MINISTRY OF PUBLIC HEALTH OF UKRAINE
BUKOVINIAN STATE MEDICAL UNIVERSITY
APPROVED
on the cathedral meeting of the
Department of patient care and higher nurse education
"______"___________________200___.
minute № ____
Head of department
Associate professor
Plesh I.A.
METHODICAL GUIDELINES
for 3 – year students of the medical faculty
rd
MODULE 2
THE MAIN DUTIES AND PROFESSIONAL SKILLS OF NURSE
AT THE SURGICAL DEPARTMENT
SEMANTIC MODULE 2
TRAUMATISM AND DAMAGE.
DESMURGY.
Topic:
Clean and purulent wounds
Subject: Nursing practice
3rd-year students of Medical faculty
Speciality: "General medicine" – 7.110101
7.110104 – "Pediatrics"
Duration - 2 hours
Methodical guidelines composed by:
Professor R.I. Sydorchuk
Assoc. professor O.Y. Khomko
Assistant R.P. Knut
Chernivtsi – 2008
AIM:
1. To know classification of wounds, biology of a wound process, kinds of a
surgical treatment of a wound. To be able to determine phases of a course of
a wound's process and a kind of a wound healing. To know methods and
engineering of realization of a primary surgical treatment of a wound.
2. To receive concept about infected wounds, To familiarize with features of a
course of a wound process of contaminated wounds. To familiarize with
modern methods of complex treatment of contaminated wounds. To learn to
apply agents to local treatment of such wounds and to acquire principles of
their surgical treatment.
3. To determine the basic clinical and laboratory attributes of disease, to
acquire algorithm, principles of diagnostics and treatment of damages of a
forward abdominal wall, bodies of abdominal cavity.
PROFESSIONAL MOTIVATION:
1. Wounds are one of kinds of damages which extremely wide-spread both in
peace and in a wartime. In many cases they are a principal cause of a
disability and a lethality. The history of surgery is a history of treatment of
wounds. For any other purpose in surgery agents of treatment and their
combinations, as for treatment of wounds were not offered so much. And in
modern conditions annually there are many new methods of treatment of an
above named pathology. Despite of it, the problem of treatment of wounds,
in particular purulent, remains not up to the end decided.
2. Despite of appreciable progress of surgery, the problem of treatment of
purulent wounds to nowadays remains actual in connection with formation
antibiotic resistances cultures of the microorganisms, expressed allergization
and immunodepressive influences on the population.
3. The trauma of a stomach concerns to damages extremely dangerous to life
and is accompanied by a high lethality. It caused by damage of vitally
important organs, and also complexity of diagnostics. Therefore doctors of a
surgical structure should know main principles of diagnostics and treatment
of traumatic damages of a stomach.
BASIC LEVEL:
TYPES OF WOUNDS
According to aetiology, the types of wounds are:
1. Incised wounds.
2. Chopped wounds.
3. Lacerated wounds.
4. Contused wounds.
5. Bruise wounds.
6. Flesh wounds with defect of skin.
7. Puncture wounds
8. Bites wounds.
9. Ischemic or necrotic wounds.
10. Gunshot wounds.
Rapid healing of the wound, particularly rapid skin cover, is the ideal
objective - the first intention of the surgeon. This is brought about by joining
together the edges of the wound by sutures, clips, or by adhesive materials, film or
tape.
Alternative methods of closure used to achieve protection against infection
by skin cover include delayed primary suture, secondary suture, and skin grafting.
Most wounds may be treated by wound excision and primary suture of the
skin (with drainage if needed), within 6 hours of injury. Each layer is tackled in
turn and devitalised tissue is carefully trimmed away. The object of wound
excision is to convert the injury from a jagged lacerated wound into one which
approximates to the incised wound. However, a certain amount of damaged but
recoverable tissue remains in the wounds, and for this reason it is usually unwise to
attempt complicated repairs of deep structures such as tendons and nerves in these
wounds. As soon as the skin wound is soundly healed, probably in 4 to 6 weeks'
time, a formal secondary repair of any divided tendons and nerves can be carried
out.
THE PHASES OF WOUND HEALING
The lour basic processes which take place in wound healing are:
1. Phase of traumatic inflammation. Immediately after disruption of tissue
integrity either by accidental trauma or by surgeon's knife, inflammation starts.
After a transient: vasoconstriction, all local small vessels dilate. As dilatation
occurs, capillaries become abnormally permeable to proteins and plasma leaks into
the site of injury. The blood vessels undergo transient vasoconstriction followed by
vasodilatation. Platelets become adherent and with clotting factors form a
haemostatic plug to stop bleeding from the small vessels. 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 PEG and PEG, 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 ceils produce a variety of prostaglandins. These
prostaglandins seem to be the final mediators of acute inflammation and may play
a chemolactic role for white cells and fibroblasts. Aspirin and indomethaein are
potent inhibitors of prostaglandin biosynthesis and the antiinflammatory action of
these drugs actually results 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 blood. As the granulocytes die, 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 monocytes 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.
2. Phase of demolition (pyogenic for secondary wound healing).
The dead tissue cells liberate their autolytic enzymes. Similarly
disintegrating polymorphs liberate proteolytic enzymes. The mononuclear cells
along with 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 vascularisation and b) stage of devascularisation.
Stage of vascularisation. 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 204 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 pan 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 specialised 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 205 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 hydroxylysine. Other fibrous tissues such as elaslin do not
contain significant amount of hydroxyproline.
Fibroblasts are also thought to be responsible for the production of
mucopolysaccharide ground substance.
Stage of devascularisation. In this stage fibroplasia proceeds and some
vessels undergo atrophy, whereas others show endarteritis obliterans, that means
their lumens become obliterated due to ultimate proliferation. So the granulation
tissue looks pale at this stage, which is known as devascularisation.
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 hyalinisation
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.
4. Epithelisation. While dead material is being removed from deeper areas,
important events occur at the edges of epithelial wounds. In skin wounds, the
epidermis immediately adjacent to the wound edge begins thickening within 24
hours after injury.
Epithelisation of the wound mainly occurs by proliferation and migration of
the marginal basal cells lying close to the wound margin. There is no regeneration
of hair follicles, sebaceous and sweat glands in the new epidermis. 206
In case of the wounds with skin loss, healing of the skin layer is of
importance not only in its own right but because the healing of deeper structures,
such as the tendons and bones, can only take place satisfactorily in the presence of
an intact skin cover. Furthermore, the longer any exposed surface remains raw the
greater will be the deformity and disability. In all wounds with skin loss therefore,
the skin loss should be repaired as soon as is practicable and as follows:
1. Clean incised wounds with skin loss - primary grafting.
2. Lacerated wounds with skin loss - wound excision and primary grafting.
BITES
Bites of animals such as the horse, cat, and dog require the usual treatment
of wounds. Where there is the slightest suspicion that the animal is suffering from
rabies, the bite should be freely excised. If possible, the responsible animal should
be kept under observation, or, if it has been killed, Negri bodies should be sought
in the brain.
Human Bites. Because the wound becomes contaminated with so many
types of bacteria a human bite can prove very dangerous to life or limb. Although
not strictly a bite, a common type of injury of this kind is an incised, wound over
the knuckles resulting from a clenched fist of one combatant striking the front teeth
of his opponent. The joint is usually penetrated, but the track closes when the
fingers are extended. In such a case the wound must be excised.
GUNSHOT WOUNDS
Mechanism. The amount of damage caused by bullets is dependent on the
kinetic energy (KB) released by the bullet as it traverses tissue. The energy can be
calculated from the formula KE = 0.5mv2 where m is the mass and v the velocity
of the bullet.
The low velocity bullet from a pistol, travelling below 1,500 feet per second,
produces injury by its direct effect on tissue by laceration and crushing, within the
narrow confines of the bullet track. The high velocity bullet has a much greater
lethal potential. Tissue necrosis occurs several centimeters on either side of the
bullet track due to the associated shock-wave and a phenomenon known as
cavitation. The penetrating high velocity bullet releases energy which is absorbed
by adjacent tissue particles, imparting to them an acceleration which flings them
forwards and outwards producing the temporary cavity (Fig.1).
Fig.1. Gunshot wound. Cavitational destructive effect
due to the energy oj the high velocity missile
Tissue necrosis occurs especially in muscle at some distance from the bullet
track and forms a perfect culture medium for pathogenic organisms sucked in from
the entrance and exit wounds by the negative pressure in the cavity.
The amount of damage caused by a high velocity bullet is also dependent on
the density and structure of the target organ. Comparatively, little damage occurs
in the through and through wound of a lung, whereas the passage of such a bullet
through or sometimes close to the liver may completely shatter that organ. All
bullet injuries should undergo the operation of wound debridement, which literally
means to debridle or unleash. The entrance and exit wounds, frequently of only
small diameter, do not indicate the considerable damage that may have occurred to
the deeper structures within. The higher the velocity of the bullet, the greater the
area of damage around the bullet track, and the greater the accompanying tissue
necrosis and oedema.
FACTORS OF THE 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 :
a) 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 syndrome, cirrhosis, chronic inflammatory conditions, etc.
b) Vitamin A is required for proper epithelialisation, which may be
hampered due to its deficiency.
c) 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. They may be
depleted in intestinal fistulas.
3. Hormones:
a) Corticosteroids. The effects of this hormone on granulation tissue
formation and wound contraction have been discussed above.
b)Desoxycorlicosterone acetate and anabolic steroids like testosterone are
also concerned with increase in the speed of wound ealing.
The following conditions delay or hamper the quality of wound healing.
These are :
4. Anaemia.
5. Uraemia.
6. Jaundice.
7. Diabetes. 8. Blood dyscrasias.
9. Malignant disease.
10. 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 Lunger are due to
arrangements of collagen bundles in the dermis. The wounds right angle to these
lines lend 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 vascularised. 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 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
ave 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, jeopardises 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.
STUDENTS’ INDEPENDENT STUDY PROGRAM
I.
Objectives for Students’ Independent Studies
You should prepare for the practical class using the existing textbooks and
lectures. Special attention should be paid to the following:
Theme 1. Wounds and wound's process. Prophylaxis of development of an
infection into the wound. Treatment of clean wounds.
1. Definition of concept of a wound;
2. Classification of wounds;
3. Principles of wound's healing, features of each phase of a wound
process;
4. Definition of concept of an primary surgical treatment of a wound, initial
and secondary seams;
5. A technique of realization of an primary surgical treatment of a
contaminated wound;
6. Indications to performance of an primary surgical treatment and
applying of a different kind of seams.
Theme 2. Infected wounds.
1. Definition of concept "wound";
2. Definition of concept " a primary surgical treatment of wounds ", "
initial and secondary seams ";
3. Classification of wounds;
4. Principles of wound's healing, features of each phase of a wound
process;
5. A technique of realization of an initial surgical treatment of
contaminated wounds;
6. Indications to performance of an initial surgical treatment and applying
of different kinds of seams.
7. The basic characteristics of the general condition of the patient, ways of
their definition;
8. Conditions which assist development of a pyesis of a wound;
9. Principles of antibacterial therapy;
10.Principles of a surgical treatment of contaminated wounds (their
advanced processing);
11.Methods of a stimulation of processes of regeneration;
12.Local and general treatment of contaminated wounds.
II.
Tests and Assignments for Self – assessment
Multiple Choices.
Choose the correct answer/statement:
1. Secondary infection of wounds is probably at infringement corrected
asepsises:
A. At the moment of granting the first medical service;
B. During a dressing;
C. During operation;
D. During reception of a wound;
E. All answers true.
2. The penetrating wound of abdomen refers wound with damage:
A. Skin;
B. A subskin fat;
C. Muscles;
D. Parietal peritoneum;
E. Visceral peritoneum.
3. What wound is healed faster others:
A. Incized;
B. Chopped;
C. Bite;
D. Contused;
E. Gunshot.
4. For freshen wounds typically all without:
A. Pain;
B. Bleeding;
C. Defect of tissues;
D. Sensations of twitching in a wound;
E. Hiatus
Real-life situations to be solved:
5. The patient for the fourth day after appendectomy had throbbing pain in the
region of a postoperative wound, the body temperature increased, the
leukocytosis is observed.
What complication has arisen at the patient?
6. After the transferred traffic accident to the patient of 63 years old in
conditions of a dressing room of admitting room have not washed out a
cavity of a wound a solution of oxidizers, did not drain a wound, and on
have indistinctly sewed up.
Whether doctors have correctly arrived? What possible complications it is
necessary to wait in the postoperative period?
III.
Answers to the Self-Assessment:
1. B;
2. D;
3. A;
4. D
5. Postoperative wound infection.
6. Incorrectly. Development of anaerobic surgical infection.
IV.
References:
Essential reading:
1. Gostishchev V.K. General surgery /The manual. – M.: GEOTAR-MED,
2003. – 220p.
2. Lectures prof. B.I. Dmitriev from Odessa State Medical University.
3. Surgery: Text-book for English medium medical students / S.I.
Shevchenko, O.A. Tonkoglas, I.M. Lodyana, R.S. Shevchenko. –
Kharkiv: KSMU, 2001. – 344p.
4. Kushnir R. Ya. General surgery /Lectures.- Ternopil, Ukrmedknyha,
2005.- 308 p.
5. Butyrsky A. General surgery /The manual.- Simpheropol: publishers
CGMU, 2004.- 478 p.
Further reading:
1. Oxford handbook of clinical surgery / Edited by G.R. Mc Latchie, D.J.
Leaper, 2002.- 930 p.
V.
Students’ Practical Activities:
Theme 1. Wounds and wound's process. Prophylaxis of development of an
infection into the wound. Treatment of clean wounds.
 Work 1. Work 1. To provide and warn development of a wound infection;
 Work 2. To estimate a course of a wound process;
 Work 3. To impose and remove seams.
Theme 2. Infected wounds.
 Work 4. To carry out an primary surgical treatment of infected wounds;
 Work 5. To carry out necrectomy of purulent wound;
 Work 6. To carry out a dressing of an infected and purulent wound with
application of modern antiseptics;
VI.
Seminar Discussion Of Theoretical Questions And Practical Work:
VII. The initial level of knowledge and skills is checked by the decision of
situational problems (tasks) from each theme, answers to tests such as
"Step", constructive questions etc.
Students must know:
 Wounds: definition, classification.
 Frame of a wound and a course of a wound process in a clean wound.
 The characteristic of separate types of wounds and a first aid at them.
 Conditions of occurrence of an infection in a wound, elimination of these
conditions.
 Frame of a clean wound.
 The initial surgical treatment of a wound.
 Kinds of initial seams.
 Treatments of a clean wound in the postoperative period.
 Contaminated wounds.
 Course of a wound process in a purulent wound.
 The surgical treatment of a purulent wound, kinds of secondary seams.
 Treatments of a purulent wound according a phase of a wound process.
 Kinds of a drainage of a purulent wound.
 Concepts about a traumatism.
 Clinical symptoms of the closed damage of soft tissues, skull, a thorax, organs
of abdominal cavity.
 Prophylaxis of development of a traumatic shock, a pheumothorax, an internal
bleeding.
 Features of first-aid treatment and transportation of patients at these damages.
Students should be able to:
 To apply occlusive bandage at penetrating damage of a thorax
 To diagnose phases of a wound process;
 To determine a kind of wound's healing;
 To take a material for cytologic and microbiological researches;
 To render the first medical aid at wound;
 To apply and remove sutures.
 To carry out a dressing of a purulent wound with application of modern
antiseptics;
 To impose an immovable bandage.
 To allocate the basic clinical attributes of damage of a forward abdominal
wall, hollow and parenchymatous organs of abdominal cavity;
 To make the circuit of diagnostic search;
 To estimate results of laboiratory - instrumental methods of diagnostics;
To prove main principles of treatment of separate damages of a stomach (an
abdominal wall, hollow and parenchymatous organs).