RCSI Handbook
of Clinical Surgery
for Finals FOURTH EDITION
Senior Editors
Gozie Offiah
Arnold Hill
CRC Press
Taylor & Francis Group
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Contents
Eponymous Microvignette
7
Chapter 1
Principles of Surgery
9
Chapter 2
Hernias
33
Chapter 3
Upper Gastrointestinal Surgery
47
Chapter 4
Hepatobiliary Surgery
73
Chapter 5
Colorectal Surgery
99
Chapter 6
Inflammatory Bowel Disease
139
Chapter 7
Peripheral Vascular Disease
153
Chapter 8
Breast Disorders
179
Chapter 9
Endocrine Disorders
193
Chapter 10
Urology
219
Chapter 11
Cardiothoracic Surgery
241
Chapter 12
Major Trauma
253
Chapter 13
Plastic Surgery
269
Chapter 14
Orthopaedic Surgery
291
Chapter 15
Neurosurgery
315
Chapter 16
Otorhinolaryngology (ENT)
335
References 364
3
Senior Editors:
Prof Arnold Hill
Head of School of Medicine and Professor of Surgery,
Royal College of Surgeons in Ireland
Dr Gozie Offiah
Senior Lecturer in Surgery, Royal College of Surgeons in Ireland
Text and Image Editors:
Dr Roisin Tully – Clinical Lecturer, Royal College of Surgeons in Ireland
Dr Ryan Roopnarinesingh - Clinical Tutor, Royal College of Surgeons in Ireland
Illustrators:
Dr Kevin Quinlan
Dr Eoin Kelleher
Authors:
Dr Joan Lennon
Dr Michael Quirke
Mr Firas Ayoub
Contributors:
Dr Roisin Tully
Dr Tahir Abbasi
Dr Ryan Roopnarinesingh
Mr Waqas Butt
Dr Melanie Cunningham
Mr Edrin Iskander
Dr Raluca Mitru
Mr Ghazi Ismael
Dr Arielle Coomara
Mr Moataz Khogali
Dr Daniel Creegan
Dr Kulsoom Nizami
Dr Nauar Knightly
Mr Monim Salih
Dr Donata Lankaite
Dr Anneela Shah
Dr Celia Fernandez
Mr Igor Soric
Dr Emily Rutherford
Dr Emma Tong
Dr Evan Fahy
Dr Mark Twyford
Dr Jill Mulrain
Mr Thavakumar Subramaniam
Mr Mohammed Ben Husien
Mr Prasanna K Venkatesh
Dr Rachel Wu
Dr Hind Zaidan
Mr Nawar Masarani
Mr Ahmed Hussain
Dr Sherif Mamdouh
Dr Lindi Snyman
Dr Eilish Galvin
Dr Sheila Duggan
Consultant Expert Reviewers:
Dr Fiona Kiernan
Prof Frank Cunningham
Dr Carolyn Power
Prof Raghu Varadarajan
Dr Kevin Quinlan
Prof Martin Corbally
Dr Daniel Kane
Mr Peter Naughton
Mr Enda Hannan
Dr Criona Walshe
Mr Anthony Hoban
Mr Barry O’Sullivan
Mr Wail Mohammed
Prof James Paul O’Neill
Dr Azlena Ali Beegan
Mr Colm Power
Dr Niamh Adams
Prof Tom Walsh
Dr Cyrille Payne
Prof Ciaran Bolger
Mr Amr HA Nour
Prof Frank Murray
Mr Peter O’Leary
Dr Aoibhlinn O’Toole
Mr Andrew Coveney
Prof John O’Byrne
Dr Liz Concannon
Mr Niall Davis
Dr Gerard Kelly
Mr Seamus McHugh
Dr Ciaran Stanley
Mr Muhammad Hamid Majeed
4
Preface
The RCSI Handbook of Clinical Surgery for Finals is designed for RCSI medical
students in their final year attending the three RCSI medical schools in Dublin,
Bahrain and Malaysia; with the objective of addressing the knowledge and skills
that a student needs to pass surgery final medical year exams. These core
knowledge and skills are the same needed to be a competent doctor in clinical
practice. There has been excellent feedback from the first three editions of the
book from students in RCSI and other Irish medical schools.
This new edition of the RCSI Handbook of Clinical Surgery for Finals was reviewed
by several experts in the individual specialities. We have also added relevant
surgical anatomy to the chapters that will be useful and will add context to your
reading. This RCSI Handbook of Clinical Surgery for Finals should be used as an
adjunct to all clinical attachments and formal taught programme material. It has
been designed as a handbook, rather than a textbook, so as to be useful at the
patient bedside and in the library. We are proud to be part of the RCSI Handbook
of Clinical Surgery for Finals and wish you the best of luck with your final exams.
Arnold Hill & Gozie Offiah
July 2019
5
Acknowledgements
The editors of this book are grateful for the contribution of all the authors, expert
reviewers and illustrators. We would also like to thank all the patients who consented
for their images to be used in this handbook. We would also like to extend our gratitude to the students who engaged in a focus group session as well as the numerous
students who provided feedback to the new edition of this book. This has formed a
vital part of our endeavour to provide a comprehensive and up to date text.
Copyright © 2019 Royal College of Surgeons in Ireland
All rights reserved. No part of this publication may be reproduced, distributed, or
transmitted in any form or by any means, including photocopying, recording, or other
electronic or mechanical methods, without the prior written permission of the publisher, except in the case of brief quotations embodied in critical reviews and certain
other non-commercial uses permitted by copyright law. For permission requests,
write to the publisher.
The information in this book is the opinion of many different authors and contributors,
and is derived from multiple references at the discretion of each contributing author
and reviewer. Clinical surgery and medicine are ever-changing fields. The editors,
authors and contributors of RCSI Handbook of Clinical Surgery for Finals have made
every effort to provide information that is accurate and complete as of the date of
publication. However, in view of the rapid changes occurring in medical science, as
well as the possibility of human error, there may be some technical inaccuracies,
typographical or other errors. The information contained herein is provided “as is”
and without warranty of any kind. The contributors to this book including the RCSI
disclaim responsibility for any errors or omissions or for results obtained from the use
of information contained herein.
6
EPONYMOUS MICROVIGNETTE
Vignette
Sign:
Who were they?
42 year old male gets
Beck’s Triad of
struck in the chest with
Cardiac
a baseball bat during
Tamponade
an assault. He presents to Emergency Department and it is noted that he has
decreased heart sounds
on auscultation,
hypotensive and
distension of the JVP is
noted in the neck.
Claude Schaeffer Beck was a pioneer
American cardiac surgeon, famous for
innovating various cardiac surgery
techniques, and performing the first
defibrillation in 1947
35 Year old female
Charcot’s
presents to Emergency
Cholangitis
Department with Right
Triad
Upper Quadrant pain. She is of increased adiposity, is noted to have scleral icterus and has been
complaining of fever and intermittent chills at home.
A French neurologist and professor of
anatomical pathology. Charcot has been
referred to as “the father of French
neurology and one of the world’s
pioneers of neurology”
50 year old male presenting Murphy’s Sign
with Right Upper Quadrant of cholecystitis
pain for the last 24 hours.
On examination of his abdomen the doctor firmly placed a hand at the costal margin in the right upper abdominal quadrant and asked him to breath in, however this caused the patient to catch his breath due to pain.
An American physician and abdominal surgeon
noted for advocating early surgical
intervention in appendicitis appendectomy
In addition to general surgical operations,
such as appendectomy, cholecystostomy,
bowel resection for intestinal obstruction,
and mastectomy, he performed and described
innovative procedures in neurosurgery,
orthopedics, gynecology, urology, plastic
surgery, thoracic surgery, and vascular surgery
A 20 year old male
McBurney’s
presented with generalised Point
abdominal pain, nausea and vomiting over 12 hours that localised to the right
Iliac fossa.
Upon examination the
physician pressed on a
point 1/3 the way on a line
from the Anterior Superior
iliac Spine to the umbilicus
which ilicited a pain
response.
Charles Heber McBurney, MD was an
American surgeon who described the point
of greatest tenderness in appendicitis, which
is now known as McBurney’s point.
His name has been associated with at
at least 15 medical eponyms
7
EPONYMOUS MICROVIGNETTE
Vignette
Sign:
82 year old elderly female
Colles’ Fracture
presents after falling on an outstretched hand having tripped getting out of her pew in church. On examination she is seen
to have a ‘Dinner fork deformity” of her left wrist. X-ray confirmed an extracapsular fracture of the distal radius with dorsal angulation (apex volar)
.
.
8
Who were they?
Abraham Colles
(23 July 1773 – 16 November 1843)
was professor of anatomy, surgery and
physiology at the
Royal College of Surgeons in Ireland.
His teaching career was highly successful,
and drew crowds of students to RCSI.
He enhanced the reputation of the surgical
profession, so that it was no longer
considered inferior to medicine. This was the
era of surgery prior to anaesthesia, antisepsis,
and antibiotics; so treatments were relatively
crude with high mortality from bleeding and
infections.
37 year old female
Pemberton’s
presented to clinic with
Sign
symptoms of fatigue, constipation and weight gain. She had also noticed a central neck lump which
has been getting bigger
over the last few months
and has become quite large.
On examination the
surgeon asked her to raise
her hands over her head
and hold them there. After
about 1 minute the
woman’s neck veins began
to protrude, her face
became flushed and she
became short of breath
Dr.Hugh Pemberton an English physician
who was a pioneer for diabetes, thyrotoxicosis
and peripheral vascular
disease in England in the 1920’s
62 year old male presenting Baker’s Cyst
to orthopaedic clinic with pain, swelling and stiffness
behind his right knee. On examination there was a visible and palpable mass
in the popliteal fossa and some joint line tenderness. Ultrasound confirmed a
popliteal cyst.
William Morrant Baker was an English
physician and surgeon
Baker became Sir James Paget’s assistant for
many years perfecting his trade
He resigned his post as surgeon in 1892 due
to his own locomotor ataxia condition
PRINCIPLESOF
OFSURGERY
SURGERY
PRINCIPLES
Chapter 11
Chapter
Principles of Surgery
Principles of Surgery
9
PRINCIPLES OF SURGERY
Contents:
• History taking
• Differential diagnosis of the acute abdomen
• Common management principles in an acute abdomen
• Incisions
• Surgical drains
• Nutrition in surgical patients
10
PRINCIPLES OF SURGERY
HISTORY TAKING - COMMON SURGICAL SYMPTOMS
Pain:
SR.COPD.SARAH mnemonic works for all causes of pain and can be used for other
symptoms too – use it while you work out your differential diagnoses.
Ø
Site:
— “Where is the pain?” “Point to where the pain is?”
Ø
Radiation:
— “Does the pain move or spread-out anywhere?”
— Gallbladder disease: around to right side of your back / shoulder-tip.
— Pancreatic disease: straight through to the back.
— Ureteric disease: Loin to groin.
— Character: If necessary, give examples but avoid leading questions
— “How would you best describe this pain?”
— Sharp like a needle / burning or stinging / dull or throbbing.
— Restless / prefer to lie still (colicky pain).
Ø
Onset:
— When did it start?
— Suddenly / gradually.
Ø
Periodicity
—Time of day: night (PUD vs Gallstone)
— Worse after eating fatty food.
— “Does the pain build up and get worse over minutes / hours?”
(Crescendo pain)
— Always the same? Improve / disimprove?
Ø
Duration
— “How long have you experienced the pain?”
Ø
Severity (out of 10)
— Maximum pain and baseline pain.
Ø
Associated symptoms:
— Vomit: quantity / quality.
— PR Bleed / Melena: Black, tarry and sticky stool.
— Haematemesis: Vomit any bright red blood? Small black bits like
tea-leaves or coffee grounds in your vomit?
— Dysuria: stinging when you urinate.
— Tenesmus: feeling of not fully emptying bowels after a bowel motion.
Ø
Relieving factors:
— Pancreatitis: Relieved when sitting forward.
— Analgesia / food.
Ø
Aggravating factors:
— Worse after a deep breath? Worsened by walking or moving?
Ø
History of this symptom:
— “Have you experienced this type of pain before?”
11
PRINCIPLES OF SURGERY
UPPER GI SYMPTOMS
Dyspepsia
Ø Persistent or recurrent abdominal pain or abdominal discomfort centered in the
upper abdomen.
Ø “Discomfort” refers to a subjective, negative feeling that does not reach the
level of pain according to the patient.
Dysphagia
Ø Subjective sensation of difficulty or abnormality of swallowing.
—
New or long-standing?
—
Worsening or staying the same?
—
Able to swallow fluids / solids only?
Ø Able to swallow saliva?
Gastro-oesophageal reflux / heartburn
Ø Bitter tasting / sour fluid in throat or mouth.
—
Ask how frequent it occurs, association with food.
—
Relieving factors (lying flat, food avoidance).
Haematemesis
Ø Coffee grounds represent old or low volume gastric bleeding.
Ø Dark red blood is either variceal or arterial
Ø Blood appearing only after repeated vomiting (“blood-streaked vomitus”)
usually represents traumatic oesophageal cause or gastritis.
LOWER GI SYMPTOMS
Altered bowel habit
Ø May indicate underlying bowel cancer or inflammatory bowel disease.
Ø May be change in frequency, constipation or change in stool consistency.
Rectal bleeding
Ø Haemorrhoids or anal bleeding: bright red in colour and only on wiping?
Ø Rectal bleeding: on the surface of the stool?
Ø Colonic bleeding: dark red in colour, mixed up with the stool, or with clots?
Ø
Ø
Proximal colonic bleeding: is stool maroon red in colour and loose?
Dyschezia: “Is it painful?” Painful bleeding would suggest an anal fissure.
Haemorrhoids are not typically painful unless thrombosed
Tenesmus
Ø Feeling of not fully emptying bowels after a bowel motion. Suggests low
rectal tumour.
12
PRINCIPLES OF SURGERY
HEPATOBILIARY SYMPTOMS
Jaundice
Ø Yellow discolouration of the sclera and skin due to hyperbilirubinaemia.
—
Ask for itch, dark urine and pale stool in every case.
—
Itch suggests posthepatic obstruction.
Ø Ask when the patient last felt well.
_______________
PERIPHERAL ARTERIAL DISEASE SYMPTOMS
Claudication
Ø Pain in calf, thigh or buttock precipitated by exercise and relieved by rest due
to inadequate blood flow.
—
Claudication distance: “How far can you walk before needing a rest?”
—
“How long do you typically rest for before recommencing walking?”
—
“When did the pain on walking first begin?”
—
“Did your leg go suddenly cold and then recover with the onset of calf
pain on walking?”
Rest pain
Ø Severe, burning pain in limb affected by inadequate arterial flow, present at
rest. Pain is neuropathic in nature due to neuronal ischaemia.
—
“Worse at nighttime?”
—
“Do you have to hang your leg over the side of the bed?”
—
“Do you have to walk around your room at night to relieve the pain?”
_______________
UROLOGY SYMPTOMS
Dysuria
Ø Pain on micturition.
—
Burning when you pass water?
—
Pain in lower abdomen?
—
Nocturia, frequency.
Haematuria
Ø Blood in the urine
Ø “Does the blood occur at the start of urination?” (Suggests bladder origin)
Ø “Does the blood appear at the end of urination, or during urination?”
(Suggests prostatic or penile origin)
13
PRINCIPLES OF SURGERY
DIFFERENTIAL DIAGSOSIS OF ACUTE ABDOMEN
Illustrated by Kevin Quinlan: regional differential diagnosis of an acute abdomen
14
PRINCIPLES OF SURGERY
Formulating differential diagnoses and approach to history taking
Ø Formulate a differential diagnosis as the history progresses.
Ø Ask targeted questions which help to rule-in or rule-out your differential diag
noses as you proceed through your history.
Ø You should ask 2-3 questions about each differential diagnosis to show the
examiner that you are considering the likely causes for the patient’s
presentation.
—
These are all “leading questions” for typical symptoms of each disease –
with practice you will be able to frame them with “open questions” and
use your own style of history taking.
Differential diagnosis of epigastric pain:
Ø Peptic ulcer disease / Gastritis
—
Constant pain, aggravated by movement (inflammation).
—
Heartburn.
—
Melena.
—
Haematemesis / coffee-ground vomit.
—
Duodenal ulcer: usually woken up with pain. Eating / milk relieves pain.
Ø
Pancreatitis
—
Epigastric pain radiating through to the back.
—
Constant pain, aggravated by movement (inflammation).
—
Relieved when sitting forward.
—
History of this pain before? After alcohol? History of gallstones?
Ø
Gastro-oesophageal reflux (GORD)
—
Heartburn
—
Epigastric pain radiating to chest.
—
Relieved with gaviscon or cool drinks.
Ø
Cardiac (MI / pericarditis)
—
Chest pain, tightness or discomfort.
—
Radiation to left arm, shoulder or jaw.
—
Short of breath / sweaty (diaphoresis) / anxiety.
—
Any history of heart trouble such as a heart attack or angina?
Ø
Ruptured AAA
—
Abdominal pain radiating to back.
—
Dizzy, light headed, or sweaty.
—
Collapse / loss of consciousness.
—
Any history of poor circulation to your legs or heart disease?
—
Ever diagnosed with an aneurysm?
15
PRINCIPLES OF SURGERY
Differential diagnosis of right upper quadrant (RUQ) pain
Biliary colic
— Ingestion of a fatty meal prior to pain.
—
Crescendo: pain waxes and wanes.
—
Colicky: restless with rapid escalation pain, bending over or moving to find
a position of comfort.
—
Pain usually lasts less than 6 hours.
Ø
Ø Cholecystitis / Cholangitis
—
Ingestion of a fatty meal prior to pain.
—
Radiation around the right side to your back / right shoulder / shoulder-tip.
—
Pain lasts more than 24 hours. Constant pain, aggravated by movement
(inflammation).
—
Jaundice: dark urine, pale stools, yellowing of eyes and skin, pruritus.
—
Cholangitis:
¾ Charcot’s triad: 1) pain; 2) fever / chills; 3) jaundice.
¾ Reynold’s pentad: 4) shock, hypotension; 5) confusion.
—
Murphy’s sign (+ve in Cholecystitis) tenderness & inspiratory arrest upon
deep palpation of the costal margin along the mid-clavicular line as the
patient takes a deep breath in.
Ø Hepatitis
—
Constant pain, aggravated by movement (inflammation).
—
Medication history, travel history and social history (alcohol and drugs
of abuse).
Ø Pneumonia
—
Diaphragmatic irritation from lower lobe pneumonia may cause right
(or left) upper quadrant pain
—
Short of breath.
—
Productive cough.
—
Chest / RUQ / LUQ pain: pleuritic and sharp / knife-like.
Differential diagnosis of left upper quadrant (LUQ) pain
Ø Left lower lobe pneumonia
Ø Splenic abscess / infarction
Ø Gastritis
Ø Gastric ulcer
Ø Herpes zoster
16
PRINCIPLES OF SURGERY
Differential diagnosis of Umbilical pain
Ø Appendicitis (see RIF pain)
Ø Small Bowel Obstruction (Diffuse abdominal pain)
Ø UTI (cystitis)
—
More lower abdominal / pelvic pressure.
—
Dysuria, pyuria, haematuria, frequency.
_______________
Differential diagnosis of Right / Left flank pain
Ø Renal Colic (as per Ureteric Colic – see RIF pain)
Ø Pyelonephritis
—
UTI & systemic features: fever, rigors, N/V.
—
Constant dull pain (inflammatory).
Ø Musculoskeletal:
Ø Sciatica
Ø Lumbar Disc
Ø Bony metastases
_______________
Differential diagnosis of diffuse abdominal pain
Ø Gastroenteritis
—
Diarrhoea +/- blood / mucus.
—
Vomit.
Ø Acute Mesenteric ischaemia
—
Risks: elderly, atrial fibrillation, cardiovascular disease, history of chronic
mesenteric ischemia.
—
Ask for associated vomiting, diarrhoea, ileus.
—
Typically very severe pain unrelieved by analgesia.
Ø
Chronic mesenteric ischaemia
—
Post-prandial pain.
—
Weight loss.
—
Change in bowel habit.
Ø
Bowel obstruction
—
Vomit. Green in colour (bilious) or brown (faeculent).
—
Constipation. Obstipation (no flatus in complete obstruction).
—
Distension.
—
Perforation (sudden)
17
PRINCIPLES OF SURGERY
—
—
- On exam: decreased resonance on percussion;
SBO (high): first, bilious vomit; later, constipation.
LBO (low): first, constipation; later, faeculent vomit. On exam: distension,
tympanic abdomen, high pitched bowel sounds.
Differential diagnosis of right iliac fossa (RIF) pain
Ø Appendicitis
—
Migratory umbilical pain to RIF pain.
—
Worse on movement or coughing (inflammation).
—
Fever, chills, rigors.
—
Nausea / Vomiting.
—
Anorexia i.e. lack of appetite
—
Deep tenderness at McBurney’s point: 1/3rd distance from ASIS to the
umbilicus. Also rebound (peritonitis).
—
Rovsing’s sign: LIF palpation increases RIF pain.
—
Obturator sign: lie supine, flex hip & knee 90°. Examiner passively
internally rotates the hip, causing pain. Retrocaecal appendicitis can inflame the obturator internus, which stretches with this manoeuvre.
—
Psoas sign: lie on side with knees extended. Examiner passively extends
thigh, causing abdominal pain. Retrocaecal appendicitis can inflame ileo-psoas. DDx: psoas abscess.
Ø Ectopic pregnancy
—
Full menstrual history:
¾ LMP (first day of last menstrual period).
¾ Illicit normal cycle & for patient.
¾ Menorrhagia?
¾Period late / irregular bleeding?
¾Pregnant?
¾ PV bleeding between period?
—
Dizzy / faint / hypotension.
—
Dyschezia (painful bowel motion due to blood collecting and irritating
the Pouch of Douglas).
Ø Ruptured ovarian cyst
—
Full menstrual history:
¾ LMP (first day of last menstrual period).
¾ Period late / irregular bleeding?
¾ Pregnant?
¾PV bleeding between period?
—
Sudden onset (unlike appendicitis).
—
Vomit (Vomiting with severe pain suggests ovarian torsion).
18
PRINCIPLES OF SURGERY
Ø
Pelvic inflammatory disease
—
Ask for symptoms associated with ruptured ovarian cyst.
—
Fever.
—
Vaginal discharge.
—
Full sexual history necessary.
19
PRINCIPLES OF SURGERY
Ø Inguinal hernia
—
“Lump in the area before this pain began?”
—
“Lump there all the time or does it come and go?” (incarcerated or not).
—
“Lump swollen and tender now?”
—
“Lump gone in the morning and appears during the day?”
—
Dragging sensation.
—
Strangulation: constant pain. On exam: fever, tachycardia; localized
tenderness, irreducible hernia.
Ø
Ureteric stone
—
Severe pain.
—
Radiate from ‘loin to groin’
—
Restless with the pain.
—
Haematuria.
—
Dysuria, urgency.
—
Vomit.
Ø Inflammatory bowel disease
—
Change in bowel motion. What is normal for you?
—
Haematochezia / bloody diarrhoea.
—
Systemic symptoms:
¾ Weight loss.
¾ Joint pain.
¾ Eye trouble.
¾ Skin rash.
_______________
Differential diagnosis of left iliac fossa (LIF) pain
Ø Diverticulitis
—
Change in bowel motion. What is normal for you?
—
Haematochezia / bloody diarrheoa.
—
Fever, chills, rigors. Anorexia.
—
Prior colonoscopy? Any abnormalities found?”
Ø Ectopic pregnancy
Ø Ruptured ovarian cyst
Ø Pelvic inflammatory disease
Ø Inflammatory bowel disease
Ø Ureteric stone
_______________
20
PRINCIPLES OF SURGERY
Differential diagnosis of Suprapubic pain
Ø Urine retention
Ø UTI
Ø Prostatitis
Ø Pelvic inflammatory disease
Ø Inflammatory bowel disease
Ø Osteitis pubis
21
PRINCIPLES OF SURGERY
Illustrated by Kevin Quinlan: essential components of the regional differential diagnosis
of an acute abdomen.
22
PRINCIPLES OF SURGERY
ACUTE ABDOMEN INVESTIGATIONS
To rule in:
To consider if indicated
Bedside
Vitals
Urine Output
Urine Dipstick
ECG
Capillary Glucose
Urine
Urine Culture & Sensitivity
β-hCG
Amylase
Stool / Swab
Culture & sensitivity
Blood
FBC: Hb; WCC; platelets.
CRP
Blood Culture & Sensitivity
U+E: Urea, Creatinine
Ca2+
Albumin
LFT
Coagulation screen
Type & Screen
Amylase
ABG: lactate
Glucose
Troponin
β-hCG
Imaging
Ultrasound (US):
• Abdomen
• Pelvis
CXR erect
PFA
CT +/- contrast:
• Abdomen / pelvis
• Angiography
• KUB
MRCP
Shock
Hypovolaemia, retention.
UTI, haematuria, bilirubinuria
MI
DKA
UTI
Ectopic pregnancy
Pancreatitis
If indicated
Hb: Anaemia. WCC: Infection.
Platelets: surgery prep.
Infection
Sepsis/SIRS
AKI, dehydration.
Ureteric stone, Pancreatitis
Malnutrition, Pancreatitis
Hepatobiliary, Pancreatitis
Surgery prep; liver dysfunction
Surgery prep; blood loss
Pancreatitis (3x Upper Limit
of Normal)
Lactate: ischaemia, sepsis
DKA
MI
Pregnancy, ectopic pregnancy
Abdo: Hepatobiliary, AAA,
appendicitis, complicated
pancreatitis.
Pelvic: Ectopic pregnancy,
ovarian cyst.
Perforated viscous
Obstruction:
Small Bowel Normal : < 3cm
Large Bowel Normal : < 6cm
Caecum/Sigmoid Normal: <9cm
Obstruction, perforation site.
Mesenteric ischaemia
Renal/ureteric stone, AAA
If no CBD stone seen on US
23
PRINCIPLES OF SURGERY
Invasive
Endoscopic US (EUS)
Percutaneous Cholangiography
OGD / Colonoscopy
Diagnostic Laparoscopy
24
If no CBD stone, but dilated CBD on MRCP.
Biopsy of pancreas
If ERCP fails
PUD / IBD
If still unknown
PRINCIPLES OF SURGERY
ACUTE ABDOMEN TREATMENT
to consider if indicated
Bedside
O2
Ins / Outs
NPO
IV access
Urine Catheter
IV fluids:
• Hartmann’s (Na+ Lactate)
• 0.9% Na+Cl- & 20 K+Cl(if vomiting)
• 5% Dextrose 2L
As either/both of:
1. Replacement IV fluids
2. Maintenance IV fluids
NGT nasogastric tube
• Wide bore to decompress
obstruction
/ relieve vomiting.
• Fine bore to feed.
Medical
Anti-emetic
Analgesia per WHO ladder
Antibiotics
(empiric, then specific)
Prophylaxis
PPI
VTE venous
thrombo-embolism
• TEDS thrombo-embolic
deterrent stockings
• Hydration, early mobility
• LMWH (e.g. Enoxaparin
20-40 mg sc od)
Definitive
Conservative
Medical
Endoscopic
Interventional Radiology
Surgery
To treat
If hypoxia
Monitor U.O.; retention
See IV fluids section in Chapter 2.
Contraindications:
• Opioids in SBO (constipation).
• NSAIDs in PUD / AKI / asthma.
Prevent PUD / gastritis
DVT PPx
25
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
INCISIONS
INCISIONS
Illustrated by Kevin Quinlan: common open and laparoscopic scars.
Illustrated by Kevin Quinlan: common open and laparoscopic scars.
26
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
Laparoscopic
Appendicectomy
Laparoscopic
Cholecystectomy
Laparoscopic
left nephrectomy
Laparoscopic resection
left sided colonic tumour
27
PRINCIPLES OF SURGERY
DRAINS
1. Drains remove collections of blood (drainage of haemothorax), fluid (ascitic
drain), pus (drainage of empyema or subphrenic abscess) or air (pneumothorax).
2. Drains prevent accumulation of fluid around the operative site (eg bile after
biliary surgery)
3. Complications:
a. Damage underlying structures by migration or misplacement.
b. A route for infection.
Note: Generally drains are removed when nothing further is coming out or when
contents of drain fall below 30/50ml depending on site in 24hr
Types of drains:
Ø Identify these drains during your clinical attachment.
Ø Open passive drains: provide a conduit for drainage of secretions.
— Yates, Penrose.
Ø Closed passive drains: siphon effect of gravity and capillary action.
— Robinson, nasogastric tube, ventriculoperitoneal shunt, chest tube
(tube thoracostomy).
Ø Closed active drains: generate active suction.
— “Redivac” drain, “Minivac” drain.
Ø T – Tube
— Rarely used. Post open exploration of the bile duct after intraoperative
cholangiogram.
— Superseded by ERCP.
— Decompresses the bile duct system and make sure there are no
further stones.
— It is brought out percutaneously.
— Should drain 600 ml per day initially and slowly reduce.
— After 10 days the tube will form a fibrotic reaction with the skin and
it will close.
— Before removing it clamp it for 24 hours and look for signs of obstructive jaundice.
28
PRINCIPLES OF SURGERY
NUTRITION IN SURGICAL PATIENTS
Ø
Ø
Ø
Timely nutrition reduces catabolic state and skeletal muscle wasting.
Pre-existing malnutrition is common in surgical patients.
Advanced malignancy, sepsis from appendicitis or diverticulitis, prolonged
vomiting, bowel obstruction while patient is nil per os (NPO), all lead to excessive catabolic states and require early nutritional support.
Poor nutrition leads to the following:
Ø Impaired albumin production.
Ø Impaired wound healing and collagen deposition.
Ø Skeletal muscle weakness (ICU myopathy).
Ø Reduced neutrophil and lymphocyte function.
Body Mass Index (BMI) is the most commonly used measure of nutrition.
Ø Weight / height 2.
Ø 18-25 kg/m2 is normal, <15 underweight, >30 obese.
Ø Grip strength is a useful measure of skeletal muscle strength.
Ø Albumin and transferrin levels are poor indicators of nutritional state.
Ø Prealbumin has been shown to be a useful test of nutritional status and progress, although not routinely done in clinical practice.
Types of nutritional support
Ø Oral
— Always the preferred route. Start oral feeding early and avoid excessively long preoperative fasting and post-operative fasting.
— Promotes normal GI flora and mucosal balance.
— Chewing gum has been found to stimulate and improve GI function.
Ø Nasogastric or nasojejunal
— Nasojejunal tubes used if nasogastric tube is not possible, e.g.:
severe vomiting, gastric resection, gastric outlet obstruction.
Ø Feeding gastrostomy or jejunostomy
29
PRINCIPLES OF SURGERY
PRINCIPLES OF SURGERY
— Gastrostomy:
for patients with
○ Gastrostomy:
for
functioning GIT,
but cannot
patients
with swallow / anorexia.
functioning GIT, but
(PEG = percutaneous
endoscopic
cannot swallow
/
gastrostomy).
anorexia.
— Jejunostomy:
to bypass
stomach
(PEG
=
(e.g. ulcers).percutaneous
endoscopic
gastrostomy).
○ Jejunostomy: to
bypass stomach
(e.g. ulcers).
Illustrated by Kevin Quinlan: Gastrostomy.
Illustrated by Kevin Quinlan: Gastrostomy.
➢ Total parenteral nutrition (TPN)
○ May be
given to(TPN)
patients in whom the oral AND nasogastric/jejunal
Ø Total parenteral
nutrition
route
not possible.
— May
be is
given
to patients in whom the oral AND nasogastric/jejunal
For is
example,
extensive bowel resection, severe catabolic state with
○ route
not possible.
fistula
and bowel
resection
as Crohn’s
disease.
— For
example,
extensive
bowelsuch
resection,
severe
catabolic state with
○
Peripheral
TPN
must
be
given
through
a
large
diameter vein.
fistula and bowel resection such as Crohn’s disease.
○
Hyperosmolar
solution
can
lead
to
tissue
damage
if extravasation
— Peripheral TPN must be given through a large diameter
vein.
occurs.
— Hyperosmolar
solution can lead to tissue damage if extravasation
○ More commonly given via central vein.
occurs.
— More commonly given via central vein.
Image by Kevin Quinlan & Azlena Ali Beegan: PICC line (with consent).
Ø Central TPN:
¾ Hickmann line (dedicated tunneled catheter).
¾ PICC line (Peripherally Inserted central venous catheter).
¾ Risks of central venous catheterization include:
— Haematoma / haemorrhage.
— Line superinfection / infection to surrounding soft tissues.
— Line obstruction / kinking / malplacement.
— Damage to surrounding structures from malplacement, including:
— Pneumothorax.
— Air embolism.
— Cardiac dysrhythmias.
— Carotid artery dissection.
30
PRINCIPLES OF SURGERY
Ø TPN associated complications:
¾ Hyperosmolarity.
¾ Lack of glycaemic control.
¾ Nutrient deficiencies.
¾ Liver dysfunction, cholestasis and pancreatic atrophy.
¾ Fluid overload.
Ø Patients on TPN require
¾ Daily urea, electrolytes and glucose until stabilised on TPN.
¾ Liver function test (LFTs) twice weekly.
¾ Magnesium, Copper, Manganese, Zinc, Phosphate weekly.
31
NOTES
32
HERNIAS
HERNIAS
Chapter 22
Chapter
Hernias
Hernias
33
HERNIAS
Contents:
•
General Principles
•
Inguinal Hernia
•
Femoral Hernia
•
Other Hernias
•
Consent for Inguinal Hernia Repair
34
HERNIAS
GENERAL PRINCIPLES
Definition
Ø
A hernia is an abnormal protrusion of the contents of a cavity through a
weakness in its containing wall.
Aetiology
Ø
Congenital
— Persistent processus vaginalis (inguinal).
— Persistent umbilical opening.
Ø
Acquired
— Caused by a weakened abdominal wall and / or increased intra-
abdominal pressure.
— Weakened abdominal wall.
¾ Ageing
¾ Previous surgery (incisional hernia)
¾ Steroid use
¾ Postoperative surgical site infection
¾ Smoking
— Increased intra-abdominal pressure.
¾ Pregnancy
¾ Obesity
¾ Ascites
¾ Chronic cough
¾ Heavy lifting
Contents of a hernia
Ø
Peritoneal lining.
Ø
Omentum and/or bowel.
Herniae can be:
Ø
Reducible
— Contents re-enter containing cavity (usually the abdomen) either
spontaneously or with manipulation.
Ø
Irreducible / Incarcerated
— Hernia persists despite manipulation.
— May be due to a narrow hernia “neck” (“small defects are more dangerous than large defects”).
— At risk of strangulation.
Ø
Obstructed
— Kinked bowel Ò obstruction +/- strangulation of bowel segment.
Ø
Strangulated
— Ischaemia of the bowel within the incarcerated/obstructed hernia.
— Decreased lymphatic flow Ò increased venous pressure Ò
increased bowel oedema Ò impeded arterial inflow Ò infarction.
35
HERNIAS
Types of hernia to know about.
Ø
Inguinal hernia (>75% of all hernias)
Ø
Femoral hernia (<10% of all hernias)
Ø
Umbilical hernia
Ø
Periumbilical
Ø
Incisional
Ø
Spigelian
Ø
Obturator
_______________
Unusual hernia types
Illustrated by Kevin Quinlan: Richter’s Hernia.
Ø
Ø
Ø
36
Richter’s hernia: only part of the bowel circumference is trapped within the
hernial sac. As a result there is a partial bowel obstruction with vomiting but
the patient continues to pass flatus. Richter was surgeon in 1778.
Sliding hernia: a retroperitoneal structure such as the colon or urinary bladder slides down and forms the wall of the hernial sac.
Pantaloon hernia: both a direct and indirect hernia occur together.
HERNIAS
Illustrated by Kevin Quinlan: hernia types.
INGUINAL HERNIA
Epidemiology
Ø
Male : Female = 12:1
Ø
Two peaks in incidence: congenital < 5 years old; acquired > 50 years old.
_______________
Types of inguinal hernia
Ø
Can be direct or indirect according to their surgically defined relationship to
the inferior epigastric artery.
—
Indirect hernias are in the inguinal canal, descending to the scrotum.
¾ Leave the abdomen via the deep inguinal ring to follow an oblique course through the inguinal canal.
¾ The peritoneal sac may represent a patent or re-
opened processus vaginalis.
¾ May extend to the tunica vaginalis surrounding the testis.
Ø
Direct hernias protrude anteriorly through transversalis fascia (Hasselbach’s triangle).
Ø
Pantaloon hernia describes a combination of both.
37
HERNIAS
Location of an inguinal hernia
Ø
Above and medial to the pubic tubercle
—
Direct: Medial to the inferior epigastric artery.
—
Indirect: Lateral to the inferior epigastric artery.
Ø
Essential to understand inguinal and femoral hernias in detail.
Ø
Inguinal canal runs from the deep to superficial ring.
Ø
Inguinal ligament runs from ASIS to pubic tubercle.
Ø
Deep inguinal ring
— Formed through transversalis fascia.
— Lies 1-2 cm above the midpoint of the inguinal ligament.
Ø
Superficial inguinal ring
Ø
Formed through a v-shaped defect in external oblique aponeurosis.
Ø
Lies above and medial to the pubic tubercle.
Ø
Hasselbach’s triangle
— Inguinal ligament inferiorly.
— Inferior epigastric artery laterally.
— Rectus sheath medially.
— Direct hernias protrude directly through Hasselbach’s triangle
— Indirect hernias lie “in” the canal through a weakness in the
processus vaginalis
38
HERNIAS
Ø
Boundaries of the inguinal canal
—
Anterior wall
¾ External oblique aponeurosis covers entire canal and internal oblique covers the lateral one-third.
—
Posterior wall
¾ Conjoint tendon medially, transversalis fascia entire canal.
—
Superior wall
¾ Internal oblique and transversus abdominis (conjoint muscle).
—
Inferior wall
¾ Inguinal ligament.
Illustrated by Kevin Quinlan: inguinal canal.
Ø
Contents of the inguinal canal
—
3 Vessels
¾ Testicular artery & vein (Pampiniform plexus of veins)
¾ Artery & vein to the vas
¾ Cremasteric artery & vein
—
4 Nerves
¾ Nerve to the cremaster
¾ Sympathetic nerves
¾ Ilioinguinal nerve
¾ Genital branch of genitofemoral nerve
—
3 Fasciae
¾ External spermatic fascia
¾ Cremasteric fascia
¾ Internal spermatic fascia
—
3 Others
¾ Spermatic cord
¾ Vas deferens
¾ Lymphatics
39
HERNIAS
Clinical features
Ø
Patient may describe a lump.
Ø
Usually not symptomatic until exacerbated.
Ø
Symptoms are typically exacerbated by any condition which raises intra
abdominal pressure (chronic cough, obesity, constipation).
Ø
When exacerbated, cause dragging / aching sensation.
Ø
Indirect inguinal hernia: Usually asymptomatic in the morning, then symptoms develop throughout the day as the hernia moves down the canal.
An indirect hernia with a large deep ring defect behaves like a direct hernia.
Ø
Direct inguinal hernia: abdominal wall lump appears immediately on standing.
Diagnosis
Ø
Clinical examination is the method of diagnosis.
—
Examine systematically looking for the presence of a cough-
impulse and reduction of the hernia to it’s opening defect.
—
Once reduced, the location of the deep ring can be determined.
—
Differentiation between direct / indirect hernias often intraoperative.
—
Remember to stand the patient.
Ø
Ultrasound / CT
—
May be useful if equivocal diagnosis / obstruction suspected.
_______________
Management
Ø
Conservative
—
Elderly with significant morbidity.
—
Annual risk of incarceration 2-3 / 1,000 hernias per year.
Ø
Operative (Open / Laparoscopic Herniorrhaphy)
—
Congenital inguinal hernia should be repaired at the earliest possible opportunity because of increased risk of incarceration,
strangulation and testicular ischaemia.
—
Symptomatic inguinal hernias in adults should be repaired.
—
Open Lichtenstein tension free repair
¾ Utilises a patch of non-absorbable mesh to strengthen the posterior wall of the inguinal canal.
¾ Local anaesthesia plus sedation, or general anaesthesia.
—
Laparoscopic herniorrhaphy
¾ Indications are bilateral hernias or a recurrent hernia.
¾ The two main techniques are:
- Totally extraperitoneal (TEP) repair and transabdominal preperitoneal patch (TAPP) repair,
both of which require the use of mesh and are
considered tension-free repairs.
40
HERNIAS
Complications of inguinal hernia repair
Ø
Scrotal haematoma.
Ø
Wound infection.
Ø
Urinary retention.
Ø
Chronic pain / paraesthesia in the scrotum (or labium majora in females)
from damage to the ilio-inguinal nerve.
Ø
Testicular atrophy caused by inadvertent damage to the testicular artery.
Ø
Recurrence rates less than 1%.
— Infection most important risk for recurrence.
— Poor operative technique.
— Avoidance of mesh for reinforcement of weak musculature.
— Conditions such as chronic cough, constipation or bladder outlet
obstruction also contribute to recurrence.
_______________
FEMORAL HERNIA
Epidemiology
Ø
Female > male.
Ø
< 10 % of all hernias.
Ø
30% of all hernia repairs in women and < 1% of all hernia repairs in men.
Ø
More common in later life (>70 years).
_______________
Surgical anatomy
Ø
Boundaries of the femoral triangle
— Inguinal ligament superiorly.
— Medial border of sartorius muscle laterally .
— Medial border of adductor longus medially.
— Iliacus, psoas, pectineus and adductor longus form the floor.
— Superficial fascia and great saphenous vein form the roof.
Ø
Contents of the femoral triangle
— From medial to lateral (VAN): femoral vein, femoral artery, femoral
nerve.
Ø
Boundaries of the femoral canal
— Anteriorly: Inguinal ligament.
— Medially: lacunar ligament.
— Laterally: femoral vein.
— Posteriorly: pectineal ligament.
Ø
Contents of the femoral canal
— Lymph node (Cloquet’s node) and fat.
Ø
Location of femoral hernias
— Below and lateral to the pubic tubercle.
41
HERNIAS
Clinical features
Ø
Small lump immediately below the inguinal ligament and just lateral to its
medial attachment to the pubic tubercle.
Ø
Cough impulse rarely detected due to the narrow neck of the hernial sac.
Ø
Due to the narrow neck of a femoral hernia it is more likely to strangulate but
localizing signs are usually absent.
Ø
30% present with a small bowel obstruction.
_______________
Differential diagnosis
Ø
Femoral canal lipoma.
Ø
Saphena varix (SFJ varices).
Ø
Femoral lymph node.
Ø
Femoral artery aneurysm.
Ø
Femoral artery pseudoaneurysm (post angiography).
Ø
Sarcoma (leio- or rhabdomyosarcoma)
_______________
Management
Ø All femoral hernias should be surgically repaired.
42
HERNIAS
OTHER HERNIAS:
UMBILICAL HERNIA
True umbilical hernia
— Always congenital.
— Through umbilical cicatrix.
— May close spontaneously by 3 years of age.
— Following this there is little likelihood of improvement and surgical
repair should be considered.
Ø
Periumbilical
— Always acquired.
— Not through the umbilicus itself.
— Common in obese patients and multiparous women.
Ø
Management
Ø
True umbilical hernia should be surgically repaired after 3 years of age.
Ø
Periumbilical occasionally strangulate
— Risk / benefit assessed on a case-by-case basis.
_______________
INCISIONAL HERNIA
Ø
Ø
Up to 10% of laparotomy incisions eventually herniate.
Predisposing factors
— Postoperative wound infection.
— Abdominal obesity.
— Poor muscle quality (smoking, anaemia).
— Multiple operations through the same incision.
— Poor choice of incision.
— Inadequate closure technique.
Clinical features
Ø
Lump & defect: vary from small (more dangerous) to complete defects.
Ø
Incisional hernias may be asymptomatic at presentation but tend to progressively enlarge.
Ø
Rarely, they may cause strangulation.
Management
Ø
Repair is usually indicated for pain or strangulation.
Ø
Mesh used for larger defects (> 4 cm).
_______________
43
HERNIAS
SPIGELIAN HERNIA
Ø
Defect between lateral border of the rectus abdominis and linea semilunaris.
Ø
The hernial sac comes to lie interstitially between the layers of internal and
external oblique and transversus abdominis.
Ø
Difficult to diagnose.
Ø
Usually requires imaging (CT).
Ø
Direct surgical repair indicated.
Ø
Spiegel was a surgeon in the 1600s.
Illustrated by Kevin Quinlan: Spigelian Hernia.
______________
OBTURATOR HERNIA
Ø
Defect through obturator canal (lateral pelvis into thigh).
Ø
Causes medial thigh pain in cutaneous distrIbution of the obturator nerve.
Ø
Very challenging diagnosis - CT usually required.
Ø
High risk of obstruction.
Illustrated by Kevin Quinlan: Obturator Hernia.
44
HERNIAS
CONSENT FOR INGUINAL HERNIA REPAIR
Ø
Introduce yourself to the patient.
Ø
Ensure correct patient and correct side. Mark the correct side.
Ø
Establish what the patient knows about the procedure.
_______________
Explain the procedure
Ø
Hernias form when an area of the abdominal wall is weakened.
Ø
The bowel pushes out against the weak area in the abdominal wall, forming
a bulge.
Ø
Most hernia repairs are performed under general anaesthetic but may also
be performed using a combination of regional anaesthetic and sedation.
Ø
Can be performed using the laparoscopic or open method.
_______________
Open inguinal hernia repair
Ø
The surgery:
— The operation can be done as a day case. If you develop any complications you may have to spend longer in the hospital.
— A 5cm incision is made in the groin area.
— The intestines are placed into their correct position by excising the
hernial sac near the spermatic cord and repairing the weak area.
— The weak area is strengthened using a synthetic mesh (Tension free Lichtenstein repair).
Ø
Risks of the procedure:
— General risks of surgery and general anaesthesia: Nausea, vomiting, sore throat after the anaesthetic, cardiac, respiratory, DVT, PE risks depending on comorbidities.
— Risks specific to the procedure which are rare but include:
¾ Damage to blood vessels which may result in bleeding or a haematoma (collection of blood). The latter may settle
down on its own but require a repeat operation.
¾ Testicular atrophy (risk < 1%): if the the testicular artery is
damaged then the testicle itself may get damaged.
¾ Infection of the wound or mesh, requiring antibiotics. An infected mesh requires surrgical removal.
¾ Damage to nerves resulting in pain in the groin or the scrotum. This may resolve after the operation but in rare cases may persist. It happens in approx 4% cases.
¾ Recurrence (1%).
Ø
Post-operative care
—
The patient should not drive or operate machinery for 24 hours.
—
Routinely the patient is prescribed painkillers, but not antibiotics.
—
Avoid heavy lifting for 6-8 weeks.
45
NOTES
46
UPPER GASTROINTESTINAL SURGERY
Chapter 3
Upper Gastrointestinal Surgery
Illustrated by Kevin Quinlan: Oesophago-gastro-duodenoscopy
Contents:
•
Benign Oesophageal Disorders
•
Oesophageal Motility Disorders
•
Oesophageal Cancer
•
Gastric Cancer
•
Upper GI Bleeding
47
UPPER GASTROINTESTINAL SURGERY
BENIGN OESOPHAGEAL DISORDERS
GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)
Definition
Ø
A condition which develops when the reflux of stomach contents into the
oesophagus causes troublesome symptoms and/or complications
Ø
GORD can be separated into erosive and non-erosive disease
Ø
Also defined as an oesophageal pH of <4 for > 4% of a 24-hour period on pH
monitoring.
Epidemiology
Ø
GORD is the most frequently diagnosed upper GI disorder
Ø
Most common in middle aged adults
Pathophysiology
Ø
Reduced lower oesophageal sphincter tone
Ø
Increased intragastric pressure
Risk Factors
Ø
Family history of GORD, elevated BMI, heavy alcohol use, smoking pregnancy
Clinical features
Ø
retrosternal discomfort or heartburn
Ø
Acid reflux into pharynx
Ø
Commonly worse at night and after large meals.
Ø
Dysphagia may occur if there is associated ulceration or a stricture.
Ø
Globus (feeling of lump in throat).
Ø
Pulmonary aspiration (nocturnal coughing; hoarse voice)
Ø
may be associated with hiatus hernia
Complications
Ø
Ulceration
Ø
Stricture formation
Ø
Barrett’s oesphagus
Investigations
Ø
OGD should be performed in all new cases over the age of 45 to exclude
malignancy
Ø
Over the age of 45 reflux can be confirmed by 24h continuous pH monitoring.
Peaks of pH change must correspond to symptoms.
48
UPPER GASTROINTESTINAL SURGERY
Treatment
Ø
Medical
— Reduce acid reflux.
¾ Reduce smoking and weight.
— Counteract acid secretion.
¾ Proton Pump Inhibitors
— Symptomatic relief with antacids (e.g. Gaviscon).
— Increase gastric and oesophageal emptying.
¾ Promotility agents, e.g. metoclopramide
10mg tds PO.
Ø
Surgical
— Nissen’s Fundoplication: Wrapping fundus of the stomach around
the intra-abdominal oesophagus to augment high pressure zone
— Indicated for:
¾ Persistent symptoms despite maximal medical therapy.
¾ Large volume reflux with risk of aspiration pneumonia.
¾ Complications of reflux, including stricture and severe ulceration.
PEPTIC ULCER DISEASE
Definition
Ø
Injury leading to mucosal breakdown to the submucosa within the lower
oesophagus, stomach or duodenum
Introduction
Ø
Lifetime prevalence in general population estimated at 5-10%
Ø
Commonest sites: first part of the duodenum, gastric antrum, and lesser
curve of the stomach.
Ø
Incidence on decline likely due to widespread use of potent anti-secretory
medications and treatment of Helicobacter pylori.
Ø
Role of surgery is limited to the management of resistant ulcers and emergency management of perforated or bleeding ulcers.
Aetiology
Ø
Helicobacter Pylori, and the use of NSAIDS are the main risk factors for
both gastric and duodenal ulcers.
Ø
H. pylori infection leading to ulceration is poorly understood but likely is due
to inflammation initiated by H. Pylori and sustained by the combined effect
of gastric acid and pepsin secretion upon the mucosa of upper GIT.
Ø
Other Risk Factors: smoking, alcohol, Psychosocial stress, steroids
49
UPPER GASTROINTESTINAL SURGERY
Gastrinoma.
— Known as Zollinger-Ellison syndrome.
— Consists of islet cell tumor, secreting gastrin in association with acid hypersecretion and severe PUD.
— The majority of Zollinger-Ellison tumors are sporadic.
— Some occur in association with the multiple endocrine neoplasia
syndrome type 1 (MEN1).
Ø
Clinical Features
Ø
Often non-specific symptoms, nausea, epigastric pain.
Ø
If bleeding, Can present with haematemesis, melaena, and/or acute abdomen
Ø
Duodenal ulceration
— Hunger pains, nocturnal pain/early morning hours
— Relieved by food; pain is often cyclical
Ø
Gastric ulceration
— Postprandial pain. Pain triggered by food.
— Associated with weight loss and anorexia
— Pain less cyclical.
Complications “Anterior ulcers perforate / posterior ulcers bleed”
Ø
Bleeding
— Acute upper GI bleeding
— iron deficiency anaemia due to chronic low level bleeding
Ø
Perforation
Ø
Gastric Outlet obstruction
— Chronic scarring around pylorus
— always consider gastric malignancy as cause of outlet obstruction
Diagnosis and investigations
Ø
Oesophagogastroduodenoscopy (OGD)
— Biopsy urease test, known as CLO test (Campylobacter-Like Organism).
— Gastric antral mucosal histology
— Less commonly bacterial culture.
Ø
Urease testing
— To assess for presence of H. pylori can be performed on antral biopsies from gastroscopy or as a CO2 breath test.
Ø
Urea breath testing (UBT)
Ø
Stool antigen testing.
Ø
Serology.
Ø
Fasting serum gastrin levels- If Zollinger-Ellison syndrome suspected.
50
UPPER GASTROINTESTINAL SURGERY
Management
Ø
The control of predisposing factors:
— Eliminate proven H. Pylori infection by triple therapy.
1-2 weeks course of two antibiotics (eg. Amoxicillin 1g BD
and Clarithromycin 500mg BD) with proton pump inhibitor,
initially BD for 1-2 weeks, then continued OD for another
4-6 weeks.
Ø
Diminish irritant effects of acid-pepsin.
— Achieved with antacid drugs or alginate preparations.
Ø
The use of mucosal protective agents.
— eg. Sucralfate
Ø
The reduction of acid secretion:
— Proton pump inhibitors (omeprazole).
— H2 receptor blocking drugs (cimetidine, ranitidine).
Managing complications of peptic ulcer disease
Haemorrhage:
Ø
Typically results from erosion of a duodenal ulcer through the posterior wall
of the duodenum into the gastroduodenal artery.
Ø
See upper GI Bleed Section at the end of the chapter for more detail on
acute management
Perforation:
Ø
Declining incidence with advances in medical management.
Ø
Duodenal perforation is more common than gastric ulcer perforation.
Ø
Patients present with severe abdominal pain and peritonitis.
Ø
Diagnosis made by the presence of free air under the diaphragm on an
erect CXR.
Ø
The patient must be adequately resuscitated and a nasogastric tube should
be placed.
Ø
Treatment Ò surgical repair of the perforation. Usually, the ulcer is oversewn and secured with a plug of omentum.
Gastric outlet obstruction:
Ø
The pylorus/pre-pyloric area are common sites of chronic ulceration.
Ø
Healing with fibrosis leads to stricture formation and pyloric stenosis.
Ø
Patients present with episodic and projectile vomiting unrelated to eating.
Ø
On examination patients are dehydrated and undernourished
Ø
Abdominal examination reveals the presence of a succussion splash.
Ø
Biochemical analysis reveals a hypochloraemic hypokalemic metabolic
alkalosis.
Ø
PFA may demonstrate a hugely dilated stomach.
Ø
Management involves initial aggressive resuscitation.
Ø
Operative intervention aims to prevent further ulceration and establish gastric drainage.
51
UPPER GASTROINTESTINAL SURGERY
Surgical options include gastro-enterostomy and pyloroplasty or rarely a partial
gastrectomy.
BARRETT’S OESOPHAGUS
Definition
Ø
The replacement of the stratified squamous epithelium of the distal oesophagus with columnar epithelium by metaplasia
Introduction
Ø
Incidence of cancer in Barrett’s
— 1% per year develop adenocarcinoma
Ø
Follow-up: Regular endoscopic surveillance with systematic biopsy
Aetiology
Ø
A consequence of prolonged gastro-oesophageal reflux
Management
Metaplasia and dysplasia:
Ø
Medical or surgical reflux treatment do not usually lead to regression of
metaplasia.
High grade dysplasia and cancer:
Ø
Should be treated by resection in patients fit for oesophagectomy.
Ø
50% of patients with high-grade dysplasia will develop invasive adenocarcinoma.
_______________
52
UPPER GASTROINTESTINAL SURGERY
DYSPHAGIA AND ODYNOPHAGIA
Dysphagia
Ø
Difficulty swallowing
Causes of Dysphagia
Ø
Congenital: e.g. Oesophageal atresia
Ø
Acquired:
— Luminal: bolus, foreign body, oesophageal web, Plummer-Vinson
syndrome occurs in people with long-term (chronic) iron deficiency anaemia
— Intramural: Carcinoma, stricture, achalasia, GORD, oesophagitis,
oesophageal dysmotility disorder, scleroderma
— Extramural: Hilar lymphadenopathy, pharyngeal pouch, retrosternal goitre, lung carcinoma
— Neurological: Stroke, Myasthenia Gravis, Motor Neuron Disease
Odynophagia
Ø
Painful swallowing
Ø
Causes of Odynophagia:
— Trauma: Radiation, oesophageal burn, oesophageal rupture
— Foreign Body: Oropharyngeal or oesophageal
— GORD: Oesophagitis, oesophageal ulceration
— Infective: Pharyngitis, tonsillitis, oesophagitis (HSV/Candida), abscess
— Neoplasia: Pharyngeal/Laryngeal/Oesophageal carcinoma
— Motility-related: Achalasia, oesophageal dysmotlity disorders
— Other: Scleroderma
53
UPPER GASTROINTESTINAL SURGERY
Key Questions in Dysphagia History:
Symptom
Consideration
Degree of dysphagia
Solids, liquids, or both
complete Inability to swallow liquids is
a medical emergency & requires hospital admission
Progressive dysphagia is suspicious for malignancy
Sudden onset while eating suggests bolus
obstruction
Benign stricture formation due to reflux
Onset & duration of dysphagia
Long history of dyspepsia, reflux
and progressive dysphagia
Weight loss
Malignancy or poor feeding.
zenker diverticulum Pharyngeal pouch, Achalasia
Nocturnal cough
Haematemesis
Bleeding oesophageal lesion Peptic ulcer
may cause oesophageal stricture
Fatigue (due to anemia)
Anaemia is associated with Plummer-Vinson
syndrome, where it is linked with presence of
oesophageal web.
Anaemia could result from acute or chronic
blood loss.
Breathlessness
Bronchogenic carcinoma,
Symptom of anaemia
Recurrent aspiration pneumonia
Metastatic lung disease
Neurological symptoms
Oesophageal motility disorder
Polio
Myasthenia gravis
Bulbar palsy
Syringomyelia
54
UPPER GASTROINTESTINAL SURGERY
Investigations for Dysphagia
Investigation
Consideration
Bloods
Upper GI Endoscopy (+/- biopsy)
Barium Swallow
FBC (anaemia), U&E (dehydration)
1st line investigation
Used to diagnose dysmotility disorders
(‘Bird’s beak or ‘Rat’s tail’ appearance in achalasia)
Used to assess coordination and strength of
peristaltic movement in the oesophagus and
also the sphincter pressures.
Naso-oesophageal wire containing pH
probe placed in lower oesophagus for 24 hours
Used to diagnose GORD
DeMeester score is a composite measure
of reflux episodes and length of occasions
that pH is measured <4
Primary lung cancer
Mediastinal mass
Large retrosternal goitre
Air-fluid level in the mediastinal shadow,
which is often suggestive of the dilated oesophagus seen in achalasia
Aspiration pneumonia
Staging of oesophageal tumours
Staging of oesophageal tumours
& detecting submucosal disease
Manometry
pH Studies
Chest X-ray
CT Thorax Abdomen & Pelvis
Endoscopic USS
55
UPPER GASTROINTESTINAL SURGERY
HIATUS HERNIA
Illustrated by Kevin Quinlan: Sliding and rolling hiatus hernia
Definition
Ø The presence of part of or all of the stomach within the thoracic cavity, typically by protrusion through the oesophageal hiatus in the diaphragm
Introduction
Ø Very common with the majority being asymptomatic
Ø More common in females
Ø May or may not be associated with GORD
Ø Risk factors: Obesity
56
UPPER GASTROINTESTINAL SURGERY
Types
Ø
Type I: ‘Sliding hernia’
— Most common type (80%)
— Associated with GORD.
— Gastro-oesophageal junction slides up into the chest which can cause lower oesophageal sphincter to become less competent
Type II: ‘Rolling hernia’ or para-oesophageal hernia
— May result in volvulus or become incarcerated and cause obstruction
— Gastro-oesophageal junction remains in the abdomen but a bulge of
stomach herniates up into the chest alongside the oesophagus
— As the gastro-oesophageal junction remains intact, gross acid reflux
is less common
Ø
Clinical Features
Ø Mostly asymptomatic
Ø Dyspepsia & symptoms of GORD
Diagnosis & Investigations
Ø Chest X-ray (lateral chest shows air fluid level in posterior mediastinum)
Ø Barium swallow
Ø OGD (visualises mucosa but cannot reliably exclude hiatus hernia)
Ø CT scan (in emergencies)
Management
Conservative/Medical:
Ø Reduce acid production (stop smoking, lose weight, reduce alcohol)
Ø Counteract acid secretion (PPIs, antacids, mucosal protectants)
Ø Promote oesophageal and gastric emptying. Pro-motiliants (e.g. metoclopramide)
Surgical:
Ø Rarely required
Ø Indicated if persistent symptoms despite maximal medical therapy
Ø Elective procedure of choice is laparoscopic reduction of the hernia and
fixation (gastropexy)
Ø Occasionally achieved with a fundoplication (e.g. Nissen’s) if GORD symptoms predominate
Ø Rolling hiatus hernia should be repaired even if asymptomatic as it may
strangulate (which has a high morbidity and mortality rate), which needs
prompt surgical repair
57
UPPER GASTROINTESTINAL SURGERY
OESOPHAGEAL MOTILITY DISORDERS
Causes
Primary:
Ø Achalasia
Ø Diffuse oesophageal spasm
Secondary:
Ø Autoimmune rheumatic disorder (eg scleroderma)
Ø Chagas disease
American trypanosomiasis, is a tropical parasitic disease
caused by Trypanosoma cruzi. It is spread mostly by insects
Ø Diabetes mellitus
known as Triatominae, or "kissing bugs"
Ø Amyloid
Ø Intestinal pseudo-obstruction
Ø Myasthenia gravis
ACHALASIA
Definition
Ø Characterised by a high lower oesophageal sphincter (LOS) pressure and
failure of the relaxation of the sphincter. There is associated poor peristalsis
throughout the oesophagus.
Presentation
Ø Usually presents as difficulty swallowing and retrosternal chest pain.
Epidemiology:
— Usually affects people aged 25-60 years.
— 5% in childhood.
— Prevalence of 10 cases per 100,000.
Pathogenesis and aetiology
Ø Unknown, but there is a definite neurological defect involving Auerbach’s
myenteric plexus, with the vagi showing axonal degeneration of the dorsal
motor nucleus and nucleus ambiguous.
Investigations
Ø Endoscopy
Ø Barium swallow: Produces a false negative in 1/3 of patients.
Ø Dilation of the esophagus. The following features may be seen:
— Narrow oesophago-gastric junction with “bird-beak” appearance caused by the persistently contracted LOS
— Aperistalsis
— Poor emptying of barium
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UPPER GASTROINTESTINAL SURGERY
Manometry
Ø Absence of peristaltic waves in oesophagus.
Ø High resting intra-oesophageal pressure, impaired relaxation.
Ø Normal resting pressure is 0-30 mmHg.
Complications of achalasia
Ø Nocturnal aspiration.
Ø Bronchiectasis.
Ø Lung abscess.
Ø Carcinoma in 3%. Squamous cell carcinoma type in mid oesophagus.
Treatment of achalasia
Ø Balloon dilatation – works in about 70%, 3% risk of perforation.
Ø Heller’s cardiomyotomy – reflux after myotomy is common.
Ø Injection of botulinum toxin – injection into LOS, limited long term success.
_______________
DIFFUSE OESOPHAGEAL SPASM
Presentation
Ø Dysphagia for solids and liquids
Ø Atypical chest pain (may mimic angina-like chest pain)
Diagnosis
Ø Difficult, but manometry may reveal ‘nutcracker’ or ‘corkscrew’ oesophagus
with high amplitude peristalsis of long duration.
Treatment
Ø Nifedipine and reassurance.
_______________
CHAGAS DISEASE
Ø Chronic infection with Trypanosoma cruzi, a parasite native to Brazil.
Ø Causes destruction of intramuscular ganglion cells.
Ø Clinical picture is very similar to achalasia.
Ø It is also associated with cardiomyopathy, megacolon, megaduodenum
and megaureter.
_______________
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UPPER GASTROINTESTINAL SURGERY
SCLERODERMA AND OESOPHAGEAL DYSMOTILITY
Ø 80 % have oesophageal involvement.
Ø Oesophagitis is seen in CREST (Calcinosis, Raynaud’s, Oesophagitis, Scleroderma and Telangiectasia) syndrome.
Ø Adynamic oesophagus and reflux cause stricture.
Ø The lower oesophageal sphincter is found to be hypotensive on manometry,
unlike achalasia.
Ø Treatment: medical or a partial fundoplication.
OESOPHAGEAL TUMOURS
Aetiology
Ø Rare before the age of 50.
Ø At least half occur in the lower one third of the oesophagus with only 15%
occurring in the upper one third of the oesophagus.
Ø The aetiology of oesophageal carcinoma depends on the type of carcinoma.
Adenocarcinoma
Ø Rapidly increasing incidence in Europe, North America and Australia and has
squamous cell carcinoma in some of these areas.
Ø ♂:♀, 5:1
Ø The main pathological pathway is likely due to chronic GORD, causing metaplasia from squamous cell mucosa to specialised columnar epithelium
(Barrett’s oesophagus). This metaplasia then progresses to low grade dysplasia, then high-grade dysplasia, and eventually adenocarcinoma.
Ø Adenocarcinoma is relatively insensitive to radiotherapy and therefore surgery is the mainstay of treatment.
Squamous cell carcinoma
Ø Most common histological subtype globally, however, Incidence slightly reducing in western world.
Ø Commonest in Japan, northern China, and South Africa
Ø ♂:♀, 3:1.
Ø Pathogenesis typically initiated by carcinogenic substances in direct contact
with the oesophageal mucosa
Ø Associated with smoking, alcohol intake, diet poor in fresh fruit and vegetables, chronic achalasia, chronic caustic strictures and dietary nitrosamines (found in processed meat).
Ø May occur anywhere in the oesophagus.
Ø Squamous cell carcinomas are sensitive to radiotherapy and may be treated
with either radiotherapy or surgery.
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UPPER GASTROINTESTINAL SURGERY
Risk factors associated with oesophageal cancer
Adenocarcinoma
Squamous Cell carcinoma
Barrett’s oesophagus
GORD
Obesity
High fat intake
Cigarette smoking
High alcohol intake
High alcohol intake
Cigarette smoking
Nitrosamines in diet
Vitamin A, C deficiency
Coeliac disease
Strictures and webs
Achalasia
Peptic ulcer disease
Clinical features
Ø
Dysphagia with weight loss
— Any new symptoms of dysphagia, especially over the age of 45, should be assumed to be due to a tumour until proven otherwise.
Ø
Haematemesis
— Rarely the presenting symptom.
Ø
Incidental/screening
— Occasionally identified as a result of follow-up/ screening for Barrett’s metaplasia, achalasia, or reflux disease.
— Presence of high grade dysplasia in Barrett’s is associated with the presence of an occult adenocarcinoma in 30%.
Ø
Features of disseminated disease
— Cervical lymphadenopathy.
— Hepatomegaly due to metastases.
— Epigastric mass due to para-aortic lymphadenopathy.
Ø
Symptoms of local invasion
— Dysphonia in recurrent laryngeal nerve palsy.
— Cough and haemoptysis in tracheal invasion.
— Neck swelling in superior vena cava (SVC) obstruction.
— Horner’s syndrome in sympathetic chain invasion.
Diagnostic Investigations
Ø
OGD and biopsy.
Ø
Barium swallow only indicated for failed intubation or suspected post-
cricoid carcinoma (often missed by endoscopy).
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UPPER GASTROINTESTINAL SURGERY
Staging investigations (TNM Staging)
Ø
Local staging:
— Endoluminal ultrasound scans to assess depth of invasion.
Ø
Regional staging
— CT TAP to evaluate local invasion, locoregional lymphadenopathy, liver disease.
— Diagnostic Laparoscopy to assess for peritoneal disease.
Ø
Disseminated disease
— PET scanning may be used to exclude occult disseminated disease in patients otherwise considered for potentially curative
treatment.
Treatment - Multidisciplinary team discussion essential
Endoscopic Treatment
— Radiofrequency ablation, endoscopic mucosal resection, and endoscopic submucosal dissection are endoscopic techniques,
which are increasingly being used to treat early tumours.
Ø
Surgical:
— Surgery can be a single modality treatment for early tumour stages without nodal involvement (≤T2N0), and for failed endoscopic treatments.
— Surgery is combined with neoadjuvant therapy for more advanced oesophageal cancer
— Surgical resection is by oesophagectomy, which typically involves removal of most of the oesophagus, as well as the cardia ,and lesser curve of the stomach.
Ø
Common procedures are:
— Ivor Lewis Procedure (2 stage oesophagectomy):
¾ 2 stages- an abdominal stage and a thoracic stage, which
can use open or minimally invasive approaches.
¾ eg. laparoscopic mobilization of the stomach and distal
oesophagus, followed by thoracoctomy, thoracic lymphadenectomy, and intra-thoracic anastomosis
— McKeown Procedure( 3 stage oesophagectomy)
¾ Preferred for tumours proximal to the carina
¾ 3 stages: abdomen, thorax, and neck stages
— Transhiatal resection
¾ Abdomen - neck opened
— Neoadjuvant therapy with chemotherapy and radiotherapy may
help to downstage the tumour and allow surgical intervention.
Ø
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UPPER GASTROINTESTINAL SURGERY
Chemotherapy:
— In locally advanced disease (T3-T4), or in tumours with nodal involvement (N1-N3), chemotherapy or chemoradiotherapy must
be considered in addition to surgical management.
— Consider in metastatic disease
¾ improves survival compared to supportive management but
must weigh against side effects and quality of life
— Potentially curative.
— Good for adenocarcinoma.
—
Patient has to be relatively fit to tolerate it.
Ø
Radiotherapy:
— Better for squamous cell carcinoma.
— May cause strictures or fistulation.
Ø
Palliative:
— For patients with inoperable disease, symptom control and improvement of dysphagia is the mainstay of treatment
— Dysphagia can be treated by endoluminal self-expanding metal
stenting (SEMS). Risks include: perforation and stent migration
— Laser treatment
¾ Good for short, intrinsic tumours to restore swallowing.
¾ It may need repeating.
¾ Carries risk of perforation
Ø
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UPPER GASTROINTESTINAL SURGERY
GASTRIC TUMOURS
Classification and Aetiology
Ø
Gastric adenocarcinoma
Ø
Gastro-oesophageal junctional adenocarcinoma
Ø
Gastrointestinal stromal tumours (GISTs)
Ø
Neuroendocrine tumours (carcinoid tumours)
Ø
Lymphoma
Pathology
May arise from the tissues of the following:
Ø
Mucosa (adenocarcinoma)
— Commonest
— Age of incidence >50y
— ♂♀, 3:1
Ø
Connective tissue of the stomach wall (previously known as leiomyoma
or leiomyosarcoma, but part of the spectrum of disease called gastrointestinal stromal tumours (GISTs).
Ø
Neuroendocrine tissue (carcinoid tumours).
Ø
Lymphoid tissue (lymphomas).
Adenocarcinoma Risk Factors
Ø
Chronic gastric ulceration related to H. pylori.
Ø
Diet rich in nitrosamines (smoked or fresh fish, pickled fruit).
Ø
Epistein-Barr Virus
Ø
Family history of gastric cancer
Ø
Blood type A
Symptoms
Ø
Dyspepsia (new onset of dyspepsia over the age of 45 should be considered to be due to adenocarcinoma until proven otherwise).
Ø
Weight loss, anorexia, and lethargy.
Ø
Occasionally presents as acute upper GI bleeding.
Ø
Dysphagia uncommon unless involving the proximal fundus and
gastro-oesophageal junction.
Signs
Ø
Ø
Ø
Anaemia (iron deficiency due to chronic blood loss).
Palpable epigastric mass.
Palpable supraclavicular (Virchow’s) lymph node (Troisier’s sign). Suggests
disseminated disease.
Diagnosis and investigation
Ø
Diagnosis usually by gastroscopy and biopsy
— Barium meal may be required if gastroscopy contraindicated.
64
UPPER GASTROINTESTINAL SURGERY
Staging investigations include
— CT TAP to assess for distant metastases and local lymphadenopathy.
— Endoluminal ultrasound to assess for local disease.
— Diagnostic laparoscopy (for patients considered for potential resection) to exclude small volume peritoneal metastases.
Ø
Treatment
Ø
Surgical excision remains the gold standard treatment to provide cure.
Ø
Most patients present with advanced disease and therefore may not be
suitable surgical candidates.
Ø
Overall patient fitness, as well as tumour stage (according to TNM), determines suitability for surgery.
Ø
Surgical interventions include a total or partial gastrectomy with lymph
node dissection. Open and minimally invasive techniques can be used
Ø
Chemotherapy can be used for disseminated disease, but has no impact
on survival if used alone.
Ø
Palliation may be achieved with limited radiation therapy.
Ø
Palliative gastrojejunostomy for symptom control may provide good symptomatic relief.
Partial/Total Gastrectomy Complications:
Ø
Early
—
Haemorrhage
—
Acute pancreatitis
—
Anastomotic leak
—
Duodenal stump disruption
—
Respiratory compromise
Ø
Late
—
Dumping syndrome.
¾ General weakness, light-headedness, sweating
¾ Early: rapid transit of hyperosmolar solutions
¾ Late: hypoglycaemia due to increase insulin secretion
—
Bile reflux and vomiting
—
Diarrhoea
—
Recurrent stomal ulceration
—
Metabolic abnormalities.
¾ Iron deficiency
¾ Vitamin B12 deficiency
Prognosis:
Ø
Overall prognosis remains poor.
Ø
Five-year survival for patients with stage I disease (limited to mucosa) is
66%.
Ø
10% five-year survival with stage III disease (regional lymph node involvement).
65
UPPER GASTROINTESTINAL SURGERY
CONSENT FOR OESOPHAGO-GASTRO-DUODENOSCOPY
Illustrated by Kevin Quinlan: Oesophago-gastro-duodenoscopy
Explain to patient what the procedure involves
Ø
Inspection of the upper GI tract (oesophagus, stomach and upper intestine)
with a flexible endoscope (a tube smaller than the size of your little finger
with a camera in it).
Ø
The team will be able to take photographs, make videos and take samples
of the tissues, this is painless. These samples will be investigated and the
photographs can be filed with your permanent records.
Ø
Tell the patients to assume that they will be in the endoscopy department
from 1-3 hours (emergencies will have priority).
Ø
Explain to patient they can opt to be sedated or they can opt not to have
sedation and instead have a local anaesthetic throat spray and remain
awake for the procedure.
Intravenous sedation
Ø
Typically given IV Midazolam (a benzodiazepine) as sedation
Ø
Be cautious for benzodiazepine overdose
Ø
Always have Flumazenil (benzodiazepine antagonist) available
— They will be slightly drowsy and relaxed but not unconscious. They may not be able to remember the procedure.
— They can breathe normally throughout the procedure through their nose.
66
UPPER GASTROINTESTINAL SURGERY
— If you opt for sedation you may not operate machinery, drive, consume alcohol, or sign legally binding documents for 24 hours
after receiving the medication and you need someone to accompany you home. very IMPORTANT
Preparation for the OGD
Ø
The stomach must be empty, therefore no eating for 6 hours before the endoscopy. Small amounts of water are safe up to 2 hours before endoscopy. Tell patient routine medications may be taken; however
if they are currently on medications to reduce acid in the stomach please
stop these 2 weeks before the scheduled endoscopy.
Ø
Tell patient to please inform the staff if they are taking any blood thinning
agents like aspirin, warfarin, NOACs or clopidogrel. Also inform of any
allergies to latex or sedative drugs.
Risks associated with the procedure.
Ø
Note: these are extremely rare (1 in 2000 cases)
Ø
Perforation of the esophagus or lining of stomach
Ø
Bleeding
Ø
Damage to teeth
Ø
Risks associated with sedation
Ø
Aspiration
Ø
Numbness, risk of scalds
Ø
Sore throat.
67
UPPER GASTROINTESTINAL SURGERY
UPPER GASTROINTESTINAL BLEEDING
Key Facts
Ø
Bleeding from oesophagus, stomach or duodenum (Above Ligament of
Trietz)
Ø
Haemetemesis: Vomiting of blood
Ø
Melaena: Black ‘tarry’ stools due to digestion of Hb by intestinal bacteria
Ø
PUD is the most common cause (35-50%)
Ø
Variceal bleeding should always be high on the list of differentials as it is the
cause of up to 9% of upper GI bleeds and can be rapidly fatal
History
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Haemetemesis & melaena
Haematochesia in 15% (brisk upper GI bleed)
Abdominal pain (PUD/gastritis)
Heartburn, reflux, dyspepsia (background of PUD)
Dysphagia, weight loss (Upper GI malignancy)
Features of chronic liver disease e.g. Jaundice (Oesophageal varices)
Features of anaemia (fatigue, syncope, dyspnoea, chest pain)
Background of PUD, chronic liver disease, varices, GI malignancy
Previous endoscopy
Medications: Aspirin/Plavix, Warfarin/NOAC, NSAIDs, steroids
Physical Exam
Ø
Vitals (tachycardia, hypotension, tachypnoea, reduced urine output)
Ø
Reduced cap refill, cool extremities, reduced JVP, reduced GCS
Ø
Visible active bleeding (haemetemesis/melaena)
Features of chronic liver disease
— Ascites, jaundice, spider naevi, gynecomastia, caput medusae,
hepatomegaly
Ø
Abdominal exam
— Tenderness? Guarding? Masses?
Ø
PR exam
— Masses? Fresh blood? FOB positive?
Ø
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UPPER GASTROINTESTINAL SURGERY
Differential Diagnosis
Oesophageal
Gastric
Duodenal
Varices
Malignancy
Ulcer
Oesophagitis
Mallory-Weiss tear
Varices
Malignancy
Ulcer
Gastritis
Dieulafoy lesion
Ulcer
Malignancy
Vascular malformation
(such as aorto-enteric
fistula)
Investigations
Ø
FBC
— Check Hb and platelets
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Ø
U&E
— Disproportionately raised urea to creatinine
Coagulation screen
—
Check for underlying coagulopathy/INR
LFTs
— Evidence of chronic liver disease or liver mets
— Derrangement resulting in coagulopathy
Group & cross-match 4 units
Erect Chest X-ray, ECG, ABG
NG tube & aspirate
— Can help determine if upper GI or lower GI bleed
OGD
CT angiography/Angiography
Management of Unstable Upper GI Bleed
Ø
ABCDE: Protect airway, high flow O2
Ø
Keep NPO
Ø
IV cannula x2 (Large Bore)
Ø
Send full bloods as above (including group & save +/- cross-match)
Ø
IV fluids
— Bolus 10-20ml/kg if hypotensive
Ø
Urinary catheter
— Monitor hourly ins/outs
Ø
Transfuse with cross-matched blood
— Maintain Hb >8g/dL (10 if cardiovascular disease)
— Consider O negative blood if unable to wait for type specific blood
Ø
Correct clotting abnormalities
— Consider Vit K, FFP, PCC if high INR
Ø
IV PPI infusion
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UPPER GASTROINTESTINAL SURGERY
Ø
Ø
Ø
— Reduce rebleeding & operative intervention for bleeding PUD
IV octreotide/vasopressin
— Reduces portal pressures in variceal bleed
Sengstaken Blakemore tube may be required in massive variceal bleed
(Found in the fridge - ward/theatre/resus)
Inform the following:
— Senior colleague
— Surgical on call
— Endoscopy
— Anaesthetics
— HDU/ICU
— Operating theatre
Ø
Urgent OGD for diagnostic & therapeutic purposes
— Therapeutic options include:
¾ Adrenaline injection
¾ Heater probe coagulation
¾ Sclerotherapy
¾ Banding of varices
Ø
Surgery may be required if:
— Massive haemorrhage requiring ongoing resuscitation
— Failed endoscopic management
— Rebleeding
Rockall Score:
0
1
Age (A)
<60
60-79
Shock (B)
Nil
HR>100
Co-morbidity
Nil major
(C)
Diagnosis
Mallory-Weiss
All other Dx
(D)
tear
Evidence of
None
Bleeding (E)
Risk of mortality post-GI bleed:
<3 = Good prognosis
>8 = Poor prognosis
70
2
3
80+
SBP<100
IHD/CCF,
Renal/liver
major morbidity failure
GI
malignancy
Blood,
spurting vessel,
adherent clot
NOTES
71
NOTES
72
HEPATOBILIARY SURGERY
Chapter 4
Hepatobiliary Surgery
73
HEPATOBILIARY SURGERY
Contents:
•
Jaundice
•
Gallbladder Disease
•
Pancreatitis
•
Pancreatic Carcinoma
74
HEPATOBILIARY SURGERY
JAUNDICE
Key Facts
Ø
Ø
Normal serum Bilirubin 3-17mmol/L
Jaundice is clinically present at >35mmol/L
Aetiology: Jaundice is categorised based on the site of the underlying cause/disease.
Pre-hepatic (Haemolytic) – Unconjugated hyperbilirubinaemia
— Autoimmune haemolytic anaemia.
— Congenital (e.g: hereditary spherocytosis, sickle cell disease).
— Transfusion reactions.
— Drug toxicity.
Ø Hepatic
— Hepatic unconjugated hyperbilirubinaemia.
a mutation in the UGT1A1 gene which
¾ Gilbert’s
results in decreased activity of the
bilirubin uridine diphosphate
¾ Crigler-Najjar syndromes.
glucuronosyltransferase
— Hepatic conjugated hyperbilirubinaemia.
¾ Viral hepatitis.
¾ Alcoholic liver disease.
¾ Toxic drug jaundice.
¾ Metastatic disease.
¾ Dubin-Johnson Syndrome
¾ Rotor Syndrome
Ø Post-hepatic (obstructive)
— Intraluminal.
Choledocholithiasis occurs when a gallstone
blocks the common bile duct and bile cannot flow
¾ Choledocholithiasis
past it, instead backing up into the liver
— Mural abnormalities.
¾ Biliary stricture
¾ Primary sclerosing cholangitis
— Extrinsic compression of the bile ducts.
¾ Carcinoma of the head of pancreas, ampulla of Vater
or bile duct.
¾ Chronic pancreatitis
¾ Enlarged lymph nodes in porta hepatis.
¾ Mirizzi’s syndrome: external biliary compression from a stone impacted in the neck of the gallbladder.
Ø
75
HEPATOBILIARY SURGERY
History and Presentation
Ø Have you noticed any change in the colour of your urine or bowel
motions?
— Dark urine with pale clay colour stool is classically associated with
obstructive jaundice.
Ø
Ø
Ø
Ø
Ø
Do you have any pain? Can you describe the pain?
— Any pain associated with jaundice should be explored and noted:
— Is it?
Intermittent and severe:
¾ Biliary colic and CBD stones
Dull pain in the RUQ:
¾ Viral hepatitis and cholestatic jaundice
Painless:
¾ Carcinoma of the pancreas, haemolytic anaemia.
Associated fever or preceeeding flu-like illness: Chlorpromazine is a phenothiazine (FEEN-oh-THYEa-zeen) that is used to treat psychotic disorders such
¾ Infective hepatitis
as schizophrenia or manic-depression in adults.
Chlorpromazine is also used in adults to treat nausea
and vomiting, anxiety before surgery, chronic hiccups,
acute intermittent porphyria, and symptoms of
tetanus.
Are you on any medications?
— Recent medications should be recorded.
— Many drugs can cause cholestatic jaundice even after one dose e.g:
Chlorpromazine.
Ø Do you have any other symptoms such as fever, itching or tiredness?
— Lethargy and general malaise along with a flu-like illness may be
associated with hepatitis.
— Ascending cholangitis (Charcot’s triad):
¾ RUQ pain
¾ Jaundice
¾ Fever and rigors
— Cholestatic/Obstructive jaundice is often accompanied by pruritus
Ø
Ø
Ø
Ø
76
Social history
— Contact with known hepatitis carriers
— Blood transfusion,
— Intravenous drug abuse
— Risky sexual practices
Foreign travel
— Asia and the Far East increases risk of hepatitis A.
Excessive Alcohol intake
HEPATOBILIARY SURGERY
Physical Examination
General inspection
— Signs of liver cirrhosis:
¾ Asterixis/Liver flap (hepatic encephalopathy)
¾ Clubbing
¾ Dupuytren’s contracture
¾ Leukonychia
¾ Palmar erythema
¾ Bruises (bleeding tendencies)
¾ Gynaecomastia
¾ Muscle wasting
¾ Spider naevi (>3 in area of Superior Vena Cava distribution
pathological)
Ø
Abdominal examination
— Abdominal signs of cirrhosis:
¾ Ascites - Hypoproteinaemia or intra-abdominal malignancy
¾ Caput medusae - Due to portal hypertension associated with chronic liver disease.
¾ Splenomegaly.
¾ Hepatomegaly is common in both hepatic and posthepatic
jaundice. Note the size and texture of the liver:
— Large, tender and smooth liver in liver failure.
— Large and irregular may indicate the presence of
metastases.
¾ Murphy’s Sign: Place your right hand at the right costal margin in the mid-clavicular line and ask the patient to take a deep breath in. If pain causes cessation of
inspiration this is a positive test. It suggests gallbladder
inflammation.
Ø
Courvoisier’s law: A painless, palpable gallbladder in a patient with jaundice is
unlikely to be due to gallstone disease and may suggest malignant obstruction
of the ducts
Complete the examination with a digital rectal examination
Note: Acute cholecystitis does not cause Jaundice. In order for Jaundice to be
present with gallstone disease, the gallstone disease must be causing some
sort of blockage (eg, ascending cholangitis, Mirizzi Syndrome, choledocholithiasis etc)
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HEPATOBILIARY SURGERY
Investigations for a jaundiced patient:
Haematology and Biochemistry
Ø
Liver function tests (LFTs)
Unconjugated bilirubin
Haemolytic
Hepatocellular
Obstructive
↑
↑
Normal
↑↑
Alkaline phosphatase
Normal
Normal
Gamma glutamyl transferase
Normal
Transaminase
Normal
↑
Lactate dehydrogenase
Normal
↑
↑
↑↑
Normal
Normal
Full blood count
— Elevated WCC with acute cholecystitis or cholangitis
Ø Urea, Creatinine and electrolytes
— To assess hydration and guide fluid resucitation.
— Hepatorenal syndrome
Ø Coagulation profile
— PT/APTT are markers of liver function.
— Vitamin K deficiency with obstructive jaundice impaires function of
clotting factors II, VII, IX, X causing an increased PT.
They are vitamin K dependent factors
Ø Hepatitis serology
— Hepatitis A, B and C.
Ø Autoantibodies (AMA, ANA, Anti-SM)
— Performed in suspected autoimmune hepatitis or primary biliary
cirrhosis.
Ø Amylase
— Acute or chronic pancreatitis due to lower CBD stone
Ø Urinary analysis
— Presence of bilirubin in urine can be tested with a simple ward
dipstick test.
Ø
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HEPATOBILIARY SURGERY
Imaging
Ultrasound
— Cholelithiasis.
— Dilated biliary ducts (intra and extrahepatic) associated with
obstruction
— Architectural disturbances of the liver itself associated with liver
parenchymal disease.
— Pancreatic masses.
Ø
Magnetic resonance cholangiopancreatography (MRCP)
— For suspected extrahepatic obstruction with no cause seen on
ultrasound.
Ø
Liver
Ledt Kidney
Gallstone with
sludge in biliary
tree
Image by Anthony Hoban: MRCP (with consent)
79
HEPATOBILIARY SURGERY
Image by Anthony Hoban: ERCP (with consent)
Contrast-enhanced CT
— Preferable to ultrasound if neoplastic obstruction is suspected
— Better definition of mass lesions and general location of CBD
obstruction.
— Detailed pancreatic imaging
Ø
Liver biopsy
Ø When no extrahepatic cause of jaundice is found (ie: No duct dilatation,
No evidence of haemolysis).
Ø May indicate the cause of liver dysfunction or provide histological proof
of metastatic disease.
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HEPATOBILIARY SURGERY
Management
General treatment
— Correct dehydration.
— Monitor urinary output.
— Check clotting times.
¾ Vitamin K should be administered if PT is prolonged
— Ensure adequate nutrition.
¾ Dietitian review
¾ Enteral feeding
¾ Rarely surgical gastrostomy or jejunostomy tube
Ø Specific treatment cuts the muscle (sphincter) between the common
— Acute presentation bile duct and pancreatic duct.
¾ ERCP +/- Sphincterotomy +/- Stent insertion
¾ Percutaneous transhepatic cholangiogram
¾ Surgical drainage
— Elective presentation
¾Haemolytic jaundice
— Steroids for autoimmune cases
— Splenectomy
¾ Obstructive jaundice
— ERCP for asymptomatic uncomplicated stones.
— Surgical drainage.
¡ Cholecystojejunostomy for failed interventional
treatment The surgical formation of a communication between the
gallbladder and the jejunum
—Surgical resection.
 Whipple’s pancreaticoduodenectomy
for pancreatic tumours
¾ Hepatic jaundice
— Treat the causative agent and support liver function.
— Transplantation in specific circumstances.
Ø
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HEPATOBILIARY SURGERY
GALLBLADDER DISEASE
Key Facts
Ø Present in 10% of people >50 years of age
Pathological Features
Ø Bile has three major components:
— Bile salts
— Phospholipids
— Cholesterol
Ø
Types of gallstones:
— Pure cholesterol 10%
— Pure pigment 10%
— Mixed 80%
Predisposing conditions
Ø Increasing age
Ø Female
Ø Obesity
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HEPATOBILIARY SURGERY
Ø
Ø
Ø
Ø
Ø
Multiparity
Chronic haemolytic disorders
Long term parenteral disorders
Rapid weight loss
Previous surgery (e.g: vagotomy or resection of terminal ileum)
Common Presentations
Ø Asymptomatic Gallstones
— In the US, approx 30% of patients with cholelithiasis come to surgery.
— The current practice is to operate only on symptomatic patients.
Biliary Colic / Gallstone colic
— Intermittent severe epigastric pain, usually associated with
restlessness, nausea and vomiting.
— Mostly resolves in few hours.
Ø
Acute Cholecystitis
— 80% of cases results from obstruction of the cystic duct by a gallstone
impacted in Hartmann’s pouch.
— Severe, continuous right upper quadrant pain.
— Often radiates to the back.
— Usually associated with anorexia and pyrexia.
Ø
Murphy’s sign: Tenderness over gallbladder during inspiration.
Complications of acute cholecystitis:
— Empyema or abscess of the gallbladder.
— Perforation with biliary peritonitis.
— Gallstone ileus via a cholecystoenteric fistula.
— Jaundice due to compression of the adjacent common bile duct by
pressure (Mirizzi syndrome).
Ø
Chronic Cholecystitis
— The most common form of symptomatic gallbladder disease.
— Clinical examination may be unremarkable.
— During an attack, patients may report RUQ tenderness.
— Adequate analgesia and routine elective cholecystectomy is sufficient
in most patients.
— Medical management is rarely advised
— Ursodeoxycholic acid reduces cholesterol in bile by inhibiting cholesterol secretion and is occasionally used to reduce gallstone size.
Ø
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HEPATOBILIARY SURGERY
Mucocele
— Stones in the neck of the gallbladder, bile is absorbed, but mucus
secretion continues, producing a large tense globular mass in the right
upper quadrant.
Ø
Ø
Empyema
— Abscess of the gallbladder.
Ascending/Bacterial Cholangitis
— A bacterial infection of the biliary tract, which arises from obstruction
of the ducts.
— Causes of cholangitis include
¾ Principal: choledocholithiasis, biliary stricture, neoplasm.
¾ Less common: chronic pancreatitis/pseudocyst, ampullary
stenosis.
— Choledochlithiasis: Approx. 15% of patients with stones in the gallbladder are found to harbor calculi within the bile ducts. It is therefore common for patients to present with cholangitis due to choledocholithiasis despite a previous cholecystectomy.
— The symptoms of cholangitis (Charcot’s triad) are:
¾ RUQ pain
¾ Jaundice
¾ Fever and rigors
— Treatment is with IV fluids, antibiotics and to relieve the obstruction.
— The following options should be considered:
¾ ERCP and endoscopic sphincterotomy. Unlikely to be successful in patients with large stones (>2 cm).
¾ Percutaneous cholangiography is used where an ERCP
is unsuccessful.
¾ When the common duct is explored surgically through a
choledochotomy, a T tube is usually left in the duct. This (now
uncommon) technique allows for repeat cholangiograms and
extractions of residual stones.
Ø
Differential diagnosis
The differential diagnosis for gallstones includes other common causes of an acute
abdomen:
Acute peptic ulcer (especially duodenal) with or without perforation
Ø History of epigastric pain relieved by food or antacids.
Ø Acute pancreatitis, especially if cholecystitis is accompanied by an elevated
amylase.
Ø Acute appendicitis in patients with a high caecum
Ø
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HEPATOBILIARY SURGERY
Ø
Ø
Severe RUQ pain with associated high fever and local tenderness may develop in Fitz-Hugh-Curtis syndrome (acute gonococcal perihepatitis).
Medical causes of RUQ pain include right lower lobe pneumonia or a myocardial infarction
Diagnosis and investigation
Ø Bloods
— FBC
— CRP
— U&E - biochemical signs of dehydration
— LFTs - An elevated bilirubin and an elevation in the canalicular enzymes (Alkaline phosphatase and gamma glutaminase) may be
transient or as a result of a stone impacted in the CBD.
— Blood culture (if pyrexia)
— Serum amylase - in acute presentations
¾ Amylase may be elevated in the event of a gallstone pancreatitis
Ø Ultrasound. Procedure of choice; identifies stones, determines wall thickness,
and assesses ductal dilatation.
— Ultrasonographic Murphy’s sign.
Ø MRCP
— If the ducts are found to be dilated on ultrasound the next investigation is to perform an MRCP.
— This can more accurately identify stones in the duct or other causes
of the obstruction in the biliary tract.
— If a stone is identified the patient can then proceed to either an ERCP
or percutaneous cholangiography.
Treatment of Acute Cholecystitis
Ø Patients are initially treated with:
— Analgesia
— IV fluids
— Antibiotics
— Oral intake is restricted
Ø Then either:
— Manage the patient expectantly (with continued antibiotics and supportive care) and plan an elective cholecystectomy after approx
6 weeks
— Perform cholecystectomy during the index admission unless there
are specific contraindications to surgery (eg, serious concomitant
disease).
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HEPATOBILIARY SURGERY
Cholecystectomy
— Routinely laparoscopic; often as a day case.
— Immediate or interval cholecystectomy
— Indicated for:
¾ Symptomatic gallstones
¾ Asymptomatic patients at risk of complications (diabetics,
history of pancreatitis, long-term immunosuppressed).
— Risks of laparoscopic cholecystectomy.
¾ Conversion to open operation, >5%
¾ Bile duct injury, <1%
¾ Bleeding, 2%
¾ Bile leak, 1%
— Contraindications to laparoscopic cholecystectomy
¾ Generalized abdominal sepsis
¾ Major bleeding disorders
¾ Late pregnancy
¾ Intra abdominal malignancy
Ø
Consent for laparoscopic cholecystectomy
Consent taking of a patient for a laparoscopic cholecystectomy includes outlining
not only how the procedure itself is done and the indications involved but also any
complications that may arise. Consent should be taken by the surgeon performing the
operation.
Ø Introduction to patient and explanation of what you are going to discuss.
Ø Assess patient’s current level of understanding of procedure/indication/etc.
Ø Explanation of procedure:
— Procedure occurs under general anaesthetic in order to relax the
patient’s muscles and to prevent them from experiencing discomfort or
pain.
— 3-4 small incisions will be made in the abdomen, 1 for the camera and
others for surgical instruments (demonstrate on patient’s abdomen).
— The patient’s abdomen will be insufflated with gas (carbon dioxide) to
allow the surgeons to better visualize the anatomy.
— The surgeons will remove the gallbladder through the umbilical incision.
— The patient will be woken up by the anaesthetist and taken to the
post-operative recovery room. They will feel quite drowsy.
— Preoperative preparation for the patient includes fasting from midnight the night before the procedure and they may be asked to
hold some of their medications.
Ø Discuss the indications for the procedure.
Ø Discuss possible complications of the procedure:
— General to laparoscopy: pain, bleeding, infection.
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HEPATOBILIARY SURGERY
— Postoperative complications including atelectasis, shoulder tip pain,
thromboembolic events (DVT/PE), urinary tract infection, wound infection.
— Specific to laparoscopic cholecystectomy:
¾ 5% risk of conversion to open cholecystectomy, requiring
larger incision and possibly longer recovery time.
¾ <1% risk of damage to the CBD requiring a second operation
(choledochojejunostomy).
¾ Bile duct leak leading to jaundice and requiring placement of
percutaneous drainage tube.
¾ Retained bile duct stones.
¾ Mortality risk 0-1%
Ø If the procedure is done on day case basis, patient may go home on the day
of surgery; otherwise they may be in hospital longer if a complication occurs.
They should return to ordinary activity by day 5-10 post-op.
Ø May require readmission or visit to GP if the patient develops fever, severe
pain/nausea/vomiting, or if they notice yellowish colour to their skin or eyes.
Ø Assess the patient’s overall understanding of information and ask if they have
any questions.
Illustrated by Anthony Hoban: Liver, pancreas, gallbladder and biliary tree.
87
HEPATOBILIARY SURGERY
PANCREAS
ACUTE PANCREATITIS
Key Facts
Ø Pancreatitis is an inflammatory process of the pancreas, resulting in release of
inflammatory cytokines and pancreatic enzymes (amylase, trypsin, lipase etc),
initiated by pancreatic injury.
Ø It can vary from a mild attack to developing into full blown SIRS (systemic
inflammatory response syndrome)
Epidemiology:
Ø It is a common acute illness, with an annual incidence ranging from 10 to 40
per 100,000.
Ø Overall mortality should be less than 10% of patients admitted with acute
pancreatitis, with a mortality rate around 30% in those with severe disease.
Aetiology: (“ I GET SMASHED” mnemonic)
Ø Idiopathic
Ø Gallstones (60%) It is hypothesized that gallstone obstruction of the ampulla
of Vater allows bile reflux into the pancreatic duct thus activating enzymes in
the pancreas. Small stones may cause a transient obstruction prior to passing,
while larger stones tend to become impacted in the distal end of the common
bile duct.
Ø Ethanol / Alcohol (30%).
Ø Trauma
Ø Steroids
Ø Mumps and other infections
— Hepatitis A, B or C.
— Coxsackievirus.
— HIV.
Ø Autoimmume
Ø Spider bites / Scorpion stings
Ø Hypertriglyceridemia / Hypercalcaemia
Ø ERCP
Ø Drugs and toxins.
— Metronidazole, tetracycline,
— Azathioprine, mercaptopurine.
— H2 blockers.
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HEPATOBILIARY SURGERY
Presentation
Ø
Ø
Ø
Ø
Ø
Sudden onset of epigastric pain radiating through to the back.
Relief may sometimes be obtained by sitting forward.
Nausea and vomiting.
Clinical examination depends on the severity of the attack but ranges from
mild epigastric tenderness with minimal associated systemic features to those
with florid SIRS (tachycardic and hypotensive) and generalised peritonitis.
Left flank ecchymosis (Grey-Turner’s sign) and periumbilical ecchymosis
(Cullen’s sign), seen in haemorrhagic pancreatitis.
The severity of the attack and the associated mortality from acute pancreatitis is
determined by different scoring systems (RANSON criteria, Glasgow Imrie criteria and
APACHE scoring systems). The greater the numbers of criteria present the higher the
associated mortality.
Ø
RANSON criteria
— Criteria on Admission:
¾ Age > 55
¾ WCC > 16 x 109/L
¾ Glucose > 10 mmol/L
¾ LDH > 350 IU/L
¾ AST > 250 IU/L
— After 48 hr of admission:
¾ Fall in hematocrit>10%
¾ Increase urea >1.98mmol/L ¾ Calcium <2 mmol/L ¾ pO2 <8kPa
¾ Base deficit >4 mmol/L
¾ Fluid needs >6 L/48 hrs —
—
—
—
0-2 point:
3-4 points:
5-6 points:
>7 points:
1 point
1 point
1 point
1 point
1 point
1 point
1 point
1 point
1 point
1 point
1 point
1% predicted mortality rate (MR)
15% predicted MR
40% predicted MR
100% predicted MR
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HEPATOBILIARY SURGERY
Glasgow criteria
— It is scored through the mnemonic, PANCREAS:
¾ P - paO2 <8kpa
¾ A - Age >55 years old
¾ N - Neutrophilia - WCC >15x10(9)/L
¾ C - Calcium <2 mmol/L
¾ R - Renal function, Urea >16 mmol/L
¾ E - Enzymes: LDH >600 iu/L; AST >200 iu/L
¾ A - Albumin <32g/L (serum)
¾ S - Sugar: blood glucose >10 mmol/L
— Score > 3: severe pancreatitis (organ failure, complications, surgical
intervention)
— Score < 3: mild pancreatitis (minimal organ dysfunction, supportive
care only)
Ø
Differential Diagnosis
Ø Differential diagnoses of acute pancreatitis
— Gastritis
— Peptic ulcer disease
— Biliary Colic
— Cholecystitis
— Choledocholithiasis
Investigations
Bedside - ECG, urine dipstick.
FBC, LFTs, Electrolytes, Calcium, Urea, Albumin, Glucose.
Amylase - above 3 times normal level (i.e. > 300) supports diagnosis. Level
is not an indicator of severity and can be normal on admission. In acute on
chronic pancreatitis amylase increase is often absent.
Lipase and urinary amylase - can also be used and stays elevated longer.
CRP useful indicator of progress and response to treatment
Arterial blood gas - pH, PO2, lactate.
Imaging
— Chest X-ray: to rule out free air under diaphragm.
— Abdominal X ray may demonstrate a ‘sentinel loop’ of dilated adynamic small bowel in the center of the abdomen. It may also demonstrate a ‘ground-glass’ appearance of a peritoneal exudate. Not
routinely indicated.
— Ultrasound abdomen should be performed within 24 hours of presentation to determine the presence or absence of gallstones.
— CT used to judge severity/complications, usually considered at 4-5
days after presentation in mild to moderate cases.
— Endoscopic ultrasound should be considered for patients without an
identified aetiology as this may demonstrate biliary microlithiasis
Ø
Ø
Ø
Ø
Ø
Ø
Ø
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HEPATOBILIARY SURGERY
— MRCP: sometimes considered to rule out choledocholithiasis and
abnormalities of biliary and pancreatic ducts.
Terminology relating to acute pancreatitis
Ø
Mild acute pancreatitis
— Minimal organ dysfunction and an uneventful recovery.
Severe acute pancreatitis
— Associated with organ failure and/or local complications such as
necrosis, abscess or pseudocyst.
Ø
Ø
Acute fluid collections
— Occur early in the course of acute pancreatitis.
— Situated in or near the pancreas.
— Always lack a wall of granulation or fibrous tissue.
Ø
Pancreatic necrosis
— Diffuse or focal areas of non-viable pancreatic parenchyma.
— Typically associated with peripancreatic fat necrosis.
Acute pseudocysts
— Collection of pancreatic juice surrounded by a wall of fibrous or granulation tissue.
Ø
Pancreatic abscess
— Circumscribed intra - abdominal collection of pus arising in close
proximity to the pancreas, but containing little or no pancreatic necrosis, which arises as a consequence of acute pancreatitis.
Ø
Management
Mainly conservative/supportive:
Ø Close monitoring in ICU if severe.
Ø Oxygen
— maintain saturations above 94%.
Ø IV fluid resuscitation:
— Manage distributive shock and therefore reduce complications/organ
failure.
— Maintain urine output above 0.5ml/kg/hr.
Ø Appropriate analgesia.
Ø Proton pump inhibitors.
Ø Antithrombotic prophylaxis.
Ø Nil per oral initially
Ø Nasogastric tube if severe vomiting and ileus.
Ø Nutrition
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HEPATOBILIARY SURGERY
— Enteral feed is preferable to prevent translocation of gut bacteria and
prevent secondary septic complications, sometimes requires nasojejunal tube.
— Parenteral nutrition (TPN) required if enteral feed not tolerated due to
ileus and vomiting.
Ø Role of antibiotics
— rarely indicated unless infectious aetiology or infected pancreatic
necrosis, (imipenem/meropenem is antibiotic of choice)
Ø Urgent ERCP and stone extraction
— Indicated for proven bile duct stones causing obstruction and pancreatitis.
Treatment of early complications
Ø
Ø
Ø
Ø
Severe pancreatitis (score ≥3) HDU/ITU admission for optimisation of fluid
balance, respiratory, cardiovascular and renal support.
Radiological guided drainage of fluid collections, necrosis and abscesses may
be required.
Surgical debridement/necrosectomy rarely carried out for infected necrosis
and has very poor prognosis.
Cholecystectomy should be performed after recovery in patients with gallstone pancreatitis, to prevent recurrent attacks. In mild to moderate cases
it is also recommended to do it in the same admission.
Complications of Acute Pancreatitis:
Ø
Local
—
—
—
—
—
—
Peripancreatic fluid collections.
Pseudocyst - collection of sterile fluid within lesser sac.
A pseudocyst has no epithelial lining of it’s own.
Abscess - either pancreatic or peripancreatic.
Necrosis/gangrene.
Splenic vein thrombosis/Haemorrhage from major vessels.
Systemic
— Renal - hypovolaemia + direct damage from vasoactive peptides and
inflammatory mediators.
— Respiratory - ARDS, pleural effusions (transudative - low albumin or
exudative -inflammatory mediators), pneumonia.
— Cardiac - hypovolaemia, arrhythmias.
— Liver derangement.
— Haematological - DIC.
— Metabolic:
¾ Hyperglycaemia
Ø
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HEPATOBILIARY SURGERY
¾ Hypocalcaemia - saponification of calcium salts, reduced
PTH, calcitonin release.
— Intestinal - haemorrhage, ileus.
— Death
CHRONIC PANCREATITIS
Key Facts
Ø
Ø
Ø
Chronic pancreatitis is characterized by recurrent or persistent abdominal
pain and pancreatitis.
Often associated with exocrine or endocrine or pancreatic insufficiency.
Chronic inflammation causes glandular atrophy, duct ectasia, microcalcification and intraductal stone formation with cystic changes secondary to duct obstruction.
Pathological Features
Ø The process may affect the whole or part of the gland (focal).
Ø Chronic inflammatory changes cause progressive disorganization of the pancreas.
Ø Glandular atrophy and duct ectasia.
Ø Microcalcification and intraductal stone formation with cystic changes secondary to duct occlusion.
Causes
Ø
Ø
Ø
Ø
Recurrent episodes of acute pancreatitis, usually alcohol induced or can be a
chronic progressive process itself.
Secondary to pancreatic duct obstruction.
— Pancreatic head tumours or cysts
— Pancreatic duct strictures
— Congenital pancreatic anomalies
— Cystic fibrosis
Autoimmune diseases.
— Primary biliary cirrhosis
— Primary sclerosing cholangitis.
Idiopathic.
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HEPATOBILIARY SURGERY
Clinical Features
Recurrent or chronic abdominal pain.
— Typically epigastric radiating to back, worse after food and alcohol.
Ø Fat malabsorption resulting in steatorrhoea and malabsorption of fat soluble
vitamins.
Ø Weight loss and anorexia.
— Due to protein malabsorption.
Ø Insulin dependent diabetes mellitus.
— secondary to loss of Beta cell function.
Ø
Investigations
Ø Abdominal X-Ray
— May show calcification.
Ø Ultrasound abdomen
— Pancreatic duct dilatation.
Ø CT scan pancreatic protocol
— Pancreatic anomalies, tumors, cysts.
Ø MRCP
— Ductal abnormalities.
Ø ERCP
— Pancreatic duct strictures, calculi, dilated segments.
— Sometimes involvement of pancreatic head can lead to CBD stricture
and obstructive pattern of LFTs.
Ø Endoscopic ultrasound combined with aspiration cytology/biopsies
— To differentiate chronic pancreatitis from tumors and other pathologies.
Ø Faecal elastase to check exocrine function.
Management
Ø Treat causative agent.
— Stop alcohol / Cholecystectomy / Treat autoimmune disease.
Ø Dietary modifications.
— Reduce fat, adequate carbohydrate and proteins.
Ø Enzyme supplements.
— Creon.
Ø Acid suppressive therapy.
Ø Insulin may be required for diabetic control.
Ø Adequate analgesia.
— Patients may require opiates.
Ø Patients who continue to have pain may be considered for:
— Endoscopic therapy.
— Extracorporeal shock wave lithotripsy.
— Celiac nerve block.
— Denervation surgery.
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HEPATOBILIARY SURGERY
Surgery
— Only considered for patients who fail medical therapy.
— Surgery can be performed to decompress/drain an obstructed pancreatic duct, resect the affected part or treat reversible causes
like strictures, stones, tumor etc.
— Surgical options include:
¾ Pancreaticoduodenectomy (Whipple’s procedure),
¾ Partial or distal pancreatectomy.
¾ Pancreaticojejunostomy.
— The choice of operation depends upon the size of the pancreatic duct
and the parts involved.
Ø
PANCREATIC CANCER
Key Facts
Ø 80% cases of pancreatic cancer occur in the 6th and 7th decades of life.
Ø Risk factors include smoking, alcoholism, diabetes and chronic pancreatitis.
PathologIcal Features
Ø 90% are ductal adenocarcinomas
Ø 7% are cystic neoplasms
Ø 3% islet cell tumors
Presentation
Ø Carcinoma head of pancreas most commonly presents with obstructive jaundice. Gall bladder is typically palpable. (courvoisier’s law: in case of obstructive jaundice, if gallbladder is palpable it is unlikely to be due to stones).
Ø Epigastric or left upper quadrant pain.
Ø Nausea, vomiting, anorexia and weight loss could be feature of malignancy.
Ø Rarely it can present for the first time with an episode of acute pancreatitis or
thrombophlebitis migrans.
Ø Metastatic disease can cause hepatomegaly and intractable back pain due to
invasion of celiac plexus.
Investigations
Ø FBC, LFTs to look for obstructive pattern.
Ø Tumour markers CA 19-9.
Ø Ultrasound abdomen.
— Assess for gallstones and bile duct dilatation.
Ø CT scan
— Assess for pancreatic masses, local invasion and metastasis.
Ø Endoscopic ultrasound
— Accurate in detecting small pancreatic lesions and peripancreatic
nodes.
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HEPATOBILIARY SURGERY
US or CT guided fine needle aspiration cytology
— Can help with tissue diagnosis.
Ø ERCP
— Can be done to get brushings for cytology.
— Can also help relieve biliary obstruction via stent insertion.
Ø PET scan
— Can help to differentiate neoplastic from nonneoplastic lesions and
also help to exclude metastatic disease.
Ø Laparoscopy
— For staging and assess for peritoneal disease.
Ø
Management
Majority of tumours are not amenable for curative resection because of locally
advanced disease, metastasis or co morbidities of the patient.
Palliation is aimed at relief of obstructive jaundice as it can cause liver failure,
hepatic encephalopathy and hepatorenal syndrome.
Decompression of biliary system is achieved by:
— ERCP and stenting.
— Percutaneous biliary drainage, PTC and internal stenting or insertion
of an internal-external drainage catheter.
— Surgical drainage by cholecystojejunostomy or choledocho-
jejunostomy.
Ø If locally advanced tumour causes duodenal obstruction, it can be bypassed
with a gastrojejunostomy.
Ø Opiate analgesia required for pain relief and sometimes needed for celiac
plexus block.
Ø Curative resection involves pancreaticoduodenectomy (Whipple’s procedure)
Ø Whipple’s procedure involves resection of part of stomach, duodenum, pancreatic head and neck, gall bladder and part of bile duct along with clearance of draining lymph nodes. Restoring continuity of the GI
tract involves three anastomosis, gastrojejunostomy, choledochojejunostomy and a pancreaticojejunostomy.
Ø 5 year survival of 12% in patients with resectable disease.
Ø
Ø
Ø
Endocrine Tumors of Pancreas
Ø The commonest endocrine pancreatic tumour is an insulinoma
Ø Clinical Features
— Symptoms of hypoglycaemia when fasting with associated symptomatic relief following glucose replacement.
Ø Pathological Features
— Approximately 90% of insulinomas are single and benign rendering
them operable. They occur with equal frequency in the head, body
and tail of the pancreas. Malignancy is only diagnosed by the presence of metastatic disease.
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HEPATOBILIARY SURGERY
Diagnosis & investigation
— Confirming hyperinsulinism makes the diagnosis.
— Abdominal CT scanning and selective pancreatic arteriography help
to localize the lesion.
Ø Treatment
— Surgical resection.
Ø
97
NOTES
98
COLORECTAL SURGERY
Chapter 5
Colorectal Surgery
99
COLORECTAL SURGERY
Contents:
•
Acute Appendicitis
•
Diverticular disease
•
Colorectal Cancer
•
Bowel Obstruction
•
Perianal Disorders
•
Anal Cancer
•
Types of stomas
•
Stoma Complications
100
COLORECTAL SURGERY
ACUTE APPENDICITIS
Key Facts
Ø One of the most common causes of the acute abdomen as well as one of the
most common indications for emergency abdominal surgery.
Ø Located at the base of the caecum where the taenia coli converge. Its blood
supply is from the appendiceal artery, a terminal branch of the iliocolic artery.
Ø Has an immunological function
Ø Peak age of incidence is early teens to early twenties.
Ø Lifetime risk is 8.6% in men and 6.7% in women.
101
COLORECTAL SURGERY
Pathological Features
Ø Initial inflammation may be followed by localised ischemia, perforation and the
development of a contained abscess or generalised peritonitis.
Ø Usually due to appendiceal obstruction:
Ø Feacolith, lymphoid hyperplasia, infectious process. Or the presence of a
benign or malignant tumour.
_______________
Ø
Surgical anatomy of the inflamed appendix
— Commonly retrocaecal, but may be pelvic, retroileal, or retrocolic.
Clinical features
Symptoms
Signs
Abdominal pain starting centrally
and moving to the RIF
Pyrexia
Pain exacerbated by movement
Tachycardia
Nausea, vomiting, anorexia
Diarrhoea
Abdominal tenderness
Tenderness maximally over McBurney’s point
Ø The initial visceral pain afferent nerve fibres are at level T8 –T10 (level of
the umbilicus) and the following well-localized pain is due to the inflammation
of the adjacent peritoneum.
Ø Pelvic and rectal examination very useful especially when diagnosis is unclear.
Special Tests
Rosving’s Sign: Palpation of LIF causes
pain worse in RIF
Psoas Sign: Discomfort upon
hyperextension of the right hip, indicating
an inflamed retroperitoneal, retrocaecal
appendix (see note 1)
Obturator Sign: Pain in RIF as a result of
flexing and internally rotation the right hip,
usually seen in a pelvic appendix
102
Illustrated by Kevin Quinlan:
McBurney’s point is two-thirds along
a line from the umbilicus to the
ASIS.
COLORECTAL SURGERY
Differential diagnosis
Terminal ileal pathology:
Crohn’s ileitis, TB
Special populations:
Meckel’s Diverticulitis
Gastroenteritis
1.Children: Mesenteric
adenitis
2. Older adults: Caecal tumour
Retroperitoneal pathology:
renal colic, pancreatitis
Gynaecological pathology:
ovarian cyst, ectopic, PID, ovarian torsion
_____________
Investigations
Ø
Acute Appendicitis is a Clinical Diagnosis
Bedside: o
o
MSU
(dipstick,
culture &
sensitivity).
Beta hCG
Alvarado Score:
Bloods: Imaging: o
o
o
o
FBC
(leukocytosis)
CRP.
Beta hCG.
Symptoms Score
Abdominal Pain 1
Anorexia 1
Nausea/vomiting
1
Signs
Tenderness in RIF 2
Rebound Tenderness 1
Temperature >37.5 1
LAB values
Leucocytosis >10,000 2
Neutrophils >75% 1
o
Pelvic US (if there is concern
over ovarian pathology ).
CT Abdo/Pelvis where there
is a question over the
diagnosis or pathology.
—
—
—
Score 0-3: Low risk.
Score 4-6: Observe / may need intervention
Score 7-9: Male: Proceed to
appendectomy. Female: Diagnostic laparoscopy.
—
Best employed as a tool in excluding appendicitis
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COLORECTAL SURGERY
Management
Ø
Resuscitation
— IV access & IV fluids.
— Analgesia.
— Antibiotics (IV or PO). According to local guidelines.
— DVT Prophylaxis.
Definitive management of acute appendicitis
— Open or laparoscopic appendectomy.
— You may expect up to 15% of appendectomies to be negative for
appendicitis.
— IV antibiotics on induction; continued antibiotics only indicated for
perforation.
Ø Definitive management of an appendix mass or appendix abscess
— IV antibiotics.
— If symptoms settle, delayed (interval) appendicectomy after 6 weeks.
— If symptoms fail to settle, may need urgent appendicectomy.
— Appendix abscess may be amenable to CT-guided drainage.
Ø
Antibiotics alone for the management for uncomplicated appendicitis
— This is an area of much interest and research
— At present antibiotics are not recommended for routine use. This
is due to many unanswered questions; patient selection, recurrent
attacks, missed neoplasm (Salminen, 2011).
— Antibiotics are an option for those unfit for surgery.
Ø
Principles of appendicectomy are as follows:
— Open: Gridiron or Lanz incision centred at McBurney’s point (mostly in
children <30Kg),
— Laparoscopic approach: umbilical port, port in LIF, suprapubic port
(this is considered is gold standard).
— Appendix is carefully located.
— The mesentery of the appendix is divided and ligated.
— The appendix is clamped and tied at the base and
excised.
— Some surgeons invaginate the stump using a purse-string in the wall
of the caecum round the base of the appendix.
— Conversion to open appendicectomy in 10%.
Ø
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COLORECTAL SURGERY
Complications of acute appendicitis
Ø
Ø
Ø
Ø
Perforation (localized or generalized).
RIF ‘appendix’ mass (usually appendicitis with densely adherent caecum
and omentum, forming a ‘mass’).
RIF abscess (usually due to perforated retrocaecal appendicitis).
Pelvic abscess (usually due to perforated pelvic appendicitis).
105
COLORECTAL SURGERY
DIVERTICULAR DISEASE
Definition
Ø
Ø
Ø
Ø
106
Acquired outpouchings of sac-like mucosal projections through the colon wall.
Typically affects the sigmoid colon, but may affect any part of the GI tract.
Diverticulosis describes the presence of diverticula.
Diverticular disease describes clinically significant diverticulosis be it bleeding,
infection, perforation.
COLORECTAL SURGERY
Epidemiology
Ø Male: Female 1:1.
Ø Prevalence: Becoming more common in younger populations 50%
in over 50 years.
Ø Approximately 4-15% of patients with diverticular disease will develop diverticulitis.
Aetiology
Ø
Ø
Ø
Low fibre diet increases intraluminal colonic pressure resulting in herniation of
the mucosa through the muscularis layer.
Typically occur at entry point of nutrient arterioles between taenia coli.
No muscle layer is involved in acquired diverticula as compared to all 3 colonic muscle layers being involved in congenital diverticula.
Clinical presentation
Ø
Asymptomatic:
— Majority found incidentally at colonoscopy or barium enema.
Ø
Painful diverticulosis:
— Intermittent LIF pain, constipation, diarrhoea.
Ø
Acute diverticulitis:
— “Left sided appendicitis”.
— Symptoms: LIF pain, diarrhoea / constipation, nausea.
— Signs: Fever, tachycardia, tender LIF, guarding / rebound.
— Neutrophilia, elevated WCC, elevated CRP.
Diverticular bleeding:
— Painless.
— Spontaneous with no prodromal symptoms.
— Large volume, bright rectal bleeding due to rupture of a peridiverticular submucosal vessel.
Ø
Complications
Pericolic and paracolic abscess:
— Suppurative process from persistent colonic inflammation leading to
pericolic abscess
— Extension to paracolic space causes paracolic abscess
— Symptoms: Commonly LIF pain that is unresolving, nausea, vomiting,
systemically unwell (weight loss, night sweats).
— Signs: Spiking / swinging fever, sepsis.
Ø
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COLORECTAL SURGERY
— Treatment: antibiotics, radiologically-guided percutaneous / open
drainage and washout +/- resection of diseased segment of bowel.
Ø Peritonitis:
— Purulent peritonitis: perforation of a paracolic or pericolic abscess.
— Faeculent peritonitis: free perforation of diverticular segment.
Ø Diverticular fistula:
— Perforation into adjacent structures of chronically inflamed segment of
colon / pericolic abscess.
— Typically posterior vaginal vault (colovaginal) or bladder (colovesical).
— Colovesical fistula presents with recurrent UTIs, pneumaturia and
debris in urine.
Ø Stricture formation:
— Chronic inflammation causes luminal narrowing.
— May lead to bowel obstruction.
Diagnosis and Investigations of Acute Presentation of Diverticulitis -
Bloods: o
o
o
o
Imaging: FBC – WCC and neutrophil
elevation
U&E – identify pre-renal
failure, electrolyte disturbance
from diarrhoea.
CRP – monitor response to
treatment
Blood cultures- if sepsis is
suspected.
o
o
o
o
o
Erect CXR – if perforation suspected.
PFA – if bowel obstruction suspected
(rarely needed).
CT Scan with IV contrast – for
identification of complications.
CT Scan with oral or rectal contrast
(not for acute diverticulitis or
perforation)
CT Angiography with rectal bleeding.
+ selective vessel embolisation.
Hinchey Classification:
1A Paracolic phlegmon
1B Pericolic / mesenteric abscess
108
II
Diverticulitis with walled-off abscess
III
Purulent peritonitis (perforated abscess cavity)
IV
Faeculent peritonitis
COLORECTAL SURGERY
TREATMENT OF ACUTE DIVERTICULITIS
— Uncomplicated Diverticulitis.
— Hinchey Classification I / II / III.
Medical Management:
— IV antibiotics.
— Bowel rest, supportive management
with IV fluid therapy and analgesia.
— Radiologically-guided drainage
of abscess.
—
—
—
—
—
Failure
Free perforation.
Fistula.
Refractory to medical treatment.
Undrainable abscess.
Hinchey III / IV.
Surgical Management:
— Laparoscopy & washout.
— Resection of the diseased
segment of bowel
(Hartmann’s Procedure).
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COLORECTAL SURGERY
COLORECTAL CANCER
Key Facts
Ø
Ø
Ø
Ø
Colorectal cancer is the 3rd commonest form of cancer.
Most common GI malignancy.
Male: Female 3:1.
Peak age of incidence 55–75y.
Risk factors
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Polyposis syndromes (including FAP, HNPCC, juvenile polyposis). Note most
cases are sporadic rather than inherited.
Strong family history of colorectal carcinoma.
Chronic ulcerative colitis or colonic Crohn’s disease.
Diet poor in fruit and vegetables.
Diet rich in red meat, processed meats, animal fat.
Obesity.
Smoking, heavy alcohol use, Type 2 DM.
Pathological Features
The predominant type is adenocarcinoma.
Classified as well, moderately, or poorly differentiated.
Colorectal carcinomas metastasize via the lymphatics.
Haematogenous spread is predominantly to the liver.
Most colorectal carcinomas arise from pre-existing adenomas.
Adenomatous polyps
— Localized lesion protruding from the bowel wall into the lumen.
— Histologically there are three types of adenomas;
¾ Tubular adenomas (70%)
¾ Villous adenomas (10%)
¾ Tubulo-villous adenomas (20%)
— Villous adenomas have the greatest potential for malignant transformation and the potential is proportional to the size of the lesion.
Ø Serrated adenomas also predispose to colorectal cancer and can look like
hyperplastic polyps. So, all polyps that look hyperplastic must be biopsied.
Ø
Ø
Ø
Ø
Ø
Ø
110
COLORECTAL SURGERY
Morphology
Ø
Ø
Ø
Colorectal cancer may occur as
— Polypoid
— Ulcerating
— Stenosing
— Infiltrative tumour mass
Distribution
— Rectum - 30%
— Descending & sigmoid - 45%
— Transverse - 5%
— Right-sided - 20%
Synchronous carcinoma at time of diagnosis 3-5%.
Clinical Features
Right-sided lesions:
—
Iron deficiency
anaemia.
Left-sided lesions:
—
—
PR bleeding –
mixed with stool.
Change in bowel
habit
Distal lesions:
—
—
PR Bleeding –
blood on surface of stool.
Tenesmus –
difficult, painful defecation,
sensation of incomplete
evacuation
Illustrated by Kevin Quinlan:
colon.Left-sided lesions:
Emergency presentations
— 40% of colorectal carcinomas will present as emergencies commonly
with large bowel obstruction.
— Perforation with peritonitis.
— Acute PR bleeding.
Ø
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COLORECTAL SURGERY
Diagnosis and investigations
Elective
— PR examination or rigid sigmoidoscopy and biopsy.
— Colonoscopy and biopsy. Important to visualise as far as the caecum
to exclude synchronous lesions (present in 3-5%).
— CT colonography if colonoscopy not possible.
Ø
Ø
Emergency: CT scan with oral and IV contrast.
Staging investigations
Ø
Ø
Ø
Ø
Local extent
— Colon cancer – CT scan.
— Rectal cancer - pelvic MRI +/- endoanal US to assess T-stage (TNM).
Presence of metastases
— CT thorax/abdomen/pelvis is gold standard.
— PET scan may be used to evaluate equivocal lesions.
Synchronous tumours - colonoscopy or CT colonography.
Tumour marker (CEA) is of no use for diagnosis or staging, but can be used to
monitor disease relapse.
Pathological staging
Ø
Duke’s classification
— A - confined to bowel wall only
— B - through bowel wall
— C - positive lymph nodes
— D - metastases
Ø TNM staging
— T – bowel wall
■ T1 – invades submucosa
■ T2 – invades muscularis propria
■ T3 – invades through muscularis propria to sub serosa or
adjacent organs
■ T4 – invades visceral peritoneum
— N – lymph nodes
■ N0 – no lymph node invasion
■ N1 – 1-3 nodes involved
■ N2 – 4 and more nodes involved
— M – distant metastasis
■ M0 – no distant metastasis
■ M1 – distant metastasis present
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COLORECTAL SURGERY
Management
Potentially curative treatment
Ø
Ø
This is for up to 80% of cancers and is indicated for resectable tumours with
no evidence of metastases.
The goal of surgery with curative intent is complete removal of the tumour,
the major vascular pedicle and the lymphatic drainage basin of the affected
colonic segment.
Operative options
— Right / transverse colon - right/extended right hemi colectomy.
— Left colon - left hemi colectomy.
— Sigmoid/upper rectum - high anterior resection.
— Lower rectum - low anterior resection or abdominoperineal resection
(APR). APR usually for lesions < 5cm from the anal verge. APR involves removing the anal canal and sphincter complex, while leaving a permanent end colostomy in the LIF.
— Anorectal - APR.
Ø
Ø
Ø
Ø
Ø
Preoperative (neoadjuvant) chemo radiotherapy for rectal cancer reduces
local recurrence. The role in colon cancers in yet unclear and is decided on a
cases by case bases with MDT involvement.
Adjuvant chemotherapy is offered for tumours with positive lymph nodes or
evidence of vascular invasion, with the goal of eradicating micro metastases.
A course of oxaliplatin-containg agents is generally used.
Hepatic or lung resection may be offered to patients with resectable metastases and resectable primary tumour.
Note that a laparoscopic approach to colonic resection is now standard in
many centres.
Palliative treatment - For unresectable metastases or unresectable tumours.
Ø Chemotherapy.
Ø Endoluminal stents with self- expanding metal stents for obstructing colon
tumours.
Ø Transanal ablation of rectal obstructing tumours.
Ø Surgery for untreatable obstruction, bleeding, or severe symptoms. Options
include a defuctioning colostomy or ileostomy, internal bypass.
Follow-up
Ø
Ø
Ø
Outpatient review - history and examination, PR, CEA.
Colonoscopy at 1 year, every 3 to 5 years thereafter (ESMO Guidelines).
CT scans annually for 3 years.
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COLORECTAL SURGERY
BOWEL OBSTRUCTION
Definition:
Mechanical blockage arising from a structural abnormality that presents a physical
barrier to the progression of gut content.
Ø
Ø
Ø
Can be classified into small bowel obstruction (SBO) or large bowel obstruction (LBO). The obstruction can be complete (nothing passes through)
or incomplete (or partial, when gas and liquid stool may pass distally).
May present in an acute or sub acute manner.
Ileus is the hypo mobility of the GI tract in the absence of a mechanical obstruction. Common in postoperative patients.
Obstruction can be Complicated or non-Complicated
Ø Non-complicated obstruction can often be managed conservatively with close
observation.
Ø Complicated bowel obstruction presents as complete obstruction
Ø Closed loop obstruction, bowel ischemia, necrosis or perforation) and often
requires surgery.
— Closed-loop obstruction = intestine (usually small bowel) obstructed at
2 ends, which can rapidly progress to ischemia, necrosis and perforation (4-6 hours). Urgent diagnosis and treatment is crucial.
Clinical Presentation
Symptoms:
o Abdominal Pain
o Constipation
o Vomiting
• Bilious (SBO)
• Faeculent (distal SBO and LBO)
o Cannot pass flatus (obstipation)
o Abdominal distension
114
Signs:
o Distension (pronounced and
early in LBO)
o Tenderness
o Rigidity / guarding
o High pitch / absence of bowel
sounds
o DRE – empty rectum
COLORECTAL SURGERY
Aetiology: small or large bowel obstruction
Small bowel obstruction
Large bowel obstruction
Adhesions
Colon cancer (20% of colon cancer),
Hernia
Hernias
Malignancy
Diverticulitis
Intussusception
Volvulus
Stricture (Crohn’s Disease, Radiation,)
Intussusception
Meckel’s diverticulum
Stricture
Aetiology: intraluminal, intramural or extrinsic
Intraluminal:
o
o
o
o
Illustrated by Daniel Kane:
aetiology of bowel obstruction.
Foreign body
Gallstone
Faecolith
Faecal impaction
Mural:
o Tumours (LBO)
o Strictures
o Volvulus
o Intussusception
o Functional: ileus, aganglionic segment,
atresia
Extrinsic:
o Adhesions
o Hernias
Other causes:
o Endometriosis.
o Drugs: antimuscarinics, opioid analegesia.
o Ogilvie syndrome / Pseudo-obstruction: post-operative obstruction without a
mechanical cause.
o Superior mesenteric Artery syndrome: duodenum is compressed between SMA
and aorta. Often presents with irretractable vomiting.
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COLORECTAL SURGERY
Diagnostic imaging:
Image by Niamh Adams: PFA of small bowel obstruction.
Erect CXR: Rule out a co-existing perforation (but only 60% sensitive).
PFA:
— Dilated loops of small bowel (valvulae conniventes) or large bowel (haustrations)
— Air/Fluid Levels.
— 3,6,9 rule: The small bowel should be 3cm or less, the large bowel 6cm
and the caecum 9cm or less on PFA.
Ø CT Scan with oral/IV contrast: To establish the cause of the obstruction.
Ø
Ø
Management
Ø Drip & Suck.
Ø Begin IV fluids.
Ø Insert a wide bore NG tube. Decompress the stomach and then leave on free
drainage.
Ø NPO, analgesia, urinary catheter, I/O chart
Ø Electrolyte management is essential given the underlying intestinal dysfunction.
Ø The initial approach should be conservative, as the definitive treatment will
vary depending on the cause.
Ø If bowel is ischaemic, it will have to be resected.
Ø An end-to-end anastomosis may be possible or the patient may require
loop or end stoma.
116
COLORECTAL SURGERY
Specific management:
Ø Tumour: resection / chemotherapy / radiotherapy / balloon dilation / stenting.
Ø Strictures: dilatation / resection of abnormal segment.
Ø Adhesions: adhesiolysis.
Ø Hernias: repair hernia.
Ø Volvulus: colonoscopy & pneumatic decompression.
PERIANAL DISORDERS
Ø
The internal sphincter is composed of circular, non-striated involuntary muscle
supplied by autonomic nerves.
Ø
The external sphincter is composed of striated voluntary muscle supplied by
the pudendal nerve.
Ø
Extensions from the longitudinal muscle layer support the sphincter complex.
Ø The superior part of the external sphincter fuses with the puborectalis muscle,
which is essential for maintaining the anorectal angle, necessary for continence.
Ø
The upper 2/3 of the anal canal is lined by columnar epithelium. The lower
third of the anal canal is lined by sensitive squamous epithelium.
Ø
Blood supply to the anal canals upper 2/3 is the superior rectal artery that is
from the inferior mesenteric artery. The inferior rectal artery a branch from the
internal pudendal artery supplies the lower 1/3.
Ø
Lymphatic drainage of the upper two thirds of the anal canal drains to internal
iliac lymph nodes. While lower third of the anal canal goes to inguinal lymph
nodes. This is important in squamous cell carcinoma of the anal canal.
117
COLORECTAL SURGERY
HAEMORRHOIDS
Ø
Haemorrhoids are normal vascular and connective tissue columns that exist
in three columns on the anal canal: 2, 7 and 11 o’clock (when patient in the
lithotomy position)
Illustrated by Kevin Quinlan: haemorrhoids.
Ø
Internal Haemorrhoids
— Above the dentate line.
— Covered by mucosa.
— Painless.
— Bleed and prolapse.
Ø
External Haemorrhoids
— Below the dentate line and covered by the anoderm.
— May thrombose and cause pain and itching.
Aetiology
Ø
Ø
Ø
Poorer dietary habits and constipation.
Prolonged straining.
Increased intra abdominal pressure e.g.: pregnancy.
Four degrees of haemorrhoids
Ø
Ø
Ø
Ø
118
First degree – bleed only, no prolapse below the dentate line.
Second degree – prolapse, but reduce spontaneously.
Third degree – prolapse and have to be manually reduced.
Fourth degree – permanently prolapsed may strangulate.
COLORECTAL SURGERY
Management
Examination
Ø
Ø
Ø
Ø
Exclusion of other causes of rectal bleeding, especially colorectal malignancy,
is the first priority.
Digital rectal examination (DRE) to look for prolapse and skin tags, to assess
sphincter tone and to exclude other anal conditions. If DRE is very painful
think of the possibility of anal fissure or intersphincteric abscess.
Proctoscopy.
Consider sigmoidoscopy to rule out rectal/colonic pathology
Conservative
Ø Important measures to manage the clinical manifestations of haemorrhoids
include: only evacuating when the natural desire to do so arises, minimise
straining or lingering (e.g. reading on the toilet), the addition of stool softeners
and bulking agents to ease the defecator act, increased dietary fibre and
increased physical activity.
Ø Topical analgesics and steroids such as mixed hydrocortisone/lidocaine
may be beneficial but should not be used for longer than a week.
Ø Sitz baths used in warm water three times a day.
Ø Injection Sclerotherapy (first and second degree haemorrhoids).
Ø Rubber band ligation (second degree haemorrhoids).
Ø Trans anal haemorrhoidal dearterialisation (second and third degree haemorrhoids).
Operative Management
The indications for haemorrhoidectomy include:
Ø Third- and fourth-degree haemorrhoids.
Ø Second-degree haemorrhoids that have not been cured by non-operative
treatments.
Ø Fibrosed haemorrhoids.
Ø Intero-external haemorrhoids when the external haemorrhoid is well defined.
Types of haemorrhoidectomy
Ø Open (Milligan-Morgan)
Ø Closed (Ferguson)
Ø Stapled
119
COLORECTAL SURGERY
Thrombosed external haemorrhoids:
Ø
Ø
Can cause excruciating pain, and patients will often present acutely.
Surgical evacuation of the haemorrhoid with excision of the skin overlying the
thrombosed haemorrhoid can produce immediate relief.
Patients should be referred for colonoscopy when presenting with rectal bleeding even
when symptoms strongly suggest haemorrhoids.
ANAL FISSURE
Ø
Ø
An anal fissure (synonym: fissure-in-ano) is a longitudinal split in the anoderm
of the distal anal canal that extends from the anal verge proximally towards,
but not beyond, the dentate line.
It is one of the most common causes of anal pain and anal bleeding.
Aetiology
Primary
— Local trauma, such as passage of hard stool, prolonged diarrhoea,
vaginal delivery, or anal sex.
— Usually start with a tear in the anoderm within the distal half of the anal
canal. The tear then triggers cycles of recurring anal pain and bleeding.
Ø
Secondary anal fissures
— Inflammatory bowel disease (e.g., Crohn’s disease).
— Granulomatous diseases (e.g., extra pulmonary tuberculosis, sarcoidosis).
— Malignancy (e.g., squamous cell anal cancer, leukaemia).
— Communicable diseases (e.g., HIV infection, syphilis, chlamydia).
Ø
Types of Anal Fissure
Ø
Acute
— Less than 6 weeks of onset.
Chronic
— Longer than 6 weeks or features on examination showing fibrosis,
fibrotic edges and perianal skin tag.
Ø
120
COLORECTAL SURGERY
Clinical features
Ø Pain is the predominant symptom. The pain is usually exacerbated by defecation.
Ø Occasionally bleeding or presence of perianal skin tag.
Ø Rarely pruritus ani.
Examination
Ø Anal fissures can be visualised by gentle parting or spreading of the buttocks
with eversion of the anal verge.
Ø Digital rectal examination is usually painful and examination is precluded by
spasm.
Ø Do not attempt if patient is in severe pain.
Management
Best prevented- healthy bowel habit, high fibre diet and adequate fluids.
Conservative
Ø
Ø
Ø
Ø
Ø
Ø
Relief of constipation.
Local wound care (warm sitz baths).
Analgesia.
Severe perianal and rectal pain.
Associated with constitutional symptoms of fever and malaise.
Purulent discharge if the abscess spontaneously drained.
Investigations
Ø
Pelvic CT or MRI if required. Often clinical diagnosis.
Management
Management of acute anorectal sepsis is primarily surgical, including careful
examination under anaesthesia, sigmoidoscopy and proctoscopy, and adequate
drainage of the pus.
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COLORECTAL SURGERY
ANAL FISTULA
Ø A fistula is a chronic abnormal connection between two epithelial lined surfaces.
Ø Usually lined with granulation tissue but may be epithelialized
Ø Anorectal fistula is the chronic manifestation of the acute perirectal process
that forms an anal abscess.
Ø When the abscess ruptures or is drained, an epithelialized track can form that
connects the abscess in the anus or rectum with the perirectal skin.
Aetiology
Ø
Ø
Ø
Ø
Ø
Ø
Anorectal abscess
Crohn’s disease
Lymph granuloma venereum
Radiation proctitis
Rectal foreign bodies
Primary perianal actinomycosis
Clinical features
Ø Intermittent rectal pain.
Ø Chronic purulent drainage and a pustule-like lesion in the perianal or buttock
area.
Ø Intermittent and malodorous perianal drainage and pruritus.
Examination
Ø
Ø
Ø
Perianal skin may be excoriated and inflamed.
The external opening may be visualized, or palpated as induration just below
the skin.
Under experienced hands a fistula probe can be passed through the fistula to
identify its internal opening using a proctoscope or sigmoidoscope.
Clinical assessment
Ø
Ø
122
Full history.
Examination including proctosigmoidoscopy is essential.
COLORECTAL SURGERY
Types of anal fistula (Parks’ classification)
Primary track can be:
1. Intersphincteric
2. Trans-sphincteric
3. Extrasphincteric
4. Suprasphincteric
Anal fistulae can be low or high,
depending on whether the internal
opening is above or below the
puborectalis.
4
2
1
3
Illustrated by Kevin Quinlan: anal fistula primary tracks.
Goodsall’s rule
‘’All fistula tracts with external openings within 3 cm of the anal verge and posterior to
a line drawn through the ischial spines travel in a curvilinear fashion to the posterior
midline. All tracks with external openings anterior to this line enter the anal canal in a
radial fashion.’’
ANTERIOR
POSTERIOR
Illustrated by Kevin Quinlan: Goodsall’s rule for anal fistula tracts.
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COLORECTAL SURGERY
Management
Ø The goal of surgical therapy is to eradicate the fistula while preserving faecal
continence.
Ø Examination Under Anaesthesia (EUA), is part of the assessment prior to
definitive treatment.
Ø Done to identify the external and internal openings.
Surgical options
Ø Fistulotomy done if the fistula lies entirely below the puborectalis, with laying
open the fistulous tract. The wound then heals gradually by secondary intention.
Ø Fistulectomy excision of the fistula tract is another option for low anorectal
fistula.
Ø Seton insertion either loose, tight or chemical. Draining setons are used as
cutting setons are too painful. Setons are used for high anorectal fistula. The theory is to achieve a staged fistulotomy by placing a seton suture that
is sporadically tightened so as to gently cut through the tract and muscle while
allowing healing and fibrosis to develop between divided muscles, thus preserving sphincteric function and faecal continence.
Ø Advancement flap.
Ø Plugs and glues.
124
COLORECTAL SURGERY
PILONIDAL SINUS AND ABSCESS
Ø In Latin ‘pilus’ means hair and ‘nidus’ means nest.
Ø A sinus is a blind ending tract, usually lined with granulation tissue that leads
from an epithelial surface into the surrounding tissue, often into an abscess
cavity.
Ø Intergluteal pilonidal disease is an infection of the skin and subcutaneous
tissue at or near the upper part of the natal cleft of the buttocks.
Aetiology
Ø
Ø
The theory is that it is an acquired disease rather than congenital.
These cases have occurred in locations that would be subject to local trauma
from hair, such as on the hands of barbers and animal groomers.
Pathogenesis
Ø
Ø
Ø
Ø
Ø
The specific mechanism is unclear, although hair and inflammation are contributing factors
Loose hair tends to gather toward the natal cleft due to the anatomy and the
suction of the buttocks on movement.
This draws hair deeper into the pore, and the friction causes the hairs to form
a sinus.
Once the pore becomes infected, an acute subcutaneous abscess develops,
spreads along the tract, and may discharge its contents through a pilonidal
sinus in the skin cephalad to the natal cleft.
A recurring or chronic infection can also develop in the affected area due to a
retained hair or infected residue.
Clinical features
Ø Asymptomatic.
Ø Acute; with pain, swelling and purulent discharge. Fever and malaise if not
drained.
Ø Chronic; is pilonidal sinus appearing after treatment of an acute pilonidal
abscess or those at first presentation with or without an abscess. With recurrent or persistent drainage and pain.
Examination
Ø
Ø
Asymptomatic; one or more primary pores (pits) in the midline of the natal
cleft and/or a painless sinus opening cephalad and slightly lateral to the cleft.
Acute or chronic disease; a tender mass or sinus draining mucoid, purulent,
and/or bloody fluid can be identified. A hair may occasionally be seen 125
COLORECTAL SURGERY
protruding from a sinus opening. Secondary tracts or pits can be identified
lateral to the midline in patients with chronic or persistent complex disease.
Investigations
Ø The condition is a clinical diagnosis and no imaging or laboratory tests are
required.
Treatment
Ø
Skin hygiene and hair exfoliation is important in preventing recurrence.
Surgery
Acute:
Ø incision and drainage of the pilonidal abscess. Laying open of would. Will
usually require second operation once healed to excise remaining sinus.
Definitive:
Aims to obliterate the epithelialised sinus tract and heal the wound.
Different debatable techniques include:
— Excising the sinus tract with primary closure of the wound, this is further
divided in midline closure and off-midline closure. The latter is being
more
— Favoured recently due to relatively lower risk of recurrence and infection.
Ø Excising the sinus tract with laying open the wound, to allow healing by secondary intention.
Ø Bascom’s operation; lateral to midline incision, to curette the deep cavity and
excision of the primary midline pits. Primary closure of the midline incisions
and lateral wound left to heal by secondary intention.
Ø Karydakis procedure; semi lateral ‘d- shaped’ incision incorporating the sinus
tract down to the presacral fascia. The flap of tissue on the vertical wound side
is mobilised and brought to the convex wound edge and sutured in layers over
a drain.
Ø
Ø
Recurrent pilonidal sinus
Ø
126
Rotational flap procedures are recommended, e.g.: z plasty, modified
Limberg flap.
COLORECTAL SURGERY
ANAL CANCER
Risk factors
Ø Female
Ø Infection with HPV (T16 & T18)
Ø Lifetime number of sexual partners
Ø History of anorectal condyloma
Ø Cigarette smoking
Ø Receptive anal intercourse
Ø Infection with HIV
Anal intraepithelial neoplasia (AIN)
Ø Precursor to invasive squamous anal carcinoma.
Ø The level of AIN (I,II,III) is dependent on the degree of cytological atypia and
its depth in the epidermis.
Ø High proportion of AIN III (Bowen’s Disease) progresses to carcinomas.
Anatomy of the anal canal defining the types of tumours
Ø Two categories of tumours arise in the anal region.
Ø Tumours that develop from mucosa (glandular, transitional or nonkeratinizing
squamous) are termed anal canal cancers.
Ø Tumours that arise within the skin at or distal to the squamous mucocutaneous junction are termed perianal or anal margin cancers.
Lymphatic drainage
Ø Tumours originating above the dentate line, similar to rectal cancers, drain to
the perirectal and paravertebral nodes.
Ø Tumours arising below the dentate line spread primarily to the superficial
inguinal and femoral nodes.
Types of Anal canal Tumours
Ø Squamous Neoplasms
— Condylomata Acuminatum
— Anal Intraepithelial Neoplasia
— Bowen’s Disease
— Squamous cell carcinoma
Ø Adenocarcinoma
— Anorectal adenocarcinoma
— Paget’s Disease
Ø Melanoma
Ø Neuroendocrine Tumours
Ø Mesenchymal Tumours
Ø Malignant Lymphoma
127
COLORECTAL SURGERY
Clinical features
Ø Rectal bleeding (approx. 45% of presentations), pain, rectal mass
Ø Examination of anal verge can reveal the lesion. Cancer of the anal canal
may not be visible, although extensive lesions may protrude to the anal verge.
Careful examination under anaesthesia is required to allow biopsy.
Ø Histology of the biopsied lesion is essential to confirm diagnosis and to determine the tissue of origin, as the treatment for SCC varies from that of
adenocarcinoma.
Ø CT, MRI and endoanal ultrasound are useful and essential in assessing the
extent of the lesion and staging the tumour.
Management
Ø
Ø
Ø
It is important to detect anal cancer at an early stage, as extensive local invasion and metastatic disease are associated with a poor outcome.
Multidisciplinary treatment of anal cancer is essential with surgeon and radiotherapist involved in assessment and treatment.
Staging (TNM) is important for prognosis and also guides treatment approaches. Therefore, it is important to confirm lymph node involvement
histologically by biopsy of accessible suspected nodes.
Treatment
Ø Wide surgical excision: for early well-circumscribed superficial (T1N0) carcinoma.
Ø Chemo radiotherapy: for anal canal and T2, T3, T4 tumours.
Ø Abdomino-perineal resection of anus and rectum; in advanced disease, for
chemo-radiotherapy.
Ø Sphincter sparing treatment is currently being extensively invetigated.
128
COLORECTAL SURGERY
STOMAS
An ostomy (stoma) is a purposeful anastomosis between a segment of the
gastrointestinal tract and the skin of the anterior abdominal wall.
Can be temporary or permanent.
LOOP ILEOSTOMY
Illustrated by Kevin Quinlan: loop ileostomy
Clinical features
Ø
Ø
Ø
Loop of ileum in the RIF may be supported by a bridge or rod.
2 lumens present: active proximal spouted lumen and inactive distal lumen.
Contents: liquid or soft effluence.
Clinical relevance
Ø
Ø
Usually a temporary stoma.
Usually performed to defunction bowel and protect newly formed anastomoses e.g. in the following situations:
— Risk of anastomotic leak
— Sepsis
— Patient unstable
— Chemotherapy / radiation
— Perianal Crohn’s disease (to promote healing)
129
COLORECTAL SURGERY
Associated colorectal surgery
Low Anterior Resection
— Portion of rectum and/or
sigmoid colon excised and
anastomosis formed.
— Anal sphincter present.
— May require Ileostomy.
Ø
Illustrated by Kevin Quinlan: anterior resection
END ILEOSTOMY
Illustrated by Kevin Quinlan: end ileostomy
Clinical features
Ø
Ø
Ø
Ø
130
Proximal end of ileum in RIF.
Spouted.
Single lumen.
Content: liquid / soft effluence.
COLORECTAL SURGERY
Associated surgery
Ø Panproctocolectomy
— Colon, rectum, and anus removed
— Results in permanent end ileostomy
— May have ileo-anal J-pouch procedure later if anal canal is functional. (this
is only in restorative proctocolectomy where the anus is preserved)
— Indications: IBD, Familial Adenomatous Polyposis (FAP).
Illustrated by Kevin Quinlan:
panproctocolectomy
Ø Total colectomy.
— Surgery from caecum to rectum.
— Rectum and anus present.
— Patient can later undergo a completion proctectomy and
ileo-anal J-pouch.
— Can be reversed.
— Indications: IBD emergency, large bowel obstruction, colorectal cancer.
Illustrated by Kevin Quinlan:
total colectomy
131
COLORECTAL SURGERY
Ø Ileo-anal J-pouch
— Ileum folded in J-shape and stapled
together to make a pouch, which is then
attached to the anus.
— Temporary loop ileostomy to protect newly formed pouch.
— Often performed after
restorative proctocolectomy where the anus is preserved.
— Pouchitis is a complication that presents with diarrhoea and pain. Treatment involves metronidazole.
Illustrated by Kevin Quinlan: J-pouch
END COLOSTOMY
Illustrated by Kevin Quinlan: end colostomy
Clinical features
Ø Proximal end of resected colon in the LIF.
Ø Single lumen, flush with skin – no spout.
Ø Content: solid effluence.
132
COLORECTAL SURGERY
Associated surgeries
Abdominoperineal resection (AP resection).
— Resection of sigmoid colon, rectum and anus.
— No anal canal.
— Permanent end colostomy.
— Indication: low rectal cancer.
Ø Hartmann’s procedure.
— Resection of sigmoid colon and upper rectum.
— Can also have a mucous fistula between rectum and abdominal skin.
Hence this end colostomy and mucous fistula may appear like a loop
colostomy.
— This end colostomy can be reversed, i.e., be temporary.
— Indications = emergency surgery:
■ Complications of sigmoid colon cancer.
■ Diverticular disease complications.
Ø
LOOP COLOSTOMY
Ø
Ø
Ø
Ø
Ø
Loop of colon in LIF or above umbilicus.
2 lumens present: active proximal spouted lumen and inactive distal lumen.
Solid effluence.
Usually temporary stoma.
Indications: Same as Loop ileostomy, therefore loop colostomy rarely done.
DEFUNCTIONING STOMA
Ø
Ø
This is a temporary stoma often used in rectal cancer surgery. It is created
when anastomosis is created following intestinal resection in order to protect
the anastomosis and allow for optimal healing conditions.
When healing is achieved the stoma is reversed and normal bowel continuity
is regained.
STOMA COMPLICATIONS
—
—
—
—
—
Stoma stenosis
Stoma retraction
Stoma necrosis
Parastomal hernia
High output stoma
133
COLORECTAL SURGERY
STOMA STENOSIS
— Stoma stenosis is narrowing or constriction of the stoma or its lumen.
— This condition may occur at the skin or fascial level of the stoma.
Aetiology
—
—
Causes include hyperplasia, adhesions, sepsis, and radiation of the intestine before stoma surgery, local inflammation, hyperkeratosis,
and surgical technique.
Stoma stenosis frequently is associated with Crohn’s disease.
Clinical Presentation
—
—
—
With GI stoma stenosis, bowel obstruction frequently occurs
signs and symptoms are abdominal cramps, diarrhoea, increased
flatus, explosive stool, and narrow-calibre stool.
The initial sign is increased flatus.
Management
high-fiber food
—
—
Conservative therapy includes a low-residue diet, increased fluid intake,
and correct use of stool softeners or laxatives for colosto¬mies.
Partial or complete bowel obstruction and stoma stenosis at the fascial
level require surgical intervention.
STOMA RETRACTION
— In stoma retraction, the stoma has receded about 0.5 cm below the skin
surface.
— Retraction may be circumferential or may occur in only one section of
the stoma.
Aetiology
— Stoma retraction is most common in patients with ileostomies.
— The usual causes of stoma retraction are tension of the intestine or obesity.
— Stoma retraction during the immediate postoperative period relates to
poor blood flow, obesity, poor nutritional status, stenosis, early removal
of a supporting device with loop stomas, stoma placement in a deep
skinfold, or thick abdominal walls.
— Late complications usually result from weight gain or adhesions.
134
COLORECTAL SURGERY
Clinical features
— A retracted stoma has a concave, bowl-shaped appearance.
— Retraction causes a poor pouching surface, leading to frequent peristomal skin complications.
Management
— Typical therapy is use of a convex pouching system and a stoma belt.
— If obtaining a pouch seal is a problem and the patient has recurrent
peristomal skin problems from leakage, stoma revision should be considered.
NECROSIS
Aetiology
— Blood flow and tissue perfusion are essential to stoma health. A stoma
may be affected by both arterial and venous blood compromise.
— The cause of necrosis usually relates to the surgical procedure, such
as tension or too much trimming of the mesentery, or vascular compromise.
— Other causes of vascular compromise include hypovolemia, embolus,
and excessive oedema.
Clinical features
— Stoma necrosis usually occurs within the first 5 postoperative days.
— Discoloration may be cyanotic, black, dark red, dusky bluish purple, or
brown.
— The stoma mucosa may be hard and dry or flaccid.
— The stoma may have a foul odour.
— Associated complications may include stoma retraction, mucocutaneous separation, stoma stenosis, and peritonitis.
Management
— Superficial necrosis may resolve with necrotic tissue simply sloughing
away.
— But if tissue below the fascial level is involved, surgery is necessary.
— A transparent two-piece pouching system (stoma bag) is recommended for frequent stoma assessment.
— The pouch may need to be resized often.
135
COLORECTAL SURGERY
PARASTOMAL HERNIA
—
—
—
Parastomal hernias are incisional hernias in the area of the abdominal
musculature that was incised to bring the intestine through the abdominal wall to form the stoma.
The intestine or bowel extends beyond the abdominal cavity or abdominal muscles; the area around the stoma appears as a swelling
or protuberance.
They may completely surround the stoma (called circumferential hernias) or may invade only part of the stoma.
Aetiology
— Parastomal hernias can occur any time after the surgical procedure but
usually happen within the first 2 years.
— Patient-related risk factors include obesity, poor nutritional status at the
time of surgery, presurgical steroid therapy, wound sepsis, and chronic
cough.
— Risk factors related to technical issues include size of the surgical
opening and whether surgery was done on an emergency or elective
basis.
— Recurrences are common if the hernia needs to be repaired surgically.
HIGH OUTPUT STOMA
— Stoma output > 1500mls-2000 mls / 24 hours (NB look at stoma output chart).
Aetiology
— Surgery that results <200cm residual small bowel and no colon.
— Intra-abdominal sepsis.
— Intestinal obstruction at stoma site. Investigate with CT scan.
— Enteric infection (clostridium difficile).
— Recurrent disease in the remaining bowel.
— Radiation enteritis.
— Medication (sudden withdrawal of steroids, opiates, administration of
prokinetics, laxatives).
136
COLORECTAL SURGERY
Complications
— Water & sodium depletion (thirst, postural hypotension, headaches,
nausea).
— Sodium depletion, so kidneys trying to conserve sodium. Results in
urine output < 800 ml/day, renal impairment and urinary sodium < 20
mmol/litre.
— A urine sodium concentration can be low before serum sodium levels
change. His urine spot sodium was 8mmol/litre.
— Hypo magnesia serum magnesium <0.7mmol/litre.
— Malnutrition (due to malabsorbtion / food avoidance) with a low albumin.
— Frequent emptying of stoma bag / leakage / skin care problems. Can
lead to excoriation.
Management
—
—
—
—
—
50% will be transient, managed with oral restriction of hypotonic liquids
Reduce mortality with loperamide and codeine phosphate
Replace electrolytes (sodium and magnesium)
Treat intra-abdominal sepsis if present
30% may need TPN
137
NOTES
138
INFLAMMATORY BOWEL DISEASE
Chapter 6
Inflammatory Bowel Disease
139
INFLAMMATORY BOWEL DISEASE
Contents:
• Crohn’s Disease
• Ulcerative Colitis
140
INFLAMMATORY BOWEL DISEASE
Introduction
— Inflammatory Bowel Disease (IBD) is a term that incorporates 2 major
disorders, Ulcerative Colitis (UC) and Crohn’s Disease (CD)
— These two disorders have distinct pathology but show some clinical
overlap.
— Less than 10% of patients with inflammatory bowel disease (IBD) have
an extra-intestinal manifestation at initial presentation. However, approximately 25% of patients will develop these in their lifetime.
— The aim of treatment in IBD is firstly to induce remission and then
to prevent future flare ups (i.e. maintain remission)
Ulcerative Colitis
Crohns Disease
Inflammatory disorder of the mucosa
and superficial submucosa of the colon
only
A chronic, non-caseating
granulomatous disease
Rectum always affected
May extend proximally to involve a
amount of the large colon
Characterised by a full thickness inflammatory process that can affect
any part of the GIT from the lips to the
anal margin
Associated with several variable extra-intestinal disorders
Backwash ileitis – in 20% with
pancolitis the terminal ileum may
also be involved
Epidemiology
Ulcerative Colitis
Ø Typically occurs in the late teens and early twenties with an equal distribution between genders.
Ø 6 – 8% of patients have affected 1st degree relative.
Ø Multitude of studies examining environmental and familial risk factors but
without causal association.
Ø Results from poorly defined interactions between genetic and environmental factors.
141
INFLAMMATORY BOWEL DISEASE
Crohns Disease
Ø Increasing incidence in Ireland (3.1 – 20.2. / 100,000)
Ø Prevalence is now similar to ulcerative colitis (approx. 200/100,000).
Ø More common in Caucasians.
Ø Onset in teens and twenties.
Ø Smoking is a risk factor.
Pathology
Ulcerative Colitis
— The inflammation is usually confined to the mucosa and superficial submucosa.
o Granular, hypervascular, oedematous mucosa.
o Mucosal ulcers (aphthous) and crypt abscesses form.
o Acute neutrophil infiltration occurs.
— Residual islands of intact but oedematous mucosa may project into the bowel
lumen (“pseudopolyposis”).
— Fibrosis of the mucosa and submucosa results in loss of haustration (‘lead
pipe colon’).
— Long-standing disease predisposes to dysplastic changes in the epithelium
and development of adenocarcinoma.
Crohn’s Disease:
Sites affected:
Small bowel involvement in 80% (terminal ileum in particular).
Large bowel alone in 20%.
Both large and small bowel in 50%.
Perianal disease in over 30%.
Upper GIT in 5 to 15%.
— Crohn’s disease is a chronic inflammation which is transmural (i.e. it affects
the entire thickness of the bowel wall).
— The wall becomes markedly thickened by oedema, but the epithelium remains remarkably intact being marked with deep fissuring ulcers which
results in cobblestoning.
— One or more discrete areas of bowel may be affected in what are termed ‘skip
lesions’.
— Crohn’s disease is characterized by the presence of non-caseating granulomas. These contain multinucleated giant cells and are scattered through the bowel wall and regional lymph nodes.
— Long-standing inflammation leads to progressive fibrosis of the thickened
bowel wall and elongated strictures.
— Perforation, abscesses and fistulae are some “fistulising” sequelae of transmural inflammation.
142
INFLAMMATORY BOWEL DISEASE
Clinical Features:
Ulcerative Colitis
Image by Niamh Adams: toxic megacolon.
Toxic Megacolon
c. Diff infection
**Surgical Emergency**
— Massively dilated colon with
patchy necrosis.
— Systemically ill with high fever,
marked tachycardia and dehydration.
— Culminates in perforation and fatal
peritonitis unless emergency
colectomy is performed.
Pancolitis
—
—
—
—
—
May have backwash ileitis.
Systemically unwell.
Hypokalaemia due
to impaired water and
sodium absorption.
Hypoalbuminema:
negative acute phase
reactant from systemic
response and decreased
oral intake.
Anemia from blood
loss and inflammatory
response.
Left-sided
— To splenic flexure.
— Larger stool volume.
— Blood & mucous.
— More severe
systemic complications.
Proctitis
— Commonest presentation.
— Bloody diarrhoea.
— Mucus mixed with diarrhoea.
— Rectal pain and tenesmus.
— Urgency.
— Associated weight loss, anergia, loss of appetite.
Illustrated by Kevin Quinlan: Colon.
143
INFLAMMATORY BOWEL DISEASE
Crohn’s Disease
Clinicopathological Features
Mucosal inflammation causes diarrhoea which, if the colon is involved, may
be streaked with mucus and blood.
— If small bowel is inflamed, diarrhoea occurs and digestive and absorptive functions may be compromised.
— Extensive disease results in general malabsorption causing protein calorie malnutrition, iron and folate deficiency and anaemia.
— In children, Crohn’s disease may cause marked growth retardation.
— Excess bile salts in the faeces cause colonic irritation (and more diarrhoea) while diminished recirculation of bile salts may result in
gallstone formation.
— Involvement of the terminal ileum may reduce vitamin B12 absorption
but serious deficiency usually occurs only after surgical resection.
Ø
Transmural inflammation
— Crohn’s disease of the terminal ileum may mimic acute appendicitis.
— At appendicectomy, the terminal ileum is visibly inflamed and the bowel
wall abnormally thick to palpation.
— Serosal inflammation may cause a diseased segment of bowel to adhere
to adjacent abdominal structures.
— Several complications may occur if these become matted together by the
inflammatory process.
• Adhesions
• Tough, fibrotic bands of connective tissue may cause bowel obstruction.
— Perforation
• Free perforation is rare
• Contained perforation may occur which causes localised pericolic or
pelvic abscess formation
— Fistula
• Develop between diseased bowel and other hollow viscera causing
typical clinical phenomena
Ø
Perianal problems
— Superficial ulcers with undermined edges are relatively painless.
— Fistulation through the posterior wall of the vagina may lead to rectovaginal fistula and continuous leakage of gas and/or faeces per
vagina.
— Perianal disease is frequently associated with dense, fibrous stricturing
at the anorectal junction.
— Incontinence may develop as a result of destruction of the anal sphincter musculature because of inflammation, abscess formation,
Ø
144
INFLAMMATORY BOWEL DISEASE
fibrotic change and repeated episodes of surgical drainage.
— In severe cases, the perineum may become densely fibrotic, rigid and
covered with multiple discharging openings (watering-can perineum).
the result of multiple fistulae extending from the urethra to open within the perineum
Upper GI Tract
— The upper GI tract may be affected less frequently and may consist
of oral ulceration, dysphagia with oesophageal involvement or upper abdominal pain and, perhaps, gastric outlet obstruction with
gastroduodenal involvement.
Ø
Given the above, CD has a wider variety of clinical presentations than UC:
Ø
Ø
Ø
Ø
Inflammatory features
— Fever
— Malaise
— RIF pain
— Weight loss
— Growth retardation
Fistulising features
— Ileo-enteric (ileoileal / ileocolic) presents with tender mass, fever.
— Peritonitis may occur if there is free perforation.
— Cysto-enteric fistula may present with pneumaturia.
— Entero-vaginal fistula may present with faeculent discharge.
— Entero-cutaneous may present with cutaneous discharge and cellulitis.
Stenosing features
— Colicky abdominal pain
— Small bowel obstruction
— Weight loss (“food fear”)
Perianal disease
— Fissures and fistulas
145
INFLAMMATORY BOWEL DISEASE
Extra-intestinal manifestations
“A PIE SAC”
A
P
I
E
S
A
C
– Aphthous Ulcers.
– Pyoderma Gangrenosum.
(eye) – Iritis, Uvetits, Episcleritis.
– Erythema Nodosum.
– Sclerosing cholangitis / Sacroilitis.
– Arthritis.
– Clubbing of the fingers.
Illustrated by Kevin Quinlan:
extra-intestinal manifestations
of IBD.
Extra-intestinal manifestations of CD and UC
Musculoskeletal system
• Arthritis: ankylosing spondylitis isolated joint involvement.
• Hypertrophic osteoarthropathy: clubbing, periostitis.
• Miscellaneous manifestations: osteoporosis, aseptic
necrosis, polymyositis.
Dermatologic
•
and oral systems
•
•
•
Reactive lesions: erythema nodosum, pyoderma
gangrenosum, aphthous ulcers, necrotising vasculitis.
Specific lesions: fissures, fistulas, oral Crohn’s disease, drug rashes.
Nutritional deficiencies: acrodermatitis enteropathica,
purpura, glossitis, hair loss, brittle nails.
Associated diseases: vitiligo, psoriasis, amyloidosis.
Hepatobiliary system
•
•
•
Primary sclerosing cholangitis, bile-duct carcinoma.
Associated inflammation: autoimmune chronic active
hepatitis, pericholangitis, portal fibrosis, cirrhosis,
granulomatous disease.
Metabolic manifestations: fatty liver, gallstones associated with ileal Crohn’s disease.
Ocular system
• Uveitis/iritis, episcleritis, scleromalacia, corneal ulcers, retinal vascular disease.
Metabolic system
• Growth retardation in children and adolescents, delayed sexual maturation.
Renal system
146
• Calcium oxalate stones.
Endosco
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§ to Stool culture to
§
Stool
culture
therapy.
associated
with
a fall
eliminate the
§
MR Enterography
eliminate
in serumthe
albumin
possibility of an possibility of an
colitis: infectious colitis:
§ infectious
Faecal calprotectin
- Campylobacter - Campylobacter
§ - Stool
culture to- Shigella
Shigella
- Amoebiasis
the
- eliminate
Amoebiasis
ofdifficile
an - Clostridium difficile
- possibility
Clostridium
sigmoidoscopy
sigmoidoscopy
Common
to both
**Mucosa is
Common
**Mucosatois both
 hyperaemic and
 hyperaemic and
infectious colitis:
- Campylobacter
- Shigella
- Amoebiasis
- Clostridium difficile
Specific to CDSpecific to CD
Specific to CD
Endoscopy:
Endoscopy:
Specific to CD
§
OGD :
OGD :
If upper
If upper GI symptoms
areGI symptoms are
present.
present.
May reveal deep May reveal deep
Endoscopy:
ulcers and
longitudinal ulcerslongitudinal
and
cobblestone
mucosa
in the mucosa in the
§ cobblestone
OGD :
duodenum,
stomach
or,
duodenum,
or,
If upper GI stomach
symptoms
rarely,are
in the oesophagus.
rarely, in the oesophagus.
present.
May reveal deep
longitudinal ulcers and
cobblestone mucosa in the
duodenum, stomach or,
rarely, in the oesophagus.
§
Imaging:
Imaging:
Small bowel enema
§
Small bowel§enema
o Areas
structuring dilatation.
and pre-stenotic dilatation.
o Areas of structuring
andofpre-stenotic
tendirregular
to be narrowed,
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and
when
o Areas tend toobe Areas
narrowed,
and when
terminal
ileum
is terminal ileum is
involved
theresign
mayofbe
a string sign of Kantor.
involved there may
be a string
Kantor.
§
CT with contrast
§Imaging:
CT with contrast
demonstrate
fistulae,abscesses
intra-abdominal
§
Small
enemao Can
o bowel
Can demonstrate
fistulae,
intra-abdominal
and abscesses and
bowel
thickening
or dilatation.
o bowel
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dilatation.
or dilatation.
§ tend
MR enterograpy
o Areas
to be narrowed, irregular and when terminal ileum is
§
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o may
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there
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sign
ofsmall
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o Effective
showing
small
bowel
stricturing
in
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patients.in young patients.
Small bowel
is examined
contrast
given
through a NJ tube.
§
CT o
withSmall
contrast
bowel o
is examined
by contrast
given by
through
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tube.
§ demonstrate
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o Can
fistulae, intra-abdominal abscesses and
§
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o enterocutaneous
Inorpatients
with enterocutaneous
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§
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demonstrate the anatomy
and the
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and allow
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o adequate
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forsmall
futureplanning
surgery.
§
o Small bowel is examined by contrast given through a NJ tube.
Fistulography
o In patients with enterocutaneous fistulae, fistulography helps
demonstrate the anatomy and complexity of fistulae and allow
adequate planning for future surgery.
147
INFLAMMATORY BOWEL DISEASE
Management:
•
•
Therapy
The choice of Medical Treatment depends on the severity of flares,
disease extent, symptoms and the risk of long-term complications
BOTH diseases are highly catabolic and involvement of MDT including dieticians/nutritionists is crucial
Indication
Used in
Local therapy
— Used in all grades of
—
(suppositories, foam disease severity or liquid enema)
— Ideal for proctitis
— Corticosteroid or
— Foam enemas extend
5-aminosalicylic acid up to splenic flexure
(5-ASA) preparations
— Induce and maintain
remission
Systemic corticosteroids —
(oral prednisolone,
—
budesonide, intravenous
hydrocortisone)
—
Since UC more
commonly affects the
rectum, this therapy
is more common in
UC but also used in CD
Additive to local therapy — CD and UC to
Induce remission induce remission.
for moderate or
severe exacerbations
Not commonly used in
maintenance therapy
due to side effects
Systemic therapy –
— Long-term maintenance
Non-immunologic therapy to minimise
— 5-ASA preparations relapse
(sulfasalazine,
— Acute therapy for
mesalazine or pancolitis
olsalazine)
— Both UC and CD
Systemic Therapy –
— Long term maintenance
Immunologic therapy to minimise
— Azathioprinerelapse
— 6-mercaptopurine
— Acute therapy for
— Anti-TNF: Infliximab, pancolitis
Adalimumab, Golimumab
Anti Integrin (anti alpha1beta7): Vedolizumab
— Anti interleukin IL12/23
— Both UC and CD
148
INFLAMMATORY BOWEL DISEASE
1. Subtotal Colectomy with ileostomy
—
—
—
—
—
Safest operation in the emergency situation.
Most of the diseased colon is removed, but the patient is left with an
inflamed rectal stump.
Months later, when the patient is well, this may be revised
Alternatively, rectum may be retained and treated with local therapy plus
surveillance, though cancer risk remains.
Crohn’s colitis accounts for 8 per cent of such procedures for acute
colonic disease.
2. Restorative proctocolectomy (Ileal pouch-anal anastomosis/
Park’s pouch)
—
—
—
—
—
—
A sphincter-preserving operation avoiding permanent ileostomy.
Entire colon and rectal mucosa is excised and a pouch reservoir is
fashioned from a loop of terminal ileum.
The pouch is brought into the pelvis and anastomosed to the upper
anal canal.
A temporary ileostomy is usually retained for a few months to allow
healing.
Many patients have excellent continence.
May get “pouchitis” which is inflammation within the neo-rectum.
3. Pan-proctocolectomy with permanent ileostomy
— Includes removal of rectum and entire colon.
— Generally recommended for elderly patients in whom sphincter-
preserving procedures are inadvisable.
149
INFLAMMATORY BOWEL DISEASE
Crohn’s Disease:
1.
Ileocecal resection:
Usual procedure for terminal ileal Crohn’s with a primary anastomosis between
the ileum and the ascending or transverse colon
2.
Segmental Resection:
Short segments of small or large bowel strictures can be performed. This is
usually a preferred method of treatment when there is a complication of the
disease e.g. perforation or fistula formation
3.
Stricturoplasty:
Multiple areas of stricture formation in CD can be treated by a local widening
procedure of endoscopic dilatation to avoid small bowel resection
Note: This is not usually used for a colorectal stricture
4. Subtotal Colectomy with ileostomy :
Crohn’s colitis accounts for 8 per cent of such procedures for acute colonic disease.
Pre Op Preparation –
— The patients overall medical condition should be optimized by correcting anaemia, fluid depletion, electrolyte imbalance, and malnutrition prior to surgery
where possible.
—
Patients with UC/CD who require surgery may be on one or more immunosuppressive drugs or biologic agents (e.g., infliximab). Most immunosuppressive drugs can be discontinued just before surgery without negative effects however this should be discussed with at an MDT meeting.
— Abdominal Imaging : CT Enterography / MR Enterography are very accurate in
assessing lesions and complications (abscess/fistula) in Crohn Disease.
— Patients who undergo abdominal surgery for UC/CD are at a moderate-to-high
risk for developing a venous thromboembolism due to systemic inflammation.
They should receive thrombo-prophylaxis.
150
NOTES
151
NOTES
152
PERIPHERAL VASCULAR DISEASE
Chapter 7
Peripheral Vascular Disease
153
PERIPHERAL VASCULAR DISEASE
Contents:
—
Peripheral Arterial Disease
—
Acute Limb Ischaemia
—
Abdominal Aortic Aneurysm
—
Varicose Veins
—
Deep Vein Thrombosis
—
Leg Ulcers
—
Carotid Disease
—
The Diabetic Foot
154
PERIPHERAL VASCULAR DISEASE
PERIPHERAL ARTERIAL DISEASE (PAD)
Definition: Chronic insufficiency of the arterial blood supply of the limbs (most
commonly the legs) due to stenosis or occlusion of the vessels
Ø Primary pathological cause is atherosclerosis
Ø Less common causes include fibromuscular dysplasia, vasculitides (Buerger’s
disease, Takayasu arteritis), radiation-induced vascular injury
Symptoms:
Ø Intermittent Claudication: Muscular pain (most commonly in calves and/or buttocks) brought on by exercise and relieved by rest
— Caused by demand for oxygen by muscles during exertion in the context of reduced blood supply
Ø Critical Limb ischaemia:
— Rest pain > 2 weeks
Pain in the forefoot when lying flat at night, classically relieved by
hanging leg over side of bed
— Tissue loss (ulcers, gangrene, necrosis)
Ø Pallor of the lower limb
Ø Reduced temperature of the lower limb
Ø Burning sensation, paraesthesia
Ø Leriche Syndrome: Occlusion at bifurcation of aorta causing classical triad
— Buttock/thigh claudication
— Absent/reduced femoral pulses
— Erectile dysfunction
Rutherford-Fontaine Classification
I
Asymptomatic
II
Intermittent Claudication: Can be further classified into IIA (claudication distance>200m) and IIB (claudication distance<200m)
III
Rest Pain
IV
Tissue Loss (ulcers, gangrene, necrosis)
Differential Diagnoses to consider apart from Intermittent Claudication:
Ø Spinal stenosis
Ø Osteoarthritis
Ø Nerve root entrapment (e.g. Sciatica)
155
PERIPHERAL VASCULAR DISEASE
Key Features on History Taking:
Where is the pain? When did it begin? (Essential to distinguish between chronic
limb ischaemia and acute limb ischaemia)
Is it worse by walking?
How far can you walk before you need to stop? (Claudication distance)
Does the pain go away when you stop?
Does the pain ever occur at rest? At night? Relieved by hanging over the edge of
the bed?
Noticed any change of colour or temperature of your legs?
Have you noticed any black areas or sores on your leg that won’t heal?
PAD risk factors – Are you a smoker? Do you have high cholesterol? etc. (see
below)
Risk Factors:
Ø Non modifiable factors (male, age>55, family history of vascular disease)
Ø Smoking (most important risk factor)
Ø Hypertension
Ø High Cholesterol
Ø Diabetes
Ø Previous Stroke / Myocardial infarct / Angina
Ø Hyperhomocysteinemia
Investigations:
Ø Ankle-Brachial Pressure Index (ABPI): Ratio of peak systolic doppler ankle
pressure to arm pressure
ABPI interpretation
1.1-0.9 Normal
0.9-0.5 Intermittent claudication
<0.5 Rest pain
<0.3 Tissue loss
>1.1 Calcified arteries (typically seen in diabetics) False elevation
Ø Duplex Ultrasound
Ø CT Angiogram/MR Angiogram
Ø Digital Subtraction Angiography DSA
156
PERIPHERAL VASCULAR DISEASE
Management:
Ø Conservative (Risk factor modification)
— Smoking cessation (CRUCIAL)
— Physical exercise
— Dietary modification
Ø Medical
— Antiplatelet therapy (Aspirin, Clopidogrel)
— Statin: lowers cholesterol, improves walking distance, reduces rate of
major vascular events
— Control BP
— Tight glycaemic control
— Cilostazol: Phosphodiesterase inhibitor which causes vasodilation – for
symptom relief in intermittent claudication only
— Pentoxifylline – xanthine derivative – for symptom relief in intermittent
claudication only
Ø Endovascular:
— Angioplasty +/- stenting –In many cases procedures can be performed
as day case procedures. Procedures can also be performed under local
anaesthesia
Ø Surgical:
— Bypass procedures used for disease not best managed via endovascular techniques
— Can use synthetic graft (e.g. PFTE/Dacron) or vein graft-the best option- (e.g. GSV)
— Examples: Fem-pop bypass, fem-distal bypass, aorto-bifem bypass,
axillo-bifem bypass, fem-fem crossover
— Amputation if non-viable limb
Illustrated by Kevin Quinlan: Balloon angioplasty of arterial atherosclerosis
157
PERIPHERAL VASCULAR DISEASE
ACUTE LOWER LIMB ISCHAEMIA
Definition: Abrupt interruption in perfusion that threatens viability of the lower limb
Causes
Ø Acute thrombus with pre-existing atherosclerosis (Acute-on-chronic Ischaemia)
— Often patient has a history of claudication.
— Usually no obvious source of emboli
Ø Embolus
— Classically lodges at branching points of vessels.
— Cardiac sources account for 70-80% of emboli (mural thrombus after MI,
arrhythmias, infective endocarditis, prosthetic heart valves, atrial myxoma).
— Can occur from pre-existing atheromas or arterial aneurysms.
— Blue toe syndrome- Atheroembolic debris resulting in distal small arterial
occlusion with blueish discoloration of distal foot
— Paradoxical emboli can occur from intracardiac shunts (e.g. PFO) or AV
malformations.
Image by Dr.Nauar Knightly of ‘Blue Toe Syndrome’ (with consent)
Ø Other causes
— Direct arterial trauma.
— Intra-arterial drug injection.
— Aortic dissection.
— Popliteal aneurysm.
— Iatrogenic.
158
PERIPHERAL VASCULAR DISEASE
Clinical Features (6 P’S): Pain, pallor, pulselessness, perishing cold, paraesthesia,
paralysis
Complications if untreated
Irreversible tissue damage within 6 hrs: Limb loss, mortality
Types of Amputation:
Ø Digital
Ø Ray- if gangrene extends to forefoot
Ø Transmetatarsal- used if several toes are gangrenous
Ø Below knee amputation (BKA)
Ø Through knee amputation
Ø Above knee amputation (AKA)
Management
Ø If clear evidence of acute ischaemia on history and exam, do not delay definitive treatment.
Ø Patients usually have other significant comorbidities: IHD, renal disease.
Ø Give O2.
Ø IV access and fluids if dehydrated.
Ø Bloods – FBC, U&E, coag, troponin, glucose, group & save.
Ø CXR.
Ø ECG- looking for cardiac cause.
Ø Analgesia- Morphine.
Ø Give unfractionated Heparin
— Stat dose of 5000 IU then infusion of 1000 IU/hr.
— Be sure there are no contraindications to Heparin use.
— Check aPTT in 4-6 hrs.
— Aim for aPTT 60-90.
Ø Definitive treatment depends on severity of ischaemia
— Irreversible ischaemia (petechial haemorrhages, hard muscles)– amputation.
— If limb is swollen/tender with loss of power or sensation – consider amputation if there are life threatening systemic complications.
— If an obvious embolus is the cause, perform urgent embolectomy +/ fasciotomy. A Fogarty catheter is used to extract the embolus.
— If limb is viable – can continue IV Heparin + CT angio or perform angiography (stop Heparin 4 hrs before). Thrombolysis +/- angioplasty
can then be performed. Be sure no contraindications to thrombolysis.
159
PERIPHERAL VASCULAR DISEASE
Complications of Reperfusion
Ø Reperfusion injury.
Ø Rhabdomyolysis:
— Elevated K+, elevated CPK, renal impairment, myoglobinuria.
— Treat with aggressive IV fluids, diuresis with Mannitol, alkalinisation of
urine.
Ø Compartment syndrome – prevent and treat with 4-compartment fasciotomy
160
PERIPHERAL VASCULAR DISEASE
ABDOMINAL AORTIC ANEURYSMS
llustrated by Kevin Quinlan: Infra-renal abdominal aortic aneurysm
Definition: abnormal localized dilatation of aorta exceeding normal diameter by
>50% or diameter >3cm.
Ø AAA is a true aneurysm: Contains all 3 layers of vessel wall
— Transmural inflammatory change, abnormal collagen remodelling, loss
of elastin and smooth muscle cells, resulting in aortic wall thinning and
progressive expansion
Ø Male: female 9:1.
Ø Prevalence- 4% in males >65yrs.
Ø 95% of AAA’s are infrarenal
Ø Described as either fusiform or saccular
Ø >80% of patients with ruptured AAA die before reaching hospital
Ø 50% of patients with ruptured AAA who arrive will not survive surgery
161
PERIPHERAL VASCULAR DISEASE
Risk Factors:
Ø Risk factors as for PVD
— 10-fold increased risk in smoking.
— 50% increased risk in poorly controlled HTN.
— Increased expansion and rupture risk associated with smoking and
uncontrolled HTN.
Ø Collagen and elastin defects e.g. Marfan’s, EDS.
Ø AAA diameter > 5.5cm and expansion rate >0.5cm/6 months associated with
increased risk of rupture.
Ø Aortitis - from bacteraemia, endocarditis, mycotic aneurysms.
Surveillance (Current UK screening/surveillance guidelines)
3cm – 4.4cm
Annual surveillance USS
4.5cm – 5.4cm
3 monthly USS surveillance
5.5cm or greater
Surgery
The rate of expansion is directly related to size of aneurysm
Clinical Features
Ø Most are asymptomatic: <50% detected on exam by a pulsatile and expansile
mass in abdomen.
Ø 40% detected incidentally on imaging for other reason.
Ø There is an associated increased risk of peripheral aneurysms, particularly
popliteal aneurysm
Ø Symptoms arise from aneurysm expansion, rupture or peripheral embolism
include:
— Abdominal/back/flank pain.
— Distal peripheral embolization or ischaemia.
— Upper G.I. Bleeding from aortoenteric fistula.
— Syncope or shock with large pulsatile mass, ecchymoses or death from
a ruptured AAA.
Differential Diagnosis
If patient presents with sudden onset abdominal/back/flank pain:
Ø Ischaemic bowel
Ø Perforated PUD
Ø Pyelonephritis
Ø Nephrolithiasis
Ø Acute pancreatitis
Imaging
Ultrasound
Ø Best initial imaging modality
162
PERIPHERAL VASCULAR DISEASE
Ø 98% accuracy
Ø Non-invasive
Ø Does not define extent of aneurysm
Ø Inadequate for planning repair
CT abdomen with IV Contrast
Ø Highly accurate in determining size and extent of aneurysm
Ø Defines relationship of AAA to renal arteries
Ø Can tell if AAA is leaking
Ø Determines suitability of endovascular repair
Elective Repair
Ø Open surgical repair
— Uses a synthetic (Dacron) graft to repair aneurysm.
— Long midline incision (laparotomy).
— Aorta clamped below renal arteries where possible to prevent renal
ischaemia.
— Graft can be straight if iliac arteries not involved or bifurcated if iliac
arteries involved.
—
3-7% mortality
Ø Endovascular aneurysm repair (EVAR)
Insertion of a stent over aneurysmal segment.
— Small groin incisions (may be vertical or transverse)
— Does not require cross clamping of aorta.
— Procedure carried out under direct radiological guidance.
— Uses high doses of nephrotoxic contrast.
— Reduced early mortality.
— High early re-intervention rate if endoleak occurs.
— Requires lifelong surveillance post-op for endoleak.
Complications of AAA Repair
Ø Early
— Death.
— Haemorrhage- uncontrolled vessels or anastomotic breakdown
— Myocardial ischaemia- 20% of patients
— Cardiac arrhythmias.
— Cardiac failure
— Bowel ischaemia- may present with abdominal pain, bloody diarrhoea.
Urgent laparotomy if evidence of peritonitis
— Abdominal compartment syndrome
— Atelectasis, ARDS, RTI
— Endoleak (EVAR)
— Renal dysfunction- pre-existing renal disease, nephrotoxic contrast/
antibiotics, prolonged hypotension/ dehydration, use of NSAIDs
— Limb ischaemia
163
PERIPHERAL VASCULAR DISEASE
— Wound infection- reduced by prophylactic antibiotics
— Impaired sexual function
Ø Late
— Graft infection- usually needs to be removed.
— Graft limb occlusion- within 30 days, may present with acute ischaemic
limb.
— Aortoenteric fistula
— Endoleak (EVAR)
Endoleak: An endoleak is persistent blood flow into an aneurysmal sac after EVAR
is performed.
Type I Leak at attachment sites of graft
Type II Filling of aneurysmal sac by collateral vessels (IMA, Lumbar)
Type III Leak through defect in graft
Type IV Leak through fabric of graft due to porosity
Type V Expansion of aneurysm sac without evidence of leak on imaging
Other Aneurysms:
Ø Thoraco-abdominal
— Often asymptomatic.
— Can present with chest pain, back pain, acute aortic regurgitation, acute
cardiac failure.
— Widened mediastinum on CXR.
— Rupture is rare without pre-existing symptoms.
— 20% mortality with elective repair.
— Endovascular repair may be used (Fenestrated or Branched Grafts)
Ø Femoral
— Presents with pulsatile groin swelling +/- lower limb ischaemia.
Ø Popliteal
— Mostly asymptomatic but bilateral.
— Can cause acute limb ischaemia.
Ø Carotid
— Pulsatile neck swelling.
— May have neurological or pressure symptoms.
— Diagnosed with carotid duplex scan.
Ø Iliac
— Mostly asymptomatic.
— Rupture may be missed as acute abdomen or renal colic.
Ø Visceral
— Splenic artery aneurysms most common.
164
PERIPHERAL VASCULAR DISEASE
RUPTURED AAA
Clinical Features:
Ø Presentation may be delayed if rupture is contained within retroperitoneal space.
Ø A contained leak may initially be haemodynamically stable but can proceed
rapidly to rupture.
Ø Longstanding leak causing aortoenteric fistula can present with high output
cardiac failure and GI bleed.
Ø Sudden onset abdominal/back/flank pain.
Ø Sudden collapse with hypotension.
Ø May have a history of AAA under surveillance.
Ø Pulsatile abdominal mass is not always palpable.
Management
Ø Airway
Ø Breathing (give 15L 100% O2 via non-rebreather mask)
Ø Circulation (Wide bore IV Access X2, give IV Fluids)
— Bloods (FBC, U&E, coag, group & cross-match 10 units)
— Request platelets & FFP
— Urinary catheter: monitor urinary output
Ø Do not aggressively hydrate: Allow permissive hypotension to avoid worsening
a rupture
Ø Analgesia
Ø Alert vascular surgeon, anaesthetist, theatre, ICU
Ø Gain consent for surgery
Ø If not a candidate for surgery: analgesia & palliative care
— Based on age, co-morbidities, extent of aneurysm, patient’s wishes,
family’s wishes
Ø To aid diagnosis and allow planning of repair: CT Angiogram
Ø If a candidate for open/endovascular repair: Urgent transfer to theatre
Ø ICU care post-op
165
PERIPHERAL VASCULAR DISEASE
VARICOSE VEINS
Image by Azlena Ali Beegan: Varicose veins (with consent)
The venous system of the leg is comprised of three groups
1. Superficial veins- Great and small saphenous systems (GSV, SSV) and
tributaries.
2. Deep venous system- veins running between the muscular compartments
of the leg.
3. Perforators in the calf and thigh- connect superficial and deep systems.
Ø Blood passes from the superficial to the deep systems via perforators.
Ø Backflow is prevented by the presence of valves in the deep and perforator
veins.
Ø Varicose veins (VVs) are tortuous dilated segments of veins associated with
venous hypertension caused by incompetent valves.
Ø Typical varicose veins are superficial branches of the long and short saphenous
system.
Ø More common in females
166
PERIPHERAL VASCULAR DISEASE
Risk factors for varicose veins
•
•
•
•
•
Advancing age
Prolonged standing
Elevated BMI
Smoking
Sedentary lifestyle
•
•
•
•
•
•
High oestrogen states
Pregnancy
Pelvic masses
Previous DVT
Ligamentous laxity
Lower limb trauma
Clinical Features: Patients may present with worsening symptoms or complications
or cosmetic concerns.
Symptoms:
Ø Pain
Ø Heaviness of leg
Ø Oedema- worse in evening, hot weather
Ø Dry skin
Ø Tightness
Ø Itching
Complications
Ø Stasis dermatitis/Eczema
Ø Phlebitis
Ø Lipodermatosclerosis- fibrosing dermatitis of subcutaneous tissue
Ø Skin pigmentation- due to haemosiderin deposition
Ø Ulceration
Ø Bleeding
Diagnosis & Investigations
Ø Typically a clinical diagnosis
Ø Always examine the abdomen to assess for an abdominal/pelvic mass
Ø Trendelenburg test and Perthes test can help clinically identify point(s) of incompetence
Ø Ultrasound Duplex of superficial and Deep veins: Gold standard to define anatomy and levels of incompetence.
Management
Ø Conservative
— Leg elevation
— Exercise
— Weight loss
Ø Medical
— Compression stockings
— Sclerotherapy- laser, foam
— Topical agents for skin changes (i.e. moisturising creams)
167
PERIPHERAL VASCULAR DISEASE
Ø Surgical
— Radiofrequency ablation
— Laser ablation
— Local stab avulsions
¾ Open ligation +/- GSV stripping
Ø Indications for surgery
— Cosmetic
— Symptomatic
— Prevent complications
Ø Complications of surgery
— Nerve injury resulting in area of pain/paraesthesia/numbness
— Deep venous thrombosis (DVT)
— Recurrence
— Bruising/haematoma
— Bleeding
— Wound infection
168
PERIPHERAL VASCULAR DISEASE
DEEP VENOUS THROMBOSIS
Virchow’s triad
Factors contributing to thrombosis
1. Stasis of blood flow
2. Endothelial injury
3. Hypercoaguability
Risk factors for Deep Vein THROMBOSIS
Trauma, Travel (long-distance flights)
Hormones (OCP, HRT)
Road traffic accidents (fractures)
Operations
Malignancy
Blood disorders: Factor V Leiden, protein C/S deficiency, antithrombin deficiency
Obesity, Old age, Orthopaedic surgery
Serious illness (prolonged hospital stay)
Immobilisation, Inadequate hydration
Smoking
Clinical Features
Ø Limb swelling
Ø Pain
Ø Warmth
Ø Erythema
Ø Homan’s sign- calf pain on dorsiflexion of foot (unreliable and should not be
performed due to risk of embolisation).
Ø May have mild pyrexia and tachycardia.
Ø May be asymptomatic
Ø Complications of DVT: PE, chronic venous insufficiency, venous gangrene.
Diagnosis & Investigations
Ø D-dimers: Sensitive but not specific
Ø Duplex scan- investigation of choice for DVT.
Ø CTPA- best for suspected PE.
Prophylaxis:
Ø Prophylactic low molecular weight heparin
Ø TEDS
Ø Mobilisation
Ø Hydration
Ø Smoking cessation
Ø Stop OCP 4-6 weeks pre-op
169
PERIPHERAL VASCULAR DISEASE
Wells Probability Score for DVT
Ø Active malignancy (1)
Ø Paralysis, paresis or recent plaster immobilisation of lower limbs (1)
Ø Localised tenderness along deep venous system (1)
Ø Entire leg swollen (1)
Ø Calf swelling >3cm & larger than asymptomatic side (1)
Ø Pitting oedema (1)
Ø Collateral superficial veins (1)
Ø Previously documented DVT (1)
Ø Alternative diagnosis as likely as DVT (minus 2)
Interpretation:
DVT likely: 2 points or more
DVT unlikely: 1 point or less
Treatment
Ø Uncomplicated DVT.
— Therapeutic LMWH then switch to Warfarin for 3-6 months.
Ø Complicated DVT
— IV unfractionated Heparin or LMWH while converting to Warfarin.
— Thrombolysis or thrombectomy- if severe thrombosis.
— IVC filter.
¾ Inserted percutaneously via jugular/femoral vein to catch and
prevent PE’s
¾ Used in recurrent PE despite treatment, if contraindications to
anticoagulation and if anticoagulation can’t be used during
major surgery
¾ Risks of IVC filter placement- air embolism, arrhythmias, pneumo/haemothorax, IVC obstruction, bleeding
Thrombolysis
Ø Agents include streptokinase, urokinase, recombinant tPA.
Ø Administered via catheter as a low dose intra-arterial infusion.
Ø Indications
— Acute limb ischaemia.
— Venous thrombosis.
— Acute surgical graft occlusions.
— Thrombosed popliteal artery aneurysm.
Ø Contraindications
— Bleeding disorders.
— Current peptic ulcer.
— Recent haemorrhagic stroke.
— Recent major surgery.
— Evidence of muscle necrosis- may cause reperfusion injury
170
PERIPHERAL VASCULAR DISEASE
Ø Complications
— Allergy.
— Catheter leak, occlusion.
— Bruising.
— Major bleed or stroke.
CAROTID ARTERY DISEASE
Ø CVA- rapidly developing neurological deficit lasting >24 hrs.
Ø TIA- acute episode of focal neurological deficit that resolves within 24 hrs.
Ø Carotid artery stenosis occurs in 10% of people 80-89 yrs.
Clinical Features: Symptomatic carotid disease:
Ø CVA
— Completed stroke.
— Stroke in evolution- progressive neurological deficit over days and weeks.
— FAST criteria”
¾ Facial droop
¾ Arms: can they raise them and keep them elevated
¾ Speech slurred?
¾ Time: call for help if one of these signs are present
Ø TIA
— Can have a transient change in facial expression, drooping of the corner
of the mouth, dribbling.
Ø Amaurosis fugax- transient monocular visual loss, like a curtain coming down
over eye.
Ø Cerebral hypoperfusion
Diagnosis & Investigations
Ø Carotid duplex scan- screening test of choice, but can be difficult to perform if
vessels calcified.
Ø Carotid MR angiography.
Ø Cranial CT/MR angiography.
Ø Cardiac Echo / Telemetry – Useful in excluding cardiac source of embolic stoke
Management
Medical
Ø Antiplatelet agents- Aspirin, Plavix
Ø Anticoagulants- use in non-cardiac emboli is controversial.
Ø Smoking cessation.
Ø BP control.
Ø Tight glucose control.
Ø Statin.
171
PERIPHERAL VASCULAR DISEASE
Surgical / Endovascular
Ø Carotid Endarterectomy / Carotid Stent
— Indications
¾ 50-99% stenosis with recent TIA/CVA
¾ Consideration of intervention if asymptomatic but >70% stenosis in younger patients and low interventional risk
— Contraindications
¾ Severe neurological deficit after cerebral infarction.
¾ Occluded carotid artery.
¾ Severe comorbidities.
Carotid Endarterectomy
Ø Can be performed under GA or LA.
Ø Incision along anterior border of sternocleidomastoid muscle.
Ø Shunting of carotid artery following clamping can allow for ongoing cerebral
perfusion during surgery
Ø Endarterectomy is carried out in a smooth plane in the media of the artery.
Ø A smooth tapering endpoint on internal carotid is obtained.
Ø Endarterectomy is most commonly closed with a synthetic patch
Ø Post-op:
— Observe for haematoma that may compromise airway
— Antiplatelet therapy
— Monitor blood pressure post-operatively (may be labile)
Ø Complications of surgical treatment
— CVA- increased risk in stenting vs endarterectomy.
— MI- increased risk in endarterectomy vs stenting.
— Death.
— Wound haematoma- in endarterectomy can cause airway obstruction.
— Recurrent stenosis.
— Cranial nerve injury
¾ Vagus – vocal cord paralysis, dysphagia
¾ Hypoglossal – deviation of tongue
172
PERIPHERAL VASCULAR DISEASE
LEG ULCERS
Image by Azlena Ali Beegan: Mixed arterial & venous ulcer (with consent)
Causes
Ø Venous
Ø Arterial
Ø Mixed arterial & venous
Ø Neuropathy
Ø Diabetes
Ø Vasculitic- Buerger’s disease, Takayasu’s arteritis
Ø Malignancy- consider if ulcer does not heal with adequate medical management
Ø Infection
Ø Lymphedema
It is important to ask about both arterial and venous risk factors for ulceration
173
PERIPHERAL VASCULAR DISEASE
Clinical Features of Arterial & Venous Ulcers
Arterial
Venous
Site
Distally i.e. digits
Medial gaiter region
Edges
‘Punched out’, well defined
Sloped
Depth
Deep
Superficial, shallow
Size
Small
Large
Base
Necrotic
Granulation tissue
Margin
Regular
Irregular
Cause
Arterial insufficiency
Venous hypertension
Surrounding features
Features of PVD
Features of chronic
(pallor, hair loss, trophic
venous insufficiency
changes, onychogryphosis,
(oedema, haemosiderin,
cool, weak/absent pulses,
lipodermatosclerosis,
prolonged cap refill)
VVs)
As per chronic PVD in
4-layered profore
Management
patients with critical limb
dressing
ischaemia
Leg elevation
Venous support stockings
Skin graft
ABx if infection
Consider VV surgery if
possible once ulcer healed to reduce recurrence rate
174
PERIPHERAL VASCULAR DISEASE
THE DIABETIC FOOT
Features of the diabetic foot include
Ø Ulceration
Ø Infection
Ø Sensory neuropathy
Ø Poorly healing wounds
Aetiology of diabetic foot:
Ø Small & medium vessel disease
Ø Sensory neuropathy resulting in unnoticed tissue damage
Ø Autonomic neuropathy resulting in reduced sweating, which leads to dry, cracked skin and infection
Risk Factors for Diabetic Foot:
Ø Previous ulcers
Ø Diabetic neuropathy
— Stocking distribution.
— Charcot’s joints. bone and joint changes that occur secondary to loss
of sensation
Ø Associated Peripheral arterial disease
— Diabetic patients usually have calcified peripheral arteries.
— ABI may be falsely elevated
Ø Calluses.
Ø Living alone.
Ø Evidence of other diabetic complications e.g. Renal/visual impairment.
Clinical Features
Ø Ulcers commonly on pressure points (toes, heels).
Ø Evidence of sensory loss.
Ø If arterial disease is present, foot may be cool with reduced/absent pulses.
Ø Secondary infection of ulcer +/- cellulitis.
Ø ABI may be falsely elevated- calcified vessels. Toe Pressures are a useful
useful adjunct in determining perfusion in this population
Investigations
Ø ABIs / Toe Pressures
Ø Duplex USS
Ø CT Angio / MR Angio if co-existing arterial disease suspected
Ø Check blood glucose level and HBA1c, renal function, BP
175
PERIPHERAL VASCULAR DISEASE
Management
Ø Best done at a specialist multidisciplinary clinic.
Ø Regularly inspect feet.
Ø Appropriately fitted footwear & avoid walking barefoot.
Ø Chiropodist for debriding calluses and for nail care.
Ø If infected ulcer:
— Broad spectrum antibiotics.
— +/- Debridement of dead tissue.
— +/- Amputation of non-viable digits if adequate arterial supply for healing
of amputation
— X-ray/MRI to rule out underlying osteomyelitis.
Ø Consider revascularization if significant arterial disease.
Ø Consider amputation if no response to medical or other surgical treatments.
Neuropathic Ulcers
Ø Caused by trauma unnoticed by patient.
Ø Punched out appearance.
Ø Located over pressure points or calluses.
Ø Surrounded by inflammatory tissue.
Ø Frequently painless due to neuropathy.
176
NOTES
177
NOTES
178
BREAST DISORDERS
Chapter 8
Breast Disorders
179
BREAST DISORDERS
Contents:
• Breast cancer
• Breast cancer screening
• Benign breast disease
• Breast reconstruction
180
BREAST DISORDERS
BREAST CANCER
Key facts
Ø Most commonly occurring cancer in women.
Ø Commonest in western world: 1 in 12 lifetime risk for women.
Ø Incidence increases with age.
Ø Rare before the age of 25.
Ø Less than 1% occurs in men.
Aetiology
Ø Increasing age
Ø Genetic:
— Positive family history (particularly a first degree relative)
— BRCA 1 and BRCA 2 genes (about 70% chance of developing breast
cancer before age of 80)
— Inherited mutations in many other genes (CHEK-2, PALB 2, etc)
— Previous breast or ovarian cancer.
Ø Other factors related to exposure of estrogen:
— Early menarche
— Late menopause
— Nulliparity
— Obesity
— Hormone replacement therapy (HRT) for >10 years.
Ø Breast conditions:
— Ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS)
are both associated with increased risk of developing breast cancer. DCIS is a precursor of invasiveness in the ipsilateral breast.
— LCIS although not a premalignant change in itself, is regarded as a
marker for development of malignant disease in either breast.
— Atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia
Pathological features
Ø Virtually all cancers of the breast are adenocarcinoma.
Ø The commonest form: Invasive Ductal Carcinoma (75%).
Ø Other forms:
— Invasive lobular carcinoma
— Medullary carcinoma
— Tubular carcinoma
— Mucinous carcinoma
— Inflammatory breast cancer
— 70% express estrogen (ER) or progesterone (PR) receptors.
181
BREAST DISORDERS
INVASIVE DUCTAL CARCINOMA (IDC)
Ø Most common histological subtype of breast cancer: accounts for 75% of all
mammary tumours.
Ø Tumours are graded 1 – 3 according to the degree of nuclear atypia and tubule
differentiation.
INVASIVE LOBULAR CARCINOMA (ILC)
Ø About 10% of all invasive breast cancers are invasive lobular carcinomas
Ø Tend to be multicentric and can be bilateral.
Ø Size frequently underestimated radiologically.
DUCTAL CARCINOMA IN-SITU (DCIS)
Ø
Ø
Ø
Ø
Ø
Ø
Pre-malignant condition.
40-50% of DCIS may progress to invasive carcinoma if left untreated
Mammogram frequently shows microcalcifications.
Pathologically graded: low, intermediate, and high grade.
DCIS is treated with wide local excision with clear margins. Mastectomy is
needed for large lesions and multicentric disease. High grade DCIS is treated
with postoperative radiotherapy after lumpectomy (but not mastectomy).
Axillary surgery is not needed.
Clinical features
Ø Breast lump:
— Commonest symptom
— Usually painless
— Hard irregular lump
— Can be immobile, tethered or fixed (attached to chest wall).
Ø Nipple abnormalities:
— Bloody discharge
— Recent nipple inversion (involvement of Cooper’s ligament), distortion or
deviation.
Ø Skin changes:
— Dimpling, tethering, rash, colour change or ulceration.
— Late presentation may be with skin ulceration or tumour ulcerating through the skin.
— Peau d’orange: sensation of the texture of an orange peel arises as a
result of tumour invasion of the dermal lymphatics causing dermal oedema.
182
BREAST DISORDERS
Classical signs of breast carcinoma:
Hard irregular breast lump
Skin tethering or dimpling
Recent nipple inversion
Bloody nipple discharge
Skin ulceration
Peau d’orange
Investigations
Ø All breast lumps or suspected carcinomas are investigated with Triple Assessment
Ø Triple assessment results must be discussed at the multidisciplinary meeting
(MDM)
CLINICAL
History and breast exam
TRIPLE
ASSESSMENT
PATHOLOGICAL
FNAC
Needle core biopsy
Open wire guided excisional
biopsy
RADIOLOGICAL
Mammogram
Ultrasound
MRI Breast
183
BREAST DISORDERS
Ø Triple Assessment
— Clinical assessment
¾ Accurate history & breast examination.
— Radiological assessment
¾ Mammogram
— Over 35 years old.
— Two-view, lateral and oblique.
— Suspicious findings: mass, microcalcifications, stellate/spiculated
mass.
— Overall sensitivity 77 - 95%.
— For women <35 the sensitivity of mammography is low due to the
high density of the breast tissue which obstructs the view.
¾ Ultrasound Breast
— Used to assess lesions or lumps identified on physical exam or mammogram. Also used to assess the lymph nodes
¾ MRI Breast
— Used in lobular carcinoma to assess the extent of the disease, multicentricity, and the opposite breast.
Ø Pathological assessment
¾ Fine needle aspiration cytology (FNAC)
— Performed in the outpatient clinic/US-guided.
— Mainly used to aspirate benign cysts.
— Does not distinguish between invasive and non-invasive.
— Not used very much in diagnosis.
¾ Needle core biopsy
— Performed under local anaesthetic.
— Finds receptor status, differentiates between invasive carcinoma and
in situ carcinoma.
— Gene profile tests- Oncotype Dx, used to determine the clinical usefulness and patient benefit of adjuvant chemotherapy
¾ Open wire guided excisional biopsy (if core biopsy fails)
— Performed under general anaesthetic.
— Wire placed under radiological guidance into the area of abnormality
used as a guide for the surgeon.
Ø Staging investigations (not routinely done unless positive lymph nodes)
— Once a diagnosis of cancer is made, staging includes:
¾ Staging CT scan (thorax, abdomen, and pelvis)
¾ Liver ultrasound/Bone scan/LFTs/Serum calcium
184
BREAST DISORDERS
AJCC TNM (Tumour, Node and Metastases) Classification
Stage (Simplified)
TNM
5 – year survival
I
T1, N0
> 85%
IIA
T1N1, T2N0
> 70%
IIB
T2N1, T3N0
IIIA
T3N1, T1-3N2
IIIB
<50%
T4, peau d’orange,
ulceration, satellite
metastases
IIIC
T1-3 with any N3
IV
Distant metastases
< 20%
TNM stage with associated prognosis
T/N/M
Stage
Description
T (Primary)
Tis
T0
T1
T2
T3
T4
Carcinoma in Situ
No primary tumour located
Tumour < 2 cm
Tumour 2 – 5 cm
Tumour > 5 cm
Extension to chest wall
N (Nodes)
N0
N1
N2
N3
No nodal involvement
Mobile ipsilateral axillary nodes
Fixed ipsilateral axillary nodes
Ipsilateral supraclavicular nodes
M (Metastases)
M0
M1
No metastases
Distant metastases
185
BREAST DISORDERS
Management:
Surgery
Ø Mainstay of non-metastatic disease.
Ø Breast conserving surgery (wide local excision)
— Commonest procedure.
— Provided breast is adequate size and tumour location is appropriate to ensure clear margins.
— Usually combined with external beam radiotherapy to residual breast to
reduce risk of local recurrence.
Ø Simple mastectomy
— Best local treatment and cosmetic result for:
— large tumours (especially in small breast)
— late presentation with complications such as ulceration
— Also used for multicentric disease or where there is widespread disease.
— Performed with reconstruction at the same time (immediate) or later stage
(delayed). Options include:
¾ Implant reconstruction:
— Tissue expanders
— Saline/silicone implants
¾ Autologous:
— Free flap: Deep inferior epigastric perforator (DIEP) flap
— Pedicle flap: Latissimus dorsi (LD) flap
Flap Reconstruction
Deep Inferior Epigastric
Artery Perforator (DIEP)
Latissimus Dorsi Flap (LD)
Free flap (no muscle)
186
Uses abdominal skin, fat
and attached vessels
Pedicled flap (uses muscle)
Can adapt with patient’s
weight changes
Implant usually needed
for volume
Simultaneous “tummy tuck”
May affect strength
and function on relevant side
BREAST DISORDERS
Ø Surgical management of regional lymph nodes
— Sentinel node biopsy:
¾ One or two nodes primarily draining tumour is identified by radioactive tracer (technetium 99) and blue dye injected around
tumour.
¾ Sentinel node is described as ‘hot and blue’ as a result of the accumulation of both the radioactive material and the blue dye due
to lymphatic drainage.
¾ If positive nodes identified, then a full axillary clearance is required.
¾ Avoids major axillary surgery where not necessary.
— Axillary node clearance:
¾ Involves 3 levels: lateral to, behind and medial to the pectoral muscles
¾ Associated with risk of ipsilateral arm lymphoedema 20-40% and
axillary numbness 80%.
¾ Potential nerve complication:
— Long thoracic nerve (winging of the scapula).
— Thoracodorsal nerve.
Ø Surgery for metastatic disease
— Limited for symptomatic control of local disease for example mastectomy
for fungating tumour, wedge resection of metastatic lesions in liver or lung.
187
BREAST DISORDERS
Medical Treatment
— In non-metastatic disease, medical therapy is utilised to reduce the risk of
systemic relapse, usually after primary surgery as adjuvant therapy.
— Occasionally used as a treatment of choice of elderly or those unfit/
inappropriate for surgery.
— Endocrine
— Hormonal therapy:
¾ Tamoxifen for 5 - 10 years
— Selective Estrogen Receptor Modulator/(ER) antagonist
— Used in ER +ve patients (premenopausal)
¾ Anastrozole (Arimidex):
— Aromatase inhibitor
— Used in ER +ve patients (postmenopausal)
— Caution with osteoporosis due to side effect of reduced
bone density
— Targeted Therapy:
¾ Trastuzumab (Herceptin):
— Antibody directed at Her-2/neu receptors.
— Used in HER2 receptor positive patients
¾ Lapatinib:
— Tyrosine kinase inhibitor, binds to the tyrosine kinase
domains of EGFR and Her2-neu receptors inhibiting
signal transduction
— Used in HER2 receptor positive advanced breast cancer patients in combination with other medical treatments
Ø Chemotherapy
— Offered to some patients with tumours that have spread or are at high
risk of spreading/recurrence:
¾ +ve nodes, poor grade, large tumours, young patients, positive oncotype dx, high recurrence rate
— Oncotype DX test:
¾ Genomic test that analyzes the activity of a group of 21 genes that can affect how a cancer is likely to behave and
respond to treatment.
¾ It is a prognostic test (information about how likely (or unlikely) the breast cancer is to recur and predictive test
(likelihood of benefit from chemotherapy) in early stage ER
+ve breast cancer patients
— Examples of chemotherapy agents:
¾ CMF: Cyclophosphamide, methotrexate, 5-FU
¾ CA: Cyclophosphamide, anthracycline
¾ Taxane based: Paclitaxel, docetaxel
188
BREAST DISORDERS
Ø Radiotherapy
— Offered to some patients with:
¾ Breast conservation surgery, high grade tumour, large tumour (≥5cm), 1 – 4 lymph nodes positive, positive surgical
margins.
Ø Palliative treatment in metastatic breast cancer (for symptom management and
to increase survival time):
— Sites of metastases: lymph nodes, lung, liver, bones, brain.
— Endocrine therapy: as above.
— Chemotherapy: as above.
— Radiotherapy: to reduce pain of bony metastases or symptoms from
cerebral or liver disease
_______________
BREAST CANCER SCREENING
Ø
Ø
Ø
Ø
BreastCheck is an Irish government-funded programme.
The aim is to reduce deaths from breast cancer by diagnosing and treating the
disease at an early stage.
Women aged 50 to 69 are offered a free mammogram in two year intervals.
Screening mammography is is used to identify features in the breast suspicious
for malignancy for e.g. spiculated calcification and microcalcification.
189
BREAST DISORDERS
BENIGN BREAST DISEASE
FIBROADENOMA
Ø
Ø
Ø
Ø
Ø
Benign overgrowth of one lobule of the breast, epithelial and fibrous component.
Most common under 30, but may occur at any age.
Features: Painless, mobile, discrete lump.
Diagnosis: Ultrasound followed by core biopsy.
Treatment: Excision if >3cm, for cosmesis, or symptomatic.
BREAST CYSTS
Ø
Ø
Ø
Ø
Ø
Fluid filled cysts – May be clear, yellow, green, milky or brown in colour
Benign.
Features: Round symmetrical lumps, discrete or multiple, often painful.
Diagnosis: Fine needle aspiration, triple assessment to exclude malignancy.
Treatment: Aspiration if symptomatic.
FIBROCYSTIC DISEASE
Ø Noncancerous breast lumps which can sometimes cause discomfort.
Ø Often periodically related to hormonal influences from the menstrual cycle.
Ø Occurs between 15-55 years.
Ø Features: Swelling, ‘lumpy’ breasts, multiple breast cysts.
Ø Diagnosis: Triple assessment to exclude malignancy.
Ø Treatment: reassurance; proper fitting bra, evening primrose oil to relieve discomfort
BREAST INFECTIONS
Ø Lactational infections
— Due to staphylococcal infection.
— Treatment: with oral antimicrobial and aspiration if abscess present
Ø Recurrent mastitis and duct ectasia
— Chronic inflammation of the subareolar mammary ducts.
— Associated with smoking.
— Bacteria rarely found
— Presentation: Recurrent greenish-yellow nipple discharge or breast
abscess.
— Treatment: Broad spectrum antibiotics and drainage of the abscess
FAT NECROSIS
Ø Necrosis of the adipose tissue in the breast as a result of traumatic injury for
example trauma from seat belt following a road traffic accident
or post breast reduction or post radiotherapy
190
BREAST DISORDERS
GYNAECOMASTIA
Benign growth of the breast tissue in males usually due to imbalance in the
estrogen levels compared to androgens in the breast leading to increased estrogenic activity.
In young males: Cannabis is the most common cause.
In elderly men: Spirinolactone is the most common cause.
Examples of other causes:
— Hypogonadism (Kilnefelter’s syndrome), hyperthyroidism, chronic liver
disease
— Neoplasms secreting estrogens or their precursors
— Medications: Estrogen, cimetidine, anabolic steroids/androgens
Ø Management:
— Exclude neoplasm (mammography +/- core biopsy).
— Conservative: Tamoxifen
— Surgery: If symptomatic
Ø
Ø
Ø
Ø
191
NOTES
192
ENDOCRINE DISORDERS
Chapter 9
Endocrine Disorders
Illustrated by Kevin Quinlan: Exophthalmos.
193
ENDOCRINE DISORDERS
Contents:
• Goitre
• Differential Diagnosis of Neck Swelling
• Investigation and Surgical Management of Thyroid Disorders
• Thyrotoxicosis
• Graves Disease
• Thyroid Cancer
• Hyperparathyroidism
• Pheochromocytoma
• Cushing Disease
• Conns Syndrome
194
ENDOCRINE DISORDERS
GOITRE
Ø The term goitre refers to enlargement of the thyroid gland.
_______________
Anatomical Review
Ø The thyroid is formed from two triangular lobes (the left and right) connected by
a central isthmus overlying the 2nd and 3rd tracheal rings.
Ø Found between the levels of C5 - T1, invested within the pretracheal fascia.
Illustrated by Kevin Quinlan: surgical anatomy of the thyroid.
Ø Arterial Supply
— Inferior and superior thyroid arteries.
Ø Venous drainage
— Superior, middle and inferior thyroid veins.
Ø Lymphatic Drainage
— To the prelaryngeal, pretracheal and paratracheal nodes.
— Lateral parts of the gland drain to deep cervical nodes.
Ø Important Nearby Anatomical Structures
— The external laryngeal branch of the superior laryngeal nerve (vagal
branch) passes medial to the superior portion of the gland to innervate
cricothyroid muscle
195
ENDOCRINE DISORDERS
The recurrent laryngeal nerve (vagal branch in root of neck/superior mediastinum) lies between the trachea and oesophagus, emerging medial to
the inferior portion of the gland. Passes along the medial surface of each thyroid lobe before entering the larynx behind the inferior cornu of the thyroid
cartilage. Thus very vulnerable during thyroid and parathyroid operations.
— To the prelaryngeal, pretracheal and paratracheal nodes.
— Lateral parts of the gland drain to deep cervical nodes.
— Important Nearby Anatomical Structures
— The external laryngeal branch of the superior laryngeal nerve (vagal
branch) passes medial to the superior portion of the gland to innervate
cricothyroid muscle
— The recurrent laryngeal nerve (vagal branch in root of neck/superior
mediastinum) lies between the trachea and oesophagus, emerging
medial to the inferior portion of the gland. Passes along the medial
surface of each thyroid lobe before entering the larynx behind the inferior cornu of the thyroid cartilage. Thus very vulnerable during thyroid
and parathyroid operations.
Ø
Ø Central Control:
Illustrated by Kevin Quinlan: central control of thyroid hormones.
Thyroid Function Tests (TFT)
TSH
T4
Hyperthyroidism
¨
¨
Hypothyroidism
¨
¨
Ø Thyroid Hormones increase metabolism, growth, development and catecholamine effects.
196
ENDOCRINE DISORDERS
TYPES OF THYROID DISEASE
1. Graves’ Disease: A syndrome consisting of hyperthyroidism, goitre, eye disease and pretibial/localised myxoedema (see Graves’ Disease section).
2. Hashimoto’s Thyroiditis: Chronic autoimmune thyroiditis.
— It is more common in women (7:1) .
— High thyroid peroxidase (TPO) and thyroglobulin antibodies.
— Hypothyroidism is characteristic.
— Surgery rarely required.
3. Amiodarone induced: May cause both hyper- and hypothyroidism.
— Due to the inhibition of mono-deiodination of T4 (reducing T3 production), the blocking of T3 receptors and a direct toxic effect
leading to follicular destruction.
4. Iodine Deficiency
a. This may present with a diffuse goitre.
b. Usually painless and slow growing.
c. Areas with low naturally occurring iodine levels & no dietary supplements.
5. Cystic Thyroid Nodule / Simple Cyst: 50% of solitary thyroid nodules. Often an incidental finding. Common cause of thyroid pain & dysphagia (sudden haemorrhage or haemorrhagic infarction of cyst).
6. Thyroglossal cyst: not found in the gland itself. These are a midline structure
which move with protrusion of the tongue. They form in the thyroglossal duct
and may be found at any point along this structure. 40% present in adulthood.
Excised using the Sistrunk procedure (excise cyst, tract and the central part of
the hyoid bone).
7. Thyroiditis: Acute suppurative thyroiditis is extremely rare and is managed
with antibiotics and surgical drainage as appropriate.
a. Acute
b. Subacute (de Quervain’s) An often painful, usually self limiting condition involving enlargement of one or both lobes. Inflammatory markers may be raised. Sometimes biochemical or clinical evidence of hyperthyroidism. Anti-inflammatory treatment sometimes required. Occasionally steroids are necessary.
c. Chronic (Reidels’s) This condition may mimic malignancy presenting
as a woody hard thyroid swelling. It is characterised by a dense fibrous
inflammatory infiltrate and may coexist with conditions such as sclerosing cholangitis or retroperitoneal fibrosis. Open exploration and
biopsy may be necessary for diagnosis and resection of the isthmus
may be required in the event of a compromised airway.
197
ENDOCRINE DISORDERS
DIFFERENTIAL DIAGNOSIS OF A NECK SWELLING
Posterior triangle
Anterior triangle
Congenital
Cystic hygroma:
Branchial cleft cyst:
Zenker’s Diverticulum Inflammatory
Post-viral lymphadenopathy
(most neck
Bacterial / Suppurative lymphadenopathy:
lumps)
• Mycobacteria,
• Actinomycosis,
• Brucellosis
HIV
Neoplastic
Metastatic
• Lung, oesophagus,
breast, SCC of the
aerodigestive tract
Salivary gland
• 80% in parotid
Lymphoma
Lipoma
Midline
Thyroglossal
cyst.
Thyroid
Carotid Body tumours /
Chemodectoma
Illustrated by Kevin Quinlan: anatomy of the neck.
Purple = posterior triangle. Yellow = anterior triangle.
I – VI = anatomical levels to describe the location of a cervical lymph node.
198
ENDOCRINE DISORDERS
INVESTIGATION & SURGICAL MANAGEMENT OF THYROID DISORDERS
Biochemical
Thyroid function tests
Evaluation of thyroid status is essential. This includes TSH and T4. It may, however,
also be necessary to measure T3 separately.
TSH
T4
Low
Normal
Low
High
Diagnosis
Subclinical/sub-biochemical hyperthyroidism
TSH is appropriately suppressed. Check T3 to rule out T3-
thyrotoxicosis. Requires monitoring as 5% progress to clinical
hyperthyroidism. Repeat thyroid function tests in 8 weeks.
Treat if:
Ø
Atrial fibrillation
Ø
Symptomatic hyperthyroidism
Ø
Osteoporosis in postmenopausal women
Ø
Multinodular goitre
Hyperthyroidism
Normal High
Drug related often a cause. Check for administration of heparin,
amiodarone, propranolol and glucocorticoids. May also indicate
peripheral resistance or autoimmune thyroid pathology.
High
Normal
Subclinical/sub-biochemical hypothyroidism
Commonest in women >60
Treat if:
Ø
Pregnant
Ø
Symptomatic
Ø
Hyperlipidaemia and/or atherosclerosis
High
Low
Hypothyroidism
Autoantibodies
Ø Autoantibodies are more likely to be elevated in Graves Disease.
— Anti TSHR Ab: Anti-thyrotropin receptor antibodies
— Anti Tg Ab: Antithyroglobulin antibodies
— Anti TPO Ab: Anti-thyroid peroxidase antibodies
199
ENDOCRINE DISORDERS
Imaging
Ultrasound
Ø Ultrasound (US) is the imaging of choice in thyroid pathology as it is non-
invasive and does not expose the patient to radiation. Ultrasonic features:
More Likely Malignant
—
—
—
—
—
—
Solid
Irregular margins
Microcalcifications
Increased vascularity
Size > 5cm
Lymphadenopathy
More Likely Benign
— Cystic
— Smooth
— Macrocalcifications
Surveillance of a Single Nodule
Ø <1 cm: Most likely no need for FNAC
Ø >1 cm and suspicious for malignancy: FNAC
Biopsy
Ø Fine Needle Aspiration Cytology (FNAC) under US guidance is usually performed. This is graded similarly to breast cytology, i.e. British Thyroid association, Th1 to Th5 or the Bethesda system (USA).This will not show the
gland’s architecture, but a core biopsy is more risky in the thyroid gland.
Ø If FNAC does not demonstrate malignancy in a suspicious lesion, repeat in 6
months. If there is still no evidence of disease, malignancy is unlikely.
Ø Follicular cells are worrisome: 25% will have underlying malignancy. FNAC
cannot determine if a follicular lesion or hurthle cell variant (the only benign
thyroid tumours) is benign or not. These patients require lobectomy and the entire lesion needs to be examined histologically to exclude capsular or
lymphovascular invasion (the determinants of malignancy).
200
ENDOCRINE DISORDERS
Nuclear imaging - Scintigraphy
Ø Uses technetium. This form of imaging does not exclude or confirm cancer.
Ø “Hot” nodules demonstrate technetium uptake. Unlikely to be cancer.
Ø “Cold” nodules: no technetium uptake.10% chance of malignancy.
CT Neck (non contrast) if there is a suspicion of malignancy or retrosternal
extension.
Ø Also assesses lymphadenopathy / invasion of local structures.
MDT discussion
Ø Important in managing patients with goitre and thyroid nodules. Input from
surgeons, endocrinologists, histopathologists and radiologists.
_______________
Indications for thyroidectomy (the 4 C’s)
Ø
Ø
Cancer
Ø Cosmesis
Compression of adjacent
Ø Carbimazole (or other medical structures treatment) failure
201
ENDOCRINE DISORDERS
THYROTOXICOSIS
A hypermetabolic syndrome due to elevated thyroid hormone levels.
Symptoms of thyrotoxicosis
Ø Sweats, tremors, palpitations
Ø Weight loss despite increased appetite
Ø Insomnia
Ø Anxiety
Ø Heat intolerance
Ø Diarrhoea
Ø Oligomenorrhoea
Signs of thyrotoxicosis
Ø Extremities
— Fine tremor
— Palmar erythema
— Acropachy, hands and feet (looks like clubbing; unique to Graves’
disease)
— Onycholysis
— Warm & sweaty
— Fast, irregular pulse
— Graves’ dermopathy / pretibial myxoedema. 15% of those with eye
signs. Was more common, now rarer due to earlier treatment.
Ø Face
— Graves’ Ophthalmopathy:
¾ Proptosis, Exophthalmos, chemosis
¾ Ophthalmoplegia
— Any cause of hyperthyroidism:
¾ Lid lag
¾ Lid retraction
— Alopecia
Causes of thyrotoxicosis
Ø Graves’ Disease
Ø Toxic multinodular goitre
Ø Solitary toxic nodule
Ø Thyroiditis
— Hashimoto’s
— Post partum
— De Quervain’s
Ø Amiodarone
Complications of thyrotoxicosis
Ø Increased risk of atrial fibrillation
Ø Osteoporosis
Ø Thyroid storm
202
ENDOCRINE DISORDERS
Investigation of thyrotoxicosis
ECG
Ø May demonstrate either sinus tachycardia or atrial fibrillation. The patient may
require cardiac monitoring.
Biochemical
Ø TFTs: Hyperthyroidism (high fT4, low TSH). TSH suppression correlates well
with the severity of disease.
Ø TPO may be elevated but is a non-specific marker of autoimmune attack.
Ultrasound
Ø Will allow evaluation of goitre or nodules, if any are present.
Scintigraphy
Ø Diffuse uptake: Graves’
Ø Patchy uptake: TMN
Ø Single area of uptake: Solitary nodule
_______________
Management of thyrotoxicosis
Ø
Ø
Ø
Propranolol: Sufficient beta blockade must be established in order to minimise
the cardiac effects of thyrotoxicosis. Propranolol used mostly.
Anticoagulation if atrial fibrillation is present and not controlled.
Carbimazole can be used in an acute setting. A high initial dose may be tapered following repeat TFTs.
NB: Achieving euthyroid status before surgery is essential to avoid precipitating a
thyroid storm
203
ENDOCRINE DISORDERS
Definitive management of thyrotoxicosis
Graves’ Disease
Carbimazole for 18 months. If disease is refractory,
consider Radioiodine treatment or Surgery. If thyroid
orbitopathy Surgery preferable to radioiodine therapy.
Toxic Multinodular Goitre
Radioiodine therapy is the preferred approach, followed by Surgery, particularly in the presence of a
large gland with pressure symptoms or retrosternal
extension.
Solitary adenoma
Surgery is the preferred approach, followed by Radioiodine treatment.
Thyroiditis
Analgesia, preferably NSAIDs.
Beta blockade.
Steroids tapered over two weeks.
GRAVES’ DISEASE
Graves’ Disease is an autoimmune syndrome
comprising:
—
—
—
—
—
—
Hyperthyroidism.
Goitre.
Thyroid eye disease.
Pretibial/localised myxedema.
TSH receptor antibodies.
Most commonly occurs in women
aged 20 – 40 years old.
Illustrated by Kevin Quinlan:
exophthalmos,
pretibial myxoedema
Signs & symptoms specific for Graves’ disease
Ø Smooth, diffusely enlarged goitre with bruit
Ø Thyroid eye disease
— Proptosis/Exophthalmos
— Periorbital oedema
— Conjunctival injection
— Ophthalmoplegia (look up to stretch
inferior rectus to provoke as the
inferior rectus muscle becomes fibrous
and tight. The same manoeuvre may be
accompanied by a measurable increase
in intraocular pressure).
204
Illustated by Kevin Quinlan:
thyroid bruit,
thyroid acropachy
ENDOCRINE DISORDERS
Ø Extremities:
— Acropachy
— Onycholysis
— Pretibial myxoedema
Ø Nonspecific hyperthyroidism signs/symptoms
_______________
Investigating Graves’ disease
Ø TFTs: high free T4; low TSH. TSH correlates well with the severity of disease.
Ø Autoantibodies:
— TSH receptor antibodies positive.
— TPO antibodies: up to 80%.
— Thyroglobulin antibodies: up to 70%.
Ø Scintigraphy will demonstrate increased uptake
Management of Graves’ disease
Is based on a two-pronged attack; providing symptomatic relief and definitively
treating the underlying pathology. Definitive treatment options include Medication
(Carbimazole / PTU), Radioactive Iodine and Surgery.
Medical
Ø Beta-blocker for symptom relief.
Ø Carbimazole acts to block the action of TPO, which prevents the formation
of thyroid hormone. Requires 18 months of treatment starting with a high dose
and titrating down.
Ø Propylthiouracil (PTU) (10x less potent than carbimazole). Blocks conversion
of T4 to T3.
— If someone can’t tolerate carbimazole being lowered, consider moving
forward with therapy.
¾ At 18 months, often 50% remission.
¾ If relapse, move on to surgery or radioiodine.
Ø Side effects of Carbimazole / PTU
— Teratogenicity (thus PTU preferable in pregnancy)
— Agranulocytosis
— Hepatotoxicity
— Rash, urticarial, arthralgia.
Radioactive Iodine
Ø First line treatment in USA. Opposite in Europe.
Ø Transient hyperthyroidism may occur as gland is destroyed.
Ø 2-5% risk of hypothyroidism per annum after treatment.
Ø Need life-long follow up to check for this.
Ø Side Effects of Radioactive iodine Treatment
— Hypothyroidism
— Transient thyroiditis
— Transient worsening of graves ophthalmopathy
205
ENDOCRINE DISORDERS
Thyroidectomy (complete removal of thyroid gland) or Subtotal thyroidectomy (risk
of recurrence proportionate to the volume of gland remaining
Ø Patient should be euthyroid prior to surgery (decreases vascularity of gland.
Lugol’s iodine may help in this respect).
Ø Indications:
— Cancer
— Compression of adjacent structures: thyroid mass effect
— Carbimazole (or other medical therapy) failure
— Cosmesis / severe ophthalmopathy
Ø Benefits:
— avoids long term risks of radioactive iodine
— provides tissue for histology
Ø Children, young women and pregnant women (second trimester) ideal candidates
Ø If Graves ophthalmopathy is present, total thyroidectomy is indicated.
206
ENDOCRINE DISORDERS
THYROID CANCER
Proportions of Different Thyroid Cancers (approximate values)
Papillary carcinoma
80%
Follicular carcinoma
10%
Medullary carcinoma
4%
Anaplastic carcinoma
<3%
Papillary Thyroid Cancer
Epidemiology
Ø Incidence of 12.5 per 100,000.
Ø Female: male ratio of 2.5:1.
Ø Most commonly occurs in those aged 30 - 50 years old.
Risk Factors
Ø Radiation exposure.
Ø Family history.
Pathological features
Ø Unencapsulated.
Ø May be partially cystic.
Ø Papillae consisting of one or two layers of tumour cells surround
a well-defined fibrovascular core.
Ø Follicles and colloid typically absent.
Ø Approximately one half will contain psammoma bodies.
Metastatic Activity
Ø 2-10 percent of patients will have metastatic disease at presentation.
Ø Of these, two thirds have pulmonary disease and a quarter skeletal disease.
Ø Rarer sites include brain, kidneys, liver and adrenals.
Prognostic Factors
Ø Age: Younger age at diagnosis is a positive prognostic factor.
Ø Tumour size: Smaller tumour size is a positive prognostic factor.
Ø Soft tissue invasion: The presence of this is a negative prognostic factor.
Ø Distant metastases: The presence of these is a negative prognostic factor.
Ø Overall, the prognosis in papillary cancer is good. One series demonstrated a
6% mortality for patients with non metastatic disease over 16 years.
207
ENDOCRINE DISORDERS
Follicular Thyroid Cancer
Epidemiology
Ø Female: male ratio 3:1.
Ø Most commonly in 50 – 70 year olds..
Risk Factors
Ø Radiation exposure
Ø Family history.
Ø Iodine deficiency.
Pathological Features
Ø Well differentiated tumour of the thyroid epithelium.
Ø Capsulated.
Ø Colloid may be present, and is a positive prognostic indicator.
Ø Hurthle Cell and Insular variants somewhat more aggressive.
Metastatic Activity
Ø Lymphatic involvement seen in 8-13% of cases.
Ø Distant metastases seen in 10-15% of patients.
Ø Typically spreads haematogenously to bone (lytic lesions) and lungs.
Ø May also involve the brain, liver, bladder and skin.
Ø Metastases may be hormonally active, leading to hyperthyroidism.
_______________
Medullary Thyroid Cancer
Ø
Ø
Ø
Ø
Ø
Ø
Ø
Ø
A neuroendocrine tumour of the parafollicular or C cells of the thyroid gland.
The production of calcitonin is a feature. CEA may also be expressed by medullary cancers.
Flushing and diarrhoea will be present if calcitonin levels are high.
Thyroid function tests usually normal.
May be sporadic or occur as part of an inherited syndrome (MEN2).
Sporadic: 80% of cases with a slight female preponderance. Present with a
single nodule and often cervical lymphadenopathy.
Familial: As part of MEN-2.
Prior to surgical treatment, patients must be evaluated for other neuroendocrine
tumours prior to surgical intervention
Anaplastic Thyroid Cancer
Ø
Ø
Ø
Ø
Ø
Ø
208
Undifferentiated tumours of thyroid follicular epithelium.
Aggressive; disease specific mortality approaching 100%.
Typically in older women and presents with a rapidly enlarging neck mass.
About 20% will have synchronous differentiated cancers.
Early palliative care input important.
Usually no indication for surgical intervention. Chemotherapy and radiotherapy
may be used to provide symptomatic relief.
ENDOCRINE DISORDERS
CLINICAL PRESENTATION & MANAGEMENT OF THYROID CANCER
Signs and Symptoms
Ø Appearance of thyroid node/neck lump
Ø History of rapid growth
Ø Fixation of a thyroid node to over or underlying structures
Ø New onset hoarseness or vocal cord paralysis
Ø Ipsilateral cervical lymphadenopathy
Ø May be an incidental finding on imaging
Investigations
Ø ECG
Ø Biochemical
— Thyroid function tests
— FBC, U&E, LFTs
Ø Imaging
— Ultrasound
— Scintigraphy
— Staging CT may be necessary. NB If you suspect cancer, do NOT use
contrast in your CT: delays / interferes with radioiodine.
Ø Pre-surgical workup
— As the mainstay of treatment is surgery, it is important to evaluate. a
patient’s fitness for surgery.
— Anaesthetic review is often indicated.
— Patients may require an Echocardiogram
Treatment
Ø Multidisciplinary Meeting (MDM): Treatment is largely determined by histological type. Radiological and endocrinological input are paramount in
planning treatment. Most suspected thyroid cancers are discussed at MDM.
Ø Thyroidectomy
— Mainstay of treatment. Thyroid lobectomy in smaller cancers.
— Modified radical neck dissection if clinical or radiological (US,CT, Radioiodine scan) evidence of metastatic disease.
Ø Thyroidectomy complications
— Early: Strap haematoma, transient hypoparathyroidism (8%), hypocalcaemia, side effects of anaesthesia, seroma, laryngeal nerve
injuries, vocal cord paresis.
— Intermediate: Infection.
— Late: Permanent hypoparathyroidism (2%).
Ø Radiotherapy
— May use radioiodine following surgery and MDM to control occult disease (micro-metastases).
— External beam radiation used in anaplastic cancer to reduce tumour
size and symptoms but does not improve survival.
209
ENDOCRINE DISORDERS
Ø Medical Management
— Following total thyroidectomy, patients will require lifelong thyroid hormone replacement using a higher dose than for replacement therapy
in order to supress TSH as differentiated thyroid tumours are hormone
dependant.
210
ENDOCRINE DISORDERS
PRIMARY HYPERPARATHYROIDISM
Aetiology
—
—
—
—
—
85% of cases, due to a solitary adenoma.
10-15% of patients will have enlargement of multiple glands, sometimes
in the context of MEN syndromes.
Parathyroid cancer and ectopic adenomas are rare (occasionally intrathoracic).
Now seen more commonly due to widespread serum auto-analysis
(serendipity syndrome)
Incidence 3/1000 general population. 21/1000 in women 55-75 yrs.
Presentation
Ø Mostly asymptomatic. Often just an incidental finding of hypercalcaemia.
Ø Clinical features and complications of hypercalcaemia:
System
Symptoms & Signs
Complications
Renal
STONES
– renal; polyuria, polydipsia
Urinary tract stones, renal
insufficiency
Psychiatric /
Neurological
MOANS
– psychiatric;
Parasthesia, reduced deep
tendon reflexes
Depression, dementia,
psychosis
Skeletal
BONES
– bone pain
Arthritis (pseudogout),
osteopenia / osteoporosis /
osteitis fibrosa cystica (due to
bone resorption), pathological
fractures
GIT
GROANS
– abdominal pain,
constipation, vomiting
Pancreatitis, PUD
Generalised
FATIGUE OVERTONES
– fatigue, malaise, weakness,
muscle cramps
Cardiovascular
Hypertension, dysrhythmias,
short QT
211
ENDOCRINE DISORDERS
The Diagnosis is Biochemical
Ø Diagnostic:
— Corrected Calcium high.
— PTH high.
— Increased 24 hour urinary calcium excretion. This helps exclude
familial hypocalcuric hypercalcaemia.
Ø Imaging of the gland responsible aids planning minimally invasive surgery and
can help in cases of ectopic parathyroid glands.
— Sestamibi
— Ultrasound
Management
Acute: Correction of serum calcium is essential.
Ø IV access and administer IVF. May require between 5-7 L per day.
Ø Monitor urine output.
Ø Furosemide may be used once adequate hydration achieved.
Ø Avoid bisphosphonates if surgery is anticipated.
Definitive: Parathyroidectomy
Ø The four parathyroid glands are typically pea-sized and found on the posterior
aspect of the thyroid gland.
Ø Isolating the responsible gland prior to surgery may allow for a minimally invasive technique to be employed.
Ø Intraoperative PTH measurement can provide evidence of curative surgery.
Ø Serum calcium must be monitored during the postoperative period.
_______________
Treatment
Treat underlying cause
— Parathyroidectomy of
— Phosphate binders 3.5 glands
— Diet change
— Remaining ½ gland can
— Parathyroidectomy be left in the neck or
implanted into the upper
arm
MALIGNANT HYPERPARATHYROIDISM (Ectopic PTH).
Ø Parathyroid hormone related peptide (PTHrP) can be secreted by some malignant tumours: small cell carcinoma of the lung; breast carcinoma; renal
cell carcinoma.
212
ENDOCRINE DISORDERS
PHAEOCHROMOCYTOMA
Ø
Ø
Ø
Ø
Ø
Catecholamine producing tumours of the neural crest.
Arise from chromaffin cells of the adrenal medulla (phaeochromocytoma) or
sympathetic ganglia (catecholamine-secreting paragangliomas).
Rare: Incidence of 2 - 8 million per year.
Most common in the fourth and fifth decade of life.
May occur as part of familial syndromes such as MEN and VHL.
Rule of 10s (now a controversial rule, but a useful learning tool)
10% bilateral
10% normotensive
_______________
10% extra-adrenal
10% malignant
10% recur
10% calcificy
10% children
10% familial
Presentation
Ø Classic Triad: Episodic headache, sweating and tachycardia.
Ø Sustained or paroxysmal hypertension (85-95% of patients).
Ø Headache (up to 90%).
Ø Generalised sweating (60-70%).
Ø Other: palpitations, tremor, pallor, panic attacks, weakness and dyspnea.
Ø Increased availability of imaging has led to an increase of asymptomatic presentation.
_______________
Diagnosis
Ø 24 hour urine collection of fractionated catecholamines and metanephrines: the
most specific (98%) and sensitive (98%) test for diagnosis.
Ø Plasma fractionated metanephrines have a high false positive rate. Only examine in patients with a high index of suspicion.
Ø CT/MRI imaging to locate the tumour. MIBG scan may be useful for metastatic
or ectopic disease (paraganglionoma in islets of Zukerkandle).
Treatment
Ø Mainstay of treatment is total adrenalectomy (partial resection is indicated in
bilateral disease).
Ø Prior to treatment, substances known to provoke phaeochromocytoma paroxysms must be avoided (metoclopramide, glucagon and histamine).
Ø Alpha adrenergic blockade 10-14 days prior to surgery to control hypertension
and to encourage volume expansion.
Ø Beta adrenergic blockade 2 to 3 days prior to surgery, once sufficient alpha
blockade is achieved.
Ø Laparoscopic resection is possible in approximately 90% of patients.
Ø Malignant tumours can only be identified by their metastatic activity, which
commonly involves local organs. Distant metastases may occur up to 20 years
following resection. As such, patients require long term follow up.
213
ENDOCRINE DISORDERS
CORTISOL EXCESS, CUSHING’S DISEASE
Clinical Features
Ø Weight gain (buffalo hump; truncal obesity)
Ø Muscle wasting (lemon on a stick)
Ø Striae
Ø Facial plethora (moon facies)
Ø Thinning of the skin, easy bruising
Ø Mood changes: lethargy, depression, suicidal ideation, psychosis
Ø Menstrual irregularities
Ø Hirsutism in women, hair loss in men
Ø Glucose intolerance, diabetes
_______________
Causes
Ø Iatrogenic
Ø Primary adrenal disease
— Unilateral: Adrenal adenoma (10%) or carcinoma.
— Bilateral: ACTH independent bilateral adrenal hyperplasia.
Ø Secondary adrenal disease
— Cushing’s Disease
ACTH secreting pituitary adenoma.
Ø Ectopic ACTH secretion
_______________
Diagnosis
Ø Cortisol levels
— High. Morning peak and midnight nadir pattern is lost.
— 24 hour urinary cortisol elevated.
Ø Overnight dexamethasone suppression test
— 1 mg dexamethasone given.
— In normal patients, morning cortisol will be low.
Ø High dose dexamethasone suppression test
— 2mg dexamethasone given QDS for 24 hours.
— To distinguish Pituitary or ectopic source of ACTH dependant Cushing’s syndrome. Pituitary will still show some inhibition. Ectopic
will not.
— This will not inhibit primary adrenal or ectopic disease and cortisol
levels will be unaffected.
Ø ACTH
— High in patients with pituitary adenomas, ectopic production.
— Low in primary adrenal disease.
Ø CT/MRI in order to localize tumours.
214
ENDOCRINE DISORDERS
Treatment
Ø Iatrogenic
— Taper and stop exogenous glucocorticoids
Ø Adrenal adenoma
— Surgical excision, unilateral adrenalectomy
Ø ACTH independent bilateral adrenal hyperplasia
— Bilateral adrenalectomy
Ø Cushing’s Disease
— Transsphenoidal resection
Ø Ectopic ACTH secreting tumours
— Excision
_______________
Post-Operative Management
Ø Following surgical resection of adrenal glands, patients will require cortisol
replacement.
Ø Even following unilateral excision, cortisol levels may take several months to
recover.
Ø Patients may be administered hydrocortisone in the postoperative setting and
switched to oral agents, such as prednisolone.
Ø Following bilateral adrenalectomy, patients will require lifelong cortisol and
mineralocorticoid replacement.
Ø Patients should be counseled about the risk of an Addisonian crisis and be
given suitable advice regarding illness and medical alert jewellery.
CONN’S SYNDROME
(Primary Hyperaldosteronism)
Usually autonomous aldosterone secretion by adrenocortical tissue (Zona
Glomerulosa).
Commonly a single benign adenoma. Occasionally micro or macronodular bilateral
disease. Aldosterone secreting cancer extremely rare.
Clinical Features
Ø Hypertension
Ø Hypokalemia (not always)
Ø Hypernatremia (not always)
Ø Metabolic alkalosis (not always)
Ø Fluid retention
Ø Reduced Plasma renin activity (PRA)
Complications
Ø Hypertension
Ø Cardiac arrhythmias
Ø Cardiac fibrosis
Ø Increased cardiac mortality.
215
ENDOCRINE DISORDERS
Diagnosis
Ø Biochemical – Failure of aldosterone suppression with sodium load or Fludrocortisone suppression test.
Ø Plasma aldosterone / renin ratio.
Imaging
Ø CT / MRI (Adrenal vein sampling with measurement of aldosterone cortisol and
renin. This allows localisation. Particularly useful when bilateral findings on CT)
General
Ø Monitor BP, electrolytes, ABG, ECG, ECHO.
Treatment
Ø Treatment of Conn’s syndrome with a solitary adenoma is laparoscopic retroperitoneal adrenalectomy.
Ø Small lesions may allow partial adrenalectomy.
Ø Treatment of bilateral disease dependant on localisation studies. If bilateral
secretion probably best managed by medical therapy with aldosterone agonists
(spironolactone or eplerenone).
216
217
NOTES
218
UROLOGY
Chapter 10
Urology
219
UROLOGY
Contents:
• Urinary Tract Stones
• Acute Urinary Retention
• Common Urological Devices
• Benign Prostatic Hyperplasia
• Adenocarcinoma of the Prostate
• Renal Neoplasms
• Transitional Cell Carcinoma
• Testicular Tumours
• Acute Testicular Pain
220
UROLOGY
URINARY TRACT STONES
Ø More common in males.
Ø Peak age is 20 -50 years.
Ø Majority of urinary tract stones are radiopaque.
Types of stones
Ø Calcium stones
Ø Almost always cause symptoms when in ureter.
Ø Represent 75% of all urinary tract stones.
Ø
Ø
Ø
Ø
Staghorn calculi (struvite stones, triple phosphates stones)
Composed of calcium phosphate, ammonium and magnesium.
Usually located in the renal pelvis and calyces.
15% of all urinary tract stones and strongly associated with recurrent UTIs.
Ø Uric acid stones
Ø Radiolucent stones, but visible on non-contrast CT.
Ø Cysteine stones (relatively rare)
— Genetic predisposition
Predisposing factors for developing urinary tract calculi
Ø Dehydration / poor fluid intake
Ø Hyperparathyroidism
Ø Idiopathic hypercalciuria
Ø Disseminated malignancy
Ø Sarcoidosis
Ø Hypervitaminosis D
Ø Familial metabolic causes, Cystinuria, errors of purine metabolism, hyperoxaluria, hyperuricosuria, xanthinuria.
Ø Infection
Ø Impaired urinary drainage, e.g. pelvi-ureteric junction (PUJ) obstruction, ureteric stricture, and extrinsic obstruction.
221
UROLOGY
Symptoms
Ø Sudden onset of severe, stabbing, intermittent loin to groin pain (i.e. Flank,
abdomen, groin and genitals)
Ø Might be associated with rigors, nausea, vomiting, fever and tachycardia/
palpitations.
Ø Rarely, macroscopic (visible) haematuria.
Signs
Ø Renal angle tenderness.
Ø Suprapubic tenderness.
Ø Pyrexia.
Caveat: Beware of elderly patient presenting with suspected renal colic as it is
always important to consider a symptomatic abdominal aortic aneurysm (AAA) in the
differential diagnosis.
Investigations
1. Blood tests:
— Full Blood Count/Complete Blood Count - A Raised WCC suggests superimposed infection
— Urea and Electrolytes - Deranged renal function test indicating renal impairment.
— C Reactive Protein – Inflammation marker suggesting superimposed infection
— Serum Corrected Calcium – High levels precipitating stone formation
— Phosphate & uric acid levels - High levels precipitating stone formation
— Parathyroid Hormone - Levels if clinically appropriate
2.
—
—
—
3.
—
—
—
—
222
Urine Test:
Urine dipstick showing microscopic haematuria or evidence of concurrent UTI
Mid-Stream Urine to exclude the presence of an infection.
24 hour calcium and urate (If clinically appropriate e.g. recurrent stone former)
Radiological
Plain film X-Ray of the kidneys, ureters and bladder (KUB) may show the presence of the stone in approximately 70% of cases.
Non-contrast CT Kidney, Ureters and Bladder (CT KUB) is gold standard imaging for nephrolithiasis and will help determine the site, size of the stone
and will confirm/exclude the presence of complications.
Renal ultrasound to assess for hydronephrosis
Non-contrast MRI in pregnancy
UROLOGY
Treatment
Ø Analgesia (NSAIDS superior to opioids)
Ø Antiemetic
Ø Hydration
Ø Alpha-blocker e.g. Tamsulosin (Medical expulsive therapy)
Note - Majority of stones < 5 mm in size will pass spontaneously over a 6 week period
(NB need analgesia on discharge, for example diclofenac PO or suppositories)
Indications for active treatment of stone include:
— Presence of urosepsis
— Stones with a low likelihood of spontaneous passage (e.g. >6mm)
— Persistent pain despite adequate analgesia
— Persistent obstruction
— Renal insufficiency
Options for definitive treatment include:
Ø Extracorporeal shock wave lithotripsy (ESWL)
— Renal colic may be complication due to fragmentation of bigger
stone.
Ø Endoscopic stone retrieval (Retrograde rigid/ flexible ureteroscopy i.e. Scope
through Urethra -> Bladder -> Ureter).
Ø Percutaneous Nephrolithotomy (PCNL)
— Access gained percutaneously through renal, calyces. Good option for Staghorn Calculus.
Ø Open nephrolithotomy/ureterolithotomy.
NOTE:
Obstruction and sepsis due to renal stones is a urological emergency.
Any Hydronephrotic / Infected/ Anuric kidney needs urgent decompression before any
definitive removal of stones.
This can be done by percutaneous nephrostomy +/- antegrade stenting or retrograde
insertion of ureteric stent
Male Urinary Tract – Illustrated by Kevin Quinlan
223
UROLOGY
ACUTE URINARY RETENTION (AUR)
Epidemiology
Ø 13:1 male to female ratio.
Ø Overall incidence rate of 6.8 per 1000 years.
Ø Increases with age: 60-year-old men have a 20% chance of developing AUR
over a 20 year period.
Predisposing factors:
Ø Obstruction (#1 cause)
Ø Benign prostatic hyperplasia (BPH) is the most common underlying condition in
men.
Ø Constipation.
Ø Haematuria causing clot retention.
Ø Cancer (prostate / bladder / pelvic cancer in women).
Ø Urethral stricture.
Ø Urolithiasis.
Ø Infection: cystitis, prostatitis, urethritis.
Ø Phimosis (especially paediatric patients)
Ø Prolapse in women: cystocoele / rectocoele.
Ø Post-operatively / post-partum.
Ø Medication
¾ Antimuscarinics (decreased bladder sensation & detrusor contractility).
¾ Sympathomimetics (increased muscle tone).
¾ Opioids (decreased bladder sensation).
Ø Neurologic impairment
(Interrupted motor / sensory neural supply)
¾ Spinal cord injury: demyelination, infarction, trauma.
¾ Mass: epidural abscess / metastasis.
¾ Guillain-Barré syndrome.
¾ Diabetic Neuropathy.
¾ Stroke.
¾ Cauda equina syndrome.
Ø Dyssynergia (incomplete urinary sphincter relaxation).
Ø Inefficient detrusor muscle
¾ Most often in patients with baseline obstructive urinary symptoms.
Ø Trauma to pelvis, urethra, penis.
224
UROLOGY
Symptoms
Ø Inability to pass urine.
Ø Lower abdominal / suprapubic discomfort.
Ø Restlessness / distress / delirium.
Ø Above symptoms less pronounced (acute-on-chronic urinary retention).
Ø Overflow incontinence (acute-on-chronic urinary retention).
Signs
Ø
Ø
Ø
Ø
Ø
Ø
Suprapubic tenderness.
Enlarged palpable bladder that is dull to percussion.
Genitalia & catheter obstruction.
DRE: BPH, mass, perineal sensation, anal tone.
Pelvic exam (females): pelvic mass.
Neurological exam: neurological impairment.
Investigations
Ø Bedside
Ø Bladder ultrasound: inability to pass urine and volume > 300ml is indicative.
Ø Urinary catheterisation (volume of urine) is diagnostic & therapeutic (high clinical suspicion of AUR). Monitor urine output and post-void residual volumes
thereafter for progress / oliguria / recurrence.
— If a large volume Is drained (i.e.>1L) after catheterisation it is important to monitor the patient’s blood pressure and weight
Ø Urine
Ø Urinalysis.
Ø Urine culture & sensitivity (infection).
Ø Serum
Ø Urea & creatinine (renal failure).
Ø FBC (infection, haematuria)
Ø Do NOT check PSA – false positive in AUR.
Ø Evaluate cause (e.g. BPH, see next section).
Ø No cause found on initial evaluation = Urodynamics by a Urologist.
Treatment
Ø Most managed as outpatients after bladder decompression. Hospitalisation for
urosepsis, malignancy, clot retention and acute kidney injury.
225
UROLOGY
Bladder decompression:
Ø Urethral catheterisation.
¾ Contraindications
— Recent urological surgery: radical prostatectomy, urethral reconstruction.
— Pelvic fracture (Perineal Bruising, blood at tip of meatus etc)
¾ Types
— 1st line: 14 to 18 French catheter.
— Urethral stricture: smaller 10 to 12 French catheter.
— Enlarged prostate: larger 20 to 22 French catheter with a firm coude tip. (A larger catheter enables you to bypass enlarged prostate more easily)
¾ Complications
— Urge sensation (Rx with antimuscarinics)
— Leakage / Blockage
— Urethral trauma / strictures (males).
— Infection / abscess / fistula
— Urinary sphincter damage / incontinence
— Haematuria.
— Transient hypotension.
— Post-obstructive diuresis.
Self-intermittent catheterisation (SIC):
— Fewer complications, increased spontaneous voiding.
— Inpatients with expected temporary AUR.
— Outpatients with SIC competency with recurrent acute-on chronic
urinary retention requiring long-term catheterisation.
Suprapubic catheterisation (see illustration below).
— For patients with contraindications to / failed urethral catheterisation
/ long-term catheterisation.
— Usually inserted by Urologist / Surgeon.
— If emergency, bladder distension can be temporarily relieved by
suprapubic needle aspiration,
— 2% mortality and 10% morbidity.
Ø Trial without catheter (TWOC, if indicated) after 2 doses of alpha-blockade.
Ø Treat cause (e.g. BPH, see next section).
226
UROLOGY
COMMMON UROLOGICAL DEVICES
Urinary Catheter
Illustrated by Kevin Quinlan: 3-way urinary catheter
1.
2.
3.
4.
3L irrigation bag to irrigate intravesical blood and prevent clot formation in the
setting of significant frank haematuria.
Syringe to inflate intravesical catheter balloon with water to prevent the catheter coming out. It is very important that the catheter is inserted beyond the point of achieving catheter urine flow so that the balloon is not inflated in the urethra.
Urine drainage bag.
3-way urinary catheter (2-way urinary catheters are more common and only
have 2 connections for the urine drainage bag and balloon inflation).
227
UROLOGY
Suprapubic Catheter
Illustrated by Kevin Quinlan: suprapubic catheter (see text above).
Nephrostomy
Illustrated by Kevin Quinlan: Nephrostomy. On physical exam, the wound can be found in/near
the renal angle. This is inserted by an interventional radiologist in the setting of urinary tract
obstruction causing hydronephrosis.
228
UROLOGY
BENIGN PROSTATIC HYPERPLASIA
Ø Benign enlargement of the prostate gland.
Ø Occurs in men over 50 years of age.
Ø By the age of 60 years, 50% of men have histological evidence of BPH.
— Symptoms graded according to International Prostate Scoring
Symptom (IPSS) score
Symptoms: Classified as storage and voiding Voiding related
— Hesitancy.
— Poor flow.
— Intermittent stream.
— Dribbling
— Sensation of poor bladder emptying.
— Sensation of poor bladder emptying.
— Double voiding
— Enuresis
Storage related
— Frequency.
— Nocturia.
— Urgency.
— Urge incontinence.
— Nocturnal incontinence
Signs
Ø Homogenous enlargement of the prostate on digital rectal exam.
Ø Palpable bladder if in retention.
Ø Always assess neurological status to exclude neurological aetiology.
Investigations
Ø Serum creatinine: Might be raised if acute or chronic obstruction.
Ø Urine analysis: to exclude superimposed infection.
Ø PSA: to exclude malignancy.
Ø Urinary flowmetry and post void residual measurement.
Ø Cystoscopy: to exclude bladder disease.
Ø Transrectal ultrasound and biopsy: to exclude malignancy.
Ø Renal ultrasound to rule out upper tract deterioration/ hydronephrosis.
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UROLOGY
Treatment
1. Conservative:
For men with mild symptoms and reasonable flowmetry.
2. Medical treatment:
- Alpha-adrenergic antagonists - inhibits alpha receptors within the smooth muscles of the prostate and bladder neck.
- 5-Alpha reductase inhibitors - Inhibits conversion of Testosterone to dihydrotestosterone (DHT). It shrinks the prostate by 25-50% if used for >6
months.
3. Surgical treatment:
(Reserved for those with any of the complications or symptoms not responding
to medical therapy)
- Transurethral resection of the prostate (TURP).
- Millin’s open retropubic prostatectomy/ Da Vinci Robotic Millin’s Prostatectomy
- Transurethral incision in the prostate (TUIP).
- Laser ‘prostatectomy’.
- Microwave thermotherapy ablation of the prostate.
- Embolization.
- Urolift
- Aquablation (in a clinical trial setting)
Complications of the disease
— Haematuria.
— UTI.
— Stone formation.
— Acute retention of urine.
— Chronic retention of urine.
— Overflow incontinence.
— Obstructive irreversible renal failure.
Complications of surgery
— Haemorrhage: Primary or secondary. Watch out for clot retention.
— Sepsis: either due to bacteraemia or wound infection.
— Incontinence: due to damage of external sphincter.
— Retrograde ejaculation (75%) and impotence (up to 10%).
— Urethral strictures: prolonged catheterisation and recurrent instrumentation.
— TUR syndrome / dilutional hyponatraemia: due to excessive glycine absorption during TURP through venous sinuses of the prostate. TURP
syndrome is managed in an ICU setting.
230
UROLOGY
ADENOCARCINOMA OF THE PROSTATE
Key Facts
- The most common non-cutaneous malignant tumour in men older than 65.
- Almost all are adenocarcinomas
- Most arise in the peripheral zone of the prostate (Hence palpable nature on
DRE)
- Associated with family history, increasing age and race
Staging (TNM)
Ø T (Tumour):
— T1 = neither palpable nor detectable by imaging.
— T2 = palpable, but confined to the prostate.
— T3 = extension through prostatic capsule.
— T4 = invasion of adjacent structures.
Ø N (Lymph node): N0 = node negative. N1 = node positive.
Ø M (Metastasis): M0 = negative. M1 = positive for metastases.
Grading:
Gleason is a classification of the histological pattern based on the degree of glandular
de-differentiation
i.e. Well differentiated -> Poorly differentiated/Anaplastic
Calculation - Most common histological pattern score + the second most
common histological pattern score = Gleason Score
Gleason score (range between 2 and 10) appears to correlate well with the likelihood
of spread and the prognosis.
Ø Gleason score < 3 = low grade.
Ø Gleason score > 7 = high grade.
Spread:
Ø Locally to the bladder and the seminal vesicles.
Ø Haematogenous to the bones (generally sclerotic rather than lytic lesions).
Symptoms & signs
Ø Lower urinary tract symptoms (LUTS) in most cases.
Ø Metastases symptoms: bone pain, pathological fractures, and features of hypercalcaemia.
Ø Digital rectal exam may reveal firm irregular, “craggy” prostate.
Investigations
Ø Serum PSA - Screening test with high sensitivity, but low specificity. It is an
indication to consider prostate biopsy.
Ø Transrectal ultrasound (TRUS) and biopsy with prophylactic PO ciprofloxacin
+/- IV gentamicin if additional risk factors for infection such as diabetes
Ø Pelvic and prostate MRI - To detect the presence of extracapsular extension
231
UROLOGY
Ø Isotope bone scan - to assess for bone metastases.
Ø Staging CT TAP in high risk cases.
• PSMA PET scan
Treatment
Consider before treatment:
- Disease stage and grade (low, intermediate, high-risk)
- Patient’s age
- ECOG performance status
- Co-morbidities
Early disease with life expectancy > 10 years
Active surveillance with monitoring or PSA, DRE and MRI findings. Repeat biopsies as
indicated to assess for disease progression
Ø Radical prostatectomy
Ø Suitable for early disease (T1, T2 and T3) and life expectancy of >10 years.
Ø Involves removal of the gland and seminal vesicles down the external sphincter
mechanism.
Ø High risk of incontinence and erectile dysfunction (ED) post-op, but 95% are
continent by 12 months.
- Surgical options: Open, Laparoscopic, Robotic (DaVinci)
Ø
Radical radiotherapy
— Suitable for T1, T2 and T3 tumours.
— Complications include LUTS, proctitis, cystitis and ED.
Ø
Brachytherapy
— Gaining widespread acceptance for T1 and T2 tumours.
— Lower complications rate (localized intense radiation dose).
Early disease with life expectancy < 10 years
Ø Conservative treatment / watchful waiting if no signs of disease progression
(monitor PSA).
Ø Consider TURP if obstructive symptoms are an issue.
Metastatic disease
Ø Aim is palliation
Ø Hormonal therapy might be considered in androgen dependant tumours:
1. Luteinizing hormone-releasing hormone (LHRH) agonist.
232
UROLOGY
Ø
2.
Ø
Side effects include hot flushes, lethargy, osteoporosis, cardiovascular dysfunction and loss of sexual function.
Antiandrogens.
Side effects include gynaecomastia and nipple tenderness.
RENAL NEOPLASMS
Benign
— Adenoma
— Angioma
— Angiomyolipoma
• Simple cysts
Malignant
— Renal cell carcinoma
Wilms’ tumour (nephroblastoma in children)
— Transitional cell carcinoma: renal pelvis & collecting system.
— Squamous carcinoma of the renal pelvis
.
ADENOCARCINOMA OF THE KIDNEY
Ø Accounts for 75 % of all renal neoplasms.
Ø Strong male predominance with male: female ratio of 3:1.
Ø Tumour can extend into renal vein and metastasise to the lungs and bones.
Presentation
Ø Majority present as an incidental finding on imaging
Can present as incidental finding on abdominal ultrasound or CT.
- Classic Triad of Abdominal Mass, Haematuria and Flank Pain (<10% patients)
Ø Painless haematuria with or without clot pain.
Ø Rapidly developing varicocele is a rare but impressive sign.
Ø May present late with symptomatic deposits in the lungs and bones.
Ø Atypical features: (known as the great mimicker) persistent fever, polycythaemia, anaemia, nephrotic syndrome, pyrexia of unknown origin (PUO)
Ø May be associated with a paraneoplastic syndrome e.g. Secretion of Renin
causing hypertension & EPO causing a Polycythaemia
Investigations
Ø Haematological / Biochemical:
- FBC to check for anaemia.
- Urea & Creatinine to check be the renal function.
- Serum Corrected Calcium and ALP as may elevated indicating bone metastasis.
Ø Radiology:
- Renal ultrasound
- Triphasic CT of kidneys to confirm the site and size of the mass and to exclude any local metastasis.
- Pre- and post-contrast enhancement of a renal mass is indicative of malignancy on a triphasic CT scan of the kidneys
- Isotope bone scan if clinically or biochemically indicated.
- CT TAP to stage. CT brain if neurological symptoms
233
UROLOGY
Treatment
Ø Partial or radical nephrectomy if the tumour is confined to the kidney. Clamp
time crucial in preservation of renal function in partial nephrectomy/ metastectomy.
Ø Partial or radical nephrectomy via open, laparoscopic or robotic approach.
Ø Responds poorly to radiotherapy or conventional chemotherapy.
Ø Partial response rates of 15–20% can be achieved with immune modulators
such as interferon, interleukin, tyrosine kinase inhibitors and checkpoint inhibitors such as nivolumab in palliative patients with good performance status.
TRANSITIONAL CELL CARCINOMA OF THE URINARY BLADDER
Ø Considered the commonest form of bladder cancer in the developed world.
— Squamous cell is the most common in the developing world
Ø Strong male predominance is observed with a ratio of 3:1.
Ø Smoking (especially in women) is a major risk factor.
Ø It is also associated with exposure to aromatic hydrocarbons, e.g. workers in
the petrochemical, industrial dye, rubber industries and chimney sweeps.
Ø Other forms of bladder cancer include:
- Adenocarcinoma: relatively rare.
- Squamous cell carcinoma: in areas of endemic Schistosomiasis or in patients with chronic inflammation from long term catheterisation.
Presentation
Ø Painless visible haematuria (bladder cancer until proven otherwise).
Ø Lower urinary tract symptoms.
Ø Clot colic.
Ø Urine retention.
Investigations
Ø Urine cytology: May reveal malignant cells.
Ø Flexible cystoscopy under local anaesthesia is used to visualize the bladder.
Ø Transurethral resection for histological diagnosis, grade and stage.
Ø Imaging to detect local disease and distant spread: ultrasound, CT, MRI.
234
UROLOGY
Treatment
Ø Superficial Transitional Cell Carcinoma
Transurethral resection of bladder tumour (TURBT)
+
Intravesical chemotherapy (via a urinary catheter) with mitomycin C (reduces
the risk of tumour recurrence but not disease progression)
This is either given as a single once of dose or as a weekly instillation for 6
weeks.
Note - Recurrence is common so regular cystoscopic surveillance is performed.
Ø Carcinoma in situ (CIS)
Ø Requires thorough therapy to prevent invasive TCC.
Ø Intravesical immunotherapy with BCG can be effective as it upregulates host
immune response against the tumour.
Ø 6 cycles of BCG are given as induction and this is followed by a maintenance
BCG programme for up to 3 years.
Ø Needs close cystoscopic surveillance with regular bladder mapping with biopsies.
Ø Invasive Transitional Cell Carcinoma
- Curative therapy can be offered with neoadjuvant chemotherapy and radical
cystectomy (Urinary diversion will be required via Urostomy/Ileal Conduit).
Neobladder can be fashioned in younger patients with a good performance
status
- Radical radiotherapy (In patients unfit for cystectomy) is an option however
side effects of radiation cystitis and proctitis are unfavourable for patients.
Prognosis
Ø Poor prognosis in invasive disease.
- 40 – 50 % 5-year survival in muscle invasive tumour.
235
UROLOGY
TESTICULAR TUMOURS
Ø Associated with testicular maldescent.
Ø Lymphatic spread is to the retroperitoneal and intrathoracic lymph nodes.
Ø Common types include seminomas and non seminomatous germ cell tumours
(NSGCT).
Ø Less common tumours include lymphomas and interstitial tumours.
Seminoma:
—
—
—
Non-Seminomatous Germ Cell Tumour :
(NSGCT)
Peak incidence is 30 – 40
— Peak incidence is 20 – 30 year of age.
year of age
Presents as smooth, firm and
— Haematogenous spread most
homogenous swelling. commonly to lungs, brain, and liver
Lymphatic spread is more
common than haematogenous.
Presentation
Ø The commonest presentation is painless palpable hard testicular mass.
Ø Occasionally, the predominant symptoms are those of metastatic disease.
Note – Lymphatic Spread of testis is to the PARA-AORTIC lymph nodes and so inguinal lymphadenopathy is NOT a clinical sign unless there is scrotal
involvement.
Investigations
Ø Urgent scrotal ultrasound is mandatory for any testicular mass.
Ø Serum tumour markers, LDH, B-HCG and AFP may be elevated suggesting
metastatic disease in NSGCTs.
Ø Computerized tomography (CT) and magnetic resonance imaging (MRI) are
the most useful means of detecting secondary deposits.
Staging
Ø Royal Marsden Staging System:
- Stage 1: testis lesion only – no spread.
- Stage 2: nodes below the diaphragm only.
- Stage 3: nodes above the diaphragm.
- Stage 4: pulmonary or hepatic metastases.
Treatment
Ø Orchidectomy is the mainstay of treatment.
Ø Seminomas are radiosensitive.
Ø NSGCTs are chemotherapy sensitive.
236
UROLOGY
ACUTE TESTICULAR PAIN
Causes include:
Ø Testicular torsion until proven otherwise.
Ø Torsion of the testicular appendix “Morgagni’s Hydatid”.
Ø Acute epididymo-orchitis.
Ø Idiopathic scrotal oedema.
TESTICULAR TORSION
Ø Peak age is 12 – 18 years.
— ‘bell and clapper’ deformity: testis is free to rotate due to a deficient attachment to the tunica vaginalis in the scrotum.
— Salvage depends on the time of intervention and degree of torsion.
Presentation
Ø Sudden onset of severe, constant, unilateral scrotal pain.
Ø May be associated with nausea, vomiting and abdominal pain.
Ø The testes is severely tender, lies high and transverse in the scrotum.
Ø The absence of the ipsilateral cremasteric reflex is a key sign.
Management
Ø Analgesia.
Ø Immediate scrotal exploration is required to salvage the testis. (6 hour window
to save testicle)
Ø Scrotal colour duplex ultrasound: if immediately available or where symptoms
have been present for days and testicular viability is unlikely.
Ø Immediate scrotal exploration is required to salvage the testis.
Ø A viable testicle is distorted and fixed.
Ø A clearly non-viable testicle is excised.
Ø The contralateral testicle is also fixed in cases of torsion (orchidopexy) to
reduce the risk of a “bell and clapper” deformity.
TORSION OF THE HYDATID OF MORGAGNI
Ø Difficult to differentiate from testicular torsion clinically.
— Symptoms are due to torsion of the testicular appendix “Hydatid of Morgagni” or the epididymal appendages.
Ø The cremasteric reflex should be preserved.
Management
Ø Analgesia and scrotal exploration is mandatory.
Ø Excise the appendage.
237
UROLOGY
ACUTE EPIDIDYMO-ORCHITIS
Ø Common organisms include Chlamydia trachomatis, Neisseria gonorrhoea in
the young (sexually-transmitted infections (STI).
Ø Escherichia coli and Proteus occur in chronic bladder outflow obstruction or
urinary tract instrumentation.
Ø It is also associated with adolescent mumps.
Management
Ø Scrotal elevation, local ice therapy, and oral NSAIDs may help.
Ø Antibiotics therapy is prescribed according to local guidelines for STIs and
non-STIs infections
238
NOTES
239
NOTES
240
CARDIOTHORACIC SURGERY
Chapter 11
Cardiothoracic Surgery
241
CARDIOTHORACIC SURGERY
Contents:
• Work up for Cardiothoracic Surgery
• Coronary Artery Bypass Grafting
• Valvular Heart Disease
• Pneumothorax
• Chest Tube insertion
• Other notes on thoracic surgery
242
CARDIOTHORACIC SURGERY
Preoperative investigations for Cardiothoracic Surgery:
1. Full History & Exam (including full neurological exam, NYHA & GOLD scoring
systems)
2. ECG
3. CXR (AP And Lateral)
4. Pulmonary Function Tests
— FEV1 important to assess patient’s ability to undergo lung reducing surgery
— Include a Diffusion Capacity of the Lung for Carbon Monoxide (Effected with
Fibrosis and Emphysema)
5. Cardiopulmonary exercise test
6. CT Thorax +/- Contrast
7. Carotid Doppler Ultrasound to assess for carotid atherosclerotic disease
8. Trans-oesophageal Echocardiogram (TOE)
— Assessment of valves including degree of prolapse/stenosis
— Assessment for Regional wall motion abnormalities
9. Coronary Angiography:
— A planned CABG or those undergoing valvular surgery who would benefit
from surgical revascularisation in the same operation.
— May consider revascularisation before surgery in stable angina
10. Pulmonary Wedge Capillary Pressures (Via Right heart catheterisation): Before
complex valvular surgery.
11. Cardiac MRI (if specified by surgeon)
12. Dental Review (If surgery on valves)
Coronary Artery Bypass Grafting:
Indications for surgery
—
—
—
—
—
>70% left main stem stenosis.
Symptomatic patients with >70% proximal LAD stenosis.
Symptomatic patients with >70% disease in all three vessels
Concomitant valvular disease which requires replacement
Vessel Disease (as above) in a diabetic
Procedure:
— Performed via median sternotomy. A piece of conduit (saphenous vein, left
internal mammary artery, radial artery) is anastomosed to the coronary artery
beyond the lesion and then to the ascending aorta.
243
CARDIOTHORACIC SURGERY
Selection of conduits
— Venous grafts
— The long saphenous vein is the most
common vein used as a conduit.
Standard “Triple Bypass” includes:
The 10 year patency rate is 50-60%.
- Left internal mammary artery — Arterial grafts
(LIMA) to Left anterior descending — The left internal mammary
(LAD)
artery/internal thoracic artery is
- Portion of harvested Long
the conduit of choice for left anterior
Saphenous Vein from Aorta to descending artery. The 10 -year
Circumflex artery
patency rate is 90%.
- Portion of harvested Long
— Radial artery can also be used
Saphenous Vein from Aorta to as a second choice but is prone to
Distal right coronary artery (RCA)
vasospasm.
Complications:
— Death, 0–1% in low risk patients.
— Stroke, 1–2% in low risk patients.
— Re-sternotomy for bleeding or tamponade 5%.
— Chest infection, atrial fibrillation, wound infection, renal failure.
Prognosis:
— In untreated patients with symptoms severe enough to warrant coronary angiography, 10% have an acute MI within 1 year and 30% have an acute MI
within 5 years. Hospital mortality of MI is 7–10%.
— In three-vessel disease, the 5y survival is 50%, lower if LV function is impaired.
— Left main stem disease has a 2-year survival of 50%.
244
CARDIOTHORACIC SURGERY
Surgery of the Heart Valves:
Choice of Valve Type:
Mechanical:
Bio-prosthesis: (Bovine/Porcine)
— Life Long (>20 years)
— Requires Warfarin
— Noisy (Metallic Click)
— Shorter Life (10-15 years)
— No need for warfarin
— Silent
Aortic Stenosis:
Syncope
Triad of Symptoms –
Aetiology:
— Calcific Degeneration
— Bicuspid Valve
— Rheumatic Disease
Angina
Dyspnoea
Clinical Features:
— Ejection Systolic Murmur loudest in aortic region and radiates to carotids
— Heaving Apex Beat
Diagnosis:
— ECG may show LV Hypertrophy
— ECHO needed to assess degree of stenosis
Indications for intervention:
1. Gradient of flow across the valve
2. Symptomatic Aortic Stenosis
Mode of intervention:
— Open via thoracotomy
— Transcatheter Aortic Valve Implantation (TAVI)
Prognosis:
— When combined with coronary artery disease, aortic stenosis is associated with
a high risk of sudden death.
— Post-operative prognosis is good.
— Type of valve used is of importance to length of patency.
245
CARDIOTHORACIC SURGERY
MITRAL REGURGITATION (MR)
—
Second most common valvular lesion.
Aetiology
— Mitral valve prolapse due to ischaemia (Papillary muscle dysfunction/Chordae
Tendinea rupture)
— Rheumatic disease.
— Infective endocarditis.
— Connective tissue disorders.
Clinical features
— Holosystolic murmur loudest at apex +/- third heart sound that can radiate to
axilla
— Acute MR
— Signs of CCF.
— Chronic MR
— Exertional dyspnoea.
— Orthopnoea.
— Displaced apex beat.
— Atrial Fibrillation in 80%.
Diagnosis
— Transthoracic, < transoesophageal echocardiogram.
Indications for surgery
— Acute MR.
— Severe chronic MR.
Mode of surgery
— Open Valve replacement
— Endovascular MitraClip if surgery contraindicated
— Prognosis
— Mortality of untreated severe MR is 5% per year.
— Operative mortality is 2–3% for low risk cases.
Prognosis
246
— Mortality of untreated severe MR is 5% per year.
— Operative mortality is 2–3% for low risk cases.
CARDIOTHORACIC SURGERY
MITRAL STENOSIS (MS)
— Prevalence <1%.
Clinical features
— Rumbling mid-diastolic murmur at apex
— Signs of RH Failure (Due to increased pulmonary vascular resistance)
— Atrial fibrillation.
— Left parasternal heave.
— Tapping apex beat.
Note many patients may be asymptomatic
Diagnosis
— CXR shows splaying of carina (enlarged LA)
— Transthoracic, transoesophageal echocardiogram.
—
—
—
Mode of surgery
Percutaneous Valvotomy
Open Mitral Valve replacement
Prognosis
— Poor once symptoms of heart failure are present.
AORTIC REGURGITATION (AR)
Aetiology
— Rheumatic disease.
— Infective endocarditis.
— Aortic dissection.
— Marfan’s syndrome & other connective tissue disorders.
— Large vessel vasculitis
Clinical features
— Early diastolic murmur.
— Acute AR (endocarditis)
— Signs of left ventricular failure (LVF).
— Chronic AR
— Often asymptomatic.
— Wide pulse pressure (Corrigan’s/Water Hammer Pulse).
Diagnosis
— CXR shows cardiomegaly.
Indications for surgery
— Acute AR is a surgical emergency.
— Chronic AR
— LV dilatation >5.5cm.
Prognosis
— Acute AR has a poor prognosis.
— Chronic AR has a good outcome until failure occurs (50% 2 year mortality).
— Operative mortality is 3–5%
247
CARDIOTHORACIC SURGERY
PNEUMOTHORAX
Definition
— Presence of air in the pleural space with varying degrees of secondary lung
collapse.
Classification
— Primary spontaneous pneumothorax: Occurs without obvious reason or
apparent lung disease.
— Secondary spontaneous pneumothorax: Due to a known underlying lung or
systemic disease.
— Traumatic pneumothorax: The result of iatrogenic or non-iatrogenic blunt and/
or penetrating chest interventions and injuries.
PRIMARY SPONTANEOUS PNEUMOTHORAX
Key Facts
— More common in tall, young men.
— More common on the right side.
— Caused by rupture of small sub pleural blebs.
— Usually found in the apex.
Clinical Features
— Dyspneoa.
— Chest pain.
— Tachypnoea.
— Hyperresonant hemithorax.
— Absent breath sounds.
Investigations
— Chest X-Ray (CXR).
— CT provides a more accurate estimate of the size of pneumothorax.
Complications
— Tension pneumothorax.
— Pneumomediastinum.
— Haemopneumothorax.
— Recurrent pneumothorax.
Management
— Conservative if small (<20%) pneumothorax and asymptomatic. Oxygen, repeat
CXR.
— Needle aspiration if >2 cm rim of air seen
— Chest tube insertion (4-5th intercostal space in the mid-axillary line) indicated if
aspiration fails.
248
CARDIOTHORACIC SURGERY
Surgery
Video Assisted Thorascopic Surgery (VATS) is being increasingly used for Bullectomy and pleurodesis
Recurrence rate
— Less than 2% following surgery.
SECONDARY SPONTANEOUS PNEUMOTHORAX
Aetiology
— Underlying lung or systemic disease.
— Chronic airway and alveolar diseases: e.g. severe asthma, cystic
fibrosis, emphysema, bullae and cysts.
— Systemic connective tissue diseases: e.g. rheumatoid arthritis, ankylosing spondylitis, scleroderma, Marfan and Ehlers Danlos syndromes.
— Malignant lung and chest diseases: e.g. bronchial cancer, sarcoma.
—
Notes on Thoracic Surgery:
1. Pleurodesis
- Kaolin Talc Insufflation (Snowstorm) promotes inflammation and pleural
adherence
- Pleural Stripping with parietal pleura stripped off in order to create raw
surface for inflammatory adhesive reaction
- Post-operative pyrexia is common and is seen as a sign of success associated with inflammation
- DO NOT do Pleurodesis if someone may be considered for a lung transplant.
2. Empyema
- May be associated with infection post thoracic surgery OR spontaneous
following a pneumonia.
- Approximately 40% associated with streptococcal species
- Symptoms/Signs include persistent pyrexia, dyspnoea and pleuritic chest
pain
- Decortication of the empyema may be necessary if medical management
has failed.
CHEST TUBE INSERTION (TUBE THORACOSTOMY)
—
—
—
The insertion of a chest tube into the pleural cavity to drain air, blood, pus,
or other fluids.
Allows for continuous, large volume drainage until the underlying pathology
can be more formally addressed.
A “safe triangle” has been described as the preferred site of insertion.
249
CARDIOTHORACIC SURGERY
Illustrated by Kevin Quinlan: borders of the “safe triangle” in the axilla.
Technique
— Inserted in the 4-5th intercostal space just anterior to the mid-axillary line, just
above the rib to avoid the neurovascular bundle
— Blunt dissection of the subcutaneous tissues is used to access the pleural
space. Keep dissection tools on the upper edge of the rib to avoid the neurovascular bundle on the underside of the rib above.
— Chest tube is inserted under direct vision and attached to an underwater seal.
— To avoid water entering the pleural space, never lift the underwater seal above
the level of the bed.
— Chest tubes should not be clamped.
Confirmation of tube placement
— Bubbling of air in the underwater chamber.
— Oscillation of fluid in the tube connecting the chest tube to the underwater seal
with patient’s respiration.
— Chest X-Ray.
250
NOTES
251
NOTES
252
MAJOR TRAUMA
Chapter 12
Major Trauma
253
MAJOR TRAUMA
Contents:
• Advanced Trauma Life Support (ATLS)
• Thoracic Trauma
• Abdominal Trauma
254
MAJOR TRAUMA
THE ADVANCED TRAUMA LIFE SUPPORT (ATLS®) SYSTEM
Ø
Ø
Ø
The international standard for care during the ‘golden hour’ following trauma.
Emphasises that injury kills in certain reproducible time frames in a common
sequence: loss of airway, inability to breathe, loss of circulating blood volume,
expanding intracranial mass.
The primary survey (ABCDEs) with simultaneous resuscitation is emphasized.
Image by Anthony Hoban: Trimodial pattern of mortality following trauma
Primary Survey: The goal of primary survey is to Identify and treat
life-threatening conditions according to priority (ABCDE).
Note :
1.
2.
Always THINK of the cohort of person you are treating as the elderly, children,
athletes and the multi-morbid respond in different ways to shock.
Always remember to reassess after any intervention by monitoring vitals and
clinical response
Ø Airway maintenance with cervical spine protection.
— Assess the airway for patency. If the patient can speak, airway is not
immediately threatened although this is not always the case e.g. Burns
victims
— Consider secretions, foreign body, mandibulofacial fractures (e.g. Le
Fort Fractures) and tracheal/laryngeal fractures if there is airway impairment in a semi conscious/unconscious patient
— Protect the spinal cord using manual in-line immobilization and immobilization devices if available if there is a suspected C-spine injury
(Consider Age, Mechanism of trauma, clinical neck pain or numbness in extremities)
255
MAJOR TRAUMA
—
—
—
Perform jaw thrust +/- chin lift (if C-spine clear)
Consider nasopharyngeal/oropharyngeal airway
Note: If a patient can tolerate one of these airway adjuncts it is likely that
they may need a more definitive airway.
If patient unable to maintain airway integrity, secure a definitive airway
(orotracheal, nasotracheal, cricothyroidotomy).
Ø Breathing and ventilation
— Administer 100% O2 using a non-rebreathing mask/reservoir.
— Full cardiorespiratory exam - Inspect for tracheal deviation, distended
neck veins, chest wall expansion & symmetry, respiratory rate, and thoracic wounds.
— Percuss and auscultate chest.
— Identify and treat life-threatening conditions: tension pneumothorax, open
pneumothorax, flail chest with pulmonary contusion, massive haemothorax.
Ø Circulation with haemorrhage control
— Look for signs of shock (drowsiness, cold clammy skin, reduced capillary
refill, hypotension, tachycardia)
— Hypotension is usually due to blood loss.
¾ Chest, abdomen, retroperitoneum, pelvis, long bones (‘blood on the floor and five more’).
— Control external bleeding with pressure.
— Obtain IV access using two 14G cannula.
— Send blood for cross-match, FBC, coagulation profile and U&E.
— Commence bolus of warmed Hartmanns solution
— Unmatched, type-specific blood (O negative) only for immediate life-
threatening blood loss.
— Consider surgical control of haemorrhage (laparotomy, thoracotomy).
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MAJOR TRAUMA
Source: ATLS Version 9 Chapter 3 “Shock” – “Haemorrhagic Shock”.
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MAJOR TRAUMA
Ø Disability
— Perform a rapid neurological evaluation using the AVPU method (Alert,
responds to Vocal stimuli, responds only to Painful stimuli, unresponsive
to all stimuli) or the Glasgow coma scale (GCS).
— After excluding hypoxia and hypovolemia, consider changes in level of
consciousness to be due to head injury.
Ø Exposure/environment control
— Undress patient for through examination.
— Prevent hypothermia by covering with blankets/warming device.
— Use warm IV fluids.
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MAJOR TRAUMA
The Trauma Triad of Death:
Hypothermia
Coaguloapthy
Acidosis
Ø Adjuncts to primary survey
— Monitoring. Pulse, non-invasive BP, ECG, pulse oximetry.
— Urinary catheter (after ruling out urethral injury).
— Diagnostic studies. X-rays (lateral cervical spine, AP chest, and AP pelvis), ultrasound scan, CT scan, diagnostic peritoneal lavage.
Ø Secondary survey
— Begin the above only after the primary survey is completed and while
sufficient resuscitation is being carried out.
— Take history using AMPLE method (Allergy, Medication, Past medical
history, Last meal, Events of the incident).
— Perform a head-to-toe physical examination and continue to reassess
all vital signs. Perform any specialized diagnostic tests that may be required.
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MAJOR TRAUMA
THORACIC TRAUMA
Image by Niamh Adams: Tension Pneumothorax
N.B.: Tension pneumothorax is a clinical diagnosis. You should never see an X-ray like this!
Key features
Ø Thoracic injuries account for 25% of deaths from trauma.
Ø Fifty per cent of patients who die from multiple injuries also have a significant
thoracic injury.
Ø Open injuries are caused by penetrating trauma from knives orgunshots. Closed injuries occur after blasts, blunt trauma, and deceleration. (Road traffic
accidents (RTAs) are the most common cause.
Management - primary survey
Ø Identify and treat major thoracic life-threatening injuries.
Tension pneumothorax
Ø Clinical dagnosis – no imaging.
Ø Air enters the pleural space via injury to the lung or the chest wall.
Ø Expanding pneumothorax impedes venous return to the heart.
Ø Respiratory distress, tachycardia and hypotension.
Ø Decreased movement
Ø Hyperresonant percussion note
Ø Absent breath sounds over affected hemithorax.
Ø Trachial deviation – Late sign
Ø Perform immediate needle decompression
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MAJOR TRAUMA
Insert a 14 guage cannula into the 2nd intercostal space in the mid-clavicular line.
Then, insert surgical chest drain into the fifth intercostal space between the anterior
and midaxillary line. Finally, attach an underwater seal drain
Open pneumothorax
Associated with a large chest wall defect >3cm.
(Air flows through path of least resistance i.e. If thoracic opening >2/3 diameter of
trachea)
Ø Occlude with a three-sided dressing. This creates a valve that allows air out of
the pleural cavity but not into it.
Ø Follow by immediate insertion of an intercostal drain through a separate incision.
Flail chest
2 or more ribs fractured in 2 or more locations.
Ø Results in paradoxical motion of the chest wall. Restricted chest wall movement and underlying lung contusion result in hypoxia.
Ø If the segment is small and respiration is not compromised, nurse patient in HDU with adequate analgesia. Encourage early ambulation and vigorous
physiotherapy. Do regular blood gas analysis.
Ø In more severe cases, endotracheal intubation with positive pressure ventilation is required.
Massive haemothorax
Ø Accumulation of >1500 mL of blood in pleural cavity.
Ø Suspect when shock is associated with dull percussion note and absent breath
sounds on one side of chest.
Ø CXR may show a “white out” in the hemi-thorax
Ø Simultaneously restore blood volume and carry out decompression by inserting
a wide bore (>32Ch) chest drain.
Ø Consider need for urgent thoracotomy to control bleeding if there is continued
brisk bleeding and need for persistent blood transfusion.
Ø Consult with a regional thoracic center immediately.
Cardiac tamponade
Ø Most commonly results from penetrating injuries, but blood can also accumulate in pericardial sac after blunt trauma.
Ø Recognized by haemodynamic instability. Tachycardia, pulses paradoxus
Ø BECKS TRIAD: Hypotension, raised JVP and faint heart sounds.
Ø If critically ill with suspected tamponade, perform ‘blind’ pericardiocentesis and
call cardiothoracic or general surgeons to consider emergency thoracotomy.
Ø If unwell, but responding to treatment, arrange urgent transthoracic echo and
eFAST scan in emergency department
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MAJOR TRAUMA
Management - secondary survey
Ø Perform an in-depth examination.
Ø In stab injuries, expose the patient fully and position them so that you can assess the entire chest.
Ø Get an erect CXR looking for pneumo-/haemothorax
Ø Treat with a chest drain if large or symptomatic or in any patient likely to require
mechanical ventilation.
Potentially life threatening injuries:
Pulmonary contusion
Ø Most common potentially lethal chest injury.
Ø Risk of worsening associated consolidation and pulmonary oedema.
Ø Treat with analgesia, physiotherapy, and oxygenation.
Ø Consider respiratory support for a patient with significant hypoxia.
Tracheobronchial rupture
Ø Suspect when there is persistent large air leak after chest drain insertion. Seek
immediate (cardiothoracic) surgical consultation.
Ø Thoracic CT scan usually diagnostic.
Blunt cardiac injury (myocardial contusion/traumatic infarction)
Ø Suspect when there are significant abnormalities on ECG or echocardiography.
Ø Seek cardiological/cardiothoracic surgical advice.
Thoracic Aortic Injury – Transection / Partial transection
Ø Most common area affected is the proximal descending aorta, where the mobile
aortic arch is fixed at the ligamentum arteriosum
Ø Patients survive immediate death if the haematoma is contained.
Ø Suspect when history of decelerating force and where there is widened mediastinum on CXR.
Ø Thoracic CT scan is diagnostic.
Ø Consider Cardiothoracic and/or Vascular surgical referral.
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MAJOR TRAUMA
Image by Anthony Hoban: Extrauminal blood at the aortic arch (with consent)
Image by Anthony Hoban: Bowel in left hemi-thorax (with consent)
Diaphragmatic rupture
Ø Usually secondary to blunt trauma in restrained car passengers (seat belt compression causes ‘burst’ injury commonly on the left side).
Ø Suspect in patient with a suitable history and a raised left hemidiaphragm on
CXR.
Ø Penetrating trauma below the fifth intercostal space can produce a perforation.
Ø Commonly missed on CT scans. Laparoscopy is diagnostic in cases where
diaphragmatic injury is highly suspected.
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MAJOR TRAUMA
ABDOMINAL TRAUMA
Key features
Abdominal injuries are present in 7–10% of trauma patients. These injuries, if
unrecognized, can cause preventable deaths.
Blunt trauma
Ø Most frequent injuries are spleen (45%), liver (40%), and retroperitoneal haematoma (15%).
Ø Blunt trauma may cause:
— Compression or crushing, causing rupture of solid or hollow organs.
— Deceleration injury due to differential movement of fixed and non-fixed
parts of organs, causing tearing or avulsion from their vascular supply,
e.g. liver tear and vena caval rupture.
Ø Blunt abdominal trauma is very common in Road Traffic Accidents where:
— There have been fatalities.
— Any casualty has been ejected from the vehicle.
— The closing speed is >50mph.
Penetrating trauma
This may be caused by:
Ø Stab wounds and low velocity gunshot wounds.
— Cause damage by laceration or cutting.
— Stab wounds commonly involve the liver (40%), small bowel (30%), diaphragm (20%) and colon (15%).
Ø High velocity gunshot wounds transfer more kinetic energy and cause further
injury by cavitation effect, tumble, and fragmentation of ammunition.
— Commonly involve the small bowel (50%), colon (40%), liver (30%), and
vessels (25%).
Management
Primary survey of the abdomen
Ø Any patient persistently hypotensive despite resuscitation, for whom no obvious
cause of blood loss has been identified by the primary survey, can be assumed
to have intra-abdominal bleeding.
Ø Focused Abdominal Sonography for Trauma (FAST) scanning is used as part of
primary survey
Ø If the patient is stable, an emergency abdominal CT scan is indicated.
Ø If the patient remains critically unstable, an emergency laparotomy is usually
indicated.
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MAJOR TRAUMA
Secondary survey of the abdomen
Ø History
— Obtain from the patient, other passengers, observers, police, and emergency medical personnel.
Ø Mechanism of injury
— Seat belt usage, steering wheel deformation, speed, damage to vehicle,
ejection of victim, etc. in automobile collision.
— Velocity, calibre, presumed path of bullet, distance from weapon, etc. in
penetrating injuries.
Ø Prehospital condition and treatment of patient.
Physical examination
Ø Inspect anterior abdomen which includes lower thorax, perineum, and log roll
to inspect posterior abdomen.
— Look for abrasions, contusions, lacerations, penetrating wounds, distension, evisceration of viscera.
Ø Palpate abdomen for tenderness, involuntary muscle guarding, rebound tenderness, gravid uterus.
Ø Percuss to elicit subtle rebound tenderness.
Ø Assess pelvic stability.
Ø Penile, perineum, rectal, vaginal examinations, and examination of gluteal
regions.
Investigations
Ø Blood and urine sampling.
Ø Plain radiography
— Supine CXR is unreliable in the diagnosis of free intra abdominal air.
Focused assessment sonography for trauma (FAST)
Ø It consists of imaging of the four Ps.
— Morrison’s pouch, pouch of Douglas (or pelvic), perisplenic, and pericardium.
Ø It is used to identify the peritoneal cavity as a source of significant haemorrhage.
Ø It is sensitive but is user dependent
Ø It does not adequately show retroperitoneal bleeding and also is not specific
for sites of intra-abdominal bleeding.
Diagnostic peritoneal lavage (DPL)
Ø Superseded by FAST and CT scanning.
— Aspiration of blood, GI contents, bile, or faeces through the lavage catheter indicates laparotomy.
— This is rarely performed and is mentioned as reference only.
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MAJOR TRAUMA
CT
Ø
Ø
The investigation of choice in hemodynamically stable patients in whom there
is no apparent indication for an emergency laparotomy.
It provides detailed information relative to specific organ injury and its extent
and may guide/inform conservative management.
Indications for resuscitative laparotomy
Ø Blunt abdominal trauma.
Ø Unresponsive hypotension despite adequate resuscitation and no other cause
for bleeding found.
Indications for urgent laparotomy
Ø Blunt trauma with positive DPL or free blood on ultrasound and an unstable
circulatory status.
Ø Blunt trauma with CT features of solid organ injury not suitable for conservative
management.
Ø Clinical features of peritonitis.
Ø Any knife injury associated with visible viscera, clinical features of peritonitis,
haemodynamic instability, or developing fever/signs of sepsis.
Ø Any gunshot wound.
266
NOTES
267
NOTES
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PLASTIC SURGERY
Chapter 13
Plastic Surgery
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PLASTIC SURGERY
Contents:
• Malignant melanoma
• Basal cell carcinoma
• Squamous cell carcinoma
• Burns
• Wound healing
• Dupuytren’s disease
• Hand trauma
• Upper limb compression neuropathy
• Compartment syndrome
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PLASTIC SURGERY
MALIGNANT MELANOMA
Definition
Ø A malignant neoplasm of melanocytes
Incidence
Ø Global incidence doubled in last 20 years
Ø 4 – 5% of all skin cancers
Ø 80% of skin cancer deaths
Risk factors
Ø Pale skin, freckles, fair hair
Ø Multiple benign naevi
Ø Atypical naevi
Ø UV exposure, sunburns
Ø Family history of malignant melanoma
Ø Immunosuppression
Presentation
Ø The American System: ‘ABCDE’ system
— Asymmetry, Border, Colour, Diameter, Evolution
Ø Metastatic melanoma may present with palpable lymph nodes. It may be the only
clinical finding as the primary site of the melanoma may not be clinically evident
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PLASTIC SURGERY
Ø The Glasgow system (7-point checklist):
— Score of ≥ 3 needs specialist referral
Major (2 points)
Minor (1 point)
Change in size
Diameter ≥ 7 mm malignant melanoma
Irregular pigment
Inflammation
Irregular border
Oozing/bleeding/crusting
Pathological Subtypes
272
Itching/altered sensation
PLASTIC SURGERY
Staging
Ø Breslow thickness
— Depth of the tumour – distance measured in mm from the epidermis to
the maximum depth of the tumour
— Single most important prognostic variable
Ø Breslow thickness: 5 – year survival
Depth
5-Year Survival (%)
In situ
95 – 100
< 1 mm
95 – 100
1 – 2 mm
80 – 95
2 – 4 mm
60 – 75
> 4 mm
50
Management
Ø Specific investigations
— Excision biopsy with a 2 mm margin, (not a punch biopsy) for histopathology diagnosis
— A staging CT scan to out-rule metastatic disease for tumours ≥1mm thickness (I would say for “all stage 3 disease and is considered in
stage 2 disease”)
— Baseline blood tests
Ø Surgery
— Wide local excision is performed with a margin of 1-3 cm, depending on
the Breslow thickness of the tumour
— Sentinel lymph node biopsy for tumours with ≥ 0.8 mm Breslow thickness, in the absence of regional lymphadenopathy and recommended by Melanoma MDT
— The presence of metastatic disease in the sentinel node mandates completion lymphadenectomy
Ø Adjuvant therapy
— Immunotherapy (Interferon) – for metastatic or recurrent disease, however trials of its efficacy are still ongoing
— Immunomodulators (Ipilimumab) – for metastatic disease
Ø Local recurrence
— Isolated chemotherapeutic limb perfusion has been demonstrated to aid
in patients with multiple recurrences isolated to one limb. It can reduce
the recurrence rate and the overall survival
— CO2 laser and curettage may also benefit
Ø Radiotherapy
— For metastatic disease and palliative symptom control, i.e. bone or brain
metastases
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PLASTIC SURGERY
BASAL CELL CARCINOMA VERSUS SQUAMOUS CELL CARCINOMA
BCC
Definition/
> Malignant neoplasm of the
Epidemiology
> Malignant neoplasm of the
Also known as ‘rodent ulcer’
> Most common
non-melanoma skin cancer
(NMSC)
> More common age
> 40 & Caucasians
> Slow growing; metastases
is rare
> Cause extensive local
damage if left untreated
SCC
> Malignant neoplasm of
keratinising cells of the
epidermis
> Second most common
NMSC
> Higher mortality than
BCC
> More common age > 50 & Caucasians
> Metastases in SCC are
more common than
BCC; spread via
lymphatics
> Lesions on the lip, ears and perineum metastasise early; poorer prognosis
Risk factors
> Exposure to sunlight (i.e. working outdoors)
> Fair skin, light hair, blue/green eyes
> Male preponderance
> Family history
> Immunosuppression
> Smoking
> Previous BCC
Prevention
> Primary – minimising sun exposure, protective clothing and
sunscreen
>Secondary – Early detection and appropriate management (regularly examining patients with previous BCC and biopsy of
any suspicious skin lesions to confirm diagnosis)
Presentation
> Shiny,
translucent/pearly pink/skin
coloured papule/nodule
> The lesion may also be tan,
black or brown and may be
confused with a mole
> Open sore that bleeds,
oozes or crusts and remains
open for 3 or more weeks.
May ulcerate.
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> Hyperkeratotic indurated
crusted nodule
> Reddish, scaly
patch/plaque
> Ulcerated
> May bleed
PLASTIC SURGERY
BCC
> A reddish patch or irritated
area, which may crust or itch
> Telangiectasia
> A white, yellow or waxy
scar-like area with poorly
defined borders and shiny,
taut skin may represent a
more aggressive tumour
SCC
Treatment
> Depends on the size,
depth and location of the
tumour
> Surgical excision –
Simple excision or Mohs
micrographic surgery
> Cryotherapy/curretage
> Radiotherapy – for medically
unfit
> Topical creams (Imiquimod
5% or Fluorouracil 5% (5-FU)) –
for smaller superficial lesions
> Excision of primary
tumour with a 5 mm-10 mm
clearance margin
> Block dissection of
affected lymph nodes
if lymphatic involvement
> Radiotherapy – for
unresectable tumours,
unfit for surgery or local
control of distant
metastases
> Cryotherapy/curettage
> Topical creams (Fluorouracil 5% (5-FU)) –
for smaller superficial lesions
Prognosis
> Good, with ~ 95% of
patients remaining disease
free at 5 years in those
with clear margins
> Previous BCC diagnosis
increases risk of having
recurrent BCC’s within 3 years
by ~ 40%
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PLASTIC SURGERY
BURNS
Aetiology
Ø Most thermal burns are caused by a flame, boiling water or contact with hot
objects, e.g. hot stove
Ø Chemical burns are much less common and most often occur with
— Industrial chemicals, e.g. splashes or inhalation of fumes
— Household chemicals, e.g. caustic soda
Ø Electrical burns act like thermal burns: heat is produced. Injury is proportional to
the voltage of the source
Ø Cold thermal injury occurs in frostbite
Emergency burn care
— Stop the burning process
— Flames: stop drop and roll, remove from burning source
— Scalds: remove wet clothing
— Cool the burn:
¾ Cool running water for at least 20 minutes
¾ Do not use ice
¾ Wet towels work less efficiently and should be changed regularly to ensure they are cold
¾ Manage as per ATLS guidelines
Severity of burn injury depends on multiple factors
— Depth
— Size
¾ Calculated as a percentage of the total body surface
— Location
— Patient risk factors
Assessing depth and size of the burn
— Depth
¾ Epidermal
— Erythematous/bright red, shiny
— Brisk capillary refill, painful to touch
— Heals within a few days with simple dressings.
¾ Partial thickness
— Dark red, blotchy, may have blisters
— Slow capillary refill, may not have any sensation
— May heal with dressings, but if there is mixed depth, some require surgery.
¾ Full thickness
— Leathery appearance, usually white
— No capillary refill or sensation
— Most require excision and reconstruction
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PLASTIC SURGERY
Illustrated by Azlena Ali Beegan and Kevin Quinlan: Depth of Burns
— Size – Total Body Surface Area (TBSA)
¾ Wallace rule of 9’s, less accurate:
— Each entire arm (posterior and anterior surface) is worth 9%, each
leg is 18%, anterior and posterior trunk is 18% each, etc. The head
is 9% and the perineum is 1%
— Lund-Browder chart:
¾ The most accurate method
¾ Note: that there are different percentages for small
children as the head is proportionately larger
— For small burns, the “palm rule” can be useful, the patient’s palm,
(not the assessor) is worth ~1%
Burn resuscitation
Ø Burns cause vasodilation and increase vascular permeability
Ø This causes oedema and loss of circulating fluid
Ø May lead to organ failure. The burn area itself also has a direct loss of fluid due
to evaporation
Ø Fluid resuscitation in first 24 hours is paramount to improve mortality and morbidity. Indicated in adults with >15% and children with >10% TBSA burns
The Parkland formula is the gold standard for guiding fluid replacement:
4mls Hartmann’s solution X Bodyweight (kg) X % TBSA
Ø Half of the fluid is given in the first 8 hours and the other half in the next 16
hours
Ø Response should be monitored by urine output
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PLASTIC SURGERY
Management
Ø General:
— Early aggressive fluid resuscitation is key
— Early enteral feeding in more severe burns
— Drug therapy in burns includes IV analgesics and sedatives for the
patient’s comfort
— Tetanus immunisation is given routinely and antibiotics are usually
administered topically due to no blood supply to the burn eschar
— Proton pump inhibitors: to reduce the incidence of associated stress ulceration
— Consider DVT prophylaxis
Ø Conservative treatment:
— For small superficial or mixed partial thickness burns
— Simple dressings changed infrequently to allow healing
Ø Surgery:
— For deeper burns or full thickness burns
— The burn is excised down to healthy viable tissue
— Usually the wounds are reconstructed using a split thickness skin
graft
— For specialised areas such as the hand and face, full thickness skin
graft may be indicated
Complications
Ø Circumferential burns can act like a tourniquet and reduce blood supply to the
affected limb resulting in ischaemia
— Treatment is by escharotomy (incision through the eschar/burn) to
release the stricture and restore circulation to the compromised
extremity
Ø Respiratory complications
— Upper airway burns that cause oedema and obstruction of the
airway
— Inhalation injury causing decreased gas exchange
Ø Renal compromise occurs secondary to acute tubular necrosis
— Because of the hypovolaemic state, blood flow decreases to the
kidneys causing ischaemia
— If persists, renal failure may ensue with severe metabolic acidosis
and myoglobinuria
Ø Infection
— The most serious threat to further tissue injury and possible sepsis
— Survival may be dependent on the prevention of wound contamination
— Burns may be protected from contamination by application of topical
antibiotics with or without dressings
— Excision of the burn and adequate skin coverage is the primary goal
for these wounds
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PLASTIC SURGERY
WOUND HEALING
Classification
Ø Primary intention – May be further subdivided into the following categories:
— Immediate closure of incised wound through apposition of wound
edges
— Delayed primary closure in cases where time is allowed for oedema or infection to resolve before definitive wound closure
Ø Secondary intention – Wound healing occurs by concomitant wound contraction
and migration of fibroblasts and keratinocytes from the wound edges
Phases of wound healing
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PLASTIC SURGERY
Abnormal scarring
Hypertrophic
Keloid
Abnormal proliferation of scar tissue
limited to original wound margins
Abnormal proliferation of scar tissue
extending beyond original wound margins
Hypertrophic more common than keloid More common in dark-skinned populations
and often have family history
Occur within 8 weeks of injury, grows
rapidly and regresses over time
Persist for many years and often do not
regress spontaneously
Typical locations are areas where
there is scar tension such as
pre-sternal region, shoulders and
crossing joint surfaces
May develop after minor trauma such as
acne scars or ear piercing
Type III collagen
Type I and II collagen
May lead to pruritus due to increased
numbers of mast cells
Treatment modalities may be combined
and include pressure garments, silicone
sheeting and topical silicone gel, intralesional corticosteroid injection, excision
and radiation (each of which carry high risk
of keloid recurrence)
Disordered wound healing
Ø Factors affecting wound healing
— Local factors:
¾ Infection, vascularity, trauma, radiation therapy, denervation
— Systemic factors:
¾ Congenital – Ehlers-Danlos, Werner syndrome, Epidermolysis bullosa
¾ Acquired – Nutritional deficiency, steroid use, immunosuppression, diabetes mellitus, hypothyroidism,
smoking
Ø Pathologic wound healing
— Acute failure of wound healing:
¾ Post-operative separation of a surgical incision
¾ Local causes – Haematoma, seroma, infection, oedema,
excess tension
— Chronic failure of wound healing:
¾ Failure to achieve anatomical/functional integrity over 3
months
¾ Common causes – Diabetes mellitus, venous stasis,
ischaemic tissue, pressure necrosis, osteomyelitis,
hidradenitis suppuritiva, pyoderma gangrenosum, occult
malignancy, e.g. SCC/Marjolin’s ulcer
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PLASTIC SURGERY
Wound management
Reconstructive Ladder
Algorithm of reconstructive options applied to manage wounds or defects that
advocates the initial use of less complicated techniques with progression to more
complex strategies when necessary
Ø Skin grafts:
— A graft is a subunit of tissue transferred from one part of the body
to another without its own blood supply, e.g. skin, bone, cartilage
Split thickness skin graft
Full thickness skin graft
Epidermis with a variable amount of dermis
Epidermis with the entire dermis
Harvested from thigh or buttock
Harvested from eyelids, postauricular
area, supraclavicular area and less commonly flexor creases of the elbow,
buttock or groin
Deep dermis is preserved at donor
site to allow healing by secondary intention
Donor sites are areas with thin skin and
allows direct closure of the donor defect
Recipient site must have reasonable blood
supply for skin graft to ‘take’ and the graft
is usually tacked to the recipient site around
the edges and covered for a week without
any dressing change
Requires good blood supply for survival
and graft take
If there is insufficient graft to cover the
recipient site the graft may be meshed to
allow it to spread out over a wider area
Used to cover more sensitive areas, e.g.
nose or eyelids, when pigment matching
or to allow for growth of child
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PLASTIC SURGERY
Ø Flaps:
—
—
282
A flap is a subunit of tissue that is transferred from one part of the
body to another with its own blood supply
Differs from skin graft in that it does not rely on revascularisation
from the recipient bed
PLASTIC SURGERY
DUPUYTRENS DISEASE
Definition
Ø An abnormal, benign and progressive fibroproliferative disorder affecting the
fascial layers of the digits and palm
Epidemiology
Ø Caucasians, most commonly in northern Europeans
Ø Autosomal Dominant inheritance with variable penetrance
Ø Male predominance, with approximately 7 to 10 times greater incidence
Ø Peaks between 40 and 60
Associated Conditions
Ø Idiopathic
Ø High alcohol intake
Ø Liver cirrhosis
Ø Diabetes mellitus
Ø Epilepsy
Presentation
Ø Discrete nodules
Ø Longitudinal cords which may result in finger contractures
Ø Affects the palm and most commonly the ring and small fingers
Dupuytren’s Diathesis
Ø An aggressive cohort which has an earlier onset of disease and an early recurrence
Ø Three classic findings:
— Knuckle Pads Ò Garrod pads
— Foot Involvement Ò Ledderhose disease
— Penis Involvement Ò Peyronie’s disease
283
PLASTIC SURGERY
Surgical Indications
Ø MCPJ Contracture Ò Usually correctable
— Interference with daily activities
— If contracture >30° to 45°
Ø PIPJ Contracture Ò Difficult to fully correct
— Early intervention
Ø Contracture causing maceration or hygiene difficulties
Ø If patient is not able to have both the digit and palm simultaneously on the table
surface (Table Top Test)
Management
Complications (Surgery)
Ø Hematoma formation
Ø Recurrence
Ø Neurovsascular injury
Ø Finger Stiffness
Ø Complex Regional Pain Syndrome
284
PLASTIC SURGERY
HAND TRAUMA
Tendon injuries
Ø Flexor Tendon Injuries:
— Commonly result from volar lacerations and may be associated
with neurovascular injury
— Surgical repair
— Early hand therapy and ROM exercises is extremely important
Ø Extensor Tendon Injuries:
— Commonly from dorsal lacerations
— If injury proximal to uncturae tendinum, may be a normal range of
motion as disruption to extensor mechanism is masked
— Surgical repair
Fractures
Ø Rigid fixation allows for early movement
Ø Aim to move hand early to reduce stiffness
Amputations
Ø Indications for replantations:
— Thumb, multiple digit or whole hand amputations
— Transmetacarpal and partial hand amputations
— Any amputated part in a child
Ø Relative indications:
— Sharp injuries at elbow, proximal forearm or humeral-level amputations
— Single digit amputations distal to flexor digitorum superficialis (FDS) insertion
— Single-digit amputations in athletes/musicians/persons needing full
complement of fingers and cosmesis
Ø Management of the amputated part:
— Amputated part Is wrapped in moist saline gauze
— Placed in a waterproof ziplock plastic bag and placed in icy water
— Get Xray to outrule fracture extension
Ø Management of patient:
— Stabilise
— Optimise
— Surgical repair
Ø Post-operative:
— Keep patient and digit warm and well perfused
— Urine output >0.5ml/kg/hr
— Look for changes in the color of digit
— Postoperative use of therapeutic heparin/LWMH
— Could use continuous brachial plexus blockade to ensure analgesia effect and prevent microvascular thrombosis
— Examine finger every hour, and if any change from baseline, notify
the surgeon as may need to go back to theatre
285
PLASTIC SURGERY
UPPER LIMB COMPRESSION NEUROPATHY
MEDIAN NERVE
Ø Carpal tunnel syndrome
— Most common mononeuropathy of upper limb
— Mechanical compression in the fixed rigid space of the carpal tunnel
Ø Aetiology:
— Compression by ganglion cyst, anomalous flexor pollicis longus
(FPL) muscle or persistent median artery
Ø Risk factors of carpal tunnel syndrome:
— Female sex, diabetes mellitus, pregnancy, rheumatoid arthritis,
hypothyroidism, wrist fracture or dislocation, or arthritis that deforms
the small bones in the wrist,
Ø Carpal tunnel anatomy:
— Boundaries – Scaphoid and trapezium radially, pisiform and hook of
hamate ulnarly, transverse carpal ligament forms the roof, carpal
bones form floor
— Contents – Median nerve, FPL, FDS x 4, Flexor digitorum profundus (FDP) x 4
Ø Presentation:
— Pain and paraesthesia of thumb, index and middle fingers worse at
night and relieved by shaking hands
Ø Clinical exam:
— Thenar muscle wasting and weakness of abduction
— Thenar sensory disturbance spared due to innervation by palmar
cutaneous branch
— Special tests: Phalen’s, Tinel’s and Durkan’s tests. Pen touch test
can be used to isolate abduction
Ø Electromyography studies:
— Aid in diagnosis and localisation of nerve compression site
— Prolonged motor and sensory latencies and reduced conduction
velocities are diagnostic for carpal tunnel syndrome
Ø Management:
— Conservative treatment:
¾ Analgesia/NSAIDs/ Corticosteroid injection
¾ Splint in neutral position continuously at night time
— Surgery:
¾ Open carpal tunnel release
Ø Post-operative Complications:
— Infection, haematoma, scar tenderness, complex regional pain
syndrome, incomplete resolution of symptoms due to ‘double-crush’
phenomenon, injury to palmar cutaneous branch and recurrent
motor branches of median nerve
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PLASTIC SURGERY
ULNAR NERVE
Ø Cubital tunnel syndrome
— Compression at multiple sites at/adjacent to cubital tunnel
Ø Ulnar tunner syndrome
— Compression in Guyon’s canal
Ø Presentation:
— Hypaesthesia/Paraesthesia of little and ulnar half ring fingers and
dorsoulnar hand
— Sensory disturbance at dorsoulnar hand is spared in ulnar tunnel
syndrome innervated by dorsal sensory branch of ulnar nerve
— Weakness of grip strength and intrinsic wasting in advanced cases
causing functional issues with fine motor control
— Tinel’s test – Positive over site of compression
— ‘Ulnar paradox’ – more likely to get clawing with distal compared to
proximal ulnar nerve compression due to sparing of the FDP
Ø Management:
— Conservative treatment:
¾ Analgesia/NSAIDs
¾ Splint wrist in neutral
— Surgery:
¾ Decompression of cubital tunnel or ulnar tunnel as per
site of compression
RADIAL NERVE
Ø Posterior interosseous syndrome
— compression at/adjacent to radiocapitellar joint
Ø Radial tunnel syndrome
— compression at radial tunnel running from radiocapetellar joint to
the distal edge of the supinator
Ø Wartenberg syndrome
¾ compression of superficial sensory branch of radial
nerve
Ø Diagnosis:
— Gradual weakness of finger and wrist extensors
— Posterior interosseous syndrome – Motor symptoms predominates
— Radial tunnel syndrome – Pain predominates
— Wartenberg syndrome – Pain and paraestesia is exacerbated by
pinch grip
Ø Management:
— Conservative treatment:
¾ Analgesia/NSAIDs
¾ Splint/Steroid injection
— Surgery:
¾ Nerve exploration/decompression
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PLASTIC SURGERY
COMPARTMENT SYNDROME
Description
Ø Surgical Emergency!
Ø Raised pressure within a closed anatomical space, which as it continues to
rise, will eventually compromise tissue perfusion resulting in necrosis as a result
of microvascular compromise
Ø Can occur in the lower limb (below knee, most common), thigh, forearm, foot
and hand
Presentation
Ø Pain out of proportion to the injury (most significant) and worse on passive stretch of the compartment muscles
Ø Parasthesia
Ø Pallor (may be present)
Ø Arterial pulsation may still be felt but pulselessness tends to be a sign of irreversible damage
Ø Paralysis of the muscle group may occur
Causes
Ø Blunt trauma
Ø Crush injury
Ø Fractures; tight cast
Ø Burns
Ø Penetrating trauma; Vascular Injury
Ø Malignancy
Diagnosis
Ø Clinical suspicion
Ø Measurement of intracompartmental pressures
— Comparment pressure of > 40 mmHg or > 30 mmHg with clinical suspicion (can be measured using Stryker needle and is
especially useful in unconscious patients)
— Difference between diastolic pressure and compartment pressure of
< 30 mmHg
— Follow the trend of pressures
Management
Ø Prompt and extensive fasciotomies within 4-6 hours of symptom onset
Ø If the extremity is being compressed by dressings, reduce them
Complications
Ø Muscle fibrosis and death Ò Volkmann ischaemic contracture
Ø Nerve injury and dysfunction
Ø Myoglobinuria and renal failure Ò Aggressive IV fluid resuscitation
Ø Amputation Ò consider if muscle groups necrotic at fasciotomy
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PLASTIC SURGERY
INFECTIOUS FLEXOR TENOSYNOVITIS
Infection of the tendon and synovial sheath leading to inflammatory products in the
potential space between the visceral and parietal paratenon. Infectious source may be
from local trauma, spread from surrounding soft tissues, or haematogenous spread.
Progresses from exudative (Stage 1) to suppurative (stage 2) to septic necrosis of
the tissue (Stage 3) if not treated promptly. Complications include rupture of tendon
sheath, compartment syndrome, ischemia and necrosis.
Kanavel’s Cardinal Signs:
-Tenderness on percussion/palpation over the flexor sheath
-Finger held in slight flexion
-Pain on passive extension
-Fusiform swelling
Management:
Surgical Emergency —early antibiotics plus surgical intervention
Antibiotics
—initially empiric guided by clinical findings and tailored if
possible
Surgery
—almost was required to decompress the flexor space
-Stage 1:
Tendon sheath irrigation and drainage +/- debridement
-Stage 2/3:
Debridement of tendon sheath and necrotic tissue*
*Brunner’s incision- ‘Z’ shape incision allows surgical access to tendon sheath and
avoids contracture and functional complication of a linear incision
TRIGGER FINGER (Stenosing flexor tenosynovitis)
This occurs due to difficulty in the tendon to pass through a relatively stenosed fibroosseus canal due to thickening of the first annular (A1) pulley overlying MCP joint.
This leads to an inability to smoothly flex or extend the affected digit with associated
painless locking of the finger in flexion or extension which may only be overcome with
passive manipulation. The cause is unknown but may due to overuse or repetitive use.
Management:
Conservative/medical
-Limit exacerbating activities and use splinting
-May involve a trial of NSAIDs
-Local glucocorticoid injection if above fails
Surgical
—reserved for those that fail conservative treatment/glucocorticoid
injections
-Surgical release of the A1 pulley ligament
-US-guided percutaneous or Open approaches
*complications from surgery: infection, digital nerve damage, bowstringing of the flexor
tendon, scarring of the tendon
289
NOTES
290
ORTHOPAEDIC SURGERY
Chapter 14
Orthopaedic Surgery
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ORTHOPAEDIC SURGERY
Contents:
• Principles of Orthopaedics
• Upper Limb Injuries
• Lower Limb Injuries
• Pelvic Fractures
• Septic Arthritis
• Back Pain
• Osteoarthritis
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ORTHOPAEDIC SURGERY
LEARNING OBJECTIVES
By the end of this chapter you should be able to
ü Describe the basic principles of fracture management
ü Describe the basic management of distal radius,
humerus, scaphoid, ankle, tibial, and pelvic fractures
ü Describe the classification of hip and ankle fractures and determine treatment according to
classification
ü Describe the diagnosis and management of septic
arthritis, compartment syndrome and cauda equina
syndrome
ü Describe the diagnosis and management of hip
and knee osteoarthritis
Greenstick
Wedge Comminuted
Open
Transverse
Avulsion
Oblique Non-displaced
Oblique
Displaced
Spiral
llustration by Kevin Quinlan: Fractures
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ORTHOPAEDIC SURGERY
PRINCIPLES OF ORTHOPAEDICS
Definitions
Ø Fracture = a break in the continuity of bone cortex whether complete or incomplete
Ø Closed fracture = no communication with external environment
Ø Open fractures = communication of fracture site with external environment by
breach in skin
Ø Reduction = manipulation of fracture to restore normal alignment at the fracture
site
Ø In medical notes, the ‘#’ symbol may be used for the word ‘fracture’
Ø Fracture – dislocation = there is a fracture associated with joint dislocation (complete loss of contact of the joint surfaces)
Principles in Fracture Treatment
Ø Reduction of fracture
Ø Immobilisation - cast/ splint/ internal or external surgical device
Ø Rehabilitation – mobilisation and exercise
Why do we reduce fractures?
Ø Stabilise the fracture
Ø Reduce pain
Ø Preserve blood supply
Ø Restore anatomical relationships
Ø Aid in bone healing and remodeling
Ø Avoid deformity / malunion
Ø Reduce chance of non-union
Ø Reduce risk of osteoarthritis
Fracture Reduction
Ø Open or closed reduction
— Open - Fracture site exposed surgically. The fracture is then usually
immobilised by internal fixation with plates and screws, or other
surgical fixation devices. This is generally referred to as open reduction and internal fixation (ORIF)
— Closed – the fracture is reduced manually without surgically exposing the fracture site. This may be done with the patient awake
or under general anaesthetic. Immobilisation may then be done with
a cast, brace or a surgical device place percutaneously or through
an incision remote to the fracture site (e.g. percutaneous wires, or
intra medullary nailing).
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ORTHOPAEDIC SURGERY
General fracture Management
Ø Follow ATLS (Advanced Trauma Life Support) guidelines - treat life threatening
injuries first!
Ø Provide adequate analgesia
Ø Always check neurovascular status before and after interventions
Ø Fracture dislocations need to be reduced ASAP
Ø Wounds require antibiotics, and tetanus cover.
Ø Irrigation of wounds may need to be done in the operating theatre, e.g. the
wounds of open fractures.
Ø Reduction promotes healing and reduces pain
Ø A backslab type cast, rather than a full cast is applied initially to allow room for
swelling.
Ø Obtain X–rays. 2 views , 2 joints (above and below), 2 eyes (confer with a colleague/senior)
Ø Unstable fractures and poorly reduced fractures nearly always require operative
intervention
Stages in fracture healing
1. Tissue destruction and haematoma formation (immediate)
2. Inflammation and cellular proliferation (acute)
3. Callus formation (few days to weeks)
4. Consolidation (few weeks to months)
5. Remodelling (months up to more than 1 year)
Factors adversely affecting healing of fractures
General
Specific
Ø Age
Ø Degree of local trauma
Ø Poor nutrition
Ø Inadequate reduction and immobilization
Ø Smoking
Ø Infection
Ø Drugs
Ø Location of fracture
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ORTHOPAEDIC SURGERY
UPPER LIMB INJURIES
DISTAL RADIAL FRACTURE
Key Facts
Ø Most common orthopaedic injury with bimodal distribution.
— Younger patients: high-energy mechanisms, fall from height, RTA,
sports injury
— Older patients: low-energy mechanisms e.g. Fall from standing
position.
Ø 50% intra-articular
Ø DRUJ (Distal radio-ulnar joint) injuries must be evaluated
Ø Radial styloid fracture indication of higher energy.
Risk Factors
Ø decreased bone mineral density
Ø female sex
Ø caucasian
Ø early menopause
Most common mechanism is fall onto outstretched hand (FOOSH) with wrist in
dorsiflexion
Presentation
Ø Wrist deformity, swelling, pain, bruising and loss of function.
Ø Neurovascular exam is important; median nerve symptoms are common, carpal
tunnel compression (13%-23%)
Ø Eponyms:
— Colles Fracture
• Extra-articular distal radius fracture with dorsal angulation (apex
volar), dorsal displacement, radial shift and radial shortening.
• Classical “dinner fork” deformity
— Smith Fracture (reverse Colles)
• Extra-articular fracture with volar angulation (apex dorsal) of distal
radius with a “garden spade” deformity or volar displacement of
hand and distal radius.
• Fall onto flexed wrist with forearm fixed in supination.
• Unstable treated with volar buttress plate
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ORTHOPAEDIC SURGERY
Treatments
Ø Non-operative:
— Nondisplaced or minimally displaced fractures.
— Low demand patients e.g. significant surgical risk patient, demented.
— Displaced fractures can be treated with closed reduction under
sedation or anaesthesia to improve fracture alignment
Ø Operative:
— Indications include: High energy injuries, secondary loss of function, articular ‘step-off’ or gap, metaphyseal comminution or bone loss, loss of volar buttress with displacement (e.g. Smith’s
fracture), DRUJ instability, open fractures.
— Techniques include:
• Percutaneous wiring
• Kapandji intrafocal wiring
• External fixation (especially in open fractures)
• ORIF (Dorsal plating or volar plating)
Complications
Ø Median nerve dysfunction
Ø Malunion/ nonunion
Ø Posttraumatic osteoarthritis
Ø Tendon rupture. Most commonly extensor pollicis longus (EPL)
Ø Complex regional pain syndrome CRPS (previously known as reflex sympathetic dystrophy)
Ø NB: If clinically obviously displaced fracture: check neurovascular status, relocate the fracture and place in backslab before x-ray.
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ORTHOPAEDIC SURGERY
HUMERAL FRACTURE
Key Facts
Ø Increased incidence in older population is related to osteoporosis.
Ø 300,000 per year ( more common than hip fractures)
Ø 85% are undisplaced
Ø 2:1 female-to-male ratio likely related to issues of bone density.
Mechanisms of injury
Ø Fall onto outstretched hand from standing height typically in old, osteoporotic
women
Ø Younger patients present following high-energy trauma e.g. RTA.
Ø Other mechanisms: electrical shock, seizure, direct trauma (greater tuberosity
fracture), malignancy.
Presentation
Ø Pain in shoulder or proximal arm with arm held close to chest.
Ø Swelling, tenderness, reduced range of motion and crepitus.
Ø Possible paraesthesia or numbness of lateral arm over deltoid (regimental patch), secondary to axillary nerve injury
Neer Classification
Ø Based on number of fragments displaced. Ranges from one to four part. Also
may have articular subtypes.
Ø The four described fragments include: greater tuberosity (GT), lesser tuberosity
(LT), surgical neck (SN).
Ø The classification then describes not the number of fracture lines but is based
on displacement. 1-part fractures are minimally displaced (<45°angulation or
<1cm displacement) A way of remembering this is, in minimally displaced fractures, the humerus can still be thought of as one complete part ‘1-part’)
Ø For each number of parts that is displaced (e.g. GT, LT, SN) the classification
goes up by 1 part. Thus a 2-part has one fragment displaced, a 3-part has 2
fragments displaced.
Treatment
Ø Non-operative treatment
— Minimally or non-displaced fractures
— Immobilisation with broad arm sling, shoulder immobiliser, humeral
brace, U slab or hanging cast
Ø Operative treatment
— Any significant displacement of 2 part or more fractures
— ORIF or intramedullary nail as option
— 3 part or more fractures are unstable and are almost always surgically treated.
— Primary shoulder arthroplasty is an option for elderly patients
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ORTHOPAEDIC SURGERY
Complications
Ø Vascular injury (5-6%); axillary artery most common site
Ø Neural injury (Brachial plexus, axillary nerve injuries)
Ø Myositis ossificans
Ø Joint stiffness
Ø Avascular necrosis
Ø Nonunion/malunion
CLAVICULAR FRACTURE
Key Facts
Ø Fall or direct blow to lateral shoulder
Ø 75% occur in middle of clavicle, 20% lateral/distal clavicle
Treatment
Ø Middle third— Most treated conservatively with broad arm sling.
— ORIF for: Open fractures, significant displacement or shortening,
skin tenting by fracture, neurovascular injury Ø Lateral/ Medial third
— Non displaced- Sling
— Displaced- ORIF
Complications
Ø Neurovascular injury- brachial plexus
Ø Pneumothorax
Ø Non Union
Ø Operative complications:
— Infection
— Paraesthesia secondary to supraclavicular nerve injury
— Vascular injury, pneumothorax
SHOULDER DISLOCATION
Anterior dislocation – most common
Ø Trauma- Forced abduction and external rotation, or a direct all on the shoulder.
Ø Shoulder looks “square”- loss of normal contour
Ø Patients supports arm with other arm
Treatment
Ø Reduction of dislocation with various methods
Ø Assess neurovascular status before and after reduction – Axillary nerve sensation
— External rotation technique – the patient’s arm is adducted with
the elbow flexed, the forearm is then gently and very slowly externally rotated.
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ORTHOPAEDIC SURGERY
—
—
Stimson technique The patient lays prone trolley with arm hanging
off the side with a weight and allowed to drop toward the ground
Cunningham The clinician sits in front of the patient who is in a
comfortable sitting position. The patient places the hand of the
dislocated shoulder on the clinician’s shoulder who then rests one
arm on the patient’s elbow crease while gently massaging the patient’s biceps, deltoid and trapezius to encourage relaxation. The
patient is then encouraged to pull the shoulder blades together
while straightening the back.
Posterior dislocation
Ø Epileptic seizure/Electrocution. Fall on outstretched arm, while arm is in an
internally rotated, flexed, adducted position.
Ø Arm held in internal rotation, unable to externally rotate. Can palpate humeral
head posteriorly
Do not miss a posterior dislocation. Look for the ‘lightbulb sign’
and always get 3 X-ray views of the shoulder
Ø Humeral head defect <25% of articular surface + duration of injury <3 weeks:
closed reduction can be tried
Ø Otherwise: surgical intervention may be best
SCAPHOID FRACTURE
Ø FOOSH (Fall on outstretched hand)
Ø Tender at anatomical snuffbox
Ø Treat on clinical suspicion- repeat X-ray at two weeks. If still no fracture,
perform CT/MRI
Ø Risk of AVN. More proximal fractures = higher risk AVN
Scaphoid fractures
may not be visible
on initial X-ray.
Treat based on
clinical suspicion
and repeat X-rays at
2 weeks
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LOWER LIMB INJURIES
NECK OF FEMUR FRACTURES (HIP FRACTURES)
Key Facts
Ø Commonest site of fracture in elderly
Ø 80% occur in women
Ø Bimodal distribution: Majority in elderly, minority in young patients (road traffic
accident/ high energy trauma)
Ø Other risk factors
— Caucasian
— osteoporosis/osteopenia
— Diabetes mellitus
— recurrent falls
— tobacco and alcohol use
Ø Presentation:
— Pain and unable to weight bear on the affected limb
— shortened and externally rotated limb
Ø If high clinical suspicion but x-ray unequivocal perform CT or MRI (gold standard)
Classification of Hip Fractures
Illustration by J Mulrain
INTRACAPSULAR
FRACTURES
Any fracture in the yellow
shaded area shown
These must be classified
according to Garden
classification to determine
whether to:
fix the fracture, with
cannulated screws or
dynamic hip screw (DHS)
or replace it (hemiarthroplasty or Total hip
arthroplasty)
EXTRACAPSULAR
FRACTURES
Any fractures in the green
shaded area shown
Includes: intertrochanteric
and sub-trochanteric
fractures
These must be fixed, they
cannot be replaced.
Fix using Dynamic hip
screw (DHS)
or intramedullary nail
The joint capsule
demarcates the area for
intra-capsular fractures.
The femoral HEAD can
also be fractured and
these fractures should not
be confused with intracapsular NECK of femur
fractures. These fractures
are classified differently
altogether.
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ORTHOPAEDIC SURGERY
Classification of intracapsular neck of femur fractures
Garden Classification
Illustration by J Mulrain
GARDEN I
GARDEN II
GARDEN III
GARDEN IV
Incomplete fracture
Complete fracture
Complete fracture
Complete fracture
Not displaced but
IMPACTED
Non-displaced
fracture
Partially displaced
Fully displaced
-risk of avascular
necrosis of the
femoral head
after fixation, so
replacement by
hemi arthroplasty
or total hip
arthroplasty is
recommended
High risk AVN
Should be
treated with
hemiarthroplasty
or total hip
arthroplasty
Called ‘valgus
impacted’ - due to
valgus deformity at
the neck
In very young
patients fixation
rather
than replacement
may still be
attempted
302
In very young
patients fixation
rather than
replacement may
still be attempted
ORTHOPAEDIC SURGERY
Ø Complications
— AVN of femoral head
— Osteoarthritis
— Non-union
— Mortality (pre-injury mobility is the most significant determinant
of postoperative survival)
— Wound infection
— Haematoma
— DVT/PE
Hip fractures should be operated on the day of, or day after admission
to improve patient outcomes
SLIPPED UPPER FEMORAL EPIPHYSIS (SUFE)
Ø
Ø
Ø
Ø
Paediatric/adolescent presentation
Not usually associated with trauma
Instability of the proximal femoral growth plate
Presentation can include hip pain, thigh pain, knee pain; limp (acute or chronic);
decreased ROM of the hip; shortening of the affected limb is possible
Do not miss: often presents as knee pain. Always examine
the joint above and below the site of pain
X-Ray features:
Ø Displaced femoral head: posterior and inferior to femoral neck, within the limits
of the acetabulum
Management:
Ø Non weight bearing with crutches, and typically includes surgical fixation
Ø Fixation of the unaffected side may be a necessary preventative measure
ANKLE FRACTURES
Key Facts
Ø Ankle = complex hinge joint composed of articulations among the fibula, tibia
and talus held by ligaments.
Ø Usual mechanism of injury include torsional (foot inversion) or axial loading (fall
from height)
Clinical Presentation
Ø Pain, swelling of ankle, clinical deformity, non-weight bearing on ankle.
Ø Fractures can involve just 1 malleolus, both medial and lateral malleoli (bimalleolar), or all three ‘malleololi’ i.e. medial, lateral, and posterior malleoli
(trimalleolar)
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ORTHOPAEDIC SURGERY
Classifications
Ø Denis-Weber classification
— Based on level of fibular fracture; the more proximal the injury,
greater risk of syndesmosis disruption and instability.
Denis-Weber classification
Illustration by J Mulrain
Normal ankle
joint
The syndesmosis
(shown in grey)
consists of the
ligament complex
at the distal
tibiofibular joint
and the lower
thickened portion
of the intraosseus
membrane. As it
is ligamentous it
is not visible on
X-ray
304
Weber A
Fracture line (red)
below the level of
the syndesmosis
Weber B
Fracture at the
level of the
syndesmosis
Usually treated
in below knee
walking cast
Some possibility
of syndesmosis
disruption and
instability
Needs surgical
fixation if significant
displacement, or
non-weight bearing
in below knee cast
if non-displaced
Weber C
Fracture above
the level of the
syndesmosis
High likelihood
of syndesmosis
disruption
and instability
Needs surgical
fixation
ORTHOPAEDIC SURGERY
Maisonneuve Fracture
Medial malleolar fracture OR a deltoid
ligament rupture with a fracture
at proximal third of fibula.
It may be associated with
a syndesmosis injury
Always remember to examine
the knee as well as the ankle.
Complications of ankle fractures
Ø Malunion, nonunion
Ø Osteoarthritis
Ø Infection
Ø Prosthesis failure
Ø DVT
TIBIAL FRACTURE
Key Facts
Ø Mechanism: High-energy: young people with sporting injuries/fall from height
Ø Common site for open fractures as the tibia lies just below the skin. (Also poor
blood supply- affects healing)
Ø Susceptible to compartment syndrome
Treatment
Ø Conservative - undisplaced and closed
Ø Surgical - Unstable fractures or open fractures
— Locking plate
— Intramedullary nail- Most Common
— External fixation
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ORTHOPAEDIC SURGERY
Open Fractures
Ø A fracture where there is a skin breech allowing exposure of the fracture to the
external environment.
Ø The skin breech may even be a small puncture near the fracture. Examine for
associated neurovascular injury. Large skin defects need immediate plastic surgery involvement
Management of open fractures
— Check and document neurovascular status
— reduce fracture, recheck n/v status
— remove only gross contamination
— photograph
— place dressing over wound
— place in backslab
— give i.v. antibiotics and tetanus prophylaxis
— arrange for early surgical management
(immediate/ within 12 h/ within 24h)
Open tibial fractures:
— also monitor for compartment syndrome
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ORTHOPAEDIC SURGERY
COMPARTMENT SYNDROME
Key Facts
Ø An orthopaedic emergency
Ø Increased pressure in an osseofascial compartment
above the capillary pressure which may lead to irreversible neural and muscular damage. Permanent damage occurs if not treated within 4 to
6 hours.
Ø The diagnosis is clinical. In patients who cannot
report pain e.g. ICU patients, or if there is clinical
uncertainty a compartment pressure monitor may be
used
Symptoms
— PAIN
— Pain out of proportion to the injury
— Do not simply try to manage pain with
increasing opioid use. Look for signs
of compartment syndrome and plan to operate immediately if signs are present and other short term
measures (below) fail
Signs
Compartment
syndrome is a
clinical diagnosis.
Pain is the hallmark
symptom as well
as increased pain
with passive stretch
of the affected
muscles.
Neurovascular
symptoms are NOT
part of the initial
diagnosis as these
are late signs
Surgery should be
performed within 1
hour of diagnosis
— Swollen ‘tense’ limb / muscle compartment
— Pain worsens with passive stretch of the affected muscle compartment, e.g. passive plantarflexion of the ankle increases
pain in the anterior leg
Treatment
—
—
—
Remove all circumferential dressings - split and remove casts,
backslabs, splints, and even bandage dressings
Maintain a normal blood pressure – avoid hypotension (improves
circulation to the affected compartment)
If symptoms do not resolve within 30 minutes, surgical decompression by fasciotomy must be performed. This must be
done within 1 hour of diagnosis
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ORTHOPAEDIC SURGERY
PELVIC FRACTURES
Key Facts
Ø Apart from pubic rami and insufficiency fractures, pelvic fractures indicate a
major trauma to the patient.
Ø In young patients this may be from high energy trauma e.g. RTA.
Ø In the elderly major trauma is most often caused by a fall from standing height.
Ø An x-ray of the pelvis is part of the ‘trauma series’ of X-rays (Chest, C-spine,
AP pelvis) required in the initial assessment of polytrauma cases. Some centres
with adequate facilities have replaced trauma series X-rays with trauma CTs
Ø Mortality 15-25% for closed fractures, as much as 50% for open fractures.
Ø Haemorrhage from venous plexus is leading cause of death, especially in open
book pelvic fracture.
Ø Associated injuries include thoracic and intra-abdominal injuries with genitourinary or gastrointestinal injuries and other fractures.
Ø Multidisciplinary approach with early general surgeon/ vascular surgeon or
urologist involvement when suspect other injuries
Reduce haemorrhage into the pelvis by applying a pelvic binder for
unstable pelvic fractures
“close the tap”
Types
Ø Isolated pelvic fractures are usually stable. If the fracture doesn’t extend to
acetabulum early mobilization, bed rest and analgaesia usually suffice. If extends into acetabulum may require operative management.
Ø Multiple ring fractures usually unstable. They also have a significant probability
of massive haemorrhage. Early stabilization with pelvic binder essential. Definitive treatment with an external fixator or ORIF within 72 hours.
Ø Lateral compression, anteroposterior compression, vertical shear, or a combination of forces are involved. So-called open book fractures can be especially serious.
Initial Management:
Ø ATLS guidelines
Ø Apply pelvic binder or bedsheet around the pelvis at the level of the GREATER
TROCHANTERS
Ø Some vertical shear type fractures may require traction – get specialist help
Ø Two Large IV Cannulae and Warm Crystalloid + O negative blood
Ø Crossmatch 4-6 units
Avoid “springing” the pelvis as this may disrupt any pre-formed clot
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ORTHOPAEDIC SURGERY
Complications:
Ø Death from haemorrhage
Ø Osteoarthritis
Ø Urogenital Injury
Ø DVT/PE
SEPTIC ARTHRITIS
Key Facts
Ø An orthopaedic emergency –chondral damage and risk of sepsis and death
Ø Adult/ paediatric
Ø Native/ prosthetic joint
Ø ‘spontaneous’ or post procedure
Ø Usually spreads haematologically but may develop from contiguous osteomyelitis/ skin puncture
Ø Usually Staph Aureus/Gonococcus/Strep
Ø Red, hot, swollen, painful joint
Ø Painful to move
Ø Fever and rigors
Investigations
Ø FBC , CRP, Blood cultures, Joint aspirate and X ray
Ø Kocher’s criteria in children
Treatment
Ø IV Flucloxacillin and Benzylpenicillin (or according to local hospital guidelines)
Ø Refer to Orthopaedics ASAP for surgical washout of joint
BACK PAIN
Ø Lower back pain is very common
Ø Need to rule out AAA, Cauda Equina, Spinal Cord Compression, metastatic
disease
Ø Perform an ASIA (American Spinal Injury Association) assessment
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ORTHOPAEDIC SURGERY
CAUDA EQUINA SYNDROME
Ø Acute compression of the cauda equina usually by herniated intervertebral disc,
fracture or other lesion resulting in typical symptoms. If not urgently surgically
treated may result in permanent urinary and faecal incontinence
Ø Signs and symptoms – may include:
— Pain - lower back /buttocks/posterior thighs, legs
— Paraesthesia
• saddle/perineal/perianal
• bilateral buttocks, posterior thighs/legs/feet
— Weakness – legs/feet
BACK PAIN RED FLAGS
Back pain symptoms
Ø Night pain
Ø Progressive unrelenting pain
Associated symptoms – legs/ perineum
Ø Altered perineal/perianal sensation
Ø Sphincter disturbance; retention or incontinence of urine/faeces
Ø Lower limb weakness
Ø Bilateral lower limb symptoms
Systemic symptoms
Ø Trauma
Ø Systemic symptoms eg weight loss
Patient factors
Ø Previous Ca History
Ø <20 years of age , >55 years of age
— Sphincter disturbance – urinary or faecal incontinence or retention
Ø Diagnosis
— urgent MRI Lumbar spine
Ø Treatment
— Urgent surgical decompression
Time from clinical suspicion of Cauda Equina Syndrome to MRI
is paramount: delays may have huge clinical and medicolegal
consequences.
Order and discuss the MRI promptly and document the timeline
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ORTHOPAEDIC SURGERY
SCIATICA
Ø Pain and/or parasthaesia caused by irritation or compression of the sciatic nerve
Ø Pain usually radiates from the lower back through the buttock and lower limb on
the affected side.
Ø Pain can become very severe and easily exacerbated by activities of daily living
such as prolonged sitting, coughing or sneezing
Ø Disc protrusion or herniation is the most common cause of the pain
Ø Rule out more sinister manifestations including spinal stenosis, space occupying lesion, spinal infection, trauma, cauda equina, spondylolisthesis
Ø Sciatica can be self-limiting, or may be treated with anti-inflammatories, physiotherapy, and surgery in rare cases
OSTEOARTHRITIS
Key Facts
Ø Osteoarthritis is a form of non-inflammatory arthritis
Ø May represent failed attempt of chondrocytes to repair damaged cartilage
Ø Most common form of arthritis
— Knee is most commonly affected joint
— Other includes hips, ankles, facet joints of vertebrae etc
Ø Osteoarthritis can either be either
— Primary: intrinsic defect, genetic predisposition
— Secondary: trauma, infection or congenital.
Presentation
Ø Pain and stiffness
— especially in the morning, on movement and increasing with age/
chronicity of condition
Ø Swelling
Ø Reduced range of movement.
Characteristics of osteoarthritis on radiographs
Ø Joint space narrowing.
Ø osteophyte formation
Ø Subchondral sclerosis
Ø Subchondral cysts
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ORTHOPAEDIC SURGERY
Treatments
The primary goal of treatment is to manage pain
Ø Nonoperative
— Analgaesia
— Lifestyle modifications
— Physiotherapy
— Weight loss
— Corticosteroid joint injections
Ø Operative
— Arthroscopic debridement is not routinely inidicated in osteoarthritis
— Total joint arhroplasty for advanced disease with disabling pain
refractory to conservative measures
— Total hip and total knee replacement/ arthroplasty are among the
most commonly performed elective procedures
TOTAL HIP ARTHROPLASTY (THA) ‘Hip Replacement’
Ø Involves replacing the femoral head (ball) and acetabulum (socket) with artificial
prostheses
Ø These may be cemented or non-cemented or a combination – e.g. non cemented acetabulum and cemented femur
Ø THA risks:
— Infection
— Nerve injury (e.g. Sciatic)
— Intra-operative fracture
— Dislocation
— Leg length discrepancy
TOTAL KNEE ARTHROPLASTY (TKA)
Ø Involves replacing the surface of the distal femur and proximal tibia with artificial
prosthesis +/- patellar resurfacing.
Ø TKA Risks:
— Infection
— nerve injury (Peroneal)
— intra-operative fracture
— Chronic pain
— instability
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NOTES
313
NOTES
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NEUROSURGERY
Chapter 15
Neurosurgery
315
NEUROSURGERY
Contents:
• Brain Tumours
• Intracranial Injuries
• Spinal Injuries
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NEUROSURGERY
BRAIN TUMOURS
Key Facts
Ø 2% of cancer related deaths.
Ø Cerebral metastasis is the most common brain tumour.
Ø Primary brain tumours may arise from cells of the brain parenchyma or from its
intracranial linings.
Ø Brain tumours are the second most common solid cancer in children, comprising 15-25% of all paediatric malignancies.
Ø Location
— Adults = supratentorial
— Children = infratentorial
Clinical presentation
Ø Symptoms and signs of brain tumours depend on the location (supra or infratentorial) size, degree of brain invasion and infiltration and surrounding
brain oedema.
Ø The most common presentation of brain tumours are: headache,vomiting
(symptoms of raised intracranial pressure (ICP)) and progressive neurological deficit.
Ø Supratentorial tumours:
— Symptoms due to increased ICP
¾ Headache (especially early morning)
¾ Nausea/vomiting
¾ Diplopia
¾ Decreased vision
¾ Papilloedema
¾ Progressive focal deficit – “mass effect”
¾ Weakness
¾ Dysphasia (speech difficulty)
¾ Altered level of consciousness
— Headache (may occur with or without raised ICP).
— Usually associated with vomiting and blurring of vision .
— Irritative symptoms: Seizures, neck stiffness, photophobia, irritability, cranial nerve palsies.
— Mental status changes (depending on the location of the lesion )
¾ Depression
¾ Lethargy
¾ Apathy
¾ Confusion
Ø Infratentorial tumours (posterior fossa tumours)
— Symptoms secondary to increased ICP due to hydrocephalus
¾ Headache
¾ Nausea/vomiting
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NEUROSURGERY
¾ Papilloedema
¾ Gait disturbance/ataxia
¾ Vertigo
— Cerebellar signs:
¾ Truncal ataxia (vermian tumour)
¾ Intention tremor
¾ Dysmetria
¾ Slurred speech
¾ Nystagmus
— Brain stem involvement
¾ Multiple cranial nerve palsies
¾ Weakness of extremities
Pathogenesis
Ø Unknown
Ø Radiation
Ø Immunosuppression – lymphoma
Ø Hormonal – meningioma
Ø Alteration of genetic expression (Mutation in p53 gene )
Ø Genetic - neurofibromatosis, Von Hippel-Lindau syndrome, Turcot’s syndrome.
Diagnosis and investigation
Ø History (symptoms, past history of cancer, rate of progression of symptoms)
Ø Physical examination (neurological findings)
— A detailed neurological examination is very important in localising
the tumour.
Ø Radiological Investigations
— CT
— MRI is the best imaging modality
¾ Pre and post Gadolinium MRI
¾ Perfusion -weighted MRI Regional (Blood flow)
¾ Magnetic Resonance Spectroscopy(MRS)
¾ Functional imaging: fMRI
— Degree and pattern of contrast enhancement often aids diagnosis.
Ø CSF cytology
— CNS lymphoma: abnormal cells
— Germ cells tumours: positive occasionally for markers
Ø Serum Markers
— Blood serum tumour markers (beta HCG and alpha fetoprotein) are
positive in intracranial germ cells tumours.
Ø Imaging outside the CNS is unnecessary since CNS primary tumours do not
tend to metastasise due to the blood brain barrier
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NEUROSURGERY
Pathology
Ø There are over 120 different types of brain tumours.
Ø Common brain tumours include:
Ø Gliomas (Neuroepithelial tumours)
— Astrocytomas (grade 1-4)
¾ Majority of primary brain tumours – 50%
¾ Grades from low to highly malignant
• Low grade astrocytoma 2nd + 3rd decades
• Anaplastic astrocytoma 4th decade
• Glioblastoma multiforme 5th + 6th decades
¾ Site
• Cerebral hemisphere in adults
• Cerebellum and brain stem in children.
¾ Death in glioblastoma multiforme is usually less than
a year.
Grading and survival of astrocytic gliomas
WHO
Burger system
Median survival
1
Pilocytic astrocytoma
Curable
2
Low grade astrocytoma
7-9 years
3
Anaplastic astrocytoma
2-3 years
4
Glioblastoma multiforme (GBM)
9-12 months
— Oligodendroglioma
¾ Arise from oligodendrocytes.
¾ Primarily tumour of the adults – 40 years
¾ Most common site is frontal lobe.
¾ Common presentation is seizure .
¾ Both low grade & high grade (anaplastic)
¾ CT scan brain demonstrates calcification in 90%
of cases.
— Ependymoma
¾ Origin is ependymal cell lining in ventricle
¾ Common in children
¾ Site is floor of 4th ventricle.
¾ Both low grade and anaplastic
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NEUROSURGERY
Ø Nerve Sheet Tumours
— Acoustic Neuroma
¾ Arise from superior vestibular division of the 8th cranial
nerve.
¾ 75% of cerebellopontine (CPA) angle tumours are schwannomas
¾ Benign
¾ Mostly in adults.
¾ Presents with hearing loss, tinnitus and dysequilibrium.
Ø Neuronal Tumours: Ganglioglioma, Gangilocytoma, Neuroblastoma
— Medulloblastoma
¾ Childhood malignant tumour
¾ Origin in the roof of the 4th ventricle.
¾ Presents with obstructive hydrocephalus and cerebellar
signs.
Ø Meningial Tumours
— Meningioma: 20%
¾ Origin is from arachnoid cap cells
¾ Slow growing
¾ Usually benign
¾ Common sites are falx cerebri and convexity on sphenoid bone.
¾ Female to male nation is 2:1. The peak age is 40 yrs.
¾ High frequency in patients with neurofibromatosis-2
Ø Pituitary adenoma
— Functioning
¾ Sexual dysfunction
¾ Galactorrhoea- Prolactinomas
¾ Acromegaly -GH adenomas
¾ Cushing syndrome -Cortisol secreting tumour
— Non-functioning
¾ Mass effect
¾ visual disturbance such as bitemporal hemianopia due
to their proximity to the optic chiasm.
Ø Tumour like malformations
— Craniopharyngioma
¾ Majority are children (Peak age 5-10 years of age)
¾ Benign
¾ Presents with visual dysfunction, hypothalamic alteration
and hydrocephalus.
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NEUROSURGERY
— Colloid Cyst:
¾ Benign
¾ Arise in anterior 3rd ventricle
¾ Hydrocephalus is common
¾ Presents with a headache
Ø Metastatic Tumours
— Most common brain tumour
— Common primary sites are:
¾ Lungs - 50%
¾ Breast
¾ GIT melanoma
¾ Renal
— Route of metastasis: haematogenous
— Survival for cerebral metastasis is from 2-9 months
— Management is mostly palliative
Treatment
Ø The options for treatment of a brain tumour depend on several factors
— Location
— Type of tumour
— Overall health of the patient
Ø Surgery
— The goals of surgery are as follows:
¾ Diagnosis (History)
¾ Obtain a histological diagnosis
¾ Treatment (resection/debulking/decompression/CSF
diversion)
— Curative mostly for benign tumours
— Debulking of tumour is usually followed by adjuvant radiotherapy
¾ e.g. higher grade gliomas
— Stereotactic tissue biopsy performed when surgery is not possible
— New surgical photodynamic techniques
¾ Fluorescence image guided surgical resection (FIGS)
• Photosensitisers are administered preoperatively
and accumulate selectively in the tumour.
• Visible tumour is then surgically removed under
white light.
• Blue light longpass filter is then used to allow the surgeon to visualise and remove as much of the
remaining residual tumour as possible
• The more of the tumour resected, the better the
prognosis (effective treatment to patients with high
grade tumours)
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NEUROSURGERY
Ø Radiotherapy
— External beam radiotherapy
— Goal of radiation treatment is to cause cell death or to stop cell
replication.
— In certain tumours it can be curative and in the majority of cases it
will prolong survival.
— Stereotactic radiosurgery delivers a large dose of radiation to the
tumour in one dose, based on imaging that has accurately outlined
the lesion (useful in well defined tumours such as meningiomas).
Ø Chemotherapy
— Increasingly being used for primary brain malignancies
— Most common is temozolomide
¾ Alkylating agent
¾ Good penetration of the blood brain barrier
— Certain regimens in combination with radiotherapy have shown a
survival benefit in gliomas compared to controls.
— Chemotherapy can be used also in the treatment of oligodendrogliomas.
Ø Other therapies
— Corticosteroids
¾ Reduce mass effect
— Anticonvulsant therapy to treat seizure.
— DVT/PE prophylaxis
¾ Clots occurs in 20-30% of patients with brain tumours.
¾ This is due to release of thromboplastin when the brain
is injured.
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NEUROSURGERY
INTRACRANIAL INJURY
Key Points
Ø Must be promptly and systematically assessed.
Ø Intracranial injuries are surgical emergency
Ø Seek senior advice early.
Aetiology of Head Injuries
Ø Haemorrhagic
— Epi/extradural
— Subdural
— Subarachnoid haemorrhage (SAH)
— Parenchymal haemorrhage
Ø Non-haemorrhagic
— Diffuse axonal injury (DAI)
¾ Effacement of sulci, ventricular enlargement
¾ Leads to profound coma and death in approximately
80%
— Contusion
— Coup/contrecoup
Ø When assessing a head injury, the following factors should be considered
— whether it is penetrating
— whether a fracture is present
— whether depressed bone fragments are present
Munro-Kelly Doctrine
Ø The skull is essentially a rigid box
Ø It has room for three things
— Brain
— Blood
— CSF
Ø If one of these volumes increases, the others must reduce.
Ø Like any anatomical structure with an abundance of capillaries, the brain has an
autoregulation system.
Ø ICP should be <15 mmHg
Ø As pressure increases, capillary blood flow remains the same, up until a point.
Ø This protective mechanism is lost in TBI and the system becomes pressure
dependent
Ø As intracranial pressure rises, CSF acts as a buffer and will be sacrificed first
Ø Blood is the next component to be lost as autoregulation fails. This leads to
hypoxic brain injury.
Ø Herniation of brain tissue may occur.
Ø Cushing’s Triad: Hypertension, bradycardia and irregular respiration.
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NEUROSURGERY
Cerebral Herniation
Ø Uncal
Ø Central
Ø Subfalcine
Ø Tonsillar/Coning
Assessment of Head Injury
Ø ABCDE as per ATLS guidelines
Ø GCS
— Serial data should be gathered and a neurological observation chart
kept.
Ø History
— May need to obtain collateral from ambulance personnel, police
or witnesses
— Establish mechanism of injury
¾ In falls, establish height
¾ In road traffic accident, establish speed, seat belt usage,
position of patient before and after accident.
Ø Examination
— Trauma survey as per ATLS guidelines
— Bruising:
Image by Wail Mohammed: Raccoon Eye (with consent)
Image by: Wail Mohammed:
Battle sign (with consent)
324
NEUROSURGERY
— Bleeding
¾ Scalp: SCALP: Skin, connective tissue, galea aponeurotica, loose areolar tissue (LAT) and periosteum.
¾ The blood vessels are in the LAT: supratrochlear, supraorbital, superficial temporal, posterior auricular
and occipital. If cut, these vessels can’t shrink back so
will bleed heavily.
Investigations
Ø The aim of assessment is to prevent secondary brain injury as a result of hypoxia. Investigations should not be delayed.
Ø Early communication with senior staff, including anaesthetics, and liaising with
specialist centres is an important component of management.
¾ Imaging
— CT non contrast
— MRI, CT or MR angiography may be used to provide further information regarding brain parenchyma and intracranial vasculature.
Management
Ø Position the patient with their head up.
— Reduces cerebral blood volume.
— Ensure nothing is impeding venous return; ties,collers..etc
Ø If there is a suspicion of raised ICP, invasive monitoring may be necessary.
Ø Airway management is essential and patients with head injuries often require
ventilation.
Ø Sedation.
Ø Hypertonic saline may be administered to reduce ICP.
Ø Mannitol and diuretics.
Ø Obtain early neurosurgical advice and consider transfer to specialist centre.
Ø Patients may require surgical decompression
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NEUROSURGERY
EXTRADURAL HAEMORRHAGE
Mechanism of Injury
Ø Impact injury .
Ø Blow injury (Pterion most common)
Presentation
Ø Classic but rare lucid interval.
Ø May be conscious or unconscious
Ø Bleeding occurs between the skull and dura mater.
Ø Space occupying.
Ø Middle meningeal artery (MMA) affected in 80% of cases.
Ø Signs include fixed, dilated pupil on the affected side (CN III damage).
Ø Can lead to uncal/transtentorial herniation, which leads to respiratory arrest
Ø CT Brain features:
— Biconvex/lentiform disc.
— Midline shift.
— Ventricular compression.
— Will NOT cross sutures.
Image by Wail Mohammed: Extradural haemorrhage (with consent)
Treatment
Ø Craniotomy and evacuation of hematoma.
Ø Coagulate the bleeding vessel.
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NEUROSURGERY
SUBDURAL HAEMORRHAGE
Ø Between dura and arachnoid (ruptured bridging veins)
Ø Can be acute, subacute or chronic, the latter having a better prognosis.
Mechanism of Injury
Ø Acceleration/Deceleration or Shearing injuries
Ø In 50% of chronic cases, no discrete cause is found.
Ø Prognosis is poor
Presentation
Ø Confusion.
Ø Delerium.
Ø Headache which gradually becomes worse.
Ø Symptoms from raised ICP.
Ø CT Brain features:
— Will cross suture lines
but not the falx cerebri or
tentorium cerebelli.
— Crescent shaped.
— Chronic bleeds may be
isodense to the brain.
Image by Wail Mohammed: Subdural haemorrhage (with consent)
Risk Factors
Ø Elderly (cerebral atrophy increases tension on bridging subdural veins)
Ø Alcoholics (cerebral atrophy)
Ø Anticoagulated patients
Treatment
Ø Depends on size, onset and patient factors.
Ø Small SDHs may be treated conservatively, larger ones may require evacuation
of the clot by catheter or craniotomy.
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NEUROSURGERY
SUBARACHNOID HAEMORRHAGE
Ø Bleed between pia and arachnoid matter due to arterial or venous origin.
Causes
Rupture of cerebral aneurysms in circle of Willis arteries
Rupture of vascular malformation (AVM,AV fistula)
Vasculitis
Drugs
Cerebral venous sinus thrombosis
Tumours
Trauma : the most common cause
Presentation
(Non-traumatic)
Sudden onset headache
Pain at its worst on onset
Often presents without build up (but beware herald bleeds)
Signs of raised ICP (not always)
Vessels Involved
(Aneurysmal)
Middle cerebral
Anterior Cerebral
Anterior inferior /Posterior inferior cerebellar AICA/PICA
Anterior communicating
Posterior Communicating
Investigations (Non-traumatic)
Ø Non-contrast CT
— Blood within the cisterns (CSF Spaces )
— Can be associated with communicating hydrocephalus
Ø LP (if CT is negative): xanthochromia
Ø CT Angiogram
Ø Cerebral formal angiography
Image by Wail Mohammed: Subarachnoid haemorrhage (with consent)
Treatment of Aneurysmal subarachnoid haemorrhage
Ø Coiling
Ø Clipping
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NEUROSURGERY
SPINAL INJURY
General Principles
Ø Chief concern relates to underlying neurological injury to spinal cord, nerve
roots or cauda equina
Ø Protect: Assess level of current injury
Ø Prevent: take precautionary measures to prevent further injury occurring.
General anatomy pointers
Ø Spinal cord ends at L1/L2
— Any injury distal to this involves the cauda equina not the cord.
Ø All the lumbar and sacral segments of the cord lie between T10 and L1.
Ø Phrenic nerve arises from C3,4,5
— Cord section proximal to C3 leads to respiratory arrest.
Ø C2 and C3 supply the vertex and occiput.
Ø C5 - T1 supply the brachial plexus.
Assessment of injuries to vertebral column
Clinical history and examination : high yield information of structures involved
XRay and CT define bony anatomy clearly
MRI used for soft tissues (post ligamentous complex, intervertebral discs, nerve
roots, spinal cord).
“Stability”
— Ability of spine to bear further physiological load
— “Instability” implies further damage may occur leading to greater
deformity and/ or pain and/or neurological deficit.
Ø Stability of a vertebral injury can be measured on CT / Xray
Ø Measure in terms of “Columns of Denis”
— Unstable = 2 or more columns are disrupted / at least 50% loss in
vertebral height.
Ø
Ø
Ø
Ø
Illustrated by Wail Mohammed: Vertebral columns
329
NEUROSURGERY
Clinical examination
Ø Full neurological examination with additional reflexes needed.
Ø Ascertain whether “complete” or “incomplete” neurological injury.
— Complete:“No motor or sensory function more than 3 segments
below the level of the injury”
¾ Alternatively, “no motor or sensory function in lowest
sacral segments”.
— Incomplete: Preservation of sacral function, toe flexion, sphincter
contraction.
Ø Always document perianal sensation (sensory) and anal tone (motor) and presence of anal reflex separately.
Ø Motor (myotomes)
— myotome = muscles supplied by a particular spinal nerve root
— Find the spinal cord level supplying the motor nerve to ascertain the
level of injury.
MRC grading for strength examination
Grade
Strength
0
no active contraction
1
flicker of contraction
2
contraction producing movement if gravity eliminated
3
weak contraction and movement against gravity
4
Active movement against some resistance
5
full resistance, full strength
NT
Ø Sensory (dermatomes)
— Dermatome = area of skin mainly supplied by a single spinal nerve
— Nipple line T4
— Middle finger C7
— Lower limbs
¾ “You stand on S1, sit on S3 and the first three lumbars
run down to the knee”
Ø Reflexes
— Deep tendon reflexes
¾ absent to 4+
— Anal reflex (“wink”)
¾ stimulation of perineum = anal contraction
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NEUROSURGERY
SPINAL CORD SYNDROMES
Ø Anterior cord syndrome
— Anterior O of cord affected
— Burst fracture with extrusion of fragments into canal / trauma to
anterior spinal artery.
— Dorsal columns preserved
¾ proprioception
¾ vibration sense
¾ light/Fine touch
— Motor: Complete paralysis
— Sensory: Light touch and pain loss
— Worst prognosis
Ø Central cord
— Hyperextension injury.
— Commonest syndrome.
— Upper limbs affected more severely than lower limbs.
— Worse prognosis
Ø Posterior cord
— Post ligamentous complex injuries.
— Rare.
— Loss of posterior column function (vibration, proprioception).
Ø Brown-Sequard
— Unilateral facet joint trauma causing hemitransection of cord.
— Ipsilateral loss of motor and proprioceptive function.
— Contralateral loss of pain and temperature sensation as spinothalamic tracts cross over in the lower cord.
— Best prognosis.
Ø Cauda Equina syndrome
— Compression of the cauda equina.
— Essentially a peripheral nerve compression.
— Contrast it with a conus medullaris compression (which is distal
cord compression at sacral segments).
— Causes
¾ Large Central / Paracentral disc herniation
¾ Neoplasms
¾ Infection
¾ Trauma
— Bladder dysfunction most consistent finding
¾ Overflow urinary incontinence with large residual volumes.
— Areflexic, asymmetrical lower limb flaccid paralysis.
— Asymmetrical lower limb sensory changes.
— “Saddle anaesthesia” (loss of perianal sensation) due to affected
sacral nerve roots.
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NEUROSURGERY
— Anal reflex and bulbocavernosus reflexes may be present or absent
depending on the level of the compression.
— Surgical decompression within 48 hours necessary.
Initial Management of spinal injuries
Ø
Ø
Ø
Ø
Ø
332
Utmost caution in turning and lifting the patient.
Spine should be stabilized with collar /brace /spinal board .
Hypotension and hypoventilation must be treated
Careful attention to body temperature
Nasogastric tube and urinary bladder should be passed.
NOTES
333
NOTES
334
OTORHINOLARYNGOLOGY (ENT)
Chapter 16
Otorhinolaryngology (ENT)
335
OTORHINOLARYNGOLOGY (ENT)
Contents:
• General ENT
• Otology
• Rhinology
• Head and Neck Oncology
• Surgical procedures in ENT
336
OTORHINOLARYNGOLOGY (ENT)
Symptom:
Description:
Notes:
Otalgia
Pain in the ear
Referred pain: pathology affecting anatomy with shared sensory pathways
Mainly oropharynx/larynx
Otorrhea
Discharge from the ear
Often associated with infection
Clear/blood stained/purulent?
Hearing loss
Timeline important
Sudden onset: urgent attention
Tinnitus
Perception of sound in
Character: ringing/pulsatile?
the ear: no external stimuli
Vertigo
Hallucination of movement
True vertigo: rotary
Central/peripheral cause?
Establish triggers + duration
Triggers: sudden movement, spontaneous, ongoing infection
Facial nerve
Palsy/anaesthesia/
paraesthesia
Pathology may originate from the ear
Facial nerve: intrinsically related to
middle/inner ear anatomy
Terminal branches: possible parotid gland
pathology
Common Symptoms: Nose
Symptom:
Description:
Notes:
Epistaxis
Nose bleeding
Document risk factors:
Anticoagulants/HTN/Bleeding disorders/
Trauma
Site/Volume/Duration
Anterior bleed: from anterior nasal septum
Posterior nasal cavity bleed: clots often
swallowed/coughed up
First aid measures undertaken?
Nasal
Blockage
May be unilateral/bilateral
Can interfere with sleep/exercise
Acute nasal obstruction post trauma: r/o
septal haematoma
Rhinorrhea
Nasal discharge
Clear/mucopurulent/blood stained?
Seasonal/perennial?
Clear rhinorrhea with recent head trauma/
nasal surgery: possible CSF leak
Anterior/postnasal drip?
Associated respiratory symptoms?
337
OTORHINOLARYNGOLOGY (ENT)
Epistaxis
Nose bleeding
Document risk factors:
Anticoagulants/HTN/Bleeding disorders/
Trauma
Site/Volume/Duration
Anterior bleed: from anterior nasal septum
Posterior nasal cavity bleed: clots often
swallowed/coughed up
First aid measures undertaken?
Intermittent unilateral epistaxis, nasal blockage and atypical facial pain: concerning
for a sino-nasal or postnasal space malignancy
Common Ontological Symptoms: Head and Neck
Symptom:
Description:
Notes:
Pain
Anatomical location
Referred pain most often to the ear
Odynodysphagia
Painful/difficulty
swallowing
Timeline, liquids-solids?
Dysphonia
Impaired inability
to vocalize
Stridor
High pitched sound:
Inspiratory: laryngeal obstruction
partial airway obstruction Expiratory: tracheobronchial obstruction
at or below level
Biphasic: subglottic/glottic obstruction
of larynx
Dyspnoea
Neck mass. non healing ulcer
Trismus
338
Associated breathlessness?
Several causes:
Malignant/benign conditions
“lockjaw” Spasm of jaw
Quinsy
muscles (tetanus)
causing mouth to remain
tightly closed
OTORHINOLARYNGOLOGY (ENT)
GENERAL ENT
Foreign body in the ear
Ø Common in the paediatric population
Ø Patient may present with otitis externa or perichondritis
Ø Removal can be attempted if child is compliant: prevent iatrogenic tympanic
membrane perforation
Ø If child is not compliant, removal can be done under general anesthetic
Ø Insects in the ear should be first killed with an oil based solution and then removed
Foreign body in the nose
Ø Unwitnessed foreign body insertion should be investigated with lateral nasal,
inspiratory and expiratory chest x-ray
Ø All nasal foreign bodies should be removed on an urgent basis to prevent aspiration
Ø Removal under general anaesthetic is indicated if initial attempts fail
Ø Bronchoscopy is indicated if nasal foreign body is aspirated during removal or
not visible under anaesthesia
Foreign body in the upper oesophagus
Ø Fish bone, dentures, coins and many others
Ø Often obstructing oesophagus at 4 constricted sites
— Level of the cricoid cartilage
— Arch of aorta
— Left main bronchus
— Diaphragm
If the foreign body is a battery, this is an ENT Emergency requiring immediate
removal to prevent chemical burn
ACUTE TONSILLITIS
Key facts
Ø Tonsils are paired lymphatic organs part of the Waldeyer ring and are thought to
have a protective/immune role
Ø Each tonsil has a fibrous capsule and is separated from the pharyngobasilar
covering of the superior constrictor muscle by a layer of areolar tissue
Ø Blood supply to the tonsils is through the external carotid artery branches:
— Superior Pole:
• Ascending pharyngeal artery
• Lesser palatine artery
— Inferior Pole:
• Facial artery branches
• Dorsal lingual artery
• Ascending palatine artery
Ø Venous drainage is a diffuse peritonsillar plexus that drains into the lingual and
pharyngeal veins that anastomose with the internal jugular vein
339
OTORHINOLARYNGOLOGY (ENT)
Pathogens
Ø Predominantly viral (influenza, parainfluenza, adenovirus, enterovirus)
Ø Streptococcus pneumonia
Ø H. influenzae
Ø Anaerobes
Symptoms
Ø Sore throat
Ø Odynodysphagia
Ø Otalgia (referred pain)
Ø Dysphonia
Ø Trismus
Ø Painful cervical lymphadenopathy
Ø Pyrexia
Ø Malaise
Signs
Ø Hyperaemic tonsils
Ø Peritonsillar erythema
Normal Tonsils
InflamedTonsils
Ovula
Tonsil
Illustrated by Carolyn Power:
normal/inflamed
Diagnosis
Ø Clinical
Ø Referred to hospital in cases of no oral intake, severe dehydration, sepsis or
airway concerns
Ø Hospital referred cases are investigated with FBC, CRP, liver function and Monospot (Glandular fever)
Complications of acute tonsillitis;
Ø Local & Spread of infection; Quinzy, Parapharyngeal abscess, retropharyngeal
abscess, chronic tonsillitis, acute otitis media.
Ø Rheumatic fever & post-streptococcal glomerulonephritis & scarlet fever.
Management
Ø Most cases are managed in the community with analgesia, bed rest and continued oral intake
Ø Oral antibiotics are often prescribed if symptoms are persistent
Ø If hospital referred, intravenous antibiotics, fluids and analgesia
Ø First line antibiotics: penicillin
Ø Tonsillectomy indicated if 7 or more episodes in 1 year
Avoid Ampicillin and Co-Amoxiclav
in monospot positive cases:
Risk of hypersensitivity maculopapular
rash
340
OTORHINOLARYNGOLOGY (ENT)
HEAD AND NECK ABSCESSES
PERITONSILLAR ABSCESS (QUINSY)
Ø Clinical diagnosis: peritonsillar swelling, trismus and a deviated uvula
Ø This is a complication of tonsillitis
Ø Urgent incision and drainage under local anaesthetic is indicated
PARAPHARYNGEAL ABSCESS
Ø A deep neck space infection
Ø Symptoms: sore throat, odynodysphagia and lateral neck mass
Ø Diagnosed on CT neck
Ø Management involves incision and drainage under general anaesthetic and
intravenous antibiotics
RETROPHARYNGEAL ABSCESS
Ø Retropharyngeal space is from skull base to T3 vertebral level in the mediastinum
Ø Patient often presents with a sore throat, neck stiffness, odynodysphagia and
stridor
Ø A large abscess in a child can compromise the airway
Ø A lateral neck x-ray will show soft tissue widening at level of C2 and C6 +/- CT
Scan to confirm diagnosis
Ø Abscess should be drained urgently under general anaesthetic to prevent spread to the mediastinum causing mediastinitis
Ø Intravenous antibiotics are indicated
Ø Intubation or an emergency tracheostomy should be considered in cases of
airway compromise
341
OTORHINOLARYNGOLOGY (ENT)
OTOLOGY
PINNA (AURICULAR) HEMATOMA
Key facts
Ø Complication of direct trauma to the anterior pinna
Ø Shearing of blood vessels from the perichondrium to the cartilage leads to hematoma formation.
Ø Persistent hematoma between the perichondrium and cartilage could lead to
avascular necrosis of the cartilage
Ø Immediate management is indicated to prevent long standing deformity (cauliflower ear)
Symptoms
Ø Pain
Ø Pinna laceration
Ø Bleeding
Ø Hematoma
Management
Ø Urgent incision and drainage under local anaesthetic
Ø Splinting to prevent reformation of hematoma at incision site
PROMINENT EARS
Key facts
Ø Pinna malformation during intrauterine development
Ø Can be bilateral or unilateral
Ø Associated with psychological sequelae due to bullying in school or teen years
Symptoms
Ø Cosmetic appearance
Ø Psychological
Management
Ø Operative intervention is to prevent bullying
Ø Done prior child commences school
Ø Pinnaplasty or otoplasty are cosmetic procedures aimed to augment the over
projection of the cartilage
342
OTORHINOLARYNGOLOGY (ENT)
OTITIS EXTERNA
Key facts
Ø Infective inflammation of the external auditory canal
Ø Bacterial overgrowth is due to skin maceration from moisture exposure, canal
trauma or obstruction
Ø Loss of protective lipid layer lining the canal
Predisposing factors
Ø Water exposure (swimmers)
Ø Immunosuppression
Ø Retained foreign body
Ø Auditory canal stenosis
Ø Dermatological conditions (eczema, psoriasis, dermatitis)
Ø Canal trauma (cotton bud)
Pathogens
Ø Pseudomonas aeruginosa
Ø Staphylococcus aureus
Ø Fungal (aspergillus, candida)
Symptoms
Ø Otalgia
Ø Otorrhea (muco-purulent, green)
Ø Hearing loss in the affected ear
Ø Fullness
Signs
Ø Canal oedema and erythema
Ø Muco-purulent discharge filling the canal
Ø Tympanic membrane may not be visible due to canal oedema
Management
Ø Aural toilet under microscope visualisation
Ø Extensive canal oedema may prevent topical treatment from infiltrating the
canal.
Ø If tympanic membrane is not visible due to canal oedema, a topical antibiotic
laced wick is inserted
Ø If a wick is placed, a second review after 2 days is indicated.
Ø Once canal oedema is reduced, topical antibiotic drops can be commenced.
Ø Routine analgesia is required
Ø Intravenous antibiotic therapy for immunocompromised patients due to risk of
infective spread to the pinna or skull base (malignant otitis externa)
343
OTORHINOLARYNGOLOGY (ENT)
ACUTE OTITIS MEDIA
Key facts
Ø Acute infective inflammation of the middle ear
Ø High incidence in children age 3 -7
Pathogens
• Viral
Ø Streptococcus pneumonia
Ø Haemophilus influenza
Ø Moraxella catarrhalis
Symptoms
Ø Otalgia and hearing loss
Ø Otorrhoea following tympanic perforation
Ø Coexisting nasal symptoms
Signs
Ø Middle ear effusion
Ø Bulging inflamed tympanic membrane
Ø Tympanic membrane perforation and otorrhoea
Ø Nasal endoscopy is indicated in adults
Management
Ø Analgesia
Ø Oral antibiotics
Ø Nasal decongestants
Complications of acute otitis media:
— Extracranial Intratemporal:
— Tympanic membrane (TM) perforation
— Acute Mastoiditis & Subperiosteal abscess
— Facial Nerve Palsy
— Labyrinthitis
— Petrositis
— Tympanosclerosis (conductive hearing loss)
Intracranial:
— Meningitis
— Extradural abscess
— Subdural abscess
— Brain abscess
— Lateral sinus thrombosis (may lead to internal jugular vein thrombosis and cavernous sinus thrombosis)
—
344
OTORHINOLARYNGOLOGY (ENT)
OTITIS MEDIA WITH EFFUSION
Key facts
Ø Chronic accumulation of non-purulent effusion within the middle ear and mastoid air cell system
Ø The commonest cause of conductive hearing loss in children
Ø Predisposing factors; Eustachian tube dysfunction, Craniofacial abnormalities,
Cleft palate, Adenoid hypertrophy, Allergic rhinitis, Recurrent AOM, Passive
smoking, Bottle feeding.
Symptoms; asymptomatic, hearing loss, tinnitus, aural fullness
Signs;
Ø Air bubbles or fluid level behind the drum
Ø Amber yellow drum
Ø Retracted drum
Investigations;
Ø Hearing assessment
Ø Tympanogram
Treatment;
Ø Watchful waiting for at least 3 months
Ø Ventilation tube insertion If the effusion is persistent
Complications of OME;
Ø Hearing loss
Ø Retraction pockets
Ø Cholesteatoma
Ø Tympanosclerosis
Chronic suppurative otitis media
Key facts
Ø Persistent inflammation of the middle ear or mastoid cavity
Ø Characterised by recurrent or persistent ear discharge (otorrhoea) through a
perforation of the tympanic membrane
Ø Assumed to be a complication of acute otitis media. Frequent URTI and poor
socioeconomic conditions (overcrowded housing, and poor hygiene and nutrition) may be related to the development of chronic suppurative otitis media
Ø The most commonly isolated microorganisms are Pseudomonas aeruginosa
and Staphylococcus aureus
Ø To improve symptoms of otorrhoea; heal perforations; improve hearing; and
reduce complications, with minimum adverse effects of treatment
345
OTORHINOLARYNGOLOGY (ENT)
CHOLESTEATOMA
Key facts
Ø An expanding keratinizing squamous epithelium within the middle ear
Ø Locally destructive
Ø Has a tendency to recur after surgical management
Classification
Congenital
Ø Due to a persistent epidermoid ectoderm. Presents as an white anterior attic
mass/pearl behind an intact tympanic membrane in the 1st year of life.
Ø Disease can be extensive if diagnosed later in childhood
Acquired
Aetiology
Ø It is normal for squamous epithelium to migrate from the surface of the tympanic
membrane outwards along the external auditory canal
Ø Constant negative middle ear pressure results in a retraction of the pars flaccida
to form a retraction pocket
Ø Keratin builds up within the retraction pocket and may get infected or expand
further into the middle ear
Symptoms
Ø Painless foul smelling discharge
Ø Hearing loss secondary to ossicular erosion
Ø Vertigo (erosion of the vestibular organ)
Ø Tinnitus
Ø Facial nerve palsy
Ø Meningitis – intracranial extension
Signs
Ø Attic retraction with keratin build up observed on otoscopy or micro-otoscopy
Investigation
Ø Audiogram
Ø High resolution CT Temporal bone (inadequate views of the temporal bone with
CT Brain alone)
Management
Ø Aural toilet and topical antibiotic treatment
Ø Mainstay of treatment is operative
Ø Mastoidectomy to remove disease
Ø If disease (cholesteatoma) is causing intracranial complications (meningitis,
cerebral abscess), urgent mastoid exploration is indicated
346
OTORHINOLARYNGOLOGY (ENT)
ACOUSTIC NEUROMA
Key facts
Ø Common benign tumour of the cerebellopontine angle
Ø Benign tumour arising from the schwann cells
Ø Often unilateral. Bilateral is seen in neurofibromatosis type 2 (NF2)
Symptoms
Ø Unilateral sensorineural hearing loss
Ø Tinnitus
Ø Vertigo
Ø Facial nerve palsy
Ø Headaches
Ø Ataxia
Ø Raised CSF (papilloedema, altered consciousness)
Investigation
Ø Audiology (unilateral SNHL)
Ø MRI of the Internal auditory meatus
Management
Guided by tumour size, growth rate, hearing level and patient preference
Ø Conservative
Ø Stereotactic radiosurgery
Ø Surgery
347
OTORHINOLARYNGOLOGY (ENT)
RHINOLOGY
EPISTAXIS
Local causes
Ø Idiopathic
Ø Traumatic (nasal bone or septum fracture, foreign body, digit trauma)
Ø Inflammatory (rhinitis)
Ø Neoplastic
Ø Iatrogenic
Systemic causes
Ø Anticoagulation drugs
Ø Inherited bleeding disorders
Ø Acquired coagulopathy (liver failure, vitamin K deficiency, platelet dysfunction)
Ø Hypertension
Symptoms
Ø Anterior bleeding (via nostrils)
Ø Posterior bleeding (ingestion of blood)
Signs
Ø Circulatory shock
Ø Bleeding on anterior nasal inspection
Ø Posterior bleeding visible on nasal endoscopy
Ø Hematoma noted on posterior pharyngeal wall on oral examination
Blood vessels involved
Ø 90% of bleeds originate from Littles area (Kislebach’s plexus) – anterior-inferior
naso-septal anastomosis
Ø Internal and external carotid artery branches
Ø Ophthalmic artery (Internal carotid artery)
Ø Anterior and posterior ethmoid arteries
Ø Greater palatine and superior labial artery (Internal maxillary artery)
Ø Sphenopalatine
Investigation
Ø Full blood count (haemoglobin and platelets); Coagulation screen; Renal function; Group and hold or cross match
Ø Chest x-ray and ECG (preoperative assessment)
348
OTORHINOLARYNGOLOGY (ENT)
Management
Ø Most cases are managed in the community
Ø Head flexed forward and nasal alar compression for 15 minutes
Ø Profuse bleeding or failure of conservative measures indicate hospital assessment
Ø Gain intravenous access
Ø Correct coagulopathy if medically indicated or contributing factor such as hypertension
Ø Anterior bleeding can be visualised and cauterised (silver nitrate or electrocautery)
Ø Anterior nasal packing
Ø Posterior nasal packing
Ø Oral antibiotics are indicated with nasal packing to prevent sinusitis, otitis media
(Eustachian tube obstruction) and cavernous sinus thrombosis
Ø Persistent bleeding may require operative intervention
Ø Functional endoscopic sinus surgery (FESS) with sphenopalatine artery ligation
Ø Anterior ethmoid artery ligation
Ø External carotid artery ligation
ALLERGIC RHINITIS
Key facts
Ø Ig E mediated type 1 hypersensitivity reaction in the nasal mucous membranes
Ø Can be seasonal or perennial
Ø Allergen – Ig E interaction triggers release of prostaglandins, leukotriene and
other factors that cause nasal mucosal oedema, increased capillary permeability and rhinorrhoea
Typical allergens
Ø Pollens
Ø Mould
Ø House dust mite
Ø Animals (cats, dogs, birds)
Symptoms
Ø Rhinorrhoea
Ø Nasal itch
Ø Epiphora (watery eyes)
Ø Nasal obstruction
Ø Post nasal drip
Signs
Ø Mucosal oedema
Ø Turbinate hypertrophy
Ø Nasal polyps (variable)
349
OTORHINOLARYNGOLOGY (ENT)
Investigations
Ø Skin prick test
Ø Total plasma Ig E and RAST
Management
Ø Managed in the primary care setting once diagnosis established
Ø Avoid allergen
Ø Oral antihistamines
Ø Topical steroid nasal sprays
Ø Oral steroids if symptoms severe
Ø Desensitisation (oral or injection depot) to proven pollen allergy
Ø Surgical intervention to reduce nasal obstruction (Septoplasty, turbinate reduction) for better aeration or access for topical therapy
Ø Coexisting sinusitis should be treated
NASAL POLYPS
Key facts
Ø Polyp formation secondary to inflammatory nasal mucosal oedema
Ø Often at middle meatus
Ø Inflammatory process may be due to allergy, chronic infection or idiopathic
Symptoms
Ø Nasal blockage
Ø Rhinorrhoea
Ø Post nasal drip
Ø Large polyps can be visible at nasal nares or cause intercanthal widening
Signs
Ø Visible polyps on nasal endoscopy
Investigations
Ø Allergic rhinitis investigations (skin prick, Ig E and RAST)
Ø CT of paranasal sinuses
Ø Biopsy if suspicious of malignancy
Management
Ø Medical management is first line if not suspicious of malignancy
Ø Intranasal steroid spray +/- tapering oral steroids
Ø Surgical management if failed medical therapy causing persistent nasal blockage
Ø FESS and polypectomy
Ø Continue medical management postoperative
Ø Long term recurrence is inevitable
350
OTORHINOLARYNGOLOGY (ENT)
Sinusitis
Ø Paranasal sinuses are maxillary, frontal, ethmoidal and sphenoidal.
Ø Obstruction of paranasal sinus openings either in the middle meatus or superior
meatus can lead to secretion retention within the sinuses and reduced aeration
Local causes
Ø Infective rhinitis or upper respiratory tract infection
Ø Allergic or nonallergic rhinitis
Ø Nasal polyposis
Ø Retained foreign body
Ø Anatomical variations (deviated nasal septum, abnormal uncinate process and
turbinate hypertrophy)
Ø Tumour
Ø Fractures involving paranasal sinuses
ACUTE RHINOSINUSITIS
Ø Acute inflammation of the sinuses, most often the maxillary sinuses.
Ø Often during upper respiratory tract infection
Ø Infective inflammation leads to mucosal oedema, increased mucous production
and sinus cilia dysfunction
Ø Subsequent obstruction of sinus openings lead to mucus stasis and secondary
bacterial infection
Ø Fungal sinusitis is rare but may affect immunocompromised patients
Symptoms
Ø Nasal blockage
Ø Malaise
Ø Pyrexia
Ø Atypical facial pain
Ø Upper molar pain
Signs
Ø Nasal mucosal oedema and erythema
Ø Mucopurulent pus in the middle meatus
Investigations
Ø Flexible nasal endoscopy under local anaesthetic vasoconstrictor spray (cophenylcaine)
Ø Raised inflammatory markers (WCC, CRP/ESR)
Ø CT of paranasal sinuses (gold standard)
Management
Ø Antibiotics
Ø Analgesia
Ø Nasal decongestant to aid aeration of sinuses and prevent secretion stasis
Ø Failure of medical therapy may indicate FESS
351
OTORHINOLARYNGOLOGY (ENT)
CHRONIC RHINOSINUSITIS
Ø two or more of the following (1 of them should be nasal discharge or obstruction):
— Mucopurulent drainage (anterior, posterior, or both),
— Nasal obstruction (congestion),
— Facial pain-pressure-fullness, or
— Decreased sense of smell.
Ø Endoscopic findings of discharge, edema or polyps in the middle meatus
Ø CT scan changes
Ø Duration of symptoms > 12 months
Complications of sinusitis
Ø Orbital complications – Chandler’s classification
— Preseptal cellulitis
— Orbital cellulitis
— Subperiosteal abscess
— Orbital abscess
— Cavernous sinus thrombosis
Ø Pott’s Puffy tumor
— A life threatening complication
— Osteomyelitis of the frontal bone with subperiosteal abscess causing swelling and edema over the forehead and scalp.
Ø Intracranial complications
— Meningitis
— Extradural abscess
— Subdural abscess
— Brain abscess
— Cavernous sinus thrombosis
Ø Mucocele
— Accumulation of sterile mucus with increased viscosity
— Expansion of cyst can cause bony erosion and displacement of adjacent structures such as the orbit
— Diagnosis on CT
352
OTORHINOLARYNGOLOGY (ENT)
HEAD AND NECK ONCOLOGY
Relevant anatomy
Oral cavity subsites
Ø Lip
Ø Alveolar margin
Ø Floor of mouth
Ø Buccal mucosa
Ø Anterior 2/3 tongue
Ø Hard palate
Ø Retromolar trigone
Larynx (voice box)
Ø Supraglottic subsites
— Inferior surface of the epiglottis to the vesibular folds (false vocal cords)
Ø Glottic subsites
— Contains vocal folds (true vocal cords) and 1cm below them
Ø Subglottis
— Inferior border of the glottis to the inferior border of the cricoid cartilage
Pharynx
Ø Nasopharyngeal borders
— Roof with sphenoid sinus superiorly
— Lateral walls include the Eustachian tube, torus tuberis and fossa of Rosenmuller
— Inferior border – free border of the Soft palate
Ø Oropharyngeal subsites
— Posterior 1/3 tongue and vallecula
— Soft palate and uvula
— Palatine and lingual tonsil
— Posterior pharyngeal wall from the free border of the soft palate downwards
to the horizontal plane of the vallecula
Ø Hypopharyngeal subsites
— Posterior pharyngeal wall (from the level of epiglottis to cricoid cartilage
— Piriform sinus
— Postcricoid region
353
OTORHINOLARYNGOLOGY (ENT)
Key facts
Risk factors
Ø Tobacco use (smoking and chewing)
Ø Excessive alcohol intake
Ø Human papilloma virus (HPV)
Ø Radiation exposure
Ø Previous head and neck cancer
Ø Betel nut (paan) chewing
Aetiological factors
Ø HPV types considered high risk: 16,18,31,33,35,39,45,51,52,56,58,59,66
Ø 90% HPV 16 targeting reticulated tissue of the tonsils (lingual and palatine)
354
OTORHINOLARYNGOLOGY (ENT)
HUMAN PAPILLOMA VIRUS
Ø Key facts
— HPV type 16 (90%) is most commonly seen in squamous cell carcinoma
(SCC) of the head and neck
— The virus targets the reticulated epithelium of the tonsils (lingual and palatine tonsils)
— Affects a younger patient population
— HPV-mediated SCC is associated with superior prognosis including a lower
rate of recurrence and higher overall survival
— Gardasil vaccine is for type 6,11,16,18
— HPV is a double stranded DNA
— Viral DNA is within nucleus of infected epithelium and infects stratified squamous epithelium, which have a high proliferation capacity
— HPV oncogenes E6 binds to p53 (tumour suppressor gene) and E7 binds to
Rb (retinoblastoma)
— High number of HPV-DNA replication occurs once cell is close to the surface
Investigations
Ø Hematological investigation
Ø Radiological (chest x-ray, CT neck and thorax, MRI and PET imaging)
Ø Laryngoscopy and oesophagoscopy for biopsy and rule out second primary
Ø Biopsy of lesion for tissue histology
Ø Fine needle aspiration cytology for suspicious nodal enlargement
Nutritional status
Ø 40% are clinically malnourished on presentation
Ø Increased risk of aspiration pneumonia
Ø Consider nasogastric tube feeding in the immediate setting
Ø Percutaneous endoscopic or radiological inserted gastrostomy tube for long
term use
Airway concerns
Ø If concerned about an acute airway obstruction due to tumour, consider urgent
endotracheal intubation, emergency cricothyroidotomy or tracheostomy
Speech rehabilitation
Ø Electrolarynx
Ø Blom singer valve with tracheo-oesophageal puncture
Staging
Ø Tumour node metastasis (TNM) system
355
OTORHINOLARYNGOLOGY (ENT)
Management outline
Ø Multidisciplinary meeting discussion
Ø Single modality or combined therapy
Ø Surgical resection
Ø Radiotherapy (primary or adjuvant therapy)
Ø Concurrent chemotherapy
Ø Palliative care
LARYNGEAL CANCER
Function of the larynx
Ø Phonation
Ø Prevent aspiration during deglutition
Histological subtypes
Ø Squamous cell carcinoma (90%)
Ø Variants of SCC (spindle cell ca, verrucous ca, basaloid ca, adenosquamous ca)
Ø Neuroendocrine tumours (carcinoid tumour)
Ø Lymphoma
Ø Metastasis (regional or distant)
Treatment
Ø Stage I and II can be treated with single modality therapy (surgery vs radiotherapy)
Ø Stage III and IV often require combined therapy:
— Surgery and adjuvant radiotherapy
— Surgery with adjuvant chemotherapy and radiotherapy
— Chemotherapy and radiotherapy
Surgical options
Ø Transoral laser microsurgery
Ø Hemilaryngectomy with voice preservation
Ø Supraglottic, or supracricoid laryngectomy
Ø Total laryngectomy
ORAL CANCER
Histological subtypes
Ø Squamous cell carcinoma (90%)
Ø Variants of SCC (spindle cell ca, verrucous ca, basaloid ca, adenosquamous ca)
Treatment
Ø Surgery with or without radiotherapy is preferred for oral cavity cancer
Ø Adjuvant radiotherapy is considered for positive margins or perineural invasion
Ø Modified radical neck dissection is indicated in cases of positive nodal metastasis
356
OTORHINOLARYNGOLOGY (ENT)
OROPHARYNGEAL CANCER
Ø Majority are squamous cell carcinoma
Ø Risk factors include alcohol, smoking and HPV infection
Management
Ø Early stage is treated with single modality
Ø Advanced stage can be treated with concurrent chemotherapy and radiotherapy
Ø Salvage surgery
NASOPHARYNGEAL CARCINOMA (NPC)
Ø A genetic predisposition to environmental carcinogens leading to malignant
transformation of nasopharyngeal epithelial cells
Ø South East Asia and Chinese population have high incidence of NPC
Ø NPC often arises from the fossa of Rosenmuller and spreads via direct extension
Clinical features
Ø Epistaxis
Ø Nasal obstruction
Ø Neck mass
Ø Cranial nerve dysfunction
Ø Unilateral middle ear effusion
Staging
Ø Different from oral and oropharynx as primary treatment is chemo-radiotherapy
Investigation
Ø Biopsy of post nasal space examination under anesthesia
Ø Panendoscopy
Ø CT Neck, Thorax and MRI skull base
Ø PET imaging
Management
Ø Radiotherapy is the mainstay of treatment
Ø Concurrent chemotherapy is used for disease with an advanced stage
357
OTORHINOLARYNGOLOGY (ENT)
SURGICAL PROCEDURES
TONSILLECTOMY
Indications
Ø Recurrent tonsillitis. Documented episodes of community managed tonsillitis or
requiring hospital care
— 7 episodes in 1 year
— 5-6 episodes per year over 2 years
— 3 episodes per year over 3 year
— 2 or more episodes of peritonsillar abscess
Ø Suspected neoplasm
Ø Gross enlargement causing dysphagia or sleep apnea.
Ø Part of a staged surgical procedure
Complications
Ø Bleeding (primary or secondary)
Ø Pain including referred pain to the ear
Ø Teeth damage
Ø General anesthetic complications
Ø Temporomandibular joint dislocation
Ø Infection
Ø Pulmonary complications (pneumonia, embolism)
Management of tonsillectomy bleed
Ø Airway, breathing circulation
Ø Persistent bleeding or if the patient is hemodynamically unstable, emergency
operative
Ø Sporadic or intermittent bleeding in a hemodynamically stable patient can be
managed with a trial conservation period
Ø Conservative management includes:
— Hospital admission for observation
— Check FBC, group and screen
— Nil per oral
— Intravenous fluids
— Intravenous antibiotics
— Analgesia
— Hydrogen peroxide gargles
358
OTORHINOLARYNGOLOGY (ENT)
VENTILATION (TYMPANOSTOMY) TUBES
Key facts
Ø small tube inserted into the tympanic membrane in order to keep the middle ear
aerated for a prolonged period of time.
Indications
Ø Otitis media with effusion
Ø Recurrent acute otitis media
Ø Persistent Eustachian tube dysfunction
Ø Barotrauma
Ø Acute otitis media with bulging tympanic membrane or facial paralysis
Types
Ø Grommet tube
Ø T-shaped tube ( stay for longer duration)
Complications
Ø Otorrhea
Ø Residual tympanic membrane perforation
Ø Tympanosclerosis
Ø Injury to incudostapedial joint
Ø Bleeding ( High dehiscent jugular bulb)
Ø Tube blockage
Ø Early extrusion of tube
MASTOIDECTOMY
Key facts
Ø Operative procedure to gain access to mastoid air cells, middle and inner ear
structures
Indications
Ø Cholesteatoma
Ø Chronic suppurative otitis media
Ø Acute mastoiditis
Ø Temporal bone malignancy
Ø Cochlear implant surgery
Types
Ø Cortical mastoidectomy
Ø Radical mastoidectomy
359
OTORHINOLARYNGOLOGY (ENT)
Complications
Ø Facial nerve dysfunction
Ø Hearing loss (of varying severity including dead ear)
Ø Tinnitus
Ø Vertigo (Due to lateral semicircular canal damage or fistula formation)
Ø Intracranial complications (meningitis, subdural or extradural abscess)
Ø Sigmoid sinus thrombosis
PAROTIDECTOMY
Indications for superficial parotidectomy
Ø Benign parotid tumours or low grade malignant tumours involving the superficial
lobe
Ø Preservation of facial nerve
Indications for total parotidectomy
Ø High grade parotid gland malignancy
Ø Deep lobe involvement
Ø Facial nerve involvement
Complications
Ø Facial nerve paresis
Ø Bleeding and formation of hematoma
Ø Greater auricular nerve dysfunction leading to loss of sensation of the ear lobe
Ø Frey’s syndrome (gustatory sweating due to regeneration of damaged auriculotemporal nerve. This results in aberrant parasympathetic innervation of
cutaneous sweat glands)
Ø Sialocele
Ø Cutaneous salivary gland fistula
NECK DISSECTION
Key facts
Ø Surgical excision of the cervical lymph nodes
Ø Management of head and neck malignancy
Ø The type of neck dissection undertaken depends on the anatomical location of
the primary tumour and nodal status
Types
Ø Radical neck dissection
o Excision of node level I - V
o Sternocleidomastoid (SCM)
o Internal jugular vein
o Spinal accessory nerve
360
OTORHINOLARYNGOLOGY (ENT)
Ø Modified radical neck dissection
o Excision of node level I - V
o Type 3 Spinal accessory nerve, internal jugular vein and SCM are spared
o Type 2 Spinal accessory nerve and internal jugular vein are spared
o Type 1 Spinal accessory nerve is spared
Ø Selective neck dissection
o Involves excision of nodes at risk of disease metastasis
Complications
Ø Wound infection and breakdown
Ø Flap necrosis
Ø Frozen Shoulder syndrome due to sacrifice of spinal accessory nerve
Ø Vagus nerve injury
Ø Marginal mandibular nerve injury
Ø Hematoma
Ø Thoracic duct injury leading to chyle leak and fistula
Ø Cerebral and facial oedema due to internal jugular vein ligation
Ø Respiratory complications (pneumothorax, phrenic nerve injury, embolism, pneumonia)
Ø Major vessel damage (carotid artery)
361
NOTES
362
NOTES
363
REFERENCES
1. Dabbas N, Adams K, Pearson K, Royle G., 2011. Frequency of abdominal wall hernias: is
classical teaching out of date? JRSM Short Rep 2011; 2:5.
2. Davis BS, Dunn DP, Hostetler VC., 2017. Beyond hernias: a multimodality review of abdominal
wall pathology. Br J Radiol 2017; 90:20160719.
3. Balla A, Batista Rodríguez G, Buonomo N, et al., 2017. Perineal hernia repair after abdominoperineal excision or extralevator abdominoperineal excision: a systematic review of
the literature. Tech Coloproctol 2017; 21:329.
4. World Society of Emergency Surgery (WSES): Guidelines for emergency repair of complicated
abdominal wall hernias, update (2017)
5. INTERNAL CLINICAL GUIDELINES, T. 2014. National Institute for Health and Care Excellence: Clinical Guidelines. Dyspepsia and Gastro-Oesophageal Reflux Disease: Investigation and Management of Dyspepsia, Symptoms Suggestive of Gastro-Oesophageal
Reflux Disease, or Both. London: National Institute for Health and Care Excellence (UK)
6. LORDICK, F., MARIETTE, C., HAUSTERMANS, K., OBERMANNOVA, R. & ARNOLD, D.
2016. Oesophageal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and
follow-up. Ann Oncol, 27, v50-v57.
7. PENNATHUR, A., GIBSON, M. K., JOBE, B. A. & LUKETICH, J. D. 2013. Oesophageal carcinoma. Lancet, 381, 400-12.
8. RAHMAN, M. W., SUMON, S. M., AMIN, M. R. & KAHHAR, M. A. 2013. Rockall score for risk
stratification in adult patients with non-variceal upper gastrointestinal hemorrhage. Mymensingh Med J, 22, 694-8.
9. SCHLOTTMANN, F. & PATTI, M. G. 2017. Primary Esophageal Motility Disorders: Beyond
Achalasia. Int J Mol Sci, 18.
10. Roy-Chowdhury, N., Chopra, S. and Grover, S. (2018). Diagnostic Approach to the Adult
with Jaundice or Asymptomatic Hyperbilirubinemia. [online] Uptodate.com. Available at: https://
www.uptodate.com/contents/diagnostic-approach-to-the-adult-with-jaundice-or-asymptomatichyperbilirubinemia?search=jaundice&source=search_result&selectedTitle=1~150&usage_
type=default&display_rank=1 [Accessed 30 Oct. 2018].
11. Swaroop Vege, S., Whitcomb, D. and Grover, S. (2018). Clinical Manifestations and Diagnosis of Acute Pancreatitis. [online] Uptodate.com. Available at: https://www.
uptodate.com/contents/clinical-manifestations-and-diagnosis-
of-acute-pancreatitis?search=acute%20 pancreatitis&source=search_
result&selectedTitle=2~150&usage_type=default&display_rank=2 [ Accessed 30 Oct. 2018].
364
REFERENCES
12. Freedman, S., Whitcomb, D. and Grover, S. (2018). Clinical Manifestations and Diagnosis of Chronic Pancreatitis in Adults. [online] Uptodate.com. Available at: https://
www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-chronic-
pancreatitis-in-adults?search=chronic%20pancreatitis&source=search_
result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 30 Oct. 2018].
13. Uptodate.com. (2018). Clinical Manifestations, Diagnosis, and Staging of Exocrine Pancreatic Cancer. [online] Available at: https://www.uptodate.com/contents/clinical-
manifestations-diagnosis-and-staging-of-exocrine-pancreatic-cancer?search=pancreatic%20
cancer&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
[Accessed 30 Oct. 2018].
14. Liang MK, Anderson RE, Jaffe BM, Berger DH., The appendix. In: Schwartz’s Principles of
Surgery, 10th ed, Schwartz SI, Brunicardi CF (Eds), McGraw-Hill Companies, New York
2015.
15. Salminen P, Paajanen H, Rautio T, Nordström P, Aarnio M, Rantanen T, Tuominen R, Hurme
S, Virtanen J, Mecklin JP, Sand J, Jartti A, Rinta-Kiikka I, Grönroos JM. Antibiotic Therapy
vs Appendectomy for Treatment of Uncomplicated Acute Appendicitis: The APPAC Randomized Clinical Trial. JAMA. 2015;313(23):2340.
16. Up to date- Management of Acute Appendicitis
17. Up to date- Overview of the management of primary colon cancer
18. PathologyOutlines.com, Inc. Anus and perianal area, Cornish T, Gonzalez R, Ladoulis C,
Riddle N, Rishi A, Weisenberg E Revised: 31 August 2018, (c) 2002-2018,
19. Peppercorn, M. and Kane, S. (2018). Clinical Manifestations, Diagnosis and Prognosis
of Crohns Disease in Adults. [online] Uptodate.com. Available at: https://www.
uptodate.com/contents/clinical-manifestations-diagnosis-and-prognosis- of-crohn-
disease-in-adults?search=crohns%20disease%20adult&source=search_r
esult&selectedTitle=2~150&usage_type=default&display_rank=2 [Accessed 30 Oct. 2018].
20. Fleshner, P. (2018). Surgical Management of Ulcerative Colitis. [online] Uptodate.
com. Available at: https://www.uptodate.com/contents/surgical-management-of-
ulcerative-colitis?search=ulcerative%20colitis%20treatment&source=search_
result&selectedTitle=4~150&usage_type=default&display_rank=4 [Accessed 30 Oct. 2018].
21. Alguire, P. and Scovell, S. (2018). Overview and management of lower extremity chronic
venous disease. [online] UpToDate. Available at: https://www.uptodate.com/contents/
overview- and-management-of-lower-extremity-chronic-venousdisease?search=chronic%20
venous%20 insufficiency&source=search_result&selectedTitle=1~150&usage_
type=default&display_rank=1 [Accessed 28 Oct. 2018].
365
REFERENCES
22. Neschis, DG. and Golden, MA. (2017). Clinical features and diagnosis of lower extremity peripheral artery disease. [online] UpToDate. Available at: https://www.uptodate.
com/contents/clinical-features-and-diagnosis-of-lower-extremity-peripheralartery-disease?search=peripheral%20arterial%20disease&source=search_
result&selectedTitle=1~150&usage_type=default&display_rank=1[Accessed 28 Oct. 2018].
23. Chaer, R. (2018). Endovascular repair of abdominal aortic aneurysm. [online] UpToDate. Available at:https://www.uptodate.com/contents/endovascular-
repair-of-abdominal-aortic-aneurysm?search=abdominal%20aortic%20
aneurysm&source=search_result&selectedTitle=7~150&usage_
type=default&display_rank=7 [Accessed 28 Oct. 2018].
24. Eidt, J. (2018). Open surgical repair of abdominal aortic aneurysm. [online] UpToDate.
Available at:https://www.uptodate.com/contents/open-surgical-repair-of-abdominal-aorticaneurysm?search=abdominal%20aortic%20 aneurysm&source=search_
result&selectedTitle=6~150&usage_type=default&display_rank=6 [Accessed 28 Oct. 2018].
25. Berger, J. and Davies, M. (2018). Overview of lower extremity peripheral artery disease. [online] UpToDate. Available at:https://www.uptodate.com/contents/overview-oflower-extremity-peripheral-artery-disease?search=vascular%20surgery&source=search_
result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 28 Oct. 2018].
26. Genes Dis. 2018 May 12;5(2):77-106. doi: 10.1016/j.gendis.2018.05.001. eCollection 2018
Jun. Breast cancer development and progression: Risk factors, cancer stem cells, signaling
pathways, genomics, and molecular pathogenesis. Feng Y, Spezia M, Huang S, Yuan C, Zeng Z, Zhang L, Ji X, Liu W, Huang B, Luo W, Liu B, Lei Y, Du S, Vuppalapati A, Luu HH,
Haydon RC, He TC, Ren G.
27. Am Soc Clin Oncol Educ Book. 2018 May 23;(38):457-467. doi: 10.1200/EDBK_201313.
New and Important Changes in the TNM Staging System for Breast Cancer. Hortobagyi GN1,
Edge SB1, Giuliano A1.
28. Breast Cancer Treatment (PDQ®): Health Professional Version. Authors PDQ Adult Treatment Editorial Board. Source PDQ Cancer Information Summaries [Internet]. Bethesda
(MD): National Cancer Institute (US); 2002-.2018 May 31.
29. Surg Pathol Clin. 2018 Mar;11(1):17-42. doi: 10.1016/j.path.2017.09.003. Epub 2017 Dec 1. A
Diagnostic Approach to Fibroepithelial Breast Lesions. Tan BY1, Tan PH2.
30. J Adolesc Health. 2018 Sep 29. pii: S1054-139X(18)30281-7. doi: 10.1016/j.
jadohealth.2018.06.028. [Epub ahead of print]The Effect of Surgical Treatment for Gynecomastia on Quality of Life in Adolescents. Nuzzi LC, Firriolo JM, Pike CM, Cerrato FE, DiVasta AD, Labow BI.
366
REFERENCES
31. Ross, D., Burch, H., Cooper, D., Greenlee, M., Laurberg, P., Maia, A., Rivkees, S., Samuels,
M., Sosa, J., Stan, M. and Walter, M. (2016). 2016 American Thyroid Association Guidelines
for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis.
Thyroid, 26(10), pp.1343-1421.
32. Tuttle, R. (2018). Differentiated thyroid cancer: Overview of management. [online] Uptodate.
com. Available at: https://www.uptodate.com/contents/differentiated-thyroid-cancer-overviewof-management?topicRef=7860&source=see_link [Accessed 15 Oct. 2018].
33. Fuleihan, G. and Silverberg, S. (2017). Primary hyperparathyroidism: Clinical manifestations. [online] Uptodate.com. Available at: https://www.uptodate.com/contents/
primary-hyperparathyroidism-clinical-manifestations?search=hyperparathyroidism&source=
search_result&selectedTitle=3~150&usage_type=default&display_rank=3 [Accessed 15 Oct.
2018].
34. Young, W. (2018). Clinical presentation and diagnosis of pheochromocytoma. [online] Uptodate.com. Available at: https://www.uptodate.com/contents/clinical-
presentation-and-diagnosis-of-pheochromocytoma?search=pheochromocytoma&source=
search_result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 15 Oct.
2018].
35. Nieman, L. (2018). Primary therapy of Cushing’s disease: Transsphenoidal surgery and
pituitary irradiation. [online] Uptodate.com. Available at: https://www.uptodate.com/contents/
primary-therapy-of-cushings-disease-transsphenoidal-surgery-and-pituitary-
irradiation?search=Cushing%27s%20disease%20pituitary&source=search_
result&selectedTitle=1~150&usage_type=default&display_rank=1 [Accessed 15 Oct. 2018].
36. Light, R. W. 2018. Primary spontaneous pneumothorax in adults. 4/5/2018 ed. UpToDate.
Available at - https://www-uptodate-com/contents/primary-spontaneous-pneumothoraxin-adults?search=pneumothorax&source=search_result&selectedTitle=1~150&usage_
type=default&display_rank=1#references
37. Kumar, P, Clark, M, Camm, AJ and Bunce NH (2012) “ Cardiovascular Disease”, Clinical
Medicine (ed.8), page 723-751
38. Aranki, S, Aroesty, J (2018) . Coronary Artery Bypass Graft Surgery: Graft Choices . 28/6/2018 ed. UpToDate. Available at https://www-uptodate-com/contents/coronary-arterybypass-graft-surgery-graft-choices?topicRef=90757&source=see_link
39. Nishimura, R.A, Otto, C.M, Bonow,R.O, et al (2017). 2017 AHA/ACC Focused Update of the
2014 AHA/ACC Guideline for the management of patients with valvular heart disease: A
report of the AHA/ACC task force on clinical practice. 15/3/17 ed. AHAjournals.Org. Available
at - https://www.ahajournals.org/lookup/doi/10.1161/CIR.0000000000000503
40. American College of Surgeons Committee on Trauma (2012) “Initial Assessment and Management”, Advanced Trauma Life Support (ed.9), page 2-28
367
REFERENCES
41. American College of Surgeons Committee on Trauma (2012) “ Thoracic Trauma”, Advanced
Trauma Life Support (ed.9), page 94-110
42. American College of Surgeons Committee on Trauma (2012) “Abdominal and Pelvic Trauma”, Advanced Trauma Life Support (ed.9), page 122-147
43. Raja, A and Zane, R.D (2018). Initial Management of Trauma in Adults. 30/5/2018 ed. UpToDate. Available at - https://www-uptodate-com. /contents/initial-management-of-traumain adults?search=major%20trauma&source=search_result&selectedTitle=1~150&usage_
type=default&display_rank=1
44. British Association of Dermatologists [Available from: http://www.bad.org.uk/healthcareprofessionals.
45. Buzaid AC, Gershenwald JE. Tumor node metastasis (TNM) staging system and other prognostic factors in cutaneous melanoma [Available from: https://www.uptodate.com/
contents/tumor-node-metastasis-tnm-staging-system-and-other-prognostic-factors-in-
cutaneous-melanoma.
46. Hettiaratchy S, Papini R. Initial management of a major burn: II—assessment and resuscitation. 2004;329(7457):101-3.
47. Hettiaratchy S, Papini R. Initial management of a major burn: I—overview. 2004;328(7455):1555-7.
48. Notebook G. NICE urgent referral guidance for suspected malignant melanoma [Available
from: https://www.gpnotebook.co.uk/simplepage.cfm?ID=-221249461.
49. Rutkove SB. Overview of upper extremity peripheral nerve syndromes [Available from:
https://www.uptodate.com/contents/overview-of-upper-extremity-peripheral-nerve-syndromes.
50. Thornton JF, Gosman AA. Skin Grafts and Skin Substitutes and Principles of Flaps. Selected
Readings in Plastic Surgery. 2004;10(1):78.
51. British Orthopaedic Association. (2017), British Orthopaedic Association | BOA Standards for
Trauma (BOASTs), Audit Standards for Trauma.
52. British Orthopaedic Association and British Geriatrics Society. (2007), “The care of patients with fragility fracture”, available at: https://www.bgs.org.uk/sites/default/files/content/
attachment/2018-05-02/Blue Book on fragility fracture care.pdf.
53. National Institute for Health and Care Excellence. (2014), “Osteoarthritis: care and management”, Osteoarthritis: Care and Management, available at:https://doi.org/nice.org.uk/
guidance/cg177.
54. National Institute for Health and Care Excellence. (2016), “Fractures ( non-complex): assessment and management”, NICE.Org.Uk.
368
REFERENCES
55. Rockwood and Green´s. (2015), Fractures in Adults, Wolters Kluwer, available at:https://doi.
org/10.1684/ejd.2011.1531.
56. Kumar, P, Clark, Jarman P.(2012) “Neurological Disease”, Clinical Medicine (ed.8), page
1067 – 1150
57. Lissauer T, Clayden G, Newton R W, Stevens M (2012) Illustrated Textbook of Paediatrics;
Chapter on Malignant Disease: Brain Tumours (ed.4) page 372
58. Singer R J, Ogilvy C S, Rordorf G (2018) Clinical management and diagnosis of aneurysmal
subarachnoid haemorrhage & Treatment of aneurysmal subarachnoid haemorrhage. [UpToDate]
Available at :
a. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-aneurysmalsubarachnoid-hemorrhage?search=subarachnoid%20hemorrhage&source=search_
result&selectedTitle=1~150&usage_type=default&display_rank=1
b. https://www.uptodate.com/contents/treatment-of-aneurysmal-subarachnoid-
hemorrhage?search=subarachnoid%20hemorrhage&source=search_
result&selectedTitle=2~150&usage_type=default&display_rank=2
59. Sataloff, R.T. and Sclafani, A.P., 2015. Sataloff’s Comprehensive Textbook of Otolaryngology: Head & Neck Surgery: Facial Plastic and Reconstructive Surgery (Vol. 3).
JP Medical Ltd.
60. Bull, P.D. and Clarke, R., 2002. Lecture notes on diseases of the ear, nose and throat. Blackwell Science.
61. Scholes, M.A. and Ramakrishnan, V.R., 2015. Ent Secrets. Elsevier Health Sciences.
62. Woo, P., 2009. Stroboscopy. Plural Publishing.
63. Hussain, S.M. ed., 2018. ENT, Head & Neck Emergencies: A Logan Turner Companion.
CRC Press.
369
INDEX
A
Abdominal Aortic Aneurysms
Abdominal Trauma
Achalasia
Acoustic Neuroma
Acute Abdomen Investigations
Acute Abdomen Treatment
Acute Appendicitis
Acute Epididymo-Orchitis
Acute Lower Limb Ischaemia
Acute Otitis Media
Acute Pancreatitis
Acute Rhinosinusitis
Acute Testicular Pain
Acute Tonsillitis
Acute Urinary Retention (Aur)
Adenocarcinoma Of The Prostate
Adenocarcinoma Of The Kidney
Allergic Rhinitis
Anal Cancer
Anal Fissure
Anal Fistula
Ankle Fractures
Aortic Regurgitation (Ar)
161
264
58
347
23
25
101
238
158
344
88
351
237
339
224
231
233
349
127
120
122
303
247
B
Back Pain
Barrett’s Oesophagus
Basal Cell Carcinoma Versus Squamous Cell Carcinoma
Benign Breast Disease
Benign Oesophageal Disorders
Benign Prostatic Hyperplasia
Bowel Obstruction
Brain Tumours
Breast Cancer
Breast Cancer Screening
Breast Cysts
Breast Infections
Burns
370
309
52
274
190
48
229
114
317
181
189
190
190
276
C
Carotid Artery Disease
Cauda Equina Syndrome
Chagas Disease
Chest Tube Insertion (Tube Thoracostomy)
Cholesteatoma
Chronic Pancreatitis
Chronic Rhinosinusitis
Clavicular Fracture
Clinical Presentation & Management Of Thyroid Cancer
Colorectal Cancer
Commmon Urological Devices
Compartment Syndrome
Compartment Syndrome
Conn’s Syndrome
Consent For Inguinal Hernia Repair
Consent For Oesophago-Gastro-Duodenoscopy
Cortisol Excess, Cushing’s Disease
Crohn’s Disease
Ct
171
310
59
249
346
93
352
299
209
110
227
288
307
215
45
66
214
141
264
D
Deep Venous Thrombosis
Defunctioning Stoma
Differential Diagnosis Of A Neck Swelling
Differential Diagsosis Of Acute Abdomen
Diffuse Oesophageal Spasm
Distal Radial Fracture
Diverticular Disease
Drains
Ductal Carcinoma In-Situ (Dcis)
Dupuytrens Disease
Dysphagia And Odynophagia
169
133
198
14
59
294
106
28
182
283
53
E
End Colostomy
End Ileostomy
Epistaxis
Epnoymous Microvignette
Extradural Haemorrhage
132
130
348
6
326
371
INDEX
F
Fat Necrosis
Femoral Hernia
Fibroadenoma
Fibrocystic Disease
190
41
190
190
G
Gallbladder Disease
Gastric Tumours
Gastro-Oesophageal Reflux Disease (Gord)
General Ent
Goitre
Graves’ Disease
Gynaecomastia
82
64
48
339
195
204
191
H
Haemorrhoids
Hand Trauma
Head And Neck Abscesses
Head And Neck Oncology
Hepatobiliary Symptoms
Hernias General Principles
High Output Stoma
History Taking - Common Surgical Symptoms
Human Papilloma Virus
Humeral Fracture
118
285
341
353
13
35
136
11
355
298
I
Incisional Hernia
Incisions
Infectious Flexor Tenosynovitis
Inguinal Hernia
Intracranial Injury
Invasive Ductal Carcinoma (Idc)
Invasive Lobular Carcinoma (Ilc)
Investigation & Surgical Management Of Thyroid Disorders
372
43
26
289
37
323
182
182
199
J
Jaundice
75
L
Laryngeal Cancer
Learning Objectives
Leg Ulcers
Loop Colostomy
Loop Ileostomy
Lower Gi Symptoms
Lower Limb Injuries
356
293
173
133
129
12
301
M
Malignant Hyperparathyroidism (Ectopic Pth).
Malignant Melanoma
Mastoidectomy
Median Nerve
Mitral Regurgitation (Mr)
Mitral Stenosis (Ms)
212
271
359
286
246
247
N
Nasal Polyps
Nasopharyngeal Carcinoma (Npc)
Neck Dissection
Neck Of Femur Fractures (Hip Fractures)
Necrosis
Nutrition In Surgical Patients
350
357
360
301
135
29
O
Obturator Hernia
Oesophageal Motility Disorders
Oesophageal Tumours
Oral Cancer
Oropharyngeal Cancer
Osteoarthritis
Otitis Externa
Otitis Media With Effusion
Otology
44
58
60
356
357
311
343
345
342
373
INDEX
P
Pancolitis
Pancreas
Pancreatic Cancer
Parapharyngeal Abscess
Parastomal Hernia
Parotidectomy
Pelvic Fractures
Peptic Ulcer Disease
Peripheral Arterial Disease (Pad)
Peripheral Arterial Disease Symptoms
Peritonsillar Abscess (Quinsy)
Phaeochromocytoma
Pilonidal Sinus And Abscess
Pinna (Auricular) Hematoma
Pneumothorax
Primary Hyperparathyroidism
Primary Spontaneous Pneumothorax
Principles Of Orthopaedics
Prominent Ears
143
88
95
341
136
360
308
49
155
13
341
213
125
342
248
211
248
294
342
R
Radial Nerve
Renal Neoplasms
Retropharyngeal Abscess
Rhinology
Ruptured Aaa
287
233
341
348
165
S
Scaphoid Fracture
Sciatica
Scleroderma And Oesophageal Dysmotility
Secondary Spontaneous Pneumothorax
Septic Arthritis
Slipped Upper Femoral Epiphysis (Sufe) Shoulder Dislocation
Spigelian Hernia
Spinal Cord Syndromes
Spinal Injury
Stoma Complications
374
300
311
60
249
309
303
299
44
331
329
133
Stoma Retraction
Stoma Stenosis
Stomas
Subarachnoid Haemorrhage
Subdural Haemorrhage
134
134
129
328
327
T
Testicular Torsion
Testicular Tumours
The Advanced Trauma Life Support (Atls®) System
The Diabetic Foot
Thoracic Trauma
Thyroid Cancer
Thyrotoxicosis
Tibial Fracture
Tonsillectomy
Torsion Of The Hydatid Of Morgagni
Total Hip Arthroplasty (Tha)
Total Knee Arthroplasty (Tka)
Transitional Cell Carcinoma Of The Urinary Bladder
Treatment Of Acute Diverticulitis
Trigger Finger
Types Of Thyroid Disease
237
236
255
175
260
207
202
305
358
236
312
312
234
109
289
197
U
Ulnar Nerve
Umbilical Hernia
Upper Gastrointestinal Bleeding
Upper Gi Symptoms
Upper Limb Compression Neuropathy
Upper Limb Injuries
Urinary Tract Stones
Urology
Urology Symptoms
287
43
68
12
286
296
221
222
13
V
Varicose Veins
Ventilation (Tympanostomy) Tubes
166
359
W
Wound Healing
279
375
NOTES
376