SURGERY

Jeremy Chee
Faith Leong
(Information from Washington added on to ChinYeeedited-Andres)
2013 spellchecked version

Pre-operative Care
Peri-Operative Principles
General Anesthesia
Local and General Anesthesia
Blood Products
Post-Operative Care
Fluid Management
Surgical Nutrition
Post-Op Pyrexia
Post-Op Pulmonary Problems
Cardiovascular Problems
Wound dehiscence
Other Post-Op Complications
Surgical Techniques
Wound Healing
Suturing and Skin Closure
Surgical Drains
Surgical Dressings
Abdomen
Abdominal Trauma
Abdominal Incisions
Abdominal Masses
Approach to Abdominal Masses
Approach to Abdominal Pain
Acute Appendicitis
Perforated Ulcer
Mesenteric Ischemia
Approach to Intestinal Obstruction
Small Bowel Obstruction
Large Bowel Obstruction
Approach to Bleeding GIT
Upper BGIT
Lower BGIT
Variceal Bleed
Groin Hernia
Groin Lumps
Abdominal Stomas
Upper GI
The Esophagus
Approach to Dysphagia
GERD
Barretts Esophagus

1
5
6
7
8
9
10
10
11
11
12
13
16
17
17
18
19
20
21
23
25
27
27
28
30
31
32
34
34
35
36
39
41
42
43
45
46

Achalasia
Esophageal Cancer
Peptic Ulcer Disease
Gastric Carcinoma
Hepatobiliary and Pancreas
Approach to Jaundice
Approach to Cirrhosis
Approach to Ascites
Gallstones
Acute Cholecystitis
Choledocholithiasis
Mirizzis Syndrome
Cholangitis
Recurrent Pyogenic Cholangitis
Cholangiocarcinoma
Acute Pancreatitis
Chronic Pancreatitis
Pancreatic Carcinoma
Liver Hemangioma
Simple Liver Cyst
Hepatocellular Carcinoma
Liver Metastases
Pyogenic Liver Abscess
Amoebic Liver Abscess
Colorectal
Inflammatory Bowel Disease
Benign Colonic Polyps which may not be so benign
Familial Adenomatous Polyposis, Hereditary Non-polyposis
Colorectal Cancer
Colorectal Carcinoma
Diverticular Disease
Hemorrhoids
Anal Fistulae
Anal Fissures
Breast
Breast Assessment
Approach to Breast Lump
Approach to Nipple Discharge
Breast Pain
Breast Cancer
Gynaecomastia
Pagets Disease of the Nipple

46
47
49
51
55
58
58
59
61
63
63
64
65
66
67
70
71
73
73
74
76
76
77
78
81
81
82
86
88
89
89
90
92
93
93
94
99
99

Lumps and Bumps

Approach to Lumps and Bumps
Lipoma
Sebaceous Cyst
Ganglion
Basal Cell Carcinoma
Squamous Cell Carcinoma
Malignant Melanoma
Neurofibroma
Dermoid Cyst
Seborrhoeic Keratosis
Hemangioma
Kaposis Sarcoma
Fibrosarcoma
Neck Lumps
Anatomy of the Neck
Cervical Lymphadenopathy
Salivary Glands
Salivary Gland Swellings
Approach to Salivary Gland Swellings
Sialolithiasis
Salivary Gland Tumours
Thyroid
Thyrotoxicosis
Thyroglossal Cysts
Thyroid Gland
Multiple Endocrine Neoplasia
Surgery in Thyroid Disease
Vascular
Anatomy of Lower Limb Arteries
Arterial Assessment
Acute Limb Ischemia
Chronic Limb Ischemia
Treatment of Chronic Limb Ischaemia
Diabetic Foot
Abdominal Aortic Aneurysm
Varicose Veins
Venous Ulceration
Venous Thrombosis

100
102
103
104
105
107
109
112
113
114
114
115
115
116
120
122
123
124
125
127
128
129
134
135
136
137
138
140
144
145
146
148
150
152

!
PERIOPERATIVE PRINCIPLES
ASA Grading
Medical co-morbidity increases risk a/w anaesthesia & surgery
ASA accurately predicts morbidity and mortality
50% of patients presenting for elective surgery are ASA grade 1
Operative mortality for these patients is less than 1 in 10,000.
Grade Definition
I Normal healthy individual
II Mild systemic disease that does not limit activity
Severe systemic disease that limits activity but is
III
not incapacitating
Incapacitating systemic disease which is
IV
constantly life-threatening
Moribund, not expected to survive 24 hours with
V
or without surgery

Mortality (%)
0.05
0.4
4.5
25
50

Respiratory function
Lung function tests predict the type and severity of lung disease
Can predict risk of complications and postoperative mortality
Tests fall in to three categories
o Lung volumes (spirometry)
o Airway caliber (peak flow rate)
o Gas transfer (ABG)
Arterial blood gases may be invaluable
Cardiac function
Chest x-ray (presence of cardiorespiratory symptoms or signs)
ECG (ischemia or previous infarct)
Echocardiography (cardio anatomy and function)
Exercise test
Renal function
Glomerular filtration rate is the gold standard test of renal function
Can be calculated by measuring creatinine clearance rate
Requires 24-hour urine collection
Use of serum creatinine may be inaccurate in patients with:
o Obesity, Oedema, Pregnancy, Ascites

PRE-OPERATIVE CARE

Pre-operative Investigations
The request for pre-operative investigations should be based on:
Factors apparent from the clinical assessment
The likelihood of asymptomatic abnormalities
The severity of the surgery contemplated
5% of patients have abnormalities on investigations not predicted
0.1% of these investigations ever change the patients management
70% of pre-operative investigations eliminated without adverse effect
Investigations:
CXR
ECG
FBC
PT/PTT
U/E/Cr
Random blood glucose
Urinalysis
Blood gases (ABG)
Lung function tests

Recommendations are based on:

Age
ASA Grade of patient
Grade of surgery

Preoperative anaemia
Tissue oxygenation is dependent on
o Arterial oxygen content
o Capillary blood flow
o Position on the oxygen dissociation curve
Haemoglobin concentration affects all of these factors
o Anaemia reduces arterial oxygen content
o Reduced plasma viscosity increases capillary blood flow
o Increases 2,3 DPG and shifts dissociation curve to the right
Both anaemia and polycythaemia increase postoperative mortality
Perioperative haemoglobin concentration of approximately 10 g/dl is ideal

1!

!
Anaesthetic Risk

Operative Risk

Conditions rendering patients at increased anaesthetic risk

Difficult airway
Obesity
o HDU bed post op
o Increased M&M
Cardiac disease
o Revised cardiac risk index
High-risk surgery
Ischaemic heart disease
At least 6 months after AMI risk of post op AMI
History of congestive heart failure
History of cerebrovascular disease
Insulin therapy for diabetes mellitus
Renal impairment
o Hypertension
Assess degree of HTN and end organ damage
Respiratory disease
o Bronchospasm
o URTI
o Atelectasis
o Smoking
o Bronchopneumonia
o Hypoxaemia
o Respiratory failure
o Pulmonary embolism
Gastrointestinal disease
o GERD
o Liver function
Renal failure
Diabetes
o Wound healing and infections
Haematological disorders
Allergic reactions

As above, and:

PRE-OPERATIVE CARE

Obstructive Jaundice
Coagulation disorders
o Reduces the absorption of fat soluble vitamins
o Reduces production of factors II, VII, IX, X
o Disorders can be reversed with Fresh Frozen Plasma or Vitamin K
Reduced wound healing
Increased risk of infection
Hepato-renal syndrome
o Acute renal failure in patient with jaundice
o Probably due to systemic endotoxaemia
o Requires adequate hydration and diuretics
o Value of mannitol unproven
Altered drug metabolism
o Half-life of many analgesics is prolonged (e.g. morphine).
Chronic renal failure
Chronic renal failure affects multiple organ systems
Effects that need to be considered by both surgeons and anaesthetists
include
o Electrolyte disturbances
o Impaired acid-base balance
o Anaemia
o Coagulopathy
o Impaired autonomic regulation
o Protection of veins, shunts and fistulae

2!

!
Pre-Op Assessment

Reduce morbidity and mortality associated with surgery

Prevent unnecessary cancellations
Reduce hospital stay

Aim of preoperative planning

Obtain informed consent for the procedure
Assess pre-existing medical conditions
Plan pre and postoperative management of these conditions
Issues that should be discussed
Time of admission and starving instructions
Management of usual medication
Any specific pre-operative preparation that may be required
Transport to theatre
Any specific anaesthetic issues
Anticipated duration of surgery
Likely recovery period
Need for drains, catheters
Likely discharge date
Need for dressing change or specific postoperative care
Follow up requirements
Likely date of return to work or full activity
Important medical diseases that increase morbidity and mortality
Ischaemic heart disease
Diabetes mellitus
Congestive cardiac failure
Endocrine dysfunction
Hypertension
Chronic renal failure
Cardiac arrhythmias
Nephrotic syndrome
Chronic respiratory disease
Obstructive jaundice
Advantages of pre-admission clinic
Allows pre-operative optimisation of patients
Reduces duration of hospital stay
Reduces risk of unnecessary cancellations
Guidelines minimise unnecessary preoperative investigations

PRE-OPERATIVE CARE

Informed consent

Patients autonomy must be respected at all times

This could adversely affect outcome or result in their death
Patients must be given sufficient information to make these decisions

Types of consent
Express consent - oral or written
o Needed for most investigations or treatments with risks attached
o e.g. consent for operation
Implied consent
o Non-written consent when patient co-operates with a particular action
o e.g. physical examination
Information required for valid consent
When obtaining consent patients should be informed of:
o Details of diagnosis and prognosis with and without treatment
o Uncertainties about the diagnosis
o Options available for treatment
o The purpose of a proposed investigation or treatment
o The likely benefits and probability of success
o Any possible side effects
o A reminder that the patient can change his or her mind at any stage
o A reminder that the patient has the right to a second opinion
The person who obtains consent must be:
o Suitably trained and qualified
o Have sufficient knowledge of the proposed treatment and its
risks
Children
At age of 16 years a child can be presumed to have the capacity to
decide on treatment
Below the age of 16 years the child may have the capacity to decide
depending on their ability to understand what the treatment involves
If a competent child refuses treatment a person with parental
responsibility may authorise treatment which is in the child's best
interests

3!

!
Premedication and Induction
Principles of premedication
Anxiolysis
Analgesia
Amnesia
Antiemetic
Antacid
Anti-autonomic
Adjuncts
Induction
Induction agents are usually administered intravenously
Distributed to organs with a high blood flow (e.g. brain)
Have rapid onset and without maintenance would have rapid recovery
Perioperative Monitoring
Airway management
General anaesthesia removes muscle tone
Methods of maintaining airway include
o Manual methods (e.g. Jaw thrust)
o Endotracheal tube
Complications of endotracheal intubation
Failure to intubate & loss of airway control
Unrecognised oesophageal intubation

Accidental intubation of a main bronchus

Trauma to the larynx, trachea or teeth

Pulmonary aspiration
Disconnection or
blockage of the tube
Tracheal stenosis

Hypothermia
Hypothermia develops rapidly during general anaesthesia
Heat loss can be reduced by use of:
o Warming blanket
o Warm intravenous fluids
o Warm fluid to irrigate body cavities
o Forced air warming

Monitoring during anaesthesia

Accurate monitoring of vital signs
Facilities for cardiopulmonary resuscitation
Monitoring of the following is considered essential for all patients:
o Temperature
o Oxygen content of
o Heart rate
inspiratory gas mix
o Blood pressure
o End-tidal carbon dioxide
o ECG
o Pulse oximetry
Alarms should indicate
o Oxygen supply failure
o Ventilator disconnection
The following may be considered for major surgery
o Invasive blood pressure monitoring
o Central venous pressure
o Urine output
Recovery from anaesthesia
Causes of failure to breath after general anaesthesia include:
o Obstruction of airway
o Central sedation due to opiates or anaesthetic agent
o Hypoxia
o Hypercarbia
o Hypocarbia due to overventilation
o Persistent neuromuscular blockade
o Pneumothorax
o Circulatory failure leading to respiratory arrest
Postoperative nausea and vomiting
Mechanisms of postoperative nausea and vomiting
Chemoreceptor trigger zone
Vestibular apparatus
Vagal sensory neural endings

Prevent Injury
Ensure patient is appropriately fastened to table
Movement of patient should be coordinated
Preserve Circulation

PRE-OPERATIVE CARE

4!

!
GENERAL ANAESTHESIA
Ideal inhalational anaesthetic agent
Preparation
Easily administered
Boiling point above ambient
temperature
Low latent heat of vaporization
Chemically stable
Compatible with soda-lime,
metals and plastics
Non-flammable
Cheap

Pharmacodynamic
High potency - allows high FiO2
High therapeutic index
Analgesic

Pharmacokinetic
Low solubility
Rapid onset, rapid offset,
adjustable depth
Minimal metabolism
Predictable in all age groups
Adverse actions
Minimal toxicity
Minimal unwanted effects nausea, vomiting, cardiac
arrhythmias
No toxicity with chronic lowlevel exposure of staff

Adverse effects of inhalational anaesthetic agents

Cardiovascular
Central nervous system
Decreased myocardial contractility
Increased cerebral blood
flow
Reduced cardiac output

Reduced cerebral
Hypotension
metabolic rate
Arrhythmias

Increased risk of epilepsy

Increased myocardial sensitivity to

Increased ICP
catecholamines
Respiratory
Depress ventilation
Laryngospasm and airway
obstruction
Decreased ventilatory response to
hypoxia and hypercapnia
Bronchodilatation

PRE-OPERATIVE CARE

Others
Decreased renal blood flow
Stimulate nausea and
vomiting
Precipitate hepatitis

Maintenance of anaesthesia
Balanced anaesthesia has three aspects to it
o Hypnosis = suppression of consciousness
o Analgesia = suppression of physiological responses to stimuli
o Relaxation = suppression of muscle tone and relaxation
MAC = Minimum alveolar concentration (required to keep 50% of
population unresponsive)
Specific anaesthetic agents
Halothane
Potent anaesthetic but poor analgesic agent (MAC = 0.75)
Can be used for gaseous induction in children
Isoflurane
Potent anaesthetic but poor analgesic agent (MAC = 1.05)
Less cardiotoxic but causes greater respiratory depression
Nitrous oxide
Weak anaesthetic agent (MAC = 103)
Cannot be used as an anaesthetic agent alone without causing hypoxia
Used in anaesthesia mainly for its analgesic properties
Muscle relaxants
Depolarizing agents (suxamethonium)
Used during induction of anaesthesia
Side effects:
o Histamine release producing a 'scoline rash'
o Bradycardia
o Somatic pain resulting from fasciculation
o Hyperkalaemia
o Persistent neuromuscular blockade = 'scoline apnoea'
o Malignant hyperpyrexia
o Increased intra-ocular pressure
o Increased gastric pressure
Non-depolarizing agents (vecuronium)
Act over 2-3 minutes and effects last for 30 minutes to one hour
Competitive antagonism of acetylcholine receptor
Used for muscle relaxation

5!

!
LOCAL AND REGIONAL ANESTHESIA
Local anaesthesia
Reduces membrane permeability to sodium
Act on small unmyelinated C fibres before large A fibres
Reduce pain and temperature sensation before touch and power
Lignocaine
Lignocaine is a weak base (pKa=7.8)
Has a duration of action of about one hour
o With addition of adrenaline duration of action increased to 2 hrs
Main toxicity is on central nervous and cardiovascular systems
Plain lignocaine should be used for local anaesthesia in digits and
appendages (adrenaline containing solutions can cause tissue ischaemia)

Postoperative epidural infusions

Attenuates postoperative stress response
Improves postoperative pain control
Reduces incidence of postoperative pulmonary complications
Allows more rapid return of gastrointestinal function
Reduces duration of hospital stay
Opioid alone
Allows opioid analgesia
without sedation
No motor or sympathetic
blockade
Itch is common
Serious respiratory
depression can occurs after
stopping infusion
Combination of LA and opioid
Synergy between sites of action
Reduced doses of both drugs
Optimal analgesia possible

PRE-OPERATIVE CARE

Local anaesthetic alone

Potential for complete
anaesthesia
No sedative effects or
respiratory depression
Sympathetic and motor
blockade are common
Cardiovascular side effects
can occur

Spinal and epidural anaesthesia

Spinal anaesthesia
- local anaesthetic or opiate into CSF below termination of cord at L1
Epidural anaesthesia
- local anaesthetic or opiate into fatty epidural space
Both can produce good anaesthesia for up to 2 hours
The quality of the block is often better with a spinal
Epidural anaesthesia is technically more demanding
Contraindications
Pre-existing neurological disease
Coagulopathy
Complications
Timing
Characteristic
Hypotension
Immediate
LA toxicity
High Blockade
Urinary retention
Headache
Local infection
Early
Meningism
Epidural haematoma
Backache

Spinal
Common
Rare
Occasional
Common
1-5%
Almost never
Uncommon
Almost never
Common

Epidural
Less common
Occasional
Occasional
Less common
Never unless dural puncture
Uncommon
Very rare
Very rare
Common

Hypotension
Sympathetic outflow form spinal cord occurs between T1 and L2
Blocked to varying degrees in both spinal and epidural anaesthesia
In hypovolaemic patients there is a greater risk of hypotension
Hypotension during spinal and epidural anaesthesia usually requires fluid
resuscitation
Post spinal headache
Seen following in 1 - 5% of spinal anaesthetics, usually due to CSF leak
In most patients is settles after about 3 days
Headache is characteristically occipital, worse on standing and relieved
by lying down
Initial treatment is with bed rest, simple analgesia and fluids
If persists consider 'blood-patch' (patients own blood injected into
epidural space)

6!

!
BLOOD PRODUCTS
Cross Matching
Blood grouping
Patients red cells grouped for ABO and Rhesus antigens
Serum tested to confirm patients ABO group
Antibody screening
Detects atypical red cell antibodies in recipients serum
Crossmatching
Tests donor red cells against patients serum
Blood products
Whole blood
Packed red cells
Granulocyte concentrates
Platelet concentrates
Human plasma - fresh frozen plasma / freeze-dried plasma
Plasma protein fraction
Human albumin 25%
Cryoprecipitate
Clotting factors - Factor VIII / IX
Immunoglobulins
Complications of blood transfusion
Early
Haemolytic reactions
(immediate or delayed)
Bacterial infections from
contamination
Allergic reactions to white cells
or platelets
Pyogenic reactions
Late
Infection - cytomegalovirus / hepatitis
Immune sensitization
Iron overload

PRE-OPERATIVE CARE

Circulatory overload
Air embolism
Thrombophlebitis
Citrate toxicity
Hyperkalaemia
Clotting abnormalities

Acute haemolytic or bacterial transfusion reactions

Due to acute haemolysis or bacterial contamination
May occur after infusion of small volume of incompatible or infected blood
Associated with high morbidity and mortality
In unconscious patient bleeding due to DIC may be only sign
Most ABO mismatched transfusions are due to human error
o Usually occurs soon after start of transfusion
o Patient feels unwell and agitated
o Symptoms include back pain and pain at infusion site
o Associated with shortness of breath, rigors
o Examination will show hypotension, oliguria and bleeding from
venepuncture sites
o Urinalysis will show haemoglobinuria
Management
Discontinue transfusion immediately and remove giving set
Check unit of blood against patients identity
Give intravenous crystalloid
Consider transfer to the intensive care unit
Take blood for FBC, plasma haemoglobin, clotting, blood cultures and
repeat grouping
Give broad spectrum antibiotics
Monitor urine output and ECG
Anaphylaxis
Usually occurs soon after start of transfusion
May be seen in IgA deficient patients reacting to transfused IgA
Presents with circulatory collapse and bronchospasm
Management
Discontinue transfusion and remove giving set
Maintain airway and give oxygen
Administer adrenaline, chlorpheniramine, salbutamol
If the patient is IgA deficient any further transfusion must be carefully
planned

7!

!
FLUID MANAGEMENT
Daily requirements
For the average 70 Kg man
Total body water 60% of body weight
40% is in the intracellular and 20% in the extracellular compartments
The plasma volume is 7%
The extravascular volume is 13%
+
Total body Na is 4200 mmol (50% in ECF)
+
Total body K is 3500 mmol (only about 50-60 mmol in ECF)
Normal osmolality of ECF is 280 295 mosmol/kg
Fluid replacement
Fluid replacement = fluid deficit + maintenance fluid + ongoing losses
*70ml of blood per kg

Composition of crystalloids
Hartmanns
N/S
Dextrose
Sodium (mmol/l) 131
150
30
Chloride (mmol/l) 111
150
30
Potassium
5
Nil
Nil
(mmol/l)
Lactate (mmol/l)
29
Nil
Nil
Calcium (mmol/l) 2
Nil
Nil
3L of Dextrose saline is not equivalent to 2L 5% Dextrose and 1L Normal
saline
3L Dextrose Saline = 3L water and 90 mmol sodium
2L 5% Dextrose saline + 1L Normal saline = 3L water and 154 mmol
sodium

Fluid deficit
Fluid deficit in dehydration (ml/l) = body weight x % dehydration
Maintenance requirements
Daily maintenance fluid requirements (Holliday-Segar formula)
o 0-10 kg is 100 ml/kg/day
o 10-20 kg is 1000 ml + 50 ml/kg for each kg > 10
o >20 kg is 1500 ml + 25 ml/kg for each kg > 20
Replacement of losses
Pre-operative or pre-admission
o Ongoing losses
o Nasogastric aspirate
o Vomit, diarrhoea
o Stoma, drains, fistula etc.
Most surgical ongoing losses are rich in sodium and should be replaced
with 0.9% saline
Insensible losses
Faeces approximately 100 ml/ day
Lungs approximately 400 ml/ day
Skin approximately 600 ml/ day

POST-OPERATIVE CARE

0.45% saline/5% dextrose for replacement and maintenance needs

o Maintenance + replacement fluid over 24hr
st
o given in 1 8hr, over the next 16 hrs in acute GE
o Replacement slower in meningitis and DKA
0.22% saline/5% dextrose used for maintenance in patients with renal,
liver, cardiac failure
Isotonic 0.9% saline used for resuscitation
o Fluid bolus 20ml/kg over 20 min for severe dehydration

Electrolyte requirements
Na: 2-3 mmol/kg/day
K: 1-2 mmol/kg/day
Ca: 3-5 mmol/kg/day
Glucose: 3 g/kg/day
Assessment of adequacy of resuscitation
Clinical history and observations Pulse, blood pressure, skin turgor
Urine output oliguria < 0.5 ml/kg/hr
CVP or pulmonary capillary wedge pressure
Response of urine output or CVP to fluid challenge
A fluid challenge should be regarded as a 200-250 ml bolus of colloid
This should be administered as quickly as possible
A response in the CVP or urine output should be seen within minutes
The size and duration of the CVP response rather the actual values
recorded is more important

8!

!
SURGICAL NUTRITION
Malnutrition causes:

Delayed wound healing, Reduced ventilatory capacity,

Reduced immunity and increased risk of infection

Nutritional assessment
Clinical assessment
o Weight loss, BMI
o 10% = mild malnutrition
o 30% = severe malnutrition
Anthropometric assessment
o Triceps skin fold thickness
o Mid arm circumference
o Hand grip strength

Blood indices
o Reduced serum
albumin, prealbumin
or transferrin
o Lymphocyte count
End-of-bedogram

Methods of nutritional support

Use gastrointestinal tract if available
Prolonged post-operative starvation is probably not required
Early enteral nutrition reduced post-operative morbidity
Enteral feeding
Prevents intestinal mucosal atrophy,
Supports gut associated immunological shield
Cheaper than TPN and has fewer complications
Polymeric liquid diet
o Short peptides, medium chain triglycerides and polysaccharides
o Vitamins and trace elements
Elemental diet
o L-amino acids, simple sugars
o Expensive and unpalatable; High osmolarity cause diarrhoea
Enteral feed can be taken orally or by NGT
Nasoenteral tube - usually fine bore
Long term feeding can be by:
o Surgical gastrostomy, jejunostomy
o Percutaneous endoscopic gastrostomy (PEG)
o Needle catheter jejunostomy
Rate of infusion often started at low rate and increased
Strength of initial feed often diluted and strength gradually increased

Parenteral nutrition
Intestinal failure = A reduction in functioning gut mass below the minimal
necessary for adequate digestion and absorption of nutrients
Useful concept for assessing need for TPN
Can be given by either a peripheral or central line
Indications for total parenteral nutrition
Absolute indications
o Enterocutaneous fistulae
Relative indications
o Moderate or severe malnutrition
o Acute pancreatitis
o Abdominal sepsis
o Prolonged ileus
o Major trauma and burns
o Severe inflammatory bowel disease
Monitoring of parenteral nutrition
Feeding lines should only be used for that purpose
Drugs and blood products should be given via separate peripheral line
5% patients on TPN develop metabolic derangement
Nutrition should be monitored:
o Clinically Weight
o Biochemically twice weekly
o FBC, U+Es, LFTs,
2+
2+
22+
o Mg , Ca , PO4 , Zn
o Nitrogen balance
Blood cultures on any sign of sepsis
Metabolic complications of parenteral nutrition
Hyponatremia
Hypokalaemia
Hyperchloremia
Trace element and folate deficiency
Deranged LFTs
Linoleic acid deficiency

Complications of enteral feeding

Malposition and blockage of tube
Gastroesophageal reflux
Feed intolerance
POST-OPERATIVE CARE

9!

!
POST-OP PYREXIA
Category
Wind

POD
1-2

Water
Walking
Wound
Wonder Drugs

3-5
4-6
5-7
7+

POST-OP PULMONARY PROBLEMS

Description
the lungs, i.e. pneumonia, aspiration, and pulmonary
embolism
urinary tract infection, related to indwelling catheter
deep vein thrombosis or pulmonary embolism
Surgical site infection
drug fever, infections related to intravenous lines or
reaction to blood products

Assessment of patient
Adequate assessment requires a full clinical examination
Respiratory complications often associated with breathlessness, cough
and chest pain
Wound infections may show erythema, purulent discharge or dehiscence
Abdominal pain, distension and ileus may suggest a collection
Calf pain and tenderness may suggest a DVT
Appropriate clinical signs may be present
Investigation
Useful investigations may include:
o Chest x-ray
o ECG
o Arterial blood gases
o Ventilation / perfusion scan
o Abdominal ultrasound or CT scan

Lack of alveolar ventilation

o Hypoventilation (airway obstruction, opiates)
o Bronchospasm
o Pneumothorax
o Arteriovenous shunting (collapse, atelectasis)
Lack of alveolar perfusion
o Ventilation-perfusion mismatch (pulmonary embolism)
o Impaired cardiac output
Decreased alveolar diffusion
o Pneumonia
o Pulmonary oedema

Atelectasis
Significant atelectasis is more often seen
o In those with pre-existing lung disease
o With upper rather than lower abdominal incisions
o Obese patients
o Cigarette smokers
The basic mechanisms leading to atelectasis are:
o Increased volume of bronchial secretions
o Increased viscosity of secretions
o Reduced tidal volume and ability to cough
Treatment
Intensive chest physiotherapy
Nebulised bronchodilators
Antibiotics for associated infection
Pneumonia
Aspiration pneumonitis
Aspiration of gastric contents results in a chemical pneumonitis
Most commonly seen in apical segments of right lower lobe
If unrecognised or inadequately treated it can result in a secondary bacterial
infection
Secondary infection is usually with gram-negative and anaerobic organisms
Treatment
Tilt table head down and suck out pharynx
Consider intubation and endotracheal suction
Prophylactic antibiotics should be given
No evidence that steroids reduce inflammatory response

POST-OPERATIVE CARE

10!

!
CARDIOVASCULAR PROBLEMS

Hypotension
Hypovolaemia
Ventricular failure
Cardiogenic shock
Arrhythmias
Conduction defects
Hypertension

Causes of perioperative arrhythmias

Physiological disturbances
o Acidosis
o Hypercapnia
o Hypoxaemia
o Electrolyte imbalance
o Vagal manoeuvres
o Hypovolaemia
Pathological disturbances
o Myocardial ischaemia or infarction
o Pulmonary embolus
o Phaeochromocytoma
Pharmacological causes
o General anaesthesia
o Local anaesthetic toxicity
o Positive and negative inotropes

WOUND DEHISCENCE

Affects about 2% of mid-line laparotomy wounds

Serious complication with a mortality of up to 30%
Due to failure of wound closure technique
o Broken sutures or slipped knots
o Inadequate muscle bites
Usually occurs between 7 and 10 days post operatively
Often heralded by serosanguinous discharge from wound
Should be assumed that the defect involves the whole of the wound

Management
Opiate analgesia
Sterile dressing to wound
Fluid resuscitation
Early return to theatre
Resuture under general anaesthesia
Exact technique is variable
Interrupted or mass closure with non-absorbable sutures often used
The use of 'deep tension' sutures is controversial
Believed by some to strangulate muscle and weaken the closure
Also painful and associated with increased risk of infection

Causes of postoperative hypertension

Pain
Pre-existing hypertension
Hypoxaemia
Hypercapnia
Positive inotropic drugs
Hyper-reninemia

POST-OPERATIVE CARE

11!

!
OTHER POST OP COMPLICATIONS
Causes of postoperative hepatic dysfunction
Increased bilirubin load
o Blood transfusion
o Haemolysis
o Haemolytic disorders
o Abnormalities of bilirubin metabolism
Hepatocellular damage
o Pre-existing hepatic disease
o Viral hepatitis
o Sepsis
o Hypotension
o Hypoxaemia
o Drug-induce hepatitis
o Congestive cardiac failure
o General anaesthetic induced hepatic necrosis
Extra-hepatic biliary obstruction
o Gallstones
o Ascending cholangitis
o Pancreatitis
o Common bile duct injury
Causes of postoperative renal failure
Prerenal (hypoperfusion)
o Shock (hypovolaemia, cardiogenic, septic)
o Renal artery disease
Renal (direct injury)
o Acute tubular necrosis (following prerenal, drugs, myoglobin)
o Glomerulonephritis
o Interstitial nephritis
Postrenal (obstruction)
o Bladder outflow obstruction
o Single ureter (calculus, tumour)
o Both ureters (bladder malignancy)

POST-OPERATIVE CARE

Urinary tract infections

10% of patients admitted to hospital have a urinary catheter inserted
Risk of catheter-related infection depends on:
o Age and sex of patient
o Duration of catheterisation
o Indication for catheterisation
Bacterial colonisation of catheters is common
If catheter required for more than 2 weeks 90% patients will develop
bacteriuria
Commonest organisms are Enterobacter and enterococci
Does not require treatment unless patient is systemically unwell
Infection can be prevented by:
o Maintaining closed drainage system
o High infection control standards
o Preventing backflow from catheter bag
Postoperative confusion
Occurs in 10% of postoperative patients
Associated with increased morbidity and morality
Leads to increased duration of hospitalisation
Clinical features include
o Reduced level of consciousness
o Impaired thinking
o Impaired memory
o Abnormalities in perception
o Disturbed emotion
o Psychomotor disturbance
Causes
Hypoxia - respiratory disease, cardiac failure, arrhythmia
Trauma - head injury
Infection - intracranial, extracranial
Neoplasia - primary and secondary cerebral tumours
Vitamin deficiency - Thiamine (Wernicke's encephalopathy), B12
deficiency
Endocrine - hypothyroidism, hyperthyroidism, Addison's disease
Degenerative
Vascular - CVA, TIAs
Drugs
Metabolic derangement

12!

!
WOUND HEALING
Skin anatomy
Skin has natural tension lines
o Incisions placed along these lines -- heal with narrower and
stronger scar
More favourable cosmetic result
Pathophysiology of wound healing (3 phases)
Acute inflammatory phase
st
o 1 2-5 days
o Bleeding stops (hemostasis) - platelet clot + scab formation
o Inflammation - opens blood ss and cleanses wound
Proliferative phase (cell proliferation + deposition of extracellular matrix)
o 5 days to 3 weeks
o Granulation -- angiogenesis + fibroblasts synthesizing ECM
Pink and granular! (due to rich network of capillary
vessels)
o Contraction of wound - due to myofibroblasts
o Epithelialization
Maturation phase (remodelling of ECM)
o Occurs from 3weeks to 2 years!
o Increase in tensile strength
o Formation of avascular scar
o Scar tissue only 80% as strong as normal tissue
st
Strength increases rapidly over 1 7 days
Full maturation of scar takes up to 12months
Time required to regain strength depends on tissue type
and thickness
Bowel - 1month
Skin - 6 months
Abdominal incisions through muscle layers take
3-4 months b4 they no longer require suture
support
Close with either loop nylon that persists
in the wound
or a strong, slowly absorbing suture
material such as PDS
Superficial skin wounds require little support
Close with quickly absorbable suture
material or stapler

SURGICAL TECHNIQUES

Classification of wound healing

Primary intention (oppose skin)
o Uncontaminated wounds with minimal tissue loss
o Wound edges can be easily approximated
(sutures/staples/adhesive strips) w/o excessive tension
o Heals by rapid epithelialization with minimal granulation tissue
Secondary intention
o Wounds with substantial tissue loss
o Edges cannot be apposed w/o excessive tension
o Leave open and allow to heal from bottom up by granulation
tissue, epithelialization and contraction
o Takes much longer, more intense inflammatory response
o Scar quality and cosmesis poor result (Butt abscess
saucerization/ulcers)
Delayed primary intention
o A period of healing by secondary intention - control infection/
reduce tissue edema; Close by primary intention!
Rate of healing
Site
o Scalp and face heal v quickly
o Bone and intestine can regenerate with no/minimal loss of fx
o Cardiac - little regenerative potential
o Nerve - partial fx may be regained through slow neuronal growth
Age - rate of healing declines with age
Causes of delayed wound healing
Local factors
o Wound infection/dirty
o Dead tissue
wound
o Surgical technique
o Hematoma
o Ischemia (Acute; Damage to
o Excessive mobility e.g.
vascular ss; Sutures too tight)
Situated over a joint
o Previous irradiation
o Foreign body
General factors
o Age - elderly
o Chronic diseases
Cardiorespiratory disease; Diabetes Mellitus; Vascular
disease (Atherosclerosis, Venous disease)
Anaemia, Renal/liver failure, Obesity, Malnutrition
Immunosuppressive disease e.g. AIDS
o Drugs - Steroids, Immunosuppressive drugs
13!

!
Ideal conditions for wound healing
Absence of things
o No infx or foreign body
Surgical factors
o Accurate apposition of tissue in layers (eliminating dead space)
o No excess tension
Vascular factors
o Good blood supply, good hemostasis, prevent hematoma
Wound dehiscence
Failure of wound healing
Partial or total disruption of any or all layers of operative wound
Evisceration (burst abdomen) = extrusion of abdominal viscera
o Usually preceded by blood-stained fluid
Mgt
o Resuscitation, reassurance, analgesia
o Protection of organs with moist sterile towels
o Re-operation and closure
Incisional hernias - @ sites of partial dehiscence
Classification of wounds
Depth
o Superficial - only epidermis and dermis
No granulation tissue, no scar
E.g. Superficial burn/ graze
o Deep
Involves layers deep to the dermis
Healing process: migration of fibroblasts, granulation
tissue formation, scar formation
If deep wound not closed with good approximation - can
cause contractures (problem)
Related to the rate of surgical site infections
Principles of wound closure
Optimize wound healing & cosmesis
Incise along natural tension lines
Avoid hematoma and obliterate potential spaces -- use of surgical drain
Eliminate all dead tissue & infx
Avoid excess wound tension, ensure good blood ss
Handle tissues gently
Use appropriate suture material
Choose appropriate closure technique
SURGICAL TECHNIQUES

Classification of surgical wounds

Class
Definition
Class I
Operative wound clean
Clean
Non-traumatic, with no
inflammation encountered
No break in technique
Respiratory, gastrointestinal
and genitor-urinary tracts not
entered

Class II
Clean contaminated

Class III
contaminated

Class IV
Dirty infected

Operative wound cleancontaminated

Non-traumatic wound with
minor break in technique
Gastrointestinal, respiratory or
genitor-urinary tracts entered
without significant spillage
Wound contaminated
Fresh traumatic wound from
clean source
Major break in technique
Gross spillage from the
gastrointestinal tract
Entrance into the genitourinary or biliary tracts
Incision encountering acute
non-purulent inflammation.
Operative wound dirty
Traumatic wound from dirty
source or delayed treatment
Fecal contamination
Foreign body
Retained devitalized tissue
Operative wound w/ acute
bacterial inflammation or
perforated viscus
Operative wound where clean
tissue is transected to gain
access to a collection of pus

Examples
Vascular, Neurological,
Endocrine, Eye, Orthopedic
procedures (unless: trauma III,
old wound IV, amputation II),
Skin ( mastectomy,
lumpectomy, lesions, lipoma,
cosmetic, I&D IV, old wounds
III, inflamed III, infected IV)
Exploratory Lap (no bowel
involvement II) (herniorrhaphy)
Thoracic procedures
GI procedures (including:
laparoscopy, colonoscopy,
gastroscopy, cholycystectomy)
GU procedures
Ear surgery
Nose/Oropharynx
Inflammation
Gross spillage
Fresh accidental wound

Infected
I&D abscess
Wound debridement

14!

!
Scar formation
Factors influencing scar formation
o Individual genetic make up
o Race
o Anatomical site
o Wound tension
o Age
o Placement of incision
o Surgical technique
To minimise the degree of postoperative scarring:
o Incisions should run along Langer's lines
o The finest suture possible should be used
o Tension should be avoided
o Sutures should be removed as soon as possible
o Traumatic wounds should be clean and edges excised
o Exposure to sunlight should be avoided in the early
postoperative period
Management
1. If large defect -- takes very long to heal, conservative mgt not
recommended as scar will be large, ugly and granulation tissue may
overgrow
2. Reconstruct
o Secondary closure -- allow for healthy granulation tissue to form,
excise the edges to rebleed wound, appose the skin and re-stitch
with a strong stitch
o Skin graft (partial thickness for large wounds)
o Rotation flap
o Muscle flap with blood ss
o Free flap with microvascular reconstruction -- re-perfuse

SURGICAL TECHNIQUES

Problematic scars
Contractures
Result if scars shorten
Particularly seen in badly aligned scars not corresponding to Langer's
lines
Can reduce joint mobility
May require a z-plasty or skin graft
Depressed scars
Result if skin becomes attached to deep tissue
Can be treated by release of normal skin from margins of scar
Scar is then de-epithelialized and skin edges closed over the top
Keloid and hypertrophic scars
All scars become red and thickened during the normal healing process
After several months maturation results in flattening of the wound
In some scars collagen formation is excessive
Results in elevated and red scar
If confined to wound = hypertrophic scar
If extends beyond wound into normal tissue = keloid scar
Seen particularly in patients of Afro-Caribbean origin
Particularly affects scars on the presternal and deltoid areas
Treatment is often difficult
Treatment options include:
o Intra-lesional steroid injections (e.g. triamcinolone)
o Compression dressings with elasticated compression garments
o Silastic gel therapy
o Excision and radiotherapy
o Laser therapy

15!

!
SUTURING AND SKIN CLOSURE

Staples, skin clips

Sutures - interrupted or continuous
Subcuticular sutures
Self-adhesive steristrips
Glue
Adequate apposition of tissues under the skin may eliminate the
requirement for skin closure

Choosing sutures
To hold a wound together in good apposition until such time as the natural
healing process is sufficiently well established to make the support from the
suture material unnecessary and redundant.
Properties of suture material
Size of suture
Absorption rate
Type of needle
Handling characteristics and
knotting properties
Properties of materials
Suture materials vary in their physical characteristics
o Monofilament sutures (e.g. polypropylene) are smooth
The slide well in tissues but if handles inappropriately
they can fracture
o Multifilament sutures (e.g. polyglactin) are braided
They have a greater surface area
They are easier to handle and knot well
Absorbancy - depends on duration of support required
o Non-absorbable e.g. Prolene (polypropylene)
o Absorbable e.g. Vicryl (polyglactin)
Synthetic vs biological (biological - have unpredictable length of time
persistence in tissues + strength and have )
Absorbable
Non-Absorbable
o Polyglycolic Acid (Dexon) o Polyamide (Nylon)
o Polyglactin (Vicryl)
o Polyester (Dacron)
o Polydioxone (PDS)
o Polypropylene (Prolene)
o Polyglyconate (Maxon)
o Silk, Linen, Stainless Steel
o Catgut
Ideal suture material =
o Have good handling characteristics
o Not induce a significant tissue reaction
o Allow secure knots
o Have adequate tensile strength
o Not cut through tissue
o Be sterile, non-electrolytic, non-allergenic, cheap
SURGICAL TECHNIQUES

Classification of needles
Shape
o Straight
o Curved
o Circular
o J-shaped
Type (point of needle)
o Conventional cutting needle
o Reverse cutting needle
o Round-body taper-point needle
o Taper cutting needle
o Blunt point needle
Thickness
o Should be appropriate to weight of suture
o Choice of a larger or smaller curved needle may aid suture
placement
Large for large bites of tissue e.g. Abdominal closure
Small for accurate placement e.g. Vascular anastomosis
Common errors of suture use
Too many throws. Increases foreign body size. Causes stitch abscesses
Intra-cuticular rather than subcuticular sutures causing hypertrophic
scars
Holding monofilament sutures with instruments reduces tensile strength
by over 50%
Holding butt of needle causes needle and suture breakage
Timing of suture removal
Vary according to site
o Areas that are very mobile - may req longer to heal
o Face 4-5 days
o Scalp 6-7 days
o Hands and limbs 10days
o Abdominal wounds 10-20days

16!

!
SURGICAL DRAINS

SURGICAL DRESSINGS

Drains are often made from inert silastic material

They induce minimal tissue reaction

Purpose of surgical drains

Minimise dead space in a wound e.g. Axillary clearance, mastectomy,
thyroidectomy
When there is risk of leakage e.g. Pancreatic surgery, bowel
anastomosis
To drain actual fluid collections e.g. Subphrenic abscess
To divert fluid away from blockage or potential blockage
o Biliary T-tube, suprapubic urinary catheter, ventricular CSF drain
To decompress and allow air to escape e.g. Chest drain
Classifying surgical drains
Open (into dressing) vs closed (into container)
o Closed = reduce risk of infx
Suction vs non-suction (passive gravity drainage)
o Suction = better drainage but may damage adjacent
organs/structures e.g. Bowel - precipitate leak
Open drains
Closed drains
Include corrugated rubber or
Consist of tubes draining into a
plastic sheets
bag or bottle
Drain fluid collects in gauze
They include chest and
pad or stoma bag
abdominal drains
Increase the risk of infection
The risk of infection is reduced
Active drains
Active drains are maintained
under suction
They can be under low or
high pressure

Dressings - provide optimal healing environment for wounds

Moist
Infection free, with minimal slough
Free of chemicals and foreign bodies e.g. Dressing fibres
At optimum temperature
Reduce wound disruption - minimum change in dressings
Correct pH (4.8 - 6)
Requirements of dressings
Provide protection from infx and trauma
Allow debridement - chemical and mechanical
Be absorbent and remove excess exudates while keeping wound moist
Maintain temp & gaseous exchange
Comfortable and cosmetically acceptable
Stimulate healing
Inexpensive and easy to change

Passive drains
Passive drains have no suction
Function by the differential
pressure between body cavities
and the exterior

Complications of drains
Infx via drain track
Injury to adjacent structures by drain e.g. Bowel
Anastomosis leakage
Retraction of drain into the wound
Bleeding by erosion into blood vessel
Pain e.g. Chest drain irritating diaphragm
Herniation @ drain site

SURGICAL TECHNIQUES

17!

!
ABDOMINAL TRAUMA
Assessment of abdominal trauma
Can be difficult due to altered sensorium (head injury, alcohol), altered
sensation (spinal cord injury), injury to adjacent structures (pelvis, chest)
Differentiate between penetrating and blunt trauma
Indications for immediate laparotomy
Unexplained shock (third spacing) with strongly suspected intraabdominal injury
Rigid silent abdomen (i/o + perf viscus)
Evisceration, gunshot wounds, stab wounds with implement in-situ
Obvious signs of peritoneal irritation
Radiological evidence of
o Intraperitoneal gas
o Ruptured diaphragm
Positive result on peritoneal lavage
FAST (Focused Assessment for the Sonographic assessment of Trauma)
U/S for intraperitoneal fluid
Probe placed on pericardial, RUQ, LUQ, suprapubic region
o Detects fluid in subphrenic, subhepatic spaces or Pouch of
Douglas in hypotensive patient
o Confirms need for emergency laparotomy
Advantages
Disadvantages
Portable
Does not image solid parenchyma, retroperitoneum,
Can be done in <5min diaphragmatic defect or bowel injury
Can be used for serial Compromised in uncooperative, obese patient w
exam
substantial bowel gas
No contrast/radiation
Operator dependent
Cannot differentiate blood from ascites
Not conclusive; may need alternatives
CT Scan
Advantages
Precisely locate intra-abdominal lesions pre-op
Evaluate retroperitoneum
Non-invasive
Possibility of conservative tx

ABDOMINAL TRAUMA

Disadvantages
Expensive
Time consuming
Use of contrast

Peritoneal Lavage
Indication
Contraindication
Equivocal clinical examination
Absolute indication for laparotomy
Difficulty in assessing patient
already exists
Persistent hypotension despite Previous abdominal surgery or infx
adequate fluid resuscitation
Gravid uterus; Morbid obesity
Multiple injuries
Coagulopathy
Advantages
Disadvantages
Reveal or exclude presence of Morbidity wound complications,
intraperitoneal hemorrhage
intraperitoneal injury, viscus injury
Discover bowel perforation
False negative rate 2%
Method
o Ensure that catheter and NGT are in place
o Under LA make vertical sub-umbilical incision dividing linea alba
o Aspirate any free blood or enteric contents from peritoneal cavity
o If no blood aspirated infuse 1L of normal saline and allow 3 min to
equilibrate
o Place drainage bag on floor and allow to drain
o Send 20 ml to laboratory for measurement of RBC, WCC and
microbiological examination
Positive result
3
o Red cell count > 100 000 / mm
3
o White cell count > 500 / mm
o Presence of bile, bacteria or faecal material
o Frank blood >5ml
Damage Control Surgery
Ensure hypothermia, coagulopathy and severe acidosis is not
exacerbated
o Injury severity score >25
o Core temperature < 34C
o Arterial gas pH <7.1
Principles
o Control hemorrhage
o Remove dead tissue
o Control contamination
o Lavage abdominal cavity
o Close abdomen without tension (can use Bogota bag)
o Send to SICU for rewarming, ventilation, restoration of perfusion,
correction of deranged biochemistry commence nutrition
o Second look laparotomy allows definitive treatment

18

!
ABDOMINAL INCISIONS
Abdominal incisions
They must allow adequate access to the abdomen
They should be capable of being extended if required
Ideally muscle fibres should be split rather than cut
Nerves should not be divided
The rectus muscle has a segmental nerve supply
It can be cut transversely without weakening a denervated segment
Above the umbilicus tendinous intersections prevent retraction of the
muscle

Midline incision
Midline incisions are the commonest approach to the abdomen
The following structures are divided:
o Skin
o Linea alba
o Transversalis fascia
o Extraperitoneal fat
o Peritoneum
The incision can be extended by cutting through or around the umbilicus
Above the umbilicus the Falciform ligament should be avoided
The bladder can be accessed via an extraperitoneal approach through
the space of Retzius
The wound can be closed using a mass closure technique
The most popular sutures are either non-absorbable or absorbable
monofilaments
At least 1 cm bits should be taken 1 cm apart
Requires the use of one or more sutures four times the wound length
Paramedian incision
A paramedian incision is made parallel to and approximately 3 cm from
the midline
The incision transverse:
o Skin
o Anterior rectus sheath
o Rectus - retracted laterally
o Posterior rectus sheath - above the arcuate line
o Transversalis fascia
o Extraperitoneal fat
o Peritoneum
The potential advantages of this incision are:
o The rectus muscle is not divided
o The incisions in the anterior and posterior rectus sheath are
separated by muscle
The incision is closed in layers Takes longer to make and close
Had a lower incidence of incisional hernia (when sutures were not so
good)

ABDOMINAL INCISIONS

19

!
ABDOMINAL MASSES

Physical signs of abdominal masses

Signs of hepatomegaly
Mass descending below right costal margin and costal angle
Moves with respiration and cannot get above it
th
Dullness to percussion up to the level of the 8 rib in the mid-axillary line
Signs of splenomegaly
th
Mass descending below the left 10 rib and enlarging in a line towards
the umbilicus
Often has a palpable notch on the medial border
Moves with respiration and cannot get above it
Dullness to percussion
Can be brought forward by lifting the lower ribs
Cannot be felt bimanually or balloted
Signs of a renal mass
Mass lies in paracolic gutter
Moves with respiration but usually only lower border is palpable
Can be felt bimanually or balloted; not dull to percussion

Signs of an enlarged gallbladder

th
Mass arising from below the tip of the right 9 rib
Smooth and hemi-ovoid in shape
Moves with respiration
Dull to percussion
Cannot feel space between mass and liver
Signs of an enlarged urinary bladder
Hemi-ovoid smooth mass arising from the pelvis
Can extend above umbilicus
Non-mobile and dull to percussion
Does not bulge into the pelvis
Cannot be felt on rectal examination
Signs of an ovarian cyst
Smooth mass arising from the pelvis
Mobile from side-to-side but not up and down
Dull to percussion
Palpable fluid thrill
Lower extremity can be felt on pelvic examination

APPROACH TO ABDOMINAL MASSES

20

!
APPROACH TO HEPATOMEGALY

Physical examination
o Normal
Impalpable in adults; 2FB below right costal margin in infants
o Features
Enlarged mass extending downwards below right costal
margin
Gross hepatomegaly - may fill subcostal angle and
extend below left costal margin
Moves with respiration
Dull to percussion - may extend above normal upper
level of 5th right intercostal space
Specific features to aid diagnosis
o Edge
Smooth - fatty liver/micronodular cirrhosis/congestive
cardiac failure
Knobbly - metastatic/macronodular cirrhosis
o Consistency - hard if mets
o Tenderness (occurs with distention of capsule)
Hepatitis
HCC
CCF/AV malformation
o Pulsatility only in TR
Always feel for associated splenomegaly and lymphadenopathy
o Causes of hepatosplenomegaly
Cirrhosis (portal HTN)
Polycythaemia
Leukaemia
Amyloidosis
o Causes of hepatosplenomegaly + lymphadenopathy
Lymphoma

APPROACH TO ABDOMINAL MASSES

Causes of hepatomegaly
Smooth generalized enlargement
Congestion due to cardiac failure
Micronodular cirrhosis
Reticuloses
Hepatic vein obstruction (BuddChiari syndrome)
Infective hepatitis
Cholangitis
Portal pyaemia
Amyloidosis

Knobbly generalized enlargement

Secondary carcinoma
Macronodular cirrhosis
Polycystic disease

Congenital
Riedels lobe (right lobe)
Polycystic liver disease

Cirrhosis (often shrunken)

Chronic viral hepatitis
Alcoholic
Rare: biliary, cardiac,
hemochromatosis, Wilsons

Inflammatory
Infective hepatitis
Viral - Hepatitis viruses, EBV,
CMV, HIV
Bacterial - pyogenic abscess, TB
Parasite - amoebiasis, malaria
Portal pyaemia and liver abscess
Leptospirosis (Weils disease) or
actinomycosis
Vascular
Right heart failure
Tricuspid regurgitation
Budd-Chiari syndrome

Localised swelling
Riedel's lobe
Hydatid cyst
Liver abscess
Hepatocellular carcinoma

Metabolic
Fatty liver
Amyloid/Gauchers disease
Neoplastic
Primary -- HCC
Secondary mets
Hemopoietic disease & reticuloses
Lymphoma Hodgkins
disease & NHL
Leukaemia
Polycythaemia

21

!
Causes of a palpable gall bladder
Obstruction of the cystic duct
o Stone in Hartmann's pouch
o Cholangiocarcinoma
Obstruction of the common bile duct
o Carcinoma of the head of the pancreas/periampullary carcinoma
Courvoisier's law
'If in the presence of jaundice the gallbladder is palpable, the obstruction
of the bile duct causing the jaundice is unlikely to be due to a stone.'
Stones causes a thickened non-distensible gall bladder; leading to
fibrosis (longstanding process)
Causes of splenomegaly
Infection
Bacterial - typhoid, typhus, TB
Viral - glandular fever
Protozoal - malaria, kala-azar

Congestion
Portal hypertension
Hepatic vein obstruction
Congestive heart failure

Cellular proliferation
Myeloid and lymphatic leukaemia
Pernicious anaemia
Polycythaemia rubra vera
Spherocytosis
Thrombocytopenia purpura
Myelosclerosis

Others

APPROACH TO ABDOMINAL MASSES

Causes of a renal mass

Hydronephrosis
Pyonephrosis
Perinephric abscess
Hypernephroma
Nephroblastoma
Solitary cyst
Polycystic disease
Causes of a right iliac fossa mass
Appendicitis
Tuberculosis
Carcinoma of the caecum
Crohn's disease
Iliac lymphadenopathy
Psoas abscess

Amyloidosis
Gaucher's disease
Felty's syndrome
Angioma
Lymphosarcoma

22

!
APPROACH TO ABDOMINAL PAIN
History
Pain

A/w

Frequency
Site and radiation
Onset
Character:
o Colicky obstruction of the bowel or ureters
o Sharp peritonitis
Aggravating and relieving factors:
o Relationship to meals, movement, defecation
o Patient lies perfectly still peritonitis
o Patient leans forward pancreatitis
Fever
GIT symptoms
o Bloating/distension
o Nausea/vomiting
Amount, colour, contents, presence of blood,
relationship to eating/pain
GI infections, small b/o, increased ICP
o Reflux
Acid brash, water brash, heartburn, hematemesis
Gastritis, PUD
o Bowel habits
Constipation/diarrhea ask about frequency, stool, what
kind of change
Bowel obstruction, biliary tract problems
o PR bleed
Melena/Hematochezia ask about colour of blood,
relationship to stool
Cancer, diverticulosis
LOW/LOA malignancy or depression
o If appetite increased: malabsorption of hypermetabolic state
Liver
o Jaundice, pruritus, sclera, variceal bleeding, pale stools, tea
coloured urine, hepatic encephalopathy
Urinary syndromes possible post-op pain related
o FUNDSHIP (frequency, urgency, nocturia, dribbling, poor stream,
hesitancy, incontinence, pis-en-deux) + ARU
o Hematuria

APPROACH TO ABDOMINAL PAIN

Tenderness localized to:

RHC
Epigastric region
Cholangitis
RHC pain, fever,
jaundice
+ shock, altered mental
Acute cholecystitis
Biliary colic, nausea,
vomiting, pain
(Murphy+)
Hepatitis
Jaundice
Liver abscess
Pyelonephritis
Fever, pain radiating to
back, nausea,
tenderness
I/O or perf colon

Peptic ulcer
Dull, burning pain
after/unrelated to meals,
relieved with antacids,
episodic. Radiation to back =
perforation
Pancreatic pain
Steady epigastric pain, may be
partially relived by sitting up
and leaning forwards.
Radiation of pain to back,
vomiting common.

LHC
Splenic pain
Infarct/aneurysm
(due to AF or emboli)
Atypical AMI
Perf colon
Pyelonephritis

Biliary colic (cystic duct)

Sharp, severe, constant pain
that lasts for hours. Hx of
episodes.
Colonic pain
Relieved by passing motion
Gastric cancer
Early satiety

Right flank

Left flank
Umbilical region

Renal colic
Severe, colicky pain,
constant pain in the
renal angle, radiation to
the groin.
Right iliac fossa
Appendicitis
Perf Cecum

Bowel obstruction
Colicky pain. Frequent (2-3
mins) small bowel, less
frequent (10-15 mins) large
bowel. Associated with
vomiting, constipation,
abdominal distension.
Pancreatitis
Appendicitis

Crohns
Terminal ileitis

Renal colic
Severe, colicky pain,
constant pain in the
renal angle, radiation
to the groin.
Left iliac fossa
Diverticulitis
(sigmoid)
PID, salpingitis

AAA Rupture
Radiates to back, shock,
hypotension

23

!
PMHx
Biliary/Liver disease
o Gallstones, biliary colic, jaundice, hepatitis, chronic liver disease
Pancreatic disease
o Assess risk factors (I GET SMASHED)
o Possible pancreatic pseudocyst formation from pancreatitis
Hematological disease
o Sickle cell anemia associated with biliary diseases due to
pigment gallstones
Autoimmune diseases - pancreatitis
Surgical/medical history
o Adhesion I/O
o Biliary strictures
Comorbidities
o HTN, Hypercholesterolemia, DM, strokes, cancers
Medications
Drug allergies
NSAIDS/Steroids ulcers
Nitrates reflux inducing
Antivirals, diuretics pancreatitis
TCM acute liver failure
Social history
Travel / eating
Food allergies
Smoking/alcohol
Family history
Cancer
GERD problems
Liver problems
Hereditary diseases

APPROACH TO ABDOMINAL PAIN

Investigations
Lab
o FBC, UECr, INR/PTT
o LFT / Amylases / Lipases
Imaging
o Ultrasound
o CTAP
o Endoscope
o CXR
Functional Disorders
Upper abdominal discomfort after meals, often associated with a sensation of
fullness, belching, nausea, early satiety or inability to finish a meal are typical
features of functional disease.
Irritable bowel syndrome due to spasm of the intestine and gives rise to upper or
lower generalized abdominal pain. There is usually associated constipation
and/or diarrhoea, and defecation may relieve the pain.
Structural disorders
Peptic ulcer disease usually gives rise to upper abdominal pains worse on
hunger, relieved by food and sometimes waking the patient up at night.
Stomach cancer can give rise to similar pains but usually of shorter duration and
associated with loss of appetite and weight.
Gallbladder give rise to very severe upper abdominal pain lasting up to several
hours, sometimes going to the back or right shoulder. There may also be
darkening of the skin and eyes (jaundice) or of the urine.
Renal colic is due to a stone passing down from the kidneys. It results in
excruciating pain lasting up to hours, usually in one loin but often going into the
lower abdomen and groin on the same side. The urine may turn dark due to the
presence of blood.
The acute abdomen
The pain of acute appendicitis is often generalized initially but becomes
concentrated in the right lower abdomen. This pain is constant and becomes
increasingly severe. It may get worse on touching the abdomen, on movement or
even on breathing or coughing. There may be vomiting and fever.
The pain from perforated ulcer is similar in character but occurs in the upper
abdomen.
In intestinal obstruction, there is generalized abdominal pain which comes in
waves (colic). The abdomen becomes distended and vomiting occurs. Stools and
flatus are not passed.

24

!
ACUTE APPENDICITIS

Acute abdominal pain is defined as previously undiagnosed pain of <72

hours duration

Causes of right iliac fossa mass

Appendix mass
Crohn's disease
Caecal carcinoma
Mucocele of the gallbladder
Psoas abscess
Pelvic kidney
Ovarian cyst

Causes of right iliac fossa pain

Appendicitis
Mesenteric adenitis
Urinary tract infection
Non-specific abdominal pain
Pelvic inflammatory disease
Renal colic
Ectopic pregnancy
Constipation

Etiology
Obstruction of appendiceal lumen
o Fecaliths: Calcium salts and fecal debris collect around nidus of
faecal material within appendix
o Lymphoid hyperplasia: a/w inflammatory and infective disease
Crohns/UC
GE, URTI
o Less common: TB, parasites, tumor
Increased intraluminal pressure
o Due to continued mucosal secretion and bacterial overgrowth
o Wall thins, lymphatic and venous obstruction occurs
Necrosis and perforation develops when arterial flow is compromised
The risk of perforation is:
o Less than 10 years old = 50%
o 10-50 years old = 10%
o Over 50 years old = 30%
Clinical features of appendicitis
Central abdominal pain moving to localized tenderness in right iliac fossa
o Right iliac fossa peritonism
o Percussion tenderness is a kinder sign of peritonism than rebound
o Rovsing's sign = pain in RIF on palpation of the LIF
Nausea, vomiting, anorexia (should precede pain in order to exclude i/o)
Associated with
o Low-grade pyrexia
o LOA
o +/- diarrhea or constipation
o +/- irritative voiding symptoms & hematuria (due to inflamed
appendix near bladder/ureter)
APPROACH TO THE ACUTE ABDOMEN

Physical examination
RIF (McBurneys point - 2/3 from umbilicus to ASIS) tenderness
Rebound tenderness, rigidity & guarding
May have palpable RIF mass (periappendiceal abscess or phlegmon)
May have LIF tenderness (situs inversus or lengthy appendix)
Cough sign: RIF pain on coughing (localized peritonitis)
Rovsing sign: RIF pain with palpation of LIF (peritoneal irritation)
Obturator sign: RIF pain with internal rotation of flexed right hip (pelvic)
Psoas sign: RIF pain with passive extension & active flexion of right hip
Infants/children may present with inflamed hemiscrotum
o Due to migration of pus through patent processus vaginalis
o Often mistaken for acute testicular torsion
Differential diagnoses
Gastrointestinal disease
Gastroenteritis
o Characterized by nausea and vomiting before onset of pain
o A/w malaise, high fever, diarrhea and poorly localized pain
o WBC count usually normal
Mesenteric lymphadenitis
o No rebound tenderness or muscular rigidity usually
o Self-limiting inflammation of mesenteric LNs in RIF
o A/w viral infections
Meckels diverticulitis
o Clinically indistinguishable, but usually in infants
o PUD, diverticulitis, cholecystitis
Urologic diseases
Pyelonephritis
o High fevers, rigors, costovertebral pain, tenderness
o Diagnose by urinalysis + culture
Ureteric colic
o Classical loin to groin pain, little localized tenderness, hematuria
o XR-KUB often shows stones
O&G
Pelvic inflammatory disease
o S/S may be indistinguishable
o Pain usually bilateral, may have vaginal discharge
o Do transvaginal US to visualize ovaries & tubo-ovarian abscesses
Ectopic pregnancy (do urine pregnancy test)
Ovarian cysts (do transvaginal/transabd US)
Ovarian torsion (sudden, acute intense pain with simultaneous frequent
and persistent vomiting)
25

!
Investigations
Appendicitis is essentially a clinical diagnosis
Predictors of appendicitis in patients with abdominal pain
o Raised inflammatory markers
o Clinical signs of peritoneal irritation
o Migration of abdominal pain
Bloods
FBC: Total white cell count (inflammation)
UECr
CRP (trends inflammatory process)
Blood c/s
Pre-op prep
o PT/PTT
o GXM
Urine
UFEME - may have pyuria (TRO UTI) and haematuria (TRO urolithiasis)
Pregnancy test (TRO ectopic pregnancy)
Imaging
Erect CXR
CTAP
o Distended, thick-walled appendix with inflammatory streaking of
surrounding fat, pericecal phlegmon or abscess
o Right lower quadrant free air indicates perforation
Ultrasound
o Useful in women of child-bearing age to exclude O&G causes;
may be helpful in the assessment of an appendix mass or
abscess

Management
NBM, IV fluids/analgesia/anti-emetics e.g. Maxolon, correct electrolyte
imbalances
Opiate analgesia does not mask the signs of peritonism
Active observation
o In cases of diagnostic doubt
o Active observation reduces negative appendicectomy rate
without increased risk of perforation
Conservative treatment for appendiceal mass/abscess
o When omentum wraps around inflamed appendix and contained
the inflammatory process
Inflammation localized to RIF, patient pyrexial with
palpable mass
o Symptomatic Rx + Abx + monitor patient and size of mass Do
surgery only when mass has reduced in size and patient is
stable (less inflammation = easier surgery)
o Give IV
o Fluids, analgesia and antibiotics
o Appendicular abscess suspected Incision & drainage
Definitive treatment: appendectomy
o IV roc/Flagyl
o Diagnostic laparoscopy should be considered particularly in
young women
o Open appendicectomy is usually performed via a Lanz incision
and muscle splitting approach

Alvarado scoring system

A score below 5 is strongly against a diagnosis of appendicitis,
while a score of 7 or more is strongly predictive
1. Migratory right iliac fossa pain
1 point
2. Anorexia
1 point
3. Nausea and vomiting
1 point
4. Right iliac fossa tenderness
2 points
5. Rebound tenderness
1 point
6. Fever
1 point
7. Leukocytosis
2 points
8. Shift to left (segmented neutrophils) 1 point

APPROACH TO THE ACUTE ABDOMEN

26

!
PERFORATED ULCER
Clinical features
Most occur in patients with pre-existing dyspepsia
10% have no previous symptoms
Classic presentation is with:
o Sudden onset epigastric pain
o Rapid generalization of pain
o Examination shows peritonitis with absent bowel sounds
10% have an associated episode of melaena
10% have no demonstrable gas on an erect chest x-ray
Water soluble contrast enema may confirm perforation
Management
Most patients require surgery after appropriate resuscitation
Conservative management may be considered if significant co-morbidity
More likely to fail if perforation is of a gastric ulcer
Preoperative preparation
Fluid resuscitation with CVP or Swan Ganz monitoring
Analgesia
Antibiotics
Nasogastric intubation
Operation
Oversew of ulcer
Oversew perforation with omental patch
o Use 2/0 synthetic absorbable.
o Take 1 cm bites either side of ulcer
Thorough wash out and irrigation of peritoneal cavity with 0.9% saline
All gastric ulcers require biopsy to exclude malignancy
Definitive ulcer surgery probably not required
50% patients develop no ulcer recurrence
Postoperatively patients should receive H. pylori eradication therapy
Outcome
Operative mortality depends on four major risk factors
o Long period from perforation to admission
o Increasing age
o Coexisting medical disease
o Hypovolaemia on admission
APPROACH TO THE ACUTE ABDOMEN

MESENTERIC ISCHEMIA

Occurs as result of either SMA or SMV occlusion

nd
Affects bowel from 2 part of duodenum to transverse colon
o 50% embolic arterial occlusion
o 25% atheromatous arterial occlusion
o 10% venous occlusion
o Whatever the underlining aetiology reduced capillary flow causes
intestinal necrosis
Overall mortality is approximately 90%

Clinical features
Severe central abdominal pain out of proportion to clinical signs
Vomiting and rectal bleeding may also occur
No single clinical feature provided conclusive evidence of the diagnosis
o As a result the diagnosis is difficult and often delayed
o Early diagnosis requires a high index of suspicion
May also be evidence of an embolic source (e.g., recent MI, arrhythmia)
o May also be other features of atherosclerotic disease
History of intestinal angina leading to food fear
chronic mesenteric ischemia
o 75% have ischaemic heart disease
Investigations
No single investigation provides pathognomic evidence
Raised WBC
ABG may show a metabolic acidosis
Serum amylase is raised in 50% of patients
Abdominal x-ray may be normal early in the disease process
o Late features include dilated small bowel and 'thumb printing'
due to mucosal oedema
Mesenteric angiography may confirm the diagnosis
Management
Papaverine infusion into the SMA may be beneficial
Laparotomy allows:
o Confirmation of diagnosis and assessment of extent of ischaemia
o Opportunity to revascularize SMA
o Resect necrotic small intestine
Revascularization may be achieved by embolectomy, graft/bypass or
endarterectomy
Resection and primary anastomosis may be possible
27

!
APPROACH TO INTESTINAL OBSTRUCTION
Causes
Intraluminal
Mechanical

Functional

Foreign body
Bezoar
Mural
Strictures 2 to:
Divert, Crohns, RT
Extraluminal
Volvulus
LN compression
SMA syndrome
Paralytic ileus (post-op, inflammatory, ischemic, metabolic,
hypothyroid/opiate induced)
Hirschsprungs disease (absent ganglia in Auerbachs plexus)
Ogilvie syndrome (in severely ill patients)

Types
Small Bowel I/O
Adhesions
Herniae

Ileocecal tumor
Intussusception

Impacted stool
Gallstone ileus
Tumors
Intussusception
Adhesions
Hernia

Large Bowel I/O

Cancer
Post-divert strictures

Sigmoid
volvulus

History
4 cardinal symptoms
o Pain (Usually colicky - 4-5 days duration)
Complete obstruction: constant sharp pain
Volvulus: acute onset severe pain
o Vomiting
Ask if projectile; Color - bilious/feculent
o Abdominal distention
o Constipation (vs normal frequency)
Ask if obstipated - no flatus even! (severe)
Other pertinent history
o Previous surgeries
o Underlying or previous GIT disorders
Previous Ca, IBD
o Symptoms of GI bleed - melena/frank PR bleed
o Symptoms of GI infection
o Recent change in bowel habits - frequency, tenesmus, stool
calibre
o Suspicion of malignancy - LOW/LOA
o Family history of cancer
o Risk factors for ischaemic bowel - atherosclerosis, heart disease,
previous CVA
ABDOMINAL EMERGENCIES

Physical Exam
Vitals
General inspection
o Hemodynamic stability - HR, BP
o Cachexia
o Febrile?
o Confusion/AMS
o Toxic-looking/sepsis
o Abdo distention
Abdomen
o Distention
o Scars - previous surgery
o Visible peristalsis -- severe obstruction
o Signs of peritonitis - guarding, rebound tenderness vs SNT abdo
o Masses, herniae
o Bowel sounds
Initially hyperactive (peristalsis trying to pass obstruction),
later sluggish or absent
Tinkling BS = SBIO
o Succussion splash + epigastric tenderness = gastric outlet
obstruction
DRE - look for stools felt, masses
Acute management
Resuscitate if necessary
o Monitor vitals - IDC to monitor urine O/P
NBM (bowel rest) + IV drip (correct dehydration)
NG tube on constant suction
Correct electrolyte imbalances, replace K+
Start broad-spectrum Abx (as IO affects normal translocation of bacterial
flora)
Rule out any surgical emergencies (history/PE/inx)
o Obstructed hernia
o Volvulus (sigmoidal, caecal, gastric)
o Closed loop obstruction
o Ischemic bowel with necrosis (impending perf)
o Perforation/peritonitis -- do erect CXR to look for free gas

28

!
Investigations
Bloods
FBC
o TW for infx
o Hb for anemia
UECr
rd
o Dehydration 2/2 vomiting or intra-luminal 3 space loss
(damaged enterocytes unable to reabsorb)
ABG
o Acidosis from bowel ischaemia
o Alkalosis due to vomiting (esp for GOO/pyloric stenosis)
Pre-op
o PT/PTT; GXM - 4 pints of blood
o ECG & cardiac enzymes
Imaging
Erect CXR - look for free gas under diaphragm, any aspiration pneumonia
AXR
o Riglers sign (obvious bowel wall due to extraluminal air)
o Erect to look for air-fluid levels (>6 is significant)
o Supine
Look for bowel dilation on radiograph (>3cm sig for small
bowel, >5 for large bowel)
Jejunum & proximal ileum - centrally located, stack of
coins appearance
Distal ileum - lead pipe appearance
Colon - incomplete bands/haustrations
o Sigmoid volvulus - coffee bean + parrots beak sign
o Closed loop obstruction - distal lesion with very distended
caecum (thinnest wall, most prone to distention up to 12cm);
ileum not dilated
o Bowel ischaemia +/- necrosis -- gas in bowel wall
(pneumatosis intestinalis) due to gas gangrene
o Rectal gas absent may mean complete obstruction
(may require KUB to see)
Barium enema
o Gastrografin preferred if risk of perf (avoid barium peritonitis)
Colonoscopy contraindicated (risk of perf)
CT colonography

ABDOMINAL EMERGENCIES

Definitive management is cause-dependent

Obstructed hernia -- herniorrhaphy
Sigmoid volvulus
o Ryles tube decompression
o Flexible sigmoidoscopic decompression with sigmoid colectomy
and formation of double-barrel colostomy with secondary
reanastomosis
Closed loop obstruction (if due to distal tumor)
o Resect bowel + primary anastomosis with proximal defunctioning
(loop) colostomy
o Hartmanns procedure (sigmoid resection with end colostomy +
rectal stump w 2ndary anastomosis) if bowel too
inflamed/edematous to anastomose (high risk of leak)
Ischaemic bowel (at watershed areas e.g. splenic flexure, rectosigmoidal jx)
o Ischaemia alone can cause paralytic ileus
o Supportive mgt - NBM, drip & suck, abx while waiting for
collaterals to re-supply bowel and for peristalsis to begin
o Surgical intervention indicated if bowel is non-viable i.e.
Necrosis/gangrene
nd
Requires 2 laparotomy after initial resection 2-3/7 later to
ensure bowel margins are clear (no gangrenous gut left)
o Perforation (usually at thin-walled caecum)
Usually occurs due to ischaemic of distended bowel (>12cm)
Emergency laparotomy: resect lesion and perforated
bowel with generous peritoneal lavage
Type of resection - hemi-colectomy vs total colectomy
dependent on site of lesion
Continue abx after surgery (dirty surgery)
o Intussusception
Children - usually due to hypertrophic Peyers patches
Rx = administer barium enema and watch
intussusception reduce on fluoroscopy
Elderly - usually due to polyp or Ca (barium enema
unlikely to work/high recurrence)
Rx - surgical is first-line
o Post-op paralytic ileus (>3 days post-op)
Drip and suck, wait for peristalsis to restart
Oral Gastrografin: hyperosmotic - causes intraluminal
osmosis, can re-establish peristalsis
Other prokinetic agents - erythromycin, metoclopramide
(Maxolon), cisapride

29

!
SMALL BOWEL OBSTRUCTION
Mechanical obstruction
Aetiology
Small bowel obstruction accounts for 5% of acute surgical admissions
Adhesions (60%), Strangulated hernia (20%), Malignancy (5%), Volvulus
(5%)
Pathophysiology
Proximal dilatation occurs above obstructing lesion
Results in the accumulation of gas and fluid and reduced reabsorption
Dilation of the gut wall produced mucosal oedema
This impairs venous and then arterial blood flow
o Intestinal ischaemia eventually results in infarction and
perforation of that segment of bowel
o Ischaemia also results in bacterial and endotoxin translocation
o The overall effect is progressive dehydration, electrolyte
imbalance and systemic toxicity
Clinical feature
Colicky central abdominal pain
Vomiting - early in high obstruction
Abdominal distension - extent depends on level of obstruction
Absolute constipation - late feature of small bowel obstruction
Dehydration associated with tachycardia, hypotension and oliguria
Features of peritonism indicate strangulation or perforation
Investigation
Supine abdominal X-ray shows dilated small bowel
Valvulae conniventes (plicae circulares) stack of coins
Erect abdominal film rarely provided additional information
Management
Resuscitation prior to surgery
o May require more than 5 litres of intravenous crystalloid
o Adequacy of resuscitation should be judged by urine output or
central venous pressure
o Surgery in under resuscitated patient is associated with
increased mortality
o Exact procedure will depend on underlying cause

ABDOMINAL EMERGENCIES

Indications for surgery

If features of peritonism or systemic toxicity present, need to consider
early operation
o Absolute
o Relative
Generalized peritonitis
Palpable mass lesion
Localised peritonitis
'Virgin' abdomen
Visceral perforation
Failure to improve
Irreducible hernia
If obstruction presumed to be due to adhesions and there are no features
of peritonism
o Conservative management for up to 48 hours is often safe
o Requires regular clinical review
Incomplete obstruction
Previous surgery (intestinal obstruction)
Advanced malignancy
Paralytic ileus
Functional obstruction most commonly seen after abdominal surgery
Also associated with trauma, intestinal ischaemia, sepsis
Absorption of fluid, electrolytes and nutrients is impaired
Significant amounts of fluid may be lost from the extracellular cmpt
Clinical features
Usually history of recent operation or trauma
Abdominal distension is often apparent; usually no pain
If no nasogastric tube in-situ vomiting may occur
Flatus will not be passed until resolution of the ileus
Auscultation will reveal absence of bowel sounds
Investigation
Plain abdominal x-ray may show dilated loops of small bowel
Gas may be present in the colon
Water soluble contrast study to distinguish mechanical or functional
Management
Bowel should be handled as little as possible
Fluid and electrolyte derangements should be corrected
Sources of sepsis should be eradicated
Nasogastric tube
No drugs are available to reverse the condition
Usually resolves spontaneously after 4 or 5 days

30

!
LARGE BOWEL OBSTRUCTION

15% colorectal cancers present with obstruction

Most patients are over 70 years old
Risk of obstruction greatest with left sided lesions
Usually present at a more advanced stage
25% have distant metastases at presentation
Perforation can occur at site of tumour or in a dilated caecum

Clinical presentation
Caecal tumours present with small
bowel obstruction
o Colicky central abdo pain
o Early vomiting
o Late absolute constipation
o Variable extent of distension

Left sided tumours present

with large bowel obstruction
o Change in bowel habit
o Absolute constipation
o Abdominal distension
o Late vomiting

Investigation
Plain supine abdominal x-ray will show dilated large bowel (Haustrations)
Small bowel may be dilated depending on competence of ileocaecal valve
If doubt over diagnosis or site of obstruction consider a water soluble
contrast enema
Colonoscopy; CT Colonography
Management
All patients require
At operation
o Adequate resuscitation
o Full laparotomy should be
o Prophylactic antibiotics
performed
o Consenting and marking
o Liver should be palpated for
for potential stoma
metastases
formation
o Colon should be inspected
for synchronous tumours
Appropriate operations include:
o Right sided lesions right hemicolectomy
o Transverse colonic lesion extended right hemicolectomy
o Left sided lesions various options
Three-staged procedure
Defunctioning colostomy
Resection and anastomosis
Closure of colostomy

ABDOMINAL EMERGENCIES

Two-staged procedure
Hartmanns procedure
Closure of colostomy

One-stage procedure
Resection, on-table lavage and primary anastomosis
Three stage procedure will involve 3 operations!
Associated with prolonged total hospital stay
Transverse loop colostomy can be difficult to manage
With two-staged procedure only 60% of stomas are ever reversed
With one-stage procedure stoma is avoided
Anastomotic leak rate of less than 4% have been reported
Irrespective of option total perioperative mortality is about 10%
Sigmoid Volvulus
Volvulus = rotation of the gut on its own mesenteric axis
o Produces partial or complete intestinal obstruction
o Blood supply compromised resulting in intestinal ischaemia
o Venous congestion leading to infarction can occur
o Arterial supply rarely compromised
o Long narrow based mesentery predisposes to volvulus
Clinical features
Large bowel obstruction pain, constipation and vomiting
Disproportionate abdominal distension
50% patients have had a previous episode
Severe pain and tenderness suggests ischaemia
Plain abdominal x-ray may show a large bean shaped loop of large
bowel arising from pelvis
If diagnostic doubt consider a water soluble contrast enema
Will demonstrate site of obstruction
Management
Resuscitation with intravenous fluids is essential
Conservative management can be attempted if no clinical features of
ischaemia
o Sigmoidoscopy can be both diagnostic and therapeutic
o Flatus tube can be inserted and left for 2-3 days
o 80% of patients will settle with conservative management
o If decompression occurs no emergency treatment required
50% further episode of volvulus within 2 years
If decompression fails or features of peritonitis
o Sigmoid colectomy and primary anastomosis
o Hartmanns procedure
o Paul Mikulicz Colostomy

31

!
APPROACH TO BLEEDING GIT
History
Nature
of bleed

Amount
Etiology
clues

Complx

Comorb

Upper
Lower
Hematemesis
Hematochezia
- fresh red (variceal, AV malform) - mixed with or coating stool
- coffee grounds (ulcer, gastritis) - torrential/drops, any clots
Melaena
- bright/dark red
- above ligament of Treitz
- mucous
- fresh (jet black with sheen,
- relation to defecation
tarry, liquid consistency) vs
stale (black grey, dull, mixed w
normal stool, particulate) vs iron
(greenish hue)
st
1 Episode?
Measurement cup/bowl?
Frequency?
Ulcer/gastritis/erosions
TRO UBGIT
- Hx dyspepsia, ulcer (past
- Melaena, hematemesis, coffee
OGD)
grounds vomitus
- Drugs (NSAIDs, steroids,
- Hx of PUD, gastritis, varices, Ca
antiplatelets, anticoags)
stomach
Varices
Bleeding divert/angiodysplasia
- Hx of CLD
- Torrential, stops spontaneously
Mallory-Weiss tear
- Altered clots
- Binge drinking w severe
CRC
retching
- constitutional symptoms
Malignancy
- change in bowel habits, tenesmus
- LOW, LOA, malaise
- occult bleed from anemia
- Early satiety
- fam Hx
- Dyspepsia
Colitis
- Infective: fever/chills/rigors/n/v/
pain/travel/food etc
- Inflammatory: UC/Crohns
Hemorrhoids
- blood coating stools, pain
- Hx of constipation, hard stools,
chronic straining, low fibre
Coagulopathy
Anemia
- Postural giddiness, SOB, lethargy, effort tolerance, palpitations, CP
Dehydration & shock
- Thirst, confusion, pallor, urine output
Elderly, CLD, renal disease, IHD

ABDOMINAL EMERGENCIES

Associated symptoms
Fever
GIT symptoms
o Abdominal bloating/distension
o Nausea/vomiting
Amount, colour, contents, presence of blood,
relationship to eating/pain
GI infections, small b/o
o Reflux
Acid brash, water brash, heartburn, hematemesis
Gastritis, PUD
o Bowel habits
Constipation/diarrhea ask about frequency, stool, what
kind of change
Bowel obstruction
o PR bleed
Melena/Hematochezia ask about colour of blood,
relationship to stool
CRC, diverticulosis
LOW/LOA malignancy or depression
o If appetite increased: malabsorption of hypermetabolic state
Liver
o Jaundice, pruritus, sclera, variceal bleeding, pale stools, tea
coloured urine, hepatic encephalopathy
o CLD
Urinary syndromes possible post-op pain related
o FUNDSHIP (frequency, urgency, nocturia, dribbling, poor stream,
hesitancy, incontinence, pis-a-deux) + ARU
o Hematuria
Fam + Personal Hx
IBD, IBS, CRC
Cancer
GERD problems
Liver problems
Hereditary diseases
Comorbidities DM

Social Hx
Alcohol excess diarrhea and
pancreatitis
Smoking Crohns, CRC
HIV risk factors
immunocompromised host
Contact history similar
symptoms

Drug Hx
Medications as above
Drug allergies

32

!
Physical Examination
Vitals
o BP & postural BP, HR
o Conscious level/confusion - GCS
General inspection
o Pallor, cold, clammy peripheries
o Cachetic? Jaundice?
o Stigmata of CLD
Abdomen
o Any tenderness, mass
o Hepatosplenomegaly, ascites -- CLD
o DRE - melaena (fresh vs stale) or frank blood
Investigations
Vitals assess state of shock, conscious level
FBC, UECr, INR/PTT
LFT
GXM

ABDOMINAL EMERGENCIES

Management
Resuscitation
o Airway (intubate nasal prongs), Breathing (oxygen), Circulation
(ECG)
o 2 large-bore IV cannula in antecubital fossa
o Take blood for investigations - FBC, UECr, LFT, PT/PTT, GXM
(4 pints)
IV fluids/crystalloids - 1 pint N/S over 1/2 - 1hr if patient
is in shock
May follow with more if req
Beware fluid overload in patients with renal/heart failure
Correct any coagulopathy - if patient is on
Antiplatelets e.g. aspirin - consider platelet replacement
Anti-coagulants e.g. warfarin / PT/PTT prolonged consider FFP +/- Vit K
Adjunct
o NG tube if hematemesis (therapeutic and diagnostic)
contraindicated if variceal bleed suspected
o Catheterization i/o monitoring
o IV omeprazole (80mg bolus)
o IV somatostatin/octreotide, IV abx, Vit K for Varices
Monitor
o HR, BP, Urine output, mental status
Emergency OGD/Colonoscopy
o Indications:
Persistent shock after resuscitation
Ongoing BGIT
Suspected variceal bleed
o Role:
Diagnostic: Identify source of bleeding
Therapeutic: Injection of ulcer, ligation/sclerotherapy,
cauterization
Laparotomy and on-table lavage + angiogram in crazy LBGIT

33

!
UPPER BGIT
Causes
Peptic ulcer (50%)
Gastric erosions
Oesophageal or gastric varices

LOWER BGIT

Mallory-Weiss tear
Angiodysplasia
Dieulafoy malformation
Gastric neoplasia

Management
Aggressive fluid resuscitation is important
o Circulating blood volume restored with crystalloid
o Cross-matched blood should be given when available
All patients require closed monitoring in an HDU or ITU environment with
central and arterial pressure monitoring
Proton-pump inhibitors
Bleeding peptic ulcer
80% bleeding stops spontaneously
25% require intervention for recurrent bleeding within 48 hours
Duodenal ulcer bleeding usually from gastroduodenal artery
o Close gastroduodenotomy as a pyloroplasty
o Consider truncal vagotomy and pyloroplasty
o All patients should be given H. pylori eradication therapy post op
o If a pyloroplasty will be difficult because of large ulcer consider
Poly-a gastrectomy
Gastric ulcer consider local resection or partial gastrectomy
All patients require early endoscopy ( intervention) to determine:
Site of bleeding
Features of recent bleed
o Ooze from ulcer base
Continued
o Clot covering ulcer base
bleeding
o Black spot in ulcer base
o Visible vessel
Endoscopic therapy
Laser photocoagulation using the Nd-YAG laser
Bipolar diathermy; Heat probes
Adrenaline or sclerosant injection
Indications for surgery
Continued bleeding that fails to respond to endoscopic measures
Recurrent bleeding / gastric ulcer bleed
Patients > 60 years
Cardiovascular disease with predictive poor response to hypotension
ABDOMINAL EMERGENCIES

Accounts for 20% cases of acute gastrointestinal haemorrhage

Most cases settle spontaneously without the need for emergency surgery

Causes
Diverticular disease
Angiodysplasia
Inflammatory bowel disease

Ischaemic colitis
Infective colitis
Colorectal carcinoma

Angiodysplasia
Acquired malformation of intestinal blood vessels
o 80% lesions occur in the right side of the colon
o Often associated with cardiac valvular disease
Dilated vessels or 'cherry red' areas may be seen at colonoscopy
Bleeding may be visible during capillary phase of angiogram
Investigation
Most patients are stable and can be investigated once bleeding stops
In the actively bleeding patient consider:
o Colonoscopy
Rate of bleeding for detection
o Sigmoidoscopy
Investigation
Rate of bleed
o OGD TRO varices
Radiolabel red cell scan
0.1 ml/min
o Emergency exploratory
Mesenteric angiography
1.0 ml/min
laparotomy
Non-selective
aortic
angiography
6.0 ml/min
o Selective mesenteric
Colonoscopy
Any
angiography
Intraoperative endoscopy
Any
(can be on table)
o Radionuclide scanning
Uses technetium-99m labeled red blood cells
Management
Acute bleeding tends to be self-limiting
Consider selective mesenteric embolization if life threatening
haemorrhage
If bleeding persists perform endoscopy to exclude upper GI cause
Proceed to laparotomy, consider on-table lavage and panendoscopy
o If right-sided angiodysplasia perform a right hemicolectomy
o If bleeding diverticular disease perform a sigmoid colectomy
o If source of colonic bleeding unclear perform a subtotal
colectomy and end-ileostomy

34

!
VARICEAL BLEED

Suspect variceal UBGIT in patients with history of variceal bleed, chronic

alcohol intake, jaundice or stigmata of CLD

Primary prevention
Bleeding from varices more likely if poor
hepatic function or large varices
Primary prevention of bleeding is
possible with blockers like propanolol
o Prevents varices formation
o Reduces risk of bleed by 40-50%
Band ligation may also be considered
Predictors of hemorrhage:
o Site: varices at gastroesophageal
jx have thinnest coat of tissue
- highest risk of rupture & bleed
o Size (fraction of lumen occupied
and shape of varices)
o Childs score
o ESRH; Previous bleed

Secondary prevention
70% patients will have a rebleed; 30% in first 6wks
Ablation regimen
o Endoscopy with initial
ligation/sclerotherapy
o Subsequent endoscopic
monitoring and repeated
ligation/sclerotherapy as
required to completely
ablate varices
If patient bleeds again and
ablation fails
TIPSS; Surgical shunt
*The mortality of a variceal bleed is
approximately 50%

Active bleeding
Resuscitation should be as for other causes of upper GI haemorrhage
o Airway - endotracheal intubation to protect airway, prevent
aspiration, facilitate OGD
o Breathing - supplemental oxygen
o Circulation - 2 large-bore IV cannula in proximal veins
Infuse crystalloids while awaiting bloods - N/S
Assess: Vitals, hydration status, Mental state
Investigations: Blood tests - GXM 4 pints, FBC, UECr, LFT, PT/PTT
IV regimen
o IV somatostatin/octreotide
Acts as splanchnic vasoconstrictor decreases portal
flow & portal pressures (not given in ulcer bleed)
Also inhibits secretion of gut hormones that portal flow
o IV omeprazole - acid suppression
in intragastric pH clot stability, aids hemostasis
Decrease formation of stress ulcers
o IV antibiotics (Roc/flag)
Infection a strong prognostic indicator in acute variceal bleed
Abx reduces risk of rebleed & mortality
Lactulose may be used to decrease GI transit & ammonia absorption
ABDOMINAL EMERGENCIES

Endoscopy should be performed to confirm site of haemorrhage

o To confirm diagnosis and institute management
o Needs to be done emergently, as soon as patient is stabilized
o Note: half of pts with known esophageal varices have upper GI
bleed from an alternative source - need to do thorough
endoscopy
o Emergency endoscopic therapy includes:
Endoscopic banding of varices (best)
Intravariceal or paravariceal sclerotherapy (higher
morbidity)
Only for large gastric varices
Temporary tamponade with Sengstaken-Blackmore tube for 12 hrs
(repeat endoscopy after)
o Should be considered as a salvage procedure if first endoscopy
fails; always protect airway first
o Inflate gastric balloon and pull upwards against CE jx - balloon
will compress perforator veins entering esophagus from stomach,
decreasing esophageal variceal bleed
o Tamponade is 90% successful at stopping haemorrhage
o Unfortunately 50% patients rebleed within 24 hours of removal of
tamponade
o A Sengstaken-Blackmore tube has three channels
Inflation of gastric balloon, inflation of oesophageal
balloon, aspiration the stomach
If endoscopic methods fail need to consider:
o Transection or devascularization
o Porto-caval or mesenterico-caval shunting
Emergency shunting associated with 20% operative
mortality and 50% encephalopathy
Transjugular intrahepatic porto-systemic shunting
(TIPSS)
Radiologically-guided
Stent between branches of hepatic and portal
venous circulation
In patient with good Childs score (A is best; its for
CLD/cirrhosis) only to avoid ppt encephalopathy
Reduces risk of rebleeding but increases risk of
encephalopathy
Mortality of the procedure ~1%
Surgery portacaval/mesocaval/splenorenal shunt
Sugiura procedure

35

!
GROIN HERNIA
A hernia is a protrusion of an organ through the wall that normally
contains it
The two main aetiological factors for acquired hernias are
o Increased intra-abdominal pressure (e.g. straining or lifting)
o Abdominal weakness (e.g. advancing age or malnutrition)
A hernia consists of:
o A sac, its coverings, its contents
Hernias can be:
o Reducible
o Irreducible
Narrow neck or adherent contents to sac wall
o Obstructed or incarcerated
Obstructed but viable intestine
o Strangulated
Venous drainage from sac contents compromised
Clinical features
The hernia often increases in size on coughing or straining
It reduces in size or disappears when relaxed or supine
Examination may show it to have a cough impulse and to be reducible
o Irreducible but non-obstructed hernias may cause little pain
o If the hernia causes obstruction colicky abdominal pain,
distension and vomiting may occur
The hernia will be tense tender and irreducible
o If strangulation occurs the lump will become red and tender
Diagnosis is usually based on clinical features

Mortality of strangulated hernia repair

The peak incidence of hernia strangulation is approximately 80 years
In those with acute onset of a hernia the greatest risk is in the first 3
months
Risk of strangulation depends on type of hernia
o Femoral is approximately 40%
o Direct inguinal is approximately 3%
Operative mortality remains at approximately 10%
o Is ten times greater than that following an elective repair
Risk of death is dependent on:
o Age and presence of necrotic bowel requiring resection

ABDOMINAL HERNIA

Femoral hernias
Account for 7% of all abdominal wall hernia
Female : male ratio is 4:1
Commonest in middle aged and elderly women
Much less common than inguinal hernias but are as common as inguinal
hernias in older women
Anatomy of the femoral canal
Anterior border is the inguinal ligament
Posterior border is the pectineal ligament
Medial border is the lacunar ligament
Lateral border is the femoral vein

Management of femoral hernia

All uncomplicated femoral hernias should be repaired as an urgent
elective procedure
Three classical approaches to the femoral canal have been described
o Low (Lockwood)
o Transinguinal (Lotheissen)
o High (McEvedy)
Irrespective of approach used the following will be achieved
o Dissection of the sac
o Reduction / inspection of the contents
o Ligation of the sac
o Approximation of the inguinal and pectineal ligaments
36

!
Inguinal hernias
Male : female ratio is 12:1
Elective : emergency operation 12:1
Peak incidence is in the 6th decade
65% inguinal hernias are indirect
In females inguinal hernias are as common as femoral hernias
Anatomy
Inguinal canal lies between the superficial and deep inguinal rings
o Deep ring lies deep to the mid-inguinal point
In men it contains vas deferens & testicular artery & veins
In women it contains the round ligament
o Anterior border is the external oblique aponeurosis
o Posterior border is the transversalis fascia
o Inferior border is the inguinal ligament
o Superior border is the conjoint tendon - the lower fibres of
internal oblique and transversus abdominis
Indirect hernias arise lateral to the inferior epigastric vessels
o Bulges directly ant though a weakened fascia: Hesselbachs
triangle, post to the inguinal canal
o Hesselbachs : inf. Epigastric art., rectus abd, inguinal ligament
Direct hernias arise medial to the inferior epigastric vessels
Classification of inguinal hernias (Nyhus)
Type 1 Indirect hernia with normal internal ring
Type 2 Indirect hernia with dilated internal ring. Posterior wall intact
Type 3 Posterior wall defect
A: Direct inguinal hernia
C: Femoral hernia
B: Indirect inguinal hernia, internal ring dilated
Type 4 Recurrent hernia
Indirect Hernia
Neck lies lateral to inferior epigastric
artery, out of Hesselbachs triangle

Direct Hernia
Neck lies medial to inferior epigastric
artery, within Hesselbachs triangle

Reduces upwards, laterally & backwards Reduces upwards & straight backwards
Controlled after reduction by pressure
over the deep ring
May descend down the scrotum

Controlled after reduction by pressure

over the superficial ring
Does not descend down the scrotum

Narrow; strangulation at superficial ring

Rarely causes strangulation

Does not readily reduce on lying down

More common in young adults & infants

Readily reduces on lying down

More common in old men

ABDOMINAL HERNIA

Techniques of inguinal hernia repair

Herniotomy involves removal of the sac and closure of the neck
Herniorrhaphy involves a form of reconstruction to
o Restore the disturbed anatomy
o Increase the strength of the abdominal wall
o Construct a barrier to recurrence
Shouldice or Liechtenstein now regarded as 'gold standard'
Laparoscopic hernia repair should be reserved for bilateral or recurrent
hernia
Complications of hernia repairs
Urinary retention
Scrotal haematoma
Damage to the ileoinguinal nerve
Ischaemic orchitis
Recurrent hernia
Recurrent inguinal hernia
Recurrence rate varies with herniorrhaphy technique and duration of
follow up
Factor involved in recurrence include:
o Inadequate preoperative selection
o Type of hernia
o Type of operation
o Postoperative wound infection
Recurrent hernias should be repaired using a mesh technique
Can be performed as either an open or a laparoscopic procedure
Patients should be consented for a possible orchidectomy
Differentials of inguinal and femoral hernias
Inguinal hernia
Femoral hernia
Femoral hernia
Inguinal hernia
Vaginal hydrocele
Lymphadenopathy
Hydrocele of the cord Saphena varix
Undescended testis
Ectopic testis
Lipoma of the cord
Psoas abscess
Psoas bursa
Lipoma

37

!
Umbilical hernias
Two types of umbilical hernia occur in adults
True umbilical hernias are rare
o Occur with abdominal distension (e.g. ascites)
Para-umbilical hernias are more common
o Occurs through the superior aspect of the umbilical scar
Female : male ratio is 5:1
Usually contain omentum
Neck is often tight and the hernias are often irreducible
Differential diagnosis
Cyst of the vitello-intestinal duct
Urachal cyst
Metastatic tumour deposit (Sister Joseph's nodule)
Management
Management of true and para-umbilical hernias is similar
Surgery is usually performed through a infra-umbilical incision
Occasionally the umbilicus needs to be excised
Contents of the hernia are reduced
Defect in linea alba can be repaired with:
o An overlapping Mayo repair
o A mesh repair
Epigastric hernia
Arises through a congenital weakness if the linea alba
Hernia usually consists of extra-peritoneal fat from near to falciform
ligament
Male : female ratio is 3:1
Strangulation is rare
Can be repaired with either sutures or a mesh
Spigelian hernia
Occurs at the lateral edge of the rectus sheath
Interparietal hernia in the line of the linea semilunaris
Usually occurs at the level of the arcuate line
Obturator hernia
Occurs in the obturator canal
Usually asymptomatic until strangulation occurs
May complain of pain on the medial aspect of the thigh
Vaginal examination may allow identification of a lump in the region of
the obturator foramen
ABDOMINAL HERNIA

Incisional hernia
Occurs through the scar from a previous operation
1% of all transparietal abdominal incisions result in a hernia
Account for 10% of all abdominal wall hernias
Partial dehiscence of all deep fascial layers occurs
Skin remains intact
Most develop within a year of surgery
Symptoms are often minimal with cosmetic appearance the main concern
Most are wide necked but strangulation can occur
Aetiological factors
Preoperative
o Increasing age
o Malnutrition
o Sepsis
o Uraemia
o Jaundice
o Obesity
o Diabetes
o Steroids

Operative
o Type of incision
o Technique and materials used
o Type of operations
o Use of abdominal drains
Postoperative
o Wound infection
o Abdominal distension
o Chest infection or cough

Management
CT or ultrasound may clarify muscular defect and hernial sac content
The elderly or infirm may be helped by an abdominal wall support
If surgery is required the following should be considered
o Fascial closure or mayo-type repair using sutures
o A 'keel repair' using sutures
o A mesh repair using polypropylene or PTFE
o Mesh can be placed as a sublay, onlay or inlay
The results with mesh are superior to suture repairs
o Composite meshes may offer reduced risk of complications
o A sublay mesh repair may have the lowest recurrence rate
Special types of hernia
Richter's hernia
o Partial enterocele
o presents with strangulation and obstruction
Maydl's hernia
o W loop strangulation
o Strangulated bowel within abdominal cavity
Littre's hernia
o Strangulated Meckel's diverticulum
o Can cause small bowel fistula
38

!
GROIN LUMPS
Hydrocele

Epididymal Cyst

Points from examination:

Very swollen scrotum; uniformly enlarged
Cannot define testis well; no separable from testis
Maybe firm, tense or lax
Maybe transilluminable if acute (less in chronic hydrocele)
Can get above the mass; the superficial ring is distinct

Points from examination:

Small mass separate from testis; can get above it
Firm; maybe loculated; transilluminable if large cyst
Often multiple in the head of epididymis
May occur as a complication of vasectomy (spermatoceles)

Definition of hydrocele:
Excess accumulation of fluid in processus vaginalis (fold of peritoneum
as testis descends; usually patent for fluid to accumulate)
o

Types of 1 hydrocele:
Vaginal hydrocele:
o Only in tunica vaginalis & does not extend into the cord
Hydrocele of the cord
o Mass around the cord; attached distally to the testis
o Difficult to distinguish from irreducible inguinoscrotal hernia
o May extend up and beyond
Congenital hydrocele: patent processus vaginalis filled with peritoneal
fluid
Infantile hydrocele: hydrocele of cord and congenital hydrocele
o

Types of 2 hydrocele
From testicular tumours
From torsion
From trauma
From orchitis (any inflm)
Treatment options:
Conservative:
o Watch & wait or Aspiration [tend to reaccumulate]
o
o Must exclude a 2 cause
Surgical:
o Lords plication of the sac
o Jaboulays operation to evert the sac

OTHER GROIN LUMPS

Treatment:
Conservative [mainstay]
Surgical: if painful, very large or frequent recurrences. Complicated by
operative damage and fibrosis of epididymis subfertility
Varicocele
Points from examination:
Best noticed on palpating the standing patient
Mass is separate from testis; can get above it
Feels like a bag of worms; +ve cough impulse
Not transilluminable
Definition:
Dilated, tortuous pampiniform plexus
98% on Left side: left vein is more vertical, connects to left renal vein,
longer than right one, often lacks a terminal valve
Causes:
Idiopathic in younger males around puberty
In older men with retroperitoneal disease: RCC
Treatment options:
Conservative: risk of infertility
Surgical:
o Transfemoral radiological embolization with coil or sclerosant
o Excise the surrounding veins via high retroperitoneum, inguinal
or laparoscopic approach

39

!
Testicular Torsion (Surgical emergency)
Testicular Tumor
Points from examination:
Inseparable from the testis; can get above i
Hard, nodular, irregular, non-tender
Not transilluminable (but maybe a/w hydrocele)
DDx:

Chronic infection with scarring

Long standing hydrocele with calcification,

Classification:
Mostly seminomas or teratomas
o Seminomas: 30-40YO, normal tumour markers, Rx with RT to
paraaortic nodes and CT according to staging
o Teratomas: 20-30YO, AFP/ BHCG raised in 90%, Rx with CT
Others: embryonal carcinoma, choriocarcinoma, yolk sac tumour, Leydig
cell tumours (10% malignant ; a/w gynaecomastia), Sertoli cell tumour
(a/w gynaecomastia), Lymphoma (look for lymphoma elsewhere; poor
prognosis)
Treatment:
Staging, excision of whole testis with combination chemotherapy

OTHER GROIN LUMPS

Clinical features:
Children/ teenagers
acute abdomen (T10 innervation) & acute scrotum a/w vomiting
swollen and tender scrotum, testis is high in scrotum; pain worsen by
lifting testis up
Previous attacks of self-limiting pain; ppt by trauma, cycling, straining,
coitus
DDx:

Epididymitis
Torsion of testicular appendage (pea coloured lump through scrotum)
Strangulated inguinoscrotal hernia

Cause:
Maldescended testis hanging like a bell clapper within tunica vaginalis
Treatment:
Emergency exploration if Doppler US ve for flow or clinical suspicion
o Untwisting (lateral) of affected testis and orchidopexy of both
testis to scrotum
o Warm up with warm pad to see reperfusion or check with doppler
after untwisting [4h before ischaemia]
If dead, excise and replace with prosthesis

40

!
ABDOMINAL STOMAS

A stoma is a surgically created communication between a hollow viscus

and the skin
Functionally they can be end, loop or continent stoma

Indications
Input: feeding (PEG)
Output: decompression/lavage, defunctioning/diversion, draining
Stoma siting
Over the rectus sheath (decrease risk of prolapse)
Away from:
o Surgical incision risk of wound contamination and infection
o Skin creases or bony prominence allow flushing with skin to
prevent leakage
o Old hernia scars risk of hernia
Easy accessibility
Ensure compatible with the clothing worn by the patient
Ideally should be marked preoperatively by stoma nurse
Colostomy
RUQ or LIF
Flushed with skin
Firm brown fecal output
Larger diameter of stoma

Ileostomy
RIF
3cm sprout as ileal contents corrosive
Watery greenish ilieal output
Small diameter

Types of stomas
Permanent (end colostomy)
When no distal bowel remaining
Low rectal/ anal tumor requiring abdomino-perineal resection
Panproctocolectomy without ileal pouch anal anastomosis e.g. FAP
Usually sited on the left side with a single opening
Temporary
Decompression
relief of large bowel obstruction causing proximal dilatation
Defunctioning to protect a distal bowel anastomosis
o Previously contaminated bowel
o Technical considerations e.g. after low anterior resection, where
risk of anastomotic leakage is high
o Usually loop ileostomies or colostomies with 2 openings
(ileostomies usually on the right side, colostomies in the
epigastric/hypochondriac [transverse colostomy] or left side)
To rest an inflamed distal portion e.g. acute Crohns
Complications
Functional disorders
Excess action (stoma diarrhea)
o Distal colostomy should produce solid faeces
o Ileostomy will produce 500-700 ml/day of liquid effluent
o If excess output consider
Inflammatory bowel disease
Para-intestinal sepsis
Subacute obstruction
o Correct electrolyte and water imbalance
Reduced action
Consider simple constipation or obstruction
Structural complications
Necrosis especially if tension over stoma intra-op
Detachment
Prolapse refashion stoma
Parastomal herniation refashion stoma
Stenosis refashion stoma
Recession
Ulceration
Fistula formation
Skin excoriation due to corrosive ilieal output

GASTROINTESTINAL STOMA

41

!
THE ESOPHAGUS
Anatomy
25cm long muscular tube
o Starts @ cricoid cartilage (C6) linking oropharynx - upper
esophageal sphincter is formed by cricopharyngeus muscle
To stomach @ T10
o LES is not an anatomical sphincter but a physiological one
Increased tone of muscularis propria
Fibres of right diaphragmatic crus looping around cardioesophageal jx that contract during
coughing/sneezing/any increase in intra-abdo pressure
to prevent reflux
Angle of His where esophagus joins stomach -- acts as
valve
Intra-abdo pressure is higher than intra-thoracic pressure
3 narrow points
o Cricopharyngeus muscle (15cm from incisors)
o Carina where left bronchus crosses esophagus (27cm from incisors)
o Esophagus passes through diaphragm (40cm from incisors)
Structure: mucosa, submucosa, muscularis propria, adventitia (no serosa
except for short segment of intra-abdominal esophagus)
o Muscularis propria is striated muscle in upper 1/3, striated and
smooth in lower 1/3, smooth in lower 1/3
Blood supply
o Upper 1/3: inferior thyroid artery ; brachiocephalic veins
o Middle 1/3: esophageal branches of aorta ; azygos veins
o Lower 1/3: esophageal branches of left gastric a. ; left gastric v.
Physiology of swallowing
Oral
Mastication forms bolus on dorsum of tongue
Tongue contracts upwards and backwards - bolus pushed against
hard palate
Soft palate elevates to close nasopharynx
Further elevation of tongue pushes food into oropharynx
Pharyngeal
Epiglottis falls back + pharyngeal muscles contract to bring larynx
upwards -- makes laryngeal inlet smaller such that it is closed off
by epiglottis
Pharyngeal muscles contract to propel food bolus pass the relaxed
cricopharyngeus into esophagus
Esophageal Involuntary contractions of muscularis propria -- peristaltic waves
to propel food bolus!
UPPER GASTROINTESTINAL SURGERY

42

Mechanical

Neuromuscular

!
APPROACH TO DYSPHAGIA
Oropharyngeal
Coordination
- Stroke
- Parkinsons disease
- Brainstem tumors
Nerve & muscle dysfx
- Degenerative conditions
e.g. ALS, MS
- Peripheral neuropathy
- Myasthenia gravis
- Myopathies e.g.
Myotonic dystrophy
Tumors
Inflammatory masses e.g.
Abscess
Esophageal webs
Pharyngeal pouch
Anterior mediastinal mass

Esophageal
Achalasia
Spastic motor disorders
e.g. Diffuse esophageal spasm,
hypertensive LES
Scleroderma

Intrinsic structural lesions

- Tumors
- Strictures secondary to inflammation/
radiation/chemicals/medication
- Lower esophageal rings/esophageal webs
- Foreign bodies
Extrinsic structural lesions
- Vascular compression (aorta/LA)
- Mediastinal mass - thyroid/enlarge LN

Others e.g. Esophagitis due to reflux, infection,

RT, medication or chemicals
History
Is there odynophagia (pain a/w difficulty swallowing)
o Signifies some form of esophagitis: infectious (candida/herpes)
or post-RT or chemical-induced (usually alcohol) or reflux
o Esophageal spasm
o Scleroderma
o Pain occurs late in achalasia and ca esophagus
Diffx oropharyngeal from esophageal dysphagia
o Oropharyngeal
Complains of difficulty initiating swallowing
May be a/w choking, coughing, nasal regurgitation
Voice may be nasal (bulbar palsy)
Cause is usually neuromuscular rather than mechanical
(most commonly stroke)
UPPER GASTROINTESTINAL SURGERY

Esophageal
Pt c/o food getting stuck in throat or chest
Note: pts localization of symptom usually does not
correspond to actual site of pathology
Can be due to neuromuscular dysfx or mechanical obs
Diffx mechanical from neuromuscular dysfx
o Mechanical
More difficulty swallowing solids than fluids
May have regurg of undigested food
Recent onset of dysphagia that is progressively
worsening + LOW = high suspicion for esophageal ca
Intermittent symptoms suggest webs/rings
o Neuromuscular
More trouble swallowing fluids than solids
Dysphagia is long-standing and slowly progressive
Intermittent symptoms suggest diffuse esophageal
spasm, nutcracker esophagus
May have hx of stroke or neuromuscular dz
History of predisposing conditions
o Reflux symptoms
i.e. Retrosternal burning pain (heartburn), sour acid reflux into
mouth (acid brash), excessive salivation (water brash),
aggravated by lying down
o Caustic chemical ingestion e.g. Suicidal swallowing sulfuric acid
o Smoking, chronic alcohol ingestion
o Radiation to chest
o Medical hx
o S/S of systemic disease e.g. Stroke, scleroderma, Parkinsons
Systemic review
o LOW - occurs in ca and achalasia (but onset much later in
achalasia)
o Complications
S/S of anaemia - bleeding from tumor?
S/S of aspiration pneumonia - fever, cough, SOB
Tumor spread
o Hoarseness of voice (RLN)
o Fever, cough, hemoptysis (tracheo-esophageal fistula)
o Hematemesis (invasion into aorta)
o Neck lump (LN mets)
o

43

!
Physical examination
General condition
o Vitals (HR/BP) - pt may be hypovolemic due to
vomiting/decreased fluid intake
o Cachetic? - nutritional status
o Conjunctival pallor - bleeding from tumor, esophagitis ulcerations
o Scleral icterus/jaundice? Mets to liver
o Dehydration - mucus membranes
Disease
o Cervical LNs (esp Virchows nodes)
o Scars/RT marks on abdo/chest
o Any masses in abdo
o Hepatomegaly? Ascites?
o PR exam for melaena (UBGIT 2/2 esophageal ca)
Complications of disease
o Signs of pneumonia - febrile, toxic, lung creps, decreased air
entry (usually over right lower lobe)
Treatment
o Enteral
NGT feeding
Gastrostomy/jejunostomy
o Parenteral - TPN
Initial management
Stabilize
o Resus if hemodynamically unstable
o IV fluids + correct any electrolyte imbalances
o Feed with fluids if patient can tolerate (i.e. Only solid foods are
the problem), otherwise - tube feeding or TPN (may have to
correct state of malnutrition)
o Keep NBM if even fluids are not tolerated
o Treat any aspiration pneumonia - NBM, NGT, IV abx
Investigate for underlying cause - treat

UPPER GASTROINTESTINAL SURGERY

Investigations
Diagnostic
o Barium swallow
Adv: Less invasive than OGD, esp when suspecting
webs or divert where OGD may cause perforation
But if pt has high risk of aspiration - barium
swallow is dangerous
Visualize obstructive lesion
Shouldering of a stricture
o Benign: smoother contour
o Malignant: abrupt right-angled contour
Birds beak sign of achalasia
Visualize any pouch/diverticulum
Diffuse esophageal spasm - corkscrew
appearance
o OGD
Adv: direct visualization of lesion, able to take biopsy in
suspected malignancy
Adv: can be therapeutic i.e. Stop any bleed, stent lumen
o Manometry -- gold standard for diagnosing achalasia
Criteria: 1) absence of peristalsis 2) very high LES
pressure 3) absence of relaxation @ LES on swallowing
food
o Videofluoroscopic examination of swallowing (VFES) or flexible
endoscopic examination of swallowing (FEES)
Can assess oropharyngeal dysphagia (neuromuscular
causes) by looking for penetration and aspiration of
various consistencies of food during swallowing
Supportive
o Bloods
FBC - Low Hb (anaemia 2/2 chronic tumor bleed); high
TW in aspiration pneumonia
UECr - electrolyte disturbances 2/2 vomiting, poor intake,
raised creat/urea in dehydration (creat will be raised
more than urea in dehydration/prerenal failure)
o Imaging
CXR - consolidations in aspiration pneumonia
24hr probe monitoring: if pt c/o reflux S/S but no signs on OGD
o diagnostic test for reflux

44

!
GASTRO-ESOPHAGEAL REFLUX DISEASE

Affects approximately 40% of the adult population

Due to acid or bile reflux
Delayed oesophageal clearance also important
Gastric hypersecretion rarely implicated
Poor correlation between symptoms and endoscopic evidence of
oesophagitis
o 20% patients with oesophagitis are symptom free
o Most gain symptomatic relief with conservative treatment
o 30% of patients with symptoms have no endoscopic evidence of
mucosal injury

Causes of GERD
Loss of LES function
Delayed gastric
emptying
Increased intra-abd
pressure
Motor failure of
esophagus
Drugs causing
smooth muscle
relaxation

Natural barriers to gastro-oesophageal reflux

Lower oesophageal sphincter
Basal tone
Adaptive pressure changes
Transient lower oesophageal sphincter
relaxation
External mechanical factors
Flap valve mechanism
o Cardio-oesophageal angle
o Diaphragmatic pinchcock
o Mucosal rosette
Distal oesophageal compression
o Phreno-oesophageal ligament
o Transmitted abdominal pressure

Conservative treatment
Lifestyle modification
Drug treatment
Stop smoking
H2 antagonists
o Symptomatic relief in 60% at 6 wks
Avoid alcohol
o Endoscopic evidence of healing in 40%
Lose weight

Proton
pump inhibitors
Raise head of
o
80% healing at 8 weeks in H2
bed
antagonist resistant disease
o More than 20% relapse
o Life-long therapy often required
Management of strictures
TRO malignancy
Treat using balloon dilatation
Treat underlying reflux
UPPER GASTROINTESTINAL SURGERY

Presentation
Heartburn
Acid brash (reflux)
Symptoms occurring after food, and aggravated by lying flat
Long-standing stricture causing disease, odynophagia
Pulmonary symptoms due to aspiration
Chest pain mimicking anginal pain
Diagnosis
History TRO cardiac and malignant cause
OGD - provides histological confirmation and grading
o Look for peptic stricture, esophagitis, Barretts, hiatal hernia
o Savary-Miller grading of oesophagitis
1. Isolated (or sometimes multiple) erythematous or erythematoexudative erosion(s), covering a single mucosal fold
2. Multiple erosions covering several mucosal folds, partly
confluent but never circumferential
3. Circular extension of erosive and exudative lesions
4. (a) Ulcer
(b) Fibrosis (leading to stenosis and brachyesophagus)
5. Presence of cylindric cell epithelialization acquired in the form
of a disc, strip or sleeve
Barium swallow and follow through for motility disorders
24-hour pH monitoring - probe placed 5 cm above lower oesophageal
sphincter (LOS) Diagnostic
Oesophageal manometry (motility disorder)
Surgical options
Indications:
o Failure of medical therapy; Recurrent symptomatic relapse
o Esophagitis with frank ulceration or stricture
o Complications of reflux esophagitis (Barretts, aspiration)
Fundoplication
o Mobilization of gastric fundus, tension free wrap around 50 Fr
oesophageal bougie, wrap suture line of less than 3 cm
o Partial fundoplication is associated with less dysphagia and
fewer gas related symptoms (anterior 90/180, posterior 270)
Complications:
o Perforation of the esophagus
o 3% develop dysphagia
o 11% develop gastric bloat (difficulty burping)
o Failure of treatment
45

!
BARRETTS ESOPHAGUS
Features
Intestinal metaplasia of the oesophageal epithelial lining (stratified
squamous epithelium converted to mucus-secreting columnar epithelium
with goblet cells)
Associated with long-term reflux an adaptation mechanism where
intestinal epithelium withstands exposure to acidic reflux better than
oesophageal epithelium
Diagnosed on endoscopy and histology:
o The squamocolumnar junction (or Z line) is visible on endoscopy
as gastric and intestinal type epithelium is pink and granular in
appearance, but stratified squamous epithelium is smooth and
pale
o If the squamocolumnar junction is above the gastro-oesophageal
junction (where gastric folds begin) (i.e. they do not align) and
biopsy of the junction shows intestinal metaplasia, the patient is
diagnosed to have Barretts oesophagus
Short segment Barretts is defined as the squamocolumnar junction
being <3cm above the gastro-oesophageal junction, while in long
segment Barretts the distance between the two junctions is >3cm.
Classic Long segment Barretts is associated with more severe reflux, as
well as higher risk of dysplasia and subsequent adenocarcinoma
development than short segment Barretts
Risk of development of adenocarcinoma is about 10-15% in 10 years
Management
Treatment of underlying reflux
Lifestyle changes, acid suppression, surgery etc
Endoscopic surveillance
If patient has high grade dysplasia, it should be treated (see below),
otherwise to undergo intensive surveillance (q3mths for at least one
year) to detect cancer development
Treatment of high-grade dysplasia
Endoscopic therapies to ablate the dysplastic tissue e.g. photodynamic
therapy, laser therapy, argon plasma coagulation will not remove all
dysplastic cells thus potential for malignancy still remains
Oesophagectomy is the only definitive treatment to remove all dysplasia,
but is associated with high morbidity and mortality
Possibility of endoscopic mucosal resection as a treatment modality
UPPER GASTROINTESTINAL SURGERY

ACHALASIA

Due to reduced number of ganglion cells in myenteric plexus

o Abnormal peristalsis
o Failure of LES to relax
o Affects body and distal esophagus
Aetiology is unknown but a neurotropic virus may be important

Clinical features
Commonest in patients between 40 - 70 years
Male : female ratio is approximately equal
Presents with dysphagia, weight loss, regurgitation, retrosternal chest pain
10% of patients develop squamous carcinoma after 15-25 yrs
Investigations
CXR - widening of mediastinum, air / fluid level and absence of gastric
fundus gas bubble
Barium Swallow proximal dilatation & residue, small tertiary
contractions and distal Birds Beak narrowing
Manometry - absent primary peristaltic wave & non-propulsive tertiary
contractions; high pressure at LES
Endoscopy TRO 'pseudoachalasia' due to submucosal carcinoma
o Tight lower oesophageal sphincter which relaxes with gentle pressure
Differential diagnosis
Diffuse oesophageal spasm
Infiltrating carcinoma
Hypertrophic LES

Scleroderma
Chagas' disease

Treatment options
Conservative
Injection of botulinum toxin
Rider Moeller Pneumatic Balloon inflated to 300 mmHg for 3 minutes
o 40% dysphagia free at 5 years
Surgical: Laparoscopic Heller Cardiomyotomy
Splitting of muscular wall at LES
85% will have an improvement in symptoms at 5 yrs
10% develop oesophageal reflux; 3% will develop oesophageal stricture
Some combine cardiomyotomy with an antireflux operation

46

!
ESOPHAGEAL CANCER

rd

3 most common GIT cancer, especially in males

o 70% are squamous cell carcinomas in the upper or middle 1/3
o 30% are adenocarcinomas in lower 1/3
Overall 5 year survival is very poor and is at best 20%
Less than 50% patients are suitable for potentially curative treatment
Of those undergoing 'curative' treatment less than 40% survive 1 year
Overall prognosis - 80% mortality at 1yr, 5yr-survival <10%

Risk factors
Squamous cell carcinoma
o Alcohol 2x / tobacco 10x
o Achalasia (2-8%)
o Diet high in nitrosamines
o Coeliac Disease
o Aflatoxins
o Genetic Tylosis (keratosis)
o Trace element deficiency o High incidence in Transkei,
molybdenum
Areas of Northern China and
o Vitamin deficiencies - A & C
the Caspian littoral region
o Plummer-Vinson (webs)
o Fe-deficiency anemia
Adenocarcinoma
o 15% associated with Barrett's Oesophagus
o Reflux; Smoking 10x
Pathology
Site

o 10% in upper 1/3

o 60% in middle 1/3
o 30% in lower 1/3
3 growth patterns
o Fungating (60%)
o Ulcerative (25%)
o Infiltrative (15%)
Tumor spread
o Direct extension into adj strs
o Vascular invasion
o Lymphatic spread
Common sites of mets: liver, lungs, bone

UPPER GASTROINTESTINAL SURGERY

Clinical features
Progressive dysphagia, insidious onset
o Retrosternal discomfort/indigestion
Dysphagia first solid then liquid
Pain develops late
Anaemia +/- melaena or hematemesis (occult bleed usually)
Vocal cord paralysis - left more than right
Aspiration pneumonia
Respiratory symptoms due to overspill or occasionally a tracheaoesophageal fistula
Weight loss
Assessment
Diagnosis confirmed by:
Endoscopy plus biopsy
/ cytology
Barium swallow

Resectability and fitness for surgery

assessed by:
Chest x-ray
Lung function tests(FEV1 > 1L)
Liver ultrasound
Endoscopic ultrasound
Bronchoscopy
Laparoscopy
Thoracic CT

Staging
T:
Tis does not breach basement membrane
T1 does not invade muscularis, T2 does
T3 invades adventitia, T4 invades surrounding strs
N:
according to number of regional nodes involved
M:
nonregional LN involvement vs distant mets

Feeding in esophageal obstruction

Feeding via oropharyngeal route is preferred unless passage is
obstructed or it is unsafe (high risk of aspiration)
If able to pass NG tube around tumor -- feed via NG
o Also consider problems with long-term NG placement
o Consider PEG placement for long-term feeding
PEG = percutaneous endoscopic gastrostomy (scope in
stomach - can poke tube percutaneously)
If unable to pass tube/scope around tumor - consider open gastrostomy
Total parenteral nutrition (TPN) an option but more complications and
higher cost
Relief of obstruction (above) can enable oral feeding but dysphagia will
return as tumor grows
47

!
Investigations
Diagnosis
o Barium swallow - high accuracy in showing mucosal irregularity
and annular constrictions but no histo diagnosis
o OGD - allows biopsy with histo confirmation
Staging
o Endoscopic Ultrasound
If endoscope can pass around lesion - EUS is good for T
staging and can identify enlarged LNs
o CXR
Presence of lung mets, pleural/pericardial effusion
Aspiration pneumonia
Tracheal deviation or extrinsic compression of
tracheobronchial system
Widened superior mediastinum in upper tumor
Raised hemidiaphragm if phrenic nerve involved
o CT or MRI of thorax with extension to liver and adrenals -- TNM
o Bronchoscopy - exclude bronchial involvement
o Laryngoscope to assess for vocal cord paralysis
o Bone scan - bony mets
Supportive
o FBC - Low Hb (anaemia), high TW (aspiration pneumonia)
o UECr - electrolyte disturbances from vomiting/poor
intake/dehydration (crea>>urea)
o LFTs - low albumin in malnutrition states
Management
3 modalities available: surgery, chemo, RT (use singly or in combination)
Aims: curative vs palliative (half of cancers unresectable on ppt)
o Surgical Rx usually is performed with curative intention, but can
also achieve good long-term palliation of symptoms
Choice of treatment depends on patient factors like age, co-morb,
nutritional state, life expectancy and cancer prognosis
Curative treatment:
o Pre-op neoadjuvant chemoRT, esophagectomy, post-op
adjuvant chemoRT (for responsive tumors)
Radiotherapy
Improved survival compared to surgery for SCC (radiosensitive)
Usually given together with chemo
o External beam radiotherapy or Brachytherapy
Complications: fistula, strictures
UPPER GASTROINTESTINAL SURGERY

Chemotherapy
5-FU and cisplatin, given as neoadjuvant and adjuvant
Surgery
Only 40% tumours are resectable (but curative in early lesions
o Operative mortality now less than 10%
o Should not be done in patients with mets or contraindications
Operative approaches
o Endoluminal surgery for early lesions
o Esophagectomy
Need 10 cm proximal clearance
Total gastrectomy via thoracoabdominal (Adeno CA)
Subtotal two-stage oesophagectomy (Ivor-Lewis)
Subtotal three-stage oesophagectomy (McKeown)
Transhiatal oesophagectomy
Complications:
Intraop injury to lungs, thoracic duct, RLN
Early: respi (atelectasis, pneumonia),
mediastinitis from anastomotic leak
Late: reflux, strictures
Palliative treatment
Aim to relieve obstruction and dysphagia with minimal morbidity
Surgical debulking
Oesophageal stenting
o Endoscopic or radiological placement most commonly practiced
o Atkinson tube is the most commonly placed endoscopically
o Requires dilatation with risk of oesophageal perforation
o Complications of stents and tubes:
Oesophageal perforation
Tube displacement or migration
Tube blockage due to ingrowth or overgrowth
Endoscopic laser fulguration
o Produces good palliation in over 60% of cases
o May need to be repeated every 4 to 6 weeks
o Associated with oesophageal perforation in about 5% cases
Radiation: for unresectable, bleeding, painful lesions
o External beam radiotherapy
o Brachytherapy
Diathermy; Alcohol injection; Photodynamic therapy

48

!
PEPTIC ULCER DISEASE

Incidence about 100 per 100,000 per year

68% of patients are over 60 years of age

An imbalance between mucosal protective mechanisms against acid, and

aggressive forces that damage the gastric mucosa
Aggressive forces: gastric activity and pepsin activity
Protective mechanisms: mucus secretion, bicarbonate secretion, robust
mucosal blood flow to remove protons, epithelial regenerative capacity,
prostaglandin secretion by mucosa to maintain blood flow
Etiology
H. pylori (Gram-negative spiral flagellated bacterium, produces urease)
Causes a local inflammatory reaction and secretes enzymes that break
down the gastric mucosal barrier, and also enhances gastric acid
secretion and decreases bicarbonate production
90% patients with duodenal ulcer, 70% patients with gastric ulcer
60% patients with gastric cancer
NSAIDs
Impair mucosal prostaglandin production (through non-selective COX
inhibition) prostaglandins are important for mucosal bicarbonate and
mucin production and inhibiting gastric acid secretion, as well as
maintaining mucosal blood flow
Accounts for most of the rest of ulcer disease not caused by H. pylori
30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a
clinically significant ulcer i.e. symptomatic, bleeding
Other factors
Vices: Cigarette smoking, Alcohol
Steroids and anticoagulants do not increase the risk of ulcer formation,
but increase the risk of bleeding in an existent ulcer

UPPER GASTROINTESTINAL SURGERY

Presentation
Incidentally detected on OGD
Symptoms of dyspepsia
o Ulcer-like dyspepsia: pain in the upper abdomen
o Dysmotility-like dyspepsia: non-painful discomfort in the upper
abdomen, associated with upper abdominal fullness, early
satiety, bloating, belching, nausea
o Unspecified dyspepsia: Pain is usually worse with food in a
gastric ulcer, while it is relieved by food in a duodenal ulcer
Bleed (presenting with haematemesis (coffee-grounds vomitus) or melaena)
Perforation
o Sudden generalized abdominal pain aggravated movement
o Board-like rigidity, guarding (signs of peritonism)
o Erect CXR will show air under diaphragm
Investigation
Endoscopy (OGD)
o Diagnostic
Confirm ulcer disease & localize ulcer
Biopsy - TRO malignancy
Biopsy antral tissue - for CLO (campylobacter-like
organism to test for H. pylori)
o Prognostic
Forrest classification (or endoscopic stigmata of recent
hemorrhage ESRH) bleeding risk
Ia: spurting (arterial)
-- 90%
Ib: non-spurting ooze (venous)
-- 20%
IIa: non-bleeding w visible vessel
-- 40%
IIb: non-bleeding ulcer w adherent clot -- 20%
IIc: ulcer w hematin-covered base
-- 10%
III: ulcer w clean base
-- 5%
o Therapeutic

Injection with adrenaline -- to create edema and

tamponade effect
Thermal coagulation with heater probe
Hemostatic clipping (endoclip)
Argon plasma coagulation
Microscopy silver or Giemsa staining of antral biopsies
Culture difficult and requires special culture techniques
CLO rapid urease test colour changes due to change in pH
13
14

C or C breath test Ingested radioactive urea is broken down to CO2

Serology detected immunologically using an ELISA
49

!
Conservative Management
Gastro-protection:
Proton Pump inhibitors
20mg omeprazole OM
Promotes ulcer healing even with ongoing NSAID use
90 - 100% healing at 2 months
Low recurrence on long term maintenance
H2 Antagonists
Give 40mg BD famotidine if allergic to omeprazole
65% healing at 1 mth, 85% healing at 2
If stop treatment - 90% recurrence at 2yr
If maintenance therapy - 20% recurrence at 5 years
H. Pylori eradication
Two weeks amoxicillin, clarithromycin and omeprazole
o If allergic to penicillin, substitute amox with metronidazole
o Document eradication with endoscopy + CLO, urea breath test or
stool serology (after 6 wks)
o 80% cured with dual or triple therapy
o Treatment failure occurs in up to 20% - go for quadruple therapy
(add bismuth)
The number of complications however remain unchanged
o May be increasing due to increased NSAID use in elderly
o Bleeding and perforation still have mortality of >10%
Surgical Management
Gastric ulcer
Indication for surgery:
Failure to heal after 3 months conservative therapy
Dysplasia/ carcinoma
Recurrence
Persistent bleed/perf
Surgery (if prepyloric ulcer - can treat like duodenal ulcer):
Oversew bleeding vessel
Gastrectomy

UPPER GASTROINTESTINAL SURGERY

Duodenal Ulcer
Indications:
Persistent bleeding (e.g. Erosion of posterior D1 ulcer into
gastroduodenal artery)
Perforation - contained or free
Gastric outlet obstruction - patient presents with vomiting of undigested
food not long after meal + succussion splash positive + air-fluid levels on
AXR + hypokalemic hypochloraemic metabolic alkalosis with paradoxical
aciduria
Failure of medical management (ulcer does not heal)
Surgical options for duodenal ulceration:
Oversew bleeding vessel with omental patch repair
Reduce acid production by the stomach via Truncal vagotomy
o Cephalic phase reduced by vagotomy
o Antral phase reduced by antrectomy
May require gastric drainage procedure to overcome effects of vagotomy
on gastric drainage
Surgical Procedures
Open surgical procedures
Truncal vagotomy with:
o Pyloroplasty
o Gastrojejunostomy
o Antrectomy
Highly selective vagotomy
Anterior seromyotomy and
posterior truncal vagotomy
Post gastrectomy complications
Percentage
Diarrhoea
16
Dumping
14
Bilious vomiting
10
Iron deficiency anaemia 12
B12 deficiency
14
Folate deficiency
32
Recurrent ulceration
2

Laparoscopic peptic ulcer operations

Thoracoscopic truncal vagotomy
and pyloric stretch
Highly selective vagotomy
Posterior truncal vagotomy with:
o Selective anterior
vagotomy
o Anterior seromyotomy
Post vagotomy complications
Percentage
Diarrhoea
2
Dumping
2
Bilious vomiting <2

50

!
GASTRIC CARCINOMA
Epidemiology
th
th
Gastric carcinoma 5 in men, 8 in women in Singapore
Incidents increases after 50yo
Risk factors
Environmental
o Diet low in Vitamin C; preserved food, nitrosamines, polycyclic
hydrocarbons
o Alcohol, Smoking
o Occupational exposure: asbestos, heavy metal, rubber
Genetic - Blood group A, , e-cadherin mutation, family history, HNPCC
Precursor states
Post gastrectomy (Bilroth II)
o Chronic exposure of gastric mucosa to biliary, pancreatic &
intestinal secretions @ anastomotic zone, >15yrs after surgery
Gastric polyps
o Inflammatory polyps - highest risk (75-90%)
o Adenomatous polyps - 10-20% risk, increased if large (>2cm)
&/or villous histology
Chronic gastritis
Hypertrophic gastritis - inflammatory disease of gastric epithelium - up to
10% risk of malignant change
Pernicious anemia - autoAbs to parietal cells with achlorhydria - 2-10%
risk of gastric ca
PUD -- <1% risk of malignant change
H. Pylori infection -- 3-6x increased risk

Clinical presentation
Asymptomatic
o Most present late and are not amenable to radical surgery
o Upper GI endoscopy should be considered in all with dyspeptic
symptoms over 40 years
Symptomatic -- very non-specific
o Abdo pain
o Dysphagia - a/w proximal cancers
New onset dysphagia in >35yo should be cause for
concern
o Nausea, vomiting, anorexia (and LOW)
o Palpable mass
o Early satiety
Complications (bleed, block, burst, burrow)
o Bleed
Anaemia - SOB, CP, decreased ET, palpitations, fatigue,
postural giddiness
UBGIT - coffee grounds vomitus / melena
o Block
Gastric outlet obstruction - projectile vomiting shortly
after meal
Vomiting, aspiration pneumonia, dehydration,
hypokalemic hypochloremic metabolic alkalosis with
aciduria
Malnutrition
o Burst
Perforation - peritonism
o Burrow
Fistulas
Metastasis - LOA/LOW/malaise

Morphology Borrmanns classification

Type I (3%): non-ulcerated, polypoid, growing intraluminally
Type II (18%): Ulcerated, circumscribed with sharp margins
Type III (16%): Ulcerated, margins not sharply circumscribed
Type IV (63%): Diffuse, infiltrating, may be ulcerated, may infiltrate
extensively (entire stomach) - linitis plastica
Location
30% pylorus/antrum
20% body
37% cardia
12% entire stomach
UPPER GASTROINTESTINAL SURGERY

51

!
Histology
Adenocarcinoma (90-95%)
Lauren classification
Intestinal type *more common overall
o Occurs in high risk population (i.e. Older, male)
o Distal 1/3 of stomach; arise from mucosa
o H. pylori --> chronic gastritis --> intestinal metaplasia -->
dysplasia --> carcinoma
o a/w ERB2, ERB3 receptor stimulation
Diffuse type
o Occurs in low risk population - younger, female
o Proximal 1/3, cardio-esophageal jx; arise from submucosa
o More aggressive, invasive growth pattern - rapid submucosal
spread
o Present later, worse prognosis
Transmural and lymphatic spread w early mets
o Associated with K-sam oncogene
If detected early (early gastric ca)
o Confined to mucosa and submucosa
o Good prognosis and survival regardless of size, LNs status,
histological grade
Leiomyosarcoma (2-3%)
Arises from the smooth muscle of the stomach wall
Lymphatic spread is rare
75% present with an upper gastrointestinal bleed
60% have palpable abdominal mass
Diagnosis can be confirmed by endoscopy and CT scanning
Partial gastrectomy; 5-year survival is approximately 50%
Gastric lymphoma (1%)
Stomach - commonest extranodal primary site for non-Hodgkin's lymphoma
Clinically presents similar to gastric carcinoma
70% of tumours are resectable; 5-year survival is approximately 25%
Both adjuvant radiotherapy and chemotherapy may be useful
Sister Mary Joseph Nodule
Presents as firm, red, non-tender nodule a/w advanced malignancy
Results from spread of tumour within the falciform ligament
90% of tumours are adenocarcinomas
Commonest primaries are stomach and ovary

UPPER GASTROINTESTINAL SURGERY

Spread
Direct extension - to neighbouring organs
Lymphatic spread
o Regional nodes i.e. Perigastric nodes
o Virchows node, Umbilical nodes - Sister Mary Joseph node
Hematogenous spread
o Liver (look for hepatomegaly with ascites & jaundice on PE)
o Lung (SOB?)
o Bone (pain over the axial skeleton/spine)
o Brain (changes in behavior)
Peritoneal seeding
o Omentum - omentum caking
o Parietal peritoneum
o Ovaries Krukenbergs tumor
o Cul-de-sac (Blumers shelf)
Investigations
Requires a combination of preoperative investigations & intra-op assessment
Diagnostic
Staging
OGD confirms diagnosis,
Endoscopic ultrasound may allow
site & extent of tumour
assessment of intramural tumour
penetration (gold standard)
Visualize and biopsy
CXR
Usually ulcer with
heaped up edges
CT will assess nodal spread and
extent of metastatic disease
Laparoscopy will identify peritoneal
seedlings occult on CT (1/5)
Supportive
FBC - low HbUECr - if vomiting -- electrolyte disturbances
(low K, low Cl, acid-base balance)
LFTs - as a marker of nutritional status (<35 is poor); liver metastases
-hCG (beta-human chorionic gonadotropin), CA-125, and CEA
(carcinoembryonic antigen)
TNM staging
Tis Carcinoma in situ (does not breach BM) N0 No LNs involved
T1 Tumor limited to mucosa & submucosa N1 1-6 regional LNs
T2 Tumor invades muscularis mucosa
N2 7-15 regional LNs
T3 Tumor penetrates serosa
N3 >15 regional LNs involved
T4 Tumor invades adjacent structures
Prognosis if generally very poor
Overall 5 year survival is approximately 5%
Survival is 70%, 32%, 10% and 3% for Stages 1,2,3 and 4 respectively
52

!
Management
Principles
A tumour is considered resectable if confined to stomach or N1 or N2
nodes (less than 6 nodes) involved (Stage I and II)
o Nodes less than 3 cm from tumour = N1 nodes
o Nodes greater than 3 cm from tumour = N2 nodes
If tumour and N1 nodes resected = D1 gastrectomy
If tumour and N2 nodes resected = D2 gastrectomy
Even in patients with incurable disease surgery may palliate symptoms
Chemoradiotherapy may reduce relapse and improve survival
Chemotherapy/Radiotherapy
Adjuvant therapy
5-flurouracil with chemotherapy
5-flurouracil with epirubicin for advanced dz
Neoadjuvant therapy
5-FU and cisplatin can be used to downstage unresectable locally
advanced disease -- significant increase in resectability
For resectable disease: pre-op 5-FU, cisplatin, doxorubicin, methotrexate
followed by intraperitoneal 5-FU --> improved resection rates, response
rates, median survival

UPPER GASTROINTESTINAL SURGERY

Curative
Surgery
- Wide resection of the tumor to negative margins (at least 6cm)
- En-bloc excision of regional LNs & any structures involved by local invasion
- Choice btwn subtotal (1/3 of stomach left) and total gastrectomy
Proximal tumors
o Total or proximal subtotal possible
o Total gastrectomy with Roux-en-Y esophagojejunostomy preferred
avoid post-op morbidity of reflux esophagitis and
impaired gastric emptying (a/w prox subtotal gastrect)
o Tumors of GE jx
may require esophagogastrectomy with cervical or
thoracic anastomosis
Midbody tumors
o Generally req total gastrect to achieve adequate margins
Distal tumors
o Distal subtotal gastrect - superior post-op nutritional status and
quality of life (maintains gastric remnant - residual reservoir fx)
and hence preferred if adequate margins can be obtained
Diffuse-type tumors - total gastrectomy
- Reconstruction
Billroth I: end to end gastroduodenostomy
o Rarely done as it is difficult to mobilize duodenum up to
anastomose with residual stomach
Billroth II: gastrojejunostomy
o No protection against biliary reflux into stomach
Roux-en-Y
o Prevents biliary reflux
o Involves 2 anastomoses -- higher chance of leak

53

!
Complications of gastrectomy
Early
Bleeding, Infx, Anastomotic leak
Late
Nutritional disturbances (30%)
o Prolonged iron, folate, vitamin B12, calcium, vitamin D deficiencies
o Can result in anemia, neuropathy, dementia and osteomalacia
(respectively)
o Supplementation required - B12 injx, Fe supplementation
Early satiety -- further nutritional status deterioration
Retained antrum syndrome
o Prox subtotal gastrect - too much antrum left behind -- increased
acidity in residual stomach -- formation of marginal ulcers on
jejunal end of anastomosis
Dumping syndrome
o Due to loss of reservoir fx & pylorus - rapid emptying of highosmolar carbo load into small intestine
o Most common after Billroth II reconstruction
o Early (within 30mins)
Nausea, epigastric distress, explosive diarrhea,
vasomotor symptoms (dizziness, palpitations, flushing,
diaphoresis)
Relieved by recumbence or saline infusion
o Late (1-4hrs)
Symptoms are primarily vasomotor
Hormonal response to high simple carbo loads results in
hyperinsulinaemia and reactive hypoglycaemia
Hypoglycaemic s/s relieved by carbohydrate ingestion
o Tx: smaller volume meals, increased frequency, avoid simple
carbohydrates, liquids should be taken 30mins after solids
Alkaline reflux gastritis
o Most commonly a/w Billroth II
o Triad of constant epigastric pain, nausea, bilious emesis
Vomiting does not relieve pain, not a/w meals
o Endoscopy: inflamed, beefy red, friable proximal mucosa +/- bile
reflux
o No mechanical obstruction (diffx from loop syndromes)
o Rx
Non-surgical: frequent meals, antacids, cholestyramine
Surgical: Roux-en-Y gastrojejunostomy (preferred)

UPPER GASTROINTESTINAL SURGERY

Roux stasis syndrome (up to 30% of patients after Roux-en-Y)

o Chronic abdo pain, nausea, vomiting aggravated by eating
o Functional obstruction - due to disruption of peristalsis in
duodenum & altered motility in gastric remnant
Loop syndromes - mechanical obstruction of either afferent or efferent
limbs of Billroth II
o Afferent loop (duodenal) syndrome
Caused by bowel kink/volvulus/internal herniation
Severe abdo pain, non-bilious emesis (no bile in NG
aspirate)
Elevated bilirubin/amylase
Acute complication: duodenal stump blowout progressive dilation,
peritonitis/abscess/fistula
Chronic complication (with partial obstruction) - blind
loop syndrome
Steatorrhea, B12, folate, iron deficiency (due to
lack of B12 and fat absorption) (B12 bound to R
factor digested by proteases, B12 released to
bind to IF to be absorbed)
o Efferent loop syndrome
Abdominal pain and bilious emesis
o Rx: remove adhesions, revise anastomosis, bowel resection,
conversion to Roux-en-Y
Intestinal hurry
o Inadequate reservoir fx -- poor digestion -- phytobezoar formation
Post-vagotomy diarrhea
o Watery and episodic
o Rx: anti-diarrheals, reduce excessive fluid intake, reduce lactose
intake

Palliative
Objective: Prevent obstruction, bleeding, perforation, relieve pain
Obstruction: endoscopic laser ablation, surgical resection (subtotal/total),
bypass
Bleed: angioembolization
Pain: external beam radiotherapy (also for low-level ongoing bleed)
Prognosis -- stage-dependent
Stage I: 90% 5yr survival
Stage II: 70%
Stage III: 40%
Stage IV: 0%
54

Hepatic

Pre-hepatic

Normal serum bilirubin <17umol/L (1mg/dL)

Serum bilirubin >35umol/L (2mg/dL)
o clinically detectable jaundice/icterus (yellowing of skin & sclera)

Pathogenesis
- Increased production of
unconj bilirubin by
reticuloendothelial sys
- Excessive destruction of
RBCs (hemolysis)
exceeds ability of liver to
conjugate
- unconj bili accumulates
in blood
- No increase in conj bili in
blood --> none will be
found in pee
- Increased amt of
urobilinogen in gut
reabsorbed & overflow
into systemic circulation - excreted by kidneys
- Hepatocellular damage
-hepatic ability to
conjugate bilirubin drops
- less excreted into
canaliculi
- Both unconj and conj
bilirubin accumulate in
blood

Causes
Hereditary
- G6PD deficiency
- Thalassemia
- Hereditary
spherocytosis
- Sickle cell anaemia

Symptoms and signs

- Normal urine/stools
- May have anaemic
symptoms
- Unconj hyperbilirubinaemia
- Raised LDH, decreased
haptoglobin
- Peripheral blood film if
Acquired
malaria suspected
- Malaria
- Direct Coombs test for
- Incompatible blood
autoimm
transfusions
- Stool ova/cyst/ parasites for
- Mechanical heart
malaria
valves
- Hemolytic uraemic
syndrome (in acute
renal failure)
- Autoimmune SLE
- Infectious - viral
- Mixed signs: urine may be
hepatitis,
dark with normal stool
EBV/CMV, TB
- LFT - raised AST/ ALT
- Cirrhosis / CLD disproportionate to ALP/GGT
alcoholic, viral,
- In cirrhosis decreased
metabolic or
albumin, raised INR
infiltrative
- AFP to exclude malignancy
- Hepatotoxic drugs
- Do viral hepatitis serology
e.g. Paracetamol
(HBV - anti-HBc, HBsAg,
O/D, TCM
HCV - anti-HCV, HCV RNA,
- Autoimmune e.g.
HAV - Anti-HAV)
SLE
- Autoimmune (ANA, anti- Hereditary inability
dsDNA)
to conjugate or
- Metabolic screen excrete
ceruloplasmin or 24hr Cu
urine O/P
- Do abd U/S: look for surface
nodularity, increased
echogenicity in cirrhosis,
signs of portal HTN
(splenomeg & ascites)

HEPATOBILIARY AND PANCREATIC SURGERY

Obstructive

!
APPROACH TO JAUNDICE

- Obstruction of intrahep
or extrahep bile ducts,
preventing excretion of
conjugated bilirubin
- No pigment -- pale
stools + conj bili builds
up in blood and
excreted in pee dark
tea-colored pee
- Hepatic and post-hep
forms co-exist e.g. CBD
stones can also cause
biliary cirrhosis, tumor
deposits or cirrhosis can
destroy liver tissue and
compress intrahepatic
ducts

Intraluminal
- gallstones/
parasites e.g.
Ascaris
lumbricoides

- Tea-colored pee, pale

stools, intense pruritus
- Conj hyperbilirubinaemia
- Increased ALP/GGT
disproportionate to AST/ALT

Mural
- Biliary strictures
post-ERCP or
gallstones of
chronic
pancreatitis
- PBC - intrahepatic
bile ducts
- PSC - intra&extra
hepatic ducts
- Cholangitis/
choledochal cyst/
distal cholangio
CA

Do abdo U/S
- If ducts dilated (>8mm) do
ERCP/MRCP/PTC
- If not dilated further
serological testing e.g. For
AMA, p-ANCA (PSC), ANA,
anti-SMA

Extraluminal
- Ca head of
pancreas
- Other periampullary ca
- Mirizzis syndrome

RBCs reach end of life in circulation after ~120 days -- destroyed in

reticuloendothelial system -- porphyrin ring of Hb disrupted; iron is
recycled for further Hb synthesis -- bilirubin-globin reaches liver (lipidsoluble; water-insoluble)
Liver: Bilirubin conjugated with glucuronic acid in hepatocytes -- excreted
in bile as water-soluble bilirubin glucuronide
Bowel: Bilirubin reduced by bacteria to colourless urobilinogen -- majority
excreted in faces where it is broken down to urobilin and stercobilin -colors stool brown
o Small amt reabsorbed from intestine - portal venous sys - liver -re-excreted as bile into gut
o Some reach systemic circulation and excreted in pee
Urine exposed to air - urobilinogen ox to urobilin (darker)

55

!
History
Onset
o Acute (days)
Gall stone disease, Acute hepatitis
Acute Budd-Chiari syndrome, hemolysis
o Subacute (weeks to months)
Pancreatic and hepatobiliary malignancy
Intrahepatic cholestasis
RHF
o Recurrent episodes gallstone disease
o Resolution? if yes, benign obstruction; painless progressive = Ca
Associated symptoms
o Fever (Chills and rigors)
Sign of inflammation/infection
Cholangitis, viral hepatitis, cholecystitis, Mirizzis syndrome
o RUQ pain
Cholangitis, acute hepatitis, Budd Chiari, Mirizzis
Lack of pain + gradual onset + obstructive suggests
pancreatic/bile duct/periampullary malignancy/
drug/autoimmune
o Confusion sepsis (cholangitis) or hepatic encephalopathy
o Easy bruising
Ask about gum bleeding, nosebleeds, easy bruising
coagulopathy can be caused by liver failure.
Jaundice can also be due to hemolysis DIC, malaria
o Back pain
Viral hepatitis and severe hemolysis
o Dark urine/pale stools
Excessive conjugated bile appearing in urine
May not distinguish obstruction from hemolysis
o Pruritus
Cholestatic picture
Bile duct obstruction, drug induced
o Weight loss (Malignancy, chronic liver disease)
Travel History
Hep A/B
Liver flukes
Medications and vaccines
Current and previous
medications
Hep A and B vaccinations

Gynae
Liver disease in pregnancy
Family history
Liver disease, hepatitis, blood disorders
Hemochromatosis, Wilsons disease,
Gilberts syndrome
Hemolytic anemias sickle cell, G6PD
deficiency

HEPATOBILIARY AND PANCREATIC SURGERY

Associated risk factors

Viral hepatitis
o Needle and blood exposure, tattoos, sexual history (number of
partners, barrier protection), vaccination history
o Travel/eating/shellfish history
o Immunosuppressive therapy
Alcoholic hepatitis
Acute liver failure
o Paracetamol/herbal remedies causing acute liver failure
Cholestatic jaundice
o Cholelithiasis history of gallstones, post-prandial RUQ pain
Hemolytic anemia, gastric bypass surgery (risk factors)
o Hepatic/biliary surgery (Risk of biliary strictures
o Previous pancreatitis
Formation of pancreatic pseudocyst compression
o Sickle cell anemia
Ischaemic cholangiopathy sickling in end arteries
o Ulcerative colitis (a/w primary sclerosing cholangitis)
Complications
Ascending cholangitis
o Charcot's triad is classical clinical picture
Intermittent pain, jaundice and fever
o Cholangitis can lead to hepatic abscesses
o Need parenteral antibiotics and biliary decompression
o Operative mortality in elderly of up to 20%
Clotting disorders
o Vitamin K required for gamma-carboxylation of Factors II, VII, IX, XI
o Vitamin K is fat soluble. No absorbed.
o Needs to be given parenterally
o Urgent correction will need Fresh Frozen Plasma
o Also endotoxin activation of complement system
Hepato-renal syndrome
o Renal failure post intervention
o Due to gram negative endotoxinaemia from gut
o Preoperative lactulose may improve outcome
o Improves altered systemic and renal haemodynamics
Drug Metabolism
o Half-life of some drugs prolonged. (e.g. morphine)
Impaired wound healing
Fat malabsorption steatorrhea, vitamin deficiency coagulopathy
Liver decompensation encephalopathy, hepatic fetor, ascites
Gallstone pancreatitis abdominal pain radiating to back with n&v
56

!
Investigation of Jaundice
Blood results
FBC infection/anemia
Prolonged PTT
UECr
Hepatitis serology
Amylase, Lipase
Blood cultures if febrile
Cancer markers: CA19-9, CEA
LFT
o Bilirubin ( in direct), rarely >100umol/L in pre-hep causes, can
be much higher in obstruction
>1000 - late malignant dz
Direct > indirect; normal 3:7
o ALP/GGT > 2 x AST/ALT (obstructive)
o 5 x ALP/GGT < AST/ALT (hepatic)
o AST/ALT raised in acute viral hep
AST:ALT = 2:1 alcoholic hepatitis
o Albumin may be reduced
Urinalysis findings
Conjugated bilirubin
Urobilinogen

Haemolysis
normal
increased

Hepatocellular
normal
normal

Obstruction
increased
nil

Ultrasound
Normal CBD <8 mm diameter; abnormal if >10mm
CBD diameter increase with age and after previous biliary surgery
For obstructive jaundice ultrasound has a sensitivity 70 - 95% and
specificity 80 - 100%
o GB stones or sludge; thickened GB wall, pericholecystic fluid,
duct dilation, liver consistency
o Demonstrates dilated biliary system and site of obstruction
Unable to detect distal CBD stone well; CT preferred if
malignancy + staging
o Demonstrates fattiness/cirrhosis of liver
CT AP (Tri-phasic)
Stages and assesses operability of tumours
Demonstrates intra-hepatic lesions e.g. Tumor/abscess/cyst which can
then be biopsied under radiological guidance
Assess intrahepatic ducts
Delineate pancreatic mass - ca vs chronic pancreatitis hard to diffx
o CT is preferred if malignancy is suspected (ca head of
pancreas/periampullary tumor - can stage TNM)
HEPATOBILIARY AND PANCREATIC SURGERY

HIDA Radionuclide scanning

99

technetium iminodiacetic acid (HIDA); taken up by hepatocytes and

actively excreted into bile; allows imaging of biliary tree
o Failure to fill gallbladder = acute cholecystitis
o Delay of flow into duodenum = biliary obstruction
Now mainly used for biliary atresia
Endoscopic retrograde cholangiogram (ERCP)
Per oral endoscope cannulate ampulla of Vater in D2
o Diagnostic:
Localization/nature of obstruction
Visualize any tumor
Biopsy or brush cytology
o Therapeutic:
Stone extraction or stenting for decompression
Complications
o Pancreatitis
o Duodenal perf
o Ascending cholangitis
Percutaneous transhepatic cholangiography
Cannulates a dilated bile duct
May be req if ERCP is impossible
Can introduce stent - decompress bile duct & resolve jaundice
Lower risk of bleed but higher infx risk
MRCP (magnetic resonance cholangiopancreatography)
Non-invasive, high-res imaging of biliary tree
But no therapeutic purpose
Summary
Exclude pre-hepatic cause: haptoglobin level, reticulocyte level, Coombs
test
Liver synthetic fx: PT & albumin
Hepatocellular damage: AST/ALT, GGT
Bile duct obstruction: ALP/GGT, US of HBS, MRCP, ERCP, PTC; CT for
pancreatic lesion
Intrahepatic mass: U/S or CT with needle biopsy

57

!
APPROACH TO CIRRHOSIS

Definition: consequence of chronic hepatic injury with healing by

regeneration and fibrosis.
Fibrosis leads to further cell damage and destruction of hepatic
architecture, progressing to liver failure and portal HTN

Etiology
Parenchymal
o Alcoholic
o Viral (Hep B, Hep C)
Metabolic
o Fe overload - hemochromatosis
o Cu overload - Wilsons disease
Biliary
o Primary biliary cirrhosis (autoimmune)
o Secondary to prolonged biliary obstruction
Hepatic venous outflow obstruction
o Budd-Chiari Syndrome (hepatic vein occlusion)
o Severe chronic CCF (cardiac cirrhosis)
Others
o Chronic active hepatitis in autoimmune disease
o Schistosomiasis e.g. In Egypt
o Nutritional - protein-deficient diet
o Idiopathic (cryptogenic)
o Parental nutrition related (possible due to fat content)
o Non-alcoholic steatohepatitis (NASH)
Consequence
Hepatocellular failure
Portal HTN
Ascites
Malignant change
Clinical features
Gynaecomastia
Testicular atrophy
Amenorrhea
Spider naevi
Finger clubbing
Palmar erythema (hyperestrinism - failure of liver to inactivate estrogen)

HEPATOBILIARY AND PANCREATIC SURGERY

APPROACH TO ASCITES
Causes of ascites
Transudate (<30g/L protein)
Cardiac: CCF, RHF, TR, constrictive
pericarditis
Abdo: CLD (low albumin)
Renal: ESRF, nephrotic syndrome
(loss of albumin)
GIT: protein losing enteropathy

Exudate (>30g/L protein)

Cirrhosis
Malignancy
Infective cause - TB
Chylous ascites

Pathogenesis in cirrhosis
Raised portal pressure -- transudation of fluid into peritoneal cavity alone
does not cause ascites (not seen in pre-hepatic obstruction of the portal
venous sys)
Liver damage -- low albumin -- low plasma osmotic pressure -- deficient
reabsorption of ascetic fluid
o A/w increased aldosterone levels and Na retention
Increased lymphatic pressure in a cirrhotic liver -- lymph transudation
from liver surface
o Also present in post-hepatic block e.g. Hepatic veins/IVC
Physical Examination
Abdominal distention
Peripheral stigmata of CLD and portal HTN
o Clubbing, jaundice/scleral icterus, spider naevi etc.
Signs of fluid overload - LL/sacral edema, bibasal crepitations
Other signs of malignancy - cachexia
Flank dullness -- shifting dullness -- fluid thrill
Investigations
Peritoneal tap (see below)
o SAAG (serum albumin-ascites gradient) = serum albumin conc ascitic albumin conc
Normal = </= 1.1
> 1.1 -- ascites 2/2 portal HTN (i.e. Due to increased
hydrostatic pressure)
If (absolute) albumin level is high - CCF/Budd-Chiari
syndrome; if albumin is low - cirrhosis
CT AP (triphasic) - look for liver pathologies e.g. HCC that can develop
on background of cirrhosis

58

!
Rx of ascites
Conservative
o Low salt, high protein diet + fluid restriction
o Diuresis - spironolactone +/- thiazide or loop diuretic
o Drip - IV albumin

Peritoneal tap/paracentesis
o Role
Diagnostic: send fluid for FEME, protein, microbiology,
cytology
Therapeutic: relieve discomfort and diaphragm splinting
due to distention
o Indications
Failed medical treatment
Symptomatic
o Procedure
Aseptic technique, LA, U/S guidance
May insert pigtail catheter via Seldinger technique
Open drain into stoma bag
o Complications: patient loses protein
Replace 10g albumin/L of ascitic fluid removed
Surgical
o Shunt surgery
Anastomosis of portal vein/SMV to IVC
Peritoneovenous shunting
Portacaval shunting
Trans-jugular intrahepatic portosystemic shunt (TIPSS)
Under radiologic control
Involves the creation of an intrahepatic
portosystemic shunt
o Hepatic vein is cannulated via the
internal jugular vein
o Intrahepatic portal vein punctured
percutaneously
o Guide wire passed from portal to hepatic
vein
o Stent is then passed along guide wire
But porto-systemic shunts predispose to
encephalopathy - pt has to be maintained on
low-protein diet forever and must be Childs A
o Liver Transplantation
For intractable ascites secondary to hepatic cirrhosis

HEPATOBILIARY AND PANCREATIC SURGERY

GALLSTONES
Gallstones are found in 10% men and 20% women
Prevalence increases with advancing age
o 10-20% become symptomatic
Female, Fatty, Fertile, Forty, Flatulent
Pathophysiology
10% of gallstones are radio-opaque
Cholesterol stones result from a change in solubility of bile constituents
Bile acids act as a detergent keeping cholesterol in solution
Bile acids, lecithin and cholesterol result in the formation of micelles
o Biliary infection, stasis and changes in gallbladder function can
precipitate stone formation
o Bile is infected in 30% of patients with gallstones
o Gram-negative organisms are the most common isolated
Three types of stones are recognized
o Cholesterol stones (15%)
40-50 y/o
Risk factors for increased cholesterol secretion: obesity,
hyperlipidaemia, increased estrogens
Risk factors for decreased GB emptying: GB malignancy
must be excluded
o Pigment stones (5%)
black (found in GB) or brown (found in ducts)
Risk: increased secretion of bilirubin into bile e.g.
Chronic hemolysis, CLD, TPN, gallbladder stasis,
infection with bacterial degradation of biliary lipids
(insoluble pdts)
o Biliary sludge = microlithiasis suspended in bile
Predispose to stone formation, pre-stone condition
On US - layering in biliary tree
o Mixed stones (80%)
Variant of cholesterol stones
Bile is often supersaturated with cholesterol
This favours the formation of cholesterol microcrystals

59

!
Clinical Course
Asymptomatic (80-95% of gallstones)
o Risk of symptom occurrence is 1-2% per year, greatest risk
within 1st 5yrs of diagnosis
o Majority of patients do not require removal of stones or GB -expectant management
o Role of surgery in the asymptomatic patient
Predisposing cause for GB stasis e.g. GB mass with
suspicion of malignancy (polyp, porcelain GB) -prophylactic surgery
Immunocompromised - abnormal presentation, difficult to
detect
Patients with chronic hemolytic disease (e.g. Sickle cell
anaemia) - ~50% chance of symptomatic disease in their
lifetime
Symptomatic
o Biliary colic
Typically epigastric or RHC pain (may radiate to inferior
angle of right scapula or tip of right shoulder)
Waxing-waning in character but rarely pain-free intervals
between waves of pain (unlike ureteric colic)
Often triggered by meals - oily
Lasts for few mins-hrs; resolves spontaneously
Associated with N/V (relieved by vomiting), bloating,
abdominal distention flatulent dyspepsia
Biliary colic is herald symptom for risk of further
sequelae
o Acute cholecystitis
o Mucocoele (hydrops) of GB or empyema
o Mirizzis syndrome
o Choledocholithiasis with obstructive jaundice
o Cholangitis +/- sepsis
o Acute pancreatitis
o Fistula formation and passage into gut -- gall stone ileus
(subacute IO)

HEPATOBILIARY AND PANCREATIC SURGERY

Investigations
Laboratory
FBC, UECr, Amylase, Lipase , PT/PTT, Hepatitis serology, blood
cultures if febrile, Cancer markers: CA19-9, CEA, LFT, Albumin
Urinalysis for conjugated bilirubin and urobilinogen
Imaging
Plain AXR (but only 10% of stones are radio-opaque)
US HBS - investigation of choice for gallstones
o More sensitive than CT scan for stones (5mm cuts)
o Features of stone: strong echogenic rim with posterior acoustic
shadowing
o Bile in GB should be a black homogenous patch, otherwise -sludge
CT scan
o Not usually done for stones in particular, done when diagnosis is
uncertain and looking for other causes
Magnetic Resonance Cholangiopancreatography (MRCP)
o Cuts taken to construct biliary tree, w/o contrast
o Resolution comparable to ERCP, plus its minimally invasive preferred unless pt requires therapeutic interventions
Endoscopic Retrograde Cholangiopancreatography
o Diagnostic + therapeutic
Stone removal (balloon catheter or Dormia basket)
90% success, 8% morbidity
Sphincterotomy (to relieve obstruction + stone removal)
Stenting
o High level of complications
Pancreatitis 2-3%, cholangitis 1-2%
Hemorrhage 2-3%, perforation into bile duct/duodenum
0.5-1%
o Therefore, risk and benefits must be assessed and patients must
be selected carefully
Percutaneous transhepatic cholangiography (PTC)/biliary drainage
(PTBD)
o Tube into liver under radiologic guidance into a dilated biliary
duct
o Rarely done now unless
High obstruction which cannot be seen well on ERCP
Therapeutic purpose: drainage of obstructed system that
ERCP failed to drain from below
HIDA scan - only used in biliary atresia
60

5 criteria for normal cholangiopancreatogram (ERCP/MRCP/IOC)

o No filling defects
o Normal intrahepatic ducts
o Smooth CBD w normal diameter (no stricture/narrowing or dilation)
o Tapering of distal CBD (rat-tailing)
o Good and free flow of contrast into duodenum

Perioperative management of obstructive jaundice

Preoperative biliary decompression improves postoperative morbidity
Broad spectrum antibiotic prophylaxis
Parenteral vitamin K +/- fresh frozen plasma
IV line & catheter
o Pre-operative fluid expansion
o Need careful post-operative fluid balance to correct depleted
ECF compartment
Management
Asymptomatic
No surg required unless pt has indication (e.g. GB polyp, hemolytic
anaemia, immunocompromised)
Counsel symptoms - biliary colic, acute cholecystitis, obstructive jaundice
Symptomatic
Initially: ERCP Therapeutic, but if failed, consider:
o Open cholecystectomy + exploration of CBD
o Laparoscopic exploration of CBD
o Mechanical lithotripsy (80% successful after failure of ERCP)
o Extra-corporeal shockwave lithotripsy
o Chemical dissolution with cholesterol solvents
Administered via T Tube or nasobiliary catheter
25% complete response and 30% partial response
o If retained stones after CBD exploration need to consider:
Early ERCP or Exploration via T tube tract at 6 weeks
Cholecystectomy only definitive Rx for symptomatic GB stones (Open or
lap - lap has shorter hospital stay, less pain & post-op complications)
o Risk of lap
Conversion to open ~5% (due to abnormal anatomy,
difficult/complicated dissection/iatrogenic injury)
Conversion rate higher if there is ongoing infection e.g.
Cholecystitis/pancreatitis
o Risks of both
Injury to surroundings - bowel and biliary strs e.g. CBD
Spilled bile - peritonitis & sepsis
Infection and bleeding
HEPATOBILIARY AND PANCREATIC SURGERY

ACUTE CHOLECYSTITIS

90% cases result from obstruction to the cystic duct by a stone

Increased pressure within the gallbladder results in inflammation
Secondary bacterial infections occurs in 20%
Most common organisms are E. coli, Klebsiella and strep. faecalis

Presentation
Constant pain (usually greater than 12 hours duration) in RUQ
o Radiating to inferior angle of scapula
Fever, tachycardia
Murphy's sign - guarding in right upper quadrant on deep inspiration
o Possible palpable GB (omentum or empyema)
Complications of acute cholecystitis
Hydrops
o Tense GB filled with mucus (sec to cystic duct obstruction)
o If pressure exceeds capillary blood pressure - GB wall necrosis
Empyema
o GB filled with pus due to bacterial infx of stagnant bile
o Patient usually toxic, surgery required
Gangrene & perforation
o Localized perforation -- abscess confined by the omentum
o Free perforation -- generalized peritonitis, sepsis, requires
emergency laparotomy
Fistula formation - cholecystenteric
o Most commonly to duodenum, 2nd colon, 3rd stomach
o Occurs after repeated attacks of acute cholecystitis
o Usually asymptomatic
o On AXR, may see aerobilia (40%) i.e. Accumulation of air
o Rx if symptomatic: cholecystectomy and fistula closure
Gallstone ileus
o Due to cholecystenteric fistula passing into enteric lumen
o Causes intermittent bouts of SBIO (1-2% of all IOs)
Most common site of obstruction is terminal ileum
Small stones usually pass w/o symptoms
o Mortality is 10-15%, mainly in elderly patients
o Rx
Small bowel enterotomy proximal to the point of
obstruction is usually required to remove stone
Immediate cholecystectomy not warranted, <4% of
patients will have further symptoms
61

!
Investigation
Ultrasound is the initial investigation of choice
o Presence of gallstones / sludge
o Distended thick-walled gallbladder
o Pericholecystic fluid
o Murphy's sign demonstrated with ultrasound probe
CT as above, with the addition of fat stranding
** LFTs usually normal and no jaundice
Will show failure of isotope uptake by gallbladder
Management
Conservative (80% patients improve with conservative treatment)
Resuscitate ABC
Septic workup (blood c/s)
NBM, IV fluids, opiate analgesia
Empirical IV roc/flagyl
80% patients improve with conservative treatment
If fit, should be considered for a laparoscopic cholecystectomy
Surgery
Pre-operative ERCP is indicated if:
o Recent jaundice
o Abnormal liver function tests
o Significantly dilated common bile duct
o Ultrasonic suspicion of bile duct stones
Evidence now suggests that early surgery (less than 72 hours) is safe
o Less fibrosis, easier to operate on edematous DB
o No need for readmission; decreased length of hospitalization
o Slightly higher rate of conversion to open chole or injury of
adjacent structures
o But depends on severity of illness, response to resus and IV abx,
and logistical factors
Std practice: Delayed/interval cholecystectomy (6-8wks) if presentation
delayed >3 days after symptoms, if gallbladder if palpable or if WBC >18
If patient unfit for surgery, percutaneous cholecystotomy may be beneficial
o In moribund patients not fit for surgery who have failure of
systemic therapy i.e. IV Abx
o Usually done under LA, percutaneous with radiological guidance
o Drains GB and alleviates inflammation --> better outcomes
o Particularly useful in acalculous cholecystitis
Ill patients with prolonged stay + fasting + TPN biliary
stasis + dehydration bile infection
Maintenance before emergency cholecystectomy
HEPATOBILIARY AND PANCREATIC SURGERY

62

!
CHOLEDOCHOLITHIASIS
Presents with: Obstructive jaundice + Biliary colic
Investigations
Bloods
FBC -- TW must be trended for any sign of inflammation
Amylase -- CBD stone may cause pancreatitis
LFTs -- raised bilirubin (direct/conjugated), ALP raised > AST/ALTs
Imaging
US HBS
o Stones in GB
o Gallstone in CBD (but only visible in 50% due to obscuring gas in
duodenum)
o Dilated CBD (normally 5mm or less)
>10mm is abnormal
EUS/MRCP/ERCP or PTC -- can confirm intraductal stones
Management
If not sure about stone -- less invasive investigation e.g. EUS/MRCP
If likelihood of CBD stone is high -- ERCP with stone removal
If ERCP successful -- plan for lap chole
If ERCP failed -o Patient well, can tolerate another ERCP -- try again (+/- stent in
between to drain bile)
o If not -- (Intra-operative cholangiogram) operative removal
Open CBD exploration
Lap CBD exploration
If no facility to do ERCP - open or lap cholecystectomy with IOC and
CBD exploration

MIRIZZIS SYNDROME
Pathology
Gallstone in Hartmanns pouch (infundibulum of GB) compressing the
common hepatic duct resulting in obstructive jaundice
o Compression effect is physical (stone) and also contributed by
the surrounding inflammation
One of the caveats to Courvoisiers law (in the presence of jaundice, a
non-tender enlarged GB is unlikely to be due to stones)
o Because stones causing obstruction occurs in chronic
cholecystitis - gallbladder wall is thickened -- no distention
possible
Grading
Grade I - no fistula, only extrinsic compression of CHD
Grade II - fistula formation with common bile duct, with the fistula <1/3
diameter of the CHD
Grade III - fistula 1/3 to 2/3 diameter of CHD
Grade IV - fistula >2/3 diameter of CHD
Management
Grade I & II - attempt lap chole
Grade II - IV - open cholecystectomy with CBD exploration

Indications for surgical stone removal

(i.e. Not suitable for ERCP)
Stone problems
o Stone >25mm
o Intrahepatic stone
o Large number of stones
o Impacted stone
Duct problems
o Duct pathology
o Tortuous duct
o Previous bilroth II surgery (anatomy no can do ERCP)

HEPATOBILIARY AND PANCREATIC SURGERY

63

!
CHOLANGITIS
Presentation
Classically: Charcots triad (Fever, RUQ pain, jaundice)
Reynolds pentad: Charcots triad + altered mental status and
hemodynamic instability (esp in elderly)
Surgical emergency!
Pathology
Obstruction to biliary system -- stagnant bile gets infected
Causes:
o Choledocholithiasis (60%)
o Benign strictures
o Malignancy - pancreatic (extramural) or biliary e.g.
Cholangiocarcinoma (intramural)
Common organisms - Gram negative bacteria + anaerobes
o Klebsiella, E.coli, Enterobacter, Enterococcus
Management
Resuscitation
o ABC - obtain good IV access and fluid resuscitate as appropriate
o Bloods + C/S
o Close monitoring
Vitals in ICU/HD
Urine output - put in-dwelling catheter (IDC)
If patient has shock that does not respond to fluid
challenge -- CVP line insertion
Antibiotics - IV rocephin, flagyl; add imipenem if patient in shock
Biliary decompression & definitive Rx
o Investigate for cause of obstruction - U/S or CT scan
U/S HBS preferred if suspecting stones
o Decompression commonly performed using ERCP
Primary objective = Decompression - stenting or
nasobiliary drain can be used
If cause of obstruction i.e. Stone is found - can be
treated/removed Success rate 90%
o Definitive Rx dependent on
Medical condition of patient
Success of biliary decompression
Logistical considerations
o Choices for definitive Rx
Lap or open cholecystectomy +/- intra-operative
cholangiogram (IOC done in cholangitis)
HEPATOBILIARY AND PANCREATIC SURGERY

CBD Exploration
Based on site and cause of obstruction
o Cholangiogram - inject dye to image higher ducts
o Choledochoscopy - scope to see large biliary ducts, cannot
image higher ducts, not as sensitive (but can remove stone)
Removal of stone
o Manual = forceps to grasp stone
o Flushing out of stones
o Dredging stones with ballon catheter or Dormia basket
o Lithotripsy
Consider use of biliary stent or T tube after stone removal (If significant
instrumentation of biliary sys during operation would result in swelling &
edema of biliary system -- post-op obstruction and build-up of bile -higher risk of biliary leakage)
o Stent -- removed later by endoscopy
o T-tube (usually after CBD exploration)
o Horizontal limb in CBD, vertical limb leading out
o Functions as pressure release valve - most of bile flows through
into distal CBD, only diverted out if there is obstruction to flow
o Allows for post-op cholangiogram to check for remaining stones
(POD9-10) before removal
Normal: Free flow of contrast into duodenum, no residual
stones, no free leak of contrast into duodenum
If normal - release anchoring stitch and pull gently
If stones are present, leave tube in for 4-6 wks to form a
fibrous tract -- allows for instrumentation of tract with
scope to remove stones
Consider biliary bypass if
o Multiple stones, CBD >2cm diameter, or strictures present (as
chronically dilated CBD unlikely to function normally after
removal of obstruction)

64

!
RECURRENT PYOGENIC CHOLANGITIS
AKA cholangiohepatitis
Pathophysiology
Helminth infx (e.g. Ascaris/clonorchis) -- epithelial damage -- predispose to
seeding of coliforms into biliary system -- stone formation -- recurrent cholangitis
Recurrent bacterial cholangitis
Intrahepatic pigment stones
Intrahepatic biliary obstruction

Management
Treat current infx
Biliary drainage - stent
Definitive (surgical) biliary drainage - e.g. Roux-en-Y
choledochojejunostomy above the level of strictured CBD
Prognosis = death in approximately 20% of patients over 5-6yrs

History
Recurrent attacks of cholangitis
o 1-2 episodes of fever, jaundice, RUQ abdo pain/yr
o Hx of previous biliary surg/endoscopic procedures/perc drainage
Complications of recurrent pyogenic cholangitis
o Cirrhosis with portal HTN (secondary biliary cirrhosis)
o Cholangio CA
DDx: primary sclerosing cholangitis
Investigations -- for diagnosis & complications
Bloods
o FBC
o LFT with ALP>ALT/AST
o PT: may be normal or increased (prolonged cholestasis causes
fat malabsorption & Vit K deficiency)
Important TRO increased PT / correct with parenteral
Vitamin K before any invasive procedures e.g. PTC
o Blood C/S: can guide choice of Abx
Stool ova parasites: freq a/w clonorchis infx -- treat if present
Imaging
US HBS
o Segmental biliary dilation
o Hepatolithiasis
o Liver abscess
ERCP/PTC - to delineate biliary tree
CT scan

HEPATOBILIARY AND PANCREATIC SURGERY

65

!
CHOLANGIOCARCINOMA
Arises from bile duct epithelium, occurs anywhere along biliary tree
Tumors usually locally invasive (spread microscopically along bile ducts)
Metastasize to involve liver & peritoneum
Site

Intrahepatic - 25%
Extrahepatic upper duct a.k.a. Hilar/Klatskin tumor
Extrahepatic lower duct

Bismuth Classification
Type I: below confluence of L & R hepatic ducts
Type II: tumor involves confluence of L & R hepatic duct
Type IIIA/B: involving common hepatic duct & either L or R hepatic duct
Type IV: multicentric or involving confluence and both hepatic ducts
Associations and Risk Factors
Age
Related to chronic cholestasis
o Primary sclerosing cholangitis (inflammation, destruction,
scarring of bile ducts)/ulcerative colitis
o Hepatolithiasis
o Parasitic infection - Opisthorchis and Clonorchis species
o Carolis disease (multifocal segmental dilation of large
intrahepatic bile duct)
Bile duct adenoma
Choledochal cyst
Thorotrast exposure
Presentation
Painless jaundice (only painful if there is cholangitis)
Acholic stools (pale)/tea-colored pee
Advanced s/s:
Abdominal pain, LOW, Fatigue/malaise, Hepatomegaly
Investigations
Bloods
LFTs to confirm increased bilirubin
CA 19-9 > 100ul/ml (good sensitivity of 89%, specificity 86%)
o Usually used for pancreatic ca
CA 125

HEPATOBILIARY AND PANCREATIC SURGERY

Imaging (from simplest least invasive to more advanced less invasive)

Diagnostic:
o *CT AP - to delineate mass and define its relation to liver
o *MRCP - look at tumor, r/s to key vessels & intrahepatic mets
o U/S - look at bile duct masses, dilation, assess extent of tumor
involvement within the liver and portal vein
o EUS with FNA - lower bile duct strictures and masses
Diagnostic and therapeutic
o *ERCP
Diagnostic - biopsy for histological analysis!
Distal tumors vs small pancreatic carcinomas
But if obstruction is complete - may not be able
to delineate upper limit of tumor
Therapeutic - decompression of the biliary tree
If cholangitis is present or if bilirubin very high
o PTC - when MRCP/ERCP fails/cannot delineate the upper limit
Diagnostic - FNA cytology
Therapeutic: decompression (may be palliative)
Curative Treatment
Surgery only chance for long-term cure
Tumour is resected and biliary reconstruction is performed
1 in 4 tumors resectable
o Extent of tumor, vascular invasion, hepatic lobar atrophy,
metastatic lobar atrophy, metastatic disease
Contraindications to surgery:
o Distant mets
o Cant resect both lobes of liver
Bilateral or multifocal intrahepatic disease
Unilateral hepatic vascular invasion w contralateral
ductal spread
o Vessels involvement
Invasion of portal vein trunk or hepatic artery (proximal
vessel that supplies both lobes)
Bilateral involvement of hepatic artery or portal vein branches
Prognosis for resectable disease (5yr survival)
Intrahepatic ~40% ;
Distal ~40%
Perihilar 10-30% -- early lymphatic spread (LNs at portal hepatis)
Palliation
ERCP or PTC biliary stenting
Bilateral drainage for hilar cholangiocarcinoma
Surgical bypass can be performed
66

!
ACUTE PANCREATITIS
Aetiology
Gallstones and alcohol account for 80% cases of acute pancreatitis
Gallstones less than 5mm diameter are more likely to cause pancreatitis
than larger ones
Less than 5% patients with gallstones develop pancreatitis
Aetiological factors can be summarized as follows:
o Idiopathic - 20%
o Obstruction
Choledocholithiasis 40%
Ampullary or pancreatic tumours
o Pancreatic structural anomalies
o Toxins
Alcohol 40%
Drugs Steroids, NSAIDs, diuretics, sulphonamides
o Trauma (Accidental or Iatrogenic)
o Metabolic abnormalities
Hyperlipidemia 7%
o Infection (Mumps)
o Vascular anomalies
Epidemiology
80% have mild disease
40% of those with severe disease develop infected pancreatic necrosis
The mortality associated with infected necrosis is about 40%
50% of deaths occur within first week due to multi-organ failure
Pathophysiology
Final common p/w - inappropriate activation of proenzymes stored within
zymogen granules in pancreatic cell
o Trypsin is implicated as it activates most of the proenzymes
secreted by the pancreas
Activated lytic enzymes destroy pancreatic acinar cells -- release potent
cytokines attract neutrophils & macrophages pro-inflamm cytokines
Cytokine cascade amplifies local inflammatory response + results in
systemic inflammatory response: T<36 or >38, HR > 100, RR >20, TW>15)
May progress to sepsis and septic shock and multi-organ dysfunction
Gallstones obstruct pancreatic duct -- interstitial edema -- impairs blood
flow to acinar cells -- ischaemic cellular injury -- predispose to enzyme
activation
Alcohol generates free radicals during metabolism - direct injury
o May sensitize pancreas to injury by other agents
HEPATOBILIARY AND PANCREATIC SURGERY

Clinical features
Sudden onset constant epigastric pain radiating to the back
o Tenderness may be localised to epigastrium or generalized
o Palpable pseudocyst or phlegmon
o Abd distension due to ileus
Alleviated by sitting up and leaning forward
N/V, anorexia, fever, dehydration
Elicit etiology!
Differential diagnosis includes
o PUD (ask PMHx of dyspepsia)
o Perf viscus
o Acute cholecystitis / hepatitis assess jaundice/hepatitis
o Mesenteric ischaemia
o AMI (ask CP, diaphoresis, palpitations)
Ecchymoses of retroperitoneal haemorrhage are rare and appear late
o Cullen's sign, Grey Turner's sign
Causes of hyperamylasaemia
Perforated peptic ulcer
Cholecystitis
Generalized peritonitis

Intestinal obstruction
Mesenteric infarction
Ruptured AAA
Ruptured ectopic pregnancy

Diagnosis
Serum amylase (normal = 100)
o >3x upper limit of normal (sensitivity 60%, specificity 95%) or >1000iu/l
o Raised between 12-72 hrs not useful in late diagnosis
o 20% cases of pancreatitis have normal serum amylase
(particularly alcoholic aetiology)
Serum lipase more sensitive and may remain elevated longer
o >3x upper limit of normal has higher sensitivity and good specificity
o Rises within 8 hrs of onset, returns to normal after 7-10 days
Urine diastase (similar to lipase)
Features suggestive of a gallstone aetiology include:
o Female sex
o Bilirubin > 25 umol/L
o Age more than 50 years
o AST > 100 IU/L
o Amylases > 4000 IU/L
o ALP > 300 IU/L

67

!
Severity stratification and etiology
Imaging
Erect CXR - look for free gas, pleural effusion, pulmonary infiltrates,
ARDS complete whiteout

AXR
o
Sentinel loop sign or colon cut off sign -- due to ileus (functional
spasm due to nearby inflammation)
o
Calcification in chronic pancreatitis

US HBS - Can visualize biliary tree and pick up gallstones, can visualize
diffusely enlarged and hypoechoic pancreas
o
Alternatively - MRCP/EUS/ERCP if stone is likely
CT AP - if looking for complications of pancreatitis (1 wk or more later), if
other findings unequivocal
A Normal
B Focal or diffuse glandular enlargement
Small intra-pancreatic fluid collection
C Any of the above
Peripancreatic inflammatory changes
Less than 25% gland necrosis
D Any of the above
Single extrapancreatic fluid collection
25-50% gland necrosis
E Any of the above
Extensive extrapancreatic fluid collection
Pancreatic abscess
More than 50% gland necrosis
Laboratory
FBC - TW, hematocrit
UECr - Urea, any electrolyte imbalances or dehydration
LFTs - AST, albumin, to look for obstructive picture in gallstone pancreatitis
LDH
ABG - PaO2, base excess
Ca/Mg/PO4 with albumin - hypercalcemia etiology
Fasting lipids - hyperlipidaemia etiology
ECG & cardiac enzymes - to exclude AMI
Danger signs in 1st few hours
Encephalopathy
Hypoxaemia
Tachycardia >130/min, hypoBP <90mmHg, hematocrit >50
Presence of ecchymoses signs
Oliguria <50mls/hr, azotemia
HEPATOBILIARY AND PANCREATIC SURGERY

Prognostic factors (identify severe pancreatitis)

Ranson's criteria (>=3 is severe)
On admission
Within 48 hours
o Age > 55 yrs
o Haematocrit fall >10%
o WCC > 16,000
o Urea rise >0.9 mmol/l
o LDH > 600 U/l
o Calcium < 2 mmol
o AST > 120 U/l
o pO2 < 60 mmHg
o Glucose > 10 mmol/l
o Base deficit > 4
o Fluid sequestration > 6L
APACHE II score
Multivariate scoring system (assesses ICU patient condition)
Measure objective parameter - vital signs and biochemical analysis
Account for premorbid state and age
Can be used throughout course of illness
C-Reactive Peptide
At 48hrs, if >210mmHg - more likely to be severe
More than 3/7 - useless as other confounding factors enter
Complications of acute pancreatitis
Local
Necrosis +/- infection
Pancreatic fluid collections
Colonic necrosis
Gastrointestinal haemorrhage
Splenic rupture

Systemic
Hypovolaemia and shock
Coagulopathy
Respiratory failure
Renal Failure
Hyperglycaemia
Hypocalcaemia

Course of disease
75% mild course, will recover unless comorbidities cause deterioration
20-25% severe outcome, 1/3 of these eventually die (mortality overall <10%)
o Death is bimodal
Early (within 1/52) - due to SIRS and severe organ failure
Late - usually due to infection & resultant sepsis -- MOF
Timing of intervention in pancreatitis
All patients should undergo ultrasound within 24 hours of admission
If confirms gallstones and severe pancreatitis consider ERCP in 48 hrs
If not stable after 1 wk Contrast enhanced CT to assess pancreatic necrosis
If suspicion of infection - CT guided aspiration
Consider pancreatic necrosectomy if
o Clinical deterioration
o Bacteriological proof of infection
Antibiotics do not prevent infected necrosis in acute necrotizing pancreatitis
Operative mortality >40%
68

!
Supportive treatment of pancreatitis
Monitor (after resuscitating)
o If severe -- HD/ICU monitoring
o Fluid resuscitate with crystalloids
o Monitor vitals (SpO2, BP, HR, Temp), urine O/P and CVP
NBM (bowel rest) and IV fluids
o NGT decompression if required (severe vomiting, ileus or
gastroparesis)
o Acid suppression (IV omeprazole) to protect against stress ulcer
formation
o NBM for at least 2/7 until more stable - restart clear fluids if
tolerated (mild disease)
o Correct any dehydration and electrolyte abnormalities
(hypocalcemia, hypoglycaemia)
Analgesia
o No NSAIDs - can worsen pancreatitis & cause renal failure
o Use opioids - tramadol/pethidine (just not morphine)
Abx (?)
o Current practice not to give for pancreatitis
o Two situations to give - cholangitis or infection of necrosis or
abscess (CTAP + TW)
Imipenem for infected (or fluoroquinolones); IV Roc/flag
for cholangitis
Support for organ failure
o Hypoxaemia -- ventilate with PEEP (positive end-expiratory
pressure)
o Acute renal failure -- Dialysis & CVP monitoring
o Hypotensive -- fluid resuscitate + inotropes
ERCP may be of benefit within the first 48 hours in patients with
predicted severe disease
Monitor for complications & manage
Treat etiology
Avoid alcohol
Stop any offending meds
Control hyperlipidaemia
Biliary pancreatitis - cholecystectomy
If mild, can do cholecystectomy in same admission
1 in 5 patients with biliary pancreatitis will have recurrence, 1/4 - 1/2 of
these will occur in the next month

HEPATOBILIARY AND PANCREATIC SURGERY

Local

Acute fluid collections (35%)

Pseudocyst (15%) = persistent fluid collection walled off by fibrosis -- no
epithelial-lined surface >6cm for >6wks
o Presents as GOO, infx, peritonitis, hge (due to erosion of
vessels), persistently raised amylase (after resolution of
pancreatitis)
o Usually resolve spontaneously (half). Even if they dont, dont
poke them intervention at 6 weeks
o U/S, CT, ERCP
o Check for duct anatomy and fistula
Abscess = fluid collection of pseudocyst
Pancreatic necrosis - CT shows areas of no IV contrast uptake
Infected necrosis - CT shows gas bubbles, positive culture on FNA (CT
or US guided)
Chronic pancreatitis (with endocrine or exocrine insufficiency)

Systemic complications
Peritoneal sepsis
Pancreatic ascites -- massive fluid accumulation of fluid in peritoneum
Intra-abdominal hge -- erosion of vessels, usually splenic
Multi-organ failure - ARDS, ARF, hypovolemic shock, DIVC
Intervention for local complications
ERCP
o Indications: severe pancreatitis/pt not improving, evidence of
ductal stones, concomitant cholangitis
CT-guided aspiration of pancreatic necrosis
o Differentiate between sterile and infected necrosis - to consider
surgery if patient deteriorating
Role of surgery
o Infected necrotic pancreas - mortality 100% w/o op -- do
necrosectomy/resection of pancreas
o Sterile necrotic pancreas (necrosectomy)
Delay surgery till as late as possible for demarcation of
necrotic areas (repeated surgeries if required)
Surgery can be open, lap, endoscopic or percutaneous
o Diagnostic uncertainty
o Complications e.g. Intra-abdominal hge
Nutritional support
Pancreatitis is associated with a catabolic state
Evidence that early enteral nutrition is safe (Nasojejunal feeding limits
pancreatic secretion, preferred over oral or nasogastric feeding)
69

!
CHRONIC PANCREATITIS

Chronic inflammatory disease of the pancreas

o Results in irreversible destruction of both the endocrine &
exocrine pancreatic tissue
o Pancreas may appear macroscopically normal

Aetiological factors
Alcohol
Tobacco
Pancreatic duct strictures
Pancreatic trauma
Hereditary pancreatitis
Tropical pancreatitis
Epidemiology
Male to female ratio is approximately 4:1
Mean age of onset is approximately 40 years
Clinical progression
Early stages of the disease episodes of acute pancreatitis
Late stage of disease is characterized by pancreatic fibrosis &
calcification
Pancreatic duct dilatation and stricture formation occurs
o Cysts form within the pancreatic tissue
Chronic pancreatitis increases the risk of pancreatic carcinoma
Clinical features
Local chronic pain is the principal symptom in most patients
o Usually epigastric, sub-costal and radiating to the back
o Pain may be continuous or episodic
o Often interferes with life and may lead to opiate abuse
Nausea and vomiting
Weight lost may occur + Decreased appetite
Loss of exocrine function produces malabsorption and steatorrhoea
Loss of endocrine function results in diabetes
Complications:
o Pancreatic pseudocyst
o Fistulae
o Ascites
o Pancreatic cancer

HEPATOBILIARY AND PANCREATIC SURGERY

Investigation
Serum amylase is often normal
Plain abdominal x-ray may show pancreatic calcification
CT or MRI is the most useful investigation for imaging the pancreas
May confirm pancreatic enlargement, fibrosis and calcification
ERCP has a high sensitivity for detecting chronic pancreatitis
MR pancreatogram will outline the state of the pancreatic duct
Pancreatic function test rarely provide useful information
o Direct tests - e.g. secretin-pancreozymin test, Lundh test
o Indirect tests - e.g. serum trypsin, faecal fat analysis
On imaging criteria it can be difficult to differentiate chronic pancreatitis
from carcinoma
Treatment
Treat underlying cause (e.g. alcohol, ductal stricture)
Low fat diet and alcohol abstention is essential
o Surgery is associated with significant morbidity and mortality
Does not arrest loss of endocrine and exocrine function;
used for:
Persistent local complications e.g.
Pseudocyst/fistulae/local obstruction of
CBD/duodenum 2/2 fibrosis
Pain relief - pancreatectomy, celiac plexus block,
thoracic splanchnicectomy
If performed is aimed at:
Removing any mass lesion
Relieving pancreatic duct obstruction
Mass lesion can be removed by
pancreaticoduodenectomy or a Beger procedure
Duct obstruction can be relieved by
Puestow procedure - side-to-side pancreaticojejunostomy
Pancreaticojejunostomy
Frey procedure
Disease confined to pancreatic tail may require distal
pancreatectomy
Surgery relieves symptoms in 75% of patients
Symptomatic
o Analgesia (avoid opiates to prevent addiction
o Pancreatic enzyme supplements may
Reduce steatorrhoea
Reduce frequency of painful crises
o Control blood sugar with insulin
70

!
PANCREATIC CARCINOMA

More than 80% of cases occur between 60 and 80 years of age

Male : female ratio is 2 : 1
Median survival for unresectable disease is 6 months (80% of patients)
Overall 5-year survival <5%

Clinical features
Asymptomatic (incidental screening finding) vs symptomatic
Most are gradual - dull, mid-epig pain, malaise/fatigue, nausea, LOW, LOA
30% present with painless progressive obstructive jaundice
Head of pancreas or periampullary
Pancreatic body/tail (late)
- Obstructive jaundice (painless with - Celiac and mesenteric plexus invasion
palpable GB, +/- cholangitis) dull constant pain in epigastrium
icterus, pruritus, stool/pee
radiating to back
changes (note: Courvoisier sign in - Malaise, LOW, LOA, nausea
periampullary tumors)
- Exocrine insufficiency if duct obstructed - Duodenal obstruction
steatorrhea/malabsorption
- Bleeding upper GIT - Metastatic symptoms: ascites, bone
hematemesis/melaena
pain, SOB, dyspnea
- Constitutional - Paraneoplastic syndromes migratory
LOW/LOA/malaise, nausea
thrombophlebitis in 6%
Pathology
Most commonly ductal adenocarcinoma (75% head, 20% body, 5% tail)
Neuro-endocrine tumours of the pancreas (PNET)
o Often produce hormones causing defined clinical syndromes
o Non-functioning tumours have increased risk of malignancy
Insulinoma
Gastrinoma
Commonest PNET
Presents with Zollinger-Ellison
syndrome
Presents with:
o Impaired consciousness
Causes intractable peptic ulcer
o Personality change
disease at unusual or multiple
o Sweating and fainting
sites, resistant to normal therapy
attacks in 30%
20% patients develop diarrhoea
Fits occur in 30% of patients
& weight loss
Associated with
Diagnosis confirmed by
hypoglycaemia, symptoms
increased serum gastrin on
relieved by food
secretin stimulation
Diagnosis confirmed by
Also need to confirm gastric
increased insulin and CRP
hypersecretion
10% tumours are malignant
60% tumours are malignant
HEPATOBILIARY AND PANCREATIC SURGERY

Associations
Well-known: Cigarette smoking, alcoholism & industrial carcinogens
Disease states: Chronic pancreatitis
Genetic factors (K-ras, p16), familial cancer syndromes (FAP, Von Hippel
Lindau, hereditary breast ca, Gardners syndrome)
Investigations
Differentiate with peri-ampullary tumor
Duodenum (best outcome), bile duct or ampullary duct
Better tumor biology; present earlier with obstructive jaundice (better prognosis)
Computerized tomography (most useful)
Spiral CT has improved on resolution of conventional CT
Has sensitivity of greater than 95% for detection of pancreatic tumours
Contrast-enhanced triple-phase imaging is modality of choice
Features:
o Hypoattenuating indistinct mass that distorts normal architecture
of pancreas, bile & pancreatic duct dilation in head of pancreas
tumors (double duct sign)
o Look for evidence of extra-pancreatic spread - TNM staging:
regional LNs, liver mets, ascites
o Determine resectability of tumor: no distant mets, preserved fat
plane btwn mass and SMV/portal vein, no tumor encasement of
celiac, hepatic or superior mesenteric artery
Ultrasound
Abdominal ultrasound has sensitivity of about 80% for the detection of
pancreatic cancer; Detects level of biliary obstruction, excludes
gallstones and may identify pancreatic mass
Doppler ultrasound allows assessment of vascular invasion
Staging
CT AP - T, N staging + liver mets
EUS - T, N
CXR + CT thorax - lung mets
Bone scan - if there is suspicious signs and symptoms
Laparoscopy
o Laparoscopy will identify liver or peritoneal metastases in 25% of
patients deemed resectable after conventional imaging
o Laparoscopic ultrasound has improved predictability of resection

71

!
Curative Management
Resectional surgery
Resection is the only hope of cure (15% tumours are resectable)
o Tumour size (<4 cm)
o Presence of ascites, nodal, peritoneal or liver metastases
o Patent veins (superior mesenteric and portal which run behind &
emerge from top)
o Definable fat plane between tumour and SMA and celiac axis
Pre-operative biliary drainage of unproven benefit
Has not been shown to reduce post-operative morbidity or mortality
High recurrence rate
Whipple's operation
Octreotide given for one week to reduce pancreatic secretion
Preceded by staging laparoscopy to confirm absence of peritoneal mets
Remove head of pancreas, CBD, GB, duodenum, prox 15cm jejunum,
distal stomach
Head of pancreas and duodenum excised followed by:
o End to side pancreaticojejunostomy
o End to side hepaticojejunostomy
o Duodenojejunostomy
Mortality - 2-7%; morbidity up to 30% (mostly mild)
Postoperative chemotherapy may improve survival
Complications
Intra-op/early
Late
Injury to liver, kidney, bowel
Long-term exocrine
insufficiency - steatorrhea,
Bleeding, infection/sepsis
malabsorp (Vit ADEK) 30%
Pancreatitis
Endocrine insufficiency DM
Anastomotic leak (5-20%)
(10%)
o may cause fistula formation or
Gastric stasis in PPPD
pseudocyst
Diarrhea resulting from
Intra-abdominal abscess
autonomic nerve injury during
Biliary anastomotic breakdown
LN dissection
GIT/Op-site hemorrhage
Pylorus-preserving proximal pancreaticoduodenectomy
Preserves gastric antrum and pylorus
Compared with Whipple's procedure
o Reduced morbidity, no change in mortality
o Fewer post gastrectomy symptoms
o Less entero-gastric reflux
o Improved post-operative nutrition
May be associated with gastric stasis & increased risk of local recurrence
HEPATOBILIARY AND PANCREATIC SURGERY

Palliative Management
85% of patients are not suitable for curative resection
Palliation of symptoms can be achieved either surgically or
endoscopically
Surgical palliation has initially higher complication rate
Produces better long-term symptom control.
Palliative treatment should achieve:
o Relief of jaundice by either endoscopic stenting or surgery
o Prevention of duodenal obstruction by gastrojejunostomy
o Relief of pain by coeliac plexus block
External biliary drainage now rarely required
Palliative chemotherapy (e.g. gemcitabine) controversial
Endoscopic stenting
Achievable in over 95% of patients
Complications include bleeding, perforation, pancreatitis
Mortality less than 3%
20% develop duodenal obstruction
Patency of plastic stents often only 3 to 4 months
Can be improved with the use of self-expanding wall stents
Palliative surgery
Biliary drainage can be achieved by choledocho- or cholecystojejunostomy
10% will develop duodenal obstruction
Triple bypass
o Choledocho/hepatico-/cholecysto-jejunostomy
o Gastrojejunostomy
o Jejuno-jejunostomy (prevents food reflux into biliary tree)

Removes risk of duodenal obstruction and often avoid recurrent jaundice

Analgesia
Pain occurs in over 80% with advanced
malignancy
Can be palliated with:
o Slow release morphine
o Coeliac nerve block
o Thoracoscopic section of
splanchnic nerves

72

!
LIVER HEMANGIOMA
Epidemiology
Prevalence of up to 20%
Female: male - 3:1
Pathogenesis
Congenital vascular malformation
Enlarges by ectasia (dilation)
Presentation
Incidental finding, Usually small & asymptomatic
o Most less than 5cm
o If large (>5cm) - may have nonspecific abdo symptoms e.g.
Upper abdo fullness or vague abdo pain
Mass effects
o Compression on surrounding organs
Pain - due to stretching of liver capsule
Rupture (<1%)
Kasabach-Merritt syndrome (for large hemangiomas)
o Consumptive coagulopathy + thrombocytopaenia
Heart failure
o Secondary to large AV shunt
Note: Malignant transformation does not occur
Diagnosis - radiological
US HBS
o Well-defined, lobulated, homogenous, hyperechoic mass (may
have hypoechoic regions - hemorrhage, fibrosis, calcifications)
o Compressibility of lesion is pathognomonic
Triphasic CT
o Slow enhancement of rims during arterial & portal-venous phase
o Enhancement progresses towards the centre of the lesion
o Brightest in delayed phase
o Note: biopsy contraindicated -- may precipitate severe hemorrhage

SIMPLE LIVER CYST

Epidemiology
Prevalence 1-3%
9:1 female predominance for symptomatic cysts
Half of cysts are solitary
Pathogenesis
Congenital malformation when an aberrant bile duct loses
communication with the rest of biliary tree & becomes progressively
dilated (fluid within cysts is not bilious)
No solid component, no septa
o Mixed cysts with septations are suggestive of malignancy
Note: cysts that communicate with biliary system = choledochal cysts
Presentations (with complications)
Torsion
Bleeding & rupture
Mass effect
o IVC compression
o Cholestasis due to CBD compression
o Portal HTN
Fistula formation with duodenum
Malignant change -- rare
Treatment if symptomatic
Aspirate
Ethanol sclerotherapy (painful)
Fenestration (open or lap) i.e. Unroofing of cyst
Excision/resection

Treatment - only if symptomatic or complicated

Follow-up/observation
Surgical
Indicated when symptomatic, complications or unable to exclude malignancy
Possible role for prophylactic surgery in large, lateral, inferior lesions
Higher risk for rupture!
HEPATOBILIARY AND PANCREATIC SURGERY

73

!
HEPATOCELLULAR CARCINOMA
th

Singapore: 4 most common cancer in men; Male : female ratio = 4:1

Peak presentation is 40 years; usually with background of cirrhosis
Aetiology
Types: Fibrolamellar (non-cirrhotic, non hepatitic) vs non-fibrolamellar (cirrhotic)
Cirrhosis
Alcohol
Viral hepatitis - particularly
NAFLD
Hepatitis B and C
Anabolic steroids
Metabolic triad:
Primary liver diseases - e.g.
alpha-1 anti-trypsin deficiency,
primary biliary cirrhosis
Wilsons disease,
Mycotoxins - e.g. aflatoxin
hemochromatosis
produced by Aspergillus flavus
Clinical presentation
Asymptomatic
Suspect in any patient with cirrhosis with evidence of clinical deterioration
Detected during screening for chronic hep B carriers
Symptomatic
Local
o
o
o
o

RUQ dull, persistent pain (secondary to capsular stretch)

RUQ mass - hepatomegaly
Low grade pyrexia (tumor necrosis)
Jaundice is a late feature
Compression/invasion of intrahepatic ducts
Lymphadenopathy at porta hepatitis
Pre-existing cirrhosis
Constitutional: Malaise, LOW, LOA
Tumor rupture:
o Haemobilia or haemoperitoneum are often the immediate cause
of death pallor with shock
o Severe abdo pain + peritonism
o U/S, DPL, then treat with Transarterial Embolization
Liver decompensation
o Background of existing HCC + CLD/cirrhosis especially
n
o Liver f - jaundice/pruritus, coagulopathy, edema, encephalopathy
o Portal HTN - ascites, LL edema, hematemesis, melena (varices)
o Hepatorenal syndrome in late stages
Metastases
Paraneoplastic syndromes
o Bone pain
o High metabolic demands hypoglycaemia
o Dyspnea
o Tumor produces EPO erythrocytosis

HEPATOBILIARY AND PANCREATIC SURGERY

Investigations
As most tumours cause symptoms late, screening of high risk patients advocated.
Laboratory
FBC (low Hb from BGIT, raised TW from spontaneous bact peritonitis)
rd
UECR (dehydration, 3 spacing, diuretics for ascites, contrast nephropathy)
LFT (albumin, bilirubin, ALP, transaminases)
Hepatitis Markers
Alpha-fetoprotein - produced by the yolk sac & liver
o Normal <5; WHO criteria >400
o Progressive increases in serum levels in 70-90% of HCC
o Slightly increased and often fluctuating serum levels also seen in
hepatitis, cirrhosis, pregnancy, teratoma
o In HCC serum levels correlate with tumour size
Rate of increase in serum levels correlate with tumor growth
Tumour resection results in a fall in serum concentrations
Serial assessment useful in measuring response to tx
Imaging
CT Triphasic - Conventional or lipoidal enhance
o Arterial phase
Contrast in aorta/ any bleed & HCC
IVC and portal vein are dark
o Portal venous phase (most CT scans taken @ this phase)
Portal vein as bright as aorta
Visualize metastasis
o Delayed phase
Contrast drains out - none of the vessels in liver are lit up
Visualize hemangioma (also rim enhancement in others)
o Characteristic features of HCC
Enhancement in arterial phase (due to hepatic arterial ss)
Rapid contrast washout in portal venous phase - hypodense
Dynamic MRI scan - greater detail
Hepatic angiogram (reveals abnormal blood vessels)
Lipiodol and post-lipoidal CT with hepatic angiogram
o CT scan a week later
WHO Criteria for HCC:
o Lipiodol will be retained in HCC
(a) Risk factors for HCC
even after many days - tumor
e.g. HBV/HCV carrier
has no Kupffer cells
(b) Characteristic CT
Staging
triphasic findings:
Lung: CXR, CT thorax
Hypervascular lesion
CT AP: liver, adrenals, peritoneum, LNs
(c)
Raised AFP (>400)
Bone: Bone scan if indicated

74

!
Screening for chronic hepatitis carriers
6 monthly - yearly U/S with AFP levels
o Frequency of screening controversial, but should be increased in
high risk pts (i.e. HBeAg positive, high HBV DNA levels)
Important to detect smaller and resectable HCCs -- increases survival
from 26 to 88 weeks (~6 months to 2yrs)
Remember to screen family for Hep B carrier status! Especially if famhx
is positive
o U/S
Operator dependent
May miss certain areas of liver where imaging is difficult
Not a/w with radiation exposure
o AFP
Not perfect as 1 in 5 (20%) of HCC will not have raised
AFP
o Combining both increase sensitivity and specificity!
Surgery for hepatocellular carcinoma
Only about 20% patients are suitable for surgery
Surgical resection
Surgical resection involves either hemi-hepatectomy or segmental resection
Presence of field change effect in the cirrhotic liver -- new tumor can
develop in remnant liver
o Fine balance between adequate resection margins and
preservation of sufficient functional liver to prevent liver failure
o Good immediate and short-term results, but long term <30% 5yr
survival due to occurrence of new primaries in cirrhotic liver
Most tumours are unresectable to:
o Stage of disease
Metastatic or multicentric not suitable
o Fitness for op
o Liver function
Advanced cirrhosis
ICG test pre-op must <15% remains after 15mins for >3
segments removed (major resection)
CT liver scan program to calculate residual function
o Involvement of major vessels
o Crazy portal HTN (increased resistance to flow)
The presence of cirrhosis increases the operative mortality (to >20%)
o Consider only Childs A and good Childs B
After resection, 5 year survival is typically 30-60%
The 5-year recurrence rate is over 80%
HEPATOBILIARY AND PANCREATIC SURGERY

Child-Pugh Classification of CLD

Measure
Albumin, g/l
Coagulation PT INR
Bilirubin, mol/l
Distension Ascites
Encephalopathy
Points
5-6
7-9
10-15

Class
A
B
C

1 point
>35
<1.7
<34
None
None

2 points
28-35
1.71-2.20
34-50
Mild
Grade I-II

3 points
<28
> 2.20
>50
Moderate to Severe
Grade III-IV (or refractory)

One year survival Two year survival

100%
85%
81%
57%
45%
35%

1) Prognosis
2) Strength of medical treatment
3) Necessity of liver transplant

Liver transplantation
Useful for unresectable disease confined to the liver
Operative mortality is often 10-20%
After transplantation, 5-year survival is less than 20%
Milan criteria for transplantation (>75% 5yr survival if followed!)
o Single tumor 5cm or smaller OR 3 or less tumors, > 3cm
o No evidence of gross vascular invasion
o No regional nodal or distant metastasis
Problems with availability of donor organ - disease may no longer by
suitable for transplant when organ is available
o Possibility of bridging therapy such as radiofrequency ablation
to shrink disease and prevent progression until organ is available
In HBV carriers - risk of reinfection of donor liver (esp if HBeAg positive,
high HBV DNA levels)
o Can be aggressively treated with anti-viral drugs 2 months before
o Anti-HBV Ig long-term after transplant
Palliative therapy
Loco-regional
o Radiofrequency ablation (RFA) - best among the 3
o Percutaneous ethanol injx
o Cryotherapy
Intra-arterial
o Transarterial chemoembolization TACE
o Transarterial embolization TAE
o Selective intrahepatic radiation - Yttrium-90
Systemic
o Sorafenib improves median survival by 3 months
(limited results + expensive)
75

!
LIVER METASTASES

PYOGENIC LIVER ABSCESS

50% patients with colorectal cancer develop liver metastases

20% have metastases at time of initial surgery
25% develop metastases within 5 years of a 'curative' resection
Median survival with metastases is about one year

Presentation
Mets to liver parenchyma
History - Incidentally found on f/u for cancer
- Hard mass/heaviness
- Pain on rupture
O/E
- Hard, irregular nodular hepatomegaly
- Jaundice is late sign
Invx
Both obstructive and transaminitis

Mets to porta hepatis LNs

S/S of obstructive jaundice
- Scleral icterus
- Tea-colored urine, pale stools
- Progressive early jaundice
- Hepatomegaly may be absent
Obstructive in early stages

Detection of metastases
Ultrasound will detect lesion more than 0.5 cm in diameter
CT allows assessment of resectability
Intra-operative ultrasound superior to extra-corporeal scanning
Elevated tumour marker - CEA, CA 19.9, CA 242
Investigation: Triphasic CT
Hypodense on arterial phase Mets are usually hypovascular (c.f. HCC)
Spread by portal vein contrast uptake on portal venous & delayed phases
Liver resection for metastatic disease
Resectional surgery is only chance of cure for patients with liver mets
Only 10% of patients w metastases suitable for 'curative' hepatic resection
Aim is to resect tumour with more than 1 cm margin by segmentectomy,
lobectomy or hepatectomy
5 year survival 35% and 10 year survival 20%
Relative indications
Single lobe involvement
Less than three lesions without
evidence of satellite lesions
No invasion of inferior vena cava
More than 20% of liver spared
Palliation of liver metastases
Cryotherapy
Hepatic artery infusion therapy
Laser photo-coagulation

Relative contra-indications
Hilar & coeliac nodal
involvement
Distant metastases
Poor cardiovascular reserve
Pre-operative portal vein
embolization - atrophy of
segments to be excised
Neoadjuvant chemotherapy

HEPATOBILIARY AND PANCREATIC SURGERY

Usually seen in elderly patients (more common in SG than amoebic)

Can be multiple or solitary
Arise as a result of biliary sepsis
Mortality is high as diagnosis is often delayed
Commonest organisms involved - E. coli, Klebsiella, Proteus and
Bacteroides species, strep milleri, enterococcus/bacter

Aetiology
Portal pyelophlebitis - appendicitis, diverticulitis or pelvic infections
Biliary disease - cholecystitis, ascending cholangitis or pancreatitis
Trauma - blunt or penetrating or iatrogenic
Direct extension - empyema of the gall bladder, subphrenic or
perinephric abscess
Septicaemia
Infected liver cysts or tumours
Clinical features
Patients are generally systemically unwell
Severe abdominal pain usually localised to right hypochondrium
Swinging pyrexia, rigors and weight loss
25% present with jaundice
Examination shows an hypochondrial or epigastric mass
30% have a pleural effusion
Investigation
Serology shows a raised TW, increased ESR and deranged LFTs
Hepatitis markers TRO hepatitis
Blood c/s, melioidosis, stool ova/cysts/parasites
Tumor markers
Aspirates for cytology, staining, c/s
Chest x-ray often shows a raised right hemidiaphragm & pleural effusion
Ultrasound will localised the abscess and will guide drainage
CT triphasic TRO tumor; irregular+necrotic, multi-loculated, rim-enhancing
Management
Early: resus, vitals monitoring with i/o charting
Antibiotics 1st 2/52 IV; next 4/52 PO
Percutaneous drainage under ultrasound guidance if >3cm
If biliary obstruction will need to consider decompression
Open surgery if failure of resolution with percutaneous drainage or
intraperitoneal rupture (esp w gallstones/multiple abscess/ascites)
76

!
AMOEBIC LIVER ABSCESS

Prognosis in uncomplicated cases is good (<1%)

Due to infection with the protozoan parasite Entamoeba histolytica

o Transmitted by the faecal-oral route
10% of affected patients develop liver abscesses
Liver abscesses can be solitary or multiple
o 80% of abscess develop in right lobe of the liver
Can present several years after intestinal infection

Clinical features
Presents with malaise, persistent pyrexia and weight loss
Right hypochondrial pain is often mild
o Tender hepatomegaly
Less than 20% of patients present with diarrhoea
NO jaundice or sepsis
Complications can arise as a result of abscess rupture or extension of
infection peritonitis
Complications occur in 5% patients and include:
o Amoebic empyema
o Hepato-bronchial fistula
o Lung abscess
o Pericarditis
o Peritonitis
Investigations
Serology shows raised WCC and ESR
o Latex agglutination assay positive in more than 90%
o Sigmoidoscopy, stool microscopy and rectal biopsy may identify
the organism
Chest x-ray may show a raised right hemidiaphragm, atelectasis or
abscess
U/S HBS
o Aspiration produces a typical 'anchovy sauce' appearing pus
o Pus is odourless and sterile on routine culture
CT Tri-phasic
Management
Metronidazole is the antibiotic of choice
o If ineffective chloroquine and dehydroemetine may be
considered
Ultrasound guided aspiration may be useful
o In pregnancy, or suspicion of secondary infection
o Symptomatic distension or fever
o Esp in impending rupture
HEPATOBILIARY AND PANCREATIC SURGERY

77

!
INFLAMMATORY BOWEL DISEASE
Causes of colonic inflammation
Infection - bacteria, viruses,
parasites
Ulcerative colitis
Crohn's' disease
Ulcerative colitis
Peak age of onset 20 - 35
yrs
Characteristic feature acute mucosal inflammation
with crypt abscesses

Radiation enteritis
Ischaemic colitis
Microscopic colitis
Drug-induced colitis

Crohns disease
Incidence is increasing possibly
due to increased recognition
Characteristic feature - patchy
transmural inflammation with noncaseating granuloma

Epidemiology
Bimodal distribution
o Young: 2nd and 3rd decades of life
o Middle: 5th and 6th decades of life
Equal gender predominance
Genetic association
Higher prevalence among Ashkenazi Jews and in cooler climates
e.g. Scandinavia, UK, Germany
Pathophysiology
Both Crohn's disease and ulcerative colitis have some pathophysiological
features in common
Both result from inappropriate activation of the mucosal immune system
This process is driven by the normal luminal flora
May result from defective barrier function of the intestinal epithelium
Genetic factors contribute to susceptibility as demonstrated by:
o Variable prevalence in different populations
o Increased incidence in first degree relatives
o Increased concordance in monozygotic twins
o Concordance in site and type of disease in affected families
Possible environmental factors include:
o Smoking
o Use of NSAIDs
o Luminal flora

Pathological features
Crohn's disease
Skip lesions - penetrating
Can affect entire GIT (mouth, terminal ileum)
Rectum normal in 50%
Terminal ileum involved in 30%
Discretely ulcerated mucosa
Serositis common
Fibrous shortening
Strictures common
Enterocutaneous or intestinal fistulae in 10%
Anal lesions in 75% (fistulae, fissures)
Possible malignant change
Macroscopic: bowel is thick-walled & nodular
(cobblestone appearance) with creeping fat,
mesenteric thickening and deep linear ulcers
Microscopic: transmural involvement, noncaseating granulomas (pathognomonic, but
only present in 2/3)

History
GIT symptoms
Non-specific symptoms
Abdo pain
LOW/LOA/fatigue
D/N/V
Fever
Bloating, distention
Anemia
Bloody stools with mucus and pus
Malnutrition
Crohns fistula
Extra-intestinal
manifestations
Colovesical fistula or colo-ovarian fistula:
e.g. Skin
fecaluria, pneumaturia, feces per vagina/PID
O/E: usually normal (may have extra-intestinal manifestations)
DDx

COLORECTAL SURGERY

Ulcerative colitis
Lesions continuous - superficial
Begins in rectum, expends prox
Rectum always involved
Terminal ileum involved in 10%
Granulated ulcerated mucosa
Normal serosa
Muscular shortening of colon
Fibrous strictures rare
Fistulae rare
Anal lesions in <20%
Malignant change well recognized
Macroscopic: granular appearance
of mucosa, loss of vascular
markings, pseudopolyps
interspersed with areas of shallow
ulceration
Microscopic: only mucosal and
submucosal involvement; crypt
abscesses

Gastroenteritis (Exclude by doing stool microscopy and culture)

o Bacterial: E coli/ campylobacter/ salmonella/ shigella
o Parasitic: Entamoeba histolytica
o Viral: rotavirus
Other infective causes: diverticulitis, TB colon
Ischaemic colitis; Bleeding diverticulosis; Ca colon
78

!
Clinical features of inflammatory bowel disease
Ulcerative colitis
30% disease confined to rectum
15% develop more extensive disease over 10 years
20% total colonic involvement from onset
Patients generally fall into following categories:
o Severe acute colitis
o Intermittent relapsing colitis
o Chronic persistent colitis
o Asymptomatic disease
Assessment of disease severity
o Mild = < 4 stools per day. Systemically well
o Moderate = > 4 stools per day. Systemically well
o Severe = > 6 stools per day. Systemically unwell
o Systemic features: tachycardia, fever, anemia, hypoalbuminaemia
Endoscopic grading of ulcerative colitis
0 = normal
1 = loss of vascular pattern or granularity
2 = Granular mucosa with contact bleeding
3 = Spontaneous bleeding
4 = Ulceration
Crohns disease
Clinical features depend on site of disease
50% have ileocaecal disease, 25% present with colitis
Systemic features are more common than in ulcerative colitis
Extraintestinal manifestations
Associated with disease activity
Skin
o Erythema nodosum
o Pyoderma gangrenosum
Joints
o Asymmetrical nondeforming arthropathy
Eyes
o Anterior uveitis
o Episcleritis
o Conjunctivitis
Hepatobiliary conditions
o Acute fatty liver
Thromboembolic disease
COLORECTAL SURGERY

Unrelated to disease activity

Joints
o Sacroiliitis
o Ankylosing spondylitis
Hepatobiliary conditions
o Primary sclerosing
cholangitis
o Cholangiocarcinoma
o Chronic active hepatitis
o Gallstones
Amyloid
Nephrolithiasis

Medical management of inflammatory bowel disease

Treatment depends on
o Type, site, severity of disease
Different drugs may be used for active disease and those in remission
5-Aminosalicylic acid
Used in mild / moderate ulcerative colitis and Crohn's disease
5-ASA block production of prostaglandins and leukotrienes
Mesalazine is conjugated to prevent absorption in small intestine
Topical preparation may be used in those with left-sided colonic disease
Maintenance therapy of proven benefit in those with ulcerative colitis
Of unproven benefit in those with Crohn's disease
Corticosteroids
Often used in those in whom 5-ASA therapy is inadequate
o Also used in those presenting with acute severe disease
Can be given orally, topically or parenterally
Use should be limited to acute exacerbations of disease
o Of no proven value as maintenance therapy in either ulcerative
colitis or Crohn's disease
o Use must be balanced against side effects
Immunosuppressive and immunomodulatory agents
Often used in those in whom steroids cannot be tapered or discontinued
Agents used include:
o Azathioprine - effective in both UC & Crohn's disease
o Methotrexate - effective in Crohn's disease
o Cyclosporin
o Infliximab - anti-TNF-alpha therapy

79

!
Surgery for Crohns Disease

Surgery for Ulcerative Colitis

Indications for surgery - Crohns disease

Absolute
Perforation with generalized peritonitis
Massive haemorrhage
Carcinoma
Fulminant or unresponsive acute severe colitis

Indications for surgery

20% of patients with ulcerative colitis require surgery at some time
30% of those with total colitis require colectomy within 5 years

Elective
Chronic obstructive symptoms
Chronic ill health or debilitating diarrhoea
Intra-abdominal abscess or fistula
Complications of perianal disease
Surgery should be as conservative as possible
No evidence that increased resection margins reduce risk of recurrence
If possible improve preoperative nutritional state
Surgical Options
Limited resections
30% undergoing ileocaecal resection require further surgery
Strictureplasty often successful
Bypass procedures rarely required

Emergency
Toxic megacolon
Perforation
Haemorrhage
Severe colitis failing to respond
to medical treatment

Elective
Chronic symptoms despite
medical therapy
Carcinoma or high grade
dysplasia

Surgical options
Emergency
Elective
Total colectomy
Panproctocolectomy & Brooke ileostomy
with ileostomy
Panproctocolectomy & Kock continent ileostomy
and mucus
Total colectomy and ileorectal anastomosis
fistula
o Maintains continence but proctitis persists
Restorative proctocolectomy with ileal pouch
o Need adequate anal musculature
o Need for mucosectomy unclear
o May need defunctioning ileostomy
Pouch design
Functional results of ileoanal pouch
Mean stool frequency six per day
Perfect continence
o During day
(90%)
o At night
(60%)
Gross incontinence
(5%)
Morbidity
50% develop significant complications
Small bowel obstruction
(20%)
Pouchitis
(15%)
Genitourinary dysfunction
(6%)
Pelvic sepsis
(5%)
Fistula
(5%)
Pouch failure
(6%)
Anal stenosis
(5%)
Larger capacity pouches reduce stool frequency

COLORECTAL SURGERY

80

!
BENIGN COLONIC POLYPS WHICH MAY NOT BE SO BENIGN

A polyp is a pedunculated lesion

o Not all polyps are tumours
o Not all polypoid tumours are benign
o Not all benign tumours are polypoid

Classification of large bowel polyps

Epithelial
Mesodermal
Adenomas - tubular,
Lipoma
villous, tubulovillous
Leiomyoma
Metaplastic polyps
Haemangioma

Hamartoma
Juvenile polyps
Peutz-Jeghers
syndrome

Juvenile polyps
Commonest form of polyp in children
Can occur throughout large bowel but are most common in the rectum
Usually present before 12 years
o
Prolapsing lump or rectal bleeding
Not pre-malignant, treated by local endoscopic resection
Peutz-Jeghers syndrome
Rare familial disorder
Polyps found throughout gut but most common in the small intestine
o Presents in childhood with bleeding, anaemia or intussusception
Circumoral pigmentation and intestinal polyps
Polyps can become malignant
Metaplastic polyps
Small plaques approximately 2 mm in diameter
Not pre-malignant
Adenomas
Benign epithelial neoplasm (pre-malignant)
o Risk of malignancy increases with size
o Malignancy more common in villous rather than tubular lesions
Most adenomas are asymptomatic
o p/w bleeding, mucous discharge or prolapse
o Villous adenomas may produce hypokalaemia but this is rare
Diagnosis is often by sigmoidoscopy or colonoscopy
o Full colonoscopy essential to exclude other lesions
Treatment is by transanal excision or colonoscopic snaring
o Patients require regular colonoscopic surveillance
COLORECTAL SURGERY

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

<1% of colorectal cancers

Definition: >100 adenomatous polyps all over colon & APC mutation
o Attenuated FAP <100 polyps, usually about 30
Autosomal Dominant mutation of APC gene on 5q21
p/w symptomatically but non-specifically with: loose stools, diarrhea,
lower abdominal pain, weight loss, passage of blood and mucus

Clinical Manifestations
Gastrointestinal: >100 Colonic polyps in 50% of 16yo, 90% of 45yo
o Also presents in stomach, duodenum and periampullary
Extra-gastrointestinal manifestations:
o *Eye: Congenital hypertrophy of retinal pigmented epithelium
o Bone: Osteomas
o Skin: Epidermoid cysts, Lipomas
o Thyroid: Papillary Thyroid Cancer
o Desmoid cancers (treated with chemoRT), Adrenal cortex tumor
Surveillance
Genetic testing (confirm plus chop become cancer)
At-risk members: yearly colonoscopy from 12yo + 5-yearly OGD
o 80% detected by screening BUT 20% asymptomatic
Treatment
Prophylactic proctocolectomy w ileal pouch anal anastomosis (formation
of reservoir pouch) at ~20yo
Subtotal colectomy if rectum no polyps (NB surveillance of rectal stump)

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC)

80% becomes cancer, accounts for 8% of colorectal cancers
Genetics: microsatellite instability due to mutated mismatch repair gene
Left sided in Asians, Right sided in Westerners
Polyps tend to be flat, villous; often poorly differentiated
Lynch I familial colonic cancer
Lynch II associated with other GIT or urogenital cancers
o Endometrial cancer, and also gastric, ovarian, small bowel,
hepatobiliary, and renal pelvis/ureter cancers
Diagnosis
The Amsterdam clinical criteria identifies candidates for genetic testing,
and genetic testing can make a diagnosis of Lynch syndrome.
o 3 or more family members are diagnosed with colorectal cancer
o 2 are first degree relatives & 2 successive generations affected
o 1 or more of the colon cancers is diagnosed under age of 50
o 0 FAP (familial adenomatous polyposis) is excluded

Surveillance 1-3yrly colonoscopy starting at 20 years old

81

!
COLORECTAL CARCINOMA

Colorectal cancer is most common cancer in Singapore

40% are rectal and 60% are colonic tumours
3% patients present with more than one tumour (=synchronous tumours)
A previous colonic neoplasm increases the risk of a second tumour
(=metachronous tumour)

Pathology
Almost all tumours are adenocarcinomas
90% of tumours are sporadic
8% a/w HNPCC and 1% a/w FAP
1% arise in association with long-standing ulcerative colitis (>10 years)
Risk factors
Sporadic colorectal cancer (85%)
o Older age
o Obesity
o Male sex
o Smoking
o Cholecystectomy
o Hx of colorectal polyps/cancer
o Ureterocolic anastomosis
o Familial colorectal cancer (20%)
o Diet rich in meat and fat
Colorectal cancer in inflammatory bowel disease (1-2%)
o Ulcerative colitis
Adenomatous polyps (villous, >2cm, multiple)
Hereditary colorectal cancer (5-10%)
o FAP and its variants (Gardners and Turcots syndromes)
o Hereditary non-polyposis colorectal cancer (HNPCC)
o Hamartomatous polyposis syndromes (Peutz-Jeghers)
Site
20% in cecum and ascending colon
5% in transverse colon
15% in descending colon and proximal sigmoid
60% in distal sigmoid and rectum
Morphology
Polypoid (more common in right colon)
Scirrhous (annular apple core in left colon)
Ulcerated
Nodular

COLORECTAL SURGERY

Pathogenesis
APC pathway (adenoma-carcinoma sequence)
Accounts for 80% of sporadic colorectal carcinomas
Adenomas: 70% tubular, 10% villous, 20% tubulovillous
o Most cancers believed to arise within pre-existing adenomas
o Risk of cancer greatest in villous adenoma
Characterized by chromosomal instability
Stepwise accumulation of mutations in a series of oncogenes and tumour
suppressor genes (APC DCC K-RAS p53)
1. Loss of the APC suppressor gene on 5q21 (congenitally absent
in patients with familial adenomatous polyposis APC)
APC is required to break down beta-catenin; with the
loss of APC, beta-catenin accumulates and activates
various genes in the nucleus (such as MYC and cyclin
D1) which promote cell proliferation
2. K-RAS (12p12) mutation follows the loss of APC an activating
mutation that causes the RAS to keep delivering mitotic signals
and prevent apoptosis
3. Loss of tumour suppressor gene at 18q21
4. Loss of p53 late in carcinogenesis
The molecular evolution of colon cancer through this pathway occurs
through a series of morphologically identifiable stages:
localised epithelial proliferation small adenoma
large dysplastic adenoma carcinoma in-situ invasive cancer
Defects in DNA mismatch repair
Involved in 10-15% of sporadic cases
Accumulation of mutations, but due to a different mechanism, and
without clearly identifiable morphologic correlates i.e. no adenomas
Due to mutations in one of the five DNA repair genes (MSH2, MSH6,
MLH1, PMS1, PMS2) of which MSH2 and MLH1 are the most commonly
involved in sporadic colorectal carcinomas
o Loss of DNA mismatch repair results in microsatellite instability
which affects coding or promoter regions of genes involved in
cell growth such as the BAX gene and the type II TGF- receptor
Tumours that arise from this pathway have a better prognosis than
tumours that arise from the APC pathway

82

!
Clinical presentation
History
Right sided
Occult presentation
Iron deficiency anaemia
due occult GI Blood loss
Weight loss
Right iliac fossa mass

Left Sided
Mass effect
Abdominal pain
Alteration in bowel habit
Rectal bleeding + mucus
Tenesmus

Complications in 40% of patients

Bleed
Iron deficiency anaemia - SOB, CP, decreased ET,
palpitations, fatigue, postural giddiness
LBGIT (blood and possible mucus)
Block
Change in bowel habits (<3x/week = constipation)
Progressive constipation, possible spurious diarrhea
Mucoid stools
Change in consistency of stools
Tenesmus
Burst
Perforation peritonism super super super super super pain
Burrow Colovesical fistulae (fecaluria, pneumaturia, recurrent UTI)
Metastasis Constitutional symptoms LOA/LOW/malaise
Examination
Abdominal Mass
DRE (rectal mass)
o Hard, non-tender, polypoid, irregular, contact bleeding
o Distance from anal verge >7cm (internal anal sphincter)
Screening
Screen asymptomatic population for pre-disease state (based on
observational studies)
o Prevalent and lethal disease
o Precursor can be detected early (long asymptomatic period)
o Early detection makes a difference (can institute treatment)
o Safe, effective, feasible test available
FOBT (detection)
o Test for heme component broken down by upper GIT
Colonoscopy (prevention)
o Allows for polypectomy
o Recommended after 40yo (official is 50), once every 10 years

COLORECTAL SURGERY

Investigation
Diagnostic
Colonoscopy (98% accuracy)
o Diagnostic:
Visualize (size and location) and biopsy lesion
Enables detection of synchronous lesions
(polyps 30%, cancers 5%)
o Therapeutic: e.g. polypectomy, stenting of obstructed colon
o Ensure good bowel prep (PEG for renal impaired, Oral fleet)
o Risks: Perforation, Bleeding, Failure to complete
CT colonography (95% accuracy) second line
o Spiral CT (IV contrast, air, contrast enema) 6mm polyps
Double-contrast barium enema (barium + air)
o Not adequate for diagnostic purposes, may miss small lesions
Classically can see an apple core lesion
o In patients presenting with large bowel obstruction single contrast
enema (after rigid sigmoidoscopy) is the investigation of choice
o Barium prep: bisacodyl oral or magnesium salt
o Risks: inssipation of barium stones
Staging
CT scan of the abdomen and pelvis
o Local T staging & invasion into bladder, ureter, uterus
o Staging of regional and no-regional lymph node involvement
o Metastases to the liver, peritoneal seeding, omental kinking
o Ascites, hydroureter/hydronephrosis, intestinal obstruction
CXR + CT scan of the chest
Bone scan if appropriate
Endoscopic ultrasound, or transrectal ultrasound for rectal tumour
o T staging to determine depth of involvement by tumour
o Can also assess local lymph node status
Monitoring
FBC for low Hb, together with iron studies
rd
UECr: fluid and electrolyte abnormalities from vomiting or 3 space
losses (intraluminal); assess risk of contrast nephropathy
LFT: derangements caused by metastasis (though these changes will
only occur late) raised bilirubin, ALP
PTT/GXM: for surgery
CEA (used only for trending)
o >90% of tumours produce CEA
o Compare pre-op, immediate post-op, and follow up for recurrence
o Causes of false positive raised CEA:
smoking, pregnancy, bronchitis, cholangitis and cancers of the
stomach, lung, breast, pancreas, cervix, bladder and kidney
83

!
Surgical pre-operative measures
Bowel prep
o 3 days low residue diet, NBM day before op
o Bowel clearance with PEG
Prophylactic antibiotics
o Cefuroxime and Metronidazole 30min before induction of
anaesthesia
Heparin anti-coagulant

Principles of Surgery for the Colon

5 cm proximal and 5 cm distal clearance for colonic lesions
Radial margin should be histopathologically free of tumour if possible
Lymph node resection should be performed to the origin of the feeding vessel
En Bloc resection of adherent tumours should be performed
Preferentially segmental colectomy with intraoperative decompression
Depending on site of lesion surgical options are:
o Caecum, ascending colon, hepatic flexure Right hemicolectomy
o Transverse colon Extended right hemicolectomy
o Splenic flexure, descending colon Left hemicolectomy
o Sigmoid colon High anterior resection

Principles of Surgery for Rectum

Because it is so common:
o Upper rectum: where the tenia coli coalesce into a single
longitudinal muscle layer.
o Rectum measures ~12 to 15 cm in length and contains three
valves
o Middle rectal valve be located 9 to 10.5 cm from the anal verge
At anterior peritoneal reflection: the anterior cul-de-sac
Lesions at or beneath the middle rectal valve are
considered to lie in the extraperitoneal portion of rectum
o Anorectal junction
Anatomically at dentate line 3 cm from anal verge
Surgically 2cm above dentate line, at proximal edge of
anal sphincter 5cm from anal verge
Clearance margins
o 5 cm proximal and 2 cm distal clearance for higher rectal lesions
o 1 cm distal clearance for super low rectal lesions is adequate
o Radial margins are very important
o Local recurrence reduced by performing total mesorectal
excision (TME)
COLORECTAL SURGERY

Surgical options
o Sphincter-sparing (with temporary defunction ileostomy)
Low Anterior Resection (Upper Rectum)
If distal margin >2cm above sphincter complex,
which is 2 cm above dentate line, which is 3 cm
from anal verge (total 7cm from anal verge)
Ultra Low Anterior Resection (Lower Rectum)
If distal margin 1cm above sphincter complex
o Sphincter-sacrificing
Abdomino-perineal resection
For lower rectal cancers or invasion into external
sphincter complex
Anus and sphincter complex dissected with
creation of end colostomy
o Even for the lowest of rectal cancers, using a combination of
neoadjuvant chemo/radiation, total mesorectal excision, and
intersphincteric proctectomy and colonic J-pouch to anal
anastomosis, sphincter preservation can be achieved for most
patients.
o Unless the rectal tumor involves the external sphincter muscle,
there is no oncologic need to remove it, and following resection of
the tumor, gastrointestinal tract continuity can be restored.
Reconstruction
o Formation of colonic J pouch to improve function
o Coloplasty creation of a pouch
Extended resections for locally advanced, adherent tumors
o Consider neoadjuvant therapy to downstage
Stoma creation
o Defunctioning loop ileostomy/colostomy due to increased risk of
an anastomotic leak & also poorer blood supply to anastomosis
o A defunctioning stoma does not protect against anastomotic leak,
but mitigates against disastrous complications of faecal peritonitis
should a leak occur
o Closed in 2-6/12 after check with Gastrografin reveals no leak

Operative complications
Intra-op

Early (<30d)

Late (>30d)

Damage
to other
organs
e.g. ureters

Wound infection; Bleeding; Abscess

Anastomosis breakdown/leak
faecal peritonitis
Early stoma complications

Diarrhoea
Impotence (pelvic nerves)
Adhesions (I/O)
Anastomotic stricture
Late stoma complications
84

!
Adjuvant Chemoradiotherapy
Principles
Adjuvant therapy for T2 and above
Neoadjuvant for T3 and above
Chemoradiotherapy
o Good evidence for T3 tumours, CRM<2mm: benefits > risk
o Only for rectal cancers because of the radio risk

Staging
Dukes (more important)
Stg
A

Description
Tumor confined to bowel wall with no extension into
extrarectal/ extracolic tissue, no LN mets

5yr surv
75%

Invades past muscularis propria into extrarectal/

extracolic tissue, no LN

55%

Chemotherapy
5FU and folinic acid is effective as adjuvant therapy
Given for both colon and rectal cancers

LN mets present
C1: only nearby nodes involved (paracolic LNs)
C2: continuous string of LN involved up to proximal
resection (LN at base of mesentery)

Radiotherapy
Colon cancers, and tumors of the upper rectum, do not have tendency
for local failure and therefore, except in specific situations, are not
treated with radiation also radiation may harm intra-abdominal organs
Tumors at or below the level of the middle rectal valve are considered to
be extraperitoneal, and depending on their stage, may be treated with, in
addition to surgery, radiation and chemotherapy to help in reducing local
recurrence rates and maximizing the odds of achieving a sphinctersparing operation.
Risk factors for local recurrence include:
o Local extent of tumour
o Nodal involvement
o Circumferential margin status
o Risk of local recurrence can be reduced by radiotherapy
Can be given either preoperatively or postoperatively
Preoperative radiotherapy given as short course immediately prior to
surgery
o Reduces local recurrence
o Increases time to recurrence
o Improves 5-year survival

C1:40%
C2:20%

Distant mets/ extensive local mets such that surgically Poor

incurable

TNM made easy

T
1 Invades Submucosa
2 Invades Muscularis propria
3 Penetrates muscularis into surrounding
4 Penetrates to visceral peritoneum
N 1 Mets in 1-3
2 Mets in 4 or more
M 0 No
1 Yes (a = only 1 organ or site, b = good luck to you)

Follow-up
Follow-up visits 3-monthly for the first 2 years, then 6-monthly for the
next three years, and subsequently yearly, measure CEA at each visit
Yearly colonoscopy
CXR and liver ultrasound to detect metastases

COLORECTAL SURGERY

85

!
DIVERTICULAR DISEASE
Pseudodiverticulum - acquired herniation of colonic mucosa & submucosa
through the colonic wall, with covering of colonic serosa
Diverticulosis coli presence of acquired pseudodiverticula
Diverticular disease symptomatic diverticulosis coli
Diverticulitis inflammation of diverticula
Features
Increases with age
Risk factors dietary fibre & genetics
Majority are asymptomatic; 10-30% are symptomatic
Classically at the mesenteric border but usually circumferential
o Majority are in the sigmoid colon, right sided genetic
o Asians: 40% right, 60% left, Caucasians: 20% right, 80% left
Pathogenesis
Increased intraluminal pressure a/w lack of dietary fibre
Degenerative changes in colonic wall a/w weakening of collagen w age
o Usually at point of entry of terminal arterial branches where
serosa is weakest
Staging (for acute diverticulitis)
Severity staging by CT scanning may allow not only the selection of patients
most likely to respond to conservative treatment, but may also predict the risk of
failure of medical therapy and of secondary complications after initial
conservative treatment.
Hinchey Classification for acute diverticulitis
Stage 1

Pericolonic /
Mesenteric abscess
(small)

Stage 2

Pelvic / retroperitoneal
abscess (large)
Purulent peritonitis
(fm perf diverticulitis)

Stage 3
Stage 4

- Conservative: ABx, NBM, IV fluids

- Surgery: 1 stage surgery after acute
episode resection of affected bowel
segment with primary anastomosis

- Percutaneous drainage
- Elective 1 stage surgery
- 2 stage operation Hartmanns
procedure (partial colectomy + diverting
end colostomy & rectal stump formation)
Faecal peritonitis
2 re-anastomosis 3 months later
(fm ruptured diverticula)

COLORECTAL SURGERY

Presentation
Acute diverticulitis
Typical presentation: 50yo male with fever, localized abdominal
tenderness and GI symptoms, commonly diarrhea
Symptoms
Signs
Pain: usually at LLQ (sigmoid), colicky
Vitals: usually low grade
constant; relieved by defecation
fever + tachycardia
GI symptoms: N/V/C/D
Abdo exam: tenderness
Urinary symptoms e.g. Urgency
+/- palpable mass
Differentials
o GI: appendicitis, colitis (including GE & IBD), mesenteric adenitis/
ischaemia, ca colon, IBS
o Uro: UTI, renal colic, renal tumor, renal cyst, hydronephrosis
o Obgyn: PID, ectopic pregnancy, torsion of cyst/ovary, endometriosis
Investigations
o Bloods: FBC
TWC raised + raised ESR
o Imaging
Erect CXR: look for free air under the TRO perf
AXR: look for air-fluid levels in an abscess, I/O
CT scan (CTAP, triple contrast)
Contrast enema NOT recommended due to the
risk of barium peritonitis
Visualize diverticula elsewhere (but not the one
that is inflamed)
Confirm colitis (suggests divert) - mesenteric fat
infiltration, concentric bowel thickening
Spot abscess, free gas, segmental colonic thickening
Cannot differentiate Hinchey III and IV because
shit and pus look the same on CT
Sigmoidoscopy not recommended due to risk of perf
Laparoscopy if diagnosis in doubt
Management
o Conservative
NBM, IV fluids, IV rocephin, flagyl
Antispasmodics/analgesia/antipyretics
Fibre supplements + stool softeners when oral feeds are
restarted
Colonoscope after acute inflammation has subsided ~6wks
Confirm diagnosis, TRO colon cancer
Not to be done immediately due to risk of colonic
perforation
o Surgical -- see Hinchey classification
86

!
Chronic diverticulitis
Presentation
o Recurrent LIF pain
o Irregular bowel habits with passage of mucus (due to edema)
o Due to healing by strictures and adhesions -- I/O may result
Management
o Colonoscopy should be done to rule out ca colon
o Conservative mgt as above
o Surgery considered if severe/recurrent
Diverticular abscess
Presentation (may follow acute diverticulitis)
o Localized tenderness & guarding
o Palpable mass that may be detected on DRE
o Swinging fever
Investigations: identified on CT scan (air-fluid levels)
o Can diffx inflammatory phlegmon and abscess
Management: Percutaneous CT/US guided abscess drainage
Generalized peritonitis secondary to perforation
Presentation
o Acute onset continuous abdominal pain; guarding, rigidity
o Vomiting; Febrile + tachycardic
Investigations
o FBC raised TWC, raised Hb
o UECr dehydration
o CXR free gas
o CTAP TRO other causes e.g. PUD, appendicitis, ischaemic bowel
Management: Resuscitate (ABC) then surgery (refer Hincheys)
Obstruction
Small bowel I/O
o Usually temporary, due to adhesions of enteric loop to acute
diverticulitis inflammation
o Conservative - drip and suck, surgery considered if does not resolve
Large bowel I/O
o Occurs with recurrent acute diverticulitis
o Presents as colicky abdominal pain, constipation & distention
o Investigation: CT - dilated bowels proximal to stenosis
o Differential: Ca colon
o Management: NBM, drip & suck; resection + primary anastomosis

COLORECTAL SURGERY

Hemorrhage
80% self-limiting, but 40% will have recurrent bleed
Presentation
o Usually elderly with high density of sigmoid diverticula
o Massive bleed - torrential; altered blood with clots (not melena)
o Colicky pain as blood is irritative & causes spasm
o Syncope from seeing blood, haha
Invx as per LBGIT and mgt
o Assess vitals, resus if required
o Always always PR and proctoscope to rule out piles
o Rule out UBGIT - history + NGT
o Correct any coagulopathies - drug-induced or congenital or
acquired disease
o CT mesenteric angiography
Diagnose, localize bleed and intervene angioembolization
But low success rate -- bleed usually stops
spontaneously - no active bleed for blush to form
o Colonoscopy - may be able to find active bleed but intervention
may be difficult
o Exploratory laparotomy
Wash out rectum - exclude rectal bleed
Colonoscope small bowel (small incision at ileocecal jx) make sure theres no blood
Colonoscope large bowel + wash out - resect bleeding
segment
Fistula
Vesicocolic (most common)
o PMHx of chronic diverticulitis + UTI
o Hx of dysuria, frequency, hematuria, pneumaturia, fecaluria
o Investigations
Urine tests:
Dipstick/UFEME
Urine c/s
Imaging
Cystoscopy - cystitis
KUB air in bladder
o Differentials - other causes of fistula
Ca colon, ca bladder
Crohns
Post-irradiation necrosis (e.g. Ca prostate)
o Management: resection of diseased colon + closure of fistula
Colovaginal not pleasant
Coloenteric enteritis and malnutrition
87

!
HEMORRHOIDS
Presentation
Affect 50% of population over the age of 50 years
Painless bright red rectal bleeding (coating, dripping)
Prolapsing perianal lump
Acute pain due to thrombosis
Faecal soiling or pruritus ani
Anatomy
Abnormal swelling of the anal cushions causes dilatation and
engorgement of the arteriovenous plexuses
Internal hemorrhoids are not supplied by somatic sensory nerves and
therefore cannot cause pain - internal hemorrhoids can produce perianal
pain by prolapsing and causing spasm of the sphincter complex around
the hemorrhoids
Internal hemorrhoids can also cause acute pain when incarcerated and
strangulated
Pathogenesis
80% of patients have high resting anal pressure
o Dilatation of venous plexus
o Distension of AV anastomoses
o Displacement of anal cushions

Treatment
All should have high residue diet
Lifestyle modifications less straining
Local preparations rarely produced long-term clinical benefit
Outpatient
Conservatively treat with Daflon
Surgical options for first and second degree haemorrhoids include:
o Injection with 5% phenol in arachis or almond oil
o Rubber band ligation
Inpatient
Treatment options include:
o Dilatation and banding; Haemorrhoidectomy
Haemorrhoidectomy is usually performed as an open procedure (3)
Secondary infection and postoperative pain may be reduced with oral
metronidazole
Anal stenosis may develop if adequate skin bridges are not maintained
Other haemorrhoidectomy techniques include closed or stapled
procedures
o Reduced operating time
o Less postoperative pain
o Shorten hospital stay, More rapid return to normal activity

Classification
Haemorrhoids are often classified as internal or external
Internal haemorrhoids arise above the dentate line
Banov grading of internal hemorrhoids
Description
Rx
I
Hemorrhoids do not prolapse Lifestyle modifications; meds (Daflon)
improves venous tone
II
Hemorrhoids prolapse on BO Rubber band ligation
but reduce spontaneously
Injection sclerotherapy
(phenol emollient oil)
III Hemorrhoids prolapse on BO Staple hemorrhoidectomy
but manually reduced
IV Hemorrhoids are prolapsed,
Excision ( due to high recurrence)
cannot be reduced

ANAL AND PERIANAL CONDITIONS

88

!
ANAL FISTULAE
Anal fistulae are abnormal communications, hollow tracts lined with granulation
tissue connecting the primary opening inside the anal canal to a secondary
opening in the perineal skin. They are usually associated with anorectal
abscesses (obstruction of ducts infection).
Conditions associated with multiple anal fistulas:
1. Crohns disease
2. TB
3. Actinomycosis
4. Hydra-adenitis suppurativa
Goodsalls Law
Posterior :
(All fistula tracts with external openings within 3 cm of the anal verge and
posterior to a line drawn through the ischial spines)
o Curvilinear
o Internal opening in posterior midline (at level of dentate line)
Anterior :
o Straight tracts
Tracts closer to anal verge = simpler, shorter
Tracts further away = transphincteric, long, high tracts

ANAL FISSURES
A painful linear tear or crack in the distal anal canal, which, in the short term,
usually involves only the epithelium and, in the long term, involves the full
thickness of the anal mucosa.

Most will heal because of good blood supply (within 1 day / 2 days)
If they dont heal: usually due to spasm of internal sphincter muscle

Features of a chronic anal fissure:

1. Boat shaped
2. Punched out
3. Exposing internal sphincter
4. Sentinel skin tag
5. Hypertrophic anal papilla
Management
Internal anal sphincterotomy
o Definitive for chronic anal fissure
o
But do not cut through muscle irreversible
Medical sphincterotomy (reversible)
o GTN paste, botulinum toxoid injections

Investigations
Endoanal U/S (H2O2 aided for hyperechoic effect) to view course of
fistula tract
MRI able to visualise entire pelvis, beyond the sphincter complex
CT/fistulography (in emergency situation) for complex fistulas / unusual
anatomy
Management
Fistulotomy (for simple, short tracts) cut & lay open tract
Fistulectomy core along tract & remove tract entirely
Seton for complex, long, high tracts

ANAL AND PERIANAL CONDITIONS

89

!
BREAST ASSESSMENT
Modified sweat gland that lies in the subcutaneous tissue of the anterior chest
wall between superficial and deep layers of the superficial fascia
The base of each breast extends from the lateral border of the sternum
to the mid-axillary line, from the second to the sixth rib
The axillary tail pierces the deep fascia and enters the axilla
Lymphatic drainage
Axillary nodes 75% of ipsilateral breast drains to the axillary nodes
o 40-50 nodes: Anterior, posterior, medial, lateral, apical
o Drains into supraclavicular and jugular nodes
o Levels:
Level I: lateral to pectoralis minor
Level II: posterior to pectoralis minor
Level III: medial to pectoralis minor, up to apex of axilla
Internal mammary nodes--20% of drainage from the ipsilateral breast
o Drains upper and lower inner quadrants
o About 4 nodes per side, with one node in each of the first three
interspaces and one in the fifth or sixth interspace
Interpectoral (Rotters nodes) between pec major and pec minor
Symptoms requiring specialist referral
Lumps (any new lump, even one in pre-existing nodularity)
Asymmetrical nodularity persisting after menstruation
Breast abscess
Persistently refilling or recurrent cysts
Axillary lymphadenopathy
Breast pain
o Pain associated with a lump
o Persistent unilateral pain in a postmenopausal woman
Nipple discharge
o All women aged over 50 years, or women <50 with:
o Women aged below 50 years with:
Bilateral discharge sufficient to stain clothes
Blood-stained nipple discharge
Persistent discharge from a single duct
Family history

BREAST SURGERY

Symptoms that may indicate breast cancer

Breast lump

Breast pain

Change in breast size or shape

Arm lymphedema

Dimpling of the breast skin

Involution or inversion of nipple

Axillary lymphadenopathy
Nipple discharge or bleeding
Ulceration of the breast skin
Bone or abd pain / jaundice

Triple assessment
Clinical Exam
Features of lump that are highly suspicious for breast cancer
o Surface: irregular or nodular
o Edge: poorly defined
o Consistency: firm (rather than hard, usually)
o Tenderness: non-tender
o Fluctuation: usually not
o Fixation: to skin or underlying chest wall
Nipple involvement - either in the lump or concurrent nipple changes
o Lymphadenopathy
Pathological
FNAC
o Less invasive, less painful, smaller wound (23G needles), does
not require LA
o But only cells are obtained with no histology cannot
differentiate between in-situ cancer and invasive cancer, requires
skilled cytopathologist
o If FNAC shows malignant cells, do frozen section intraop before
proceeding with surgery (recommended).
Core biopsy (gold standard)
o Core biopsy is more invasive, requires local anaesthetic, will
result in a larger wound (14G needle), more painful, risk of
complications higher (because biopsy needle is a spring-loaded
firing mechanism, improper angling may result in puncture of the
lung or heart), more ex as requires tissue processing.
o But can obtain tissue specimen, can stain for ER/PR status
better diagnostic value especially for metastatic disease
because first line treatment is chemoRT
o Usually done intra-op
o Can be guided by radiology - US or stereotactic guidance
90

!
Breast imaging (esp for symptomatic patients)
Mammography ***most sensitive!
Screening in asymptomatic women >40yo or symptomatic women >35yo
o Breast tissue in younger women is denser - more difficult to pick
up abnormalities
2 views: craniocaudal (CC) & mediolateral oblique (MLO)
o Look at axilla on MLO for any enlarged LNs
Features of malignancy
o Pleomorphic microcalcifications
Heterogenous appearance
Segmental, closely grouped or arranged in a linear
pattern (ductal distribution)
o Underlying density
o Spiculated mass or stellate lesion with poor outline or comet sign
- 95% due to malignancy
o Architectural distortion, tent sign, nipple changes
Abnormalities:
o Spiculated masses
Soft tissue mass with spicules extending into
surrounding tissue, 95% due to invasive cancer
DDx: DCIS, fibromatosis or fat necrosis
o Stellate lesions
Localised distortion of the breast parenchyma with no
perceptible mass lesion
DDx: radial scar, invasive Ca, DCIS, surgical scar
o Circumscribed masses
Analyzed according to density, outline and size
DDx: Fibroadenoma, cyst, medullary carcinoma,
abscess
o Microcalcification
Debris within the duct wall or lumen
Sole feature of 33% of screen-detected cancers
Malignant usually linear or branching
Benign is usually rounded and punctate
DDx: invasive cancer, DCIS, fibroadenoma, fat necrosis
BI-RADS Assessment
0: Incomplete
1: Negative
2: Benign finding(s)
3: Probably benign (short term follow up recommended)
4: Suspicious abnormality
25-74%
5: Highly suggestive of malignancy
75-99%
BREAST SURGERY

6: Known biopsy proven malignancy

Breast ultrasound
First investigation in pts <40yo, pregnant or lactating
Other uses:
o Guide procedures e.g. Biopsy, drainage of abscess, cyst aspiration
o Evaluate consistency - cystic vs solid - & margins
o Localisation of lesion seen in only one mammographic projection
o Evaluation of a palpable mass when mammogram is negative
o Evaluation in mammographically-difficult areas e.g. Chest
wall/axilla
Downsides
o Operator-dependent, non-standardized techniques, poor resolution
o Cannot see microcalcifications
Features of malignancy
o Markedly hypoechoic, may have thick echogenic halo
o Irregular edges due to destruction of surrounding strs
o Hypoechoic shadowing - posterior acoustic shadow
o Taller than its width (fir-tree appearance), invasion of fascia
o High central vascularity
Abnormalities:
o Cysts
Smooth walls; Sharp anterior and posterior borders
Black hypoechoic centres without internal echoes
o Solid lesions (have internal echoes)
Malignant
Benign
Heterogenic, hypoechoic
Isoechoic or hypoechoic patterns
Irregular edges
Smooth well defined borders
Cast hypoechoic shadows
Cast no hypoechoic shadows
Screening
Normal risk,
asymptomatic
Increased risk

HRT therapy

40-49 YO
Annual mammogram
50-64 YO
Biannual mammogram (by invitation)
>65 YO
Optional 2 yrly mammogram
Start screening 5 yrs
Monthly BSE
before onset of breast dz in 6 mthly CBE & U/S breast
youngest family member
Annual mammography
40-49 YO
Annual mammogram
50-65 YO
Biannual mammogram up to 5 yrs after cessation
of HRT

91

!
APPROACH TO BREAST LUMP
History
Lump-related
o Site & number
o Painful vs painless
o Onset: when + why was it first noticed
o Progression: change in size
o Overlying skin changes: Erythema, Dimpling, Swelling, Asymmetry
o Single lump ddx: fibroadenomas, cysts, fat necrosis, cancer
Any nipple changes (retraction) or discharge (blood, colour?)
Any other lumps anywhere else - other breast/axilla/neck
Estrogen exposure
o Menarche/menopause/perimenopausal
o Use of HRT/OCP
o Number of children (+ before 30), breast-feeding (>6mths)
Other risk factors
o Previous breast disease
Treated cancer
Previous atypical ductal hyperplasia / LCIS
o Family history of breast cancer or ovarian or CRC
(possible Lynch II)
Both paternal and maternal side (BRCA)
If yes - age of diagnosis, bilateral?
o Exposure to ionizing radiation esp RT for previous breast dx
o Daily alcohol intake (especially before age of 30)
Systemic review
o LOA/LOW, fever, bone pain, shortness of breath
Malignant
- Ductal Ca (~70%)
- Lobular Ca (~20%)
- Others e.g.
Mucinous, tubular
(~10%)

Benign
- Congenital
abnormalities
- supernumerary
nipples
- Hypoplasia

Painless
Older age group: Breast cancer
Younger age group:
- Fibroadenoma
- Cyst
- Area of fibroadenosis
BREAST SURGERY

Aberrations of normal
development and
involution (ANDI)
- Fibroadenomas
- Breast cysts
- Sclerotic/fibrotic lesions

Painful
- Area of
fibroadenosis
- Cyst
- Abscess (usually in
the lactating)

Non-ANDI
- Infective
- Lipomas
- Fat necrosis

- Fat necrosis
(post-trauma)
- Periductal mastitis
- Carcinoma (rare)

Physical Examination
Lump
o Size, tenderness, site: quadrant
o Surface: smooth/irregular/nodular
o Edge: poorly/well-defined, temperature
o Consistency: hard/soft/firm, fluctuation
o Fixation: skin or underlying chest wall (in 2 directions)
General appearance
o any asymmetry in the breast contours,
o any obvious skin changes
o peau dorange infiltration of malignant cells into lymphatics
causing edema (not compression), erythema, puckering
o any scars of previous operation or procedure e.g. punch biopsy
Look for nipple changes (7 Ds):
Discolouration
Depression
Displacement
Discharge
Deviation
Destruction
Duplication
Manoeuvres:
o Ask patient to raise her arms (to see the axilla and underside of
breasts, and accentuate any tethering to skin dimpling)
o Ask the patient to contract the pectoralis major (push her hands
against her hips) may reveal a previously unnoticeable lump if
tethered to both skin and muscle
o Press arms down & lean forward the rest of the breast will flop
fwd. but not the CA that is attached to underlying muscle
Pain Surface
Some- Smooth
times
Indistinct
NO!! Smooth/
bosselated
Irregular

Consistency
Soft to hard

Mobility
Not fixed

Mixed/fluctuant Not fixed

Rubbery
Very mobile
Stony hard

Triple Assessment
Clinical: history and PE
Radiological:
Ultrasound (if <35yo) or
mammography
Pathological

Age
30-55; especially
perimenopausal
Wide: 20-55
Young:15-25

May be
35+
tethered/fixed

Diagnosis
Cyst
Nodularity
Fibroadenoma
Cancer

Management
If all 3 assessments suggest a benign lump -F/U with physical exam for 1 year to ensure
lump is stable or regresses
If all 3 concordant for malignancy -- stage & treat
If mixed -- further workup e.g. Excisional biopsy

92

!
APPROACH TO NIPPLE DISCHARGE
Causes
Colour of discharge
Red or pink (blood + serum)
Clear yellow (serous)

Green, brown, black (cell debris)

Purulent, foul-smelling
Thin, white fluid (milk)

Cause
Ductal papilloma (benign)
Ductal carcinoma
Ductal papilloma
Duct ectasia (= periductal mastitis)
Cyst
Ductal carcinoma
Duct ectasia
Mastitis/abscess
Galactorrhoea/lactation

History
Is the discharge true?
o Exclude other conditions may mimic e.g. eczema, Pagets, etc.
Is the discharge significant?
o Spontaneous or only on pressing (spontaneous is sig)
o Intermittent or persistent (persistent is sig)
o Relation to breastfeeding (significant if >1yr after stopping)
Is the discharge worrisome?
o Unilateral or bilateral (unilateral more worrisome)
o Discharge from multiple ducts or single duct (single duct more
worrisome)
o Nature of discharge (bloody more worrisome)
o Age of the patient (more worrisome in older patient >60)
Is it troubling the patient?
Investigation
Discharge for cytology to detect malignant cells
Mammography/ US of both breasts to detect any underlying malignancy
Histology of biopsied lesion if found on imaging
Ductography, ductoscope & biopsy
Management
If malignancy found, manage malignancy
Excision for intraductal papilloma (microdocholectomy, total ductal
excision, hookwire localised excision) scarring may affect other ducts
Antibiotics for mastitis/abscess + incision and drainage for abscess
Conservative management for most other pathologies unless discharge
persists and is troubling patient microdochectomy of offending duct
BREAST SURGERY

BREAST PAIN
Cyclical mastalgia
Usually bilateral, affects upper outer quadrant
Mostly minor and accepted by many women as 'part of normal life'
Average age of onset is 24 years
No consistent hormonal abnormality
Prolactin levels may be increased
Essential fatty acid profiles may be abnormal
Treatment
80% require no treatment other than reassurance
Treatment should be considered if:
o Symptoms for more than 6 months
o For >7 days per cycle
Evening primrose oil (EPO)
o Require treatment for at least 4 months
o 50% response rate
o 1% complications - nausea
Danazol
o 80% response rate
o 25% complications - acne, weight gain, hirsutism
o Requires mechanical contraception
Bromocriptine
o 50% response rate
o 20% complications - postural hypotension
Tamoxifen effective but not licensed for use in mastalgia
Non-cyclical mastalgia
Affects older women
Average age = 45 yrs
Usually unilateral, often localised
True non-cyclical mastalgia
o Usually has a musculoskeletal cause
o Rarely cancer
Treatment
Support bra & NSAID

93

Breast cancer affects 1:12 women

It is the commonest cause of cancer death in women, 6% of female deaths

Risk Factors
Age (increases with increasing age with two peaks as mentioned)
Genetic:
o Family history: maternal & paternal (breast or ovarian cancer,
especially if in first degree relative, young onset <40 YO, bilateral
cancer in relative affected)
o Known BRCA1 (on 17q; maternal side) or BRCA2 (both sides),
o Li-Fraumeni syndrome involving p53 mutation) or HNPCC
High oestrogen exposure:
o early menarche <12YO, nulliparity, late childbearing at >30YO,
late menopause >55YO
o Oral contraceptive usage (pure oestrogen type)
o HRT (>5yrs, small increase in risk; reduced when stopped)
Previous breast disease:
o Previous breast cancer (10X)
o Previous biopsy with atypical ductal hyperplasia or LCIS (7-10X)
Ionizing radiation to breast (previous RT)
Alcohol consumption (daily)

WHO Classification
Non-invasive

Ductal

Epithelial
Lobular

!
BREAST CANCER

Spread
Local: skin & subcut tissues, underlying ribs and muscle (chest wall)
Lymphatics: axillary, internal mammary LNs, supraclavicular LNs
Haematogenous: lungs, liver, brain, bone, adrenals, ovaries

BREAST SURGERY

IDC
- 70-80% of invasive breast Ca
- Includes all cancers that
cannot be subclassified into a
specialised type no special
type
- Poorer prognosis than a
carcinoma of specialised type
- 2/3 express ER/PR,
- 1/3 overexpress C-erbB2
ILC
- 5-10% of invasive cancers
- 10-20% multicentric and/or
bilat
- Cells morphologically similar to
cells of LCIS: monomorphic,
bland round nuclei
- Cells invade individually into
stroma (due to loss of Ecadherin, a cell-adhesion
molecule)
- Similar prognosis to IDC

Others

Specialised Epithelial types

- Medullary, colloid (mucinous), tubular, papillary
- Better prognosis than IDC

Nonepithelial

Presentation
Asymptomatic: detected on mammographic screening
Local:
o Self-detected lump in the breast (>1/3 of patients)
o Nipple change: distortion, destruction, retraction, deviation,
discharge, eczema
o Overlying skin changes e.g. peau dorange, tethering (means
mass is still mobile but overlying skin will be indented when
moving the lump), fixation (means the mass is not mobile), even
fungating ulcer
o Other lumps in axilla
Pain is uncommon.
Constitutional: LOW, LOA
Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone,
brain, adrenals)

DCIS = malignant
- From terminal duct lobular unit,
- Cause distortion of lobules,
- Do not invade BM
- Non-palpable, detected microcalcifications
- 35% multicentric, occult invasive in 10-20%
- Progress to CA within 10 yrs ~30% risk;
considered malignant
- Good prognosis if treated
- Tx similar to IDC
LCIS = RF
- From terminal duct lobular unit (like DCIS)
- Do not distort lobular architecture
- Usually presents with a lump, seldom
detected by mammogram
(microcalcifications)
- 60-80% multicentric and bilateral
- Not premalignant, but a marker for
increased risk of invasive disease in both
breasts (7-10x increased risk)
- If ca develops, will be IDC usually, occurs
>15 years after diagnosis
- Usually proceed with excision biopsy.

Invasive

Inflammatory carcinoma
- Presents as erythematous. enlarged, swollen breast w/o palpable mass
- Histologically not specialised
- Diffuse invasion of breast parenchyma by ca cells blocking numerous dermal
lymphatic spaces swelling
- No histo features of inflammation
- Very poor prognosis, rapidly fatal
Primary nonepithelial malignancies of the breast arising from supporting
stroma comprise an important minority of breast neoplasms, including primary
breast sarcomas, therapy-related breast sarcomas, the phyllodes tumors,
primary breast lymphomas and angiosarcomas

94

!
Diagnosis and assessment
Most symptomatic cancers present as a painless lump
Breast pain is an uncommon presentation of breast cancer
Diagnosis is by Triple Assessment
o Clinical Evaluation Lump and regional nodes
o Imaging (ultrasound <35 years old or mammogram >35 years)
o Cytology or Histology
Imaging is reported as BI-RADS
Can help divide it into:
o DCIS or early Breast Cancer (max with small mobile axillary LNs)
o Locally advanced BC (matted LNs, skin and rib involvement)
o Continue to stage to look for metastasis in advanced BC
Prognostic factors
To select appropriate therapy according to prognosis
To allow comparison of treatment between similar groups of patient at
risk of recurrence or death
To improve the understanding of the disease
Patient factors
Age: Younger women have poorer prognosis of equivalent stage
Comorbidities
Social Support
Tumor factors
Tumour size: Diameter of tumour correlates directly with survival
Histological type (some associated with improved prognosis)
o Tubular, Cribriform, Mucinous, Papillary, Micro-invasive
Histological grade (for scoring of grades [1,2,3] )
o Tubule formation, Nuclear pleomorphism, Mitotic frequency
Lymph node status
o Single best prognostic factor
o Correlation between number & level of nodes involved & survival
Lymphatic / vascular invasion
o 25% operable breast cancers have lympho-vascular invasion
o Double risk of local relapse; risk of short term systemic relapse
o Presence confers a poorer prognosis
Metastases: Distant metastases worsen survival

BREAST SURGERY

Predictive factors (predict response to a Tx):

C-erbB2/Her-2 positivity indicates more aggressive tumour
ER or PR positivity is good predicts 90% response to treatment with
tamoxifen; also means tumour is less undifferentiated
p53 mutation NOT for prog purpose.
Staging Investigations:
CXR (for lung metastases; look for isolated hyperdensity)
CT thorax , abdomen (for liver and adrenal metastasis)
Bone scan
LFT (raised ALP) + Hepatitis screen (may flare up with chemoTx)
CT or MRI brain if patient symptomatic
T stage
Tis: Carcinoma in-situ,
Pagets with no tumour
T1a: 0.1-0.5cm
T1b: 0.5-1.0cm
T1c: 1.0-2.0cm
T2: 2 to 5 cm
T3: >5cm
T4a: Chest wall
T4b: Inv skin
T4c: 4a+4b
T4d: Inflammatory

N stage
M stage
N1: Mobile ipsilat axillary nodes M1: distant mets
N2: Fixed/matted ipsilat axillary
N3:
N3a Ipsilat infraclav nodes
N3b Ipsilat int mammary nodes
N3c Ipsilat supraclav nodes

Stage 0 Stage I Stage II

Stage III

Stage IV

Tis

T1N0

T2N0, T3N0
*skin, rib inv., matted LNs M1
T0N1, T1N1, T2N1 T3 N1
T0N2, T1N2, T2N2, T3N2
Any T, N3
T4, any N

5yr life

90%

60%

DCIS

Early Breast Cancer

80%

10%

Locally advanced BC

Advanced BC

95

Palliative Surgery
Indications
o Bleeding, fungating, infected tumor toilet mastectomy
o Fixation of pathological fractures
o Decompression of spinal cord compression
o Surgical excision of brain metastases
BREAST SURGERY

Early

Surgical options for the breast

Wide Excision + radiotherapy (breast conserving surgery, std of care)
o Removal of tumour with clear margins, while achieving good
cosmetic result
o Contraindications: [Nodal status does not influence decision for
WE or SM]
1. Multifocal (tumour originates from 1 tumour and breaks
off) +/- Multicentric (synchronous tumours)
2. No metastatic disease
3. Appropriate tumour size-to-breast ratio (to achieve good
cosmetic result) - not about T staging anymore
4. Patient must agree to post-operative radiotherapy (daily
RT in hosp)
5. CI to RT
a. PREGNANT (the only absolute CI)
b. No CT disorder underlying inflammation may get
worse
c. Previous RT to the chest
o Central lumpectomy: Must remove nipple-areolar complex
o Overall survival at 25 years for WEAC comparable to SMAC,
with Slightly higher local recurrence rates (for WEAC: 1% per
year, 4% in 5 years)
o Higher risk in younger patients as cancer tends to be more
aggressive
Simple Mastectomy
o Removal of breast tissue, nipple-areolar complex, & overlying skin
o Indications
Contraindication to wide excision
Patient prefers to remove entire breast
o If done for DCIS, dont need to give adjuvant therapy
o Reconstructed with rectus abdominis or latissimus dorsi
S/E: abnormal sensation of breast, no breastfeeding

Complications of surgery

Late

Aims of breast cancer surgery

To achieve cure if excised before metastatic spread has occurred
To prevent unpleasant sequelae of local recurrence

Haemorrhage (POD1)
Wound Infection (POD3)
Seroma formation (accumulation of serum) in 50%
Flap ischemia
Cosmetic deformity
Complications of Axillary Clearance:
- Lymphoedema RT to axilla is contraindicated with AC as it worsens
oedema
- Cellulitis even in minor trauma, due to lymphoedema. Need to clean
even minor wounds with antiseptic solution + prophylactic ABx
- Shoulder stiffness require physiotherapy
- Intercostobrachial nerve transection numbness over inner aspect of arm

Sentinel node biopsy

SLN is representative of the rest of the axilla; if the SLN is negative for
tumour cells, then the rest of the axillary nodes should be negative
Done in any breast surgery
Aims to accurately stage the axilla without the morbidity of axillary clearance
Can be located following the injection of radioisotope, blue dye, or a combo
Can be injected in peritumoural, subdermal or subareolar site
Positive node sent for frozen section
o If -ve do not clear axilla; if +ve, perform axillary clearance
Axillary Clearance
30-40% of patients with early breast cancer have nodal involvement
The aims of axillary surgery is to:
o To eradicate local disease
o To determine prognosis to guide adjuvant therapy (nodal stage)
Surgical evaluation important and should be considered for all patients
with invasive cancer
o Routinely done in clinically palpable LN or T3 (5cm)
o Previous surgery which may disrupt lymphatic flow
Levels of axillary clearance are assessed relative to pectoralis minor
o Level 1 - below pectoralis minor
o Level 2 - up to upper border of pectoralis minor (routine)
st
o Level 3 - to the outer border of the 1 rib
Benefits of axillary clearance
Axillary clearance both stages and treats the axilla
Surgical clearance possibly gains better local control
Avoids complications of axillary radiotherapy
96

!
Chemotherapy (polyCT with 3 drugs; 4-6cycles, eliminate micrometastasis)
Neoadjuvant
Shrink tumors for conservation surgery as well as to downstage locally
advanced cancers before mastectomy
70% tumours show a clinical response; in 2030% it is complete
o 80% of these patients still have histological evidence of tumour
o Surgery required even in those with complete clinical response
Complications: as for CT drug, e.g. mouth ulcers, N/V, hair loss,
immunosuppression (main disadvantage pre-op)
Adjuvant
Start 3 weeks after surgery
o For T1c and above
o Surgical margins <1mm or invasive
o T1b with lymphovascular invasion
o +ve nodal status
Premenopausal patients tend to have better response to chemotherapy
than hormonal therapy (vice versa for postmenopausal patients)
Main active agents: anthracyclines (e.g. doxorubicin, epirubicin) and the
taxanes (e.g. paclitaxel, docetaxel)
Common regimens: CMF (cyclophos, methotrexate, 5-FU)
Palliative
Anthracyclines & taxanes are the mainstay
Helps to reduce load of disease to alleviate symptoms, increase survival
Radiotherapy
Adjuvant
To decrease local recurrence rate
Indications:
o Usually done 6 weeks after Wide Excision
o High risk of local recurrence: T3 (5cm) OR 4 LN +ve
o 1-3 LN in any young pre-menopausal woman
Targeted at breast with or without internal mammary,
infra/supraclavicular LN (Axillary LN are tackled during Surgery)
Contraindications:
o Pregnancy, previous RT, patient choice
o No chemo, no WE
Regimen consists of 25 to 30 cycles in total, 1 cycle per day from Mon Fri over 5-6/52 until max dose (no repeat RT for recurrences)
Complications: radiation injury (e.g. pneumonitis, skin changes), risk of
cancers 1 in 2000 in 20yrs
Palliative: Brain mets; Bone mets to painful areas / impending fractures
BREAST SURGERY

Hormonal Therapy
Used largely in post-menopausal patients basically principle is to give therapy
which tumor responds best to
Adjuvant therapy to eradicate micrometasis
o Can also be used as palliation or preventive treatment in high
risk patient
o Reduces risk in contralateral breast
For ER/PR +ve will have 90% response
Preferred for postmenopausal women
May render patient postmenopausal for better response to HT via
medical ablation with LHRH-a or surgical oophorectomy
Selective oestrogen receptor modulators (SERMs): Tamoxifen
50% reduction in recurrence, 25% reduction in mortality
Taken daily for 5 years
Contraindications:
o PMHx of CVA/DVT ; Immobile patients
Side effects:
o Menopausal symptoms (hot flushes, etc.)
o Endometrial cancer (0.1% per year)
o Deep vein thrombosis
Aromatase inhibitors: Anastrozole, letrozole, exemestane
Inhibit peripheral conversion of testosterone and androstenedione to
oestradiol (still present in post-menopausal women)
Only suitable for post-menopausal patients as use of these agents will
cause overactivity of the HPA axis in premenopausal women
Side effects:
o Musculoskeletal pain; Osteoporosis
Targeted Therapy
Herceptin (trastuzumab)
targets Her-2-neu a.k.a. C-erbB2 receptor (an epidermal growth factor
receptor [EGFR] that is overexpressed in 18-20% of cancers)
Used in C-erbB2 positive tumours, early or late stage
Her-2-neu indicates worse prognosis Herceptin improves prog to
normal
Side effects of Herceptin:
o cardiomyopathy & CCF ; pulmonary toxicity
o infusion reactions ; febrile neutropaenia
Avastin:
Targets vascular endothelial growth factor [VEGF] receptor, used in
advanced cancer
Lapatinib: Targets Her-1 and Her-2, used in advanced cancers
97

!
Treatment by tumour stage
DCIS
WE (+radiotherapy) vs SM
Core biopsy and SLN biopsy
hormonal therapy (if WE) to reduce recurrence at surgical site;
tamoxifen reduces overall breast cancer risk by 50% in both breast

Biochemical measurements
ER positivity predicts for response to endocrine manipulation
C-erb-B2
o Likely to be resistant to CMF chemotherapy & hormonal therapy
o Respond to anthracycline and taxols
Proteases: Urokinase and cathepsin D found in breast cancer

Early breast cancer (stage 1 & 2)

T2 or less (<5cm), N1 or less (no nodes or non-fixed nodes)
SMAC, or WEAC with postop RT
Adjuvant therapy to destroy systemic micrometastases
o CT if tolerable and/or HT if ER/PR +ve
Chemo
Intermediate
No chemo
T >20mm, N >1 11mm < T < 20mm, N=0 T <10mm, N=0
High grade = chemo
o Premenopausal pt chemotherapy + hormonal
o Postmenopausal pt hormonal + chemotherapy

Recurrent breast cancer

Most local recurrences are symptomatic, a/w development of metastases
Restaging is therefore essential
Commonest sites for ductal carcinoma are liver, bone and lung
o Lobular carcinoma less predictable often spreading to bowel,
retroperitoneum etc
Recurrence whilst on adjuvant tamoxifen consider:
o Further surgery for
Isolated 'spot' recurrence after mastectomy
Local recurrence in the conserved breast
o Radiotherapy if not previously given
o Change of hormonal agent to anastrozole or megestrol acetate

Locally advanced breast cancer (stage 3)

T3 or T4, N2 or N3
Surgical resection dependent on size of tumour and resectability
Systemic therapy:
o Neoadjuvant chemo
Downstage inoperable tumour (and predicts tumor
response)
eliminate micrometastasis
o Adjuvant therapy after resection
CT & HT (depends on the histology)
Usually not done if patient has completed the course of
chemo during neoadjuvant phase
Advanced breast cancer (stage 4) aim for disease control
Distant metastases: treat symptoms and prevent potential problems
Minimal locoregional therapy except for palliative purposes
o May reduce mets!
Systemic therapy CT, HT, TT
Mets specific:
o Bone: RT to painful areas, Fixation/RT to impending fractures,
Decompression if cord compression
Treat hypercalcemia from mets
o Brain: RT
o Pleural: drain effusion
o Liver (usually liver failure > obstructive jaundice)
BREAST SURGERY

98

!
GYNAECOMASTIA

Due to enlargement of both ductal and stromal tissue

'True' gynaecomastia = enlarged breast glandular tissue
'Pseudo' gynaecomastia = excess adipose tissue
Benign and often reversible, presents as unilateral non-tender enlargement

Aetiology
Idiopathic
Physiological
(estrogen
excess)
Pathological

Neonatal
Puberty (may be painful)
Senile
Primary Testicular Failure
Endocrine Tumors
o Anorchia
o Testicular
o Klinefelter's Syndrome
o Adrenal
o Bilateral Cryptorchidism
o Pituitary
o Acquired Testicular Failure
Non-Endocrine Tumours
o Mumps
o Bronchial carcinoma
o Irradiation
o Lymphoma
Secondary Testicular Failure
o Hypernephroma
o Generalized hypopituitarism
Hepatic Disease
o Isolated gonadotrophin
o Cirrhosis
deficiency
o Hemochromatosis
Drugs
o Oestrogens and oestrogen agonists - digoxin, spironolactone
o Hyperprolactinaemia - methyldopa, phenothiazines
o Gonadotrophins
o Testosterone target cell inhibitors - cimetidine, cyproterone
acetate

PAGETS DISEASE OF THE NIPPLE

Presentation
Eczematoid change of the nipple +/- surrounding areola
Burning, pruritus, hypersensitivity, with crusting exudate
May have palpable mass (60%)
Work-up
Mammography to identify other areas of involvement
Pathologic diagnosis - core biopsy of nipple and underlying tissue
Almost always accompanied by an underlying malignancy - invasive
ductal ca or DCIS
Prognosis
Related to tumor stage
Treatment
Surgery + RT

Classification (Simon's)
Grade 1 - Minor breast enlargement without skin redundancy
Grade 2a - Moderate breast enlargement without skin redundancy
Grade 2b - Moderate breast enlargement with skin redundancy
Grade 3 - Gross breast enlargement with breast ptosis
Management
Reassurance that it is a benign and self-limiting condition
Investigate:
o Thyroid function tests, testosterone/LH
LFT, alpha-FP, beta-HCG
Medical: Danazol may reduce breast size in 80% of patients
Surgery: Excision can be considered if gynaecomastia is painful or cosmetically
embarrassing (small = periareolar incision)
BREAST SURGERY

99

!
APPROACH TO LUMPS AND BUMPS
Inspection
Number: solitary / multiple
Site: take reference from bony
points
Shape / Symmetry:
o Hemispherical, Round,
Exophytic

Size
Scars
Colour & skin changes?
o Sinuses, discharge
o Ulceration
o Erythema / cellulitis

Palpation (Ask patient: Is area painful?)

Overlying skin temperature
Consistency
o Hard > Firm > Tense > Soft
Tenderness

Mobility
Surface:
o Fully mobile in all directions?
o Smooth/Irregular/
o Fixed and immobile?
Rough
o Mobile only in certain directions?
Margins clearly defined?
Relations to surrounding tissues (over lump in 2 perpendicular planes)
o Attached to skin? muscle / tendon / bone?
o If appears to be attached to muscle:
Ask patient to tense muscle;
Reassess mobility in the 2 planes
Intramuscular or below the muscle, it will
disappear.
Above the muscle it will be more prominent.
Fixed to muscle, it will become less mobile.
Fluctuant? (for small / medium lumps)
o Pagets sign: Rest 2 fingers on opposite sides of lump, press
down on middle of lump +ve: Feel fingers moving apart

Special tests
o Transillumination [Use pen torch on one side]
o Pulsatility (only for some sites, e.g. Neck, abdomen)
Expansile: fingers pushed apart
Transmitted: Fingers pushed in same direction (upwards)
o Slip sign if lipoma is suspected
Tends to slip away from the examining finger on gentle
pressure
o Compressibility / reducibility [if AVM, haemangioma, hernia
suspected]
Reducible: Disappears on pressure, reappears with
opposing force (hernia)
o Auscultation only for certain sites / lesions (e.g. neck, abd, etc.)

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Request I would like to complete my examination by

Examine the draining LNs
If sebaceous cyst / lipoma Looking for other lumps elsewhere
Ganglion Looking for other lumps elsewhere + Asking for hand
dominance + Taking an occupational history
Characteristics of lumps:
S: site, size, shape, scars, skin changes, surface
E: edge, expansibility/ pulsatility
C: colour, consistency, compressibility
T: tenderness, temperature, transilluminability
O: others [fluctuance, fluid thrill]
R: reducibility, relationship to each other
Ulcers:
Base: granulation tissue, slough, fascia, muscle, bone
Edge: sloping (healing), punched out, undermined,
rolled (BCC), everted (SCC)
Discharge: serous, sanguinous, haemoserous, purulent
Mr. X is a young Chinese gentleman
On inspection, there is a (single) (hemispherical) lump on the (dorsum of the
forearm)
It measures <take out ruler> (x by x cm)
There are (?scars, sinuses, ulceration, or discharge seen, nor overlying or
surrounding skin changes)
Is the lump tender?
On palpation, the overlying skin is (not) found to be warm. It is (non-tender)
The surface is (smooth), with clearly-defined margins
The consistency is firm, and it is (non-fluctuant)
The lump is (not) attached to the overlying skin, and it is non-pulsatile.
It (appears to be attached to underlying muscle, as it is mobile horizontally but
not longitudinally)

100

!
Symptoms and signs

Diagnostic significance

1. Lump in or on the skin

Character of the
ulcer margin

Benign ulcers-the margin is only slightly raised by inflammatory

oedema. The base lies below the level of normal skin
Malignant ulcers-these begin as a solid mass of proliferating
epidermal cells, the centre of which eventually becomes necrotic and
breaks down. The margin is typically elevated 'rolled' and indurated
by tumour growth and invasion

Behaviour of the
ulcer

Malignant ulcers expand inexorably (though often slowly), but may go

through cycles of breakdown and healing (often with bleeding)

Size, shape and surface

features
Revealed by inspection-is the
lesion smooth-surfaced,
irregular, exophytic (i.e.
projecting out of the surface)?
Depth within the skin
Superficial and deep
attachments. Which tissue is
the swelling derived from?

Epidermal lesions such as warts usually have a surface

abnormality but deeper lesions are usually covered by normal
epidermis. A punctum suggests the abnormality arises from
an epidermal appendage, e.g. epidermal (sebaceous) cyst

Tends to reflect the layer from which lesion is derived and

therefore the range of differential diagnosis (i.e. epidermis,
dermis, hypodermis or deeper)

4. Colour and pigmentation

Normal colour
If a lesion is covered by normal-coloured skin then the lesion must lie
deeply in the skin (e.g. epidermal cyst) or deep to the skin (e.g.
ganglion)

Character of the margin

Discreteness, tethering to
surrounding tissues, threedimensional shape

A regular shaped, discrete lesion is most likely cystic or

encapsulated (e.g. benign tumour). Deep tethering implies
origin from deeper structures (e.g. ganglion). Immobility of
overlying epidermis suggests a lesion derived from skin
appendage (e.g. epidermal cyst)

Red or purple

Consistency
Soft, firm, hard, 'indurated',
rubbery

Soft lesions are usually lipomas or fluid-filled cysts. Most

cysts are fluctuant unless filled by semi-solid material
(e.g.epidermal cysts), or the cyst is tense (e.g. small
ganglion).
Malignant lesions tend to be hard and irregular ('indurated')
with an ill-defined margin due to invasion of surrounding
tissue. Bony-hard lesions are either mineralised (e.g. gouty
tophi) or consist of bone (e.g. exostoses)

Redness implies increased arterial vascularity, which is most common

in inflammatory conditions like furuncles. Vascular abnormalities
which contain a high proportion of arterial blood such as Campbell de
Morgan spots or strawberry naevi are also red, whereas venous
disorders such as port-wine stain are darker. Vascular lesions blanch
on pressure and must be distinguished from purpura which does not

Deeply pigmented

Benign naevi (moles) and their malignant counterpart, malignant

melanomas, are nearly always pigmented. Other lesions such as
warts, papillomata or seborrhoeic keratoses may become pigmented
secondarily. Hairy pigmented moles are almost never malignant.
Rarely, malignant melanomas may be non-pigmented (amelanotic).
New darkening of a pigmented lesion should be viewed with suspicion
as it may indicated malignant change

Pulsatility

Pulsatility is usually transmitted from an underlying artery

which may simply be tortuous or may be abnormal (e.g.
aneurysm or arteriovenous fistula)

Emptying and refilling

Vascular lesions (e.g. venous malformations or

haemangiomas) empty or blanch on pressure &then refill

Transilluminability
Temperature
2. Pain, tenderness and
discomfort

3. Ulceration (i.e. loss of

epidermal integrity with an
inflamed base formed by
dermis or deeper tissues)

Lesions filled with clear fluid such as cysts 'light up' when
transilluminated
Excessive warmth implies acute inflammation, e.g. pilonidal
abscess
These symptoms often indicate acute inflammation. Pain also
develops if a non-inflammatory lesion becomes inflamed or
infected (e.g. inflamed epidermal cyst). Malignant lesions are
usually painless
Malignant lesions and keratoacanthomas tend to ulcerate as
a result of central necrosis. Surface breakdown also occurs in
arterial or venous insufficiency (e.g. ischaemic leg ulcers),
chronic infection (e.g. TB or tropical ulcers) or trauma,
particularly in an insensate foot

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

5. Rapidly
Keratoacanthoma, warts and pyogenic granuloma may all develop
developing lesion rapidly and eventually regress spontaneously. When fully developed,
these conditions may be difficult to distinguish from malignancy.
Spontaneous regression marks the lesion as benign
6. Multiple,
In certain rare syndromes, multiple similar lesions develop over a
recurrent and
period. Examples include neurofibromatosis and recurrent lipomata in
spreading lesions Dercum's disease. Prolonged or intense sun exposure predisposes a
large area of skin to malignant change. Viral warts may appear in
crops. Malignant melanoma may spread diffusely (superficial
spreading melanoma) or produce satellite lesions via dermal
lymphatics
7. Site of the
lesion

Some skin lesions arise much more commonly in certain areas of the
body. The reason may be anatomical (e.g. pilonidal sinus, external
angular dermoid or multiple pilar cysts of the scalp) or because of
exposure to sun (e.g. solar keratoses or basal cell carcinomas of
hands and face)

8. Age when
lesion noticed

Congenital vascular abnormalities such as strawberry naevus or portwine stain may be present at birth. Benign pigmented naevi (moles)
may be detectable at birth, but only begin to enlarge and darken after
the age of 2

101

!
LIPOMA
Inspection
o Can be single, often multiple
o Usually at neck, trunk
o Hemispherical may appear lobulated
o Scars Implies recurrent lipoma
Palpation
o Smooth or lobulated on firm pressure bulging between strands of
fibrous tissue)
o Soft / firm (depending on nature of fat)
o Well defined edges (may not be regular; series of curves corresponding
to each lobule
o Pseudo-fluctuance if large lipomas are not liquid; but fat may be liquid
o Mobile in all directions (if subcutaneous)
o Positive slip sign; No transillumination / thrill
o Usually in the subcutaneous tissue. [check attachment skin & muscle]
Background Information
Definition: Benign tumour consisting of mature fat cells (distended with fat
from over-activity)
o Malignant change does not occur
o Liposarcomas arise de novo; occur in older age (deeper tissues
retroperitoneal, deep tissues of thigh, subscapular)
Liposarcoma classification
1. Well-differentiated
2. Myxoid, round cell (poorly differentiated myxoid)
3. Pleomorphic liposarcoma
Clinical features
o Can occur at all ages (not common in children)
o Slow-growing, never regress
o May be multiple: lipomatosis (multiple continuous lipomata)
Occur in buttocks / neck
Can cause distortion of subcutaneous tissues.
Treatment
o Non-surgical watch & wait
o Surgical If patient wants it removed (Pain / peripheral neuropathy
Dercums disease, Cosmesis)
Can be removed under LA
Nuchal lipomas (back of the neck): extremely fibrous septae:
difficult to excise
If close to joint: LA may not be possible (may communicate
with joint)
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Variants of lipomas / syndromes associated with lipomas

o Adiposis dolorosa (Dercums disease)
Multiple painful lipomas in limbs, sometimes trunk
Associated with peripheral neuropathy
Angiolipomas: prominent vascular component
o Hibernomas: brown fat cells
o Cowdens disease associated with:
Thyroid cancers
Lipomas
Palmoplantar keratoses
Multiple facial papules
Oral papillomatoses
o Bannayan-Zonana syndrome rare AD dz: lipomas with
macrocephaly and haemangiomas, intestinal polyps

Mr. X is a young Chinese gentleman

On inspection, there is a hemispherical lump over the right scapula
It measures 10 by 8 cm
There are no scars, punctum, ulceration, or discharge seen, nor any overlying
or surrounding skin changes
On palpation, the overlying skin is not warm, it is non-tender
The surface is lobulated, and its margins are not well-defined
The consistency is soft, and it is fluctuant
The lump is not attached to the overlying skin
It is mobile in all directions with a positive slip sign
It is not transilluminable
I would like to complete my examination by looking for other similar lumps
My provisional diagnosis is a lipoma
My differential diagnosis is: large sebaceous cyst

102

!
SEBACEOUS CYST
Inspection
Usually solitary (can be multiple), Hemispherical
Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles)
Variable size ; few mm to 4-5 cm
May have bluish discolouration, May exhibit plastic deformation on palpation
Punctum in apex: in 50%
Palpation
Normal Temperature, non-tender (unless inflamed)
Smooth surface
Well-defined margins (lies in subcutaneous fat)
Tense consistency, may stretch overlying skin ( plastic deformation)
Non fluctuant, not transilluminable
Attached to skin, not attached to deeper structures, mobile in all directions
Background Information
2 histological types (Arise from infundibular parts of hair follicles)
o Epidermal cyst: from infundibular portions of hair follicles
o Trichilemmal cyst: from hair follicle epithelium (most common on
scalp), frequently multiple (AD inheritance)
Definition: Distension of sebaceous glands w sebum from blockage of opening
Clinical features
o Occur in all age groups, rarely present before adolescence
o Slow growing, may appear suddenly at adolescence
o May become infected: acutely painful, sudden increase in size
o May spontaneously discharge contents through punctum, regress
Point of fixation & discharge along a hair follicle
Point gets pulled inwards on enlargement of the mass
creates punctum
Sebaceous horn may form from hardening of slow discharge
from wide punctum
Treatment: excision / curettage along with base +
histological assessment
Complications
1. Infection (discharge)
2. Ulceration
3. Calcification (trichilemmal cyst) (may lead to cyst hardening)
4. Sebaceous horn formation, [hardening of a slow discharge of sebum from a
large, central punctum.]
5. Malignant change
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Treatment
Non-surgical: leave alone (if small, asymptomatic).
Surgical
o Complete excision of cyst and contents under LA.
o Prevention of recurrence: by removal of elliptical portion of skin
containing punctum along the Langers lines.
o If at the angle of jaw, be careful of the facial nerve during operation.
Damage to zygomatic branch can cause eye ulceration.

If lump is increasing in size, what to exclude?

o Malignancies: BCC, Malignant melanoma.
Cocks peculiar tumour (complication)
o Proliferating trichilemmal cysts that can grow to large size, ulcerate

may become infected, open, granulating & edematous

Boggy, painful, discharging swelling

solitary, 90% occur in scalp

o often mistaken for SCC scalp; Angry, malignant-looking (malignant
transformation rare)

Heaping up of granulation tissue from the lining of the cyst

burst through skin, giving everted appearance

regional lymphadenopathy may be present

Gardners syndrome (If multiple lumps found)
o Genetic disorder associated with:

Multiple osteomata of skull & epidermal cysts

Adenomatous polyposis of large bowel & CRCs

Desmoid tumours

Thyroid cancers

Mr. X is a young Chinese gentleman

On inspection, there is a single hemispherical lump in the middle of the forehead just
above the eyebrows
It measures 1 by 1 cm in diameter
There is a visible punctum over the lump
There are no scars, sinuses, ulceration, or discharge seen, nor any overlying or
surrounding skin changes
On palpation, the overlying skin is not warm. It is non-tender.
The surface is smooth, with clearly-defined margins
The consistency is firm, and it is non-fluctuant
The lump is attached to the overlying skin
It is mobile in all directions
Slip sign is negative
I would like to complete my examination by
Looking for other lumps elsewhere
My provisional diagnosis is a sebaceous cyst
My differentials are:
Lipoma / Dermoid cyst

103

!
GANGLION
Inspection
Single; may have overlying scar [recurrent mass]
Hemispherical, flattened,
Near joint capsules, tendon sheaths (90% on wrist, hand ventral / dorsal)
Variable (0.5 6 cm)
Palpation
Normal temperature, non-tender
Smooth surface with Well-defined margins
May be multilocular
Soft & fluctuant if large > firm consistency if small
Weakly transilluminant. (gelatinous material)
Mobility:
o Should assess mobility in 2 perpendicular planes, then with
underlying muscles tensed (less mobile when tensed)
o Not attached to overlying skin (mobile over it)
o Attached to fibrous structures of origin [to joint capsule, tendon
sheath, intramuscular septum, fixed when tensed]
Reducibility: may slip between deep structures when pressed (appears
falsely reduce into joint)
Request
Other similar lumps; ask dominant hand, occupation
Background Information
Definition: Cystic myxomatous degeneration related to synovial lined cavity
[joint capsule or tendon sheath]
Origin controversial: pockets of synovium communicating with joint, tendon
sheath / degeneration of mucoid fibrous tissue
Site:
o Can occur anywhere in body
o Common in areas of fibrous tissue (e.g. around joints, esp. Dorsal >
Volar wrist @ scapholunate joint)
Most common soft-tissue mass in the hand
Types:
o Simple
o Compound chronic inflammation distends tendon sheath above
and below the flexor retinaculum.
o Occult
o Interosseous
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Clinical features
Majority between 20 and 60
years (rare in children)
Grow slowly over months /
years
Non painful

Differentials
Bursae (soft)
Cystic protrusion of synovial cavity in OA
(joint will be abnormal)
Benign giant cell tumours of flexor sheath
(Pigmented Villonodular Synovitis)
Lipoma
Sebaceous cyst

Treatment
Non-surgical
Watch & wait, usually may disappear after a few months.
Aspiration + 3/52 of immobilisation (successful in 30-50%). High chance of
recurrence 6-12/12 later.
Surgical
Complete excision to include neck of ganglion at site of origin. Along
Langers lines.
Complications
o Wound complications: Scar, haematoma, infection
o Recurrence <10%
o Damage to adjacent neurovascular structures.
o Stiffness & Contractures

Mr. X is a young Chinese gentleman, who is alert and comfortable

On inspection, there is a single hemispherical lump on the dorsum of the left wrist
It measures 3 by 2 cm
There are no scars, ulcerations, or discharge seen, nor any overlying or
surrounding skin changes
On palpation, the overlying skin is not warm. It is non-tender
The surface is smooth, with clearly-defined margins
The consistency is soft, and it is fluctuant
The lump is not attached to the overlying skin
It appears to be attached to underlying muscle, as it is mobile horizontally but not
longitudinally
It is transilluminant
I would like to complete my examination by Looking for other similar lumps
Asking Mr. X for his hand dominance Taking an occupational history
My provisional diagnosis is a ganglion
My differential is a
1. Bursa
2. Cystic protrusions of synovial cavity of arthritic joints
3. Benign giant cell tumours of flexor sheath

104

!
BASAL CELL CARCINOMA
Most common skin malignancy in Singapore
Inspection
Single (often multiple)
Commonly found on the face, (above line drawn from angle of mouth to
earlobe)
Hair-bearing, sun-exposed skin (especially around the eye)
Lesions raised above the skin:
o Nodular/ nodulo-ulcerated type (most common):
Pearly, rolled edges [smooth, glistening, slightly transparent]
May be pigmented, with telangiectasia over the lump
May have central ulceration; erode facial structures if
advanced
o Cystic: large cystic nodule
Lesions not raised:
o Pigmented: contains melanin; confused with malignant melanoma
o Sclerosing: flat or depressed with ill-defined edges; maybe ulcerated
o Bush-fire / Cicatricial: multiple superficial erythematous lesions with
pale atrophic areas
o Superficial: erythematous scaly patches
Base:
o May be covered with coat of dried serum & epithelial cells
o If deep: may expose deeper tissues (bone, muscle, etc.), covered
with poor-quality granulation tissue
o On face: may erode deep into facial structures
Palpation (Important to palpate for mobility: fixation and deep local invasion)
Normal temperature, may be painful / itchy
Firm / solid consistency
should be mobile over underlying structures, confined to skin
o If fixed, immobile deeper invasion
Regional LAD (metastases are extremely rare, to rule out SCC)
+ Ask about pre-disposing factors

Xeroderma pigmentosum (familial, associated with failure of

DNA transcription)
Gorlins syndrome (rare autosomal dominant cancer)
o Acquired
Sunlight (especially UV light; UV-B range)
Carcinogens (smoking, arsenic)
Previous RT
Malignant transformation in previous skin lesions
(e.g. naevus sebaceous)
Clinical features
o In elderly people (incidence increases with age)
o Rare in dark-skinned races
o Males > females
o Grow very slowly; months / years typically
o May spread radially leaving central scar
o Persistent nodule / ulcer with central scab (repeatedly falls off, reforms)
o May have itch / pain
o If neglected: deep infected ulcer

Macroscopic appearances
Above the skin:
o Nodular
o Nodulo-ulcerative / Deeply eroding ulcer
(rodent ulcer)
o Cystic
Not raised above the skin:
o Pigmented
o Geographical / cicatricial / bush-fire
(advancing edge, healing centre)
o Sclerosing (flat / depressed tumour, illdefined edge)
o Superficial (erythematous scaly patches)

Microscopic features
Most commonly
islands and nests of
basaloid cells in
dermis
High mitotic rates,
peripheral palisading
(islands arranged
radially with long
axes in // alignment)

Background Information
Locally invasive carcinoma of basal layer of the epidermis
Does not metastasize, but can infiltrate adjacent tissues
Common in sun-exposed skin
Pre-disposing factors:
o Congenital (rare)
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

105

!
Origin of various appearances:
o Tumour always starts as a nodule
o When central epithelium dies, ulcer develops (nodulo-ulcerative)
Edge rolled raised up and rounded (but not everted) (may
be only clue to diagnosis)
o If centre of tumour does not necrose / ulcerate: nodule enlarges
cystic appearance
Not really cystic: solid and non-fluctuant
o If pigmented brown by excess melanin: pigmented BCC
o Geographical appearance:
When nodule first ulcerates, rolled edge is circular
Shape becomes irregular as malignant cells spread
As ulcer heals: irregular, raised edge around flat white scar
bush-fire BCC

Mr. X is an elderly Chinese gentleman

On inspection, there is a single hemispherical lump just above alar of the nose
It measures 2 by 2 cm
The edges of the lump are well defined, with a pearly, rolled appearance
There is a small area of pigmentation on the periphery of the lump, and fine
telangiectasia are seen over the lump
There are no visible scars, ulceration, or discharge seen, nor any other overlying
or surrounding skin changes
On palpation, the overlying skin is not warm. It is non-tender.

Differentials
SqCC
o Especially if ulcerated
o But if rolled edge: more likely BCC
Keratoacanthoma (adenoma sebaceum, molluscum pseudocarcinomatosum)
o But scar will be deep (see below)
If pigmented: malignant melanoma (rare in Singapore)
Treatment
Raised above skin: excision with 0.5 cm margin (maximum)
Not raised above skin: wider margin of excision, especially if at inner
acanthus of eye, nasolabial fold, nasal floor, ear
o Frozen section may be needed to ensure adequate excision
Alternative:
o RT
Eyes, ears, nasolabial fold lesions: Mohs chemosurgery
o Staged chemosurgery, histological assessment of margins &
electrodessication

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

The surface is smooth

The consistency is firm
The lump arises from the skin
It is freely mobile over the underlying tissues
My provisional diagnosis is basal cell carcinoma
My differentials include SqCC, keratoacanthoma
I would like to complete my examination by
Examining for cervical lymphadenopathy (although very rare in BCC)

106

!
SQUAMOUS CELL CARCINOMA
Inspection
Single (may be multiple)
More common on sun-exposed skin head, neck, arms, hands, trunk
may be of considerable size (> 1 cm)
Round nodule or Circular ulcer or Irregular/ exophytic/ fungating mass
Well defined edges:
o everted (excessive growth raises it above skin)
o dark, red-brown colour (very vascular)
May have central ulceration, Base:
o Necrotic tumour; may be covered with coagulated blood / serum
o Granulation tissue: tends to be pale, unhealthy
o Deep tissues may be exposed
o Depth: variable (may be very deep; especially in soft tissue)
o Can be copious, bloody, purulent, foul-smelling discharge
Surrounding tissue may be oedematous, thickened
Palpation
normal temperature, not tender
usually mobile
o If immobile: invasion into deep structures
Request for:
Examination of local lymph nodes (5% at time of presentation)
o Often enlarged (but may not contain tumour even if enlarged can
be from infection)
Examination for sites of metastases
o Respiratory: lung (pleural effusion)
o Abdominal: liver (hepatomegaly)
Take a history looking for predisposing factors (see below)

Background Information
Carcinoma of the cells of the epidermis forming superficial keratinous
squamous layer
Local invasion into epidermis, dermis, adjacent tissues, & lymphatic spread
to LNs
Microscopy:
o Tongues of tumours cells spreading in all directions
o Epithelial pearls nest of squamous epithelium, cells are arranged
in concentric circles surrounding a central focus of acellular keratin
Clinical features
o Incidence increases with age (usually elderly male)
o Predisposition:
Congenital:
Xeroderma pigmentosum (AD, failure of DNA
transcription)
Acquired
n
Env : sunlight, Irradiation, Chemicals
Pre-existing lesions: Solar keratosis, Bowens
disease
Chronic ulcers: old burns, chronic venous ulcers
Immunosuppression (post-transplant, HIV)
o Usually has been growing for 1 2 months before being noticed
Begins as small nodules on skin
As enlargement occurs, centre necroses, sloughs
Nodule turns into ulcer
Ulcer initially circular with prominent everted edges
Subsequently enlarges & changes to any shape
Bleeding (more common with SCC than BCC)
Discharge
Pain (invasion of deep structures)
Lymphadenopathy
Complications
Infection
Bleeding (massive / fatal if erosion into large vessel)
Treatment (depending on site of lesion)
Wide-excision with 1 cm margin
Radiotherapy (if unresectable, nodal spread)
+ Block dissection of regional lymph nodes (if involved)
Eyes, ears, nasolabial fold lesions: Mohs chemosurgery
o Staged chemosurgery, histological assessment of margins &
electrodessication

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

107

!
Lesions Associated with SqCC

Mr. X is an elderly Chinese gentleman

Marjolins ulcer

SqCC arising in long-standing benign ulcer / scar

o Commonest ulcer: venous ulcer
o Commonest scar: burns
Very similar in appearance to classic SqCC, but may not
be so florid

On inspection, there is a single irregular ulcer on the dorsum of the right

st
nd
hand, proximal to the 1 & 2 MCP joints

Very slowly growing, may progress to SqCC

red, scaly irregular plaque on the trunk
o if on the penis, vulva or oral cavity = erythroplasia
of Queyrat
Intraepidermal carcinoma
o a/w visceral malignancies in 5-7 yrs time esp if
area of skin has not been exposed to the sun
HPV has been found in some lesions
Microscopically
o Epidermis (Atypical keratinocytes)
o Basal layer is intact
Treatment: excision (SqCC will grow eventually)

The base of the ulcer is shallow and contains red granulation tissue.

Multiple yellow-grey to brown scaly tumour

o Small, hard,
o Begin with thickening of skin
On sun-exposed skin of elderly patients
25% may undergo change to SqCC
Microscopically: hyperkeratosis, atypical dividing cells in
prickle cell layer (irregular acanthosis), focal
parakeratosis, basal layer atypical only (vs atypia in whole
epidermis in SqCC)
Treatment:
o Non-surgical: cryotherapy, topical chemotherapy
(5-FU)
o Surgical: curettage of affected skin

My provisional diagnosis is squamous cell carcinoma

Bowens
disease
(SqCC in situ)

Solar (actinic)
keratosis
(SqCC in situ)

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

It measures 1.5 by 1.5 cm. The edge of the ulcer is well-defined, red and
heaped up.

There are no scars, or discharge seen, nor any surrounding skin changes.
On palpation, the surrounding skin is not warm. It is non-tender
The edges are firm
The lump arises from the skin
It is fixed and immobile

My differentials are
o Benign: Keratoacanthoma, infected seborrhoeic wart, solar acanthosis,
pyogenic granuloma
o Malignant: BCC, malignant melanoma, solar keratosis
I would like to complete my examination by
Examining the local lymph nodes for lymphadenopathy
Taking a history looking for sites of metastases
Examining the abdomen and lungs for signs of metastases

108

!
MALIGNANT MELANOMA
Inspection
Usually single (may have satellite lesions around primary lesion)
Limbs, head & neck, trunk, subungual, mucocutaneous junction, mouth, anus
Any colour: pale pink, brown, black, purple (rich blood supply)
Clearly defined but irregular
May ulcerate, discharge
May have surrounding halo: brown (pigment), pink (inflammation)
Types:
o Superficial spreading melanoma (70%):
Legs of women and backs of men
Red, white, blue in colour
Irregular edge
o Nodular type melanoma (15-30%):
On trunk
Polyploidal and raised
Smooth surface with irregular edge
Frequently ulcerated
o Lentigo maligna melanoma:
On face or dorsum of hands & forearms
Underlying lesion is flat, brown-black with irregular outline
Malignant area is thicker and darker
o Acral lentiginous melanoma:
More common in Asians and Blacks
On hairless skin: subungual area, palms, soles
Irregular area of brown/ black pigmentation
o Others: amelanotic melanoma, intra-cranial melanoma, retinal
melanoma
Beware of the man with the glass eye and hepatomegaly
Palpation
Normal Temperature, Non-tender
Surface
o If small: smooth epithelium
o If ulcerates: covered with crust (blood + serum)
o If bleeding, / infected: wet, soft, boggy
Firm consistency (small satellite nodules feel hard)
Mobile, moves with skin over deeper structures
Request
Palpation for regional lymphadenopathy
Palpation for other subcutaneous nodules (lying along course of draining
lymphatics)
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Background information
4 commonest types of malignant melanoma
Superficial spreading melanoma (70%)
Nodular melanoma (15 - 30%)
Lentigo maligna melanoma
Acral lentigous melanoma
Microscopic features
Consists of loose nests of melanocytes in basal cell layer:
Invade epidermis (leading to destruction, ulceration) & deeper into dermis,
subcutaneous fat
Clinical Features
Very rare before puberty (usually > 20 years old)
Equally in both sexes (but distribution different see below)
> 25% arise de novo
o Change in surface, size, colour, Halo, satellite nodules
o Ulceration, bleeding
o Itch, No pain
o Lymphadenopathy
Symptoms of distant metastases: LOW, SOB, jaundice
o Lymphatogenous spread to: regional LN
o Haematogenous spread to: Lungs [pleural effusion], Liver
[hepatomegaly], Brain [focal neurological signs] & Skin and
subcutaneous tissues
Predisposing Factors
Congenital / non-modifiable
o Light skinned race
o Xeroderma pigmentosum
o Dysplastic naevus syndrome (B-K mole, FAMM syndrome) 100%
risk if 2 family members affected
o Large congenital naevi
st
o FHx in 1 degree relatives (1.5X risk)
Acquired / modifiable
o Sunlight exposure
o Pre-existing skin lesions
Lentigo
> 20 benign pigmented naevi (3 x risk)
o Previous melanoma (3.5 x risk)

109

!
Features of pigmented skin lesion suspicious of malignancy
Asymmetry
Bleeding & ulceration (late)
Change in: colour, size, shape, surface, number (early)
o Surface:
Loss of normal surface markings (e.g. skin creases) around
lesion
Skin may become rough / scaly
Itchy with pale-pink halo (inflammation)
o Size:
Growth of newly-formed / long-standing mole
Increase in edge, width, thickness
o Colour:
Becoming darker
Halo of brown discolouration in skin around the lesion
Patchy colour change (black, to blue-purple vascularity)
Occasionally colourless: no melanin production
o Number:
Satellite nodules of tumour around the lesion
Enlarged inguinal, axillary lymph nodes
Diameter >6mm
Elevation (flat plaque nodule)
Request
Examine draining lymph nodes
Take a history for:
o Cardinal symptoms of malignant change in a mole
Rapid increase in size
Itching
Bleeding
Change in colour / shape / thickness
o Predisposing factors

Staging by depth of invasion

Clarks levels of invasion
Level
Extent of Tumour
I
II
III
IV
V

Epidermis only
Invades papillary dermis
Fills papillary dermis
Invades reticular dermis
Subcutaneous tissue invasion

5-Year
Survival
98%
96%
94%
78%
44%

Breslows thickness (different in absolute depth of invasion, LN involvement)

Breslow Thickness
10-Year Survival
< 0.76 mm
92%
< 3 mm
50%
< 4 mm
30%
LN Involvement
< 40% (8 yr)

Prognosis generally poor above 3 types of staging, or other indicators of

poor prognosis:
o Elderly, Male
o Lesions on trunk
o Ulceration
o Depigmentation, amelanotic
o Aneuploidy, high mitotic index

Differentials
Benign
o Moles (pigmented naevus melanocytes, melanin)
o Freckles (normal number of melanocytes, melanin from each)
o Lentigo ( melanocytes, normal amount of melanin from each)
o Pigmented seborrhoeic keratoses
o Dermatofibroma
o Thrombosed haemangioma
Malignant
o Pigmented BCC
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

110

!
Treatment
Prevention (VERY IMPORTANT):
o Avoidance of causative factors
Surgical excision with wide margins down to deep fascia
o Main lesion:
< 0.76 mm: excise with 1 cm margin
0.76 1.0 mm:
excise with 2 cm margin
> 1.0 mm: excise with 3 cm margin
o Nodal spread:
If clinical suspicion, biopsy or FNAC of lymph nodes
If palpable: therapeutic block dissection
Palliation / adjuvant for distant metastases
o Intralesional BCG therapy
o Immunotherapy: vaccines (raises anti-melanoma response),
monoclonal antibody, cytokine interferon therapy

Superficial
Spreading

Nodular

Lentigo Maligna

Acral Lentiginous

70%

15-30%

Rare

Trunk

Face;
Dorsum of hand /
forearm

Hairless skin (palms,

soles, subungual
area)

Site

: Back
: Legs

Colour

Red, white,
blue
Most often
(varying
black
pigmentation)

Edge

Irregular

Shape

Palpable, but Thick, polypoid,

Flat
thin
raised

Surface -

Remarks -

Mr. X is a middle aged Chinese gentleman

On inspection, there is a single flat-looking lesion over the right foot
It measures 2 by 4 cm
It is variegated in appearance, and exhibits red, white, and black discolouration
The margins are clearly-defined and irregular
There are no scars, nor any surrounding pigmentation, erythema, or ulceration,
bleeding, or discharge
On palpation, the overlying lesion is palpable. It is not warm. It is non-tender
The surface is smooth, and its consistency is firm
The lump is attached to the skin, and moves with it over deeper structures
My provisional diagnosis is malignant melanoma
My differential diagnoses are: BCC, pigmented naevus
I would like to complete my examination by

Brown / black

Regular outline Irregular

Brown / black
Irregular

Take a history for: cardinal symptoms of malignant change, and any

predisposing factors

Flat

Smooth

Frequently
ulcerated,
bleeding

Arises from patch

of Hutchinsons
Lentigo
Malignant area
usually thicker,
darker
Area seldom
ulcerates

Rare type
Often
misdiagnosed as
haematoma,
paronychia

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Examining for regional lymphadenopathy

111

!
NEUROFIBROMA
Inspection
Often multiple
Anywhere in skin, subcutaneous
tissues, e.g. forearm
Spherical / Pedunculated /
Fusiform (long axes lie along
length of limb)
Rarely more than few cm
Comment on any caf-au-lait spots

Palpation
normal temp., Non-tender
Smooth, Well-defined
Soft/ fleshy, rubbery consistency
Non-fluctuant
If in subcutaneous tissue: mobile
within it
Move most freely perpendicular to
course of nerve

Request
Look for other similar lesions & other manifestations of NF-1: caf-au-lait
spots, axillary freckling, Lisch nodules, optic glioma
o
Measure the BP (HPT 2 to phaeochromocytoma, CoA, RAS)
Examination of cranial nerve VII & VIII (acoustic neuroma)
Background Information
Sporadic Neurofibroma
Benign tumour containing mixture of elements from peripheral nerves:
o Neural (ectodermal); Fibrous (mesodermal)
Often multiple
History
o Any age (but usually adult)
o Symptoms: usually cause no discomfort, rarely disfiguring
o If related to nerve trunk, may be tender
Patient may get tingling sensations in distribution of nerve
Histology
o Schwann cells: appear as bundles of elongated wavy spindle cells
o Collagen fibrils, myxoid material
o Often not encapsulated (unlike neurilemmomas)
Complications of Neurofibroma
o Pressure effects: spinal cord, nerve root compression
o Deafness: involvement of VIII
o Neurofibrosarcoma (only in NF-1): 5-13 %
o Intra-abdominal effects: obstruction, chronic GI bleeding
o Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis
Treatment (single neurofibroma)
o Non-surgical: leave alone if asymptomatic, patient agreeable
o Surgical: indicated only if malignancy suspected
Local re-growth common (cannot be surgically detached
from underlying nerve)
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Neurofibromatosis I (Von Recklinghausens disease)

AD, neurocutaneous syndrome; chr 17
Characterised by pigmentary changes,

tumours, and skeletal, vascular dysplasias

o Fibroma 2 NF or 1 plexiform NF
o Iris hamartomas (Lisch Nodules)
o Bone: dysplasia, pseudoarthrosis
o Relatives
o Optic glioma
o Macules >6; >15mm post-pubertal
o Axillary freckling

Neurofibromata of all
sizes (few mm to large
subcutaneous nodules),
related differently to skin
o Within skin
o Tethered to skin
o Pedunculated

Plexiform Neurofibroma (elephantiasis neurofibromatosis)

Very rare
Excessive overgrowth of neural tissue in subcutaneous layers, giving tissue
swollen oedematous appearance
o Often mistaken for lymphoedema, but lymphatic drainage is normal
Can result in severe deformity: diffuse enlargement of peripheral nerve with
skin involvement
Mr. X is a young Chinese gentleman
On inspection, there are two spherical, pedunculated masses on the back
One measures 2 cm, and the other 0.5 cm in diameter
They are pink in colour, with well-defined margins
There are no scars, sinuses, ulceration, or discharge seen, nor any surrounding
skin changes
On palpation, they are not warm and non-tender
Their surfaces are smooth, and are firm, and rubbery
They are attached to the skin, and are mobile over the deeper tissue layers
My provisional diagnosis is neurofibromata
I would like to complete my examination by
"Looking for other similar lesions
Looking for manifestations of neurofibromatosis
Examining the cranial nerves

112

!
DERMOID CYST
Inspection
Usually single
Ovoid / spherical
Site:
o Congenital, 1-2 cm usually
Along lines of fusion of ophthalmic & maxillary facial
processes
Inner & outer ends of upper eyebrow
o Acquired, 0.5-1 cm usually
Beneath skin likely to be injured e.g. fingers
Scars often present
Palpation
Not warm, maybe tender if infected
Smooth surface, Well-defined margins
Consistency
o Congenital: Soft (not tense / hard)
o Acquired: Hard & tense (sometimes stony hard)
Fluctuant (if large)
Mobile over deeper tissues
o Deep to skin, in subcutaneous tissue
i. Congenital: Not attached to skin or underlying structures
ii. Acquired: may be tethered to scar
Background Information
A dermoid cyst is a cyst deep to the skin, lined by skin
2 different methods of formation:
o Congenital: Accident during antenatal development
o Acquired: Implantation of skin into subcutaneous tissue by injury
Treatment
Congenital
o Surgical treatment; complete excision
o Full extent should first be established with X-ray / CT
Midline cysts may communicate with CSF; must exclude
bony defect
Acquired
o Complete excision of cyst

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Clinical features
Congenital (suspect if in child, young adult)
o Formed intra-utero, when skin dermatomes fuse
o Occur at any point in mid-line, common in neck / face / nose
Particularly along lines of fusion of ophthalmic &
maxillary facial processes
Also: inner & outer ends of upper eyebrow
o May be seen at birth
o Distends a few years later, becomes obvious; few symptoms
other than cosmetic problems
o Rarely infected
Acquired Implantation dermoid (suspect if in adult Browse pg 60)
o Develop when piece of skin survives after being forcibly
implanted into subcutaneous tissue
Often by injury: cut, stab, etc.
o Symptoms
Small, tense lump
Painful and tender (in areas subjected to repeated
trauma)
Local effects (e.g. problems with grip / touch if on finger)
Also rarely infected
o Differentials
Sebaceous cyst (look for old injury, presence of scar
near cyst: more likely dermoid)
Ms. X is a young Chinese girl
On inspection, there is a single ovoid lump just above the lateral edge of the left
eyebrow
It measures 3 by 2 cm
There are no scars, ulceration, or discharge seen, nor any overlying or
surrounding skin changes)
On palpation, the overlying skin is not warm. It is non-tender.
The surface is smooth, with clearly-defined margins
The consistency is firm, and it is fluctuant
The lump is not attached to the overlying skin or underlying tissues.
It is fully mobile in all directions.
My provisional diagnosis is a congenital dermoid cyst
My differentials are: sebaceous cyst, lipoma

113

!
SEBORRHOEIC KERATOSIS

HAEMANGIOMA

(Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma)

Inspection
Often multiple
Any part of skin; most found on
back & face
Round / oval
Light brown black
stuck on appearance; appears
warty
Varying size; Few mm to 2-3 cm
Distinct margins
Request to look for similar lesions
elsewhere

Palpation
No warmth, no tenderness
Rough surface (sometimes
papilliferous)
More firm than surrounding skin
Attached to skin
Special tests
o May be picked off gently
reveals patch of pale-pink
skin, 1-2 surface capillaries
(bleed slightly)
o (DONT DO THIS IN
EXAM)

Background Information
Benign outgrowth of basal layer of epidermis raised over normal layer
Microscopy:
o Hyperkeratosis (thickening of keratin layer)
o Acanthosis (thickening of prickle cell layer)
o Hyperplasia of variably pigmented basaloid cells
Clinical features
Occur in both sexes
More common in elderly people
Begin as a patch,
o increases in area, size over months / years
o May not increase in thickness
o May suddenly fall off: leave pale-pink patch of skin
Complications:
o May become disfiguring, catch on clothes
o May get infected (may imitate SCC, pyogenic granuloma)
o Seldom bleeds (may cause it to change colour to brown)
Leser-Trelat sign: Sudden onset of multiple seborrhoeic keratoses may imply
visceral malignancy
Treatment
Non-surgical (Can be left alone as it is benign)
Surgical for cosmetic reasons, etc.
o Superficial shaving (lies above level of normal epidermis)
o Cautery
LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Background Information
Vascular malformations
o Types
Capillary: of cases, include the cutaneous haemangiomata,
telangiectasias
Predominantly venous: venous angioma
Deeper levels of subcutaneous tissue, may extend
into muscle / joint
May have distended veins over the surface of the
mass
Empty with pressure, may have bruit
Predominantly lymphatic: lymphangioma circumscriptum
o Features
Develop as abnormal proliferation of embryonic vascular
network
Hamartomas
May ulcerate, induce hyperkeratosis in overlying stratum
corneum
Many forms of cutaneous haemangiomata: (see table)
o Strawberry naevus (cavernous haemangioma)
o Port-wine stain (naevus flammeus)
o Spider naevus
o Campbell de Morgan spot
Also
Telangiectasias
o Dilatation of normal capillaries
o Can be secondary to irradiation
o Can be part of hereditary haemorrhagic telangiectasia (Osler-RenduWeber syndrome)
Autosomal dominant disease
Overt and occult haemorrhage can present as haematuria,
haematemesis, melaena, epistaxis, iron-deficiency anaemia
Vin ros patch
o Congenital intradermal vascular abnormality
o Mild dilatation of vessels in sub-papillary dermal plexus
o Can occur anywhere, gives skin pale-pink colour
o Associated with other vascular abnormalities (e.g. haemangiomata,
AV fistulae, lymphoedema)
o Usually not disfiguring
114

!
KAPOSIS SARCOMA
Inspection
Purple papules and plaques
Solitary, but usually multiple
Site: limbs, mouth, tip of nose/ palate or anywhere on the skin or mucosa
Request to take a history of previous transplantation or current underlying
immunocompromisation.
Background information
Derived from capillary endothelial cells or from fibrous tissue
Linked to HHV-8
Types:
o Classic Kaposis Sarcoma
Confined to skin of lower limbs of elderly Jews
Not fatal
o AIDS associated Kaposis Sarcoma
AIDS defining; Found in 1/3 of AIDS patients
nd
1/3 develops a 2 malignancy e.g. leukaemia/ lymphoma
o Endemic (African) Kaposis Sarcoma
Aggressive and invasive fatal tumour
Good response to chemotherapy
o Translation- associated Kaposis Sarcoma
Following high dose immunosuppressive therapy
Often regress when treatment is ended
Treatment
Conservative if asymptomatic. Start anti-retrovirals if HIV +ve
Surgical: local radiotherapy amd chemotherapy (IFN- alpha, doxorubicin,
intralesional vinblastine)

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

FIBROSARCOMA
Inspection
Single; Usually limbs (but can be anywhere)
Spherical or hemispherical
If large, vascular: may make skin shiny & pink
May have
o Sinuses & Discharge
o Ulceration
o Erythema / cellulitis
Palpation
Usually feel warmer (abnormal blood supply)
May be tender
Smooth surface (may be bosselated covered with knobs)
Well-defined margins (indistinct if fast-growing, invasive)
Firm / hard consistency (rarely stony hard; do not ossify)
Usually fixed
May pulsate, have audible bruit, palpable thrill (may be very vascular)
Request to test for distal neurological status (for invasion of nerve)
Background Information
Fibrosarcoma is one of the commonest mesodermal soft tissue malignant
tumours
o Pure benign fibroma is very rare
History
o More common in elderly (but can occur any age)
o Common complaints
Growth: disfigurement, interference with ROM
Pain
Weakness (infiltration of other structures)
General debility
Prognosis: generally good

115

!
ANATOMY OF THE NECK

The neck is composed of two triangles on each side anterior and

posterior triangles
The anterior triangle is bounded by the lower border of the mandible
superiorly, the midline anteriorly, and the anterior border of the
sternocleidomastoid posteriorly
The posterior triangle is bounded by the posterior border of the
sternocleidomastoid anteriorly, the anterior border of the trapezius
posteriorly, and the clavicle inferiorly
In general, enlarged lymph nodes are the most common cause of a
lump in the neck, regardless of location

Masses by location
Midline
1. Submental lymph node
2. Thyroglossal cyst
3. Thyroid nodule in the isthmus
4. Sublingual dermoid cyst
5. Plunging ranula (retention cyst of the sublingual)
6. Rarely, hyoid pathology e.g. bursa
Anterior Triangle
1. Lymph node along anterior border of sternocleidomastoid (levels II, III,
IV)
2. Thyroid nodule
3. Submandibular gland mass (see later section on Salivary gland swellings)
4. Branchial cyst + fistula
5. Chemodectoma (carotid body tumour)
6. Carotid aneurysm
7. Pharyngeal pouch
8. Laryngocoele (rare; an air-filled, compressible structure seen in glassblowers)

Thyroglossal Cyst
Epidemiology:
Equal in males and females. Occurs mostly in children and adolescents but up to
one-third occur in patients older than 20 years.
Pathology:
Cystic expansion of the remnant thyroglossal tract (embryological origin of the
thyroid which descends from the foramen caecum on the tongue).
Features:
Smooth, rounded, cystic lump. Usually asymptomatic but may become infected.
75% are in the midline while 25% are slightly to the left or right.
Approach:
Check of lump moves with swallowing as well as tongue protrusion
Complications:
1. Infected with sinus formation and seropurulent discharge (occurs with
incision or rupture of cyst)
2. Malignant change (carcinoma of the thyroglossal duct)
Histology:
Cyst with columnar or squamous epithelial lining which may be ciliated.
The cyst may also contain thyroid and lymphoid tissue. If malignancy occurs, it is
usually a papillary carcinoma (~90%).
Treatment:
Sistrunk procedure resection of the (a) cyst and (b) mid-portion of the hyoid
bone in continuity and resection of a (c) core of tissue from the hyoid upwards
towards the foramen caecum (remove the entire tract to prevent recurrence!)

Posterior Triangle
1. Lymph node (mainly) level V and supraclavicular lymph node groups
2. Cystic hygroma
3. Cervical rib
4. Brachial plexus neuroma/schwannoma

NECK LUMPS

116

!
Dermoid Cyst

Branchial Cyst/Fistula

Pathology:
Can be congenital or acquired.
Congenital developmental inclusion of epidermis along lines of fusion
of skin dermatomes (seen in younger patients, present since birth).
Locations include:
o medial and lateral ends of the eyebrows (internal and external
angular dermoid cysts)
o midline of the nose (nasal dermoid cysts)
o midline of the neck and trunk
Acquired due to forced inclusion of skin into subcutaneous tissue
following an injury, usually on fingers. Seen in older patients, no previous
history of mass, history of trauma to area (may have associated scar).

Epidemiology:
Affects both sexes equally, usually in young adults in their 20s.

Histology:
Cyst lined by epidermis, with evidence of adnexal structures such as hair follicles,
sebaceous glands and sweat glands.
Features:
Small non-tender mobile subcutaneous lump, may be fluctuant, skin-coloured or
bluish.
Management
- Imaging investigations (e.g. XR, U/S, CT) are important especially for cysts
on the skull as they can communicate with cerebrospinal fluid.
- Complete surgical excision of the cyst.
Plunging Ranula
Pathology:
A pseudocyst associated with the sublingual glands and submandibular ducts.
Ranulas (frog mouth) can be congenital or acquired after oral trauma.

Pathology:
A branchial cyst is thought to develop because of failure of fusion of the
embryonic second and third branchial arches. It is lined by squamous epithelium.
Features:
- Occurs anterior to the upper or middle third of the sternocleidomastoid
muscle.
- Smooth firm swelling that is ovoid in shape, with its long axis running
downwards and forwards.
- May be fluctuant, usually not transilluminable (due to desquamated epithelial
cell contents).
- Look for fistula in this area a branchial fistula will run between tonsillar
fossa and the anterior neck, passing between the external and internal
carotid arteries.
- Fine needle aspiration of the cyst will yield opalescent fluid with cholesterol
crystals under microscopy.
- May be complicated by recurrent infections purulent discharge, fixation to
surrounding structures.
Management:
- If fistula present, perform fistulogram to delineate course.
- Surgical excision of the cyst where possible. (perc drainage rarely
permanently successful)
If fistula/sinus present, inject Bonneys blue dye into tract prior to surgery to
allow accurate surgical excision.
- Treatment of infection with antibiotics.
- Complications: cyst recurrence; chronic discharging sinus.

Typically appears as a blue-grey dome-like swelling beneath the tongue.

A large ranula can present as a neck mass if it extends through the mylohyoid
musculature of the floor of the mouth termed a plunging ranula.
Treatment:
- Complete resection if possible, often in continuity with assoc sublingual
gland (but often difficult due to close association with the lingual nerve and
submandibular duct).
- If complete resection not possible, marsupialisation (de-roofing the cyst so
that it opens into the floor of the mouth) and suturing of the pseudocyst wall
to the oral mucosa may be effective.
- Incomplete removal leads to recurrence.
NECK LUMPS

117

!
Chemodectoma

Pharyngeal Pouch

Pathology:
A chemodectoma is a tumour of the paraganglion cells (paraganglionoma) of the
carotid body located at the bifurcation of the common carotid artery (into the
internal and external carotids).
They are usually benign, but locally invasive; the risk of malignancy is 10%, with
metastasis to local lymph nodes (no histopathological features for malignancy,
thus malignant nature can only be diagnosed by presence of metastasis).

Pathology:
A herniation of the pharyngeal mucosa (pulsion diverticulum) through its
muscular coat at the weakest point Killians dehiscence between the
cricopharyngeus muscle and the lower inferior constrictor muscles.

Features:
- Solid, firm mass at the level of the hyoid bone (where the bifurcation is) be
gentle during palpation as pressure on the carotid body can cause vasovagal
syncope.
- Mass is pulsatile but not expansile, due to transmitted pulsation from carotids.
- Due to close association with carotid arteries, lump can be moved side to side
but not up and down.
- May be bilateral.
Differentials:
- Main differential is carotid artery aneurysm
- Aneurysm can occur at any level but carotid body tumour occurs at the level of
the hyoid bone.
- If suspecting aneurysm, (a) listen for bruit, look for (b) signs of Horners
syndrome, (c) examine the rest of the peripheral vascular system.
Investigation:
- DO NOT PERFORM FNA
- Angiography (gold standard) shows a hypervascular mass displacing the
bifurcation. May also show vessel compromise by tumour invasion, and
undetected synchronous tumours.
- CT and/or MRI can be used to delineate tumour anatomy in relation to
surrounding structures; CT reveals homogenous mass with intense
enhancement following IV contrast administration.

Features
- Occurs in older patients
- A cystic swelling low down in the anterior triangle, usually on the left
- Squelching sound on deep palpation
- Patient complains of
o halitosis,
o regurgitation of undigested food with coughing
o dysphagia in the neck,
o
hoarseness,
o weight loss
- Complications: aspiration pneumonia; diverticular neoplasm (<1%)
Diagnosis by barium swallow
Treatment
- Leave it alone if small and asymptomatic
- Minimally invasive treatment: endoscopic cricothyroid myotomy
- Surgical approaches (several available)
o Diverticulectomy + cricothyroidotomy (diverticulectomy
associated with risk of mediastinitis, dangerous)
o Diverticulopexy (done in high risk patients, involves suspending
the lumen of the pouch in the caudal direction so that food and
secretions cannot enter the pouch; as the diverticulum is still
present, the risk for malignancy still remains)

Treatment:
- Surgical excision with pre-operative embolization (reduces bleeding and
complications, and facilitates resection); any enlarged ipsilateral lymph nodes
are also removed due to the small possibility of malignancy
- Radiotherapy is an effective alternative for patients who are unfit for surgery or
whose tumours are too large.

NECK LUMPS

118

!
Cystic Hygroma

Cervical Rib

Pathology:
A cystic hygroma is a congenital cystic lymphatic malformation found in the
posterior triangle of the neck, probably formed during coalescence of primitive
lymph elements. It consists of thin-walled, single or multiple interconnecting or
separate cysts which insinuate themselves widely into the tissues at the root of
the neck.

Features:
- Usually more symptoms than signs as it causes thoracic outlet syndrome
(diagram below)
- A hard mass in the posterior triangle at the root of the neck
- Symptoms/signs:
o Arterial: pallor, gangrene or necrosis of the tips of the fingers
o Venous: oedema, cyanosis
o Neurological: complaints of radicular symptoms (pain,
paraesthesia), wasting of the small muscles of the hand
- Adsons test can be done ask patient to extend neck and rotate it towards
side of symptoms radial pulse will be diminished, occasionally with
reproduction of radicular symptoms in the limb

Features:
- 50-65% present at birth, but occasionally may present later in childhood or
adulthood
- cystic swelling that is soft, fluctuant, and compressible (usually into another
part of the cyst), located in the posterior triangle at the root of the neck
- Classically brilliantly transilluminable
- A large cyst may extend deeply into the retropharyngeal space
Complications:
- Cystic hygroma seen on prenatal ultrasound in the first trimester suggests
chromosomal abnormality (50% of foetuses, usually trisomy 21) or other
structural abnormalities (33% of foetuses with no chromosomal abnormality,
usually congenital heart anomalies)
- May obstruct delivery
- Compressive problems after delivery respiratory, swallowing
Management:
- Radiological investigations e.g. CXR, CT to delineate extent of cyst
- Non-surgical treatment aspiration and injection of sclerosant (usually
unsuccessful)
- Surgical excision partial (to alleviate symptoms) or complete

NECK LUMPS

Diagnosis by CXR
Neuroma/Schwannoma
Features:
- Slow growing tumour arising from peripheral neural structures of the neck e.g.
brachial plexus, cervical plexus, vagus nerve, phrenic nerve, etc.
- Fusiform, is mobile in plane perpendicular to axis of nerve but not parallel
- Usually benign
- May be Tinels positive tap on the mass for any paraesthesia occurring in
distribution of the nerve
- DO NOT PERFORM FNA excruciatingly painful

119

!
CERVICAL LYMPHADENOPATHY

Causes:
Cancer (3): SCC, NPC, Adenocarcinoma
Lymphoma
TB
Infective

Neoplastic

Inflammatory

There are six levels of lymph nodes in the neck, and different structures drain to
different groups of nodes:
Ia
submental
Ib
submandibular
II
long internal jugular vein from skull base to bifurcation of
carotids (includes jugulodigastric nodes)
III
along internal jugular vein from carotid bifurcation to omohyoid
IV
along internal jugular vein from omohyoid to clavicle
Va
Posterior triangle
Vb
Supraclavicular
VI
Tracheo-oesophageal groove (not palpable)
VII
Superior mediastinum
Drainage:
Oral cavity and oropharynx levels I III
Thyroid and larynx levels II VI
Nasopharynx II V (usually upper neck level II and high level V)
NECK LUMPS

Viral (esp 1-2cm firm LN. No need Abx unless obvious infx)
Epstein-Barr virus, cytomegalovirus (infectious mononucleosis);
HIV
Streptococcus, Staphylococcus, Klebsiella (from intraoral pathology
e.g. dental abscess, tonsillitis)
Tuberculosis
Toxoplasma; Actinomycosis
Mets Head and neck primary
Nasopharyngeal carcinoma
Oral cavity, oropharynx, larynx, hypopharynx, thyroid, etc.
Other primary sites (4Bs)
Bowel (stomach, colon), breast, bronchus (lung), balls
(testicular). Also UL.
Primary lymphoma
SLE
Kikuchis (necrotising lymphadenitis occurring in young females,
presenting as painful cervical lymphadenopathy)
Sarcoidosis

History
Age
RF for CA: smoking, alcohol. Betel nut
The lump itself
o onset, duration, associated symptoms, lumps elsewhere
o Pain: inflammatory > CA
o Growth pattern / rate of growth:
last few days = infx / inflammatory / haemorrhage into cyst
last few months = CA
Constitutional symptoms
o Fever, malaise, arthralgia, myalgia (viral prodrome);
o Night sweats, low-grade fever (TB, B symptoms of lymphoma);
o Loss of appetite, loss of weight (chronic infection, malignancy)
Local symptoms intra-oral diseases e.g. tooth decay, oral/tongue ulcer,
tonsillitis. Use of dentures.
Past medical history cancer, TB (contact? Diagnosed? treated or
untreated?)
Social history: travel and contact history, sexual history for HIV, oral sex
120

!
Physical examination
Inspection
o Site, size, shape, surface: erythema, discharging sinus (multiple
lymph node enlargement with discharging sinuses can be TB or
actinomycosis; sulphur granules seen in actinomycosis)
Is there any pain? I am going to feel the lump, if any pain, let me know
o Palpate from behind, one side at a time start at submental,
then submandibular, preauricular, postauricular, along anterior
border of sternocleidomastoid, supraclavicular, posterior triangle,
lastly occipital. Use pulps of the fingers in a gentle rolling
movement.
o Tenderness to palpation
Consistency hard, matted nodes are more suspicious for malignancy
o Fixation to overlying skin or underlying structures
Potential drainage sites:
Upper LN (5) : MOUTH!!, face, scalp, thyroid, salivary glands
Lateral LN: thyroid
Lower LN: UL, Breast, Lungs, Abdomen (if Virchows), Oesophagus
Susp lymphoma (3): axilla, parotid, inguinal + liver/spleen
To complete the examination:
Formal ear, nose, throat examination especially looking at the post-nasal
space for nasopharyngeal carcinoma (NPC being the most common
cancer causing enlarged cervical lymph nodes)
Full respiratory and abdominal examination especially if supraclavicular
lymph node found
Examination of the thyroid gland
Examination of lymphoreticular system other lymph node groups, liver,
spleen
Breast examination in female patient

NECK LUMPS

Investigations
Fine needle aspiration
o Able to definitively diagnose CA and TB. (still the possibility of
false positive and false negative results)
o Only lymphoma requires excision Bx to diagnose (to be done
after FNAC)
o Do not do excision Bx first as it can compromise resection later if
LN mets is from H&N CA, because LN mets counted as locally
advanced dz (still resectable).

Radio: CT, ultrasound (esp thyroid), MRI (mainly CA as pre-op w/u)

o to assess nature of lump, extent, other enlarged nodes that are
not clinically palpable, and can be used to visualise primary
tumour if present

Panendoscopy: to look for synchronous tumors as smoking/alc affect

squamous cells
o Nose airway: nasolaryngoscopy, bronchoscopy
o Mouth CE junction: OGD

Management
According to FNAC results
Malignant work up for primary if present (e.g. squamous cell carcinoma
look for oral cavity, skin, ENT, lung malignancy; adenocarcinoma
look for breast, GI tract malignancy) and treat as appropriate
Infective/Inflammatory treat underlying condition

121

!
SALIVARY GLAND SWELLINGS

Anatomy of the Submandibular Gland

Anatomy of the Parotid Gland

Surrounded by tough fibrous capsule the parotid sheath (thus mumps

is painful as the gland swells within a tight envelope)
Sandwiched between the posterior border of the ramus of the mandible
and the mastoid process
Important structures that pass through the gland in order from lateral to
medial:
o Facial nerve and its branches
o Retromandibular vein (formed as the maxillary veins drain into
the superficial temporal vein)
o External carotid artery (branching into its two terminal branches,
the superficial temporal and maxillary arteries)
Nerve supply:
o Parasympathetic secretomotor supply from auriculotemporal
nerve carrying postganglionic fibres from the otic ganglion
(preganglionic fibres from inferior salivary nucleus);
o Somatic sensory supply of the gland from auriculotemporal
nerve; sensory supply of the capsule from the great auricular
nerve.
Parotid duct (of Stensen) runs 5cm across the masseter (surface
marking: along the line joining the intertragic notch to the midpoint of the
philtrum), drains into the mouth opposite to the upper second molar tooth
Histology: predominantly serous acini, many ducts (other glands have
few ducts)

SALIVARY GLANDS

Consists of a large superficial part & a small deep part that are
continuous with one another around the free posterior border of the
mylohyoid
The deep part of the gland is closely associated with the lingual nerve
(with the attached submandibular ganglion) above it, and the hypoglossal
nerve and submandibular duct below it surgery may injure these
nerves
Nerve supply: parasympathetic secretomotor supply from lingual nerve
carrying postganglionic fibres from the submandibular ganglion
(preganglionic fibres in superior salivary nucleus)
Submandibular duct (of Wharton) arises from the superficial part of the
gland, runs forwards deep to mylohyoid and drains into the oral cavity at
the sublingual papilla just adjacent to the frenulum
Histology: mixed serous and mucous acini, few ducts

Anatomy of the Sublingual Gland

A small almond-shaped gland sitting just under the mucosa of the floor of
the oral cavity
Each gland has 15 or so ducts, half of which drain into the
submandibular duct, the rest draining directly into the oral cavity
Nerve supply is similar to the submandibular gland
Histology: almost solely mucous acini, few ducts

122

!
APPROACH TO SALIVARY GLAND SWELLINGS
History
About the lump: onset, duration, progress, associated symptoms
o If pain is present, is it precipitated by food ingestion? (suggestive
of sialolithiasis)
o Intermittent swelling a/w food (inflammatory)
Symptoms of infection e.g. fever, malaise; if considering mumps, ask
about testicular pain and swelling (orchitis), abdominal pain (pancreatitis)
Any noticed asymmetry of the face incomplete closure of the eye on
one side, drooping corner of the mouth, drooling
Does the patient have symptoms of Sjogren: xerostomia (e.g. cannot eat
a piece of biscuit or bread without water), xerophthalmia
History of connective tissue disease e.g. rheumatoid arthritis, SLE
Physical examination
Inspect
Put yourself at the level of the patients face and look from front for any
asymmetry with an obvious mass on one side
o Parotid mass is located between the angle of the jaw and the ear
o submandibular mass is located just under the mandible
Look for scars parotidectomy scar runs anteriorly to the ear, below the
earlobe and around posteriorly before looping forward again under the
jaw
Look for fistula/sinus
Look at the patients face for asymmetry (facial nerve palsy)

Other tests
Examination of the duct openings:
o Using a torch and a tongue depressor, examine opposite the
second upper molar tooth (opening of the parotid duct), and
under the tongue (opening of the submandibular duct)
o Look for (1) red inflamed opening, (2) discharge-purulent, (3)
visible stone.
o For the parotid duct, can palpate the duct along the masseter for
stone, and look for discharge inside the mouth while palpating
Tonsillar fossa: enlargement of deep lobe of the parotid (in
retropharyngeal space) pushes tonsils and arches aside see
asymmetry of the arches
Palpate the gland openings for stones.
Bimanual palpation of the submandibular gland
Facial nerve examination
Suspicious features of malignancy:
1. Facial nerve involvement
2. LN involvement
3. Skin involvement: eg Hyperaemic
hot skin over lump
1+2+3 = CA until proven otherwise
Causes of swelling of the parotid
Parenchymal
swelling

Is there any pain? I am going to feel the lump, if any pain, let me know
Palpate from behind
Palpate the obviously enlarged gland:
Check for warmth, tenderness, consistency, surface, margins
Fixation to underlying structures for parotid, ask pt to clench the teeth
to contract the masseter, then try to move the gland
Fixation to overlying skin
Palpate the contralateral gland for any swelling
Palpate for cervical lymphadenopathy
Investigations
FNAC: malign vs benign
CT: confirm salivary gland (vs LN)
o esp parotid multiple swelling likely LN (DDx Warthin)

SALIVARY GLANDS

Pain
Fixation to underlying structures or
skin
Hard consistency
Irregular surface or ill-defined border

Nonparenchymal
swelling

Neoplasia

Benign
- pleomorphic adenoma
- Warthins (10% bilateral)
Malignant tumours
Lymphoma and leukaemia: bilateral
Sialolithiasis
Mumps: bilateral
HIV
Acute sialadenitis Chronic recurrent sialadenitis
Sjogrens syndrome: bilateral
Sarcoidosis: bilateral
Alcoholic liver disease
Acromegaly
Diabetes mellitus
Malnutrition
Pancreatitis

Stones
Infection/
Inflammation
Autoimmune
Infiltration
Systemic
disease:
bilateral
Lymph node
Facial neuroma
Temporal artery aneurysm
Skin and soft tissue swellings e.g. sebaceous cyst, lipoma

123

!
SIALOLITHIASIS
Epidemiology
Stones of the salivary gland that may be impacted within the gland itself
or in the duct.
Usually occurs in males more than females, and between the ages of 30
and 60.
80% occur in the submandibular gland (due to its higher mucus and
calcium content with a long duct, and slow flow of the saliva against
gravity); 10% occur in the parotid, 7% sublingual.
Most submandibular gland stones occur in the duct, while 50% of parotid
stones occur in the gland itself.
80-95% of submandibular stones are radio-opaque and can be seen on
an X-ray of the floor of the mouth, and 60% of parotid stones are radioopaque.
Presentation
Complete obstruction
o Acute pain & swelling of the gland involved at meal times, rapid
onset within minutes of starting to eat, resolves about an hour
after the meal.
Partial obstruction
o Occasional symptomatic episodes interspersed by asymptomatic
periods of days-weeks, chronically enlarged mass in
submandibular region
Cx: sialadenitis, and even abscess formation worsening of symptoms
of pain and redness; systemic symptoms such as fever, chills; purulent
discharge from duct opening
Stone may be palpable along the duct or at the opening of the duct

Management
General measures:
o Good hydration, good oral hygiene, soft diet, avoid sour food
(increase salivation)
o Massage of the gland, milking the duct, application of moist hot
towel
o Lifestyle changes: activities that exacerbate the pain eg. Blowing
instruments
o Analgesia NSAIDs such as ibuprofen
If sialadenitis present:
o Antibiotics usually to cover Staph and Strept e.g. Augmentin
o Refer specialist treatment if symptoms persist for several days,
or sialadenitis persists despite antibiotic therapy
Surgical removal
o Transoral removal of stones for submandibular duct stones (50%
can be removed thus), less for parotid duct stones
o If stones cannot be removed via transoral surgery or is
intraglandular, partial gland resection can be performed
Other options: Lithotripsy, wire basket removal, sialoendoscopy

Investigations
CT scan (Noncontrast) can pick up almost all stones when fine cuts are
requested
Plain X-rays can pick up radio-opaque stones
Sialogram (rarely done as it is invasive and technically demanding; CT is
better. Contraindicated in acute sialadenitis and contrast allergy.)

SALIVARY GLANDS

124

!
SALIVARY GLAND TUMOURS

PLEOMORPHIC ADENOMA

Epidemiology (80% rule for parotid)

80% occur in the parotid, of which 80% are benign (80% of the benign
tumours are pleomorphic adenomas)
10% occur in the submandibular, of which 60% are benign (95%
pleomorphic adenoma)
15% occur in minor salivary glands, of which 50% are benign (all benign
tumours are pleomorphic adenomas)
0.3% occur in sublingual glands, of which all are malignant
Pathology
Adenomas (benign)
Pleomorphic adenoma
Warthins tumour

Epithelial
Carcinomas (malignant)
Adenoid cystic ca
Pleomorphic adeno CA
Mucoepidermoid ca
Acinic cell ca
Adeno CA
Squamous cell ca
Undifferentiated

Non-epithelial
Haemangioma
Lymphangioma
Neurofibroma
Neurilemmoma
Lipoma
Sarcoma
Malignant lymphoma

Epidemiology:
Most common benign tumour
85% occur in the parotid gland
Equal sex ratio, occurs in younger patients (<50 years old)
Histology:
Very heterogeneous appearance, containing epithelial cells surrounded by loose
stroma with islands of chondromyxoid (mesenchymal components), and
interspersed islands of myoepithelial cells. The tumour appears to be
encapsulated, but histology shows multiple sites of capsular penetration by
tumour cells.
Features:
Slow-growing, painless swelling occurring in the lower pole of the parotid
Irregular and lobulated surface, texture of cartilage (slightly harder than
Warthins)
Does not invade or metastasise
Cx
o Malignant transformation (carcinoma ex pleomorphic) if left for
10-15 years (1-6% risk)
o If not completely excised, can recur due to frequent capsular
penetration (recurrence rate of 2%)
Diagnosis by clinical, FNAC, + MRI
Treatment surgical excision (sufficient margin)
- Parotid: Superficial parotidectomy for superficial tumour; if tumour is deep or
large, total parotidectomy with preservation of the facial nerve (or any way
possible as long as margins are sufficient)
- Submandibular: Total gland excision together with adjacent connective tissue,
sparing lingual and hypoglossal nerves

SALIVARY GLANDS

125

!
WARTHINS TUMOUR AKA PAPILLARY CYSTADENOMA LYMPHOMATOSUM

TREATMENT OF SALIVARY GLAND CANCERS

Epidemiology:
Only occurs in the parotid gland (10% of parotid tumours)
More common in males than females (4:1)
Occurs in older patients (>50 years)
Related to cigarette smoking

Parotid:
Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated
it (may be grafted with great auricular nerve)
Radical neck dissection if neck nodes positive
Postoperative radiotherapy
If localised in superficial lobe
Superficial parotidectomy only (if sufficient margin)
+ RT (in higher grade tumor / adenoid cystic may have spread to nerves)

Histology:
Consists of cleft like or cystic spaces lined by two-tiered epithelium,
containing mucin, surrounded by a stroma of well-developed lymphoid
tissue with germinal centres.
Features:
Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail
(inferior)
Invariably benign with no risk of malignant change
10% bilateral (check contralateral side)
Diagnosis by clinical, FNA + MRI
Treatment
Can be left alone if absolutely certain that the entire mass is composed
of only Warthins tumour cells, since there is no malignant potential
Superficial parotidectomy if causing trouble to patient
MALIGNANT TUMOURS
Tumor grade
Nerve involvement
Most common malignancies
Mucoepidermoid (34%) - most common malignant tumour in the parotid.
Younger patients.
Adenoid cystic carcinomas (22%) most common in the submandibular,
sublingual and minor salivary glands. Equal sex ratio, can occur in any
salivary gland, in older patients (usually >60 yrs). Tends to spread along
nerves.
Malignant pleomorphic adenoma
o Usually occurs in pre-existing pleomorphic adenoma, rarely de
novo
o Worst prognosis of any salivary gland tumour
o 30-70% recurrence and metastasis rate
SALIVARY GLANDS

Submandibular:
Radical excision of gland with lymphatic clearance of submandibular
triangle
Radical neck dissection if neck nodes positive
Postoperative radiotherapy
Complications of parotidectomy
Immediate (within 24 hrs)
Intraoperative facial nerve transection lower motor neurone palsy (in
surgery to the submandibular gland, damage to the hypoglossal and/or
lingual nerves can occur intraoperatively)
Reactionary haemorrhage: early post-op bleeding due to displacement of
a clot in a BV / slippage of a ligature
Early (1 to 30 days)
Wound infection
Skin flap necrosis
Temporary facial weakness (neuropraxia of facial nerve)
Salivary fistula
Division of great auricular nerve loss of sensation over pinna
Trismus (inability to open mouth due to spasm of masseter)
Late (more than 30 days)
Wound dimple, cosmetic problems
Hyperaesthesia of local skin
Freys syndrome (gustatory sweating syndrome / auriculotemporal syndrome)
o Increased sweating and redness of facial skin when eating
o Auriculotemporal nerve: symp branches (sweat glands of the
scalp), parasympathetic branches (parotid gland secretion)
o due to reinnervation of divided sympathetic nerves to the facial
skin sweat glands by fibres of the secretomotor branch of the
auriculotemporal nerve
126

!
THYROTOXICOSIS
Aetiology and diagnosis
Affects 2% women and 0.2% of men
o Graves, Toxic nodular goitre, Toxic solitary nodule, Thyroiditis
Serum free T4 is normally increased
o Serum total T4 can be variable due to changes in serum levels of
thyroid binding globulin
o Occasionally free T3 is increased in T3-toxicosis
Diagnosis of thyrotoxicosis can be confirmed by the measurement of
TSH level
o A normal TSH excludes the diagnosis (except in rare case of
TSH secreting pituitary tumours)
Clinical features of thyrotoxicosis
Palpitation,
Myopathy
tachycardia,
Tiredness and
cardiac
lethargy
arrhythmias,
Weight loss Heat
cardiac failure
intolerance
Sweating, tremor Diarrhoea and
Hyperkinetic
vomiting
movements
Irritability
Nervousness
Emotional disturbance

Behavioral
abnormalities
Ophthalmic signs
Irregular menstruation
and amenorrhoea
Pretibial myxoedema
Thyroid acropachy
Vitiligo
Alopecia

Graves' disease
Usually occurs in women between 20 and 40 years
Immunological disorder due to release production of thyroid stimulating
IgG antibodies
Bind to TSH receptor stimulating thyroid hormone production
Produces a diffuse goitre
Clinically patients have features of thyrotoxicosis often with eye signs:
o Exophthalmos and proptosis - usually bilateral
o Diplopia due to weakness of external ocular muscles
o Chemosis and corneal ulceration
Pretibial myxoedema
Occurs in 1-2% patients with Graves' disease
Painless thickening of the skin in nodules or plaques
Usually occurs on shins or dorsum of foot
Strongly associated with ophthalmopathy

THYROID SURGERY

Thyroid acropachy
Occurs in less than 1% patients with thyrotoxicosis
Closely resembles finger clubbing
Almost all patients also have ophthalmopathy or pretibial myxoedema
Treatment of thyrotoxicosis
Rapid symptomatic relief can be achieved with beta-blockers
Thyroid function can be reduced by
o Anti-thyroid drugs
o Radioactive iodine
o Surgery
Anti-thyroid drugs
Inhibit synthesis of thyroxine by reducing incorporation of iodine into
tyrosine residues
Most commonly used drugs are carbimazole and propylthiouracil
Used short-term (3-4 months) prior to definitive treatment (radioiodine or
surgery)
Used long-term (12-24 months) induce remission in Grave's disease
40% of patients with Grave's disease respond to carbimazole
Side effects of carbimazole include agranulocytosis, aplastic anaemia,
hepatitis
o Patients need to be warned to seek medical attention if they
develop sore throat etc.
Advantage - no surgery or the use of radioactive materials
Disadvantages
o Treatment is prolonged
o Failure rate after 2 years treatment is approximately 50%
o Impossible to predict which patients will remain in remission
o Some goitres enlarge during treatment
Radioactive iodine
131

I is commonest isotope used

400 MBq renders 50% patients hypothyroid but about 20% remain
hyperthyroid
Contraindicated in children, pregnancy and breast feeding
Pregnancy should be avoided for 4 months after treatment
Advantage - no surgery or prolonged drug therapy
Disadvantages
o Isotope facilities must be available
o 80% hypothyroid at 10 years
o Indefinite follow up required
127

!
Surgery
Indications for surgery in Grave's disease are:
o Relapse after adequate course of anti-thyroid drugs
o Large goitre
o High T4 levels at diagnosis (>75 pmol/l)
Subtotal thyroidectomy is treatment of choice.
Preserves about 4g (10%) of thyroid tissue
Patients must be euthyroid prior to operation
Advantages - goitre is removed and cure rate is high
Disadvantages
o 5% develop recurrent thyrotoxicosis
o 20% develop postoperative hypothyroidism
o 0.5% develop parathyroid insufficiency
Thyroid storm
Uncommon life-threatening exacerbation of thyrotoxicosis
Has a mortality of 50%
Precipitating factors
Thyroid surgery
Radioiodine
Withdrawal of antithyroid drugs
Iodinated contrast agents
Acute illness (e.g. stoke, infection, trauma)
Clinical features
Severe thyrotoxicosis
Fever
Delirium
Seizure or coma
Jaundice

THYROID SURGERY

Treatment
Propylthiouracil 600mg loading dose
Lugol's iodine at least one hour later
Beta-blocker
Supportive measures
Treatment of precipitating cause

THYROGLOSSAL CYSTS
Epidemiology
Thyroglossal cysts are usually found in subhyoid portion of tract
75% present as midline swellings
Remainder can be found as far lateral as lateral tip of hyoid bone
The cyst elevates on protrusion of the tongue
Male : female ratio is approximately equal
40% present < 10 years of age
65% present < 35 years of age
Often present as an infected cyst due lymphoid tissue in the cyst wall
Pathology
Cystic expansion of the remnant thyroglossal tract (embryological origin
of the thyroid which descends from the foramen caecum on the tongue).
Features
Smooth, rounded, cystic lump.
75% are in the midline while 25% are slightly to the left or right.
Usually asymptomatic but may become infected.
Complications
Infected with sinus formation and seropurulent discharge (occurs with
incision or rupture of cyst)
Malignant change (carcinoma of the thyroglossal duct)
Histology
Cyst with columnar or squamous epithelial lining which may be ciliated.
The cyst may also contain thyroid and lymphoid tissue. If malignancy
occurs, it is usually a papillary carcinoma (~90%).
Treatment
Sistrunk procedure resection of the (a) cyst and (b) mid-portion of the
hyoid bone in continuity and resection of a (c) core of tissue from the
hyoid upwards towards the foramen caecum (remove the entire tract to
prevent recurrence!)
If infected aspirate cyst rather than incise
o Prevents formation of thyroglossal fistula

128

!
THYROID GLAND
Anatomy
Structure
nd th
2 lateral lobes joined by an isthmus overlying the 2 -4 tracheal rings
Strap muscles are superficial to the thyroid gland - sternothyroid,
sternohyoid; platysma also
Nerves and vessel
Superior thyroid artery from external carotid
st
Inferior thyroid artery from thyrocervical trunk (1 part of subclavian A)
External laryngeal nerve - ss the cricothyroid muscle
o Controls pitch of voice
o Runs close to superior thyroid A
Recurrent laryngeal nerve - ss all the other intrinsic muscles of the larynx
o Runs close to branches of inferior thyroid
o Very important to localize/visualize nerve and not damage it
Embryology
Thyroglossal tract from foramen caecum of tongue (midline, jx of anterior
2/3 and posterior 1/3)
o Descends close to hyoid bone, expansion at caudal end of the
tract forms the thyroid gland
Parathyroid glands - 2 superior, 2 inferior, behind the lateral lobes
Presentation
Goitre (not all anterior masses are goitres)
Solitary nodule
MNG - 1 vs 2 lobes
Diffuse - physiological or Graves
Thyroid function change
Hypo/Eu/Hyperthyroid
Graves, Hashimotos, Toxic
adenoma/MNG
Malignant changes
Mets to LNs
Bony pain - atypically for follicular ca
o Proceed to exclude other
CAs that have bone mets

THYROID SURGERY

Aims of assessment:
Exclude cancer
Address issues of thyroid fx
Look for complications mass effect
Cosmesis - is patient
bothered by lump?

History
Rate of growth can diffx benign and malignant disease
o Anaplastic ca is fast growing
Onset; duration; progression
o Overnight appearance is unlikely to be malignant - more likely to
be bleeding into a cyst
o A/w pain - unlikely to be malignant (hemorrhage into cyst)
o A/w URTI - unlikely to be malignant
Thyroid functional status Hyperthyroid vs hypothyroid vs euthyroid
Hyperthyroid
Metabolic: LOW, increased appetite
Heat intolerance
Increased sweating
Proximal myopathy (Graves)
Bowel changes - diarrhea, frequent BO
CVS - tachycardia, atrial fibrillation
Oligomenorrhea/amenorrhea
Behavioural changes - easily irritable,
emotional liability, insomnia
Fine tremor
Loss of outer third of eyebrows

Hypothyroid
Decreased appetite weight gain
Cold intolerance
Dry skin
Muscle fatigue
Constipation
Bradycardia
Menorrhagia
Slow though, speech & actions,
depression, dementia, lethargy
Carpal tunnel syndrome
symptoms

Mass effects
o Swallowing difficulty due to weight of gland as trachea rises
o Airway
Dyspnea on lying down
Stridor due to airway narrowing, especially on coughing
o Recent onset hoarseness of voice (appearing after the goitre)
Due to RLN invasion (benign growths do not invade)
Previous thyroid disease or investigations
o If yes - on what meds, any ADRs
o Any radioactive iodine
o Ask for FNAC (poked) or US (jelly)
Etiology
o Family history
Dyshormonogenesis
Papillary ca
20% medullary carcinomas a/w MEN 2 Syndrome or FAP
o Autoimmune disease
o Radiation exposure
Due to RT or nuclear fallouts
33% will be malignant - affects threshold for total thyroidectomy
Increased incidence of thyroid malignancy - usually papillary
Most occult (<1.5 cm diameter) and multifocal
Usually good prognosis
129

!
Physical Examination
Objectives:
1. Confirm abnormality in the thyroid gland
2. Determine if there is a diffuse enlargement (smooth vs nodular - MNG) or
solitary nodule
3. Examine structures around the thyroid
4. Assess thyroid status of patient
IPPE

- Ask for how to address them -- hoarseness

- Shake their hands -- warm/sweaty
- Exposure: neck & clavicles
Inspect
- Lump: Size, shape, site (midline/anterior triangle)
- Skin and color changes, scars
- Swallow and stick out tongue tests
- Any distended neck veins/raised JVP
Palpate
*Always ask for tenderness first
Thyroid
Front:
Back:
- Lump: inferior border - Thyroid ask patient to protrude tongue/
- Trachea: deviation
swallow again with your hands on gland
from midline
- features of lump: size, tenderness,
consistency, mobility
Thyroid status
- diffuse enlargement -- smooth or nodular
Hands:
- Cervical LNs
Fine tremor
Acropachy (pseudoclubbing) and onycholysis
Palmar erythema and sweating
Pulse - tachycardia or Afib in hyper, bradycardia in hypo
Eyes:
Hypo - loss of hair on outer-third of eyebrows
Lid retraction/exophthalmos/chemosis/proptosis
Assess for lid lag & ophthalmoplegia (H - diplopia @ up & out)
Neuromuscular: Prox. myopathy, reflexes, pretibial non-pitting edema
Percuss/ - Percuss sternum only if you cant see the inferior border
auscultate - Auscultate if there are signs of thyrotoxicosis/large pulsatile goitre
Wish list Limb exam - proximal myopathy, reflexes, pretibial myxoedema
Cardiovascular exam - for signs of heart failure
Assess the patients biochemical thyroid status
?Pembertons sign
Present
Function - clinically euthyroid, hyperthyroid or hypothyroid
Any evidence of thyroid eye disease or pretibial myxedema (Graves)
Any goitre (nodular or diffuse), any retrosternal extension
THYROID SURGERY

Differential diagnoses:
1. TRO Cancer (only
10-20% of nodules is
malignant)
2. Follicular adenoma
3. Cyst (simple, colloid,
or haemorrhagic)
4. Dominant nodule of a
multinodular goitre

Clinical features suspicious of malignancy:

1. Male gender (thyroid nodules less common in
male but more likely to be malignant)
2. Age <15yrs or >60yrs (majority of nodules occurs
rd
th
in 3 to 6 decades likely benign)
3. History of head and neck radiation or thyroiditis
4. Family history of thyroid cancer (or MEN2,
Gardners syndrome, FAP)
5. Rapidly enlarging nodule
6. Hard, single nodule and/or nodules fixed to
surrounding structures
7. Hoarseness (i.e. recurrent laryngeal n. invasion)
8. Cervical lymphadenopathy
9. Other symptoms of invasion e.g. haemoptysis,
stridor, dysphagia

Investigation
Biochemical assessment
Thyroid functional status - Free T4 and TSH
Thyroid Antibodies - anti-thyroglobulin and anti-microsomal
If suspicion of MEN2 Syndrome will need 24 hr urinary catecholamine
estimations to exclude phaeochromocytoma prior to surgery
CEA and Calcitonin for Medullary Thyroid CA (+ve fam Hx)
CXR; CT Thorax
Chest radiography and thoracic inlet views if obstructive symptoms
Isotope scanning
131
123
99

I , I or Tch scanning provides functional assessment of thyroid

Nodules classified as cold, warm or hot
o Unable to differentiate benign and malignant nodules
o Most solitary thyroid nodules are cold
o Most cancers arise in cold nodules
o Risk of cancer in a cold nodule is 10-15%
o Risk of tumour in a hot nodule is negligible
Scintigraphy of minimal use in evaluation of solitary thyroid nodules
Useful in recurrent thyroid swellings and retrosternal goitres
Ultrasound
Solitary vs dominant nodule; solid vs cystic lesions (consistency)
o Most sonographically solid lesions are benign
o Cancer can occur in the wall of a cystic lesion
Features that might suggest malignancy are:
o Hypoechogenicity, Microcalcification, Irregular margins
o Increased nodular flow (vascularity) on Doppler
o Regional lymphadenopathy
Measurement of nodule, detection of subclinical nodule

130

!
ENT examination of vocal cords
Fine needle aspiration cytology
Should be first line investigation of the solitary thyroid nodule
Accuracy improved if performed under ultrasound guidance
With experienced cytologist diagnostic accuracy can be >95%
Possible cytopathological diagnoses are:
o Benign (thyroiditis, dominant nodule of MNG)
o Malignant (papillary, medullary, anaplastic, mets)
o Suspicious (follicular, Hurthle cell change in follicular lesion)
o Inadequate repeat FNAC
Can distinguish benign & malignant tumours except follicular neoplasms
Diagnosis of follicular carcinoma depends on capsular visualization
If follicular neoplasm on FNA lesion will require surgical excision
False negative rate less than 5% in most institutions
Definitive FNA cytology allows:
o Non-operative treatment with benign disease
o Appropriate surgical treatment of thyroid cancers at initial op
o Surgery can be avoided in anaplastic tumours and lymphomas
o Reduces total number of thyroid lobectomies
o Increases yield of thyroid cancers
Indications for surgery after FNA cytology
All proven malignant nodules
All cytologically diagnosed follicular neoplasms
All lesions exhibiting an atypical but non-diagnostic cellular pattern on
cytology
Cystic nodules which recur after aspiration
When on clinical grounds the index of suspicion of malignancy is high
even if the cytology report suggests it is benign

Benign thyroid tumours

Most are follicular adenomas
Papillary adenomas are rare
All papillary tumours should be considered malignant
Follicular adenoma
Of all follicular lesions - 80% benign and 20% malignant
They are smooth and discrete lesions with glandular or acinar pattern
They are encapsulated usually 2-4 cm in diameter
Adenomas cannot be differentiated from carcinoma on FNA cytology
Requires histological assessment of capsular invasion
Various histological types are described:
o Embryonal - rudimentary acini. No Colloid
o Foetal
o Simple
o Colloid - Well formed acini. Much colloid
o Macrofollicular, Microfollicular
Toxic adenoma
Account for 5% of cases of thyrotoxicosis
Female : Male ratio is 9:1
Presentation - 54% with a nodule and 37% with thyrotoxicosis
95% of toxic adenomas are benign
Thyrotoxicosis not usually associated with eye signs
Hot nodule on scintigraphy
Treatment is by thyroid lobectomy
Require post-operative thyroxine until suppressed gland returns to
normal
Malignant thyroid tumours
Differentiated thyroid cancer accounts for 80% of thyroid neoplasms
Female : Male ratio is 4:1
Usually presents as solitary thyroid nodule in young / middle age adult
Nodule more likely to be malignant in man or child
Papillary and follicular tumours are biologically very different
Comparison of papillary and follicular tumours
Papillary tumours
Follicular tumours
Multifocal
Solitary
Unencapsulated
Encapsulated
Lymphatic spread
Haematogenous spread
Metastasize to regional nodes Metastasize to lung, bone and brain

THYROID SURGERY

131

!
Differentiated thyroid carcinoma
Proportion
Age

Medullary carcinoma

Anaplastic carcinoma

Lymphoma

10%

7%

3%

5%

40-50 years

>50 yrs for sporadic type; 20-30 years for

familial

60-70 years

>50 years

Papillary carcinoma

Follicular carcinoma

75%
25-40 years

F:M ratio

3:1

3:1

1:1

3:2

2:1

Risk
factors

- Radiation exposure
- Polyposis syndromes (FAP,
Gardners, etc)
- Positive family history in 5%

- Follicular adenoma is NOT

a risk factor
- Iodine deficiency may be
associated

- Significant family history in the familial type

MEN2 (AD, complete penetrance, associated
with parathyroid adenoma and
phaeochromocytoma see notes below)

- Longstanding goitre
- History of previous
differentiated thyroid ca
(30% of anaplastic ca)

- History of lymphoma
or MALT elsewhere
- Hashimotos
thyroiditis (60X
increased risk)

Patho
features

- Characteristic Orphan Annie nuclei,

- Follicular structures similar
nuclear pseudoinclusions
to normal thyroid
- Papillary architecture with
- Diagnosis of cancer made
psammoma bodies
on evidence of capsular or
- Tall cell variant (nuclear features of
vascular invasion (vs
papillary ca in follicular lesion) behaves follicular adenoma)
like papillary ca, worse prognosis
- Hurthle cell variant poor

- Arise from parafollicular C cells (which

produce calcitonin)
- Distinctive deposits of acellular amyloid
material altered calcitonin collections
- Multicentric C-cell hyperplasia may be seen in
familial cases

- Small blue round cells

that are highly
anaplastic may
resemble lymphoma

- FNAC may suggest

lymphoma but
definitive diagnosis
requires trucut or
excision biopsy
- Almost always nonHodgkins B-cell

Clinical
features

- Sporadic cases usu solitary, worse prognosis

- Familial cases multicentric, better prognosis
- Aggressive growth; spread via local,
lymphatic, haematological routes
- 95% produce calcitonin, 80% produce CEA
- Unilat LN in 60-80%, contralat LN in 40%
- Always exclude MEN2 serum calcium, 24hr
urinary catecholamines

- Large bulky mass

involving neck
structures locally
advanced
- Aggressive growth
- Multiple metastases
probably present at
presentation

- Usually presents as
rapidly enlarging
goitre with
compressive
symptoms
- 60-80% aggressive
and 30% more
indolent

Surgical resection
- Hemithyroidectomy for selected low-risk patients (see below)
- Total thyroidectomy for the majority
- LN clearance: tracheo-oesophageal nodes cleared, and neck
dissection if neck nodes are positive
- For suspicious lesion hemithyroidectomy with histology, KIV TT

Surgical resection
- Aggressive resection total thyroidectomy
with level VI node clearance
- Sampling of cervical and mediastinal nodes
and modified dissection where positive

Palliative therapy for

compressive effects
- Chemotherapy to
shrink tumour
- Surgical debulking
- Tracheostomy

Chemotherapy and/or
radiotherapy
depending on type of
lymphoma

Adjuvant therapy
- Radioactive iodine at ablative levels to ablate remnant thyroid and
any cancer tissue (only for total thyroidectomy)
- External radiotherapy (only shown to have good results in pts with
locally advanced follicular ca)

No good adjuvant therapy

Median survival <6mths

Dependent on histo,
stage, treatment, etc.

Slow-growing tumour
Spread by lymphatics
30-50% multicentric
LN involvement in 80% of disease at
diagnosis (level VI first)

- Solitary
- Haematologic spread to
bone, lung, liver, brain
- LN involvement in 10%
(rare)

- Very good prognosis

- Poor prognostic factors (AMES): Age>40, presence of metastases,
extra-thyroid invasion, size>4cm
Treatment

TSH suppression give L-thyroxine, suppress TSH to <0.005U/L

Follow-up
- Check TSH levels
- Thyroglobulin as a tumour marker of recurrence
- Radioactive iodine scan to detect recurrence, followed by ablation
5yr survival

95% in low-risk pts, 88% in intermediate-risk pts, 50% in high-risk pts

Slightly worse for follicular ca

THYROID SURGERY

Follow-up
- Thyroxine replacement (not for TSH
suppression but to maintain euthyroid state)
- Serum calcitonin and CEA six mths after
surgery (if normal, considered cured 5% 5yr
recurrence)
- High calcitonin screen for residual or
metastatic disease, treat surgically, with RT or
chemo as appropriate
60-70%

132

!
Risk stratification
Patient factors: Age >45 years old is high risk; Gender male high risk
Tumour factors:
o Size nodule >4cm has higher risk
o Histology tall cell variant of papillary ca and Hurthle cell variant
of follicular ca are considered unfavourable
o Extrathyroidal extension into surrounding structures worse
o Lymph node or distant metastases worse
Scoring systems
AMES Age, Metastases, Extent, Size
AGES Age, Grade (Histological), Extent, Size) rarely used as
histological grading is not commonly performed
MACIS Metastasis, Age, Completeness of resection, Invasion, Size
Patients can be divided into three groups:
Low risk low risk patient and low risk disease (i.e. no high risk features)
Intermediate risk low risk patient with high risk disease, or high risk
patient with low risk disease
High risk high risk patient and high risk disease

Risk helps to guide treatment low risk patients can undergo

hemithyroidectomy without ablative radioiodine therapy post-op, while
high risk patients undergo total thyroidectomy with post-op ablative RAI
treatment; treatment in intermediate risk patients is tailored to the
disease, but usually is similar to that in high risk patients
5 year survival is also prognosticated by the risk: low risk patients have a
survival of 95-98%, intermediate risk patients 88%, and high risk patients
50%

Management
Surgery
Therapeutic
o Hemi vs total
Diagnostic
o For lymphoma - incisional biopsy needed to type the lymphoma
(incidentally, Rx for lymphoma is RT only)
o For follicular/Hrthle cell lesions
To diffx benign and malignant, capsular invasion has to
be seen
Lobectomy is done

THYROID SURGERY

Total thyroidectomy vs thyroid lobectomy for differentiated tumours

Arguments for total thyroidectomy
(Treatment, monitoring, recurrence, low mortality)
Multifocal disease occurs in opposite lobe in 50% cases
Total thyroidectomy reduces risk of local recurrence
Ablation with radioiodine is facilitated
Serum thyroglobulin can be used as a tumour marker for progression or
recurrence
In experienced hands, morbidity of total thyroidectomy is low
Arguments for thyroid lobectomy
Many patients do not require radioiodine
Progression to undifferentiated carcinoma is rare
Significance of micro-foci in contralateral lobe is uncertain
No evidence that more extensive procedure is associated with better
prognosis
Higher incidence of hypoparathyroidism after total thyroidectomy
Complications of thyroidectomy
Haemorrhage
Wound Complications
o Sepsis
o Hypertrophic scarring
Respiratory Obstruction
o Laryngeal mucosal oedema/hematoma
o Clot deep to strap muscles
o Bilateral incomplete recurrent laryngeal nerve palsies
o Tracheomalacia
Nerve Damage
o Recurrent laryngeal nerve palsy
o Incomplete - cord moves to midline
o Complete - cord in cadaveric position
o Preoperative cord inspection is essential
o 3% population have asymptomatic recurrent laryngeal nerve
palsy
Hypocalcaemia
Thyroid Crisis
o Fulminating
Pneumothorax
hyperthyroidism
Air Embolism
o
Hyperpyrexia
Recurrent hyperthyroidism
o
Arrhythmia
Hypothyroidism
o Cardiac Failure
133

!
Lymph node clearance
Tracheo-oesophageal groove (level VI) node clearance usually done
Radical neck dissection or modified radical neck if:
o Tracheo-oesophageal groove nodes histologically positive for
cancer
o Clinically positive nodes in the neck palpable or enlarged on
ultrasound
Radical neck dissection
The removal, en-bloc, of the entire ipsilateral lymphatic structures of the
neck, from the mandible superiorly to the clavicle inferiorly, from the
infrahyoid muscles medially to the anterior border of the trapezius
laterally
Classic radical neck dissection (Criles) internal jugular vein,
sternocleidomastoid muscle, and accessory nerve are resected.
Structures not resected: carotid arteries, vagus nerve, hypoglossal nerve,
brachial plexus, phrenic nerve
Modified radical neck dissection
o Type I: one of the three structures not removed, usually
accessory nerve
o Type II: two of the structures not removed accessory and IJV
o Type III: all of the three structures not removed
o Extended radical neck dissection: resection of lymph nodes
and/or structures not included in the classic neck dissection
Complications of radical neck dissection:
o Injury to nerves vagus (vocal cord paralysis), cervical
sympathetic chain (Horners), mandibular branch of facial (lower
lip weakness)
o Haematoma bring back to OT to find source of bleeding and
stop it
o Salivary fistula (usually when pt has received RT to the neck,
and if the upper GI tract was opened during the surgery)
infection can result
o Wound infection risk factors: previous irradiation, if upper
aerodigestive tract is opened during surgery with salivary
contamination, salivary fistula
o Carotid blowout risk factors: infection, irradiation resus,
apply constant pressure all the way to the OT!
o Poor healing usually in irradiated skin; weakest point is the
junction of the trifurcate incision

THYROID SURGERY

MULTIPLE ENDOCRINE NEOPLASIA

A group of inherited diseases resulting in proliferative lesions (hyperplasia,
adenomas, carcinomas) of multiple endocrine organs.
Features:
Tumours occur at younger age than sporadic cancers
Multiple endocrine organs involved, either synchronously or
metachronously
Multifocal tumours in each organ involved
Tumour usually preceded by asymptomatic stage of endocrine
hyperplasia
More aggressive and higher chance of recurrence compared to sporadic
type of tumours in the same organs
MEN 1
Autosomal dominant inheritance
Gene involved is the tumour suppressor gene MEN1 located on
chromosome 11q13 where mutations cause loss of function of the gene
Three Ps:
o Parathyroid (95%) hyperparathyroidism from hyperplasia of
parathyroid glands
o Pancreas (>40%) aggressive metastatic tumours (e.g.
gastrinoma, insulinoma), leading cause of death in MEN 1 patients
o Pituitary (>30%) most commonly prolactin-secreting
macroadenoma; some have growth hormone-secreting tumours
MEN 2
Autosomal dominant inheritance
Gene involved is RET protooncogene at 10q11.2 where activating
mutations occur
Two distinct groups of disorders:
MEN 2a (Sipple syndrome)
o Medullary carcinoma of the thyroid (almost all)
o Phaeochromocytoma (50%, of which less than 10% malignant)
o Parathyroid hyperplasia and hyperparathyroidism (30%)
MEN 2b (William syndrome)
o Thyroid and adrenal involvement like MEN 2a, but no
hyperparathyroidism
o Neurocutaneous manifestations: ganglioneuromas on oral
mucosa, lips eyelids
Other features: Marfanoid habitus, SCFE, delayed puberty
134

!
SURGERY IN THYROID DISEASE
Indications for surgery:
Cannot be treated medically - failed or unsuitable
Cancer
Compression on neighbouring structures
Cosmesis
Compliance/cost problems with long-term medical therapy (but patient
may still require long-term therapy after op if he/she becomes
hypothyroid or is still hyperthyroid)
Child-bearing (not a very strong indication since medical therapy can still
be given, but not RAI)
Types of surgery available:
Hemithyroidectomy removal of one lobe of the gland, including the
isthmus and the pyramidal lobe; usually for suspicious thyroid nodules
Total thyroidectomy entire gland removed completely; usually done in
MNG
Subtotal thyroidectomy
o Conventional subtotal thyroidectomy leave a thumb-sized
amount (about 4-6g) of remaining thyroid tissue on both sides
o Harley-Dunhill subtotal thyroidectomy leave a thumb-sized
amount on one side with removal of the rest of the gland
Total versus subtotal thyroidectomy (for hyperfunctioning thyroid disease)
Result of total thyroidectomy is always hypothyroidism, thus the patient
will require life-long thyroid replacement and follow-up
problems with compliance, cost, inconvenience
Results of subtotal thyroidectomy (at 5 years):
o 60-70% euthyroid (do not require medication but still have to be
followed up closely)
o 16-20% hypothyroid (usually becomes evident within 1 year of
surgery)
o 8-10% hyperthyroid (percentage increases proportionately with
time failure of surgical therapy)
Difficulty in managing post-operatively and in the long term as
patients need close monitoring (better off to just replace everyone after
TT?), but weigh this against the benefits of not requiring any medication
(for which there is a good chance)

THYROID SURGERY

Complications of thyroid surgery: (Mostly Hs, one I and one T)

Immediate (<24hrs)
Haemorrhage with haematoma formation
o Haematoma forms in the paratracheal region, mostly below the
strap muscles compression of airway if not released (DIE)
o Cut the subcuticular stitches and also the stitches holding the
strap muscles opposed to let the blood drain out
Hoarseness or airway compromise from recurrent laryngeal nerve injury
o Risk of nerve injury is <1%
o Unilateral nerve injury for hemithyroidectomy, bilateral nerve
injury for total or subtotal thyroidectomy
o Bilateral nerve palsy = compromised airway = tracheostomy
Hyperthyroidism
o Resection of gland can release large amounts of stored thyroid
hormone into bloodstream
o May result in thyroid storm (see Management of thyroid storm)
Tracheomalacia
o Floppiness of trachea resulting from chronic compression
o Requires intubation to secure airway
Intermediate (1 day to 1 mth)
Infection
Hypoparathyroidism leading to hypocalcaemia
o Risk of permanent hypoparathyroidism is 1-4% (only in total or
subtotal thyroidectomies)
10-20% of patients may have temporary Ca2+
Important to check the serum calcium levels POD 1,3,5
o Signs of hypocalcaemia paraesthesia around the mouth,
difficulty breathing, carpopedal spasm, Chvosteks sign (spasm
of the facial muscles on tapping the facial nerve), Trousseaus
sign (carpopedal spasm on inflating BP cuff over arm)
o Dangerous as it can cause laryngeal spasm & airway compromise
o Check serum calcium together with albumin to get corrected
calcium! Measured serum calcium + 0.02 (40 Albumin)
o Replacement: 5mmol/6h if symptoms mild, 10ml of 10% calcium
gluconate over 30 minutes if severe
o Hypocalcaemia may also occur due to hungry bone syndrome
after thyroidectomy in long-standing thyrotoxicosis
Late (more than 30 days)
Hypothyroidism
Hyperthyroidism (failed treatment)
Permanent hypoparathyroidism
Hypertrophic scarring or keloid formation ask patient have prev keloids
135

!
ANATOMY OF LOWER LIMB ARTERIES

External iliac artery continues as the femoral artery after crossing the
inguinal ligament (surface landmark: the mid-inguinal point i.e. midway
between the pubic symphysis and the anterior superior iliac spine)
The femoral artery then divides into the superficial femoral and the
profunda femoris (or deep femoral) arteries about 4cm below the inguinal
ligament
o The profunda femoris supplies compartments of the thigh via 2
main branches, the medial & lateral circumflex femoral arteries
o The superficial femoral runs distally and passes through the
adductor hiatus to reach the popliteal fossa, where it changes its
name to become the popliteal artery
The popliteal artery divides into the anterior tibial artery and the posterior
tibial (also called tibioperoneal trunk by some), and the posterior tibial will
give off the peroneal artery
o The anterior tibial crosses into the anterior compartment of the
leg and supplies the muscles there, and then continues as the
dorsalis pedis in the foot (surface landmark: one third of the way
down a line joining the midpoint of the two malleoli to the cleft
between the first and second toes)
o The posterior tibial supplies the posterior compartment of the leg
and passes posterior to the medial malleolus (surface landmark:
one third of the way down a line joining the medial malleolus to
the heel) before dividing into medial and lateral plantar arteries to
supply the sole of the foot

Refer to diagram important to know the arrangement of the anterior tibial,

posterior tibial and peroneal vessels at the trifurcation as you may be asked to
read an angiogram of these vessels.
From lateral to medial: Anterior tibial, Peroneal, Posterior tibial

VASCULAR SURGERY

136

!
ARTERIAL ASSESSMENT
Clinical Assessment
Claudication
Calf or thigh pain precipitated by exercise
o Usually occurs after predictable distance
o Described as 'cramp' or 'tightness'
o Relieved by rest
Progression of symptoms is important - worsening or improvement
o Impact on social function should be identified
Need to differentiate form spinal stenosis (shop window vs park bench
o Also causes exercise induced leg pain
o Usually associated with neurological symptoms and relieved by
spinal flexion
Peripheral pulses can be present in patients with intermittent claudication
Critical limb ischaemia
Characterized by rest pain
Occurs when foot is elevated (e.g. in bed)
Improved with foot dependency
May be associated with ulceration or gangrene
Foot pulses are invariably absent
Non-invasive testing of arterial patency
Arterial investigations are used to:
Confirm the clinical impression of arterial disease
Assess disease severity
Preoperative planning of surgical or radiological interventions
Duplex ultrasound
Combined pulsed doppler and real time B mode ultrasound
Allows imaging of vessels and any stenotic lesion
Flow and pressure wave form can be also be assessed
Doppler wave forms from normal and diseases arteries
In normal individuals a 'triphasic' wave is obtained
Rapid antegrade flow during systole
Transient reverse flow in early diastole
Slow antegrade flow in late diastole

VASCULAR SURGERY

Hand-held Doppler
Reflection of an ultrasound wave off a stationary object does not change
its frequency
Reflection off a moving object results in a change of frequency
The change in frequency is proportional to velocity or blood flow
Hand held 8 MHz doppler probe is used to assess arterial system
Measurements can be made at rest and after exercise
Ankle-brachial pressure index (ratio of best foot systolic to brachial
systolic pressure)
o Normal >1.0
o Claudication 0.4 -0.7
o Critical Ischaemia 0.1-0.4
In normal individuals pressures do not fall flowing exercise
o In claudicants the ABPI falls and recovery is delayed
o In diabetic lower limb pressures are falsely elevated due to
calcification in the vessel wall
Toe pressures
Provides accurate assessment of distal circulation
Not influenced by calcification in pedal vessels
Medical calcification particularly seen in diabetics
Normal toe pressures are 90-100 mmHg
Toe pressure less than 30 mmHg suggests critical limb ischaemia
Invasive vascular assessment
Angiography
Usually performed using digital subtraction techniques
Catheter inserted using Seldinger technique
Femoral artery is commonest site of venous access
Generally safe procedure performed under local anaesthetic
Potential complications include:
Contrast-related
Technique-related
o Anaphylactic reaction
o Haematoma
o Toxic reactions
o Arterial spasm
o Deterioration in renal
o Sub-intimal dissection
function
o False aneurysm
o Arteriovenous fistula
o Embolization
o Infection
CT angiography
Required intravenous contrast and ionizing radiation
Spiral CT and reconstruction can provide detailed images
Particularly useful for the assessment of aneurysmal disease
137

!
ACUTE LIMB ISCHEMIA

Defined as a sudden decrease in limb perfusion that causes a potential

threat to limb viability (manifested by ischemic rest pain, ischemic ulcers,
and/or gangrene) in patients who present within 2/52 of the acute event
(if >2/52, it is considered chronic ischaemia).Effects of sudden arterial
occlusion depends on state of collateral supply
Collateral supply in leg usually inadequate unless pre-existing occlusive
disease

Aetiology of acute limb ischaemia

Embolism (60-80%)
o Arising from:
Left atrium in patients in atrial fibrillation
Mural thrombus after myocardial infarct
Prosthetic and diseases heart valves
Aneurysm or atheromatous stenosis
Tumour, foreign body, paradoxical
o Lodging commonly at
Bifurcation of the femoral artery (most common site)
Trifurcation of the popliteal artery (next most common
site in the lower limb)
Aortic bifurcation
External and internal iliacs
Acute Thrombosis
o Thrombosis of a previously stenotic but patent artery
(atherosclerotic vessel)
o Resulting ischaemia is usually less severe than in an embolic
occlusion, because collaterals have had time to form
Other
Trauma
Dissecting aneurysm
Raynaud's Syndrome
Clinical features of limb ischaemia
Fixed staining is a late sign
Objective sensory loss requires urgent treatment
Need to differentiate embolism from thrombosis
Important clinical features include
o Rapidity of onset of symptoms
o Features of pre-existing chronic arterial disease
o Potential source of embolus
o State of pedal pulses in contralateral leg
VASCULAR SURGERY

Pain
Develops acutely; starts off in a distal part of the extremity and then
progresses proximally, increasing in severity with time
Further progress leads to decrease in pain as the nerves die off from ischaemia
Important to ask for any previous claudication pain (10% of claudicants can
develop acute ischaemia due to thrombosis of the stenosed vessel)
Paraesthesia
Starts off with paraesthesia (develops relatively early in the course of
ischaemia) and develops to complete loss of sensation
Progression: Light touch Vibration Proprioception (late) Deep pain
Pressure sense
Pallor; Perishingly cold
Assess skin colour, temperature (Perishingly cold), and capillary refill
The limb may still be slightly pink though pale, but in severe ischaemia it can
be marble-white (especially in embolus where there are no collaterals)
Other colours: Pale Cyanosis Mottling Fixed cyanosis and mottling
Mottling/Marbling (patches of blue on white): deoxygenation of stagnated
blood; surrounding areas of pallor are due to vasoconstriction
Duskiness: due to deoxygenation of stagnated blood; if there is fixed staining
(i.e. does not blanch on pressure) then the limb is non-viable
The discolouration usually affects a large part of the distal limb e.g. the toes,
foot; rarely does it only affect one toe (more in chronic ischaemia)
The site of arterial occlusion is usually one joint above the line of demarcation
between normal and ischaemic tissue
Pulselessness
If able to feel one good pulse (PT or DP), quite unlikely that the limb is ischaemic
If unable to feel, assess with a handheld Doppler the arterial and venous flow
in the limb there can still be flow without a palpable pulse
Also feel the pulses on the other limbs gives a clue as to whether the cause
is embolic or thrombotic (see below)
Paralysis
Initial: heavy limb, Late irreversible ischemia: muscle turgidity
Total paralysis occurs late and usually indicates that the limb is non-viable
Intrinsic foot muscles > Leg muscles (toe mvmts produced by leg muscles
detect late)
Can assess viability of muscle by making a cut viable muscle will be shiny &
twitches in response to flicking, while dead muscle will be dull & will not twitch
Dangerous to save dead muscle as reperfusion can cause circulation of toxic
metabolites in the muscle
138

!
Severity of ischemia

Management of acute ischaemia

Three categories: viable, threatened and non-viable

Viable: No immediate threat of tissue loss
Threatened: Salvageable if revascularized promptly
Non-viable: Limb cannot be salvaged and has to be amputated, no
emergency to operate. Patient may require revascularisation to allow
lower amputation or help the amputation to heal

Initial

Severity depends on:

capability of existing collaterals to carry blood around occlusion
location of obs relative to no. of axial arteries (pop=1, fem=2, tib=3)
extent of obs: larger lose more collaterals
duration
Pain
Capillary refill
Motor deficit
Sensory deficit
Arterial Doppler
Venous Doppler
Treatment

Viable
Mild
Intact
None
None
Audible
Audible
Urgent
work-up

Threatened
Severe (rest pain)
Delayed
Partial
Partial
Inaudible
Audible
Emergency surgery

Non-viable
Variable (anaesthesia)
Absent (fixed stain)
Complete
Complete
Inaudible
Inaudible
Amputation

Investigations
Pre-operative investigations
FBC, U/E/Cr, PT/PTT, GXM
CXR and ECG if patient is older than 40 yrs old
If suspecting an AMI with mural thrombus, do cardiac enzymes
Biochemical abnormalities (muscle necrosis): K, CK, lactic acidosis
Angiogram
Can be done in pts with viable limb; in pts with threatened limb there is
no time for angiogram may do on-table angiography
High clinical probability of embolism does not need angiography
Useful in
1. confirming an occlusion,
2. cause thrombotic or embolic
3. pinpointing the level of occlusion and the anatomy
VASCULAR SURGERY

Doppler to analyze viability and level of obstruction

Heparinize (5000mg bolus then 1000mg/hr) & analgesia
Improve perfusion (foot dependency, avoid heel pressure, max O2 sat)
Treat associated cardiac disease (CHF, AF)

Identifiable source
Claudication hx
Physical findings
Angiography

Embolic
Present AF, recent AMI
Negative
Contralat pulses present
White limb (no blood)
Minimal atherosclerosis,
sharp cut-off, few collaterals

Thrombotic
Less common
Positive
Contralat pulses diminished
Dusky limb (collaterals)
Diffuse atherosclerosis,
irregular cut-off, collaterals

Emergency embolectomy
Under LA, but monitor for AMI, AF, arrhythmia & hyperK after reperfusion
Transverse arteriotomy performed over common femoral artery
Fogarty balloon catheter is inserted into artery until distal to the clot, then
balloon is inflated to trawl clot out of the artery
If embolectomy fails - angiogram + consider bypass graft/thrombolysis
Convert to full warfarin (INR 2.5) before stopping heparin
Complications: reperfusion injury (edema, compartment syndrome calf
pain and inability to dorsiflex ankle do a 3 compartment fasciotomy)
Embolectomy has a 20% mortality, almost full success rate
Intra-arterial thrombolysis
Arteriogram and catheter (multiple side hole) advanced into thrombus
o Urokinase 5000u/hr + heparin 250u/hr for 6 hours
o Alternative thrombolytic agents include streptokinase or tissue
plasminogen activator (tPA)
Repeat arteriogram at 6 -12 hours
Advance catheter and continue thrombolysis for 48 hours or until clot lysis
Indicated for embolism in diseased artery easier than trawling
Contraindications
o Absolute: CVA (2m), active bleeding (10d), intracranial trauma (3m)
o Relative: CPR (10d), major trauma (10d), uncontrolled HTN
Angioplasty of chronic arterial stenosis may be necessary
Complications:
o Mortality of 1-2%; Bleeding (CVA, retroperitoneal)
Thrombolysis has a 10% mortality, only 35% successful
139

!
CHRONIC LIMB ISCHEMIA
Most common cause is atherosclerosis with gradually developing diffuse stenosis
of the peripheral arteries resulting in diminished blood supply to the lower limb
(imbalance between supply and demand). Multiple collaterals form to bypass the
obstructed vessels as a compensatory mechanism.
Intermittent claudication
Epidemiology of claudication
5% of males older than 50 years have intermittent claudication
5% of claudicants progress to critical ischaemia each year
75% of patients remain stable and show clinical improvement
Peripheral vascular disease is an independent risk factor for
cardiovascular disease
At 5 years of follow-up
o 10% claudicants and 50% of those with critical ischaemia have
had an amputation.
o 20% claudicants and 50% have died usually from ischaemic
heart disease
Calf claudication:
Usually affects the superficial femoral near to the
adductor hiatus, or the popliteal artery
Foot claudication:
tibial & peroneal arterial disease, but rarely do
patients with claudication due to atherosclerosis get
foot pain alone (more common in Buergers)
Thigh claudication: common femoral artery or aortoiliac disease
Leriches syndrome occlusion of the aortoiliacs, and composed of a
classical tetrad of buttock claudication, impotence in men, absent femoral
pulses (and distal pulses), and occasionally presence of aortoiliac bruits.
Assessment of claudication
History to assess disability associated with symptoms (claudication distance)
o Neurogenic claudication usually must flex spine, variable distance,
pulse present, parasthesia present
Exclude rest pain or tissue loss
Doppler studies to measure pressures and assess wave forms

VASCULAR SURGERY

Critical limb ischaemia

Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks
+/- Tissue loss (Gangrene or ulcers over the toes or feet)
Objective indication of poor vascular supply to the lower limbs
(a) Ankle brachial pressure index <0.5
(b) Toe pressure index < 0.3
(c) Toe pressure <30 mmHg, Ankle pressure <55mmHg
Rest pain
Severe pain in the distal portion of the lower limb (usually toes, foot but
may involve more proximal areas if disease is severe) occurring at rest
(calf pain without toe pain is not)
Pain is aggravated or precipitated by lifting the limb, relieved by
dependency of the limb many patients sleep with the leg hanging over
the side of the bed to relieve the pain
So severe as to disturb sleep at night blood supply as pt is not in
dependent position and decrease BP during sleep
Not easily controllable with analgesia requires opioids to control pain
Ischaemic ulcers (most are neuroarteriopathic ulcers)
Usually arise from minor traumatic wounds with poor healing
Often painful
Most often occur on the tips of the toes, bunion area, over the metatarsal
heads (ball of the foot), lateral malleolus (as opposed to venous ulcers
that occur over the medial malleolus)
Usually deep, dry, punctate (unlike venous ulcers that tend to be
superficial, moist, diffuse)
May become infected cellulitis / abscess, and spread to involve the
underlying bone and joints osteomyelitis, septic arthritis
Gangrene
Cyanotic, anaesthetic tissue associated with or progressing to necrosis
Occurs when arterial blood supply falls below that which is necessary to
meet minimal metabolic requirements
Dry hard, dry texture. Often has a clear demarcation between viable
and necrotic tissue. Occurs in patients with atherosclerotic disease. Safe
and can be allowed to autoamputate after demarcation with precautions
against infection.
Wet = infected dry gangrene. Moist, swollen, frequently blistered. Often
occurs in diabetics with decreased sensation and unrecognised trauma,
requiring an emergency surgical debridement or amputation.
140

!
History
Claudication = muscular pain, reproducible, increased on walking/dec w rest
Which part of the lower limb does the pain occur in depends on level of
obstruction
Nature of the pain, Radiation, Severity
Aggravating factors exertion
Relieving factors rest (just standing is sufficient)
Associated symptoms e.g. impotence in Leriches
Duration: When did pain first start (>2/52?)
Progress since first noticed until currently (worsening pain, ing areas of
lower limb affected, pain on less exertion, rest pain)
Current claudication distance
How has symptoms affected lifestyle e.g. impaired mobility
Any rest pain
Site, nature, severity
Aggravating factors raising the limb
Relieving factors putting limb in a dependent position
Able to relieve with normal analgesics? Or require opioid analgesia?
How long has rest pain lasted for requiring opioid analgesia (if > 2 wks,
considered a feature of critical limb ischaemia)

Drug history
Aspirin and statin intake commonly prescribed for vasculopathy
Any allergies to contrast (for angiography)
Ergots
Social history
Premorbid function and current function
Social support and home condition (need to climb stairs?)
Physical examination
Look

Any ulcer or gangrene in the lower limb?

Ask about onset of ulcer/gangrene
Progress (stable, or increasing in size, getting worse)
If ulcer, any preceding trauma? Ill-fitting shoes? Altered sensation in the
foot? Does patient take care to protect foot? Pain?
Redness/swelling/warmth in surrounding skin? Purulent/foul-smelling
discharge from the ulcer?
If gangrene, is it wet or dry? Redness/swelling/warmth in surrounding
skin? Any feeling in the toe involved? Any sensory changes in the other
normal toes, foot, limb?
Any systemic signs of infection fever, chills, rigors, malaise
Risk factors (Arteriopathy)
Diabetes mellitus take a full diabetic history including other
complications
Hyperlipidaemia / Heart disease (IHD) / Stroke (CVA)
Smoking (very strong RF; 3-6X risk of claudication, higher than the risk
for IHD)
Family history
VASCULAR SURGERY

Colour of the lower limb

o White (pallor); pink (normal); blue/dusky (cyanosed); mottled
Trophic changes
o Loss of hair
o Dry, shiny skin
o Nail changes
o Wasting
Presence of any diabetic dermopathy
Presence of ulcer
o Look carefully at the entire lower limb, including the heels (ask pt
to flex at the knee) & between the toes
o Site of the ulcer
o Venous ulcers form at the medial malleolus
o Arterial ulcers are more distal, usually between the toes, and at
pressure points such as the lateral malleolus;
o Neuropathic ulcers form at areas such as the ball of the foot & heel
o Size, shape, Edges (punched out arterial; sloping venous), Base
o Depth of the ulcer (can see underlying tendon? Down to bone?)
o Appearance of the base Necrotic? Granulating (beefy-red)?
Sloughy?
o Any discharge pus, blood?
o Surrounding skin
o Erythema (cellulitis) there may be an underlying abscess
(confirm on palpation)
o Blistering, purplish colour (possibility of necrotising fasciitis)
Presence of gangrene
o Wet (infected) or dry (not infected)
o Extent of gangrene (level of demarcation)
(If the patient has diabetes, may see deformities Charcots joint)
141

!
Feel

Move
Warmth of the skin
o Use the dorsum of the fingers of both hands to simultaneously
run up the patients feet to the shins and thighs bilaterally
o Compare the temperature on both sides (note if one side is
cooler)
o If one limb feels cool, feel for the level where the skin becomes
warm
Capillary refill
o Press hard on a toe for a few seconds, then release
o Normal capillary refill should be 2 seconds or less
o If a toe is blue, check for blanchability (fixed staining = dead toe)
Palpating the ulcer if present
o Any surrounding tenderness (infection)
o Bogginess of surrounding tissue (may have abscess formation)
o See if any discharge from the ulcer when palpating
Pulses compare both legs. Check regularity of pulses. Grading of
pulses: 2+ normal; 1+ diminished (but may be normal for popliteal);
negative if not felt
o Feel the distal pulses and work your way proximally
o Posterior tibial pulse: one-third of the way down a line joining the
medial malleolus to the heel
o Dorsalis pedis pulse: just lateral to the ext hallucis longus
tendon/ one third of the way down a line joining the midpoint of
the two malleoli to the cleft between the first and second toes
o Popliteal pulse: Ask patient to bend the knee ~60-90 degrees,
then palpate deeply in the popliteal fossa with the fingers of one
hand pressing the fingers of the other. Thumbs on the tibial
tuberosity. [If the pulse is very well felt, suspect a popliteal
aneurysm]
o Femoral pulse: Midpoint of the line joining the pubic symphysis
to the anterior superior iliac spine (mid-inguinal point), just below
the inguinal ligament
o Abdominal aorta

VASCULAR SURGERY

Buergers test
Lift both legs together to compare
Holding the heel of the foot, with the pts LL straightened, slowly lift the
entire LL, looking at the colour of the toes
Stop when the toes become pale (white)
Estimate the angle the lower limb makes with the horizontal this is the
Buergers angle
Normal lower limb can be raised to 90 degrees without turning white; if
the Buergers angle is less than 30-40 degrees, this indicates critical
ischaemia
There may be venous guttering of the lower limb at this angle as well
Hold for 1 min (to induce ischemic environment)
If the patient is lying near the side of the bed, tell the patient that youre
going to put his leg over the edge of the bed before gently abducting the
hip and then letting the leg drop over the edge of the bed
Look at the leg for reactive hyperaemia (the leg turns purple-red) due
to ischemic env causing increased acidity and triggering autonomic
response
Complete the exam
Examine the rest of the pulses
Offer to auscultate over the femoral and popliteal arteries for bruits
Examine the abdomen for any abdominal aortic aneurysm
Measure the ankle-brachial pressure index (ABPI)

142

!
Investigations
Ankle-brachial pressure index

How the ankle-brachial pressure index is done

o Lie patient supine (so that ankle pulse will not increase sec to
dependency)
o Brachial pressure is measured with a blood pressure cuff around
the arm and a Doppler probe at the brachial artery cuff is
inflated until the arterial signal is obliterated, then slowly deflated
until the signal just starts being detected, at which the pressure
is recorded
o Ankle pressures are measured in a similar manner, with the cuff
around the calf and the Doppler at the dorsalis pedis and
posterior tibial arteries one reading for each artery
o The ankle pressure to be used for each leg is the higher of the
two taken
o This ankle pressure is then divided by the brachial pressure (the
higher of the two brachial pressures for both upper limbs) to get
the ankle-brachial pressure index
Interpreting the values
o Normal ABPI is > 0.9 (can be more than 1.0 as ankle pressures
tend to be higher than brachial;
o ABPI between 0.5 - 0.9 occlusion, often associated with
claudication
o ABPI <0.5: Critical ischaemia Rest pain
o if >1.25, suggests non-compressible calcified vessel esp seen in
DM patients
do Toe pressure index instead (every value minus 0.2)
Accuracy of the index
o ABPI below 0.9 has 95% sensitivity and 100% specificity for
detecting angiogram-positive peripheral arterial disease and is
associated with >50% stenosis in one or more major vessels
Exercise treadmill testing
o Measure ABPI before and after patient exercises on a treadmill
o If the ABPI falls by >0.2 claudication

VASCULAR SURGERY

Arterial Duplex ultrasound

Non-invasive test, good alternative to angiogram
Duplex (means 2 modalities) = 2D ultrasound plus Doppler ultrasound
(measures flow and waveforms)
Normal arterial flow waveform should be triphasic (rapid antegrade flow
reaching a peak during systole, transient reversal of flow during early
diastole, and slow antegrade flow during late diastole.); biphasic &
monophasic waves are abnormal
Distal to stenosis: rate of rise is delayed, the amplitude decreased, and
the transient flow reversal in early diastole is lost
A twofold increase in peak systolic velocity compared with the velocity in
an adjacent segment of the artery usually signifies a stenosis of 50% or
more
Can define anatomy of occlusions and also look for relatively good
arteries distally for landing zone of bypass graft
Angiogram (arteriogram)
Invasive and associated with risks of
bleeding from arterial puncture,
dissection
damage to artery with worsening ischaemia
Usually only done if planning intervention e.g. angioplasty, stenting
Preparing for angiogram:
o Take informed consent from patient
o Ask about contrast allergy, asthma, renal disease, metformin
o Investigations: FBC (platelets impt), PT/PTT, UECr
Angiogram with digital subtraction the images of the underlying bone
are removed so as to better visualise the arteries (if the bones are visible,
then it is a normal angiogram, without digital subtraction)
Basic laboratory investigation
FBC, UECr, PT/PTT, septic workup: bld c/s, wound c/s
Fontaine system
Stage I: Asymptomatic
Stage IIa: Mild claudication
Stage IIb: Moderate to severe claudication
Stage III: Ischaemic rest pain
Stage IV: Ulceration or gangrene

143

!
TREATMENT OF CHRONIC LIMB ISCHEMIA
Conservative (for claudicants)
Mainstay for all cases of claudicants, esp. foot and calf claudicants
RF control
o Assessment and treatment to optimise control of CVS risk
factors cardiologist
o Antiplatelets [e.g. aspirin] and statins (target lipid levels are much
lower)
o Smoking cessation
Exercise training to stimulate collateral formation symptoms get better
o Exercise at least half to one hour every day
o Walk until pain comes, rest 2-3 minutes, walk again
o Keep a walk diary recording daily claudication distance in paces
o Supervised exercise 3X/wk helps. Advice to exercise alone does not.
Patient education:
o Teach patient to go to ED if symptoms of critical ischaemia arises
o Podiatrist to teach foot care
Medications
o Praxilene and Cilostazol shown to increase claud dist - Ex.
o Use of Vasteral (methoxyphylline) is controversial
Monitor regularly with measurement of ABPI
Indications for intervention in peripheral vascular disease
Disabling claudication or Critical limb ischaemia
Arteriography is essentially a preoperative investigation
Three options are:
o Stenting
o Percutaneous angioplasty
o Bypass surgery
Intervention (endovascular or surgical)
At least 6 months of conservative treatment first; mainly for aortoiliac
disease
Monitor claudication distance & ABPI usually intervene if claudication
distance <50m (poor QOL, almost critical limb ischemia)
Confirm disease outline with CT angiogram or angiogram
If parameters improve but then plateau, discuss with patient about
whether he can accept the level of symptoms, and the risks of
intervention
Usually do angioplasty rather than bypass as it is less invasive, though
may not be as effective in treating the symptom
VASCULAR SURGERY

Percutaneous transluminal angioplasty

Angioplasty of the aorto-iliac segment has a 90% 5 year patency
Angioplasty of the infra-inguinal vessels has a 70% 5 year patency
Angioplasty only effective for focal stenotic lesions and better for large
vessels. Problem with angioplasty is that it is not long-lasting
restenosis can occur
New method: subintimal angioplasty if lumen is so occluded that guide
wire cannot pass through, the guidewire is threaded into the subintimal
space to create a dissection around the occluded segment, and this
space is then angioplastied to create a channel parallel to the actual
lumen for blood to flow through
Complications occur in less than 2% of patients
o Acute thrombosis; Distal embolization
o Wound haematoma; Arterial wall rupture
Bypass surgery
Only used when lesions cannot be treated by angioplasty
Types of bypass graft include:
Biological grafts
o Autograft: Long saphenous vein or Internal mammary artery
o Allografts: Dacron coated umbilical vein
Synthetic grafts
o Dacron
- woven or knitted
+/- albumin coated
o Woven grafts - smaller pores.
No preclotting required
o Velour
- Polyfluorotetraethylene (PTFE)
Choice of graft material
Determined by long term patency rates
Autologous vein is best graft material but not always available
Interposition of vein between PTFE graft and artery at distal anastomosis
can improve long term patency
Reasons for graft failure
Less than 30 days - technical failure
30 days to 1 years - neointimal hyperplasia at distal anastomosis
More than 1 years - progression of distal disease
Amputation
Indications: Dead (necrotic), dangerous (gangrene, infection), damn
nuisance (non-functional, bad smell, pain)
Level of amputation depends on vascularity of the limb; indications
(where the infection is etc)
Try to preserve function must revascularize to ensure good healing
144

!
DIABETIC FOOT

Foot problems are common in type-1 and type-2 diabetics

20-40% of diabetics have peripheral neuropathy
Many also have features of peripheral vascular disease
o 15% of diabetics develop foot ulceration
Diabetes is the leading cause of non-traumatic lower limb amputation

Pathophysiology
The diabetic foot results from a combination of neuropathy and
ischaemia
Neuropathy has sensory, motor and autonomic components
o Sensory loss results in loss of protective sensation and
unnoticed foot injuries
o Loss of motor control to the small muscles of the feet results in a
claw foot deformity
Autonomic neuropathy leads to vasomotor denervation and
arteriovenous shunting
o This compromises the ability to direct blood flow to the capillary
beds
Ischaemia can affect both the large and small vessels
o Large vessels disease results in atheroma of the femoral,
popliteal and tibial vessels
o Small vessel disease affects the microcirculation
Other contributing factors include:
o Poor vision
o Cerebrovascular disease
o Limited joint mobility
o Peripheral oedema
In patients with foot ulceration healing is impaired
o Impaired fibroblast function
o Deficiency in growth factors
o Abnormalities of the extracellular matrix

VASCULAR SURGERY

Management
Prevention of complications is preferable to the need for active
management
Patients should be monitored and self-care encouraged
They should be educated about
o Washing
o Care of cores and calluses
o Toenail cutting
o Suitable footwear
In those with ulceration assessment should be made of:
o Infection
o Vascular insufficiency
Management of infection
Wound swabs often show both gram-negative, gram-positive and
anaerobic bacteria
Osteomyelitis if usually due to Staph. aureus
Plain radiography or MRI may demonstrate the extent of the infection
The threshold for antibiotic use should be low
The antibiotics used should be based on culture sensitivities
Surgery may be required if progression despite antibiotic treatment
Management of vascular insufficiency
All patients with diabetic ulceration should undergo
non-invasive vascular assessment
The ABPI should be calculated
o This may be falsely elevated due to arterial calcification
o Normal values may still be recorded in diabetics with significant
major vascular disease
Revascularization should be considered if arterial insufficiency is present
Diabetics have a predisposition for disease in medium-sized vessels
especially at the popliteal trifurcation
o The distal pedal vessels are often spared
Femoro-distal bypass grafting may be required

145

!
ABDOMINAL AORTIC ANEURYSM

AAA = localised abnormal dilatation of a blood vessel wall or the heart;

diameter >3cm
More prevalent in elderly men, Male : female ratio is 4:1
Risk factors hypertension, peripheral vascular disease, family history
Accounts for 2% male deaths above the age of 55 years
o Mortality of emergency operation is greater than 50%
o Mortality of elective surgery is less than 5%

Natural history
AAA diameter expands exponentially at approximately 10% / year
Risk of rupture increases as aneurysm expands (5 yr risk)
o 5.0 5.9 cm = 25%
o 6.0 6.9 cm = 35%
o More than 7 cm = 75%
Overall only 15% aneurysms ever rupture; 85% die from unrelated cause
95% infrarenal, but may extend to common iliac arteries
Usually fusiform in shape (vs saccular), containing mural thrombus
Screening
AAA are suitable for screening as elective operation of asymptomatic
aneurysms can reduce mortality associated with rupture
Probably males over 65 years especially hypertensives
Single US at 65 years reduces death from ruptured AAA by 70% in
screened population
Clinical features (75% are asymptomatic)
Possible symptoms:
Rupture presents with
Epigastric pain
Sudden onset
abdominal pain
Back pain
Hypovolaemic
Malaise and
shock
weight loss (with
inflammatory
Pulsatile
aneurysms)
epigastric mass

Rare presentations:
Trash feet
Aorto-caval
fistula
Primary aortointestinal fistula

Indication for operation

Rupture
Symptomatic aneurysm
Rapid expansion 10% a year
Asymptomatic > 5.5 cm exact lower limit controversial

VASCULAR SURGERY

Pre-operative investigation
Need to determine
o Extent of aneurysm
o Fitness for operation (Pre-op)
Ultrasound, conventional CTAP and more recently spiral CT
o Determines aneurysm size, relation to renal arteries,
involvement of iliac vessels
Most significant post op morbidity and mortality related to cardiac
disease
o If pre-operative symptoms of cardiac disease need cardiological
opinion
May need thallium scan or cardiac catheterization
Cardiac revascularization required in up to 10% patients
Endovascular aneurysm repair
Morbidity of conventional open aneurysm surgery related to:
o Exposure of infra-renal aorta
o Cross clamping of aorta
Endovascular repair may be associated with:
o Reduced physiological stress
o Reduced morbidity & mortality
Technique
Complications
Three main types of graft
Graft migration
o Aorto-aortic
Endovascular leak
o Bifurcated aorto-iliac
Graft kinking
o Aorto-uniiliac graft with femoro Graft occlusion
femoral crossover and
contralateral iliac occlusion
Popliteal artery aneurysms
Defined as a popliteal artery diameter greater than 2 cm
Account for 80% of all peripheral aneurysms
o 50% are bilateral
o 50% are associated with an abdominal aortic aneurysm
o 50% are asymptomatic
Symptomatic aneurysms present with features of:
o Compression of adjacent structures (veins or nerves)
o Rupture
o Limb ischaemia due to emboli or acute thrombosis
Treatment is by proximal and distal ligation
Revascularization of the leg with a femoropopliteal bypass
With a symptomatic popliteal aneurysm 20% patients will undergo an
amputation
146

!
Management
Ruptured AAA
Very high mortality nearly 100% if frank rupture (will not get to ED in
time)
Most of the patients who reach the ED (about 50% reach ED alive) have
a leaking AAA with a tamponade effect by the retroperitoneal structures
High suspicion in unstable hypotensive patient complaining of severe
sharp pain radiating to the back; may feel a pulsatile mass in the
abdomen

Stabilise patient resuscitation with fluid and blood products

o Do not intubate as neuromuscular blocking agents will reduce
tamponade effect, worsening haemorrhage
Call for vascular surgeon
Bring to OT for open repair quickly isolate the aorta and clamp it
proximally
o can be clamped for about 30 minutes without significant visceral
ischaemia
o AAA is incised, the surrounding haematoma and mural thrombus
within the AAA are cleared out
o Synthetic graft (Dacron polytetrafluoroethylene) is placed
within the aorta and the vessel wall closed up over the graft i.e.
the graft forms the lumen of the aorta
Mortality rate of repair operation in this setting is about
50%
Most common complication postoperatively is renal insufficiency can
be reduced by giving frusemide or mannitol pre-operatively before
anaesthesia induction

Non-ruptured AAA
Time available for investigation of size of AAA and related anatomy
Indications for surgery:
o Aneurysm > 5.5 cm in largest diameter [risk of surgery outweighs
that of AAA]
o Increase in diameter of more than 1cm per year
o Symptomatic aneurysm back pain, tenderness on palpation,
distal embolism, ruptured/leaking aneurysm
Patients fitness for surgery needs to be properly assessed because it is
a major operation need to optimise CVS function
Operation is the same except that it is done under elective setting
Mortality is <5% in the elective setting, serious morbidity ~10%
VASCULAR SURGERY

Endovascular stenting
An alternative to open repair which is less invasive, can be done under
GA
Mortality ~1%, but serious morbidity rate is similar to open repair: 10%
Involves deployment of a non-porous stent within the aneurysm to form
the lumen of the aorta requires adequate neck proximally and good
landing site distally
Not as good results as open surgery; need to do an angiogram every 6
months to check position of stent (ensure not migrated)
Complications of surgery
Intraoperative/early
Acute myocardial infarction most patients already have atherosclerotic
disease of coronary vessels and are at risk of AMI (responsible for 5060% of mortality)
Stroke (due to hypotension or embolism)
Renal insufficiency
Colon ischaemia occurs in 2-6%
Trash foot embolism of thrombus from the aneurysm
Infection of graft
Spinal cord ischaemia (quite uncommon)
Haemorrhage
Late

Aortoenteric fistula frank PR bleeding, torrential

Late infection of prosthetic graft material
Sexual dysfunction

Post-operative investigations:
FBC: Hb and plt (blood loss and consumptive coagulopathy)
UECr: renal insufficiency or contrast nephropathy
KUB: check position of stent

147

!
VARICOSE VEINS

Varicose veins affect

o 20-25% of adult females
o 10-15% of adult males

Assessment of varicose veins

History
o Poor correlation exists between symptoms and signs
o Cough, tap and thrill tests are inaccurate
o Important to identify those with history of DVT or lower limb
fracture
o If history of DVT need preoperative investigation with duplex
scanning
Examination
o Identify distribution of varicose veins - long saphenous (LSV) vs
short saphenous (SSV)
o Confirm with tourniquet testing & hand held-doppler probe (5
MHz)
o Recurrent varicose veins need duplex ultrasound
Indications for duplex scanning
Suspected short saphenous incompetence
Recurrent varicose veins
Complicated varicose veins (e.g. ulceration, lipodermatosclerosis)
History of deep venous thrombosis
Indications for varicose vein surgery
Most surgery is cosmetic or for minor
symptoms
Absolute indications for surgery :
o Lipodermatosclerosis leading to
venous ulceration
o Recurrent superficial
thrombophlebitis
o Bleeding from ruptured varix

VASCULAR SURGERY

Surgical Options
LSV surgery
Saphenofemoral junction (SFJ) found 2 cm below and lateral to pubic
tubercle
Flush ligation of the LSV: Individually divide and ligate tributaries of LSV
o Superficial circumflex iliac vein
o Superficial inferior epigastric vein
o Superficial and deep external pudendal vein
Check that femoral vein clear of direct branches for 1 cm above and
below SFJ
Stripping of LSV reduces risk of recurrence
o Only strip to upper calf.
o Stripping to ankle is associated with increased risk of saphenous
neuralgia (association with saphenous nerve)
Post-operative care:
o Elevate foot of bed for 12 hours
o Class 2 varix stocking should be worn for at least 2 weeks
SSV surgery
Saphenopopliteal junction (SPJ) has very variable position
Preoperative localisation with duplex ultrasound
Identify and preserve the sural nerve
Stripping associated with risk of sural nerve damage
Subfascial ligation inadequate
Perforator surgery
Significance of perforator disease is unclear
Perforator disease may be improved by superficial vein surgery
Perforator surgery (e.g. Cockett's and Todd's procedure) associated with
high morbidity
Subfascial endoscopic perforator surgery (SEPS) recently described
Not indicated for uncomplicated primary varicose veins
May have a role in addition to saphenous surgery in those with venous
ulceration

148

!
Endovascular laser treatment
Laser energy deliver via narrow laser fibre to obliterate the vein
Causes heat injury to vessel wall
Usually performed under local anaesthesia
Clinical and symptomatic improvement seen in 95% patients
Patient satisfaction high and early return to work is possible
Complications include paraesthesia and skin burns
Recanalization seen in less than 10% patients
Radiofrequency ablation
Uses high frequency alternating current delivered via a bipolar catheter
Placed intraluminally under duplex guidance
Local heating results in venous spasm and a collagen seal
Performed under general anaesthesia
Long saphenous vein accessed at the knee using Seldinger technique
90% vein occlusion achieved in first week after treatment
Associated with less pain than open surgery
o Improved quality of life and earlier return to work
Complications include paraesthesia and skin burns
Recurrence rates are similar to open surgery

Recurrent varicose veins

15 - 25 % of varicose vein surgery is for recurrence
Outcome of recurrent varicose veins surgery is less successful
Can be avoided with adequate primary surgery
Reasons for recurrence
Inaccurate clinical assessment
o Confusion as to whether varicosities are in LSV or SSV
distribution
o Can be avoided with use of hand held doppler
Inadequate primary surgery
o 10% cases SFJ not correctly identified
o 20% cases tributaries mistaken for LSV
Failure to strip LSV
Injudicious use of sclerotherapy
o 70% of those with SF incompetence treated with sclerotherapy
alone will develop recurrence
Neovascularization
o With recurrent varicose vein need to image with duplex or
varicography

Sclerotherapy
Only suitable for below knee varicose veins
Need to exclude SFJ or SPJ incompetence
Main use is for persistent or recurrent varicose veins after adequate
saphenous surgery
Sclerosants
o 5% Ethanolamine oleate
o 0.5% Sodium tetradecyl sulphate
Recently foam ( mixture of air / sclerosant) has been shown to be more
effective
Different to sclerosants used for haemorrhoids
Needle placed in vein when full with patient standing
Empty vein prior to injection
Apply immediate compression and maintain for 4-6 weeks
Do not exceed maximum volume
Injection about 5 sites possible
Complications of sclerotherapy
Extravasation causing pigmentation or ulceration
Deep venous thrombosis
VASCULAR SURGERY

149

!
VENOUS ULCERATION

Leg ulceration is common

Most are due to venous hypertension
o 40% of venous ulcers are due to superficial venous disease
Rare causes include:
o Rheumatoid arthritis
o Malignancy
o Syphilis
Surgical correction of superficial venous disease often results in healing

Assessment
Clinical assessment should
o Identify previous DVT
o Assess arterial disease
o Identify varicose veins and underlying valvular incompetencies
Assessment requires
o Clinical examination
o Hand held doppler assessment
o Possible duplex scanning
Venous hypertension
Affects 1-2% of population
Due to chronic venous insufficiency and distal vein hypertension
Usually due to post thrombotic syndrome
Can be due to primary valvular incompetence

Causes of chronic venous insufficiency

Gravitational reflux
Venous insufficiency classified as primary or secondary
Primary insufficiency has no obvious cause of valvular dysfunction
Insufficiency results in early refilling of venous pool after muscle
contraction
o Causes progressive and sustained increase in calf vein pressure
= Ambulatory venous hypertension
o Results in capillary dilatation and leakage of plasma proteins
Compartmental pressures
Incompetent perforating veins exposes superficial veins to high
pressures during muscle contraction
= hydraulic ram effect
o Produces localised venous hypertension and filtration oedema
o Continues until tissue pressures rise to restore equilibrium
Leucocyte trapping
Accumulation of leucocytes occurs in dependent limbs of those with
venous hypertension
Trapping of WC associated with activation
o Hypoxic endothelial cells stimulate adherence of WC
o Activate WC release O2 radicals, collagenases and elastases
which injure surrounding tissue
Evaluation of venous insufficiency
History of chronic venous insufficiency
Exclude other causes of leg ulceration
Signs of venous hypertension
Perimalleolar oedema
Pigmentation
Lipodermatosclerosis

Eczema
Ulceration

Doppler ultrasonography
Used to assess presence of venous reflux
LSV, SSV and perforators should be assessed
Patency of femoral and popliteal veins should be checked
Flow augmented by compression of calf, deep inspiration or Valsalva
manoeuvre
Duplex ultrasonography
Allow anatomical and functional assessment
Flow rate and anatomy can be measured
VASCULAR SURGERY

150

!
Treatment of venous ulceration
Compression
Elastic compression stockings
o Provide graduated compression
o Produce local alteration of microvascular haemodynamics
o Minimal effect on deep vein dynamics
o Do not cure hypertension - Protect skin from the effects
o Occlusive arterial disease is a relative contraindication
Gel paste gauze boots
CircAid
External pneumatic compression
Drug treatment
Systemic agents - minimally effective
o Zinc
o Fibrinolytic agents
o Pentoxifylline
Topical agents - not recommended
o Antibiotics
o Free radical scavengers
o Hydrocolloid dressings

Marjolin's ulcer
Marjolin's ulceration is a squamous cell carcinoma arising at sites of
chronic inflammation
Recognized underlying causes include:
o Chronic venous ulceration
o Burns
o Osteomyelitis sinuses
Usually a long-period between injury and malignant transformation
o This period may be 10-25 years
40% occur on lower limb
Malignant change is usually painless
Nodal involvement is uncommon
Diagnosis is confirmed by biopsy of the edge of the ulcer
Management involves adequate excision and skin-grafting or amputation

Surgery
Aims of venous ulcer surgery are:
o Cure venous hypertension
o Heal the ulcer
Combination of superficial venous surgery and compression may be
beneficial
Surgical options include:
o Skin grafting
o Free flap grafting
o Superficial vein stripping
o Perforating vein interruption
o Valve plasty
o Thrombolysis, dilation, stenting

VASCULAR SURGERY

151

!
VENOUS THROMBOSIS

Venous thrombosis is significant cause of morbidity and mortality

Pulmonary embolus accounts for 10 - 25 % of hospital deaths
At least 20% patients with a DVT develop a post-thrombotic limb
o 80% of calf DVTs lyse spontaneously without treatment
o 20% of calf DVTs propagate to the thigh and increased risk of
PE

Pathophysiology
Thrombus formation and propagation depends on Virchow's triad
o Venous stasis (immobility)
o Hypercoagulable state (drugs or malignancy)
o Endothelial damage (external compression)
Risk of venous thrombosis during surgery
Low risk
o Minor surgery (<30 min) + no risk factors other than age
o Major surgery (> 30 min) , age <40 yrs + no other risk factors
Moderate risk
o Major general, urological, gynaecological, cardiothoracic,
vascular or neurological surgery + age >40 yrs
o Major medical illness or malignancy, trauma or burn
o Minor surgery, trauma or illness with prev DVT, PE or
thrombophilia
High risk
o Fracture or major orthopaedic surgery of pelvis, hip or lower limb
o Major pelvic or abdominal surgery for cancer
o Major surgery, trauma or illness with prev DVT, PE or
thrombophilia
o Major lower limb amputation
Risk factors for venous thrombosis
Patient Factors
- Age
- Puerperium
- Obesity
- High-dose oestrogen therapy
- Varicose veins - Previous DVT or PE
- Immobility
- Thrombophilia:
- Pregnancy
- Antithrombin III deficiency

VASCULAR SURGERY

- Protein C deficiency
- Protein S deficiency
- Antiphospholipid antibody
- Lupus anticoagulant

Potential for DVT can be investigated by thrombophilia screen

FBC and blood film
>Clotting studies - APPT / PT / TT
Reptilase test
Protein C & S and Antithrombin III assay
Lupus anticoagulant
Prevention of thromboembolism
Prevention of stasis
Early mobilization
Graduate compression stockings (reduce incidence of DVT by 50%)
o The stocking profile should be
18 mmHg at the ankle
14 mmHg at the mid-calf
8 mmHg at the upper thigh
Intermittent pneumatic compression (e.g. Flowtron boots)
Pharmacologically reduce hypercoagulable state
Heparin
Unfractionated heparin (MW = 15 kDa) 5000u 3x daily
Low Molecular Weight Heparin (MW = 5 kDa) Enoxaparin 20 or 40 mg
daily
Potentiate Antithrombin III by inactivating activated clotting factors
o Unfractionated heparin anti-Xa activity = anti IIa activity
o Low Molecular Weight Heparin = anti-Xa activity 4x > anti IIa
Does not have significant effect on APPT
Reduce DVTs by 70% and PEs by 50%
Side effects of unfractionated Heparin
o Osteoporosis
o Idiosyncratic thrombocytopenia
New drugs
New drugs useful in DVT prophylaxis include
o Thrombin inhibitors (e.g. hirudin)
o Specific factor Xa inhibitors (e.g. fondaparinux)
Factor Xa inhibitors may be more effective than LMWH
Current recommendations for DVT prophylaxis
Assess for clinical risk factors and overall risk of thromboembolism
Should receive prophylaxis according to degree of risk
o Prophylaxis should continue until discharge
Low risk patients should be mobilized early
Moderate risk patients should receive specific prophylaxis
152

!
Clinical features of DVT
Many are asymptomatic
Clinical features depends on site of venous occlusion
Classical clinical features of a calf DVT are:
o Calf pain and tenderness
o Pyrexia
o Persistent tachycardia
Homan's sign = pain on passive dorsiflexion of the ankle
Occlusion of the ilio-femoral vein can result in venous gangrene
(phlegmasia cerulea dolens)
Investigation of suspected DVT
D-dimers
A fibrin degradation product that can be assayed in plasma
Levels raised in the presence of recent thrombus
A negative result almost excludes the presence of venous thrombosis
Decision to proceed to venography or ultrasound often based on D-dimer
result
Venography
Gold standard, Will identify both calf vein and proximal thrombus
Painful and time consuming investigation.
o 2-3% of patients develop contrast reaction
Ultrasound
Technique has three components - all operator dependent.
o Venous compressibility
o Detection of Doppler flow
o Visualization of clot
Able to exclude femoro-popliteal or major calf DVT in symptomatic
patients

Treatment of venous thrombosis

Prevention of pulmonary embolus
Restore venous and valvular function to prevent the post thrombotic limb
Anticoagulation
Initially with unfractionated or low molecular weight heparin
Followed by oral anticoagulation
Surgical thrombectomy
Considered in massive ilio-femoral thrombosis associated with
phlegmasia cerulea dolens
o Good early results with 62% complete and 38% partial clearance
of ilio-femoral segment
o Unfortunately re-occlusion common
o Thrombolysis of unproven benefit
Pulmonary embolism
Investigations of possible pulmonary embolus
Arterial blood gases - hypoxia, hypocarbia but may be normal
ECG - Signs of right heart strain - classically S1Q3T3
CXR - Show oligaemia + central pulmonary markings and excludes other dx
Ventilation / Perfusion scanning - May confirm or refute diagnosis
Pulmonary angiography and echocardiography
Spiral CT might replace pulmonary angiography
Lower limb investigations for DVT as above
Management of pulmonary embolus
If high degree of suspicion but stable:
o Anti-coagulate with heparin or LMWH
o Oxygen, analgesia, colloid to increase CVP
o Warfarinise for at least 3 months
If haemodynamically unstable:
o Consider pulmonary thrombolysis via pulmonary artery catheter
o If thrombolysis contraindicated consider pulmonary embolectomy
Inferior vena caval filters
Inserted percutaneously usually via femoral vein
Indicated if:
o Recurrent pulmonary emboli despite adequate anti-coagulation
o Extensive proximal venous thrombosis and anticoagulation is
contraindicated

VASCULAR SURGERY

153