus precludes gastrointestinal feeding, parenteral
nutrition should be initiated using an intravenous cannula placed in a large-calibre high-flow
central vein. Solutions of synthetic aminoacids mixed with hypertonic solutions of glucose are
primarily used with blood sugar levels frequently monitored and kept below 200 mg/100 ml.
Sudden intolerance of a previously well-tolerated glucose load is an early sign of sepsis and a
careful search should be made for source of infection and its adequate cine. 500 to 1000 ml of
fat emulsion is also given twice a week to prevent the development of essential fatty acid
deficiencies. There always remains a high risk intravenous sepsis at the site of intravenous
cannula, the site of which should be changed every 48 to 72 hours.
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5. Gastric decompression.— Majority of patients with more than 20% of total body
surface area bums will develop a reflex paralytic ileus during the 1st 24 hours. Intestinal motility
is gradually lost after 12 hours of bum injury. Vomiting in such a patient carries a high risk of
pulmonary aspiration. That is why patients with major bums require introduction of a nasogastric
suction to effectively decompress the stomach and upper small intestine until intestinal motility
can be demonstrated. Moreover patients with major burns are at risk of haemorrhagic gastritis
due to increased stress. So gastric aspirates should be monitored frequently for the presence of
frank blood. Antacid may also be instilled through the nasogastric tube to prevent superficial
erosions of the gastric mucosa. Cimetidine, a H2 receptor antagonist which suppresses gastric
acid secretion may be used in this connection to prevent or to treat stress gastritis.
6. Treatment of G. I. complications.— As mentioned in gastric decompression
cimetidine may be introduced through nasogastric tube to prevent occurrence of acute ulceration
of the stomach and duodenum. This is almost always required with bums more than 35% of
body surface. When gastrointestinal motility returns, the antacid may be given orally till the
extent of bum is reduced by healing or by grafting to less than 35% of body surface. 400 mg of
Cimetidine may be given parenterally every 4 hours if there is intestinal ileus and G. I. feeding
is contraindicated. If major upper gastrointestinal haemorrhage occurs, the patient should be
promptly treated with iced saline solution lavage. When haemorrhage cannot be controlled by
conservative means, surgical operation is indicated. The abdominal incision may be placed on
the bum wound. After opening the abdomen gastrotomy or duodenotomy is performed to see
the bleeding ulcer and to achieve haemostasis by oversewing the base of the ulcer. During closure,
the subcutaneous tissue and the skin are left open to prevent soft tissue infection. Blood volume
replacement should always be considered in these cases.
Acute ulceration of colon usually heal by itself when bum wound has been adequately
taken care of.
III. LOCAL TREATMENT.—
1. First-aid measures.— The patient should be immediately removed from source of
heat. Cold clean water should be applied to the burned area immediately and is continued
every 5 minutes.
2. Burn wound care.— After proper resuscitation, attention should be directed to the
burn wound. It should be cleansed with a surgical detergent and all loose nonviable skin should
be trimmed away. The second-degree bums or partial thickness bums usually present as vesicular
lesions. The overlying blister should be punctured and the upper nonviable skin is removed.
Such debridement should usually be performed without anaesthesia, but with tremendous aseptic
care. At the time of wound cleansing, the entire wound should be inspected. Silver nitrate must
be used soon after injury, before bacteria have proliferated on the wound. Although gram-positive
organisms are slightly less susceptible to silver nitrate, true resistance does not occur. Its most
serious disadvantages are the associated electrolyte imbalances. Cerium nitrate has been shown
to be an effective topical antimicrobial drug and currently is undergoing clinical evaluation.
Majority of the topical antimicrobial agents appear to be equally effective in controlling burn
wound infection when applied early before heavy colonization has occurred. Only mafenide
acetate is able to penetrate the eschar and is capable of suppressing dense bacterial proliferation
beneath the eschar surface. It is particularly effective against clostridia. The main disadvantage
of this medicine is that it results in hyperchloraemia which is compensated for by an increase in
ventilation and subsequent respiratory alkalosis.
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The nonviable skin of the third-degree or whole thickness bum injury is known as the eschar.
Usually the eschar remains tightly adherent to the underlying subcutaneous tissue and its removal
may cause significant pain and severe haemorrage. So only loose eschars are removed initially
without anaesthesia and blood loss. The remaining eschar is left intact and bacterial colonization
is prevented by applying topical chemotherapeutic agent. Following cleansing and debridement
the topical agent of choice is applied. The choice is now in front of the surgeon to adopt either
exposure method or closed method of treatment.
In EXPOSURE METHOD, the burned area is left uncovered and the topical agent is applied
every 12 hours. A crust forms on the surface of the wound to protect the raw area. This crust
later on separates. The date of separation depends on the depth of the bum. This method is
particularly suitable for bums of the head, face and neck, though it may be applied in case of
bums of the body or trunk.
In CLOSED METHOD, the wound is covered by dressings in 3 layers. The inner layer is
nonadherent and antiseptic and it is either oily based 'tulles' or water based cream. Tulles usually
contain topical chemotherapeutic agent e.g. chlorhexidine, soframycin or nitrofurazone. Such
dressing does not tend to adhere and cause less pain at the time of change of dressing. 0.5%
silver nitrate soaks may be used and such occlusive dressings are changed 2 or 3 times daily
and kept always moistened by application of additional 0.5% silver nitrate solution. The second
layer is of ordinary sterile cotton gauze and the 3rd layer is the cotton bandage.
In case of burned hand, the part is enclosed in polythene bag. The band is elevated and
active exercise is encouraged to reduce oedema and to maintain full range of movement to
prevent contracture to develop.
In case of bums of the face and scalp, the exposure method is applied and 1% povidone
iodine lotion is applied daily.
Even with open treatment topical therapy is essential as this prevents organism to penetrate
the eschar and ultimately extend down to the viable-nonviable tissue interface. At this site further
microbial proliferation takes place. The topical agents should be used selectively to meet the
individual patient's wound care needs. In this respect Sulfamylon bum cream, silvadene bum
cream and 0.5% silver nitrate soak have been introduced which have good bacteriostatic effect.
Particularly Sulfamylon bum cream is effective against pseudomonas organisms. Sulfamylon is
chemically mafenide acetate and this may be applied for open treatment of bum wounds. This
cream has proved effective against a wide range of gram-positive and gram-negative organisms
as well as most anerobes. This drug actively diffuses through the eschar providing protection in
the depth of the eschar at the interface between the viable and the nonviable tissues. Silvadene
is chemically silver sulphadiazine. It has essentially the same bacterial spectrum as the sulfamylon
cream. Betadine is also very popular nowadays which is a water soluble topical antiseptic
complex of polyvinyl pyrolidone (povidone) iodine. It is effective against wide range of grampositive and gram-negative organisms as well as some fungi. Serum nitrate is also being used
recently in bum dressing especially in full thickness bums. It offers a hard effect in the burned
skin and reduces some of the cell-mediated immunosuppression that occurs in bum.
If the bum wound becomes very much infected, its treatment depends on the extent and
depth of the septic process. In these cases often systemic antibiotic therapy is required depending
on the culture and sensitivity result available from the bum wound. If the infection is focal or
even multifocal, antibiotic solution can be infused directly into the infected wound. A solution
of carbenicillin is infused every 12 hours beneath the eschar using a No. 20 spinal needle. If
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73
focal infection spreads deep into the subcutaneous tissue, excision of the infected wound should
be advised. Prior to such excision, two subeschar injections of carbenicillin are carried out 6
hours apart.
3.
Skin grafting.— The goal of bum wound care is the timely closure of bum wound.
When the bum wound is covered with red and finely granular granulation tissue with a surface
bacterial count of less than 105/Sq. cm of wound surface and absence of residual nonviable
tissue, it is ready for split thickness skin graft (autograft). At this time the dressings are removed
in the operation theatre. Warm packs are applied and autograft skin is applied directly to the
areas. Pinch grafts are often applied in bum cases.
As wound maturation proceeds, crusts separate from areas of second-degree bum and the
eschar loosens and sloughs from areas of third-degree bum. These processes can be hastened by
daily wound care. In case of full thickness bums the eschar takes about 2 to 3 weeks to separate. If
healthy granulation tissue is seen after separation of eschar, early skin grafting should be performed
to prevent scarring and contractures. Sometimes following the eschar separation the wound may
not be very healthy. Skin grafting (autograft) is not ideal in these cases. During the time interval
between the eschar separation and when the wound is ready for autograft, the open wound of
granulation tissue can be temporarily covered with a homograft or heterograft. This is known as
physiologic dressing or biologic dressing. The homograft is usually obtained from cadavers and the
grafts are spread on fine mesh gauze that is thinly impregnated with petrolatum and then
refrigerated for upto 2 weeks. Usually porcine heterograft is used. Synthetic skin substitutes may
also be used. Polymer of polyvinyl alcohol, polyurethane foam, collagen films etc. are being used
as synthetic skin substitutes. A bilaminate membrane has been recently introduced which is
composed of a temporary silastic epidermis and porous collagen chondroitin 6-sulphate fibriller
dermis. Following grafting, the dermal component is encroached with fibroblasts and vessels from
the wound bed, whereas the silastic epidermis remains firmly adherent, but can be removed when
autograft is available for transplantation. The advantages of the temporary biologic dressings
are — (i) that they contribute to the prevention and control of infection, (ii) that they preserve
healthy granulation tissue, (iii) that they decrease evaporative water loss, (iv) that they cover
exposed sensory nerves and therefore decrease pain, (v) that they protect neurovascular tissue
and tendons and (vi) that they maintain proper joint function. When adherence of the temporary
biologic dressing is decreased, the granulation tissue may be assumed to be in optimal condition
for autograft. These biologic dressings are removed within 5 days and are replaced with new
physiologic dressing until autografting can be accomplished. During changing of such dressings
further debridement of the wound is possible to make the wound more tidy.
Some clinicians utilise these biologic dressings to immediately cover superficial seconddegree bums. This decreases hospitalization, but one must be sure that the wound is indeed a
partial thickness and not a full thickness bum.
As soon as the bum wound has been adequately prepared by the use of temporary
physiologic dressings as described above, it should be covered with the patient's own skin
(autograft). The biologic dressing is removed in the operation theatre and following the
establishment of haemostasis by application of warm packs, autograft skin is applied directly to
the bum wounds from where biologic dressings have been removed.
About the type of autograft whether partial thickness or full thickness skin graft is to be
used, a dictum should be remembered — 'the thicker the skin, the better the cosmetic result'
and 'the thinner the skin, the better the take'. When the area to be grafted is more and the
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donor sites are limited, mesh or expanded grafts should be utilised. In this the lifted skin grafts
are placed on plastic carriers. A series of parallel incisions is made in the sheet graft, allowing
expansion of upto 6 times the area of the original donor site. These are now directly applied to
the wound. Mesh graft is covered with occlusive dressings which are kept wet with antimicrobial
solution e.g. 0.5% silver nitrate. The small interstices of the mesh grafts are rapidly filled by
epithelialization within 4 to 8 days resulting in a somewhat thinner but physiologically functional
skin cover. Such mesh grafts should not be used on the face, hands, feet and flexion creases as
these are not cosmetically good and cannot withstand recurrent trauma.
EXCISION of the bum wound is an attractive alternative to the conventional treatment
mentioned above. Excision of the bum wound with immediate skin graft coverage may shorten
hospital stay, but this should be weighed against the disadvantages like anaesthetic risk, blood
loss and operative stress. Such excised wounds are also susceptible to infection. Recently method
of tangential excision has been introduced. Successive thin layers of bum tissue are removed
with a guarded skin knife or dermatome until all nonviable tissue has been excised as indicated
by uniform capillary bleeding from the entire wound. Such wound is closed by autografting. A
modification of tangential excision has been proposed in which successive layers of bum tissue are
dissected off till first sign of capillary bleeding appears. Now the wound is covered with biologic
dressing with an antimicrobial solution. The patient is again brought to the operation theatre on
the 4th day for further excision if necessary. The patient is again taken to the operation theatre
7 days later to remove the biologic dressing and to apply autograft.
4.
Physical therapy and rehabilitation.— The major local problem of bums is formation
of contractures and deformities. To prevent these problems a progressive physical therapy programme
should be started immediately after hospital administration. In this programme the care is
adopted to maintain normal range of joint movements in and around bum areas. Various
exercises are conducted in the direction opposite to that of anticipated deformity. Prolonged
immobilization must be avoided. Early movement following skin grafting should be encouraged.
Splints may be manufactured to maintain anticontracture positions during sleep. Upper
extremities are more susceptible to the deleterious effects of contracture formation than the lower
extremities. Daily range of movement evaluation and appropriate daily exercises achieve
maximum potential range of movement in joints underlying both second and third degree bums.
Complications of thermal burn.—
1.
Curling ulcer.— Stress ulceration of the stomach and duodenum which is known as
Curling's ulcer is come across in major thermal bum. Serial endoscopic examination has shown
that 85% of patients with bums exceeding 35% demonstrate superficial mucosal disease within
72 hours of injury. This mucosal disease heals in majority of patients (80%) within 1 week. Only
in 20% of patients the disease may progress to frank gastric and duodenal ulcers which usually
become first evident 96 hours after injury. Curling's ulcers are often multiple and are found
simultaneously in the stomach and duodenum. These lesions heal following successful
resuscitation and initiation of enteral feeding. Until the bum wound is healed, 30 ml antacid is
administered each hour through nasogastric tube to maintain the gastric pH above 5. The dosage
can be increased if gastric acidity persists below this level. Cimetidine is equally effective in
preventing Curling ulcer and in patients who cannot tolerate antacid. Clinical trial suggests that
early enteral feeding may be as effective as antacids and histamin H2 antagonists. In rare cases
who require surgery for severe haemorrhage or perforation of Curling's ulcer, vagotomy and
gastric resection has produced the best immediate and long term survival.
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2. Acute pancreatitis.— This occurs in patients with extensive bums with an incidence as
high as 30% in those requiring treatment in intensive care unit. The peculiarity is that the
abdominal pain is often absent and this condition is only suggested by increasing fluid
requirement and new onset of hyperglycaemia. Measurement of amylase excretion rate appears
to be the most sensitive laboratory diagnostic test. Treatment is general supportive measures,
nasogastric aspiration and parenteral nutrition.
3. Acute acalculous cholecystitis.— This complication occurs occasionally in burned patients
in two forms. In one form, the gallbladder is infected by haematogenous seeding from a primary
source in the septic bum wound. The other presentation occurs in critically ill patients with
marked dehydration, ileus, hypematraemia and hyperosmolarity. In this form the gallbladder
and bile are often sterile. Jaundice and abdominal pain may suggest this condition. Physical
examination is difficult in burned patient. Ultrasonography is quite helpful in diagnosis by
showing thickened gallbladder wall, sloughing mucosa and intraluminal gas in the gallbladder.
Once the diagnosis is established, cholecystectomy is indicated to avoid rupture of the
gallbladder. Tube cholecystostomy may sometimes be used in unstable and critically ill patients.
4. Superior mesenteric artery syndrome.— Very occasionally the superior mesenteric artery
may obstruct the transverse portion of the duodenum, so that enteral elementation becomes
impossible with duodenal obstruction.
Gastric decompression and intravenous nutrition are often sufficient to relieve this condition.
5. Non-occlusive ischaemic enterocolitis — is occasionally recognized in severely burned
patient. The lesion is usually located in the distal small bowel and colon and resembles the
lesions of Curling's ulcer in the upper G. I. tract. The lesions may bleed or perforate, but if the
patient recovers, healing of the bowel often occurs with stricture formation.
Nasogastric aspiration and intravenous infusion should be started immediately. Occasionally
laparotomy and caecostomy may be necessary to avoid infarction and perforation of the colon.
6. Myocardial infarction — may occur in old burned individuals. Infarction usually occurs
toward the end of the 1st week after bum. It may be due to increased cardiac output at this
time exceeding the ability of the diseased heart to meet its own perfusion and infarction occurs.
All patients with major burns should be monitored electrocardio-graphically.
Short-acting infusable drugs e.g. dopamine or dobutamine are preferable to long acting drugs
e.g. digitalis. Adequate intravascular volume must be maintained to meet the perfusion
requirements of the wound and visceral organs. Beta-adrenergic blocking agents should not be
used to treat cardiac disease in burned patients. Increased after load is treated with intravenous
nitroprusside or nitroglycerin.
TREATMENT OF ELECTRICAL INJURY.— As a first-aid measure the electric current
should be stopped. If the patient is lying unconscious one must exclude presence of cardiac arrest
and cardiopulmonary resuscitation should be started. Fluid estimates based on cutaneous injury
will definitely lead to underresuscitation, so adequate fluid replacement should be achieved.
Intravascular volume deficits are replaced with Ringer's lactate solution sufficient to maintain a
urinary output of 50 to 75 ml/hr. Urinary output should be increased to 100 ml/hr. by raising the
fluid infusion rate if the patient has grossly visible myoglobinuria. In this case 12.5 g mannitol
may be added to each litre to Ringer lactate solution. As soon as haemodynamic stability is
attained, operative treatment should be considered. Cutaneous electrical injury should be debrided,
cleared and topical antimicrobial burn creams are applied. Mafenide acetate is preferred for
electrical injuries because of its superior ability to penetrate injured tissue deeply and its unique
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anticlostridial spectrum. Stony hard oedema of muscle compartments should require immediate
exploration. Similarly absence of peripheral pulses distal to the site of electrical contact require
immediate exploration. Arteriography may also be helpful in determining the need for exploration
— narrowing of the arteries indicates exploration. A complete neurologic examination must be
performed on admission and at schedule intervals thereafter to note the presence and time of
occurrence of neurologic deficits. Although visceral injury is rare, liver necrosis, intestinal
perforation, focal pancreatic necrosis have been reported in patients with high voltage electrical
injury. Compression fracture of vertebra may also occur owing to tetanic contractions at the time
of electrical contact. Fractures of long bones may result from falls due to electric shock. Late
complications include delayed haemorrhage from even moderate sized blood vessels due to
'arteritis' produced by electrical injury. Cardiopulmonary arrest is common in this type of injury.
When the exposed limb is explored, all muscles which may be involved by electrical current
should be exposed. Meticulous debridement is required so that all necrosed tissues are excised.
The wounds are packed loosely and kept open for further check up in the operation theatre
after 24 to 48 hours.
TREATMENT OF CHEMICAL BURNS.— As a first-aid measure, it is essential to irrigate
the affected areas with copious amounts of clean water. The only exception is phenol bums
where water may accelerate absorption, so polyethylene glycol should be used. Common pit falls
in the treatment of chemical bums is failure to remove all contaminated clothings and delay in
water lavage. Wound irrigation should be carried out for at least 30 minutes or even more. In
some cases a continuous shower for 24 hours may be needed. There are several chemical agents
for which more specific treatment is necessary. Hydrofluoric acid injury is an occupational hazard
of glass workers and the treatment consists of prolonged irrigation with benzalkonium chloride
solution and excision of any tissue with frank necrosis. Bums caused by phenol should be washed
with polyethylene glycol or glycerol to remove residual phenol. It must be remembered that if
there is extensive skin damage in chemical bums, early excision is necessary to limit extension
of tissue damage. Once healthy tissue is exposed skin grafting should be done.
Cold injuries.— Cold injuries can be broadly classified into 2 groups — (a) frost bite and
(b) acute cold injuries from industrial accidents.
(a) Frost bite injuries mainly affect the extremities exposed to very cold object or climate.
The depth of injury is difficult to assess and these injuries are usually managed by conservative
means such as rapid exposure to warm water. Surgery is usually not required.
(b) Cold injuries from industrial accident may occur due to exposure of a part of the body
to liquid nitrogen or other such liquid which will cause epidermal or dermal destruction. It
must be remembered that the human tissue is more resistant to cold injury than to heat injury.
Assessment of depth of injury is difficult, so surgery is rarely required unless a proper assessment
can be made about the depth of injury.
Ionizing radiation injury.— These injuries can be divided into 2 groups — localized injury
which is much more common and whole body radiation injury. The localized radiation damage is
preliminary treated conservatively until and unless the true extent of the tissue injury can be
assessed. If there be any ulcer, excision and coverage of the part with vascularized skin is required.
Whole body radiation may be lethal depending on the dose of the radiation. When it is lethal
it causes a slow and unpleasant death. In case of non-lethal radiation injury one can come across
immune system dysfunction and even systemic damage to the gut mucosa. Management of
these injuries is mainly supportive.
7
BOIL, ABSCESS, CARBUNCLE,
CELLULITIS AND ERYSIPELAS
BOIL (FURUNCLE)
Definition.— It is an acute staphylococcal infection of a hair follicle with perifolliculitis.
Such infection usually proceeds to suppuration and central necrosis.
Clinical features.— It starts with a painful and indurated swelling which gradually extends.
It is associated with tremendous tenderness and surrounding oedema. After a couple of days,
there will be softening at the centre, on the summit of which a small pustule appears. It bursts
spontaneously discharging greenish small amount of slough. After this a deep cavity develops
lined by granulation tissue, which heals by itself.
A blind boil ’ is one which subsides without suppuration. A 'stye' is similar infection of an
eyelash follicle.
Sites.— (i) Boils are common on the back and neck.
. (ii) Furuncle of the external auditory meatus is very painful as the skin is almost attached
to the underlying cartilage and there is hardly any space for swelling, which develops with
considerable tension inside it giving rise to exquisite pain.
(iii)
Infection of the perianal hair follicle is perianal boil which when ruptures results in a
perianal sinus or fistula.
Complications.—
(a) Boil may lead to cellulitis, particularly in those whose power of immunity is less.
(b) Boils may also lead to infection of the neighbouring hair follicles where numbers of
hair follicles are too many (e.g. axilla) leading to hydradenitis.
(c) Boils usually secondarily infect the regional lymph nodes.
Treatment.—
1. The general health of the patient has to be improved, as boils often occur in individuals
with debility and ill-health.
2. Incision is usually unnecessary as the pustule is very small. Only a touch of iodine on
the skin pustule will hasten necrosis of the overlying skin and help the pus to drain out.
3. If escape of pus does not occur spontaneously or with application of iodine, removal
of the affected hair allows ready escape of pus.
4. Antibiotic is usually not required. It is only indicated when multiple boils appear or if
boils recur.
5. After escape of pus the part should be cleaned twice with a suitable disinfectant e.g
hexachlorophene. This discourages development of further boils.
6. If boils are recurrent, diabetes should be excluded.
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ABSCESS
Definition.— An abscess is a collection of pus in the body.
There are three varieties of abscess seen in surgical practise — 1. Pyogenic abscess, 2. Pyaemic
abscess and 3. Cold abscess.
1. PYOGENIC ABSCESS.—
This is the commonest variety of abscess. Organisms gain entry to form abscess by (i) direct
infection from outside due to penetrating wounds, (ii) local extension from adjacent focus of
infection, (iii) lymphatics and (iv) blood stream or haematogenous.
Pathology.— The suppurative infection gradually leads to cell death and liquefaction. Both
tissue cells and those of the exudate are killed by the toxins of pyogenic organisms. Liquefaction
of the dead tissue is caused by proteolytic enzyme released from the dead polymorphonuclear
leucocytes. The resulting yellow alkaline fluid is called ‘pus’. It contains both disintegrating and
living leucocytes and living and dead bacteria.
An abscess is a cavity filled with pus and lined by a pyogenic membrane. This pyogenic
membrane consists of dead tissue cells and a wall of granulation tissue consisting for the most
part of phagocytic histiocytes.
As recovery starts this pyogenic membrane is converted into fibrous tissue and the cavity
is gradually covered with granulation tissue which transforms into collagen fibres.
Sometimes the abscess cavity persists, which becomes firm and contains sterile pus. The firmness
is due to thickness of its wall. This is known as 'antibioma'. This is due to continuous administration
of antibiotics. The lump may even be hard, when it may mimic a carcinomatous lump.
Clinical features.—
Cardinal features of acute inflammation are usually present. These are —
(a) Redness or rubor — there is redness over the area particularly before localization of the
abscess. This is due to hyperaemia.
(b) Pain or dolor — a throbbing pain is characteristic of presence of pus.
(c) Heat or calor — the inflamed area is hot due to hyperaemia (cf. in cold abscess this is
not present and that is why it is called 'cold').
(d) Swelling or tumor — due to presence of pus inside the abscess cavity.
(e) Impairment of function or functiolaesa — the function of the part is definitely impaired.
This is more obvious when an abscess occurs near a joint, when movement of the joint will be
painful and patient tries not to move the joint.
Of these 5 signs and symptoms importance should be given to pain, redness and heat.
Presence of pus is detected by —
(i) the temperature becomes elevated;
(ii) there is brawny oedema with induration when the pus is deep seated (e.g. in the breast,
parotid gland and ischiorectal fossa);
(iii) when the pus becomes superficial, fluctuation test will be positive.
Special Investigations.— Nowadays various sophisticated investigations have been
introduced to correctly locate and accurately diagnose abscess cavities in different parts of the
body. The various methods are —
(a)
Conventional radiology is only successful when there is air or gas with pus. This
examination then reveals fluid levels e.g. subphrenic abscess, lung abscess etc. Sometimes
presence of pus is suggested by opacity e.g. in the nasal antrum, pleural cavity etc.
BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS
79
(b) Isotope scanning is helpful in locating collection of pus or site of infection by
accumulation of radio-active technetium after its intravenous injection. This is mostly used as
diagnostic stool in demonstrating brain abscess, hepatic abscess and osteomyelitis. Similarly radio­
active gallium scan is sometimes used to detect pelvic, perinephric, mediastinal or subphrenic
abscesses.
(c) Ultrasound is of considerable value in the diagnosis of gallbladder stones or empyema
and also to detect abscesses in the liver or spleen.
(d) CT scan is particularly helpful to distinguish between abscess and tumour by showing
necrotic centre in case of abscess. It is helpful to locate abscess cavity inside the abdomen as
also in the brain.
Treatment.—
1. In the initial stage, when the pus is not localized, conservative treatment may be
advised. The affected part is elevated and given rest. A suitable antibiotic should be started.
2. When the pus has been localized, it should be drained. The old adage holds true today
also ‘where there is pus, let it out’.
So the basic principle of treatment of an abscess is — (i) to drain the pus, (ii) to send a
sample of pus for culture and sensitivity test and (iii) to give proper antibiotic.
DRAINAGE OF PUS.— This is usually done by surface anaesthesia with ethyl chloride
spray. In cases of deep abscesses, general anaesthesia may be required.
Incision.— Drainage of pus can be obtained by (a) free incision or by (b) Hilton's method.
(a) Free or liberal incision.— In this technique a liberal incision is made on the most
prominent part of the abscess so as to cause least damage to the surrounding healthy tissue. It
should be placed on the most dependent part also, so that gravity will help drainage. Incision
must be adequate (liberal) for easy drainage of pus and to avoid chronicity.
If any important structure like nerve or vessel is liable to be present in the depth, the incision
should be made parallel to these structures. This incision should be bold through the skin,
subcutaneous tissue and deep fascia. The muscle should be incised along the line of the fibres.
(b) Hilton's method.— This method is chosen when there are plenty of important structures
like nerves and vessels around the abscess cavity, which are liable to be injured. This is
particularly employed in places like neck, axilla or groin.
In this technique the skin and subcutaneous tissue are incised on the most prominent and
most dependent part of the abscess cavity. A pair of artery forceps or sinus forceps is forced
through the deep fascia into the abscess cavity. The blades are gradually opened and the pus is
seen to be extruded out. The forceps is now taken out with the jaws open to increase the opening
in the deep fascia. A finger is introduced to explore the abscess cavity.
Exploration.— After the incision has been made upto the abscess cavity and some amount
of pus has been extruded, a finger is inserted into the abscess cavity and all the walls of the
loculi are broken. There must not be any loculus unbroken as this will lead to chronicity. All
loculi are broken into one cavity, for complete drainage.
Counter-incision.— When the most prominent part is not the most dependent part, complete
drainage of pus is not possible with a single incision. So a counter-incision is required at the
most dependent part to facilitate drainage by gravity. In this technique, through the first-made
incision on the most prominent part, a sinus forceps is passed to the most dependent part. The
blades are slightly made apart, then with a knife a fresh incision is made on the skin between
the tips of the sinus forceps.
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Drainage.— A corrugated rubber drain is usually used for drainage of an abscess cavity.
When counter-incision is used, the drain extends from the first incision to the counter-incision.
When the surrounding granulation tissue is bleeding too much, a roller gauze should be
packed inside the wound and it can be kept for 48 hours. Some surgeons believe in instilling
local antibiotic into the abscess cavity.
Follow-up.— Rest to the affected part is very important postoperative measure. This
expedites healing.
Proper antibiotics selected by culture and sensitivity test should be started immediately.
After 48 hours the dressing or drain should be removed. Fresh dressing is done everyday
with acriflavine lotion and sterile gauze. If the cavity has to be packed, the packing should be
made gradually lighter to help the cavity to heal.
Vitamins should be given to the subjects, who are thought to be suffering from this deficit.
Vitamin C should be given to all cases as this helps in wound healing. Vitamin B complex
should be given when tetracycline is used as antibiotic.
Operations on Different Abscesses
Abscess of the neck.—
This usually results from suppuration of the regional lymph nodes. It may occur from
extension of the alveolar abscess.
For cosmetic reason horizontal incision along the natural crease is preferred. Only when the
abscess runs along the direction of the stemomastoid, an incision along its anterior border is
made.
The abscess is drained by Hilton's method.
Abscess of the axilla.—
This abscess is also caused by suppurative lymphadenitis. Sometimes axillary abscess may
occur from boils affecting many hair follicles or sweat glands.
With fully abducted arm the incision is made % an inch behind the anterior fold of the
axilla. At this place there is no important structure. Moreover the pus is usually located behind
the pectoralis major muscle. Drainage of pus is usually done by Hilton's method.
Abscess of the groin (inguinal abscess or bubo).—
Such abscess also occurs as a sequel of suppurative condition of the inguinal lymph nodes.
The lymph nodes here are distributed in two sets. The medial group of horizontal lymph nodes
is involved from infection of the external genitalia. The vertical group is involved from infection
of the lower limb.
Incision.— For the medial group of horizontal lymph nodes, a transverse incision along the
most prominent and dependent part of the abscess cavity is made.
For the vertical group, a vertical incision along the abscess is preferred parallel to the femoral
vessels so as to protect these vessels. An added advantage of this incision is that the wound is
likely to gape when the thigh is bent, thus providing better drainage.
Popliteal abscess.—
This abscess is caused by 3 conditions — (i) suppuration of the regional lymph nodes, (ii)
osteomyelitis of the lower end of the femur or upper end of the tibia and (iii) infection of the
local cellular tissue.
It is essential that one must exclude the possibility of popliteal aneurysm before making an incision.
BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS
81
Cases are not unknown when leaking aneurysm with surrounding inflammation was incised
with mistaken diagnosis of abscess with disastrous result.
Incision.— This is made slightly medial to the lateral border of the popliteal space parallel
to the biceps tendon. Obviously this incision is on the lateral side on the popliteal space. Care
must be taken not to injure the lateral popliteal nerve.
Gluteal abseess.—
This abscess is often caused by infection of a haematoma. Intragluteal injection in the form
of intramuscular administration of various drugs may cause gluteal abscess. In older days quinine
injection was a common cause.
Incision.— A free incision is made over the most prominent and dependent part of the abscess
along the fibres of the gluteal maximus — downwards and laterally. Counter-incision may or
may not be required.
Iliac abscess.—
It is also due to infection of a haematoma within the iliac muscle. Clinically it mimics very
closely an appendicular abscess. But it is slightly lateral to the usual position of appendicular
abscess. Moreover Rovsing's sign is absent here.
Incision.— It is made just above and parallel to the iliac crest. The structures are cut right
upto the abscess cavity along the line of incision. Care must be taken not to open the peritoneal
cavity, moreover it is obliterated by adhesions.
Deltoid abscess.—
Such abscess is usually caused by infection of haematoma or intramuscular injection.
Incision.— A free longitudinal incision is made over the most prominent part of the abscess
in the direction of the deltoid muscle fibres. A counter-incision at the most dependent part
becomes sometimes necessary.
Abscess of the sole and heel.—
Such abscess is usually caused by the prick of a thorn or a needle or secondary to acute
osteomyelitis of the calcaneum.
Incision.— A free incision is made on the most prominent part of the swelling along the
lateral or medial margin of the sole. So scar from healing of drainage wound remains away
from the weight bearing areas. Sometimes such abscess is a 'collar-stud' one with superficial
and deep parts connected through a small nick in the plantar fascia. So care must be taken to
drain the deep part as well by extending incision on the plantar fascia.
2. PYAEMIC ABSCESS.—
In this condition multiple abscesses develop from infected emboli in pyaemia.
Pyaemia is a condition characterized by formation of secondary foci of suppuration in various
parts of the body. These foci are caused by the lodgement of septic emboli, consisting of a
clump of organisms, infected clot or vagitations, formed as the result of breaking up of an infected
thrombus. Pyaemia is occasionally associated with conditions like acute osteomyelitis, acute
inflammation of intracranial sinus and acute bacterial endocarditis.
Such pyaemia is also seen in acute appendicitis when the infective emboli pass into the
portal venous system and cause portal pyaemia (forming multiple pyaemic liver abscesses).
Three terms should be understood by the students in this connection —
A.
BACTERAEM1A.— This term merely indicates that bacteria are circulating in the blood
stream. It probably occurs in every infection and particularly after every tooth extraction due to
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caries and major traumatic wounds. This condition is of little clinical significance, as the organisms
are usually rapidly destroyed. That is why bacteraemia is usually transient and may last only a
few moments, as the reticuloendothelial system localizes and destroys these organisms under
favourable conditions. Occasionally bacteraemia may be the means by which apparently isolated
infections arise in internal organs e.g. osteomyelitis, pyelonephritis (descending type) etc.
B. SEPTICAEMIA.— This is a condition characterized not only by the presence of bacteria
in the blood as shown by blood culture, but also by the development of certain clinical
manifestations due to liberation of toxins by those bacteria. These clinical manifestations are
mainly pyrexia, rigors, hypotension, intravascular coagulation defects and petechial
haemorrhages. In every case of septicaemia there is some local focus of infection from which
organisms enter the blood stream. As soon as this local focus of infection is removed, the bacteria
soon disappear from the blood. The major routes by which bacteria reach the blood are — (i) by
direct extension into an open vessel, (ii) by release of infected emboli following thrombosis of a
biood vessel in an area of inflammation and (iii) by discharge of infected lymph into the
bloodstream following lymphangitis.
In the absence of systemic disease, beta-haemolytic Streptococci (Strep, pyogenes) are the
most frequently responsible organism. Septicaemia may be caused by alpha haemolytic
Streptococci (Strep, viridans), as a consequence of subacute bacterial endocarditis. Many specific
diseases e.g. typhoid fever and brucellosis are also septicaemic phase of infection.
Treatment is immediate administration of suitable antibiotic found out by at least 3 blood
cultures together with an aminoglycoside and metronidazole (all intravenously). Blood
transfusions, plasma expanders and hydrocortisone should be given.
C. TOXAEMIA.— In this condition toxins, either chemical or bacterial, circulate in the
blood stream. These produce toxaemic symptoms.
The features of pyaemic abscess —
(a) These are generally multiple.
(b) These abscesses commonly occur in the subfascial plane.
(c) These abscesses are non-reacting in nature i.e. acute features like calor, rubor, dolor
are absent.
(d) Constitutional disturbances are tremendous with high fever, rigor and toxaemia.
(e) Such abscesses may occur in the viscera e.g. spleen or kidneys. Death may occur from
such abscesses in the vital organs like brain or heart.
Treatment is to administer the suitable antibiotic parenterally as quick as possible. The
antibiotic is chosen by culture and sensitivity test of the organism of the pus. The superficial
abscesses should be drained. A careful search should be made to locate the source of infection,
which should be treated as soon as possible.
3. COLD ABSCESS.—
As the name suggests this abscess is 'cold' and non-reacting in nature. It does not produce
hot and painful abscess as seen in pyogenic abscess. Brawny induration, oedema and tenderness
are conspicuous by their absence. Only when this is associated with secondary infection a few
of these features may be present.
Cold abscess is almost always a sequel of tubercular infection anywhere in the body
commonly in the lymph nodes, bone and joint. Caseation of lymph nodes forms the cold abscess.
The commonest sites are at the neck and axilla. On palpation soft and matted nodes are usually
palpable.
BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS
83
Sites.—
(i) While the neck and axilla are the commonest sites, the other sites are —
(ii) Loin from caries spine.
(iii) At the side of the chest wall from tuberculosis of ribs.
(iv) At the back of the chest wall or side of the chest wall or even anterior part of the chest
wall through the lateral or anterior cutaneous nerve, branches of intercostal nerve from the
posterior mediastinal group of lymph nodes. So cold abscess may travel a long distance along
definite anatomical plane or tracing a nerve or a vessel.
(v) Near the ends of the long bones and joints from bone and joint tuberculosis.
Treatment.— Once the diagnosis is confirmed, full antitubercular regime should be started.
If the cold abscess continues to be present, aspiration may be attempted obliquely through the
normal surrounding skin and not through the most prominent and most dependent part as this
will invariably cause sinus formation. Aspiration may be followed by local instillation of I.N.H.
solution.
If the local abscess still persists, the affected group of lymph nodes should be excised as a
whole. A word of caution is highly important, that an incision should not be made on a cold abscess
for drainage, as it almost always invites secondary infection and forms a persistent sinus.
CARBUNCLE
Definition.— It is an infective gangrene of the subcutaneous tissue due to Staphylococcal
(Staphylococcus aureus) infection. Gram-negative bacilli and Streptococci may be found
coincidentally.
•
Sites.— Carbuncles are mostly seen on the back, in the nape of the neck where the skin is
coarse and vitality of the tissue is less.
The shoulders, the cheek, dorsum of the hand are the other rare sites. Hirsute portions of
the chest and abdomen may also be involved.
Pathology.— When the invading staphylococci penetrate the deeper layers of the skin and
the subcutaneous fat, a carbuncle is formed. This consists of a series of communicating
abscesses, which discharge by separate openings on the surface. That is why the surface is
sieve-like. Individual compartments in the carbuncle are maintained through persistence of
fascial attachment to the skin. Carbuncles may be more extensive than they appear. There is a
central large slough, surrounded by a rosette of small areas of necrosis. In untreated cases
infection may extend widely with fresh openings appear on the surface, which coalesce with
those previously formed. Under treatment when the central slough is drained off, fibroblastic
reactions start from the surrounding granulation tissue and carbuncle heals with a characteristic
induration.
Clinical features.— It generally affects males above 40 years of age. Often the subject is
diabetic.
It commences as painful and stiff swelling which spreads very rapidly with marked
induration. The overlying skin becomes red, dusky and oedematous. Subsequently the central
part softens and multiple vesicles appear on the skin. Later on these vesicles transform into
pustules. These pustules subsequently burst allowing the discharge to come out through several
openings in the skin producing a sieve-like or cribriform appearance, which is pathognomonic of
carbuncle. These openings enlarge and ultimately coalesce to produce an ulcer. At the floor of
A CONCISE TEXTBOOK OF SURGERY
the ulcer lies the ashy-grey slough. Finally the slough separates leaving an excavated granulation
tissue, which heals by itself. When the resistance of the individual is poor in diabetic subject,
the sloughing process may extend deeply into the muscle or even bone.
Constitutional symptoms and toxaemia vary according to the degree of the resistance of
the individual and efficacy of the treatment.
Treatment.—
(i) Improvement of the general health of the patient should be brought about.
(ii) Proper antibiotic should be started immediately from the culture and sensitivity test.
If the surface openings have not formed, a synthetic penicillin e.g. erythromycin may be used.
At this time a paste composed of anhidrous magnesium sulphate and glycerin may be applied
or S. S. Mag Sulph powder is used on a moisten cotton and placed on the affected area. This
will exercise a valuable osmotic affect and will not only reduce oedema but also will help to
burst the carbuncle. Hot compress is helpful before bursting. It may be supplemented by infra­
red or short wave diathermy.
Operation may be required (a) when toxaemia and pain persist even after a course of
antibiotics and (b) when the carbuncle is more than 2Yi inches in diameter. It must be remembered
that incision is never made unless there is softening in the centre.
Technique.— A large cruciate incision is made extending upto the margin of the inflammatory
zone. Sloughs should be cleared with a piece of gauze. Epices of the four skin flaps are generously
excised. The wound is covered with vaseline gauze or sofratulle dressing. The part should be
kept in perfect rest for a week and antibiotic is continued till resolution.
CELLULITIS
Definition.— It is a non suppurative inflammation spreading along the subcutaneous tissues
and connective tissue planes and across intercellular spaces. The term is a misnomer, as the
lesion is one of the connective and interstitial tissue and not of the cells.
The causative organism is mostly the Streptococcus pyogenes, though a variety aerobic and
anaerobic bacteria may produce cellulitis.
Pathology.— The organism usually gains access through a wound or scratch or following
surgical incision. There is wide spread swelling and redness at the area of inflammation, but
without definite localization. Initially the site of inoculation becomes red. Gradually the skin
swells and becomes shiny. In severe infections blebs and bullae form on the skin. Central necrosis
may occur at a later stage.
Clinical features.— There is varying degree of fever and toxaemia.
The affected part is very much swollen and painful. Diabetic individual often suffers from
cellulitis.
On examination, the affected part is warm, swollen and tender. There is pitting oedema
and brawny induration. The surrounding lymph vessels may be seen as red streaks due to
lymphangitis.
The regional lymph nodes will be enlarged and tender with acute lymphadenitis.
Treatment consists of (i) rest and elevation of the part to reduce oedema.
(ii) Appropriate antibiotic preferably broad spectrum should be administered.
(iii) Failure of inflammatory swelling to subside after 48 to 72 hours suggests that an abscess
has developed. In that case incision and drainage of the pus should be accomplished.
BOIL, ABSCESS, CARBUNCLE, CELLULITIS AND ERYSIPELAS
85
ERYSIPELAS
Definition.— It is an acute inflammation of the lymphatics of the skin or mucous membrane.
The causative organism is usually Streptococcus haemolyticus group A (Strep, pyogenes).
Pathology.— The organism usually gains entrance through a minor wound like a scratch,
which may escape notice, but a break in the surface is always present.
The disease spreads from the site of inoculation and the advancing margin becomes bright,
red and slightly raised above the general surface. The margin itself is irregular in outline. Just
beyond the sharp margin the lymphatics are crowded with streptococci. The margin shows acute
congestion. The lymph spaces of the corium of the skin are crowded with cells. The inflammatory
cells are mainly lymphocytes and wandering mononuclear cells. It should be remembered that
whereas in ordinary streptococcal infections the characteristic defence cell is the
polymorphonuclear leucocyte, in erysipelas this cell is small mononuclear cell. The centre of the
patch shows little change. There is notable absence of pus formation. Following the fading of
the inflammation, brown discolouration of the skin may remain.
Clinical features.— The condition which predisposes this disease are debilitating state
and poor health.
The condition commences as a rose-pink rash which extends to the adjacent skin like a
drop of grease spreading on a piece of paper. The vesicles appear sooner or later over the rash
and rupture. Serous discharge comes out from these vesicles. Fever and other constitutional
symptoms may be present with varying degrees. When it affects skin below which there is loose
areolar tissues e.g. orbit, scrotum etc., there is considerable swelling of the part due to oedema
of the subcutaneous tissues and thus very much resembles cellulitis.
To distinguish between a true erysipelas and a cellulitis, the following points in favour of
erysipelas should be borne in mind :— (i) The typical rosy rash disappears on pressure and
feels stiff ; (ii) The raised rash of erysipelas has a sharply defined margin, which is better felt
than inspected ; (iii) The vesicles of erysipelas contain serum in contradistinction to the cellulitis
in which they contain pus; (iv) In case of the face, Milian's ear sign is significant in which
erysipelas can spread into the pinna (being cuticular affection), whereas cellulitis cannot spread
to the pinna due to close adhesion of skin to the cartilage of the ear (without any areolar tissue).
Comj >lica I ions.—
1. Sloughing or gangrene rarely occurs particularly in grossly debilitated or diabetic
individuals.
2. Lymphoedema may rarely occur due to lymphatic obstruction, which occurs more in
parts containing loose areolar tissues e.g. eyelids or scrotum.
SPECIAL INFECTIONS
In this chapter I shall mainly discuss the granulomatous inflammations. Granulomatous
inflammation produces highly distinctive pattern of tissue response which forms 'granuloma'.
This granuloma is a tumour-like proliferation of granulation tissue. The granulomatous inflammation
is classically, though not exclusively, 'chronic'.
Classification of granulomas.— According to the type of central degeneration, granulomas
are classified into various types :—
1. CASEOUS.— The necrotic centre of the granuloma is soft and friable which accounts
for the use of the term 'caseous'. Although the best example is tuberculosis, yet other conditions
may present caseous necrosis e.g. histoplasmosis, tularemia etc.
2. GUMMATOUS.— In this form, necrosis is mainly due to ischaemia. Such an area is
finally transformed into a mass of cellular debris. Such lesion is characteristically seen in the
tertiary stage of syphilis.
3. SUPPURATIVE.— In certain infections due to bacteria and fungi (e.g. actinomyces,
blastomyces) large numbers of polymorphonuclear leucocytes are present in the central necrotic
portion.
4. FIBRINOID.— Although the exact pathogenesis is poorly understood, it is most
probably a manifestation of tissue hypersensitivity. Fibrinoid necrosis appears in the
granulomatous nodules which are seen in rheumatoid arthritis and rheumatic fever.
GRANULOMATOUS DISEASES
These can be classified into 4 groups —
1. Infective —
(a) Bacteria e.g. tuberculosis, leprosy, syphilis.
(b) Fungi e.g. actinomycosis, blastomycosis, histoplasmosis.
(c) Viruses e.g. cat-scratch disease.
2. Foreign body reaction —
(a) Exogenous e.g. silica, dusting powder granuloma.
(b) Endogenous e.g. gouty tophus, xanthogranuloma.
3. Hypersensitivity, e.g. rheumatic nodules, giant-cell arteritis.
4. Unknown aetiology e.g. Crohn's disease.
TUBERCULOSIS
The two chief methods of infection are inhalation and ingestion.
1.
Infection by inhalation is by human type of tubercle bacillus in the form of tiny droplets
spread out by cough of the tuberculous patients. After inhalation or air-borne infection one of
SPECIAL INFECTIONS
87
the three routes may be followed —
(i) Direct spread to the lungs.
(ii) Through the tonsils the infecting organisms are spread to the cervical groups of lymph
nodes causing tuberculous lymphadenopathy.
(iii) The infecting organisms ultimately enter the blood stream and may involve any organ
in the body e.g. the bone, joints, the kidneys, the bladder, the testis, the peritoneum, the brain
and the eye.
2. Infection by ingestion may occur due to ingestion of milk containing bovine form of
tubercle bacilli coming from tuberculous cow. However this type of infection is almost unknown
nowadays as pasteurization of milk has been enforced by law. It is often due to ingestion of
cough or infected material of human type of tubercle bacilli that this type of infection may
occur. Tuberculosis of the intestine is often due to such infection. This infection may spread to
the retroperitoneal groups of lymph nodes, follow the lymphatic path and may ultimately reach
the blood stream.
3. A rare form of infection is through the skin (cutaneous spread) in those engaged in
occupations e.g. pathologists, butchers, nurses etc. Lupus vulgaris is the lesion commonly seen
through this spread.
Pathology.— The initial lesion is the miliary tubercle, a tiny collection of histiocytes which
develop into epitheloid cells. The histiocytes are members of the reticuloendothelial system which
are derived locally from the primitive mesenchyme of the connective tissues, from lining cells
of the sinuses in the liver, spleen, lymph nodes and bone marrow. These histiocytes retain a
high degree of power of phagocytosis, amoeboid movement and independent proliferation. These
cells ingest bacteria and cell debris so that their cytoplasms swell and individual histiocytes
gradually assume epitheloid appearance which are known as epitheloid cells. The epitheloid cell
has a large vesicular nucleus and a clear cytoplasm and a few processes which may anastomose
with the neighbouring cells to form an epitheloid reticulum. In addition to the epitheloid cells,
one or more cells may be seen situated usually toward the centre, but occasionally at the
periphery of the tubercle. These cells are much bigger than the epitheloid cells and contain
many nuclei (20 or more) characteristically grouped. These cells are called foreign body giant
cells and usually contain tubercle bacilli. These cells are apparently formed by the fusion of a
number of epitheloid cells. Though giant cells are characteristic of tuberculosis but these are
also found in syphilis and actinomycosis and even around foreign bodies e.g. a piece of silk
suture. In fact this represents a foreign body reaction.
For the first few days the tubercle consists entirely of the epitheloid cells and giant cells. By
the end of a week lymphocytes begin to make their appearance. These are small dark cells with
darkly staining nuclei and scanty cytoplasm, identical in structure with the lymphocyte of the
blood. These cells are derived from the perivascular lymphatic sheath or lymphoid tissue and
are one of the principal sources of gamma globulins.
The tubercle is non vascular. There is no formation of new blood vessels. This lack of
vascularity influences in the production of caseation which begins to appear in the centre of the
tubercle follicle by the end of the second week. The cells in the centre undergo necrosis and
fuse together to form granular structureless cheesy material. This coagulation necrosis is partly
due to action of the bacterial toxins which are produced by disintegration of tubercle bacilli.
The fibroblasts proliferate forming a fibrous zone around the tuberculous area walling it, so
that the caseous area becomes enclosed in a fibrous capsule. So a typical TUBERCLE is formed
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88
by a central zone of caseation surrounded by epitheloid cells and foreign body giant cells, which
are further surrounded by a zone of lymphocytes and around that lies the fibrous zone which
encircles the tubercle follicle. Tubercle bacilli may remain viable for long periods within this
tubercle follicle. Due to influence of antitubercular drugs the tubercle bacilli die and the fibrous
tissue gradually invades the tubercle follicle in which the epitheloid and giant cells are also
destroyed, converting it into a fibrous mass which is known as healed tubercle. In untreated
cases caseation occurs. Caseation may be followed by liquefaction. This is usually associated
with high multiplication of the bacilli. So this liquified material, which is known as cold abscess,
has a high infectivity when discharged. The cold abscess is so named, because it produces a
soft swelling without the signs of acute inflammation. The wall of the abscess is lined by granular,
caseous material which contains tubercle bacilli. The outer layers consist of granulation tissue.
The fluid inside the cold abscess is not true pus, but consists of fatty debris, floating in a serous
fluid, intermingled with a few necrotic cells. It is usually sterile on ordinary culture.
The course of the disease is profoundly influenced by the use of the antitubercular agents.
Clinical features.— Detail symptoms and signs are described in any standard Text Book
of Medicine. Only regional tuberculosis is described in this textbook in appropriate chapters.
Treatment.—• Students are referred to the author's 'Undergraduate Fractures & Orthopaedics'
page 193 for General Treatment. Various local treatments are discussed in the appropriate
chapters.
SYPHILIS
It is a venereal disease caused by infecting organism, treponema pallidum, a delicate spiral
organism (spirochaete) of 6 to 15 pm in length. Due to advent of various antibiotics which are
effective against this organism, there has been a dramatic decline in incidence of this disease.
The disease is transmitted by direct contact from a surface lesion containing the organisms. So
the disease remains infective in the primary and secondary stages for first 2 years. After that
the disease may remain in the person's body but ceases to be infective. The organism dies rapidly
on drying, so early lesions are mostly seen in moist areas e.g. external genitalia, anus and mouth.
The disease is divided into four stages — 1. Primary syphilis, 2. Secondary syphilis, 3.
Tertiary syphilis and 4. Latent syphilis.
1.
Primary syphilis.— A sore or hard chancre (Hunterian chancre) gradually develops
at the site of entry of infecting organisms. This takes about 3 to 4 weeks (incubation period) to
develop. It first develops as an indurated papule, which gradually becomes eroded and forms
into a hard chancre (Hunterian chancre). It is characteristically hard, shallow and non-bleeding
ulcer, which is oval or round in shape. Its edge is raised and hyperaemic extending into dusky
red oedematous surrounding skin. This primary chancre is often seen on the inner surface of
the prepuce or glans of the penis and even in the coronal sulcus, where it may be missed if the
prepuce is not fully retracted. In case of females the chancre is hardly seen from outside as it
often involves the innerside of labia minora or even the cervix, which the patient may not be
aware of. While genital chancres are always painless, extragenital chancres may be painful and
may occur in the anal or perianal region, lip, tongue, nipple etc. Extragenital chancres are also
relatively softer than their genital counterparts.
Regional lymphatic involvement is a very characteristic feature. The lymph nodes become
enlarged, remain discrete with rubbery consistency. These are always painless.
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89
Diagnosis is mainly confirmed by finding infecting organism in the clear exudate from the
lesion by dark-ground microscopy. It must be remembered that serum tests do not become
positive for 2 to 3 months after the appearance of chancre. So negative results of these serum
tests cannot exclude primary syphilis.
2. Secondary syphilis.— This stage appears in 2 to 3 months after the primary syphilis,
the actual range is about 1 month to 6 months.
The commonest manifestation of secondary syphilis is a generalized rash dull red or coppery
in colour. This rash is characteristically pleomorphic showing macular, roseolar, papulo-squamous
and even other varieties. The next important manifestation is the appearance of snail-track ulcers,
which are formed by coalescence of small, round and superficial erosions in the mouth. Condyloma
lata is another characteristic manifestation of this stage of syphilis. These are wart-like growths
which are teemed with treponemes and are seen in the mucocutaneous junctions e.g. anus, vulva
and perineum. A generalized painless lymphadenopathy also occurs at this stage. The most
characteristic finding is enlargement of epitrochlear and suboccipital groups of lymph nodes
which are almost always present. Less common symptoms include sore throat, 'moth-eaten'
alopecia, bone and joint pains, iritis, hepatitis etc. There may be constitutional symptoms e.g.
malaise, headache, backache and pyrexia. Occasionally acute meningitis, cranial nerve or spinal
nerve palsies may occur due to irregular pachymeningitis.
3. Tertiary syphilis.— Many cases spontaneously recover in the secondary stage. Only
35% of untreated syphilitics will develop tertiary syphilis. At this stage syphilis mainly affects
the blood vessels. There is a perivascular collection of lymphocytes and plasma cells. Plasma
cells are the characteristic element in the reaction to the treponema pallidum. The inner coat of
the small arteries is concentrically thickened, which is known as syphilitic endarteritis obliterans
which results in ischaemia of the tissue. In the tertiary stage the lesions may be localised or
diffuse.
The localized lesion, the gumma is of surgical significance.This is an accumulation of
granulation tissue with central necrosis due to syphilitic hypersensitivity reaction. Sloughing or
caseation of the centre causes formation of a gummatous ulcer. This is a painless punched out
ulcer with wash-leather slough on the floor. Microscopically surrounding the necrotic or the
caseous centre there are lymphocytes and plasma cells which are further surrounded by
proliferating fibroblasts and definite fibrous tissue. To the naked eye gumma appears as a yellow
homogeneous mass surrounded by fibrous tissue. When near the surface ulceration almost always
occurs.
Diffuse manifestations of this stage of syphilis may involve almost any structure. Some may
suffer from neurosyphilis, some from cardiovascular syphilis etc.
Serum tests are always positive in this stage of syphilis.
4. Latent syphilis.— Sometimes syphilis may remain symptomless and latent following
untreated secondary stage. The serum tests are always positive in these cases.
Congenital syphilis.— Treponema pallidum from an infected mother may cross the
placental barrier to enter foetal circulation. Thus congenital syphilis is come across. Congenital
syphilis can be divided into 2 groups — (i) early congenital syphilis and (ii) late congenital
syphilis.
(i)
EARLY CONGENITAL SYPHILIS.— The manifestations in this group appear within
a few weeks in the new bom. There may be generalized rash and mucous erosions as seen in
secondary syphilis. There may be syphilitic rhinitis with nasal discharge which interfere with
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90
suckling. Loss of weight, periostitis, osteochondritis, hepatosplenomegaly and basal meningitis
are the various manifestations. Affection may be so severe as to cause death in early infancy
due to syphilitic pneumonia.
(ii)
LATE CONGENITAL SYPHILIS.— The characteristic manifestations of tertiary syphilis
may occur in old children or puberty in this condition. These are often called stigmata or late
congenital syphilis. Hutchinson's classical triad should be remembered in this respect. These include
interstitial keratitis, 8th nerve deafness and Hutchinson's teeth — band-shaped deformity of the
upper central incisors. Other classical signs of late congenital syphilis are saddle nose, sabre
tibia, Clutton's joint (painless effusion with various subluxations commonly affecting the knee
joint), perforation of the palate and parietal bossing.
Treatment.— Penicillin is the antibiotic of choice in syphilis. Procaine Penicillin G 6 lacs
units daily for 15 days is highly effective in early syphilis. In case of late syphilis the same dose
should be prolonged upto 3 weeks. Serological tests should be performed at regular intervals
for 20 years after treatment to be confirmed about the cure of the disease.
Those patients who are allergic to penicillin, tetracycline, erythromycin and cephaloridine
are the useful antibiotics for this condition. Doxycycline is a very useful drug and should be
used in the dose of 100 mg thrice daily for 15 days.
Jarisch Herxheimer reaction.— Some patients after first injection often develop malaise, pyrexia
and rigors for a few hours. This reaction is seen only in early syphilis and not in late syphilis.
Prednisone 10 mg 4 times daily for 3 days may be given before penicillin injection to prevent
this reaction.
To prevent congenital syphilis the same dose of procaine penicillin G should be given to
the mother for 15 days as early as possible in pregnancy.
ACTINOMYCOSIS
It is a chronic, suppurative granulomatous disease caused by a fungus-like organism
Actinomyces Israelii. It is an anaerobic gram-positive filamentous organism.
It has been established that A. Israelii may be recovered from the oral mucosa, tonsillar
crypts, dental cavities and pharynx of many normal persons. The method of infection is not
definitely known. Entry into the tissue is resumed to result from trauma or ulceration or by
tooth extraction. It is not known whether additional factors like hypersensitivity is necessary for
subsequent evolution.
The actinomyces grow in the human tissues in the form of yellow colonies which are easily
seen in the pus as 'sulphur granules' by the naked eye. When these granules are crushed under a
cover glass and examined unstained, two elements may be distinguished — branching mycelial
elements and club forms. The filaments are gram-positive and constitute greater part of the
body, whereas the clubs are gram-negative pear-shaped bodies which form a fringe around the
periphery of the colony of the body. The filaments are arranged in radiate fashion from the
centre part of the granule. The characteristic radial arrangement is responsible for the familiar
term 'ray fungus'. The clubs probably represent a means of defence against the invading
organism.
Three clinical forms of actinomycosis are encountered. In more than half the cases the
initial lesion involves the tissues of the face and neck including the mandible (facio-cervical
type), in the remainder cases the lungs and the gastrointestinal tract are involved with equal
SPECIAL INFECTIONS
91
frequency. The basic pathology is a subacute pyogenic inflammation with considerable induration
and multiple sinus formation.
1.
FACIO-CERVICAL actinomycosis.— The lower jaw is more frequently involved, which
may be adjacent to a carious tooth. A firm mass slowly develops. It is characteristically seen
over the angle of the mandible. It is frequently painless. The connective tissue, the muscle and
the bone are successively destroyed and
replaced by granulation tissue. An
abundant fibrous tissue reaction may
lead to brawny induration in the affected
area. Gradually softening occurs at few
places with appearance of abscesses,
which ultimately burst to form multiple
sinuses. So the overlying skin becomes
indurated and bluish in colour with
openings of numerous sinuses. The pus
is usually thin and contains sulphur
granules which are diagnostic.
2.
mainly the caecum or appendix is
affected. In the submucosa flat grey
nodules appear, which turn into a large
firm mass, readily mistaken for
malignancy. Suppuration within it forms
Fig.8.1.— Facio-cervicai actinomycosis.
multiple abscesses. Ultimately the
abdominal wall is involved with multiple
sinuses discharging thin pus with sulphur granules.
The liver is the second organ affected by this disease. It is involved either by direct extension
or by blood borne infection through portal vein. The lesion is a honey-comb mass within the
liver which resembles a sponge saturated with pus.
3.
LUNGS are involved by direct spread from the neck downwards or from abdomen
upwards. Lungs may be affected by aspiration of the fungus. The lung becomes riddled with
abscess cavities surrounded by abundant fibrous tissue. Gradually the chest wall may be involved
with multiple sinuses.
Spread.— Actinomycosis is not known to spread. Sometimes the lesion may rupture into a
vessel to cause blood borne metastases in distant organs e.g. the liver, the brain, the heart,
kidney, spleen and ovary. Spread by lymphatics is unknown.
Treatment.— A. Israelii are sensitive to penicillin, lincomycin and tetracycline. If penicillin
is used a prolonged intensive course should be given 10 mega units daily in the beginning
reducing to 4 mega units daily later on.
LEPROSY
It is an infectious disease which is mainly seen in the tropical and subtropical countries. It
is caused by Mycobacterium Leprae, an acid-fast bacillus almost similar to tubercle bacillus.
The source of infection is not the skin but mainly from nasal secretions of patients with
92
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lepromatous leprosy. But it requires some other factors associated with poverty and lack of
hygienic conditions.
Pathology.— According to the resistance of the host two extreme varieties of leprosy are
noticed — lepromatous leprosy and tuberculoid leprosy. There are of course a spectrum of ranges
between these two extreme varieties which are known as border-line-lepromatous or borderline-tuberculoid varieties.
Lepromatous leprosy.— When there is least resistance from the host, the bacteria multiply
with little cellular response. The subcutaneous tissues are loaded with masses of bacteria with
little cellular response except a few macrophages and a few lymphocytes.
Tuberculoid leprosy.— In this type the tissue responses are strong and one can see localized
lesions where bacilli are not numerous with the presence of epitheloid cells, foreign body giant
cells and many lymphocytes almost like a tubercle. It must be remembered that tuberculoid
leprosy causes early and severe deformity but localized, whereas lepromatous leprosy causes
mild and late deformities but are wide spread. The most severely deformed patients are those
affected by border-line forms.
Clinical features.— Though it is a systemic infection, leprosy presents predominantly as
an infection of the skin, upper respiratory tract and peripheral nerves. The characteristic feature
of this disease is its predilection to affect the surface of the body, particularly the cool areas.
Warm areas like the axilla, gluteal clefts etc. usually remain unaffected. The testis is affected
though the ovary and deeply placed organs remain unaffected. The upper respiratory tract like
lining of the nose is severely involved. As leprosy does not affect the vital organs of the body,
it does not become fatal.
One of the most characteristic features of leprosy is its effect on nerves. Cellular infiltrate
may be seen localized around nerve fibres in the skin. The superficial nerves e.g. posterior
auricular, superficial temporal and even ulnar nerves become swollen and tender. Anaesthesia
that results from involvement of cutaneous nerves is an important point in diagnosis and often
becomes the first sign of leprosy. It must be understood that the disfigurement of hands and
feet which are often seen in leprosy is not due to the disease itself, but to the damage and
misuse which follows loss of pain sensation.
Systemic symptoms such as malaise, fever and joint pain may occur. Occasionally rhinitis,
iridocyclitis, swollen and tender lymph nodes and acute epididymoorchitis may be noticed.
Treatment.— In the beginning medicine is quite effective and it has become possible to
cure this disease medically. Diaminodiphenyl sulphone (Dapsone, DDS) is the selective
bacteriostatic drug for this disease. 50 to 100 mg daily of this drug should be prescribed to the
patients till they become bacteriologically negative. It usually takes a long time of therapy about
3 years for tuberculoid leprosy and about 10 years or more in case of lepromatous leprosy. DDS
resistant cases have been found in increasing numbers particularly among lepromatous type of
leprosy who have received smaller doses of DDS or the treatment has been terminated before
cure.
The other anti-leprosy drugs are rifampicin, ethionamide and clofazimine. So a combination
of drugs has been chosen by W.H.O. to tackle these resistant cases. DDS 100 mg and clofazimine
50 mg daily with supervised doses of rifampicin 600 mg and clofazimine 300 mg monthly for 2
years is usually recommended. Ethionamide in the dose of 250 mg daily can be given as
alternative to clofazimine.
Surgery is only recommended for various deformities of leprosy.
SPECIAL INFECTIONS
93
AIDS
Pathology.— Acquired Immune Deficiency Syndrome (AIDS) has been the topic of the day,
though surgeons are not so much concerned with this disease, as it is not a surgically curable
disease. It is caused by a virus — Human Immune Deficiency Virus (HIV I and II). It is not an
ordinary virus and it has a sinister capability of destroying T-cells and thus devastating the
entire immune system. This virus is present in most body fluids of the patients particularly in
the blood and semen. Spread of infection is mostly by sexual contact or through transfusion of
infected blood. The foetus of an infected mother is also involved.
Clinical features.— The patients usually remain asymptomatic for 1 or 2 months. Even if
symptoms do occur they are often non-specific.
General symptoms.— The patients often suffer from fever, malaise, lethergy, myalgia,
lymphadenopathy and sore throat in about 30% of cases. There may be thrombocytopenia.
Chest symptoms.— Life threating pneumonia may occur due to opportunistic infections.
Pneumonia due to Pneumocystis Carinii is a quite common presentation of AIDS, though fungi,
atypical micobacteria and other organisms may be responsible.
Skin manifestations.— Kaposi's sarcoma is a frequent manifestation of aids. It is presented as
purplish or bluish or brownish nodules particularly on the limbs. In due course the nodules
ulcerate and the disease disseminates widely. Some patients of AIDS present with severe
necrotising Herpes simplex. A few patients present with other non-specific skin infections e.g.
folliculitis, intertrigo and eczema.
Abdominal lesions.— 'Gay Bowel Syndrome' refers to procto-colitis due to enteric organisms
including shigella, salmonella, giardia, E. histolytica. The most common presentation of AIDS
patients is cramping abdominal pain with diarrhoea. Persistent diarrhoea can be due to HIV
infection only. If Kaposi's sarcoma involves G.I. tract, there may be G.I. bleeding. There may be
retroperitoneal lymphadenopathy which may cause intestinal obstruction or intussusception.
Laparotomy may be indicated for perforation, obstruction and bleeding.
Neurological manifestations.— About 40% of patients show neurological symptoms, of which
meningitis is the commonest. Meningitis may occur due to direct effect of AIDS virus or may
be caused by cryptococcus, mycobacteria, toxoplasma, fungi and Herpes simplex. Cerebral
lymphoma and subacute encephalitis are also seen in these cases. CT scan is particularly helpful
in diagnosing cerebral lymphoma.
Diagnosis.— As many patients remain asymptomatic and the symptoms are also non-specific,
diagnosis is mainly confirmed by finding antibodies to the virus detected by tests of high
sensitivity and specificity. It must be remembered that a positive antibody test only means that
the person has been exposed to the virus and only 50% of sero-positive patients will progress to
full blown AIDS patients.
Treatment.— No specific treatment has been invented of this disease. Prevention is the
main treatment today. The HIV virus mutates very fast and that is why it has not been possible
to develop a successful vaccine against AIDS.
CYSTS
A soft fluctuant swelling containing fluid in a sac lined by epithelium or endothelium is
called a cysf. The word 'cyst' is derived from a greek word meaning 'bladder.'
Classification.— Two types of classification of cysts are known in surgical practise.
I. In the FIRST TYPE OF CLASSIFICATION the cysts are broadly divided into two varieties
— 1. True cysts and 2. False cysts (pseudocysts).
1. True cysts are lined by epithelium or endothelium, though if infected it may be lined
by granulation tissue. The fluid of a true cyst may be either of the following two varieties —
(i) It is usually serous or mucoid and varies in colour from almost colourless to brownstaining due to presence of altered blood. Cholesterol crystals are often present in the fluid.
(ii) The content may be porridge or toothpaste-like due to accumulation of desquamated
epithelium within the secretion. Such content is usually found in dermoid, epidermoid, branchial
cysts and sebaceous cysts.
2. False Cysts or Pseudocysts.— These may be of the following types :—
(i) Exudation cysts.— Such cysts develop from exudation of fluid and are limited in
anatomical spaces e.g. pseudopancreatic cyst (encysted collection of fluid in the lesser sac), fluid
of tuberculous peritonitis lined by adherent coils of intestine, vaginal hydrocele, bursa.
(ii) Degeneration cysts.— Such cysts develop as degeneration in the centre of a malignant
tumour due to haemorrhage or ischaemic necrosis or colliquative necrosis. Apoplectic cyst is an
example of this type.
II. The SECOND TYPE OF CLASSIFICATION of cysts is based on whether it is congenital
or acquired type.
1. Congenital cysts are of following varieties :—
(a) Sequestration dermoid.— This type of cyst develops at the line of closure of embryonic
clefts due to burial of dermal cells in this fusion line. The usual sites are in the midline of the body
(particularly in the neck), at the outer angle of the orbit (angular dermoid), in the upper part of
the anterior triangle of the neck (which is known as branchial cyst, developed due to persistence
of precervical pouch after fusion of the branchial clefts).
(b) Tubulo-embryonic or tubulo-dermoid cyst.— Such cysts develop in the tract of an
ectodermal tube e.g. thyroglossal cyst from the thyroglossal duct; post-anal dermoid from
post-anal gut; ependymal cyst in the brain; pituitary cyst arising from non-obliterated part of
Rathke's pouch.
(c) Cysts of embryonic remnants.— Certain cysts develop from embryonic tubules or ducts
which normally disappear. The examples of such cysts are cysts of the urachus and vitellointestinal duct; hydatid of Morgagni from remnants of paramesonephric ducts; cyst from the
remains of mesonephric duct (Wolffian body) which is known as organ of Giraldes.
CYSTS
95
2. Acquired cysts.— The various types of acquired cysts are as follows :—
(a) Retention cyst.— Such cyst develops due to retention of secretion of a gland due to
obstruction of its duct. The common examples are sebaceous cysts, cysts of the breasts, mucous
cysts of the lips and cheeks, pancreatic cyst, parotid cyst, Bartholin's cyst etc.
(b) Distension cyst.— Such cyst develops from distension of normal acini or follicles of
a gland e.g. thyroid cyst, ovarian cyst. Lymphatic cyst and cystic hygromas are also included
in this variety as such cysts also develop due to distension of lymph sacs or lymphatics.
(c) Exudation cyst.— This type of cyst develops due to exudation of fluid into an
anatomical space already lined by endothelium e.g. vaginal hydrocele, bursa and pseudopancreatic cyst. It is noteworthy that these are usually false cysts according to the previous
classification.
(d) Degeneration cyst.— These are degeneration cysts mentioned under the group of
false cysts (see above).
(e) Cystic tumours e.g. dermoid cyst of the ovary, cystadenomas of the ovary,
cystadenoma of the breast etc.
(f) Implantation dermoids.— Such cysts develop when squamous epithelium of the skin
is driven in by a penetrating wound. Such cysts are usually seen in the finger, hand, or sole of
the foot.
(g) Traumatic cyst.— Sometimes haematoma within the muscles, fascia or subcutaneous
tissue may resolve into a cyst. Such cyst contains straw-or brown-coloured fluid containing
cholesterol crystals and is usually lined by endothelium.
(h) Parasitic cysts.— In this group the commonest is hydatid cyst developed from
infestation of Taenia Echinococcus. Such cysts are mostly seen in the liver or lung though they
may be seen in other parts of the body as well. Besides hydatid cyst other cysts in this group
are — cysticercosis due to infestation of taenia solium. The cysticercus is the intermediate stage
of the parasite. This is mainly a disease of the pig, though human beings are rarely affected.
The cysts can occur in any organ. In the brain they produce pressure symptoms. These cysts
are often calcified, so X-ray can diagnose. Excision is the only treatment.
Trichiniasis or cysts of Trichinia spiralis mainly affect the muscle.
Clinical features of a cyst.—
HISTORY.— A few points are particularly noted in history —
(i) Duration of the swelling.— Whether the swelling is present there from birth or it is
of recent origin.
(ii) How did the swelling appear — whether spontaneous, following injury or a disease?
(iii) Pain.— Whether the cyst is painless or painful? Painful cyst is mainly inflammatory
or indicates presence of secondary infection.
(iv) Growth of the cyst.— How fast is the growth of the swelling?
(v) General health.— If the swelling is associated with anaemia, anorexia and cachexia
possibility of cystic tumour or degeneration cyst should be considered.
Physical Examination.—
INSPECTION.—
(i)
Site is highly important as dermoid cyst is often diagnosed by the site alone. Certain
congenital cysts are also diagnosed easily by the site alone.
(ii)
Number is also important as multiple cysts are characteristically seen in sebaceous
cysts.
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96
(iii)
Surface and margin.— Smooth surface and regular margin are characteristic features of
a cyst.
PALPATION.—
(i) Surface and margin.— Palpation reveals smooth spherical surface with regular margin.
(ii) Consistency.— A cyst is usually soft in consistency. When the fluid inside the cyst
remains under tension, the consistency may be even hard, but the centre of the swelling will
yield on pressure (this is not possible in case of a soild tumour).
(iii) Fluctuation.— A cyst is a fluctuating swelling.
(iv) Fluid thrill.— In case of a big cyst fluid thrill test will be positive.
(v) Translucency.— While a few cysts are brilliantly translucent as they contain clear fluid
e.g. cystic hygroma; but a few cysts are not translucent as they do not contain clear fluid and
instead contain pultaceous material or blood e.g. dermoid cyst, sebaceous cyst and cystic
tumours.
Effects of a cyst.—
(a) A cyst may press on neighbouring structures particularly the blood vessels to cause
venous congestion and varicosity of veins e.g. ovarian cyst causing varicose veins of the lower
limb.
(b) Cyst may press on neighbouring ducts e.g. choledochal cyst pressing on the common
bile duct.
Complications.—
(i) Infection.— This is the commonest complication of a cyst. When infected it becomes
painful. Gradually it will adhere to the surrounding structures. Later on an abscess may develop,
which if untreated will discharge on the surface resulting in an ulcer or a sinus.
(ii) Haemorrhage.— Haemorrhage inside a cyst is also very common. When a cyst becomes
suddenly painful, haemorrhage into the cyst should be suspected. Such haemorrhage may
cause fatal e.g. sudden haemorrhage into a thyroid cyst may cause pressue on the trachea
which may lead to fatal consequences.
(iii) Torsion.— Certain cysts are notorious for this complication e.g. ovarian dermoids.
This may lead to abdominal emergencies.
(iv) Calcification.— In case of certain long standing cysts calcification of wall is not
uncommon. A few cysts are particularly prone to such complication e.g. hydatid cyst and
cysticercosis.
A few important and common cysts are discussed below :—
DERMOID CYST
A dermoid cyst is a cyst which lies deep to the skin and is lined by skin. So a dermoid cyst
can be called an epidermal cyst. These cysts are lined by squamous epithelium and contain
pultaceous or tooth paste-like material which contain desquamated epithelial cells.
There are four types of dermoid cyst :
(i) Sequestration dermoid.
(ii) Implantation dermoid — Acquired variety.
(iii) Tubulo-dermoid.
(iv) Teratomatous dermoid
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97
SEQUESTRATION DERMOID
This is a congenital variety of dermoid cyst, which is formed by inclusion of epithelium
buried at the line of embryonic fusions. So these are found along the lines of fusion of the two
embryonic segments.
Pathology.—
This cyst is lined by stratified squamous epithelium with hair, hair follicles, sebaceous
glands and sweat glands. It contains white pultaceous tooth paste-like desquamated material
with or without hairs. It is mixture of sebum, sweat and desquamated epithelial cells.
Common sites are.—
1. At the midline of the body particularly in the neck.
2. External angular — just above the outer canthus of the eye.— At the line of fusion of
the frontonasal and maxillary processes.
3. Post auricular — behind the ear — at the site of fusion of the mesodermal hillocks.
4. On the skull at the site of fusion of the skull bones.
5. At the midline of the face particularly at the root of the nose.
Origin.—
At the line of embryonic fusion, a few ectodermal cells are sequestrated into the deeper layer.
Ultimately these cells proliferate and liquify to form a sequestration dermoid cyst. Such cyst lies
almost near the mesoderm from where the bones develop, that is why indentation is often found
in the underlying bone. Sometimes the cyst starts in the mesoderm so that there may be
prolongation of the cyst through the bone and a portion of the cyst may remain intracranial.
Clinical Features.—
HISTORY.—
Duration.— The cyst may be noticed at birth, but is usually seen a few years later — the
time taken to form the cyst.
SYMPTOMS.—
A painless swelling, which is slowly growing is the main symptom. Cosmetic disfigurement
is the main complaint. Such cyst hardly becomes big enough to cause any serious mechanical
disability and rarely may become infected.
LOCAL EXAMINATIONS.—
(i) Site.— The site is very peculiar as this must be at the embryonic fusion.
(ii) Size and shape.— Such cyst hardly attains a size bigger than 2 cm in diameter. It is
usually ovoid or spherical in shape.
(iii) Surface — is smooth.
(iv) Punctum.— A dermoid cyst does not have a punctum which is always found in
sebaceous cyst.
(v) Consistency.— Such cyst feels soft. It may indent with pressure as the content is
thick pultaceous material, mixture of sebum, sweat and desquamated epithelial cells.
(vi) Compressibility or reducibility.— This cyst can neither be compressed nor be reduced
(cf. meningocele).
(vii) Relations.— Dermoid cyst is not attached to the skin. This cyst is also free from
underlying structures. There may be bony indentation when the bone lies exactly deep to the
cyst. This can be palpated by moving the base of the cyst with a finger (See Fig. 1.3, page 2
of 'Surgical Short Cases' by the same author).
7
A CONCISE TEXTBOOK OF SURGERY
98
(viii) Transillumination test — is always negative.
(ix) While lying above the cranial bones such cyst may have intracranial connection.
X-RAY.— This may show a depression in the bone underlying the cyst or a gap. Such gap
may be present when there is an intracranial extension or a fibrous band may pass through this
bon)' gap and connect the cyst with the underlying duramater.
Complications.—
(i) Infection.
(ii) Suppuration.
(iii) Ulceration.
(iv) Pressure symptoms to the surrounding structures.
Treatment.—
Complete excision of the cyst is the treatment of choice. This should be done under general
anaesthesia as the cyst has to be dissected from the sensitive pericranium moreover there may
be intracranial extension.
If preliminary X-ray shows a gap in the underlying bone, the operation has to be delayed
to give an opportunity for spontaneous closure.
If there is intracranial extension, osteoplastic flap should be removed for excision of the
intracranial part.
IMPLANTATION DERMOID
It is an acquired dermoid and arises from indriven epithelium beneath the skin due to a
puncture injury e.g. needle prick or thorn prick.
Common sites are —
(i) Palm of the hand.
(ii) Any part of the finger.
(iii) Particularly pulp or tip of the finger.
(iv) Sole.
Such dermoid is quite common in gardeners, tailors and women.
Pathology.—
Such cyst is usually lined by stratified squamous epithelium .
The content is white cheesy material formed by desquamated
epithelial cells and sebum. Hair is usually absent.
Clinical features.—
HISTORY.—
A history of puncture injury is usually available. In some cases
the patient often forgets of such injury.
SYMPTOMS.—
A swelling in the finger or palm is usually the presenting
feature. The cyst may be slightly painful.
EXAMINATIONS.—
A tense cystic swelling is found in the finger or palm. As the
cyst is quite tense, the consistency is often firm or even hard. There
may be a scar on the skin overlying the cyst. Fluctuation is very Fig.9.1.— An implantation
difficult to elicit as the cyst is small and tense.
dermoid in the finger.
CYSTS
99
The most important clinical feature is the presence of a tense cyst in the finger or palm with
a previous history of a punctured wound.
Complications.—
(i) Infection.
(ii) Suppuration.
(iii) Bursting.
Treatment is complete excision of the cyst.
TUBULO-DERMOID
This is also an epidermal cyst, but such cyst develops from an unobliterated portion of a
congenital ectodermal duct or tube.
Pathology.—
The cyst is formed by accumulation of secretion of the lining ectodermal cells of the
unobliterated portion of an embryonic duct.
Examples.—
(i) Thyroglossal cyst — develops from the thyroglossal duct. It is the commonest example
of tubulo-dermoid cyst.
(ii) Post-anal dermoid — develops from remnant of neurenteric canal or post-anal gut.
But it is now regarded as a simple form of teratoma.
(iii) Ependymal cyst in the brain — from the sequestration of cells derived from the
infolding neuroectoderm.
TERATOMATOUS DERMOID
This is a cystic swelling develops from the totipotent cells with ectodermal predominence.
Such cyst usually contains mesodermal elements like bone, cartilage etc. Hairs are almost
always present in such cyst. So the usual contents are bone, cartilage, tooth, hair and cheesy
material.
Common sites are —
(i) Ovary — ovarian cyst.
(ii) Testis — teratoma.
(iii) Mediastinum — mediastinal cyst.
(iv) Retroperitoneum —• retroperitoneal cyst.
(v) Post-anal dermoid.
.
SEBACEOUS CYST
Sebaceous glands are present in the skin. These glands secrete sebum which keeps the skin
soft and oily. The duct of the sebaceous gland mainly opens into the hair follicle and rarely
may open directly on to the skin. If the duct or the mouth of the sebaceous gland becomes
blocked, the gland becomes distended with its own secretion and forms a sebaceous cyst. So
this is a retention cyst and is most accurately called 'epidermoid cyst' since such cyst is lined
by superficial squamous cells.
Pathology.—
Such ,cyst is lined by squamous epithelium and contains sebum which is yellowish
A CONCISE TEXTBOOK OF SURGERY
100
pultaceous material with unpleasent smell. Such material contains sebum, fat and desquamated
epithelial cells.
Common sites.—
A sebaceous cyst can be seen anywhere in the body but most commonly seen in those parts
where there are plenty of sebaceous glands. Such sites are —
(i) The scalp.
(ii) Face.
(iii) Scrotum. The characteristic feature here is — that the cysts are multiple and when
well formed they feel solid.
There is no sebaceous gland in the palm or sole, so sebaceous cyst is never seen in these
areas.
Clinical features.—
(i) It is a typical cystic swelling which is spherical in shape. Its size varies from a few
millimetres to about 5 cm. in diameter. The surface is smooth and there is a bluish or blackish
spot or punctum which indicates the blocked opening of the duct.
(ii) Such cyst is
always fixed to the
skin, so the overlying
skin cannot be lifted off
the
swelling
(cf.
dermoid cyst and
lipoma). The consis­
tency is cystic. Due to
presence of sebum there
may be indentation due
to pressure with finger
tip. If the cyst is a big
one, fluctuation test
may
be
positive
otherwise it is difficult
to perform. This cyst is
free from underlying
Fig.9.2.— Shows two sebaceous cysts of the scalp. Note that punctum cannot
structures and it can be
be seen which is a common finding of a sebaceous cyst of the scalp.
moved easily with the
skin.
(iii) Transillumination test is almost always negative.
(iv) The swelling is usually not tender. In case it is tender, the cyst is obviously infected.
Treatment.—
Total excision of the cyst is the treatment of choice. If the cyst is infected, preliminary
antibiotic treatment should be given and the excision is only possible when the infection has
subsided.
If the cyst is a small one it can be excised under local anaesthesia.
Two kinds of procedure may be adopted —
(a)
Dissection method.— An elliptical incision is made on the skin including the punctum.
The cyst is gradually dissected from the surrounding skin till the entire cyst can be removed
CYSTS
101
intact. It must be remembered that the whole of the cyst wall must be removed, otherwise
recurrence is inevitable. Such dissection method is particularly applicable when the cyst was
infected previously since this will make the cyst wall well defined and thick.
(b)
Incision-avulsion technique.— Under local anaesthesia an incision is made through the
skin into the cyst. Some contents of the cyst are squeezed out. The cyst wall is then held with
a pair of dissecting forceps and the cyst is carefully avulsed out.
TREATMENT OF SCROTAL SEBACEOUS CYST.—
(i) If it is solitary — excision of the cyst should be performed.
(ii) If the cysts are multiple affecting a part of the scrotal skin — that part of the scrotal
skin including the sebaceous cysts should be excised.
(iii) If the cysts are multiple and scattered all over the scrotal skin — the whole of the
scrotal skin should be excised and the testes have to be placed in pockets made in the
subcutaneous tissue at the medial side of the respective thigh.
Complications.—
(i) Infection.— The sebaceous cyst is very prone to infection. When it is infected, the
overlying skin becomes red. A sebaceous cyst may be repeatedly infected.
Once infected, antibiotic treatment should be started. If the infection subsides, excision of
the cyst should be carried out as mentioned above.
If infection does not subside with antibiotic treatment, it should be incised and the pus and
semiliquid foetid material are expelled. Now the cyst wall is gradually dissected out or avulsed
under antibiotic cover.
(ii) Ulceration.— This complication arises when an infected cyst ruptures by itself and
discharges its contents. The ulcer is covered by granulation tissue. It may look like an
epithelioma. When the sebaceous cyst of the scalp ulcerated, excessive granulation tissue forms
resembling fungating epithelioma. This is called the Cock's peculiar tumour (See Fig. 3.68 of
'A Manual On Clinical Surgery').
(iii) Sebaceous horn.— Slow discharge of sebum from a wide punctum sometimes hardens.
This forms the sebaceous horn (See Fig. 3.69 of 'A Manual On clinical Surgery').
(iv) Calcification.— This is a rare complications though it is seen in the sebaceous cyst
of the scrotum.
(v) Malignancy.— Very rarely malignancy may develop which is often in the form of
basal cell carcinoma.
COMMON TUMOURS AND
MISCELLANEOUS LESIONS
OF THE SKIN
Definition of a tumour.— A tumour or 'neoplasm' is a growth of new cells which
proliferate without relation to the needs of the body. The most important two processes which
play part are abnormal reproduction and abnormal differentiation. So abnormal behaviour is
of greatest significance. It must be remembered that the term 'tumour' should be reserved for
new growths only and should not be used for any 'swelling' either inflammatory or traumatic.
In that way the term 'neoplasm' is more appropriate.
A few definitions should be clearly understood in respect of tumours —
Metaplasia.— It is a condition in which there is a change in one differentiated tissue so
that it resembles another type of a similarly differentiated tissue. The word 'differentiated'
should be noted, as it excludes tumour as a form of metaplasia. Examples of squamous
metaplasia are that simple columnar epithelium of gallbladder in chronic cholecystitis especially
if accompanied by stones may be converted to squamous epithelium which is a precancerous
condition. Similarly transitional epithelium of renal pelvis and bladder in chronic infection
particularly with presence of stones may be converted to squamous epithelium. These
metaplasias mostly occur due to chronic irritation. Columnar metaplasia is relatively uncommon
and is sometimes seen in cervical erosion when squamous epithelium of ectocervix is replaced
by a simple columnar epithelium.
Dystrophy.— This is defined as a disorder, usually congenital, of the structure or function
of an organ or tissue. The alternative term dysplasia may also be used for such an abnormal
development of tissue. Dyscrasia literally means a bad mixture and is now used only by
haematologists to describe any blood disorder of uncertain aetiology.
Anaplasia.— It sometimes happens that a malignant tumour consists merely of a diffuse
mass of irregular cells which do not resemble any normal tissue. Such complete undifferentiation
is called 'anaplasia'. In this case the tumour is so poorly differentiated that they defy recognition
i.e. the parent tissue is very poorly reproduced.
Teratomas.— These are tumours arising from totipotential cells i.e. the cells capable of
differentiating into any of the tissues of the body. So representatives of each of the three germ
layers (e.g. ectoderm, endoderm and mesoderm) must be present before a teratoma can be
diagnosed. Though in most cases one particular tissue overgrows all the others. Teratomatous
dermoid is one type of these tumours which may be seen in the ovary, testis, superior
mediastinum, retroperitoneum and in the presacral area. Malignant change may occur. Such
dermoid contains hair, teeth, muscle, gland tissue etc. A peculiar type, known as sacrococcygeal
teratoma, may develop into a part of a foetus and is considered as 'foetus in foetu'.
The tumours are broadly divided into two groups — 1. Benign or innocent and 2.
Malignant. Though a great practical importance is given to this classification, yet intermediate
types of behaviour exist in certain tumours which do not fall properly in either of these two
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
103
categories. The characteristics of the two groups must be considered —
1. Benign or innocent tumours.— The cells which constitute this type of tumour show
no tendency to invade the surrounding tissues. The excessive accumulation of cells produces
an expanding lesion which causes atrophy of the surrounding tissues which form a capsule
around such tumour. So presence of a capsule is a characteristic feature of a benign tumour.
Benign tumours proliferate slowly and show little evidence of mitosis. The arrangement of the
cells closely resembles that of the parent tissue — well differentiated. In nutshell the
characteristics of benign tumours are —
(i) These tumours are well circumscribed and possess capsules.
(ii) Benign tumours are usually smaller in size than malignant ones. Though a few
benign tumours are known for their huge sizes e.g. ovarian cystadenoma, uterine fibroids etc.
(iii) The rate of growth of benign tumour is generally slow and it usually exists for a
longer period of time.
(iv) Benign tumours usually produce symptoms due to the swelling and pressure effects
on the surrounding structures.
(v) A few benign tumours are known to secrete hormones which produce symptoms in
that way e.g. islet-cell tumours of the pancreas, phaeochromocytoma, adrenal cortex adenoma
giving rise to Cushing's syndrome, Conn's syndrome or adrenogenital syndrome.
(vi) Ulceration and haemorrhage are rare in case of benign tumours.
(vii) Benign tumours never metastasise.
2. Malignant tumours.— The hallmark of malignant tumours is invasiveness. The tumour
edge is therefore ill-defined in contrast to the well-defined encapsulated margin of benign
tumours. It is this infiltrative capacity which gives it the name 'cancer' (the crab). Excluding the
locally malignant group, all malignant tumours metastasize.
The characteristic features of malignant tumours are —
(i) Invasiveness as mentioned earlier.
(ii) Malignant tumour is known for its rapid growth. It increases in size very rapidly.
(iii) Malignant tumour almost always metastasizes either by direct spread or by lymphatics
or through blood stream or by transcoelomic implantation.
(iv) Microscopically malignant tumours show much mitotic activity. There is nuclear
enlargement with hyperchromatism. This type of tumour is characterized by failure of cells to
differentiate normally. 'Pleomorphism' in one word is characteristic of this tumour.
(v) This tumour is often associated with anaemia, malnutrition and cachexia due to
excess of blood loss, marrow replacement by metastasis, malabsorption and sometimes due to
toxic product of necrotic tissue circulated in the body and destruction of liver tissue by multiple
hepatic metastases.
(vi) These tumours are more prone to ulceration and haemorrhage.
(vii) A few malignant tumours are known to secrete hormones e.g. hypernephroma
secreting erythropoietin, oat-cell tumours may produce Cushing's syndrome etc.
A comparison of the main features of benign and malignant tumours are given below:—
Benign
1. Age — may occur at any age.
2. Size.— Usually of small size, but
occasionally enormous.
Malignant
1. Age — is usually seen after 40 years.
2. Size.— Usually of large size.
A CONCISE TEXTBOOK OF SURGERY
104
3. Growth.— (i) Slowly-growing; (ii)
Expansive type of growth; (iii) The
progress of growth is erratic with a
tendency to cease.
4. Histological structure.— (i) Welldifferentiated; (ii) Well-formed stroma
with Little tendency to haemorrhage and
necrosis; (iii) Cells regular. Few mitoses.
5. Fixity.— Benign tumours are usually not
fixed to the surrounding structures.
6.
The surrounding structures are not
involved.
7. Benign tumours usually do not show
tendency towards haemorrhage and
ulceration.
8. Metastasis.— Metastases never occur.
9. Cause of death.— Usually not fatal. If
death occurs, it is due to mechanical
pressure - and obstructive effects.
Endocrine adenomata
may
have
hormonal effects.
3. Growth.— (i) Rapidly growing; (ii)
Invasive type of growth; (iii) The progress
is usually relentless until death occurs.
4. Histological structure.— (i) Less welldifferentiated and sometimes completely
anaplastic; (ii) Stroma often poorly
formed. Haemorrhage and necrosis are
common; (iii) Cells are often pleomorphic.
Mitosis often numerous.
5. Malignant tumours are usually fixed to
the surrounding structures due to local
invasion.
6. Involvement of surrounding structures is a
characteristic feature e.g. in case of
malignant tumour of the parotid gland
the facial nerve is often involved and
paralyzed.
7. Malignant tumours show more tendency
towards haemorrhage and ulceration due
to increased vascularity.
8. Metastasis.— Metastases frequent.
9. Cause of death.— Almost invariably fatal
if untreated. Cause of death a
combination
of
mechanical
and
destructive effects, together with blood
loss, secondary infection, starvation etc.
Various types of malignant tumours.—
1. Careinoma-in-situ.— When a malignant tumour has no invasion, the lesion is called
carcinoma-in-situ. The microscopic changes represent an early morphological indication that a
carcinoma or any malignant tumour is beginning to develop. Examples of this condition is
mostly seen in the epithelium particularly in the stratified squamous epithelium of the skin,
mouth and cervix.
2. Locally malignant tumours.— These tumours show prominent local invasion, but
distant metastases are insignificant. The prominent examples are adamantinoma and
craniopharyngioma.
3. Dormant cancer.— Rarely cancers may remain dormant for sometime, even for a
few years, after which they suddenly grow aggressive. These cases are called dormant cancers.
It is often said that these tumours are probably show growing and that is why remain dormant
for a considerable period of time until they are provoked by trauma or intercurrent illness or a
change in hormonal balance e.g. pregnancy or psychological trauma or even after operation
when they start growing as typical malignant tumours.
4. Latent cancer.— The typical example of this condition is prostatic cancer. It is a
relatively uncommon disease. Nevertheless, it is said that if the prostate is routinely sectioned
in cases of all necropsies dying of other diseases, the incidence of prostatic cancer appears to be
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
105
high. In cases of patients of over 90 years of age the incidence is about 100%. This incidence
falls to 70% between the ages of 80 to 90 years and 25% in patients of 50 to 60 years. These
lesions are latent, many presumably remain so until death occurs from another cause.
DIFFERENT VARIETIES OF BENIGN AND MALIGNANT TUMOURS
Tissue of Origin
Benign
Locally Malignant Malignant
Epithelium.—
1. Covering and protective
epithelium.—
(a) Squamous.
(b) Transitional.
(c) Columnar.
2. Compact secreting
- epithelium.—
Squamous-cell
papilloma.
Transitional-cell
papilloma.
Columnar-cell
papilloma.
Adenoma. If cystic,
cystadenoma or
papillary cyst­
adenoma.
3. Other epithelial Tumours
include.—
Connective Tissue.Fibrous tissue.
Nerve sheath.
Fat.
Smooth muscle.
Striated muscle.
Synovium.
Cartilage.
Bone.
Osteoblast.
Osteoclast.
Mesothelium.
Blood vessels and
lymphatics.
Meninges.
Neuroglia.
Chromaffin tissue.
Lymphoid and Haemato­
poietic tissue.
Squamous-cell
carcinoma.
T ransitional-cell
carcinoma.
Adenocarcinoma.
Adenocarcinoma. If
cystic, cystadenocarcinoma.
Basal-cell carcinoma.
Salivary and mucous
gland tumours. Carci­
noid tumours (argentaffinoma). These are
difficult to classify in
terms of behaviour.
Fibroma.
Neurofibroma.
Lipoma.
Leiomyoma.
Rhabdomyoma.
Synovioma.
Chondroma.
Fibrosarcoma.
Neurofibrosarcoma.
Liposarcoma.
Leiomyosarcoma.
Rhabdomyosarcoma.
Malignant synovioma.
Chondrosarcoma.
Osteoma.
Osteoclastoma.
Mesothelioma.
Benign haemangioma
and lymphangioma.
Meningioma.
Astrocyoma.
Oligodendroglioma.
Ependymoma.
Carotid body tumour.
Osteogenic sarcoma.
Malignant osteoclastoma.
Malignant mesothelioma.
Angiosarcoma.
Lymphangio-sarcoma.
Malignant meningioma.
Malignant astrocytoma.
Oligodendroglioma and
ependymoma.
Malignant carotid body
tumour.
Lymphosarcoma.
Reticulum cell-sarcoma.
Hodgkin's disease.
Benign lymphoma.
106
A CONCISE TEXTBOOK OF SURGERY
Tissue of Origin
Benign
Locally Malignant
Malignant
Foetal trophoblast.—
Embryonic Tissue.—
Hydatidiform mole.
Follicular lymphoma.
Multiple myeloma.
Leukaemias and polycythaemia vera.
Chorion-epithelioma.
Totipotential cell.
Pluripotential cell.
Benign teratoma.
Malignant teratoma.
Kidney.
Liver.
Nephroblastoma.
Hepatoblastoma.
Unipotential cell.
Retina.
Hind-brain.
Sympathetic ganglia
and adrenal medulla.
Embryonic Vestiges.—
Notochord.
Enamel organ.
Parapituitary residues.
Branchial cyst.
Hamartoma.—
Melanotic.
Angiomatous.
'Exostoses' and
'Ecchondroses'.
Neurofibromatosis.
Tuberous sclerosis.
Retinoblastoma.
Medulloblastoma.
Ganglioneuroma.
Neuroblastoma.
Chordoma.
Adamantinoma.
Craniopharyngioma.
Branchiogenic carcinoma.
Benign melanoma.
Benign angioma.
Malignant melanoma.
Angiosarcoma.
Neurofibroma.
Glioma.
Chondrosarcoma.
Neurofibrosarcoma.
Malignant glioma.
AETIOLOGY OF MALIGNANT TUMOURS.—
The cause of cancer is not known. A few factors are often incriminated to cause cancer. But
the cause is not one for all cancers. Cigarette smoking is often held responsible for cancer of the
lung, but it has got nothing to do with malignant melanoma or cancer of the breast. The various
agents which may be responsible for cancers in the body are described below.
1.
HYDROCARBONS.— By far the most important of the chemical compounds
responsible to initiate carcinoma is the polycyclic hydrocarbon. Sir Percival Pott observed that
cancer of the skin is more common in men who worked with tar and suggested it to be the
causal agent. By painting tar on a rabit's ear everyday for over 6 months, carcinoma developed
at the end of that time. Thus malignant tumour was produced at will. Tar is a highly complex
substance containing a variety of chemical agents. A hydrocarbon benzpyrene was isolated from
tar and showed that it had a high degree of carcinogenic activity. It was considered that 1 : 2 :
5 : 6 - dibenzanthracene is the main component which is responsible to cause cancer. To be
more precise 1 : 2 - benzanthracene has practically no carcinogenic effect, but the attachment of
a new benzene ring in the 5 : 6 position gives it great carcinogenic power.
Another of the carcinogenic hydrocarbons is the cholanthrene group. It was found that
cholanthrene and methyl cholanthrene are among the most powerful carcinogenic agents known.
Both methyl cholanthrene and benzpyrene contain 1 : 2 - benzanthracene ring system, though
this ring is almost completely lacking in carcinogenic activity.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
107
The carcinogenic azocompounds is the second group which have now been overshadowed
by the carcinogenic hydrocarbones. The carcinogenic property of azocompounds first came to
light as a result of investigation into the action of scarlet red, an azodye as a stimulant of
wound healing. This acts at a distance and only on the liver, the main organ of metabolism in
the body. However its carcinogenic action on the liver is manifested only when there is
deficiency in riboflavin.
Another well known example is the aniline dye cancer of the urinary bladder, in which
the carcinogen is beta naphthylamine. This tumour not only occurs in aniline dye workers, but
also can be readily induced in the dog.
2. SEX HORMONES.— Due to structural resemblance between the carcinogenic
hydrocarbons and the female sex hormones, there is possibility that these hormones may be
carcinogenic. Oestrogen does not act on the skin, but it acts on the mammary epithelium which
is normally under the influence of ovarian stimulation. In normal woman the output of oestrogen
is rhythmical. Though it is said that when the supply is constant and prolonged cancer may
result, yet it seems that oestrogens require co-operation of one or more additional agencies.
The most essential factor is probably heredity. While describing heredity as a cocarcinogen, only
genetic factor does not work. There may be a nongenic Bittner milk factor, which is viral in
nature.
In the prostate there seems to be little doubt that an endocrine dysfunction is an aetiologic
factor. The serum acid phosphatase and urinary 17-ketosteroid levels are elevated which are
indicators of androgen secretion as well. The remarkable beneficial effects of castration and
administration of oestrogen on prostatic cancers also signify this.
3. FiADIATIONS.— Various forms of radiations may act as carcinogens. The early workers
in the X-ray department suffered radiation dermatitis followed by cancer of the skin of the
hand after many years. Osteosarcoma has been reported in bones subjected to radiation for
bone cyst and giant-cell tumour. Multicentric carcinoma of the breast developed in patients
irradiated 10 years previously for Hodgkin's disease of the chest. Many survivors of the
Hiroshima atomic blast ultimately suffered from leukaemia. Cancer of the thyroid has also
developed long time after irradiation of the neck for some other reason.
4. VIRUSES.— Peyton Rous first showed that a cell-free filtrate of a fowl carcinoma
could produce a new tumour when injected into another fowl. The active agent seemed to be
a virus. Later on in 1936 Bittner found that when new bom mice of a high mammary cancer
strain were fostered by mothers of a low cancer strain, the tumour incidence was greatly
reduced. On the other hand new bom mice of a low strain when fostered by mothers of a
high strain showed an increased incidence of breast cancer. The tumour developed when the
animal reached early adult life. He described an 'agent' transmitted through the mother's milk
which was responsible for such mammary cancer. He described it as transmissible milk factor
which is nothing but a virus.
Co-Carcinogens.— Whatever may be the carcinogenic agents there may be some factors
which help the cancers to develop. A match may start a fire, but the material must be
inflammable; a little damp or high breeze may extinguish the flame. The various factors which
probably help carcinogens to form cancers are —
(i)
Heredity.— Majority of the cancer patients give familial history. A familial tendency is
always noticed.
(ii) Chronic irritation.— Radiation is an irritant causing inflammation, but it is also a
108
A CONCISE TEXTBOOK OF SURGERY
carcinogen. Cancer may develop in the scars of old bums. The 'Kangri cancer' of the abdominal
wall in the natives of Kashmir who wear a hot basket of charcoal under their clothes for purposes
of warmth is a result of thermal irritatior..
(iii) Trauma.— When a tumour develops, the patient often recalls having received trauma
at that part before. This is particularly seen in cases of osteosarcoma. But often this relation
has no meaning as the patient's attention has either been directed to the part by the injury
where malignant tumour has already started or that haemorrhage into the tumour has caused
an increase in the size of tumour. It cannot be denied that injury may cause cell destruction
followed by regeneration and this may serve as a promoter where an initiating carcinogen has
already produced a condition of latent cancer.
(iv) Diet.— Thiamine deficiency may activate the virus which may be a carcinogenic one. It
has been noticed that those people with a high incidence of cancer in the liver, the diet is very
low in vitamine. Fats cooked at high temperatures might have carcinogenic properties. At the
end it must be confessed that though very little is known about this subject yet it deserves mention.
(v) Geography.— Incidence of certain cancers is very high in a few countries. Cancer of the
liver is a rare disease in most countries, though it is very common in Java and South Africa.
Burkitt's tumour has also a very definite geographic distribution. Whereas carcinoma of stomach
is so common in Japan, but carcinoma of breast is not so frequent there. Many factors are
responsible for this geographic variation e.g. diet, climate, actinic radiation etc.
SPREAD OF MALIGNANT TUMOURS
There are few subjects of greater importance to the surgeon or more intriguing to the
pathologists than the spread of tumours. Infiltration into the surrounding tissues is a salient
feature of all malignant tumours. The invading cells come across various natural passages,
which then afford an easy route for the malignant cells for further spread. The most important
structures involved in this way are the lymphatics and blood vessels. In both of them the
malignant cells are carried to distant sites. If these cells survive and multiply, a distinct mass of
tumour is produced at this distant site. This is known as metastasis.
Various routes of spread of malignant tumours are :— 1. Local or direct spread; 2. Invasion
by lymphatics; 3. Through blood vessels; 4. Through serous cavities; 5. Natural passages and
6. Inoculation.
1.
Local or direct spread.— Direct infiltration of the surrounding tissues is a
characteristic feature of all malignant tumours. This means that the microscopic extent of a
malignant tumour is more than its microscopic extent. The cancer cells are amoeboid and
motile. The cancer cells are free because of greatly reduced adhesiveness, which in turn seems
to be due to deficiency of calcium in the cell membrane. The cells of benign tumours are
incapable of movement as they are firmly adherent to one another by cell adhesiveness. It has
been suggested that invasiveness of cancer cells is due to hyaluronidase which these cells
produce. Hyaluronidase breaks down resistance of the viscid ground substance which contains
hyaluronic acid. This facilitates invasion into the normal tissue.
The invading cancer cells tend to follow natural clefts or tissue planes and gradually move
in the line of least resistance. Dense fascial sheaths may form barriers which confine malignant
cells for sometimes. This is a well known fact in case of osteosarcoma where periosteum resists
cancer cells to invade surrounding soft tissues for quite sometime. Cartilage is also resistant to
tumour infiltration.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
109
2. Invasion by lymphatics.— Carcinoma shows a particular tendency to invade the
local lymphatics at an early stage. Sarcomata on the other hand, rarely spread via lymphatics.
Carcinoma cells readily enter lymphatics and pass through lymphatics by either permeation
or embolism.
Permeation is the growth of column of tumour cells along the lumen of the vessel. The tumour
cells grow progressively within the lumen of the lymphatics as a solid cord. Sometimes the
central area of the malignant cord may undergo necrosis and even disappear, while the advancing
ends proliferate. Eventually the cord of cells reaches the draining lymph nodes by blocking the
main ducts, the lymph is diverted to adjacent channels and in this way there may be retrograde
deviation of tumour cells. Lymphatic permeation may cause local dermal oedema which produces
the 'peau-d-orange' appearance seen in breast cancer. Through this lymphatic permeation, the
entire skin of the chest wall may be a sheet of confluent carcinoma, producing cancer-en-cuirasse.
The cancer cells stimulate perilymphatic fibrosis, but this does not stop advancement of lymphatic
permeation. In malignant melanoma black spots are seen along the track of lymphatics which
are nothing but intermediate deposits left by lymphatic permeation in its way from the primary
growth towards the regional lymph nodes. Such lymphatic permeation is seen to advance through
the peribroncheal and periarterial lymphatics in bronchogenic carcinoma and through the
perineural lymphatics in carcinoma of the prostate.
Embolism.— Of much greater importance is the spread of carcinoma cells along the
lymphatics by embolism. The regional and distant lymph nodes are early involved by the process
of lymphatic embolism.
In case of lymph nodes, the metastases are at first confined to the subcapsular space. At
this stage the node is not enlarged. Gradually the tumour cells permeate the sinusoids and
replace the parenchyma. Direct spread from node to node is not seen usually as the capsule of
the lymph node is not penetrated till late stage. Lymphatic spread of carcinoma is primarily
embolic. All the lymph from the abdominal organs reach the thoracic duct, which finally opens
into the left jugular vein. Tumour cells thus pass from lymph to blood stream by this route.
Spread along the thoracic duct explains those cases in which cancer of the G. I. tract is associated
with pulmonary metastasis while the liver remains clear. Moreover, familiar involvement of the
supraclavicular lymph nodes is due to tumour emboli lodging behind the valves near the
termination of the duct, thus blocking the duct. From here permeation of the tumours in the
retrograde manner involve the supraclavicular lymph nodes (Virchow's nodes). Retrograde
embolism occurs when the main lymphatic is blocked due to permeation. This explains
involvement of left supraclavicular group of lymph nodes (which is known as Troisier's sign) in
cancer of the G. I. tract, lungs and even testes due to retrograde embolism when the thoracic
duct is blocked. Sometimes the entire length of the thoracic duct is filled with tumour, the
obstruction leading to chylothorax and chylous ascites.
Though less importance is given to the posterior or dorsal spinal lymph path by which
tumour cells may pass up or down for considerable distances, this may explain the upward
passage of tumour cells from the prostate and downward passage of cancer cells from the breast.
This pathway has now been overshadowed by Batson's vertebral system of veins.
3. Spread through blood vessels.— Malignant cells invade small vessels or venules,
become detached and are then carried by the blood stream to some distant site, where they
come across a capillary network. At this site the emboli become impacted, proliferate and develop
into secondary tumour. A second method of blood borne metastasis is by way of the lymphatics.
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All lymphatics drain into the venous circulation and tumour emboli pass through the lymphatics
into the venous circulation. It is difficult to assess how much blood spread is due to primary
venous invasion and how much is secondary to lymphatic involvement. In case of sarcoma,
there is no doubt that invasion is primarily venous, as lymphatic spread is quite uncommon. In
case of carcinomata blood spread occurs sometime after lymphatic involvement and it is quite
possible that much of the blood stream invasion is secondary to lymphatic spread.
Four groups of veins may be invaded :
(i) The systemic veins are frequently invaded by sarcoma as also by carcinoma. Carcinoma
of the thyroid and renal carcinoma are notorious for venous invasion. In case of the latter
there is a tendency for the tumour to grow as a solid column along the lumen of the vein.
Similarly the testicular tumours, particularly the teratomas, distend the spermatic vein by
tumour permeation.
(ii) Pulmonary veins are often invaded by metastatic tumours only when the pulmonary
capillary network is bypassed. Thus the tumour cells reach the left side of the heart from
where they are distributed to the systemic circulation. This is the explanation for the cases in
which there are systemic metastases without apparent involvement of the lungs.
(iii) The portal system of veins is invaded by the tumours of the G.I. tract and pancreas.
The tumour emboli ultimately lodge in the capillaries of the liver, where secondary tumours
are quite common.
.
(iv) The vertebral system of veins of Batson pass up inside the spinal canal and anastomose
with the sacral, lumbar, abdominal and thoracic veins. There are frequent reversals of flow in
this intercommunicating system as a result of coughing, straining and increase of intra-abdominal
pressure, as these veins are valveless. This route may serve to explain the spread of carcinoma
of the prostate to the vertebral column and of bronchogenic carcinoma to the brain.
The commonest organ in which blood borne metastasis occurs in the liver. Not only the G.I.
tract cancers regularly metastasise there, but also carcinomata of the lungs, breast, genitourinary
system, melanomata and sarcomata do also metastasise there. It seems that the liver affords an
excellent nutritional medium for tumour cells.
The next most common site for blood borne metastasis is the lung. It is particularly involved
in cases of carcinomata of the breast, kidney, thyroid, testicular tumours and sarcomata.
Bones are involved third after liver and lungs. Osseous metastases may be osteolytic or
osteosclerotic. In case of the former there are areas of translucency in the bone found
radiologically. The serum alkaline phosphatase level is normal, but sometimes there is sufficient
demineralization to lead to severe hypercalcaemia and renal failure. Ultimately there may be
pathological fracture. Usually carcinoma of the lung, breast, kidney and thyroid show
predilection to bony metastases which are osteolytic in nature. Carcinoma of the prostate often
produces osteosclerotic metastasis particularly in the vertebrae and pelvic bones. In these cases
the secondaries are found as more radio-opaque areas in X-ray. There is raised serum alkaline
phosphatase level, while the serum calcium and phosphate levels remain normal. There is also
a raised level of serum acid phosphatase. Both the primary lesion and skeletal metastases
serve to produce this enzyme, which may possibly be responsible for the characteristic
osteosclerosis of prostatic cancer.
It must be remembered that the areas of bone which contain red bone marrow are usually
involved by metastases e.g. vertebrae, ribs, skull, sternum, pelvic bones and ends of long bones.
The brain is not infrequently the seat of secondary tumours by blood borne metastasis. Lungs
are often the primary source followed by carcinoma of the breast and melanomata. It has been
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
111
postulated that there is a direct communication between the bronchial veins and vertebral plexus
which may explain frequency of lung cancer to produce brain metastasis.
4. Spread through serous cavities (transcoelomic spread).— When a tumour invades
the serosal layer of a viscus, it causes local inflammatory response with a small effusion in the
serous cavity. The cells become incorporated into the fibrinous exudate and are then detached.
They are swept into the effusion. These tumour emboli settle diffusely on its wall, proliferate
and set up in 'seedlings'. The commonest example of transcoelomic spread is seen in cases of
gastric, colonic and ovarian carcinomata. In gastric and colonic cancer there may be
transperitoneal spread to the ovaries, which are known as Krukenberg tumours. Both ovaries
are enlarged with smooth surface and the substance of the ovary is almost replaced by a mass
of mucoid carcinoma. The primary is often a mucoid cancer of the stomach or colon or
occasionally of the breast. Some authorities attribute this to retrograde lymphatic spread as the
surfaces of the involved ovaries are smooth and free of seedling deposits. However most
workers are in the favour of transcoelomic spreads, as the mucoid cancers penetrate easily and
it makes possible for the cells to be detached and deposited on the surface of the ovary and
ultimately invade into the substance of the ovary. Mucoid cancer tends to stimulate a dense
stromal reaction and this may account for the thickened surface.
Transpleural spread occurs in some cases of lung and breast cancer.
The similar type of spread is seen in case of primary cerebral tumours down the
subarachnoid space to the spinal theca. There is no lymphatic in the cerebrospinal space.
Implantation of tumour cells by transcoelomic spread can be accepted without reserve in this
particular case. Seedlings of this type are characteristic of medulloblastoma, though it may also
occur in other malignant gliomata and even in secondary tumours of the brain.
5. Spread along natural passages or epithelial-lined spaces.— The tumour cells
may be carried along such passages as the bronchus and ureter to become implanted at a distant
site to form new growth. It is common in cases of papilloma of the renal pelvis, where this
tumour may spread along the ureter even into the bladder. Sometimes a cancer on the lower lip
may initiate similar type of cancer on the opposing surface of the upper lip.
6. Inoculation.— It is a well known fact that clumsy surgical technique may allow
implantation of cancer cells on to the adjacent incised tissues and it is quite possible that there
may subsequently develop a new tumour. Such spread of tumour can also occur while taking
biopsy. In one case a carcinoma of the breast was removed and a skin flap was taken from the
thigh to close the large gap. A few months later a nodule having the same structure as the
breast cancer developed in the scar on the thigh.
The only common tumours are discussed below :—
BENIGN TUMOURS
PAPILLOMA.-
Papilloma is a common benign sessile or pedunculated tumour composed of squamous
epithelium. It always contains a core of connective tissue element which contains blood vessels
and lymphatics. It is a simple overgrowth of all layers of the skin. A papilloma may arise in
any situation from epithelial surface — either from epidermis or from mucous membrane. The
various examples are :—
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1. From the epidermis — papilloma of the skin.
2. From mucous membrane —
(a) Squamous cells.— It may arise in the tongue, cheek, lip, oesophagus etc.
(b) Transitional cells — pelvis of the ureter, bladder etc.
(c) Columnar cells — Colon and rectum (commonest), stomach, small intestine etc.
3. From the wall of the duct e.g. breast.
4. From the wall of the cyst e.g. ovary or breast.
Papilloma of the skin.—
A cutaneous papilloma may be either of the (i) squamous cell type or (ii) basal cell type.
SQUAMOUS CELL PAPILLOMA.— There are four varieties of such papilloma.
(i) Congenital papilloma.— It is usually present since birth or may appear in early life.
It is often of brownish colour.
(ii) Infective papilloma or infective wart (Verruca vulgaris).— It is a common papilloma
which probably arises from virus infection. It may be single or multiple and may disappear
spontaneously. Such papilloma is seen in children or adolescents. It particularly affects the
fingers, palm and the sole.
Infective wart as mentioned earlier may regress by itself, but may recur after removal.
When it occurs in the sole of the foot (plantar wart) it may be difficult to differentiate from a
com.
(iii) Soft papilloma, which is often seen on the eyelids of elderly people.
(iv) Keratin horns.— This is due to excess keratin formation and is also seen in old people.
BASAL CELL PAPILLOMA (syn. Seborrhoeic or senile wart; Seborrhoeic Keratosis).— This
condition is seen in persons of middle or old age. These occur in numbers on trunk, face,
arms and arm pits. These are raised brownish warts. This tumour is slow growing, beginning
as a minute patch which gradually increases in area. The lesion is present for months or years.
Senile warts gradually increase in area but not in thickness. They may suddenly fall off
uncovering a pale pink patch of skin.
They have a distinct edge and a rough surface (papilliferous surface) and the size varies
from a few millimetres to 2.3 cm in diameter. It is slightly harder and stiffer than normal skin.
Treatment.—
Papillomata are usually excised for cosmetic reasons.
In case of plantar warts patients often come to the clinician to get relief of pain while
walking. Following measures may be adopted —
(i) Socks may be changed to cotton variety.
(ii) Application of formaldehyde at nights on the wart may cure the condition.
(iii) Sometimes silver nitrate application also cures the condition.
(iv) Curettage or excision should be carried out if the above measures fail.
ADENOMA.
A benign tumour of glandular tissue is called an adenoma. Adenoma usually arises from
secretory gland. It consists of a dense mass of acini lined by exuberant epithelium which may
be columnar or cuboidal in type. Adenoma of endocrine gland often shows no acini, but is
composed of uniform polygonal or sphenoidal cells arranged in solid groups. Adenomata are
usually encapsulated, the capsules of which are produced as the result of pressure atrophy of
the surrounding parenchyma. Adenoma may be found in any glandular organ, of which the
breast, prostate and endocrine glands are the common sites, though this may also be seen in the
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
113
secreting glands of bronchi. In adrenal cortex and prostate this tumour is often multiple and it
is difficult to decide whether the condition is neoplastic or merely nodular hyperplasia.
Adenoma, when arises from secretory glands of mucous membrane, often becomes
pedunculated and is then called a 'polypus'. This is particularly common in the large intestine
and it is frequently multiple. In the hereditary condition of 'polyposis coli' thousands of these
tumours are present in the colon and also rectum. This tumour often tends to be malignant
which becomes evident by the larger cells, hyperchromatic nuclei and mitosis.
There are two other variants of adenoma :—
(i) Fibroadenoma.— In the breast the specialised connective tissue surrounding the glandular
epithelium is usually involved in the adenoma whenever it occurs here. This overgrowth is due
to an excessive stromal reaction. Two types have been described — the hard pericanalicular
fibroadenoma and soft intracanalicular fibroadenoma. In the pericanalicular type the ducts are
surrounded by dense connective tissue. In the intracanalicular type the looser connective tissue
is impinged into the ducts which become elongated and slit-like. In this variety the connective
tissue shows rapid growth and the tumour may attain a very large size, which is known as
giant fibroadenoma (Brodie's tumour).
(ii) Cystadenoma.— Sometimes adenoma forms elaborate cystic spaces into which
papillary ingrowths of neoplastic epithelium occur. These are known as papillary cystadenoma,
which is most common in the ovary and is also seen in the pancreas, parotid gland and rarely
in the kidney. Two types are usually found — one in which the epithelium secretes serous fluid
(serous cystadenoma) and the other type in which mucin is produced (pseudomucinous
cystadenoma).
FIBROMA.—
It is a rare tumour. It consists of collections of fibroblasts between which there is variable
amount of collagen. Two varieties of fibroma are usually described — 'hard' or 'soft'. Hard
fibroma has more collagen, whereas the soft fibroma is predominantly cellular. Soft fibroma is
more common in the subcutaneous tissue of the face and appears as soft brown swelling.
Fibroma is also seen in the stomach, ovary and skin.
Many fibromas are combined with other mesodermal tissues such as fat (fibrolipoma),
muscle (fibromyoma), nerve sheath (neurofibroma, which may be multiple as in Von Reckling­
hausen's disease).
A few unusual types of fibromata e.g. desmoid tumour, myxofibroma (myxomatous change
in fibroma) or myxoma (when this change is marked) may be seen.
MYOMA.—
This tumour is not common. It is the benign tumour of the muscle. Myoma may be of
two types depending on whether the striated muscle is involved (rhabdomyoma) or unstriped
or smooth muscle is involved (leiomyoma).
Rhabdomyoma.— This is a tumour of the striated muscle and is extremely rare. It may turn
into malignant rhabdomyosarcoma particularly in young children.
Leiomyoma.— This tumour is much commoner than rhabdomyoma. The usual sites are
uterus, stomach, intestine and skin. This tumour may be multiple. A leiomyoma is composed
of whorls of smooth muscle cells interspersed with variable amounts of fibrous tissue. The
muscle element to certain extent may be replaced by fibrous tissue wli«_n it is called
fibroleiomyoma or fibroid. A leiomyoma may undergo cystic change or may be the seat of
dense calcification.
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114
Treatment.— Treatment of papilloma, adenoma, fibroma and myoma is excision. The
operative technique of such removal of tumour depends on its site. When the growth is superficial
excision of the tumour is performed through skin incision. When the tumour is inside a viscus
e.g. large intestinal polyp, excision is performed with the help of diathermy snare through a
colonoscope. Excision of such tumour may require removal of part or whole of the viscus from
which it has originated.
LIPOMA
A lipoma is one of the commonest and most benign of all tumours. It is composed of fat
cells of adult type. It can occur anywhere in the body, that is why it is often called as 'universal
tumour' or 'ubiquitous tumour'. But the common sites are the subcutaneous tissue of (i) the
trunk, (ii) the nape of the neck and (iii) the limbs.
Varieties.— Mainly there are three varieties — 1. Encapsulated variety, 2. Diffuse variety
and 3. Multiple lipomas.
1. Encapsulated lipoma is the commonest tumour. The details of this tumour is described
below.
2. Diffuse variety.— This is a rare variety and does not possess the typical features of
lipoma, hence it is often called 'pseudolipoma'. It is seen in the subcutaneous and intermuscular
tissues of the neck. It is not a typical tumour but an overgrowth of the fat in this region. It does
not possess the capsule which is typical of a lipoma. It gives rise to a disfiguring swelling of the
neck. It is often found in persons taking excessive alcohol.
Treatment.— Excision of the excess of fat if it is required by the patient due to cosmetic
reason.
3. Multiple lipomas.— Such variety is not uncommon. It is often called lipomatosis. The
tumours remain small or moderate in size and are sometimes painful as these often contain
nerve tissue and are called neurolipomatosis. These are mostly seen in the limbs and in the trunk.
Lipomata of different sizes and shapes may be seen. Macroscopically and microscopically these
are no different from solitary lipoma. Dercum's disease (adiposis dolorosa) is a variety of this
condition in which there are tender lipomatous swellings particularly affecting the trunk.
A few lipomas MAY CONTAIN OTHER TISSUES and are named accordingly —
(i) Fibrolipoma — when a lipoma contains an excessive amount of fibrous tissue.
(ii) Naevolipoma — when a lipoma contains excessive vascularity with telangiectasis of
the overlying skin.
(iii) Neurolipoma — when a lipoma contains nerve tissue. It is often painful.
Complications.— A lipoma when present for a long time may undergo certain changes.
This is particularly true in cases of lipoma in the subcutaneous tissue of the thigh, buttock or
a retroperitoneal lipoma. Such changes are —
(i) Myxomatous degeneration.
(ii) Saponification.
(iii) Calcification.
• (iv) Malignant or sarcomatous change. Though liposarcoma is not uncommon, yet a lipoma
turning into liposarcoma is not so common.
Clinically a lipoma can occur in different anatomical situations. According to this a
lipoma can be classified into —
(i) Subcutaneous type.— This is the commonest variety. Although any part of the body
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
115
can be affected, yet it shows particular tendency to occur in the back, nape of the neck and on
the shoulders. Subcutaneous lipoma is usually sessile, but occasionally may become
pedunculated. The characteristic features of such lipoma are described below.
(ii)
Subfascial lipoma.— Lipoma may occur under the palmar or plantar fascia and is
often mistaken as tuberculous tenosynovitis. Such lipomas may also occur in the areolar layer
under the epicranial aponeurosis in the scalp. Subfascial lipoma can be confused with a
dermoid cyst, particularly so, as such lipoma can also erode the underlying bone as the
dermoid cyst.
Treatment is urgent excision of the tumour.
(iii) Intermuscular lipoma.— Such lipoma occurs between the adjacent muscles and
becomes firmer on feel when the adjacent muscles contract. Mechanical interference with the
action of the muscles is often complained of. Fibrosarcoma is also common in such situation
and is difficult to differentiate from this condition clinically. Intermuscular lipoma is mostly
seen in the thigh or around the shoulder.
Treatment is early excision as it is difficult to differentiate from fibrosarcoma.
(iv) Subserous lipoma.— This is rare and is sometimes found beneath the pleura or
peritoneum. When it is beneath the pleura it presents as a benign thoracic tumour.
Retroperitoneal lipoma is also rare and is often misdiagnosed as hydronephrosis, pancreatic
cyst or teratomatous cyst. A retroperitoneal lipoma may attain a big size. Very occasionally
one may find a lipomatous mass rather than a lipoma at the fundus of the sac of a femoral
hernia. This is a condensation of extraperitoneal fat rather than a typical lipoma.
(v) Submucous lipoma is also rare. It may occur in the respiratory or elementary tract.
It has also been seen in the tongue. In the respiratory tract it may cause respiratory obstruction.
In the intestine it may lead to intussusception.
(vi) lntra-articular — inside the joint. It is extremely rare.
(vii) Subsynovial lipoma.— Such lipoma occurs deep to the synovial membrane. It is
seen in the knee joint. In this case it is often compared with Baker's cyst or a bursitis.
(viii) Parosteal lipoma — occurs under the periosteum of a bone.
(ix) Extradural lipoma.— This is a type of spinal tumour. Intracranial lipoma does not
occur as there is no fat in the extradural tissue within the skull.
(x) Intraglandular lipoma.— There are 3 glands in which a lipoma may be seen — (i)
the breast, (ii) the pancreas and (iii) under the renal capsule.
SUBCUTANEOUS (ENCAPSULATED) LIPOMA.
Pathology.— It consists of normal fat, which is arranged in lobules separated by fibrous
septa and enclosed in a delicate capsule. A lipoma is usually small but it may attain a very big
size although still remaining benign. From its capsule fibrous bands pass to the overlying skin,
that is why when a lipoma is moved, the overlying skin becomes dimpled.
Microscopically, it shows plenty of adult fat cells.
Clinical features.—
HISTORY.—
(i) Age.— Lipoma may occur at any age, but is not commonly seen in children.
(ii) Duration.— Usually it is a long standing tumour, but the exact duration may not be
discovered as it may remain without being noticed for months. It is an extremely slow growing
tumour.
SYMPTOMS.— Painless swelling which is present for a long time is the main complaint.
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EXAMINATIONS.—
(i)
Position.— Lipoma can occur anywhere in the body and it should be always kept in
mind in the differential diagnosis of a swelling. It is more common in the upper limbs, around
the shoulder, in the neck and in the back.
(ii) Colour.— The skin overlying the
tumour is usually normal. Only in case of very
large lipoma, the skin may be stretched with
dilated veins seen over the tumour. But such
feature is more common in case of
naevolipoma or haemangioma.
(iii) Temperature and tenderness.— There
is no increased temperature and no tenderness.
(iv) Size and Shape.— Lipoma may be
seen in all sizes. There is no definite shape of
a lipoma but it is usually lobulated. The
lobules can be seen and felt on the surface.
Lipoma is usually round or egg-shaped.
(v)
Surface.— This is smooth and
lobulated.
The edge is soft, compressible and
Fig.10.1.— Subcutaneous lipoma at the lower end of
often
slips
away from the examining finger.
forearm — not a very common site (Courtesy Dr. Yogesh
This
is
called
'slip sign'. This sign is helpful
Salphale).
to differentiate this condition from a cyst, in
which case the edge does not slip away from the palpating finger, but yields to it.
(vi) Consistency.— Lipoma feels typically soft but does not fluctuate.
(vii) Transdlumination test may be positive. This is the only condition which may
transilluminate even though it is not a cyst.
(viii) Mobility.— A lipoma is freely mobile over the deeper structures. The underlying muscle
has to be made taut and the lipoma is moved both along the long axis of the fibres of the
underlying muscles and at right angles to those. The overlying skin is also not fixed to the lipoma,
so that the skin can be lifted up off the tumour. When the underlying muscle is made taut, such
lipoma becomes more prominent indicating that it is superficial to that muscle. But when the
overlying skin is lifted up or the lipoma is moved, the overlying skin will show dimples due to
the attachment of fibrous septa from the capsule of the lipoma to the overlying skin.
Treatment.— A lipoma should always be excised. Mostly the patient wants it for cosmetic
reason, but even if there is no other complaint, it should be excised due to its various complications.
Incision is made on the overlying skin preferably along the Langer's lines. The incision is
deepened till the capsule of the lipoma is reached. Now the dissection is continued sideways by
dividing the fibrous septa over'the capsule and its attachments to the surrounding tissues. Then
a finger is insinuated and the whole lipoma is enucleated out.
Haemostasis of the resulting cavity is ensured. Some deep sutures may be applied to obliterate
the cavity. The overlying skin is closed with or without drainage.
HAEMANGIOMA
A haemangioma is a developmental malformation of blood vessels and not a typical tumour.
So it is considered to be an example of 'Hamartoma'. Such theory can be explained by the facts
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
117
that (i) haemangioma is often present since birth and (ii) it never turns malignant.
Types of haemangioma.—
There are mainly three types of haemangioma —
1. Capillary haemangioma — arising from capillaries.
2. Venous or cavernous haemangioma — arising from the veins.
3. Arterial or plexiform haemangioma — arising from arteries.
Haemangioma may occur anywhere in the body though it is more common in the skin and
subcutaneous tissues.
1. Capillary Haemangioma.— Mainly three varieties of capillary haemangioma are seen
— (a) Strawberry angioma (Strawberry naevus), (b) Port-wine stain, (c) Salmon patch.
(a) STFtAWBERRY ANGIOMA.—
Characteristic features.—
(i) The typical history is that the red mark is noticed after 1 to 3 weeks of birth. This
red mark gradually increases in size for a few months till it takes a typical strawberry or raspberry
like swelling.
(ii) The subcutaneous tissue as well as the skin is often involved. Sometimes muscles
may be affected. Very rarely submucous strawberry angioma has been seen when it is prone to
alarming haemorrhage.
(iii) Clinically the swelling is compressible.
(iv) After the first birthday the angioma gradually regresses in size and involusion may
be completed by the age of 7 to 8 years.
(v) On examination.— This is bright or dark red in colour. This slightly protrudes from
the skin surface and appears as a sessile haemisphere. The surface is irregular and there may be
small areas of ulceration covered with scabs. Strawberry angioma is soft. It is compressible. It is
not pulsatile. Sustained pressure will squeeze most of the blood out of the haemangioma leaving
it collapsed. As soon as the pressure is released refilling occurs quickly. It is usually seen in the
skin and is freely mobile with the skin.
(b) PORT-WINE STAIN.—
Characteristic features.—
(i) It is usually present since birth and does not show any change for the rest of the life.
The size gradually varies in proportion to the whole body. Colour may alter.
(ii) It is common on the face and at the shoulders, neck and buttock.
(iii) This is deep purple-red in colour which may become paler in later life.
(iv) There is no definite swelling but it is a diffuse vascular deformity.
(v) With pressure the colour diminishes in intensity, but when the pressure is released
the colour of the naevus takes time to reappear as the feeding vessels are also abnormal.
(c) SALMON PATCH.—
Characteristic features.—
(i) This is present since birth.
.
(ii) It usually disappears before the first birthday.
(iii) It is mostly seen over the forehead or occiput or anywhere in the midline of the body.
Treatment.—
(i)
Wait and watch policy should be adopted, as majority of the capillary haemangiomas
disappear on their own.
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(ii) If the lesion exists even after 8 years and the patient and the parents insist on cosmetic
treatment, the followings may be tried.
(a) Excision of the lesion with skin grafting.
(b) Carbondioxide snow application.
(c) Injection of hot water or hypertonic saline or sclerosing agent may be tried if
strawberry angioma persists.
(d) X-ray therapy has not proved very successful, yet may be considered in failure
cases. It causes disturbance of growth, necrosis of skin, pigmentation and ulceration.
(e) Injection of steroids.
Sturge-Weber syndrome.— A facial port-wine stain may be associated with haemangioma of
the ipsilateral cerebral haemisphere which may lead to Jacksonion epilepsy.
2.
Cavernous Haemangioma.— It consists of multiple dilated venous channels. It is a
spongy swelling.
CHARACTERISTIC FEATURES.—
As soori as the pressu ^m <>V° ^ SWe ^ n^
(i) Conservative treatment is more often
required in the form of —
Fig. 10.2.— Cavernous haemangioma.
(a) Injection of sclerosing agent into the
lesion. In this respect 3% sodium morrhuate is quite effective otherwise boiling water or hypertonic
saline may be tried. The injection is given once a week for a few times upto 6 weeks if necessary.
(b) Cautery treatment may be applied to the haemangioma. A needle is pushed into
the haemangioma and its end is touched with a diathermy node.
(ii) Surgery is a better treatment if the swelling is small and localized. The feeding vessels
are first ligated and the whole lesion is excised. Diathermy may be used to control haemorrhage.
Such excision may be made easier with preliminary conservative treatment.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
119
3. Arterial Or Plexiform Haemangioma.— It is a type of congenital arteriovenous fistula.
There is pulsatile swelling of arteries and the veins become arterialized i.e. tortuous and thick
walled and pulsatile — feeling like a bag of pulsating earthworms. This is often called cirsoid
aneurysm. Such cirsoid aneurysm is commonly seen on the forehead or in the scalp over the
temporal region.
Treatment.—
(i) Ligation of feeding vessels.
(ii) Therapeutic embolisation of the feeding artery.
(iii) After ligation of feeding vessels excision of the lesion with diathermy.
Spider naevus.—
It is a solitary dilated skin arteriole feeding a number of small branches which grow in
radial manner.
It is an acquired condition and is associated with some generalized disease. Such spider naevus
appears on the upper half of the trunk, face and arms. Peculiarly enough this is the drainage
area of superior vena cava though its relationship cannot be explained. Spider naevus fades
completely when compressed with the finger.
Spider naevus is usually associated with hepatic disease (particularly hepatic cirrhosis or
tumours destroying the liver) and tumours producing oestrogen.
GLOMUS TUMOUR (SYN. GLOMANGIOMA).—
Glomus tumour is a rare, benign and exquisitely painful small tumour of the skin and
subcutaneous tissue. This usually occurs on the extremities particularly in the nail-beds of the
hands and feet.
The GLOMUS is a specialized arteriovenous anastomosis surrounded by large pale cells
which are called glomus cells. Between these cells there are numerous medullated and nonmedullated nerve fibres, though the latter outnumber the former. Such glomus is most abundantly
present in the region of the nail-bed at the tips of the fingers and toes and the palmar surface of
phalanges. Glomangioma obviously is more common in these sites.
The function of the glomus is supposed to be concerned with heat regulation.
The glomus tumour or the glomangioma is a benign and circumscribed tumour blue
or reddish in colour. This is usually quite small and it seldom exceeds 1 cm in diameter.
Pathology.—
This tumour consists of tortuous vascular channels in the walls of which there are large
pale cells of the epitheloid type with clear or vacuolated cytoplasm. The cells may be clumped
in large masses without any definite lumen. Plain muscle fibres intervene between the lumen
and the clumps of epitheloid cells. Abundant nerve fibres mainly nonmyelinated variety are
seen between the epitheloid cells and these are responsible for exquisite pain which is the most
important symptom of suqh tumour.
Clinical features.—
1. Age.— This tumour usually occurs in the 5th decade, though it may be seen at all stages.
2. Site.— The common sites have been discussed earlier in this section.
3. Single or multiple.— Typically this lesion is single, though a familial multicentric has
been noticed which is usually not so painful as the single variety.
4. Colour.— Colour varies from deep red to purple or blue. There is variation is colour
with change in temperature.
5. Pain.— This is by far the most prominent symptom of this condition. It may occur
A CONCISE TEXTBOOK OF SURGERY
120
either spontaneously or with pressure or with trauma. The pain is stabbing or burning in nature.
Pain has a radiating character and is usually caused by touch or slight pressure. Pain is probably
caused by dilated glomus vessels pressing on the numerous nerve endings.
Differential Diagnosis.—
1.
2.
3.
4.
5.
phalanx.
Subungual melanoma.
Squamous papilloma.
Granuloma pyogenicum.
Subungual granuloma from chronic infection.
Subungual sprouting granulation tissue resulting from chronic osteomyelitis of the distal
Treatment.—
Since the tumour is radioresistant, the only treatment of choice is excision or removal of the
tumour. When encapsulated, the tumour may be shelled out. If there is no obvious capsule, wide
excision is indicated. Removal of the tumour gives complete and permanent relief to the patient.
LYMPHANGIOMA
Origin.— Lymphangioma, like haemangioma, is congenital in origin. Localized cluster of
dilated lymph sacs in the skin and subcutaneous tissues which cannot connect into the normal
lymph system grows into lymphangioma.
Types.— Mainly there are 2 types of lymphangioma — (a) superficial variant presents as
circumscribed lesion which appears as small blisters and slightly elevated skin patches. These
lesions are called lymphangioma circumscriptum.
.
(b)
Deep lesions are large, cystic, translucent and may be seen in the neck, mediastinum or
axilla. These are called cystic hygromata.
Clinical features.—
Age.— Lymphangiomata are present since birth.
SYMPTOMS.—
Usually the disfigurement is noticed by the child's parents. Sometimes small vesicles may
leak clear fluid. Occasionally the vesicles may be rubbed with the clothes, get infected and become
painful. Otherwise this lesion is painless.
ON EXAMINATION.—
(i) Sites.— Lymphangioma circumscriptum are found at the junction of the limbs and
at the junction of the neck with the trunk i.e. around the shoulder, axilla, buttock and groin.
Cystic hygromata are commonly seen in the neck, axilla, mediastinum etc.
(ii) Colour.— Skin vesicles contain clear fluid and looks yellow or watery. When such
vesicle contains blood they turn brown and even black.
(iii) Size.— Lymphangioma circumscriptum are small lesions, whereas cystic hygromata
are big lesions.
(iv) Consistency.— Lymphangioma is soft and spongy. These are translucent swellings.
Fluctuation and fluid thrill are present.
(v) Regional lymph nodes usually do not enlarge until and unless the lesion gets infected.
Treatment.—
Surgical excision is the treatment of choice. Radiotherapy has no place. When excision is
complete there is no chance of recurrence and cure is complete and permanent. Sometimes
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
121
complete excision becomes difficult and excision remains incomplete. Even then this condition
is rarely associated with recurrence.
HAMARTOMA
The term hamartoma was first coined by Albrecht in 1904. The term 'hamartoma' is derived
from a greek word which means 'fault' or 'missfire'. Its original meaning was 'missing the mark
in spear throwing'.
A hamartoma is a developmental malformation consisting of a tumour-like overgrowth in
which the tissues of a particular part of the body are arranged haphazardly, usually with an
excess of one or more of its components. A large number of common lesions fall into the general
category of hamartoma.
Common lesions included in this group are benign pigmented moles, majority of angiomas
and neurofibromas. A very well known example of hamartoma is the isolated cartilaginous mass
found in the substance of a lung. On section it is found to be composed of mature hyaline
cartilage with clefts lined by respiratory epithelium and surrounding the cartilaginous mass
there is connective tissue and smooth muscle. There is no true capsule.
THE CHARACTERISTIC FEATURES OF HAMARTOMA ARE —
(i) Most hamartomata are present at birth or in early years of childhood. But usually
only those on exposed areas like the skin and mouth will be recognized as early as this. Other
tumours will be recognized late, though no doubt the original nidus was present at birth.
(ii) Its growth is co-ordinated with that of the surrounding tissues and growth stops
after adolescence.
(iii) It may regress, which is typically seen in strawberry haemangioma.
(iv) It may be multiple — typical example being neurofibroma.
(v) There is no capsule around a hamartoma. It grows alongwith its surroundings, so
there is no question of any connective tissue condensation.
(vi) Hamartoma is not a tumour, but it is quite possible for a tumour to develop in a
hamartoma.
(vii) For all practical purposes the lesion is benign and it hardly changes into malignancy.
(viii) Hamartoma may be associated with an obvious chromosomal abnormality.
Examples are —
(a) Vascular hamartoma — known as haemangioma.
(b) Benign naevus.
(c) Angiomatous syndromes (often multiple) — (i) hereditary haemorrhagic telangiectasia,
(ii) Sturge Weber syndrome — in which there is combined haemangioma over one-half of the
face and haemangioma of the ipsilateral cerebral hemisphere.
(d) Glomus tumour.
(e) Lymphangioma.
(f) Neurofibroma (Von Recklinghausen's disease). 1
(g) Skeletal hamartoma — solitary exostosis and diaphyseal aclasis.
(h) Adenoma Sebaceum.
NEUROMAS
Neuromas are of mainly two varieties — true and false.
False neuromas are those which arise from the connective tissue covering the nerve fibre
or from the nerve sheath. Neurilemmoma and neurofibroma are included in this group.
A CONCISE TEXTBOOK OF SURGERY
122
True neuromas are extremely rare and are only seen in connection with the sympathetic
system. The sympathetic system originates from the neural crest and develops along 2 lines :—
(a) Primitive neuroblasts and adult sympathetic cells which may give rise to tumours such as
neuroblastoma and ganglioneuroma respectively, (b) Chromaffin tissue situated mostly in the
adrenal medulla and may produce tumours known as pheochromocytoma.
NEURILEMMOMA (SYN. SCHWANNOMA)
Lots of controversies are still existing about neurilemmoma arising from schwann cell of the
neurilema and neurofibroma. It must be remembered that whereas schwann cells are derived
from the neural crest, neurilemmoma is ectodermal in origin.
Neurofibroma arises from elements of perineurium and endoneurium and are mixtures of
ectoderm and mainly mesoderm.
Neurilemmoma is a benign, well encapsulated tumour which forms a single, round or
fusiform firm mass on the course of one of the larger nerves. Schwannomas are white to grey,
firm, circumscribed well capsulated lesions. Multiple lesions may occur on the same nerve or
may be distributed throughout the body. The commonest site is the acoustic nerve. Such
neurilemmomas are occasionally seen in the posterior mediastinum and in the retroperitoneal
space. In the peripheral nerves, the sensory branches are affected more frequently.
PATHOLOGY.— Microscopically it consists of schwann cells. The long slender cells form
twisted band and have elongated nuclei which show palisading arrangement or are arranged in
whorls. Basically two types of tissue can be noticed in such a tumour — fascicular and reticular
tissues. The fascicular tissue presents a solid complex appearance almost like an exaggerated
tactile corpuscle, known as Verocay body. The reticular tissue consists of loosely arranged schwann
cells in an open network of tiny cysts and reticulin fibres.
The neurilemmoma is essentially a benign lesion and does not show any tendency to
malignant transformation.
TFtEATMENT. - Excision of the tumour is the treatment of choice. As the tumour displaces
the nerve, it can b' easily dissected from the nerve without damaging it.
NEUROFIBROMA
This tumour arises from the connective tissue of the nerve sheath. This is a developmental
disorder and is often considered as Hamartoma and not a typical tumour. Such disorder often
runs in families.
Majority of the neurofibromas arise from endoneurium, the innermost connective tissue
covering of the nerve fibre. The endoneurium is covered by perineurium and epineurium, which
remain usually unaffected.
Followings are the varieties of neurofibroma. Varieties :
1.
Local Or Solitary Neurofibroma.— Single neurofibroma is usually found in the
subcutaneous tissue. It is usually seen in the extremities e.g. median nerve, ulnar nerve etc.
Cranial nerves may be involved e.g. acoustic neuroma.
Clinical features.— A swelling is the main presenting feature. Such swelling may be painful.
Paraesthesia or pain likely to occur from pressure of the tumour on the nerve fibres.
On examination, it is a smooth firm swelling of the skin and subcutaneous tissue which
occurs along the course of a nerve. Its margins are well defined. The swelling can be moved
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
123
sideways but cannot be moved longitudinally along the long axis of the nerve. The swelling
may be tender. There may be paraesthesia along the sensory supply of the nerve involved. There
may be weakness of the muscles supplied by the nerve. Both the area of sensation and the muscle
power of the nerve involved should be examined.
It may be associated with other types of neurofibroma.
Solitary neurofibroma may occur in other sites than skin. These are —
(i) In the cranial nerve, particularly the 8th cranial nerve.
(ii) Dorsal nerve root or ganglion.
(iii) Intramuscular.
(iv) In the bone — exceedingly rare.
Complications.—
(i) Cystic degeneration;
(ii) Sarcomatous changes may occur.
Differential diagnosis.—
(i) Lipoma;
(ii) Fibroma;
(iii) Large lymph nodes;
(iv) Haemangioma;
(v) Some cystic lesions, as neurofibroma may undergo cystic degeneration. These are
sebaceous cyst, dermoid cyst, subcutaneous bursae.
Treatment.— Excision of the neurofibroma without injuring the nerve concerned is the
treatment of choice. Sometimes it may not be possible to save the nerve while resecting the tumour.
In such cases excision may accompany resection of
the involved portion of the nerve and then end-toend anastomosis of the divided nerve is performed.
Recurrence is a problem after resection.
Sarcomatous changes may occur in the recurrence.
2. Generalized Neurofibromatosis
(SYN. VON RECKLINGHAUSEN’S DISEASE
OF NERVE).— In this condition there are
multiple neurofibromas arising from the cranial,
spinal and peripheral nerves. This is an autosomal
dominant inherited disease. Neurofibroma
basically comprises of 2 types — type I, which is
also called Von Recklinghausen's disease and type
II,
which was previously called acoustic
neurofibromatosis. Type I is a relatively common
disorder and 50% of patients give a definite
family history. In type I a gene (NF-1) has been
mapped out in chromosome 17q 11.2. The NF-2
gene is located on chromosome 22q 12.
Pathology.— On gross examination, the
neurofibromas vary from spherical to cylindrical
masses. They may or may not be encapsulated.
Microscopically, they are composed of a Fig. 10.3.— Generalised Neurofibromatosis.
124
A CONCISE TEXTBOOK OF SURGERY
proliferation of all the elements in the peripheral nerve including Schwann cells and fibroblasts.
Typically these components are dispersed in a loose disorderly pattern, often in a loose myxoid
stroma. Elongated serpentine Schwann cells predominate with their slender, spindle-shaped nuclei.
It must be remembered that neurilemmomas composed entirely of Schwann cells which virtually
never undergo malignant transformation. On the other hand neurofibromas of Von
Recklinghausen's disease may become malignant in about 10 to 15% of cases. Malignant
transformation is more common in large tumours attached to the large nerve of the neck and
extremities. The superficial lesions rarely become malignant.
The cutaneous pigmentations, the 2nd major component of this syndrome, are present in
over 90% of patients. Most commonly they appear as light brown macules with smooth borders
often located overlying the nerve trunks. These are called cafe an lait patches. It should be
considered that if more than 5 such patches are present over 1.5 cm in diameter, the patient is
likely to have neurofibromatosis.
A wide range of associated abnormalities have been reported in these patients. Pigmented
iris hamartoma also called Lisch nodules are often present. These do not produce any symptoms
but are helpful in establishing the diagnosis.
The most common associated abnormalities perhaps are skeletal lesions which include
erosive defects due to contiguity of neurofibroma to the bone, scoliosis, intraosseous cystic lesions,
subperiosteal bone cysts and pseudoarthrosis of the tibia. Other abnormalities found in
neurofibromatosis are meningiomas, gliomas, pheochromo-cytomas and medullary thyroid
cancers. 5 to 20% of patients with pheochromocytomas have neurofibromatosis.
Although some patients with these conditions have normal mentality, yet there is a tendency
of reduced intelligence. If occurs in gastrointestinal tract, intestinal obstruction or G.I. tract
haemorrhage may result.
Clinical features.— Multiple nodules of varying sizes can be seen scattered over the face,
neck, trunk and limbs. Majority of the neurofibromata are present at birth. Gradually they increase
in number and size during life. The nodules vary in consistency from soft to hard. Each nodule
has a distinct margin. Neurological abnormalities are not common. But such abnormalities should
be looked for.
Pigmentation of the skin is often associated with. The pigment is melanin and the pigmented
patches are called cafe au lait patches. These are the diagnostic features of Von Recklinghausen's
disease. This is due to common neuroectodermal origin of the endoneurium and melanocytes.
Such pigmentations are seen in the skin around the swelling or over the swelling.
There may be associated skeletal deformities e.g. kyphosis, scoliosis.
In 5% of cases malignant change (sarcomatous) becomes evident.
Complications.—
(i) Cystic degeneration.
(ii) Sarcomatous change.
Treatment.— The swellings are so numerous that excision of all the tumours is impossible.
Indications for excision are :
(a) When one swelling is large enough,
(b) When one swelling is painful,
(c) When one is causing pressure symptoms,
(d) When one is causing mechanical discomfort,
(e) When there is suspicion of malignancy.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
125
Barring the above indications surgery is not considered in this case.
The students must remember that there is another condition called Von Recklinghausen's
disease of bone (syn. osteitis fibrosa cystica). This is hyperparathyroidism due to excessive
parathyroid hormone secretion and it is characterized by pathological fracture, recurrent renal
calculi and peptic ulcer. It may be associated with other endocrine abnormalities.
3.
Plexiform
Neurofibromatosis
(SYN.
PACHYDERMATOCELE).—
It
is
an
excessive overgrowth of neural tissue in the subcutaneous fat and makes the tissue look
oedematous. It is a rare condition. It is more commonly seen in connection with branches of the
trigeminal nerve (5th cranial nerve). Occasionally this condition may be seen in the extremities
and the scalp. Fibromyxomatous degeneration of the nerve sheaths is often accompanied with.
Clinically there is a big swelling with the overlying skin thickened and oedematous. It
becomes folded and pendulous. It looks like a mass hanging from the face. It presents a horrible
look. On palpation one may feel the thickened nerves like thrombosed veins. There may be
pigmentation of the skin. Plexiform neurofibroma may occur alongwith generalized
neurofibromatosis. Very rarely it may undergo sarcomatous change.
4.
Elephantiasis
Neurofibromatosa.—
It is a severe form of plexiform neuro­
fibromatosis affecting the subcutaneous nerves of the limbs particularly the lower ones. It is a rare
condition and often congenital. The overlying skin becomes coarse, dry and thickened like an
elephant's skin (hide). The subcutaneous tissue becomes
greatly thickened and fat is replaced by fibrous tissue.
Other causes of elephantiasis are :
(a) Filariasis,
(b) N o d u l a r
leprosy (elephantiasis
graecorum),
(c)
Occlusion
of lymph drainage due
to (i) excision of
draining lymph nodes
e.g.
brawny
arm
following
radical
mastectomy,
malig­
nancy or (ii) radio­
therapy.
(d) A r t e r i o venous fistula.
5.
Cutaneous
N
e u r o f i b r o
­
(SYN.
MOLLUSCUM FIBROSUM).— These are also
multiple subcutaneous
nodules sessile or
pedunculated over the
matosis
126
A CONCISE TEXTBOOK OF SURGERY
chest, abdomen or back. When these occur on the scalp it is called turban tumour. It occurs in
connection with the terminal filaments of cutaneous nerves. The nodules are small, firm, discrete
and multiple. There is no hypertrophy of the skin. There may be associated pigmentation of the
skin.
Treatment.— Large swellings may be excised.
Neurofibroma may occur anywhere in the body but the followings require special mention :
A. Acoustic neuroma.— It grows from the auditory nerve sheath at the internal auditory
meatus. The first symptom is unilateral deafness, followed by tinnitus, vertigo and headache.
Gradually the tumour enlarges and presses upon the adjacent nerves e.g.
(a) 7th cranial nerve or facial nerve causing facial muscle weakness.
(b) 6th cranial nerve or abducent nerve — causing squint.
(c) 5th cranial nerve or the trigeminal nerve — causing trigeminal neuralgia or
anaesthesia. Ultimately the tumour may press on the cerebellum causing cerebellar symptoms
and signs with increased intracranial pressure.
Treatment is excision of the acoustic neuroma through posterior fossa craniotomy.
B. Dumb-bell shaped neuroflbroma — arising from the dorsal nerve root partly inside
and partly outside the intervertebral foramen. Root pain and paralysis are the main features.
This may be a schwannoma or neurofibroma.
C. Amputation neuroma or stump neuroma.— It occurs as a fusiform swelling at the
end of the divided nerve after amputation. It consists of fibrous tissue and nerve fibres. There
are proliferating axons and reparative proliferation of neurolemmal cells. Such neuroma is a
painful condition. There will be tingling and numbness particularly due to irritation by an artificial
limb due to pressure on the neuroma.
Treatment.— Prophylactic.— During amputation the nerve should be divided above the
proposed level of bone section.
Curative.— Once the condition has developed treatment is excision of the neuroma.
MALIGNANT TUMOURS
BASAL CELL CARCINOMA (SYN. RODENT ULCER)
This is a locally invasive carcinoma of the basal layer of the epidermis. It is of low grade
malignancy. This is particularly liable to occur in fair and dry skinned people constantly exposed
to sunlight. Elderly subjects are usually affected.
Aetiology.—
1. Elderly people are usually affected. The patients are in middle or late age.
2. It affects males more often than females.
3. It is particularly seen in the white residing in tropical countries.
.
4. It grows very slowly, often over a course of many years.
5. Exposure to sunlight seems to be an important aetiologic factor, that is why this lesion
is usually confined to the face.
6. Rodent ulcer is particularly prevalent in Australia and is confined to white people of
the labour class whose skin is exposed to the bright sunlight of high actinic value.
7. It is seldom seen in the dark skinned people.
8. The tumour is frequently multiple and the multiple growths may be confined to one
area or may occur in different areas.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
127
9.
Multiple, basal cell carcinomas may develop in persons following prolonged
administration of arsenic usually in the form of liquor arsenicalis. Arsenic was also previously
used in skin ointments.
10.
90% of basal cell carcinoma is seen in the face above a line from the comer of the
mouth to the lobule of the ear. The commonest site being around the inner canthus of the eye.
Pathology.—
Macroscopic features.— Although it is called rodent ulcer, many of the lesions are non­
ulcerated. The different macroscopic types are :—
(i) Deeply eroding ulcer on rodent ulcer. Such an ulcer has a typical rolled edge (not
everted), often beaded and the floor showing scabbing over some areas and breaking at others.
(ii) Nodular type.
(iii) Cystic type — a large semi-transparent nodule with darkly translucent colour as it
contains oedematous fluid with a network of fiery red blood vessels on the surface.
(iv) Pigmented nodule.
(v) Field fire or Forest fire or Geographical variety — with advancing edge and healing
centre. It has an irregular raised edge around flat white scar.
Microscopic features.—
It consists of densely packed islands of darkly stained cells which extend down from the
epidermis, although often no connection with the epidermis may be seen. The cells on the
periphery of the islands are more deeply staining and have 'palisade' arrangement. There are
no cell nests or keratinrzation. Prickle cells are also absent. Mitotic figures are usually absent.
Stromal component is composed of benign fibrovascular tissue and chronic inflammatory cells.
Basal cell carcinomas have varying rates of growth. Some remain small for long period of
time, while others grow rapidly and destroy large areas.
Origin.—
*
As mentioned earlier the common belief is that the basal cell carcinoma arises from the basal
layer of the epidermis. But occasionally a basal cell tumour arises from the basal cells of the hair
follicles and sweat glands. Such tumours are mostly seen in the scalp and adolescents are the
usual victims. Such tumour is called 'turban tumour' or 'epithelioma adenoides cysticum'.
Spread.—
Basal cell carcinoma usually spreads by local invasion. It gradually destroys the tissue it comes
in contact with. That is why this tumour is called 'rodent ulcer'. Lymphatic spread is not seen, so
the regional lymph nodes are not enlarged. Similarly blood spread is also extremely rare.
Clinical features.—
SYMPTOMS.—
The principal complaint is of a persisting lesion — either an ulcer or a nodule. It is not
painful in the beginning, though it may itch. The lesion grows slowly and a little bleeding may
be complained of. If untreated rodent ulcer becomes quite big and deep. It then may cause pain
and bleeding and may become infected.
Basal cell carcinoma is more known for its multiplicity.
LOCAL EXAMINATIONS.—
(i)
Site.— Though no site is exempted, yet 90% of basal cell carcinoma is seen on the
face above the line drawn from the angle of the mouth to the lobule of the ear. The common
sites are :
A CONCISE TEXTBOOK OF SURGERY
128
(a) Around inner canthus of the eye.
(b) Around outer canthus of the eye.
(c) Nose.
(d) On and around nasolabial fold.
(e) On the forehead — more common
in females.
In fact, the rodent ulcer may be seen more
commonly in places of the face over which tear
rolls down. That is why it is aptly called a 'Tear
cancer'.
This lesion is also seen in the scalp, neck, arms
and hands (i.e. the exposed areas of skin).
(ii)
The lesion.— The tumour always
starts as a nodule. Gradually the centre of the
nodule dies and an ulcer results. Such an ulcer
has a rolled edge i.e. raised and rounded (not
everted cf. epithelioma). As the growth spreads, Fig. 10.6.— A typical case of basal cell carcinoma
at the upper part of the face. Note its rolled out
the shape of the ulcer becomes irregular. An
margin which is typical of this condition.
Fig. 10.7.— A typical basal cell carcinoma at its
commonest site.
irregular raised edge around a flat white
scar is sometimes called a field fire or
geographical basal cell carcinoma. When
the ulcer erodes deeper structures, the
edge becomes more prominent, but does
never become everted.
The floor of a rodent ulcer is covered
with a coat of dried serum and epithelial
cells. If this sheds off, the ulcer will bleed.
The base of the ulcer consists of the
tissue which the tumour is eroding, either
fat or muscle or bone.
If the centre of the nodule dies an ulcer
is formed, if it does not die the nodule
continues to develop. The nodule gradually
becomes large and may look cystic. But it
should be remembered that being a solid
tumour, it cannot be truely cystic, though
'cystic rodent ulcer' term can be used. It is
neither fluctuant nor does it contain typical
fluid inside it, though some oedematous
fluid may be present.
(iii)
Regional lymph nodes — are
usually not enlarged. If these are enlarged
the diagnosis should be reconsidered.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
129
TREATMENT.—
I.
RADIOTHERAPY.— Superficial
radiotherapy will cure over 90% of all basal
cell carcinomas.
Contraindications to radiotherapy are —
(i) If the lesion is very close to the
eye.
(ii) If the lesion is on the back of the
hand.
(iii) If the lesion adheres to cartilage
or bone.
II. SURGERY.—
Indications.—
(i) Where radiotherapy is contra­
indicated. Fig. 10.8.— Rodent ulcer in front of the pinna.
(ii) Recurrence after radiotherapy.
(iii) Appearance of a new lesion adjacent to previously treated area.
Excision of the growth with healthy tissue margin at the circumference and at the depth
should be performed. About 3 to 5 mm of healthy tissue should be excised with the tumour in
all 3 dimensions.
The defect can be closed by simple direct suturing if the growth is a small one. It may
require partial or full thickness skin graft to cover the defect. Rotation flaps or pedicle grafts
may be used for better cosmetic result.
III. CRYOSURGERY has recently been used but its efficacy is yet to be proved.
IV. LOCAL CHEMOTHERAPY.—• 5-fluorouracil cream has been applied locally. It has not
been successful in majority of cases. It may be tried in small flat nodules.
V. LASER beam destruction of the tumour is being performed in a few sophisticated centres.
BASO-SQUAMOUS CARCINOMA In this condition epithelioma like changes take place at the margins of a basal cell carcinoma.
Such lesion often occurs in the skin which was exposed to radiotherapy previously. Such lesion,
on careful examination will show an everted edge. The lesion is friable and necrotic.
Regional lymph node metastasis is a very characteristic feature of this condition.
Diagnosis is confirmed by biopsy.
Treatment.— It is according to the squamous cell carcinoma.
SQUAMOUS CELL CARCINOMA (SYN. EPITHELIOMA, EPIDERMOID
CARCINOMA).—
Origin.—
This is a carcinoma of the cells of the epidermis that usually migrate outwards to the surface.
It is the prickle cell layer from which squamous cell carcinoma usually starts.
(a) Squamous cell carcinoma can occur de novo in the skin.
(b) This may occur in a few pre-existing lesions of the skin —
(i) Long standing chronic ulcers (e.g. Marjolin's ulcers) following bum, venous ulcer,
old scar etc.
(ii) Senile Keratosis.
A CONCISE TEXTBOOK OF SURGERY
130
(iii) Bowen's disease.
(iv) Leukoplakia.
(v) From skin exposed to irradiation.
(vi) Chronic skin lesions e.g. lupus vulgaris (cutaneous tuberculosis), eczema, wart.
(vii) Exposed to prolonged irritation by various chemicals e.g. dyes, tar, soot, pitch etc.
Scrotal cancer is common in chimney sweepers and in those whose clothes get
soaked with oil or tar.
(c)
Very rarely squamous cell carcinoma may develop from a basal cell carcinoma, which
is known as baso-squamous carcinoma.
Sites.— Such tumour may develop in any place where there is squamous or transitional
epithelium. It is mostly seen in —
(i) Anywhere in the skin particularly in the dorsum of the hands, in the face, limbs etc.
(ii) At the junction of the skin and mucous membrane e.g. the lip, nostril, eyelid, penis
and vulva.
(iii) It is also seen in the mucous membrane lined by stratified squamous epithelium e.g
tongue, mouth, oesophagus and vagina.
(iv) It is occasionally seen even from columnar epithelium e.g. in the bronchus,
gallbladder etc. In such places it usually occurs following metaplasia.
(v) It may occur where there is transitional epithelium following metaplasia e.g. pelvis
of the kidney, ureter and urinary bladder.
Predisposing factors.—
A few conditions have always been incriminated to excite or induce development of
epithelioma. These conditions are —
(a) Bowen's disease.
(b) Senile Keratosis.
(c) Lupus vulgaris.
(d) Xeroderma pigmentosum.
(e) Exposure to sunlight or irradiation.
(f) Chronic irritations such as —
(i) Leukoplakia.
(ii) Bum, scar, venous ulcer, osteomyelitis sinus (Marjolin's ulcers).
(iii) Continuous heat by a charcoal burner (Kangri) applied to the abdomen or back
of the thighs may cause typical Kangri cancer of Kashmir.
(iv) Sleeping on oven bed is often a habit of Tibetans, which may cause Kang cancer of
buttocks, heels and elbows.
(v) Prolonged irritation of the skin by certain chemicals e.g. pitch, tar. Cancers of scrotal
skin is common in chimney sweepers.
Pathology.—
TYPES.— Two types are usually seen — 1. Proliferative type and 2. Ulcerative type. By far
the ulcerative variety is commoner.
Macroscopic features.— These have been described in the clinical features.
Microscopic features.— There are solid columns of epithelial cells which are seen growing
down into the dermis, separated from one another by connective tissue. These expand into bulb­
like masses, which on section may appear detached. In course of time the cells nearest to the
centre being the oldest undergo degenerative changes and converted into a hyaline structureless
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
131
mass of keratin. This is the process of keratinization. The mass of keratin looks red with eosin
stain. This is surrounded by normal-looking squamous cells presenting the characteristic 'prickle­
cell' appearance and these are arranged in concentric manner as seen in 'onion skin'. This whole
appearance is called 'celTnest' or 'epithelial pearl'.
This 'cell-nest' or 'epithelial pearl' is quite
characteristic feature of epidermoid carcinoma,
but this may be absent in (i) rapidly growing
tumour and (ii) in mucous membranes e.g.
oesophagus and urinary bladder where
cornification is not seen.
Another typical feature of this malignant v.
tumour is infiltration of the dermis by chronic
inflammatory cells particularly plasma cells.
This is almost always present and this may
represent an immune defence reaction against gPNuDB^^L
the tumour.
Spread.—
1. Local spread — by continuity and
contiguity.
2. Lymph spread occurs by embolism and
permeation. Lvmph node involvement varies : .
with the site of the primary lesion. It is late in
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case of tumours in the hand or from a scar or
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from chronic ulcer. But it is early seen in cancer Rg.l0.9.- Squamous cell carcinoma behind
of the foot and in cancer of the face and neck.
the pjnna
3. Blood spread occurs very rarely and
even if it occurs it takes place in very late stage.
.
Clinical features.—
HISTORY.—
(i) Age.— Usually this tumour is
seen above 40 years of age and the incidence
increases with the age.
(ii)
Occupation.— Cancer of the
scrotal skin is common in chimney sweepers
and also occurs in engineers whose clothes
become soaked in oil. Prolonged exposure to
sunlight also causes such lesion.
(iii) Duration.— Usually the swelling
is present for one month or few months, as
the growth shows variable growing capacity.
SYMPTOMS.—
(i)
A nodule or an ulcer is the main
presenting symptom. There may be complain
Fig. 10.10.— Squamous cell carcinoma on the
of bleeding which is more common in
lower lip.
epithelioma than in basal cell carcinoma.
r
132
A CONCISE TEXTBOOK OF SURGERY
(ii) The tumour is usually painless. It only becomes painful if it invades deeper structures.
(iii) Sometimes enlarged lymph nodes are the main complaint and the patient may be
ignorant of the primary lesion.
LOCAL EXAMINATIONS.—
(i) Sites.— These have been discussed earlier.
(ii) Temperature and tenderness.— The ulcer has a normal temperature and is usually
not tender.
(iii) Size and shape.— Squamous carcinoma begins as a small nodule. As they enlarge
the centre becomes necrotic and sloughs out. Thus an ulcer develops. Such an ulcer is oval or
circular in shape and the size varies extremely.
(iv) Edge.— This carcinoma has raised and everted edge. This shows excessive tissue
growth over and above the normal surface.
(v) Floor — is covered by necrotic tumour, serum and blood. There may be some
granulation tissue but this is pale and unhealthy. Some deeper structures may be exposed, such
as muscle, tendon, cartilage or bone.
(vi) Base — of the ulcer is indurated. This is the pathognomonic sign of an epithelioma.
(vii) Mobility.— In early cases epithelioma can be moved with the skin over the underlying
structures. Once the tumour has been fixed to the underlying structures, it cannot be moved. If
the tumour has invaded a muscle in the depth, the tumour can be moved with the muscle
relaxed. But if the concerned muscle is made taut, the tumour cannot be moved.
(viii) Regional lymph nodes.— This may be enlarged and such examination is highly
important. If enlarged, it may not be due to lymph metastasis but may be due to secondary
infection. It must be noted that about l/3rd
cases of such palpable lymph nodes are
caused by infection and usually subside
after treatment of the primary lesion. But
until it is proved otherwise, it should be
assumed that the palpable lymph nodes are
due to metastasis.
TREATMENT.— Treatment can be
divided into two groups —
A. Treatment of the primary lesion and
B. Treatment of the secondary lymph nodes.
A.
Treatment of the primary
lesion.—
I. SURGERY.—
Wide excision is the treatment of choice
once the diagnosis is confirmed by biopsy.
Excision of the growth should be performed
with 2 cm of the normal tissue surrounding
the tumour. In case of tumour involving
finger, toes and penis, amputation is
indicated.
Fig.10.11.— Ulcerated squamous cell carcinoma on
Indications.— Surgery is particularly
the dorsum of the hand.
indicated —
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
(i)
(ii)
(iii)
(iv)
133
When the lesion is of large size.
When the lesion has involved muscle, cartilage or bone.
When the facility of radiotherapy is not adequate.
Recurrence of the growth after radiotherapy.
n. RADIOTHEFtAPY.—
Superficial radiotherapy will cure 80% of early lesions. Different forms of radiotherapy may
be applied when there is adequate facility according to the size and type of the tumour. Such
methods are deep X-ray therapy, radium needles and moulds.
Indications.—
(i) When the condition of the patient is not satisfactory for surgery.
(ii) When the growth is small.
(iii) When the growth has not involved muscles, cartilage or bone or is not close to eyes.
B. Treatment of the secondary lymph nodes.—
(i) When there is no enlarged regional lymph node — regular follow-up is advised, till
the nodes become enlarged and palpable. If the nodes are never enlarged, no treatment should
be advised. When the lymph nodes become enlarged and palpable, a biopsy should be performed.
If metastatic, block dissection should be performed.
(ii) When the lymph nodes are already palpable and enlarged — this may occur due to
secondary infection or metastasis. A biopsy should be performed. In case of metastasis, if the
lymph nodes are mobile and resectable, radical block dissection is justified. If the biopsy shows
secondary infection, a course of antibiotic should be given.
(iii) If the lymph nodes are enlarged, hard and fixed to the surrounding structures,
palliative radiotherapy is the only treatment available.
GLANDULAR CARCINOMA.—
These tumours arise from secreting epithelium or from underlying glands. These are usually
seen in the G. I. tract, breast, kidney, gallbladder, prostate, thyroid and uterus.
Pathology.— The pattern of invasion beneath the basement membrane into the deeper
structures is similar to that found in squamous cell carcinoma. But in this case, the groups of
cancer cells, instead of producing keratin, tend to arrange themselves into acinar structures
containing a central lumen into which secretion pours. The cells surrounding this lumen may be
columnar, cuboidal, polygonal or spheroidal. According to differentiation and arrangement of the
tumour cells glandular carcinoma can be subdivided into — 1. Adenocarcinoma, 2. Carcinoma
simplex, 3. Most undifferentiated carcinoma and 4. Colloid or mucoid carcinoma.
1. ADENOCARCINOMA.— The best differentiated cancers in this group show excellent
acinus formation, which resembles normal glandular structure. The walls of such acini are
composed of layers of cells which invade the surrounding tissues.
2. CARCINOMA SIMPLEX.— In case of less differentiated tumours there are merely
clumps of cells surrounded by a stroma. There is no attempt at central cavitation to produce
acini and thus no glandular structure is recognizable. The calls are mostly polygonal or spheroidal
in shape. This type is most commonly seen in the breast, where the cancer clumps are often
surrounded by a dense fibrous stroma.
3. MOST UNDIFFERENTIATED CARCINOMA.— In this variety the tumour is diffuse
and the cells are arranged in sheets — typical of anaplasia. It is difficult to differentiate this
tumour from squamous cell cancer or sarcoma.
134
A CONCISE TEXTBOOK OF SURGERY
4.
COLLOID OR MUCOID CARCINOMA.— It is a variety of carcinoma simplex which
contains demonstrable mucus. There is large accumulation of mucus in the cytoplasm of the
cells, so that the nucleus is compressed on to the cell wall. This type of cell is typically called a
signet-ring cell, which resembles an adult fat cell. In some adenocarcinoma there is so much
mucus formed that it infiltrates into the stroma, which appears as a basophilic lake, in the midst
of which disintegrating tumour tissue can be seen. This is another type of mucus secreting or
mucoid carcinoma.
The mucoid cancer presents as a bulky, gelatinous and mucoid mass. The mucus tends to
stimulate considerable fibrous tissue reaction near it. Mucoid cancers are notorious for the
ease with which they spread locally.
These tumours are seen in the large bowel, stomach, lung and rarely in the breast.
„ According to the stromal reaction, glandular carcinoma is subdivided into scirrhous, atrophic
scirrhous or encaphaloid variety.
SCIRRHOUS CARCINOMA is mostly seen in the breast. The reaction of the invaded tissue
to the carcinoma is so stimulated that a fibrotic and hard tumour is produced. In the breast this
results in retraction of the nipple and dimpling of the skin due to the presence of scirrhous
carcinoma. Though scirrhous carcinoma is most commonly seen in the breast, yet it is also seen
in the stomach (in prepyloric cancer where there is considerable thickening of the wall and in
case of Linitis plastica). This variety is also seen in colon in annular variety. It should be noted
that although the fibres seen in scirrhous carcinoma gives the impression of an attempt by the
host to strangle the tumour cells, but this does not appear to be the case in practise. In fact
prognosis of scirrhous carcinoma is as poor as that of the encephaloid variety.
ATROPHIC SCIRRHOUS.— In this variety the fibrous tissue element is more, so that the
tumour becomes very hard in consistency. The prognosis is better than scirrhous variety.
ENCEPHALOID (OR MEDULLARY) CARCINOMA.— In this variety there is little stroma
in relation to the cell bulk. The growth is soft in consistency. Such tumour is often seen in the
large bowel or caecum (cauliflower type) or in the breast (during lactation).
TRANSITIONAL CELL CARCINOMA.—
These tumours arise from transitional epithelium, which is seen in the renal pelvis, ureter
and urinary bladder. Macroscopically this tumour takes papillomatous appearance, which differs
from its benign counterpart in having a broader base and showing invasion. Benign papilloma
and carcinoma merge so imperceptibly into one another that is often impossible to define the
line of malignancy.
Microscopically, the tumours vary from well differentiated columns of transitional epithelial
cells to highly anaplastic cells sheets in no way different from other undifferentiated neoplasms.
Squamous metaplasia is sometimes noted.
MARJOLIN’S ULCER.—
Marjolin's ulcer is the name given to a squamous carcinoma which arises in a chronic benign
ulcer or scar.
The commonest ulcer to become malignant is a long standing venous ulcer. The scar which
may show malignant change is the scar of an old bum.
THE SPECIAL FEATURES.—
(a) It is a slow growing malignant lesion, probably due to less vascularity of the region.
(b) Edge of such an ulcer is not always raised and everted.
(c) Painless — such lesion is almost always painless and is often ignored by the patient.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
135
(d) Such carcinoma is less malignant than a typical squamous carcinoma.
(e) There is no lymphatic metastasis — as the lymphatics are destroyed or occluded by
the previous chronic lesion of the skin. Lymphatic metastasis only occurs when surrounding
normal epithelium is invaded.
TREATMENT.— Even though it is less invasive and slower in growth, the treatment is
almost same as squamous cell carcinoma arising de novo.
I- Surgery.— This is the main stay of the treatment. Wide excision of the lesion alongwith a
margin of at least 1 cm is excised. The gap is made good by either partial or full-thickness skin graft.
If the growth is a big one involving distal part of the limb, amputation is advised.
When such a big ulcer lies in the proximal part of the limb, excision of the growth only
with surrounding tissue leaving the part of the ulcer which seems to be still benign, followec
by skin grafting may be tried. Recurrence following such treatment should call for amputation.
II.
Radiotherapy.— This tumour being absolutely radioresistant, there is no place of such
therapy.
THE MELANOMAS
Melanomas are melanin containing tumours develop either from melanocytes or melanoblasts.
Physiology.— The pigment melanin is formed from the amino acid tyrosine. The pigment
melanin is normally found in :—
(i) The skin — in coloured people the whole body and in the white the nipple, areola,
perineum and axilla.
(ii) Choroid of the eye.
(iii) Substantia Nigra.
(iv) Leptomeninges.
(v) Adrenal medulla.
(vi) Telachoroidea.
Tyrosin is an amino acid and is converted by oxidation to dehydroxyphenylalanine
(D.O.P.A.). Such oxidation is performed by the enzyme tyrosinase which is present in the
melanocytes. DOPA reaches the pigment forming cells, where it is converted into melanin by
the enzyme dopa oxidase. The pigment forming cells are the melanoblasts and melanocytes.
The melanocytes are the mature cells. These melanocytes are concerned with both synthesis and
carriage of melanin. Melanocytes are dopa-positive cells. These melanocytes usually appear as
clear cells in the epidermis, but in malanotic condition they are increased in number with
pigmentation.
The origin of the melanoblasts is controversial. There are two views :
(a) The epidermal theory.— The melanoblasts in this theory are merely epithelial cells
which have the power of forming pigments, that these proliferate in the basal layer of epidermis
and penetrate into the underlying dermis where they may become cut off from their source of
origin. The process may be arrested in any stage, but in each case the resulting lesion is a
naevus.
(b) The neurogenic theory.— This appears complex and farfetched. According to this theory
the melanoblasts are believed to origin in the region of the neural crest. Early in the embryonic
life they migrate with the peripheral nerve to their final position in the basal layer of the
epidermis. These are dopa-positive cells and may be pigmented or non pigmented.
Melanoblasts and melanocytes are capable of producing pigments as they contain dopa
136
A CONCISE TEXTBOOK OF SURGERY
oxidase. They are located in the epidermis. The cells are dendritic and they actually communicate
with each other by these dendritic processes. They lie intercalated between the basal cells of the
epidermis.
Melanoblasts transfer their pigment to dermal macrophages which are known as melanophores.
These are only pigment carriers and being dopa-negative they cannot produce pigment.
Production of melanin is controlled by certain hormones. These are —
(a) M. S. H. (Melanocyte-stimulating hormone), which is formed in the anterior lobe of
the pituitary. This is the main hormone which controls synthesis of melanin.
(b) A. C. T. H., to a slight extent, may have some influencing effect in the production of
melanin.
(c) Sex hormones, both oestrogen and androgen.
BENIGN MELANOMAS (SYN. MOLES, PIGMENTED NAEVUS, FRECKLES).—
The most common benign lesion is a 'naevus' or a 'mole'. Although many of these may be
present since birth others appear later in life. This is an example of controlled overgrowth so
that the growth is caused by excess stimulation rather than excessive growth. That is why such
lesion should be better called a Hamartoma of melanocytes. Depending on the nature of further
proliferation, benign melanoma can be classified into following varieties.
Varieties of benign melanomas.—
1. Hairy mole.— This is a common variety. It is flat or slightly raised above the level of
the skin. It has a smooth or slightly warty epidermal covering. It has hairs growing from its
surface. There are also sebaceous glands which may become infected. This causes increase in
swelling and tenderness.
2. Non-hairv or smooth mole.— This is also very common. The surface is not elevated.
The epithelium is smooth. There is no hair growing from its surface.
3. Blue naevus.— It is an uncommon variety of naevus. It is a type of mole which
occurs deep in the dermis. The thick overlying layers of the dermis and epidermis mask the
colour of the melanin and make it look blue. The overlying skin is often smooth and shiny. It is
more often seen in children. It is commonly seen on the face, dorsum of the hand, feet and
buttocks of babies (Mongolian spot). Microscopically the melanin containing cells are situated
deep in the dermis in the pattern of whorls or in strap-like manner.
4. Junctional naevus.— If the growth and movements of melanocytes stop before
they have all migrated into the dermis, there will be clusters of cells of various stages of
maturity in the epidermis and dermis. This lesion is called a 'junctional naevus', because it is
centred around the junctional or basal layer of the epidermis. Junctional moles are immature
and unstable and can turn malignant. In fact majority of the malignant melanomata begin in
junctional naevi.
It is a smooth or elevated naevus of all shades. Such lesion may occur anywhere in the
body either from the birth or may appear later in life. Junctional naevus occurs more commonly
on the palm, soles, digits and genitalia. In fact any naevi occurring in these areas should be
considered as junctional naevi. Hence there is higher incidence of malignant melanoma in these
sites.
Microscopically, there is proliferation of melanocytes at the epidermal junction. The cells
have clear cytoplasm, dark nuclei and varying amounts of melanin. About 90% of malignant
melanomata develop from this group of the naevus.
Malignant change is evidenced by — (i) Increase in size, (ii). Increase in pigmentation, (iii)
COMMON TUMOURS AND MISCELLANEOUS LESIONS- OF THE SKIN
137
Satellite pigmented spots, (iv) Ulceration, crusting or haemorrhage, (v) Microscopic features are
hyperchromasia, anaplasia, mitotic figures and subepithelial spread.
5. Compound naevus.— From the above description it becomes clear that two distinct
varieties of melanoma are available — intradermal and junctional. When intradermal and
junctional features are both present in one mole, it is called a 'compound naevus'. The intradermal
component is inactive and incapable of multiplication, but the junctional component is responsible
for this lesion being potentially malignant.
6. Juvenile melanoma.— A mole showing junctional activity before puberty is called a
‘juvenile mole'. The reason for a special name of such a mole is that microscopically it looks so
active that it is often thought to be malignant, but ultimately it turns into a mature intradermal
mole and not to a malignant melanoma.
It is usually found in young children and face is the commonest site.
7. Hutchinson’s Freckle (Lentigo).— It is worthy of special note. This term is used to
describe a large area of dark pigmentation. It is commonly seen on the face and neck in elderly
people. The surface is smooth but there may be raised rough nodules with junctional activity
and may turn malignant. There are two stages of the disease : In the macular stage, the lesion is
smooth and light brown with irregular borders. In the tumour stage, there is induration and the
histologic features of melanoma. Because the background pigmentation is so dark, areas of
malignant change giving rise to increase in pigmentation may pass unnoticed.
Two special features of this lesion should be remembered — (i) its late development and
(ii) its high incidence of malignant change. But it carries a better prognosis.
Treatment.— It is better to excise a benign mole. The reasons are (i) for cosmetic purpose,
(ii) if its position makes it liable to repeated trauma (though there is no evidence that trauma
causes malignant change), (iii) If the lesion is suspected to be a junctional naevus occurring in
the palms, soles or external genitalia and (iv) if history suggests malignant change e.g. more
pigmentation, development of erythema, increase in size or consistency, change in surface
characteristics, i.e. scaling, oozing, crusting, bleeding, erosion and some subjective symptoms
like itching, burning etc.
After excision of the lesion with a margin of normal skin, the lesion is set for histological
examination.
MALIGNANT MELANOMA.—
By definition the term malignant melanoma refers to a malignant lesion originating in the
melanoblasts. Precursors of melanocytes arise in the neural crest. These cells migrate to the areas
including the skin, meninges, eyes and upper oesophagus during foetal life. In each of these
locations melanocyte shows its potentiality to develop malignant melanoma. Skin is the most
common site of malignant melanoma and it represents about 4% to 5% of all skin malignancies.
About 25% of cases are seen in each of the head and neck, lower extremity and trunk. 11% are
seen in the upper extremities. The remainder involves the genitalia. It should be remembered
that in whites subungual melanomas are more frequent.
All melanomas originate from the melanoblasts at the dermal-epidermal junction, but the
cells may not contain melanin at all times and therefore some lesions may be amelanotic.
Origin.— A malignant melanoma may arise —
(i) In a pre-existing pigmented naevus (90%), either in a junctional naevus, compound
naevus or in a Hutchinson's Lentigo.
(ii) De novo in apparently normal skin (10%).
A CONCISE TEXTBOOK OF SURGERY
138
AETIOLOGY.—
(i) Age.— Patients of any age may develop malignant melanoma, but it is extremely
rare before puberty. The average age at the time of diagnosis is probably late forties.
(ii) Sex.— Women develop melanoma slightly more than men. Melanomas in women
are more common in lower extremities. Women have a better prognosis than men with equivalent
lesions. Presence of oestrogen receptor on malignant melanocytes has been evaluated extensively.
Oestrogen receptor binding as well as detection of these receptors have been found using
immunofluorescent technique. In other series it has been found that the oestradiol-binding
component in melanoma most likely represents an artefact and that true oestrogen receptors are
absent from this tumour. Controversy also exists about the relationship of melanoma and
pregnancy, which is discussed below.
(iii) Race.— It is more common in the whites, who are more exposed to sunlight. It is
more frequent in Australia, but it is very rare in Negroes. Individuals with Celtic ancestry
appear to show highest predilection for development of this disease. When Celtic people migrate
to more temperate climates, the incidence of melanoma increases. This is the reason why this
condition is particularly common in Australia. In general, melanoma is commoner in Caucasians
than in Asians and black populations. Risk of malignant melanoma is in the ratio of 20 : 1 in
whites to blacks.
(iv) The role of ultraviolet light in the aetiology of melanoma is debatable issue. But it is
accepted to certain extent that both the incidence of melanoma and subsequent mortality can be
correlated with the degree of sunlight exposure. Probably severe sun bums early in life correlate
best with increased risk of melanoma. So sun block is recommended, particularly in fair-skinned
children may reduce the risk of developing melanoma. Again the fact that melanoma does occur
in sites not exposed to the sun, e.g. mucous membrane sites, exposure to sunlight is not clearly
the only aetiologic factor.
(v) A genetic factor alongwith environmental one seems to play a role in malignant
melanoma formation. Abnormalities in chromosomes 1, 6 and 9 have been noticed in malignant
melanoma patients.
(vi) Site.— Palms, soles and external genitalia are the common sites. It may also occur
beneath the nail when it is called subungual melanoma. This is more often seen in the thumb
or great toe. Melanoma may also be seen in choroid of the eye or even in meninges. Malignant
melanoma is also noticed in the rectum and anal canal.
(vii) Role of trauma.— Though there is a tendency to believe that repeated trauma to a
naevus may turn it into malignant melanoma, yet definite evidences are yet to be received.
(viii) Role of pregnancy.— Similarly pregnancy is also alleged to provoke malignant
change in a naevus. Oestrogen has got some influence in producing melanin pigment and it is
true that pregnancy has a bad influence on the course of the malignant melanoma. But
pregnancy has probably little influence in provoking malignant change in a naevus. According
to a few studies women diagnosed with melanoma during pregnancy fare no worse than their
non-pregnant counterparts. Whereas in other studies it had been shown that the pregnant
patient had an increased incidence of lymph node metastasis, but there was no significant
difference in the time to development of distant metastatic disease nor any difference in long
term survival.
(ix) Steroid hormones may have influence to produce malignant melanomas.
PATHOLOGY.—
Microscopical features.— With the development of malignant melanoma there is increase in
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
139
junctional activity and the cells increase in size. The proportion of nucleus to cytoplasm is
increased, the nucleolus is enlarged, hyperchromatism is present and mitoses are observed. The
cytoplasm is often vacuolated with fine melanin granules to mimic Paget cell. These changes
extend throughout the epidermis. In determining whether a naevus has become malignant or
not the surface layers of the epidermis are examined for invasion by cells which are vacuolated.
Invasion of the dermis is indicated by the presence of circular or polyhedral cells with abundant
spongiocytoplasm and fine pigment granules.
The tumour cells may form small cluster in the subepidermal lymphatics — dreadful
indication of early stage of lymphatic spread. Subepidermal zone is invaded by inflammatory
cells mostly lymphocytes. This is always suggestive of malignant change. In fully developed
melanoma the large tumour cells in the dermis often show alveolar arrangement, the groups
being separated by a fine stroma.
PATHOLOGICALLY, malignant melanoma of the skin can be divided into 4 histopathologic
types — 1. Lentigo Maligna Melanoma (LMM), 2. Superficial Spreading Melanoma (SSM), 3.
Acral Lentiginous Melanoma (ALM) and 4. Nodular Melanoma (NM). The junctional melanomas
which constitute
the first 3 groups
Clark's Levels
proliferate
in
horizontal direc­
tion
initially
0-1
Epidermis
along
the
S
S
dermoepidermal
1.0s
Papillary
junction, which
s
*3
Dermis
is known as
radial
growth
5> 2.0Reticular
phase.
This
0
Dermis
precedes dermal
ft
invasion which
I
3.0fi
is known as
vertical
growth
8ubeutaneous
I 4.0► Tissue
phase.
Vertical
M
growth
is cs
associated with
5.0-1
both
invasive
features
and
metastatic capa­
bilities. Only in Fig.10.12.— Shows different levels of invasion of malignant melanoma. Both Clark’s
levels and Breslow’s depth of invasion (mm) have been shown in this diagrammatic
nodular mela­
figure.
1, 2, 3, 4, 5 indicate corresponding levels I, II, III, IV, V of Clark. Remember that
noma
vertical
depth of invasion of malignant melanoma is the most important single criterion to indicate
growth occurs
the prognosis of the disease.
early.
1. Lentigo Maligna Melanoma (LMM).— This type is more often seen in older
individuals in the sixth to eighth decades of life. This lesion consists predominantly of spindle­
shaped malignant cells. Pagetoid cells are usually not seen in this lesion. This is presented as a
thin melanoma and that is why it is associated with a better prognosis. This lesion is mostly
140
A CONCISE TEXTBOOK OF SURGERY
seen on sun-exposed skin, particularly the face. The most characteristic histologic finding is
solar elastosis.
2. Superficial Spreading Melanoma (SSM).— It is the commonest of all melanomas. It
occurs on both sun-exposed and nonexposed areas of the skin. This lesion has pagetoid cells with
both junctional activity and upward growth that causes bulging of the epidermis. The epidermis
is not atrophic as seen in LMM, rather it is more hyperplastic, which is characteristic. Prognosis
is definitely worse than LMM.
3. Acral Lentiginous Melanoma (ALM).— This lesion is more common among blacks
and more commonly seen on the palms, soles and in subungual position. It has got some
histologic characteristics of LMM and some of SSM. This lesion is devoid of pagetoid cells.
On the contrary there is marked junctional proliferation with large atypical melanocytes with
long dendritic processes. Both atrophic epidermal changes and solar elastosis are absent.
Mucous membrane presentation is most commonly seen on the vulva; however it is also seen
in the anus, penis, clitoris, vagina, sinuses and oral cavity. This lesion has a particularly poor
prognosis almost like nodular melanoma and in the mucous membrane sites the prognosis is
even worse (5-year survival rate is less than 20%). It is the commonest type of melanoma
found in Japan.
4. Nodular Melanoma (NM).— In this variety, growth in the horizontal direction is almost
absent and vertical growth predominates.
So this is the most malignant form. The
pigmentation is generally uniform and
the borders are well circumscribed.
Ulceration occurs early. It is seen in
younger individuals and it may occur in
any part of the body. It presents as
convex palpable lesion. Malignant
melanoma can be STAGED according to
Clark's level of invasion (according to the
original paper by Clark and associates in
1969). Level I (in situ) applies when all
tumour cells are above the basement
membrane. Level II has tumour extension
into the papillary but not the reticular
dermis. In level III the tumour cells reach
the interface between the papillary and
reticular dermis. Level IV refers to
tumour cells reaching the reticular
dermis. In level V tumour cells invade
the subcutaneous fat.
In 1970, Breslow noted that the
tumour thickness itself is the best single
prognostic indicator for localized
melanoma. Fig. 10.12 depicts a schematic
Fig. 10.13.— Superficial spreading melanoma.
diagram of both Clark's levels and
Breslow's depth of invasion of the tumour.
Breslow introduced staging by measuring maximal thickness of the lesion at the centre of it.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
141
Stage I is categorized by thickness 0.75 mm or less; Stage II — 0.76 to 1.50 mm; Stage III — 1.51
to 3.00 mm; Stage IV — more than 3.00 mm. It is a reliable and important determinant of the
therapy and prognosis. A close correlation exists between tumour thickness and prognosis.
A lesion less than 0.76 mm thick is considered to be a 'thin melanoma' and the prognosis is
extremely good. Lesions of 0.76 to 4 mm are generally considered as intermediate thickness lesion
and 10-year mortality rate is approximately 20% to 40%. Lesions more than 4 mm thickness are
considered as 'thick melanoma' and 10-year mortality rate is approximately 70%.
Spread.— This malignant tumour kills patients by producing wide spread metastasis.
1. LOCAL EXTENSION.— Malignant melanoma spreads initially by local extension by
continuity and contiguity.
From the original site of the tumour the tumour cells grow peripherally in the junctional
layer and in this way melanotic halo is produced. Malignant melanoma has a tendency to form
satellite nodules in the skin and such nodules develop progressively at greater distance from the
original tumour. Such nodules develop from 2 types of spread — (i) local spread and (ii) lymphatic
spread — through lymphatic permeation the tumour cells grow along the lymphatics and form
nodules at greater distances.
The deep fascia acts as a strong barrier and malignant melanoma hardly infiltrates the deep
fascia.
2. LYMPHATIC SPREAD.— This is the commonest spread of malignant melanoma. The
tumour cells reach the regional lymph node by embolism and permeation. The importance of
regional lymph node metastasis cannot be overemphasized. It is the most common presentation
of metastatic melanoma and is associated with a poor prognosis. When nodal metastasis is present,
the patient's survival may be less than half that of patients without nodal involvement. It should
be remembered that by
the time the regional
nodes
are
detected
clinically, 70% to 80% of
patients will have distant
metastases.
Satellite
nodules are seen in the
transit
between
the
primary growth and
regional lymph nodes.
Secondary lymphoedema
may occur due to early
involvement
of
the
regional lymph nodes.
In malignant mela­
noma of the eye there is
no lymph spread.
3. BLOOD SPREAD —
Blood spread is a late
event and may be absent
until nearly the end. The
skin is a common site of
A CONCISE TEXTBOOK OF SURGERY
142
metastasis. Secondary growths appear in the skin early. Liver, lungs, bones and brain may be
involved by blood borne metastasis. The most common sites of distant metastases are the lungs
and the liver, though the brain, the bones, gastrointestinal tracts or other sites may be involved.
Such metastasis may appear early or many
years after diagnosis. The predilection of
melanoma for Central Nervous System (CNS)
metastasis is well known and may be due to
the embryologic similarity of the origin of the
melanoma cells and neural cells. Any
neurologic manifestation in a patient with a
history of melanoma should arouse suspicion
of metastasis to the brain.
After first recurrence, subsequent
recurrences are more likely to be distant rather
than regional. Once melanoma has
metastasized to distant organ, it becomes
widely disseminated very soon. However
some patients develop extensive local and
'
regional recurrences without visceral
._4,t involvement and these patients survive for
I®! KP
decades after resection of these lesions,
jg&c
i"!
CT examination of the chest will reveal
lung metastasis. Bone scan is t h e most
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s e n s i t i v e s t u d v t o detect m e t a s t a t i c disease t o
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.
.
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skeleton, tndoscopv is particularlv helpl
1'^“' , . • t o d e t e c t metastasis in the G.l. tract where
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oesophagus, rectum, anal canal and small
intestine are mostly involved. The lesion may
Fig. 10.15— Malignant melanoma at the sole of
the foot
P^YP^d mass whi<* causes occult
bleeding or intussusception; or may be
ulcerating mass which may occasionally
perforate. Melanoma may metastasise to the adrenal glands which can be diagnosed by CT
scanning. MRI (Magnetic Resonance Imaging) is particularly helpful to detect CNS metastasis
which is quite common in this disease. Some unusual sites may be involved by blood spread e.g.
the small intestine, the heart and the breasts.
Sometimes liver has been metastasized even after many years of removal of the eye due to
malignant melanoma.
be
CLINICAL FEATURES.—
CARDINAL SYMPTOMS OF MALIGNANT CHANGE IN A MOLE OR NAEVUS.—
1. Increase in size.— The patient usually complains that a long standing mole has suddenly
shown rapid growth within last few days. Such increase in size occurs in all directions. The
moles become wider and thicker.
2. Change in colour.— The malignant mole becomes darker. Such colour change is often
patchy. Some areas may show increased vascularity. Sometimes malignant melanoma does not
show pigment and such lesion is called amelanotic melanoma.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
143
3. Bleeding.— The overlying epithelium becomes
ulcerated and often breaks down with minor injury. This
tends to bleed. These changes are particularly noticed when
the growth has become malignant.
4.
Evidence of local spread.— Tumour cells
gradually invade the surrounding skin to produce a halo,
which indicates appearance of malignancy. Gradually the
malignant cells permeate through the intradermal
lymphatics and cause satellite nodules at a little distance
away from the primary tumour. Gradually more satellite
nodules develop at greater distances.
5. Enlarged regional lymph nodes.— This indicates
that the growth has turned malignant.
SYMPTOMS.— When benign mole shows the cardinal
symptoms of malignant change, malignant melanoma is
the most probable diagnosis. Malignant melanoma is not
painful. It often itches. Sometimes the patient may
complain of lymph node enlargement, that means swelling Fig.10.16. Melanoma of the left cheek,
in the groin, axilla or neck according to the region of the primary tumour.
Only in late cases one may complain of weight loss, dyspnoea or jaundice (due to hepatic
involvement).
Local examinations.—
(i) Sites.— Majority of the melanomata are seen in the palms and soles of the feet. Other
parts of the limbs and head and neck may be involved. It is also seen at the mucocutaneous
junctions e.g. the mouth and the anus.
(ii) Colour.— It may be of any colour from brown to black. More blackish is the colour,
more chance is there of malignancy, as malignant melanocytes produce more pigments. But the
students are cautioned that melanomas may be seen without pigmentation and such growth is
known as amelanotic melanoma and this causes tremendous confusion, so far as the diagnosis
is concerned.
(iii) Temperature and tenderness.— A malignant melanoma is no warmer and not tender.
(iv) Surface.— When small, the surface may be smooth, but as it attains larger size, ischaemic
necrosis, small ulcers, crusts etc. are seen on the surface. Bleeding is quite common on the surface
and the surface of a big melanoma looks wet, soft and boggy.
(v) Consistency.— The tumour feels firm. The small satellite nodules may feel hard.
(vi) Mobility.— The tumour moves with the skin as it arises from the skin. It can be easily
lifted up from the deeper structures.
(vii) Surrounding skin.— A halo and/or satellite nodules may be seen in the surrounding
skin.
(viii) Regional lymph nodes — are often enlarged in a case of malignant melanoma.
General examination.— One should examine the lungs, liver and brain and the whole
extent of the skin from the primary tumour to the regional lymph nodes. In the first three organs
melanoma may spread through blood. Black nodules may be seen in the skin anywhere between
the primary tumour and the regional lymph nodes. This is due to lymphatic permeation.
One should be aware of one clinical type i.e. Amelanotic Melanoma, which is rather pinkish.
144
A CONCISE TEXTBOOK OF SURGERY
On careful inspection one may find slight
pigmentation at the base. It carries a bad
prognosis even worse than nodular
melanoma with quick regional lymph node
metastasis.
Non-cutaneous
melanomas.—
Melanocytes originate from neural crest and
undergo migration during embryonic life
and may be found in non-cutaneous sites.
These sites include—
(i) Mucous membranes (specially the
oral cavity and nasal sinuses, the genitalia,
rectum and anal canal).
(ii) Melanomas are also rarely seen in
viscera e.g. oesophagus, adrenal glands and
lungs. Mucous membrane melanomas are
more aggressive with high mortality rates.
(iii) Ocular melanomas are the most
non-cutaneous melanomas and account for
approximately 4% of all melanomas. This
type of melanoma also shows predilection
for Caucasians. Lesions are usually found
in the uveal tract (Iris, ciliary body and
Fig.10.17.— Nodular amelanotic melanoma of the
choroid), which contains melanocytes in
great toe.
normal human beings. These uveal
melanomas do not metastasise to regional nodes as uveal tract does not have lymphatic drainage.
The common metastatic site is the liver. Treatment is either photocoagulation, partial ocular
resection or enucleation.
(iv) Very rarely meningeal or dural melanomas are seen.
Clinical staging.— Clinically melanoma can be staged as follows :
Stage I — refers to the primary tumour only.
Stage II — refers to primary tumour + presence of satellites ('in-transits') or enlarged regional
lymph nodes. When there is only satellite, it is staged as Ha. If only regional lymph nodes are
enlarged, the lesion is staged as lib. If a lesion is present with both satellites and enlarged regional
lymph nodes, the lesion is staged as Ilab.
Stage III — refers to lesion with distant metastasis, that means the disease has spread further
than the regional lymph nodes.
SPECIAL INVESTIGATIONS.— This is mainly aimed at staging of the disease, as the
lesion is diagnosed with confidence only by excisional biopsy. There is no method to detect
presence of micrometastasis, which would have otherwise helped in the proper treatment.
Depending on the suspicion of metastasis various investigations can be performed e.g. Computed
Tomography, Ultrasonography, endoscopy for oesophageal metastasis, bone scans to detect bone
metastasis, Magnetic Resonance Imaging (MRI) for CNS metastasis etc. Lymphangiography to
detect lymph node metastasis is of no definite value as this often produces false positive or
negative result.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
145
Excision biopsy is the main stay of
diagnosis and should be encouraged in
preference to incision biopsy.
Histopathology plays a key role in
determining prognostic indicators and the
natural history of a particular melanoma.
The thickness of the melanoma is the most
important prognostic factor. The type of
melanoma, whether it is nodular,
superficial spreading, lentigo maligna or
acral, does not have much significance in
survival. The lentigo maligna melanoma,
which was previously thought to have a
good prognosis has shown no difference
in 5-year mortality compared to other
histogenic types of melanoma of equal
thickness.
In melanoma, the extent of
malignancy at the time of diagnosis is also
an important prognostic factor. Patients
with localized diseases of the skin have
better prognosis than patients with disease
involving first-order lymph nodes and in­
transit lesions. When nodal metastasis had
occurred, the prognosis is based on the
number of lymph nodes involved. Patients Fig. 10.18.— Pigmented basal cell carcinoma of the cheek
with distant metastasis involving visceral
simulating a melanoma,
organ, the skeleton or the central nervous
system have a very grave prognosis.
Differential diagnosis.—
A few conditions mimic melanoma. These are :—
(i) Pigmented basal cell carcinoma.
(ii) Keratoacanthoma.
(iii) Pyogenic granuloma.
(iv) Cafe-au-lait patch.— This is patchy pigmentation associated with neurofibromatosis or
sometimes pheochromocytoma. This is light to dark brown pigmentation.
(v) Peutz-jegher's syndrome.— This is a familial condition characterized by circumoral
pigmentation and multiple intestinal polyposis. Pigmentations are seen on the lips, in the buccal
mucous membrane and around the mouth.
(vi) Kaposi's sarcoma.
(vii) Glomus tumour.
(viii) Angioma.— This may rarely mimic melanoma. Its compressibility and blanching on
pressure help in differentiating this lesion from melanoma.
(ix) Histiocytoma.
(x) Pigmented senile warts.
10
146
A CONCISE TEXTBOOK OF SURGERY
(xi) Pigmented squamous papilloma.
(xii) Epithelioma (particularly if the lesion is amelanotic melanoma).
TREATMENT.—
A.
SURGERY.— This is the main treatment of malignant melanoma. The following
modalities of surgical treatment can be offered.
1. Excisional biopsy with a margin of 2 to 5 mm of surrounding healthy skin is indicated
for most pigmented lesions. Incisional biopsy, better be avoided, may be required in extremely
large lesions. There is no evidence to suggest that this increases dissemination.
2. In case of Clark's level I or Breslow's stage I excisional biopsy with a very small margin
of normal skin is all that is required. These tumours are very unlikely to metastasize and rarely
recur if a margin of 2 cm clearance is achieved. To determine the excision margin, it is better to
remember that for the lesion which is impalpable, palpable or frankly nodular, the clearance
margin should be 1 cm, 2 cm or 3 cm respectively. It has been found out by randomized trials
that excision with more clearance margin does not offer a better local recurrence rate.
3. When the tumour extends below the papillary dermis Clark Level IV, a 5 cm margin
beyond the lesion should be excised. It is of no use excising the deep fascia. The gap is covered
by split skin graft taking skin from the contralateral limb. Skin grafting from the ipsilateral limb
is avoided as there is every possibility of recurrence. A split skin graft is preferred as local
recurrence will be clearly seen through the graft.
4. In case of digits or toes, amputation is indicated. If the lesion is located in the proximal
half of the digit, disarticulation is performed at the level of the corresponding tarsometatarsal or
carpometacarpal joint.
At present the trend is towards conservatism but the margins should be excised to give a
local recurrence to zero. This is 1 cm for lesions less than 1 mm thick; 1.5 cm for lesions 1 to 2
mm thick; 2 cm for lesions more than 2 mm thick and 3 cm for lesions more than 4 mm thick.
Positron emission tomography (PET) is now applied in sophisticated institutions to detect
malignant cells in early stages and to detect metastasis which is otherwise not so detectable. But
computer tomography and magnetic resonance imaging, which are being used in majority
institutions, are also quite effective in staging the disease of malignant melanoma.
5. Block dissection of the nodes.—
(i) The major problem regarding the surgical treatment of lymph nodes focuses on the
uninvolved regional lymph nodes. The problem is whether the surgeon should perform an
immediate elective node dissection as soon as the diagnosis of malignant melanoma is made or
to wait for the clinical evidence of node involvement. Immediate elective node dissection does not
improve the survival rate and it should be restricted to those patients for whom follow-up is a
problem. Only for thick lesions (more than 2 mm in tumour thickness) consideration should be
given to prophylactic node dissection for increased survival rate. In these cases it may be more
sensible to perform only node sampling and full regional node dissection is only restricted to
those with histological metastasis in the lymph node.
(ii) When there is obvious regional lymph node involvement either clinically or
lymphangiographically these have to be resected by block dissection. One must be very radical
in such block dissection e.g. in case of inguinal lymph node involvement one should also resect
the iliac group of lymph nodes.
Only when the primary lesion is close to the lymph nodes e.g. on the face or neck, near the
axilla or the groin, the primary tumour is excised alongwith block dissection of the regional
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
147
lymph nodes in continuity (mono block procedure). This is the best radical treatment for malignant
melanoma. But this is not always advocated if the primary tumour is well away from the regional
lymph nodes.
Recurrence.— Local recurrence is often the manifestation of residual disease not excised
with the primary tumour and it may represent the outgrowth of satellite lesions which are common
with melanoma. Locally recurrent disease is defined as cutaneous or subcutaneous disease arising
within 5 cm of the primary site after complete excision of the primary lesion. The risk of local
recurrence obviously increases with the thickness of the lesion. These local recurrences are managed
surgically. These are excised widely with more than 5 cm margin around the lesion.
Regional recurrence.— The most common manifestation of regional recurrence is involvement
of lymph nodes. When a patient presents with lymph node metastasis, it is wise to re-stage the
patient with Computed Tomography (CT) scan, because the risk of visceral metastasis increases.
If lymph node metastasis is present in the absence of distant metastatic disease, radical resection
of the involved lymph nodes is advised.
In-transit recurrence between the primary lesion and the first order lymph nodes is also a
regional recurrence. It should be managed by complete surgical removal. Re-staging should be
performed and systemic therapy should be considered.
Another option for patients with this regionally recurrent melanoma is hyperthermic limb
perfusion (isolated limb perfusion). In this process the arterial supply and the venous drainage
of the extremity are surgically isolated. High dose of chemotherapy is perfused into the involved
limb under hyperthermic conditions (at 40°-41°C). Melphalan is the mostly used chemotherapy
and its response rate is more than 80%. This treatment is usually well tolerated, though at times
toxicity can be so severe that amputation may be necessary. The major role of this hyperthermic
perfusion is to avoid amputation in patients with advanced regional disease in the absence of
visceral metastasis. This is a definitive treatment of in-transit metastasis, non-resectable recurrence
or non-resectable tumours. It can be used to convert advanced non-resectable lesions to operability.
It can be used as adjunct to surgical excision for regionally confined poor prognosis melanoma.
Isolated limb perfusion is currently the treatment of choice for recurrent melanoma which is
confined to an extremity and it has been proved useful in dealing with local and in-transit
metastases. It may be used prophylactically in melanomas more than 1.5 mm thickness, where the
incidence of local recurrence and in-transit metastasis has been reduced, though overall survival
appears to remain the same.
B.
SYSTEMIC TREATMENT OF MELANOMA.— SYSTEMIC CHEMOTHERAPY
should be considered as a palliative measure, if the disease has spread beyond the first-order
lymph nodes. The single agent which has the greatest efficacy is dacarbazine (DTIC). Different
combinations of drugs have been used and multiple drug regimens are even better. In pulmonary
involvement systemic chemotherapy is definitely ideal. This regimen is observed over a 40 days
interval and if additional metastatic lesions are not evident, removal of the remnants with
continuation of postoperative chemotherapy should be the treatment of choice. In approximately
10% of patients metastatic disease is detected in bones. External fixation followed by radiation
and chemotherapy is the most accepted method of treatment. Metastatic lesion in G.I. tract may
require surgical intervention alongwith chemotherapy. Similarly in adrenal metastasis,
adrenalectomy alongwith chemotherapy works good. In case of CNS metastasis, solitary brain
metastasis may be managed by surgical excision, but in case of multiple metastasis, whole brain
radiation and adjuvant systemic chemotherapy is advised.
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A CONCISE TEXTBOOK OF SURGERY
IMMUNOTHERAPY is gradually receiving more and more acceptance in the treatment of
this disease. Interleukin-2 (IL-2) and alpha-interferon have been used systemically in the
treatment of metastatic disease. High dose alpha-interferon reduces mortality when given for
patients who have had surgical clearance of nodal metastasis. High dose IL-2, a T-cell growth
factor, has been used to treat patients with metastatic melanoma. Most recent reports suggest
a response rate of 35% including some complete responses. This is the single most effective
immunotherapeutic regimen evaluated in humans to date. Monoclonal antibody therapy has
been used but is yet to prove its efficiency. Tumour vaccine protocols appear to have survival
benefit in some patients.
RADIOTHERAPY.— Melanoma is not a radiosensitive tumour and therefore adjuvant
radiotherapy is not commonly advocated. It is however used in cases with nodal metastasis
where complete surgical excision has been in doubt, particularly in the head and neck region, but
its effect on improving survival is as yet unproven. Radiotherapy is used in higher dose of 400
to 800 rads. Radiotherapy has been used as an adjuvant method in the treatment of bone and
cerebral metastasis. In these areas palliation can be achieved and pain relief is worthwhile product
of this therapy.
SARCOMA
This is a rare tumour (1% of all malignant tumours) in comparison to carcinoma. Sarcoma
also differs from carcinoma in the age incidence. Sarcoma usually occurs in the 2nd and 3rd
decades and in fact may occur at all ages.
The macroscopic appearance of a sarcoma varies considerably. Most tumours appear as a
fleshy mass. The consistency of the tumour varies and depends on the relative proportion of the
fibrous and vascular tissue. Haemorrhage commonly occurs due to presence of thin walled veins.
In some places the tumours almost surround the venous spaces. This explains the reason for early
blood borne metastasis in sarcoma and its grave prognosis.
Comparison between carcinoma and sarcoma is described below : —
Carcinoma
1. Age.— Common in middle and old age.
A very common tumour.
2. Structure.— (a) Typically arranged in
groups and columns, except in the most
anaplastic tumours.
(b) Stroma often well-formed.
Haemorrhage and necrosis less
extensive, except in anaplastic tumours.
3. Growth pattern.— Often somewhat
slowly growing.
4. Metastases.— (a) Lymphatic metastasis is
early.
(b) Blood-borne metastases usually
evident a little later.
Sarcoma
1. Age.— Occurs at all ages of life;
Common in younger people. A much less
common tumour.
2. Structure.— (a) Arranged in diffuse
sheets intimately related to the stroma,
(b) Stroma nearly always poorly-formed
and inadequate for the growth of the
tumour.
Haemorrhage and necrosis extensive,
3. Growth pattern.— Growth is ususally
very rapid.
4. Metastases.— (a) Lymphatic spread is
rare. '
(b) Blood-borne metastases appear very
early.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
149
(c) Commonest seat of blood-borne
(c) Commonest seat of metastasis is the
metastasis is the liver. Other organs often
lung. Other organs may also be involved.
involved are the lungs, brain, bones,
Skeletal deposits are rare.
kidneys and adrenals.
5. Radiosensitivity.— Many are highly
5. Radiosensitivity.— Almost completely
radio-sensitive.
radioresistant.
There are more than 20 types of soft tissue sarcomas each with distinguishing histologic and
biologic behaviour. Soft tissue sarcomas may develop at any site in the body. These are not
encapsulated but possess a pseudocapsule of compressed malignant and normal cells. These
tumours have tendency for local infiltration along fascial planes. If local excision is performed,
local recurrence is quite high upto 70 to 80%. Distant metastases occur mainly by haematogenous
route most frequently to the lungs. Some of these tumours e.g. synovial sarcoma,
rhabdomyosarcoma etc. may metastasize to regional lymph nodes in 10 to 20% of cases. However
early lymphatic spread is uncommon.
Types of sarcomas.—
Cell of Origin
Types of Tumours
Fat cell
Liposarcoma
Fibroblast
Fibrosarcoma
Histiocyte
Malignant fibrous histiocytoma
Smooth muscle
Leiomyosarcoma
Rhabdomyosarcoma
Striated muscle
Osteoblast
Osteosarcoma
Chondrosarcoma
Chondroblast
Endothelium of blood vessels
Haemangiosarcoma
Lymphangiosarcoma
Endothelium of lymph vessels
Synovial cells
Synovial sarcoma
Pluripotential mesenchyme
Malignant mesenchymoma
Ectoderm (peripheral nerve)
Malignant neurilemmoma
Uncertain
Kaposi's sarcoma
Malignant granular cell tumour
Clear-cell sarcoma of tendon
sheath and aponeuroses
Osteosarcoma is the most common tumour of all sarcomas. Of soft tissue sarcomas
liposarcomas, fibrosarcomas, malignant fibrous histiomas and rhabdomyosarcomas occur more
frequently about 16% each, whereas other sarcomas are infrequent.
Fibrosarcoma.—
It is a common soft tissue sarcoma. It is the malignant counterpart of fibroma. It differs
from the benign tumour in that it infiltrates the surrounding tissues and metastasizes. It can
occur anywhere in the body particularly in muscle sheaths, scars and in fibrous epulis. An
important diagnostic feature that distinguishes a fibrosarcoma from a cellular fibroma is the
irregular and pleomorphic appearance of the individual cells. There is always evidence of
mitotic activity. The more the tumour becomes malignant, it shows greater cellular
pleomorphism, nuclear hyperchromatism and mitotic activity; giant-cells are quite common.
Collagen formation becomes scanty. The most anaplastic tumours show no collagen and the
cells are spindle-shaped (spindle-cell sarcoma) of varying lengths. There are dilated veins
150
A CONCISE TEXTBOOK OF SURGERY
over the tumour to suggest malignancy. On palpation the tumour feels warm and pulsation
may be detected (pulsatile fibrosarcoma). Haemorrhage and necrosis are common features of
most sarcomata, as the stroma is delicate and the vascular supply inadequate to meet the
demands of the tumour.
DIAGNOSIS.—
1. Biopsy is essential to establish the diagnosis. Excisional biopsy is used for lesions upto
3 cm in size. Incisional or wedge biopsy is used for larger lesions. Needle biopsy may be used
but often insufficient tissue is obtained to make a definitive diagnosis. The staging system is
based on 4 parameters : T, N, M and G (referring to tumour size, regional lymph node involvement,
distant metastasis and histological grade of the tumour).
2. Chest films, tomograms and/or computed tomographic scans are necessary to exclude
pulmonary metastasis.
3. Angiography may demonstrate tumour vessels characteristic of malignant tumours and
to determine relationships of the sarcoma and blood vessels.
TREATMENT.—
SURGERY.— The treatment of choice for fibrosarcoma and all soft tissue sarcomas is adequate
surgical resection. Wide excision is essential because these sarcomas spread by infiltration along
muscle and fascial planes. The surgical modalities are — (i) wide local excision, (ii) muscle group
excision and (iii) amputation.
(i) The wide local excision must be three dimensional to obtain margins in all directions
around the tumour. The surgeon should be incising through the normal tissues all the times and
should remove the sarcoma surrounded by normal tissue.
(ii) Muscle group excision may be used for some sarcomas requiring removal of all involved
muscles from their origins to insertions.
(iii) Generally the amputation site is above the joint of the involved muscle groups. As wide
local excision and muscle group excision often fail to provide a recurrence free survival, amputation
has often been the recommended treatment of choice.
RADIOTHEF^APY.— These tumours are relatively radioresistant. Radical high-dose precision
radiation therapy (6,000 to 7,000 rads in 6 to 7 weeks) with or without limited surgical excision
has been effective in. treating patients with early to moderately advanced soft tissues sarcomas.
The local recurrence rate following this type of treatment is about 20 to 25%. Amputation should
be recommended in all of these recurrent cases with lesions of the extremity. Sarcoma of bone is
comparatively sensitive to radiotherapy, which is often used before amputation.
Combination with CHEMOTHEFtAPY.— Combination of selected surgery, irradiation and
chemotherapy has been successful as reported in a few series. However this treatment has
produced marked improvement in embryonal rhabdomyosarcoma in children. The most
effective chemotherapeutic combination is VAC (Vincristin, Actinomycin D and
Cyclophosphamide) for 1 to 2 year period. Though irradiation and chemotherapy have added
significantly to our therapeutic armamentarium, adequate surgical excision remains the
treatment of choice. When total surgical excision is not feasible, limited resections may be
followed by irradiation and possibly chemotherapy.
Desmoid tumour.—
Desmoids are usually located at the anterior abdominal wall arising from the musculoaponeurosis of the rectus abdominis muscle and its sheath. This tumour is particularly frequent
in women during child bearing age and may have its onset near the time of pregnancy. This
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
151
tumour may also arise in surgical scar. Extra-abdominal desmoids occur most often in the region of
the shoulders and thighs and are more aggressive than their abdominal counterparts.
This tumour is benign and does not metastasize to distant organs, though it has a great
tendency for local recurrence.
TREATMENT is wide surgical excision. If not amenable to surgical resection, this can be
treated by radical dose irradiation. Large non resectable tumours may be controlled by irradiation.
Synovial sarcoma.—
This is the most common soft tissue sarcoma of the hands and feet particularly in young
adults. This tumour usually occurs in the vicinity of joints, but seldom involves the synovial
lining of the joint itself.
This tumour appears as a soft, painless swelling with sarcomatous changes. Lymph node
metastases occur in 20% of cases.
Diagnosis is established by excision and biopsy of the tumour.
Kaposi’s sarcoma.—
It is a malignant blood vessel tumour which is multicentric in origin. About 75 to 85% of
cases the primary tumour arises in the skin. It occurs predominantly in adult males.
Irradiation is the treatment of choice, though surgery and chemotherapy may be used in
selected cases.
MISCELLANEOUS LESIONS OF THE SKIN
CORN
It is a localised hyperkeratosis of the skin. It usually occurs at the sites of pressure e.g. on the
sole and toes. There is usually a homy induration of the cuticle with a hard centre. Com may be
painful particularly when it is rubbed. Com has a tendency to recur after excision. A corn has a
deep central core which reaches the deeper layers of dermis.
TREATMENT.—
(i) Some preventive measures may be taken such as using soft shoes or soft pads at the
pressure points of the sole.
(ii) Salicylic acid in collodion on successive nights may be applied.
(iii) Central local applications have been effective such as Comae or Carnation cap.
(iv) If these measures fail and the com is painful, it should be excised with particular care
to take off the deep root of the central core. This often prevents recurrence.
WARTS
Warts are patches of hyperkeratotic overgrown skin. Such overgrowth of skin is often
stimulated by vims.
Warts may occur at any age but are most common in children, adolescents and young adults.
The symptoms are usually disfiguring. Multiple warts in the fingers may interfere fine movements.
Warts are only painful if they are rubbed or become infected.
Once warts appear, they may persist for many years or regress spontaneously. Sometimes
family history may be obtained.
Three types of warts may be seen :—
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152
1. The common warts, which have been described above.
2. Senile warts.
3. Venereal warts or papilloma accuminata.
Venereal warts are often seen in the coronal sulcus of the penis, in the anal region, scrotum
and in the perineum. These are multiple and moist warts with offensive serous discharge.
Venereal warts are treated by (i) fulguration with diathermy or (ii) by podophyllin — 10 to
20% solution with tincture benzoin is used.
HYPERTROPHIC SCAR
In this condition both the intensity and duration of the active phase of scar formation are
increased. This is characterized by hypertrophy or proliferation of mature fibroblasts or fibrous
tissue without any proliferation of blood vessels. A scar may undergo hypertrophy which remains
localized and after a time slowly regresses. Even in severe hypertrophy the scar does not become
worse after 12 weeks.
Characteristic features of hypertrophic scars are :—
1. It is common in young individuals.
2. Scars crossing the natural skin creases (Langer's line) are more vulnerable to produce
hypertrophic scar. Infection or excessive tension may produce hypertrophic scar.
KELOID
The main distinguishing feature between a keloid
and a hypertrophic scar is that in keloid the normal
surrounding tissue is affected by spread. The
hypertrophic scar never gets worse after 6 months,
but a true keloid continues to get worse even after a
year. It is characterized by proliferation of immature
fibroblasts and also immature blood vessels. A keloid
has claw-like processes. It looks smooth, pink and
raised patch. A keloid is unsightly, often tender to
touch and always itch. The most characteristic feature
of keloid is that it recurs even when it is excised.
AETIOLOGY.— There are a few aetiological
factors which may cause keloid. These are :
1.
Colour
Fig.10.19.— Keloids on the back — not a keloid formation. Negroes are commonly affected,
very common place.
2. It is a familial condition.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
153
3. It is more common in women.
4. Tuberculosis plays a role in aetiology. Patients with tuberculosis often suffer from keloid
formation.
5. Local factors e.g. if the incision crosses the Langer's line keloid formation is more common.
6. Dislocation of hair follicles is also a factor which is more often seen in burns.
TREATMENT.— Treatment is extremely difficult.
Conservative treatment.—
1. Intrakeloidal injection of steroids is helpful and should be considered as the best treatment.
Injection Kenacort seems to be quite good in this regard.
2. Intrakeloidal hialuronidase injection may be tried.
3. Intrakeloidal injection of Vitamin A has given some better result.
4. Intrakeloidal injection of Methotrexate has been used with some success.
5. Deep X-ray therapy has also debatable success. It suppresses further proliferation of
immature fibroblasts and blood vessels. So it may stop further growth of the keloid and stop itching.
6. Ultrasonic therapy has recently been tried with some success.
Surgery.—
1. Excision and resuturing is often followed by recurrence. Preoperative radiotherapy and
postoperative radiotherapy prevents recurrence rate but the total efficacy of such treatment is not
very much encouraging.
2. Shaving away the excess scar tissue and then resurfacing the area by a thin skin graft,
though advocated by a few surgeons to give encouraging results, yet such treatment has never
produced good results by large. Care should be taken not to extend the incision into the normal
tissue at any point.
SOLAR KERATOSIS (SYN. SENILE KERATOSIS)
Prolonged exposure to sunlight will cause hyperkeratosis of the skin, which is known as solar
keratosis. This condition often takes malignant change.
HISTORY.—
(i) The patients are usually above middle age. They have usually worked out of doors for
many years.
(ii) Patient notices appearance of thickened patches of the skin. These may occur in multiple.
(iii) These are usually seen on the face, backs and on the hands.
EXAMINATIONS.—
The thickened patches are yellowish-grey or sometimes brown in colour. Usually the lesions
are less than 1 cm in diameter. They have a dry hard scale on the surface of the lesion.
It is a hard lesion which is firmly adherent to the skin.
Careful watch must be kept to note if the lesion is undergoing malignant change or not. If
the patch or nodule is tethered to the underlying structures, it is turning to malignancy.
Lymph nodes are never palpable in solar keratosis as such. If regional lymph nodes are
palpable, it is sure that the lesion has turned malignant.
KAPOSI’S SARCOMA
In this condition multiple bluish nodules occur especially on the limbs. It is a rare condition
of cutaneous sarcoma. It is usually associated with generalized lymphosarcoma. It is a slow
growing tumour.
A CONCISE TEXTBOOK OF SURGERY
154
This condition is mainly seen in middle age or above.
Males are predominantly involved. This is more common
in Italy and in Eastern Europe. It is also seen in Africa.
The nodules usually first appear in the skin of the
lower limb. In the beginning they may be slightly red
coloured and painless. In course of time the nodules
enlarge and gradually become bluish. They become
ulcerated and infected. Signs of systemic lymphosarcoma,
enlarged lymph nodes and hepatosplenomegaly are the
characteristic features of this condition.
Treatment.— These tumours are sensitive to
radiotherapy and chemotherapy.
BOWEN’S DISEASE
Fig.10.20.— Bowen’s disease at the back
shows large area of ulceration due to
carcinomatous change.
The main interest of this disease is that it is
precancerous. It usually presents as a cluster of flat, pink,
papular patches which are covered with crust. The patches
and the adjacent skin are brown and they look thick. When
the crusts are removed the papules can be seen with oozy
and bloody surface. This condition is often considered to
be eczema by the patients. This condition pathologically
mimics Paget's disease of the breast.
Biopsy must be taken immediately to confirm the
diagnosis.
PYOGENIC GRANULOMA
In all wounds capillary loops at the base form the granulation tissue. If chronic infection
stimulates the capillary loops to grow too vigorously a protruding mass develops covered with
epithelium. This is a pyogenic granuloma. It is dull red, soft or firm and more or less pedunculated
nodule which grows rapidly to about 2 cm in diameter. The patient usually complains of a rapidly
growing swelling on the skin which bleeds easily and discharges serous or purulent fluid. The
growth is so rapid that it attains about double the size in a few days.
Pyogenic granuloma can occur anywhere in the skin but is most commonly seen on the face,
the fingers and the toes, the parts which are likely to be injured. Although they are not typically
painful they are slightly tender. These are usually soft and are slightly compressible. The lump
bleeds easily when touched. Regional lymph nodes may be enlarged when such lesion is highly
infected.
Treatment is excision.
MOLLUSCUM SEBACEUM (Keratoacanthoma)
It is a peculiar benign tumour which often affects (the exposed areas) the face, lips or the
hands in old individuals. It presents as a solitary firm hemispherical nodule. It grows rapidly and
attains a full size of approximately 2 cm in diameter within a few weeks. The top of the tumour
often ulcerates (See Fig. 10.15) and forms a crust, which when removed shows a crater beneath.
COMMON TUMOURS AND MISCELLANEOUS LESIONS OF THE SKIN
155
At this stage an
ulcer with raised
margin may be
mistaken as everted
margin, so that the
lesion resembles an
epitheliomatous
ulcer (squamous
cell
carcinoma).
Malignant trans­
formation of the
lesion is almost
unknown.
TREATMENT.—
Spontaneous
healing is some­
times noticed. The
lesion may be
curetted and silver
nitrate may be
applied to the
crater for cure. The
Fig.10.21.— Molluscum Sebaceum affecting the outer margin of the eyelid. Note the
best treatment is of raised margin and central umbiiication which are the typical features of this condition.
course excision of
the growth, which also permits histopathological examination to exclude squamous cell carcinoma.
ULCER, SINUS AND
FISTULA
ULCER
An ulcer is a break in the continuity of the covering
epithelium — skin or mucous membrane. It may either follow
molecular death of the surface epithelium or its traumatic
removal.
EXAMINATION OF AN ULCER
The students are referred to the author's 'A Manual On
Clinical Surgery' Chapter III for detail discussion on this
subject. Here only the important points of local examination
will be discussed.
An ulcer has a margin or edge which takes characteristic
shape in a particular form of ulcer. It has a floor which means
the exposed surface of the ulcer and it has a base on which
the ulcer rests. Base is better felt than seen.
Edge.— This is an important finding of an ulcer which
by itself not only gives a clue to the diagnosis of the ulcer
but also to the condition of the ulcer. In a spreading ulcer, the
edge is inflamed and oedematous whereas in a healing ulcer
the edge, if traced from the red granulation tissue in the
centre towards periphery, will show a blue zone (due to thin
growing epithelium) and a white zone (due to fibrosis of the
scar).
Five common types of ulcer edge seen in surgical practice
are;—
(i)
Undermined edge — is mostly seen in tuberculosis.
The disease causing the ulcer spreads in and destroys the
subcutaneous tissue faster than it destroys the skin. The
overhanging skin is thin friable, reddish blue and unhealthy,
Fig. 1 1 . 1 . — Diagrammatic repre­
(ii) F*unched out edge — is mostly seen in a gummatous
sentation of different types of edge of ulcer or in a deep trophic ulcer. The edge drops down at
ulcers. A.- Undermined edge; B.right angle to the skin surface as if it has been cut out with a
Punched out edge; C - Sloping edge;
punch. The diseases which cause the ulcers are limited to the
D.- Raised and pearly-white beaded
ulcer itself and do not tend to spread to the surrounding
edge; E - Rolled out (everted) edge.
tissue, (iii) Sloping edge is seen mostly in healing traumatic
ULCER, SINUS AND FISTULA
157
or venous ulcer. Every healing ulcer has a sloping edge, which is reddish purple in colour and
consists of new healthy epithelium, (iv) Raised and pearly-white beaded edge — is a feature
of rodent ulcer. This type of edge develops in invasive cellular disease and becomes necrotic at
the centre, (v) Rolled out (Everted) edge — is a characteristic feature of squamous cell carcinoma
or an ulcerated adenocarcinoma. This ulcer is caused by fast growing cellular disease, the growing
portion at the edge of the ulcer heaps up and spills over the normal skin to produce an everted
edge.
During palpation consistency of the edge should be noted. Marked induration of the edge is
a characteristic feature of a carcinoma be it a squamous cell carcinoma or adenocarcinoma. A
certain degree of induration or thickness is expected in any chronic ulcer, whether it is atrophic
ulcer, gummatous ulcer or a syphilitic ulcer.
Floor.— This is the exposed surface of the ulcer. When floor is covered with red granulation
tissue, the ulcer seems to be healthy and healing. Pale and smooth granulation tissue indicates
a slowly healing ulcer. Wash-leather slough (like wet chamois leather) on the floor of an ulcer is
pathognomonic of gummatous ulcer. One must be very careful to note what is there at the floor
of an ulcer. A trophic ulcer penetrates down even to the bone, which forms the floor in this
case. A black mass at the floor suggests malignant melanoma.
Base (On which the ulcer rests).— The students must understand the difference between
the floor (i.e. exposed surface within the ulcer) and the base (on which the ulcer rests and it is
better felt than seen) of an ulcer. If an attempt is made to pick up the ulcer between the thumb
and the index finger, the base will be felt. Slight induration of the base is expected in any chronic
ulcer but marked induration (hardness) of the base is an important feature of squamous cell
carcinoma and Hunterian chancre.
CLASSIFICATION OF ULCERS.—
Two types of classification of ulcers are possible :—
I. Clinically and II. Pathologically.
I. CLINICALLY, an ulcer may be either —
(a) Spreading' — when the surrounding skin of the ulcer is inflamed and the floor is
covered with slough without any evidence of granulation tissue; or
(b) Healing — when there is granulation tissue in the floor of the ulcer, the surrounding
skin is not inflamed and the edge shows bluish outline of growing epithelium, moreover, there
is slight serous discharge; or
(c) Callous — when there is pale granulation tissue in the floor, there is considerable
induration at the base, edge and surrounding skin. This ulcer shows no tendency towards healing.
n. PATHOLOGICALLY, the ulcers are classified into three main headings — A. Non-specific
ulcers, B. Specific ulcers and C. Malignant ulcers.
A.
Non-specific ulcers.— There are various causes of such ulcers. According to the cause
these ulcers are classified as below —
1. Traumatic ulcer — can be either (i) mechanical e.g. dental ulcer of the tongue from
jagged tooth, from pressure of a splint etc. or
(ii) Physical — from electrical or X-ray bum or
(iii) Chemical — from application of caustics.
2. Arterial ulcer — as occurs in atherosclerosis, Buerger's disease and Raynaud's disease
(primary and secondary).
3. Venous ulcer — e.g. venous ulcer in post-phlebitic limb.
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A CONCISE TEXTBOOK OF SURGERY
4. Neurogenic ulcer.
5. Infective ulcer.— Pyogenic ulcer and Baimsdale ulcer are included in this group.
6. Tropical ulcer.— These ulcers occur in the legs and feet of the people in the tropical
countries. Infection by Vincent's organisms (bacteroides fusiformis) in a small abrasion may
cause such ulcer. Ulcers associated with mal-nutrition, anaemia, avitaminosis and rheumatoid
arthritis are also included in this group.
7. Cryopathic ulcer.— Ulcers due to chilblains and cold injury are included in this group.
8. Martorell's ulcer (hypertensive ulcer ).
9. Bazin's ulcer (erythrocyanoid ulcer).
10. Diabetic ulcer.
11. Miscellaneous ulcers.— Ulcers may be associated with (i) polycythemia, (ii) leukaemia,
(iii) systemic sclerosis, (iv) ulcerative colitis, (v) poliomyelitis, (vi) arteriovenous fistulae, (vii)
Acholuric jaundice, (viii) various collagen disorders and (ix) chronic lymphoedema. Cortisone
ulcers are also included in this group.
B. Specific ulcers are seen in tuberculosis, syphilis, soft sore and actinomycosis. Meleney's
' ulcer is included in this group.
C. Malignant ulcers — e.g. epithelioma, rodent ulcer and malignant melanoma.
TRAUMATIC ULCER.— According to the cause of the trauma, the ulcer may be situated
anywhere in the body. But these ulcers occur more commonly where the skin is closely applied
to bony prominences e.g. shin, malleoli and back of the heel. Plaster sores and dental ulcer of
the tongue are included in this group.
These are small, painful and circular ulcers. Occasionally, particularly in older people, a
single ulcer confined to the lower leg is due to chronic staphylococcal infection. 'Footballer's
ulcer' on the shin is due to staphylococcal infection in an area of repetitive trauma. These ulcers
heal quickly and do not become chronic unless supervened by infection or ischaemia, which
may turn this ulcer to chronicity. The typical example of such chronic ulcer is the 'footballer's
ulcer'.
ARTERIAL ULCER.— These ulcers are caused by inadequate skin circulation. These occur
in those parts of the limbs which are subjected to repeated pressure and trauma. Prolonged
pressure on one part of the foot causes ischaemic damage to the tissues and if the circulation is
inadequate then the tissues cannot repair themselves and ischaemic ulcer develops.
These ulcers are mostly due to peripheral arterial disease and poor peripheral circulation.
Atherosclerosis of the peripheral arteries is the commonest cause of this condition. This condition
is more often seen in old people. It is due to episodes of trauma and infection that destroy the
skin which fails to heal because of poor arterial supply. These ulcers tend to occur on the anterior
and lateral aspects of the leg, on the toes, dorsum of the foot or the heel (the parts exposed to
trauma).
Buerger's disease (thromboangiitis obliterans), a disease of men between 20 and 40 years of
age, may also present with such ulcer. Patches of dry gangrene are present alongwith the arterial
ulcer.
Pain is the main complaint. These ulcers tend to be punched out and destroy the whole skin
and the deep fascia (unlike the venous ulcer) and may expose the tendons in the floor of the ulcer.
When these ulcers occur on the inner side of the ankle, the diagnosis may be confused with the
venous ulcers, but a history of intermittent claudication with discolouration of one or more toes
ULCER, SINUS AND FISTULA
159
becomes the differentiating feature. Moreover if the leg is kept elevated above the heart's level,
the ulcer shows no sign of healing and the patient will complain of pain in this position.
Arteriography is important to detect the arterial disease.
VENOUS ULCER.— This is the
commonest ulcer of the leg. The basic
cause of venous ulcer is abnormal venous
hypertension in the lower-third of the leg,
ankle and dorsum of the foot. Various
terms have been used e.g. varicose ulcer,
post-thrombotic ulcer, gravitational ulcer
etc. For further description the students
are referred to author's 'A Textbook on
Surgical Short Cases' P.154 or P.268 of this
book.
NEUROGENIC ULCER.— The
mechanism of formation of such ulcer is
repeated injury or pressure in an area
which has lost appreciation of pain. The
neurological conditions which predispose
to formation of such ulcer include
diabetes, alcoholic peripheral neuritis,
tabes dorsalis, spina bifida, leprosy,
peripheral nerve injury, paraplegia and
syringomyelia. These ulcers are painless.
These ulcers are commonly seen on
the heel and ball of the foot when the
patient is ambulatory; on the buttock and
on the back of the heel when the patient
is non-ambulatory. This ulcer starts with
callosity under which suppuration takes
place. The pus comes out and the central
hole forms the ulcer which gradually
A typical venous ulcer with ankle flare below
Fig.11.2.burrows through the muscles and the
the ulcer.
tendons to the bone. That is why this
ulcer is also called perforating ulcer.
Trophic ulcers are included in this group which are caused by various factors such as
impairment of nutrition of the tissues, inadequate blood supply and neurological deficit. Bed
sore is included in the group of trophic ulcers. These ulcers have punched out edge with slough
in the floor thus resembling a gummatous ulcer. These ulcers develop as the result of repeated
trauma to insensitive part of the body.
INFECTIVE ULCER.— For further description of pyogenic ulcer and Baimsdale ulcer the
students are referred to author's 'A Text Book On Surgical Short Cases' Chapter XIV 'Ulcers of
the leg'. Syphilitic ulcers are classified under the heading of specific group of ulcers and are not
included here.
TROPICAL ULCER.— The most characteristic feature of this ulcer is its callousness towards
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A CONCISE TEXTBOOK OF SURGERY
healing. Its edge is slightly raised and exudes copious serosanguineous discharge. This ulcer
practically retains the same size for months and years. In some cases, it destroys the surrounding
tissue and thus spreads widely. Every effort should be made to detect the cause behind the
ulcer and to treat accordingly. Otherwise it may retain its existence or even spread rapidly.
The ulcer, which develops due to infection by Vincent's organisms in a small abrasion or
breach of continuity of the skin due to trauma or insect bite, commences as a papule with a
zone of surrounding inflammation and induration. Pain is an important symptom and this is
often accompanied by acute lymphadenitis. Gradually pustules develop and burst in two or
three days forming ulcers whose edges are undermined and raised. Copious serosanguineous
discharge with considerable pain is the most important feature. The ulcer becomes indolent and
refuses to heal for months or even years. In others, it heals after a long period leaving a parchment
like pigmented scar.
CRYOPATHIC ULCERS.— Cryopathy means a condition resulting from intense cold and
chilly weather.
1. CHILBLAINS.—When the lower extremity is exposed to intense cold, blisters and
ulceration may occur particularly in the feet. This is also called pemiosis. The lesion starts as
red tender spot, which becomes a pruritic swelling later on. Blisters form in such swelling. These
blisters burst to form ulcers. These ulcers
are superficial. Such lesion results from
excessive vasoconstriction of the skin
arterioles of the affected area.
2. COLD INJURY.— This is also
known as frostbite. When any part of the
body is exposed to wet cold below
freezing point, ischaemic changes occur
in the skin and subcutaneous tissues.
Such ischaemic changes are due to
arteriolar spasm followed by stasis of
blood in the capillaries. This alongwith
exposure of the tissues below freezing
point will lead to freezing of tissues and
denaturation of intracellular protein with
destruction of enzyme systems. All of
these will cause gangrene of the full
thickness of the skin. This is known as
frostbite.
MARTORELL'S
ULCER.— This
was first described by Martorell in 1945.
These ulcers occur in patients over 50
years of age who are usually
hypertensive or atherosclerotic. A local
patch of skin on the back or outer side
of the calf suddenly necroses and sloughs
away leaving a punched-out ulcer FiS-H-3— Martorell’s ulcer. Note the typical punched-out
extending down to the deep fascia. Pain appearance 11 appears suddenly and causes considerable pain.
ULCER, SINUS AND FISTULA
161
is quite severe and may prevent the patient from sleeping. This condition may be bilateral.
Pathology is sudden obliteration of the end arterioles of the skin of this region which is
already having a sparse arterial supply from atherosclerosis. It is noteworthy that all peripheral
foot pulses are usually present. Since this is an ischaemic lesion, it has a long painful course and
may take months to heal.
BAZIN’S ULCER.— These ulcers are associated with 'erythrocyanosis frigida', which is an
exclusive disease of young women. These patients have thick ankles with abnormal amount of
subcutaneous fat, combined with an abnormally poor arterial supply to the ankle skin. The
blood supply of the lower-third of the leg and the ankle are derived from a number of fine
perforating arteries arising from the posterior tibial and peroneal arteries. In erythrocyanoid
cases these arteries may be abnormally small or even absent causing low grade ischaemia of the
whole ankle region. The patient finds that the ankle skin is abnormally sensitive to temperature
changes. When the weather is cold, the ankle is blue, cold and often tender. In hot weather
chronic reactive hyperaemia becomes evident with the ankle becomes hot, oedematous, swollen
and painful. Palpation of the leg will reveal small, superficial and painful nodules which
breakdown to form ulcers. These ulcers are small and multiple. Anything liable to cause an
ulcer (incompetent perforating vein, trauma or infection) produces its effect much more quickly
and in a more severe degree in the relatively ischaemic fat ankle. It is therefore necessary to
recognise this condition and to treat such condition as venous ulcers, traumatic or infective
ulcers more vigorously in erythrocyanoid limb.
Acute fat necrosis sometimes occurs on the back and outerside of the ankle, particularly
with chronic exposure to cold environment. This may ultimately lead to very chronic painful
ulcers. Sympathectomy may be necessary to manage such ulcer. These patients are much troubled
by chilblains. This again may be an indication for sympathectomy particularly if the patient
lives in a cold climate.
DIABETIC ULCER.—
Aetiology.—
• Slight injury to glucose laden tissue may cause chronic infection and ulcer formation.
• Ulceration in diabetes may be precipitated by ischaemia due to diabetic atherosclerosis.
• More prone to infection of glucose ladden tissue may cause ulceration.
• Diabetic polyneuropathy or peripheral neuritis may also cause ulcer formation.
Sites.—
• Toes and feet particularly the sole is the commonest site.
• Leg is also affected.
• Any other part of the body may be affected.
Nature.— Diabetic ulcer is deep and spreading.
Investigations.—
• Blood sugar estimation both fasting and post-prandial.
• Urine ketone bodies.
• Culture and sensitivity of the discharge.
• Arterial blood flow of the lower limb is measured by Doppler ultrasound.
Treatment.—
• Diabetes should be controlled.
H
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A CONCISE TEXTBOOK OF SURGERY
• Antibiotics are prescribed to control infection.
• Excision of the ulcer, debridement and skin grafting once healthy granulation tissue is
formed.
MISCELLANEOUS ULCERS.— Ulceration of the leg may be associated with (i) gross
anaemia, (ii) polycythemia, (iii) leukaemia, (iv) systemic sclerosis, (v) rheumatoid arthritis, (vi)
ulcerative colitis, (vii) poliomyelitis, (viii) arteriovenous fistulae, (ix) acholuric jaundice, (x) various
collagen disorders and (xi) chronic lymphoedema.
Cortisone ulcers are recently not uncommon finding. Cortisone ointment are often applied
to minor abrasions, eczemas and other lesions of the ankle to damp down inflammatory reaction
and therefore controlling pain. These local cortisone creams, if applied, continuously for a
prolonged period, may cause large callous ulcer with no inflammatory response. These ulcers
are difficult to treat and may require excision and skin grafting.
TUBERCULOUS ULCER.— Such ulcer usually develops due to bursting of cold abscess.
This cold abscess may form — (i) from matted tuberculous lymph nodes; (ii) From tuberculosis
of bone or joint; (iii) From submucous lesions e.g. intestinal tuberculosis or tongue tuberculosis.
CHARACTERISTIC FEATURES.—
Size and shape— Tuberculous ulcer is generally oval in shape with irregular crescentic
border.
Number — is often multiple.
Edge — is thin reddish blue and undermined.
Depth.— Tuberculous ulcer is usually shallow.
Pain.— Slight pain is often accompanied with such ulcer.
Floor.— Pale granulation tissue is seen on the floor with variable amount of discharge.
Base.— Slight induration is characteristic feature of this ulcer which indicates chronicity of
this ulcer. Base is usually attached to the pathological lesion underneath which may be lymph
nodes, bone or joint.
Lupus Vulgaris.— It is a form of cutaneous tuberculosis, occurs commonly in the face and
hand and the usual victims are the children and young adults. It starts very superficially. The
peculiarity of this ulcer is that it heals at the centre and remains active at the periphery and
thus gradually spreads like a wolf. Hence its name 'lupus', means a wolf.
Management of Lupus Vulgaris.—
• Antitubercular drugs.
• When healing is not complete, excision and skin grafting should be performed.
Investigations.—
• Chest X-ray; ESR; Examination of discharge; Biopsy, if required.
SYPHILITIC ULCERS.— Ulcers due to syphilis are seen in all the three stages of this
disease.
IN PRIMARY SYPHILIS — a hard chancre or Hunterian chancre is seen. This chancre usually
develops at the site of entry of the treponemes in about 3 to 4 weeks after exposure. The sites
are usually external genitalia, but it may occur at extragenital sites e.g. lip, tongue, nipple, perianal
region etc.
Characteristic features.— Hard chancre is usually single, painless and possesses a
characteristic indurated base, which feels like a button. It is usually shallow oval or round in
shape with a raised hyperaemic margin.
ULCER, SINUS AND FISTULA
163
It must be remembered that extragenital chancres have less indurated base and may be
slightly painful.
The regional lymph nodes are enlarged which are firm, discrete and painless.
IN SECONDARY SYPHILIS — ulcers may develop in the form of mucous patches, snailtrack ulcers or more so in the form of condylomas.
Mucous patches.— These are white patches of sodden thickened epithelium.
Snail-track ulcers.—These are multiple small, round and superficial erosions which coalesce
to form narrow, curved and shallow ulcers which are called 'snail-track ulcers'. These ulcers are
commonly seen in the mouth.
Condyloma lata.— These are fleshy, wart-like growths, mostly seen at the mucocutaneous
junctions e.g. angles of the mouth, anus, vulva etc. These are in fact raised, flat, white and
hypertrophied epithelium, which often present as fungating sessile masses. The surfaces are
moist and teemed with treponemes.
In this stage of syphilis there is generalized enlargement of lymph nodes which are painless;
particularly important are the epitrochlear and suboccipital groups of lymph nodes which are
almost always enlarged and considered to be diagnostic to some extent.
IN TERTIARY SYPHILIS.— The typical lesion in this stage is the localized gumma or
gummatous ulcer.
Gummatous ulcer.— Gumma is a syphilitic hypersensitivity reaction consisting of granulation
tissue with central necrosis. Sloughing of this necrotic tissue produces the gummatous ulcer
which is known for its punched-out indolent edge and painlessness. In the floor there is yellowish
grey gummatous tissue (wash leather slough). On healing it leaves a silvery 'tissue paper' scar.
W.R., Kahn and V.D.R.L. tests are positive. Lymph nodes are not enlarged unless secondarily
infected.
Characteristic sites of this gummatous ulcer are —
(i) Over subcutaneous bones e.g. tibia, sternum, ulna and skull.
(ii) In the scrotum particularly on its anterior surface in relation to the testis.
(iii) Occasionally in the tongue.
SOFT CHANCRE OR CHANCROID (DUCREY’S).— This condition is caused by gramnegative Haemophillus Ducreyi. It is a contagious disease. 3 to 5 days after exposure multiple
acute sores develop on the external genitalia. These are often painful. These gradually become
pustular and ulcerate to form soft sores. These ulcers are multiple, rounded, soft (cf. hard
chancre), painful and readily bleed. The edges of these ulcers are undermined.
The regional lymph nodes (inguinal lymph nodes) become enlarged and tender. They show
the features of acute lymphadenitis. Suppuration may or may not occur in these nodes. If
suppuration occurs the nodes become matted and form a fluctuant swelling with abscess (known
as 'bubo'). The overlying skin becomes red. These buboes should not be incised lest chronic
sinuses should be formed. It is better to aspirate these buboes. If suppuration does not occur
resolution is the rule.
Treatment.— Sulphonamide or cotrimoxazole two tablets twice daily for 7 to 10 days is
considered to be the best drug in this condition.
ACTINOMYCOSIS.— This condition causes multiple ulcers. At first the area becomes
indurated. Nodules appear, which soften and ulcerate in various places. The surrounding skin
often looks bluish in colour. So if multiple ulcers are found in an indurated area with bluish
colour of skin surrounding the ulcers, the condition should be suspected as actinomycosis.
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164
Diagnosis is confirmed by collecting discharged pus from the ulcers in a sterile tube. Presence
of granules, known as 'sulphur granules' in the collected pus is quite diagnostic. On microscopy
the granules consist of gram-positive mycelia (actinomyces israelii). In these granules the
peripheral filaments radiate from the central part of the granule.
Actinomycosis is seen in one of the four places — (i) Facio-cervical, which is the commonest
site, followed by (ii) thorax, (iii) right iliac fossa and (iv) liver.
MELENEY’S ULCER.— These ulcers are seen in the postoperative wounds either after
the operation for perforated viscus or for drainage of empyema thoracis. It is also found, though
rare, on the dorsum of the hand. This type of ulcer is due to symbiotic action of microaerophilic
non-haemolytic streptococci and haemolytic staphylococcus aureus. Clinically it is an undermined
ulcer with lot of granulation tissue in the floor. It is surrounded by deep purple zone, which in
its turn is surrounded by an outer zone of erythema. This particular condition is painful, toxaemic
and the general condition deteriorates without treatment.
BAIRNSDALE ULCER.
This is caused by acid-fast Bacilli-Mycobacterium ulcerans. Its deep severe form is called
'Buruli Ulcer' with extensive dermal necrosis.
Diagnosis is confirmed by examining the discharge which shows acid-fast bacilli.
Treatment is by antitubercular drugs which usually resolve the ulcer. Skin grafting may be
necessary.
RODENT ULCER.— See page 126.
EPITHELIOMA.— See page 129.
MALIGNANT MELANOMA.— See page 137.
MARJOLIN'S ULCER.— See page 134.
PRINCIPLES OF MANAGEMENT OF ULCERS.— To know the exact aetiology of an
ulcer is extremely important to be successful in treatment. A thorough history, physical
assessment of the patient and general medical condition should be considered besides the local
examination of the ulcer. This will often provide important clues to know the aetiology. The
need for other investigations will vary depending on the type of ulcer one is suspecting. Biopsy
of the lesion is extremely important to determine the exact nature of the ulcer. The principles of
ulcer management in fact include the following points —
(i) To determine aetiology;
(ii) Accurate assessment of ulcer;
(iii) To identify and to correct morbid factors e.g. anaemia, diabetes, infection etc.;
(iv) To treat underlying causes;
(v) Drainage and desloughing of the ulcer;
(vi) To avoid adherent dressings.
A clear ulcer with healthy granulation tissue exuding serous discharge should be dressed
once a day. If there is copious discharge more dressings should be done in a day. Use of woven
cotton or cellulose gauze soaked in antiseptic solutions should be discarded. Antiseptic solutions
impair capillary circulation and are toxic to granulation tissue. Ulcers can be cleaned more safely
with normal saline solution. Use of gauze dressing as packs often cause discomfort as these
expand into hard mass on absorbing fluid. In addition this type of dressings become adherent
to the granulation tissue avulsing the superficial layer of the ulcer and thereby causing further
delay in healing.
ULCER, SINUS AND FISTULA
165
The ideal dressing should be one that is soft, absorbent, non-adherent and non-allergic.
Although ideal dressing probably does not exist, but there are dressings which provide
compromise. Hydrocelluloid gel (Granuflex, Hydrogel), some of which may have a polyurethane
base and provide good wound protection. Compound forms of gel, when it comes in contact
with ulcer exudate, expands to fill the wound. It provides a good environment for wound healing
and is an effective barrier against microorganisms. These can be used particularly in leg ulcers
and pressure sores. Alginates e.g. Kalstostat or sorbsan consist of absorbent fibres composed of
a mixture of sodium and calcium salt of algenic acid. The fibres absorb fluid to form a gel-like
substance that promotes healing. Microporous polyurethene films (Liofoam) are suitable for
relatively shallow lesions. These are permeable to gasses and water vapour, but are impermeable
to microorganisms. So these dressings may be left in place for several days and are suitable for
the management of minor bums, skin graft donor sites and postoperative wounds. Such dressing
also reduces the healing time. But this type of dressing should not be used in established infection
or excess exudate.
SINUS AND FISTULA
SINUS.— A sinus is a blind track leading from the surface down to the tissues. There may
be a cavity in the tissues which is connected to the surface through a sinus. The sinus is lined
by granulation tissue which may be epithelialized.
FISTULA.— A fistula is a communicating track between two epithelial surfaces, commonly
between a hollow viscus and the skin (external fistula) or between two hollow viscera (internal
fistula). The track is lined with granulation tissue which is subsequently epithelialized. A fistula
may be an abnormal communication between vessels (arteriovenous fistula).
Sinuses and fistulae may be congenital or acquired.
Congenital sinuses and fistulae are (i) branchial fistula, (ii) tracheo-oesophageal fistula,
(iii) arteriovenous fistula, (iv) preauricular sinus etc.
Acquired sinuses and fistulae usually follow inadequate drainage of abscesses, (i) The
perianal abscess may burst on to the surface and lead to the formation of fistula-in-ano. (ii)
Acquired arteriovenous fistula — is caused by trauma or operation (for renal dialysis), (iii)
Thyroglossal fistula and (iv) Pilonidal sinus are other examples of acquired variety.
Causes of persistence of a sinus are: (1) presence of foreign body or necrotic tissue (e.g.
sequestrum or a suture material) in the depth; (2) absence of rest; (3) non-dependent drainage
or inadequate drainage of an abscess; (4) when a specific chronic infection (e.g. tuberculosis,
actinomycosis etc.) is the cause; (5) when the track becomes epithelialized; (6) sometimes there
may be a dense fibrosis around the wall of the track and the cavity preventing their collapse, as
occurs in chronic empyema; (7) presence of malignant disease.
Causes of persistence of a fistula are : once a true fistula has been formed, it seldom
shows any intention towards healing. Moreover irritant discharges such as urine, faeces, bile
etc. are passed through the fistula and prevent its healing. Obstruction of the lumen of the
viscus or tube distal to the fistula is often a main cause of persistence of fistula. One thing
should always be remembered that if the natural passage is made patent, all abnormal offshoots
heal spontaneously.
LOCAL EXAMINATIONS.— The students are referred to same author's 'A MANUAL ON
CLINICAL SURGERY' page 56 for the details of local examinations.
EXAMINATION WITH A PROBE.— This is important but should be performed with due
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166
precaution. This examination
will inform the clinician
about (i) the direction and
the depth of the sinus, (ii)
presence of any foreign body
such as sequestrum, which
will be movable, at the depth
of the wound, (iii) whether
the fistula is communicated
with a hollow viscus or not
and (iv) whether fresh
discharge comes out on
withdrawal of the probe or
not.
EXAMINATION
OF
DRAINING
LYMPH
NODES.— This examination
is always essential and
should not be missed under
any circumstances.
GENERAL
NATION.—
EXAMI­
Depending on the site
and cause of the sinus,
examination of the particular
system should be performed.
In case of a sinus in the loin,
the spine, ribs and the
kidneys should be examined
to know the exact cause of R9.H.4.- Typical diagrammatic representations of sinus and fistula to
,.
show the difference,
the lesion (tuberculous smus
following cold abscess). In case of a sinus due to chronic empyema, the chest should be
thoroughly examined. In case of a sinus due to osteomyelitis, the bone should be examined
carefully. In case of fistula around the anus a thorough examination not only of the anal canal
and rectum both manually and proctoscopically should be called for but also sigmoidoscopic
examination and examination of the whole abdomen should be performed. In case of multiple
fistulae in the perineum and scrotum, the lower urinary track should be thoroughly examined.
SPECIAL INVESTIGATIONS.—
1. Examination of the discharge — is of utmost importance to come to a diagnosis. It
should be examined macroscopically, physically, chemically, microscopically (e.g. for sulphur
granules in case of actinomycosis) and bacteriologically.
2. X-ray examination.— (a) Straight X-ray may show a sequestrum and osteomyelitic
change of the bone concerned or presence of opaque foreign body.
(b)
Injection of radio-opaque fluid (lipiodol or hypaque) into a sinus or a fistula will indicate
the depth as also cause of the sinus by delineating its course.
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167
TYPES OF PATHOLOGICAL SINUSES.—
Congenital
Umbilical
Urachal
Sacral
Coccygeal
Pre-auricular
Acquired
Pilonidal
Post-surgical
Actinomycosis
Osteomyelitis
Tuberculosis
Hydroadenitis suppurativa
CONGENITAL SINUSES
UMBILICAL SINUS.— This usually results from the continued presence of the umbilical
end of the vitelline duct. In the foetus, the vitelline duct connects the foetal midgut to the yolk
sac. This normally obliterates and disappears completely. If this duct persists in part, such sinus
develops. The morphology of the sinus tract can be delineated with a sinogram. Treatment is
excision of the sinus.
URACHAL SINUS.— In foetus the urachus connects the developing bladder to the
umbilicus. It normally obliterates by the time of birth. A persistent urachal sinus results when
the umbilical end of the urachus is not obliterated. Such sinus presents a chronic drainage of
small amount of material from the umbilicus. If the sinus is a complete one, connecting the
urinary bladder, small amount of urine may leak out from the umbilicus. Such sinus often
becomes infected. Treatment is total excision of the sinus.
PREAURICULAR SINUS.— Preauricular sinus may be unilateral or bilateral. These are
usually asymptomatic but may become infected. If infected, antibiotic and drainage are required
followed by excision when infection passes off. Complete excision is sometimes difficult because
such sinus may have ramifications which may be in proximity to the branches of the facial
nerve. This type of sinus, if uncomplicated, may be left alone. Excision is only recommended if
recurrent infection complicates such sinus.
ACQUIRED SINUSES
PILONIDAL SINUS.— This is usually found in the natal cleft. It is thought to arise from
loose hair shafts that are shed from the body and migrate to the natal cleft during walking.
These are forced into deep tissues by gluteal contractions. Such sinus is initially asymptomatic,
but with blockage and infection of the sinus a painful swelling may develop. Sometimes discharge
occurs from this swelling and pain and swelling disappear, but recur again if left untreated.
This condition may progress with formation of sinus tracks and openings. Treatment is complete
excision of the sinus alongwith its ramifications. Various techniques are being adopted e.g.
excision with primary closure or excision with healing from secondary intention. But recurrence
is the main problem.
POST-SURGICAL.— It is a commonly encountered sinus which results from non-absorbable
suture material acting as a focus of infection within the wound. It is more common after closure
of contaminated wounds. Treatment is removal of the suture.
Larger sinuses may occur as a result of postsurgical intraabdominal abscesses or anastomotic
leaks. This may form a fistula if the abscess cavity is in continuity with the bowel lumen. The
internal opening usually closes leaving a chronic discharging sinus that fails to heal due to
inadequate drainage of the abscess cavity.
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HYDROADENITIS SUPPURATIVA.— This is due to abnormality of the apocrine sweat
glands of the body which are found in the axillae, groins, perineum or around the nipples. It is
characterized by development of recurrent abscesses. The abscesses may resolve or may discharge
spontaneously forming chronic discharging sinuses. The condition may improve with antibiotics
like tetracycline, but radical surgical excision of the affected area may be required if the condition
persists.
Other sinuses have been discussed in the appropriate chapters. In the management of sinuses,
accurate detection of any associated deep abscess cavity or complex deep extensions of the
sinus tract is highly important, for successful treatment e.g. for osteomyelitic sinus, for
osteomyelitic abscess cavity must be treated to get rid of such sinus.
TETANUS
Definition.— It is a condition of toxaemia due to absorption of soluble toxin from the
wound contaminated with Clostridium tetani.
Bacteriology.— Cl. tetani is the causative organism, which is a gram-positive anaerobic
rod with terminal round spore — about 3 to 4 times wider than the bacillary body, giving rise
to a typical drum stick appearance. It is mainly found in manure and soil. It is a normal inhabitant
of the intestines of human beings and animals.
A low oxygen tension in the wound is necessary if Cl. tetani is to grow.
The exotoxin produced by the Cl. tetani, which causes tetanus, consists of 2 components—
(a) Tetanospasmin, which is a neurotoxin and acts on the motor-end plates and (b) Tetanolysin is
an oxygen labile haemolytic toxin.
INCUBATION PERIOD.— It varies from 3 days to 3 weeks but on average it is 7 days.
This period is increased in immunised persons. The incubation period is important as it indicates
the severity of the disease. The longer is the incubation period, the milder is the attack.
The interval between the first symptom and first reflex spasm, which is known as the period
of onset has also a significant prognostic value. If this interval is less than 48 hours, the condition
is almost fatal. So the incubation period is followed by the period of onset.
MODES or ENTRY.—
(i) Usually a penetrating wound due to rusty nail, splinter or thorn is the portal of entry.
In 50% of cases the wound is slight and healed before evidence of tetanus develops. Such
mild injuries may not induce significant local anoxia, but they may be accompanied by other
Infections which lower the oxidation potentiality of the tissues, at which the spores of Cl. tetani
can germinate.
(ii) Dirty abrasions may sometimes lead to this condition. Street injury which is
contaminated with dust or excreta of cows or horses may cause tetanus.
(iii) Chronic ulcers of the leg, boils, paronychia and dental extractions have also been
implicated as modes of entry.
(iv) Tetanus may follow a subcutaneous injection of an irritant drug like quinine or emetine.
(v) It is now currently seen in developed countries as a complication of narcotic addiction,
which has been called as 'urban tetanus'.
(vi) 'Tetanus neonatorum' results from contamination of the cut surface of the umbilical cord.
It is an important cause of infant mortality in developing countries. Soon the child ceases to cry
and suck followed by fever and convulsion. Severe spasm of the respiratory muscles is the
common cause of death.
(vii) 'Post-abortal tetanus' or 'puerperal tetanus' results from unsterile manipulation or
instrumentation during abortion or labour.
(viii) 'Postoperative tetanus' sometimes follows elective surgical procedure, which is often due
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to negligent breakdown in sterile technique or caused by contamination from the patient's
intestinal tract.
(ix)
Sometimes the wounds are so trifle that they are often forgotten. After months or years
due to some unknown change which produces the right conditions for Cl. tetani to multiply and
produce toxin that tetanus develops. This is known as 'latent tetanus’.
PATHOLOGY.— Manifestations of the disease are due to absorption of soluble exotoxin
from the site of infection. Implantation of tetanus pores into the wound should be followed by
an anaerobic condition in which these pores can germinate and the organisms can multiply due
to low oxygen potential of such tissue. Necrosis and devitalization of the tissue by injury to the
blood vessel and thrombosis are the contributory factors. Calcium ions derived from soil or
haemorrhage act further to reduce the oxygen potential of the tissue.
From the site of infection the toxin, liberated by the tetanus bacilli, is absorbed, and reaches
the central nervous system. How does this toxin reach the central nervous system is a question.
Various theories have been put forward :—
(a) The toxin travels through the motor nerves along their axis cylinders to reach the cord.
(b) The toxin travels through blood stream. This explains why the earlier effects e.g. trismus
or difficulty in deglutition or rigidity of neck muscles or spasms of the muscles of the face are
well away from the wound.
(c) The toxin travels through the lymphatics along the nerve trunks to the central nervous
system.
Whatever may be the route, the exotoxin ultimately reaches the cord and is fixed to the
motor cells of the anterior horn. Once it is fixed to the motor cells of the anterior horn, it cannot
be detected in the CSF and no amount of A. T. S. can neutralise this fixed exotoxin.
With fixation of exotoxin to the anterior horn cells, it causes extreme hyperexcitability of
motor neurones in the anterior horn cells. This evokes widespread reflex spasms of the muscles.
Moreover the exotoxin produced at the inoculation site inhibits the cholinesterase at the
motor end plates. This results in an excess of acetylcholine at the motor end plates, which causes
tonic muscle spasm.
CLINICAL FEATURES.—
(a) Trismus is the most common early symptom. It is often combined with pain and stiffness
of the neck, back and abdomen.
(b) Occasionally dysphagia (difficulty of deglutition) appears first. These symptoms increase
according to the severity of the attack.
(c) Gradually the patient shows a characteristically anxious expression (risus sardonicus),
in which the eye brows and the comers of the mouth are drawn up. This is due to spasm of the
muscles of the face and jaw.
(d) The muscles of the neck and trunk gradually become rigid to varying degrees and the
back is slightly arched, a condition known as opisthotonus. This rigidity is due to spasms of the
corresponding muscles which are chronic as well as tonic and the relaxation is incomplete during
the interspasmodic intervals. Psoas and abdominal muscles may rupture.
(e) Manipulation of a limb or palpation of any part of the body may increase muscular
rigidity and may bring on cramp-like pain. Initially the reflex spasms are brought on by external
stimuli e.g. moving the patient or knocking the bed. But later on they occur spontaneously at
regular and increasingly shorter intervals.
(f) Every muscle in the body is gradually thrown into intense chronic contraction, the jaws
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171
are tightly clenched, the head is retracted, the back is arched and the limbs are usually extended.
(g)
The constitutional symptoms are also seen e.g. the temperature becomes elevated, the
pulse becomes rapid and the patient may become cyanotic due to respiratory failure, which is
obviously an ominous sign.
Special types of tetanus.— After describing the common clinical manifestations of tetanus,
I would now like to mention a few special types of tetanus —
1. Acute tetanus.— In this type the incubation period is less than 10 days and the
prognosis is grave.
2. Chronic tetanus.— In this type the incubation period is about 1 month. The clinical
manifestations are less severe. These cases have often received prophylactic injections of antitoxin.
3. Delayed tetanus or latent tetanus.— In this condition the organism remains latent
in the wound for months or years. Due to certain unknown change, the organisms suddenly
find right conditions to multiply and produce toxin.
4. Local tetanus.— In this condition there are local contractures of muscles in the
neighbourhood of the wound. Often these cases had taken antitoxins or probably the exotoxin
involves only the segmental anterior horn cells of the cord.
5. Cephalic tetanus.— In this condition there is irritation or paralysis of the cranial nerves
which dominate the picture. The facial nerve is affected most often. Involvement of ocular nerve
causes ophthalmoplegia. Involvement of hypoglossal nerve causes spasm or paralysis of the
tongue. Trismus or dysphagia may also be present. This condition may be a type of local tetanus
when it follows wounds of head and face.
6. Bulbar tetanus.— In this condition there is extensive spasm of the muscles of
deglutition and respiration. This form is often dangerous as death is caused by spasm of muscles
of respiration.
7. Late tetanus.— In this condition the inoculation period is considerably prolonged.
8. Tetanus neonatorum.— This has been discussed above.
9. Recurrent tetanus.— The patient who has survived tetanus is not immune, unless
immunized. He may receive a second attack, which is known as recurrent tetanus.
TREATMENT.—
A. PROPHYLAXIS.—
1. Active immunization.—
The best way to avoid tetanus is to provide active immunization to all individuals. This is
done either by formol toxoid or alum precipitated toxoid (A. P. T.). Nowadays aluminum
phosphate-adsorbed tetanus toxoid is used. Active immunization should be given to all children
alongwith toxoids of diphtheria and pertussis vaccine (DTP) which is cumulately called the
'triple antigen'. For active immunization above 6 years of age 0.5 ml tetanus toxoid is injected
intramuscularly. For injection left deltoid region is probably the best followed by the gluteal
region. The same dose is repeated after 4 to 6 weeks and again the same dose is repeated after
6 to 12 months. Only after this 3rd injection the basic series is considered complete, following
which a 'booster' dose of same amount is injected every 4 years. Following the initial dose of
tetanus toxoid, non-immunized individual requires approximately 30 days to acquire a safe
antibody level.
(i) When a non-immunized individual receives injury, the full course as mentioned above
should be administered.
(ii) When an immunized individual receives injury, only a booster dose is administered.
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2. Passive immunization.—
(a) Equine A. T. S. (prepared from horse serum) may be given to non-immunized individual
at the time of injury so as to give an adequate cover during the period needed to establish active
immunity by the toxoid. The dose is usually 1,500 I.U. and is used subcutaneously or
intramuscularly. The disadvantages of this A. T. S. are that (i) a preliminary skin test is always
required before administration to avoid anaphylactic reactions. If the skin test is positive A. T. S.
should not be given, (ii) The effect of A. T. S. is obtained after 48 hours and the effect remains
upto 2 weeks, (iii) If the person has already received an injection of A. T. S., this time A. T. S. will
be eliminated quickly. So it is advisable to inject a larger dose in the range of about 30,000 units
and repeated every alternate day to maintain its action.
(b) Human antitetanus globulin (Humotet) (A. T. G.) is better than the previous A. T. S.,
as it is homologus antitoxin. Its protective value is 100 times more than that of A. T. S. and no
skin test is required as being a homologus antitoxin, similarly chance of anaphylactic reactions
are nil. It may be given intramuscularly or intravenously in the dose of 250 to 500 units alongwith
the tetanus toxoid to achieve immediate immunization and gives adequate cover to the patient
before active immunization provides adequate antibody level in the serum.
3. Proper debridement of the wound — If all lacerated and contaminated wounds are properly
debrided alongwith removal of all dead tissues, blood clots and foreign bodies, chance of tetanus
will be almost nil. This is probably the most important prophylactic measure as it eliminates all
favourable conditions for growth and survival of tetanus bacilli.
4. Antibiotic.— Penicillin is a bacteriostatic agent for Cl. tetani and prevents production of
exotoxin. Moreover it also acts on pyogenic organisms particularly gram-positive ones, whose
presence helps germination and multiplication of Cl. tetani. Whenever one suspects that there is
a chance of tetanus, injection penicillin should be given in large dose (10 lacs I.M. twice daily)
which has a good prophylactic value. A single dose of long-acting depot penicillin like Penidural12 is sometimes used in different centres. For those patients who are sensitive to penicillin,
tetracycline may be used.
B. TREATMENT OF ESTABLISHED CASES.—
1. Passive immunization with 4000 units of Humotet should be administered alongwith
tetanus toxoid injection. If Humotet is not available, 1 lac units of A. T. S. is given half
intravenously and half intramuscularly.
2. Antibiotics.— High dose of injection Penicillin 10 lac units every 4 hours should be
administered. It can be supplemented with Metronidazole to protect the lungs against respiratory
infections. If the patient is allergic to Penicillin, tetracycline may be used.
3. Wound care.— Surgical care of wounds should be immediate. The most important
features of surgical care are thorough cleansing and debridement. All necrotic tissues and foreign
bodies should be removed so that Cl. tetani cannot get chance for further growth and exotoxin
production. All stitches should be removed. Blood clots, foreign bodies and pus, if present,
should be cleared. The wound should be left open till the patient has recovered from convulsing
stage.
4. The patient is isolated to a quiet, dark but well ventilated room. No external stimuli
should be there to provoke painful spasms.
5. Further treatment depends upon the severity of the case —
In mild cases, where there is only tonic rigidity without any dysphagia or reflex spasm, the
patient should be sedated with promazin (200 mg I.M.) and a barbiturate (amylobarbitone) or
TETANUS
173
injection diazepam (5 to 40 mg I.V.). These drugs are usually required to be repeated 4 times in
24 hour period.
In moderately severe cases, with dysphagia and reflex spasms, but without any cyanotic
convulsions, (a) a nasogastric tube has to be passed for feeding, (b) A self retaining catheter is
passed to drain the bladder, (c) Intravenous fluid should be started, (d) An intake and output
chart should be well maintained alongwith monitoring of renal function, (e) The patient must
be sedated as mentioned above ('in mild cases'), (f) A tracheostomy should be considered if the
patient has difficulty in breathing. Suction through tracheostomy tube should be done now and
then alongwith humidification.
In very severe cases, who are having cyanotic convulsions, more care should be taken to
maintain respiration, (a) A muscle relaxant should be given in the dose of 40 mg Tubocurarine
I. V. initially and subsequent injections by I. M. (b) Following tracheostomy which is performed
gently under local anaesthesia, positive pressure respiration should be started, (c) Sedation with
pentothal sodium is necessary, (d) Nasogastric feeding should be started, (e) Elimination of
visceral stimuli such as distension of urinary bladder is avoided by continuous catheterization.
(f) Intravenous fluid and electrolytes with a good monitoring of input and output is necessary.
(g) Constant nursing care is highly important, (h) When the convulsions do not occur after the
relaxants have been stopped, usually after 14 days or so, the ventilator can be stopped.
Causes of death.— Tetanus is a lethal condition and death is generally due to respiratory
arrest.
1. Lung complications.— These are the common causes of death.
(i) Pulmonary infection, mainly bronchopneumonia.
(ii) Aspiration of pharyngeal contents into the lungs.
(iii) Vigorous spasm of the respiratory muscles with laryngeal spasm causes airway
obstruction resulting in cyanotic convulsions.
(iv) Pulmonary embolism due to dislodgement of emboli from the stagnant limbs due to
excessive sedation.
2. Death may occur from drug intoxication, particularly the barbiturates.
3. Anaemia and exhaution which may be so severe due to repeated convulsions that the
patient passes into coma and expires.
4. Hyperpyrexia and effects of exotoxin on the brain may cause death.
5. Previously, anaphylactic reactions due to use of equine or bovine tetanus antitoxin led
to death. But this cause has been eliminated with skin test and more use of Humotet.
6. Compression fracture of the vertebra, specially the thoracic vertebrae is more of a
complication rather than cause of death.
7. Complication from co-existing diseases may cause death e.g. perforation of peptic ulcer,
rupture of heart through the site of infarction etc. due to convulsions.
Results.— With modem treatment as mentioned above the death rate has been considerably
reduced to 15% in general for all ages, though mortality rate is still high in case of children and
the old.
GAS GANGRENE
Definition.— This is a rapid spreading infective gangrene of the muscles characterized by
collection of gas in the muscles and subcutaneous tissue. As this condition is caused by Clostridial
infection, it is also called 'Clostridial myonecrosis'.
Aetiology and predisposing factors.— Basically gas gangrene is most likely to develop
in wounds where there has been extensive laceration or devitalization of muscle mass with
gross contamination of the wound by soil and other foreign bodies. So two factors should play
simultaneously — (i) entry of Clostridial organisms particularly Clostridium perfringens or Cl.
Welchii and (ii) the conditions within the wound should be such that these organisms produce
toxins and are able to multiply to cause gas gangrene. These organisms usually multiply in
anaerobic conditions.
Mere presence of organisms does not produce gas gangrene. Production of gas gangrene is
only possible when these organisms are able to multiply with a layer of toxin sufficiently
concentrated to overcome the local defence of the tissue, (a) Injury to the tissue causes tissue
breakdown with lowering of tissue resistance, (b) Presence of calcium is one of the determining
factor and is derived from soil, blood clots etc. (c) Presence of secondary organisms helps to
maintain the anaerobic condition and suitable pH for growth of gas gangrene organisms.
So the predisposing factors for producing gas gangrene are —
(i) Haemorrhage and blood clot help infection especially by supplying calcium.
(ii) Contamination with soil supplies silica and calcium to the wounds. As Clostridial
organisms are present in human and animal faecal flora, contamination with manured soil
provide enough Clostridium organisms to produce gas gangrene.
(iii) Laceration and crush injuries of the tissues are essential, as the organisms cannot
multiply in healthy living tissues. Dirty splinters or fragments if contaminate the wound, chance
of forming gas gangrene increases.
(iv) Alongwith gas gangrene bacilli other organisms should also gain entry e.g.
Staphylococci, Streptococci and proteus group. Presence of aerobic bacilli in the wound utilise
the oxygen in the tissues and create an atmosphere for growth of the anaerobes.
(v) Circulatory obstruction caused by occlusion or damage of the artery or pressure on
the blood vessel by a tourniquet or a tight bandage are contributory factors.
(vi) Inadequate drainage and exudation in the muscle fibres help in the spread of infection.
(vii) Diabetes and other occlusive arterial diseases also predispose this condition.
Bacteriology'.— Gas gangrene is mainly caused by anaerobic Clostridial organisms of which
Clostridium perfringens (Cl. Welchii) is the main organism. Other Clostridial organisms are also
found e.g. Cl. oedematiens, Cl. septicum, Cl. histolyticum and Cl. bifermentans. These organisms
are found in the stools and therefore buttock, perineum and thigh wounds are more often
complicated by gas gangrene. These organisms also present occasionally as normal flora in the
GM GANGRENE
175
vagina. It is mainly the exotoxins of these organisms which produce this disease. The various
exotoxins produced by these organisms particularly Cl. Welchii are as follows —
(a) Alpha toxin (lecithinase) is a haemolytic and also a lecithinase which splits lecithin to
phosphocholine and diglyceride.
(b) Collagenase is a proteinase and breaks down collagen, the connective tissue element of
the muscle.
(c) Hyaluronidase breaks down hyaluronic acid, the substance mainly responsible cementing
of the muscle cells and forming the barrier against infection.
(d) Theta toxin — is haemolytic, lethal and necrotic, though it is weaker than lecithinase.
(e) Leucocidin — kills the leucocytes.
The anaerobic Clostridium organisms can be divided into two groups — namely
Saccharolytic and Proteolytic. Of the saccharolytic group of anaerobes, Cl. Welchii plays the main
part. The saccharolytic group of organisms grows on the sarcolemma and breaks down the muscle
glycogen into carbondioxide, hydrogen and lactic acid. Excessive production of acid may stop
the growth of the saccharolytic organism for the time being. At this stage the proteolytic group of
organisms multiplies with liberation of proteinase and formation of aminoacid in the tissues.
The aminoacid further breaks down into ammonia, sulphurated hydrogen (H2S) and other
noxious gases. Ammonia neutralizes the acid produced by the saccharolytic group. The acid is
also neutralized by profuse exudate and calcium salts.
Pathology.— Clostridial invasion affects the whole of the involved muscle from origin to
insertion producing a foul smelling necrosis of the muscle which becomes from dull red to
green and ultimately black in appearance.
The earliest pathological change is a rapidly spreading oedema of the subcutaneous tissue
and muscle with accumulation of gas. The collagen fibres become swollen, fragmented and are
ultimately broken down. The blood vessels are damaged with destruction of their endothelial
cells, which helps the necrotic process to proceed further. The muscle gradually loses its striation
and nuclei and passes through various stages of degeneration. It loses contractility and its normal
healthy colour with crepitation due to presence of gas bubbles. Gas bubbles spread along the
long axis of the muscle sheath. Ultimately the muscle becomes soft, friable and green to black in
colour due to the action of sulphurated hydrogen on iron liberated from broken down muscle
haemoglobin. The gas is chiefly hydrogen and odourless in the beginning, but soon it becomes
foetid due to the production of sulphurated hydrogen (H2S), ammonia and volatile gases by the
action of proteolytic group of organisms.
If septicaemia occurs, gas may be produced in other organs, notably the liver (known as
'foaming liver').
Various types of gas gangrene.— According to the spread along the muscles and extent of
involvement, various types of gas gangrene have been described.
1.
Clostridial cellulitis.— This is a crepitant infection involving necrotic tissue, but healthy
muscle is not involved. Cellulitis is characterized by foul smelling, seropurulent infection of a
wound. There may be local extension along fascial planes, but involvement of muscle is absent.
Clostridium perfringens may be present but the predominant organisms are proteolytic and
non-toxigenic Clostridia e.g. Cl. sporogenes and Cl. tertium.
Clostridium cellulitis has a gradual onset with incubation period 3 to 5 days. The skin is
rarely discoloured and there is little or no oedema. The spread of cellulitis may rarely be rapid
and extensive requiring immediate radical surgical drainage.
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176
2. Single muscle type.— The infection is limited to one muscle only.
3. Group type.— The gas gangrene is limited to one group of muscles e.g. extensors of the
thigh or adductors of the thigh or glutei etc.
4. Massive type.— The gas gangrene involves almost the whole muscle mass of one limb.
5. Fulminating type.— In this condition gas gangrene spreads very rapidly even beyond
the limb and is often associated with intense toxaemia with high fatal rate.
Clinical features.—
I. GENERAL.—
The patient looks anxious and anaemic. There may be rise of temperature which never
becomes hectic, on the contrary in severe cases the temperature may be subnormal. The pulse is
rapid and there is fall of blood pressure due to liberation of toxins which suppress the suprarenal
gland. The patient may be vomiting. The patient remains mentally normal.
n. LOCAL.—
In the beginning patient complains of pain in the affected limb. There is gradual swelling
and gross oedema of the part, so much so that the stitches may give way. The most characteristic
feature is profuse discharge of brownish and foul smelling fluid between the sutures. The skin
becomes discoloured — khaki to greenish due to associated haemolysis. Crepitus is always present
due to presence of gas in the muscle and subcutaneous tissue. It is often palpable and sometimes
audible with a stethoscope. If muscles are visible its colour is also noticed, which becomes green
to black.
Special Investigations.—
1. Direct microscopic examination.— A few smears are prepared from the exudate and
stained by Gram's method. Staphylococci and streptococci will be seen. The causative organisms
will be shown as thick rectangular bacilli suggesting one of the organisms — Cl. Welchii, Cl.
bifermentans etc. Spores are not usually seen in case of Cl. Welchii.
2. Cultures.— Special cultures should be made for growth of anaerobic organisms. Exudate
is directly applied and anaerobic organisms show their growth in anaerobic cultures.
Nagler reaction.— Serologically controlled toxaegenic strains of Cl. Welchii are rapidly detected
by direct plate culture of the exudate by Nagler reaction method. The test is based on the fact
that lecithinase of Cl. Welchii splits soluble lipoprotein complex of the human serum with the
formation of an insoluble precipitate of lipoids and protein, producing an opacity in the culture
medium.
3. X-ray shows gas shadows within the muscle and in the subcutaneous tissue.
Treatment.—
I. PROPHYLAXIS.— The students must understand and follow the principles of how
to prevent formation of gas gangrene. As this condition carries a considerable mortality rate,
prophylaxis should be followed very rigidly.
1. Wound excision or debridement.— All contaminated wounds should be thoroughly
debrided. The margins of the wounds should be excised, (i) All devitalized tissues and blood
clots should be removed, (ii) All dead and damaged muscles should be removed., (iii) All foreign
bodies including completely detached pieces of bones should be removed.
2. Administration of high dose of penicillin about 2 grams 4 hourly is always necessary
whenever a patient is admitted with a badly lacerated wound. This is probably one of the few
indications of prophylactic antibiotic therapy.
3. While performing wound excision tourniquet should be avoided. Similarly if plasters
GAS GANGRENE
177
are applied in case of compound fractures, care must be taken to see that the plaster is not
jeopardising the blood supply to the distal limb.
4. Whenever the wound is in tension, it is better to leave open than to apply primary
sutures under tension.
5. Passive immunization by intramuscular injection of anti gas gangrene serum (A.G.S.) of
polyvalent antitoxin of 22,500 I.U. containing 9,000 I.U. Cl. Welchii, 4,500 I.U. Cl. septicum and
9,000 I.U. Cl. oedematiens. This polyvalent serum is administered every 4 to 6 hours, if the
disease becomes established. Its prophylactic value is still debatable.
6. Active immunization has not been so popular in case of gas gangrene. Yet nowadays
toxoid precipitated with alum (A. P. T.) is injected. Two dosage of this toxoid are injected at an
interval of 2 to 6 weeks. This should be followed by a booster dose 3 to 9 months after the
previous immunization or at the time of the injury sustained by the person.
U. TREATMENT OF AN ESTABLISHED CASE.— Early and adequate surgery is the
most effective means of treating gas gangrene. Due to rapid spread of infection, a 24-hour delay
in the treatment may prove fatal.
1. Surgery :
(a) As soon as the diagnosis is established multiple longitudinal incisions for
decompression and drainage are urgently required.
(b) Aggressive surgical debridement in the form of excision of all devitalized tissues
should be carried out. In case of single muscle type, the affected muscle is completely excised. In
case of group type, all the affected portions of the muscle should be removed, till the healthy
muscles are reached, which is identified by their colour, contractility and bleeding capability.
(c) In case of massive type of gas gangrene or if early diagnosis was not made, then
amputation is the only answer.
The principles of amputation are —
(i) The tourniquet should always be avoided to minimise further circulatory damage to
the living muscles and at the same time bleeding from the muscle can be seen to judge the
viability of the various muscles.
(ii) It should be of guillotine type without closure of the stump for better drainage.
(iii) Amputation should be through a safe level well proximal to the affected muscles. That
means in case of affection of calf muscles, a mid thigh amputation should be performed.
2. Supportive treatment.—
(i) High dosage of penicillin should be administered (10 lac units every 4 hours)
immediately as soon as the diagnosis is confirmed. This should be supplemented by tetracycline
2 g daily or chloramphenicol 2 g daily or streptomycin 1 to 2 g daily. Later on the doses are
reduced according to the virulence of gas gangrene.
(ii) Blood transfusion should be started before the operation is contemplated. This is to
combat shock and anaemia. Further, crystalloid or colloid solutions may be administered
intravenously.
(iii) Anti-gas gangrene serum which has been described above as prophylactic treatment,
should be administered in an established case with the same dose repeated every 4 to 6 hours
for 3 times. So 3 ampoules of polyvalent antitoxin will be required.
(iv) Hyperbaric oxygenation has been used with some success, where this is available. The
limb is placed in the chamber of hyperbaric oxygen after the operation has been performed.
12
1A SKIN GRAFTING
Though it comes in the domain of plastic surgery, only the basic points of skin grafting,
which a general surgeon should know, will be discussed here.
Indications.— (1) Skin is the best possible dressing for a raw surface, that is why extensive
raw wound should always be covered with skin. In surgical practice extensive raw wound can
result from many conditions, of which trauma and bum deserve special mention. If this raw
wound is not grafted it scars easily with the blemishes and deformities. (2) Contracted scars in
the vicinity of the joints require excision and skin grafting. (3) Skin loss from surgically removed
malignant growths should be made good with immediate skin cover.
TAKING OF A SKIN GRAFT DEPENDS ON VARIOUS FACTORS.— (1) The recipient
area must not be avascular, (2) but there should not be any excess blood, serum or exudate to
separate the graft from the recipient area. For this, a pressure bandage is always required after
skin grafting. (3) The recipient area must be free from infection. (4) The part after skin grafting
should be immobilized to prevent displacement. (5) The nutritional status of the individual
should be satisfactory.
PREPARATION OF THE RECIPIENT WOUND.— The area is first washed with soap and
water. A soft brush may be used to clean the dirt from the surrounding skin. Then diluted
cetavlon solution is used to clean the area with sponge-holding forceps. Any slough in the wound
should be removed with great care. There should not be any crevices or hypergranulation tissue
in the wound. If present, they should be scraped off to expose a flat healthy granulation tissue
as the bed for skin graft. If there is any bleeding this should be tackled by pressure of hot saline
pack.
PREPARATION OF THE DONOR SKIN.— This area is shaved at least 24 hours before the
operation. Then the area is cleaned with ether soap and spirit. Strong antiseptics like tinct. iodine
must be avoided. The area is now dressed with sterile gauze and bandage, which will be opened
only in the operation theatre.
METHODS OF SKIN GRAFTING
Skin loss can be made good :—
(1) By local adjustment (by flaps) from the surrounding skin.
(2) By free skin grafts taken from other parts of the body.
. (3) By pedicle grafts, where the flap remains attached to the original site on one end and
the other to the place to be grafted. Occasionally an intermediate 'host' may be used where the
distance between the donor area and the recipient area is too long to be bridged. Suppose a
wound in the face is to be grafted from the abdominal wall. In this case as the distance is too
much the flap from the abdominal wall is first transferred to the forearm and then from the
forearm to the face. So the forearm acts as an intermediate 'host'.
SKIN GRAFTING
179
(1) Local adjustments from the surrounding skin (by flaps).— This method has an
obvious advantage that as the blood supply of the flap remains as it is, 'taking' of the graft is
no problem. Moreover, removal of skin from other parts of the body is also not required. That
is why it should always be used wherever possible. Methods which are commonly used are —
SIMPLE UNDERMINING.— The adjacent skin margins are freed from the underlying
subcutaneous tissue as much as possible to cover the defect without tension.
V-Y ADJUSTMENT.— This means a V-shaped incision is made a little below the wound with
its open ends towards the wound. The edges of the incision as well as of the wound are
undermined. Now the wound is closed in such a manner that the V-shaped incision is turned into
a Y-form.
ROTATION FLAP.— It can be
used to close larger defects which are
particularly of triangular type.
Smallest side of the triangle is
extended by an incision, undermined
and the skin flaps can be brought
over the defect. Here the tension is
equally distributed over a large area.
Z-PLASTY.— This is used mostly
in palms. It can be used where a linear
scar has been excised leading to a
linear skin loss.
(2)
Free Skin Grafts are of
three types:—
(a)
PARTIAL THICKNESS
SKIN GRAFT.— This is used where
the skin loss cannot be made good
by local adjustments. The grafts are
Fig. 14.1.— Rotation flap. Note how a triangular defect in the
usually taken from the anterior
scalp in Fig. A is made good by rotation flap in Fig. B.
surface of the thigh or forearm. Two
types can be used — thin grafts through the tips of the papillae (Thiersch graft) or thick grafts
(Split-skin grafts). These are nothing but different thickness of the same graft which can be lifted
with the same Humby's skin grafting knife with guarded blade. Thin grafts 'take' easily even in
the presence of slight infection.
Partial or split-thickness skin graft includes all of the epidermis and a variable part of the
dermis including the superficial layers of the corium. This graft does not take so easily as the
Thiersch graft but when take successfully they give better appearance and durability. This graft
is able to survive on compromised surfaces such as granulated wounds contaminated with bacteria,
because split-thickness skin is more reachly supplied with open blood vessels on its undersurface.
This graft is also used to cover wounds with precarious circulation and those with large areas of
skin loss from bums and other traumatic injuries. It should be remembered that dermis is about
20 times thicker than the epidermis in most areas of the body, permitting a wide differences in
graft thickness. Since only a part of the dermis is taken, the donor site will heal spontaneously
by epithelial outgrowths by remaining epithelium islands, sweat glands and hair follicles.
IB
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One point is very clear, that a rich vascular supply is essential for support of a split-thickness
graft. This graft will not survive when placed directly on bone, cartilage or bare tendon. However
muscle, fascia, peritoneum, pleura, meninges and vascularized fat will all support this type of
skin graft. As mentioned above this skin graft generally survives when placed over the wounds
containing less than 105 organisms per gram of tissues unless the organisms are streptococci,
which can rapidly dissolve transplanted skin. In this case further surgical debridement with
administration of systemic and topical antibiotics followed by placement of pig skin xenografts
or amnion allografts should be performed to eliminate infection from the recipient site and to
promote formation of healthy granulation tissue.
Patch grafting is a variant of the partial thickness skin graft. This is only applied when
presence of infection in the recipient wound gives rise to suspicion of the complete 'take' of the
partial thickness skin graft. Here the same thickness, as described above, of the skin are cut into
small squares or strips and they are grafted over the recipient wound to cover it wholly. Finally
pressure dressing is applied. No doubt that its cosmetic value is less than the split-thickness
skin graft but it 'takes' more easily even in presence of sepsis.
Technique.—• The recipient wound is first washed with normal saline. Then the sister in the
operation theatre takes off the bandages from the donor area and thus exposes it. The surgeon
cleans the area with diluted savlon. The area is draped as usual. The donor area is now made
taut with two wooden blocks. Then skin grafting knife is used to lift the skin graft. The knife is
lightly pressed and sawing movement is employed to lift the skin. Equal pressure must be
maintained all throughout the process. The blade of the knife can be so adjusted that different
thickness of the skin can be lifted. After the required size of the skin graft has been lifted, the
oozing wound is covered with penicillin gauze and bandage. The graft is now spread nicely on
the recipient wound and kept in position with fine silk suture. Vaseline gauze is now spread
over the graft. Sterile gauze pieces are placed to cover the vaseline gauze and finally these are
covered with sterile bandage keeping even pressure all throughout. This dressing is kept as
such for at least a week. If the part is over a joint, the joint should be kept immobilized.
(b)
WHOLE THICKNESS (WOLFE'S) SKIN GRAFTProcess of this skin grafting
comes actually under the domain of the plastic surgeons and general surgeons hardly perform
this operation. A full-thickness skin graft is a free graft including the entire epidermis and dermis.
This graft requires a better blood supply for survival than do split thickness grafts, because the
graft vessels are cut below the level of their dermal branching. Therefore relatively fewer cut
vessels are available to absorb nutrients from the wound bed to meet the relatively greater
nutritional needs of this thicker graft. So this graft for proper 'taking' needs early vascularization.
So disadvantages of these grafts include (i) better blood supply for their survival, (ii) limited area
that can be covered, (iii) the need to surgically close the donor site and (iv) the poor resistance
to infection, which generally precludes use of these grafts on contaminated wounds. This grafting
cannot be performed in presence of sepsis. The skin loss after excision of scar or growth can
suitably be made good by this type of skin graft. Granulating wound is unsuitable for this type
of skin graft due to the presence of some sort of infection in the wound.
Full thickness skin is best taken from locations where the skin is thin such as postauricular
area, supraclavicular area and eyelids or where skin is loose and redundant such as flexor creases
of the elbow, buttock and groin. A very important point in technique is that the graft is lifted gently
with a skin hook and removed from the subcutaneous tissue by sharp dissection. Fat should not
be left on the undersurface of the skin graft. Otherwise the capillaries are prevented from growing
SKIN GRAFTING
181
into the graft and the
graft will not 'take'.
The graft should be
carefully fixed with
accurate skin sutures to
the recipient site as
vascularisation occurs
through the edge as
well as from the deep
surface. A pressure
dressing of the 'tie
over'
variety
is
advisable. The dressing
should not be removed
before 7 to 10 days.
Technique.— Hae­
morrhage should be
arrested very meticu­
lously in the recipient
wound. It should be
done by hot saline Fig. 14.2.— Shows the technique of obtaining a whole-thickness graft. Note
packs or by fine
that it is raised without the inclusion of fat. Fbr details see the text.
ligatures. Diathermy
must not be used. The recipient wound should be mapped on a metal-foil and the donor area is
accordingly sized. Any hair-less area
can be used as a donor area. The
incision is now made vertically
straight down through the full
thickness of the skin along the
mapped margin, underlying fatty
tissue should be excluded. The edge
of the skin is now retracted by stay
sutures with fine silk to avoid trauma
to the skin edge by the use of such
instrument like dissecting forceps.
The graft is now applied to the
recipient wound and fixed to its
periphery with fine silk stitches. Short
stab wound may be made if the graft
is a large one to prevent collection of
fluids in between the graft and the
wound. Finally, pressure bandage
should always be applied and the
part is kept immobilized. First Fig.14.3.— Shows the technique of lifting‘Finch grafts'and their
dressing should be done after a week
placing on the recipient site
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A CONCISE TEXTBOOK OF SURGERY
or so. The skin margins of the donor area are undermined and approximated by silk sutures.
(c)
PINCH GRAFTS (REVERDIN).— These are small cones of skin with a surface diameter
of not more than 1/4 inch and it tapers gradually in the depth to form a shape of a cone. The
advantage is that it can be used in presence of sepsis. Due to cosmetic reason its use is being
taken over by the patch graft, as it leaves a stippled surface when it heals.
Technique.— The skin is first pierced by a straight needle vertically and a cone of skin is incised
off encircling the needle. The grafts are then transferred to the recipient raw area in rows about
1/4 inch apart to cover the entire surface. A penicillin gauze and a pressure bandage are applied.
(3)
Pedicle Grafts.— A pedicle graft is never separated from its blood supply, since
revascularization at the recipient site is allowed to develop before the original blood supply is
finally severed. Pedicle flaps, which include subcutaneous fat as well as skin, provide padding
that prevents ulceration and so are useful for
wounds such as decubitus ulcers and those that
sustain frequent trauma. Pedicle flaps may also
be used to cover bare tendons, bone and
cartilages. The graft in the form of a flap is first
created by making skin and subcutaneous
incisions along 3 sides, leaving intact the side
with the best blood supply. The flap is
undermined and then is sutured immediately to
the closeby recipient site or may be delayed i.e.
allowed to remain in its primary bed until its new
blood supply is better established. In the form of
a flap or a tube, the pedicle graft is used to even
distant sites with the help of an intermediate
'host' (see below). The donor site may be closed
by primary suturing or is covered with a split­
thickness skin graft.
These can be of three types — (i) a direct
pedicle graft, (ii) bridge pedicle graft and (iii) tube
Fig. 14.4.— Method of direct pedide graft being
pedicle graft.
used to make good the defect in the antecubital
DIRECT PEDICLE GRAFT.— This method
region.
is only applicable when the donor area can be
brought near the recipient wound. That means skin from the trunk can be used to cover wounds
of the upper limb, skin of the lower limb can be used to cover wounds of the other lower limb
(crossJimb flap ). These two parts are always kept approximated by firm bandaging or by plaster
of Paris. The flap actually consists of two parts — (a) the part for actual graft and (b) the part
which connects the recipient area to the donor area (the pedicle). The latter part is responsible
for nutrition of the former and it should be broad enough to carry the blood supply to the flap.
The bed from where the flap is raised should be covered with the surrounding skin by
undermining. If this is not possible, split skin graft can be used. After three weeks when the
flap is supposed to have established its nourishment from the recipient area, the pedicle is
divided.
BRIDGE PEDICLE GRAFT.— This means a flap is raised from the donor area with its
both ends attached to the area and the recipient wound is pushed beneath the flap and attached
SKIN GRAFTING
Fig. 14.5.— Shows the method of using a bridge pedide
graft to repair a defect of the palm.
183
to it. So the flap gains its blood supply from
the attached two ends and hence its length
should not exceed IVi times greater than its
width. This is mostly done in case of
wounds in the palm.
Technique.— Two parallel incisions are
made vertically through the whole thickness
of the skin but the fatty layer is excluded.
The flap is raised and the raw wound
beneath the flap is closed by approximating
the adjoining skin margins. Then the
recipient part is pushed beneath the bridge
and the edges of the bridge flap are sutured
to the recipient area with fine silk. The
pressure bandage is used as usual and the
part is immobilized. After 21 days the
pedicle is severed in the idea that the graft
has been vascularized from the recipient
wound.
TUBE PEDICLE GRAFT (GILLIES).— This method is contemplated only when the donor
area cannot be brought close to the recipient area. So a long flap is required and the greater part
of the flap serves as pedicle. This type of grafting finds its greatest field in the plastic surgery of
face. It is also practised in hands and feet, where
durable skin is required. As the risk of infection is
less and the blood supply is very much assured
this graft is more preferable to the conventional
whole thickness skin graft.
Technique.— The site from where the tube
lifted varies according to the requirement. But the
abdomen and anterior thoracic region in men are
the most preferred sites. The width to length
dimensions should be 7.5 cm by 17.5 cm, 8.5 cm
by 22 cm etc. The operation is performed in three
stages. Stage I consists of raising the flap, which is
attached at both ends and stitching the sides of
the flap to form a tube. The skin of the abdomen
is so obliquely incised as to get good axial blood
supply.
The skin and superficial fatty layer up to
Hg. 14-6.— Method of tube pedide graft
the membranous layer (fascia of Scarpa) are incised
being used to repair a defect of Use cheek.
and included in the tube. The bed is of course
closed by undermining the edges and suturing them. Stage II, which starts six weeks later, consists
of freeing one end, opening out that end and implanting that end to the recipient area. In Stage
III, after three weeks, the tube is severed and the raw area is thoroughly grafted.
When the recipient wound is far away from the donor site an intermediate 'host' may be
required. As for example, when the recipient wound is at leg resulting from excision of scarred
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A CONCISE TEXTBOOK OF SURGERY
osteomyelitis wound and the donor site is the abdominal skin, forearm or the wrist may be
used as an intermediate 'host'. In this case the technique is as follows:— Stage I is same as
above. Stage II starts after three weeks, when one end is incised and grafted to the host. After
three weeks the tube is 'delayed', i.e. the other end of the tube is first severed and again sutured
to see if the graft can survive from its new blood supply from the host. After one week that end
is completely severed, the end is opened up and grafted to the recipient area. In Stage III, after
three weeks the tube is cut from the host.
There are various other SPECIAL TYPES OF FLAPS containing skin and other tissues
which are used by the plastic surgeons to make good the big defects. These are:—
1. The last few years have seen the development of a new understanding of the blood supply
of the skin and how it may be harnessed. The blood supply to the skin ends with vertically running
arterioles to the undersurface of the dermis and up into the papillae. In some areas of the body,
arteries accompanied by veins run for considerable distances in the subcutaneous tissues which
can be called axial vessels. Examples of this are the superficial temporal, occipital and superficial
inferior epigastric vessels. These can be harnessed to construct arterial or AXIAL PATTERN FLAPS.
2. In certain areas of the body vessels run vertically through the subcutaneous fat from
the deep fascia. In these places inclusion of deep fascia into a cutaneous flap allows greater
Fig. 14.7 .— Lattissimus dorsi myocutaneous flap.
Pig. 14.8.— Pectoralis major myocutaneous flap.
SKIN GRAFTING
185
extension and mobility because the blood vessels perforating the subcutaneous tissue are not
disrupted. These flaps are known as FASCIOCUTANEOUS FLAPS.
3. The deep fascia in its turn is intimately linked with the underlying muscle. The rich
blood supply to muscle is mainly from one source, so that the muscle with the overlying skin
can be lifted and swung on a pedicle. This is known as myocutaneous flap.
The various types of MYOCUTANEOUS FLAPS which are commonly used are :—
(a) Lattissimus dorsi myocutaneous flap.—The arterial supply of lattissimus dorsi is the
subscapsular artery which runs down on the deep surface of the lattissimus dorsi muscle. A large
area of the skin overlying the muscle can be lifted with the lattissimus dorsi muscle. The anterior
border of the muscle is displayed and the vessels are located. The muscle is now lifted off the
chest by dividing its origins. The flap of the muscle with the overlying skin can be rotated and
pivoted on these vessels. This flap has been used for closure of the chest wall defects and defects
in the neck. It has also been used for breast reconstruction. It can be used as 'free grafts' (see
below) and transferred to many sites to cover compound wounds of the leg, scalp defects etc.
(b) Pectoralis major myocutaneous flap.— The main blood supply to the pectoralis major is
the acromiothoracic trunk, which runs on the undersurface of the muscle in a vertical direction.
An islands of skin attached to the lower part of the muscle is usually used. The pectoralis major
is detached both from its origin and insertion keeping a 5 mm of vertical strip of muscle overlying
the acromiothoracic trunk. The island of skin, the muscle mass and the vessels are swung on an
axis just below the clavicle and can reach the neck, cheek and even inside of the mouth. The
skin defect of the chest is closed by undermining edges or by application of a skin graft.
(c) Deltopectoral flap.— The internal mammary vessels have branches which perforate the
chest wall between the costal cartilages just lateral to the border of the sternum and then run
laterally towards the shoulder. The flap is dissected to incorporate the vessels from the 2nd, 3rd
and 4th costal spaces. The lower margin of the flap is along the axillary fold, where the skin is
extensile and long flap can be constructed. Careful dissection below the fascia covering pectoralis
major muscle is undertaken without damaging the perforating vessels. This flap may be transferred
to be used in the neck, face, inside of the mouth and even to reconstruct the pharynx and upper
oesophagus. The chest defect is covered with split skin graft.
(d) Groin flap.— The main vessel is the superficial circumflex iliac artery, a branch of the
femoral artery, with its accompanying vein. These vessels run 2 cm below and parallel to the
inguinal ligament towards laterally almost in a straight line. The flap is raised with a margin of
3 cm on either side of these vessels and can extend outwards over the iliac crest. The deep
fascia is included with the skin upto the sartorius muscle after which this vessel perforates the
deep fascia and care must be taken not to damage these vessels.
4.
DERMOLIPOMATOUS GRAFT.— In this graft fat alongwith dermis is used. This
ensures that the subdermal plexus remains intact. The donor sites are usually the lower abdomen
and the buttocks. Such grafts may be used on the face. This graft has been used as contourforming operation in the breast, but did not succeed much. The donor site is first marked out
according to the need. It should be remembered that these grafts shrink. The dependent edge is
usually incised and then it is undermined upto the marks. Bleeding is stopped by warm packs.
The epidermis is removed and is kept as free graft. This graft is now applied on the recipient
site and the edges are sutured in two layers. The graft is covered with dressings and reinforced
with a crepe bandage to prevent haematoma formation.
5. The fasciocutaneous, myocutaneous or axial pattern flaps can be used as FREE FLAPS
and are transferred to the recipient site without any pedicle. After placing these flaps properly
186
A CONCISE TEXTBOOK OF SURGERY
on the recipient site the
neurovascular
bundles
are
anastomosed
with
the help of operating
microscopes
(micro­
surgery).
6.
Another variation
of skin graft is to use a
flap of muscle or fascia
without overlying skin to
cover the recipient area
and then the whole thing
is covered with a split
skin graft. Indeed one of
the best beds for skin
grafts is the omentum.
This can be transferred
either as an intact pedicle
(omental graft) or a free
omentum with arterial
and venous anastomosis
Fig. 14.9.— Omental graft. Fig. A shows how to separate greater omentum from (micro-surgery) and then
the greater curvature of the stomach. Fig. B shows how to bring the omentum
covered with a split skin
through the subcutaneous tunnel to make good the chest wall defect.
graft.
CHAPTER
DISEASES OF
ARTERIES
ARTERIAL OCCLUSION
Arterial stenosis or occlusion is a common arterial disease which is mainly caused by
atherosclerosis, emboli or trauma. In various places the symptoms produced by arterial occlusion
are different e.g. in lower limb it causes intermittent claudication, rest pain and gangrene. In
the heart it causes angina pectoris and myocardial infarction. In the brain it causes transient
ischaemic attacks and hemiplegia. In the kidney it causes hypertension. In the intestine it causes
abdominal pain and infarction.
Arterial occlusion is of two types — chronic arterial occlusion and acute arterial occlusion.
CHRONIC ARTERIAL OCCLUSION
AETIOLOGY AND PATHOLOGY.—
1.
ATHEROMA.— By far the main cause of chronic arterial occlusion is atheroma. This
disease characteristically affects the large systemic arteries like the aorta and its main branches.
Although coronary and cerebral vessels are also commonly involved. Two types of atheroma
are seen —
Type I. Yellow plaques in the tunica intima.— In the subendothelial layer foam cells accumulate
and later breakdown to release fatty material into the intima, thus yellow plaques or fatty streaks
are formed. This type of pathology is not much concerned in narrowing of the arterial lumen,
but it more often causes weakening of the wall to cause dilatation or aneurysm formation.
Type II. Accumulation of fatty material in the intima with additional fibrosis.— This is more
common type and is seen in the middle and old age individuals. It is often called atherosclerosis
and causes varying degrees of arterial occlusion. The lesion is composed of a central mass of
fatty, yellow porridge-like material which consists predominantly of cholesterol and its esters
and is surrounded by dense fibrous tissue which gives it a white pearly appearance. In advanced
cases ulceration may be superadded resulting in thrombosis. The fatty material also subsequently
undergoes dystrophic calcification, which may be seen on straight X-ray.
Aetiology of this atheroma is not very clearly known, but there are theories which are almost
acceptable.
(a) In human beings atheroma is common in a few conditions accompanied by
hypercholesterolaemia e.g. hereditary hypercholesterolaemia, myxoedematous subjects, diabetics
etc.
(b) Nowadays it is held that cholesterol in the blood is not solely responsible, but it is
mainly the p-lipoprotein (which include cholesterol), which is concerned in the formation of
atheroma.
The P-lipoproteins are absorbed into the intimal layer especially in areas of endothelial
damage due to stress. Once the P-lipoprotein is in the intima, it splits up into cholesterol and its
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A CONCISE TEXTBOOK OF SURGERY
esters which are retained, whereas the other lipid components e.g. phospholipids are rapidly
removed. Normally the cholesterol is kept in solution by phospholipids. As phospholipids have
been removed, accumulation of cholesterol in the intima causes' the fibrous tissue reaction which
leads to atheroma formation.
It should be remembered that unsaturated fat of vegetable origin lowers the blood cholesterol
level. Similarly oestrogens lower the blood cholesterol level and may explain the lower incidence
of atheroma in females.
2. TRAUMATIC.— Injury to the arterial walls by fractures, adjacent missiles or continuous
rubbing may cause thrombosis formation and also narrowing of the arterial wall to cause arterial
occlusion.
Other rare causes are —
3. INFECTIVE.— Arterial damage may occur by acute inflammatory lesion in the vicinity.
These are mainly seen in small arteries. Similarly in chronic infective diseases, it may produce
endarteritis obliterans to cause thrombosis and narrowing of the vessels. This was previously seen
in cases of syphilis. But nowadays this is uncommon and sometimes seen in the arteries in the
wall of the tuberculous cavity in the lung.
4. THROMBOANGIITIS OBLITERANCE (BUERGER’S DISEASE).— See page 219.
5. RAYNAUD’S DISEASE.— See page 210.
6. POLYARTERITIS NODOSA.
7. GIANT-CELL ARTERITIS.
CLINICAL MANIFESTATIONS of chronic: arterial occlusion.—
SYMPTOMS.— PAIN is the key symptom of arterial occlusion irrespective of its site. A
careful history has to be taken regarding its mode of onset, its location, distribution and its
character. When arterial occlusion develops over longer periods of time, ischaemia is not manifested
until the demand is increased with exercise.
INTERMITTENT CLAUDICATION.— 'Claudio' means 'I limp'. Intermittent claudication is
the most common complaint of the limb due to chronic arterial occlusion. In this condition pain
is experienced during exertion and gradually disappears within minutes upon cessation of activity.
Such pain is a cramp-like pain felt in the muscles. The group of muscles which will be affected
by this pain depends on the site of arterial occlusion. This pain is due to accumulation of excessive
P substances in the muscle which are not absorbed properly due to inadequate blood supply. As
mentioned just now the pain is felt in a group of muscles and which group will be involved
depends on the site of arterial occlusion. As for example in case of aortoiliac obstruction,,
claudication is felt in both buttocks, thighs and calves. In case of iliac obstruction claudication is
felt in the thigh and calf of the same side. In case of femoropopliteal obstruction unilateral
claudication is felt in the calf. In case of Buerger's disease where the arterial occlusion is mostly
in the lower tibial or plantar arteries, claudication is felt in the foot.
On careful enquiry the patient often complains that after walking a distance, which is called
the 'claudication distance’, the pain starts. If the patient continues to walk the metabolites increase
the muscle blood flow and may sweep away the P substances produced by exercise and pain
disappears (grade I). More often the pain continues and the patient can still walk with effort
(grade II). But mostly the pain compels the patient to take rest (grade III, Boyd's classification).
The claudication distance will vary from day to day and will be altered by walking up-hill, the
speed of walking or against the wind. As the disease progresses this claudication distance will
be gradually diminished.
DISEASES OF ARTERIES
189
Intermittent claudication however less commonly occurs in the upper limb due to brachial
artery or axillary or subclavian artery occlusion. Such intermittent claudication, if at all seen, is
only complained of after such activities as writing or manual labour.
REST PAIN.— As the arterial occlusion progresses, intermittent pain of the muscle will be
supplanted by a continuous rest pain at the sites most distal of the arterial supply e.g. toes, foot,
fingers, hand etc. Characteristically this pain is worse at night and is worsened by elevation of
the extremity, whereas it is somewhat relieved by hanging the foot out of the bed or by sleeping
in a chair. This rest pain is mainly due to ischaemic changes in the somatic nerves, so it is the cry
of the dying nerves.
Application of warmth will increase the symptoms of arterial occlusion.
Other points should be noted while taking history e.g. smoking habit of the patient, cardiac
disorders if any, any history of previous trauma, familial history, occupational history, if the
patient is diabetic or not and the drug history.
PHYSICAL EXAMINATIONS.—
A.
INSPECTION.—
1. Change in colour is the most noticeable feature of an ischaemic limb. Congestion and
purple-blue cyanosed appearance particularly in dependency is noticed in chronic arterial
insufficiency. The colours are quite different from chronic congested extremity with venous
insufficiency. When the limb is elevated it becomes pallor.
2. Signs of ischaemia.— Characteristic changes due to arterial insufficiency often occur
at the most distal distribution of the concerned artery. These are thinning of the skin, diminished
growth of hair, loss of subcutaneous fat, shininess, trophic changes in the nails which become
brittle and show transverse ridges and minor ulceration on the pressure areas e.g. tips of toes,
ball of the foot, heel and malleoli. It must be remembered that ulceration from venous insufficiency
is virtually unknown below the level of the malleolus. To the contrary most ulcers from arterial
insufficiency begin over the toes or at the most distal parts of the arterial trees. Ischaemic ulcers
are never seen on the leg or about the ankle without involvement of the toes.
3. Buerger’s test.— The legs of normal individual even if they be raised by 90° remain
pink. But in case of an ischaemic limb elevation to a certain degree will cause marked pallor. The
angle between the limb at which such pallor appears and the horizontal plane is known as
'Buerger's angle' or the 'vascular angle'. If the vascular angle is less than 30°, it indicates severe
arterial occlusion.
4. Capillary filling time.— After elevating the legs, the patient is asked to sit up and
hang his leg down by the side of the table. A normal leg will remain pink. But an ischaemic leg
will change its colour from pallor to pink. This change of colour takes place slowly and is called
the 'capillary filling time'. An ischaemic limb further changes its colour and becomes purple-red.
This is due to the filling of dilated skin capillaries with blood.
5. Venous refilling.— The extremities are elevated until collapse of vein has occurred.
The extremities are then quickly lowered and the time required for the veins to refil particularly
on the dorsum of the foot or hand is noted. Normally venous refilling will occur within 10 to 15
seconds. Longer time for filling means arterial insufficiency. Time more than 1 minute denotes
severe degree of arterial occlusion.
Of course this test cannot be performed in presence of venous varicosities with incompetent
valves.
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A CONCISE TEXTBOOK OF SURGERY
6. Pre-gangrenous state.— The combination of rest pain, colour changes, hyperaesthesia
with or without ischaemic ulceration is frequently referred to as 'pre-gangrenous' state.
7. Established gangrene.— When the arterial occlusion is severe and is existing for
quite a long time, gangrenous changes will be seen. This is the final stage and it is the dry
gangrene, which is characteristic of chronic arterial occlusion. It starts peripherally in the toes and
extends proximally to involve gradually the entire foot and leg.
Line of demarcation is often seen between the gangrenous part and the normal living limb.
This line of demarcation is a line of inflammatory zone. Only in case of ainhum, this line of
demarcation is very deeply marked mainly at the base of the little or the 4th toe.
B.
PALPATION.—
1. Skin temperature of the ischaemic limb is always colder than the normal limb.
2. Capillary refilling.— The tip of the nail or pulp of a toe is pressed for a few seconds
and the pressure is then released. The time taken for the blanched area to turn pink is a crude
indication of capillary blood flow.
3. Venous refilling.— The two index fingers are placed side by side on a vein. The
fingers are now pressed firmly and the finger nearer to the heart is moved proximally keeping
the steady pressure on the vein so as to empty a short length of vein between the two fingers.
The distal finger is now released. This will allow venous refilling to be observed. This is poor in
case of ischaemic limb. This is known as Harvey’s sign.
4. Palpation of peripheral pulses — is the most important feature of the examination.
In the lower extremity, the femoral, popliteal, posterior tibial and dorsalis pedis pulses are felt
(See Fig.15.1 in the next page). In the upper extremity the brachial, radial and ulnar pulses are
felt. The integrity of the palmar arterial arch is tested by performing the Allen test. The patient
is asked to make a tight fist. The radial and ulnar arteries at the wrist are occluded. The patient
now slowly opens his hand. With the hand in a relaxed position, the integrity of the radial artery
in the hand is determined by releasing radial compression and noting the return of colour. The
manoeuvre is repeated releasing the ulnar artery while the radial artery remains compressed.
The disappearing pulse.— When peripheral pulses are apparently normal, exercising the
patient to a point of claudication may unmask the effect of arterial obstruction and the previously
palpable pulse may disappear. After rest of couple of minutes the pulse reappears. This is known
as 'disappearing pulse'. The reason is that exercise causes vasodilatation below the slight arterial
occlusion. This needs more arterial flow to the distal part, so that the arterial flow which was
already reduced cannot keep pace with the increasing demand, so that the arterial pressure falls
and the pulse disappears.
••
C.
AUSCULTATION.—
1. Arterial bruits.— A systolic bruit over an artery revealed by auscultation indicates
slight occlusion of the artery. Such systolic bruit is conducted distally.
A continuous machinery murmur indicates presence of an arteriovenous fistula.
2. An oscillometer may be of some value in case of extremities with oedema where
peripheral pulses are difficult to palpate. This instrument consists of a blood pressure cuff attached
to a manometer. This cuff is inflated to just above diastolic pressure. This evaluates pulsatile
oscillations of the artery during systolic pressure. It has an advantage that it can quantify the
degree of occlusion used at bedside or even in the office.
DISEASES OF ARTERIES
191
SPECIAL INVESTIGATIONS.—
A.
GENEFIAL INVESTIGATIONS.—
1.
Blood examination
should be performed
to exclude anaemia, diabetes, polycythemia, plipoprotein and cholesterol estimations should be
performed.
2.
Plain X-ray of the abdomen should be
performed to exclude presence of abdominal aortic
aneurysm by finding arterial calcification at its
wall.
3.
E.C.G. should always be performed to
exclude any heart problem.
B.
LOCAL INVESTIGATIONS.— These
investigations are designed to detect blood flow,
to know the site of arterial occlusion and its
degree.
1.
Doppler ultrasound.— This is based
on the shift in ultrasound frequency that arises if
an ultrasound beam is transmitted to and reflected
from moving blood cells. This is known as doppler
effect. The changes of frequency in the reflected
beam as compared with the transmitted beam are
due to the 'doppler shift'. The frequency shift is
proportional to the velocity of the blood flow. It
may be analysed audibly by listening to the
intensity and pitch of the sound and may be
recorded graphically either as a simple wave form
or as a more complete sound spectrum analysis.
The last technique makes it possible to obtain
quantitative information about the degree of
stenosis.
The second application of doppler ultrasound
is to determine systolic arterial pressure. The
doppler probe is then used as a sensitive
stethoscope over an artery distal to a pressure
cuff. The cuff is inflated to a supra-systolic level
which will cause cessation of blood flow and
hence disappearance of the doppler signal. The
cuff is gradually relaxed and the systolic pressure Fig. 15.1.— Technique of palpation of the dorsalis
is measured. This technique is often used in the pedis, posterior tibial and popliteal arteries from
above downwards.
lower extremity.
The third application of doppler ultrasound is for vascular imaging. The doppler probe is
moved over the area to image the artery. A storage oscilloscope indicates places where blood
flow is detected and thus an image of the artery is obtained. It also gives information of the
diameter of the artery, its blood flow rates and velocities.
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A CONCISE TEXTBOOK OF SURGERY
A hand-held doppler ultrasound probe is most useful in the assessment of patients with
occlusive arterial disease. This is a very essential tool. It can be used even at sites where arterial
pulse cannot be palpated. The ankle-brachial pressure-index (ABPI) is the ratio of the systolic
pressure at the ankle with that at the arm. The resting ABPI is normally about 1. Values below
0.9 indicate some degree of arterial obstruction and a value less than 0.3 suggests imminent
gangrene. It must be appreciated that re-testing after exercise is useful to detect intermittent
claudication, as ABPI may be normal at rest. This probe is useful to get an idea about the site of
stenosis.
•
2. Duplex Imaging.— In this technique a Duplex scanner uses B-mode ultrasound to
provide images of vessels. There is a second type of ultrasound, namely Doppler ultrasound, in
which the imaged vessels are isolated and the Doppler shift is obtained which is analysed by a
computer in the Duplex scanner itself. In this technique shifts can give detailed knowledge of
blood flow or turbulence inside the vessel. Some scanners have colour coding, in which various
colours indicate change in direction and velocity of blood flow. It can be considered as accurate
as angiography in a few circumstances. In terms of safety this technique is preferred to angiography
if the two tests are considered to be equally useful.
3. Plethysmography.— This is a method of assessing changes in volume due to arterial
supply to that particular part. It has applications in peripheral arterial, cerebrovascular and
venous diseases. As the pressure pulse passes through a limb segment a wave form is recorded
by plethysmography, which determines arterial pressure as well as arterial and venous blood
flow.
This method is one of the earliest methods of measuring blood flow in human limbs. Venous
outflow from a limb is briefly arrested while allowing arterial inflow to measure the volume
change in the limb which is proportional to the arterial inflow. Three systems have been used e.g.
water-filled volume recorder, air-filled volume recorder and the mercury in a silastic strain
gauze. This technique is still a good non-invasive method of measurement of blood flow. But it
has rarely been found suitable for screening method for surgery, as the surgeon is more interested
to know the site of the arterial block rather than to measure the blood flow as such. Recently
segmental plethysmography has been introduced by placing.venous occlusion cuffs around the
thigh, calf and ankle. The cuffs are inflated to 65 mm Hg and the pulsation is the quantitative
measure of the arterial diseases.
4. B-scan ultrasound.— This can be used for visualization of blood vessels as a real-time
echo. The value in the diagnosis of occlusive disease is limited when the vessel wall is extensively
calcified. This B-scan may be used as a guide for precise placement of the doppler sample so that
doppler ultrasound can be combined with this technique to get valuable information.
5. Treadmill.— Sometimes patients cannot assess the claudicating distance, which can be
proper Iv assessed by this technique. It may be used in the detection of a fall in ABPI after exercise
indii.&mg occult arterial stenosis.
b. Phonangiography.— Vibrations of low frequency in the arterial wall due to disturbances
in blood flow can be detected as a noise using a stethoscope. By analysing this sound and its
location information of atherosclerosis and stenosis may be obtained.
7.
Determination of ankle pressure.— This is one of the non-invasive techniques used
in verifying the diagnosis of ischaemic disease, in localizing the anatomic site of obstruction and
in choosing the type of operation. This is generally done with a doppler device. In patients without
DISEASES OF ARTERIES
193
arterial disease, the ankle/arm pressure ratio is 1 or higher. In claudication, it is generally between
0.5 to 1 and with more advanced degree of ischaemia it is generally less than 0.5. Segmental
pressures are obtained by application of cuffs at different levels of the leg. The pressure gradients
between the levels provide information about the location of the disease.
8.
Isotope technique.— Xenon
133 dissolved in isotonic saline is injected
intramuscularly and the clearance of
which has been used to study the* blood
flow in the calf muscles. Recently
Technetium has become the isotope of
choice though the technique remains
essentially the same. More recently «£,.
intravenous injection of isotope has been
used to get a direct arterial visualization.
'.
.•
*5^-*
-
"
.$■
r
For this a gamma camera is used to
picturise the blood flow in a limb.
9.
Electromagnetic
flow
meter.— When a column of blood moves
an electric potential is produced which is
proportional to the velocity of blood and
the magnetic field strength. The electric
potential is produced at right angles to
the flow. It bears a linear relationship to
the velocity of the blood flow. Two
electrodes are placed diametrically
opposite to each other in contact with the
arterial wall. This is the 'cuff' type of
electromagnetic
flow
meter.
The
electrodes on the surface of the artery pick
up an electromotive force induced in the
blood by its motion through the magnetic
field and feed it back to suitable electronic
amplification. Such a method can detect
the change in the rate of the blood flow
of 1%. But the greatest disadvantage of
this technique is that the artery has to be
exposed.
Fig.15.2.— Bolus of 99Tcm has been injected i.v., followed
by arterial imaging which is done by a gamma camera. This
figure is an aorto-iliac irr age showing occlusion of the left
external iliac, but patency of the common and superficial
femoral arteries, suitable for cross-over grafting.
10. Investigation for vasospasm.— In early part of Raynaud's disease or Buerger's disease
vasospasm is the main cause of arterial obstruction. It is at this stage that sympathectomy plays
its greatest role. Later on organic changes develop and sympathectomy does not do much good
to these patients. So, importance of finding out the degree of vasospasm cannot be overemphasized
to assess the value of sympathectomy. The method is nerve block with local anaesthetic e.g. the
posterior tibial nerve behind the medial malleolus, the ulnar nerve behind the medial epicondyle
or spinal anaesthesia in case of whole lower limb. Any rise of skin temperature is recorded and
is compared with the rise of mouth temperature.
13
194
A CONCISE TEXTBOOK OF SURGERY
Rise of skin temp. - Rise of mouth temp.
Brown's vasomotor index = ------------- —----- ---------------------------------------Rise of mouth temperature
Operation is only advisable when the index is 3.5 or more.
11. Oscillometry.— This is of particular value in detecting arterial pulsation at different
levels of the limb. In embolism, a sudden decrease in the movement of its needle is obtained at
the level of arterial occlusion. In thromboangiitis obliterans, if no pulsation is obtained in the leg,
amputation should be performed in the thigh. But if oscillation can be seen in the leg a lower
amputation should be advised.
12. Arteriography.— This is the most reliable method of determining the state of the main
arterial tree. This procedure gives information about the size of the lumen of the artery, the
course of the artery, constriction and dilatation of the arteries and the condition of the collateral
circulation ('Run off'). Hypaque 45 (Sodium Diatrizoate) is the contrast medium often used.
Either of the following two methods is generally used :
(a) RETROGRADE PERCUTANEOUS CATHETERIZATION.— Under local anaesthesia
with proper aseptic precaution a special needle and a cannula are introduced into the femoral or
brachial artery (Seldinger technique). The common femoral artery is used for aortoiliac, renal,
mesenteric and femoropopliteal arteriography, whereas the brachial artery is used for subclavian,
vertebral, carotid and thoracic angiography. The needle is now withdrawn and a flexible guide
wire is threaded through the cannula. The cannula is withdrawn and a polythene catheter is
passed over the guide wire into the artery for a distance.
To avert the dangers of arteriography namely (i) iodine sensitivity and (ii) dissection of the
arterial wall if the tip of the needle is partly within the wall of the artery, a trial injection of 5 to
10 ml of 45% hypaque is made. This will ascertain the position of the tip of the needle.
Either a free flush arteriography or a selective angiography is performed. In free flush
arteriography the tip of the catheter lies in the main aorta and a 'bolus' of 30 ml of the same
contrast medium is injected rapidly. Series of X-ray exposures are taken to see particularly the
whole length of the arterial tree, the origins and the adjacent part of its branches. In selective
angiogram the tip of the catheter is introduced into the corresponding artery to delineate the
artery and its branches precisely.
(b) DIRECT ARTERIAL PUNCTURE.— This method is used in carotid angiogram.
Abdominal aorta (translumbar route) may also be chosen for this method for aortoiliac and
femoropopliteal arteriography when the femoral arteries are occluded or the retrograde method
has failed to produce necessary information.
13. Digital subtraction angiography (DSA).— This technique is preferred nowadays in
specialized centres. In this technique the angiographic information is digitalised in a computer
system, for which the contrast image is subtracted from the non-required surrounding images.
The result is a greater clarity. DSA may be carried out by arterial or venous injection. The arterial
technique is more or less same as conventional angiography, only fine catheter and less contrast
medium are used. The venous technique offers less clarity than its arterial counterpart, the only
advantage is that it avoids arterial puncture. Higher volume of contrast medium is injected in a
large vein which offers even better clarity than the simple arteriography.
The more sophisticated technique is the introduction of magnetic resonance angiography
without the need of direct arterial puncture. When this technology will advance, obviously the
catheter based contrast studies will be reduced.
DISEASES OF ARTERIES
195
MANAGEMENT. — Management of cases of chronic
arterial occlusion can be best described under the
following heads —
A. Conservative methods;
B. Indirect surgery to cause vasodilatation;
C. Direct arterial surgery.
A.
('onscri'alirc methods.- About 65% patients
who first present at a vascular clinic with intermittent
claudication can be treated initially by conservative
methods. Followings are the modalities under this group.
1. Stoppage of smoking.—This often goes a long way
to stop the progression of the disease. It particularly works
wonder in case of Buerger's disease.
2. Diet.— Diet should be so planned as to reduce
weight in case of obese individuals. The diets containing
cholesterol or P-Iipoproteins should be avoided.
3. Lipid abnormalities.— As mentioned earlier raised
P-lipoprotein is probably the commonest abnormality
found in those suffering from atherosclerosis.
Cholestyramine is particularly useful which lowers
cholesterol level.
4. Proper explanation.— In cases of intermittent
claudication if the patients are properly explained that
walking is not doing any harm, the walking distance often
improves. Improvement has even seen probably due to Fig. 15.3.— Aortogram showing occlusion
establishment of adequate collateral circulation in many of left external iliac and superficial femoral
patients within a few months.
arteries
5. Exercise, if performed within limits, often reduces pain of intermittent claudication and
may help in spontaneous cure.
6. Diabetes and hypertension, if present, should be treated accordingly. Both these diseases
play a considerable role in the development of atherosclerosis.
7. Care of the feet.— This is particularly required in pre-gangrenous state, patients with rest
pain and in diabetic patients.
(i) The part should not be exposed to excessive cold or heat.
(ii) Stockinette may be used to prevent the feet from exposure to cold or to trauma.
(iii) By reducing exercise, demand of blood supply is diminished, so pain is relieved to a
great extent. This may be performed by reducing walking, stopping cycling and by wearing
shoes with high heel to diminish action of calf muscles.
(iv) Pressure to the affected foot particularly over the heel and malleoli should be avoided.
(v) Even minor trauma by amateur chiropody may start gangrene in pregangrenous toes.
So nail cutting should be done cautiously and at the same time any minor trauma should be avoided.
8. Buerger's position.— In this position the head end of the bed is raised and at the same
time the foot end of the bed is gradually lowered about 6 inches daily. This increases blood
supply to the lower extremity and may improve the condition.
9. Buerger's exercise.— In this exercise the affected lower limb is elevated for 2 minutes and
196
A CONCISE TEXTBOOK OF SURGERY
then lowered below the bed side for another 2 minutes. This process is repeated several times in
one sitting. In a day at least 3 sittings should be performed. This also improves circulation to the
affected lower limb.
10. Analgesics.— Various analgesics may be used, of which aspirin in dispersible form is
probably the best due to its antiadhesive effect on the platelets.
11. Drugs.— Drugs to combat diabetes and hypertension must be used properly. A few
antihypertensive agents, particularly beta-blockers may reduce claudication distance. An anti­
platelet agent may be used for patients with occlusive arterial disease. Aspirin in the dose of 75
mg to 300 mg daily is quite a good and easily available drug in this group. If there is raised blood
lipids, drug treatment should be used to reduce these to normal level. It must be appreciated that
vasodilators are generally ineffective. Praxilene (Naftidrofuryl oxalate) may increase the
claudicating distance by allowing a greater oxygen debt to be incurred, but the actual ultimate
benefit is quite negligible. Trental (oxpentifylline) reduces blood viscosity and thus may be of
some benefit, but not quite satisfactory.
Intra-arterial administration of vasodilator drugs at the selective site by injection has been
successful as a temporary method. The drugs used are papaverine, lignocaine and duvadilan
injections.
Paravertebral injection of local anaesthetics near the sympathetic chain has also improved
circulation of the limbs. It is also known as chemical sympathectomy. In case of lower limb, injection
is made by the side of the L2, 3 and 4 vertebrae. For upper limb, injection is made by the side
of T2, 3 and 4. If 1% lignocaine is used, the effect is only temporary. For a more lasting result
about 5 ml phenol solution in water is injected. The procedure is better carried out under X-ray
control and a small injection of contrast medium (Hypaque solution) may precede the proper
injection of phenol. The main danger is to penetrate the aorta or the vena cava which can be
detected by drawing back the piston of the syringe which will show indrawing of blood into
the syringe.
B. Indirect surf/cry to cause vasodilatation.—1.
SYMPATHECTOMY.— This operation, though not very effective in claudication, yet it
has some beneficial role in cases of rest pain and minor ulceration of the toes and fingers. It is
still very doubtful how much muscular blood supply is improved by sympathectomy, but it is
almost certain that it increases blood supply to the skin and subcutaneous tissue. Its main
indications are —
(i) Rest pain and minor ulceration, which are not amenable to direct arterial surgery. The
role of sympathectomy is probably the best in these conditions.
(ii) Buerger's disease.— In this condition sympathectomy plays a considerable role. The
result seems to be very significant if the Brown's vasomotor index is more than 3.5.
(iii) Raynaud's disease and other vasospastic conditions.— In these cases sympathectomy has
not been able to bring about considerable success.
(iv) Senile gangrene or diabetic gangrene in the elderly.— In these cases sympathectomy is
only advised where direct surgery is not feasible.
Usually one of two varieties of sympathectomy is usually performed.
(a) Lumbar sympathectomy.— This operation is performed in cases of arterial occlusions
of the lower limbs.
(b) Cervico-dorsal sympathectomy.— This is performed for arterial occlusion of the upper
limbs.
DISEASE^ OF ARTERIES
197
2. ADRENALECTOMY.— This operation is only used in cases of Buerger's disease with
some satisfactory results. Bilateral adrenalectomy should be performed.
3. MINOR SURGERIES to reduce muscular activity.— In ischaemic limb if the muscular
activity is reduced, claudication pain will be reduced to considerable extent. This can be achieved
by—
(i) Division of nerves to the gastrocnemius and soleus in the popliteal fossa. These muscles
are the muscles of the calf.
(ii) Tenotomy of the tendo-Achilles diminishes effort of the calf muscles by increasing the
length of its tendon.
C.
Divert arterial surgery.— Various surgeries can be recommended according to the
type of occlusion and the artery affected. The followings are the different types of surgery which
are used for chronic arterial occlusions.
(1) Repair of injured artery.— This is performed only when the occlusion is due to
trauma.
(i) After exposing the site of occlusion due to trauma, simple manipulation of fractured
bone ends may cure the arterial occlusion. In certain cases of arterial spasm adventitial injection
of papaverine may cure the condition.
(ii) When the artery is tom, direct end-to-end arterial suturing should be performed with
5/0 atraumatic silk.
(iii) In certain cases a segment of the artery becomes contused or lacerated. In these cases
the affected portion is removed and if this segment is small, end-to-end suturing may become
possible without any tension to the suture line. If the affected segment is long, a Dacron graft or
a reversed long saphenous vein graft may be used to make good the loss of the segment.
(2) Thromboendarterectomy.— This operation is performed when the atheromatous lesion
Fig. 15.4 .— Shows the technique of endarterectomy. See the text for details.
198
A CONCISE TEXTBOOK OF SURGERY
is short and localized and has affected a big artery like aorto-iliac occlusion or less commonly in
femoropopliteal occlusion. Though it may require more extensive operation, yet it has the
advantages of preserving the patient's own arteries and avoiding the use of a prosthesis with its
attendant risks. This operation is also called 'disobliteration' or 'reboring'.
In this operation the whole length of the obliterated segment is explored. When the affected
segment is small, a longitudinal incision is made over the diseased segment and is made deep
till the atheromatous plaque is reached. The diseased intima, atheromatous plaque and the
thrombus are removed through a plane of cleavage through the middle of the tunica media. The
arteriotomy is then closed with continuous 5/0 polypropylene (prolene) suture with or without
a vein patch graft. This patch graft is to avoid constriction following longitudinal suturing. This
is called 'Open endarterectomy'.
In case of longer diseased segment, arteriotomies are made only at the upper and lower ends
of the diseased segment. An endarterectomy loop is inserted through the lower arteriotomy and
is pushed upwards dissecting and separating the atheromatous plaque as far as the upper
arteriotomy. The atheromatous plaque is removed from the upper arteriotomy. The arterial
openings are closed after ensuring good flow. General anticoagulant therapy is instituted. This
is called 'Closed endarterectomy'.
(3) Arterial by-pass grafting.— In this technique the diseased segment is bypassed with
a synthetic graft (knitted Dacron or Teflon) or with reversed autogenous long saphenous vein graft.
Prostheses come in two types — woven and knitted. Woven grafts leak less when first exposed to
blood during surgery. Modern knitted prostheses leak even less as they are sealed with gelatin or
collagen by the manufacturer. In fact there is probably little to choose between the types of Dacron
graft to be used. All achieve fairly satisfactory results. In aorto-iliac occlusion mostly synthetic grafts
are applied, whereas in femoro-popliteal occlusion, autogenous vein graft is mainly used. A
Polytetrafluoroethylene (PTFE) graft may be used instead of autogenous vein graft. This often gives
prolonged patency. In case of aorto-iliac occlusion suture material used is monofilament
polypropylene — 2/0 or 3/0. In femoropopliteal occlusion at the groin, 4/0 or 5/0 polypropylene
is used; whereas in case of further down limb occlusion 7/0 suture material is used.
(4) Balloon transluminal angioplasty.— In this technique a balloon angioplasty catheter
is passed through the arterial stenosis. The balloon is inflated with dilute contrast medium to a
pressure of 5 to 10 atmospheres for a period of 15 to 30 seconds even upto 1 minute, after which
it is deflacted. This is repeated for a few times before withdrawal of the catheter. This balloon
is introduced into the arterial tree using the Seldinger technique. Expansion of the balloon produces
fissures in atheromatous plaques and also ruptures muscle fibres of the tunica media thus widening
the lumen and ensuring blood supply to the distal limb. This technique is mainly used in case
of arterial occlusions of the iliac artery, superficial femoral or renal artery. Gradually the endothelial
lining develops along the fissures in the atheromatous plaque within a few months.
Transluminal angioplasty and stenting.— This is particularly effective to inflate a narrowed
short occlusion. The balloon catheter is inserted over a guide wire. The balloon is positioned
within the stenosis or occlusion which is confirmed by angiography. The problem is that often
the vessel fails to stay adequately dilated after such treatment and in these cases metal stent may
be used. In this technique the balloon catheter is introduced through the expanding stent and
then the balloon is inflated. The stent becomes rigid after being expanded and keeps the vessel
widely patent. The catheter balloon is now deflated and the catheter is removed. There is also a
type of self-expanding stent, which is held compressed by a sheath of plastic before application.
WSEAStES Off- ARJERSE5
199
The stent is positioned at the site of stenosis and the plastic sheath is withdrawn. The stent selfexpands and holds the vessel lumen wide open.
This procedure is not as good as reconstructive surgery, and is only used when latter type
of surgery is not possible. However the advantage of this procedure is that it can be repeated if
stenosis recurs.
(5)
Other operative salvage procedures.— These operations should not be performed
only for intermittent claudications as gangrene or loss of limb may result if these operations fail.
(a) Femoro-femoral cross over graft.— In this technique without extensive exploration and
minimizing the operation time, an iliac artery occlusion may be relieved if the other iliac artery
is patent with a strong femoral pulse. 8 mm Dacron graft is placed in a tunnel in the subcutaneous
tissue in the lower abdomen just above the pubis from one groin to the other to connect the
common femoral arteries on each side. So that blood from the patent femoral artery is carried
through the graft to the other femoral artery of the ischaemic side.
(b) Hitch-hike femoro-popliteal-tibial graft.— This technique is adopted in cases of difficult
femoro-popliteal occlusion. A Dacron graft connects the common femoral artery to a
thromboendarterectomised upper popliteal artery. A vein graft is again connected from this
rebored upper popliteal artery to the arteries below the knee.
(c) Axillo-femoral graft.—This technique is used for pre-gangrenous limb in a poor risk
patient with bilateral iliac obstructions. 8 mm Dacron graft is placed in a tunnel in the subcutaneous
tissue extending from the axilla to the groin. In its upper part it is anastomosed with the axillary
artery in an end-to-side fashion. In its lower end it is anastomosed to the femoral artery of the
involved limb in the same fashion. By this blood flows sufficiently from the axillary artery to
revascularise the lower limb.
VARIOUS SITES OF CHRONIC ARTERIAL OCCLUSIONS
AORTO ILIAC OCCLUSION
Actiolog\ and Pathology. Patients are mostly in the 5th and 6th decades. Some degree
of atherosclerosis is almost always seen. The process may be atherosclerosis with intimal thickening
and fibrosis. The thrombus often propagates upto the level of the renal arteries, occluding one
renal artery and extending upto near the origin of the superior mesenteric artery.
Concomitant coronary or cerebral atherosclerosis occurs in 30 to 50% of patients with
symptomatic aorto-iliac disease.
Clinical lea! n res.—
SYMPTOMS.— The classical symptoms are intermittent claudication involving both buttocks,
the thighs and calves with impotence of varying severity in males. Impotence is a characteristic
feature in males with occlusion in the region of bifurcation of aorta and the internal iliac arteries
(Leriche's syndrome). Claudication may be symmetric or asymmetric, depending upon the pattern
of involvement of the iliac arteries. Rest pain and ulceration almost always indicate additional
distal disease particularly in diabetics.
PHYSICAL EXAMINATION.— The principal finding is diminution or absence of femoral pulses,
combined with absence of popliteal pulses. Pulsation of the abdominal aorta may be palpable,
but may be absent if the abdominal aorta is occluded upto the renal arteries. Systolic bruit is often
audible over the aorta or iliac arteries confirming the presence of atherosclerosis. Nutrition of the
extremities is usually normal.
200
A CONCISE TEXTBOOK OF SURGERY
Occasionally an acute episode of
severe ischaemia of toes or feet with
cyanosis and rest pain may be
complained of. The syndrome
probably arises from embolization of
fragments of atherosclerotic plaques
or thrombi dislodged from the surface
of such plaque.
Treat ment.— This depends very
much on the symptom and the
profession of the individual rather
than anything else. For example, mild
claudication in a 45 year old patient
whose
occupation
necessitates
frequent walking is a strong
indication for operation. Whereas a
retired patient of 70 with angina
pectoris and claudication does not
require operation.
CONSERVATIVE TREATMENT
consists of (i) daily exercise to the point
of claudication. This may not only
increase the walking tolerance, but
also
may
enhance
collateral
circulation. If walking is not feasible,
Fig. 15.5.— Aortogram showing complete obstruction of the a similar exercise may be advised
right common iliac artery.
indoors
(ii) Abstinence from tobacco in any form is mandatory. It is almost proved that claudication
improves when smoking is stopped and that the risk of gangrene becomes less than that of the
patients who smoke. It should be remembered that claudication progresses to gangrene 2.3 % per
year.
(iii) Alcohol may be advised for its peripheral vasodilator effect.
(iv) Drug therapy with vasodilators have very limited result.
(v) Care of the feet as mentioned earlier should be carried out rigidly in these cases.
(vi) Attempt must be made to lower blood lipid concentration by diet and drugs, but of course
with uncertain benefit.
(vii) Acetyl Salicylic acid in small doses strikingly alters platelet aggregation and may thereby
prevent intravascular thrombosis.
SURGERY.—
(1) Thromboendarterectomy.— The typical pattern of atherosclerotic involvement is extension
of disease proximally to within 2 to 3 cm from the renal arteries and distally into the common
iliac arteries stopping in about 50% of patients just beyond the bifurcation of the common iliac
arteries. Thromboendarterectomy is mainly preferred when the occluded segment is short i.e.
involving the terminal 5 cm of the aorta and the proximal part of the common iliac arteries. When
the disease is more extensive than this, by-pass graft procedure should be the operation of choice.
DISEASES OF ARTERIES
201
The abdomen may be opened through either a long right paramedian or midline or a
supraumbilical transverse incision. Transverse incision is often preferred, as it is less painful and
wound healing is much better as this incision runs parallel to the Langer's lines. The peritoneum
of the posterior abdominal wall is incised over the front of the aorta. The aorto-iliac bifurcation
is clearly dissected out, great care being taken not to damage the wall of the iliac veins which are
often firmly adherent to the adjacent arteries. The extent of the disease is now confirmed by
palpation. The arterial clamps are placed well above and below the diseased segment.
When the diseased segment is short, a long arteriotomy is made over the diseased segment
of the aorta and common iliac arteries. A plane of cleavage is found between the atheromatous
core and the outer half of the tunica media. The core is removed and the distal intima is inspected
to ensure that it is firmly attached to the media. If there is any doubt, it is safer to suture it in
place to avoid dissection.
When the diseased segment is long, this portion of the aorta is dissected clear. The aorta
proximally and the external and internal iliac artery distally are encircled with plastic tapes. 50
mg of heparin is then given by intravenous injection before occlusive clamps are applied. Usually
the external iliac clamps are applied before those of the abdominal aorta to protect from distal
embolization. Incisions are made over the distal common iliac arteries and cleavage planes between
the plaques and the media are developed. A longitudinal incision is made into the aorta above
the level of the inferior mesenteric artery and an appropriate cleavage plane between the arterial
intima and media is indentified. With an arterial stripper, the core of atherosclerotic material is
freed proximally. By blunt dissection the aortic and the iliac core can be mobilized and removed
in one piece. The calibre of the external iliac arteries should be measured by the catheters. A
diameter smaller than 16 F catheter indicates the necessity of extending endarterectomy to the
common femoral arteries.
The aortotomy incision is closed with a continuous 5/0 monofilament non-absorbable suture.
The iliac arteriotomies are closed similarly with a patch graft of either autologous saphenous vein
or prosthetic patch of knitted Dacron. The occluding clamps are sequentially removed to permit
flushing. Once blood flow is restored, heparin is neutralized with protamine, giving 1 mg for
each mg of heparin.
(2)
By-pass grafting.— This is a very popular operation in aorto-iliac disease. The superiority
of the previous operative procedure over this has not been demonstrated conclusively as con­
comitant aneurysmal disease of the aorta is a definite contraindication to endarterectomy.
Long term patency rate after either procedure ranges from 60% to 90%. But by-pass operation
is more popular in aorto-iliac disease.
Usually a Woven Dacron prosthesis is preferred because of firmer adherence of the neointima
which forms subsequently in the wall of the graft.
The proximal anastomosis is constructed in an end-to-side fashion with a continuous suture
of 4/0 monofilament suture. Soft tissue tunnels are formed by blunt dissection anterior and
parallel to the iliac vessels, through which the limbs of the prosthesis are brought parallel to the
iliac arteries. If the distal anastomosis is performed to the common femoral artery, the graft is
brought to the groin deep to the inguinal ligament. The common femoral artery is incised near
the origin of the profunda femoris artery. A continuous suture of 5/0 monofilament suture is
used for end-to-side suturing with the common femoral artery. This is done on both sides.
The major technical hazard in by-pass grafting is the formation of thrombi in the proximal
or distal arterial tree with subsequent embolization into the extremity. This is avoided by flushing
the graft before the distal anastomosis is completed.
202
A CONCISE TEXTBOOK OF SURGERY
Antibiotics in
large amounts are
always started
Extent of disease
Operation
before
the
operation and
may be repeated
aorta
if the operation is
+
aortoiliac
endarterectomy
common iliac
continued for
longer period.
(3) Balloon angi­
oplasty.— This
technique is
probably suitable
to short seg­
mental stenosis.
aortofemoral
Dacron bypass
The technique has
been described
above.
In approxi­
mately 10% of
patients serious
local complica­
external iliac
tions occur which
endarterectomy
include rupture of
external iliac
(extra peritoneal)
the vessel with
retroperitoneal
haemorrhage or
total occlusion of
the
previously
stenotic
vessel.
unilateral
iliac
femorofemoral
The long term
(poor-risk
Dacron bypass
results are not
patients)
(subcutaneous)
known as the
procedure
has
been introduced
recently.
(4) Lumbar sym­
pathectomy.— This
is indicated in
aortoiliac
axillofemoral
(poor-risk
Dacron bypass
patients
with
patients)
r\ (subcutaneous)
trophic changes
in the feet not
amenable
to
arterial
recon­
struction
ope­
rations.
fis .15.6,— Diagrammatic mgaesenAMian erf Jfoe gperatoms to be performed in various
Unfortunately,
cases off scato-SBac ©odtetoass..
the benefit of
203
DISEASES OF ARTERIES
sympathectomy are unpredictable. In many series signs of improvement were seen in only 20 to
30% of patients. There is no doubt lumbar sympathectomy increases circulation of the skin and
subcutaneous tissue, which provides some protection from trophic changes and ulceration. It
does not increase blood flow to the leg muscles.
FEMORO POPLITEAL OCCLUSION
I’utholo&v.— The most common site for atherosclerotic occlusion in the lower extremity is
the distal superficial femoral artery within the adductor canal almost near the adductor foramen.
From here occlusion extends proximally in the superficial femoral artery till the opening of a
large collateral branch or may extend upto its origin from the common femoral. Occlusion of the
profunda femoris artery is very rare, as it is not an artery of conduction, but an artery of supply.
Usually arteries of conduction are involved by atherosclerosis.
If occlusion affects the popliteal artery or its branches, more serious circulatory insufficiency
appears and ulceration and gangrene of the feet may start. This is more common in diabetics.
Clinical features.—
.
SYMPTOMS. — Intermittent claudication of the calf muscles with moderate exercise is the
main symptom.
PHYSICAL EXAMINATION reveals a normal femoral pulse but absent popliteal and dorsalis
pedis pulses. Sometimes dorsalis pedis pulse may be felt at rest, but disappears with exercise,
which is known as the 'disappearing pulse'. The nutrition of the foot is usually normal. But if
occlusive disease is present distally, it may be associated with rest pain and trophic changes in
the foot.
The risk of gangrene developing within 5 years in an extremity with claudication as the only
symptom is about 5%.
Treat incut.— Indications for operation is almost in the similar trend as in aorto-iliac disease,
i.e. it is dependent on the symptom of the patient, his age and his occupation.
CONSERVATIVE TREATMENT.— If this is chosen, it is almost similar to that described in
aorto-iliac occlusion. Only one point requires mention that a good exercise programme of walking
daily has resulted in marked improvement in claudication in at least 50% of patients within 6 to
12 months.
SURGERY.—
1. Endarterectomy.— In this disease open endarterectomy is preferred, in which the whole
length of the occluded portion of the artery is exposed by a longitudinal incision, atherosclerotic
core is removed and the arteriotomy is closed by suturing with a vein patch to prevent constriction.
Endarterectomy has not proved satisfactory in femoro-popliteal occlusive disease. That is why it
is only advocated when a suitable vein is not available for by-pass surgery.
2. By-pass grafting.— By-pass operation with autologus saphenous vein is the standard
technique. In determining the choice of operative procedure, venous by-pass is always favoured
if the saphenous vein is at least 4 mm in external diameter.
The long saphenous vein is carefully removed from the inguinal ligament to the knee joint.
This vein is now reversed to permit blood flow in the direction of venous valves without being
obstructed by them. Now it is attached with end-to-side anastomosis to the femoral and the
popliteal arteries proximally and distally respectively above and below the occlusive disease. If
the long saphenous vein is not of adequate diameter, a suitable cephalic vein is an acceptable
substitute.
3. Profundaplasty.— Recognition of the importance of the profunda femoris has laid to the
204
A CONCISE TEXTBOOK OF SURGERY
development of
the operation of
Extent of disease
Operation
profundaplasty
aimed
speci­
fically at in­
creasing
the
superficial
blood
flow
down
femoropopliteal
femoral
vein bypass
this vessel. This
vessel arises from
the
posterior
aspect of the
common femoral
artery and its
orifice is rarely
visualized
by
superficial
anteroposterior
superficial
femoral
X-ray projection.
femoral
endarterectomy
But this will be
demonstrated on
lateral projection.
Another peculiar
feature is that in
majority of cases,
if atheroma at all
superficial
involves
this
+
deep femoral
profundaplasty
artery, the athe­
±
(vein patch)
romatous
ste­
popliteal
nosis is only seen
at its origin. Only
in a few cases
such
stenosis
may extend upto
Fig. 15.7.— Operations for femoropopliteal disease : Examples of disease pattern and ^he ^'rs^ perfooperations to be performed for each case. These operations should only be done when rating artery.
the aorto-iliac segment is relatively free from disease.
This ope­
ration
of
profundaplasty is aimed at removal of atheromatous stenosis from the origin of the profunda and
then to widen the endarterectomised segment by insertion of a vein patch.
The vessel is dissected out and it is palpated to know the extent of the affected segment by
atheroma. After applying bulldog clamps to all the major branches, the diseased segment is
opened by a longitudinal incision (arteriotomy). This arteriotomy must extend upwards into the
common femoral trunk and downwards into the normal part of the artery. By endarterectomy,
the atheromatous core is removed. The distal intima is carefully examined and stitched to the
underlying media if it be needed. A saphenous vein patch is prepared and sutured into the
arteriotomy to widen the profunda artery. The bulldog clamps are now removed. Many surgeons
carry' out arteriography on the table to ensure no technical error has been made during anastomosis
0
,
mr\
DISEASES OF ARTERIES
205
and there is no obstruction of
the blood flow.
Profundaplasty operation
may be carried out in
conjunction
with
other
procedures e.g. by-pass graft
operation. Even with no
demonstrable
stenosis,
widening of the calibre of
apparently normal profunda
artery gives better results
comparable to only by-pass
operation.
4.
Lumbar sympathec­
tomy.— When claudication is
the only symptom, this
operation should not be
performed. This operation is
only indicated when trophic
changes are present and direct
arterial reconstruction is not
possible. As mentioned earlier
this
operation
provides
vasodilating effect on the skin
and subcutaneous vessels
proving some protection from
ulceration and gangrene to the
ischaemic foot.
Lumbar sympathectomy is
used in two situations —
Fig. 15.8.— Profundaplasty operation. After opening the origin of the
(i)
i4s a limb salvageprofunda femoris artery thromboendarterectomy is performed and the
procedure, as mentioned above.
opening is closed with a vein patch.
(ii)
y4s an adjunct to
reconstructive arterial procedure.— There is good evidence that the long term patency of
femoropopliteal by-pass graft is improved by simultaneous lumbar sympathectomy. However
this is not widely accepted.
5.
Amputation.— In certain cases when there is definite ischaemic change in the distal limb
with ulceration and gangrene, there is probably no way out but to amputate the distal portion
of the limb.
Level of amputation.— This is the main problem as the surgeon has to balance two opposing
factors — on one hand the more distal the amputation, the easier it is for the patient to use a
prosthesis. On the other hand, the more proximal the level of amputation, there is more likely of
primary healing. Presence or absence of pulses, arteriographic picture, the results of doppler studies
are the points to be considered. The general rule is that, when in doubt, the more proximal level
should be chosen to prevent repeated amputation.
The various types of amputation are described in the chapter of 'Amputation' (Chapter 19).
206
A CONCISE TEXTBOOK OF SURGERY
CAROTID OCCLUSIVE DISEASE—
It is mainly atherosclerosis at the origin of the internal carotid artery or a more extensive
occlusion of that artery. Occasionally there may be cerebral embolization from the heart or
fibromuscular hyperplasia of the carotid arteries or obliterative arteritis of the great vessels
(Takayasu's arteritis) or due to blunt or penetrating trauma.
In more than 75% of cases the
plaques are found at the carotid
bifurcation involving distal part of the
common carotid and the proximal
parts of external and internal carotid
arteries.
Carotid stenosis causes transient,
recurrent and progressive strokes
causing
hemiplegia
on
the
contralateral side. The classical stroke
from unilateral carotid disease is
ipsilateral blindness and contralateral
hemiplegia. There may be transient
ischaemic attacks (TIA), which mean
transient
monoplegia,
transient
hemiplegia or transient ipsilateral
blindness. These episodes clear within
minutes to hours after an abrupt
onset. Between such episodes the
patient is completely well.
Between the transient ischaemic
attack on the one hand and the
massive stroke on the other, a wide
variety of motor and sensory
syndromes are seen.
Fig.15.9.— Internal carotid arteriogram showing stenosis due to
11 cainicni. The ideal patient
atherosclerosis.
for operation is one with transient
ischaemic attack without permanent
neurologic abnormality. If the internal carotid has become totally occluded producing a major
neurologic deficit, operation performed within 6 hours after onset of symptoms may produce
dramatic recovery, though the operative mortality is considerably high. But if operation is carried
out beyond 6 hours, the result is miserable.
The operation is carotid endarterectomy followed by suturing with vein patch.
SUBCLAVIAN-VERTEBRAL DISEASE. Stenosis involving only the vertebral artery is infrequent. The disease is frequently limited
to the site of origin of the vertebral artery. The atherosclerotic plaque usually has a smooth
intimal surface here.
Symptoms are mainly due to decreased flow to the basi-vertebral system. Concomitant disease
in the basilar artery is quite frequent.
Subclavian steal syndrome is a condition in which there is atherosclerotic stenosis of the
DISEASES OF ARTERIES
207
subclavian artery proximal to the site of origin of the vertebral artery. Reduction in pressure in
the subclavian beyond the stenosis results in retrograde flow from the brain stem down the
vertebral artery to the arm (so blood is stolen from brain). The clinical picture is that of syncopal
attacks due to ischaemia of the brain stem, visual disturbances and decreased pulse and blood
pressure in the symptomatic arm. There may be a localized bruit in the supraclavicular space.
Treatment.— Subclavian exposure of the subclavian-vertebral junction is obtained through
a transverse supraclavicular incision. If the atherosclerotic plaque has a smooth surface,
endarterectomy may not be necessary and the lumen of the artery is simply widened known as
patch angioplasty with autologous saphenous vein.
Operations for subclavian steal syndrome are rarely necessary. A by-pass graft from the
ipsilateral common carotid artery to the distal subclavian artery may be necessary in symptomatic
cases. If the common carotid artery is markedly stenotic, axilloaxillary by-pass grafting may be
used.
AORTIC-ARCH OCCLUSIVE DISEASE (TAKAYASU’S ARTERITIS).—
Sometimes a non-specific arteritis affects major branches of the aortic arch and also the
thoracic and abdominal aorta. This is particularly seen in the Orient among young women. This
is known as Takayasu's arteritis, named after an ophthalmologist who described it. But occlusive
disease of the major branches of the aortic arch may also occur due to atherosclerosis in Western
Countries and also due to syphilitic arteritis. Takayasu's arteritis involves all layers of the aortic
wall with proliferation of connective tissue and degeneration of the elastic fibres. Granulomatous
lesions may also be present. Aneurysmal formations — fusiform or saccular varieties are also
noticed. It has been suggested that the disorder may be an autoimmune disease.
l linkul Icaimvs.- In case of atherosclerotic disease symptoms are mild permitting many
pathways for collateral circulation. Ischaemic symptoms of the upper extremities and brain may
occur.
In case of Takayasu's arteritis there is fever, malaise, arthritis and general arthralgia. Some
patients complain of pericardial pain and tachycardia and a few may also vomit. Later on ischaemic
manifestations are seen in the upper extremities and brain.
1
real mi n In case of atherosclerosis, multiple by-pass grafts may be required from the
ascending aorta proximally to the carotid or subclavian artery distally. Endarterectomy usually
is not possible.
In case of Takayasu's arteritis, operative treatment often proves disappointing, as both
endarterectomy and by-pass grafts are liable to reocclude. Since this disorder is an autoimmune
disease, steroids may be administered with some beneficial results. Operation is only recommended
for patients with disabling symptoms.
MESENTERIC ARTERIES OCCLUSION.—
Syndromes of visceral artery occlusion may be acute or chronic.
Acute occlusion of the mesenteric artery causes gross changes which are mainly intense muscle
contraction and bluish white rippling of the seromuscular surface. Later on the bowel relaxes and
the surface becomes pale with bluish tinge. The peritoneal covering loses shiny appearance.
Much later, gross signs of haemorrhage into the mesentery are seen and haemorrhagic infarction
becomes well manifested. The bowel wall becomes swollen and infiltrated with blood and the
mucosa becomes necrotic. Permeability to bacteria and fluid occurs and this causes purulent
peritonitis. With this there is a massive intraluminal loss of plasma and fluid. Leucocytosis goes
above 15000. Metabolic acidosis supervenes.
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Superior mesenteric artery embolization.— This is a common example of acute occlusion.
It causes (i) tremendous abdominal pain, (ii) followed by vomiting and diarrhoea with (iii)
evidence of cardiac lesion which may be the cause of embolization.
The diagnosis is confirmed by angiography.
Treatment.— Obviously immediate operation is the treatment of choice. After examining
the whole length of the bowel, one can assess the artery which has been embolized. Through a
transverse arteriotomy, Fogarty catheter is passed and embolectomy is performed alongwith
removal of propagated clot. Following restoration of blood flow, pulsation returns to the mesenteric
artery after an appropriate period of time. Now judgement is made as to whether or not the
intestine should be resected. If this is not required the abdomen can be closed.
M esenterie artery thrombosis.— This is a common example of chronic occlusion. In case
of thrombotic occlusion of the mesenteric artery, illness develops insidiously with a progressive
and steady colicky abdominal pain. This is the pain of intestinal spasm due to ischaemia. Half
of these patients will give a history of prior intestinal ischaemia manifested by weight loss, post­
prandial pain and altered bowel habits. Some may give manifestations of other atherosclerotic
occlusions.
Whenever bowel infarction is suspected, aortography should be performed. The intra-aortic
catheter is placed at the level of the first lumbar vertebra and anterior, posterior and lateral films
are taken after injecting the radio-opaque dye. In case of this disease a sharp cut of the superior
mesentery artery is seen within 1 cm of its origin.
Treatment.— Previously thromboendarterectomy was used, but as the operation is very
much time consuming and very traumatic to the already ill patient with intestinal infarction, by­
pass graft operation (with aorto-mesenteric graft) is now more popular. The infra-renal lumbar
aorta is exposed. Similarly the mesenteric artery is dissected free of its investment in the mesentery.
A saphenous vein graft is mainly used for end-to-side anastomosis from the anterior surface of
the aorta to the superior mesenteric artery.
Following revascularisation, the need for intestinal resection should be considered. A secondlook operation may be performed.
POPLITEAL ARTERY ENTRAPMENT SYNDROME.
In this condition a developmental anomaly is seen in the popliteal artery. In this case the
popliteal artery, instead of entering the popliteal fossa through the arch of the adductor magnus
muscle, enters the popliteal fossa through the muscle mass of the medial head of the gastrocnemius
muscle. Due to this developmental anomaly, the popliteal artery is exposed to repeated trauma
and severe compression by that muscle. As a result typical atherosclerotic changes appear with
occlusion and thrombosis. Sometimes a post-stenotic dilatation and aneurysm may be formed.
C'linieal features.— The main symptom is progressive intermittent claudication of the leg
and sometimes of the foot. Gradually ischaemic gangrene may develop in the toes and foot.
On examination, the usual finding is diminished or absent popliteal, posterior tibial and
dorsalis pedis pulses. Sometimes all pulses may remain normal, but disappear on dorsiflexion
of the foot. Occasionally when there is aneurysm formation, a pulsatile swelling is seen in the
popliteal fossa.
Treat inent.—
(a)
When there is no organic lesion developed in the popliteal artery, various types of
myotomy procedures can be adopted to release it from pressure.
DISEASES OF ARTERIES
209
(b)
When organic lesion has developed, only correction of anatomic abnormality will not
do and some sort of direct arterial surgery in the form of by-pass graft with autogenous long
saphenous vein or thromboendarterectomy angioplasty should be performed to restore blood flow.
ANTERIOR COMPARTMENT SYNDROME.—
Any condition, which increases fluid in the anterior compartment of the leg, causes increase
of pressure in this closed space surrounded by tough deep fascia. If such swelling continues, first
it obstructs veins. If the intracompartmental pressure exceeds aterial pressure, the arteries will be
occluded with ischaemia of the distal limb. The unyielding walls of the compartment are the
tibia, the interosseous membrane and the anterior crural fascia (deep fascia).
Such increase of intracompartmental pressure may be caused by severe exertion, trauma,
venous or lymphatic obstruction in the proximal limb or a complication of femoropopliteal by­
pass or even cardiopulmonary by-pass operation.
Clinical features.— Pain is the first and most important symptom. In the beginning it starts
as a dull ache and soon becomes severe. The pain is located in the anterior compartment of the
leg. Movement increases pain.
As the syndrome progresses, one can see erythema of the skin over the anterior compartment.
On palpation tenderness can be elicited on the anterior compartment. Dorsalis pedis pulse
may be diminished or absent, which is a relatively late sign and is seen after the loss of motor
power of the muscles of the anterior compartment. The first muscles which become paralysed are
the anterior tibial and the extensor hallucis longus, followed by extensor digitorum longus and
other muscles.
Examination will reveal in late cases loss of sensation in the area supplied by the peroneal
nerve.
Treatment.— As soon as the diagnosis is made, decompression of the compartment should
be performed by fasciotomy. The skin is incised 2 cm lateral to the shin bone and is made deep
through the subcutaneous tissue and deep fascia. The muscle bellies will be seen bulging through
the fasciotomy. The incision is extended till the compartment pressure is completely relieved. It
is better to keep the wound open and left for secondary suture. Some surgeons however close the
skin only over the bulging muscles to prevent entry of infection.
RAYNAUD’S SYNDROME
Definition.—
Raynaud's syndrome is a condition characterized by episodic attacks of vasospasm that
cause closure of the small arteries and arterioles of the distal parts of the extremities in response
to cold exposure or emotional stimuli. Classically the attacks consist of three sequential phases
— (i) intense pallor followed by (ii) cyanosis and (iii) rubor upon warming requiring 15 to 45
minutes for full recovery. However a large number of patients develop only pallor and cyanosis
during attacks.
Fingers and hands are most frequently involved, although in many patients the toes, feet,
ears, nose and lips may be similarly affected.
Aetiology.—
1.
The syndrome described by Raynaud now termed as Raynaud's phenomenon is a primary
disorder whose aetiology is still unknown. It is also termed Raynaud's disease. It is much more
common in women with a ratio of about 5 :1. 90% of patients are below 40 years of age. In men
it is usually much less severe in intensity.
14
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A CONCISE TEXTBOOK OF SURGERY
2. It may be a secondary manifestation of some other probably more serious disease. A
comprehensive list is given below but it is more often associated with Buerger's disease
(thromboangiitis obliterans), scleroderma, cervical rib or other thoracic outlet syndrome and
atherosclerosis.
DISOFtDERS IN WHICH RAYNAUD’S SYNDROME MAY BE SECONDARY ARE :
I. Immunologic and connective tissue disorders —
1. Scleroderma.
2. Systemic lupus erythematosus (SLE).
3. Rheumatoid arthritis.
4. Dermatomyositis.
5. Sjogren's syndrome.
II. Obstructive arterial diseases —
1. Arteriosclerosis.
2. Buerger's disease.
3. Thoracic outlet syndrome.
III. Environmental conditions —
1. Vibration injury.
2. Direct arterial trauma.
3. Cold injury.
IV. Drugs —
1. Ergot.
2. Betablocking drugs.
3. Cytotoxic drugs.
4. Birth control pills.
V. Miscellaneous —
1. Cold agglutinins.
2. Cryoglobulinaemia.
3. Neoplasia.
4. Neurologic disorders.
5. Endocrine disorders.
RAYNAUD’S DISEASE
Maurice Raynaud described this condition in 1862. Publication of Allan and Brown's
observations have put light in the understanding of Raynaud's syndrome. Presently there appears
little justification in attempting rigid separation of Raynaud's disease from Raynaud's phenomenon
(where Raynaud's disease is secondary to some other condition). With the passage of time incidence
of primary Raynaud's disease decreases as some associated disease process is found in more and
more patients.
' Pathophysiology.—
The arterioles penetrate the dermis at right angles with an irregular reticulate pattern and
end in a capillary network. In Raynaud's disease, vasospasm occurs with such severity that
dermal circulation momentarily ceases with the production of severe pallor. If the vasospasm is
less severe, with slowing but not cessation of dermal circulation, cyanosis appears. After some
minutes of pallor, the capillaries and probably the venules dilate due to hypoxia and
accumulation of metabolic products of regional anaerobic metabolism. This is followed by a
DISEASES OF ARTERIES
211
slight relaxation of the arteriolar spasm with entry of small amount of blood into the dilated
capillaries. This is rapidly deoxidised and this gives rise to cyanosis. This results from sluggish
flow of blood with an increase in the percentage of reduced haemoglobin in the capillaries.
When the vasospasm subsides, a reactive hyperaemia with vasodilatation develops due to
accumulation of tissue metabolite during the anoxic period and this produces redness or rubor.
Why is there the increased tendency of the dermal arterioles to vasoconstriction ? This is not
definitely known. But there are many theories.
Two types of adrenergic receptors have been identified in the blood vessels. Alpha 2-adrenergic
receptors are present in form on human platelets. A recent study evaluated that there is marked
elevation of Alpha 2-receptor activity in spastic Raynaud's disease. This increased Alpha 2adrenergic activity may prove to be the 'local vascular fault' hypothesised by Sir Thomas Lewis
50 years ago.
In majority of patients the episode of vasoconstriction is precipitated by exposure to cold. But
in about 25% of patients intense emotion may be the initiating factor. Only rarely is alone the
significant stimulus without an abnormal sensitivity to cold.
Clinical leaf tires.—
Environment has a role to play in this disease and cool damp climates may increase the
incidence of Raynaud's syndrome or may merely make the underlying abnormality clinically
apparent.
Occupation has also a big role to play in Raynaud's syndrome. Use of vibrating tools or exposure
to chronic cold increase incidence of this condition. Incidence of this condition among chain-saw
operators and miners using vibrating equipment ranges from 40% to 90%. Those who work with
earth impactors or rivetting machines which are also vibrating tools show similar incidence of
this disease. These vibrators seem to disturb the neurovascular controls in the hands. Similarly
this syndrome is reported in about 50% among food workers working in cold environment.
Females comprise 70% to 90% of cases of Raynaud's syndrome. Raynaud's disease is
commoner in younger women. Older males may develop this syndrome usually from
arteriosclerosis.
Three stages are distinctly observed with exposure to cold or emotional disturbances. These
are — (1) Stage of local syncope, (2) Stage of local asphyxia and (3) Stage of recovery.
Stage of local syncope.—With exposure to cold the digital arterioles go into spasm and the
decreased blood flow is evident by pallor or blanching (stage of blanching). This change starts at
the tip of the finger and gradually spreads towards the base.
Stage of local asphyxia.— With gradual warming there is slight relaxation of arterioles. Small
amount of blood passes to the capillaries which become dilated due to accumulation of anaerobic
metabolities from the previous stage. Slowly flowing blood becomes easily deoxygenated and
the part becomes dusky or cyanosed (stage of dusky anoxia). The fingers remain cold and numb.
Stage of recovery.— As the attack passes off and with more warming, the spasm absolutely
disappears and the arterioles relax. The oxygenated blood returns into the dilated capillaries
(under influence of anaerobic metabolites which accumulated in the first stage of pallor) and the
fingers become red (stage of red engorgement) and swollen. There may be burning sensation or pain
produced by the increased tissue tension within the digits.
This condition is commonly bilateral.
Inspection.—
No abnormality is usually detected. In late cases one may find finger tip ulceration. This is
A CONCISE TEXTBOOK OF SURGERY
212
usually associated with obstruction and not only spasm of the arterioles.
Palpation.—
(i) Fingers and hand feel cold.
(ii) Pulses at the wrist are usually normal (cf. Buerger's disease).
(iii) One must exclude other conditions which may be associated with this disease e.g.
thoracic outlet syndrome, cervical rib, scleroderma, atherosclerosis etc.
Patients with scleroderma may have visible changes in their skin and face and may complain
of dysphagia.
In long standing cases the fingers gradually waste, especially the pulps, which become thin
and pointed. Small scars may appear following necrosis of small areas of skin. Small and painful
ischaemic ulcers may be seen on the finger tips. Repeated infections (paronychia) are common
around the nails. These are painful and slow to heal.
‘ The patients may gradually get rest pain and gangrene of the finger tips.
Special Investigations.—
1. Digital plethysmography with digital blood pressure determination.
2. Arteriography.
3. Haemogram, E. S. R., Rheumatoid factor, antinuclear antibody determination.
4. Protein electrophoresis.
TREATMENT.
Conservative treatment should be tried first.
CONSERVATIVE TREATMENT.—
1. Moving to warm climate.
2. Tobacco should be avoided.
3. The part should be protected from exposure to cold.
4. Occupational exposure should be reduced.
5. A variety of vasodilator drugs have been used in this condition. One of the most
widely used drugs is Reserpine. An oral dose of 0.25 to 0.50 mg daily should be prescribed for
2 weeks. Methyldopa may be administered orally. This treatment should be continued for several
weeks. Intra-arterial injection of Reserpine 2 or 3 times yearly may be necessary. Guanethidine
has been claimed to be the most effective drug for the symptomatic treatment of this condition
in the last decade. Phenoxybenzamine and more recently prazocin and pentoxifylline are the
adrenergic blocking drugs which have been claimed to provide good result.
The calcium channel-blocking drugs have been used with success by certain investigators.
Nifedipine is the most potent peripheral vasodilator in this group and has been moderately
effective in the treatment of Raynaud's syndrome. This has produced clinical improvement in
50% to 60% of patients. The combination of Nifedipine with low dose of guanethidine or prazocin
has frequently appeared to improve results while diminishing the incidence of side effects.
Patients with spasmodic Raynaud's syndrome respond better than obstructive Raynaud's
syndrome. Prostaglandin E administered intravenously to these patients have shown benefits as
has been reported from a few hospitals of London.
OPERATIVE TREATMENT.—
There is definitely a place for vascular surgery in cases of arteriosclerosis, emboli, thoracic
outlet syndrome, aneurysm or trauma which may be associated conditions of Raynaud's syndrome.
Although CERVICO-DORSAL SYMPATHECTOMY is recommended for primary Raynaud's
disease, and though there is good immediate result, yet this is often followed by gradual recurrence
DISEASES OF ARTERIES
213
of
symptoms.
Probably
sympathectomy
produces
long term good results in
mild Raynaud's syndrome of
the spastic variety and this is
the same group of patients
who respond best to drug
therapy.
Cervico-dorsal sympa­
thectomy is of little or no
benefit in patients with
Raynaud's syndrome who
have associated connective
tissue disease.
The question of the day
is whether cervico-thoracic
sympathectomy should be
recommended in all cases of
Raynaud's syndrome or not.
Cervico-Thoracic
Sympathectomy.—
In
this
technique first, second and
Fig. 15.10 — Anatomical position of cervical sympathetic ganglia.
third thoracic ganglia are
removed preserving the
cervical portion of the stellate ganglion proximal to the level where the rami communicantes
from the first thoracic nerve join the ganglion, to avoid Homer's syndrome. So in this operation
the sympathetic trunk from the lower half of the stellate ganglion to the just below the 3rd
thoracic ganglion should be resected. As mentioned earlier initial results are usually good but
recurrence of symptoms in subsequent years is quite common.
For this reason sympathectomy is usually employed only when the symptoms are severe and
other therapy becomes ineffective.
Technique of operation.— See Figs. 8.7 & 8.8 at page 95 of Author's 'A Practical Guide to
Operative Surgery'.
Cervico-thoracic sympathectomy can be performed by one of the three following approaches:A.
ANTERIOR APPROACH.— The patient lies supine on the table. His neck is extended
by putting a sand bag between the shoulder blades. The head is rotated to the opposite side and
the hand of the corresponding side is pulled downwards. Operation on both sides can be done
in one sitting. An incision is made about 1/2 inch above the clavicle starting from the lateral
border of the sternal head of the stemomastoid muscle to the medial border of the trapezius.
After incising the skin, superficial fascia, platysma and investing layer of the deep cervical fascia,
the clavicular head of the stemomastoid is divided and the inferior belly of omohyoid is retracted
upwards to expose the scalenus anterior and the phrenic nerve. The phrenic nerve is safeguarded
and the scalenus anterior is divided at its insertion to the first rib. The subclavian artery is
exposed. It is retracted upwards with a sling. Its branches are carefully safeguarded. The supra­
pleural membrane is detached from the inner border of the first rib. The pleura is pushed
A CONCISE TEXTBOOK OF SURGERY
214
. Skin incision for cervical sympathectomy.
phrenic
drawn
medially
pleura
subclavian
Sibson's fascia is broken through with the finger taking
care not to tear the underlying pleura.
The sympathetic
chain is divided
between the
third and
fourth ganglia.
\
o J**.
! s'/
\\ \
. //
-—
11.— Steps of cervico-thoracic sympathectomy through
anterior approach.
downwards and laterally to
expose the sympathetic trunk and
the corresponding posterior ends
of the ribs. The sympathetic trunk
is divided just below the 3rd
thoracic ganglion. The proximal
divided end is drawn upwards
and all the rami communicantes
joining the 3rd and 2nd thoracic
ganglia are divided. Finally the
sympathetic trunk is divided just
below the level of the attachment
of rami communicantes to the
stellate ganglion. This operation
can also be performed above the
subclavian artery, which is
probably a better approach for the
short necked patients. But in that
case the thyrocervical trunk
should be divided between
ligatures for better exposure.
B. AXILLARY
APP­
ROACH.— The patient lies
supine with the arm abducted.
An incision, about 5 inches in
length, is made on the medial
wall of the axilla along the line of
the 2nd intercostal space. To reach
the intercostal space, the fibres of
serratus anterior have to be
divided, but generally the long
thoracic nerve lies a little
posterior to the incision and
hence less liable to be damaged.
The pleural cavity is opened and
rib-retractor is used. The lung is
drawn downwards and forwards
to expose the sympathetic chain
covered with parietal pleura. The
pleura is incised and the
sympathetic trunk is removed
according to necessity. Bleeding
vessels are secured. The lung is
inflated and the wound is closed
with an under-water seal
drainage.
C.
POSTERIOR
APP­
ROACH.— This is probably the
DISEASES OF ARTERIES
215
least popular approach for this operation. A vertical incision is made about 5 cm lateral to the
midline keeping the third rib in the centre. All muscles are divided to reach the ribs. 5 cm of
the posterior end of the 3rd rib along with the corresponding transverse process is excised
subperiosteally. The sympathetic trunk will be exposed and excised according to necessity. For
proper exposure, the 2nd and 3rd intercostal nerves may be required to be divided. The
convalescent period is much prolonged and the operation is a lengthy procedure. For this, scope
of its application is very much limited.
Complications.—
1. Main complication is perforation of pleura leading to pneumothorax.
2. On the left side, lymph fistula due to damage to the thoracic duct may occur.
3. Homer's syndrome, which is manifested by ptosis, myosis, enophthalmos and anhidrosis
of that half of the face, may occur if adequate precaution is not taken.
ACROCYANOSIS
It is a condition in which there is persistent but painless cold and cyanosis of the hands and
feet. Though this condition is often confused with Raynaud's syndrome, yet the italic words in
the first sentence are the distinguishing features from Raynaud's syndrome. The basic pathology
is the slow rate of blood flow through the skin due to chronic arteriolar constriction. This results
in a high percentage of reduced haemoglobin in the blood, in the capillaries and this is the cause
of cyanotic colour. In some patients endocrine dysfunction has been found.
This condition also affects young women. Coldness and blueness of the fingers and hands
are persistently present for many years. The extremities are never completely normal. With heat
the colour may change from deep purple to red. Episodes of blanching (which is a common
feature of Raynaud's phenomenon) is absolutely absent in this condition. The peripheral pulses
are usually normal (same as Raynaud's phenomenon). There are no trophic changes indicative
of chronic tissue ischaemia such as atrophy or sclerosis of the skin or ulceration.
Treatment.—
Avoidence of cold temperature and reassurance are often helpful. One may try vasodilator drugs.
If the condition does not respond to above conservative measures, sympathectomy may be
carried out with reasonably good results.
THORACIC OUTLET SYNDROME
The thoracic outlet syndrome is the collective name which includes (i) cervical rib syndrome,
(ii) scalenus anticus syndrome, (iii) costoclavicular syndrome, (iv) hyperabduction syndrome, (v)
pectoralis minor syndrome and (vi) first thoracic rib syndrome. The syndrome is caused by
compression of the brachial plexus or subclavian artery and/or vein in the region near the
thoracic outlet. The symptoms may arise from neural, vascular or combined compression.
Anatomy.—
The subclavian artery leaves the thoracic cage by passing over the first rib between the
scalenus anticus muscle anteriorly and the scalenus medius muscle posteriorly alongwith the
brachial plexus. It then passes under the clavicle and subclavius muscle to enter the axilla beneath
the pectoralis minor muscle. The subclavian vein passes anterior to scalenus anticus muscle and
is in intimate relation with the head of the clavicle and the most medial portion of the first rib.
A potential area of compression exists firstly in the interscalene triangle between the scalenus
anticus anteriorly, the scalenus medius posteriorly and the first rib interiorly. Distal to this area
is again a narrow space — intercostoclavicular space — between the clavicle and the first rib. In the
axilla where the pectoralis minor tendon is attached to the coracoid process, the axillary artery
A CONCISE TEXTBOOK OF SURGERY
216
may be obstructed where it
travels round the coracoid
process. During hyperabduction
the axillary vessels and the
brachial plexus are bent at an
angle of approximately 90° in this
area and are liable to be
compressed.
Aetiology.—
(i)
Cervical rib, which occurs
in approximately 1% of the
population, produces symptoms
in only 10% of cases. Symptoms
due to cervical rib are rare in
children, but are most frequently
seen in thin women in the 3rd
and 4th decades. Unusually well
developed musculature may
predispose to compression. Thin
women with long narrow necks
Fig.15.12.— Schematic diagram of the anatomy of thoracic outlet. may predispose to some variation
in the anatomy of the head and
neck. Gradual descent of the shoulder girdle perhaps from atrophy of the regional musculature
may cause onset of symptoms in the 2nd or 3rd decade.
(ii) A wide scalenus anticus muscle may narrow the space in the interscalene triangle and
may cause symptoms.
(iii) The width of the first rib is also of consideration as wider first rib may give rise to
symptoms.
(iv) Fractures of the clavicle or first rib, which produce subsequently bony callus, may lead
to small subclavian aneurysm, peripheral emboli and ischaemia of the hand.
Pathology.—
Compression of the brachial plexus usually affects its lower trunk (C8 & Tl). The ulnar nerve
is mostly involved.
Vascular symptoms may be intermittent from compression or temporary occlusion of the
subclavian artery. Claudication with exercise, pallor, sensation of coldness, numbness or
paraesthesia are the various vascular symptoms. If this condition continues, there may be
atheromatous changes in the artery or a post-stenotic aneurysm may develop. From these emboli
may be dislodged into the peripheral circulation and produce ischaemia of the fingers or hand.
Thrombosis of the .subclavian artery is a late and dreadful sequence.
Another group of vascular symptoms is due to intermittent vasoconstriction similar to that
seen in Raynaud's phenomenon. Unilateral appearance of Raynaud's syndrome should always gives
rise to suspicion of some pathology of thoracic outlet. The intricate cause is the presence of separate
sympathetic nerve for upper extremity. Usually sympathetic innervation of the upper extremity
is incorporated in the main trunks of the brachial plexus. But in only 10% of cases it comes from
a separate cord which is more prone to direct compression and irritation.
DISEASES OF ARTERIES
217
Sometimes venous hypertension of the upper extremity may result from intermittent
compression of the subclavian vein. Acute thrombosis of the subclavian vein may be a result of
thoracic outlet syndrome but the exact pathologic mechanisms are not clear.
Clinical features.—
The symptoms of thoracic outlet syndrome vary depending on whether nerves or blood vessels
or both are compressed. Majority of the patients are middle-aged females, although younger group
may be involved. Usually manifestations of compression of either nerves or the vessels dominate.
NEUROLOGIC SYMPTOMS are pain, paraesthesia and numbness usually in the fingers and
hands in the ulnar nerve distribution. Pain is of insidious onset and of general distribution. It
commonly involves the neck, shoulder, arm and hand. It may even radiate to the anterior chest
or posteriorly to the parascapular region. Paraesthesia and numbness are more specific in
distribution and mostly involve the cutaneous area supplied by C8 and T1 (ulnar nerve
distribution). Later on neurologic deficits in the form of sensory loss, motor weakness and atrophy
may develop.
SYMPTOMS OF ARTERIAL COMPRESSION are seen less frequently in about l/4th of the
cases. These include pain, numbness, paraesthesia, coldness and weakness of the arm or hand.
These symptoms are accentuated by exercise and exposure to cold. Distal embolization may
cause Raynaud's syndrome, which in late cases may produce digital ulceration and even gangrene.
The venous symptoms include oedema, venous distension, pain and cyanosis.
Physical examination.—
The signs of arterial compression may be evident by direct physical examination. There may
be differences in qualities of the pulses between the two arms when the subclavian, brachial and
radial arteries are compared.
Occasionally a subclavian and axillary aneurysm may be palpable in the infraclavicular area.
In mild forms of ischaemia one may find pallor on elevation of the arm. In more chronic
cases one may see atrophy of the skin, brittle nails or even focal ulceration.
In 5% of patients Raynaud's phenomenon can be induced by application of the cold to the
extremity.
Three diagnostic manoeuvres or tests can be applied for thoracic outlet syndrome. These are:
1. Adson's manoeuvre or test.— In this test the patient sits on a stool. The clinician feels his
radial pulse. The patient is now asked to inspire deeply, extend his head backwards and turn his
chin towards the affected side. Deep inspiration, extension of the neck and turning of the head
make the scalenus anticus muscle taut and may decrease or obliterate the radial pulse of the
affected side. The test is said to be positive if there is diminution or obliteration of the radial pulse
of the affected side.
2. Costoclavicular compressive manoeuvre or test.— Patient's radial pulse is felt. The patient
throws his shoulders backward and downward as an exaggerated military position. This will cause
reduction or disappearance of the radial pulse. This is produced by the compression of the subclavian
artery between the clavicle and the first rib. Simultaneously a subclavian bruit may be heard.
3. Hyperabduction manoeuvre.— Patient's radial pulse is again monitored. The affected arm
of the patient is now passively hyperabducted. This will cause reduction or disappearance of the
radial pulse due to compression by the pectoralis minor tendon. An axillary bruit can be heard
near the position of the pectoralis minor tendon.
In 10% of patients there may be signs of venous obstruction such as oedema and venous
distension.
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A CONCISE TEXTBOOK OF SURGERY
On auscultation one may get supraclavicular bruit.
In only 20% of patients there may be objective signs of nerve compression. The clinician
must examine the sensory system and the motor system thoroughly. Both fine sensation and
crude sensation, sensation of temperature and vibration should be tested. These will be diminished
along the medial aspect of the forearm and hand in case of nerve compression. Strength of the
muscles, particularly the intrinsic muscles of the hand innervated by the ulnar nerve, should be
tested. Muscle weakness or even atrophy is a late feature of nerve compression.
Different ial Diagnosis.—
A few conditions have to be differentiated from the thoracic outlet syndrome. These are :
1. Cervical spondylosis.
2. Cervical disc protrusion.
3. Cervical cord compression.
4. Pancoast's tumour.
5. Brachial neuritis.
6. Raynaud's syndrome or phenomenon.
7. Carpal-Tunnel syndrome.
Special Investigations.—
1. X-ray of the neck and chest.— This will demonstrate bony abnormalities e.g. cervical ribs,
bifid first rib, fusion of the first and second rib and clavicular deformities. This will also show
narrowing of the intervertebral foramina by exostosis or tumour.
2. Myelograms may be necessary to demonstrate protrusion of cervical disc or other causes
of cervical cord compression.
3. Arteriography.— This will diagnose arterial compression and exact location of it. One
may do the arteriogram while he is performing the Adson, costoclavicular and hyperabduction
manoeuvres. Arteriogram may occasionally demonstrate post-stenotic dilatation. When an
arteriogram is normal one should suspect neural compression.
4. Plethysmography may be used to know the arterial compression. By this technique one
can record changes in digit volume with each heart beat and can demonstrate obstruction of the
arterial flow.
5. Electromyographic studies may be performed to establish diagnosis of neural compression.
It is possible to detect sites of compression of peripheral nerves by recording the altered responses
of the distal muscles to proximal electrical stimuli. Nerve conduction times should be recorded
particularly through the ulnar nerve. Such conduction time will be significantly prolonged across
the thoracic outlet to the elbow and wrist. However, variability and unreliability of the nerve
conduction study have limited its usefulness in the diagnosis of thoracic outlet syndrome.
TREATMENT.—
In all cases, except those with complete vascular occlusion or poststenotic aneurysm,
conservative treatment should be given a trial.
CONSERVATIVE MANAGEMENT.— This consists of :
1. Weight reduction.
2. Exercise programme to strengthen the muscles of the shoulder girdle, particularly the
elevators. This will minimise the tendency of the shoulder to droop.
The above-mentioned conservative treatment relieves symptoms in 50% to 70% of patients.
Operation is only advised to those cases who do not respond favourably to this conservative
management.
DISEASES OF ARTERIES
219
OPERATIVE MANAGEMENT.— This is indicated to those, who do not respond to four or
more months of trial of conservative management.
Operative treatment includes (i) excision of the cervical rib, (ii) division of the scalenus
anticus muscle, (iii) resection of the clavicle and (iv) division of the pectoralis minor tendon.
(i) Excision of the cervical rib.— One of three incisions may be used for excision of the
cervical rib. These are (a) anterior supraclavicular incision, (b) posterior incision identical to that
used for an upper thoracoplasty and (c) transaxillary incision. See the treatment of cervical rib
later in this chapter for details of these operations.
If sympathectomy is indicated, the parietal pleura is stripped from the chest wall attachments
posteriorly and the sympathetic chain will be exposed for excision.
(ii) For scalenotomy operation anterior supraclavicular incision should be employed. For
further details of this operation, see page 226.
(iii) If the pectoralis minor tendon is compressing the neurovascular structures, division of
this tendon should be undertaken through the same transaxillary incision, at the same time the
first rib is resected.
Mild poststenotic dilatation of the subclavian artery usually does not progress once the
compression is relieved and frequently remains of no clinical consequence. However big aneurysm
of the artery should be excised and replaced with grafts, preferably vein graft.
Thrombosis of the subclavian artery should be treated by thromboendarterectomy or by-pass
grafting of the involved segment.
For venous compression, one has to divide the constricting bands which are merely extension
of the manubrial insertion of the stemomastoid muscle.
Occasionally the head of the clavicle may participate prominently in the compression, so that
it requires resection of the medial half of the clavicle. It is always recommended to do an operative
venogram to confirm that decompression operation has been successful. In extremely rare cases
one may find webs at the junction of the subclavian vein and internal jugular vein. This requires
venotomy and excision of the web with subsequent closure of the venotomy of the subclavian
vein.
BUERGER’S DISEASE (THROMBOANGIITIS OBLITERANS)
Buerger's disease was first described by Winiwarter in 1879, but it is Leo Buerger who
published in details this disease in 1908 and again in 1924. In reality, the classic syndrome
described by Buerger, is uncommon.
Definition.—
It is the inflammatory reaction in the arterial wall with involvement of the neighbouring vein
and nerve, terminating in thrombosis of the artery. Many cases diagnosed as Buerger's disease
are probably presenile atherosclerosis occurring in the 3rd, 4th and 5th decades of the life.
Incidence.—
The disease is found more frequently in men between 20 and 40 years of age. It is uncommon
in women, who constitute only 5% to 10% of all patients with Buerger's disease. This is more
common in the Jewish race.
Aetiology.—
A specific cause of this disease has never been demonstrated.
(i) There is a striking association with cigarette smoking and this disease. Usually 20 or more
A CONCISE TEXTBOOK OF SURGERY
220
cigarettes per day is required for this disease to occur. But it is obvious that there are so many
more smokers than patients with Buerger's disease.
(ii) There may be some hormonal influence which suggests the sex distribution. This disease
occurs rarely even in female smokers.
(iii) Patients with Buerger's disease usually come from lower socio-economic groups and they
often have poor hygiene. Fibrinogen levels are often elevated in these patients and a
hypercoagulable state has been postulated. Hyperaggregability of platelets has been reported.
(iv) Familial predisposition has been reported. A genetic factor is suggested as blacks are
rarely affected.
(v) Autonomic overactivity has also been suggested with severe peripheral vasospasm.
(vi) Recently an autoimmune aetiology has been postulated, based on the finding of both
antibodies and lymphocyte-mediated sensitivity to collagen in this disease.
(vii) There has been some association of this disease with Rickettsial disease.
It appears almost certain that some immunologic process, potentiated by cigarette smoking,
plays a major role in Buerger's disease.
Pat hology.—
An obvious inflammatory process features the Buerger's disease. The diseased artery is
usually surrounded by a dense fibrotic reaction which incorporates the adjacent vein and less
often the neighbouring nerve. This seems to be the characteristic of thromboangiitis obliterans.
The lesions in Buerger's disease are segmental and usually begin in arteries of small and
medium size. Both upper and lower extremities are affected in contrast to arteriosclerosis which
usually spares the upper extremities. In the lower extremities the disease generally occurs beyond
the popliteal arteries, starting in tibial arteries extending to the vessels of the foot. In the upper
extremities it is manifested by arterial involvement usually distal to the forearm in about 30% of
patients. Thromboangiitis has also been described in the G.I. tract, veins, lungs, heart etc.
Early in the course of Buerger's disease, the superficial veins are involved producing the
characteristic migratory, recurrent superficial phlebitis (but the larger and deep veins are seldom
affected).
The acute lesion consists of acute arteritis and periarteritis, acute phlebitis and periphlebitis.
The walls of the vessels are invaded by polymorphonuclear leucocytes. Thrombosis occurs within
the vessels with occlusion of the lumen. Giant cells are often present in the thrombus. Small
micro abscesses within the thrombus may characteristically present. These abscesses have central
foci of polymorphonuclear leucocytes. Only a segment of the vessel is involved, which may be
long or short.
In chronic lesion, the artery and the vein are bound together by fibrous adhesions. The nerve
may also be involved in the same adhesions. Involvement of the nerve is responsible for agonising
pain. The thrombus shows fibroblastic activity and endothelial proliferation. The thrombosis is
now organized into fibrous tissue. The internal and external elastic lamina of the artery are
frequently much thickened.
Clinical features.—
Thromboangiitis obliterans occurs almost exclusively in males between 20 and 40 years of
age. The typical patient is one who is a heavy smoker and had started smoking at an early age.
One should always suspect the diagnosis of Buerger's disease when a young male smoker presents
with peripheral ischaemia, particularly if the upper extremity is involved and if there is a history of
migratory superficial phlebitis.
DISEASES OF ARTERIES
221
SYMPTOMS.—
Due to the peripheral involvement, the
pedal arteries are affected earlier and the
patients complain of pain while walking at the
arch of the foot (foot claudications), somewhat
less often at the calf of the leg, but never at
the thigh or buttock (which is common in
atherosclerosis). In the upper extremity it is
the vessels distal to the wrist that are involved
so claudication is rare in upper extremity.
Pain is typical of intermittent claudication i.e.
pain is increased when the muscle is exercised
and disappears when the exercise stops.
Progression of ischaemia is similar to that
in all chronic progressive arterial occlusions.
Intermittent claudication progresses to rest
pain. Gradually postural colour changes
appear, followed by trophic changes and
eventually ulceration and gangrene of one or
more digits and finally of the entire foot or
hand requiring amputation.
Pain in Buerger's disease also results from
phlebitis and ischaemic neuritis. Gradually
rest pain is so intense that the patient cannot
sleep. Some amelioration may be achieved
by placing the affected limb in dependent
position. The limbs become rubor or red on
dependence and pallor on elevation.
One must remember of occasional involvement of the mesenteric or cerebrovascular
circulation. Symptoms may be complained of from this involvement.
Physical examination.—
INSPECTION.—
There may not be any specific finding till gangrene develops. The peculiar feature is that the
ischaemic area is usually sharply demarkated with relatively good circulation in adjacent tissues.
Before gangrene one may find signs of chronic tissue ischaemia. These include loss of hair from
the digits, atrophy of the skin and brittle nails. Gradually there may be ulceration or gangrene
of the toes commencing in the distal portion of the digit near the nail and gradually extend
proximally to involve whole of the foot or hand.
PALPATION.—
The most frequent finding is absence of posterior tibial and dorsalis pedis pulses in the feet.
Absence of the posterior tibial pulse is highly suggestive of the diagnosis especially when bilateral.
In the upper extremity the radial pulse may be absent and when bilateral it is also suggestive of
this disease.
Special Invesligations.—
ARTEFUOGF?APHY is obviously the most important investigating procedure. In arteriography,
A CONCISE TEXTBOOK OF SURGERY
222
it is the peripheral arteries which are first involved e.g. digital arteries or dorsalis pedis artery.
While the contours of large arteries are normal and smooth, there are abrupt areas of occlusion
in the arteries of the calibre of tibials, frequently surrounded by extensive collateral circulation
which has been typically termed the 'tree root' or 'spider legs' in appearance. A 'cork screw'
deformity has also been observed in peripheral arteries representing partial recanalisation of the
arteries previously occluded by thrombi.
So the characteristic arteriographic appearance of this disease is the smooth and normal appearance
of larger arteries in combination with the extensive occlusion of the smaller arteries alongwith extensive
collateral circulation.
Treatment..—
CONSERVATIVE TREATMENT has a great role to play in this disease.
(i) Every effort should be made to make the patient stop smoking. Indefinite remissions may
follow stoppage of cigarette smoking.
(ii) Various drugs have been tried with questionable value. This included vasodilator drugs,
anticoagulants, dextran, phenylbutazone and steroids. More recently prostaglandin therapy
(PGA-1) has been advocated to prevent platelet aggregation.
SURGICAL TREATMENT.—
(i) Role of sympathectomy is doubtful. Perhaps 50% of patients are significantly benefited
from this procedure. It has got a specific role in relieving pain.
(ii) Arterial reconstruction is also difficult as the distal arteries are usually involved. It may
be considered in rare cases where there is segmental proximal occlusion. Occasionally patients
with Buerger's disease develop atherosclerosis in major arteries. Such a combination may be
suspected if the popliteal pulse is absent. In these patients arterial reconstruction may be performed
on the atherosclerotic proximal arteries, which in fact causes marked circulatory improvement.
(iii) Microvascular transplantation of free omental grafts to areas not amenable to arterial
reconstruction has been successfully tried.
(iv) Amputation is the only way out when gangrene occurs. The approach is conservative
and lowest possible level should be chosen. When gangrene is confined to a toe, amputation may
be postponed, unless rest pain or infection is rather uncontrollable. Amputation should be limited
to the area of gangrene. When below-knee amputation can remove the gangrenous area, it will
not be justified to go for above-knee amputation.
Prognosis.— The risk of amputation is about 20% within 10 years after onset of symptoms.
Although this varies with the use of tobacco. In a few patients who stop smoking completely,
progression of the disease is greatly restricted.
CERVICAL RIB AND SCALENUS ANTICUS SYNDROME
Surgical Anatomy.—
The costal element may develop from the anterior part of the transverse process of the 7th
cervical vertebra. This may sometimes develop into a rib which is known as the cervical rib. In
extreme rare conditions one may find a 6th cervical rib.
Brachial plexus is formed by lower four cervical nerves (C5, 6, 7, 8) and the first thoracic
nerve. When there is a very small contribution from the first thoracic nerve (Tl), this condition
is known as prefixed brachial plexus. Cervical rib may accompany such condition. Sometimes the
brachial plexus receives a big contribution from Tl and also a small part of T2. This condition is
DISEASES OF ARTERIES
223
called postfixed brachial plexus. Such condition even with normal first thoracic rib, may cause
symptoms similar to a cervical rib.
Types of cervical ril>.—
It must be remembered that by mass radiography it has been found out that the cervical rib
(coming out from the 7th cervical vertebra) is present in 0.45% of all individuals. In more than
1/2 cases the cervical rib is unilateral. It is commoner on the right side.
Four types of cervical rib are usually found. These are :
1. Complete cervical rib.— Such rib articulates anteriorly (a) either with the manubrium
stemi or (b) with the first rib.
Incomplete varieties —
.
2. The cervical rib ends as a large bony mass.
3. The cervical rib ends tappering connected with a fibrous cord to the scalene tubercle of
the first rib.
4. There is no bony cervical rib, but its place is taken by a fibrous band which is incorporated
in the scalenus medius muscle. Obviously it cannot be demonstrated radiologically.
Pathology.—
The subclavian artery and the brachial plexus pass through a narrow triangle, termed the
scalene triangle, which is bounded anteriorly by the scalenus anterior muscle, posteriorly by the
scalenus medius muscle and inferiorly by the first rib.
When the cervical rib is present, the floor of the triangle is raised. Both the subclavian artery
and the lower trunk of the brachial plexus are raised. The lumen of the subclavian artery becomes
constricted. A small poststenotic fusiform dilatation occurs just distal to the constriction. Within
the dilatation clotting occurs on the intima and then thrombus is formed. Portions of this thrombus
may become detached and give rise to emboli. Sometimes, of course rarely, there may be proximal
extension of the thrombus, so that the opening of the vertebral artery may be involved leading
to cerebrovascular embolic episodes.
Due to presence of the cervical rib or due to postfixed brachial plexus, the lower trunk of the
brachial plexus is lifted up leading to compression of this trunk. Neurological deficiencies may
develop from such stretching or compression. Such deficiencies will be limited to the lower trunk
i.e. C8 and Tl distributions. Irritation of the periarterial sympathetic fibres or damage to the
sympathetic fibres content in the lower trunk will lead to vasomotor disturbances.
Sometimes there may not be only cervical rib or postfixed brachial plexus, but abnormally
well developed scalenus anterior muscle may elevate the first rib and compress on the subclavian
artery and the lower trunk of the brachial plexus to give rise to similar symptoms as those of
cervical rib. This is known as scalenus anticus syndrome.
Clinical features.—
Majority of the patients who present with symptoms of cervical rib and scalenus anticus
syndrome are women over 30 years of age. Slim women with long narrow neck are more
susceptible.
Various clinical types encountered with cervical rib are —
I.
CERVICAL RIB WITH NO SYMPTOMS.— As discussed earlier, while 0.45% of the
general population possess cervical rib, only a few come to the clinician with complaints. In fact
well formed cervical ribs (complete) on X-ray examination are usually without symptoms. It is
often the fibrous band or incomplete cervical rib which produces symptoms.
II. CERVICAL RIB WITH LOCAL SYMPTOMS.— Patients may present with symptoms
224
A CONCISE TEXTBOOK OF SURGERY
locally due to presence of cervical rib. They complain of pain and tenderness in the supraclavicular
fossa. On palpation a bony hard, totally fixed lump may be detected in the supraclavicular fossa.
This is obviously the cervical rib.
III. CERVICAL RIB WITH VASCULAR SYMPTOMS.—
(i) Pain.— It is a common symptom with cervical rib. It is mostly located in the forearm,
but sometimes it radiates to the upper arm. The pain is characteristic of intermittent claudication
i.e. pain appears with the use of the arm particularly when the arm is in raised position at the
time of exercise. The pain is relieved by rest. This pain is of ischaemic muscle.
(ii) The hand of the affected side is colder and paler than its fellow of the opposite side.
Sometimes the hand and the fingers may become cyanosed when it is dependent for long.
(iii) Numbness of the fingers is a very common complaint. In a long continued case there
may be ulceration or even gangrene of the fingers.
(iv) Radial pulse is sometimes as full as that of the other side. But if Adson's test is
performed or the arm is hyperabducted, the radial pulse may become feeble or even absent on
the affected side.
Sometimes a systolic bruit can be heard over the distal part of the subclavian artery.
IV. CERVICAL RIB WITH NEUROLOGICAL SYMPTOMS.— Neurological symptoms from
cervical rib is not that common. Usually the lower trunk of the brachial plexus i.e. C8 and Tl
segments are affected.
(i) Sensory disturbances may be detected along the medial aspect of the forearm, the
hand, the little finger and the medial aspect of the ring finger. Fine sensation may be lost. One
must test crude sensation, temperature sensation, vibration sensation in these parts.
(ii) Motor disturbances are also distributed along C8 and Tl. The muscles of the
hypothenar eminence and other small muscles of the hand supplied by the ulnar nerve are
usually affected. Weakness and in late cases wasting may be noticed.
Again it is emphasized that neurological symptoms are less common in cervical rib than
vascular symptoms. When a case is presented mainly with neurological symptoms alongwith
presence of cervical rib, one must exclude (i) pressure on the cervical roots in the region of the
intervertebral foramina, (ii) protrusion of intervertebral cervical disc, (iii) Carpal-Tunnel syndrome
or (iv) angulation of the ulnar nerve behind the elbow, before one comes to the conclusion that
the neurological symptoms are due to the cervical rib only.
Treatment.—
1. No symptom — no treatment.
2. CONSERVATIVE TREATMENT.— This is indicated in all cases as the first mode of
treatment. This is primarily aimed at strengthening the muscles of the shoulder girdle. Majority
of the symptoms are due to sagging down or drooping of the shoulder.
Conservative treatment includes —
(i) Use of a sling.
(ii) Physiotherapy and exercises to strengthen the muscles of the shoulder girdle and to
elevate the shoulder.
(iii) Certain analgesics.
(iv) The patient is instructed not to carry heavy weight like a bucket full of water, a heavy
shopping basket etc.
About 80% of cases are relieved of symptoms by this simple conservative management.
3. OPERATIVE TREATMENT.— Operation is advised —
DISEASES OF ARTERIES
225
(a) When conservative treatment fails.
(b) When there is vascular symptom.
(c) When there is neurological symptom.
OPERATIONS.—
A.
When cervical rib is present — extraperiosteal excision of the cervical rib together with
any bony prominence of the first rib is performed. The whole of the cervical rib must be excised
alongwith its fibrous band if present. Sometimes first rib is also excised when it is noticed that
it is compressing the subclavian artery or the post fixed brachial plexus. The periosteum of the
rib should also be excised, so that there is no chance of regeneration of the rib.
One should also perform scalenotomy i.e. scalenus anticus muscle is divided close to its
insertion.
Excision of the cervical rib.— One of the three approaches may be adopted for excision
of the cervical rib. Anterior approach is by far the most popular.
(a) ANTERIOR APPROACH.— Position.— The patient lies supine on the table. The neck is
extended by placing a sand bag between the patient's shoulders. The arm of the affected side is
drawn strongly downwards.
Technique.— The incision is made one inch above the clavicle starting in front from the
clavicular attachment of the stemomastoid muscle to the anterior border of the trapezius behind.
After incising the skin, superficial tissue and platysma, the investing layer of the deep cervical
fascia will be exposed. It is incised and the lateral border of the stemomastoid is retracted
medially to expose the scalenus anterior muscle lying behind the stemomastoid. When the scalenus
anterior muscle is exposed, a careful search should be made for the phrenic nerve, which lies in
front of the scalenus muscle but behind the prevertebral fascia. The subclavian vein is protected.
The phrenic nerve is protected and the insertion of the scalenus anterior to the first rib or into
the cervical rib, is divided. The knife edge is kept against the bone, so that the subclavian artery
is not injured. The brachial plexus is retracted gently downwards and forwards and the scalenus
medius muscle is defined. The fibres of this muscle, inserted into the cervical rib, are also divided.
The cervical rib is cleared off all attachments and the pleura must be safe-guarded. The rib is next
disarticulated from the transverse process of the seventh cervical vertebra or is divided as far
posteriorly as possible. The periosteum is never lifted off the cervical rib and it is excised along
with the periosteum.
(b) POSTERIOR APPROACH.— The incision is identical to that used for an upper
thoracoplasty. The subclavian vessels and the brachial plexus are easily exposed and are displaced
anteriorly. Cervical rib may be excised through this approach and this provides ample exposure
for reconstruction of the vessels if required.
(c) TRANSAXILLARY APPROACH.— The incision is made in the lower most portion of the
axilla from the pectoralis major anteriorly to the latissimus dorsi posteriorly. The incision is
deepened to the muscle of the chest wall. The serratus anterior and the intercostal muscles are
now exposed. The intercostobrachial nerve is saved. Dissection is continued upward and just
above the first rib one can see scalene muscles which are inserted to the first rib. The scalene
muscles are transected. The cervical rib is identified. Any attachment to the cervical rib is divided
and the cervical rib is removed in its entirety including the periosteum. If required the first rib
is also removed from the costochondral junction anteriorly to the posterior angle of the rib
posteriorly. The parietal pleura usually lies deep to the dissection. In case the pleura is punctured,
the puncture is closed around a catheter whilst the anaesthetist expands the lungs.
15
226
A CONCISE TEXTBOOK OF SURGERY
Scalenotomy.—
Position.— Same as that described for excision of the cervical rib.
Technique.— Incision is same as that applied for excision of the cervical rib. After the scalenus
anterior muscle is exposed, the phrenic nerve is protected and the insertion of the scalenus
anterior is divided from the first rib. After division of the scalenus anterior muscle the subclavian
artery and the brachial plexus will slide forward and will be relieved of compression. The
subclavian artery and the lower trunk of the brachial plexus should be examined carefully whether
they are really relieved of any stretching or compression. Sometimes the nerve trunk appears to
be stretched over the medial tendinous fibres of the scalenus medius. In this case these fibres
should also be divided.
B.
When there is no cervical rib — only scalenotomy is performed. A thorough search should
be made for presence of a fibrous band in the substance of the scalenus medius muscle or
neighbourhood. If this be present, it must be excised.
ACUTE ARTERIAL OCCLUSION
Sudden occlusion of an artery is commonly due to A. Emboli or B. Trauma.
Aetiology and Pathology.—
A.
Emboli.— The Greek word 'embolus' means 'something thrown in'. Two types of
embolization are seen — (i) cardioarterial embolization and (ii) arterioarterial embolization.
(i)
CARDIOARTERIAL EMBOLIZATION.— In about 90% of patients emboli in the lower
extremity originate in the heart. The main three causes are — atrial fibrillation, mitral stenosis
and myocardial infarction.
Atrial fibrillation is often seen in mitral stenosis cases. It may also occur from atherosclerosis
without mitral stenosis particularly in older patients.
With mitral stenosis emboli originate from thrombi which are formed in the left atrium because
of restriction of blood flow through the stenotic mitral valve. These patients may also have atrial
fibrillation which may be the cause of emboli formation.
In myocardial infarction emboli originate from mural thrombi which are formed over the
endocardial surfaces of the infarcts. Such embolization usually occurs in the first 2 to 3 weeks
following infarction.
Other rare causes of cardioarterial embolization are bacterial endocarditis and atrial myxoma.
Sites.— Majority of emboli which arise from the heart usually lodge in the arteries of the
lower extremities. These constitute more than 70% of cases. About 10% to 15% emboli lodge in
the superior extremity. About 10% of emboli lodge in the cerebral circulation intracranially.
Another 5% emboli lodge in the visceral arteries — the superior mesenteric, renal etc.
Emboli of the lower extremity usually lodge at bifurcation of major arteries where the diameter
abruptly narrows. The common sites according to frequency of occurrence are : at the bifurcation
of common femoral artery (about 35%), at the bifurcation of popliteal artery (15%), at the bifurcation
of the common iliac artery (14%), at the bifurcation of the aorta (10%). In the superior extremity
the commonest site is at the bifurcation of the brachial artery (about 10%), followed by axillary
artery near shoulder joint (4.5%).
Effects.— The result of arterial embolization is the immediate onset of severe ischaemia of the
tissues supplied by the involved arteries. If untreated, gangrene occurs in about 50% of cases
depending upon the artery involved. The peripheral nerves are very sensitive to oxygen deprivation.
DISEASES OF ARTERIES
227
Ischaemia in these peripheral nerves lead to
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arteries may originate from the atherosclerotic plaques in the abdominal or thoracic aorta.
Sometimes progressive ischaemia occurs which terminate to gangrene or repeated embolic episodes
are seen with almost complete recovery between the episodes.
B.
Trauma.— Arterial trauma may cause acute arterial occlusion. Most arterial injuries
result from penetrating wounds which partly or completely disrupt the walls of the arteries.
Penetrating injuries may be associated with fractures in the adjacent bones which cause arterial
blockage.
Most arterial injuries are either lacerations or transections of the arterial wall. Less common
injuries are arterial contusion with thrombosis. Rarer causes may be simple spasm of the arterial
wall in association with fractures and/or extensive soft tissue injuries from blunt trauma. Very
occasionally arteriovenous fistula may develop. Sometimes swelling of the surrounding soft tissues
may cause blockage of the artery within the fixed fascial compartments, which are known as a
compartmental syndrome (see above).
Clinical features.— There is nothing specific in the local clinical symptoms and signs of
arterial embolism that distinguishes it any way from other causes of acute limb ischaemia, as
mentioned above.
The best way to distinguish between arterial embolism and other causes of acute limb
ischaemia is to take proper history and to examine the rest of the patient. Valvular heart disease
and recent myocardial ischaemia account for majority of causes. Presence of atrial fibrillation
should always give rise to the suspicion of cardio-genic embolism.
.
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228
The 5 'P's are the best way to describe the clinical presentation of acute arterial occlusion.
The 5 'P's are — Pain, Paralysis, Paraesthesia, Pallor and absent Pulses.
The onset is almost always abrupt, very rarely it may be gradual. In 80% of cases there is
severe pain referred to the most peripheral portions of the limb. Alongwith the pain, the colour
of the affected extremity becomes extremely pallor or mottling due to alternate areas of pallor
and cyanosis, Neurologic symptoms carry a prognostic value. If motor and sensory functions are
intact, the extremity will survive. In majority of cases there may be some sensory disturbances
which vary from paraesthesia to anaesthesia. Paralysis, either partial or complete may occur in
this condition. Sometimes paralysis with anaesthesia may elude the clinician to divert his attention
towards neurologic disease.
PHYSICAL EXAMINATION.—
Inspection.— The affected extremity looks pale with collapsed peripheral vein.
Palpation.— Local temperature is cold below the site of lodgement of embolus. This temperature
level should coincide with the colour changes.
Palpation of arterial pulse is the most important examination to know the site of obstruction.
The pulse of the main artery if traced down, suddenly the pulsation will be lost at the point of
obstruction. There may be a tender small swelling. It should not be too difficult to determine the
level of occlusion. The guides are palpation of pulses, colour change and temperature change. It
must also be noted that at the site of lodgement of embolus the artery feels firm and often tender.
For practical purposes this means that if the common femoral pulse is absent, the embolus is
either lodged there in which case the artery becomes firm and tender or higher up most probably
in the common iliac in which case the femoral artery is soft and non tender. Similarly the
popliteal pulse becomes absent and the artery is tender when the embolism is within it. Sometimes
the popliteal pulse is full and bounding, even stronger than the normal side. This happens when
a small embolus impacts at the bifurcation of the artery below the level of the knee. The pulse
can usually be traced down to the point where it meets the obstruction; here there is often a
tender small swelling and the pulse is lost.
However the level of ischaemia does not correspond to the level of site of occlusion. An iliac
embolus produces ischaemia at the level of the hip joint, while a common femoral embolus
produces ischaemia distal to the knee. These of course vary with the effectiveness of the collateral
circulation. Palpation of muscle is important. In the early stage a doughy sensation is felt on
palpation. The importance of this feeling is that when the muscles are soft the extremity can be
salvaged with effective embolectomy, regardless of how long the embolus has been present. With
continuing ischaemia, the muscle progresses to necrosis and finally to rigor mortis, at this time
the muscles feel stiff. Palpation of stiff muscle means the necrosis has occurred. At this time
effective embolectony is not possible.
The most important aspect of physical examination is the cardiac examination, which should
not be missed.
Special Investigations.—
As soon as the patient is examined and the diagnosis is made, a critical decision is to
whether an angiography should be performed or not. If performance of angiography delays
operation beyond 4 to 6 hours of 'golden period', it should be omitted. Intraoperative angiography
is alternative, which is particularly useful where the site of embolus is uncertain.
.
E.C.G. and Chest X-ray should be performed to evaluate the presence of cardiac diseases.
DISEASES OF ARTERIES
229
TREATMENT.—
A. FOR EMBOLUS.—
Arterial embolectomv is the treatment of choice and it should be performed as early as
possible, at least before 4 to 6 hours to prevent muscle necrosis, however it does not guarantee
that claudication will not subsequently develop in the extremity.
As soon as the diagnosis is confirmed and the decision for operation is taken, Heparin, 5000
to 10000 units is given intravenously by continuous I. V. drip.
Some surgeons recommend administration of large doses of Heparin to promote lysis of
emboli and thereby improve the chances of operative success. 30000 units of Heparin is
administered intravenously as a bolus followed by doses of 2000 to 3000 units per hour by
continuous I.V. drip. If clinical improvement occurs, operation may be deferred.
OPERATIVE TECHNIQUE.— For operations on the extremities, local anaesthesia is preferred
in seriously ill patients. Only when the patient is clinically well and the anaesthetist or cardiologist
gives his approval, a general anaesthetic should be considered.
With the lower limb fully prepared and toweled as for a varicose vein operation, a longitudinal
incision is made over the common femoral artery. There is no place for cosmetically pleasing
skin-crease incision in this operation. The femoral vascular sheath is opened and more local
anaesthetic may be needed. The common femoral artery is gently freed from its bed using a
curved forceps e.g. Moynihan's cholecystectomy forceps and a tape is passed under it to lift the
artery. First 1 inch or so of the superficial femoral and the origin of the profunda femoris are
cleared sufficiently to permit the application of bulldog arterial clips. At this stage, 5000 units of
Fig.15.15.— Arteriography showing embolization of the popliteal artery in the first figure. Second figure shows
good arterial flow following embolectomy operation.
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A CONCISE TEXTBOOK OF SURGERY
heparin may be given intravenously or preferably into the pulsating proximal part of the femoral
artery, particularly if heparin is not given earlier. With the arterial sling tape, a short incision is
made over the common femoral artery, where the embolus is lodged. The embolus characteristically
pops out as soon as the lumen is entered. It is removed. It may be followed by a brisk spurt of
arterial blood, then the proximal clamp is applied with a curved Crafford coarctation clamp. The
distal thrombus is then removed with the Fogarty balloon catheter. Usually No. 5 or 6 is used. With
the balloon deflated, the lubricated catheter is passed through arteriotomy as far as possible
down the main artery. The balloon is gently inflated till resistance is felt in the syringe. The
catheter is now gently withdrawn adding slightly more saline to the balloon as the artery size
increases proximally. A long coiled black thrombus with paler pieces of embolus will then emerge
from the arteriotomy. Several passes may be needed to remove all possible thrombus and to
achieve back-bleed of arterial blood. The same manoeuvre is then repeated down the profunda
femoris artery. Each artery is clipped with a soft bulldog clamp.
If there is larger proximal thrombus, with the removal of the embolus, no spurt of arterial
blood will be seen. In this case the Fogarty catheter is inserted upwards through the arteriotomy
with the distal femoral clipped. It is passed upwards for at least 25 cm. The balloon is inflated
and the catheter is gently pulled down. Portions of the embolus and thrombus alongwith a gush
of arterial blood under full pressure will emerge through the arteriotomy. More than one pass
may be necessary.
Arteriotomy is closed with 5/0 arterial suture preferably prolene. The distal clamps are
removed first and any leaks detected is secured with further interrupted sutures. It is preferable
whenever possible not to reverse the action of Heparin at this point to aid removal of stasis
thrombus from the smaller branches.
In some complicated cases, not all of the thrombus may be removed via the common femoral
arteriotomy. In this case a medial approach to the popliteal artery below the knee and sometimes
the posterior tibial artery at the ankle may be required to be opened for full clearance of extensive
or adherent thrombus from these areas.
In late cases with doubtful limb viability and established muscle contracture, revascularization
of the limb may bring about profound metabolic acidosis from ischaemic areas. Infusion of
sodium bicarbonate solution systemically 100 mol or more should be required. Otherwise a
cardiac arrest may occur.
As with all ischaemic cases, there is risk of anaerobic infection it is advisable to give a
preventive large dose of penicillin.
In the postoperative care, the most important aspect is to see that the peripheral circulation is
adequate. Palpation of arterial pulses is the best clinical sign. Pulses which are difficult to feel can
be checked with the doppler instrument. The mode of heparin administration is important. Some
surgeons do not give heparin for 6 hours postoperatively and then to administer it by intermittent
intravenous injection in doses of 5000 units every 6 hours. Oral therapy with Coumarin derivatives
is started after 4 days and continued as long as the patients are at risk. Later on attention should
be given to the heart problems to cure these.
Intra-arterial thrombolysis.— When the ischaemia is not so severe that arterial
embolectomy is mandatory, it may be possible to treat either the embolus or thrombosis by
intra-arterial thrombolysis. Firstly an arteriography is performed and the occlusion is noted. A
narrow catheter (5F gauge) is passed into the occluded vessel and left embedded within the
clot. A thrombolytic agent is now infused for several hours. Heparin 250 units per hour is also
DISEASES OF ARTERIES
231
added to the infusing material. The common thrombolytic agents used are streptokinase,
urokinase and tissue plasminogen activator (TPA). Today TPA is mostly used because of its
relative rapidity of action. It has also least allergic side effects. Angiograms are carried out at
regular intervals to know the extent of lysis. The method is abandoned when there is no further
dissolution of clot. The main contraindications of this technique are recent stroke, bleeding
diathesis and pregnancy.
B. FOR ARTERIAL TRAUMA
The treatment is operation and depends on the type of injury to the artery. If a portion of
the arterial wall is damaged, it can be repaired with a vein patch. If the artery is through and
through divided, end-to-end suturing is the best method. If a portion of artery is contused or
lacerated, this segment should be removed and an attempt is made for end-to-end anastomosis.
If the loss of artery is more than 2 cm, direct anastomosis cannot be performed. In this case
autogenous vein graft in the form of reversed long saphenous vein is mostly used.
Ligation of an injured artery should be performed only in case of injury to the minor arteries
such as the radial or ulnar artery, neither of which is essential for limb survival provided one of
these remains uninjured.
Fat Embolism.—
It occurs after major bone fractures e.g. fracture femur, fracture tibia and fibula or in multiple
fractures. It usually occurs in 24 to 72 hours.
Pathogenesis.— It occurs from aggregation of chylomicrons derived from bone marrow.
Clinical features.— Manifestations can be described under following heads —
Cerebral.— Restlessness, disorientation, constricted pupil, drowsiness, pyrexia and ultimately
coma.
Cutaneous.— Petechial haemorrhages in the skin.
Pulmonary.— Tachypnoea, cyanosis, right heart failure, fat droplets in sputum, froth in the
mouth and nostril and finally respiratory failure.
Kidney.— Blockage in renal arteriole causing renal failure. Fat droplets in urine.
Retina.— Emboli in the retinal artery causing haemorrhages in retina detected in fundoscopic
examination.
Management.—
•
•
•
•
Ventilator support.
Heparinization.
Hyperbaric oxygen.
Low-molecular weight dextran.
Air Embolism.—
Causes.—
• Commonest cause is through I.V. drip.
• From traumatic opening of major veins suctioning air inside.
• During fallopian tube insufflation.
• During surgeries of neck and axilla.
• During antifungal pneumothorax.
About 50 ml air should be sucked in to cause air embolism. First air enter the right atrium where
it gets churned to form a foam which enters the right ventricle and blocks the pulmonary artery.
Clinical diagnosis can be made by hearing Mill-wheel murmur over the pericardium by
stethoscope.
A CONCISE TEXTBOOK OF SURGERY
232
Management.—
• Patient is placed in Trendelenburg position. A needle is introduced into the right ventricle
to aspirate air. If this is not sufficient open thoracotomy is performed to aspirate air completely
which is responsible to cause the block.
Therapeutic embolization.—
Indications.—
• To arrest haemorrhage in G.I. bleeding, urinary bleeding etc. Embolization of
gastroduodenal artery or left gastric artery in duodenal ulcer bleeding or gastric ulcer bleeding
respectively. It is also used in bleeding from oesophageal varices.
• In haemangiomas.
• In case of malignancies e.g. hepatoma, renal cell carcinoma etc.
• AV fistulas.
Materials used for therapeutic embolization.—
•
•
•
•
•
•
•
Gel foam.
Quick setting plastics.
Plastic microphones.
Wool.
Ethyl alcohol.
Stainless steel coils.
Blood clots.
Decompression Disease or Caisson’s J )isea.se.—
This condition develops from rapid decompression when an individual travels by air or goes
to high altitude or when deep sea divers come to the surface. In this case bubble of nitrogen
blocks the small vessels.
Clinical features.—
• When lung vessels are affected, chest pain or tightness or choking is complained of.
• In case of spinal cord vessels ischaemia causes neurological deficit.
• When vessels of muscles and joints are affected — it causes tremendous pain.
Treatment.—
• Instead of sudden decompression, gradual decompression is followed.
• Oxygen therapy.
GANGRENE
Definition.— Gangrene is death of a portion of the body with putrefaction. It must be
remembered that gangrene is not just necrosis or infarction, but in every case of gangrene there
should be infection with saprophytic putrifying bacteria which add rottenness to death of the part.
Types of gangrene.— There are two types of gangrene — 1. Dry gangrene and 2. Moist
gangrene.
1. DRY GANGRENE.— The characteristic features are —
(i) The part is gradually deprived of its arterial blood supply.
(ii) There is characteristic colour change — first greenish and finally black due to
haemolysis of the red blood corpusles. The term 'mummification' is applied to such dry and
shrivelled foot, which is exactly like that of a mummy.
(iii) There is mainly arterial occlusion, but the venous outflow remains unimpeded.
DISEASES OF ARTERIES
233
(iv) Occlusion of the artery is by a chronic process e.g. atheroma with superadded
thrombosis or due to an acute process e.g. embolus or ligation of one of the main arteries,
(v) There is a definite bright red line of separation appears between the living and dead
tissue. This line indicates a process of inflammation due to the contact of the dead with the still
living tissue. There is dilatation of vessels and an exudation of leucocytes. As the blood supply
of the skin and subcutaneous tissue is less abundant than that of the muscles and bone, destruction
of former will proceed further up the limb than that of the latter, so that the resulting stump will
be conical in form.
(vi) The conditions which produce dry gangrene are senile gangrene, diabetic gangrene,
Buerger's disease, Raynaud's disease, sudden vascular occlusion e.g. embolism, ligation or injury
to the vessel, frostbite and due to escharotics (strong acid or alkalis).
2.
MOIST GANGRENE is characterized by moist and oedematous limb, with colour
changes which vary among dark red, green, purple and black owing to sulphurated hydrogen
produced by the putrefactive bacteria acting upon the liberated haemoglobin due to haemolysis
and with horrible odour, which is partly due to nitrogenous products such as indol and skatol
and partly due to nonnitrogenous products e.g. sulphurated hydrogen, butyric acid and lactic acid.
The characteristics of moist gangrene are —
(i) When the vein is obstructed, so that no blood can leave the part. No fresh blood can
enter, so liquifaction and bacterial infection occur to cause moist gangrene.
(ii) The part is cold, pulseless, swollen and oedematous. The colour also changes in this
condition. The skin becomes raised into blebs which contain foul smelling fluid.
(iii) It is characterized by horrible odour.
(iv) There is little attempt at formation of a line of demarcation.
(v) Constitutional symptoms are always grave, which are almost absent in dry gangrene.
(vi) The principal conditions, which may give rise to moist gangrene, are gangrene from
acute inflammation, long-standing venous thrombosis, bed sores and gas gangrene.
Separation of gangrene.— There is always a natural attempt by the living tissue to get rid
of the dead tissue. Due to this a zone of demarcation is usually formed between the living tissue
and the dead or gangrenous part. This is due to the development of a layer of granulation tissue.
These granulations extend into the dead tissue. Ulceration follows and as the zone of demarcation
gradually becomes deeper, a final line of separation forms which separates the gangrenous part
from the living tissue.
In dry gangrene, the final line of demarcation appears in a few days and separation begins to
take place perfectly. The soft tissues are separated quickly, but the bone takes much longer time
to separate. As mentioned earlier the blood supply of the skin and subcutaneous tissue is less
abundant than that of the muscle and bone, so the line of separation appears in a conical manner.
In moist gangrene, there is little attempt at formation of actual line of separation due to more
infection and the disease spreads very rapidly up the limb. So dry gangrene is better than moist
gangrene and every effort should be made to convert moist gangrene to the dry gangrene.
Dry Gangrene
• Dry, shriveled, mummified.
• Occurs due to slow and gradual
loss of blood supply.
Moist Gangrene
• Oedematous, putrified and dis­
coloured (due to H2S).
• Occurs due to sudden loss of blood
supply.
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• Clear line of demarcation is present.
• Cannot extend proximally above
the line of demarcation.
• Causes are mainly atherosclerosis,
thromboangiitis obliterans.
• Treatment is a limited amputation.
• Line of demarcation is vague.
• Extends proximally rapidly.
• Causes are mainly emboli and
trauma leading to acute occlusion.
• Treatment is high amputation.
CAUSES OF GANGRENE
A. Arterial occlusion.—
1. Atherosclerosis (Senile gangrene); 2. Embolism (Embolic gangrene); 3. Raynaud's
disease; 4. Buerger's disease; 5. Cervical rib; 6. Syphilitic gangrene (due to endarteritis obliterans).
B. Venous obstruction.— Deep vein thrombosis.
C. Nervous diseases.—
1. Syringomyelia; 2. Tabes dorsalis; 3. Peripheral neuritis; 4. Hemiplegia; 5. Paraplegia;
6. Leprosy.
D. Traumatic gangrene.—
1. Direct injury to the main artery; 2. Indirect injury (crushing of the tissues or fractures
when bone fragments press on the main artery).
E. Infective gangrene.—
1.
Carbuncle; 2. Cancrum oris; 3. Postoperative progressive gangrene following drainage
of empyema and appendicectomy; 4. Gangrene of the scrotum (Fournier's gangrene ); 5. Gas
gangrene.
F. Diabetic gangrene.— This should be considered as a separate group as one or more
of three factors viz. arterial occlusion, infection and peripheral neuritis play simultaneously to
cause gangrene.
G. Physical gangrene.—
1.
Heat — bums and scalds; 2. Cold — frostbite; 3. Eschartics (corrosive) — acids and
alkalis; 4. Electricity; 5. X-ray (irradiation).
Special Investigations.— These are almost similar to those of chronic arterial occlusion
which have been discussed earlier.
TREATMENT.
General treatment.— This includes nutritious diet, control of diabetes, relief of pain and
care of the heart.
Local treatment.—
CONSERVATIVE TREATMENT.—
Care of the affected part.—
(i) The part should be kept dry. An attempt should always be made to keep dry gangrene
as dry as possible and try to convert moist gangrene into dry gangrene. Exposure of the part and
use of fan may help in keeping the part dry.
(ii) The part may be kept elevated, which will reduce pain.
(iii) The part should not be heated.
(iv) The part should be protected particularly the local pressure areas e.g. the heel, the
malleoli, the ball of the toes etc. Otherwise patches of gangrene may develop in these areas. A
bed-cradle, padded or Sorbo rings, foam may be used as preventive measures.
DISEASES OF ARTERIES
235
(v)
The gangrenous part should be carefully observed and toileted e.g. lifting of the crust,
removal of hard or desiccated skin, release of pus etc. Paring of nails should be done carefully,
as carelessness may increase infection in the gangrenous part to make it a moist gangrene from
the dry one.
SURGICAL TREATMENT.—
1. Sympathectomy.— See chapter 18.
2. Amputation.— It has two aspects —
(i) Limb-saving aspect.— Amputation may be required when gangrene has developed.
But a conservative approach should be adopted. With arterial disease, sympathectomy or direct
arterial surgery may more limit the extent of amputation. Thus a major amputation may be
avoided.
(ii) Life-saving aspect.— In case of a badly crushed limb or a rapidly spreading moist
gangrene and in gas gangrene, amputation is required to save life of the patient.
For further description of amputation, see chapter on 'Amputation'.
3. Direct arterial surgery.— When gangrene has developed from chronic occlusion of artery
due to atherosclerosis, it has a place. Revascularization of the limb may heal the gangrene or at
least considerably limit the level of amputation. In embolism or thrombosis also it has a definite
place in the form of embolectomy or thrombectomy. However in Buerger's disease or Raynaud's
disease it has no place.
DIABETIC GANGRENE
The diabetics possess distinct problems, which make their limbs more liable to gangrene
formation. Mainly three factors play major roles —
1. Sugar laden tissues of the diabetics lower their resistance to infection. So these patients
are more susceptible to infection. After a trivial injury to the toe, sole of the foot or the heel,
within hours or days a virulent necrotising infection may appear which spreads along the musculofascial planes. The infecting organism may often be gas producing of the Clostridial group.
Although any type of infection may occur including fungal infections.
This susceptibility to infection manifests itself in the development of carbuncles in the neck
and in different types of necrotising infections of the abdominal wall after elective abdominal
operations.
2. The second most important factor is liability of formation of atheroma in the arteries of
the diabetic patients. It is very much known that 60% of deaths of diabetics take place from
cerebral haemorrhage as a result of atherosclerotic changes in the cerebral arteries. In the lower
limb however arterial occlusive disease mainly involves the popliteal artery and its branches
down to the pedal arches. Arteries proximal to the popliteal are usually non-affected or if affected
show non-diabetic type of atherosclerosis.
3. The 3rd peculiarity of the diabetes is diabetic neuropathy. This impaires sensation and
thus involves the lower limbs to more injuries and infections. As a result of this the pressure
areas of the foot e.g. the heel, ball of the foot become complicated by trophic ulcers. Due to
neuropathy muscular involvement may also be seen in the form of loss of reflexes and deformities.
The feet may be splayed and deformed. Thick callosities may develop in the sole and if attended
by amateur chiropody, it favours entry of infection.
Clinical features.—
. • Pain and ulceration of foot.
A CONCISE TEXTBOOK OF SURGERY
236
• There may be loss of sensation.
• Peripheral pulse may be absent.
• Change of colour and temperature where gangrene is impending.
• There may be abscess formation.
Both dry and moist types of gangrene are seen in diabetics.
Dry gangrene occurs more frequently in old diabetic patients. Dry gangrene is only possible
when infection factor is minimum and occlusive factor is maximum. The gangrene slowly
progresses with a line of demarcation.
Moist gangrene is more often seen in young diabetics. Infection plays a major role to form this
type of gangrene, which is very much spreading and often lethal.
Sometimes trophic ulcers are seen at the pressure sites usually at the metatarsal heads
particularly over the first or third metatarsal head. Often
these ulcers are completely anaesthetic and hence
painless. Secondary infection is very common.
Meggitt’s classification of diabetic foot.—
Grade 0 — Foot pain only.
Grade 1 — Superficial ulcer of foot.
Grade 2 — Deep ulcer of foot.
Grade 3 — Ulcer with bone involvement.
Grade 4 — Forefoot gangrene.
Grade 5 — Whole foot gangrene.
Special Investigations.—
•
•
•
•
•
•
Blood sugar and urine ketone bodies estimate.
Blood creatinine estimation.
Pus should be sent for culture and sensitivity.
Doppler study to know arterial patency.
Angiogram to know any arterial blockage.
X-ray if osteomyelitis is suspected.
Treatment.—
CONSERVATIVE TREATMENT.—
• Diabetes should be controlled by drugs and
insulin.
• Vasodilators, dipyridamole, pentoxiphylline, low
dose aspirin etc.
• Care of foot — avoid injury, keep it clean and dry
particularly toe webs.
• Micro Cellular Rubber (MCR) foot wear may be
used.
• When there is infection, antibiotics should be
prescribed.
Fiq.15.16.—
Diabetic arteriosclerotic
3
* a. m *
Problems of diabetic foot.—
„ ,,
.,
* Callosities followed by ulceration.
J
gangrene involving the right great toe. Note
the trophic ischaemic chants in the toes
and foot.
.
* Abscess and cellulitis of foot,
* Diabetic wet gangrene.
DISEASES OF ARTERIES
237
• Osteomyelitis affecting different bones e.g. calcaneum, cuneiforms, metatarsals.
• Arthritis of joints.
SURGERY.—
Infection.— In many cases infection with Clostridia may necessitate immediate guillotine
amputation through the mid-leg or mid-thigh to prevent death from septic shock. In early cases
of course wide spread incision and drainage with debridement of the wound should be performed.
Careful localized debridement combined with intensive antibiotic therapy has often been successful
in saving the limb. The most important aspect of such debridement is removal of all necrotic
tissues. Inadequate debridement leaving deep necrotic tissues is the main cause of failure of this
technique.
Occasionally radical debridement combined with arterial reconstruction of the tibio-peroneal
artery may save the limb from almost inevitable amputation.
If gangrene has set in amputation may be required. Level of amputation will depend on level
of skin changes and Doppler study.
Trophic ulcers.— These trophic ulcers are sharply demarcated, punched out areas on the
sole of the foot found in diabetics. Treatment consists of local cleansing, protection from trauma
and avoidence of weight bearing. Care of the foot is extremely important and all possible methods
should be adopted to prevent entry of infection.
If superimposed infection occurs, the treatment is local debridement with proper antibiotic
administration.
Gangrene.— Localized dry gangrene of a toe is best treated by postponing operation and
allowing autoamputation to take place over a period of weeks. Sometimes collateral circulation
may develop during this period to permit healing of gangrene.
If spreading gangrene takes place, amputation should be called for. So far as the level of
amputation is concerned, conservative approach should be taken depending on conditions of
peripheral pulses and arteriographic picture.
Role of sympathectomy is very limited in case of diabetic gangrene.
BEDSORES
It is also called decubitus ulcer. This is so called, as this ulcer appears on the points of pressure
when a patient is long bed ridden. Though in majority of old patients who are bed ridden for
a considerable period, bedsores may invariably occur, yet there are a few predisposing factors
which cause bedsores earlier than expected time.
These factors are — (i) sensory loss of the part, (ii) malnutrition, (iii) moisture, (iv) anaemia
and (v) improper nursing.
Before formation of bedsore the area becomes red and if the change of colour persists, the
centre of the area gives way to initiate formation of bedsore.
Treatment.—
PREVENTION.— All possible methods should be adopted to prevent formation of
bedsores. These bedsores usually form over the bony prominences. The methods to prevent
bedsores are —
(i) Frequent change of posture 2 to 4 hourly is important.
(ii) The part should always be kept dry with powder. If there be soakage of the area with
sweat, urine or faeces, the part should be immediately dried followed by sprinkling of powder.
(iii) A ripple bed or water bed has now been introduced to prevent bedsore.
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A CONCISE TEXTBOOK OF SURGERY
(iv) P.V.C. blocks, foam or sheep skin may be used to protect the pressure points.
(v) Adhesive film e.g. Opsite may be used to prevent soakage of the part.
(vi) Aerosol silicone spray may also be used to keep the part dry.
(vii) The haemoglobin of the patient should be maintained at a normal level. Transfusion
of blood or packed cell may be required.
SURGICAL TREATMENT.— Only when the patient is young and otherwise healthy, operative
treatment may cure the condition. Excision of the ulcer followed by flap pedicle skin grafting is
required.
FROSTBITE
This condition occurs due to exposure to cold. This is mainly seen in the climbers and
explorers. It is sometimes seen in elderly debilitated individuals when exposed to very cold
climate.
.
Experimentally it has been demonstrated that freezing begins in the mammalian tissues
when the temperature in the deeper parts reaches 10°C and at -5°C the cells gradually become
frozen. Frostbite only occurs due to prolonged exposure to very cold weather as happened in case
of explorers in high altitudes. A different form of frostbite is produced due to acute exposures
to below 0°C, which is called 'high altitude frostbite', in this case ice crystals deposit on the
tissues.
Pathology.— The severity of frostbite has been grouped into 4 clinical types :—
(i)
In first degree frostbite there is oedema and redness of the affected part, (ii) In 2nd degree
there is formation of blisters, (iii) In 3rd degree there is necrosis of the skin, (iv) In 4th degree
there is gangrene of the extremity which requires amputation.
The basic pathology is vasospasm and damage to the vessels walls in the form of vascular
occlusion. This causes sludging of blood and wide spread thrombosis. This is followed by capillary
permeability. With rewarming there is formation of oedema.
Treatment.— Rapid warming of the tissue is the most important aspect of treatment. The
frozen tissue should be placed in warm water with a temperature of 40 to 44°C. Complete
rewarming usually takes 20 minutes. Care must be taken not to use higher temperature which
may cause gangrene instead of being beneficial.
Following rewarming the injured part is elevated to minimise formation of oedema. The
patient should be kept in a sterile environment. Blisters may be opened and necrotic skins are
removed. Antibiotic therapy and tetanus antiserum are given routinely to minimise risk of infection.
Use of intra-arterial vasodilator has markedly improved vasospasm in this condition.
Angiography may be performed to know the extent of vascular stenosis and degree of
functional vasospasm. Fast-acting vasodilator e.g. papaverine has been used with success.
Sympathectomy has been proved beneficial if it is performed within first few days. It should
not be performed too early as it may accelerate oedema formation. If sympathectomy is performed
following pick intensity of oedema, it helps in absorption of oedema and to minimise tissue
necrosis.
If thrombosis is the major problem, heparin or dextran may be used to lessen the degree of
small vessel thrombosis.
Demarcation of gangrene areas should be carefully observed for several weeks before
amputation is performed.
DISEASES OF ARTERIES
239
AINHUM
Nothing much is known about this disease. It is more often seen in male Negroes who were
always barefooted since childhood. Ainhum is also reported in countries of Central America and
the East.
The characteristic feature is appearance of a fissure at the level of the interphalangeal joint
of a toe. This fissure takes the form of a fibrous band and encircles the digit, which becomes
gradually necrotic. The most frequently affected toe is the 5th toe, which is followed in order of
frequency by the 4th, 3rd, 2nd and great toe. Sometimes the condition may be bilateral and
occasionally more than one toe may be involved.
Arterial pulsations are usually normal.
Treatment.— In the early stage when the toe has not been necrosed, longitudinal incisions,
one on the medial side and another on the lateral side may be performed through the constricting
band to release it. Z-plasty may be performed instead to relieve constriction.
When the digit becomes necrotic, amputation is the only treatment performed through the
constricting band.
ENDOVASCULAR SURGERY.—
This means surgery within the vessel. Mainly this is applied in case of peripheral vessels e.g.
femoro-popliteal, coronary, cerebral, renal etc.
Varieties.—
• Endovascular atherectomy.
• Endovascular grafts e.g. PTFE, Decron etc.
• Balloon angioplasty.—This method is particularly applied in case of short segment stenosis
in vessels like coronary vessels, renal vessels, ilio-femoral vessels.
• Angioscopy.— Inside of a vessel is visualized with small, flexible fibreoptic scope.
Irrigation is required to avoid opacification by blood.
• Intravascular stenting.— Self expanding stent may be used to expand small stenosed area
of the vessel.
• Intravascular ultrasound to know more about pathology in the lumen as well as the wall
of the vessel.
There are certain complications.—
• Rupture of the vessel.
• Sepsis of the vessel.
• Fluid overload.
• More thrombosis may develop following its use.
• Air embolism.
ANEURYSM
Definition.—
Dilatation of a localized segment of the arterial system is known as aneurysm.
Broadly, an aneurysm can be classified into three types — (a) True aneurysm, (b) False
aneurysm and (c) Arteriovenous aneurysm.
(a)
A true aneurysm is one, which contains all the three layers of the arterial wall in the
aneurysm.
A CONCISE TEXTBOOK OF SURGERY
240
(b)
A false aneurysm is one, which has a single layer of fibrous tissue as the wall of the
sac and does not contain the three layers of the arterial wall as the covering of the aneurysmal
sac. Majority of the false aneurysms follow trauma. A mycotic aneurysm (which is produced by
growth of microorganisms in the vessel wall) is usually of false variety.
Causes.—
Except traumatic aneurysm all other aneurysms are caused by weakening of the wall of the
artery. This weakness may be either congenital or acquired.
1. Congenital.—
(i) Congenital aneurysm often occurs in the cerebral blood vessels particularly in the
circle of Willis due to congenital deficiency of the elastic lamina at the sites of branching. This
is known as Berry aneurysm. These aneurysms remain symptomless till they rupture and cause
subarachnoid or intracerebral haemorrhage.
(ii) A cirsoid aneurysm is the mass of dilated pulsating serpiginous vessels — both
arterial and venous — which is found in a congenital arteriovenous malformation (See Fig. 3.42
of 'A Manual On Clinical Surgery').
(iii) Congenital arteriovenous fistula may lead to aneurysm.
(iv) A few syndromes, which are rare inherited connective tissue defects such as Marfan's
syndrome and Ehler-Danlos syndrome, may cause congenital aneurysm.
(v) Aneurysm of aorta may occasionally occur proximal to coarctation of aorta.
2. Acquired.—
Acquired varieties can be broadly classified into three groups — A. Traumatic, B. Degenerative
and C. Infective.
A- TRAUMATIC.— Majority of the traumatic aneurysms are false aneurysms and are
fusiform in shape.
(i) Direct trauma such as penetrating wound to the artery may cause such aneurysm.
(ii) Irradiation may cause aneurysm.
(iii) Arteriovenous aneurysm may develop from trauma.
(iv) Indirect trauma may cause aneurysm e.g. at the subclavian artery distal to the point
where it crosses the cervical rib.
B. DEGENEFiATIVE.— This group is by far the most common group.
(i) Atherosclerosis, with associated degenerative changes in the elastic and muscle fibres of
the tunica media, is by far the commonest cause of aneurysm. These aneurysms are most frequently
located in the abdominal aorta and the popliteal artery. This suggests that there may be particular
mechanical strains consequent upon local anatomical factors 'such as lumbar lordosis and the
repeated flexion and extension at the knee. However atherosclerotic aneurysm may occur elsewhere
e.g. in the thoracic aorta and its main branches and in the femoral artery. Most atherosclerotic
aneurysms are diagnosed in patients over 60 years of age, more common in men than in women.
(ii) A peculiar type of congenital abdominal aortic aneurysm is seen in relatively young
South African Negroes. This is attributed to congenital intimomedial mucoid degeneration.
C. INFECTIVE.—
(i) Syphilis.— The vasa vasorum becomes obstructed by intimal proliferation and this
leads to impaired nutrition of the tunica media. Syphilitic aneurysms usually follow syphilitic
arteritis. Now this is a rare entity. This is only seen in the thoracic aorta. This may be fusiform
or saccular in shape.
(ii) Acute infections may lead to aneurysmal dilatation. In about 10% of patients with
DISEASES OF ARTERIES
241
abdominal aortic aneurysm, the wall of the sac is thickened and shows extensive active chronic
inflammatory changes with plasma-cell infiltration.
(iii) Non-specific mycotic aneurysm may occur anywhere in the body. The nomenclature
is a misnomer as the cause is not due to fungus but due to bacterial infection. It is mainly caused
by staphylococcus aureus or streptococcus.
(iv) As an occasional complication of subacute bacterial endocarditis, the arterial wall
becomes weak and forms aneurysm. Infected embolus rests on the peripheral arteries and thus
produces weakening of the wall.
(v) Sometimes aneurysm is seen in an artery traversing tubercular cavity in the lung.
(vi) Aneurysm is also seen in an artery situated at the base of a peptic ulcer and is also
infective.
(vii) Arteritis — particularly polyarteritis may cause aneurysm.
According to the shape a true aneurysm may be fusiform, saccular or dissecting aneurysm.
FUSIFORM ANEURYSM occurs when there is uniform expansion of the entire circumference
of the arterial wall. This is the commonest variety and it is a spindle shaped enlargement.
SACCULAR ANEURYSM is an expansion of a part of the circumference of the arterial wall.
This is usually traumatic. When a penetrating wound in the artery does not close spontaneously,
a pulsating haematoma develops which is enclosed by fibrous tissue. Later on this saccular cavity
becomes partly lined by endothelium derived from the intima. This is how a saccular aneurysm
forms.
DISSECTING ANEURYSM occurs when the intima ruptures usually beneath an
atheromatous plaque and the blood is forced through the intima to enter between the inner and
outer coats of the tunica media. The intima and the adjacent part of the media are nourished by
diffusion of the arterial blood. The adventitia and the outer part of the media are nourished by
the vasa vasorum from intercostal and other arteries which form a plexus in the adventitia.
Split occurs between the inner part of the media and the outer part of the media. If the vasa
vasorum fails in its function because of obliteration, this leads to mucoid degeneration in the
ground substance of the media which may result in the appearance of clefts in the vessel wall.
This is one of the most common acute problems involving the thoracic aorta and is usually
associated with arterial hypertension and cystic medial necrosis of the aortic wall. The initiating
lesion is a tear in the intima through which the blood leaks into the wall of the aorta and
dissects it and hence its nomenclature.
Clinical features.—
SYMPTOMS.—
Aneurysm may be asymptomatic and it is then detected accidentally.
(i) The commonest presenting symptom is a dull aching pain. With abdominal aneurysm
there is dull pain in the centre of the abdomen.
(ii) Acute pain may be complained of if the vessel suddenly stretches.
(iii) A severe pain, bursting in nature, is complained of when an aneurysm ruptures and
a large haematoma forms.
(iv) Referred pain may be due to pressure on a nerve e.g. patients with abdominal aortic
aneurysm may present with sciatica.
(v) Some patients notice a pulsatile mass, which is a common mode of presentation for
femoral and popliteal aneurysms.
(vi) Sometimes patients may present with severe ischaemia of the lower limb. Such occurrence
16
242
A CONCISE TEXTBOOK OF SURGERY
may be seen in aortic and femoral aneurysms, though the incidence is less. But in popliteal
aneurysm such incidence is more.
(vii) Patient may present less severe ischaemia caused by emboli originating in the aneurysm.
The best example of such complication is the multiple small emboli which block the digital
arteries from a subclavian aneurysm leading to Raynaud's syndrome. In the lower limb such
emboli may cause intermittent claudication or rest pain.
(viii) Enlargement of the artery may block the vein by direct pressure or may cause it to
thrombose. The patients present with swollen blue and painful limbs. This is due to venous
thrombosis or obstruction which is more often seen in aneurysms of the aorta, femoral and popliteal
arteries which are closely related to the respective veins.
So aneurysms can cause symptoms due to expansion (acute pain), rupture (severe pain bursting
in nature), thrombosis (leading to ischaemia) or release of emboli (Raynaud's syndrome or
intermittent claudication or rest pain or even gangrene of the foot or toes).
Examination.—
(i) A pulsatile swelling exhibiting expansile pulsation in the course of an artery should be
suspected as aneurysm.
(ii) Pulsation diminishes if a pressure is applied proximal to the swelling. It refills again
in 2 or 3 beats if the proximal pressure is released.
(iii) The swelling is compressible.
(iv) A Thrill may be palpable over the swelling.
(v) On auscultation a systolic bruit may be heard over the swelling.
PRESSURE EFFECTS.—
Aneurysms exert pressure on the adjacent structures. These pressure effects are discussed in
details below.
Effects of aneurysm.—
The main menace of aneurysm is rupture which causes enormous bleeding and ultimately
death of the patient if the condition is not suspected earlier and operation is undertaken. Aneurysm
as such produces A. Effects of pressure on the neighbouring structures, B. Thrombosis and C. Emboli
formation.
A. PRESSURE ON THE NEIGHBOURING STRUCTURES.—
(i) Pressure on veins.— This leads to oedema of the distal limb. This is more commonly
seen in aneurysm of the abdominal aorta, femoral and popliteal aneurysm.
(ii) Pressure on the nerves.— This leads to altered sensation e.g. pain, numbness, tingling
and paraesthesia. Paralysis is rare.
(iii) Pressure on the bones.— This leads to erosion of the bones. Such erosion is seen in
vertebrae by aortic aneurysm. The intervertebral discs are resilient structures and do not undergo
erosion.
(iv) Pressure on adjacent organs.— Pressure of an aortic aneurysm on the oesophagus may
cause dysphagia. In case of abdominal aortic aneurysm the stomach may be pushed forward and
if the aneurysm leaks or bursts into the stomach it causes severe haematemesis.
(v) Pressure on the skin.— This stretches the overlying skin and the skin becomes red and
oedematous showing features of inflammation, as if an abscess lies underneath. Aneurysms have
been incised with the wrong diagnosis of abscess with sinister consequences. So one must be very
careful to exclude aneurysm if the abscess lies in the line of a known artery. In this case one can aspirate
first before making an incision.
DISEASES OF ARTERIES
243
B. THROMBOSIS.—
Due to formation of laminated thrombus within an aneurysm, the arterial flow to the distal
segment is diminished. Such thrombosis is very common in aneurysm and this is the reason why
arteriography is not diagnostic of aneurysm as such thrombosis does not show dilated sac in
arteriography. This leads to ischaemia of the distal limb. This is a common occurrence in popliteal
aneurysm. This has some protective influence in preventing rupture.
C. EMBOLI FORMATION.—
Emboli often originate in the aneurysm. The best example is formation of multiple small
emboli from subclavian aneurysm which block the digital arteries. Similarly emboli from the
aortic aneurysm, femoral or popliteal aneurysm may cause intermittent claudication, rest pain or
gangrene of the toes.
ISCHAEMIA IN A CASE OF ANEURYSM may be due to :
(i) Thrombosis in the aneurysm.
(ii) Occlusion of the origin of the emerging artery with
thrombosis.
(iii) Pressure of aneurysm on the nearby branches of the
artery.
(iv) Embolism from the aneurysm.
Complications of aneurysm.—
1.
Pressure
on
the
adjacent
structures.—
See above under
'Effects of aneurysm'.
2.
Thrombosis
and
emboli
formation.—
These
lead
to
circulatory insufficiency of the inferior extremity. These have been
discussed above.
3. Infection.— This may occur from organisms in the blood
stream. Signs of inflammation become evident with suppuration,
abscess formation followed by rupture.
4. Rupture.— This seems to be the gravest complication of
aneurysm. This occurs due to avascular necrosis of the vessel wall
(pressure necrosis), more commonly along the sides of the
aneurysmal sac. Rupture leads to haemorrhage. This depends on
the site of the artery involved — either retroperitoneal or
subarachnoid, or in the pleural cavity (haemothorax), in the
peritoneal cavity (haemoperitoneum), in the trachea (haemoptysis),
in the oesophagus, stomach or duodenum (haematemesis). Fig.15.17. Arteriographic
u .* • .
, ... study of a man who presented
n . . , j -,.is ushered with severe pain •
Rupture
bursting m nature and with .. . .. . f ,
r,,
r
°
severe shock.
5. Spontaneous cure.— Occasionally, particularly in saccular
with claudication. It shows
., ,_______ , ... ,
thrombosed popliteal aneurysm.
aneurysm gradual formation of clot in the sac with ultimate fibrosis may lead to consolidation.
This is seen in saccular aneurysm in the peripheral arteries.
Differential diagnosis.—
1.
Swelling over an artery.— This also leads to pulsation which is typically called 'transmitted
This pulsation is different from expansile pulsation of aneurysm. When two fingers are
placed on a pulsating swelling, in case of expansile pulsation the two fingers diverge from each
other, whereas in transmitted pulsation the two fingers diverge from each other, whereas in
pulsation'.
244
A CONCISE TEXTBOOK OF SURGERY
transmitted pulsation the two fingers are lifted up without divergence with each arterial beat
(See Figs. 3.23, 3.24 & 3.25 in 'A Manual On Clinical Surgery'). Such cases can be easily
distinguished from aneurysm by the above-mentioned test and by postural change, in which the
swelling will be shifted away from the artery so that it will lose pulsation. A pseudopancreatic
cyst often pulsates being a swelling on the abdominal aorta. When the patient is examined in the
genupectoral position the cyst falls away from the artery and consequently pulsation is vanished.
2. Swelling beneath an artery.— A swelling under an artery will lead to pulsation as the
artery is brought towards the surface. Such pulsation is seen when subclavian artery is pushed
up by the cervical rib. Very careful examination is required to distinguish this condition from a
typical aneurysm.
3. Pulsating tumours.— A few tumours are so vascular that they pulsate e.g. telangiectatic
osteosarcoma, very vascular osteoclastoma, metastasis from hypernephroma, aneurysmal bone
cyst etc. Careful investigation should be performed to differentiate such condition from typical
aneurysm.
4. An abscess.— As has been mentioned earlier in the section of 'Effects of Aneurysm' in
'Pressure on the skin', before making an incision onto a swelling, particularly in the chest wall,
in the groin, in the axilla or in the popliteal fossa, one must ask oneself 'Is it not an aneurysm?'.
See whether it is a pulsatile swelling or not.
Special Investigations.—
1. BLOOD — is examined for cholesterol level and other lipids to exclude atherosclerosis.
W. R. and Kahn test should be performed to exclude syphilis.
2. RADIOGRAPHY.—
(i) Straight X-ray may show (a) calcification of the arterial wall, (b) soft tissue shadow
or (c) bony erosion.
(ii) Arteriography is mainly performed to know about the collaterals above and below
the lesion and also to know the condition of the artery above and below the aneurysm.
Arteriography often fails to show aneurysmal dilatation due to the presence of laminated blood
clot within the sac. To decide the type of surgery needed this investigation is important.
3. OTHER INVESTIGATIONS should be performed to exclude other conditions in the
differential diagnosis and to know the general condition of the patient before undertaking major
surgery for aneurysm. Investigations to know the renal function are highly important for abdominal
aortic aneurysm.
Treatment.—
1. ARTERIAL LIGATION.— This operation is becoming obsolete nowadays, since collateral
circulation maintains blood flow through the aneurysm and if the collateral circulation is
inadequate the risk of gangrene is considered high. This procedure is however suitable for splenic
artery, intracranial aneurysm etc. where adequate surgical facilities for sophisticated surgery is
not available. The different methods of ligation are :
(i) Anel's method.— The ligature is applied just proximal to the sac.
(ii) Brasdor's method.— The ligature is applied just distal to the sac.
(iii) Hunter's method.— The ligature is applied immediately above a branch of the artery.
(iv) Wardrop's method.— The ligature is applied immediately below a branch of the artery.
(v) Antylus’ method.— Two ligatures are applied one proximal and another distal to the
aneurysmal sac.
2. WIRING OF THE ANEURYSMAL SAC.— This is indicated in elderly and poor risk
DISEASES OF ARTERIES
245
patients and in cases of difficulty placed aneurysms for operation excision as this may carry high
mortality rate.
A long fine thread of stainless steel wire (200 or 1000 feet in length of No. 3) is introduced
into the aneurysmal sac with a hypodermic needle. The wire gets coiled within the sac and this
leads to clotting, thrombosis followed by fibrosis. This may lead to consolidation.
3. WRAPPING OF THE ANEURYSMAL SAC.— A strip of fascia lata, polythene or
cellophane sheet may be wrapped round the aneurysmal sac to strengthen its wall and prevent
rupture. This may be of value in intracranial aneurysms where surgery is difficult and rupture
or such aneurysm may cause death of the patient. So wrapping and strengthening of the wall of
the aneurysm may save the patient.
4. ANEURYSMORRHAPHY (Matas' reconstructive aneurysmorrhaphy).— This is
particularly suitable in case of saccular aneurysm of arteries like femoral or popliteal. The
aueurysmal sac is totally excised and the defect in the arterial wall is closed by suturing of the
adjacent healthy arterial wall.
5. EXCLUSION AND BY-PASS GRAFTING.— This operation is performed where excision
of the aneurysmal sac is not very safe due to presence of adhesions to the neighbouring vital
structures. These vital structures may be damaged during dissection of the aneurysm. Such cases
are abdominal aortic aneurysm where inferior vena cava lies adherent and femoral artery aneurysm
where femoral vein lies adherent.
In this operation the artery is ligated above and below the aneurysm. The by-pass graft
mostly autogenous vein graft is sutured above and below the ligatures with a small opening in
the artery. Two small openings are made in the arterial wall above and below the ligatures and
the 'by-pass graft' mostly autogenous vein graft is sutured around the small openings so that the
blood flows through the by-pass graft to the distal artery. The excluded aneurysmal sac becomes
thrombosed and shrinks into fibrous mass.
6. EXCISION AND GRAFTING.— This is the most popular operation and should be performed
wherever possible. Dacron graft or autogenous vein may be used for grafting.
7. EXCISION AND END-TO-END SUTURING.— This is only possible in case of peripheral
aneurysm, where after excision of the aneurysm two cut ends can be approximated by mobilization
for end-to-end anastomosis.
ARTERIOVENOUS ANEURYSM
Communication between an artery and adjacent vein leads to arteriovenous aneurysm or
arteriovenous fistula.
Causes.—
(i) Congenital.— It is a direct 'shunt' between an artery and a vein. The lesion is commonest
in the leg, but it may occur in the arm or in the scalp. In the latter position it forms a mass of
dilated vessels known as 'cirsoid aneurysm'.
(ii) Acquired — mainly traumatic either by a penetrating wound or a sharp blow.
Communications develop between the artery and the vein lying close to each other at the time
of injury or during the process of healing communication may develop between the artery and
vein, (a) When the artery and the vein communicate directly through a short wide channel it is
called aneurysmal varix. (b) When the anastomosis becomes indirect through an intermediate sac
lying in the soft tissues it is called varicose aneurysm.
(iii) Iatrogenic.— When arteriovenous fistulas are created surgically, this is called iatrogenic
A CONCISE TEXTBOOK OF SURGERY
246
arteriovenous fistula. In current practice the most common is that used in the forearm or legs to
permit renal dialysis in the management of renal insufficiency. Arteriovenous fistulas have also
been surgically constructed to increase blood flow and patency through vascular anastomoses
such as used in venous reconstructions and limb salvage procedures. For renal dialysis it is
mostly used in the wrist or in the ankle and such temporary arteriovenous fistula is known as
cimino fistula.
A few iatrogenic fistulas may result inadvertently during operations e.g. operations on the
kidney, intervertebral discs, small bowel resection and pelvic surgery.
A few iatrogenic fistulas are made as part of operations e.g. distal splenorenal shunt, coronary
artery by-pass grafting etc.
Manifestations of Arteriovenous Anastomosis.—
A. SYSTEMIC EFFECTS.—
The pathophysiologic changes that follow a direct communication between the arterial and
venous system are demonstrated by presence of a thrill over the site of the lesion. The magnitude
of systemic symptoms is related to the size of the fistula and its position in relation to the heart.
These changes are maximum in case of a large artery. With large shunts directly into the venous
circulation, a sequence of changes occurs that is directly related to the volume of blood passing
through the fistula. Systemic effects are :
(i) Cardiac output increases.
(ii) The heart rate increases.
(iii) Diastolic arterial pressure diminishes with an increase in systolic pressure i.e. increase
of the pulse pressure.
(iv) There are elevated right and left atrial pressures.
(v) The blood and plasma volumes increase in an effort to compensate for the increased
volume of blood in the venous circulation.
(vi) Due to high cardiac output, the heart increases in size and ultimately cardiac
hypertrophy results.
(vii) Large fistulas may ultimately lead to congestive cardiac failure with pulmonary
oedema.
(viii) There is also decrease of peripheral resistance.
(ix) It has been found out that digitalis preparations are usually ineffective. So operation
is justified in these cases.
(x) The Central Venous Pressure (CVP) is often increased.
(xi) Arteriovenous fistulas may be associated with the development of bacterial
endocarditis. This also requires surgical closure of the fistula for permanent cure.
B. LOCAL EFFECTS.—
(i) Aneurysmal dilatation is usually present at the site of the fistula.
(ii) Extensive collateral circulation develops connecting the arteries above and below the
fistula. This collateral circulation can become massive and results in an increase in temperature
both of the skin and of the muscle.
(iii) When such fistula occurs in an extremity, the limb may be increased in length. Increase
in bone growth is probably due to increase in local temperature.
(iv) Presence of a thrill over the site of the lesion is quite characteristic, particularly if the
lesion is located near the surface.
(v) On auscultation, a bruit can be heard almost throughout the cardiac cycle.
DISEASES OF ARTERIES
247
(vi) The veins are enlarged and may be to certain extent arterialised.
Clinical features.—
LOCAL SIGNS.—
1. As mentioned earlier a pulsatile swelling or an aneurysmal dilatation is particularly
visible if the lesion is superficial.
2. One can find the dilated collateral circulation with increase temperature of the skin.
3. Port-wine discolouration of the skin may also be seen due to increased collateral
circulation.
4. Distended superficial veins may also be visible. The veins are often varicosed.
5. Increased length of the limb is often noticed in congenital fistula. This may be noticed
in acquired type if the fistula has developed before completion of bony growth, but this will be
less evident.
6. On palpation a thrill may be detected. Pressure on the artery proximal to the fistula
causes the swelling to diminish in size. The thrill and the bruit cease to exist.
7. Below the fistula the limb is ill-developed, it feels cooler.
8. Below the fistula muscle wasting may be noticed.
9. Below the fistula one may find ischaemic changes o£ the extremity with presence of
even indolent leg ulcer. This is due to inadequate arterial blood supply below the fistula due to
diversion of blood into the veins.
10. Auscultation reveals continuous bruit.
SYSTEMIC SIGNS.—
The signs are similar to what have been described above under the heading of 'systemic
effects'. Here one sign worths mentioning i.e. Branham's sign. If a finger is pressed on the
artery proximal to the fistula, there will be slowing of pulse rate and rise in the diastolic
pressure.
Special Investigations.—
1. Arteriography confirms the diagnosis, as the venous filling occurs with speed. This also
indicates the position of the fistula and its size.
2. Ultrasound.— The lesion and the enlarged veins can be aptly demonstrated by
ultrasonography.
Treatment.—
CONGENITAL LESIONS are not progressive, so excision is only advised for severe deformity
and recurrent haemorrhage.
The ACQUIRED LESIONS are usually progressive and operations are always required.
1. Reconstructive operation is the operation of choice. The vessels are separated. The
intervening sac is excised. The defects in the vessels walls are repaired. In difficult cases it may
be necessary to reconstruct the artery at the expense of the vein. Such reconstruction is performed
with the involved vein (which has been sacrificed) or with Dacron graft. The vein is simply
ligated above and below and the intervening part may be utilized for grafting of the artery.
2. Quadruple ligation.— When reconstruction operation is not possible, ligation of the
involved artery and vein both above and below the lesion may be performed (with four ligatures
— 2 for artery and 2 for the vein).
3. Selective intra-arterial embolization is also a useful technique for treating these lesions.
4. In majority of patients it is possible to close the fistula without any distal ischaemia and
subsequent amputations are not required.
A CONCISE TEXTBOOK OF SURGERY
248
ABDOMINAL AORTIC ANEURYSMS
Abdominal aortic aneurysms are important as they are both common and potentially lethal.
This is the most common of all aneurysms. Its incidence is about 2% in the Western population.
95% are due to atherosclerosis. It is fortunate that about 95 % of these aneurysms occur below
the origins of the renal arteries. If imtreated about 1/2 the patients die within 3 years of the
diagnosis and 2/3rds will be dead in 5 years. The most frequent cause of death is rupture of
the aneurysm.
It has been noticed that there is a steady rise in the incidence of this aneurysm, probably due
to increased longevity of mankind. Most patients are in the 6th or 7th decade. Males are more
often affected than females in the ratio of approximately 10 : 1.
Aetiology and Pathology.— As mentioned above about 95% of this aneurysm are
atherosclerotic in origin. In only minor cases other causes like Marfan's syndrome, syphilis or
trauma may be detected.
This aneurysm characteristically originates just below the renal arteries and extend distally
beyond the aortic bifurcation into the common iliacs. This seldom involves the external iliac
arteries. Small aneurysms limited to the abdominal aorta are also not uncommon. If the diameter
of the aneurysm becomes 10 to 15 cm, it may be discovered accidentally by palpation. There is
usually no impairment of peripheral circulation unless distal embolization from the laminated
thrombus lining the lumen occurs.
Clinical features.— It is difficult to know what proportion of abdominal aneurysms may
cause symptoms, but in many patients the
condition is found by chance during
routine abdominal examination. So most
of the patients remain unaware of their
abdominal aneurysms until a mass is
accidentally discovered.
Low
back
pain
may be caused by
abdominal aneurysms. Such pain is due
to tension on retroperitoneal tissues from
the aneurysm. The symptoms are very
vague. Sometimes pain may be referred
to the groin or thigh due to nerve
compression.
Virtually
any
intra­
abdominal condition may be simulated
by an abdominal aortic aneurysm e.g.
peptic ulcer, cholecystitis, pancreatitis,
appendicitis or diverticulitis.
A few patients only complain of a
pulsatile mass in the abdomen.
With
beginning
leakage
of
the
aneurysm, it may mimic acute abdominal
conditions e.g. perforated peptic ulcer,
_._„„_,,
„,
haemorrhagic pancreatitis or generalized
Fig. 15.18.— Calcification in wall of an aortic aneurysm . ...
accidentally revealed in an intravenous pyelogram.
”
‘
DISEASES OF ARTERIES
249
PHYSICAL EXAMINATION.— For abdominal aneurysm, the abdomen is palpated with
relaxed abdominal muscles while the patient is taking deep respirations. Careful palpation may
usually delineate the lateral walls of the aorta providing an estimate of its width. A pulsating
mass greater than 1 inch diameter usually establishes the diagnosis of aneurysm.
During physical examination, peripheral pulses should be carefully palpated for associated
occlusive vascular disease. Presence of a bruit over the bifurcation of the carotid artery is
particularly significant because an asymptomatic stenosis of the carotid artery may be revealed.
Leakage may occur either into the peritoneal cavity or into the duodenum or even into the
inferior vena cava. Initially bleeding is into the retroperitoneal space, where it may be contained
for- a while before it proves fatal.
Special Investigations.—
1. Blood.— Haemoglobin estimation, full blood count, ESR, grouping and cross-matching,
blood lipids, electrolytes and urea should be performed.
2. Urine analysis to exclude diabetes is essential.
3. E.C.G., liver function test and chest X-ray should be performed.
4. Straight X-ray of the abdomen is the most useful confirmatory investigation, which often
shows a thin curved line of calcification in the wall of the sac. Less frequently only a soft tissue
mass may be seen. The lateral view is particularly helpful which more clearly shows the calcific
rim or thin line of calcification in the wall of the aneurysm, which may be obscured in the
anteroposterior view by the shadows of the vertebral bodies. An estimate of the size of the
aneurysm can be obtained.
5. Aortography is not without risk and may not be very informative since many aneurysms
contain mural thrombus with a central lumen which approximates to that of a normal aorta and
may mask the true size of the aneurysm. Previously it was used to establish relationship of the
renal arteries with the aneurysm, but renal artery involvement is seen in only 1% of cases and
there is no justification to do this investigation.
However this investigation may be justified only when to be confirmed about the extent of
a suspected extensive lesion and to exclude presence of small aneurysms.
6. Ultrasound scanning has the advantage of being a non-invasive technique.
7. Computerised Tomography (CT) or Magnetic Resonance Imaging (MRI) is best to assess the
extent of the aneurysm. To know the involvement of the renal arteries by aneurysm these
investigations are more helpful than other investigations. It also assists in differentiating from
other abdominal masses.
8. Intravenous pyelography is useful not only as a test of renal function, but also because it
may reveal obstruction of one or both ureters. It should be remembered that ureteric obstruction
is more likely to be due to retroperitoneal inflammatory reaction than to external pressure due
to the aneurysmal sac.
Treatment.—
INDICATIONS FOR OPERATION.—
(i) Aneurysms smaller than 5 cm in diameter can be safely observed till they expand or
become symptomatic.
(ii) Asymptomatic aneurysm measuring more than 5 cm diameter is an indication for
operation unless there are other risks which have already shortened the life expectancy.
(iii) When the aneurysm becomes painful, an emergency operation should be contemplated,
as pain denotes impending rupture. Abdominal tenderness also denotes impending rupture.
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PREOPEFtATIVE EVALUATIONS include special investigations mentioned above, an
electrocardiogram, renal function tests (particularly clearance studies) and coagulation studies
including platelet counts. If carotid bruits are heard, cerebral angiogram may be performed. If
angina pectoris is present, coronary angiogram is indicated.
TECHNIQUE OF OPERATION.— Before anaesthesia, heparin is injected 10,000 units
intravenously. After induction of anaesthesia, a self-retaining urethral catheter is passed to monitor
urine flow during surgery and in the first few postoperative days.
A long midline incision is made to enter into the peritoneal cavity. The small intestine is
delivered out and enclosed in a sterile plastic bag or moist towels. The small intestine is packed
away on the right side of the abdomen, the descending and pelvic colon on the left side and the
transverse colon upwards. Goligher's self-retaining retractor is used to retract the abdominal
walls. Other possible causes for the patient's symptoms should be ruled out e.g. peptic ulcer,
carcinoma of the G.I. tract etc.
Now the abdominal aneurysm is assessed properly particularly noting the level of its neck
and the state of its bifurcation. The posterior parietal peritoneum is incised from the ligament of
Treitz to the pelvis below, taking care not to damage the inferior mesenteric vein. The neck of
the aneurysm is identified and a vascular clamp is applied there. This step is performed quickly
in case of leaking aneurysm. The inferior mesenteric artery is dissected out. If trial clamping leads
to cyanosis of the left colon, a cuff of the aorta should be preserved around its origin for later
reimplantation into the graft. Usually the artery is ligated and divided close to the abdominal
aorta. The common iliac arteries are next clamped.
For this, these arteries are mobilized and made
free from the inferior vena cava and iliac veins.
ANTERIOR
AORTIC
The aneurysm is now incised longitudinally
ABDOMINAL
ANEURYSM
and
mass of thrombus within it is removed.
WALL \
Bleeding from the orifices of the lumbar and
median sacral arteries is controlled by suturing
their orifices within the sac.
Now the inferior end of the aneurysmal sac
is inspected. If a ring of normal aortic tissue can
be identified proximal to its bifurcation, a tube
graft can be used. If the bifurcation is involved
VERTEBRAL
in the aneurysm or if there is aneurysmal
COLUMN
involvement of the iliacs, a bifurcation graft will
be necessary.
A woven or knitted Dacron graft may be
Fig.15.19.— Transverse scan at the level of 4 cm
used. Knitted graft should be preclotted and its
above the umbilicus shows a moderately large
use is associated with blood loss through the
abdominal aortic aneurysm with a large defect in
left lateral wall consistent with rupture. Echo-free interstices. That is why woven Dacron graft is
area in the left paravertebral region represents the more preferred.
The graft is now placed inside the aneurysmal
haematoma.
sac. The upper anastomosis is commenced in the
midline posteriorly and picks up a fold of aortic wall at the neck of the sac. The suture line now
proceeds laterally to its side and meets in the midline anteriorly. 3/0 Mersilene suture is often
used for this purpose. The graft is then occluded whilst the proximal aortic clamp is released to
DISEASES OF ARTERIES
251
test the adequacy of the suture line. Any leaks should be closed by additional sutures.
If a tube graft is used, it is of such a length that it will be under moderate tension when the
distal suture is completed. The distal anastomosis is carried out in exactly the same manner as
the proximal suture.
When a bifurcation graft is used, the common iliac arteries are transected taking care not to
damage their accompanying veins. Two points should be kept in mind at the time of distal
anastomosis — (i) the intima of the common iliac artery should be carefully anchored by the
suture so as to prevent formation of dissecting aneurysm and (ii) before completion of the distal
anastomosis it is essential to release in turn the proximal and distal clamps to dislodge any
thrombus which may be formed during operation. If required, passage of a Fogarty catheter
distally may be required.
The aneurysmal sac is now approximated around the graft and the posterior parietal
peritoneum is closed.
Left colon should be inspected and as mentioned earlier reimplantation of the inferior
mesenteric artery to the graft may be required.
POSTOPERATIVE COMPLICATIONS.— Early postoperative complications are mainly
cardiac and respiratory complications e.g. ischaemia and infarction (cardiac) and atelectasis,
lower lobe consolidation and 'shock lung' (respiratory). Haemorrhage is now not a very serious
complication and occurs provided that anticoagulation is continued beyond the immediate
postoperative period. Haemostasis must be achieved satisfactorily. Left colon ischaemia due to
lack of collateral blood supply may occur in 10% of cases. Fortunately this often resolves
spontaneously. Other early complications are haemorrhage, thrombosis of the graft, peripheral
emboli, ileus, intestinal obstruction, ischaemia of the left colon and renal insufficiency.
Late complications include graft thrombosis, false aneurysm, aortoduodenal fistula (it should
be suspected whenever haematemesis or melaena occurs in months or years after operation. A
successful outcome may be achieved by prompt operation in which aorta is separated from
duodenum, the holes are closed and some omentum is interposed between two structures).
Neurological complications include sexual dysfunction and spinal cord ischaemia. Renal failure
and infection of the graft are rarely seen.
Endoluminal stent-graft procedure.— It has been a minimally invasive recent treatment
offered by major vascular surgical centres for certain aortic aneurysms. The common femoral
arteries are exposed surgically. Under radiological control a stent-graft delivery system is guided
up into the aorta and is placed within the aortic sac. This stent-graft is placed within the aortic
body and one iliac artery. For the other iliac artery a separate single iliac-stent graft is introduced
from the opposite common femoral artery. One must be careful to see that the upper most level
of the graft and distally at both iliac levels the stent-graft should be bloodtight.
Though this method is a success in the initial stage, but lately there is a possibility of stentgraft fragmentation and leakage at the interface of vessel and stent-graft.
RUPTURED ABDOMINAL ANEURYSM.—
C linical features.— It constitutes a grave surgical emergency. Two types of rupture may
occur —
In case of anterior rupture there is free bleeding into the peritoneal cavity. This condition is
extremely fatal and only few patients can be brought to the hospital alive. Those who are brought
alive, carries a high risk of surgery due to prolonged period of hypotension and shock.
Posterior rupture produces retroperitoneal haematoma. The onset is characterized by acute
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vascular collapse, usually with a flank or abdominal pain. Sudden collapse with a pulsatile mass
in the abdomen is almost diagnostic. But frequent erroneous diagnosis as renal colic or massive
myocardial infarct or pulmonary infarct may be made. So careful abdominal palpation is very
essential in these cases.
If no operation is performed the mortality rate is 100%. If operation is performed as an
emergency procedure 50% survival should be expected.
Operative Treatment.— Operation is performed as quickly as possible, infusing 500 to
1000 ml of fluid every few minutes until serious hypotension has been corrected. It is important
to know that elevation of blood pressure should be avoided until the abdomen has been opened and
proximal control of the aorta is obtained. This must be achieved very quickly by cross-clamping
the aorta below the renal arteries. If necessary the aorta may be compressed through the lesser
omentum till infrarenal control can be obtained. Blood replacement is next considered. The
ruptured aneurysm is widely incised, intra-abdominal clots are evacuated and the renal arteries
isolated. Recently there has been renewed interest in autotransfusion using blood sucked out
from the peritoneal cavity. Stored blood should be warmed before transfusion. Low molecular
weight dextran should not be used as when excreted by the kidneys it may block the renal
tubules. Blood loss should be carefully measured and replaced. Intravenous mannitol (200 ml of
20% solution) or frusemide (Lasix) may be of value particularly in the early post-operative phase,
as renal failure is more common after this type of operation.
POPLITEAL ANEURYSMS
Among peripheral aneurysms this aneurysm accounts for 70% of cases. 2/3rds of popliteal
aneurysms are bilateral. If abdominal aorta is carefully examined, l/3rd of these cases may be
seen to accompany aortic aneurysm.
Almost all popliteal aneurysms are atherosclerotic. It usually involves upper 2/3rds of the
artery.
It usually occurs in men in 6th and 7th decades of life, half of whom are hypertensive.
Clinical features.— It is frequently symptomless and may be self-limiting due to spontaneous
thrombosis.
Two types are usually found— (a) the saccular form, may rapidly expand and rupture, (b) The
fusiform type, which is often bilateral, rarely rupture and may be complicated by distal embolism.
This aneurysm itself presents as swelling behind the knee. Symptoms and signs of progressive
enlargement include local pain, tenderness and swelling of the leg due to compression of the
popliteal vein. Sometimes this aneurysm presents with one of its complications e.g. ischaemic
ulceration of toes due to emboli, sudden onset of severe ischaemia following thrombosis or pain
and haematoma formation due to rupture. It should always be suspected and looked for in cases
with embolism of the toes where there is no other obvious source.
Treat ment.— Operation is almost always justified because of its complications of thrombosis,
embolization, gangrene and rupture. Only small asymptomatic aneurysms in the elderly patients
and thrombosed aneurysms can be left alone.
OPERATIVE TECHNIQUE.— This operation may be performed in prone position with an
incision across the popliteal crease to expose the popliteal artery with the aneurysm. Otherwise
this operation can be performed in supine position with the knee slightly flexed and the incision
is made on the medial aspect of the lower thigh extended across the knee joint into the upper calf.
DISEASES OF ARTERIES
253
The upper part of the incision may be deepened to expose the upper part of the popliteal artery.
Exposure can be improved by division of semimembranosus and semitendinosus tendons.
Once the artery is exposed and isolated it is clamped to prevent distal embolization during
operation. Various methods of reconstruction are possible. Perhaps the best is the use of saphenous
vein as a by-pass graft in association with proximal and distal ligation and total obliteration of
the sac. Another method is to lay a graft in the open sac and an end-to-end anastomosis is made
above and below the aneurysm. The aneurysmal sac is not excised because both veins and nerves
are intimately attached to its wall.
DISSECTING ANEURYSM
Aetiology.—
The term 'dissecting aneurysm' is a misnomer and it should be called 'aortic dissection'. The
basic pathology is splitting of the intima, allowing the blood to track into the aortic wall creating
a channel between the intima and the adventitia. This is one of the most common acute problems
involving the thoracic aorta. This tracking of blood into the aortic wall causes distension of the
aorta for which it is called an aneurysm. But this aneurysm develops months or years later, and
such aneurysm is not present during acute dissection.
The cause of weakening of the intima, which causes this condition is not definitely known.
Hypertension is present in about 75% of patients and hypertrophy of the left ventricle characteristic
of hypertension is present in about 90% of cases. The exact nature of degeneration of the aortic
wall is confusing. Cystic medial necrosis has been incriminated. Marfan's syndrome has also been
incriminated particularly when it occurs in younger age group. But in this syndrome there is greater
frequency of dissection in patients with coarctation or congenitally bicuspid aortic valve.
It should be emphasized that this disease is not due to atherosclerosis, which is a disease of
the intima which mostly affects the terminal part of the abdominal aorta. The aortic dissection
is a disease of the media and almost always occurs in the thoracic aorta. Its frequent occurrence in
older age group has led to confusion with atherosclerosis. A distinct abnormality of connective
tissue, known as lathyrism has been incriminated which weakens the cross-linking of collagen.
But confirmation of this condition as probable pathogenesis is still missing.
Pathology.—
Usually the tear of the intima and media is a transverse one in the aorta involving about
1/2 of its circumference. This tear is located in majority of cases (70%) in the ascending aorta, in
the aortic arch in 10% of cases and in the upper descending thoracic aorta in 20% of cases. Three
types have been recognized. In type I, the tear occurs in the ascending aorta, blood entering the
false channel extends along the arch and into the descending aorta and the dissection may extend
distally to reach the abdomen in about half the patients. Proximally the dissection may involve
origins of the coronary artery and the aortic valve attachment. In type II, which is more often seen
in Marfan's syndrome, the dissection is localized to the ascending aorta proximal to the origin
of the great vessels. In type III, the dissection commences in the descending thoracic aorta distal
to the origin of the left subclavian artery and extends distally through the chest into the abdomen.
Type II is uncommon, whereas the risks of complications are more in type I than type III.
As dissection progresses, branch vessels are sheared off, either becoming obliterated or
establishing a communication with the false lumen occluded by the dissection. Proximally the
coronary arteries may be involved. One or more aortic valve casps may be detached causing
aortic insufficiency. Distally, any artery may be involved. Involvement of carotid artery produces
A CONCISE TEXTBOOK OF SURGERY
254
brain ischaemia. Involvement of subclavian artery produces differences in blood pressure between
two arms. Involvement of intercostal arteries may cause spinal cord damage with paraplegia.
Rupture through the serosa causes major internal haemorrhage and sudden death. Rupture
into the pericardial cavity is the most common, probably because the adventitia is thin over the
intrapericardial ascending aorta. Rupture into the left pleural cavity may occur. This causes high
mortality of dissecting aneurysm. About 30% of patients die within 24 hours and about 70%
within 2 weeks and 90%, if untreated, within 1 year. This is the reason why emergency operations
are progressively adopted in the last few years for dissecting aneurysm involving the ascending
aorta.
In very fortunate cases, endothelial lining of the false lumen gives way and blood of the false
track again enters the aortic lumen. This is known as 'healed dissecting aneurysm'. Such patients
have double-barrelled aorta.
Clinical features.— The disease is 3 to 4 times more common in males. It occurs
predominently in older patients beyond the 5th decade, though it may occur in younger age group.
The most characteristic symptom of this disease is excruciating pain, reaching its pick of
intensity immediately. This pain is in the anterior chest, though back pain may occur in about
l/3rd of patients. The pain has a tendency to migrate as dissection extends distally. Pain may
radiate to the neck, arm and to the epigastrium. Only occasionally there may be absence of pain.
Collapse or syncope occurs in about 10 to 20% of cases due to ischaemia of the brain. Signs
of occlusion of other major vessels may be present. Hypertension is present in no less than 80%
of cases.
Special Investigations.—
1. Chest X-ray often shows 'widening of the mediastinum' which is pathognomonic of this
condition. Left pleural effusion may be seen due to extravasation of blood. Sometimes chest
X-ray may be normal.
2. E.C.G.— This condition is often confused with myocardial infarction. Electrocardiogram
is of particular value in differentiating these two conditions.
3. Aortography — is a conclusive evidence of dissecting aneurysm. It is unfortunate that it
may not be possible to do this investigation on acutely ill patients. Aortography shows the double
lumen of the aorta. Sometimes an emergency aortogram should be performed as soon as possible
after admission to hospital.
Treatment.—
1. DRUG THEFtAPY.— Immediate drug therapy has been highly rewarding primarily to
control hypertension and to decrease forceful contractility of the left ventricle. Intravenous arfonad
(trimetaphan) was first used. Later on sodium nitroprusside was used, though it may increase
myocardial contractility and that is why a beta-blocking drug e.g. propranolol was used in
conjunction. Nowadays the regimen which is mostly used is a combination of drugs including
arfonad, reserpin and guanethidine. Some suggested replacing guanethidine with alpha-methyl
dopa.
2. OPERATIVE TREATMENT.—
Indications For Operations.—
(i) When hypertension is not controlled by drug therapy, immediate surgery is indicated.
(ii) When the dissection is continued, which is revealed by continued pain or enlargement
of mediastinal emphysema, immediate operation is justified.
DISEASES OF ARTERIES
255
(iii) When immediate rupture seems likely, operation should be performed.
(iv) If there is aortic valvular incompetence, operation should be contemplated.
(v) Signs of proximal aortic dissection and signs of pericardial effusion are indications
for operation.
(vi) Involvement of important peripheral arteries is an indication for operation.
(vii) Nearly all patients with ascending aortic dissection should be managed surgically,
as these cases are threatened with complications like pericardial tamponad (rupture into the
pericardium), rupture into the mediastinum or acute aortic insufficiency.
OPERATION.— Complete transection of the involved aorta followed by end-to-end
reanastomosis with the outer wall of the proximal aorta and both inner and outer walls of the
distal aorta with particular care to suture the inner intimal layer with the outer layer of the
proximal aorta. The result is that the blood within the dissecting aneurysm enters the original
lumen of the aorta distally and as the distal intimal layer is thoroughly sutured with the outer
layer of the proximal aorta, chance of further dissection should be negligible. But unfortunately
as the disease lies in the tunica media, recurrence does happen.
Nowadays the whole of the dissected aorta is excised and the aortic continuity is restored
with a woven Dacron prosthesis. Both these operations are performed with median sternotomy
and cardiopulmonary by-pass.
DISEASES OF VEINS
VARICOSE VEINS
Definition.—
When a vein becomes dilated, elongated and tortuous, the vein is said to be 'varicose'.
Sites.—
The common sites of varicosity are :
1. Superficial venous system of the lower limbs — affecting either the Long Saphenous
or the Short Saphenous vein or the both.
2. Oesophageal varix (affecting veins of the gastro-oesophageal junction).
3. Varicosity of the haemorrhoidal veins (piles).
4. Varicosity of the spermatic veins (varicocele).
In this chapter we shall only discuss varicosity of the superficial venous system of the
lower limbs.
VARICOSE VEINS OF THE LOWER LIMBS
SURGICAL ANATOMY
Venous drainage of the lower limbs can be conveniently described under 3 heads — I.
Deep Veins, II. Superficial Veins and III. Perforating or communicating Veins, which connect
the superficial with the deep veins.
I. Deep Veins.—
The deep veins of the lower limb accompany the arteries and their branches. These veins
possess numerous valves. The main veins are — the posterior tibial vein and its tributaries, the
peroneal vein, the anterior tibial vein, the popliteal vein and the femoral vein.
The characteristic features of the deep veins are :
1. There are numerous valves in these veins. These valves direct the flow of the blood
upwards and prevent regurgitation of flow downwards.
2. Within the soleus muscle, which is the most powerful muscle of the calf there are
venous plexuses or sinuses. These are devoid of valves. These veins empty in segments into the
posterior tibial and the peroneal veins. These posterior tibial veins and the peroneal veins also
receive perforating or communicating veins from the superficial veins and both these perforating
veins and the soleus venous plexuses or sinuses may enter the same sites of these veins.
II. Superficial Veins.—
These veins lie in the subcutaneous fat between the skin and the deep fascia. These superficial
veins of the lower limb are the long and short saphenous veins and their tributaries.
DISEASES OF VEINS
257
LONG (GREAT) SAPHENOUS VEIN.—
It is the longest vein in the body. It begins in the medial marginal vein of the foot and ends
in the femoral vein about 3 cm below the inguinal ligament. It ascends in front of the tibial
malleolus, runs upwards crossing the lower part of the medial surface of the tibia obliquely to
gain its medial border. Then it ascends a finger's breadth behind the medial border of the tibia
upto the knee. Here it runs upwards on the posterior parts of the medial condyles of the tibia
and the femur and along the medial side of the thigh to the saphenous opening. Saphenous
opening lies about 3.5 cm below and lateral to the pubic tubercle. It passes through the cribriform
fascia of the saphenous opening and ends in the femoral vein.
There are about 10 to 20 valves in this long saphenous vein which are more numerous in
the leg than in the thigh. Of these, two valves are almost constant — one lies just before the
vein pierces the cribriform fascia and another at its junction with the femoral vein (this valve is
concerned with saphenofemoral sufficiency).
Tributaries.—
1. At the ankle:
It receives veins from the sole of the foot through the medial marginal veins.
2. In the leg :
(i) It communicates freely with the small saphenous vein.
(ii) Just below the knee it receives three large tributaries — (a) one from the front of
the leg, (b) one from the region of the tibial malleolus (which communicates with the perforating
veins) and (c) one from the calf which communicates with the small or short saphenous vein.
3. In the thigh:
(i) A large accessory saphenous vein — which communicates below with the small
saphenous vein. This receives numerous tributaries from the medial and posterior parts of the
thigh.
(ii) A fairly constant large vein, sometimes called the anterior femoral cutaneous vein
— commences from a network of veins on the lower part of the front of the thigh and crosses
the apex of the femoral triangle to enter the long saphenous vein in the upper part of the thigh.
4. Near the saphenous opening:
Just before the long saphenous vein pierces the saphenous opening it is joined by four veins—
(i) The superficial epigastric,
(ii) The superficial circumflex iliac,
(iii) Superficial external pudendal and
(iv) The deep external pudendal vein, which joins the great saphenous vein at the
saphenous opening.
Surgical importance.—
(a) As there is communication between the long and the short saphenous veins varicosity
may spread from one system to the other.
(b) At the time of operation for varicose vein, when a ligature is advised to the
saphenofemoral junction, the veins draining into the long saphenous vein near the saphenous
opening must be ligated and cut otherwise these small veins will become varicosed due to
incompetent saphenofemoral junction.
(c) In case of varicosity of the long saphenous vein, the small veins from the sole of the
foot and the ankle which drain into this venous system through the medial marginal veins
become dilated and this gives rise to swelling of ankle, which is known as 'ankle flare'.
17
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SHORT (SMALL) SAPHENOUS VEIN.—
This vein begins behind the lateral malleolus as a continuation of the lateral marginal vein
of the foot. It first ascends along the lateral border of the tendo Achilles and then along the
midline of the back of the leg. It perforates the deep fascia and passes between the two heads
of the Gastrocnemius in the lower part of the popliteal fossa and ends in the popliteal vein 3 to
7.5 cm above the level of the knee joint.
In the leg it is in close relation with the sural nerve.
This vein possesses 7 to 13 valves, one of which is always found near its termination in the
popliteal vein.
Tributaries.—
It sends several tributaries upwards and medially to join the long saphenous vein. The
most important communicating branch arises from the small saphenous vein before it pierces
the deep fascia and passes upwards and medially to join the accessory saphenous vein. This
communication may occasionally form the main continuation of the short saphenous vein.
III. Perforating or communicating veins.—
These veins communicate between the superficial and deep veins. These always pierce the
deep fascia. There are valves within these veins which under normal conditions allow blood to
b
Fig. 16.1 .— Direction of blood flow in the
deep, perforating and superficial veins. The
deep vein is shown within the muscle belly
and the perforating veins pass through the
deep fascia to link the superficial and deep
systems, a. Muscle contraction forces blood
proximally in the deep system while the valves
in the perforating vein prevent it from being
pumped from the deep to the superficial
system, b. During muscle relaxation the deep
system is refilled from the superficial system
and the distal limb. c. Muscle contraction in
the diseased limb forces blood into the super­
ficial system due to incompetence of perfo­
rating venous valves, which results in super­
ficial venous dilatation and tortuosity.
DISEASES OF VEINS
259
flow from the superficial to the deep veins. Only when these valves become incompetent blood
may flow in the opposite direction and thus leads to varicosity of the superficial veins.
When the calf muscles contract the blood is pumped upwards in the deep veins and blood
flow into the superficial veins is prevented by the valves in the perforating veins. During
relaxation of the calf muscles blood is aspirated from the superficial into the deep veins. If the
valves in the perforating vein become incompetent these veins become 'high pressure leaks'
during muscular contraction and this transmission of high pressure in the deep veins to the
superficial veins results in dilatation of the superficial veins producing varicose veins. Perforating
veins are of two types :
(a) INDIRECT PERFORATORS.— There are numerous small vessels which start from
the superficial venous system, pierce the deep fascia and communicate with a vessel in an
underlying muscle. The latter vessel in turn is connected with the deep vein. These indirect
perforators are mostly seen in the upper part of the leg.
(b) DIRECT PERFORATORS.— These veins directly connect the saphenous veins or their
tributaries to the deep veins. A few of these direct veins are constant in number and site. These
are :—
(i) In the thigh.—- Between the long saphenous and the femoral vein in the adductor canal.
(ii) In the leg.— The perforators in the leg are divided into three groups :—
(a) Medial perforating veins.— There are three constant medial leg perforators
situated in line with the posterior border of the tibia 2 inches (5 cm), 4 inches (10 cm) and 6
inches (15 cm) above the medial malleolus. The upper two enter the posterior tibial vein where
an unvalved soleal venous sinus also enters it. The importance of this is that the soleal venous
sinuses are devoid of valves. Moreover the clot arising in the soleal veins may extend into the
posterior tibial vein and then into the perforating veins thus destroying the valves of the
perforators. The lowest perforator has a short course connecting long saphenous with the
posterior tibial vein.
(b) Central perforating veins.— One or two veins connect the short saphenous system
to the veins in the gastrocnemius and soleus muscles. Whereas one enters the muscle on the
medial side close to its junction with the tendo Achilles, the other is situated further up in the
calf. These perforators are insignificant for all practical purposes.
(c) Lateral perforating veins.— There are inconstant perforators at the posterior border
of the fibula. These pass at the levels of 2 inches (5 cm), 5 inches (12 cm) and 7 inches (17 cm)
above the lateral malleolus. These are connected with the peroneal veins.
SURGICAL PATHOLOGY
Under normal conditions the blood from the superficial venous system is passed to the
deep veins through the competent perforators and from the deep veins the blood is pumped up
to the heart by the muscle pump, competent valves and negative intrathoracic pressure. But if
this mechanism breaks down, either due to destruction of the valves of the deep veins (following
deep vein thrombosis), or of the perforators or of the superficial venous system, the blood
becomes stagnated in the superficial veins which become the pray of 'high pressure leaks' and
thus becomes distended and tortuous to become varicose veins. If an individual stands motionless
for a long period of time, venous pressure at the ankle may rise to 80 to 100 mm. Hg and
gradually swelling appears. Even with modest activity of the calf muscles and with competent
venous valves, this pressure is reduced to 20 or 30 mm. Hg.
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260
Aetiology.—
1. Morphological factor.—Varicose veins of the lower limbs are the penalty the man has to
pay for its erect posture. The veins have to drain against gravity. The superficial veins have
loose fatty tissue to support them and thus suffer from varicosity. There are three types of
varicosity — primary varicose veins, secondary varicose veins and congenital varicose veins.
2. Primary varicose veins.— These are more common. This condition is mainly due to defect
in the valves. The defects may be congenital or acquired (either due to thrombosis or due to
inflammation in the veins.)
(i) Defect in the saphenofemoral valve leads to varicosity of the long saphenous vein.
(ii) Defect in the saphenopopliteal valve leads to varicosity of the short saphenous vein.
(iii) Defects in the valves of the perforators lead to varicosity of either long saphenous or
short saphenous system.
3. Secondary varicose veins occur due to venous obstruction e.g.
(i) Mechanical factors e.g. pregnancy or tumours in the pelvis (e.g. uterine fibroids,
ovarian cyst, cancers of the cervix, uterus, ovary or rectum).
(ii) Deep vein thrombosis leading to damage of the valves.
(iii) Hormonal causes — progesterone may cause varicosity in multiparous females.
(iv) Acquired arteriovenous fistula (due to trauma or deliberate shunting for dialysis).
(v) Extensive cavernous (venous) haemangioma.
(vi) Retroperitoneal lymphadenopathy or retroperitoneal fibrosis.
(vii) Iliac vein thrombosis.
4. Congenital varicose veins.— Occasionally varicose veins may develop below 20 years of
age. These cases are mostly due to either congenital arteriovenous fistula or cavernous (venous)
haemangioma.
Predisposing factors.—
(a) Prolonged standing.— During prolonged standing long column of blood alongwith
gravity puts pressure on the weakened valves of the veins. This causes failure of the valves
quickly giving rise to varicosity of the long or short saphenous vein. During prolonged standing
the calf muscles also do not work quite often so the calf pump mechanism also cannot push the
venous blood upwards.
(b) Obesity.— Excessive fatty tissue in the subcutaneous tissue offer poor support to the
veins. This leads to the formation of varicosity.
(c) Pregnancy.— Pregnancy is said to predispose the formation of varicose veins. Varicose
veins are often noticed in multiparous women. Pregnancy acts in various ways — (i) Progesterone
causes dilatation and relaxation of the veins of the lower limb. This may make the valves
incompetent. This hormonal effect is maximum in the first trimester of pregnancy, (ii) Pregnant
uterus causes pressure on the inferior vena cava, thus causing obstruction to the venous flow.
This effect is mostly seen in the last trimester of pregnancy. After each pregnancy both hormonal
and mechanical effects are removed and there is improvement of varicosity. During the
subsequent pregnancy these factors again cause the varicosities to develop in a bigger way.
That is why varicose veins are commonly seen in multiparous women.
(d) Old age.— This causes atrophy and weakness of the vein wall. At the same time with
aging the valves in the veins become gradually incompetent.
(e) Athletes.— Sometimes varicose veins are noticed among athletes. Forcible contraction
of the calf muscles may force blood through the perforating veins in reverse direction. This will
DISEASES OF VEINS
261
cause destruction of the valves of the perforating veins and ultimately lead to formation of
varicose veins. Similarly Ricksawpullers often suffer from varicose veins.
Clinical features.—
SYMPTOMS.—
(a) The commonest symptom is tired and aching sensation in the affected lower limb,
particularly in the calf, at the end of the day. The severity of symptoms depends mostly on the
extent of the high back pressure.
(b) Sharp pains may be complained of in grossly dilated veins.
(c) Some patients may suffer from cramp in the calf shortly after retiring to bed. Such
cramp is usually due to sudden change in the calibre of communicating veins which stimulates
the muscles through which they pass.
(d) Pain may be bursting or severe in nature and may be particularly localized to the site
of the incompetent perforating veins. Such bursting pain while walking indicates deep vein
deficiency.
(e) Patients may present with no other
symptom except dilated and tortuous veins of the
leg. These dilated veins may or may not be
associated with the following complications.
(f) There may be other complaints or
complications of the dilated and tortuous veins.
Such as —
(i) Ankle swelling towards evening.
(ii) The skin over the varicosities may itch.
It may be pigmented.
(iii) Eczema of the affected skin.
(iv) Venous ulceration.
(g) In the personal history one may find
that the patient is involved in a job of prolonged
standing e.g. bus or tram conductors.
LOCAL EXAMINATIONS.—
INSPECTION.—
1. When the patient stands up, the veins
become prominent. The varicosities may be either
wide spread or restricted to a single varix. When
such single varix is situated at the saphenous
opening, it is called a 'saphena varix’. It must be
distinguished from a femoral hernia. One can feel
characteristic thrill when the patient coughs. Such
varix disappears when the patient lies down.
When this varix is tapped with a finger, a fluid
thrill may be obtained in the long saphenous vein
lower down in the limb.
2. One must assess in inspection whether
varicosity has affected the long saphenous vein or the short saphenous vein or the both.
262
A CONCISE TEXTBOOK OF SURGERY
3.
The skin of the lower part of the leg should be particularly inspected to exclude oedema,
pigmentation, eczema or ulceration.
PALPATION.—
1. The dilated veins are particularly palpated. The saphena varix is palpated and presence
of cough impulse is elicited.
A FEW TESTS are performed to know the details of the varicose vein including the sites
of incompetent perforators.
2. Brodie-Trendelenburg test.— This test is performed to determine incompetency of the
sapheno-femoral valve and other communicating system. This
test can be performed in two ways. In both the methods,
the patient is first placed in the recumbent position and
his legs are raised to empty the veins. The sapheno-femoral
junction is now compressed with the thumb of the clinician
and the patient is asked to stand up quickly, (i) In first
method, the pressure is released. If the varices fill very
quickly by a column of blood from above, it indicates
incompetency of the sapheno-femoral valve. This is called
a positive Trendelenburg test, (ii) To test the
communicating system, the pressure is not released but
maintained for about 1 minute. Gradual filling of the veins
during the period indicates incompetency of the
communicating veins, mostly situated on the medial side of
the lower half of the leg allowing the blood to flow from
the deep to the superficial veins. This is also considered
as a positive Trendelenburg test and the positive tests are
indications for operation.
3. Tourniquet test.— It can be called a variant of
Trendelenburg test. In this test the tourniquet is tied
around the thigh or the leg at different levels after the
superficial veins have been made empty by raising the leg
in recumbent position. The patient is now asked to stand
Fig.16.3 — It shows a portion of
up. If the veins above the tourniquet fill up and those Trendelenburg test. Firstly the varicosedbelow it remain collapsed, it indicates presence of leg is to be raised to empty the veins.
incompetent communicating vein above the tourniquet.
Now the sapheno-femoral junction is
Similarly if the veins below the tourniquet fill rapidly compressed as in this figure with the
whereas veins above the tourniquet remain empty, the thumb of the clinician and the patient is
incompetent communicating veins must be below the asked to stand up. If the pressure is
tourniquet. Thus by moving the tourniquet down the leg continued for about 1 minute gradual
in steps one can determine the position of the incompetent filling of the veins during this period
indicates
Incompetence
of
the
communicating vein.
communicating veins. When the pressure
4. Pratt’s test.— This test is performed to know
is released if the varices feel very quickly,
the positions of the leg perforators. Firstly an Esmarch it indicates incompetency of the sapheno­
elastic bandage is applied from toes to the groin. A
femoral valve. The students are referred
tourniquet is then applied at the groin at the upper end of to Figs. 7.2 to 7.4 of author’s ‘A Manual
the elastic bandage. This causes emptying of the varicose
On Clinical Surgery’.
DISEASES OF VEINS
263
veins. The tourniquet is kept in position and the elastic bandage is taken off. The same elastic
bandage is now applied from the groin downwards. At the position of the perforator, a 'blow
out' or a visible varix can be seen. This is marked with a skin pencil.
5.
Perthes’ test (Modified).— This test is primarily intended to know whether the deep
veins are normal or not. A tourniquet is tied round the upper part of the thigh tight enough to
prevent any reflux down the vein. The patient is asked to walk quickly with the tourniquet in
place. If the communicating and the deep veins are normal the varicose veins will shrink whereas
if they are blocked the varicose veins will be more distended.
6. Schwartz’s test.— In a long-standing case if a
tap is made on the long saphenous varicose vein in the
lower part of the leg an impulse can be felt at the
saphenous opening with the other hand.
7. Morrissey’s test or Cough impulse test.— In
this test limb is elevated to empty the veins. The patient
is asked to cough forcibly. An expansile impulse if felt
in the long saphenous varicose vein, it may be presumed
that the sapheno-femoral valve is incompetent. Similarly
if the patient coughs and the sapheno-femoral junction
is incompetent a bruit may be heard on auscultation.
8. Fegan’s method to indicate the sites of
perforators.— In the standing position the places of
excessive bulges within the varicosities are marked with
a skin pencil. The patient now lies down. The affected
limb is elevated and the heel is kept supported. The
examiner palpates along the line of the marked
varicosities carefully, so that he can find gap or small pit
in the deep fascia which transmits the incompetent
perforator. This is marked with 'X'. This is the site of the
perforator. It should tally with the skin pencil mark of
the venous bulge marked before.
F,g. 16.4.- Shows how to perform
examlnations._
(i)
Examination of
exclude pregnancy or presence of any pelvic tumour as the cause of varicosity. Such varicosity
is called secondary varicosity.
Any dilated collateral veins in the abdomen should be carefully noticed. These veins develop
due to inferior vena caval obstruction particularly thrombosis. Such veins are more often seen in
the flanks communicating with the veins of the chest wall, tributaries of the superior vena cava.
(ii) Vaginal and rectal examinations are must to exclude pelvic tumours.
(iii) Peripheral arterial pulses should also be examined to exclude presence of arterial
insufficiency. Ulcers in the lower limb with presence of varicose veins may not necessarily be
the venous ulcers. Such ulcers may occur due to ischaemia from arterial insufficiency and are
known as 'arterial ulcers'. In these cases varicose vein is the second pathology and not the
cause of the ulcer.
Special Investigations.—
Various special investigations may be performed e.g. ascending phlebography, thermography,
A CONCISE TEXTBOOK OF SURGERY
264
radioisotope scanning, radioactive fibrinogen studies and ultrasonics to know the condition of
the deep vein, position of the thrombus and position of the incompetent perforators. Of the
above-mentioned methods ascending phlebography is the most practical and valuable in the
average hospitals.
Venography.— An ascending venography is performed by cannulating a vein in the foot
and by injecting a contrast medium. A narrow tourniquet is applied just above the malleoli to
direct blood flow into the deep veins. It is a useful investigating procedure for suspected deep
vein thrombosis when ultrasonography is not available.
Descending venography is performed by inserting a cannula in the femoral vein and the
contrast material is injected with the patient standing. The contrast material is heavier than
blood, so flows down the limb through incompetent valves.
Doppler ultrasound is a valuable non-invasive tool, which can be used to demonstrate
saphenofemoral or saphenopopliteal reflux, perforator incompetence and patency of deep veins.
An important recent advance in the investigation of venous disease is colour coded Duplex scanning.
It is possible with this non-invasive technique to map the superficial and deep venous systems.
Blood flow velocity can be measured. The direction of venous flow can be observed and also
the sites of valvular incompetence can be identified.
Photoplethysmography.— The probe is attached to the skin to assess venous filling of the
surface venules. The filling of these vessels indicates the pressure of the superficial veins of the
leg. The patient sits quietly until the trace stabilizes. Then he performs a series of 10 dorsiflexion
of the ankle. The venous pressure falls in the superficial veins of the leg and the skin venules
empty so the photoplethysmography trace falls. The patient then sits and the veins refill. This
refilling occurs faster in case of venous incompetence. The test can be repeated after application
of a tourniquet above the knee to occlude the long saphenous vein and then below the knee to
occlude both long and short saphenous veins. This helps to establish which set of superficial
veins is incompetent.
Duplex Ultrasound Imaging.— In this technique high-resolution B-mode imaging and Doppler
ultrasound are used to obtain images of veins as also to measure blood flow in these vessels.
Direct visualization of veins, anatomical as also functional informations are possible to get.
Modem Duplex ultrasound machines show blood flow as a colour mark that is superimposed
on the grey scale image of the vessel. This technique is most reliable in the investigation of
arteries and veins both their anatomy and physiology. The examination is performed with the
patient standing as the veins are filled in this position. The blood flow in the veins is assessed
exactly in the same way as done in case of hand-held Doppler probe. The calf is compressed to
know the upward flow of the blood towards the heart and is shown as blue in the colour flow
map. The calf is then released. Competent veins show no flow, but incompetent veins allow
reverse flow which is represented as red in the colour flow map.
COMPLICATIONS OF VARICOSE VEINS.—
1.
THROMBOPHLEBITIS.— This means inflammation of the superficial veins. In this
case the veins become red and feel like tender cords in the subcutaneous tissue.
Treatment is antibiotic. A foam rubber is placed on the inflamed vein, on which an elastic
bandage is wrapped. Such strapping is continued for a fortnight in which the patient may be
allowed to move about. At night the patient should sleep with legs elevated. After fortnight the
bandage is removed. This usually cures the patient. One may try application of thrombophobe
ointment with disputed result. In case tenderness persists after fortnight, the treatment is repeated.
DISEASES OF VEINS
265
2. PIGMENTATION.— This is particularly seen in the lower part of the leg. Brownish to
black pigmentation is noticed. This is due to haemosiderin deposits from breakdown of R.B.C.
which have come out of the thin walled veins.
3. ECZEMA (CHRONIC DERMATITIS).— Due to extravasation and breaking down of
R.B.C.s in the lower part of the leg, the skin may itch. The patient scratches which may lead to
eczema formation. Alternatively such eczema may occur following minor trauma or as an allergic
manifestation resulting from various ointment applications.
Treatment is application of ointment containing zinc oxide and coal tar twice daily. One
may try hydrocortisone or betamethazone ointment.
4. ANKLE FLARE.— This has been discussed earlier in this chapter. See page 257 & 284.
5. VENOUS ULCER.— This results more often from deep vein thrombosis than from
varicose vein only. Such ulcers are mostly found on or near the medial malleolus. Following
deep vein thrombosis when recanalization of the deep vein occurs, the valves are either destroyed
or become incompetent due to damage. The valves of the perforators are also damaged. So
venous stasis occurs mostly in the lower and medial part of the leg where there are maximum
number of perforators. Such venous stasis favours local anoxia and oedema. This leads to lipolysis
of the subcutaneous fat. These ulcers must be differentiated from arterial ulcers due to ischaemia
following atherosclerosis. The details of this ulcer have been discussed later in this chapter.
6. HAEMORRHAGE.— Haemorrhage from ruptured varicose vein is not uncommon. Such
haemorrhage may occur externally or internally in the subcutaneous tissue. This may follow
minor trauma. Haemorrhage is usually profuse.
Treatment is simple elevation of the leg and application of a firm pad and bandage.
Tourniquet is not used.
7. PERIOSTITIS.— This occurs in case of long standing cases, particularly if a venous
ulcer is formed over the medial surface of the tibia.
8. CALCIFICATION is occasionally seen in the walls of the veins which are varicosed for
many years.
9. EQUINUS DEFORMITY of the foot may result from long standing varicosity. This is
due to bad practice of the patient of walking on the toes for relief of pain due to varicosity.
After some years the Achilles tendon may be shortened and leads to such deformity.
Treatment is physiotherapy and remedial exercises.
TREATMENT of varicose veins.—
Three modes of treatment are available — A. Palliative treatment, B. Operative treatment
and C. Fegan's injection and compression treatment.
A. PALLIATIVE TREATMENT.— The treatment has a limited scope and its indications are:
1. Those who are pregnant.
2. Those who do not want operation.
3. Those who are waiting for operation.
4. Very early cases of varicosity.
This treatment consists of :
(i) Avoidance of prolonged standing.
(ii) A crepe bandage or elastic stockings are applied from the toes to the thigh. This
should be applied before getting out of the bed in the morning and should be kept till after
getting into the bed at night. So it should be worn all throughout the day and is only taken off
during sleep.
A CONCISE TEXTBOOK OF SURGERY
266
(iii) Whenever the patient sits or sleeps, the limb should be preferably above the heart
level. At least it should be always raised.
(iv) Exercise like 'bicycle riding' in the air while lying on the back, walking etc. should
be performed to strengthen the calf muscles.
B. OPERATIVE TREATMENT.— Indications of operative treatment are :
1. Positive Trendelenburg test.
2. Particularly sapheno-femoral incompetence.
Contraindications are :
1. Pregnancy.
2. Women taking contraceptive pills.
3. Thrombophlebitis.
These cases should be treated first and operation for varicose veins is postponed till the
above complications are got rid of.
There are two types of operation :— 1. Ligation; 2. Ligation with stripping.
1. Ligation.—
(a) Sapheno-femoral incompetence.— The operation is performed under general anaesthesia.
An oblique incision is made just below the groin crease starting from the femoral artery pulsation
to 5 cm medially. All the tributaries of the long saphenous vein are ligated and divided. The
long saphenous vein is now ligated flush with the femoral vein. Particular care is taken to see
that there is no intervening tributary of the long saphenous vein between the ligature and the
sapheno-femoral junction. In the process, the superficial epigastric, the superficial circumflex
iliac, the superficial and deep external pudendal tributaries are ligated and divided. The long
saphenous vein is now ligated distal to the flush ligature and it is divided between the ligatures.
(b) In case of saphenopopliteal incompetence — a ligature is applied at the short saphenous
vein 'flush' with the popliteal vein and another ligature distal to it. The short saphenous vein is
divided between the ligatures.
2. Ligation with stripping.— Stripping operation is mainly performed in long saphenous
vein. Since incompetent perforating veins are hardly found in association with the short
saphenous vein and since stripping the short saphenous vein can not only cause long standing
oedema but may also permanently damage the sural nerve, short saphenous stripping is not
practised.
Technique.— The operation of ligation is similar to that described above.
A transverse or longitudinal incision is made over the long saphenous vein just in front of
the medial malleolus. Care is taken not to injure the saphenous nerve. The long saphenous vein
is cleared from the surrounding structures and lifted with an aneurysm needle. The distal part
is ligated tightly and the ends of ligature are held with a pair of artery forceps, which is used to
lift the vein. Proximal tie is kept loose. The vein is incised between the two ligatures and olive
point of the Myer's vein stripper is pushed up through the vein and through the proximal tie to
emerge through the distal cut end of the long saphenous vein at the groin incision. This stripper
is about 73 cm long. The upper end is now pulled till the acom-head is arrested at the medial
malleolus incision. The proximal ligature here is tightened around the stripper and now the
long saphenous vein is severed between the two ligatures. The ends of the distal ligature are
cut short. The skin is sutured above the acom-head. An elastic bandage is wound from the toes
and gradually followed up, while the stripper is steadily pulled through the groin incision
severing all the tributaries and perforating veins up to the groin incision. The stripper with the
DISEASES OF VEINS
267
vein is kept aside. The skin margins of the groin incision are now sutured and dressed.
Very often the surgeon may not be lucky to push the stripper right up through the groin
incision. The stripper may be stuck somewhere in between. In these cases incision should be
made over the olive point where it is stuck, the vein is freed and the vein distal to this incision
is stripped. Again the olive point is introduced through the vein here and pushed up. Thus the
operation is performed in stages.
POSTOPERATIVE MANAGEMENT.— At the end of the operation compression bandage
is applied to the limb to prevent excessive bruising. This bandage may be replaced after 1 or 2
days with a thigh-length high-compression stocking. The advantage of this stocking is that it
can be easily removed before taking bath and can then be reapplied.
Complications after surgery.— Bruising and discomfort are the main complications. Slight
pain is often complained of which requires mild analgesic.
Sensory nerve injury in the form of saphenous nerve or its branches which accompany the
long saphenous vein may be damaged; similarly the sural nerve which accompanies the short
saphenous vein may also be damaged. But such damage never occurs in more than 1% of cases
and the area of anaesthesia is so small that it is often not located. However all patients should
be warned before surgery that small areas of numbness and tingling may occur after operation.
After varicose vein surgery motor nerve injury is extremely uncommon unless the popliteal
fossa is explored and the nerves in this region are not taken care of.
Venous thrombosis may follow varicose vein surgery, but usually resolves without any
specific treatment. Deep vein thrombosis may also occur following such surgery. Patients who
have previously suffered from deep vein thrombosis are particularly at risk and they should
receive full prophylactic measures including low-dose subcutaneous heparin in addition to
compression stockings. Patients receiving oestrogen therapy are also at higher risk of venous
thrombosis and heparin prophylaxis should be considered.
Multiple Cosmetic Phlebectomy.— Having dealt with the sources of retrograde flow it
may be required to remove a few superficial veins which may have been dilated over the years
by the unrestrained effects of increased intraluminal pressure.
Technique.— A Beaver miniature blade is used to make a tiny incision immediately over the
vein (which has been marked pre-operatively). With a fine mosquito forceps the vein is gently
taken out to the surface when it is more generously grasped with larger forceps. Fine dissection
may be required to free the varicose vein. The varicose vein is now resected by ligating both
the ends. The skin incision is closed with either subcuticular stitches or with steristrips to make
the closure 'cosmetic'.
C. FEGAN'S INJECTION AND COMPRESSION TREATMENT.— The indications are :
(1) When varicose veins are mostly confined to below knee and are caused by incompetent
perforators.
(2) Recurrent varicosity after operation.
(3) A probable alternative to surgery when the patient refuses it.
Contraindications are :
(1) Deep vein thrombosis — this must be excluded before injection treatment.
(2) Sapheno-femoral incompetence.
In this technique sclerosant like ethanolamine oleate 5% (Ethanolamine B.P.C.) or sodium
tetradecyl sulphate 3% (Thrombovar) is used to damage the intima of the vein and to produce
sclerosis later on. No doubt that intimal damage will take place only when sufficient concentration
268
A CONCISE TEXTBOOK OF SURGERY
of sclerosant is injected, yet one should be cautious not to inject more than sufficient concentration
of the sclerosant lest it may reach the deep veins and should initiate thrombosis there. The
maximum dose at one time and in one point is 1 ml. The injection should be given into an
empty vein so that its walls adhere without any intervening blood clot or thrombosis to yield a
lasting result.
Technique.— The patient is made to stand. The positions of incompetent perforators are
marked with ink. The needles of small syringes containing 1 ml sclerosant solution are inserted
into the ink-marked points. The pistons of the syringes are slightly withdrawn to see if the
venous blood is entering the syringes freely indicating that the ends of the needles are inside
the incompetent perforators. The patient is now asked to lie down on a bed. He is directed to
lift the leg concerned. Thus the veins are made empty. Now the solution is injected. Rubber
pads are pressed on the sites of injection while the needles are withdrawn. A crepe bandage is
applied from the toes to the groin keeping equal pressure throughout over the rubber pads.
Postoperatively, the patient is encouraged to walk as usual. Importance of walking
immediately after sclerotherapy and subsequent extra walking each day cannot be over
emphasized. Such walking is important to discourage clotting from spreading into the deep
veins. If the patient remains comfortable with
compressive bandage it should not be
disturbed for at least 3 weeks. The patient
must attend the outpatient clinic every week. ■■■■■H
f
After 3 weeks a new bandage is applied with
less compression for another 3 weeks, after
which the bandages are taken off. Later on
the patient will always be asked to attend
. '■
Ioutpatient at regular intervals, so that further
,
. - v' : injection may be carried out to any returning
varicosities. So sclerotherapy is a long term
policy of maintenance rather than the one­
time cure intended with surgery.
Wati §£ %
VENOUS ULCER
Venous ulceration has two main
aetiologies. Firstly, ulceration may be
associated with demonstrable varicose veins
and secondly, such ulceration may follow
thrombosis and phlebitis in the deep and
perforating veins. This second group presents
as an ulcerated oedematous leg with
demonstrable superficial varices in only
about l/3rd of cases. In all cases of this
second group there will be history of long
standing oedema of the leg.
Pathogenesis.— After the deep vein
thrombosis, if the deep venous system is
allowed to eventually recanalise itself, the
DISEASES OF VEINS
269
delicate valves will remain impregnated laterally in organised thrombosis. The result is patent
but valveless deep venous system, which transmits the gravitational pressure of the blood column
unimpeded from the level of the heart to the ankles. This is the main predisposing feature in
the pathophysiology of the postphlebitic state. However, valvular incompetence alone is not
enough to produce serious stasis sequels. It must occur through incompetent perforator veins
through which the high deep venous pressure is transmitted to the superficial veins. The location
of these perforating veins determines the predilection of ulcer formation — extending from the
malleoli upto the lower half of the leg. These perforators may have been involved in the initial
thrombosis or may become incompetent by dilatation resulting from the back pressure of the
valveless deep venous system.
Within 10 years of untreated thrombophlebitis, 50% will have venous ulcers.
Fibrinogen escapes through large pores in the venules of these patients with venous
hypertension secondary to venous insufficiency. This fibrinogen accumulation acts as a barrier
to diffusion of oxygen and other nutrients and thus develops thick, hard subcutaneous tissue.
Stasis dermatitis develops with brawny oedema, pigmentation and cutaneous atrophy. Fat necrosis,
tissue death and ulceration follow. It is not until some minor trauma which leads to a skin
break that an actual venous ulcer develops.
Special Investigations.—
Ascending functional phlebography or venography is highly important to formulate treatment
in difficult cases. It will show the size of the lumen of the deep veins, the presence of valves
and existence of high pressure leaks in the calf.
Doppler apparatus may be adopted to indicate the direction of flow in veins.
TREATMENT.—
A detailed history of development and progression of the leg ulceration must be taken.
The patient should be examined in a good light both standing and lying with both lower
limbs completely exposed. One must exclude ischaemic ulcer following arterial abnormality.
Clinical tests for long and short saphenous incompetence must be carried out. In addition the
position of the incompetent perforators should be pointed out. The dimensions and exact site of
ulceration should be recorded. The quantity and nature of discharge is noted and cultured.
A. Conservative Treatment.—
(i) Elevation of the affected limb is important. Vertical leg drainage is a simple and
valuable method of reducing and eliminating leg oedema. The patient is advised to sleep with
the legs at 90° to the horizontal plane by putting a vertical board at the end of the bed or
pushing the bed against the wall. The frequency of daily leg elevation depends on the rapidity
of oedema formation.
(ii) Passive movements to maintain the mobility of the foot and ankle.
(iii) Active movements of the calf muscles.
(iv) A firm elastic 'blue line' bandage is applied spirally from the base of the toes upto
the knee joint. While walking this bandage will alternatively stretch and relax and thus help in
venous pumping. A piece of felt or rubber with bevelled edges are cut to a size more than the
ulcer and is interposed in the bandage over the ulcer to reduce the local oedema. This bandage
must be worn whenever the patient is out of bed. The most important factor in achieving healing
of such ulcer is the use of high levels of compression. Pressure of 30 to 45 mmHg is ideal for
early healing. This can be achieved by the use of compression stockings (class 3 stocking exerts
about 30 mmHg compression at the ankle) or by bandaging. This compression should only be
270
A CONCISE TEXTBOOK OF SURGERY
applied to the ulcer region, so patients should wear below the knee stockings. Those patients
who cannot manage the stocking, can be treated by multilayer bandaging. But this bandaging
must be applied by a person trained in this procedure. The best known of these techniques is
the '4-layer bandage' used at Charing Cross
Hospital, London. In this method pressure
of 45 mmHg can be achieved at the ankle.
It has been shown that 70% of venous
ulcers are healed within 12 weeks. This
bandage must be changed once or twice a
week.
(v) Effective antibiotic from the
culture report should be prescribed
immediately. An analgesic may also be
prescribed if required.
(vi) Most exudative ulcers with
yellow or sloughy base and poor
granulation tissue require daily cleansing
and dressing until the ulcer becomes dry
with healthy granulation at the base.
Hibitane, Eusol or hydrogen peroxide may
be used for this purpose.
(vii)
Absorbent
or
adherent
dressings with spirit applications to
promote drying and scaling may achieve
this aim. Proprietory zinc and calamine Fig. 16.6.— Phlebogram showing translucent areas within
absorbent bandages have proved very
the deep veins which are nothing but thrombi.
effective. 'Calaband' and/or 'viscopaste'
have their advocates. Bandages are worn over the dressing and can be left in place upto 1
month at a time, although they are initially changed every week.
(viii) Once the ulcer is clean Orahesive powder may be applied on the surface of the
ulcer. Bandage should be continued from toes to the knee.
(ix)
80% to 90% ulcers will heal with this simple outpatient regimen. But the remaining
patients with extending or longstanding ulceration will prove resistant to this form of treatment
and will require admission to hospital.
B. Surgical Treatment.—
(a) Alongwith the previous conservative regimen, incompetent perforators and varicose
veins may be treated by surgery or sclerotherapy following which the ulcer will heal completely.
(b) Larger ulcers will need a split skin graft after the veins have been treated.
(c) Ascending phlebogram must be performed at this stage if not performed earlier to
detect incompetent calf perforating veins and evidence of damaged deep veins. Normal
phlebogram should arouse suspicion as another cause of ulceration as it is rarely produced by
simple saphenous incompetence.
(d) Subfascial ligation of Cockett and Dodd.— Once the ulcer has healed the
incompetent perforating veins should be identified and divided. An incision is made in the
lower half of the leg 2.5 cm behind the posterior border of the tibia. The incision is deepened
DISEASES OF VEINS
LINE OF
271
BORDER
OF TIBIA
ACHILLES TENDON
MEDIAL MALLEOLUS
LATERAL
'gjjg'XriNG
gastrocnemius
UPPER-
J- POSTERIOR
/BORDER OF
f FIBULA PALPABLE
THRU MUSCLE
MIDDLE
till the deep fascia is reached. The
margins are undermined. The deep
fascia is incised along the line of
incision. The margins of the deep
fascia are lifted up. The perforating
veins are ligatured under direct
vision and divided (Fig. 16.7).
(e) Linton developed a radical
surgical approach. In this technique
the superficial varicosities were
ligated and stripped with subfascial
ligation of the perforating veins.
(f) A by-pass operation may be
performed for thrombosed deep
veins. Such occlusion is relieved
before or at the same time that the
incompetent perforators are ligated.
The saphenous vein has been used
to by-pass segmental venous
occlusion of the iliofemoral or
femoropopliteal vein. For iliofemoral
occlusion,
the
contralateral
saphenous
vein
is
passed
suprapubically and anastomosed to
the affected side distal to the
occlusion. This is known as Palma
operation.
For femoropopliteal occlusion, the
obstructed segment can be by­
passed by anastomosis of the
saphenous vein to the poplitealtibial trunk below the occlusion at
the level of the knee joint.
Better assessment of a case can
be made by (i) isotope clearance
technique perhaps combined with
(ii) foot volumetric studies and (iii)
Doppler assessment of reflux. At
present, these techniques are being
combined with ascending and
■ACHILLES
TENDON
LOWER
DEEP FASCIA
SKIN FLAP WITH
SHORT SAPHENOUS VEIN
Fig.16.7.—
Cockett
and
Dodd
operation. The upper figure shows
incision. The lower figure shows that the
medial perforating veins are ligated and
divided, whereas the lateral perforating
veins are exposed.
272
A CONCISE TEXTBOOK OF SURGERY
descending phlebography. Based on these results by-pass surgery, valvular repair, valvular
insertion by-passes and artificial valvular transplantation can be selected and assessed.
(g) Valvular repair.— Venous valves in the deep veins may be repaired if their
incompetence is a consequence of primary valve failure. This may lead to successful long term
maintenance of leg ulcer healing. However these operations are technically difficult and there is
risk of thrombosis which may destroy the reconstructed valve. This valve repair was described
by Kistner. He described two types of repair — internal by incising open the vein and suturing
the valve to make incompetent valve competent. The other type is external suturing i.e. the
valves are sutured from outside the vein without opening it.
Valve transplant by autograft.— A portion of the vein which contains defective valves following
deep vein thrombosis may be replaced by transplanting a segment of axillary vein or brachial
vein of the same person which contains competent valves.
(h) The main stay of the local ulcer treatment is to cleanse the ulcer in simple water and
then to debride the ulcer to remove all sloughs. The skin of the leg becomes scaly, which should
be treated by emulsifying ointment. No local antibiotic should be used, similarly no topical
application has been shown to expedite the healing of a venous ulcer as often such applications
make the skin allergic. Only topical steroids may be applied when there are eczematous reactions
around the ulcers. Some surgeons prefer excision and skin grafting, but effectivity of this
procedure is questioned. Now microvascular free-skin flap transfer offers the prospect of bringing
healthy tissue into the areas of severely damaged ulcerative area of skin.
VENOUS THROMBOSIS
Venous thrombosis is a very common surgical problem, which has great influence on the
morbidity and mortality of surgical patients.
_
Aetiology'.— Three factors play major roles in aetiology of venous thrombosis. These are:—
(1) Stasis, (2) injury to the vessel wall and (3) hypercoagulability of the blood.
Stasis is probably the most important clinical factor to cause venous thrombosis. A reduction
of blood flow in the major veins by half has been shown immediately following induction of
general anaesthesia and in debilitating diseases. This decrease in flow persists for the duration
of anaesthesia. Clinical coagulability is raised from the overactivity of the normal blood clotting
mechanism. The increased clotting tendency encountered postoperatively may be the result of
several factors including altered blood elements associated with blood dyscrasias or polycythemia
or may be secondary to dehydration. This hypercoagulability of the blood most frequently occurs
in infection, after haemorrhage and in visceral carcinoma which may cause thrombophlebitis
migrans (Trousseau's sign). Injury to the vein wall is mainly due to trauma or infection.
A few predisposing factors are :— (i) major injuries, (ii) following operation, (iii) visceral cancer,
(iv) tobacco smoking, (v) diabetes, (vi) congestive heart failure, (vii) shock, (viii) polycythemia
vera, (ix) long period of sitting or bed rest, (x) pregnancy, (xi) infection, (xii) varicose vein, (xiii)
obesity, (xiv) using of contraceptive pills.
Nowadays great stress is being led on the hypercoagulability factor. Damage to the
endothelium leads to platelet adherence which is the start of the thrombotic process with fibrin
deposition.
RESULTS of thrombosis are as follows :—
(i)
Proximally, thrombosis extends into larger veins, where portions of clot may detach as
emboli to cause pulmonary embolism and infarction, which is fatal.
DISEASES OF VEINS
273
(ii) Locally the clot ultimately organise into fibrous tissue. While a few veins remain
obstructed following thrombosis, others may recanalise. In both these cases the venous valves
are destroyed leading to chronic venous valvular insufficiency. Occasionally calcification may
be seen in the thrombus in pelvic veins, which are known as phlebolith.
(iii) Distally thrombus causes venous obstruction, which increases distal venous pressure.
This leads to oedema. Venous collateral circulation may open up by the appearance of tortuous
superficial veins. If venous pressure increases to such an extent that it exceeds local arterial
pressure, blood flow ceases and venous gangrene occurs.
Types of venous thrombosis.—
Mainly two types of venous thrombosis are seen —
1. Thrombophlebitis.— This is mainly seen in the superficial veins, particularly in varicose
veins or in veins which have been cannulated for infusion. In these cases venous thrombosis is
associated with acute inflammatory response giving rise to pain, local swelling, redness and
tenderness. Although acute inflammatory changes occur in the vein wall, bacteria are rarely present.
2. Phlebothrombosis (deep vein thrombosis).— Here the thrombus produces little
local signs or symptoms and may be loosely attached to the vein wall, so that emboli may be
dislodged from this thrombus to cause fatal pulmonary embolism.
SUPERFICIAL VEIN THROMBOSIS (THROMBOPHLEBITIS).—
As mentioned earlier such thrombophlebitis occurs more often in varicose veins or after
intravenous infusion. This is also seen in association with polycythemia, polyarteritis, Buerger's
disease and visceral cancer. In both Buerger's disease and visceral cancer, thrombophlebitis may
affect one vein after the other and is typically known as thrombophlebitis migrans. This is known
as Trousseau's sign ( this sign is also used to indicate muscular spasm on pressure over nerve,
seen in tetany).
Clinical features.— The patients usually complain of painful cord-like inflamed area, the
inflamed vein.
Careful palpation will reveal a firm cord along the course of a nonsuperficial vein. There
may be associated redness, tenderness and local induration. Veins of the lower extremity should
be best examined in the standing position.
Treatment.— Operation is almost never required as embolization never occurs. However
thrombophlebitis may be present with deep vein thrombosis, when there will be significant
distal swelling and a phlebogram will diagnose deep vein thrombosis.
(a) Hot baths or compress may be helpful in relieving discomfort. It may also prevent
propagation of thrombus by preventing venous stasis.
(b) Elastic support or crepe bandage should be applied to the part. When it affects the
leg, walking is advised with elastic support. The patient may lie down in bed with legs elevated
above the level of the heart. However sitting or standing should be discouraged though walking
is encouraged.
(c) Anticoagulants or enzymatic clot dissolvers have little effect on the outcome.
(d) Aspirin is quite effective in this condition, though there is hardly any place of expensive
and potentially dangerous 'antiinflammatory' drugs.
(e) The role of antibiotic is debateable. While many surgeons prefer to give a short course
of penicillin or cotrimoxazole, others rule out any benefit which may be achieved due to
administration of antibiotic unless a definite septic cause is obvious. But antibiotic has got a
definite role to play in case of thrombophlebitis due to intravenous infusion.
18
274
A CONCISE TEXTBOOK OF SURGERY
Operative treatment.— Only when there is evidence of ascent of thrombi into the more
proximal vein, ligation of the vein is justified. Ligation of the long saphenous vein at the
saphenofemoral junction using local anaesthesia or short saphenous vein in the popliteal fossa
may be indicated if there is fear of propagation of thrombi proximally. Such ligation is also
required when the vein is becoming recurrent phlebitic.
DEEP VEIN THROMBOSIS (PHLEBOTHROMBOSIS) (DVT).—
The aetiology has already been considered under the heading of 'Venous Thrombosis'. The
main predisposing factors are (1) stasis, (2) increased blood coagulability and (3) injury to the
vessel wall.
Deep vein thrombosis occurs more often after operations, any debilitating illness, immobility
for a considerable period, child birth and some sort of local trauma. A peculiar condition is
'spontaneous thrombosis', which may occur without any definite reason and in this case presence
of visceral neoplasm should be excluded. Another important feature is that postoperative
thrombosis is rare before the age of 40 and is more often seen following operations on the hip
joint, on the prostate, cancer and in obese patients.
The thrombus may commence in a venous tributary of a main vein. The calf is the most
frequent site of thrombosis. From here thrombus extends in a serpentine fashion into the main
deep veins, where a portion may break off to cause pulmonary embolus. Other veins are also
involved less frequently.
Clinical features.— Patients with suspected deep venous thrombosis should be evaluated
and treated promptly in order to lessen the propagation of the thrombus, to limit the damage
to the venous valves and to reduce the potential for pulmonary embolism. Venous thrombosis
often is asymptomatic and clinical indications are present in only 40% or less of patients with
venous thrombosis.
The main symptom, which if at all present, is an aching pain. This pain is aggravated by
muscular activity at the site of the thrombus. Sometimes there is only a feeling of heaviness,
accentuated by standing. If there be a massive thrombosis there may be an extremely severe
aching at the site of thrombosis.
Swelling is another symptom, which is noticeable at the dependent part. This swelling is
usually minimal and only occasionally it may be marked.
PHYSICAL FINDINGS.— The three most important signs which may be present in a case
of deep vein thrombosis are swelling, tenderness and Homans' sign.
Swelling should be searched for with the aid of a measuring tape. In majority of cases there
is so slight swelling that it may be missed by the naked eyes. The other extremity should always
be placed side by side to compare and to exclude swelling on the affected side.
Tenderness over the thrombosed vein can be detected by careful palpation of the calf, popliteal
space and thigh (particularly the adductor canal).
Homans' sign.— Homans was the first physician to emphasize the importance of venous
thrombosis in the legs as source of pulmonary emboli. He described a test which is known as
Homans' sign. In his test passive forceful dorsiflexion of the foot with the knee extended will
elicit pain in the calf. Passive elongation of the gastrocnemius and soleus muscles causes irritative
pain in the calf when the calf veins are thrombosed.
Gentle pressure directly on the calf muscle in the relaxed position will also elicit pain. Care
must be taken to be gentle in manipulation lest it should dislodge emboli to cause pulmonary
embolism.
DISEASES OF VEINS
275
Moses' sign.— Squeezing of the calf muscles from side to side is painful in case of deep
vein thrombosis.
Various sites of involvement.—
1. Calf vein thrombosis.— The most frequent site of thrombosis is probably the veins of
the calf, particularly in the venous sinuses of the soleus muscle. If untreated, the thrombi may
propagate to involve the femoral vein or even the iliac vein. As mentioned above Homans' sign
and calf tenderness are usually present. Swelling is present in only 50% of cases and it is almost
always minimal.
2. Femoral vein thrombosis.— Quite often thrombosis of calf veins is associated with
thrombosis of the femoral veins. Sometimes there is only thrombosis in the femoral vein. This is
detected by tenderness of the thigh, particularly in the adductor canal. Swelling is usually present
at the ankle or calf level. Homans' sign may or may not be present.
3. Iliofemoral venous thrombosis.— Iliofemoral venous thrombosis may also be associated
with calf vein thrombosis. But it may occur singly. The left leg is more often involved in the
ratio of 3 : 1. The reasons may be (i) apparently longer course of the left vein, (ii) its constriction
by the right iliac artery and (iii) occasional presence of congenital web at its junction with the
inferior vena cava.
In this type there is marked swelling affecting almost the entire leg. This is due to
considerable rise in the venous pressure. Alongwith marked oedema there is also bluish
discolouration. When this bluish discolouration is associated with the pain, the process is called
phlegmasia cerulea dolens. This syndrome may progress to venous gangrene due to massive
thrombosis of all venous drainage of the limb. This should be differentiated from white leg or
phlegmasia alba dolens due to lymphatic obstruction and swelling of the lower limb.
4. Pelvic vein thrombosis.— Thrombosis of the pelvic veins is rare and often involves
branches of the internal iliac veins. This is more often seen in women with pelvic inflammatory
disease. Sometimes it may be seen in men due to involvement of the prostatic plexus. The
diagnosis is difficult unless it involves the common iliac and external iliac veins when
manifestations in the leg will be detected. Sometimes pelvic or rectal examination may help in
the diagnosis.
Special investigations.—
Since clinical symptoms and signs are not very reliable to diagnose deep vein thrombosis,
much reliance is given on special investigations.
1.
PHLEBOGRAPHY.— The patient lies on a mobile table in horizontal position. 45%
sodium diatrizoate is injected slowly into a vein on the dorsum of the great toe. A pneumatic
cuff just above the ankle directs the contrast medium into the deep veins. Another cuff at the
mid-thigh position confines the contrast medium initially to the lower leg. The amount and rate
of injection of the contrast medium is controlled by the filling of the veins as viewed on the
television screen. The patient is asked to dorsiflex and plantarflex his foot thus propelling the
contrast medium into the tibial veins. When the veins are filled films are taken of the leg in two
planes. At the end of the procedure the contrast medium is washed off from the leg veins by
injecting 100 ml of normal saline containing heparin.
Ascending functional cinephlebography can be obtained by continuous observation of the flow
of the contrast medium on the television screen as it progresses through the tibial veins. Function
of the valves can be particularly noticed. Similarly the popliteal and femoral veins can also be
assessed. The valvular function is considered to be normal when both the valve cusps are seen
A CONCISE TEXTBOOK OF SURGERY
276
Fig. 16.8.— Ascending phlebography showing normal filling
of the deep veins of the leg and thigh.
to open and close with onward flow of blood and
no retrograde flow occurs even with the Valsalva
manoeuvre.
Radionuclide phlebography.—- The venous
system can be visualized by injection of an isotope.
The definition is not as good as with contrast
phlebography, but thrombi within the thigh and
pelvic veins are readily identified. That is why this
technique has become of special value in iliac
venous system, where X-ray studies are often
Fig.16.9.— Phlebogram of the deep veins of the
difficult.
leg (tibial veins) showing translucent areas which
2. RADIOACTIVE FIBRINOGEN TEST—
indicate thrombi within the veins.
At first l31I-labelled fibrinogen was used.
Subsequently 125I-labelled fibrinogen was employed due to its softer radioaction and its
detectibility with much lighter and mobile apparatus. The thyroid gland is firstly blocked by
sodium iodide (100 mg) given orally 24 hours before the intravenous injection of 100 microcuries
of 125I-labelled fibrinogen. The scintillation counter is first placed over the precordial region and
the radioactivity over the heart is measured. The machine is adjusted so that this reading
represents 100%. The legs are elevated on an adjustable stand to decrease venous pooling and
to give access to the calf for the scintillation counter. Counting is performed along the lower
extremity at two inches interval. Preoperative counting can be compared with the postoperative
counting on the 1st, 3rd and 6th days after operation. An increase in the percentage value of 20
or more represents formation of thrombus in the deep veins of the legs.
DISEASES OF VEINS
277
The test is positive only during the
active formation or a propagation of a
thrombus. It is more valuable during the
postoperative period to detect the patients
at risk. At the time of formation of
thrombosis, its accuracy is about 90%. This
accuracy falls with established deep vein
thrombosis to about 80%.
3.
DOPPLER ULTRASONOGRA­
PHY.— This convenient and readily
available technique depends upon the
recognition of distorded flow patterns or
absence of flow in the larger veins. This
technique quite accurately detects the
presence of thrombi in those veins
proximal to the knee. The sensing probe is
placed over the femoral vein in the groin.
Normally it transmits a venous hum and
pressure on the calf will change it into a
'roar' due to increased blood flow. If there
is thrombosis in the calf veins, femoral or
popliteal veins, the 'roar' is not heard.
Fig. 16.10.— Radionudtde venogram. *. Dynamic phase, However this test is relatively insensitive
which shows filling defect in the right calf. Remainder of to calf vein thrombosis.
the right side and whole of the left skte are rearma!. b.
4.
PLETHYSMOGRAPHY.— Strain
Static phase, which shows persistence of ladfcmudide in
gauge plethysmography quantifies venous
the right catf distal to the fifag defect.
obstruction by measuring the rate at which
the calf veins empty when the pressure in a proximally placed pneumatic cuff is released. The
rate of maximum venous outflow is inversely proportional to venous resistance. By inflating a
proximal venous cuff below an occlusive tourniquet, the extent of venous reflux can also be
evaluated.
Other plethysmographic techniques have also been developed e.g. impedence plethysmography.
Significant venous obstruction decreases the venous volume changes occurring with respiration
and intermittent compression with a pneumatic thigh cuff. Liquid blood conducts electric currents
and this instrument is capable of measuring small changes in the electrical resistance of the leg
and thus assesses changes in venous volume. This instrument is however much more reliable
in making correct diagnosis of femoropopliteal and major calf-vein thrombosis than doppler
ultrasonography.
5. VENOUS PRESSURE MEASUREMENT.— A needle is inserted into a superficial vein
of the foot or ankle and this is connected to a saline solution manometer. The pressure is compared
with those in the other leg and arm. This test will however be positive in the presence of
significant venous obstruction only early in the course of the disease before sufficient collaterals
have developed.
6. DUPLEX ULTRASOUND IMAGING.— Due to direct visualization, both functional and
anatomical informations can be obtained.
278
A CONCISE TEXTBOOK OF SURGERY
PREVENTION.— Every care should be taken to prevent formation of deep vein thrombosis.
The main points to be considered in preventing deep vein thrombosis is (a) to minimise venous
stasis, (b) to avoid venous intimal injury and (c) to reduce hypercoagulability.
BEFORE OPERATION.— (i) Prevention must begin before operation. Time spent in hospital
awaiting operation should be reduced to the minimum.
(ii)
Leg elevation above the level of the heart is quite effective. A recent venographic
study has demonstrated that the contrast medium remains in the soleal veins in an average of
10 minutes in supine patients with legs in horizontal position. Elevation of legs 20° above
horizontal level causes immediate emptying of dye from the soleal veins.
DURING OPERATION.— (i) Elevation of leg during operation, if possible, is quite effective
in reducing DVT.
(ii) Hypertonic or irritating intravenous solutions should not be used into the veins of
the lower extremity. If they are to be used, it is best given by an indwelling catheter.
(iii) Use of anticoagulants e.g. heparin in small doses has competently reduced the
incidence of DVT. 5000 units of heparin is introduced subcutaneously 2 hours prior to operation
and every 8 hours thereafter for 7 days has considerably reduced the incidence of deep vein
thrombosis as diagnosed by I25I-labelled fibrinogen test.
(iv) Intermittent pneumatic compression, electrical calf stimulation and active plantar
flexion of the feet effectively prevent venous stasis in the soleal veins. During anaesthesia,
passive plantar flexion by pedalling on a motor driven board increases the mean venous
flow. External pneumatic compression is free from side effects and is relatively simple and
cheap. It is very effective in preventing venous stasis. Electrical stimulation of the calf muscles
is another physical method of prophylaxis. It appears to be a less effective measure of
prophylaxis when compared to intermittent pneumatic compression. Simple leg elevation and
plantar flexion of the feet are both inexpensive and effective in preventing venous stasis and
require minimal nursing effort.
AFTER OPERATION.— (i) Low molecular weight dextran has been used to prevent venous
thrombosis. But occasional occurrence of pulmonary oedema and increased incidence of bleeding
and haematomas has been noted after such indiscriminate use of dextran. However dextran
prophylaxis may be advantageous in a selected group of patients who are simultaneously in
need of volume replacement and prophylaxis for thrombosis. Bleeding generally is not a problem
if dosage of 1.5 g/kg body weight is not exceeded. However the risk of fluid overload especially
in the elderly patients should be considered.
(ii) Aspirin in small dose has both been able to reduce postoperative pain and prevent
DVT.
(iii) Elastic stockings have been claimed to reduce DVT by compressing the superficial
venous system which increases the velocity of venous blood flow through the deep veins thus
reducing the venous stasis. The optimal pressure gradient for elastic stockings should be 18 to 8
mm Hg from the ankle to the thigh, which increases venous flow velocity detected with Doppler
ultrasound. However the effect of an elastic stocking in prevention of deep vein thrombosis is
controversial. The available data do not provide sufficient evidence to justify its widespread
use. On the other hand these stockings if not fitted properly to ensure graded compression
from the ankle to the thigh, actually may act as a tourniquet and may increase venous stasis.
(iv) Leg elevation is obviously very important in the early postoperative days.
DISEASES OF VEINS
279
TREATMENT OF ESTABLISHED CASES.—
CONSERVATIVE TREATMENT.
(i) Bed rest.— Bed rest is indicated for about 7 days after the diagnosis is established.
This is to allow thrombi to become adherent to the vein wall. It also prevents formation of
pulmonary embolus.
(ii) Elevation of legs above the level of the heart decreases the pressure in the veins. It
relieves oedema and pain. It also increases rate of blood flow in the nonaffected veins thereby
preventing venous stasis and formation of new thrombi.
(iii) When walking is started, an elastic stocking should be used. With this the rate of
flow in the vein is increased. Standing and sitting idle should be prohibited. This prohibition
should be for no less than 6 months period.
(iv) Heparin.— This drug prevents thrombus formation by inhibiting the formation of
thromboplastin and also acts as antithrombin to inactivate thrombin. Its effectivity can be
determined by measuring clotting time and partial thromboplastin time (PTT). If clotting time
or PTT is at least twice normal, propagation of thrombi can be prevented. This can be achieved
by administering aqueous heparin in the dose of 5000 to 10000 units intravenously either
continuously or every 4 hours. This therapy is advised for variable lengths of time. It is reasonable
to use for at least 7 days. Gradually the dose is reduced over a period of 3 to 5 days. If the drug
is discontinued abruptly, new thrombosis may be formed. This is known as 'heparin rebound'.
After discontinuing heparin, oral anticoagulant therapy with coumarin derivatives should be
started.
(v) Coumarin derivatives.— These derivatives interfere with 4 factors in the clotting
mechanism, but their main effect is reduction of plasma concentration of prothrombin. So the
effect of these drugs can be determined by measuring prothrombin time, which should be less
than 10% of normal to inhibit propagation of thrombi. Warfarin is used for approximately 4
weeks after venous thrombosis or pulmonary embolism, as recurrence is likely within this period.
In case of patients with iliofemoral venous thrombosis this drug should be continued for 6
months. In case of pregnancy, this drug can pass placental barrier, whereas heparin cannot. So
these drugs should not be used during the first trimester or during the whole period of pregnancy
as bleeding complications in new bom infants may be noticed.
(vi) Fibrinolytic drugs e.g. streptokinase indirectly converts plasminogen to plasmin, which
can lyse clots in deep veins. Streptokinase is derived from streptococcal cell cultures. It is
administered intravenously over 12 hours period. Significant lysis of clot within 5 days has
been demonstrated. However allergic, pyrogenic and bleeding side effects should be considered.
Urokinase directly converts plasminogen to plasmin and it also successfully lyses clots. This
drug has been derived from foetal kidney cell cultures and its cost is considerable.
(vii) Aspirin, dipyridamole and sulphinpyrazone are the pharmacologic agents that inhibit
platelet function and have been used considerably in prevention of venous thrombosis. 1200
mg of Aspirin given daily as a preventive measure in patients following elective hip replacement
have been found to be as effective as warfarin in preventing clinically diagnosed venous
thrombosis and pulmonary embolism.
OPERATIVE TREATMENT.—
By-pass procedure.— Simple by-pass with vein or prosthetic material may be used in larger
vessels e.g vena cava and iliac veins. In this technique veins of large calibre are difficult to get,
so some sort of prosthetic material is more often used. Palma operation may be carried out
280
A CONCISE TEXTBOOK OF SURGERY
which involves mobilizing the long saphenous vein of the opposite leg, the distal end is tunnelled
across suprapubically and inserted into the affected femoral vein below the obstruction. Blood
drains from the affected leg via the long saphenous vein into the femoral vein of the opposite
side. In case of obstruction of the superficial femoral vein, the long saphenous vein is connected
to the popliteal vein of the same leg. This is known as May-Husni procedure. In majority of
patients with chronic superficial femoral vein obstruction, the blood flows along the long
saphenous vein to reach the common femoral vein, so no operation is required.
Valvular repair.— When the venous valves in the deep veins are damaged, valve repair is
possible to make them competent. This valve repair was described by Kistner. He described
two types of repair — internal by incising open the vein and suturing the valve to make
incompetent valve competent. The other type is external suturing i.e. the valves are sutured
from outside the vein without opening it.
Valve transplant by autograft.— A portion of the vein which contains defective valves following
deep vein thrombosis may be replaced by transplanting a segment of axillary vein or brachial
vein of the same person which contains competent valves. These operations are particularly
carried out who have previously suffered from deep vein thrombosis.
1. Venous thrombectomy with Fogarty catheter has been successfully applied in cases of
major veins e.g. subclavian, ilial or femoral.
2. Sometimes massive venous thrombosis in the lower limb leads to severe impairment
of blood supply to the limb leading to ischaemia and even gangrene. This is a surgical emergency
and requires quick relief of venous obstruction. This can be achieved surgically by opening the
femoral vein through an incision in the groin and removing all clots from the deep veins of the
pelvis and leg. This operation however is losing popularity and the more modem treatment is
thrombolysis — by passing a catheter into the affected vein and by infusing a fibrinolytic agent
e.g. streptokinase or tissue plasminogen activator (TPA).
3. Prevention of pulmonary embolism by surgical means has been considered. This is
particularly if the patient is already having anticoagulant treatment. Thrombectomy cannot be
said to have contributed significantly to the prevention of pulmonary embolism nor perhaps
either to the reduction of post-thrombotic stasis. However it has a real place as potential cure
for developing venous gangrene. The various methods in this group are —
(i)
Ligation of femoral vein below profunda entry; (ii) Ligation of iliac vein; (iii)
Interruption of the venous pathway to the lungs by narrowing the inferior vena cava by sutures,
coarsely serratpd clips or by inserting an umbrella filter.
Objections to these operations include (a) the risk of late stasis effect and (b) thrombus has
been demonstrated beyond these devices at postmortem in patients who have succumbed to
pulmonary embolism.
However very few surgeons now perform the above-mentioned operations. The more
modem treatment is to achieve thrombolysis by passing a catheter into the affected vein and
infusing a fibrinolytic drug such as streptokinase or tissue plasminogen activator (TPA). This is
reducing the need for operation.
4. The most effective preventive measure against secondary embolism is heparin in full
therapeutic dosage upto 60,000 units in 24 hours given by regulated drip. This regimen continued
for 7 to 10 days will largely exclude the problem and operation is only restricted to resistant or
chronic cases of small repeated embolism resulting in pulmonary hypertension. Of course as
with heparin there is the risk of haemorrhage.
DISEASES OF VEINS
281
PULMONARY EMBOLISM
Pathophysiology.— Thrombi break loose from the deep vein thrombosis, pass through the
right atrium and ventricle and lodge in the pulmonary arteries. This is known as pulmonary
embolism. Small emboli lodging in a lobar or segmental artery may cause death, but the
mechanism is not clearly known. It may be, that intense reflex bronchoconstriction and
vasoconstriction may lead to such death. Single small embolism may also result in infarction,
followed by infection, abscess and empyema.
Multiple small emboli may produce arterial obstruction to such an extent as to cause
pulmonary hypertension and right ventricular failure.
Large thrombus which lodges in major pulmonary artery may cause immediate death due
to vasovagal shock, right ventricular failure and inadequate transfer of oxygen and carbondioxide
in the pulmonary circulation.
Majority of pulmonary emboli originate in the lower extremity (85%). 5% come from pelvic
vein, vena cava or upper extremities. 10% of emboli originate from the right atrium.
Obviously there will be more risk of loosening of thrombus at the upper limit of a long
femoroiliac occlusion, where both the force of venous flow and turbulence will be greater.
Recent studies have demonstrated that both compliance and resistance change in both lungs
irrespective of whether the emboli are small or large. This may be reversed by increasing oxygen
in the inspired air or by administration of isoproterenol, suggesting that the changes are due to
contraction of the smooth muscles in the peripheral airways. As the changes are also seen in
the contralateral lung as well as in the embolised lung, it has been postulated that a humoral
mechanism is present. Moreover that unilateral and bilateral wheezing may be present clinically
following acute pulmonary embolism further supports this concept. It may be that serotonin
may possibly be responsible for this bronchoconstriction.
Clinical features.— Patients usually complain of dyspnoea, chest pain, haemoptysis and
hypotension. Dyspnoea is first to appear, followed by pain which becomes more severe in the
presence of a massive embolus lodged in the main pulmonary artery. The pain is usually
substernal and sharp, stabbing in nature, which occurs during breathing. In case of peripheral
embolus there may be pleuritic pain. Occasionally pain may be epigastric. Haemoptysis is due
to presence of infarction of segments of lung.
PHYSICAL EXAMINATIONS.— Most consistent finding is tachycardia and tachypnoea.
Shock and cyanosis are ominous signs and only seen in massive embolus. Pleural friction rubs
are heard in case of peripheral infarcts. Rales may be heard due to secondary pulmonary oedema.
Small pleural effusions are not uncommon. Dilatation of the cervical veins are due to right
ventricular failure. There may be accentuation of second pulmonary sound.
Special Investigations.—
1. CHEST X-RAY.— The most characteristic finding is diminished pulmonary vascular
markings. But unfortunately this is seen in only 50% of cases and only when the films are taken
within 24 to 48 hours, after which vascular markings may return to normal.
Since pulmonary emboli do not always cause infarction, wedge shaped infiltrate may not
be seen. In many patients the chest X-ray may remain normal throughout the course of
pulmonary embolism.
2. ELECTROCARDIOGRAM.— Though it may show certain changes, yet these are not
specific. The most common abnormality is ST segment depression followed by T wave inversion.
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A CONCISE TEXTBOOK OF SURGERY
3.
CHEMICAL
TESTS.— (i)
Elevation of serum
lactic dehydrogenase
(LDH activity), (ii)
increased
serum
bilirubin
concen­
tration and (iii)
normal serum gluta­
mic oxaloacetic tran­
saminase
(SGOT)
level
are
the
characteristic triad
seen in pulmonary
embolism. But how
much reliability can
be reposed on this
Fig.16.11.— A. Chest film is essentially normal. B. But perfusion lung scan of
triad remains a
the same case demonstrates absent perfusion to the entire left lower lobe.
question, as in one
series it was positive in omy i»7o or pulmonary emoou cases.
4. PULMONARY ARTERIOGRAPHY.— This is the most objective and reliable means of
establishing a firm diagnosis of pulmonary embolism. The procedure is to rapidly inject a radio­
opaque material into the right atrium or main pulmonary artery through a catheter pushed
through a peripheral vein. The filling defects created in the large pulmonary arteries can be
demonstrated. It also shows changes in the small vessel pattern peripherally. The only
disadvantage of this technique is that it may produce hypotension and it should be carefully
used in patients who are seriously ill.
5. PULMONARY RADIO ISOTOPE SCANNING.— Intravenous injection of radioactive
substances such as macroaggregated particles of human serum albomin tagged with 131I (10 -100
micra) or "mTc followed by scintillation scannings of the chest is a quite reliable method to
diagnose areas of decreased vascularity in the lung field due to pulmonary emboli.
Serial scanning is also of considerable value in following up of patients with pulmonary
embolism demonstrating resolution of the emboli.
TREATMENT.—
,
PROPHYLAXIS.— This has been adequately discussed in the section of 'Deep Vein
Thrombosis'.
TREATMENT OF ESTABLISHED CASES.—
CONSERVATIVE TREATMENT—
1.
Anticoagulants.— Anticoagulant therapy is the primary method in the majority of
patients once a diagnosis of pulmonary embolism is established. Heparin is administered in
large doses — 40,000 units or more daily till the clotting time is brought down to at least twice
the normal. In acute stages a continuous intravenous drip of heparin is a reliable method for
maintaining stable and sustained elevation of clotting time. Heparin also acts against reflex
bronchoconstriction in pulmonary embolism. It should be followed by oral anticoagulants for 3
to 6 months or even longer.
DISEASES OF VEINS
283
2. Fibrinolytic agents — Although much work has been done on the use of fibrinolytic
agents to lyse pulmonary emboli, there is little clear evidence about its usefulness. Streptokinase
is infused through the pulmonary angiogram cannula in an initial dose of upto 6,00,000 units,
followed by 1,00,000 units hourly for upto 3 days. It is important to maintain the treatment for
a sufficient length of time. The pulmonary arteriogram can be repeated to check the progress of
the condition. Streptokinase or more recently urokinase has been used but its effectivity is still
controversial.
3. Essential supportive treatment in the form of correction of metabolic acidosis by infusion
of sodium bicarbonate and improvement of heart function by the use of inotropic drugs should
be considered.
SURGICAL TREATMENT.
(i) Ligation or division.— An analysis has shown that femoral vein ligation is less effective
in the prevention of emboli than the use of anticoagulants.
Ligation or division of the inferior vena cava just distal to the right renal vein has been
performed to prevent passage of thrombi. The operation requires general or spinal anaesthesia.
The incidence of pulmonary embolism following this procedure is generally lower than the
reported incidence following femoral vein ligation. However this technique cannot be used in
desparately ill patients.
The ligation of a vein however results in propagation of the thrombus to the site of the
ligature from its origin. It is also complicated by oedema, pain, recurrent phlebitis and ulceration
of lower limbs,
(ii) Venous interruption.— Interruption of the veins of the lower extremity is indicated if
pulmonary embolus occurs in a patient receiving adequate anticoagulant therapy or in patients
in whom anticoagulant therapy is contraindicated. Phlebography is routinely used to localize
the thrombi. Interruption should always be performed proximal to the site of embolus. It should
be done at the vena cava level in the presence of pelvic vein and iliac vein thrombosis. Interrupted
arterial sutures are placed through the vena cava or a plastic clip (Moretz) is placed across it. A
plastic umbrella grid may also be placed into the inferior vena cava by means of a venous
catheter under radiological control.
Plication of the femoral vein may also be performed to prevent emboli from the calf from
passing upwards. The femoral vein is ligated or plicated just below the point where the profunda
vein joins it. Adequate venous return is possible through the profunda circulation.
(iii) Pulmonary embolectomy.— This operation was first performed by Trendelenburg in 1908.
Later on Kirschner in 1924 correctly performed this operation. It is now probably performed on
those few patients who, having survived a massive pulmonary embolism, are yet unable to
maintain circulation without cardiac massage. It should also be used in the event of failure of
thrombolytic treatment. Nowadays this operation is performed as an emergency procedure with
the use of cardiopulmonary by-pass. This technique clearly represents the most satisfactory
method of management available at this time for those patients who require embolectomy for
massive pulmonary embolism.
In case of chronic pulmonary embolism, selected patients can be well managed successfully
by embolectomy. In many such cases there is marked reduction in pulmonary function associated
with occlusion of more than half the pulmonary arterial bed producing pulmonary hypertension.
The mortality still remains high, even in experienced units.
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A CONCISE TEXTBOOK OF SURGERY
CHRONIC VENOUS INSUFFICIENCY
Aetiology.— There are mainly three causes of chronic venous insufficiency. These are — 1.
VARICOSE VEINS, which are discussed in detail in the beginning of this chapter; 2. Incompetent
perforators and 3. Deep vein abnormalities.
2. INCOMPETENT PERFORATORS.— There are many perforators between the
superficial and deep veins of the inferior extremity, which are also discussed in the section of
'Varicose veins'. When the valves of these perforators become incompentent, they become dilated
and produce localized dilatations at their junctions with the superficial vein which can be detected
both by inspection and palpation. Defects in the deep fascia through which these dilated
perforators pass may also be palpated. When these perforators become incompetent, high
ambulatory venous pressure developing within the deep veins of the calf during exercise is
directly transmitted through these perforators to the superficial venous system. Ultimately there
is a sustained rise in capillary pressure in the surrounding skin with the development of oedema,
induration, fat necrosis and ulceration.
3. DEEP VEIN ABNORMALITIES.— (i) Deep vein thrombosis is the main deep vein
abnormality which often causes chronic venous insufficiency. Following thrombosis, major deep
veins may become patent by recanalization, however the delicate valves will remain imprisoned
laterally in organised thrombosis. The result is the patent and valveless deep venous system
which transmits the gravitational pressure of the blood column unimpeded from the level of
the heart to the ankles. This is the main predisposing feature in the pathophysiology of the
chronic venous insufficiency, (ii) Occasionally the congenital or familial causes of varicosities
may also cause deep vein abnormalities.
However valvular incompetence alone is not enough to produce serious stasis. It must occur
with incompetent perforators through which the high deep venous pressure in the ambulatory
state is transmitted to the superficial tissues. These perforators may have been involved in the
initial thrombosis or may become incompetent by dilatation resulting from the back pressure of
the valveless deep venous system.
Fibrinogen escapes through large pores in the venules of the skin of chronic venous
insufficient lower limb. The accumulated fibrins cannot be removed due to inadequate blood
flow. This fibrin accumulation acts as a barrier to diffusion of oxygen and other nutrients. As a
result of this the subcutaneous tissue becomes thick, hard and tender, known as liposclerosis.
Fibrin was found in all the biopsies taken from patients with liposclerosis. These changes
alongwith stasis dermatitis which produces brawny oedema, cutaneous atrophy and pigmentation
ultimately lead to tissue death and ulceration.
C linical features.— An aching discomfort in the lower limb is frequently complained of.
Oedema is also seen. There may be associated varicose veins, but this condition is mainly due
to deep vein abnormalities and incompetent perforators. There may be night cramps in the
muscles of the calf and feet.
,
PHYSICAL FINDINGS.— Oedema, brawny induration, brownish pigmentation and
dermatitis are seen followed by the development of venous ulcers. All these are usually seen on
the medial aspect of the leg just above the ankle posterior and superior to the medial malleolus.
Various types of dermatitis may be seen. The venous ulcers are characteristically shallow
with surrounding rims of bluish discolouration and erythema. These may be as deep as the
deep fascia but cannot be deeper than that.
DISEASES OF VEINS
285
The ulcers may appear spontaneously or follow trivial trauma.
Special investigations are more or less like those described in 'Deep Venous Thrombosis'.
Treatment.—
CONSERVATIVE TREATMENT.—
(i) Elevation of leg.— The frequency of daily leg elevation should be charted according to
the oedema of the leg of the individual.
(ii) Active exercise.— Active exercise, particularly walking with elastic stockings. Elastic
stockings should be used whenever out of bed.
(iii) Those who have already developed venous ulcer, the treatment of venous ulcers as
described in the section of 'Venous ulcer' should be followed.
SURGICAL MANAGEMENT.—
1. Ligation and stripping of long or short saphenous vein.— This can only be performed when
its incompetency has been demonstrated by Trendelenburg test. Indications for this operation
are — (i) severe varicosities, (ii) moderate to severe symptoms of varicosities and (iii) presence
of venous ulcers even with aggressive conservative management. The operative procedure has
been discussed under 'Varicose veins'.
2. Fegan's injection of veins, followed by 6 weeks of continuous elastic compression, is also
discussed in 'Varicose veins'.
3. Ligation of incompetent perforators.— This technique is a valuable adjunct to conservative
therapy. It is particularly effective if performed before the patient has developed an ulcer. The
perforators are ligated subfascially. This techniques was first started by Dodd and Cockett.
Longitudinal incision is made 1 cm behind and parallel to the posterior subcutaneous tibial
border. The incision is made deep till the deep fascia is reached. The deep fascia is also divided
along the line of incision. The margins of deep fascia are now elevated and the perforators are
ligated flush to the deep fascia and then divided. All the tributaries joining these veins are also
ligated and divided. The skin is sutured and a pressure bandage is applied.
4. By-pass operation.— Saphenous vein has been used to by-pass segmental venous
occlusion of the iliofemoral or femoropopliteal veins. For iliofemoral occlusion the contralateral
saphenous vein is passed suprapubically and anastomosed to the affected side. A temporary
arteriovenous fistula distal to the anastomosis may ensure patency. For femoropopliteal occlusion,
the obstructed segment can be by-passed by anastomosis of saphenous vein to the poplitealtibial trunk at the level of the knee.
DISEASES OF THE
LYMPHATIC SYSTEM
n
The lymphatic system comprises of (a) the lymphatics which commence blindly in the tissue
spaces in most tissues of the body and ultimately empty their contents (lymph) in certain veins,
(b) lymph nodes and (c) epithelolymphoid tissues which are collections of lymphoid tissues in
the walls of the alimentary canal and in the spleen and thymus and this group is ignored in
this chapter.
DISEASES OF THE LYMPHATICS
Acute lymphangitis.—
Lymphangitis is inflammation of peripheral lymphatics. These appear as red streaks
progressing towards the regional lymph nodes. Gradually brawny oedema appears distally due
to coagulation of lymph within the lymphatics.
Acute lymphangitis is more frequently caused by Haemolytic Streptococci, though it can also
occur due to Staphylococcal infections. When infection occurs in the distal limb with organisms
mentioned above, such infection spreads through the lymphatics to the regional lymph nodes.
During this process lymphangitis occurs. This is often associated with enlarged and tender
regional lymph nodes which indicate their involvement. Gradually abscess may occur in the
regional lymph nodes.
Occasionally irritative lymphangitis is noticed following lymphangiography.
TREATMENT.— This condition is usually treated by conservative means. Rest to the part
with elevation and local heat is highly important. Since beta-haemolytic streptococci are the
common infecting organisms, penicillin is the antibiotic of choice, unless culture and sensitivity
tests approve other antibiotic. In case of penicillin resistant Staphylococci, cloxacillin is highly
effective. Incision is almost always contraindicated unless there is definite signs of purulent
accumulation e.g. infected blister or paronychia.
Chronic lymphangitis.—
This condition almost always follows repeated attacks of acute lymphangitis. The clinical
importance of this condition lies in the fact that acquired lymphoedema may be precipitated
due to this condition.
NEOPLASMS OF LYMPHATICS.—
Benign neoplasms.— Peculiarly benign lymphatic tumours are of developmental in origin
and so are seen in children often from birth. These tumours are often seen in the area of the
jugular buds in the neck, though these are also seen in the axilla, shoulder and groin. Localized
cluster of dilated lymph sacs in the skin and subcutaneous tissue which cannot connect into the
normal lymph system grows into lymphangioma or benign neoplasm of lymphatics.
Types.— 3 types are usually seen — (a) simple and capillary lymphangioma; (b) cavernous
lymphangioma and (c) cystic hygroma.
DISEASES OF THE LYMPHATIC SYSTEM
287
(a) SIMPLE AND CAPILLARY LYMPHANGIOMA.— This type presents as circumscribed
lesion which appears as vesicles or small blisters or slightly elevated skin patches. These lesions
are also called lymphangioma circumscriptum. These are typically seen on the innerside of the
thigh, on the shoulder or in the axilla. Lymphangiography reveals that the lesion is separate
from the main lymphatic system.
Treatment is excision, when lymphangiography confirms that the lesion is separate from the
main lymphatic. Otherwise there may be risk of chronic lymphatic fistula.
(b) CAVERNOUS (DIFFUSE) LYMPHANGIOMA.— These present as bigger lymphatic
swellings. These are often found in the face, mouth, lips (causing enormous enlargement of the
lips or macrocheilia) and in the tongue (a common cause of macroglossia). This cyst is often
interspersed among muscle fibres.
(c) CYSTIC HYGROMA.— This is the most common form of lymphangioma. This exhibits
large cyst like cavities containing clear watery fluid. Majority (75%) of the cystic hygromata are
present in the neck. 20% are seen in the axilla. Remaining 5% are found scattered in different
parts of the body — in the mediastinum, groin, pelvis and even retroperitoneum. Peculiarly a
few cervical cystic hygromata may have mediastinal extension extending as far as the diaphragm.
Macroscopically cystic hygroma consists of multiple locules filled with lymph. In the depth
the locules are quite big and towards the surface the locules become smaller and smaller in size.
Clinical features.— As mentioned earlier cystic hygroma is mostly seen in children and are
often reported to be present since birth.
Disfigurement is the main symptom. The swelling is mainly painless, though occasionally
it may be painful when it becomes infected.
These are soft swellings. Fluctuation and fluid thrill are always present. These swellings
are brilliantly translucent. Occasionally haemorrhage within the cyst renders the swelling opaque.
Regional lymph nodes usually do not enlarge until and unless the lesion gets infected.
Treatment.— Surgical excision is the only available treatment. In the neck the lesion is
removed under general endotracheal anaesthesia using transverse incision. The cysts often
encroach deep into the neck involving the vital structures. So careful dissection is required. The
cyst wall often lies close to the carotid artery, jugular vein, vagus nerve and brachial plexus. It
must be remembered that the excision must be complete to avoid any chance of recurrence. This
lesion is a developmental anomaly and is not a malignant tumour, so this condition is rarely
associated with recurrence. But as for all cysts, if cyst wall is left behind fluid may reaccumulate
to cause reappearance of the swelling. That is why macroscopically identifiable cystic wall should
be dissected away to prevent recurrence.
Kinmoth described sclerosing treatment for this lesion in adults with apparent satisfactory
result.
Radiotherapy has no place.
Malignant neoplasms.—
LYMPHANGIOSARCOMA.— This is a rare malignant tumour of the lymphatics. It is
occasionally seen in long standing cases of primary or secondary lymphoedema of the extremities.
It is more often seen in the upper limb than the lower limb. This condition has also been reported
in cases of postmastectomy lymphoedema.
This lesion first appears as a bruise or a purplish discolouration. Later on a skin nodule is
seen, on which ulcers with crusting are noticed which gradually progress to necrosis. Gradually
the whole of skin and subcutaneous tissue are involved.
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288
Microscopically the tumour is composed of neoplastic endothelial cells, with poorly defined
lymph spaces.
This tumour not only locally spreads rapidly, but also metastasises widely.
Treatment is ineffective and these tumours are uniformly fatal.
LYMPHOEDEMA
Pathology.— On an aetiological basis, lymphoedema may be divided into 2 groups :
(a) Primary lymphoedema in which there is a developmental error of the regional lymphatic
system.
(b) Secondary lymphoedema in which there is acquired pathology of the defective local
lymphatic system.
PRIMARY LYMPHOEDEMA.— Family history of primary lymphoedema is sometimes
received. Two main forms of familial (hereditary) lymphoedema are recognized — Nonne-Milroy
(Type I) and Letessier-Meige (Type II), though one type may overlap on the other. Milroy's
disease is probably inherited in an autosomal dominant manner with related abnormalities in
the gene coding on chromosome 5. The disease is characterized by brawny lymphoedema of
both legs, sometimes of the genitalia, arms and even face. Such lymphoedema develops from
birth to before puberty. It is often associated with wide range of lymphatic abnormalities on
lymphangiography. Meige's disease is almost similar to Milroy's disease, except that the
lymphoedema develops between puberty and middle age. This can be divided into three clinical
subgroups according to the age of onset of the swelling.
(i) In lymphoedema congenita, the oedema is present in birth. This was first described by
Milroy in 1892. This variety is comparatively rare and occurs in about 10% of all cases of primary
lymphoedema.
(ii) Lymphoedema praecox starts in adolescents and this constitutes 75% of patients with
primary lymphoedema. In this group is familial type D.
(iii) Lymphoedema tarda constitutes 15% of patients with primary lymphoedema and in
these cases the swelling is delayed until after the age of 35 years.
In primary lymphoedema there is some developmental fault in the lymphatic system and a
family history is found in about l/5th cases. In about 1/2 the patients the malformation is
predominantly unilateral.
Lymphangiography has demonstrated 3 basic types of malformation of this disease —
(a) Aplasia of the subcutaneous lymph trunks in the limbs is found in 13% of patients.
Formed lymphatic vessels are absent, but there are haphazardly arranged lymph spaces with
no attempt to form lymphatic channels. This is a severe malformation and is often associated
with the congenital variety.
(b) In 75% of cases the subcutaneous lymphatic trunks in the leg are hypoplastic. They
may be too small in size and number. The commonest defect in this group is presence of a
solitary lymph vessel, which ascends the limb without normal bifurcation and branching. This
may be termed solitary hypoplasia, which may extend upto the knee or even upto the groin. In
a small number of patients hypoplasia may affect the lymph nodes in the groin while the lymph
trunks remain normal.
(c) The third malformation is the varicose or dilated lymph trunks seen in 12% of patients
with primary lymphoedema. In this condition the subcutaneous tissues are filled with dilated
and tortuous lymphatics which are incompetent and allow retrograde reflux of lymph. This is
DISEASES OF THE LYMPHATIC SYSTEM
289
often associated with diffuse arteriovenous fistulae. The varicose state may extend proximally
to involve the pelvic and even para-aortic lymph trunks. This allows retrograde flow of intestinal
chyle into the groin and thigh. Chyle-filled vesicles may appear in the skin of the leg and
troublesome leak of milky lymph may develop.
The prognosis of primary lymphoedema depends on the type and extent of the malformation.
While lymphatic function is severely prejudiced in aplasia and the varicose types, hypoplastic
variety is less troublesome.
SECONDARY LYMPHOEDEMA.— This condition may follow involvement of the lymph
channels or lymph nodes by neoplastic or inflammatory process, by surgical excision or by
radiotherapy. In some areas parasitic infestation with filariasis is destructive within the lymph
nodes and may produce secondary lymphoedema. In the majority of cases of secondary
lymphoedema the disease process is a local affair in contrast to the primary lymphoedema
where the malformation is widespread over an entire limb.
Clinical features.—
Primary lymphoedema is mostly seen in adolescent girls. The swelling begins insidiously
with no apparent cause. The patient first notices a little puffiness around the ankle which
disappears after a night's rest only to return at a late stage of the next day. Gradually the
oedema progresses slowly. Severe swelling is unusual until several years have elapsed. The
most important feature is that the swelling is painless (in contrast to venous disease). The main
complaint of the patient is cosmetic appearance.
Secondary lymphoedema develops much more rapidly. Usually there is clear indication of
the local pathology (as mentioned earlier in the classification). This swelling is usually
accompanied by discomfort in the swollen tissues. Recurrent cellulitis is not uncommon. The
infection is usually streptococcal. High pyrexia and rigors are usually accompanied with.
Clinically, it may not be so easy to differentiate venous from lymphatic oedema. But skin
changes, pigmentation, atrophy and tendency to ulceration favour the diagnosis of post-phlebitic
swelling of venous origin. In a lymphoedema the skin remains usually healthy except slight
thickening, hyperkeratosis and recurrent cellulitis. Pain is an important symptom of swelling of
venous aetiology, which is rarely seen in lymphoedema.
Special in vest igat ions.—
It is often possible to diagnose and manage lymphoedema purely on the basis of history
and examination without any special investigations. But certain investigations may be required
to confirm the diagnosis to suggest management and to provide prognostic information.
A few ROUTINE TESTS are always performed. These are full blood count, urea and
electrolytes, creatinine and liver function tests, chest radiography and blood smear for
microfilariae.
LYMPHANGIOGRAPHY.— In this technique the lymphatics of the lower limb are delineated
with radio-opaque dye. Surgically, a lymphatic trunk of the dorsum of the foot is exposed.
Iodised oil contrast medium (neohydriol ultrafluid lipiodol) should be injected directly into the
exposed lymphatic trunk on the dorsum of the foot. By this contrast medium the lymph nodes
as well as lymph trunks can be well visualized radiographically. The contrast medium is warmed
and injected into the exposed lymph trunk. For a lower limb, approximately 6 ml of solution is
injected over a period of 1 hour. Too rapid injection may produce respiratory distress and
pulmonary oil embolus.
ISOTOPE LYMPHOSCINTIGFtAPHY.— This is now replacing lymphangiography.
19
A CONCISE TEXTBOOK OF SURGERY
290
Radioactive technetium-labelled protein or colloid particles are injected into an interdigital web
space, which are taken up by lymphatics. Serial radiographs are taken with a gamma camera.
This technique offers a qualitative measure of lymphatic function as also certain anatomical
details.
Fig.17.1,— First figure shows normal inguinal and iliac lymphangiograms. Second figure shows normal pelvic
lymphadenograms taken after 24 hours. Lipiodo! is cleared from the vessels, whereas nodes show normal
morphology and granularity.
COMPUTERISED TOMOGRAPHY.— Though a single axial CT slice through the midcalf
has been used as a diagnostic test for lymphoedema, yet CT is mainly used to exclude pelvic or
abdominal mass lesions.
MAGNETIC RESONANCE IMAGING (MRI) — provides clear images of the lymphatic
channels and lymph nodes, so it is an effective diagnostic procedure also to distinguish between
venous and lymphatic causes of a swollen limb.
Treatment.—
PRIMARY LYMPHOEDEMA.— In the beginning conservative management should always be
instituted.
Conservative Treatment.— This is the main stay of treatment. Only 15% of patients require
surgery.
(i)
Elevation of the limb at night by raising the footend of the bed on blocks of at least 1
foot high.
DISEASES OF THE LYMPHATIC SYSTEM
291
(ii) An efficient elastic stocking should be worn constantly by day. Control of lymphoedema
requires higher pressure (30 to 40 mmHg for arm and 40 to 60 mmHg for leg). The patient
should put on the stocking as first thing in the morning before rising and should be worn
throughout the day.
(iii) Pneumatic compression devices are available to control moderate lymphoedema.
(iv) Exercise has got some effect in reducing lymphoedema. Slow and rhythmic isotonic
movements will increase venous and lymphatic return and it also augments muscle pumps.
Exercise also helps to maintain joints mobility. When at rest the limb should be positioned
above the level of the heart.
(v) Drugs.— Benzpyrones of which the flavonoids have received some acceptance. Clinical
trials have shown to improve microcirculatory perfusion, stimulate interstitial macrophage
proteolysis and reduce erythorocyte and platelet aggregations and ultimately exert an
antiinflammatory effect. But acceptance is not overall and there are many criticizers. Diuretics
are of no value in pure lymphoedema and their prolonged use may be associated with side
effects by disturbing the electrolyte balance.
(vi) If eczema is present this is treated by triamcinolone 0.05 to 0.1%. Fungal lesion should
also be treated accordingly.
By instituting this treatment not only the progression of the oedema will be halted, but also
a considerable return towards normalcy may be achieved.
To the contrary, a long standing lymphoedema with secondarily fibrosed subcutaneous
tissue, there will be hardly any improvement with this conservative treatment. If there is recurrent
cellulitis, a prophylactic oral antibiotic may be prescribed for an indefinite period. These cases
are very much suitable for surgery.
Surgical Management.— Main indications are :
(i) Limitation of function of the limb
due to its weight and bulk is the main
indication.
(ii)
Recurrent cellulitis is also an
indication.
(iii) In case of women appearance of
swollen leg cosmetically is an indication for
surgical treatment.
Two types of operations have been
Thompson Operation
devised — 1. Excisional operations and 2.
Physiologic operations.
1. Excisional Operations.—
(a)
Homan’s operation.— Firstly the
skin flaps are elevated, then the subcuta­
neous tissue is excised from beneath the
flaps. The skin flaps are now closed
primarily as the width of the limb has been
decreased. The only complication is the
possibility of skin flap necrosis. This
Charles Operation
operation should be performed on two
Fig. 17.2- Two excisional operations for lymphoedema.
sides one after the other keeping at least
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A CONCISE TEXTBOOK OF SURGERY
six months gap between the two operations. This operation is more satisfactory in the calf,
though it can be used even on the upper limb, but must not be performed in presence of
venous obstruction.
(b) Thompson operation.— In this operation long viable skin flap is raised based on
midposterior aspect of the limb. This operation can be performed
on either the medial or lateral aspect of the limb. If both sides of
the limb are to be operated on, an interval of 3 to 6 months should
be given between the two operations. After raising the skin flap,
all the subcutaneous tissue and the deep fascia beneath this skin
flap should be excised. The anterior edge of the skin flap is now
burried deep into the muscle in close relation with the deep
vascular bundle and its related lymphatics. In this way the bulk
of the limb is reduced and the tissue tension is restored by the
overlapping procedure. The dermal lymphatic plexus is brought
in proximally to the deep lymphatic trunks, which are usually
Fig.17.3.— Omentum being
normal in primary lymphoedema.
used
cis a lymph bearing pedicle
(c) Charles’ operation.— In this operation the whole of the
to graft to the inguinal region to
oedematous subcutaneous tissue and the deep fascia are excised.
anastomose with deep lymphatics
The exposed muscle layer is covered with split thickness skin
of the inferior extremity.
graft. The main disadvantage is a tendency to hyperkeratosis in
the grafted area which occurs in about l/3rd of patients. The unstable skin frequently develops
minor infections with local ulceration and a weeping eczema state which is troublesome.
(d) Kinmonth's modification of Homan's procedure.— In this operation limb reduction is
usually first done on the medial side and then on the lateral side.
2. Physiologic Operations.—
(i) These operations aim to provide or enhance lymph drainage. Attempts have been
made to create an artificial lymph
channels
through
the
subcutaneous
tissue
using
nonabsorbable
thread
e.g.
prolene. These operations are
controversial.
(ii)
physiologic operation attempt to
link subcutaneous tissue with the
deep lymphatics or to attach
lymphatic-bearing pedicles such as
omentum (See Fig. 17.3) or small
bowel to the root of the affected
limb. Kinmonth and associates
Fig.17.4.— A.— Lymphovenous shunt with lymph node. B.— used an opened defunctionalised
Lymphatic threaded into vein. C.— Micro-surgery by anastomosing
small bowel pedicle to construct
dilated lymphatics to the vein.
a lymphatic anastomosis with
inguinal nodes. Unfortunately this operation is not suitable for most primary lymphoedema
patients.
DISEASES OF THE LYMPHATIC SYSTEM
293
(iii) Lymphovenous shunts have been used particularly in secondary lymphoedema cases.
(iv) Microsurgery.— In many sites the dilated lymphatics are anastomosed to veins by
micro-surgery. This has been more used in cases of oedema of the arm.
SECONDARY LYMPHOEDEMA.— In contrast to primary lymphoedema, secondary
lymphoedema hardly shows an improvement with conservative treatment. Surgery is the only
treatment, if it be required.
Surgical treatment.— As the pathology of the secondary lymphoedema is blockage or
destruction of the lymph nodes or lymph trunks, surgical procedures are designed to provide a
lymphatic bridge across the obstructed area or by deliberate creation of a lymphovenous shunt
just proximal to the site of obstruction.
Bridging procedures.— This can be performed by lymphangioplasty which was first introduced
by Handley in 1908 by using various artificial channels. Some surgeons implanted double nylon
strands. Some used polyethylene tubes perforated with lateral holes. These tubes were inserted
from the ankle level to the midabdominal wall. These were removed after 1 year, when it might
be expected that permanent channels had been formed by their presence. However these methods
could not be successful to bring improvement in the oedematous state.
Pedicle flaps of skin and subcutaneous tissue may be used as a lymphatic bridge across the
obstructive region. A thick pedicle from the arm may be transplanted into the thigh and
abdominal wall to by-pass the inguinal obstruction. Such method may be tried to by-pass the
axillary obstruction of post-mastectomy oedema of the arm. But the results have not been much
impressive and it has failed to gain a definite place in the surgical management of secondary
lymphoedema.
Lymphovenous shunts.— In this operation a healthy lymph node proximal to the obstruction
region is isolated, taking great care to preserve its vascular pedicle and afferent lymphatics.
This lymph node is transected through its middle. The cut surface of the distal half is then
implanted into a neighbouring vein e.g. the femoral vein in the groin. A linear venotomy is
used with circumferential suture of the capsule of the lymph node to the edges of the venotomy.
In this way the afferent lymph trunks joining the node will discharge their content directly to
the venous system. This operation provides a sound basis in reducing lymphoedema. However
long term report will be required for proper evaluation of this operation.
Excisional operations.— The excisional operations which mentioned under the surgical
treatment of primary lymphoedema may be applicable to a limb with secondary lymphoedema
if the original disease is inactive.
DISEASES OF LYMPH NODES
Before entering into the various causes of lymph node enlargement, a brief note is given
regarding lymphangiography which has an immense value in localizing lymph node enlargement
in various parts of the body, finding out the pathology of such enlargement and finally the sites
of lymph metastasis in various carcinoma (particularly malignancy of the testis) and malignant
melanoma.
Lymphangiography.— This test is of great value in finding out the causes of lymphoedema,
lymph node enlargement and sites of lymph node metastasis in various carcinoma.
Injection of patent blue dye into the web between the toes will show lymphatics on the
dorsum of the foot. One of these lymphatics is cannulated and ultrafluid lipiodol (Radio-opaque
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A CONCISE TEXTBOOK OF SURGERY
dye) is injected to visualize on X-ray the main lymphatic channels of the leg and subsequently
the lymph nodes. Irregular filling defect in the lymph node means secondary metastasis. Soap
bubble or foamy appearance is seen in Hodgkin's disease. Coarse nodular storage pattern is
seen in lymphosarcoma and marginal sunburst appearance is the feature found in reticulum
cell sarcoma.
In malignant melanoma, sometimes radio-active phosphorus is added to the radio-opaque
dye for lymphangiography. This will destroy the malignant cells in the lymph nodes. This process
is called 'endolymphatic therapy'.
At present CT scan and high resolution ultrasound have almost replaced lymphangiography
as these modalities are now generally available.
VARIOUS CAUSES OF ENLARGEMENT OF LYMPH NODES —
A. INFLAMMATORY.
(a) ACUTE LYMPHADENITIS.
(b) CHRONIC LYMPHADENITIS.
(c) GRANULOMATOUS LYMPHADENITIS — the aetiologic agents may be bacterial,
viral or fungal. From BACTERIAL origin are tuberculosis, syphilis, tularaemia, brucellosis etc;
From VIRAL origin are lymphogranuloma venereum, cat-scratch disease, infectious
mononucleosis; From PARASITOLOGICAL origin is filariasis due to infestation of Wuchereria
Bancrofti and toxoplasmosis; From FUNGAL origin are blastomycosis, histoplasmosis and
coccidioidomycosis (not actinomycosis, as lymph node enlargement is unusual in this disease).
In this group may be added condition like sarcoidosis, whose aetiology is still controversial.
B. NEOPLASTIC.—
(a) BENIGN — almost non-existent.
(b) MALIGNANT —
1. Primary.—
OLD CLASSIFICATION.—
(i) Giant follicle lymphoma;
(ii) Lymphosarcoma;
(iii) Reticulum cell sarcoma;
(iv) Hodgkin's disease.
NEW CLASSIFICATION.— The classification, which is currently used, is based on the
classification of Rappaport et al and of Lukes et al. It is as follows :
Primary malignant lymphomas can be broadly classified into two groups — (i) Diffuse
lymphomas (56%) and (ii) Nodular lymphomas (44%). The latter type is more prevalent in females
but is distinctly rare in children and blacks. But these two groups are actually types of
proliferation that any of the malignant lymphomas can exhibit at some points of their evolution.
The natural history of the disease is primarily related to the cell type in which a nodular pattern
indicates a slower evolution and a better prognosis than a diffuse one. It is also interesting to
note that most nodular lymphomas change later to a diffuse pattern but maintaining the same
cell composition.
The classification based on cell types are :
(i) Malignant lymphoma, undifferentiated type;
(ii) Malignant lymphoma, histiocytic type;
(iii) Malignant lymphoma, lymphocytic type (poorly differentiated);
DISEASES OF THE LYMPHATIC SYSTEM
295
(iv) Malignant lymphoma, lymphocytic type (well-differentiated);
(v) Malignant lymphoma, mixed type (histiocytic-lymphocytic);
(vi) Malignant lymphoma, Hodgkin's type — (a) lymphocytic predominance; (b) nodular
sclerosis; (c) mixed cellularity; (d) lymphocytic depletion.
2. Secondary.—
Metastatic lymph node enlargement is often seen from Carcinoma, Malignant Melanoma or
rarely from Sarcoma of the draining region.
C. LYMPHATIC LEUKAEMIA.
D. AUTOIMMUNE DISORDERS.—
(i) Juvenile rheumatoid arthritis (Still's disease).
(ii) Other Collagen diseases such as Systemic lupus erythomatosus, Polyarteritis nodosa
and scleroderma.
Causes of generaliy.ed lymph nodes enlargement.—
1.
2.
3.
4.
5.
6.
7.
8.
9.
Tuberculosis;
Syphilis — secondary stage;
Infectious mononucleosis;
Sarcoidosis;
Brucellosis;
Toxoplasmosis;
Hodgkin's disease;
Lymphosarcoma;
Lymphatic leukaemia.
SPECIAL INVESTIGATIONS.—
1. Blood.— Routine examination of blood is essential for (a) leucocytosis particularly
polymorphs (acute lymphadenitis); (b) lymphocytosis (tuberculosis, lymphatic leukaemia etc.);
(c) raised E. S. R. (tuberculosis, secondary carcinoma, lymphosarcoma etc.); (d) W. R. and Kahn
test (syphilis); (e) Microfilaria in the peripheral blood vessels when the patient is sleeping
(Filariasis).
2. Aspiration — of the abscess is essential for diagnosis be it a cold abscess or
lymphogranuloma inguinale. In cold abscess one will look for acid-fast bacilli. In
lymphogranuloma inguinale, pus from unruptured bubo is diluted ten times with normal saline
and sterilized at 60° centigrade, 0.1 ml of the solution is injected intradermally. Appearance of
a reddish papule within 48 hours at the site of injection indicates the test to be positive. This
test is known as Frei's intradermal test, which is specific for lymphogranuloma inguinale.
3. Mantoux test and guineapig inoculation test — are specific for tuberculosis.
4. Gordon’s biological test — is specific for Hodgkin's disease. An emulsion of the
affected lymph nodes is injected into a rabbit intracerebrally. This will initiate encephalitis within
a few days.
5. Biopsy.— This is probably the most important special investigation in this concern. Many
cases may not be diagnosed clinically and with the help of the above special investigations.
Biopsy should be called for in these cases. Under local or general anaesthesia according to the
circumstances, the isolated or matted lymph nodes are excised and examined both macroscopically
and microscopically.
6. Radiological examination.— In case of enlarged cervical lymph nodes, X-ray of the
chest is essential, not only to find out enlargement of the mediastinal lymph nodes, but also to
A CONCISE TEXTBOOK OF SURGERY
296
detect pulmonary tuberculosis or bronchogenic carcinoma as the cause of enlargement of cervical
lymph nodes. Calcified tuberculous lymph nodes may easily be seen in X-ray film. But tomography
will be essential to know particularly about the mediastinal lymph nodes.
7. Mediastinal-scanning — with Gallium 67 is sometimes performed to know whether
the mediastinal lymph nodes are involved or not.
8. Laparotomy.— This seems to be the last court of appeal in Hodgkin's disease. This is
required not only to know the clinical staging of the disease by wedge biopsy of the liver and
by biopsy of the aortic, mesenteric and iliac nodes and a small chip biopsy from iliac bone but
also by splenectomy as the spleen is involved in about 90% of cases of the abdominally involved
Hodgkin's disease and to obviate splenic irradiation due to its complications.
VARIOUS TYPES OF LYMPH NODE INVOLVEMENT ARE
Acute lymphadenitis.—
Due to acute inflammation of the drainage area, the regional lymph nodes become acutely
inflamed and the condition is known as acute lymphadenitis. The affected lymph nodes become
enlarged, painful and tender. The overlying skin becomes warm, red and brawny oedematous.
There is a varying degree of pyrexia. Due to periadenitis, which may be present in all the
severe forms, the lymph nodes may be matted together.
Chronic lymphadenitis.—
The drainage area most carefully be examined, hi the cervical group oral sepsis, recurrent
bouts of tonsillitis and lesions of the scalp are usually the common causes. In the groin, besides
infected cuts and ulcers, walking on bare and cracked feet may lead to this condition amongst
labourers. Painful enlarged lymph nodes are common findings.
BIOPSY will show hyperplasia of the reticuloendothelial cells which may be so great as to
replace the lymphoid tissue. The sinuses, both medullary and peripheral are dilated and filled
with endothelial cells. The whole process is a reticuloendothelial hyperplasia.
Tuberculous lymphadenitis.—
In majority of cases human tubercle bacilli enter the body through the tonsil of the
corresponding side. From there they move to the cervical lymph nodes, so the upper deep
cervical nodes are most often affected. There is no generalized infection, so the cervical nodes
involvement is not secondary to tuberculosis anywhere in the body. In about 80% of cases the
tuberculous process is virtually limited to the clinically affected group of lymph nodes.
Age.— This is commonly found in children and young adults. It may occur at any age. The
incidence in the young has diminished since the introduction of BCG vaccination.
The cervical nodes are most frequently involved followed by mediastinal, mesenteric, axillary
and inguinal nodes according to the order of frequency.
In tuberculosis, the lymph nodes on section show translucent, greyish patches in the early
stage. As the disease advances these become opaque and yellowish, which is the result of necrosis
and caseation. Microscopically the tubercles will be seen which consist of the epitheloid cells and
giant cells having peripherally arranged nuclei in the early stage. After one week, lymphocytes
with darkly stained nuclei and scanty cytoplasm make their appearance. By the end of the
second week caseation appears in the centre of the tubercle follicle. So in the centre of the
tubercle follicle lies eosin stained caseation surrounded by giant cells and epitheloid cells around
which remains a zone of chronic inflammatory cells e.g. lymphocyte and plasma cells, around
which are the fibroblasts.
DISEASES OF THE LYMPHATIC SYSTEM
297
TREATMENT.—
(i) Antitubercular drugs should be prescribed straightway once the diagnosis is
confirmed. Injection Streptomycin — 0.5 to 1 g I. M. daily, INH in the dose of 300 mg/day and
PAS in the dose of 5 to 15 g/day should be prescribed. The latter two drugs should be continued
for at least 1V4 years. Sometimes the organisms may acquire resistance against these drugs.
Recently Ethambutol in the dose of 25 mg/kg body weight and Rifampicin in the dose of 15
mg/kg body weight are prescribed daily for at least 9 months.
(ii) Sanitorial regime, good food, vitamin supplementation and high protein diet are the
supportive therapies which every patient with tuberculous lymph nodes should receive.
(iii) If the lymph nodes do not respond to the drug therapy or show initial response but
remain static after that, operative removal is justified. Incision is made along the Langer's line
over the affected nodes. With fine dissections the surrounding adhesions are released and the
lymph nodes are removed enmasse.
(iv) If cold abscess has been formed, it is advisable to start the antituberculous therapy
and to aspirate the abscess before it ruptures with sinus formation. Aspiration is performed with
a thick needle through the healthy skin preferably from above. Aspiration is never done through
the most prominent and the most dependent part of the abscess lest a sinus should be formed
along the path of the aspiration.
Syphilitic lymphadenitis.—
In the primary stage the lymph nodes in the groin become enlarged along with presence of
genital chancres. The nodes are painless, discrete, firm and shotty. These nodes do not show
any tendency towards suppuration. In extra-genital chancres occurring in the lips, breasts etc.
the nodes may become inflamed, painful and matted. In the secondary stage generalized
involvement of nodes may occur affecting particularly the epitrochlear and occipital groups.
The characteristics are similar to those found in the primary stage. There may be ulcers in the
mouth and various skin rash (pink macular rash appears 4 to 8 weeks after the sore followed
by the papular eruption and more severe form is the ecthymatous type in which the papule
breaks down quickly and the underlying tissues become eroded or ulcerated). In the tertiary
stage the lymph nodes are seldom involved. Other syphilitic stigmas, positive W. R. and Kahn
tests along with presence of Treponema pallidum in dark ground illumination from the primary
lesion confirm the diagnosis.
(i) W. R. and Kahn test — usually positive.
(ii) Treponema pallidum may be demonstrated in specimens obtained from the genitals
or from the mucocutaneous lesion.
(iii) Some specific tests e.g. treponemal antigen test — treponemal haemagglutination
assay or treponema pallidum immobilization test are of more diagnostic value.
Fllurlai lymphadenitis.—
The inguinal nodes are commonly affected and this condition is more often found in males.
The lymph nodes become enlarged and tender. A history of periodic fever with pain ( especially
during the full or new moon ) is very characteristic. Swelling of the spermatic cord with dilatation
of lymphatic vessels (lymphangiectasis ) is often found in filariasis. There may be thickening of
the skin of the scrotum. Microfilaria can be demonstrated in the blood drawn at night.
Eosinophilia is the rule. Biopsy of lymph nodes may reveal adult filaria.
Lymphogranuloma venereum (Syn. lymphogranuloma Inguinale).—
.
It is a type of venereal disease caused by a filtrable virus of the psittacosis-lymphogranuloma
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A CONCISE TEXTBOOK OF SURGERY
inguinale group. A history of exposure is definite, though accidental infection may occur e.g. in
surgeons operating on infected patients. The primary lesion is insignificant and is not revealed
if leading questions are not put to the patients. The PRIMARY LESION is a type of painless
herpetic vesicles on the genitals. The SECONDARY LESION occurs about 2 to 6 weeks after
exposure. Medial group of inguinal lymph nodes of one or both groins are usually involved.
The lymph nodes become matted due to periadenitis and gradually become liquified. The
overlying skin shows brawny oedema and becomes purple in colour. The liquified mass may
break down and discharge thick yellowish-white pus free from organisms. The sinuses result
which refuse to heal for months or years. In females pararectal lymph nodes are involved through
the posterior vaginal wall and an intense pararectal inflammation with dense fibrosis involve
the rectal wall. This may cause stricture of the rectum. Ischiorectal abscess and rectovaginal
fistula may develop.
(i) Frei's test is quite confirmatory. Pus from unruptured bubo of a patient suffering
from this disease is diluted 10 times with normal saline and sterilized at 60° C. 0.1 ml of this
solution is injected intradermally. Appearance of a reddish papule within 48 hours of at least 6
mm in diameter at the site of injection indicates the test to be positive. This is known as Frei's
intradermal test.
(ii) The Complement fixation test is even more sensitive than the previous one. It shows
positive result in earlier stage of the disease.
_
(iii) Biopsy is definitely very confirmative. The earliest change in a lymph node is an
accumulation of large mononuclear cells which form small solid granuloma. Ischaemic necrosis
follows with invasion of polymorphonuclear leucocytes. Gradually stellate abscesses form. A
marginal zone of epitheloid cells and fibroblasts appears.
('at-Scratch disease,—
This disease has always an association with cats, but inspite of the name, there is not
necessarily evidence of a scratch or bite. There is usually an initial skin lesion, which is often
ignored. Enlargement of the regional lymph nodes becomes the main feature of this disease.
Axillary or cervical lymph nodes are more often affected. There may be tiny abscess formation
with suppuration. The primary skin lesion is a red papule in the skin at the site of inoculation
usually appearing between 7 and 12 days following contacts. It may become pustular or crusted.
This condition is caused by a virus of psittacosis-lymphogranuloma group.
(i) The diagnosis can be confirmed by skin testing.
(ii) Biopsy of the lymph nodes will reveal early lesion of histiocytic proliferation and
follicular hyperplasia. Microscopic and macroscopic abscesses are late features.
Infectious mononucleosis (Glandular fever).—
Glandular fever is an acute febrile disease in which the common features are fever,
enlargement of lymph nodes, splenomegaly, sore throat, appearance in the blood of lymphocytes
of unusual type ('Glandular fever cells'). The causative organism is probably virus ofrickettsia group,
though controversy still exists regarding the responsible agent. The generalized lymph node
enlargement is due to intense hyperplasia without loss of architecture. The spleen shows almost
the similar picture. In almost every case there is enlargement of cervical lymph nodes and those
in the posterior triangle are affected as much as those in other groups. The enlarged nodes are
often painful and usually tender. Axillary and inguinal groups are affected less frequently than
the cervical group. Abdominal pain and tenderness are common and may be explained by
mesenteric node enlargement.
DISEASES OF THE LYMPHATIC SYSTEM
299
(i) Lymphocytosis in the blood is a very characteristic feature of this disease.
(ii) Paul-Bunnell test is diagnostic. It is the increase of agglutinins for sheep's red blood
cells during the acute phase of the disease.
Tularaemia.—
It is a highly infectious disease caused by pasteurella tularensis. The clinical picture resembles
plague and is characterized by an ulcer at the site of infection, enlargement and inflammation
of the regional lymph nodes and severe constitutional symptoms. The disease starts 3 to 5 days
after infection with prodromal symptoms e.g. severe headache, feelings of cold and rise of
temperature. The enlarged local lymph nodes show features indistinguishable from those of
tuberculosis.
Brucellosis (Syn. Undulant fever).—
This is a disease which results from infection with species of bacteria of the genus brucella.
These are small, Gram-negative, non-motile coccobacilli. The onset is gradual with early
symptoms of mild fever, malaise, headache, generalized muscular pain and mild gastrointestinal
disturbances. After some weeks or months a pyrexial attack occurs which lasts a few days to
some weeks. It is usually followed by further pyrexial episodes. With each attack there is
enlargement and tenderness of the spleen and to a lesser extent the liver. In some, lymph node
enlargement is a striking feature. There is usually an accompanying hypochromic anaemia and
leukopaenia.
The lymph node biopsy shows features of either tuberculosis or Hodgkin's disease. Presence
of large cells resembling Reed-Sternberg cells may suggest the latter condition.
Sarcoidosis.—
In this disease there are granulomatous lesions which may be found in any organ or tissue.
The most commonly affected are, in order of frequency, the lungs, the lymph nodes, the skin,
the eyes, the liver, the spleen, the salivary glands, the heart, the skeleton and the nervous system.
The characteristic lesion of sarcoidosis is an epitheloid cell granuloma or tubercle. But there is
never caseation. Probably this is the only criterion which differentiates this condition
microscopically from tuberculous lymphadenitis.
Lymph nodes seldom reach very large size, average diameter being 2 to 3 cm. Enlarged
nodes show no tenderness or periadenitis.
The Kveim test.— This is an intradermal injection of 0.15 to 0.2 ml of 10% saline suspension
of sarcoid lymph node. The positive result is shown in 4-6 weeks by the appearance at the site
of injection of a nodule with the histological pattern of sarcoid. This test is positive in 60 to 85%
of patients with sarcoidosis.
Toxoplasmosis.—
It is a disease caused by an intracellular parasite known as toxoplasma gondii. The parasite
multiplies by longitudinal fission within the endothelial and tissue cells of its hosts. When the
virulent strains are formed these cells rupture releasing the parasites which then invade fresh
cells.
Toxoplasmosis may be transmitted to the foetus in utero by an infected mother when it is
called congenital toxoplasmosis.
The clinical features of acquired toxoplasmosis can be easily described under four headings —
(i) Cerebrospinal form is characterized by meningoencephalitis, fever, severe headache,
vomiting, delirium, convulsions, deafness etc.
(ii) Lymphatic form is characterized by enlargement of one or more groups of lymph
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nodes with fever of several weeks duration and marked constitutional disturbances.
(iii) Exanthematous form presents as acute febrile illness with widespread maculopapular
rash, myocarditis and interstitial pneumonitis.
(iv) Latent form in which there are no symptoms or signs of the disease and diagnosis
can only be made by laboratory tests.
Fungal diseases.—
Fungal diseases cause chronic granulomatous process that may or may not be associated
with caseation necrosis. There may be hyperplasia of sinus histiocytes without granulation
formation.
NEOPLASMS
No where in pathology has a chaos of names so clouded as in the subject of lymphoid
tumours. The general term 'the reticuloses' is often used to indicate a proliferation of
undifferentiated cells of the lymphoreticular system. I have used both old and new classifications
to make the students understand both the views clearly.
Neoplasms of lymphoid tissue means malignant lymphoma, as benign neoplasm is almost unknown
in lymphoid tissue.
Glant-cell lymphoma.-—
This condition is also known as follicular lymphoblastoma. It is the most benign member
of this group. It is the least common and constitutes only 5% of malignant lymphoid tumours.
Age.— It usually occurs after the age of 30 years. It is virtually unknown in children.
Clinical features.— It usually presents with enlargement of one group of nodes commonly in
the neck or groin. The nodes are not adherent to one another and are freely mobile. Later on
the condition becomes generalized.
Biopsy shows excess of lymphoid follicles which replace the normal architecture. These
follicles are uniform in size and distribution. This condition is often confused with chronic
lymphadenitis. The sinusoides are obliterated in contradistinction to the dilated sinusoides
characteristics of chronic lymphadenitis.
Lymphosarcoma.—
It is the second commonest among the non-Hodgkin's lymphoma.
(i) Age.— Though it may develop in middle life or later, it is quite common among
children.
(ii) The disease commences locally involving a single node. Gradually the adjoining nodes
are involved. Gradually enlarged lymph nodes can be seen in the neck, mediastinum and
abdomen. In abdomen both retroperitoneal and mesenteric nodes are involved.
(iii) Lymphosarcoma may involve lymphoid tissue other than the lymph nodes as for
example tonsil, pharynx and bowel. The involvement of the small intestine may be so diffuse
that the bowel is converted into a stiff tube. Spleen is involved in about less than half the cases.
(iv) Presence of constitutional symptoms like loss of weight, anaemia, anorexia and
weakness are quite evident. Unexplained fever is present in about 1/4th of cases.
(v) On inspection swelling becomes evident particularly in the neck. The overlying skin
is tense and shiny with engorged veins.
(vi) Palpation reveals an irregular surface, definite but irregular margin and varying
consistency — in places soft, firm in some places and hard in a few.
(vii) Chest X-ray may show enlarged mediastinal nodes.
DISEASES OF THE LYMPHATIC SYSTEM
301
(viii)
Lymphangiography will show involved retroperitoneal lymph nodes with typical coarse
nodular pattern of lymphosarcoma.
(ix)
Biopsy reveals — the cut surface is greyish white, homogeneous and bulging. Adhesion
to surrounding nodes is characteristic feature of this condition.
Microscopically, the normal structures of lymph nodes disappear and are replaced by diffuse
arrangements of monotonously uniform large lymphoblasts with hyperchromatic nuclei and
scanty cytoplasm. The follicles have disappeared. Diffuse infiltration of the capsule and
surrounding tissue is one of the most characteristic features. Another important feature is that
there is no increase in reticulum as shown by silver stains. The reticulum fibres which are seen
in this condition represent the original content of the node and these are dispersed by the
infiltration of the neoplastic cells, so that in a given field they appear to be decreased in number.
Reticulum ceil sarcoma.—
It is the commonest among non-Hodgkin's lymphomas.
(i) Age and site are similar to those of lymphosarcoma.
(ii) Occasionally bone and even urinary bladder may be involved.
(iii) Prognosis is also same as lymphosarcoma and that the usual survival is less than 2
years.
(iv) Clinical features are more or less same as lymphosarcoma.
(v) Lymphangiography will show typical marginal sun burst appearance.
(vi) Biopsy.— Macroscopic feature is more or less same as lymphosarcoma.
The microscopic picture shows abundance of reticulum cells with faintly acidophilic cytoplasm.
The nucleus is double the size of a lymphocyte and is commonly infolded giving it a reniform
appearance. There are pseudopod like processes of both cytoplasm and nucleus. The characteristic
feature is the well distribution of silver staining reticulum which has got intimate relations to
the tumour cells either encircling groups of cells or sending fibrils between and around individual
cells.
Treatment of both lymphosarcoma and reticulum cell sarcoma.— If there is no evidence of spread
beyond the area of head and neck, radiotherapy is the treatment of choice. High dose of
radiotherapy nearing 6,000 rads and cobalt may be applied. Both these tumours are radiosensitive.
In case of generalized involvement chemotherapy with multiple drugs should be applied.
NEW CLASSIFICATIONS
Undifferentiated lymphoma.—
This is a malignant proliferation of primitive cells having scanty cytoplasm and a round or
oval nucleus with delicate cromatins and a small, distinct nucleolus. Burkitt's lymphoma is
regarded as a specific variant of this type of lymphoma. It has a peculiar geographic distribution
mostly seen in tropical Africa and New Guinea. Typically Burkitt's lymphoma affects children
and young adults. It has a great tendency of extra nodal involvement such as the jaws, ovaries,
abdominal organs, retroperitoneum and the central nervous system. Untreated cases follow a
rapid fatal course.
Microscopically, the most striking feature is the 'starry sky' pattern resulting from a scattering
of non-neoplastic histiocytes containing phagocytosed nuclear debris among a monomorphic
infiltrate of highly primitive cells.
(i)
Age.— Majority of the patients are between the ages of 4 and 8 years. Incidence
gradually decreases as the age advances and only 6% of cases are seen over the age of 21 years.
A CONCISE TEXTBOOK OF SURGERY
302
(ii) Sex.— Males are involved more than the females at the ratio of 2 : 1.
(iii) Mode of clinical presentation.— (a) Facial tumours are by far the most common
presentation, (b) The second most frequent mode of presentation is abdominal tumours. These
fall into three main categories — retroperitoneal mass, liver enlargements and ovarian tumours,
(c) Lesion in the central nervous system is the third mode of presentation with vertebral collapse
and paraplegia, (d) Intracranial lesions with cranial nerve palsies, unilateral or bilateral deafness,
increasing drowsiness and headache are the features, (e) Tumours in other sites like salivary
glands, thyroid glands, skeletal tumours (bones most frequently involved are the femur, humerus,
tibia and the ilium; the chief distinguishing feature between this tumour and osteosarcoma is
the relative absence of pain in this tumour) and breasts, (f) Involvement of peripheral lymph
nodes is characteristically rare.
Treatment.— Burkitt's lymphoma is extremely sensitive to radiotherapy, but local
radiotherapy has been followed by development of tumour in other sites. Radiotherapy to clinically
detectable tumours should be supplemented by chemotherapy to deal with disseminated tumours.
Histiocytic lymphoma.—
Lymph nodes involved by histiocytic lymphoma (reticulum cell sarcoma) may be matted
together and contain large necrotic areas. The nodal architecture is totally or partially obliterated
by proliferation of malignant histiocytes. Variations in cellular and nuclear shape are marked.
The nuclei are large and vesicular with prominent nucleoli and thick nuclear membranes. Mitoses
are common. Fibrosis with hyalinization of the stroma is sometimes prominent separating the
tumour cells in clusters of cords.
Lymphocytic lymphoma.—
The individual nodes are not adherent. They appear highly cellular and occasionally
contain areas of necrosis. In poorly differentiated variant the cells are larger than matured
lymphocytes but smaller than histiocytes. The nuclei are round, oval and irregular with focal
chromatin clumping and a distinct nucleolus. Nuclear indentations are often present. In welldifferentiated lymphocytic lymphoma the cells are similar to normal mature lymphocytes. It is
very difficult to differentiate this type of lymphoma from chronic lymphocytic leukaemia. The
clinical history, the peripheral blood count and the bone marrow findings are required to
make such distinction.
Mixed (histiocytic-lymphocytic) lymphoma.—
This designation should be restricted to tumours in which both histiocytes and lymphocytes
are present in significant amounts. A nodular pattern of growth is common in the early stage,
but majority however develop into a diffuse lymphoma of histiocytic type. Whether the concept
of a mixed lymphoma is valid one needs to be substantiated. The alternative possibility that the
lymphocytes are nonneoplastic and that they represent a reaction to the tumour.
Cllnicopathologic correlation.— The prognosis of a particular lymphoma depends on
the extension of the disease, cell type, nodular or diffuse pattern of growth and fibrosis. Stage I
lesions have good prognosis but unfortunately they comprise only l/3rd of all cases. The routine
use of lymphangiography has demonstrated that most patients with non-Hodgkin's malignant
lymphoma have widespread disease at the time of diagnosis. Spread by involvement of
contiguous lymph node groups is common in non-Hodgkin's lymphoma. It is more common in
the diffuse than in the nodular type.
In regard to cell type the average survival is longer for well differentiated lymphocytic
type, shorter for the histiocytic variety and intermediate for the poorly differentiated lymphocytic
DISEASES OF THE LYMPHATIC SYSTEM
303
type. In all groups, the survival rates are better in patients with tumours with a nodular pattern
of growth and those associated with a significant degree of stromal fibrosis. In contradistinction
to Hodgkin's disease non-Hodgkin lymphomas involve mesenteric lymph nodes quite commonly.
Non-Hodgkin lymphomas have a much greater tendency to begin or at least to present clinically
as extranodal tumours than Hodgkin's disease. The bone marrow and the spleen are the most
common sites of extranodal spread.
HODGKIN’S DISEASE
(i) Age.— The onset of this disease is about a decade earlier than lymphosarcoma and
reticulosarcoma. The incidence increases in the late 20s, but it is not uncommon in children.
(ii) Sex.— The disease is slightly more common in men than women.
SYMPTOMS.—
I.
The symptoms are more local than constitutional except in acute cases. The most
common presentation is painless and progressive, enlargement of the lymph node first detected in the
cervical group on one side and then on the other. This is followed by axillary and inguinal
lymph nodes enlargements. Retroperitoneal lymph nodes are often involved but require
lymphangiography and computed tomography (CT scan) for diagnosis. Mediastinal involvement
occurs in only 6% of patients at the time of diagnosis.
II.
Constitutional symptoms (B symptoms) such as fever, night sweat, weight loss and
pruritus usually indicate widespread involvement and poor prognosis. They may appear
simultaneously with lymph node enlargement or may precede that.
(i) A typical fever pattern is a high temperature with rigors occurring in a periodic
fashion alternating with a few days of afebrile period — PeTEbstein fever.
(ii) Malaise, weight loss and pallor are also common constitutional symptoms.
(iii) Itching of the skin or pruritus is unexplained but a quite common complaint of this
disease.
(iv) Pains in the bones and abdominal pain may be complained of. There may be rootpain and even paraplegia due to collapse of the vertebra secondary to bony metastasis. Rootpain may be due to deposits in the vertebra or pressure by retroperitoneal nodes on the nerve
roots while they come out from the intervertebral foramina. A peculiar feature of this disease is the
complaint of enhanced pain at the sites of disease induced by drinking alcohol.
(v) Pressure effects by enlarged mediastinal lymph nodes may cause venous engorgement,
cyanosis of the head and neck and difficulty in respiration due to pressure on the bronchus.
(vi)
Large masses in the abdomen can obstruct the inferior vena cava and cause oedema
of both the legs.
LOCAL EXAMINATIONS.—
(i) Site.— Any group of the cervical nodes may be affected including those in the
posterior triangle.
(ii) Temperature and tenderness.— The enlarged lymph nodes are neither warm nor tender.
(iii) Size, shape and surface.— Hodgkin's lymph nodes are ovoid, smooth and discrete. The
nodes show little tendency towards matting or softening.
(iv) Consistency.— The lymph nodes feel elastic and rubbery in consistency.
(v) Mobility.— These nodes can be moved from side-to-side, though their mobility is
rather restricted due to tethering to neighbouring structures.
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A CONCISE TEXTBOOK OF SURGERY
GENERAL EXAMINATIONS.—
(i) Other groups of lymph nodes may be enlarged.
(ii) Splenic enlargement is a significant finding of this disease and is found in not less
than 75% of cases.
(iii) Hepatomegaly is found in about 50% of cases.
(iv) Progressive anaemia is more or less constant and may be due to splenomegaly or
bony metastasis.
(v)
Sometimes jaundice is seen due to
excessive haemolysis of the red cells or
involvement of liver.
SPECIAL INVESTIGATIONS.—
(i) In blood, a picture of normochromic
normocytic anaemia is quite evident. About
l/3rd of cases show leucocytosis due to
increase in neutrophil and eosinophil.
(ii) Importance of lymphangiography has
already been discussed.
(iii) Computed tomography (CT scan) is
helpful to detect involvement of retroperitoneal
lymph nodes and mediastinal lymph nodes.
(iv) Chest X-ray also shows mediastinal
lymph node enlargement.
(v) The liver and spleen scan indicate
involvement of these organs or not.
(vi) Bono scan is of value in determining
bone involvement.
(vii) Lymph node scanning has been
performed with Gallium 67 to detect the
clinically doubtful lymph node involvement,
particularly the mediastinal group.
CLINICAL
STAGING
OF
THE
HODGKIN’S
DISEASE
:
Stage
I.—
Involvement of a single lymph node region or
involvement of a single extralymphatic organ
or site (I E).
Stage II.— Involvement of two or more
lymph node regions on the same side of the
diaphragm alone or with involvement of limited
contiguous extralymphatic organ or tissue (II E).
Stage III.— Involvement of lymph node
regions on both sides of the diaphragm, which
may include the spleen (III S) and/or limited
contiguous extralymphatic organ or site (III E, Fig. 17.5.— Histology of various types of Hodgkin's
III ES).
disease. A.- Mixed cellularity. B.-Lymphocytic
predominant and C - Nodular sclerosis.
Stage IV.— Multiple or disseminated foci
DISEASES OF THE LYMPHATIC SYSTEM
305
of involvement or one or more extralymphatic organs or tissues with or without lymphatic
involvement.
All stages are further subdivided on the basis of absence (A) or presence (B) of the following
systemic symptoms e.g. fever, weight loss more than 10%, bone pain etc.
PATHOLOGICALLY, Hodgkin's disease can be divided into four categories, which is
important so far as the prognosis of the disease is concerned. The more numerous are the
lymphocytes, the more favourable is the prognosis.
Type 1.— Lymphocyte-predominant Hodgkin's disease.
Type 2.— Mixed-cellularity — a diffuse infiltrate of lymphocytes, histiocytes, eosinophils
and plasma cells that obliterate the normal architecture.
Type 3.— Nodular sclerosis is often seen in clinical stage I and is associated with better
prognosis.
Type 4.— Lymphocytes depletion pattern — the most ominous form.
BIOPSY.— Macroscopically the lymph nodes are enlarged but remain discrete till the late
stage of the disease when they become fused. They are firm and elastic and on section shows
uniform grey translucent and moist appearance. Occasionally yellow patches of necrosis may
break the homogeneity.
Microscopically there is an early loss of the follicular pattern due to hyperplasia of the reticular
endothelial elements. Its most important feature is cellular pleomorphism. There are lymphocytes,
eosinophils, plasma cells and histiocytes — all are present in greater or lesser amount depending
on the microscopic type. The initial diagnosis depends on the presence of the Reed-Sternberg
cells, which the pathologists make careful search of. This cell is of relatively large size, its
cytoplasm is abundant either basophilic or amphophilic and two or more vesicular nuclei are
present, each having a thick nuclear membrane and a single prominent acidophilic nucleolus
surrounded by a clear halo. The two nuclei are such that one of which is the mirror-image of
the other, the so called 'mirror-image giant cell'. Cells with one nucleus should not be designated
as Reed-Stemberg cells. These may be designated as atypical mononuclear histiocytes. The ReedStemberg cells are neoplastic reticulum cells. Presence of atypical mononuclear histiocytes with
typical pleomorphism also suggests Hodgkin's disease. When the nucleus is single, it may be
convoluted or ring shaped. Besides these giant cells there are also polymorphonuclears,
eosinophils and plasma cells to add to pleomorphism. Eosinophils are particularly characterized,
being sometimes present in large numbers. In doubtful cases they may help to settle the diagnosis,
but they are not invariably present. This group of cells may be regarded as reactionary and
secondary and they do not form an integral part of the neoplastic process. There is a characteristic
increase of reticulum shown by silver-staining.
According to the cell types the Hodgkin's disease can be classified into four varieties —
In type I i.e. lymphocyte predominant type, Reed-Stemberg cells are scanty, scattered among a
large number of matured lymphocytes and sometimes accompanied by proliferation of benign
appearing histiocytes.
In type II or mixed cellularity there is a significant number of eosinophils, neutrophils, plasma
cells and atypical histiocytes that accompany the Reed-Stemberg cells and lymphocytes.
In type III or nodular sclerosis is characterized by broad collagen bands separating the
lymphoid tissue in well defined nodules. The fibrosis often centres around blood vessels. The
cytologic patterns within the nodules is one of lymphocyte predominance, lymphocyte depletion
or mixed cell type. Clumps of foamy macrophages are sometimes present. In additional to the
typical Reed-Stemberg cells there may be seen a type of giant-cell which is quite large with
20
306
A CONCISE TEXTBOOK OF SURGERY
abundant clear cytoplasm and several nuclei having complicated infoldings and inconspicuous
nucleolus. Some pathologists consider presence of these giant cells is more typical of this type
of Hodgkin's disease than the fibrosis itself. It must be remembered that practically all types
of Hodgkin's disease may exhibit some degree of fibrosis particularly after therapy.
In type IV or lymphocyte depletion there is infiltration predominantly formed by malignant
appearing histiocytes, some of which fulfil the criteria of Reed-Stemberg cells. Lymphocytes are
seen few and far between.
Treatment—
(i)
RADIOTHERAPY is the treatment of choice if the disease is confined to a single or
two contiguous node-bearing areas (Stage I) or to lymph nodes one side of the diaphragm
(Stage II). Radiotherapy has also produced a substantial number of prolonged remissions in
patients with generalized disease confined to nodal tissue (Stage III), but radical radiotherapy
is not widely used for this type of patients. Chemotherapy is generally employed in patients
who have Stage III disease or who have disease involving extranodal structures (Stage IV).
It is also used in a few patients with
stage II disease who have severe
systemic symptoms, such as fever, as an
adjunct to radical radiotherapy, but not
as definitive treatment. Megavoltage
radiotherapy allows wide areas to be
^
treated. Supradiaphragmatic disease is
treated by radiotherapy to cervical,
jgpraxillary and mediastinal nodes. Usually
"%•
^~
shields. Radiotherapy is given in the
range of 4,000 rads in divided doses
over several weeks. Infradiaphragmatic
disease is treated by fields covering
para-aortic and iliac nodes in the form
of inverted Y fields.
lot during the last decade in the
treatment of Hodgkin's disease
particularly in Stage III, Stage IV and
those with involvement of extra nodal
structures and those with systemic
symptoms (B symptoms). In 1964, a
combination of agents was devised at the
^
mLJ
I^
i . * . ‘
1
/
I’
%
\
f
V
{VHV
(MOPP) include Mechlorethamine,
Vincristine sulphate, Procarbazine and
Prednisone. Preliminary results reported Fig. 17.6.— The principal lymph nodes to be biopsied during
in 1970 were extremely encouraging. The the operation of staging in Hodgkin's disease marked
as black dots.
remission rate was superior to that
DISEASES OF THE LYMPHATIC SYSTEM
307
previously reported for single drug and even more important a substantial proportion of patients
remained continuously free of disease for 4 years even though no maintenance therapy was
given. MOPP is administered for six two weeks cycles of chemotherapy, with two weeks interval
between each period of drug administration.
Treatment Schedule.—
Each course of therapy consisted of 14 days of treatment. Vincristine Sulphate (1.4 mg/Sq.
M) and Mechlorethamine hydrochloride (6 mg/Sq. M) were given on days 1 and 8 by rapid
I.V. injection. Procarbazine hydrochloride (100 mg/Sq. M) and prednisone (40 mg/Sq. M) were
given orally daily in divided doses for 14 days and then discontinued. After each 14-day
treatment, all therapy was discontinued and was resumed two weeks later (to avoid leukaemia
or thrombocytopaenia).
A complete programme of therapy consisted of 6 to 2 — courses with a rest period after each
course.
LAPAROTOMY FOR HODGKIN’S DISEASE.— Staging Laparotomy is frequently done
for clinical staging of Hodgkin's disease. Its use is based on the following facts :
(i)
Hodgkin's disease generally begins in a single area and spreads in non-random manner
via lymphatic channels to contiguous lymph nodes and organs that have prominent lymphatic
tissue components, (ii) Selection of therapy depends on the clinical staging and for this staging
laparotomy is of immense value, (iii) Clinical staging is not frequently accurate only by clinical
examinations and there lies -the importance of staging laparotomy, (iv) Approximately 25% of
clinically staged patients will have their stage of disease increased and approximately 15% will
have their stage decreased following laparotomy.
Staging laparotomy is not applicable to all patients with Hodgkin's disease and should be performed
only in patients in whom the result may change the plan of therapy. Patients with advanced Hodgkin's
disease, clinical stage III B and stage IV do not benefit from staging laparotomy because treatment
will be combination chemotherapy. If there be splenomegaly even in advanced Hodgkin's disease,
splenectomy is of value to control cytopenias, reduce tumour burden and avoid the risk of
radiation to the left kidney and lower lobe of left lung.
Staging laparotomy consists of (i) splenectomy, (ii) liver biopsy, (iii) selective excision of
abdominal and retroperitoneal lymph nodes. Lymph nodes are removed from the coeliac axis
region, from the porta hepatis, from the small intestinal mesentery and mesocolon and pre- and
para-aortic lymph nodes, (iv) a bone marrow biopsy is obtained from the iliac crest. (V)
Oophoropexy (ovarian translocation) may be performed in pre menopausal women in whom
radiation therapy using the inverted Y port is likely. Both ovaries are removed from the potential
field of radiation. Lead shielding is an important adjunct to the protective effects offered by
oophoropexy.
Usually a midline incision is made to expose the abdomen for staging laparotomy. One
may use a long left paramedian incision. Staging laparotomy has minimal morbidity and
mortality rate less than 0.5%.
Prognosis.— 5 years survival rates for Hodgkin's disease are 85% for stage I and II, 70% for
stage III A, 50% for stage III B and 40% for stage IV.
SECONDARY CARCINOMA
Secondary carcinoma is a very common cause of lymph node enlargement in the elderly.
Secondary involvement of lymph node may also occur commonly from malignant melanoma.
A CONCISE TEXTBOOK OF SURGERY
308
HISTORY.—
(i) Age.— Patients are usually over 50 years of age. The exception is papillary carcinoma
of the thyroid in which secondary metastatic lymph nodes may be seen in children and young
adults.
(ii) Sex.— More common in men than in women.
SYMPTOMS.
(i) Painless swelling is the usual presentation. In late stages patient may complain of pain
due to involvement of nerves and surrounding structures.
(ii) General symptoms e.g. anorexia, weight loss, weakness etc.
(iii) Patients may have other complaints such as ulcer in the tongue, hoarseness of the
voice. If the primary is in the chest he may have cough or haemoptysis. If the primary is in the
abdomen he may complain of dyspepsia or abdominal pain.
LOCAL EXAMINATIONS.—
(i) Site.— The precise location of the gland may give a clue to the site of primary tumour.
Upper deep cervical nodes are involved when the primary lies in the head, face and interior of
the mouth. The middle and lower deep cervical nodes are involved when the primary is in the
larynx or thyroid. Supraclavicular lymph node enlargement indicates thoracic or abdominal
disease. When these glands (Virchow's glands) are enlarged, it is called Troisier's sign.
(ii) Temperature and tenderness.— Skin temperature is usually normal unless the tumour is
very vascular. These nodes are usually not tender.
(iii) Size and shape.— The lymph nodes are irregular, discrete and of varying sizes. Soon
they coalesce and form one large mass, so at that time the nodes are not descrete.
(iv) Consistency.— These nodes are usually hard to feel.
(v) Mobility.— As the nodes are tethered to the surrounding structures, their mobility
becomes restricted. In early stage the nodes can be moved sideways but not vertically. Later on
the nodes become absolutely fixed to the surrounding structures. Gradually the skin may be
involved and is 'pulled' towards the mass.
GENERAL EXAMINATIONS.—
(i) Other lymph nodes should be examined particularly in the pathway in search of the
primary tumour.
(ii) Discovery of the primary growth confirms the diagnosis. Whenever a patient comes with
enlarged lymph nodes it should be routine practise to examine its drainage area. The lymphatic
drainage of the body may be discussed in the following way :—
The cervical lymph nodes receive the lymphatics from the head, face, mouth, pharynx and
neck; the left supraclavicular lymph node (Virchow's) receives lymphatics from left upper limb,
left side of the chest including the breast and also the viscera of the abdomen including both
the testes.
The axillary group of lymph nodes drains the upper limb of that side and the trunk which
extends from the clavicle to the level of the umbilicus (including the breast).
The inguinal lymph node drains the whole of the lower limb, the skin of the lower part of
the abdomen below the level of the umbilicus, the penis, scrotum, perineum, vulva, anus, buttock,
lower part of the back including the terminal parts of the anal canal, urethra and vagina (the
portions which are developed from the ectoderm). That means the drainage area of the inguinal
lymph nodes extends from the level of the umbilicus down to the toes.
DISEASES OF THE LYMPHATIC SYSTEM
309
Treatment.—
(i) When the primary growth is not detected, the secondarily involved lymph nodes should
be excised.
(ii) When the primary growth is operable, the primary growth is adequately excised alongwith
excision of the involved nodes. In this case block dissection of the neck is indicated, provided
there is no clinical or investigation report that there are more distant metastases. Adherence to
the skin, to the mandible or to the larynx should not be regarded as inoperable for each of
these structures can be sacrificed provided the patient's general condition permits. Now-a-days
the surgeons are more inclined to combine radical neck dissection with simultaneous resection
of the primary lesion. This composite resection is called commando operation.
(iii) When the metastatic nodes are fixed to deeper structures and/ or there are distant metastases,
palliative deep X-ray treatment is indicated or the lymph nodes may be treated by local
radiotherapy such as insertion of radioactive gold seeds. This will reduce the size of the tumour
and relieve pain. High doses of deep X-ray therapy will cause necrosis of the mandible or the
laryngeal cartilages in cases of the cervical nodes.
BLOCK DISSECTION OF THE NECK
The incision is planned to give adequate access to all gland groups. The gland groups
which are removed en bloc are the submental, submandibular, the upper and lower deep cervical
Fig.17.7.— Shows various incisions for block dissection of the neck.
310
A CONCISE TEXTBOOK OF SURGERY
groups, the posterior
cervical group and the
supraclavicular group.
Various incisions have
been advocated by various
surgeons e.g. (i) Crile's T
incision whose horizontal
part starts on the midline
at the tip of the mandible
and curves across to the tip
of the mastoid process and
the vertical limb starts
from the midpoint of the
horizontal limb and runs
obliquely downwards to
the midline of the clavicle;
Fig. 17.8.— Shows the initial steps of block dissection operation.
(ii) Martin's double -Y
incision; (iii) Ward's Y incision in which the vertical limb extends from in front of the tragus
down to the middle of the clavicle and the curved oblique limb starts from the middle of the
vertical incision and is obliquely carried
upwards to the tip of the mandible in the
midline and (iv) two horizontal incisions are
made one at upper part of the neck, starting
from the tip of the mandible at the midline
and curves across one side of the neck to the
tip of the mastoid process and the lower
horizontal incision is made inch above the
clavicle. These two incisions are joined by
curved vertical incision joining the midpoints
of both these horizontal incisions.
The skin flaps are reflected including the
underlying platysma muscle and the
dissection of the neck structures begins in the
posterior triangle. The fibro-areolar tissue of
the posterior triangle are dissected away from
the trapezius muscle and is carried
medialward till the phrenic nerve is reached.
The lower end of the stemomastoid muscle
is divided. The muscle is retracted upwards.
The omohyoid is severed and turned aside
so that the entire carotid sheath is now
exposed. The internal jugular vein is
separated from the accompanying vagus
nerve and common carotid artery. Next the
jugular vein is divided between
Fig.17.9.- ■ Shows the anatomy of the neck at theinternal
end
of block dissection operation.
ligatures just above the clavicle. The
DISEASES OF THE LYMPHATIC SYSTEM
311
dissection proceeds upwards gradually dissecting the lymph nodes chain alongwith the internal
jugular vein and surrounding fat and fascia. Just above the level of the carotid bulb the
hypoglossal nerve is identified. In the upper portion of the neck the stemomastoid muscle is
again transected at the level of the mastoid together with the tip of the parotid gland. The
submandibular salivary gland is dissected free from its fossa. The lingual nerve and artery will
be seen at the depth. A tiny fibre of the facial nerve which innervates the lower lip will be seen
above the submandibular gland. These nerves are preserved. The spinal accessory nerve is only
sacrificed if it is involved in the growth. It is then divided in two places — in the lower neck
where it enters the trapezius muscle and in the upper neck where it enters the stemomastoid
muscle. The operation is completed with transection of the jugular vein at the extreme upper
part of the neck. The skin is closed with suction drainage.
The structures removed in the block dissection are —
(a)
The groups of lymph nodes mentioned above, (b) the stemomastoid muscle, (c) the
internal jugular vein, (d) the submental and submandibular salivary glands, (e) spinal accessory
nerve if it is involved, (f) branches of the external carotid artery or a segment of the parent
trunk itself if involved by growth. Spinal accessory nerve is preserved if not involved in growth.
Particular attention is given to preserve the following structures — (a) the vagus nerve, (b) the
hypoglossal nerve, (c) the lingual nerve and (d) the lowest branch (cervical branch) of the facial
nerve.
Modified radical neck dissection.— This operation is still not very specific. Some surgeons
feel that all the functional structures in the neck including the stemomastoid muscle, the spinal
accessory nerve and the jugular vein should be preserved, removing mainly the lymphoareolar
tissue of the anterior and posterior triangles and the submaxillary gland. Some surgeons feel
that the stemomastoid muscle should be removed to give proper exposure to the carotid sheath
and the jugular vein must be removed as the deep cervical nodes are closely related with this
vein.
Suprahyoid block dissection — may be indicated in cases of carcinoma of the tip of the
tongue, floor of the mouth and lower lip. The advantage is that both sides of the neck may be
operated on simultaneously. Mainly the submental, submandibular and upper deep cervical
nodes are removed alongwith the submental and submandibular salivary glands. The rationality
of this operation is very much questioned as the deep cervical nodes are the main lymph nodes
of the neck of which the lower group is left behind.
THE PERIPHERAL
NERVES
Structure of a peripheral nerve.—
The structure of a peripheral nerve can be compared to an electric cable. It consists of many
fibres, which are nothing but axons of the cells situated either in the central nervous system or
in the ganglion of the autonomic nervous system. Each of these fibres or axons is enclosed in a
myelin sheath, which in its turn is surrounded by a cellular sheath, known as neurilemma or sheath
of Schwann. A small bundle of these fibres is called a funiculus. Individual nerve fibres are
ensheathed and supported within the funiculus by delicate connective tissue called the endoneurium,
which is continuous with septa which pass inwards from the perineurium. Each funiculus is
surrounded by a connective tissue sheath called the perineurium. If the nerve is small, it may
consist of only a single funiculus; but if large, it consists of several funiculi held together and
invested by connective tissue, which is known as epineurium. Majority of the cerebrospinal nerves
are myelinated. The blood vessels form a plexus around the nerve before supplying.
INJURY TO THE PERIPHERAL NERVES
Pathology.—
According to the extent of the damage, injury to the peripheral nerves can be divided into
3 categories
1. Neurapraxia.— This condition is almost equivalent to concussion, in which there is
no organic damage to either the nerve fibre or its sheath, but there is a temporary physiological
paralysis of conduction through the intact nerve fibres. Neurapraxia is produced by minor
stretching or torsion or vibratory effect of a high-velocity missile passing near a nerve. There
may be sensory loss or weakness of muscle groups. During this time there is no reaction of
degeneration in the muscles. Recovery is complete, which may take a period of hours to even a
few weeks.
2. i\xonotmesis.— In this condition there is rupture of nerve fibres or axons within intact
sheaths. Wallerian degeneration occurs in the distal portion of the broken axons leaving the
nerve sheaths empty. Recovery takes place slowly by downgrowth of the axons into the empty
distal nerve sheaths. There may be some loss of nerve fibres owing to the blockage of the
downgrowing axons by intraneural fibrosis. Such intraneural fibrosis occurs at the sites of axonal
rupture and minute intraneural haemorrhages. As the sheaths remain intact, the relative position
of axons are preserved and hence the quality of the regeneration is often good. The time required
for recovery varies according to the level of the lesion — which occurs first in the muscles
nearest to the lesion and last in the peripheral skin, where the anaesthetic area decreases steadily.
In the first 10 days there is hardly any downgrowth of axons and so improvement is not seen.
After this initial delay of 10 days to fortnight, the downgrowing axons proceed distally at the
rate of about 1 mm per day (initially the rate may be 2 mm per day, which diminishes in
THE PERIPHERAL NERVES
313
course of time to 1 mm per day after about a couple of months) till they reach their endings.
On arrival at their endings there is a further delay of 3 weeks or so before the end organs
become fully recovered.
Axonotmesis usually results from a stress, occuiring in association with fractures or
dislocations or from an excessive zealed manipulation to reduce such injuries. It may also occur
from compression by tourniquets, splints or incorrect posture on the operating table. Progressive
compression from crutches, callus or scar tissue in the injured area or by repeated minor
stretching of a nerve, which is often seen in ulnar nerve by cubitus valgus or the same nerve
following fracture of the medial epicondyle may lead to this type of injury.
CLINICAL FEATURES.—
Following an injury, a picture of neurapraxia will be noticed. There is loss of sensation,
tone and power of the muscles with diminished reflex activity of the limb. Later on area of
anaesthesia and paralysis of muscles will be restricted to those which are supplied by the
damaged nerves only. This is due to resolution of neurapraxia to the surrounding nerve fibres
which are intact.
Usually after a fortnight anaesthesia of the skin area and loss of power of the muscles will
be restricted to the actual supply of the damaged nerves. Usually the total area affected is less
than the known anatomical distribution of the nerve due to the fact that a few fibres within the
nerve usually escape.
Secondary effects due to nerve damage will be seen. There may be impaired circulation due
to disuse which makes the affected portion cold and blue. There may be some trophic changes
e.g. the nail becomes brittle and the skin becomes thin. Within 3 weeks the reaction of
degeneration appears in the muscles concerned. The affected muscles no longer respond to
faradic stimulation, but they will respond to the galvanic stimulation. The polarity also changes
so that A. C. C. becomes greater than K. C. C. In late cases the muscle fibres degenerate and
progressive fibrosis replaces degenerated muscle fibres. If this occurs recovery is then impossible.
Sometimes periarticular adhesions may develop around the immobile joints to cause stiffness of
the joints.
TREATMENT.—
Treatment of axonotmesis is maintaining nutrition of the limb and to combat secondary
pathological changes due to nerve injury. This consists of maintaining of muscles and joints in
good working condition till the arrival of downgrowing axons. All affected joints are put through
full passive movements daily to prevent contracture to develop. Exercise of the paralysed muscles
is maintained by physiotherapy. Encouragement to the patient is of utmost necessity to restore
function during the period of recovery. Progress is always checked by taking records of the
electrical reactions of the muscles and skin sensitivity. Electrical reactions change back to normal
in the proximal groups first.
Failure to recover or regression after initial recovery, is an indication for exploration of the injured
nerve. This is required to deal with the perineural scar or to remove intraneural fibroma.
The rates of nerve regeneration are assessed by the following clinical data —
(a) Tinel's sign.— A light patellar hammer is used to percuss from below upwards along
the course of the injured nerve. A tingling sensation is experienced at the level of regeneration.
By the sign one can assess the downward growth of the axons or nerve fibres.
(b) The powers of the involved muscles are tested one by one, so that return of function
of the muscle at different levels are observed and thus the level of regeneration can be detected.
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(c)
Similarly the sensation of the affected skin is regularly assessed and the rate at which
the pain and touch sensitivity returns from the periphery of the anaesthetic skin is assessed to
know the level of regeneration.
Operative treatment of closed nerve injuries.— Sometimes nerve injury can occur as secondary
to fractures, but bony fragments do not injure the nerve directly and the function of the nerve
is impaired by ischaemia from injury to the blood vessels supplying the nerve. The majority of
these nerve lesions remain in continuity and are non-degenerative in type. In these cases the
treatment is directed to reduce the fracture or dislocation and a conservative treatment is given
for the nerve problem, which consists of prevention of stretching of the muscles supplied by
the nerve by proper splints and prevention of pressure sores.
In about 50% of these cases, nerve injury recovers within a few weeks. Of the other half of
the cases, about 80-90% will gradually recover, that is the proximal nerve fibres will grow down
the degenerated distal fragment. In these cases the quality of regeneration is quite satisfactory
as there is no chance of maldistribution of nerve fibres. In only 10% of cases, there may not be
any evidence of recovery at the expected time. These are the cases which will require exploration.
So when recovery does not reach the first motor branch in the expected time, which is calculated
by the recovery rate of approximately 25 mm (1 inch) in a month, exploration is indicated.
Sometimes closed injuries are associated with considerable pain and paraesthesia. This is an
indication for early exploration.
3.
Xvurotmesis.— In this condition there is partial or complete division of the nerve
fibres as well as their sheaths. Partial lesion will produce a lateral neuroma on the nerve. Complete
division will produce a terminal neuroma at the distal end of the proximal segment.
In the proximal segment of the divided nerve there will be retrograde degeneration upto
the first node of Ranvier. After an interval of 10 days to fortnight the distal ends of the axons in
the proximal segment will start to grow downwards. But by this time the gap between the
divided nerve ends has been replaced by organic clots and fibrous tissue, which prevent further
downgrowth of the axons. So suturing of the nerve is the only treatment available if restoration
of function is to be achieved.
In the distal segment of the divided nerve, Wallerian degeneration of the axons occurs,
which is described in detail below. It is only noteworthy here that the schwann cells proliferate
to form a small bulb-like projection from which these cells grow proximally towards the
downgrowing axons by chemotaxis.
In neurotmesis, the quality of regeneration is less perfect even after accurate nerve suturing.
This is due to maldistribution of axons into the distal fragment. That means regeneration of axon
sprouts into the wrong sheath. A motor nerve fibre may grow down a sheath previously occupied
by a sensory fibre. So it cannot function, as it will make no connection with the sensory endorgan. Similarly, a sensory fibre may grow down the sheath of a motor fibre and cannot make
connection with the motor end-plate. Moreover, a few axons will be wasted in the scar tissue at
the suture line. So the recovery of function will be worst in mixed motor and sensory nerves as
axons of motor fibres may be well united with sensory fibres of the distal fragment. The recovery
will be better if the nerve is pure motor or sensory nerve. Thus recovery from the radial nerve
injury at the elbow will be better than the ulnar nerve or median nerve injury at the wrist.
Neurotmesis is seen in war and severe industrial injuries with extensive soft tissue damage.
It is also sometimes associated with fractures. Cut injuries involving nerve may also cause this
type of injury.
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THE PERIPHERAL NERVES
TREATMENT.—
As mentioned above the only treatment available for neurotmesis is suturing of the divided
nerve ends. Such nerve repair can be of two types — primary nerve repair and secondary
nerve repair.
In clean tidy incised wounds when presented within 6 hours of injury immediate suturing
of the divided nerve is the ideal treatment, which is known as primary nerve repair.
In untidy contaminated wounds and in case of incised wounds when presented after 6
hours of occurrence, nerve suturing should be postponed until 3 or 4 weeks after injury. This is
known as secondary nerve repair. If a nerve is seen divided during the course of excision of a
contaminated wound, the ends of the divided nerves are approximated by a stitch of fine silk,
which prevents retraction during the waiting period. The idea of secondary nerve repair is that
— (a) infection of the recent wound does not jeopardise the healing of the nerve suture, but
that of late wound does; (b) the nerve sheath remains delicate and friable in an untidy wound
which is not an ideal tissue for suturing as it is easily tom by slightest tension. After about 3
weeks epineural fibrosis makes the sheath thicker and tougher to facilitate suturing.
DIFFERENT CLASSIFICATIONS OF PERIPHERAL NERVE INJURY
TABLE I
MRC (Medical
dysfunction :—
Research
Council
of
London)
classification
of
motor
nerve
Grade Clinical Features
MO
Ml
M2
M3
M4
M4+
M5
Complete paralysis.
Flicker of contraction.
Contraction with gravity eliminated.
Contraction against gravity alone.
Contraction against gravity and some resistance.
Strong contraction but not normal.
Contraction against powerful resistance (normal power of the muscle).
TABLE II
MRC CLASSIFICATION OF SENSORY NERVE DYSFUNCTON
Grade Clinical Features
50
51
52
53
S3+
54
No sensation.
Deep pain sensation.
Protective sensation i.e. skin touch pain and thermal sensation.
S2 with better localization alongwith old sensitivity. Hyper-sensitivity may
be present.
Object and texture recognition. Two point discrimination is not possible.
Normal sensation.
Degeneration and regeneration of nerves after division.—
DEGENERATION.—
When a peripheral nerve is divided, the distal part of the divided nerve shows degeneration,
which is typically known as Wallerian degeneration. In this degeneration — (i) the axis cylinder
becomes fibrillated; (ii) the medullary sheath breaks up into droplets of myelin and (iii) the
cells of the sheath of Schwann are converted into phagocytes which remove the remnants of
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the medullary sheath and axis cylinder or axon. The cells of the sheath of Schwann proliferate
forming a slight bulb at the commencement of the distal end from which sprouts of Schwann
cells grow proximally towards the downgrowing axons of the proximal segments by chemotaxis.
The proximal portion of the divided nerve also shows similar Wallerian degeneration, but only
upto the first node of Ranvier. After a short interval which varies from 10 days to fortnight the
axons begin to regenerate and begin to subdivide to produce an excess of end bulbs alongwith
proliferating Schwann cells to produce a swelling at the end, which is known as proximal neuroma
or terminal neuroma.
After incomplete division affecting only one side of the peripheral nerve, a lateral neuroma
or a swelling at the place of incomplete division develops due to proliferating Schwann cells
and axons. Similarly if only the central fibres of a nerve trunk are injured, a central neuroma
may develop.
REGENERATION.—
This is only possible when (i) the nerve remains intact (no complete section), (ii) when,
after complete section, the cut ends are sutured perfectly and (iii) when, only a small gap presents
between the cut ends.
SEDDON’S CLASSIFICATION OF NERVE INJURY
Motor Loss
Sensory Loss
Autonomic Function
Nerve conduction
distal to injury
Fibrillation on EMG
Recovery
Neuropraxia
Axonotmesis
Neurotmesis
Complete
Partial
Present
Present
Complete
Complete
Absent
Absent
Complete
Complete
Absent
Absent
Absent
Rapid
(Complete)
Present
2 mm/day
(Good)
Present
1 mm/day
(Always imperfect)
♦SUNDERLAND’S CLASSIFICATION
1st Degree
2nd Degree
3rd Degree
4th Degree
5th Degree
Epineurium
Perineurium
+
+
+
+
+
+
Endoneurium
Axon
++
+
+ = intact; - - severed
*
corresponds to the Seddon's classification in the way that the 1st degree is =
neuropraxia; 2nd degree = axonotmesis; 4th and 5th degree = neurotmesis.
In these successful cases, the axons regenerate crossing the gap in close application to the
Schwann cells from the proximal to the distal cut end. The Schwann cells from the neurilemma
that covers the myelin sheath proliferate actively. This proliferation occurs in the both proximal
and distal ends which move towards each other. If the gap is a small one ultimately they meet
each other and forms empty tubes for regeneration of the axons to occur. The activity of the
Schwann cells increases rapidly after the 4th day after injury and reaches its pick at about the
end of the 3rd week.
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317
Even after accurate suture the quality of regeneration is less perfect than in cases of
axonotmesis owing to wastage of a few axons in the scar tissue at the suture line and
maldistribution of a few axons. The density of the suture line is increased by local sepsis and
inflammation. Maldistribution of fibres is greatest in the case of mixed motor and sensory nerves,
as the motor fibres may enter into the empty tubule of sensory nerves and motor nerve cannot
have any action on the sensory end organ and thus wasted. Such maldistribution is also seen in
motor nerves which supply a large number of small muscles. The result is best in case of a pure
motor nerve which supplies a few groups of large muscles concerned in coarse movements e.g.
the radial nerve. The result is worse in case of mixed sensory and motor nerves supplying a
large number of small muscles concerned in fine movements e.g. the ulnar or the median nerve
at the wrist.
From the above discussion it is clear that while nerve suturing care must be taken to avoid
axial rotation of either cut end to ensure full anatomical continuity.
Following suture there is a period of week before sufficient axons arrive in the peripheral
stump to cause any reflex response to pinching. After crossing the site of severence the axons
grow down the peripheral nerve at the rate of 2 mm per day.
Regeneration is not possible (unsuccessful cases) when (i) there is a big gap between the two
cut ends and (ii) when there is considerable fibrosis between the two cut ends (probably due to
infection).
Secondary pathological changes accompanying nerve injury.—
These pathological changes mainly affect the skin, muscles, neighbouring joints and bones.
1. Skin.— The skin becomes thin and atrophic ulcers may develop. It also shows atrophic
changes e.g. thin and brittle nails etc.
2. Muscles.— (i) The affected muscles become paralysed and flaccid.
(ii) The paralysed muscles become over-stretched due to unopposed action of the
antagonist groups.
(iii) Within 3 weeks reaction of degeneration appears in the affected muscles — the
muscle fibres do not respond to faradic stimulation (with rapid make and break), but they
respond to galvanic stimulation (with slow make and break) due to increase in duration of
chronaxie.
(iv) A change of polarity is seen in the affected muscles in which A. C. C. becomes
greater than K. C. C.
(v) In late cases the muscle fibres degenerate and are progressively replaced by fibrosis,
after which recovery becomes impossible.
3. Joints.— Periarticular adhesions are gradually formed around immobile joints, which
later on become fixed in the position of contracture of this periarticular adhesions.
4. Bones.— These gradually become decalcified due to disuse.
Prevention.— Prevention of these secondary pathological changes are discussed in detail in
the section of treatment for 'axonotmesis'.
Gradation of muscle power.— The muscle power which becomes obviously lowered due
to nerve injury has been graded by numbers according to the Medical Research Council of
London. This gradation is as follows:—
0 = Complete paralysis.
1 = Flicker of contraction.
2 = Contraction with gravity eliminated.
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318
3 = Contraction against gravity alone.
4 = Contraction against gravity and some resistance.
5 = Contraction against powerful resistance (normal power of the muscle).
Signs of regeneration.— After nerve injury or nerve repair one has to assess the
regeneration of the nerve. This can be done by —
• The muscle most proximal to the nerve injury should be tested for muscle power. This
muscle is first rennervated. The most distal muscle is last rennervated.
• Tinel's sign.— Sensation is tested by mild tapping along the course of the nerve distal
to proximal. The first hypersensitive area is the regenerated area. This is called Tinel's sign. As
regeneration progresses the hypersensitive area moves distalwise.
• By EMG (Electromyographic study).— This can diagnose regeneration even before
clinical examination.
CAUSES OF PERIPHERAL NERVE LESION.— These can be divided into two primary
groups — A. Causes of single nerve involvement and B. Causes of multiple nerves involvement.
A. Causes of single nerve involvement.—
1. TRAUMATIC.— It may be due to (a) closed injury which usually causes either
neuropraxia or axonotmesis lesion of the nerve or (b) open injury which usually causes
neurotmesis.
2. INFLAMMATORY.— Herpes Zoster, leprosy, diphtheria.
3. NEOPLASTIC.— Neurofibroma, neurofibrosarcoma.
4. MISCELLANEOUS.— Tunnel syndrome, lead poisoning, arsenical poisoning,
diabetes etc.
B.
Causes of multiple nerves involvement.—
1. INFLAMMATORY.— Herpes Zoster, leprosy, diphtheria.
2. METABOLIC DISORDERS.— (a) Vitamin B Complex deficiency (Particularly Bl).
(b) Diabetes mellitus. (c) Alcoholism, (d) Porphyria.
3. IDIOPATHIC.
4. MISCELLANEOUS.— Lead poisoning, arsenical poisoning.
NERVE SUTURE
When nerve injury is associated with complex open wound, priority is given to prevent
infection to occur in the wound, as infection will mar the chance of proper nerve repair. So in
these wounds nerve repair is done as a Secondary procedure after the wound has healed free
from infection.
Primary nerve repair.—
.
Indication.— Primary nerve repair is only considered in case of very recent, clean-cut wound,
as for example, occurred after a cut by a piece of glass. It can also be performed in case of
children where the result of this primary suture is good. Under no circumstances primary nerve
repair should be ventured by an inexperienced surgeon.
Technique.— As the nerve ends have retracted and the epineurium is rather filmy, primary
suturing is a difficult affair. Irritant material, such as catgut, dexon, or silk should not be used
THE PERIPHERAL NERVES
319
for primary nerve repair as replacement fibrosis will mar the possibility of any good result. Non­
irritant suture material such as nylon or prolene should be used. Moreover if the nerve ends have
retracted proximally and distally, the original wound may have to be extended appropriately to
trace out the nerve ends. The nerve has to be mobilized and proper orientation (regarding
rotation) can be assessed by the vascular pattern on its surface. A small portion of the nerve is
resected both proximally and distally so that clean-cut ends are available for suturing.
Secondary nerve repair.—
Indication.— Delayed nerve repair is an easier operation and is always carried out except the
indications narrated under primary nerve repair. In secondary nerve repair there is no fear of
infection as the wound has already primarily healed. Moreover the epineurium has proliferated
and becomes thickened for proper insertion of sutures. Though portions of the nerve ends have
to be resected to get healthy nerve ends for suturing, yet this resection may be in smaller amount
should also be carried out in primary nerve repair. Secondary nerve suture should be performed
as soon as the wound has healed, as the chance of successful nerve suture will be diminished if
the delay increases beyond two months.
Technique.— This operation is normally carried out after the original injury has properly
healed. The nerve ends are generally burried in scar tissues. The dissection starts from the normal
tissues lying proximal and distal to the scar tissues and gradually the nerve ends are freed.
TECHNIQUE OF NERVE REPAIR IN GENERAL
An adequate incision is made to isolate the nerve ends. The nerve ends should be freed from
the scar tissue, which is called neurolysis. The approach should be made through an intermuscular
space. If scar tissue predominates and is hard to touch, it is probable that regeneration is completely
blocked. Resection and anastomosis will offer the only prospect of cure. Sometimes Faradic
stimulation of the nerve with bipolar electrodes may give valuable information in this matter.
Trimming of the nerve ends.— After mobilizing the nerve, the nerve ends are trimmed
to excise the scar tissue, the ragged or bruised ends of the cut nerve. Sometimes there may be an
end-bulb, which may be neuroma or glioma. These should also be excised. The ends should be
excised till the healthy bundles will be seen sprouting through the ends. One can even feel the
ends. Presence of any hardness there indicates fibrosis. Presence of healthy axoplasm, which will
be softer in touch, indicates that the resection has been completed and the healthy ends are now
ready for suturing.
Nerve suturing.— Non-absorbable, non-irritant suture material on an atraumatic needle is
used. The epineurium is picked up proximally and distally and the two lateral sutures are
inserted. The ends of these sutures are held with the artery forceps. An anterior and a posterior
sutures are also employed. Generally four sutures suffice and one should not be tempted to
employ more sutures unnecessarily. The lateral sutures are now cut short.
Construction of a new bed.— The sutured nerve should not be allowed to lie on scar
tissue. A new path is constructed by opening a muscle sheath and embedding the nerve within
the muscle fibres. It is better to provide a tantalum foil to warp around the sutured nerve. This
will prevent epineural fibrosis and out-sprouting which may well produce a painful scar.
Immobilization of the limb.— The limb is immobilized in a splint to prevent any strain
on the sutured nerve. This should be kept for no less than three weeks. After this, the splint is
gradually removed.
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320
Methods of approximation of shortened nerve ends.— As has already been discussed
that the two ends of the nerve should be freed and slices are removed from the ends of the
nerve until the projecting fibres are seen and the blood is freely oozing from the cut surfaces.
These slices should be done with the Bard-Parker knife or scalpel and not with the scissors as
this may cause crushing of the nerve-ends. During this process, some shortening of the nerve is
expected. So procedures must be adopted, so that anastomosis is performed without tension.
These devices are :—
(i) Mobilization.— The two ends are dissected from the surrounding structures for a
distance. Care should be taken to preserve the important branches.
(ii) Position of the limb concerned.— The position of the limb will be such that there will
be no tension in the suture line. The limb is held in this position by splints.
(iii) Transposition of the nerve.— By transpositioning the nerve, to shorten its course, may
help to minimise the tension on the suture line. This is done by bringing the ulnar nerve in front
of the medial epicondyle of the humerus or by bringing the radial nerve in front of the humerus.
(iv) Stripping and sacrificing of the branches.— If there are branches near about, it is obvious
that these will anchor the nerve and will prevent proper mobilization. In this case unnecessary
branches can be sacrificed and the important branches may be stripped and further mobilized.
Sometimes it may be necessary to separate the nerve fibres which form the branch from the main
trunk. This will definitely mobilize the main trunk which was previously anchored by branches.
(v) Anchoring the untrimmed nerve ends.— When it is obvious that the two ends of the
divided nerve cannot be brought together, the two untrimmed ends are approximated closely
by tension stitches. This can be done by positioning the limb properly (as for example, flexion
of the limb) to help their approximation. Subsequently the limb is gradually straightened so
that the nerve is stretched. When the limb is more or less fully extended, the second operation
is ventured and proper suturing of the nerve is peformed.
(vi) Bone resection.— When nerve injury is associated with an ununited fracture of the
bone, which needs some operative intervention, one may adopt this procedure. This is occasionally
carried out to repair the radial nerve when it is associated with ununited fracture of the humerus.
(vii) Nerve grafting.— Sometimes the two ends of the cut nerve can only be approximated,
if the limb is acutely flexed. In this case the result will not be good even if the two untrimmed
ends are anchored or the limb is gradually extended. These cases are suitable for nerve grafting.
The donor nerve is generally an autogenous graft from the saphenous nerve of the thigh, sural
nerve of the leg or the medial cutaneous nerve of the forearm. This type of nerve grafting does
not help to restore the motor function but can restore sensory function to some extent. The
epineurium of the graft is to be sutured with the epineurium of the host nerve. When the nerve
is of bigger calibre, cable grafts may be-used, in which nerve of same diameter is sutured in the
form of cable with the host nerve. Nerve grafting does not become successful if the intervening
gap between the nerve ends becomes a mass of dense scar tissue. Microscopic surgery in nerve
grafting is being popularised in States but its superiority is yet to be proved.
RESULTS OF THE NERVE REPAIR
The results of nerve repair, of course, depend on various factors, which will be discussed
in this section :
(A)
Preoperative.—
(i) Time.— The earlier the operation is performed, the better will be the result after the
THE PERIPHERAL. NERVES
321
chance of infection has been abolished. After two months, the chance of good result is remote.
(ii) Infection.— This will definitely mar the possibility of good result. Moreover
formation of scar tissue following infection will also lessen the possibility of good nerve repair.
(iii) Preoperative management.— Before the nerve has been sutured, the muscles, which
are supplied by the nerve, should not be kept in stretch. This will definitely decrease the
possibility of good result after nerve suturing.
(B) Operative.—
(i) The nerve affected.— It has already been discussed that the result in mixed motor
and sensory nerve is rather disappointing, whereas the result in pure motor or sensory nerve is
much encouraging.
(ii) Haemostasis.— Surgeon must be careful that haemostasis has been fully achieved
during operation.
(iii) Torsion.— This should not be allowed at the time of suturing of the nerve as this
will cause maldistribution of the nerve fibres in the distal segment.
(iv) Suture material.— It is of great importance that the suture material must be non­
irritant, such as nylon or prolene. Irritant suture material will increase fibrosis and hence disturb
good nerve regeneration.
(v) Tension.— Under no circumstances, tension should be allowed to the suture line.
(C) Postoperative.—
(i) Postoperative care.— This is highly important to keep the limb in such a position as
to give relaxation to the paralysed muscles as well as to the sutured nerve. The limb should be
immobilized in this position for at least a month, after that the limb is gradually straightened to
bring to its normal position.
(ii) Infection.— Care must be taken that the wound is not infected.
Treatment of incomplete division. Partial division of a nerve is better left alone. An
attempt at suturing of the partially divided nerve will simply initiate scar tissue formation and
will deteriorate the function of the intact portion of the nerve. There is so much overlapping in
the nervous system that even 4/5th division produces very little disability. Nerve suturing is
only indicated when partial division has resulted in a siginificant deficit.
When nerve suturing is almost impossible. — In certain circumstances, the loss of nerve
tissue is so much that there remains little chance of nerve repairing. In these cases following
methods can be adopted :
(i) Nerve implantation.— In this case, if there is any intact nerve by the side, it can be
divided and the proximal end of the previously intact nerve is anastomosed to the distal end of
the nerve concerned, e.g. the hypoglossal nerve is anastomosed with the distal end of the facial
nerve. Obviously full function cannot be expected, but again uncontrolled contractures may be
found.
(ii) Nerve grafting.— This has already been discussed.
(iii) Tendon transplantation.— When the improvement of nerve function cannot be expected,
relatively unnecessary nearby tendons are transplanted to the paralysed tendons for their
functioning. This is often done in case of radial nerve palsy.
(iv) Arthrodesis.— This is particularly done in case of lower limb where stability is more
important than mobility.
(v) Amputation.— If pressure sores and ulcers have become troublesome, one can try
sympathetic ganglionectomy. But amputation will be the last court of appeal.
21
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A CONCISE TEXTBOOK OF SURGERY
CRANIAL NERVES
1. Olfactory nerve.— This nerve is injured by fracture of the cribriform plate or by a
blow on the back of the head (contre-coup fracture). When this nerve is injured there is partial
(hyposmia) or total loss (anosmia) of smell of the corresponding side.
2. Optic nerve. — This nerve may be damaged by fracture involving the optic foramen
or by a neighbouring tumour or aneurysm. When this nerve is injured, there may be partial or
complete blindness of the affected eye.
3. Oculomotor nerve.— This nerve is sometimes injured in fracture of the skull affecting
the sphenoidal fissure. This nerve may also be involved by neighbouring tumour or aneurysm.
When this nerve is injured the main feature is dilated pupil on the affected side. With this
there may be ptosis of the upper eye lid due to paralysis of levator palpebrae superioris. There
may be proptosis or unusual protrusion of the eye ball due to paralysis of majority ocular muscles.
Diplopia and external strabismus are due to unopposed action of the external rectus and superior
oblique muscles of the eye ball which are not supplied by this nerve. There will also be loss of
accommodation due to paralysis of the sphincter papillae and the ciliaris.
4. Trochlear nerve.— It is rarely injured alone. It may be injured at the superior orbital
fissure due to fracture. This nerve supplies the superior oblique muscle of the eyeball and its
damage will lead to diplopia and deficient movement of the eye to turn it downwards and
laterally.
5. Trigeminal nerve.— It is the largest cranial nerve and is the main sensory nerve to
the face, greater part of the scalp, the teeth, the mouth and the nasal cavity. Its main motor
supply is to the muscles of mastication. It divides into 3 main branches — the ophthalmic, the
maxillary and the mandibular.
Trigeminal neuralgia.— Pain referred to various branches of the trigeminal nerve is known
as trigeminal neuralgia. In the beginning pain is first confined to one of its main divisions.
Trigeminal neuralgia occurs mostly in the middle aged women. Pain is often precipitated by
exposure to cold, eating, talking, touching certain parts of the face and even during walking.
The pain is often severe.
The cause of trigeminal neuralgia is not well known. When it occurs in younger individuals,
multiple sclerosis is a prominent cause.
Treatment.— Tegretol (carbamazepine) is the most effective drug in this condition. Surgery
is only considered when medical treatment fails. Various operative procedures have been
suggested —
(i) The trunks of the maxillary and mandibular nerves and the trigeminal ganglion itself
is injected with alcohol with varying degrees of success.
(ii) Electrocoagulation of the trigeminal ganglion has also produced some success.
(iii) Excision of the ganglion is a crude method, used for this condition.
(iv) Division of the sensory root of the nerve behind the ganglion is now the operation
of choice when pain is confined to the maxillary and mandibular nerve areas. Endeavour is
made to preserve the ophthalmic fibres which lie in the upper and medial part of the root. This
is to avoid the complications of anaesthesia affecting the surface of the eye. The motor root of
the nerve is left intact.
Open surgery is performed either through the middle fossa or the posterior fossa. Through
the middle fossa the trigeminal ganglion is approached either extra- or intradurally. Through
the posterior fossa the root of the 5th nerve is approached near the cerebello-pontine angle.
THE PERIPHERAL NERVES
323
6. Abducent nerve.— It is occasionally injured by fracture of the skull which involves
superior orbital fissure. It is rarely involved alone and may be involved with other cranial nerves.
This nerve supplies the lateral rectus muscle of the eye ball and this muscle becomes paralysed
if this nerve is injured leading to internal strabismus.
7. Faciid nerve, 8. \estibulococWear nerve, 9. Glossopharyngeal nerve and 10. \agns
nerve are less involved by trauma.
11. Accessory nerve.—
Causes of injury.—
(i) While removal of cervical lymph nodes.
(ii) Occasionally by fractures of the base of the skull involving the jugular foramen.
It supplies the stemomastoid muscle alongwith the 2nd and 3rd cervical nerves. It also
supplies the trapezius muscle alongwith the 3rd and 4th cervical nerves. Damage of this nerve
will cause complete to partial paralysis of the stemomastoid muscle and the trapezius muscle.
When the nerve is involved in the upper part of the anterior triangle of the neck there may be
paralysis of both stemomastoid and trapezius muscles. If the nerve is injured in the posterior
triangle of the neck, which is more common, only the trapezius muscle will be affected.
Clinical features.— There will be drooping of the shoulder due to trapezius paralysis alongwith
wasting of the trapezius. Trapezius paralysis also unables the patient to continue abduction of
the arm after 90°. Strength of stemomastoid muscle can be tested by asking the patient to turn
his face to the opposite side against resistance.
Treatment.— If the operative assault to the spinal accessory nerve is recognized during
operation attempt should always be made to suture it primarily. It is only in case of this nerve
that secondary suture may not be successful due to retraction of the cut ends.
12. Hypoglossal Nerve.—
Causes of injury.—
(i) It is mostly injured during excision of submandibular salivary glands particularly
due to tumours.
(ii) It is hardly injured in fracture base of the skull as it is protected by a bony butterss
which diverts the fissure of the fracture towards the foramen magnum.
Though this, nerve supplies the Styloglossus, Hyoglossus, Geniohyoid and Genioglossus,
yet its main supply is to the intrinsic muscles of the tongue.
Clinical features.— When hypoglossal nerve is injured there will be hemiparesis of the tongue
of that side, due to which there will be hemiatrophy of the tongue of the corresponding side
and if the tongue is protruded out the tip will be pushed towards the affected side due to
unopposed contraction of the muscles of the sound side. The affected side of the tongue becomes
wrinkled.
BRACHIAL PLEXUS
The lesion in brachial plexus may be either complete or partial.
Complete lesion is rare and occurs only after severe injury. It damages all the roots of the
plexus and is often fatal. In this case, there will be anaesthesia of the whole upper limb except
the upper part of the arm which is supplied by C3, 4 & 5 and by the intercostobrachial nerve.
There will be also complete paralysis of the arm and scapular muscles, occasionally the long
thoracic nerve supplying the serratus anterior or the nerve supplying the rhomboids may escape.
Incomplete lesion may be due to stabs or cuts and may affect any of the roots. But the common
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injury is due to traction or pressure, which affects either the upper or lower portion of the
plexus.
UPPER BRACHIAL PLEXUS LESION (ERB-DUCHENNE).— This injury is due to
excessive depression of the shoulder or displacement of the head or the both. It may affect new
bom babies during difficult confinements or adult by a fall of weight on the shoulder. The 51h
and sometimes the 6th cervical roots are involved. The muscles affected are biceps, brachialis,
brachioradialis, supinator and deltoid. So the limb becomes internally rotated, extended at the
elbow and pronated in the well known position of 'policeman taking a tip'. If only the 5th
cervical root is affected, there will not be any sensory change. But if the 6th nerve is also affected,
there will be an area of anaesthesia over the outerside of the arm and upper part of the outerside
of the forearm.
As the innervation of the hand is intact, functional improvement may be obtained
conservatively by maintaining full range of passive movement of the limb to prevent contracture
and the anaesthetic skin is protected to avoid pressure sores etc. In degenerative lesions at the
root level, one cannot expect regeneration. Function of the limb can be best restored by arthrodesis
of the shoulder and elbow joints. One may venture transplantation of muscles from the pectoral
groups to the humerus.
LOWER BRACHIAL PLEXUS LESION (KLUMPKE). This type of lesion can occur
when a falling person clutching at an object and hyper-abducting his arm or failing to obtain a
foot-hold on a passing bus. The first dorsal root (T() is usually affected. The result is paralysis
of the intrinsic muscles of the hand (with claw-hand and features of combined median and
ulnar nerves palsy) with anaesthesia of the inner one and half fingers. There will also be Homer's
syndrome. Very occasionally spasticity of the lower limb may be noticed associated with this
condition, which is a result of damage to the pyramidal tract from haemorrhage following
avulsion of the nerve roots.
Horner's syndrome.— This syndrome occurs due to injury to the sympathetic supply of the
face which accompanies the Tl nerve. This syndrome includes — (i) narrowing of the palpebral
fissure — drooping of the upper eyelid (ptosis); (ii) Enophthalmos due to paralysis of Muller's
muscle, in which the eyeball is recessed backwards; (iii) Myosis, i.e. contraction of the pupil
due to the damage to the sympathetic supply of the muscles of the iris and to the unopposed
action of the oculomotor nerve and (iv) anhidrosis i.e. failure of sweating on the affected side of
the face.
Treatment is conservative. Recovery of function may occur when the lesion is due to
stretching-(neurapraxia). But if the nerves have been ruptured, maldistribution of down-growing
fibres will definitely lead to considerable reduction in functional efficiency.
AXILLARY NERVE
This is also called circumflex humeral nerve, which passes through the quadrilateral space
and winds round the surgical neck of the humerus about a finger's breadth below the centre of
the deltoid muscle.
It is injured —
(i) Due to fracture of the neck of the humerus; (ii) Dislocation of the head of the humerus;
(iii) By a direct blow or (iv) Intramuscular injections.
This nerve supplies the deltoid muscle and a portion of the skin on the lateral aspect of the
arm which overlies the deltoid muscle. It also supplies the teres minor muscle.
THE PERIPHERAL NERVES
325
When this nerve is injured, the deltoid muscle will be paralysed which will be evident by
failure of abduction of the shoulder. There will be also a patch of anaesthesia over the outer
side of the arm.
LONG THORACIC NERVE (NERVE OF BELL)
This nerve arises from the 5th, 6th and 7th cervical nerve roots. This nerve supplies the
serratus anterior muscle.
j
This nerve may be injured — (i) by blows or (ii) by weight or a heavy object falling on the
shoulder or (iii) more often during operation on the breast or the chest wall.
Due to injury of this nerve the serratus anterior muscle becomes paralysed. Paralysis of this
muscle can be well demonstrated by 'winging of the scapula'. When the patient is asked to push
against the wall with outstretched hand, the vertebral border and the inferior angle of the scapula
become prominent from the chest wall — this is known as 'winging of the scapula'. The patient
also feels difficulty in raising the arm above right angle from a position in front of the body
due to inability of rotation of scapula on the chest wall owing to paralysis of the serratus anterior
muscle.
RADIAL NERVE
This is also known as musculospiral nerve.
Sites of injury.— This nerve may be injured in the axilla or in the radial groove. Its main
branch, the posterior interosseous nerve, which is concerned with supplying the extensor muscles
of the wrist and fingers, may be injured at the elbow.
Causes of injury.—
A. IN THE AXILLA —
(i) Crutch palsy — that is pressure with ill-adjusted crutch without proper handgrips.
Paresis of this nerve has occurred only after using 4 hours with this type of crutch without
handgrips.
(ii) Fractures and dislocations of upper end of the humerus, or by attempts at their
reduction.
(iii) Rarely by pressure of a new growth.
B. IN THE RADIAL GROOVE —
(i) Pressure of the arm on the edge of the operating table or on the edge over handle
of a chair or footpath after a heavy slip following excessive drink may bring about injury to the
radial nerve at this site. The latter type is known as 'Saturday night' paralysis.
(ii) Prolonged application of a tourniquet or ill-applied plaster of the middle of the
arm is also liable to damage the radial nerve.
(iii) Fracture of the shaft of the humerus is responsible for radial nerve injury in about
10% of cases.
(iv) During operation on the humerus due to nonunited fracture this nerve may be
injured at this site.
(v) Intramuscular injection of drugs may rarely injure radial nerve.
C. AT THE ELBOW (POSTERIOR INTEROSSEOUS NERVE INJURY).—
(i) Fracture of the neck of the radius or dislocation of the radius.
(ii) During operation of excision of the head of the radius.
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Clinical features.—
A. WHEN INJURED IN THE AXILLA —
1. Motor paralysis —
(i) Triceps muscle — which causes inability to extend the forearm against resistance.
(ii) Extensors of the wrist become paralysed which causes wrist drop which is
diagnostic of radial nerve injury.
(iii) Extensors of the metacarpophalangeal joints due to paralysis of the extensor
digitorum. However the patient can extend the interphalangeal joints with the unaffected
interossei muscles (supplied by the ulnar nerve) and lumbricals (supplied by the median and
ulnar nerves). So when the radial nerve is injured the patient will not be able to extend the
metacarpophalangeal joint, but will be able to extend the interphalangeal joints. So extension of
fingers on the whole is not affected.
(iv) Extensors of the all joints of the thumb (extensor pollicis longus and brevis) are
paralysed. So extension of thumb is not possible in radial nerve injury.
(v) The supinator and brachioradialis are paralysed, yet supination of the forearm is
ably performed by the biceps muscle particularly when the elbow is flexed. But supination is
completely lost when the forearm is extended. However paralysis of the brachioradialis can be
tested by asking the patient to flex the elbow joint keeping the forearm in midprone position
against resistance. This becomes difficult and the muscle will not stand out in case of
brachioradialis paralysis.
2. Sensory loss.— In radial nerve injury in the axilla anaesthesia will be present on the
dorsum of the arm, forearm and back of the hand. There will be also anaesthesia of the dorsum
of the thumb and lateral three fingers upto the proximal interphalangeal joint owing to overlap
by the ulnar nerve and median nerve.
3. Trophic changes.— These changes are usually not much.
B. INJURY IN THE RADIAL GROOVE.—
1. Motor paralysis.— This is similar to the radial nerve injury in the axilla, except that
the triceps and anconeus muscles remain unaffected. This is due to the fact that the branches
supplying all the 3 heads of the triceps and the anconeus arise from the radial nerve before it
reaches the radial groove.
2. Sensory loss.-— In radial nerve injury at the radial groove anaesthesia is limited to a
patch on the back of the hand and radial side of the thumb and the adjoining part of the thenar
eminence, the medial side of the thumb and the adjoining sides of the index middle and lateral
side of the ring finger. There is also anaesthesia on the back of the fingers upto the proximal
interphalangeal joints except in the thumb where it reaches upto the nail, as both posterior
cutaneous nerve of the arm and posterior cutaneous nerve of the forearm arise from the radial
nerve before it reaches the radial groove.
3. Trophic changes are trivial.
C. AT THE ELBOW.— Here the posterior interosseous nerve is mainly injured.
1. Motor paralysis.— The posterior interosseous nerve supplies all the muscles of the
back of the forearm which are concerned with extension of the wrist joint and extension of the
metacarpophalangeal joints of the fingers and extension of all joints of the thumb. It also supplies
the supinator muscle. So 'wrist drop' is the main manifestation of motor loss in case of injury to
this nerve.
2. Sensory loss.— The posterior interosseous being a pure motor nerve, there will be no
sensory loss at its injury.
THE PERIPHERAL NERVES
327
MEDIAN NERVE
Sites of injury. This nerve is injured either at the elbow or at wrist.
Causes of injury.—
A. AT THE ELBOW.— This nerve may be injured at the elbow —
(i) Due to supracondylar fracture of the humerus or condylar fracture or fracture of
lower end of the humerus.
(ii) Due to dislocation of the elbow which may be anterior or posterior, though posterior
dislocation is much more common.
(iii) This nerve may be injured by application of a tourniquet anywhere in the arm.
B. IN THE WRIST.— The various causes of this nerve injury are :
(i) Cut injury to the wrist from a variety of causes.
(ii) Fracture of lower end of the radius.
(iii) Dislocation of the lunate bone.
(iv) Carpal-Tunnel syndrome.
(v) Compound palmar ganglion.
Clinical features.—
A. WHEN INJURED AT THE ELBOW —
1.
Motor paralysis.— The median nerve with its anterior interosseous branch supplies
all the flexors of the wrist and fingers except the flexor carpi ulnaris and the inner part of flexor
digitorum profundus, as also the pronators of the forearm. So these muscles will be paralysed
when the median nerve is injured at the elbow. As the flexor carpi ulnaris remains active, the
hand will be deviated towards the ulnar side particularly when the wrist is flexed. Flexion of
the index finger will be fully affected though the flexion of other fingers may be carried out
with the help of the medial part of the flexor digitorum profundus which is supplied by the
ulnar nerve. Due to this when the patient is asked to clasp the hands the index finger will fail
to flex giving rise to an appearance of a 'pointing index'. The test is known as 'Ochsner's clasping
test’. Flexion of the terminal phalanx of the thumb becomes impossible due to paralysis of the
flexor pollicis longus and the patient will fail to flex the terminal phalanx of the thumb against
resistance while the proximal phalanx is being steadied by the clinician.
Paralysis of the muscles of the thenar eminence is a characteristic feature of median nerve
injury. On inspection the thenar eminence will be flattened and the metacarpal bone of the
thumb apparently comes on the same plane as the other metacarpal bones giving rise to an
appearance which is typically known as 'Simian' or 'Ape-like' hand. The abductor pollicis brevis,
opponens pollicis and flexor pollicis brevis, which constitute the thenar eminence are paralysed.
Even the first dorsal interosseous and the two lateral lumbricals are also supplied by this nerve.
While supply to the interosseous and lumbrical muscles are not very significant, yet paralysis
of abductor pollicis brevis will be evident by the pen test, in which the patient is asked to touch
a pen, which is kept at a slight higher level than the palm of the hand, with the tip of the
thumb. Paralysis of opponens pollicis will be evident by the failure of the patient to touch the
tips of the other fingers with the tip of the thumb.
As the pronators of the forearm become paralysed, pronation of the forearm becomes feeble
which will be particularly evident if the patient is asked to pronate his semiflexed forearm.
Pronation of forearm becomes almost nil after midprone position, upto which brachioradialis
can pronate the forearm.
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328
2. Sensory loss.— This will be particularly evident by loss of sensation over the lateral
half of the palmar surface of the hand and the palmar surface of the thumb and palmar surface
of the radial two and half fingers. This anaesthesia will be extended over the tip of these fingers
upto the middle of the middle phalanges on the posterior surface of these fingers and upto the
nail bed of the thumb. These areas of sensory loss of course will be gradually reduced due to
overlapping from adjacent nerves.
3. Trophic changes.— These changes are seen in the hand and affected fingers
particularly the index finger. Causalgia may be seen if there is partial injury to the nerve.
B.
WHEN INJURED AT THE WRIST.— The median nerve is more commonly injured
at the wrist. But in this case the forearm muscles will not be affected.
1. Motor paralysis.— Only the muscles of the thenar eminence will be paralysed and
wasted. These have been described above and the tests which will be positive are — (i) pen
test, (ii) opponens pollicis test and (iii) 'Ape-like' hand.
2. Sensory loss.— This is similar to that described under injury at the elbow.
3. Trophic changes — are similar to those of injury at the elbow.
ULNAR NERVE
Sin s ni injur This nerve may be injured at the elbow or at the wrist.
Causes of injury.—
A. INJURY AT THE ELBOW.— The causes are :
(i) Supracondylar fracture.
(ii) Dislocation of the elbow.
(iii) Fracture of the medial epicondyle of the humerus.
(iv) Cubitus valgus deformity — in which case this nerve becomes stretched and gets
friction at the groove on the medial epicondyle. This condition may develop many years after
malunited supracondylar fracture.
(v) This nerve may be fixed in the groove behind the medial epicondyle due to
adhesions complicating osteoarthritis which may lead to rupture of axons and progressive
interstitial neuritis, collectively known as ‘entrapment neuropathy'.
B. IN THE WRIST.— Cut injury at the wrist is not uncommon. It must be remembered
that ulnar nerve passes superficial to the flexor retinaculum and hence is more often involved
in cut injuries of the wrist.
( linical (catures.—
A. WHEN INJURED AT THE ELBOW —
1.
Motor paralysis.— In the forearm this nerve only supplies flexor carpi ulnaris and the
medial half of the flexor digitorum profundus. There will be slight deviation to the radial side
of the hand when the wrist is flexed. Moreover the tendon of flexor carpi ulnaris just above its
insertion into the pisiform bone will become impalpable when it is paralysed. There will be
weakness of flexion of the little and ring fingers particularly at the distal interphalangeal joints.
Paralysis of the muscles of the hypothenar eminence also occur due to injury to the ulnar
nerve. This nerve supplies the abductor digiti minimi, flexor digiti minimi, opponens digiti
minimi, both the heads of the adductor pollicis and sometimes a small twig to the flexor pollicis
brevis. It also supplies all the interossei probably with the exception of first dorsal interosseous
and to the third and fourth lumbrical muscles. The dorsal interossei are concerned with abduction
of the fingers, while palmar interossei adduct the fingers. Interossei alongwith the lumbricals
THE PERIPHERAL NERVES
329
flex the metacarpophalangeal joints and extend both proximal and distal interphalangeal joint.
In case of ulnar paralysis a typical claw hand or Main en griffe will be noticed particularly in
late cases. In this condition there is hyperextension of the metacarpophalangeal joints and flexion
of the proximal and distal interphalangeal joints. This deformity is due to paralysis of the
interossei and lumbricals which is characteristically evident in both ulnar and median nerve
palsy and in Klumpke's paralysis (lower brachial plexus lesion in which mostly Tl is affected).
In ulnar nerve paralysis though the first and second lumbricals are exempted yet this deformity
can be obviously noticed in ring and little fingers.
As the dorsal interossei are concerned with abduction of the fingers, if the patient is asked
to abduct the fingers against resistance, he will be unable to do so in case of ulnar nerve palsy.
The palmar interossei are concerned with adduction of the fingers. A card is placed between
the two fingers and asked to grip the card with the two fingers by adducting the fingers and
the clinician tries to pull the card. The latter can assess the strength of the palmar interossei by
the force of pull required for the purpose. This is known as the 'card test'.
Adductor pollicis is concerned with adduction of the thumb. If a patient with ulnar nerve
injury is asked to hold a book between his hand and the thumb with the thumb straight he will
fail to do so and he will try to hold the book by flexing the distal interphalangeal joint of the
thumb with the help of flexor pollicis longus. This is known as 'Froment's sign'.
As interossei alongwith lumbricals through extensor expansions are also concerned with
extension of the proximal and distal interphalangeal joints, the strength of the interossei can be
tested by asking the patient to straighten the finger against resistance while the clinician steadies
the proximal phalanx of that finger.
2. Sensory loss.— Sensory loss will be appreciated on the medial border of the hand
alongwith adjoining l/3rd of the palmar and half of the posterior surfaces and the whole of the
little finger and medial aspect of the ring finger.
3. Trophic changes.— These changes are often well evident in ulnar nerve injury.
B. INJURY AT THE WRIST.—
1. Motor paralysis.— Only the small muscles of the hand are paralysed. The various
tests relating to such paralysis have been discussed above.
2. Sensory loss.— As the dorsal cutaneous branch and the palmar cutaneous branch of
the ulnar nerve arise 5 cm above the wrist joint and middle of the forearm respectively, only
the palmar surface of the fingers will be affected.
SCIATIC NERVE
Causes <>l injury.—-
(i)
Subtrochanteric fracture of femur, (ii) Posterior dislocation of hip. (iii) Fracture of the
pelvis, (iv) Penetrating wounds.
Sciatic nerve is hardly involved totally. Incomplete injury is much more common in this
nerve. The lateral popliteal portion is affected nine times more commonly than the medial
popliteal portion as the latter passes down on the inner and deep aspects of the sciatic nerve.
THE COMMON PERONEAL (LATERAL POPLITEAL) NERVE
C auses of injury.—
Besides the causes mentioned above for injury to the sciatic nerve, which mainly involve
the common peroneal portion, this nerve itself may be injured by the following causes —
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(i) Fracture of the neck of the fibula, (ii) During subcutaneous tenotomy of the biceps tendon,
(iii) At the time of operation of excision of the upper end of the fibula, (iv) By cut injury, (v) By
pressure of plaster or splint, (vi) Rarely the origin of peroneus longus from the fibula may
entrap this nerve and press on it — 'entrapment neuropathy', (vii) Rarely during operations for
multiple ligation of the varicose vein particularly at the origin of the short saphenous vein.
Clinical features.—
Motor paralysis.— This nerve mainly supplies the extensor and peroneal groups of muscles
of the leg. So when this nerve is injured, these muscles will be paralysed resulting in the
deformities of 'foot drop' and talipes equinovarus.
Sensory loss.— There will be loss of sensation — (a) lateral side of the whole of the leg, which
is supplied by the lateral cutaneous nerve of the calf of the leg, cutaneous branch of the common
peroneal nerve, though it arises at the level of the head of the fibula and may escape injury when
common peroneal nerve is involved at the level of the neck of the fibula. The lower part of the
lateral part of the leg is supplied by the superficial peroneal (musculocutaneous) nerve.
(b) The dorsum of the foot, which is supplied by the superficial peroneal nerve, and the
cleft between the great toe and the second toe which is supplied by the anterior tibial or deep
peroneal nerve will lose sensation. The medial border of the foot is supplied by the saphenous
nerve, whereas the lateral border of the foot is supplied by the sural nerve so these portions are
exempted.
(c) The dorsum of all toes will lose sensation except lateral side of the little toe which is
supplied by the sural nerve.
SPECIAL INVESTIGATIONS.—
Assessment of nerve injury is mainly done by clinical examination, but some neurophysiological studies and imaging may be performed to get additional information.
N europhysiologieal inve stigation s. —
Skilled neurophysiologist is required to interprete the results and it takes about 2 to 3 weeks
after a nerve injury when proper neurophysiological assessment can be performed. Two tests
can be done :—
• Nerve conduction studies.— These actually record sensory or motor nerve action
potentials and the conduction velocity through the nerve is calculated for given anatomical
segment flowing of conduction. Slowing of conduction can be identified in case of compression
neuropathy.
• Electromyography (EMG).— In this test muscle axon potentials are recorded in
response to voluntary activity. Abnormalities which are typical of denervation or reinervation
can be assessed. Using these tests it is possible to distinguish between a nerve injury in which
axons have not degenerated distal to the lesion (neuropraxia) and one in which Wallerian
degeneration has occurred (axonotmesis or neurotmesis). However axonotmesis or neurotmesis
cannot be distinguished.
Electromyography helps to read the electrical activity of a muscle during rest and activity.
There is no electrical activity in an intact muscle at rest. During weak contraction it records
single action potential and in powerful contraction an interference pattern is observed due to
more action potentials. Denervated muscle shows denervation potentials which appear within 1
to 2 weeks after injury. If this does not appear by 15 to 20 days it indicates good prognostic
sign.
THE PERIPHERAL NERVES
331
EMG detects presence or absence of any nerve injury. It also indicates whether any nerve
injury is complete or incomplete and whether regeneration is taking place or not. Even the level
of nerve injury can be determined by showing the changes of denervation of the muscles supplied
by the nerve distal to the nerve injury.
Strength duration curve.— Minimum current used to elicit muscle contraction is called
'rheobase' and it is expressed in milliamperes. 'Chronaxie' is the duration of current required to
excite a muscle with double the rheobase strength, this is expressed in milliseconds. The duration
and strength of the current used to excite a muscle is plotted in a graph as the strength duration
curve. A normal muscle responds to stimuli varying in duration from 300 milliseconds to 1
millisecond without any increase in strength of the current. If the duration of current is decreased,
the strength of current is to be increased to produce contraction. So a strength duration curve
can be plotted known as nerve curve.
A totally denerved muscle needs either more strength of current or for a longer duration.
This is called a curve of denervation.
In case of partially denervated muscle shows a curve in between the above two. Assessment
of recovery can also be assessed by strength-duration curve. If recovery is occurring the curve
will show a shift to the left. On the other hand if degeneration is progressive the shift will be to
the right.
•
Magnetic Resonance Imaging (MRI) is now being used more frequently to display
peripheral nerve pathology. This imaging technique is showing promise for the future. Presently
this investigation is mainly used to know the damaged of the cervical nerve roots after brachial
plexus injury.
AUTONOMIC NERVOUS SYSTEM
Causalgia.—
.
It is a painful condition which arises from incomplete injury to the nerve. Usually the pain
starts following incomplete injury or division of the nerve, though occasionally such pain may
not appear before 2 or 3 months.
Pathophysiology.— Incomplete division of the nerve gives rise to an impulse which passes
towards sensory nerve endings where such stimuli lead to production of histamine-like substance.
Accumulation of this substance causes vasodilatation and the part becomes red, sweats profusely
and becomes increasingly painful. Gradually the trophic changes may appear.
Treatment.— The condition is so distressing that surgical interruption often becomes
necessary. According to the site, cervico-thoracic or lumbar sympathectomy may be required,
which are discussed below.
Ilyperhidrosis or excessive sweating.—
Some patients may complain of excessive sweating of the hands, axillae or even feet.
Treatment.— If the axillae are affected, local excision of the axillary skin which contains apocrine
sweat glands may be required. These are mapped out by applying sweat-sensitive starch and iodine
dusting on the axilla. In obstinate cases cervico-thoracic sympathectomy may be required.
When the hands are too much sweating, cervico-thoracic sympathectomy should be the
treatment of choice.
When the feet are sweating excessively with sodden and offensive feet, lumbar
sympathectomy is justified.
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SYMPATHECTOMY.—
INDICATIONS.— The operation of sympathectomy is carried out for the following basic
conditions :—
(1) CIRCULATORY INSUFFICIENCY OF THE LIMBS.— By far this is the most important
indication of sympathectomy. The arteries which have got smooth muscles in their walls, will
be released of their spasms due to sympathectomy. These arteries are generally medium sized,
small arteries, arterioles and arteriovenous communications. By this, there will be more blood
running through the collaterals giving rise to better 'run-off'. The limb will be warm, pain will
be less and the ulcers may show signs of regression.
The pathological conditions under this category, which are benefited by sympathectomy,
are as follows :
(a) Atherosclerosis.— Where direct reconstructive surgery is not possible, sympathectomy
finds its greatest field. The patient with 'rest pain' and an impending gangrene of the toes,
when shows no segmental blockage in arteriography but shows widespread distal blocks, is
probably a good case for sympathectomy. This will improve the condition by dilating the
collateral circulation. The foot will be warmer, 'rest pain' will be relieved to certain extent, but
unfortunately in many cases this symptomatic relief does not last for a long time. Some vascular
surgeons suspect whether sympathectomy really increases the deep collateral circulation or simply
increases vascularisation of the superficial tissue and skin. But one thing is certain, that if
amputation is at all required, previous sympathectomy will definitely limit its extent.
(b) Raynaud's syndrome.— In this condition, the role of sympathectomy is rather dubious.
The symptomatic relief is rather temporary and almost always fails to yield permanent relief.
(c) Thrombo-angiitis obliterans (Buerger's disease).— In this condition, the distal arteries
are involved while the proximal arteries remain absolutely normal with good volume of pulse.
By sympathectomy, one can only delay the progress of the disease, but cannot have a long term
good effect. This operation also limits the extent of amputation.
(2) HYPERHIDROSIS.— The result of sympathectomy is much better in this condition.
When sweating is sufficiently profuse to make one psychotic, this operation should always be
called for. The sweating will be abolished and the long term result is satisfactory.
(3) CAUSALGIA.— Sometimes the patients complain of persistent pain in the limb following
amputation or partial injury to the nerve. Sympathectomy, if carried out, may give the patient
some relief. But the anatomical or pathological reason of this relief is yet to be found out.
Anatomical Consideration of Sympathectomy.— The pre-ganglionic fibres concerned
with supplying the upper limb are derived from the upper thoracic segments of the spinal cord
— T2 to T7. These fibres reach the sympathetic trunk through white rami communicantes. In the
sympathetic trunk these fibres pass up to synapse about cells, situated mainly in the cervicothoracic ganglia, from where post-ganglionic fibres pass to the brachial plexus, mainly the lower
trunk. Most of the vaso-constrictor fibres supplying the arteries of the upper limb, emerge from
the spinal cord in the ventral roots of 2nd and 3rd thoracic nerves. So these arteries can be
denervated surgically by cutting the sympathetic trunk below the 3rd thoracic ganglion, severing
the rami