SURGERY NOTES

Adapted from Andre Tan

1
 4 86
7 86
1. TRAUMA & PERIOPERATIVE CARE 8 5. OESOPHAGEAL DISEASES 87
10 91
1. ADVANCED TRAUMA LIFE SUPPORT 13 1. ANATOMY OF THE OESOPHAGUS 96
2. ABDOMINAL TRAUMA 14 2. PHYSIOLOGY OF SWALLOWING 100
3. CARDIOTHORACIC TRAUMA 18 3. APPROACH TO DYSPHAGIA 101
4. NEUROSURGICAL TRAUMA 21 4. OESOPHAGEAL CANCER
5. MUSCULOSKELETAL TRAUMA 5. GASTRO-OESOPHAGEAL REFLUX DISEASE
6. POST-OPERATIVE COMPLICATIONS 6. BARRETT’S  OESOPHAGUS
7. SHOCK 7. ACHALASIA
102
8. PERIOPERATIVE CARE
28 6. UPPER GIT 105
2. LUMPS & BUMPS 34 108
37 1. APPROACH TO BLEEDING UPPER GIT 112
1. HERNIA 40 2. VARICEAL BLEEDING
2. SCROTAL SWELLINGS 41 3. PEPTIC ULCER DISEASE
3. APPROACH TO LUMPS & BUMPS 42 4. GASTRIC CANCER
4. LIPOMA 44 116
5. SEBACEOUS CYST 46 7. LOWER GIT & COLORECTAL DISEASES 118
6. GANGLION 48 130
7. BASAL CELL CARCINOMA 52 1. APPROACH TO BLEEDING LOWER GIT 134
8. SQUAMOUS CELL CARCINOMA 54 2. COLORECTAL CANCER
9. MALIGNANT MELANOMA 55 3. STOMAS
137
10. NEUROFIBROMA 56 4. DIVERTICULAR DISEASE
11. DERMOID CYST 58 5. INFLAMMATORY  BOWEL  DISEASE  (CROHN’S  
12. SEBORRHOEIC KERATOSIS DISEASE, ULCERATIVE COLITIS)
59
13. HAEMANGIOMA
60 140
14. PYOGENIC GRANULOMA 8. ANAL & PERIANAL DISORDERS
15. PAPILLOMA 60 142
16. KERATOCANTHOMA 61 1. HAEMORRHOIDS 144
17. KELOID (HYPERTROPHIC SCAR) 61 2. ANAL FISTULA
18. KAPOSI’S  SARCOMA 62 3. ANAL FISSURES
19. FIBROSARCOMA 63
20. PYODERMA GANGRENOSUM 9. LIVER DISEASES 145
21. RADIOTHERAPY MARKS 145
1. ANATOMY OF THE LIVER 145
3. SURGICAL INSTRUMENTS & PROCEDURES 64 2. CAUSES OF HEPATOMEGALY 146
65 3. CAUSES FOR A LIVER NODULE ON IMAGING 152
1. DRAINS 67 4. HEPATOCELLULAR CARCINOMA 152
2. CENTRAL VENOUS PRESSURE LINE 5. LIVER METASTASES 153
68
3. NASOGASTRIC TUBE 6. LIVER HAEMANGIOMA 153
4. TRACHEOSTOMY 7. SIMPLE LIVER CYSTS
70 154
5. SENGSTAKEN-BLAKEMORE TUBE (MINNESOTA 8. HEPATIC ABSCESS (PYOGENIC / AMOEBIC)
TUBE) 71 9. ASCITES
6. URINARY CATHETERISATION 72
7. CHEST TUBE 10. PANCREATIC DISEASES
155
4. ABDOMINAL SURGICAL EMERGENCIES 1. ACUTE PANCREATITIS 161
74 2. CHRONIC PANCREATITIS 162
1. APPROACH TO ABDOMINAL PAIN 75 3. PANCREATIC CANCER
2. APPROACH TO ABDOMINAL MASSES
3. INTESTINAL OBSTRUCTION (& MECKEL’S   76
DIVERTICULUM) 82
4. ISCHAEMIC BOWEL 84
5. ACUTE APPENDICITIS

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 166 203
167 203
11. BILIARY TRACT DISEASES 169 14. SALIVARY GLAND SWELLINGS 203
173 204
1. CAUSES OF JAUNDICE 175 1. ANATOMY OF THE PAROTID GLAND 205
2. APPROACH TO OBSTRUCTIVE JAUNDICE 175 2. ANATOMY OF THE SUBMANDIBULAR GLAND 206
3. GALLSTONE DISEASE 176 3. ANATOMY OF THE SUBLINGUAL GLAND
4. ACUTE CHOLECYSTITIS 4. APPROACH TO SALIVARY GLAND SWELLINGS
178
5. GALLBLADDER CANCER 5. SIALOLITHIASIS
178
6. CHOLEDOCHOLITHIASIS 6. SALIVARY GLAND TUMOURS
180 208
7. CHOLANGITIS
8. MIRIZZI’S  SYNDROME 15. THYROID DISEASES 209
9. RECURRENT PYOGENIC CHOLANGITIS
10. CHOLANGIOCARCINOMA 1. ANATOMY OF THE THYROID GLAND 211
182 2. APPROACH TO THYROID PROBLEMS 212
12. BREAST DISEASES 182 3. APPROACH TO THE SOLITARY THYROID 215
183 NODULE
1. ANATOMY OF THE BREAST 188 4. THYROID CANCERS
2. PRESENTATION OF BREAST DISEASES 189 5. SURGERY IN BENIGN THYROID DISEASE
3. APPROACH TO A BREAST LUMP 195 216
4. APPROACH TO NIPPLE DISCHARGE 195 16. PERIPHERAL ARTERIAL DISEASES 217
5. BREAST CANCER 222
6. PAGET’S  DISEASE  OF  THE  NIPPLE 1. ANATOMY OF THE LOWER LIMB ARTERIES
7. GYNAECOMASTIA 2. ACUTE LIMB ISCHAEMIA 228
3. CHRONIC LIMB ISCHAEMIA
196
13. NECK MASSES
197 17. ABDOMINAL AORTIC ANEURYSM
1. ANATOMY OF THE NECK 197
2. THYROGLOSSAL CYST 197 18. PERIPHERAL VENOUS DISEASES
3. DERMOID CYST 198 230
4. PLUNGING RANULA 199 1. ANATOMY OF THE VENOUS SYSTEM OF THE 232
5. BRANCHIAL CYST/FISTULA 199 LOWER LIMB 233
6. CHEMODECTOMA 200 2. CHRONIC VENOUS INSUFFICIENCY 236
7. PHARYNGEAL POUCH 200 3. VARICOSE VEINS
8. CYSTIC HYGROMA 200 4. VENOUS ULCERS
9. CERVICAL RIB 201
10. NEUROMA/SCHWANNOMA 19. UROLOGICAL DISEASES 238
11. CERVICAL LYMPHADENOPATHY 241
1. APPROACH TO HAEMATURIA
244
2. RENAL CELL CARCINOMA
3. BLADDER TRANSITIONAL CELL CARCINOMA 246
4. UROLITHIASIS 249
5. APPROACH TO ACUTE RETENTION OF URINE 252
6. BENIGN PROSTATIC HYPERPLASIA 256
7. PROSTATIC CANCER

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1. TRAUMA & PERIOPERATIVE CARE

1. ADVANCED TRAUMA LIFE SUPPORT

Main principles: Approach:

Treat greatest threat to life first Primary survey and resuscitation with adjuncts
Definitive diagnosis is less important Re-evaluation of the patient
Time is important – the  “golden  hour”  after  trauma  is   Secondary survey with adjuncts
when 30% of trauma deaths occur, and are Post-resuscitation monitoring and re-evaluation
preventable by ATLS Optimise for transfer and definitive care

PRIMARY SURVEY – ABCDE

AIRWAY Assessment of airway patency Establishing patent airway

Is patient alert, can patient speak? Chin-lift / modified jaw thrust (protect C-spine!)
Gurgling, stridor Remove any FBs in the mouth if possible
Maxillofacial injuries Oro/nasopharyngeal airway
Laryngeal injuries Definitive airway – endotracheal tube,
Caution: C-spine injury cricothyroidotomy, tracheostomy
BREATHING Assessment of breathing Management of breathing
Look, listen, feel: chest rise, breath Supplemental oxygen
sounds – rhythm and equality bilaterally Ventilate as required if patient requires
Rate of respiration assistance with breathing
Effort of respiration Needle thoracotomy for tension pneumothorax,
Colour of patient followed by chest tube
Percuss chest Occlusive dressing for open pneumothorax
Look for chest deformities e.g. flail chest
CIRCULATION Assessment of organ perfusion
Level of consciousness
Skin colour and temperature (cold, mottled, clammy), capillary refill
Pulse rate and character (weak, thread) – all major pulses
Blood pressure

Classes of haemorrhagic shock - gradual transition from one stage to the next
I II III IV
Bld loss : Amt (ml) <750 750-1500 1500-2000 >2000
% <15 15-30 30-40 >40
Ht rate <100 >100 >120 >140
BP Normal Normal/min low Decreased Critical
Cap refill Normal Prolonged Prolonged Prolonged
Resp rate 14-20 20-30 30-40 >35
Ur output (ml/h) >30 20-30 5-15 Oliguric-anuric
Anxious- Confused-
Mental state Sl anxious Mild anxiety
confused lethargic
Crystalloid +
Fluid replacement Crystalloid Crystalloid Blood
blood

Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis.
Hypothermia due to decreased perfusion and evaporation of sweat.
Some people have only minimal symptoms such as confusion and weakness.
Those on B-blockers, those who are athletic and in 30% of cases with shock due to intra abdominal
bleeding may have a normal or slow heart rate.

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 Management
Sources of bleeding apply direct pressure or pressure on proximal pressure point
Suspect occult bleeding e.g. intraperitoneal, retroperitoneal (pelvic #), soft tissue (long bone #)
Venous access – large bore, proximal veins
Restore circulatory volume with rapid crystalloid infusion – Ringer’s  lactate
Blood transfusion if not responsive to fluids or response is transient
Reassess frequently
DISABILITY Glasgow coma scale
Eye (E4) Verbal (V5) Motor (M6)
Spontaneous opening 4 Oriented speech 5Obeys 6
Opens to voice 3 Confused 4Purposeful 5
Opens to pain 2 Inappropriate 3Withdraws 4
No response 1 Incomprehensible 2Flexion response 3
No verbal response 1Extension response 2
No response 1
GCS: > 13 (minor); 8-13 (moderate); < 8 (severe)

AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive
Pupillary reactivity
Call for neurosurgical consult as indicated
EXPOSURE Remove all clothes
Check everywhere for injuries (log-roll to look at the back)
Prevent hypothermia
ADJUNCTS Monitoring
Vital signs – BP, pulse rate, saturation (pulse oximeter)
ECG monitoring
Arterial blood gas

Diagnostic tools
Screening X-ray films (trauma series): CXR, AP pelvis, lateral C-spine
Focused abdominal sonography in trauma (FAST)
Diagnostic peritoneal lavage

Urinary catheter
Functions: decompress bladder, measurement of urinary output
Caution in urethral injury: blood at urethral meatus, perineal ecchymosis/haematoma, high-riding
prostate

Gastric catheter (orogastric or nasogastric)

Function: decompress stomach, look at aspirate (bloody? bilious?)
Caution in base of skull fracture: CSF otorrhoea/rhinorrhoea, periorbital ecchymosis, mid-face
instability (grab the incisors and rock), haemotympanum insert orogastric tube instead of
nasogastric

SECONDARY SURVEY
When to do secondary survey: Primary survey and resuscitation completed
ABCDEs reassessed
Vital functions returning to normal i.e. no need for active resuscitation at the moment

AMPLE HISTORY Allergy

Medications
Past history
Last meal
Events leading to injury, Environment in which trauma occurred

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COMPLETE HEAD-TO- Head
TOE EXAMINATION Complete neurological examination
GCS or AVPU assessment
Comprehensive examination of eyes and ears for base of skull fractures
Caution: unconscious patient; periorbital oedema; occluded auditory canal

Maxillofacial
Bony crepitus/deformity, palpable deformity
Comprehensive oral/dental examination
Caution: potential airway obstruction in maxillofacial injury; cribriform plate # with CSF
rhinorrhoea do not insert nasogastric tube

Cervical spine
Palpate for tenderness, any step deformity
Complete neurological examination
C-spine imaging
Caution: Injury above clavicles; altered consciousness (cannot assess accurately); other severe,
painful injury (distracts from cervical spine pain)

Neck (soft tissues)

Blunt versus penetrating injuries
Airway obstruction, hoarseness
Crepitus (subcutaneous emphysema), haematoma, stridor, bruit
Caution: delayed s/s of airway obstruction that progressively develop; occult injuries

Chest
Inspect, palpate, percuss, auscultate
Re-evaluate frequently
Look at CXR
Caution: missed injury; increase in chest tube drainage

Abdomen
Inspect, palpate, percuss, auscultate
Abrasions and ecchymosis – “seat-belt  sign”
Lower rib fractures liver and spleen injury
Re-evaluate frequently
Special studies: FAST, DPL (diagnostic peritoneal lavage), CT scan
Caution: hollow viscus and retroperitoneal injuries; excessive pelvic manipulation

Perineum
Contusions, haematomas, lacerations
Urethral blood
DRE: Sphincter tone, high-riding prostate, pelvic #; rectal wall integrity; blood
Vaginal examination: blood, lacerations

Musculoskeletal – extremities
Contusion, deformity
Pain, Perfusion, Neurovascular status
X-rays as appropriate
Caution: potential blood loss is high in certain injuries (e.g. pelvic fracture, femoral shaft
fracture); missed fractures; soft-tissue or ligamentous injuries; examine  patient’s  back
ADJUNCTS & SPECIAL As required according to suspicion, but should not delay transfer
DX TESTS

FREQUENT RE- Have a high index of suspicion for injuries to avoid missing them
EVALUATION Frequent re-evaluation & continuous monitoring rapidly recognise when pt is deteriorating
PAIN MX Intravenous analgesia as appropriate

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2. ABDOMINAL TRAUMA

TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA

Solid organ injury: spleen, liver – bleeding (may be quite massive)
Hollow viscus injury with rupture
Vascular injury with bleeding

INDICATIONS FOR IMMEDIATE LAPAROTOMY

1) Evisceration, stab wounds with implement in-situ, gunshot wounds traversing abdominal cavity
2) Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation
3) Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising haemodynamics
4) Obvious signs of peritoneal irritation
5) Rectal exam reveals fresh blood
6) Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries excluded as source of bleeding)
7) X-ray evidence of pneumoperitoneum or diaphragmatic rupture

INVESTIGATIONS If patient is stable: FAST and/or CT scan

If patient is unstable: FAST and/or DPL

FOCUSED Advantages Disadvantages

ABDOMINAL Portable Does not image solid parenchymal
SONOGRAPHY IN Can be done quickly in <5min damage, retroperitoneum, diaphragmatic
TRAUMA (FAST) Can be used for serial examination defects or bowel injury
Ultrasonographic Does not require contrast, no radiation risk Compromised in uncooperative, agitated
evaluation of 4 patient, obesity, substantial bowel gas,
windows: subcutaneous air
Pericardial, Less sensitive, more operator-dependent,
R upper quadrant, cannot distinguish blood from ascites
L upper quadrant, Intermediate results require follow-up
Pelvis attempts or alternative diagnostic tests
CT SCAN Advantages Disadvantages
Only suitable for stable Able to precisely locate intra-abdominal Expensive
patient as quite long lesions preoperatively Time required to transport patient
time involved in Able to evaluate retroperitoneum Use of contrast
imaging with only Able to identify injuries that can be
patient in the room managed non-operatively
pt can collapse Not invasive
DIAGNOSTIC Positive DPL: Frank blood (>5ml) or obvious bowel contents aspirated
PERITONEAL Lavage fluid seen to exit from chest drain or urinary catheter
LAVAGE (DPL) RBC >100,000 per mm3, WBC >500, Gram stain + for bacteria in effluent
Involves making a cut
Indications Contraindications
in the infraumbilical
Any unstable patient with suspicion of Absolute indication for laparotomy exists
region and inserting a abdominal trauma or where clinical exam is Previous abdominal surgery or infections
catheter into the difficult or equivocal Gravid uterus
peritoneal cavity, Unexplained hypotension in multi trauma Morbid obesity
aspirate, then Patient requiring immediate surgery for Coagulopathy
instillation of saline and extra-abdominal injuries
re-aspiration
Advantages Disadvantages
Can promptly reveal or exclude the Morbidity involved – wound cxs
presence of intraperitoneal haemorrhage (haematoma, infx); intraperitoneal injury
Valuable in discovery of potentially lethal False negative rate of 2% when there is
bowel perforation failure to recover lavage fluid, early hollow
viscus injury, diaphragmatic injuries, injuries
to retroperitoneal structures

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3. CARDIOTHORACIC TRAUMA

There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving: cardiac tamponade, airway
obstruction, flail chest, haemothorax, and pneumothorax.

CARDIAC Clinical features

TAMPONADE Chest trauma and hypotension
Beck’s  triad (hypotension, muffled heart sounds, distended neck veins) – only in 50% of
High index of cases as hypovolaemia may prevent neck vein distension; muffled heart sounds least reliable
suspicion required Pulseless electrical activity
Kussmaul’s  signs (increased neck distension during inspiration, pulsus paradoxus)

Diagnostic clues
Enlarged cardiac shadow in CXR (globular heart – very rarely seen)

Small ECG voltages, electrical alternans = alternation of QRS complex amplitude or axis
between beats.

Pericardial fluid demonstrated on FAST or 2D-echo - definitive

Management
Aggressive fluid resuscitation – helps maintain cardiac output and buys time
Pericardiocentesis: 2D-echo guided or ECG lead-guided (Stop inserting needle when an abrupt
change in the ECG waveform is noted. If the ECG waveform shows an injury pattern (ST segment
elevation), slowly withdraw the needle until the pattern returns to normal, as this change in waveform
suggests that the spinal needle is in direct contact with the myocardium)

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AIRWAY Chin lift or jaw thrust
OBSTRUCTION Remove any foreign body manually, suction blood/secretions
Definitive airway – ETT, cricothyroidotomy, tracheostomy
FLAIL CHEST When 2 or more ribs are fractured at 2 points forming a flail segment that moves
paradoxically with breathing.
Results in hypoxaemia mainly due to underlying pulmonary contusion, contributed to by pain
with restricted chest wall movement.

Management:
Ensure adequate oxygenation and ventilation; judicious fluid therapy (avoid fluid overload);
adequate intravenous analgesia
Consider mechanical ventilation in high risk patients: shock, severe head injury, previous
pulmonary disease, fracture of >8 ribs, age > 65, >3 associated injuries
HAEMOTHORAX Chest tube insertion in the triangle of safety (bound by the lateral border of the pectoralis
major medially, a line just anterior to the mid-axillary line laterally, and the upper border of the
fifth rib inferiorly)
Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot
If blood >1500mls massive haemothorax, call urgent cardiothoracic consult
PNEUMOTHORAX
(TENSION/ OPEN)

Tension pneumothorax = develops when air is trapped in the pleural cavity under positive
pressure, displacing mediastinal structures and compromising cardiopulmonary function
It is a clinical diagnosis (CXR will only delay treatment, and may cause death) – signs of
pneumothorax, hypotension, neck vein distension, severe respiratory distress
Decreased venous return caused by compression of the relatively thin walls of the atria
impairs cardiac function. The inferior vena cava is thought to be the first to kink and restrict
blood flow back to the heart. It is most evident in trauma patients who may be hypovolemic
with reduced venous blood return to the heart.
Immediate needle thoracotomy in second intercostal space in mid-clavicular line
Followed by chest tube insertion

Open pneumothorax occurs in a large chest wall defect with equilibration between intrathoracic
and  atmospheric  pressure,  producing  a  “sucking  chest  wound”.
Cover defect with a sterile dressing, taping it down on 3 sides to produce a flutter-valve effect,
letting air out of the pleural cavity but not back in
Insert chest tube (not through the wound)

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4. NEUROSURGICAL TRAUMA

AIM: prevention of secondary brain injury (from hypotension, hypoxaemia, increased ICP etc) since neuronal death is irreversible.

PATHOLOGIES

Concussion Physiological dysfunction without anatomical or radiological abnormality (Physiological dysfunction is the first
step towards cell death, but is reversible if no further insult occurs)
Usually recovers in 2-3 hours
Contusion Small haematoma <1cm
Intracranial Extradural haemorrhage Lens-shaped haematoma outside the dura (between skull & dura)
haemorrhage Pathology: expanding space-occupying lesion
20% of patients with EDH are alert and well; underlying brain is minimally
damaged, thus drainage gives good results

Crescent shaped haematoma under the dura (between dura & arachnoid)
Subdural haemorrhage More severe than EDH (usu due to nature of injury that causes SDH to
occur – associated with higher impact, thus brain has other injuries)
Most often caused by head injury, when rapidly changing velocities within the
skull may stretch and tear small bridging veins
Generally result from shearing injuries due to various rotational or linear
forces (e.g. shaken baby syndrome, in which similar shearing forces
classically cause intra- and pre-retinal hemorrhages)
Pathology: underlying brain damage in addition to expanding SOL
Removal of blood does not solve brain damage poorer results
Traumatic subarachnoid Star shaped appearance (cisterns)
haemorrhage Usually only small amount of blood conservative tx sufficient

Intraparenchymal Any shape, size, location

haemorrhage If large haematoma, will require evacuation
Diffuse axonal Global injury of axons
injury Arises from injury that causes rotational and shearing forces (high impact injury) – rapid acceleration and
deceleration of brain in the intracranial cavity against relatively fixed points of attachment at the falx and
tentorium (e.g. RTA, falls, assaults, shaken baby syndrome)
Maximal effects at corpus callosum and brainstem
One of the major causes of unconsciousness and persistent vegetative state after head trauma
If severe, will see punctate haemorrhages at the grey-white border
Cerebral Hypoxic / Cytotoxic (cellular)
oedema (3 Decreased blood supply (oxygenation) loss of function of Na-K pump as ATP decreases increased
types) intracellular sodium cellular swelling
Conventionally thought to be resistant to any known medical treatment
Interstitial
Impaired absorption of CSF increases in transependymal CSF flow acute hydrocephalus
Also not responsive to steroid administration, and its response to osmotherapy is debatable
Vasogenic
Breakdown of blood-brain barrier proteins enter interstitial space oedema
Seen in TBI, neoplasms, and inflammatory conditions
This edema subtype is responsive to both steroid administration and osmotherapy

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PATHOPHYSIOLOGY

Monroe- The CNS & its contents (brain, CSF, blood) are enclosed in a rigid space whose total volume tends to
Kellie remain constant increase in the volume of one component will elevate pressure and decrease the
doctrine volume of one of the other elements

Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure

Compensatory mechanisms:
Hyperventilation vasoconstriction of cerebral vessels due to pCO2 blood volume
CSF pushed into spinal canal (but limited volume available)
Removal of any reversible cause of raised ICP will improve cerebral perfusion
Fixed dilated Constrictor fibres to the pupil run in the oculomotor nerve, which exits the brainstem at the upper
pupil midbrain – nerve fibres lie just under the tentorium
Uncus of the temporal lobe sits on the tentorium
In raised ICP, the uncus herniates over the edge of the tentorium, compressing the fibres of the
oculomotor nerve just below
Thus a fixed dilated pupil occurs on the side of the compression due to unopposed sympathetic
supply (dilates the pupil)
Cushing’s   A triad of: Widened pulse pressure (HTN)
reflex Irregular breathing (Cheyne-Stokes breathing)
Bradycardia

From Monroe-Kellie doctrine, MAP maintains cerebral perfusion pressure when ICP is raised.
Increase in mean arterial pressure achieved by sympathetic overdrive:
a) Increased heart rate
b) Increased contractility
c) Increased vasoconstriction – increased total peripheral resistance
(a) and (b) increase cardiac output increased BP; (c) increases BP

Baroreceptors detect abnormally raised BP and try to decrease it by triggering a parasympathetic

response via vagus nerve + Direct distortion of vagus nerve due to raised ICP heart rate
Distortion and/or increased pressure of brainstem (controls involuntary breathing) irregular
breathing and/or apnoea

MANAGEMENT

Assessment
3 important parameters: ABCs, GCS, pupil size

Minor head injury Most common

(GCS >13) Indications for admission: Persistent headache and/or vomiting
CSF leak
Neurological deficit
Skull fracture
History of loss of consciousness
Amnesia
In ward: NBM, IV drip (no dextrose saline!), no sedation, monitor GCS
If pt deteriorates CT scan
Exclude metabolic causes (e.g. hypoglycaemia)
Do septic workup (exclude sepsis)
Moderate head All will be CT-scanned at ED NES will operate if any indication to do so
injury In ward: as per mild head injury
(GCS 8 - 13)

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Severe head injury Must scan to look for reversible causes of raised ICP but stabilise patient first

Medical methods to lower ICP

Raise head of bed (improves venous drainage but could pressure of blood to the head)
Intubate and hyperventilate (the induced constriction of blood vessels limits blood flow to
the brain at a time when the brain may already be ischemic -- hence it is no longer widely
used. Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours
of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels
were returned to normal too quickly)
IV mannitol: create a hypertonic solution within the blood to draw water out of the neurons.
This helps to reduce the fluid within intracranial space, however prolonged administration
may lead to increase in ICP (must catheterise patient also; do not give if patient is unstable)
Screen for other life-threatening injuries (likely to be multi-trauma patient)

Achieve haemodynamic stability

Check for long bone fractures
FAST for bleeding into abdominal cavity
ABG to detect acidosis
Keep monitoring patient and re-investigate where appropriate

Operate if reversible cause found

Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced after blood
evacuated) [Burrhole usually not big enough to drain an acute bleed]
Evacuate clot
Insert endoventricular drain (EVD) if there is hydrocephalus

Total sedation after operation, ward in ICU

Prevents patient from struggling which will raise ICP
Depressed skull Can leave alone unless depression is greater than the thickness of the skull bone
fracture
Compound There is through-and-through skin laceration over the fracture
depressed fracture Always explore to ensure underlying dura is intact, and repair if dura is torn (since
meningitis can occur with a torn dura)

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5. MUSCULOSKELETAL TRAUMA

GENERAL POINTS
Extremity trauma tends not to be life-threatening
But occult blood loss can occur in large volumes esp in certain injuries – pelvic # (up to 3L), femoral shaft # (2L)
Need to have high level of suspicion and treat with urgency
Look out for any tachycardia, early signs of shock
Prepare to resuscitate patient

ASSESSMENT OF THE EXTREMITY

Perfusion: colour, pulses, skin temperature, capillary refill
Viability of the limb
Neurological assessment
Wounds – open or closed injury; abrasion over a fracture is considered open fracture
Soft tissue assessment
Deformity
Abnormal joint mobility – ligamentous injury around joint; in knee, highly likely that popliteal artery is injured as well

THE PULSELESS Things to consider

EXTREMITY Is pulselessness due to shock?
Arterial or venous compromise?
Is there compartment syndrome (pulselessness is a very late sign)
Any pre-existing vascular disease?

Physical examination
Any limb deformity (can result in kinking of vessels)?
Any joint instability (dislocation of a joint can result in intimal tear in the major vessel running
across it, with thrombosis and occlusion)?
Skin colour/temperature
Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent angiogram!
SOFT TISSUE Types
INJURIES Open: laceration, abrasion
Crushing
Degloving: open or closed
Closed

Wound care
Swabs of the wounds for culture and sensitivity
IV antibiotic prophylaxis
Tetanus toxoid cover
Photograph wound (to prevent re-opening of wound by every doctor that comes to see pt)
Betadine (povidone-iodine) dressing
In OT: generous debridement, irrigation (within 4-8 hours, especially in open fractures),
fracture stabilisation (internal or external fixation depending on Gustilo classification)
Leave wound OPEN
MANAGEMENT Recognise fracture and/or dislocation
OF FRACTURES Complete neurovascular examination of the limb involved before reduction
Appropriate X-rays (at least 2 planes)
Analgesia
Correction of deformity
Temporary immobilisation – backslab, malleable splint
Neurovascular examination; examine for compartment syndrome
Circulation chart

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 OPEN FRACTURES
Definition: communication between the # or fracture haematoma and the external environment

Gustilo-Andersen classification
Type I <1cm AND clean
Type II >1cm AND no extensive soft tissue damage, avulsions or flaps
Type IIIA Extensive soft tissue damage, avulsions or flaps but adequate soft tissue
coverage of bone OR High-energy trauma cause regardless of size of wound
Type IIIB Extensive soft tissue loss with periosteal stripping and exposure of bone.
Massive contamination common.
Type IIIC Arterial injury requiring repair

Management of open fractures

Stabilise patient first
Pain relief and analgesia
Cover the wound with moist gauze
Temporary immobilisation and splinting
IV broad spectrum antibiotics
Appropriate X-rays
Nil by mouth
Pre-op investigations: FBC, U/E/Cr, PT/PTT, GXM, ECG, CXR
Arrange for emergency operation
Angiogram if needed

Surgery involves
Generous debridement of the wound with irrigation to decrease bacterial load
Treat any soft-tissue injuries
Stabilise fracture – usually using external fixator

6. POST OPERATIVE COMPLICATIONS

General or specific?
Immediate, early or late?
Local or systemic?

IMMEDIATE Local
(<1 hour post-op) Damage to surrounding structures
Primary haemorrhage (either starting during surgery or following post-op in BP)
Replace blood loss and may require return to theatre to re-explore wound

Systemic
Basal atelectasis (collapse of alveoli):
bronchial secretions post-op & patient does not breathe deeply due to pain
Tx: chest physiotherapy, incentive spirometry
Shock: due to blood loss, or inadequate fluid replacement peri-operatively
AMI, pulmonary embolism
EARLY Local
(first 24-48 hours Pain, hemorrhage
post-op)
Systemic
Atelectasis (commonest cause of mild pyrexia in first 48hr)
Shock, AMI, PE
Nausea & vomiting (analgesia/anaesthesia induced)
Acute confusion: dehydration or sepsis (post-op confusion seen in 40%)

14
LATE Local
(between 48 hours Post-op paralytic ileus
to 1 month post-op) Wound or anastomotic dehiscence (POD 7 – 10)
Serosanguinous exudate
Tx: Analgesia, sterile wound dressing, fluid resuscitation, resuture under GA in OT
Mortality up to 30%
Post-op wound infection (usu within 1st week post-op)
Pain, redness, swelling, discharge, usually due to skin staphylococci
Incisional hernia
10-15% of abdominal wounds
Usu asymptomatic, but if painful, consider strangulation (uncommon due to wide neck)
RF: Obesity, poor muscle tone (old age), (increased intra-abdominal pressure (chronic
cough, straining from constipation), wound infection, multiple use of same incision site
Tx: Surgical repair of hernia if strangulated or if enlarging
Bowel obstruction due to adhesions
Fistula formation
Secondary haemorrhage: often as a result of infection (usu 1-2wk post-op)

Systemic
Fever:
Wind (atelectasis), Water (UTI), Walking (DVT/PE), Wound (infxn), Wonder drug (drug fever)
Infections (day 3-5): phlebitis, pneumonia, UTI, abscesses (subphrenic, pelvic)
Acute confusion: exclude dehydration & sepsis
DVT & PE (day 5-7)

POST-OP HAEMORRHAGE

EARLY Consumptive coagulopathy – if large volumes of blood transfused

Pre-op anticoagulation
Unrecognized bleeding diathesis
Damage to blood vessels/vascular organs

Management
FBC (plt), PT/PTT, GXM & order blood
Give protamine if heparin was used
Give FFP / platelet concentrates if clotting screen abnormal
Consider surgical re-exploration
LATE Usually due to infection damaging vessels at the operation site
Occurs several
days after surgery Management
Treat infection and consider exploratory surgery

POOR WOUND HEALING

Patient factors Wound factors Surgeon factors

Poor blood supply Wound infection Suturing under tension
Malnutrition Poor wound care Did not observe aseptic
Vitamin deficiency technique
Immunosuppressive therapy
Long term steroids
Radiotherapy
Co-morbidities e.g. DM, HIV

15
DVT/PE

Affects 25-50% of surgical patients

DVT in deep calf veins: 5-10% risk of PE
DVT in iliofemoral veins: 50-60% risk of PE

Risk Factors Prolonged bed rest, pregnancy (IVC compression)

Virchow’s  Triad Trauma, pelvic/ vascular surgery, intravenous drug use
1) Alterations to flow Congenital: protein C/ protein S deficiency, Factor V Leiden mutation, anti-
2) Endothelial injury phospholipid syndrome, homocysteinuria/homocysteinemia
3) Hypercoagulable state Acquired: liver disease, cancer (production of pro-thrombotic factors), OCP use

Presentation Post-operative fever (typically day 5-7)

Lower limb pain & swelling, discolouration: may not be at site of clot
Classic triad of PE: chest pain, dyspnoea, haemoptysis (poor sensitivity/specificity)
Others: seizures, syncope, new onset atrial fibrillation etc

Physical Examination Mild fever

Calf warmth, tender, swelling, erythema
Pitting oedema
Homan’s  sign: passive dorsiflexion of the ankle with knees flexed sharp pain in calf
(DON’T  DO:  risk  of  clot  propagation/  dislodging)

Investigations Duplex ultrasound to detect DVT

Chest x-ray: usually normal (classical findings listed below are rarely seen)
Atelectasis,
pleural effusion,
raised hemi-diaphragm

Westermark sign: dilatation of

the pulmonary vessels proximal
to the embolism, with collapse
of the distal vessels (oligemia)

Hampton hump: late sign,

wedged shaped infiltrate with
apex towards the hilum
CT pulmonary angiogram (gold standard)
Look for filling defects in pulmonary artery
V/Q perfusion scan: no longer done
Inhale radioactive isotope, do CXR to assess ventilation of lungs
IV contrast, do CXR again to assess perfusion of lungs
Look for areas of ventilation without perfusion (V/Q mismatch)
Correlate with clinical findings, calculate probability of PE
ECG
May have normal ECG with sinus tachycardia
Signs of right heart strain
Right axis deviation: S waves in lead I
Right ventricular hypertrophy: tall R waves in V1, deep S waves in V6
Right atrial hypertrophy: peaked P waves
RBBB
Classic S1Q3T3: S wave in I, Q wave in III, T inversion in III (rarely seen)
D-dimer: poor sensitivity & specificity in ruling in/ out DVT or pulmonary embolism

16
Prophylaxis/ Treatment Non-pharmacological
Use of inflatable calf pumps intra-operatively in patients undergoing long operations
Early ambulation post surgery
Thromboembolic deterrent (TED) stockings/ intermittent pneumatic leg compression

Pharmacological
Unfractionated heparin or LMW heparin – acute setting

Unfractionated heparin
Potentiates effect of anti-thrombin III, inactivates thrombin (PTT )
Onset: immediate for IV; 30 mins subcutaneously
Efficacy monitored using aPTT
Antidote: protamine sulphate
Side effects: thrombocytopaenia

LMW heparin (Clexane)

Potentiates effect of anti-factor 10a (not reflected by PTT)
Onset: immediate for IV
More predictable dose-effect relationship
Reversibility by protamine sulphate limited

Warfarin – long term (8-9 months, or until clot dissolves)

Vitamin K antagonist, inhibits synthesis of Vit K dependent factors (II, VII, IX, X)
Onset: 2 to 4 days (start by overlapping with heparin for 4 days)
Efficacy monitored using PT/INR (target INR: 2.0 to 3.0)
Antidote: vitamin K, FFP
SE: haemorrhage, hepatitis, skin necrosis (in patients with protein C/S deficiency)

Surgical
IVC filter (permanent or temporary: remove after 2 weeks of anti-coagulation)
Indications: History of recurrent DVT/PE
Free floating thombus seen on duplex scan
Patient not suitable for anti-coagulation e.g. up to 7 days post-op
Allergy to anti-coagulation

Treatment of Pulmonary Embolism

Supplemental oxygen,, intubation, mechanical ventilation
Initiate anti-coagulation
Intra-venous thrombolytics if not contraindicated
Surgical/ catheter embolectomy

Well’s Criteria Clinical feature Score

Active cancer (treatment ongoing or within the previous 6 months or palliative) 1
A set of criteria to Paralysis, paresis, or recent plaster immobilization of the lower extremities 1
determine the pretest Recently bedridden for more than 3 days or major surgery, within 4 weeks 1
probability of DVT Localized tenderness along the distribution of the deep venous system 1
Entire leg swollen 1
Calf swelling by more than 3 cm when compared to the asymptomatic leg 1
(measured below tibial tuberosity)
Pitting edema (greater in the symptomatic leg) 1
Collateral superficial veins (nonvaricose) 1
Alternative diagnosis as likely or more likely than that of deep venous thrombosis -2

High  Probability:  ≥  3  – treat as susp DVT and perform compression U/S

Moderate Probability 1 or 2 – treat as susp DVT and perform compression U/S
Low  Probability  ≤0  – D-dimer test

17
 7. SHOCK

Shock = inadequate tissue & organ perfusion to meet metabolic demands cellular hypoxia
S/S: BP, urine output, tachycardia, diaphoresis, AMS

TYPES OF SHOCK

Types Hypovolaemic Cardiogenic Neurogenic Obstructive Septic Anaphylactic

Causes Haemorrhage AMI Spinal injury Tension Infxns
Burns Dysrhythmia pneumothorax
Ruptured Cardiac
ectopic tamponade
pregnancy Pulmonary
Severe GE embolism
Acute
pancreatitis
S/S Pallor Pallor Warm skin Fever, rigors Fever, rigors
Cold clammy skin Cold clammy skin N/ heart rate Warm skin Warm skin
peri vas peri vas Neuro deficit
Invxs Hct (late) Cardiac enzymes FBC
ECG Bld C/S

GENERAL MANAGEMENT

AIRWAY Maintain airway – consider intubation if necessary

BREATHING 100% O2 via non-rebreather mask
CIRCULATION 2 large bore (14-16G) cannulae
Inotropic support
IV dopamine 5-10 g/kg/min
IV dobutamine 5-10 g/kg/min (esp for cardiogenic shock)
IV norepinephrine 5-20 g/kg/min (esp for septic shock)
MONITORING Pulse oximetry
ECG
BP
Heart rate
Urine output – catheterize patient

SPECIFIC MANAGEMENT

HYPOVOLAEMIC FBC – Hct (but inaccurate marker of acute blood loss - Hct in alcoholic binge from dieresis)
SHOCK GXM 6 units
U/E/Cr
Trop T (Cardiac enzymes)
Coagulation profile with DIVC screen (PT/PTT, D-dimer)
ABG – metabolic acidosis, lactate, base deficits = poor prognostic factor
UPT – r/o ectopic pregnancy (ask for LMP)
Examine the abdomen for any pulsatile AAA
Fluid resus: 1L crystalloid fast infusion over 1 hr
Assess response
Subsequent colloid or whole blood infusion
CVP line insertion – to guide fluid resus
CARDIOGENIC ECG, Trop T & cardiac enzymes
SHOCK Manage accordingly to cause – refer Emed book

18
OBSTRUCTIVE Tension Pneumothorax
SHOCK Decompression: insert 14G cannula over 2nd intercostals space in mid-clavicular line

Cardiac Tamponade
IV fluid bolus 500ml N/S
IV dopamine infusion 5 g/kg/min
Prepare for pericardiocentesis

Pulmonary Embolism
FBC, GXM x 6 units, U/E/Cr, D-dimer
ABG: PaO2 & N/ PaCO2, widened alveolo-arterial PO2 gradient (AaPO2 >20mmHg)
ECG
CXR (Exclude Ddx – pneumothorax, pneumonia, heart failure, tumour, rib #, pleural effusion, collapse)
Pulmonary angiogram (gold standard)
Pain relieve – use opioids with caution (resp depression)
Fluid resus & inotropic support if haemodynamically unstable
Anticoagulation:
IV heparin 5000U bolus OR subcut fraxiparine (0.4ml <50kg, 0.5ml 50-65 kg, 0.6ml >65kg)
Convert to oral warfarin later
Thrombolysis: intra pulm arterial urokinase for 12-24hrs
Surgical: complete IV ligation or partial caval interruption
NEUROGENIC Trauma – site, mechanism, force
SHOCK Neuro exam, DRE – document initial neurological deficits
Immobilize spine in neutral position
C-spine X-ray (AP & lat) – ensure visualization up to C7/T1 junction
Swimmer’s  view  (visualize  C7/T1  jn)  &  open  mouth  view  (visualize  C1/2  injury)
Thoracic & lumbar spine X-ray (AP & lat)
CT scan
MRI later
Titrate fluid resus with urine output
vasopressors if BP does not respond to fluid challenge
IV methyl Prednisolone 30 mg/kg over 15mins, followed by 5.4mg/kg/h for nxt 23 hrs
Indications – non-penetrating spinal cord injury & w/in 8 hrs of injury
Contraindications: <13YO
Pregnancy
Mild injury of the cauda equina / nerve root
Abdominal trauma present
Major life-threatening morbidity
Refer Ortho / NeuroSx
SEPTIC SHOCK SIRS = 2 of the following present: Temp >38 or <36oC
(SIRS + source of HR > 90bpm
sepsis + shock) RR > 20 breaths/min OR PaCO2<32mmHg
WCC>12000/mm3, <4000/mm3,or >10% immature forms

Identify site of infxn – UTI (indwelling cathether), gallbladder dz, peritonitis, pneumonia,
appendicitis, immunocompromised state
FBC, U/E/Cr, DIVC screen (PT/PTT, fibrinogen, D-dimer), blood C/S, ABG, CXR, ECG,
UFEME and urine C/S)
Rapid infusion 1-2L crystalloids
CVP line insertion
If no response to fluid Rx inotropic support
Noradrenaline (drug of choice) - 1 g/kg/min OR
Dopamine 5-20 g/kg/min

19
 Empirical Abx:
Immunocompetent w/o 3rd gen cephalosporin (IV ceftriaxone 1g) OR
obvious source Quinolones (ciprofloxacin 200mg)
Immunocompromised w/o Anti-pseudomonal ABx (IV ceftazidime 1g) OR
obvious source Quinolone
PLUS aminoglycoside (Gentamicin 80mg)
Gram-positive (burns, FB / IV cefazolin 2g
lines present) IV vancomycin 1g (if IVDA, indwelling cath, pen allergy)
Anaerobic source (intra- IV metronidazole 500mg
abdo, biliary, female + ceftriazone 1g
genital tract, aspiration + IV gentamicin 80mg
pneumonia)
ANAPHYLACTIC Definitions
SHOCK Urticaria – oedematous & pruritic plaques w pale centre & raised edges
Angioedema – oedema of deeper layers of the skin. Non-pruritic. May be a/w numbness & pain
Anaphylaxis – severe systemic allergic rxn to an Ag. Ppt by abrupt release of chemical
mediators in a previously sensitized patient
Anaphylactoid rxn – resembles anaphylactic rxn, but due to direct histamine release from mast
cells w/o need for prior sensitization

Common causes
Drugs – penicililns & NSAIDS commonest, aspirin, TCM, sulpha drugs
Food – shellfish, egg white, peanuts
Venoms – bees, wasps, hornets
Environment – dust, pollen
Infections – EBV, HBV, coxsackie virus, parasites

Stop Pptant
Stop administration of suspected agent / flick out insect stinger with tongue blade
Gastric lavage & activated charcoal if drug was ingested
Airway
Prepare for intubation or cricothyroidectomy – ENT/Anaesthesia consult
Fluid Rx
2L  Hartman’s  or  N/S  bolus
Drug Rx
Adrenaline Normotensive – 0.01ml/kg (max 0.5ml) 1:1000 dilution SC/IM
Hypotensive – 0.1ml/kg (max 5ml) 1:10,000 dilution IV over 5 mins
Glucagon Indications: failure of adrenaline Rx OR if adrenaline is contraindicated
e.g. IHD, severe HPT, pregnancy, -blocker use
0.5-1.0mg IV/IM. Can be repeated once after 30mins
Antihistamines Diphenhydramine 25mg IM/IV
Chlorpheniramine 10mg IM/IV
Promethazine 25mg IM/IV
Cimetidine For persistent symptoms unresponsive to above Rx
200-400mg IV bolus
Nebulised For persistent bronchospasm
bronchodilator Salbutamol 2:2 q20-30mins
Corticosteroids Hydrocortisone 200-300mg IV bolus, q 6hr

20
8. PERIOPERATIVE CARE

INPUT / OUTPUT
Normal daily intake Normal daily output
Water
Diet 2300 ml Urine 1400ml (min obligatory volume = 400ml)
Metbolism 200ml Skin loss 500ml (obligatory diffusion & vaporisation)
Sweating in pyrexia / heat can cause several litres extra loss per day
Lung loss 500ml (obligatory)
Faecal loss 100ml
Sodium
Diet 150 mmol/day Stool 5 mmol/day
(range 50 – 300 mmol) Skin transpiration 5 mmol/day (in absence of sweating)
Urine 140 mmol/day (can fall to 15 mmol/day)
Potassium
Diet 100 mmol/day Stool 10 mmol/day (obligatory)
(range 50 – 200 mmol) Skin < 5 mmol/day
Urine 85 mmol/day (rarely falls below 60 mmol/day)

DAILY GASTROINTESTINAL SECRETIONS & ELECTROLYTE COMPOSITION

Secretion Volume (L) Na (mmol/L) K (mmol/L) Cl (mmol/L) HCO3 (mmol/L)
Saliva 1 – 1.5 20 – 80 10 – 20 20 – 40 20 – 160
Gastric juice 1 – 2.5 20 – 100 5 – 10 120 – 160 Nil
Bile Up to 1 150 – 250 5 – 10 40 – 60 20 – 60
Pancreatic juice 1–2 120 5 – 10 10 – 60 80 – 120
Small bowel 2–3 140 5 Variable Variable
secretions (up to 40 in
(succus entericus) inflammatory diarrhoea)

DAILY REQUIREMENTS
Fluid 100 ml/kg/day
Na 2 mmol/kg/day
K 1-2 mmol/kg/day

PARKLAND’S FORMULA FOR BURNS DAILY CALORIC REQUIREMENTS

2-4 ml / kg (body wt) / % (BSA of burn) 2000 – 2500 kcal/day
Divide total volume into 2 halves CALORIC CONTENTS
Infuse 1st half in 1st 8h Glucose: 4 kcal/g
Infuse the rest in next 16h Protein 4 kcal/g
Start time = time of burn injury
Fats: 9 kcal/g
Fluid  of  choice  =  Hartmann’s  solution
Alcohol: 7 kcal/g

21
FLUIDS / MAINTENANCE

Body composition
Total body water = 55% body weight
Extracellular fluid = 20% body weight
Blood volume = 7% body weight
Acute blood loss required to produce shock = 25-30% of blood volume

Basal requirements Deficits Ongoing/ anticipated losses

Children have higher water content Thirsty: 1.5L deficit Insensible losses
(higher metabolic rate, greater surface Tachycardia: 3L deficit o Every 100kcal burned =
area to body weight ratio) Hypotensive: 6L deficit 30ml loss through skin
o Losses 10% for every
Holliday-Segar method: deg of fever > 37°C
1st 10 kg – 100 ml/kg/day (5ml /kg/hr) Sweat
2nd 10 kg – 50 ml/kg/day (2ml /kg/hr) GIT
> 20 kg – 20 ml/kg/day (1ml /kg/hr) Urine (normal = 0.5 – 1 ml/kg/hr)
Blood
Respirators

Components of regularly used IV fluids

0.9% NaCl/ Normal saline (NS) 9g Na in 1L / 154 mmol Na & Cl (isotonic)
Dextrose 5% (D5W) 50g glucose in 1L (200kcal; 1g glucose = 4kcal) (isotonic)
Dextrose 5% in 0.9% NaCl (D5NS) 50g glucose + 9g Na in 1L (hypertonic)
Hartmann’s  solution  /  Ringer’s  lactate Na 131 mmol/L
Cl 111 mmol/L
K 5 mmol/L
Ca 2 mmol/L
Lactate 29 mmol/L

Amount of required (KCl) infused in divided doses over 24h Sample daily IV fluid regimen
Premixed IV fluids are generally available with 20 or 40 mmol of KCl
per 500ml or 1000ml infusion bags 1L NS + 20 mmol KCl +
If concentrations of KCl > 40 mmol in 500ml are required, they 1L D5W + 20 mmol KCl +
should be given via infusion in the ICU with cardiac monitoring 1L D5W + 20 mmol KCL
Added K is not usually required in the 1st 24-48h after surgery (each bag given over 8 h)
because K is released from damaged cells
Total: 154 mmol Na + 60 mmol K
HCT

From loss of pure plasma (burns/pancreatitis/peritonitis): 1 point = 100ml loss of fluid

From loss of isotonic extracellular fluid (GIT): 1 point = 500 ml loss of fluid
From loss of pure water (evaporation from lungs): no change

CHOICE OF FLUID REPLACEMENT

If pt losing blood blood transfusion

Diarrhoea / vomiting crystalloids
Burns pt (losing protein) colloids

22
CVP MONITORING

Swan-Ganz/ pulmonary artery catheter

Pressure in RA
Pressure in PA
Pulmonary capillary wedge pressure
(indirect estimate of LA pressure)

Normal CVP = 5 – 10 mmHg

Useful in evaluating blood volume status when

fluids are administered during hypotensive shock
Administer fluids at a rate that maintains CVP at
12 – 15 mmHg (cardiac output optimal)

Ohm’s  Law:
𝑀𝐴𝑃 − 𝐶𝑉𝑃
𝐶𝑂 =     × 80
𝑆𝑉𝑅

VENTILATION

Ventilator settings
Tidal Volume = vol of air in each breath (8-12 cm3 /kg)
Rate = no of breaths delivered per min
FiO2 = amt of O2 delivered (N = 40%; the higher it is , the more O2 damage to the lungs)
PEEP = positive end expiratory pressure (opens alveoli that would otherwise collapse in expiration)
o Normal: 3 – 5 cmH2O (physiologic PEEP)
o Therapeutic PEEP can go up to 10 – 35 cmH2O (but too high impedes venous return to the heart)

Atelectasis = V/Q mismatch (shunt)

23
ACID BASE & ELECTROLYTES

Metabolic Acidosis pH < 7.35 [HCO3] < 20 mmol/L

Respiratory Acidosis pH < 7.35 PCO2 > 45 mmHg
Metabolic Alkalosis pH > 7.45 [HCO3] > 24 mmol/L
Respiratory Alkalosis pH > 7.45 PCO2 < 35 mmHg

Anion gap = [Na] – [Cl] – [HCO3]

Normal = 3-11 mmol/L
Hypoalbuminemia: anion gap in 2.5 mmol/L for every 1 g/dL of albumin
Elevated anion gap = HAGMA even in the presence of a normal pH / [HCO3]

Compensation

Metabolic [HCO3] 1 mmol/L = PCO2 1.2 mmHg

Acidosis
Expected PCO2 = (1.5 x [HCO3]) + 8 mmHg
PCO2 < expected concurrent respi alkalosis
PCO2 > expected concurrent respi acideosis

Calculate change in anion gap ( AG)

AG + [HCO3] = normal [HCO3] HAGMA
AG + [HCO3] > normal [HCO3] concurrent metabolic alkalosis
AG + [HCO3] < normal [HCO3] concurrent NAGMA

Metabolic [HCO3] 1 mmol/L = PCO2 0.7 mmHg

Alkalosis
Expected PCO2 = (0.6 x [HCO3 – 24]) + 40 mmHg
PCO2 < expected concurrent respi alkalosis
PCO2 > expected concurrent respi acidosis

Respiratory Acute: PCO2 1 mmHg = [HCO3] 0.1 mmol/L Acute: [HCO3] 1-2 mmol/L for
Acidosis Chronic: PCO2 1 mmHg = [HCO3] 0.4 mmol/L every PCO2 by 10 mmHg
Chronic: [HCO3] 4-5 mmol/L
Respiratory Acute: PCO2 1 mmHg = [HCO3] 0.2 mmol/L for every PCO2 by 10 mmHg
Alkalosis Chronic: PCO2 1mmHg = [HCO3] 0.4 mmol/L

If pH normal, check for balanced acid base disorder:

[HCO3] < 20 PCO2 < 35 Metabolic acidosis + Respiratory alkalosis

[HCO3] > 24 PCO2 > 45 Metabolic alkalosis + Respiratory acidosis
[HCO3] & PCO2 normal AG > 11 HAGMA + metabolic alkalosis
[HCO3] & PCO2 normal AG normal Normal (unlikely NAGMA + metabolic alkalosis)

24
 Hyponatremia Hypernatremia
Signs Confusion Thirst
Seizures Dehydration
Cardiac failure Confusion
Muscle weakness Coma
Nausea, anorexia Seizures
Causes Diuretics (esp thiazides) Fluid loss w/o water replacement (esp burns)
Water excess Saline excess
Diarrhoea / vomiting Diabetes Insipidus
Intestinal fistula DKA
Cardiac failure / Renal failure Conn’s  syndrome
SIADH
Addison’s  disease
Treatment Rehydration with appropriate sodium- Encourage oral intake
containing IV fluids IV fluids with low sodium content
Diuretics for cardiac failure
Fluid restriction to 1L per day

Hypokalemia
Signs Cardiac arrhythmias
Muscle weakness
Hypotonia (& GI motility
Muscle cramps Tetany
Causes Diarrhoea / vomiting
Intestinal fistula
Diuretics
Renal tubular failure
Cushing’s  /  exogenous  steroids  /  ACTH
Conn’s  syndrome   Burns
Metabolic alkalosis
Treatment Oral potassium supplements
KCl added to IV fluids
Hyperkalemia
Cardiac arrhythmias
Sudden death
paralytic ileus)
Sampling artefact (haemolysis)
Drugs (ACEI, spironolactone, suxamethonium)
Digoxin poisoning
Massive blood transfusion
KCl excess
Rhabdomyolysis
Tumour lysis
Renal failure
Addison’s  disease
Metabolic acidosis
1. Calcium gluconate 10% (50-100ml)
2. Insulin 20 units
+ 250ml 25% dextrose over 4-6 hrs
3. Diuretics
4. 2 adrenergic agonists
5. Sodium bicarbonate (50 – 100ml)
6. Resin (polystyrene sulfonate sodium)
(every g exchanges 3 mmol of Na for K)
7. Hemodialysis (definitive)

25
NUTRITION

Nutritional support should be considered for:

BMI < 18.5
Unintentional weight loss > 10% BW within last 3 – 6 months
BMI < 20 and unintentional weight loss > 5% within last 3 – 6 months
Poor oral intake for > 5 days
Poor absorptive capacity, high nutrient losses, increased catabolic rate

REFEEDING SYNDROME
Gastric emptying one of the last aspects of gut function to recover after an operation/major insult
Risk factors: low BMI, duration of reduced intake, degree of weight loss, electrolyte abnormalities
Feeding should be introduced gradually over 48 – 72 hours (Safe to start feeding at 50% of estimated protein and
calorie requirements and build up to full requirements over a 24 – 48 hour period.)

ENTERAL FEEDING
Start at 20ml/h x 6h, then increase by 20-30ml/h and repeat.

Indications:
Proximal small intestine intact & functional
Stimulation of secretory function does not worsen the condition being treated (e.g. small bowel fistula)

Contraindications:
Complete small bowel obstruction
Inadequately treated shock states (risk of intestinal ischemia)
Severe diarrhoea (slow rate of feeding)
Proximal small intestinal fistula
Severe pancreatitis

Routes:
Nasogastric tube feeding
Nasojejunal or nasoduodenal feeding (when gastric emptying is a problem)
Tube enterostomy
Percutaneous endoscopic gastrostomy
Complications: infection at PEG site, blockage/extrusion/removal, peritonitis, aspiration pneumonia

Complications of enteral feeding:

Fistulation
Wound infection
Peritonitis
Displacement & catheter migration
Blockage of tube
Aspiration pneumonia
Feed intolerance
Diarrhoea

Types of Oral Feeds:

Ensure (protein 9g /serving)
Ensure Plus (highly concentrated in calories 1.5 cal/ml & protein 13 g/serving)
Glucerna (for DM pts carbohydrates, modified fat)
Pulmocare (for COPD pts high calorie, low carb to help CO2 production)
Novasource Renal (for renal pts low protein & nitrogen content)

26
TOTAL PARENTERAL NUTRITION
Provision of all nutritional requirements by the intravenous route alone
Due to high osmolality of the mixture, TPN must be given into a central vein

TPN orders:
24 hr feeding volume 2500ml, rate 100ml/hr
5 days a week: kcal from carbohydrate 2500, kcal from fat 0
2 days a week: kcal from carbohydrate 2000, kcal from fat 500

Indications:
Critical illness: where enteral feeding is not established within 5 days
Obstruction of GIT: proximal small bowel obstruction not immediately relieved
Short bowel syndrome:
o Temporary (before adaptation) in < 3m of functional small intestine
o Permanent in < 1m of functional small intestine
Proximal intestinal fistula: facilitate fistula closure
Refractory  inflammatory  disease  of  the  GIT  (e.g.  Crohn’s,  UC)
Inability to use the GIT: pancreatitis with pseudocysts/abscess where enteral nutrition is not tolerated

Complications:
Catheter-related
o Mechanical: blockage, central vein thrombosis, migration, fracture, dislodgement
o Infective: exit-site infection, line sepsis, infective endocarditis
Metabolic
o Hyperglycaemia
o Deranged liver function: biliary stasis, enzyme induction from amino acid imbalance and excessive calorie
administration, fat deposition in liver
o Hypoglycaemia (too rapid cessation of glucose infusion)
o Hypertriglyceridemia
o Hyperchloraemic acidosis

27
2. LUMPS & BUMPS

1. HERNIA

Hernia = a protrusion of an organ through an opening in the wall of the cavity in which it is normally contained
Lifetime risk = 2-10%
Causes of abdominal wall weakness
- Congenital – normal (due to piercing structures), or patent processus vaginalis
- Acquired – trauma, surgical incision or disease
Consist of 3 parts:
- Sac: pouch of peritoneum (neck & body)
- Coverings of sac: layers of abdominal wall
- Contents

Types:
1) Inguinal (96%) indirect (85%), direct (15%) or pantaloon (direct & indirect)
2) Femoral (4%) & Richter’s  hernia (knuckle of bowel wall is strangulated but lumen is patent)
3) Incisional, Parastomal
4) Umbilical, Epigastric (herniation of extra-peritoneal fat)
5) Rare types: Spigelian (herniation of linea semilunaris: lat. border of rectus), Obturator, Lumbar, Gluteal, Internal, Sliding
(herniation of posterior peritoneum with underlying retroperitoneal structures: caecum, sigmoid, bladder)

PHYSICAL EXAMINTION (common signs)

- Location: all occur at congenital or acquired weak spots in the abdominal wall
- Reducibility: on direct pressure or lying down
- Expansile cough impulse

28
INGUINAL HERNIA: indirect or direct;

Indirect inguinal hernia:

- Most common; 65%
- Congenital; patent processus vaginalis + weakened fascia at deep ring
- Hernial sac enters the inguinal canal with the spermatic cord via the deep ring, then emerges from the superficial ring &
descends into the scrotum
- ♂ > ♀,  R>  L,  20%  are  bilateral,  children>adults

Direct inguinal hernia:

- Bulges directly ant though a weakened fascia Hesselbach’s triangle, post to the inguinal canal (med to inferior epigastric art)
Hesselbach’s  ∆:  inf.  Epigastric  art.,  rectus  abd,  inguinal  ligament

- Hernia sac is not with the spermatic cord

- Rare  in  ♀,  usually  occur  bilaterally in  ♂  with  
weak abdominal muscles and
comorbid  conditions  causing  ↑  intra-abdominal pressure

Clinical differences between indirect and direct inguinal hernia

Indirect Hernia Direct Hernia

Neck lies lateral to inferior epigastric artery, Neck lies medial to inferior epigastric artery,
out  of  Hasselbach’s  triangle within  Hasselbach’s  triangle
Reduces upwards, laterally and backwards Reduces upwards and straight backwards
Controlled after reduction by pressure over the deep ring Controlled after reduction by pressure over the superficial ring
May descend down the scrotum Does not descend down the scrotum
May cause strangulation at superficial ring (narrow) Rarely causes strangulation due to wide hernia neck
Does not readily reduce on lying down Readily reduces on lying down
More common in young adults and infants More common in old men

29
Anatomy of inguinal canal

- 4 to 6 cm long oblique passage above the inguinal ligament, from the deep to superficial rings.
- Deep inguinal ring lies in the midpoint of the inguinal LIGAMENT & is formed from a defect in the transversalis fascia.
- Superficial ring is a triangular defect in the aponeurosis of the external oblique.

Boundaries:
Ant. wall: aponeurosis of the
external oblique (reinforced in
lat. third by internal oblique)
Post. wall: transversalis fascia
(reinforced in med. third by
conjoint tendon)
Roof: arching fibres of the int.
oblique & transversus
abdominis before they merge as
conjoint tendon
Floor: inguinal ligament and
lacunar ligament medially

Contents:
Ilioinguinal nerve (L1): supplies
skin over root of penis & upper
part of scrotum or skin over mons
pubis & labia majora
♀:  round  ligament  of  the  uterus  
from uterus to labia majora
♂:  transmits  spermatic  cord  from  
abdomen to testes

Anatomy of the spermatic cord

Coverings: 3 concentric layers of fascia

Internal spermatic fascia:
derived from transversalis fascia
Cremasteric fascia & muscle:
derived from internal oblique
External spermatic fascia:
derived from external oblique

Contents:
3 Arteries:
Testicular artery
Artery to the vas deferens
Cremasteric artery
3 Nerves:
Nerve to cremaster
Autonomic nerves (T10)
Genital br of genitofemoral nerve
3 Others:
Vas deferens
Pampiform venous plexus
Lymphatics

30
Complications
Reducible  →  Irreducible  /  Incarcerated  →  Obstructed  →  Strangulated
- Irreducible/ Incarcerated hernia: contents of hernial sac cannot be replaced into abdomen
- Obstructed: loop of bowel trapped in hernial sac such that its lumen, but not blood supply, is obstructed (no ischaemia
not unduly tender, but with IO)
- Stangulated: blood supply to trapped bowel is cut off, bowel is dead or dying; 6hrs to gangrene.
(acutely tender with s/s of IO;;  exception:  Richter’s  hernia:  segment  of  bowel  is  trapped  &  ischaemic  but  lumen  is  patent
no IO)

Management

Non-surgical:
Raised intraabdominal pressure
o Weight loss, change jobs, avoid heavy lifting
o Treat medical conditions causing chronic cough, chronic constipation
Truss: for compression of reducible hernia at deep ring (poor pickup rate)
If obstructed/strangulated: NBM, IV drip, NG tube on suction, IV ABx

Surgical:
Hernioplasty/ Herniorraphy with mesh repair (open or laparoscopic)
o Immediately if suspect incarceration to prevent any bowel perforation
Principles: reduce bowel, ±excise hernia sac, reinforce posterior wall
o Lichtenstein tension-free mesh repair (lightweight, polypropylene mesh insertion & suture)
o Shouldice repair (non-mesh technique: 2 continuous back & forth sutures with permanent suture material)
Complications
o 2o to GA: AMI, CVA
o Immediate to early
1. ARU
2. Bruising , bleeding (testicular, cremasteric, artery to vas deferens, inferior epigastric, femoral arteries)
3. Injury to surrounding structures pain, parasthesia, impotence: spermatic cord (vas deferens,
testicular artery), round ligament, ilioinguinal nerve, nerve to cremaster
o Early
1. Infection of wound/ mesh
2. Haematoma (10%; no cough impulse, non-reducible, hard)
3. Wound dehiscence
4. pain
o Late
1. Chronic post-op pain
2. Recurrence of hernia (<0.5%; incomplete dissection, poor tissue, too early mobilization, uncontrolled co-
morbidities)
3. Ischaemic orchitis & Testicular atrophy from testicular artery damage or from pampiniform plexus
thrombosis

Post- operation monitoring:

o Work leave for 6/52 with avoiding of heavy lifting
o Treat any medical conditions to avoid coughing, constipation
o Early mobilization from D10
o Keep area clean and wash carefully, but able to bathe immediately
o Abx cover???

31
APPROACH TO AN INGUINAL HERNIA
1. Groin vs Inguinoscrotal
2. Risk factors:
3. Complications
4. Patient profile
5. Treatment:
6. Post-op complications
a) groin cough impulse
b) inguinoscrotal 1. cough impulse (may not be present in a large one)
2. cannot get above lump
3. cannot separate from testis
Increased intra-abdo pressure: chronic cough, BPH, chronic constipation
Also 4Cs: cirrhosis, heart failure, cancer, catheter (dialysis)
a) Obstructed/ Strangulated
b) Spontaneous rupture
c) Involved in peritoneal diseases
- Indirect: M, young, right, increase intraperitoneal fluid
- Direct: M, old, raised intraabdominal pressure
a) OPEN hernia repair!!!
b) Lap only if 1. Recurrent, 2. Bilateral (2 types of lap: TEP, TAP)
c) Conservative only if: small, easily reducible, direct hernia
a) Immediate: bruise, wound hematoma, scrotal hematoma, ARU, pain
b) Later: mesh infection, recurrence (10% /10years), nerve injury, ischemic orchitis

EXAMINATION OF AN INGUINAL HERNIA

“Please  examine  this  patient’s  groin”

Don gloves, introduce yourself and explain your intention, then expose the patient
STAND patient up, examine both sides
- Mr X is a ___ who appears comfortable at rest.
- I notice a groin / inguinoscrotal lump.
Squat down and examine!
- Inspect as per a lump: (if unable to see, ask the patient)
1. Is lump above or below the inguinal ligament? Any scrotal lump?
2. Estimate the dimensions of the lump
3. Any skin changes? Previous scars (look hard)?
4. Any lump on the other side?
5. Abdominal distension / visible abdo mass?
- Sir, could you turn head and cough? Look for Visible cough impulse (seen in large inguinoscrotal hernias)
- Sir, is there any pain over the groin area? I am going to feel the lump.
Palpate:
1. Can get above the lump?
2. Can feel testis?
3. Lump: consistency (soft, fluctuant), size, temperature, any tenderness?
4. Sir, could you turn head and cough again? Feel for Palpable cough impulse (bilaterally?)
- Sir, could you reduce the lump for me?
o Reducible: The point of reduction is  “above  and  medial  to  the  pubic  tubercle”  (superficial  ring)
o Incarcerated: The patient is unable to reduce the lump.

Lay the patient supine.  (supposing  you’re  standing  on  patient’s  LEFT)
- Reduce the hernia if patient has not done so.
- Locate the Deep inguinal ring: [vice versa for right side]
o Left  hand  define  pt’s  pubic  tubercle:  from  umbilicus  down   pubic symp. to the left 1st bony prominence
o Right hand define the ASIS
o Left hand to the midpoint of inguinal ligament 2cm above
- Keep pressure on deep ring, ask patient to sit up & support his pelvis, then swing over the bed and stand

With patient standing:

- Sir, could you turn head and cough?
o if remains reduced – indirect hernia,
o if not, direct hernia. (poor accuracy)
- Remove pressure & watch movement of hernia: slide obliquely (indirect) or project forward (direct)
- Percuss & ascultate for bowel sounds
Examine other side

Offer: Differential diagnosis:

1) Abdo exam: scars, masses, ascites, ARU, constipation, IO - Femoral hernia
2) DRE for BPH, impacted stools - Inguinal LN
3) Respiratory exam for COPD - Hydrocele of the cord (boys), or canal of Nuck (girls)
4) Ask patient for history of heavy lifting - Saphenous varix: [bluish-tinge, disappears on lying supine, also
has positive cough impulse]
- Undescended testes
- Lipoma of the cord

32
FEMORAL HERNIA
- Uncommon, but more common in females
- Rarely put up for exams as it is operated quickly;
- Femoral hernia is a marble shaped lump below the inguinal ligament and medial to femoral pulse
o usually irreducible; narrow neck risk of strangulation is high
o Usually does not have a cough impulse
- DDx:
o Skin/ soft tissue: cyst, lipoma
o Vascular masses: saphena varix, femoral aneurysm, inguinal LAD
o Hernia: inguinal hernia, obturator hernia
o Other: psoas bursa, ectopic testis

Differences between an inguinal and a femoral hernia

Inguinal Hernia Femoral Hernia
Appear through superficial ring above & medial to pubic tubercle Appears through femoral canal below & lateral to pubic tubercle
Usually reducible Usually not reducible
Expansile cough impulse usually present Expansile cough impulse usually absent
Low risk of strangulation High risk of strangulation

Anatomy of the femoral canal

- The femoral sheath is the downward protrusion of
fascia containing the femoral vessels & lymphatics
below inguinal lig.
- The medial compartment of the sheath constitutes
the femoral canal, which carries the lymphatics.
- The superior opening of the femoral canal is known
as the femoral ring.

Boundaries of the femoral ring:

Anterior: inguinal ligament
Posterior: iliopectineal ligament and superior
ramus of pubis
Medial: lacunar ligament
Lateral: femoral vein

INCISIONAL HERNIA
- Extrusion of the peritoneum and abdominal contents through a weak scar or wound on the abdominal wall
- Physical examination similar, just add:
o lifting head off the bed to exacerbate hernia
o palpate to determine the size of defect
- Similar complications as any hernia
- Risk factors:
o Pre-op: age, immunocompromised, obese/ distended abdomen, Malignancy,
o Intra-Op: poor technique of wound closure, placement of drains
o Post-op: wound haematoma, wound infx, early mobilization, post-op coughing
- Treatment options:
o Not all should undergo repair due to high risk of wound haematoma, infection, dehiscence and recurrent hernia
o Conservative:
- Offer corset or truss
- Weight loss and control the risk factors leading to
o Surgical:
- Offer if complications of hernia are present
- Control CVS & resp. disease; encourage pre-op wt loss
- Principles: dissect the sac and close the defect using mesh overlapping

UMBILICAL HERNIA/ PARAUMBILICAL HERNIA

- Uncommon b4 40YO; may grow to large size.
- Cause: defect through the linea alba 2o to stretching the fibers
o Pregnancy, ascites, cyst, fibroids, distention
- Issues of concern:
o Narrow Neck of hernia sac higher risk of strangulation/ infarction
o Fistula formation with discharge of contents may occur
- Management:
o Conservative: treat medcial co-morbidities.
o Surgical:  Mayo’s  Vest  over  pants  operation

33
2. SCROTAL SWELLINGS

ANSWER 4 QUESTIONS:
1. Can you get above the swelling?
2. Can you identify the testis and the epididymis?
3. Is the swelling transilluminable?
4. Is the swelling tender?

Cough impulse
Cannot Reducible
get above Hernia
Testis palpable
swelling Opaque
No cough impulse
Not reducible
Infantile hydrocoele
Testis not palpable
Transilluminable
Chronic haematocoele
Can get Non tender Gumma
above Tumour
swelling Testis not definable from Opaque
Torsion
epididymis
Tender Epididymo-orchitis
Acute haematocoele
Transilluminable Hydrocoele
Non-tender Tumour
swelling of testis

Testis definable from Opaque Non-tender TB epididymis

epididymis swelling of epididymis
Tender Epididymoorchitis
Transilluminable Cyst of epididymis

EXAMINATION OF THE SCROTUM

- “  Examine  this  gentleman’s  scrotum:”

- Always examine him STANDING!
Inspect
- inspect the groin and scrotum: scars and swelling
- groin incisions are usually oblique; scrotal incisions are usually in the median raphe
Palpate
- ask for any pain; when palpate, look at patient for tenderness
- palpate one testes at a time
- if palpated any swelling:
Is it tender?
Can you get above the swelling?
Can you identify the epididymis and testis lump is separate or part of them?
Is it transilluminable?
Offer to:
- Transilluminate the swelling if it is likely at hydrocele
- Continue the examine the groin if it is a inguinoscrotal hernia
- Examine the abdomen

34
HYDROCELE
- Points from examination:
o Very swollen scrotum; uniformly enlarged
o Cannot define testis well; no separable from testis
o Maybe firm, tense or lax
o Maybe transilluminable if acute (less in chronic hydrocele)
o Can get above the mass; the superficial ring is distinct

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

- Types of 1o hydrocele:
o Vaginal hydrocele:
Only in tunica vaginalis & does not extend into the cord
o Hydrocele of the cord
Mass around the cord; attached distally to the testis
Difficult to distinguish from irreducible inguinoscrotal hernia
May extend up and beyond
o Congenital hydrocele: patent processus vaginalis filled with peritoneal fluid
o Infantile hydrocele: hydrocele of cord and congenital hydrocele
- Types of 2o hydrocele
o From testicular tumours
o From torsion
o From trauma
o From orchitis (any inflm)
- Treatment options:
o Conservative:
Watch & wait or Aspiration [tend to reccumulate]
Must exclude a 2o cause
o Surgical:
Lord’s  plication  of  the  sac
Jaboulay’s  operation  to  evert  the  sac

TESTICULAR TUMOUR
- Points from examination:
o Inseparable form the testis; can get above i
o Hard, nodular, irregular, non tender
o Not transilluminable (but maybe a/w hydrocele)
- DDx:
o Chronic infection with scarring
o Long standing hydrocele with calcification,
- Classiccation:
o Mostly seminomas or teratomas
Seminomas: 30-40YO, normal tumour markers, Rx with RT to paraaortic nodes and CT according to
staging
Teratomas: 20-30YO, AFP/ BHCG raised in 90%, Rx with CT
o 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:
o Staging, excision of whole testis with combination chemotherapy

EPIDIDYMAL CYST
- Points from examination:
o Small mass separate from testis; can get above it
o Firm; maybe loculated; transilluminable if large cyst
- Often multiple in the head of epididymis
- May occur as a complication of vasectomy (spermatoceles)
- Treatment:
o Conservative [mainstay]
o Surgical: if painful, very large or frequent recurrences. Complicated by operative damage and fibrosis of
epididymis subfertility

35
VARICOCELE
- Best noticed on palpating the standing patient
- Points from examination:
o Mass is separate from testis; can get above it
o Feels like a bag of worms; +ve cough impulse
o Not transilluminable
- Definition:
o Dilated, tortuous pampiniform plexus
o 98% on Left side: left vein is more vertical, connects to left renal vein, longer than right one, often lacks a
terminal valve
- Causes:
o Idiopathic in younger males around puberty
o In older men with retroperitoneal disease: RCC

- Treatment options:
o Conservative: risk of infertility
o Surgical:
Transfemoral radiological embolization with coil or sclerosant
Excise the surrounding veins via high retroperitoneum, inguinal or laprascopic approach

TESTICULAR TORSION (Surgical emergency)

- Clinical features:
o Children/ teenagers
o acute abdomen (T10 inervation) & acute scrotum a/w vomiting
o swollen and tender scrotum, testis is high in scrotum; pain worsen by lifting testis up
o Previous attacks of self limitng pain; ppt by trauma, cycling, straining, coitus
- DDx:
o Epididymitis
o Torsion of testicular appendage (pea coloured lump through scrotum)
o Strangulated inguinoscrotal hernia
- Cause:
o Maldescended testis hanging like a bell clapper within tunica vaginalis
- Treatment:
o Emergency exporation if Doppler US –ve for flow or clinical suspicion
Untwisting (lateral) of affected testis and orchidoplexy of both testis to scrotum
Warm up with warm pad to see reperfusion or check with doppler after untwisting [4h before ischaemia]
If dead, excise and replace with prosthesis

36
3. APPROACH TO LUMPS & BUMPS

Permission: Introduce yourself “Mr.  X  is  a  young  Chinese  gentleman…”

Position: Ensure patient (and you) are comfortable “On  inspection,  there  is  a  (single) (hemispherical) lump
Exposure: Expose area to be examined fully on the (dorsum of the forearm)”
(Remember: Compare with other side if applicable) “It  measures  <take  out  ruler>  (  x  by  x  cm)”
“There  are  (?  scars, sinuses, ulceration, or discharge seen,
Inspection nor overlying or surrounding skin changes)”
1. Number: solitary / multiple
2. Site: take reference from bony points “Is  the  lump tender?”
3. Shape / Symmetry:
- Hemispherical, Round, Exophytic “On  palpation,  the  overlying  skin  is  (not)  found  to  be  warm.
4. Size It is (non-tender)”
5. Scars “The  surface is (smooth), with clearly-defined margins”
6. Colour & skin changes? “The  consistency is firm, and it is (non-fluctuant)”
a. Sinuses, discharge “The  lump  is  (not)  attached to the overlying skin,
b. Ulceration and it is non-pulsitile.”
c. Erythema / cellulitis “It  (appears  to  be  attached  to  underlying  muscle,  
as it is mobile horizontally but not longitudinally)”
Palpation (Ask patient: Is area painful?)
1. Overlying skin temperature
S: site, size, shape, scars, skin changes, surface
2. Tenderness
E: edge, expansility/ pulsatility
3. Surface:
C: colour, consistency, compressibility
- Smooth/ Irregular/ Rough
T: tenderness, temperature, transillumability
4. Margins clearly defined?
O: others [fluctuance, fulid thrill]
5. Consistency
R: reducability, relationship to each other
- Hard > Firm > Tense > Soft
6. Mobility
Ulcers:
- Fully mobile in all directions?
Base: granulation tissue, slough, fascia, muscle, bone
- Fixed and immobile? Edge: sloping (healing), punched out, undermined,
- Mobile only in certain directions? rolled (BCC), everted (SCC)
7. Relations to surrounding tissues Discharge: serous, sanguinous, haemoserous, purulent
- Move 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.
8. Fluctuant? (for small / medium lumps)
- Paget’s  sign:  Rest  2  fingers  on  opposite  sides  of  lump,  press  down  on  middle  of  lump +ve: Feel fingers moving apart

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

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”

37
Symptoms and signs
1. Lump in or on the skin
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 swellingderived from?
Character of the margin
Discreteness, tethering to surrounding
tissues, three-dimensional shape
Consistency
Soft, firm, hard, 'indurated', rubbery
Pulsatility
Emptying and refilling
Transilluminability
Temperature
2. Pain, tenderness and discomfort
Diagnostic significance
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)
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)
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)
Pulsatility is usually transmitted from an underlying artery which may simply be tortuous
or may be abnormal (e.g. aneurysm or arteriovenous fistula)
Vascular lesions (e.g. venous malformations or haemangiomas) empty or blanch on
pressure and then refill
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
38
3. Ulceration (i.e. loss of Malignant lesions and keratoacanthomas tend to ulcerate as a result of central necrosis. Surface
epidermal integrity with an breakdown also occurs in arterial or venous insufficiency (e.g. ischaemic leg ulcers), chronic infection
inflamed base formed by (e.g. TB or tropical ulcers) or trauma, particularly in an insensate foot
dermis or deeper tissues)
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)
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)
Red or purple 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
5. Rapidly developing Keratoacanthoma, warts and pyogenic granuloma may all develop rapidly and eventually regress
lesion spontaneously. When fully developed, these conditions may be difficult to distinguish from
malignancy. Spontaneous regression marks the lesion as benign
6. Multiple, recurrent and In certain rare syndromes, multiple similar lesions develop over a period. Examples include
spreading lesions neurofibromatosis and recurrent lipomata in 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 port-wine 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

39
4. 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 maybe more liquid
o Mobile in all directions (if subcutaneous)
o Positive slip sign; No transilluminance / thrill
o Usually in the subcutaneous tissue. [check attachment skin & muscle]

“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”

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 – Dercum’s  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)

Variants of lipomas / syndromes associated with lipomas

o Adiposis dolorosa (Dercum’s disease)
Multiple painful lipomas in limbs, sometimes trunk
Associated with peripheral neuropathy
Angiolipomas: prominent vascular component
o Hibernomas: brown fat cells
o Cowden’s  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

40
5. SEBACEOUS CYST
Inspection “Mr.  X  is  a  young  Chinese  gentleman…”
Usually solitary (can be multiple) “On   inspection, there is a single hemispherical lump in the
Hemispherical middle of the forehead just  above  the  eyebrows”
Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles) “It  measures  1 by 1 cm in  diameter”
Variable size ; few mm to 4-5 cm “There  is  a  visible punctum over  the  lump”
May have bluish discolouration “There  are  no  scars, sinuses, ulceration, or discharge seen,
Punctum in apex: in 50% nor any overlying or surrounding skin changes”
May exhibit plastic deformation on palpation
“On  palpation, the overlying skin is not warm. It is non-tender.”
Palpation “The  surface  is  smooth, with clearly-defined margins”
Normal Temperature, non-tender (unless inflamed) “The  consistency  is  firm, and it is non-fluctuant”
Smooth surface “The  lump  is  attached to the overlying skin”
Well-defined margins (lies in subcutaneous fat) “It  is  mobile in  all  directions”
Tense consistency, may stretch overlying skin ( plastic deformation) “Slip sign is negative”
Non fluctuant, not transilluminable “I  would  like  to  complete  my  examination  by…”
Attached to skin, not attached to deeper structures, mobile in all directions “Looking  for  other lumps elsewhere”
“My  provisional  diagnosis  is  a  sebaceous cyst”
Background Information My differentials are: Lipoma / Dermoid cyst
Sometimes considered to be similar to epidermoid cyst
o More accurate terminology: pilar / trichilemmal cysts
2 histological types:
o Epidermal cyst: from infundibular portions of hair follicles
o Trichilemmal cyst: from hair follicle epithelium (most common on scalp), frequently multiple (AD inheritance)
Arise from infundibular parts of hair follicles
Definition: Distension of sebaceous glands with 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
Sebum slowly exudes, dries and hardens into conical spike Inflamed
Sebum usually washed away – horn results only if overlying skin not washed
Cyst
Can be pulled out of skin
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

Treatment
o Non-surgical: leave alone (if small, asymptomatic).
o Surgical
Complete excision of cyst and contents under LA.
Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the lines of Langers.
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?

- Malignancies: BCC, Malignant melanoma.

Cock’s 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

Gardner’s  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

41
6. GANGLION

Inspection
Single; may have ovelying 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 which hand is dominant (may affect management)
Occupation

“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 shealth
(These 2 are normally soft in consistency. Ganglion is more tense.)

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:
1. Simple
2. Compound – chronic inflammation distends tendon sheath above and below the flexor retinaculum.
3. Occult
4. Interosseous

42
Clinical features
o Majority between 20 and 60 years (rare in children)
o Grow slowly over months / years
o Non painful

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

Treatment
o 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.
o Surgical
Complete excision to include neck of ganglion at site of origin. Along the lines of Langers.
Complications
Wound complications: Scar, haematoma, infection
Recurrence <10%
Damage to adjacent neurovascular structures.
Stiffness & Contractures

43
7. BASAL CELL CARCINOMA

– “Examine  this  gentleman’s  face”

(If the other side of the face, etc. needs to be inspected, ask the patient to turn his head – avoid moving around the patient)

“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.”
“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)
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

A = nodular
B = pigmented
C = sclerosing
D = superficial

44
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)
Xeroderma pigmentosum (familial, associated with failure of DNA transcription)
Gorlin’s  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:
o Above the skin:
Nodular
Nodulo-ulcerative  /  Deeply  eroding  ulcer  (“rodent  ulcer”)
Cystic
o Not raised above the skin:
Pigmented
Geographical  /  cicatricial  /  “bush-fire”  (advancing edge, healing centre)
Sclerosing (flat / depressed tumour, ill-defined edge)
Superficial (erythematous scaly patches)

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

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  

Differentials
o SqCC
Especially if ulcerated
But if rolled edge: more likely BCC
o Keratoacanthoma (adenoma sebaceum, molluscum pseudo-carcinomatosum)
But scar will be deep (see below)
o If pigmented: malignant melanoma (rare in Singapore)

Treatment
o Raised above skin: excision with 0.5 cm margin (maximum)
o Not raised above skin: wider margin of excision, especially if at inner acanthus of eye, nasolabial fold, nasal floor, ear
Frozen section may be needed to ensure adequate excision
o Alternative:
RT
o Eyes, ears, nasolabial fold lesions: Moh’s chemosurgery
Staged chemosurgery, histological assessment of margins & electrodessication

45
8. SQUAMOUS CELL CARCINOMA

“Mr.  X  is  an  elderly  Chinese  gentleman…”

“On  inspection, there is a single irregular ulcer on the dorsum of the right hand, proximal to the 1st & 2nd MCP joints”
“It  measures  1.5 by 1.5 cm. The edge of the ulcer is well-defined, red and heaped up.”
“The  base  of  the  ulcer  is  shallow and contains red granulation tissue.”
“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  provisional  diagnosis  is  squamous  cell  carcinoma”
“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”

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)

46
 Acquired
Envn: sunlight, Irradiation, Chemicals
Pre-existing lesions: Solar keratosis,  Bowen’s  disease
Chronic ulcers: old burns, chronic venous ulcers
Immunosuppresion (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
o Infection
o Bleeding (massive / fatal if erosion into large vessel)

Treatment (depending on site of lesion)

o Wide-excision with 1 cm margin
o Radiotherapy (if unresectable, nodal spread)
o + Block dissection of regional lymph nodes (if involved)
o Eyes,  ears,  nasolabial  fold  lesions:  Moh’s  chemosurgery  
Staged chemosurgery, histological assessment of margins & electrodessication

Lesions Associated with SqCC

Marjolin’s 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

Bowen’s disease Very slowly growing, may progress to SqCC

(SqCC in situ) 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)

Solar (actinic) keratosis o Multiple yellow-grey to brown scaly tumour

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

47
9. MALIGNANT MELANOMA

“Mr.  X  is  a  middle  aged  Chinese  gentleman…”

“On  inspection, there is a single flat-looking lesions 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…”
“Examining  for  regional  lymphadenopathy”
“Take  a  history  for:  cardinal  symptoms  of  malignant  change,  and  any  predisposing  factors”

Inspection
Usually single (may have satellite lesions around primary lesion)
Site: 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/ balck 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)

48
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 Lymphatogenouly to: regional LN
o haematogenously 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
o FHx in 1st 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)

Features of pigmented skin lesion suspicious of malignancy

1. Asymmetry
2. Bleeding & ulceration (late)
3. Change in: colour, size, shape, surface, number (early)
a. Surface:
i. Loss of normal surface markings (e.g. skin creases) around lesion
ii. Skin may become rough / scaly
iii. Itchy with pale-pink halo (inflammation)
b. Size:
i. Growth of newly-formed / long-standing mole
ii. Increase in edge, width, thickness
c. Colour:
i. Becoming darker
ii. Halo of brown discolouration in skin around the lesion
iii. Patchy colour change (black, to blue-purple ↑  vascularity)
iv. Occasionally colourless: no melanin production
d. Number:
i. Satellite nodules of tumour around the lesion
ii. Enlarged inguinal, axillary lymph nodes
4. Diameter >6mm
5. Elevation  (flat  plaque  →  nodule)

49
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

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

Staging by depth of invasion

Clark’s levels of invasion

Level Extent of Tumour 5-Year Survival
I Epidermis only 98%
II Invades papillary dermis 96%
III Fills papillary dermis 94%
IV Invades reticular dermis 78%
V Subcutaneous tissue invasion 44%

Breslow’s 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)
Also: Beahrs and Myer’s system

Prognosis generally poor – above 3 types of staging, or other indicators of poor prognosis:
a. Elderly
b. Male
c. Lesions on trunk
d. Ulceration
e. Depigmentation, amelanotic
f. Aneuploidy, high mitotic index

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

50
 Superficial Spreading Nodular Lentigo Maligna Acral Lentiginous
% 70% 15-30% – Rare
Face;
♂:  Back Hairless skin (palms, soles,
Site Trunk Dorsum of hand /
♀:  Legs subungual area)
forearm
Red, white, blue
Colour Most often black Brown / black Brown / black
(varying pigmentation)
Edge Irregular Regular outline Irregular Irregular
Shape Palpable, but thin Thick, polypoid, raised Flat Flat
Surface - Smooth - -
•  Arises  from  patch  of  
Hutchinson’s  Lentigo •  Rare  type
•  Frequently  ulcerated,  
Remarks - •  Malignant  area  usually   •  Often  misdiagnosed  as  
bleeding
thicker, darker haematoma, paronychia
•  Area  seldom  ulcerates

Pictures

51
10. NEUROFIBROMA

“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”

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 café-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: café-au-lait spots, axillary freckling, lisch nodules, optic glioma
Measure the BP (HPT 2o 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)
o 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)

52
 Neurofibromatosis I (Von  Recklinhausen’s  disease)
(Refer to paediatrics notes – neurocutaneous syndromes)
AD, neurocutaneous syndrome; chr 17
Characterised by pigmentary changes, tumours, and skeletal, vascular dysplasias
o Fibroma  ≥2 NF  or  ≥1  plexiform  NF
o Iiris harmatomas (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

53
11. DERMOID CYST

“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 nor underlying tissues.”
“It  is  fully mobile in  all  directions.”
“My  provisional  diagnosis  is  a  congenital dermoid cyst”
“My  differentials  are:  sebaceous  cyst,  lipoma”  

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
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)
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

54
12. SEBORRHOEIC KERATOSIS (Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma)

“Mr.  X  is  an elderly  Chinese  gentleman…”

“On  inspection, there is a single ovoid lesion lump on the back”
“It  measures  1 by 2 cm”
“The  margins  are  well-defined,  and  it  appears  to  be  slightly  raised  above  the  skin”  
“There  are  no  scars,  ulceration,  or  discharge  seen,  nor  any  surrounding  skin  changes”
“On  palpation, the overlying skin is not warm. It is non-tender”
“The  surface is rough and greasy; the consistency is firm”
“The  lump  arises from the skin”
“My  provisional  diagnosis  is  seborrhoeic  keratosis”
“My  differential  diagnosis  is:  pigmented  naevus,  melanoma”
“I  would  like  to  complete  my  examination  by…”
“Looking  for  similar  lesions  elsewhere”

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

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)
(DON’T  DO  THIS  IN  EXAM)

Request to look for similar lesions elsewhere

Background Information
Benign outgrowth of basal layer of epidermis
o Raised above the level of normal epidermis
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 thickeness
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
o Can be left alone as it is benign
Surgical – for cosmetic reasons, etc.
o Superficial shaving (lies above level of normal epidermis)
o Cautery

55
13. HAEMANGIOMA

Background Information
Vascular malformations
o Types
Capillary: ⅔ 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 vinosus)
o Spider naevus
o Campbell de Morgan spot

Strawberry Naevus Port-Wine Stain Spider Naevi Cambell de Morgan Spot

Inspection
Head & Neck Lips, face, mucous membranes of Upper torso, head and neck Trunk (bilat) – upper > lower
Site
(can be anywhere) mouth, shoulders, neck, buttock (drainage of SVC) Occasionally on limbs
Number May be multiple Usually single Usually multiple Usually multiple
Colour Bright red / dark red Purple-red Bright red Dark red / deep purple
Size Variable; 1-10 cm Variable Variable; few mm 1-3 mm
Edge Well-defined Well-defined – Well-defined
Sessile  →  pedunculated
Shape Variable Variable Circular, may be raised
as they grow larger
Skin May have small areas May have dilated subcutaneous
– –
Changes of ulceration with scabs veins around lesion
Palpation
Irregular, covered with
Surface Smooth – Smooth
smooth, pitted epithelium
Consistency Soft – – –
Mobility Mobile – – –
Relations Confined to skin – – –
Compressible: pressure
Special squeezes mass, leaves it
– Compressible, fade completely –
Tests collapsed: slowly refills
Not pulsatile
Background Information
Age Infants (congenital) Infants (congenital) – Middle-age  →  elderly
Gender ♂  =  ♀ – – –
•  Cosmesis •  Cosmesis •  Cosmesis
Symptoms –
•  May  ulcerate,  bleed  on trauma •  Bleeding  may  occur •  Non-tender
•  Diminishes  colour  but  doesn’t   •  Branches  fade  when  arteriole  
Pressure •  Collapses  on  pressure •  Fade  slightly
revert to normal compressed
•  Extensive, intradermal
•  Form  of  telangiectasia
•  Present  from  birth,  does  not  
•  Dilated  skin  arteriole  feeding   •  Formed  by  collection  of  dilated  
change in size
small branches (leaving radially) capillaries fed by single / small
•  Sturge-Weber syndrome: facial
Regress spontaneously •  Increase  in  number   cluster of arterioles
Remarks PWS with corresponding
(few months – 3 years) •  Associated  with  pregnancy,   •  Have  appearance  of  drops  of  
haemangioma in brain –
chronic liver disease (> 5) – sealing wax
contralateral focal fits
request for abdominal •  No  clinical  significance
•  Found  in  limbs  when  a/w  
examination
Klippel-Tranaunay Syndrome

Pictures

56
Also
Telangiectasias
o Dilatation of normal capillaries
o Can be secondary to irradiation
o Can be part of hereditary haemorrhagic telangiectasia (Osler-Rendu-Weber syndrome)
Autosomal dominant disease
Overt and occult haemorrhage can present as haematuria, haematemesis, melaena, epistaxis, iron-deficiency
anaemia
Vin rosé 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

57
14. PYOGENIC GRANULOMA

“Mr.  X  is  a  young  Chinese  gentleman…”

“On  inspection, there is a single hemispherical lump  over  the  thenar  eminence  of  the  right  hand”
“It  measures  about  0.8    cm  in  diameter,  with  clearly-defined  margins”
“It  is  bright  red  in  colour,  with  surrouding  erythema”
“There  are  no  scars,  sinuses,  ulceration,  active  bleeding  or  discharge  seen”
“I would like to proceed on to palpation”
“On  palpation, it is not warm. It is slightly tender”
“The  surface  is  smooth. The consistency is soft and fleshy”
“The  lump  is  confined to  the  skin”
“My  provisional  diagnosis  is  pyogenic  granuloma”
“My  differential  diagnoses  are  SCC,  non-pigmented  melanma”
“I  would  like  to  complete  my  examination  by…”
o “Asking  Mr.  X  for  any  previous  injuries  to  the  hand”
o “Asking  him  how  rapidly  the  lump  has  been  growing”

Inspection
Single; usu < 1 cm, bright red
o May be blood-encrusted or Ulceration
Hemispherical; may be sessile / pedunculated
Likely sites to be injured, e.g. hands, face
Bright red; long-standing lesions may be skin-coloured
May have sinuses, associated serous / purulent discharge, Erythema / cellulitis

Palpation – request to palpate: may bleed easily

May be slightly tender
o May bleed easily on palpation
Well-defined edges
Soft, fleshy consistency
Confined to skin
Slightly compressible (vascular origin)

Request
Take history for previous injury
Rate of growth of lump? (rapid growth in few days)

Background Information – Neither pyogenic nor a granuloma!

Rapidly-growing capillary haemangioma, usually less then 1 cm
Occur commonly after injury:
o Small capillary loops develop in healing wound, form granulation tissue
o When capillary loops grow too vigorously, form protruding mass, epithelisation
o Mass form called pyogenic granuloma (surface often ulcerated, infected)
Clinical features
Uncommon in children
May have history of minor injury, chronic infection (e.g. paronychia)
Rapidly-growing lump on skin,
Bleeds easily, discharges serous / purulent fluid
o Bleeding, pain stops once lump epithelises
Once nodule is completely covered, begins to shrink (rarely disappears completely)

Treatment
Surgical
o Curettage with diathermy of the base
o Complete excision biopsy
(if recurrent; malignancy e.g. amelanotic melanoma has to be excluded)
Non-surgical
o Regression is uncommon: surgical treatment best option
o Silver nitrate cautery is possible

58
15. PAPILLOMA (skin tags / fibroepithelial polyps)

“Mr.  X  is  a  young  Chinese  gentleman…”

“On  inspection, there is a (single) (hemispherical) lump on the (dorsum of the forearm)”
“It  measures  3 by 2 cm.
“The surface is papilliferous – there  is  no  ulceration  or  discharge  seen,  nor  any  surrounding  skin  changes.”
“On  palpation, the skin is not warm. It is non-tender. The  consistency  is  soft.”
“The  lump  is  attached to  the  skin”
“My  provisional  diagnosis  is:  papilloma”
“My  differential  diagnosis  is:  viral  wart”
“I  would  like  to  complete  my  examination  by…looking  for  similar  lumps,  asking  for  associated  conditions”

Inspection
Single / multiple
Variable: from raised plaque to pedunculated polyp
Site: Neck, trunk, face, anus (anywhere on skin)
Variable
Flesh-coloured

Palpation
Not warm, non-tender
Variable: smooth to papilliferous
Soft, not compressible
Arises from skin

Request
Similar lumps elsewhere
Ask for associated conditions: pregnancy, diabetes, intestinal polyposis

Background Information
An overgrowth of all layers of the skin with central vascular core
Not a neoplasm, but a hamartoma (skin tag is a more accurate term)
Increasingly common with age – may be congenital

Clinical features
Catches on cloths, rubs against other body parts
May resemble carcinoma if granulation is excessive
Complications:
o May become red, swollen, and ulcerate
o May become infarcted if injured
o May be infected (contains all skin components – sebaceous glands, etc.)

Treatment
Excision – diathermy, scissors
o Bleeding from central vascular core controlled using single suture / diathermy

59
16. KERATOCANTHOMA (adenoma sebaceum, molluscum pseudo-carcinomatosum)

Inspection
Often found on face
Usually solitary;1 – 2 cm in diameter
Hemispherical or conical, with central crater
Normal skin colour

Palpation
Firm and rubbery (central core is hard)
Confined to skin, freely mobile over subcutaneous tissues

Background information
Benign overgrowth of hair follicle cells with a central plug of keratin
Occur in adults
complain of rapidly-growing lump in skin
Not painful, but can be unsightly
Takes 2 – 4 weeks to grow, regresses in 2 – 3 months
o Central slough appears,
o surrounding skin retracts to form puckered scar
Cause is unknown (may be self-limiting benign neoplasm or post-viral infection)
Treatment:
o Conservative if asymptomatic
o Surgical excision of lesion with histology to r/o SqCC

17. KELOID (HYPERTROPHIC SCAR)

Healing by primary intention – 3 stages:

o Tissue defect filled by blood / fibrin
o Replacement by collagen and fibrous tissue
o Organisation of fibrous tissue to maximise wound strength
Most surgical scars have thin lines, but tissue response may be excessive: hypertrophic / keloid scar

Wounds prone to hypertrophic / keloid scar

o Infection
o Trauma
o Burns
o Tension
o Susceptible areas: across flexion areas, earlobes, chest, neck, shoulder

Hypertrophic scar
o any age – common 8-20  years,  ♂=♀,  all  races
o Excessive amount of fibrous tissue, but confined to scar (between skin edges)
o Located across flexor surfaces, skin creases
o Common, especially if infection / excessive tension
o Only enlarge for 2-3 months, then regress spontaneuosly
o Do not recur if excised and causative factor eliminated

Keloid scar
o puberty  to  30  years,  ♀>♂,  black,  hispanic  more  likely
o Hypertrophy and overgrowth extend beyond original wound
o Located at earlobes, chin, neck, shoulder, chest
o Due to local release of fibroblast growth factors
o Continue to enlarge 6-12/12 after initial injury
o May be tender, unsightly
o Will recur unless special measures taken

Treatment (recurrence can be as high as 55%)

o Non-surgical: mechanical pressure therapy – topical silicone gel sheets (day and night for 1 year), Intralesional steroid,
LA injections: e.g. triamcinolone with lignocaine
o Surgical: revision of scar by direct suturing, skin grafting (avoid excessive tension)

60
18. KAPOSI’S  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 immunocompromise.

Background information
Derived from capillary endothelial cells or from fibrous tisse
Linked to HHV-8
Types:
o Classic  Kaposi’s  Sarcoma
Confined to skin of lower limbs of elderly Jews
Not fatal
o AIDS  associated  Kaposi’s  Sarcoma
AIDS defining; Found in 1/3 of AIDS patients
1/3 develops a 2nd malignancy e.g. leukaemia/ lymphoma
o Endemic (African) Kaposi’s  Sarcoma
Aggressive and invasive fatal tumour
Good response to chemotherapy
o Transplation- associated  Kaposi’s  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)

19. 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

61
20. PYODERMA GANGRENOSUM

Inspect
Ulcer with a necrotis base
Irregular bluish red overhanging edges
a/w surrounding erythematous plaques with pustules

Request to examine for evidence of inflammatory bowel disease, RA

Backgound information
more common in males
pyoderma gangrenosum is associated with:
o IBD
o RA
o Myeloproliferative disorders: PRV, myeloma
o Autoimmune hepatitis
Differential diagnosis:
o Autoimmune: rheumatoid vasculitis
o Infectious: tertiary syphilis, amoebiasis
o Iatrogenic: warfarin necrosis
o Others:  Behcet’s  disease
Treatment:
o Non-surgical: treat underlying condition, saline cleansing, high dose oral or intralesional steroids.
KIV cyclosporine & antibiotics
o Surgical: serial allograft followed by autologous skin graft or muscle flap coverage when necessary

62
21. RADIOTHERAPY MARKS

Vital points on examination:

Of the underlying disease:
o Cachexia,
o masectomy scar/ wide excision scar suggest breast cancer
o obvious skin cancer,
o clubbing & other signs of chest disease suggest lung cancer
o suprapubic mass suggest pelvic tumour
o neck swellings with cranial nerve palsies head and neck tumour
of the radiotherapy:
o site of radiation
o shape: usually well defined borders
o features of active RT:
Indian ink marks, skin markings
Erythema, desquamation
o Features of previous RT:
Telangiectasia, hyperpigmentation
Complications of radiotherapy:
o Depends of site
o Look for future cancers:
Haematogenous malignancy
Thyroid cancers
Breast cancers

Background information
High energy X-rays interact with tissue to release electrons that cause local damage to DNA in adjacent cells via oxygen
dependent mechanism.
o Damage is usually irreparable, and normal cells have greater ability to repopulate than tumour cells in this setting
o If reparable, manifests as chromosomal abnormalities

Radiotherapy affects cells with:

o Rapid turnover: Skin (epidermal layers), small intestine, bone marrow stem cells
o Limited replicative ability: spinal cord, gonads

Complications:
o Early:
General: malaise, fatigue, LOA, N/V
Skin changes & temporary hair loss
Bone marrow suppresion, esp. if to long bone and pelvis
GI: diarrhea
o Late:
Skin changes
Heart: IHD
Lung: pneumonitis, pulmonary fibrosis
Bld vssl: radiation arteritis, esp to carotids necrosis, distal ischaemia and vssl rupture
CNS: spinal cord myelopathy
Uro: bladder fibrosis, Renal impairment (depletion of tubular cells)
Abdo: IO 2o to strictures & adhesions,
Genital: infertility
Endocrine: hypothyroidism
Eye: cataracts
Increase incidence of future cancers:
Haematogenous malignancy, e.g. leukemia
Solid tumours: Thyroid cancers
Breast cancers
Minimalising of side effects of radiotherapy:
o Lead shields to eyes, gonads and thyroid
o Dose fractionation (to allow recovery of normal cells)
o Prior chemotherapy (increase sensitivity of tumour cells)
o Regional hypothermia
o Radiolabelled antibody to deliver local radiation to tumour

63
3. SURGICAL INSTRUMENTS & PROCEDURES

1. DRAINS

FUNCTIONS OF DRAINS COMPLICATIONS

Drains are inserted to:
Evacuate collections of pus, blood or fluids (e.g. lymph)
Drain potential collections
Rationale:
Drainage of fluid removes further fluid collections
Allow early detection of anastomotic leaks/ haemorrhage
Leave tract for potential collections to drain after removal
Infection
Bleeding
Tissue damage- by mechanical pressure or suction
Drain failure - blocked/slipped/kinked
Incisional hernia - occurs when drain inserted through incision
wound site- create a separate incision site for drain!

TYPES OF DRAINS
Drains are often made from inert silastic material
They induce minimal tissue reaction
Red rubber drains induce an intense tissue reaction allowing a tract to form
In some situations this may be useful (e.g. biliary t-tube)

Open Active

Active drains require suction.

Corrugated drain, Yeates drain, Penrose drain
Drain fluid collects in gauze pad or stoma bag
Easier to drain infected collections
Closed
Consist of tubes draining into a bag or bottle
They include chest and abdominal drains
The risk of infection is reduced
Jackson-Pratt Drain, Redivac Drain, T-tube
Have expandable chambers to create low-pressure suction
Used when small – mod amts of drainage are expected or when a
passive drainage system won't provide adequate drainage
Tubing of the low-pressure active drainage system is placed
through a separate puncture wound or the tube may exit the edge
of the surgical wound
If the tubing isn't sutured in place, it could become dislodged
If a portion of the tube is pulled outside the skin, an air leak will
cause the chamber to fill with air & it won't drain properly.
Passive
Passive drains rely on gravity.
Passive drains have no suction, rely on gravity
Works by differential pressure betw body cavities and the exterior
Used when a mod – large amt of drainage is expected

CARE AND PREVENTION OF COMPLICATIONS OF TUBES:

Prevent Infection- maintain meticulous skin care and aseptic technique around the insertion site
Prevent blockage of the drain- do not allow bottles to fill up
Prevent slippage by securing drain carefully to skin; refix as required
Never hold a drainage collection device higher than the tube insertion site to prevent the drainage from flowing backward into the patient
Note amount of drainage daily

REMOVAL OF DRAINS
A drain is removed as soon as it is no longer required. The following are general guidelines:
Drains put in to cover perioperative bleeding and haematoma formation, can come out after 24— 48 hours.
Where a drain has been put in to drain an infection (abscess), remove it when fever settles or when there is evidence of complete drainage.

64
2. CENTRAL VENOUS PRESSURE LINE

INDICATIONS CONTRAINDICATIONS: ROUTES FOR CENTRAL VENOUS

1. Vascular access 1. Do not insert into an infected area. CANNULATION INCLUDE:
2. Total parenteral nutrition 2. Avoid infraclavicular approach to
3. Infusion of irritant drugs subclavian vein if patient has apical 1. Internal jugular vein
4. Measurement of CVP emphysema or bullae. 2. Subclavian vein
5. Cardiac catheterization 3. Avoid internal jugular vein if carotid 3. Femoral vein
6. Pulmonary artery catheterization aneurysm present on the same side. 4. External jugular vein
7. Transvenous cardiac pacing. 4. Bleeding diatheses
5. Septicaemia
6. Hypercoagulable states

CANNULATION OF THE INTERNAL JUGULAR VEIN

The internal jugular vein (IJV) is accessible, so cannulation of this vein is associated with a lower complication rate than with other approaches.
Hence, it is the vessel of choice for central venous cannulation.

Anatomy of the IJV

The vein originates at the jugular foramen and runs down the neck, to
terminate behind the sternoclavicular joint, where it joins the subclavian
vein. It lies alongside the carotid artery and vagus nerve within the carotid
sheath. The vein is initially posterior to, then lateral and then anterolateral to
the carotid artery during its descent in the neck. The vein lies most
superficially in the upper part of the neck.

Relations of the IJV

Anterior: Internal carotid artery and vagus nerve.
Posterior: C1, sympathetic chain, dome of the pleura.
On the left side, the IJV lies anterior to the thoracic duct.
Medial: Carotid arteries, cranial nerves IX-XII

Technique of IJV cannulation

Place the patient in a supine position, at least 15 degrees head-down to
distend the neck veins and to reduce the risk of air embolism. Turn the head
away from the venepuncture site. Cleanse the skin and drape the area.
Sterile gloves and a gown should be worn to avoid catheter-related sepsis.

Procedure
1. Use local anaesthetic to numb the venepuncture site.
2. Introduce the large calibre needle, attached to an empty 10 ml syringe.
3. Surface mark the internal jugular vein at the centre of the triangle formed by the two lower heads of the sternocleidomastoid muscle and the
clavicle. Palpate the carotid artery and ensure that the needle enters the skin lateral to the artery.
4. Direct the needle caudally, parallel to the sagittal plane, aiming towards the ipsilateral nipple.
5. While needle is advanced, maintain gentle aspiration.
6. When vein is entered, flush of blood appears in the syringe. Now, cannulate the vein via the Seldinger technique (below).
7. Remove syringe, holding needle firmly in place. Occlude needle to prevent air embolism or bleeding.
8. Advance guide wire, J-shaped end first, into the vessel through the needle.
9. Hold guide wire in place and remove needle. Maintain a firm grip on the guide wire at all times.
10. Use a dilator to enlarge the hole in the vein. Remove the dilator.
11. Thread tip of catheter into the vein through the guidewire.
Grasp the catheter near the skin and advance it into the vein with a slight twisting motion.
12. Advance catheter into final indwelling position. Hold catheter and REMOVE GUIDEWIRE.
13. Check lumen placement by aspirating through all the pigtails and flushing with saline next.
14. Suture the catheter to the skin to keep it in place.
15. Apply dressing according to hospital protocol.
16. The catheter tip should lie in the superior vena cava above the pericardial reflection.
17. Perform check chest X-ray to confirm position and exclude pneumothorax.

Complications
1. Pneumothorax/haemothorax
2. Air embolism - ensure head-down position.
3. Arrhythmias – This  happens  if  cathether  “irritates”  the  heart.  Avoid  passing  guidewire  too  far,  cardiac  monitoring during insertion.
4. Carotid artery puncture/cannulation - palpate artery and ensure needle is lateral to it, or use ultrasound-guided placement, transduce needle
before dilating and passing central line into vessel, or remove syringe from needle and ensure blood is venous.
5. Chylothorax- Avoid cannulating the vein on the left side as the thoracic duct lies there.
6. Catheter-related sepsis

65
CANNULATION OF THE SUBCLAVIAN VEIN

The subclavian vein (SVC) may be preferred for central venous access if
1. Patient has a cervical spine injury
2. Line is for long-term use e.g. dialysis, feeding. This site may be more comfortable for the patient.

Anatomy of the SCV

The SCV is the continuation of the axillary vein and originates at
the lateral border of the first rib. The SCV passes over the first
rib anterior to the subclavian artery, to join with the internal
jugular vein at the medial end of the clavicle. The external
jugular vein joins the SCV at the midpoint of the clavicle.

Technique
1. Place the patient in a supine position, head-down.
2. Turn the head to the contralateral side
(if C-spine injury excluded).
3. Adopt full asepsis.
4. Introduce a needle attached to a 10 ml syringe.
5. Surface mark the subclavian vein 1 cm below the junction
of the middle and medial thirds of the clavicle. Direct the
needle medially, slightly cephalad, and posteriorly behind
the clavicle toward the suprasternal notch.
6. Slowly advance needle while gently withdrawing plunger.
7. When a free flow of blood appears, follow the Seldinger
approach, as detailed previously.
8. The catheter tip should lie in the superior vena cava above
the pericardial reflection.
9. Perform check chest X-ray to confirm position and exclude
pneumothorax.

Complications
As listed for internal jugular venous cannulation. The risk of pneumothorax is far greater with this technique.
Damage to the subclavian artery may occur; direct pressure cannot be applied to prevent bleeding.

Ensure that a chest X-ray is ordered, to identify the position of the line and to exclude pneumothorax.

66
3. NASOGASTRIC TUBE

INDICATIONS [4] CONTRAINDICATIONS

1. Diagnostic a) bleeding from the upper gastrointestinal tract, haematemesis 1. Base of skull #
b) pentagastrin studies (rarely done now) 2. Oesophageal tear
3. Severe facial injury
2. Decompresssion Therapeutic a) intestinal obstruction
b) pyloric stenosis
c) haematemesis, esp in pts at risk of hepatic encephalopathy
Preventive:
d) therapeutic and prophylactic decompression after major abdominal surgery
e) prevention of further soilage after gastric perforation
f) prevention of anastomotic rupture after gastric surgery
g) prevention of obstruction of the operative field by air in the stomach
3. Nutrition a) patients with dysphagia
b) comatose or weak patients
4. Lavage a) poisoning
b) gastrointestinal bleeding

The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric tube insertion.

PRE-PROCEDURE
1. Gather equipment.
2. Don non-sterile gloves.
3. Explain the procedure to the patient and show equipment.
4. If possible, sit patient upright with head forward for optimal neck/stomach alignment. Otherwise, prop the patient up at 45 °.
5. Deflate the endotracheal tube or tracheostomy cuff
6. Determine the size of the nasogastric tube required (usually 14 – 16FG). If aspirating, use as large a tube as possible to reduce the risk of
blocking during use or the formation of a false passage during introduction; if feeding, a smaller tube may be used (eg. 8FG) because it is
more comfortable in the long term.

PROCEDURE
1. Estimate the length of the tube to be inserted: from the bridge of the nose to the tragus of the ear to the point halfway between the
xiphisternum and the navel. Mark the measured length with a marker or note the distance.
2. Examine nostrils for deformity/obstructions (eg. choanal stenosis) to determine best side for insertion. Select the largest nostril for insertion.
3. Lubricate tube with water. The nose may be lubricated with lignocaine gel.
4. Introduce the tube through the nostril horizontally in, passing the tube along the floor of the nose. Resistance may be felt as tip reaches the
nasopharynx, which is the most uncomfortable part of the procedure. In the operation theatre, when the patient is under general anaesthesia,
the  McGill’s  forceps  may  be  used  to  guide  the  tube  down.
5. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated) and advance the tube as the patient swallows. Swallowing
of small sips of water may enhance passage of tube into esophagus. If patient is uncooperative, bend his head to elicit a swallowing reflex.
6. Continue to advance the tube down the oesophagus. There should not be resistance. If resistance is met, rotate the tube slowly with
downward advancement towards the closer ear. Do not force the tube down against resistance as this may form a false passage.
7. Withdraw the tube immediately if changes occur in the patient's respiratory status, if the tube coils in the mouth, or if the patient begins to
cough or turns pretty colours.
8. Advance the tube until mark is reached (approximately 40cm). Stop.
9. Check for correct placement by attaching a syringe to the free end of the tube and aspirating a sample of gastric contents to test with litmus,
auscultating the epigastrium while injecting air through the tube, or obtaining an x-ray to verify placement before instilling any
feedings/medications or if you have concerns about the placement of the tube.
10. Secure the tube with adhesive tape.
11. Re-inflate the endotracheal tube or tracheostomy cuff if necessary.
12. If for suction, remove the syringe from the free end of the tube; connect to suction; set machine on type of suction and pressure as prescribed.
13. Document the reason for the tube insertion, type & size of tube, the nature and amount of aspirate, the type of suction and pressure setting if
for suction, the nature and amount of drainage, and the effectiveness of the intervention.

PROBLEMS AND COMPLICATIONS [5]

1. Technical 2. Gastrointestinal 3. Lung complications 4. Loss of fluids 5. Dry mouth

a) insertion into the a) Gastric erosions a) decreased ventilation & electrolytes, and parotitis
trachea choking. b) Pressure necrosis of b) aspiration pneumonia especially due to fluid
b) coiling & reentry into pharynx, oesophagus sodium, loss and
oesophagus (rare). or the external nares. potassium, mouth
c) trauma to the nose and c) Varices: traumatic chloride and breathing.
the pharynx. haemorrhage hydrogen
d) dislodgement d) GERD ions.
e) perforation of the e) Oesophageal erosions
pharynx and strictures
oesophagus

67
4. TRACHEOSTOMY

INDICATIONS FOR TRACHEOSTOMY

1. Maintenance of airway patency.
2. Protection of the airway from aspiration.
3. Application of positive pressure to the airway.
4. Delivery of high oxygen concentrations.
5. Facilitation of secretion clearance.

RELATIVE CONTRAINDICATIONS
1. Evidence of infection in the soft tissues of the neck at the prospective surgical site.
2. Medically uncorrectable bleeding diatheses.
3. Gross distortion of the neck anatomy due to hematoma, tumour, thyromegaly, high innominate artery or scarring from previous
neck surgery.
4. Documented or clinically suspected tracheomalacia.
5. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water.
6. Patient obesity with short neck that obscures neck landmarks.
7. Patient age younger than 15 years.

TYPES OF TRACHEOTOMY
1. Temporary: Portex (cuffed).
2. Permanent: Consist of inner and outer tubes made of stainless steel.

Tracheostomy is more useful in the elective setting compared to endotracheal intubation because:
1. Better tolerated.
2. Avoids risk of laryngeal stenosis
3. Avoids risk of endotracheal obstruction.

PROCEDURE

1. Position  the  patient.  Place  rolled  towel  under  the  patient’s  neck  to  hyperextend  the  neck  for  better  exposure.  

2. Clean and drape. Clean the skin of the neck from the chin to the suprasternal notch and laterally to the base of the neck and
clavicles. Drape field.

3. Identify anatomical landmarks (thyroid cartilage, cricoid cartilage).

4. Administer local anaethesia.

5. Incise skin. In the emergency setting, make a vertical incision 3cm from cricoid cartilage downwards. In the elective setting,
make a tranverse incision 4cm wide, 3cm above the suprasternal notch.

6. Dissect through the subcutaneous layers and platysma.

7. Identify the communicating branch of the anterior jugular vein, clamp and ligate the artery (ignore this in an emergency).

8. Visualise the thyroid isthmus and retract isthmus.

9. Retract cricoid cartilage upwards wth cricoid hook.

10. Incise the trachea between the 2nd and 3rd tracheal rings, making an inverted U-flap incision.

11. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks.

12. Suction of blood and secretions in the lumen.

13. Insert the tracheostomy tube.

14. Remove the obturator and insert the inner cannula.

15. Dress wound and secure to the neck using sutures and adhesive tape.

68
COMPLICATIONS

During Procedure
1. Bleeding if damage to the innominate or inferior thyroid artery.
2. Damage to surrounding structures, eg esophagus, recurrent laryngeal nerve, brachiocephalic vein.
3. Pneumothorax. Pneumomediastinum.

Immediate post-op
1. Surgical emphysema (refers to the condition that causes air to be trapped under the skin). Subcutaneous emphysema.
2. Obstruction, eg clot, mucus.
3. Bleeding.
4. Dislodgment.

Late post-op
1. Infection .
2. Obstruction, eg dislodgment of tube, crust formation from secretions.
3. Tracheal stenosis.
4. Tracheomalacia.
5. Tracheo-esophageal fistula. Wound breakdown
6. Scarring.

POST-OP CARE
1. Position patient in a propped up position.
2. Prevent obstruction by suction, saline irrigation, mucolytic agents (mucomyst, guaifenesin) and humidified air.
3. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday.
4. Unlock the metal tube every night so that the patient can cough it out if it becomes obstructed.

69
5. SENGSTAKEN-BLAKEMORE TUBE (MINNESOTA TUBE)

INDICATIONS
Oesophageal varices

CONTRAINDICATIONS
1. Base of skull fracture
2. Oesophageal tear
3. Severe facial injury

PROCEDURE - Keep SBT in fridge to make it stiff.

1. Measure the length of the tube. Test balloons. Test patency of the tube.

2. Sit the patient upright or at 45 degrees.

3. Apply local anaesthesia (lignocaine nasal spray).

4. Lubricate and insert the tube through the nose, asking the patient to swallow or drink water to aid in smoother passage of the
tube through the pharynx and oesophagus.

5. Inflate the gastric balloon slowly with 100-150ml water.

6. Check that the tube is in the stomach by:

(i) aspirating fluid and testing it with litmus,
(ii) auscultating the epigastrium while injecting air, or
(iii) doing an X-ray.

7. Traction.

8. Inflate the oesophageal balloon to 35 – 45mmHg (above portal HTN pressure): use the Y-connector piece with one arm to the
BP set and the other to the syringe to pump in air.

9. Aspirate  fluid  from  the  oesophagus  through  the  Ryle’s  tube,  or  if  using  the  Minnesota  tube,  use  the  additional  lumen  provided
(with the additional lumen for aspirating fluid in the oesophagus, the Minnesota tube decreases the likelihood of aspiration
pneumonia occurring).

10. Check the oesophageal balloon pressure hourly and release 5mins hourly.

11. Release oeophageal balloon after 24hrs.

12. Release gastric balloon after 48hrs.

13. The tube should not be used for more than 72hrs.

COMPLICATIONS
1. Aspiration pneumonia
2. Respiratory obstruction
3. Oesophageal ulceration and rupture
4. Rebleeding
5. Gastric varices not controlled

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6. URINARY CATHETERISATION

INDICATIONS FOR SHORT-TERM CATHETERISATION

1. Relief of acute retention of urine, e.g. benign prostatic hypertrophy, bladder outflow obstruction.
2. Bladder washout, e.g. blood clots causing acute retention of urine.
3. Cystourethrogram.
4. Administration of intra-vesical drugs.
5. As an adjunctive measure pre/post-operatively
a) Pre-operatively:
(i) to drain the bladder so as to improve access to the pelvis in urologic or pelvic surgery.
(ii) to allow accurate measurement of urine output in major surgery.
b) Post-operatively:
(i) to relieve acute urinary retention because post –op pain results in failure of the sphincter to relax.
6. Urinary output monitoring, e.g. in patient with hypovolaemic shock or the critically ill.

INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION

1. Refractory bladder outlet obstruction.
2. Chronic retention of urine, eg. neurogenic bladder.
3. Incontinence, e.g.  in  palliative  care  of  terminally  ill  or  patient’s  preference.

CONTRAINDICATIONS
1. Presence of urethral injury, as manifested by:
a) blood from the meatus,
b) scrotal haematoma,
c) pelvic fracture, or
d) high-riding prostate, elicited from a genital and digital rectal examination. (alternative: suprapubic drainage)
2. Urinary tract infection, as an indwelling catheter causes difficulty in treatment.

PROCEDURE
1. Gather equipment.
2. Explain  procedure  to  the  patient.  Maximize  patient’s  privacy.  Have  a  chaperone  if  performing the procedure on a member of the opposite sex.
3. Assist patient into supine position with legs spread and feet together.
4. Open the catheterization kit and catheter.
5. Prepare sterile field. Don the sterile gloves from the kit.
6. Test the balloon at the tip of the catheter.
7. Generously coat the distal portion (2 - 5cm) of the catheter with lubricant.
8. Using the non-dominant hand to come in contact with the patient and the dominant hand to use items from the kit (recall that once your hand
comes in contact with the patient, it is no longer sterile and cannot be used to obtain items from the kit), cleanse the peri-urethral mucosa with
antiseptic-drenched swabs held by forceps. Cleanse anterior to posterior, inner to outer, one swipe per swab, discard away from sterile field.
a) Male: Hold the penis and retract the foreskin. Swab the penis and surrounding area, making sure to cleanse beneath the foreskin.
b) Female: Retract the labia majora. Swab the perineum.
9. Apply sterile drape.
10. Installation of local anaesthesia.
a) Male:
(i) Smear lignocaine gel around the meatus and apply the gel gently into urethra.
(ii) Massage gel carefully down the urethra to sphincter, squeezing the meatus shut
(iii) Wait for for 5 minutes (alternatively, with less anaesthetic effect, smear gel over the catheter tip).
b) Female:
(i) Apply lignocaine gel to urethra or catheter tip.
11. In the male, lift the penis to a position perpendicular to patient's body and apply light upward traction (with non-dominant hand); in the female,
expose the external urethral orifice.
12. Gently insert tip of catheter into the meatus using forceps until 1 to 2 inches beyond where urine is noted to drain into kidney dish. If no urine
appears although the catheter seems to be in the right place, flush with sterile saline as the lumen may be blocked with gel. If this is still
unsuccessful, withdraw and reinsert.
13. Inflate balloon, using correct amount of sterile saline (usually 20 – 30mls but check actual balloon size). This process should be painless. If
patient feels pain, deflate balloon immediately and reposition catheter.
14. Gently pull catheter until inflation balloon is snug against bladder neck.
15. Connect catheter to drainage system.
16. Secure catheter to abdomen or thigh, without tension on tubing.
17. Place drainage bag below level of bladder.
18. Evaluate catheter function and amount, color, odour and quality of urine.
19. Remove gloves. Dispose equipment appropriately. Wash hands.
20. Document size of catheter inserted, amount of water in balloon, patient's response to procedure and assessment of urine.

COMPLICATIONS
1. Infection, which may lead to stone formation.
2. Stricture formation due either to faulty technique or an irritant material used in the catheter.
3. Creation of a false passage due to wrong technique of insertion.
4. Occasionally, irritation of the bladder may cause severe bladder spasms.

71
7. CHEST TUBE

Chest tubes are inserted to drain blood, fluid, or air and allow full expansion of the lungs. The tube is placed between the ribs and
into the space pleural space.

The area where the tube will be inserted is anesthetized locally. The patient may also be sedated. The chest tube is inserted through
an incision between the ribs into the chest and is connected to a bottle or canister that contains sterile water (underwater seal).
Suction is attached to the system to encourage drainage. A suture and adhesive tape is used to keep the tube in place.

The chest tube usually remains in place until the X-rays show that all the blood, fluid, or air has drained from the chest and the lung
has fully re-expanded. When the chest tube is no longer needed, it can be easily removed, usually without the need for medications
to sedate or numb the patient. Antibiotics may be used to prevent or treat infection.

INDICATIONS
1. Pneumothorax.
2. Hemothorax.
3. Drainage of pleural effusion.
4. Chylothorax
5. Drainage of empyema/lung abcesses
6. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center

CONTRAINDICATIONS
1. Infection over insertion site
2. Uncontrolled bleeding diathesis/coagulopathy

MATERIALS
1. Iodine & alcohol swabs for skin prep
2. Sterile drapes & gloves
3. Scalpel blade & handle
4. Clamp
5. Silk suture
6. Needle holder
7. Petrolatum-impregnated gauze
8. Sterile gauze
9. Tape
10. Suction apparatus (Pleuravac)/underwater seal apparatus
11. Chest tube (size 32 to 40 Fr, depending on clinical setting)
12. 1% lignocaine with epinephrine, 10 cc syringe, 25- & 22-g needles

PRE-PROCEDURE PATIENT EDUCATION

1. Obtain informed consent
2. Inform the patient of the possibility of major complications and their treatment
3. Explain the major steps of the procedure, and necessity for repeated chest radiographs

PROCEDURE
1. Determine the site of insertion. Locate the triangle of safety; bounded by the lateral border of the pectoris major, 5th or 6th
intercostal space, imaginary vertical line between the anterior and mid axillary lines.
2. Surgically prepare and drape the chest at the predetermined site of the tube insertion.
3. Locally anaesthetized the skin and rib periosteum.
4. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect through the subcutaneous tissues, just over the
top of the rib.
5. Puncture the parietal pleura with the tip of a clamp and put a gloved finger into the incision to avoid injury to other organs and to
clear any adhesions, clots, etc.
6. Clamp the proximal end of the chest tube and advance the tube into the pleural space to the desired length.
7. Look for fogging of the chest tube with expiration or listen to air movement.
8. Connect the end of the chest tube to an underwater seal apparatus.
9. Suture the tube in place.
10. Apply a dressing and tape the tube to the chest.
11. Do a chest X ray
12. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as necessary.

72
COMPLICATIONS
Damage to structures:
1. Laceration or puncture of the intrathoracic and/or abdominal organs, all of which can be prevented by using the finger technique
before inserting the chest tube.
2. Damage to the intercostals nerve, artery or vein.
3. Subcutaneous emphysema, usually at tube site.

Equipment:
4. Incorrect intrathoracic or extrathoracic tube position.
5. Chest tube kinking, clogging or dislodging from the chest wall or disconnection from the underwater seal apparatus.
6. Anaphylactic or allergic reaction to surgical preparation or anaesthesia.

Failure:
7. Introduction of pleural infection.
8. Persistent pneumothorax
9. Recurrence of pneumothorax upon removal of the chest tube.
10. Lungs fail to expand due to plugged bronchus; bronchoscopy required.

Recovery from the chest tube insertion and removal is usually complete, with only a small scar. The patient will stay in the hospital
until the chest tube is removed. While the chest tube is in place, the nursing staff will carefully check for possible air leaks, breathing
difficulties, and need for additional oxygen. Frequent deep breathing and coughing is necessary to help re-expand the lung, assist
with drainage, and prevent normal fluids from collecting in the lungs.

73
4. ABDOMINAL SURGICAL EMERGENCIES

1. APPROACH TO ABDOMINAL PAIN

RHC Epigastric LHC

Thoracic Hepatic Thoracic Others Thoracic Others

Pneumonia Hepatitis (viral, MI Pancreatitis Pneumonia Subphrenic
Pleural effusion autoimm etc) Pericarditis Pleural effusion abscess
Hepatomegaly Aortic aneurysm MI Splenomegaly
Biliary Abscess Pancreatitis
Cholangitis Gastrointestinal Gastrointestinal
Cholecystitis Others Oesophagitis PUD
Gallstone disease Subphrenic GERD Diverticulitis
abscess PUD Mesenteric
Pancreatitis Gastric outlet ischaemia
PUD obstructn
Appendicitis CA stomach

Rt Loin Periumbilical Lt Loin

Biliary (see RUQ) Gastrointestinal Others Splenic disease

Obstruction Appendicitis Aortic Aneurysm
Urological Hydronephrosis (early) Pancreatitis Urological (see Rt Loin)
Infection Nephrolithiasis I/O
Pyelonephritis Ureteral Mesenteric
Abscess obstruction ischaemia
Colitis
Others CA IBD
PKD RCC
Renal cyst TCC renal pelvis
Angiomyolipoma Bladder ca
Infarction (ureteral obstructn)

Others
Appendicitis

RIF Hypogastric LIF

Gastrointestinal O&G Gastrointestinal O&G Orthopaedics

Appendicitis Ovarian cyst Colorectal CA Ectopic Infection
Terminal ileitis Ovarian torsion pregnancy Septic hip arthritis
Meckel’s   Ectopic pregnancy Urological Abortion TB hip
diverticulitis PID ARU PID Degeneration
Mesenteric Bladder calculi Uterine rupture OA hip
ischaemia Orthopaedics Cystitis / UTI Fibroid Inflammation
Mesenteric (See LIF) complications RA hip
adenitis Adenomyosis Ankylosing spondylitis
IBD Endometriosis Reiter’s  syndrome
Colitis Inflitration
Colorectal CA 1o bone tumour (hip)
Hernia Metastasis to hip
Destruction
# - NOF, pubic rami
Radiation
Back pathologies (referred pain)

Paediatric ortho Gastrointestinal

conditions Diverticulitis
Transient IBD
synovitis Colitis
Perthes’  dz Colorectal CA
SCFE Hernia

O&G (see RLQ)

74
2. APPROACH TO ABDOMINAL MASSES

RHC Epigastrium LHC

Liver Gallbladder Liver (see RHC) Stomach Spleen Stomach

Pancreatic/periamp Cancer Massive
Massive ullary ca Pancreas Distension (GOO) Infxns Descending colon
Cancer: HCC Acute cholecystitis Pseudocyst CML Cancer
Metastases Hydrops Tumour Aorta Myelofibrosis Diverticular
Myeloprolftve dz Empyema Aortic aneurysm mass/abscess
Alcoholic liver dz Mirizzi syndrome Transverse colon Moderate Faeces
Rt ht failure/ Cancer Retroperitoneal Above causes
tricuspid regurg Ascending colon Diverticular lNpathy Portal hypt Left kidney
Cancer mass/abscess Lymphoma Lymphoprolftve dz (see Rt lumbar)
Moderate Diverticular Faeces Teratoma (lymphoma, CLL)
Above causes mass/abscess Other malignancies H’lytic  anaemia   Left adrenal gland
Lymphoprolftve dz Faeces (thal, HS)
Haemochromatosis Storage dz
Amyloidosis Right adrenal gland (Gaucher’s)

Mild Right kidney Mild

Above causes (see Rt lumbar) Above causes
Infxns: Infxns:
Viral – Hep, IMS Viral hep, IMS,
Bacterial – abscess Endocarditis
Parasitic – hydatid Autoimmune
cyst, amoebic – SLE, RA, PAN
abscess Myeloprolftve dz
Biliary obstruction – PRV, essential
Cirrhosis thrombocytopaenia
Infiltratn
– sarcoid, amyloid
Right Lumbar Umbilical Left Lumbar

Right Kidney Right adrenal gland Liver (see RHC) Pancreas Spleen (see LHC) Descending colon
Hydro/pyonephrosis (see Epigastrium) Cancer
Cancer – RCC Liver (see RHC) Stomach(see Left kidney Diverticular
Polycystic dz Epigastrium) Aorta (see right lumbar) mass/abscess
Single cyst Ascending colon Aortic Aneurysm Faeces
Amyloidosis mass Small intestine
Tuberous sclerosis, Cancer Obstruction Retroperitoneal
VHL Diverticular lNpathy
mass/abscess Mesenteric cyst Lymphoma
Faeces Teratoma
Other malignancies

RIF Hypogastrium LIF

Gastrointestinal O&G Bladder Uterus Gastrointestinal

Appendiceal Ovarian cyst/tumour Acute retention of Gravid uterus Diverticular
mass/abscess Fibroids urine Fibroids mass/abscess
TB gut Chronic retention of Tumour Ca colon/sigmoid
Ca caecum Urogenital: urine Crohn’s  dz  (terminal  
Distended caecum Transplanted kidney Ovary ileitis)
(due to distal Bladder Anal/rectal mass Cyst Faeces
obstruction) diverticulum Cancer Tumour
Crohn’s  dz  (terminal   Ectopic or Similar causes as RIF
ileitis) undescended testis mass

Orthopaedics Vascular:
Chondroma/sarcom Iliac artery
a of ilium aneurysm
Bony metastasis Iliac lymphadenitis

Skin & Msk:

Psoas abscess

75
3. INTESTINAL  OBSTRUCTION  (&  MECKEL’S  DIVERTICULUM)

Causes of IO

1. Mechanical

Intraluminal Mural Extraluminal

Impacted stool Tumours Adhesions (post-op,  Crohn’s)
Gallstone  ‘ileus’             Diverticular stricture Herniae
Foreign body Intussusception Volvulus
Bezoars (phyto-, tricho-) Crohn’s  strictures             Lymph node compression
RT strictures Superior mesenteric artery syndrome

2. Functional (give rise to megacolon)

- Paralytic ileus = hypomobility without obstruction accumulate gas/fluids
DDx mechanical/pseudo: hypo/absent BS as opposed to highpitch tinkling
1. Post-op (most common):
Physiologic ileus spontaneously resolves within 2-3 days, after sigmoid motility returns to normal. (Normal
resumption of bowel activity after abdominal surgery follows a predictable pattern: SB - within hours; stomach -
1-2 days; colon - 3-5 days)
Ileus that persists for more than 3 days following surgery is termed postoperative adynamic ileus or paralytic
ileus. Lap shorter duration of ileus than open.
Complications: Cx of immobility, catabolism due to poor nutrition
2. Sepsis
3. ischaemic (eg bowel, MI)
4. metabolic (hypoK/ hypoMg/ hypoNa, uraemia)
5. hypothyroidism,
6. opiate-induced, antacids, TCA
7. intraabd inflammation/peritonitis, biliary/renal colic, retroperitoneal hematoma
8. trauma (# rib/spine/HI)
- Pseudoobstruction = acute marked LB distension without obstruction.
Clinical picture similar to mechanical obs.
eg. Ogilvie syndrome: in severely ill patients (large bowel peristalsis disappears in ass with retroperitoneal pathology)
50% mortality if patient progresses to necrosis and perf.
- Hirschsprung’s  disease:  absent  ganglia  in  Auerbach’s  plexus

Ogilvie pseudo-obstruction in a septic elderly patient.

Note the massive dilatation of the colon, especially the right colon and cecum

Others: intestinal atresia

Small bowel IO Large bowel IO

1) Adhesions 1) Cancer
2) Herniae 2) Post-diverticulitis stricuture
3) Ileocecal tumour 3) Sigmoid volvulus
4) Intussussception Rarely adhesions (<1%)

76
HISTORY

Consider:
Is there I/O?
Is it functional or mechanical?
Is the bowel strangulated? local peritoneal inflammation
SB or LB obstruction?

4 cardinal symptoms
1. Pain:
- Usually colicky (central griping pain interspersed with periods of no/little pain), 4-5 days duration
- SB: every 2-20min, LB: every 30min or more
- Complete obstruction: constant, sharp pain
- Volvulus: sudden, severe pain
2. Vomiting:
- Pyloric: watery and acid, projectile
- High SB: greenish blue, bile stained
- Lower SB: brown and increasingly foul smelling (feculent = thick brown foul)
- LB: uncommon esp if competent ileocaecal valve, usually late symptom
3. Abdominal distension
- Usu not seen in high obs , esp if pt vomiting
- Closed loop: RIF bulge that is hyperresonant
- SB: distension in centre of abdomen
4. Constipation
- Ask about normal BO frequency
- Early in low obs, late in high obs
- Complete obstipation: cannot even pass flatus

Other pertinent history

- Symptoms of GIT bleed, infection
- Previous surgeries!!!
- Underlying GIT disorders
- Recent change in bowel habit
- Risk factors for ischaemic bowel: atherosclerotic RF, heart disease, previous stroke (see below)
- Suspicion of malignancy: LOW, LOA, previous Ca, FH of Ca

PHYSICAL EXAMINATION

Vitals: Is patient stable? Any fever? (sepsis) Hypotension, tachycardia? (dehydration)

General inspection: Abdominal distension? Cachexia? Confusion? Pale? Jaundice?
Peripheries: Look for signs of dehydration e.g. capillary refill, dry tongue
Palpate lymph nodes – Virchow, Sister joseph

Abdomen:
Dx I/O
Any distension?
Visible peristalsis? – severe obstruction (see browse)
Bowel sounds:
Mechanical: Initially hyperactive/loud resonant/ high-pitch sluggish or absent
Tinkling BS: small bowel obstruction
Ileus: hypo/absent BS
Succussion splash + epigastric tenderness: gastric outlet obstruction

Causes of I/O
SCARS from previous abdominal surgery?
Any masses
Any HERNIAE – inguinal + femoral (more likely strangulated)
DRE: any masses felt, any impacted stools?

Cx of I/O
Any signs of peritonitis: guarding, rebound tenderness, rigid

77
ACUTE MANAGEMENT
o Resuscitate if necessary
1. Maintain airway
2. Give supplementary O2 (high flow if susp ischemia)
o Monitor vitals
- Urinary catheter: monitor hourly urine output
o Drip and suck
1. NBM: rest bowel (alone does not give adequate rest as intestine produce up to 9L of fluids per day)
2. NG tube:aspirate stomach contents and then put on constant suction
3. IV drip: rehydrate and correct elec imbalance
o Start broad spectrum ABx [IO affects normal translocation of bacterial flora] – IV Ceftriaxone 1g + Metronidazole 500mg
o Correct acidosis (ischemia), replace K+ as guided by investigations

Rule out surgical emergencies (history/physical examination/investigations) if suspected, immediate consult with GS Reg
1. Obstructed and strangulated abdominal hernia
2. Volvulus (sigmoid, caecal, stomach)
3. Closed-loop obstruction (competent ileocecal valve)
4. Ischaemic bowel with bowel necrosis
5. Perforation/peritonitis

INVESTIGATIONS
Bloods
Assess complications
FBC: any infection, anemia
UECr :
Any dehydration due to:
- Intra-luminal 3rd space loss (damaged enterocytes unable to reabsorb)
- Vomiting (also assess K+ loss: can perpetuate paralytic ileus)
Acute renal failure from dehydration
ABG
- Acidosis from bowel ischaemia
- Alkalosis due to vomiting (more for pyloric stenosis in children)
ECG (+ CE X2 sets) in elderly

Pre-operative
GXM 4 pints of blood
PT/PTT

Imaging
Assess complications
Erect CXR :
1. air under diaphragm
2. aspiration pneumonia
KUB/AXR:
1. Rigler’s  Sign = double wall sign (obvious bowel wall due to extra-luminal air)
Blue arrows point to falciform ligament, made visible by a large amount of free air in the
peritoneal cavity. The red arrows demonstrate both sides of the wall of the stomach
(Rigler's sign), a sign of free air. The yellow arrow points to a skin fold.

2. Bowel ischaemia with necrosis?

Gas in bowel wall (pneumatosis intestinalis) due to gas gangrene

78
 Diagnostic
KUB (not AXR)
Dilated = 3cm SB, 5cm LB, 9cm caecum (increase risk of perf)
- Erect: air fluid levels (>6)
- Supine (better): look for small or large bowel dilatation on radiograph
Duodenum: C-shaped
Jejunum/proximal ileum: centrally located, “stack  of  coins”  (plicae circulares aka valvulae conniventes)
Distal ileum: plicae circulares disappears, lead-pipe appearance
Colon: more peripheral, incomplete bands (haustrations due to presence of teniae coli)
Gas present in rectum? No: complete obstruction (may require KUB film)
- Sigmoid volvulus? - Caecal volvulus
Coffee bean sign:

There is an air-fluid level (black

arrows) in each segment of dilated
bowel. Note also the central cleft
(white arrow) of the coffee bean.

- Closed loop obstruction? Distal lesion with v. distended cecum (thinnest wall; up to 12cm), ileum not dilated
Barium enema
- Gastrografin preferable if risk of perforation; risk of barium peritonitis (100% mortality!)
- Upper GI barium studies contraindicated
Colonoscopy done without bowel prep (not necessary, and also contraindicated, in IO)
CT colonography

DEFINITIVE MANAGEMENT (Depends on cause)

1) Obstructed abdominal hernia
Herniorrhapy Parrot’s  beak  sign  in  
sigmoid volvulus
2) Sigmoid volvulus (refer below)
Non surgical/ conservative
1.  Ryle’s  tube  decompression:  
- Gown up
- Put  end  of  Ryle’s  tube  in  a  bottle  submerged  in  water
- Insert  lubricated  Ryle’s  tube  into  anus
2. Flexible sigmoidoscopic decompression (recur in as much ast 50%. Elective laparoscopic sigmoid resection and right
hemicolectomy following endoscopic decompression is increasingly being described and performed to treat patients
with volvulus. The suggested interval between endoscopic decompression and definitive surgical intervention is 48-72
hours)
Surgical
a. Sigmoid colectomy with primary anastomosis: Primary anastomosis is performed if the divided bowel ends are viable,
peritoneal contamination is not evident, and the patient is hemodynamically stable
b. Sigmoid  colectomy  with  Hartman’s  procedure  (may  be  reversed  in  3-6/12 – depends on overall clinical condition and
ability to withstand another major surgery)
c. Sigmoid colectomy & formation of double barrel colostomy (Paul-Mikulicz procedure) with future re-anastamosis

d. Sigmoidopexy: fix sigmoid to posterior abdominal wall (rarely done as high risk of recurrence)
Other volvulus
Caecal volvulus: right hemicolectomy with primary ileocolic anastomosis is the surgical procedure of choice (not
endoscopic decompression as only successful in 15-20%. rare to create ileostomy)
Gastric volvulus: gastropexy

79
3) Closed loop obstruction (if due to distal tumour)
Resect bowel + primary anastamosis with proximal defunctioning colostomy
Resect  bowel  +  Hartmann’s/Paul-Mikulicz procedure: if bowel is too inflamed/oedematous to anastamose (high risk of
leakage)
Palliative: colonoscopy with stenting

4) Ischaemic bowel
Supportive management e.g. NBM, drip & suck, antibiotics while waiting for collaterals to re-supply bowel, re-establish
peristalsis
Surgical intervention if bowel is non-viable e.g. gangrenous or necrotic
o Will have relook laparotomy in 2-3/7 to ensure good resection of bowel margins??

5) Perforation (usually in caecum as it is thin walled)

Occurs due to ischaemia of stretched out bowel wall; >12cm dilated
Emergency laparotomy: resect lesion & perforated bowel with generous peritoneal lavage
If lesion e.g. tumour is proximal enough near to the cecum, can do extended right hemi-colectomy
If lesion is distal, may require total-colectomy with ileo-rectal anastamosis
Continue antibiotics following surgery

6) Intussusception
Children:  usually  due  to  hypertrophic  Peyer’s  patches.  Administer  barium enema: watch intussception reduce on
fluoroscopy
Elderly: usually leading point present (polyp, Ca). Barium enema unlikely to work, or if works recurrence rate is high,
therefore surgery is 1st line treatment

7) Post-op paralytic ileus (>3 days post-op)

a. Supportive management: drip & suck, wait for peristalsis to restart
b. Oral gastrograffin: hyperosmotic, causes intraluminal osmosis , can re-establish peristalsis
c. Prokinetic agents: erythromycin, metaclopromide, cisapride

80
MECKEL’S DIVERTICULUM

RULE OF 2s
- Like  the  appendix,  Meckel’s  diverticulum is a true congenital diverticulum, a vestigial remnant of the vitelline duct
- 2 inches in length, 2cm wide, 2 feet from ileocaecal valve
- Occurs  in  2%  of  the  population,  ♂>♀  in  the  ratio  of  2:1
- Usually asymptomatic but if often presents at age 2 if symptomatic
- 2 types of ectopic tissue
Pancreatic (6%)
Gastric (60%) – gastric acid secretion can produce inflammation, peptic ulceration & bleeding, strictures with
subsequent IO
May have both types of tissue or other rarer types (jejunal, colonic, rectal, hepatobiliary, etc)

PRESENTATION
- Usually asymptomatic, found incidentally during barium study or open surgery
- Symptomatic:
1) IO (most common presentation): strictures, intussusception, volvulus, omphalomesenteric band
2) Hematochezia (most common in children): usually massive & painless, due to peptic ulceration
3) Diverticulitis: may present exactly like acute appendicitis i.e. periumbilical pain radiating to RIF. Less prone to
inflammation  as  most  Meckel’s  have  wide  base,  little  lymphoid  tissue  &  are  self emptying
4) Others: umbilical fistula, tumour, perforation etc

INVESTIGATION
Blood: As per IO or lower BGIT
Imaging:
- Technetium-99m pertechnetate scan (investigation of choice): isotope given IV, taken up by gastric mucosa, detected by
gamma scan of the abdomen
- Barium studies: small bowel enteroclysis
- CT  NOT  helpful  as  hard  to  distinguish  Meckel’s  diverticulum  from  small  bowel  loops

MANAGEMENT

- NBM, IV drip, correct electrolyte imbalance

- IO: NG tube on constant suction, supine AXR
- PR bleed: PCT if necessary, gastric lavage to exclude UBGIT, OGD & colonoscopy
- Definitive treatment: surgery (open or laparoscopic)
Wide base: wedge ileal resection with anastamosis
Narrow base: resection of the diverticulum

81
4. ISCHAEMIC BOWEL

RISK FACTORS
Occlusive mesenteric ischemia
a. Embolic (most lodge in SMA) – becoming less common
i. Recent MI
ii. Dysarrhythmia (esp AF embolization)
iii. Valvular heart disease
b. Thrombosis  (Virchow’s  triad)  – becoming more common
i. Age >50
ii. CCF
iii. PVD
iv. Hypovolemia
v. Prothrombotic states – more in venous thrombosis (young)

Non-occlusive (no arterial or venous abn, due to vasospasm and constriction) – 20-30% of acute ischemia
a. Poor perfusion states
i. Hypotension
ii. Hypovolemia
iii. CCF
iv. MI
v. Renal failure
b. Compression from ext sources (eg. intraabdominal tumor)
c. Vasculitis
d. Radiotherapy
e. Vasoconstriction
i. digitalis
ii. strangulation (from volvulus/hernia)

Tissue injury can result from one of 2 mechanisms: (1) ischemic injury to the bowel or (2) reperfusion injury

2 Watershed areas:
a) Marginal artery of Drummond / Griffith’s  point:  SMA  and  IMA
b)  Sudeck’s  point:  Left  colic  artery  and  Superior  rectal  artery

Three progressive phases of ischemic colitis have been described:

a) A hyperactive phase occurs first, in which the primary symptoms are severe
abdominal pain and the passage of bloody stools. Many patients get better and
do not progress beyond this phase.

b) A paralytic phase can follow if ischemia continues; in this phase, the

abdominal pain becomes more widespread, the belly becomes more tender to
the touch, and bowel motility decreases, resulting in abdominal bloating, no
further bloody stools, and absent bowel sounds.

c) Finally, a shock phase can develop as fluids start to leak through the
damaged colon lining. This can result in shock and metabolic acidosis with
dehydration, hypotension, tachycardia and confusion. Patients who progress to
this phase are often critically ill and require intensive care.

Acute mesenteric ischemia (classical triad)

1. Acute severe abdo pain
2. No physical signs
3. Rapid hypovolemia shock

HISTORY (typical but vague) – high index of suspicion!!

Chronic
Gut claudication: post prandial colicky pain (10min to 3hr after a meal) food fear LOW and malnutrition
Blood in stools (as bowel begins to die) – maroon or bright red
Acute
Severe abdominal pain: out of proportion with examination findings: tends to be constant and central, or RIF
Blood in stools
Paralytic ileus, usu occurring in the splenic flexure (watershed area receiving blood from the most distal arterial branches)
Diarrhoea/constipation
Positive FOBT (sloughing of dead ischemia bowel) in 75%

82
PHYSICAL EXAMINATION

Initial Bowel compromise

Thin, writhing in pain Fever, Tachycardia, hypotension
No peritoneal sign Peritonism – rebound, guarding, rigid
Auscultation may reveal a bruit Nausea/vomiting
Distension a late feature, often first sign of impending bowel Malaena/hematemesis
infarction Massive abdominal distension
Back pain
Shock

INVESTIGATIONS
Bloods
1. FBC: high Hb/ Hct (due to plasma loss/ hemoconcentration), high TW >15 in 75%
2. ABG: Metabolic acidosis (persistant) – 50%
3. UECr: renal failure, hypovolemia
4. PT/PTT: hypercoagulable states (if present, can add Protein C/S, AT III)
5. Raised amylase / LDH

Imaging
- AXR
1. Submucosal hemorrhage and edema in the colon produce a characteristic thumbprinting

2. Dilated bowel from ileus

3. Intramural air/ air in portal venous system (ischemia)
4. Free air in abdomen (perf)
- CTAP:
Exclude other causes of abdominal pain
Ischemic colitis: SMA or superior mesenteric vein thrombosis, intestinal pneumatosis, portal
venous gas, lack of bowel wall enhancement in contrast CT, thumbprinting and ischemia of
other organs.
Non specific findings: distended bowel, an absence of intestinal gas, a thickened bowel wall,
mesenteric vascular engagement, ascites and air-fluid levels
- MRI as sensitive as CT
- Barium enema: stricture secondary to ischemia

- Arteriography (limited role in diagnosis):

confirm the presence and extent of occlusive disease.
AP views demonstrate collateral pathways, lateral projections show the origins of visceral
branches.
Features: dilated arteries, prominent accumulation of contrast material in the bowel
parenchymal, and dense and early venous filling
Can ppt acute ischemia: ensure that the patient is well hydrated.
Thrombosis - complete lack of visualization of the SMA and its branches (as thrombosis
usually starts at the prox end of SMA), Embolism to the SMA - filling of the proximal SMA
only with a sharp cutoff of the artery

Others
1. ECG: AF, STEMI
2. Colonoscopy: procedure of choice if the diagnosis remains unclear.
a. Ischemic colitis has a distinctive endoscopic appearance;
b. Rule out alternate diagnoses eg infx/IBD
c. Biopsies can be taken
d. Visible light spectroscopy (analyze capillary oxygen levels), performed using catheters placed through the 5 mm channel of
the endoscope, is diagnostic

MANAGEMENT
Acute
1. ABC
a. maintain airway and give high-flow O2
b. establish at least 1 large bore IV line and infuse fluids at maintenance rate (unless patient in shock)
2. Monitoring (as patients are prone to extensive peritonitis, shock, metab acidosis)
a. Urinary catheter to monitor urine output
3. Consider NGT
4. Antibiotics: IV Cephalosporin? and metronidazole

Definitive

83
5. ACUTE APPENDICITIS

HISTORY

- Classic: LOA with periumbilical pain which radiates to the RIF, followed by nausea & vomiting (in ½)
- N/V almost always occurs after pain, if it precedes pain, exclude IO
- May have diarrhoea or constipation
- Inflamed appendix near bladder/ureter may cause irritative voiding symptoms & haematuria
- Fever (late): >39deg uncommon in first 24h but common after rupture

PHYSICAL EXAMINATION

- Most  specific  physical  findings:  RIF  (McBurney’s  point)  tenderness  on  percussion,  rebound  tenderness,  rigidity  &  guarding
- RIF mass may be palpable
- LIF tenderness in patients with situs inversus or lengthy appendix extending to the LIF

- Cough sign: RIF pain on coughing (localized peritonitis)

- Rovsing sign: RIF pain with palpation of the LIF - While this maneuver stretches the entire peritoneal lining, it only causes
pain in any location where the peritoneum is irritating the muscle.
- Obturator/ Cope sign: RIF pain with internal rotation of a flexed right hip
- Psoas sign: RIF pain with hyperextension of the right hip - the inflamed appendix is retrocaecal in orientation

Atypical ppt:
- Infants/children may present with inflamed hemiscrotum due to migration of pus through patent processus vaginalis – often
mistaken for acute testicular torsion
- Retrocaecal right flank pain
- Pregnancy pushes appendix up right upper quadrant pain
- Pelvic appendix irritates bladder and rectum suprapubic pain, pain on urination, feeling of need to defaecate

CAUSES
- Obstruction of appendiceal lumen
Faecaliths: calcium salts & faecal debris collect around nidus of faecel material within appendix
Lymphoid hyperplasia:  a/w  inflammatory  (Crohn’s)  &  infective  dz  (GE,  URTI,  IMS,  measles)
Less common causes: parasites, TB, tumour, FB

DIFFERENTIAL DIAGNOSES

1) Mesenteric adenitis: self limiting inflammation of mesenteric LNs in RIF, a/w viral infections
2) Meckel’s  diverticulitis:  inflammation  of  Meckel’s  diverticulum  (see  below)
3) Terminal  ileitis:  usually  due  to  Crohn’s  disease  
4) Typhilitis/caecitis
5) Ischaemic colitis
6) Colon cancer
7) Appendiceal stump appendicitis
8) Psoas abscess

Most frequent misdiagnoses in Females: PID, followed by gastroenteritis and urinary tract infection / in Children: gastroenteritis,
followed by upper respiratory infection and lower respiratory infection.

INVESTIGATIONS

Blood: FBC, UECr, CRP, Blood culture, PT/PTT, GXM

Urine: UFEME (may have pyuria & haematuria)
Imaging: Erect CXR, CTAP - greater sensitivity/ accuracy/ NPV, abdominal U/S
AXR (limited use): fecalith, appendiceal gas, localized paralytic ileus, blurred right psoas, and free air

84
MANTRELS Score

Characteristic Score
M = Migration of pain to the RLQ 1
A = Anorexia 1
N = Nausea and vomiting 1
T = Tenderness in RLQ 2
R = Rebound pain 1
E = Elevated temperature 1
L = Leukocytosis 2
S = Shift of WBCs to the left 1
Total 10

0-3 could be discharged without imaging,

4-6 undergo CT evaluation,
> 7 receive surgical consultation

MANAGEMENT

- NBM, IV drip, correct electrolyte imbalance

- IV antibiotics: Preoperative antibiotics have demonstrated efficacy in decreasing postoperative wound infection rates
- Symptomatic relief: anti-emetics & analgesia

- Definitive treatment: appendicectomy (open or laparoscopic)

- Urgent vs Emergent:
appendectomy within 12-24 hours of presentation is not associated with an increase in hospital length of stay, operative time,
advanced stages of appendicitis, or complications compared with appendectomy performed within 12 hours of presentation
- Perforated appendix (emergent vs interval): mild symptoms and localized abscess or phlegmon on abdominopelvic
computed tomography (CT) scans initially treated with IV antibiotics and percutaneous or transrectal drainage of any
localized abscess. If the patient's symptoms, WBC count, and fever satisfactorily resolve, oral antibiotics. Delayed
(interval) appendectomy can be performed 4-8 weeks later.
- Conservative treatment for appendiceal mass: Oschner Sherren regime
Omentum naturally wraps around inflamed appendix, containing inflammatory process
Symptomatic treatment as well as antibiotics, monitor patient as well as size of mass
When mass has reduced in size, patient is stable, do surgery (less inflammation: easier)
Exceptions: very young or very old patients, or patients with suspected appendicular abscess (require incision &
drainage of pus)

Delayed diagnosis and treatment account for much of the mortality and morbidity associated with appendicitis.

The rate of perforation varies from 16% to 40%, with a higher frequency occurring in younger age groups (40-57%) and in patients
older than 50 years (55-70%), in whom misdiagnosis and delayed diagnosis are common.

Complications occur in 1-5% of patients with appendicitis, and postoperative wound infections account for almost one third of the
associated morbidity.

85
5. OESOPHAGEAL DISEASES

1. ANATOMY OF THE OESOPHAGUS

- Oesophagus is a muscular tube that is 25cm (10 inches) long

- Starts at the cricoid cartilage (C6 vertebra) from the
oropharynx and continues into the stomach at the level of T10
- Upper oesophageal sphincter = cricopharyngeus muscle
- Lower sphincter is not an anatomical sphincter, but
physiological:

(i) Increased tone of the muscularis propria at the lower

oesophageal sphincter
(ii) Fibres of the right diaphragmatic crus loop around the
cardio-oesophageal junction and contract during
coughing, sneezing etc when intra-abdominal
pressure increases, thus preventing reflux
(iii) Angle of His where the oesophagus joins the
stomach – acts as a valve
(iv) Intra-abdominal pressure being higher than intra-
thoracic pressure

- 3 narrow points along the course of the oesophagus

(i) Cricopharyngeus muscle (15cm from incisor teeth)

(ii) Carina where the left bronchus crosses the
oesophagus (27cm from incisors)
(iii) Where the oesophagus passes through the
diaphragm (40cm from incisors)

- Structure: mucosa, submucosa, muscularis propria, adventitia (no peritoneal lining except for a short segment of intra-
abdominal oesophagus) very distensible

Muscularis propria is composed of striated muscle in the upper one-third, striated and smooth muscle in the middle third, and
smooth muscle in the lower third

- Blood supply (roughly divided into thirds): Inferior thyroid artery to upper third, oesophageal branches of the aorta to the middle
third, oesophageal branches of left gastric artery to lower third

- Venous return also divided into thirds: Brachiocephalic veins (upper), azygos veins (middle), left gastric vein (lower) --- a
portosystemic anastomosis exists at the lower oesophagus thus leading to formation of varices in portal hypertension

2. PHYSIOLOGY OF SWALLOWING

- Process of mastication forms a food bolus on the dorsum of the tongue

- The tongue then contracts upwards and backwards pushing the food bolus against the hard palate

- Soft palate elevates (contraction of palatoglossus) to close off nasopharynx

- Further elevation of tongue pushes food bolus into oropharynx

- As the base of the tongue is elevated posterior, the epiglottis falls back; at the same time, the pharyngeal muscles contract to
bring the posterior surface of the larynx upwards to make the laryngeal inlet smaller closed off by the epiglottis

- Pharyngeal muscles contract to propel food bolus past the relaxed cricopharyngeus into the oesophagus

- Once in the oesophagus, involuntary contractions of the muscularis propria form peristaltic waves to propel food bolus into
stomach

86
3. APPROACH TO DYSPHAGIA

CAUSES OF DYSPHAGIA

- Dysphagia can be divided into oropharyngeal and oesophageal dysphagia

- In each anatomic region the dysphagia can be caused by neuromuscular dysfunction (impaired physiology of swallowing) or
mechanical obstruction to the lumen

Oropharyngeal Oesophageal
Functional (Neuromuscular diseases) Functional (Neuromuscular diseases)
Stroke Achalasia
Parkinson’s disease Spastic motor disorders
Brain stem tumours Diffuse oesophageal spasm
Degenerative conditions e.g. ALS, MS Hypertensive lower oesophageal sphincter
Nutcracker oesophagus
Peripheral neuropathy Scleroderma
Myasthaenia gravis
Myopathies e.g. myotonic dystrophy

Mechanical (Obstructive lesions) Mechanical (Obstructive lesions)

Tumours Intrinsic structural lesions
Inflammatory masses e.g. abscess Tumours
Oesophageal webs Strictures: Peptic (reflux oesophagitis)
(MRCP) Radiation
Chemical (caustic ingestion)
Medication
Pharyngeal  pouch  (Zenker’s  divert) Lower  oesophageal  rings  (Schatzki’s  ring)

Oesophageal webs (Plummer-Vinson)

Anterior mediastinal mass Foreign bodies

Extrinsic structural lesions

Mediastinium – retrosternal thyroid,
lymphadenopathy, Vascular compression
(enlarged aorta or left atrium)
Thoracic inlet mass
Kyphoscoliosis

Others
Oesophagitis: Reflux
Infectious (candida, herpes)
Radiation-induced
Medication-induced
Chemical-induced (alcohol)

Plummer Vinson syndrome / Paterson Brown Kelly syndrome

- Triad of dysphagia (oes web), glossitis, angular stomatitis (Fe def anemia)
- post menopausal women
- genetic and nutritional factors
- premalignant oes/hypopharynx/oral SCC
- Tx: Fe supplement, Oes dilatation

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HISTORY
I. Dysphagia: a) Difficulty initiating / Food stuck
b) Solids / Liquids initially
c) Progressive (CA, stricture) / Intermittent (webs, rings, oes spasm, nutcracker)
II. Associated symptoms: a) Odynophagia
b) Choke, cough, nasal regurgitation
c) Regurgitation of undigested food
d) Nasal voice
III. Complications
IV. RF

1. Differentiating oropharyngeal from oesophageal dypshagia

(i) Oropharyngeal
- Presenting complaint is usually of difficulty in initiating swallowing
- May be associated with choking, coughing, nasal regurgitation
- Voice may sound nasal (bulbar palsy)
- Cause of oropharyngeal dysphagia is usu neuromuscular rather than mechanical; stroke is the most common cause
(ii) Oesophageal
- Presenting complaint is that of food “getting  stuck”  in  the  throat  or  chest
- Patient’s  localisation  of  the  symptom  often  does  not  correspond  to  actual  site  of  pathology
- Can be due to either neuromuscular dysfunction or mechanical obstruction

2. Differentiating mechanical obstruction from neuromuscular dysfunction

(i) Mechanical
1. Patient complains of more difficulty swallowing solids than fluids
2. May have regurgitation of undigested food
3. Recent onset dysphagia that is progressively worsening, with loss of weight high suspicion of oesophageal cancer
- Intermittent symptoms are suggestive of webs, rings
(ii) Neuromuscular
1. Patient complains of more trouble swallowing fluids than solids
2. Dysphagia more long-standing, slowly progressive
3. Intermittent symptoms suggestive of diffuse oesophageal spasm, nutcracker oesophagus
4. May have history of stroke, neuromuscular disease

3. Is there odynophagia (pain associated with difficulty swallowing)?

(a) Oesophagitis: infectious (candida, herpes), post-radiation, chemical-induced (usually alcohol), reflux oesophagitis
(b) Oesophageal spasm
(c) Scleroderma
(d) Achalasia (occurs late)
(e) Oesophageal cancer (occurs late)
(f) Oesophageal rupture/stretching

4. Complications (3)
- Symptoms of anaemia (bleeding from tumour, or as part of Plummer-Vinson syndrome)
- Symptoms of aspiration pneumonia – fever, cough, shortness of breath esp at night
- Locally advanced tumour:
o Hoarseness (recurrent laryngeal nerve)
o Thoracic spine pain (spread posteriorly to thoracic spine)
o SOB (pleural effusion sec to lymphatic blockage by tumor infiltration)
o Fever, cough and haemoptysis (tracheo-oesophageal fistula)
o Haematemesis (invasion into aorta massive bleed) – rare
Always differentiate hematemesis from hemoptysis.
- Mets: Neck lump (LN), jaundice, bone pain

5. History of predisposing conditions (RF)

- Reflux symptoms e.g. retrosternal burning pain (heartburn), sour fluid reflux into mouth (acid brash), excessive salivation (water brash),
postural aggravation on lying down
- Caustic chemical ingestion in the past
- Medication history: Antibiotics (eg, doxycycline, tetracycline, clindamycin, trimethoprim-sulfamethoxazole), potassium chloride,
nonsteroidal anti-inflammatory drugs (NSAIDs), quinidine, emperonium bromide, and alendronate (Fosamax)
- Loss of weight occurs in cancer and achalasia (much later onset in achalasia compared to cancer)
- Smoking, chronic alcohol intake
- Radiation to the chest
- Symptoms of systemic disease e.g. stroke (focal neurological deficits), scleroderma (CREST: telangiectasia, sclerodactyly, calcinosis,
Raynaud’s),  Parkinson’s

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PHYSICAL EXAMINATION

1. General condition
- Vitals: the patient may be hypovolaemic from vomiting/decreased intake
o Nutrition: presence of cachexia
o Dehydration (mucous membranes, skin turgor, etc)
- Conjunctival pallor: bleeding from tumour, oesophagitis ulcerations, or associated with P-V syndrome
- Scleral icterus: metastases to liver

2. Disease/Causes
- Presence of cervical lymph nodes (esp  Virchow’s  node)
- Scars/marks over the chest and abdomen suggesting previous radiation
- Palpable mass in abdomen (not likely)
- Neuro examination (esp CN, PD features, myopathy)
- PR examination for malaena
- Bedside swallowing test?

3. Complications of disease
- Signs of pneumonia: patient febrile, may be toxic, lung crepitations, decreased air entry usually over right lower lobe
- Signs of mets: Hepatomegaly, Ascites

4. Treatment
- Tube feeding through NG tube, gastrostomy/jejunostomy – if aspirates seen, what is the colour?
- Total parenteral nutrition
- Surgical scars

MANAGEMENT

1. Stabilise patient
- Resuscitate if patient is haemodynamically unstable
- IV fluids (correct fluid deficits and also any electrolyte derangements)
- Feeding
o Consider feeding with fluids if patient can tolerate it (only having problems with solid food) otherwise consider tube feeding or
TPN need  to  correct  patient’s  nutritionally  debilitated state
o Keep NBM if patient cannot tolerate even fluids
- Treat any aspiration pneumonia – NBM, IV antibiotics

2. Investigate for underlying cause and treat it

INVESTIGATIONS

Diagnostic

1. Barium swallow

- Advantage of barium swallow is that it is less invasive than OGD, especially when suspecting webs, diverticula in the oesophagus
where OGD may cause perforation;
- CI in patients with difficulty initiating swallowing high risk of aspiration (therefore, give slowly and carefully)
- Visualisation of obstructive lesions:
o Shouldering of a stricture (benign strictures form a smoother contour whereas malignant strictures form a more right-angled
contour)
o Bird’s  beak sign of achalasia

Achalasia Benign stricture Carcinoma Cockscrew

- Visualisation of pharyngeal pouch or oesophageal diverticulum

- Diffuse oesophageal spasm gives a corkscrew appearance

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2. Oesophagogastroduodenoscopy (OGD)

- Advantage is direct visualisation of the lesion and ability to take tissue biopsy (especially useful in malignancy)
- May also be therapeutic (stopping bleeding from a tumour, stenting the lumen, etc)

3. Manometry

- Gold standard for diagnosing achalasia:

(i) Absence of peristalsis
(ii) Very high pressures at the lower oesophageal sphincter
(iii) Absence of relaxation at the LES on swallowing food

4. Videofluroscopic examination of swallowing (VFES) – using barium

Flexible-endoscopic examination of swallowing (FEES)

- Used to assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various consistencies of
food during swallowing
- VFES limited to cervical oesophagus (unable to exclude distal oes lesions)

Supportive

1. Blood investigations:

- Full blood count – Low Hb (anaemia from chronic blood loss)

High TW (aspiration pneumonia)

- Urea, electrolytes, creatinine – electrolyte disturbances from vomiting, poor intake; raised creat and urea in dehydration (creat will be
raised more than urea if patient has prerenal failure from dehydration)

- Liver function tests – low albumin with nutritional deprivation

2. CXR

- Consolidation (aspiration pneumonia)

3. 24-hour pH probe monitoring

- If patient complains of reflux symptoms and no signs are seen on OGD (see later section on Gastro-oesophageal reflux disease)

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4. OESOPHAGEAL CANCER

EPIDEMIOLOGY
- Third most common gastrointestinal tract cancer in Singapore (1st: CRC, 2nd: gastric)
- M > F, Adenocarcinoma more common in West whereas SCC more in East
- Increasing incidence with age
- Decreasing incidence overall, increasing in distal oes

RISK FACTORS
SCC (70%) Adenocarcinoma (30%)
Modifiable 1. Smoking (100X) 1. Smoking (10X)
2. Alcohol (2X) 2. Obesity GERD Barrett’s
3. Caustic injury [middle 1/3]
4. Diet: Hot drinks, preserved foods (nitrosamines), betel nuts;
vitamin / mineral def (selenium, vit E, beta-carotene)
Non- 1. Achalasia (2-8%) Barrett’s (30-40X, 1% per year) [distal 1/3]
modifiable 2. PV synd (10%) [upper 1/3]
3. Tylosis (AD disorder with keratosis of palms and soles)
4. Oes. diverticulum
5. Irradiation

PATHOLOGY

- 70% squamous cell carcinoma, 30% adenocarcinoma

- SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lower third and gastro-oesophageal junction
(related  to  reflux  and  Barrett’s  oesophagus)
- Overall: 10% of cancers occur in the upper third, 60% in the middle third, 30% in the lower third
- Three growth patterns:
Fungating (60%)
Ulcerative (25%)
Infiltrative (15%)
- Tumour spread: direct extension into surrounding structures, vascular invasion, lymphatic spread
- Common sites of metastases: liver, lung, bone

STAGING

AJCC 7th edition 2010

SCC and adenocarcinoma are staged separately
Subclassification of nodal (N) status according to the number of regional nodes containing metastases
Reclassification of tumors at the gastroesophageal junction (GEJ) and/ or the proximal 5 cm of the stomach that extend
into the GEJ or esophagus
Reassignment of stage groupings using T, N, M categories as well as histologic grade of differentiation (G), and for SCCs,
tumor location
Redefining of Tis (carcinoma in situ) as high-grade dysplasia
Subclassification of T4 disease based upon potential resectability of adjacent involved organs or structures

T Tis High-grade dysplasia

T1a Tumour invading lamina propria or muscularis mucosa
T1b Tumour invading submucosa but does not breach submucosa
T2 Tumour invades the muscularis propria
T3 Tumour invades adventitia
T4a Resectable tumor invading pleura, pericardium, or diaphragm
T4b Unresectable tumor invading other adjacent structures
N N1 1-2 Regional node involvement
N2 3-6
N3 7 or more
M M1 Distant metastases

Stage T N M Grade Tumor location Histologic grade (G)

0 is 0 0 1, X Any GX Grade cannot be assessed—stage
grouping as G1
I (A/B) 1-3 0 0 1-3 Any/ lower (Ib)
II (A/B) 2/3 0-1 0 2/3 Upp mid/ lower G1/2/3/4 Well/Mod/Poorly/Un differentiated

III (A-C) 1-4a 0-3 0 Any Any

IV any any 1 Any Any

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PRESENTATION

Usually of insidious onset, with earliest symptoms being non-specific  e.g.  retrosternal  discomfort,  “indigestion”,  and  most  patients  
already have advanced disease when they are diagnosed
– 75% have lymph node involvement at time of diagnosis.
– 50% of patients have unresectable cancer on presentation

Asymptomatic  from  screening  of  Barrett’s  oes  patients  (early  detection)

1. Dysphagia
- Present in 80% of patients – most common presentation
- Lack of serosa oes is distensible > 60% occlusion is needed before dysphagia occurs (Late presentation – T3/4)
2. LOW (classically withOUT LOA – patient still feels hungry)
3. Regurgitation

1+2+3 = CA oes until proven otherwise

Pain develops late and is usually due to extra-oesophageal involvement

Complications

4. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult)

5. Vocal cord paralysis (left - due to its longer course through the aortopulmonary window > right)
6. Aspiration pneumonia
7. Tracheo-oesophageal or broncho-oesophageal fistula

INVESTIGATIONS – 4 OBJECTIVES

(A) Diagnosis

1. Oesophagogastroduodenoscopy (Gold standard)

1. Allows biopsy of the lesion confirmatory histological diagnosis
2. Estimate distance from incisor (facilitates op planning)
3. Determine extent of tumor
4. Look for synchronous lesions
5. Detect complications: Bleeding (can stop the bleed!), Obstruction/Stenosis
6. Adjunct EUS (more sensitive for depth and nodal status)
[Same purposes/advantages as colonoscopy in CRC]

2. Barium swallow
- 92% accuracy in showing mucosal irregularity & annular constrictions but not able to dx malignancy with confidence
- Useful if OGD cannot pass through

(B) Staging (Look very hard for CI of surgery due to high morbidity and mortality)

i. Local
1. Endoscopic ultrasound (ideal in CA oes, rectal, stomach as structures are enclosed)
- If endoscope can pass around the lesion, good for T staging (T) – depth of invasion
- Also to identify enlarged regional lymph nodes (N) – FNA to confirm mets
Suspect LN mets if round, hypoechoic, well-defined borders
2. CT scan or MRI
- Can be used for T, N, and M staging
- CT T: local invasion, regional LN,
CT AP: liver/ adrenals mets, distant LN,
CT Neck: cervical LN
- Upper oes: CT NTAP
Lower oes: CT TAP
3. Bronchoscopy
a. Exclude direct tracheal involvement especially in tumours involving upper two-thirds of oesophagus
b. Laryngoscope : vocal cord paralysis

Look very hard for CI of surgery due to high morbidity and mortality.

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ii. Distant

1. Chest X-ray
- Mets
o Presence of any lung metastases
o Pleural and/or pericardial effusion
- Cx
o Aspiration pneumonia
o Tracheal deviation or extrinsic compression of tracheobronchial system
o Widened superior mediastinum in an upper oesophagus tumour
o Raised hemidiaphragm with phrenic nerve involvement

2. CT scan (as above)

3. PET scan / CT PET
- Distant N, M.
- Expensive ($2000!)
- Used for patients deemed fit for operation.

4. Bone scan for bony metastases

Staging laparoscopy not done!

(C)Complications

1. Full blood count – Low Hb (anaemia from chronic blood loss)

High TW (aspiration pneumonia)

2. Urea, electrolytes, creatinine

a. electrolyte disturbances from vomiting, poor intake;
b. raised Cr & urea in dehydration (Cr will be raised more than urea if patient has prerenal failure from dehydration)

3. Liver function tests – low albumin with nutritional deprivation, liver mets (rare)

4. CXR (as above)

Predictors of poor outcome: Sig LOW, Low albumin.

(D) Pre-op (operation requires thoracotomy)

1. Lung function test eg. Spirometry

a. In view of single lung ventilation during operation
b. Risk of COPD – Smoking is impt RF for CA oes (esp SCC)
FEV1??, FVC > 1.25L??
2. 2DE (in view of major op) – ideal EF>40%
3. PT/PTT, GXM
4. Usual: FBC, UECr

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TREATMENT

Principles
- Three modalities available – surgery, chemotherapy, radiotherapy – used singly or in combination
- Aims of treatment: Curative or palliative (50%)
- Surgical treatment is usually performed with curative intention, but can also achieve good long-term palliation of symptoms
- Choice of treatment depends on several patient factors: age, co-morbidities, nutritional state, life expectancy, and prognosis

Surgery
- Curative in early lesions and part of multimodal therapy in more advanced stages
- Resection should not be done in patients with distant metastases or contraindications to surgery

1. Endoluminal surgery – for early lesions (Tis, T1a); no attempt to remove any LNs (usually no LN involvement)
i. Endoscopic mucosal resection (EMR) – Cx: bleeding, perf (may be prevented with sufficient saline injection to raise the
mucosa containing the lesion), stricture
ii. Mucosal ablation using photodynamic therapy , Nd-YAG laser, or argon plasma coagulation

2. Oesophagectomy

(i) Ivor-Lewis / Lewis Tanner

Two-stage procedure involving gastric mobilisation (first stage, done through upper midline abdominal incision),
oesophagectomy and gastro-oesophageal anastomosis in the chest (second stage, through right thoracotomy incision)

(ii) Trans-hiatal
Done via two incisions – one in the abdomen and one in the neck
Blunt oesophagectomy, gastric mobilisation, and gastro-oesophageal anastomosis in the neck
Less morbidity than Ivor-Lewis as the chest is not opened, but controversial

(iii) Tri-incisional (McKeown approach)

Three incisions – abdominal, chest, and also left neck incision for gastro-oesophageal anastomosis in the neck

Performed with two-field lymphadenectomy (upper abdominal and mediastinal)

No difference in survival between trans-hiatal and I-L modalities; the stage of the cancer when the operation is performed is
a greater factor influencing survival

Radical en-bloc dissections not shown to improve survival

Oesophagectomies have high mortality (5-10%) and morbidity (25%) rates, thus patients have to be carefully selected in
order to maximise survival benefit from surgery

Complications
Dependent on extent of surgery and incisions used
- Intraoperatively, injury to lung, thoracic duct, RLN can occur

- Respiratory complications higher in thoracotomies – atelectasis, pneumonia

- Anastomotic leak and resultant mediastinitis (for chest anastomosis) most feared

- Anastomotic stricturing can also occur

- Reflux can result in the long term due to loss of the LES

3. Palliative debulking for obstructive symptoms

Radiotherapy
- Usually given in combination with chemotherapy
- Primary treatment for poor-risk patients
Palliation for unresectable lesions with obstructive symptoms, pain and bleeding
- SCCs are radiosensitive
- Modalities: External beam radiation or brachytherapy
- Obstructive symptoms may worsen temporarily after radiotherapy due to oedema
- Complications: tracheo-oesophageal fistula, stricture

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Chemotherapy
- Current regimen: 5-Fluorouracil and cisplatin
- Addition of chemotherapy to external beam radiation for unresectable cancers shown to have improved survival compared to
EBRT alone
- Chemotherapy given preoperatively and postoperatively improves survival

Overall curative treatment

Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection), oesophagectomy, and postoperative
adjuvant chemoradiotherapy for responsive tumours

Palliative treatment
1. Ablation
o Endoscopic laser fulguration (high frequency electric current)
o Photodynamic therapy is a new treatment option - use of drugs that are absorbed by cancer cells; when exposed to a
special light, the drugs become active and destroy the cancer cells
o Radiofrequency
o Cryotherapy
2. Surgical debulking
3. Bypass surgery rarely done nowadays
4. Stenting to maintain lumen patency and occlude fistulas – endoscopic / radiological?
o Cx: metallic Perf (friable tumor)
Bleeding
Risk of GERD, aspiration lifelong PPI

Feeding in oesophageal obstruction

- Feeding via oropharyngeal route is preferred unless the passage is obstructed or it is unsafe for the patient to feed via that
route (i.e. risk of aspiration)
o If still able to pass NG tube around tumour feed via NG (but also consider complications with long-term NG
placement e.g. erosions around nasal area, sinusitis);
o consider PEG placement for long-term feeding if able to get scope around tumour
- If unable to pass tube or scope around tumour,
o consider open gastrostomy
o Total parenteral nutrition is another option but has more complications, more costly
o Relief of obstruction via various techniques as listed above help to enable oral feeding, but most techniques are not
long-lasting and dysphagia will return with tumour growth

PROGNOSIS
- 80% mortality at 1 year, overall 5-year survival <10%

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5. GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD / GERD)

EPIDEMIOLOGY
Incidence in Singapore not known
Increasing prevalence, more common in males than females
Singapore Chinese > other races

PATHOPHYSIOLOGY
- Lower oesophageal sphincter is a physiological sphincter with various mechanisms that help to prevent reflux
- Some physiological reflux occurs that is rapidly cleared by peristaltic movements in the oesophagus
- GORD results from various pathophysiological factors (loss of the normal protective mechanisms, or the mechanisms are
overwhelmed) singly or in combination:
I. Motor failure of oesophagus with loss of peristalsis
II. Loss of LES function – decreased tone, hiatal hernia, iatrogenic injury
III. Increased intra-abdominal pressure – obesity, tight garments, large meal

IV. Delayed gastric emptying

- Acid incites inflammation in lower oesophagus – extent of inflammation increases with increasing duration of contact with acid
- Chronic inflammation results in  complications  of  GORD:  oesophagitis,  stricture,  Barrett’s  oesophagus

CAUSES/RISK FACTORS
- Motility disorder of oesophagus e.g. scleroderma
Malfunction of LES
Hiatal hernia (loss of normal LES mechanisms)
Drugs that cause smooth muscle relaxation e.g. calcium channel blockers, sedatives, beta agonists, anticholinergics, etc.
Coffee and smoking also cause LES relaxation.
- Chronically increased intra-abdominal pressure – pregnancy, chronic cough, obesity, constipation, etc
- Eating habits – lying down after a heavy meal
Any cause of decreased gastric emptying

PRESENTATION

- Heartburn: retrosternal pyrosis (=burning sensation in upp abdo)

- Acid brash/Regurgitation: reflux of sour gastric juices into back of mouth i.e. regurgitation
o These symptoms occur usu after food, particularly a heavy meal, and are aggravated by lying flat (posturally related)
- Other symptoms: globus (feeling of a lump at the throat), water brash (hypersalivation in response to reflux)
Chest pain (can mimic anginal pain with radiation to neck, jaw, arm), nausea high false positive

- Complications
o Long-standing disease can lead to dysphagia due to stricture formation; dysphagia can also result from an underlying
oesophageal motility disorder; odynophagia suggests oesophagitis with ulceration
o Reflux can also lead to pulmonary symptoms: chronic cough, chest infections (aspiration)

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COMPLICATIONS
1. Pain and spasm
2. Stricture
3. Shortening of oesophagus
4. Dysmotility
5. Haemorrhage (occult > frank)
6. Ulceration
7. Barrett’s  oesophagus  (see  below)
8. Schatzki’s  ring  (constrictive  ring  at  the  squamocolumnar junction composed of mucosa and submucosa)
9. Malignancy  (adenocarcinoma  arising  from  Barrett’s  oesophagus)

DIAGNOSIS

1. History!! is important as most patients with reflux are seen in the primary setting with no facilities for detailed investigation
- Exclude cardiac cause of chest pain, and exclude malignant cause of dysphagia
- GerdQ questionnaire

2. Oesophageal pH probe
- Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probe especially if oesophagitis is not seen on OGD
- Antimony probe (24hr) most commonly used; alternative is the Bravo capsule (a wireless capsule that is temporarily attached to the
oesophageal wall, 48hr)
- The probe is placed 5cm above the manometrically-determined upper limit of the LES (for the wired probe), or 6cm above the
endoscopically-determined squamocolumnar junction (for the wireless capsule)
- Diagnosis based on the percentage of time in 24hrs the pH reading is below 4 (positive if >5.5%)
- Can have false negative consider repeat test. Either one positive is diagnostic.

3. Oesophagogastroduodenoscopy
- Cannot actually diagnose reflux (poor correlation btw oesophagitis and reflux). Therefore, selective usage.
- Uses:
o Dx: Rule out gastric malignancy/ other conditions mimicking symptoms (in areas with high prevalence of gastric CA)
o Cx: Can visualise and grade oesophagitis if present, and take biopsy specimens for confirmation (see below)
o Ax: May see a hiatal hernia which is associated with reflux (though not all patients with hiatus hernia will have reflux)

4. Barium swallow and follow-through

- Not of much value in diagnosing reflux
- Ax: Can detect motility disorders that cause reflux,
- Cx: oesophageal ulceration and stricturing resulting from reflux
- Can sometimes see reflux of barium contrast into oesophagus

5. Manometry
- No value in reflux except for detecting motility disorder (tro achalasia! – will be much aggravated by surgical Tx of reflux)

GRADING OF OESOPHAGITIS

1. Savary-Miller classification
Grade I: One or more supravestibular non-confluent reddish spots, with or without exudates
Grade II: Erosive and exudative lesions, may be confluent but not circumferential
Grade III: Circumferential erosions covered by haemorrhagic and pseudomembranous exudate
Grade IV: Presence of chronic complications such as deep ulcers, stenosis, stricture
Grade V: Barrett’s  metaplasia

2. Los Angeles classification

- Relevance of classification schemes: subjective and dependent on assessment by the endoscopist; also, due to the multitude of
classification schemes available, just mentioning a grade may not have any meaning if the actual abnormalities are not described
- heartburn severity or the symptoms do not reliably predict the severity of erosive esophagitis; older patients experience less symptoms

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TREATMENT

Lifestyle

1. Diet and eating habits

Avoid coffee, chocolate, fatty foods, or anything that worsens symptoms
Do not eat 2 hours prior to sleeping
Walk after eating
Avoid excessive eating; eat small meals

2. Avoid drugs that relax LES e.g. anticholinergics, muscle relaxants, etc.

3. Weight reduction if obese

4. Elevate head of bed

5. Smoking and alcohol intake cessation

Medication

1. Acid suppression therapy: PPI (best! switch  ard  if  patient  doesn’t  respond  to  one,  rather  than  increasing  dosing  frequency)  or  
H2-receptor antagonists
May require LT tx. If patient stops PPI and symptoms recur, restart PPI first, no need to reinvestigate.

2. Prokinetics to increase LES pressure e.g. domperidone (anti-dopaminergic), metoclopramide (anti-dopaminergic + anti-
serotoninergic)

Surgical

- Indications:
Failure of medical therapy (or incomplete resolution of symptoms)
Oesophagitis with frank ulceration or stricture
Complications of reflux oesophagitis – respiratory  complications,  Barrett’s  oesophagus
Severe symptoms or progressive disease
Compliance problems - patient does not want to be on medication for life (despite good results)

- Goal of surgery:
Increase pressure at the gastro-oesophageal junction but not so much that it prevents food from entering the stomach (too
tight dysphagia)

- Surgery versus conservative treatment

Surgery has higher rates of cure and better long-term results?? / results not longstanding?
No need to adhere to strict lifestyle and diet change as well as long-term medication
Disadvantage of surgery is the associated morbidity and mortality

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- Fundoplication (mainstay of surgical therapy)
Can be done via open surgery or laparoscopic surgery (most laparoscopic now)
a. Nissen fundoplication is the most commonly done – a 360 degree (total) wrap of the fundus around the gastro-
oesophageal junction
b. Partial fundoplications can also be done in patients where oesophageal motility is poor or the oesophagus is
foreshortened; anterior 90 degrees, anterior 180 deg, and posterior 270 deg fundoplications are various options available

- Complications of surgery

1. Perforation – most feared complication, may result in mediastinitis if not promptly detected and repaired intraoperatively

2. Excessively tight wrap resulting in dysphagia

3. Excessively loose or short wrap – reflux recurs (failure of treatment)

4. “Slipped-Nissen”  body of the stomach intussuscepts through the fundoplication, creating an hourglass deformity whereby
the stomach resides both above and below the wrap; usually due to a foreshortened oesophagus unrecognised in the
first operation. Causes severe reflux as pouch above the wrap traps food and serves as reservoir.

5. “Gas  bloat  syndrome”  – patient experiences difficulty burping gas that is swallowed (gas accumulation)

- Outcome of surgery
80-90% Excellent to good (no symptoms, no medications and lifestyle changes required)
10-15% Satisfactory (some residual symptoms)
<5% Unsatisfactory
<1% Mortality
5-40% need for acid suppression therapy at 5 years due to symptoms

- Management of stricture
Rule out malignant cause of stricture by taking biopsy
1. Dilatation (variety of means available – balloon, dilators, etc)
2. Treatment of underlying reflux
3. If resistant to dilatation resection and reconstruction

Others
- Nerve stimulation? of LES to increase tone (still under research)

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6. BARRETT’S  OESOPHAGUS

FEATURES

- Intestinal metaplasia of the oesophageal epithelial lining

(stratified squamous epithelium 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

- Diagnosis:
Endoscopy and histology:

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

The gastro-oesophageal junction is defined as the point where the gastric folds begin

If the squamocolumnar junction is above the gastro-oesophageal junction (i.e. they do not align) and biopsy of the junction
shows intestinal metaplasia, the patient is diagnosed to have Barrett’s  oesophagus

- Complications:
Short  segment  Barrett’s  is  defined  as  the  squamocolumnar  junction  being  <3cm above the gastro-oesophageal junction
Long  segment  Barrett’s  the  distance  between  the  two  junctions  is  >3cm: associated with more severe reflux, as well as
higher risk of  dysplasia  and  subsequent  adenocarcinoma  development  than  short  segment  Barrett’s

Risk of development of adenocarcinoma is about 10-15% in 10 years

MANAGEMENT

1. Treatment of underlying reflux

- Lifestyle changes, acid suppression (PPI!), surgery etc
- Not shown to decrease risk of cancer still requires surveillance??

2. Endoscopic surveillance
- Not  certain  regarding  benefit  for  surveillance  if  patient  has  Barrett’s  but  no  dysplasia   if 2 scopes in a year reveal no
dysplasia, repeat OGD once every 3 years (half-yearly 3 yearly)
- Main purpose of surveillance is to pick up dysplasia
- If patient has high grade dysplasia, it should be treated (see below), otherwise to undergo intensive surveillance (3 mthly
for at least one year) to detect cancer development

3. Treatment of high-grade dysplasia

1. 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
2. Oesophagectomy is the only definitive treatment to remove all dysplasia, but is associated with high morbidity and mortality
(worth it?)
3. Possibility of endoscopic mucosal resection as a treatment modality (research still undergoing) – shown to be as good as
oesophagectomy with less morbidity and mortality

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7. ACHALASIA

FEATURES

- Abnormal   peristalsis   secondary   to   absence   or   destruction   of   Auerbach’s   (myenteric)   plexus   and   failure   of   the   LES   to   relax;;  
affects body and distal oesophagus

- Lacks nonadrenergic, noncholinergic, inhibitory ganglion cells, causing an imbalance in excitatory and inhibitory
neurotransmission. The result is a hypertensive nonrelaxed esophageal sphincter
- Aetiology unknown
- Adults, M:F = 1:1

- Patients present with dysphagia, regurgitation, weight loss, retrosternal chest pain, and recurrent pulmonary infections

- Barium  swallow  demonstrates  “bird’s  beak”  narrowing  of  distal  oesophagus  with  proximal  dilatation

- Manometric studies (required for diagnosis) show abnormally high pressures at the LES, with incomplete LES relaxation on
swallowing, and lack of progressive peristalsis (often aperistaltic)

- 1-10% of patients develop SCC after 15-25 years of disease

TREATMENT

- Mainly palliative in nature

- Non surgical treatment:

Intrasphincteric injection of botulinum toxin to block the release of acetylcholine at the level of the LES (problem is that it is
not long lasting and only used in patients not fit for surgery)

Pneumatic balloon dilatation (A balloon is inflated at the level of the gastroesophageal junction to blindly rupture the muscle
fibers while leaving the mucosa intact): about 65% of patients improve, 40% response rate at 5 years)
Calcium channel blockers and nitrates (both decrease LES pressure but do not improve LES relaxation. Used in elderly who
are not suitable for surgery/dilatation)
- Surgical treatment (primary Tx):

Laparoscopic Heller cardiomyotomy (much like Ramstedt pyloromyotomy for pyloric stenosis) – good results with 85%
symptom-free after 5 years; there is a 3% chance of developing reflux
addition of fundoplication (partial wrap) helps prevent this
Esophagectomy was the standard treatment in patients with achalasia and a markedly dilated or sigmoid-shaped esophagus
(controversial)

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6. UPPER GIT

1. APPROACH TO BLEEDING UPPER GIT

CAUSES

Variceal vs Non-variceal!

1. Peptic ulcer disease (bleeding peptic ulcer)

2. Gastritis, gastric erosions, duodenitis
3. Gastric malignancy
4. Stress ulcers from burns/ instrumentation
5. Gastro-oesophageal varices
6. Mallory-Weiss tear
7. Rare causes: AV malformation (Dieulafoy lesion) – most will stop bleeding spontaneously, aortoenteric fistula
8. Bleeding from other sources: Haemoptysis, nasopharyngeal bleeding
9. Systemic: coagulopathies, renal failure (uraemic gastritis)

HISTORY (if patient is stable)

1. Nature of bleeding

Haematemesis
- [oes] Can be fresh red blood as in variceal bleeding, Mallory-Weiss tear, AV malformation
- [gastric] Coffee grounds vomitus is altered blood (due to gastric acid) and can come from gastric ulcer, gastritis/erosions, or variceal
blood that has entered the stomach [oes]

Malaena
- Altered blood; malaena indicates bleeding from the upper GIT i.e. above the ligament of Treitz
- Different types of malaena:
(a) Fresh malaena – jet black with sheen, tarry, non-particulate (almost liquid in consistency), foul smelling, floats on water –
maroon when you spread it out on gloves
(b) Stale malaena – black-grey, dull, mixed with normal stool, occasionally particulate
(c) Iron stool – greenish hue on rubbing between gloved fingers, particulate.
- If  gloved  finger  is  stirred  in  a  cup  of  water,  malaena  will  “dissolve”  completely  with  no  sedimentation and turn the water black, but iron
stool will sedimentate and turn the water green

Frank PR bleeding
- Very  brisk  upper  GI  bleed  can  present  as  frank  PR  bleeding  as  blood  passes  down  so  fast  it  doesn’t  get  altered

2. Amount of blood

- If patient is having haematemesis, ask how much blood Cup? Bowl?

- Hematemesis: easily 1.5L of blood in stomach before vomiting out (bleeding more than pylorus can empty)

3. Aetiological clues / RF

Gastric ulcer/gastritis/erosions
- Any history of dyspepsia, gastric ulcer (any OGD done  in  the  past  showing  these  problems?  On  any  “gastric”  medications?)
- Any drugs that may predispose – NSAIDs, antiplatelets, steroids, anticoagulants, TCM
Varices
- Any history of chronic liver disease
- Previous variceal bleeds
Mallory-Weiss tear
- Binge-drinking with subsequent severe retching and vomiting leading to haemetemesis
Malignancy
- Recent constitutional symptoms e.g. LOA, LOW, malaise
- Early satiety
- Dyspepsia

4. Complications

- Symptoms of anaemia: postural giddiness, shortness of breath, lethargy, effort tolerance, palpitations, chest pain
- AMI esp.  if  it’s  an  old  patient  with  previous  history  of  IHD

5. Comorbidities

- Elderly patient (>60) high risk (Rockall score)

- Other comorbidities: liver disease, renal disease, IHD high risk (Rockall score)

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PHYSICAL EXAMINATION

1. Vitals!
- Blood pressure, heart rate stable? Any postural hypotension? (Tachycardia is an early sign of shock)
Narrowing pulse pressure (ind systolic hypotension) - check if patient is on BB!!
- RR>20
- Patient’s  conscious  level  – confused? (shock)
- Compare current vitals with vitals in ambulance, ED – is there a worsening trend?
- Urine output: renal perfusion indicates cardiac output

2. General inspection
- Pallor
- Cold clammy peripheries impending shock
- Stigmata of chronic liver disease

3. Peripheries
- Cold clammy peripheries impending shock
- LN (mets)

4. Abdomen
- Any tenderness (not very helpful), epig mass
- Distension (++ blood in stomach)

5. Digital rectal examination

- Malaena or frank blood
- tumor deposits / rectal mass

IMMEDIATE MANAGEMENT

1. Resuscitation

- ABC: Protect airway, supplemental oxygen, 2 large-bore IV cannula in antecubital fossa

Bloods:
1. FBC (Hb will not drop in first 24hrs, low plt - may not stop bleeding),
2. U/E/Cr (dehydration - raised Ur more than Cr, elec abn from vomiting)
3. PT/PTT (check and correct for coagulopathy),
4. LFT (Child's score - ind etiology and outcome) - do in alcoholic hx or liver disease
5. GXM: order in active bleed 4 pints PCT, FFP, Plt
ECG to detect any acute myocardial ischaemia/infarction, PFO
CXR: PFO, aspiration, perforation if pt complains of pain
- Infusion
- 1 pint N/S over half to one hour if patient is in shock, followed by more fluids if necessary (be wary in pts with renal & heart failure)
- Packed cells if Hb is less than 10, to keep Hb above 10g/dL
- May consider platelets if patient is on antiplatelet meds (qualitative defect in platelets - even if plt is normal, they are dysfunctional)
- FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K)

2. Adjuncts

- NG tube if patient is having haematemesis – prevents aspiration, allows gastric lavage prior to OGD (DO NOT insert if suspect varices)
- Catheterisation – monitor I/O balance esp in elderly or when large amount of fluid resuscitation required, or anticipating surgery
- Intubate if: 1) massive uncontrolled active hematemesis
2) signs of decompensation eg. obtunded

3. Early medications

- IV omeprazole 80mg bolus --> 8mg/hr infusion X 3/7

stomach pH and stabilises clot formation
regimen to prevent rebleed (normal Tx dose 40mg bd)
- If suspecting varices – IV somatostatin/octreotide, IV antibiotics
- Stop antiplatelets, anticoagulants, NSAIDS

4. Close monitoring

- Monitor for: SHOCK ( HR, BP, urine output, confusion & lethargy)
- HD with hourly para if
Elderly with many comorbidities
Hypotension

5. Emergency oesophagogastroduodenoscopy

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 Alternatively, scope the next available OGD (usually following day)

- 3 Indications:
1. Shock / hemodynamic instability (ensure BP is stable before OGD - requires sedation)
2. Active BGIT (esp hematemesis, also fresh malaena)
3. Suspected variceal bleed
Not just low Hb as emergency scope causes more stress.
- Ensure bloods are running before OGD!
- Role of endoscopy
Diagnostic:
confirm UBGIT & identify source of bleeding,
Biopsy (+ CLO test if ulcer)
Therapeutic:
1. Varices: ligation/sclerotherapy, glue
2. Non-variceal: Clip, Coag, Injection
- CI: Perforation - air sufflation during OGD will cause
abdominal compartment syndrome --> decrease venous return --> patient may DIE
splinting of the diaphragm

- Repeat OGD with greater detail if it is normal the 1st time.

Exclude haemoptysis & bleeding from nasopharynx
Look for Mallory weiss tear and posterior wall D1 bleeding ulcer (gastroduodenal artery)

Obscure overt bleed:

OGD normal Colonoscopy normal Small bowel imaging:
a) Capsule endoscopy
b) Tagged RBC
c) CT enterography
CT mesenteric angio anytime when patient becomes unstable.

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2. VARICEAL BLEEDING

PATHOPHYSIOLOGY WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT

A result of portal hypertension (i.e. portal venous pressure >20 cmH2O - Previous history of variceal bleed
or >12 mmHg – normal = 7-14 cmH2O / 5-10 mmHg) - Chronic alcohol intake
- Jaundice or stigmata of chronic liver disease
- Profuse hematemesis
MANAGEMENT OF VARICES can be divided into three categories:
1. Acute bleeding
2. Prophylaxis
3. Chronic management

I. ACUTE BLEEDING – MANAGEMENT

1. Resuscitate
- Airway, breathing, circulation
- If patient appears well, look for early signs of shock – tachycardia, postural hypotension
- Look at hydration status

2. Assess mental state

- If patient has altered mental state (encephalopathy) need to protect airway (may require intubation)

3. Vascular access, fluids/blood resuscitation, and blood investigations

- 2 large-bore IV cannula in proximal veins (cubital, EJV, IJV)
- Send bloods – GXM 4 pints, FBC, U/E/Cr, LFT, PT/PTT
- Infuse fluids
- Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9, enthusiastic transfusion can portal pressure

4. Management of severe bleeding: Sengstaken-Blakemore tube

- If hypotensive and bleeding is ongoing, may require use of Sengstaken-Blakemore tube for up to 48hr (if unable to ligate)
- Protect airway before inserting tube.
- Inflate gastric balloon and pull upwards against cardioesophageal junction (balloon will press on perforator veins entering oesophagus
from stomach, and thus decrease oesophageal variceal bleeding); oesophageal balloon is not inflated nowadays

5. IV somatostatin or S/C Octreotide (Not given in ulcer bleed)

- Mode of action: splanchnic vasoconstrictor which portal blood flow and hence portal pressures variceal bleeding
- Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow

6. Acid suppression
- Increasing intragastric pH increases clot stability, aids haemostasis
- Agents available: omeprazole (Losec), esomeprazole (Nexium), pantoprazole, etc.

7. Antibiotics
- Not given in ulcer bleed
- Risk of sepsis in patients with CLD and bleeding
- Studies have shown that cover with broad spectrum Abx (Gram neg cover) infectious cx, mortality, and also risk of recurrent bleed
- Ceftriaxone, Ciproflox 1g/day
- Preferably started before endoscopy (procedures increase bacteraemia)

8. Emergency endoscopy
- Purpose: confirm diagnosis and institute management
- Needs to be done emergently (on admission) as soon as patient is stabilised since bleeding can be torrential and life-threatening
- Intervene if ESRF present or active bleed (not electively)
- Banding/Ligation is the best modality for oesophageal variceal bleeding (sclerotherapy a/w higher morbidity e.g. mucosal ulceration)
- Gastric varices are usually too large to be banded, sclerotherapy/ Glue (Histoacryl) used instead – risk of embolism from histoacryl

9. Observation
- Keep patient in ICU!
- NBM 2-3/7
- Continue antibiotics and omeprazole
- Continue somatostatin up to the point where haemostasis is achieved or 5 days (exact ideal duration not well studied)
- Antiencephalopathy Tx: Lactulose + Cipro (clear gut to prevent absorption of NH3)
- Anticipate complications:
(a) encephalopathy – fleet and lactulose, treat hypokalaemia from vomiting
(b) aspiration – protect airway; ?benefit of gastric decompression using NG tube
(c) risks of procedure – OGD-related risks

10. Management of possible precipitants

- NSAIDs; Hepatic vein thrombosis

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If bleeding stops, home in around 1/52 Rescope before home! (ligate if rebleed)
If bleeding is not remediable by endoscopic intervention:

A. Insert Sengstaken-Blakemore tube up to 48hr (only temporary) repeat endoscopy 10-12 hours later
If rebleed after 48hr of SBT: consider surgery

B. TIPSS: Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt

- If patient in good Child’s  score, to avoid as it ppt. encephalopathy
- Constant monitoring of patient.
- Cx: encephalopathy (increased risk with bigger shunt), bleeding, thrombosis, failure (blood flow in opposite direction)
- usually temporising procedure

C. Shunt surgery
Portocaval shunts (portal vein to IVC)
– side-to-side, end-to-side
Mesocaval shunts (sup mesenteric vein to IVC)
Proximal splenorenal shunt (splenectomy with end-to-
side anastomosis of portal side of splenic vein to left
renal vein)
Distal splenorenal shunt (Warren-Zeppa shunt –
splenic vein divided, splenic side anastomosed end-to- A. Normal liver with normal blood flow. B. End to side spelnorenal shunt.
side to left renal vein) C. End to side portacaval shunt. D. Mesocaval H-graft shunt

D. Sugiura procedure: last resort

Most effective non-shunt operation
A key point is that the left gastric (coronary) vein and the paraesophageal collateral veins are preserved to permit portoazygous
collateralization, which inhibits future varix formation
Japan cited a 5.2% operative mortality and a 6.3% rate of recurrent hemorrhage. In United States, operative mortality with this
procedure has exceeded 20%, with bleeding recurring in 35% to 55% of patients.

Splenectomy
Proximal gastric devascularisation
Selective vagotomy
Pyloroplasty
Oesophageal devascularisation
Oesophageal transection

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II. PROPHYLAXIS OF VARICEAL BLEEDING

SECONDARY = Band ligation + Non-selective beta-blockers

- Best option is combination
propranolol unless CI: decrease size and prevent rebleeding
3 weekly ligation until completely obliterated

PRIMARY = Non-selective beta-blockers

(oesophageal varices with no previous history of variceal hemorrhage)

In pts with small varices with no risk of bleeding, the use of propranolol is of questionable benefit – repeat OGD to monitor varices.
- cardiac  output  by  β1 blockade  and  splanchnic  blood  flow  by  blocking  vasodilating  β2 receptors at splanchnic vasculature
- The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%, to be continued indefinitely
- The dose: determined by a 20% decrease in baseline resting HR / decrease in HR to 55 bpm / dev adverse effects
- If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives
- Band ligation/ Sclerotherapy: not used as primary prevention. as effective as treatment with propranolol

Predictors of variceal haemorrhage: [SRCPS]

1 Site: varices at the GE junction have the thinnest coat of supporting tissue and are at highest risk of rupture and bleeding

2 Size:
F1: Small straight varices
F2: Enlarged tortuous varices that occupy less than one-third of the lumen
F3: Large coil-shaped varices that occupy more than one-third of the lumen

3 Child’s  score – patients  with  higher  Child’s  score  have  higher  risk

4 Red signs:
Red wale marks (longitudinal red streaks)
(ESRH) Cherry red spots (flat discrete spots)
Haematocystic spots (raised discrete spots – resemble  “blood  blisters”)
Diffuse erythema

5 Previous variceal haemorrhage:

70% of patients will have further variceal bleeds after an index bleed (risk highest in first 48 hours after first bleed)
30% rebleed within 6 weeks; 30% rebleed after 6 weeks

III. CHRONIC MANAGEMENT

- Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapy and subsequent endoscopic monitoring and
repeated ligation/sclerotherapy as required to completely ablate varices)
- If patient bleeds again failed ablation consider surgery (as above – shunts, or Sugiura)
- LT propanolol + PPI
- Refer to Hepato for liver disease

http://www.heart-intl.net/HEART/011507/PortalHypertension.htm

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3. PEPTIC ULCER DISEASE

EPIDEMIOLOGY
- Incidence about 100 per 100,000 per year
- 68% of patients are over 60 years of age
- Overall mortality 7-10%, unchanged for last 20yrs – mostly due to ulcer bleeding esp in elderly with significant comorbidities

MAIN AETIOLOGICAL FACTORS

H. pylori
- 60% of population are positive for H. pylori by age 21
- About 10-20% of infected patients develop an ulcer
- Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers

NSAIDs
- 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 20% (6% overall) will have a clinically significant ulcer i.e. symptomatic, bleeding

Other factors
- Cigarette smoking
- Alcohol
- Steroids and anticoagulants do not increase the risk of ulcer formation, but increase the risk of bleeding in an existent ulcer

PATHOGENESIS

- An imbalance between mucosal protective mechanisms against acid, and aggressive forces that damage the gastric mucosa
- 2 Aggressive forces: gastric activity and pepsin activity
- 5 Protective mechanisms: mucus secretion, bicarbonate secretion into mucus, robust mucosal blood flow to remove protons, epithelial
regenerative capacity, prostaglandin secretion by mucosa to maintain blood flow
- H. pylori 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
- 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

PRESENTATION

1. Incidentally detected on OGD

2. Symptoms of dyspepsia
(a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom
(b) Dysmotility-like dyspepsia: non-painful discomfort in upper abdo, a/w upper abdo fullness, early satiety, bloating, belching, nausea
(c) Unspecified dyspepsia
- Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a duodenal ulcer

3. Bleed
- As above, presenting with haematemesis (coffee-grounds vomitus) or malaena

4. Perforation
- Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements
- Board-like rigidity, guarding will be present on examination (signs of peritonism)
- Erect CXR will show air under diaphragm

ENDOSCOPY (OGD)

- The most important and valuable investigation

- Roles of endoscopy:

(a) Diagnosis
Confirmation of ulcer disease
Location of ulcer
Biopsy to rule out malignancy – esp gastric (usually 6 bites)
Biopsy of antral tissue for CLO (Campylobacter-like organism) test / rapid urease test for H. pylori: biopsy tissue is placed into a
medium containing urea and an indicator such as phenol red. The urease produced by H. pylori hydrolyzes urea to ammonia, which
raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE).

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 (b) Prognostication of bleeding risk (in UBGIT)
Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH)

Forrest grade Bleeding risk

1a Spurting (arterial) 90%
1b Non-spurting, ooze (venous) 20%
2a Non-bleeding ulcer with visible vessel 40%
2b Non-bleeding ulcer with adherent clot 20%
2c Ulcer with haematin-covered base (flat spot) 10%
3 Ulcer with clean base 5%
Adherent clot must flush and remove clot --> grade ulcer again

Classical bleeding BV: posterior-D1 (gastroduodenal art)

Tx: Only pigmented spot can leave alone, the rest must intervene!

(c) Endotherapy (in UBGIT)

1. Injection with adrenaline (1:10,000 dilute to 10ml - continue with N/S if need more) or absolute alcohol – tamponade effect is the most
effective. Also vasoconstriction for adrenaline.
Inject around ulcer (4 quadrants). Cx: perforation, bleeding, necrosis, arrhythmia.
2. Coagulation (Heater probe = thermal / Argon plasma)
3. Haemostatic clipping (endoclip)

Principle: Dual modality better than single (as less risk of recurrent bleed and mortality) --> Usually Injection + Clip/Heater probe
No study proves superiority of either therapy.

Failed OGD hemostasis (after 1hr)

a) Surgery is mainstay
b) Transcatheter embolisation
a. ind: failed surgery, rebleed post-Sx (usually GDA), not fit for Sx
b. identify bleeding vessel and embolise with
i. Mechanical (non-absorbable coil eg. Titanium)
ii. Chemical (gel foam): can recannulise again in 2/52
c. Sandwich technique: embolise both prox and distal ends of vessel as bleeding can occur both ways.

Post-endotherapy:
- Monitor for rebleed = drop in Hb (not malaena / vomit blood clots as these are expected. Changes in vitals may be too late.)
- Diet individualised: usually NBM 1-2/7, 3/7 if worrisome, <1/7 if straight forward ulcer
- Re-scope  the  following  day  if  you’re  worried  about  the  outcome  from  the  first  scope  (notroutine)
- Oralise PPI after 3/7 infusion (if worrisome, can give IV bolus PPI BD)
- TCU 3-4/52 at clinic

Re-scope in 6 weeks to document ulcer healing

If ulcer still present, biopsy ulcer again
1. Histo: exclude malignancy for gastric ulcer
2. Gastric biopsy urease test (to confirm eradication of H. pylori) - not accurate if patient on triple tx
Rescope and biopsy every 6/52 until ulcer is healed resect if persistent
Confirm eradication of H Pylori: Urease breath test, Re-biopsy

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CONSERVATIVE MANAGEMENT

1. Gastroprotection

(a) Standard dose proton pump inhibitor

20mg OM
Promotes ulcer healing even with ongoing NSAID use
(b) Double dose famotidine
40mg BD
Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs are stopped; ulcers will not heal with ongoing
NSAID therapy

2. H. pylori eradication

First line triple therapy: omeprazole 40mg BD (for 6 weeks), amoxicillin 1g BD, clarithromycin 500mg BD for 7 days
In penicillin-allergic patients, substitute amoxicillin with metronidazole 400mg BD
Document eradication by endoscopy with CLO test, urea breath test or stool serology testing
Treatment failure occurs in up to 20%
- treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS, tetracycline 500mg QDS, metronidazole 400mg
BD, omeprazole 20mg BD for 7 days

SURGICAL MANAGEMENT

Indications for surgery for acute PUD:

1. Bleed: Mainstay of Tx for failed OGD hemostasis (after 1hr)
2. Perforation

Indications for surgery for chronic PUD:

1. Recurrent bleeding
2. Splitting BV difficult to clip
3. Prev episode of shock

DUODENAL ULCER

Indications  for  surgery:  ‘Patient  has  to  BUY  the  op’  

(more complications + duod ulcer will heal provided the high acid secretion of stomach is abolished)

1. Persistent bleeding (e.g. erosion of a post duodenal ulcer into GDA)

2. Perforation
3. Gastric outlet obstruction (patient presents with vomiting of undigested food not long after meal, succussion splash, air-fluid levels on
AXR; characteristic electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria)
4. Failure of medical management (ulcer does not heal)

Surgery:

1. Bleed =
a. Duodenotomy + Oversewing/Under-running the bleeding vessel
b. Antiulcer surgery (if patient stable and known case of rebleed/perf)
2. Perforation =
a. Omental patch repair + Bx (small <2cm ulcer / patient unstable)
b. Antiulcer Sx (>2cm or suspect malignancy)
(parietal peritoneum, jejunum serosa, stomach local flap)
3. Definitiveantiulcer surgery
= Duodenectomy + Vagotomy with gastric drainage procedures
- Usually done in elective setting for chronic duodenal ulcers
- Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric secretion; parietal cells also become less
responsive to histamine and gastrin, and vagal stimulus for gastrin release is abolished
- Vagotomy can be truncal, selective, or highly selective (selecting only those branches that appear to supply peptic cells. does
not require drainage as the Nerves of latarjet that supply the pyloric sphincter are not affected)
- Drainage procedures pyloroplasty (first) or gastrojejunostomy
Usually done with vagotomy as gastric emptying is decreased with denervation.
Pyloroplasty = incise pylorus longitudinally through mucosal layer then suture the incision transversely

Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)

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GASTRIC ULCER

Indications  for  surgery  ‘SELL  the  operation  to  the  patient’

(risk of malignancy if >2years)

1. Failure to heal after 3 months of conservative therapy

2. Dysplasia or carcinoma
3. Recurrence
4. Perforation, persistent bleeding

Surgery
1. Bleed =
a. Ulcerectomy (if patient unstable, old, unfit)
b. Antiulcer surgery (if patient stable, can tolerate)
2. Perforation =
a. Omental patch repair + Bx (small <2cm ulcer / patient unstable)
b. Antiulcer Sx (>2cm or suspect malignancy)
(parietal peritoneum, jejunum serosa, stomach local flap)
3. Definitive antiulcer surgery = Gastrectomy
a. Partial gastrec if distal ulcer
b. Proximal ½ ulcers may require total gastrec
Can be used in emergency bleed if patient stable, but considered antiulcer Sx as parietal cell mass and antrum (contains
gastrin containing cells) are removed.
Bancroft’s  closure (for severe inflammation/scarring that prevents dissection around pylorus. Remove all antral mucosa to
prevent marginal ulcers)

If prepyloric ulcer, can treat similar to duodenal ulcer

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4. GASTRIC CANCER

EPIDEMIOLOGY
- Fourth most common cancer in males, sixth most common in females in Singapore
- Female to male ratio 2:1
- Incidence 10-18 per 100,000 per year
- Incidence increases steeply after 50 years old

RISK FACTORS

1. Environmental
- Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons
- Smoking
- Alcohol
- Occupational exposure: asbestos, heavy metals, rubber
- Low socioeconomic status

2. Genetic
- Blood type A
- HNPCC – Lynch syndrome II
- P53 mutation
- Germline mutation of e-cadherin
- Family history of gastric cancer

PRECURSOR CONDITIONS

1. Partial gastrectomy for benign disease with Bilroth II reconstruction

- Usually occurs >15 years after surgery
- Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal secretions at the anastomotic zone

2. Gastric polyps
- Highest risk in inflammatory polyps: 75-90%
- 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology
- Also increased risk of adenocarcinoma elsewhere in the stomach

3. Chronic atrophic gastritis

- Hypertrophic gastritis (Menetrier’s  disease) – inflammatory disease of gastric epithelium, up to 10% risk of malignant change
- Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10% risk of gastric cancer

4. Peptic ulcer disease

- <1% risk of malignant change

5. H. pylori infection
- 3-6X increased risk of gastric cancer

HISTOLOGY

a) Adenocarcinomas

- Make up 90-95% of stomach tumours

- Lauren classification:
(a) Intestinal type (most common overall) – occurs in high risk population, distal third of the stomach, in older men; associated with erbB2
and erbB3 receptor stimulation
(b) Diffuse type – occurs in low risk population, proximal third and cardio-oesophageal junction, in younger and female patients; more
aggressive, present later, worse prognosis; associated with K-sam oncogene

- Early gastric cancer

Confined to mucosa and submucosa
Good survival and prognosis regardless of size, lymph node status, histological grade

b) Non-adenocarcinoma

- Make up less than 10% of stomach tumours

- Types: SCC, neuroendocrine tumour, leiomyosarcoma, GIST (gastrointestinal stromal tumor), primary gastric non-Hodgkin’s   lymphoma  
(MALT, linitis plastica) – NHL in submucosa adynamic stomach N/V more than anemia

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MORPHOLOGY

Borrmann’s  classification:

Type I (3%): Nonulcerated, polypoid, growing intraluminally

Type II (18%): Ulcerated, circumscribed with sharp margins
Type III (16%): Ulcerated, margin not sharply circumscribed
Type IV (63%): Diffuse, infiltrating, may be ulcerated; may diffuse entire
stomach (linitis plastica)

LOCATION

- 37% in cardia
- 30% in pyloric channel or antrum
- 20% in body
- 12% in entire stomach

SPREAD

- Direct extension to neighbouring organs

- Lymphatic spread
(a) Regional nodes
(b) Supraclavicular  nodes  (Virchow’s  node)
(c) Umbilical  (Sister  Joseph’s  node)

- Haematogenous spread – liver, lung, bone, brain

- Peritoneal seeding to omentum, parietal peritoneum, ovaries (Krukenberg’s tumour), or cul-de-sac / pouch of douglas
(Blumer’s  shelf  =  shelf-like tumor of ant rectal wall DDx tuberculous peritonitis)

PRESENTATION

Very non-specific symptoms and signs:

- Abdominal pain (usu late)60% 1. Asymptomatic: from histology of ulcer biopsy
- Weight loss 50% 2. Symptomatic: non specific abdominal pain, early
- Nausea/vomiting 40% satiety, N/V, LOW, LOA
- Anaemia 40% 3. Complications: s/s of anaemia, s/s of UBGIT, s/s of
- Palpable mass 30% GOO, s/s of metastasis, peritonism (perforation)
- Haematemesis/malaena 25%
- Early satiety 17%
- Metastatic symptoms late (bony tenderness, neurological deficits, etc)

New onset dyspepsia at age>35 years old should cause concern

COMPLICATIONS

- Bleeding
- Gastric outlet obstruction vomiting (dehydration, hypokalaemic metabolic alkalosis, aspiration ± pneumonia)
- Perforation
- Malnutrition

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INVESTIGATIONS

Diagnosis
OGD –visualisation and biopsy (ulcer with heaped-up edges)

Staging investigations
1. CXR/ CT thorax– lung mets
2. Endoscopic ultrasound – gold standard for T staging and good for N staging
3. CT abdo pelvis – good for T, N & M staging
4. Staging laparoscopy prior to operation – picks up small peritoneal metastases that are occult on CT scanning (up to 1/5 of
patients) upstage of disease

Complications
5. FBC – low Hb
6. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis
7. LFTs – albumin as a marker of nutritional status (alb<35 is poor); liver mets

STAGING

Tis Carcinoma in situ N0 No regional LN

T1 Tumour limited to mucosa and submucosa N1 1-6 regional LN involved
T2 Tumour invades muscularis mucosa N2 7-15 regional LN involved
T3 Tumour penetrates serosa N3 >15 regional LN involved
T4 Tumour invades adjacent structures

CURATIVE TREATMENT

SURGERY

Principles of surgery:
- Wide resection of the tumour to negative margins (at least 6cm margins)
- En-bloc excision of regional lymph nodes
- Choice between total gastrectomy and subtotal gastrectomy
Subtotal gastrectomy leaves a small portion of proximal stomach – easier to anastomose to jejunum than oesophagus since
oesophagus does not have serosa (higher risk of leak)
Subtotal gastrectomy is associated with less morbidity, better functional outcome (some residual reservoir fx preserved)
Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia, body) as well as diffuse-type tumours and
cardio-oesophageal junction tumours

- Reconstruction
Bilroth I (end-to-end gastroduodenostomy) – rarely done (diff to mobilise duodenum to anastomose with residual stomach)
Bilroth II/ Poly-A (gastrojejunostomy) – no protection against biliary reflux into stomach
Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higher chance of leak
Oesophagojejunostomy (after total gastrectomy)

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Complications of gastrectomy:

Early
1. Bleeding
2. Infection
3. Anastomotic leak
4. Injury to surrounding structures eg. pancreas

Late

1. Early satiety

2. Retained antrum syndrome

a. Not enough antrum removed acidity in residual stomach, with formation of marginal ulcers on the jejunal side of the anastomosis

3. Intestinal hurry
a. Inadequate reservoir function leads to poor digestion may have phytobezoar (veg fibre bezoar) formation

4. Dumping syndromes
a. Early dumping syndrome (1/2-1hr after meal): due to increased osmotic load from stomach into small intestine flushing, palpitations,
dizziness, nausea, diarrhoea, hypovolemia (due to rapid entry of water into small intestine)
Treat by eating small frequent meals with low carbo and high protein/fat.
b. Late dumping syndrome (1-3hr later): reactive hyperinsulinaemia alimentary hypoglycaemia (weak, sweat, dizzy).
Treat by eating more carbohydrates.

5. Biliary/intestinal reflux into stomach

a. Leads to symptoms of dyspepsia

6. Afferent limb syndrome

a. Occurs in Bilroth II/Polya reconstruction
b. Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic narrowing, or adhesions postprandial epigastric pain
with nausea, non-bilious vomiting
c. one of the main causes of duodenal stump blowout in the early postoperative period and is also an etiology for postoperative obstructive
jaundice, ascending cholangitis, and pancreatitis due to transmission of high pressures back to the biliopancreatic ductal system
d. Can be decreased by doing Roux-en-Y surgery (but may still occur)

7. Nutritional deficiency
a. Iron deficiency – mixed picture
i. Loss of intrinsic factor B12 deficiency
ii. Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid decreased iron absorption in terminal ileum
b. Need to supplement with B12 injections and iron supplements

Post-gastrectomy weight loss

10-33% of pre-op weight
due to LOA (less frequent meals) + decreased reservoir capacity of stomach

Follow-up
- 2/52-1/12: repeat OGD
- 6/12: detect local recurrence (esp if margin involved), check for B12 deficiency
- 1-2 yr: yearly OGD

CHEMOTHERAPY/RADIOTHERAPY

Adjuvant therapy
5-fluorouracil with chemotherapy
5-fluorouracil with epirubicin for advanced disease

Neoadjuvant therapy
- 5-FU and cisplatin can be used to downstage unresectable, locally advanced disease with a significant increase in resectability (61% 79%)
- For resectable disease: preoperative 5-FU, cisplatin, doxorubicin, methotrexate, followed by intraperitoneal 5-FU
improved resection rates, response rates, median survival

PALLIATIVE THERAPY
- For palliation of symptoms such as pain, bleeding, obstruction

1. Endoscopic laser ablation for obstruction

2. Embolisation for bleeding
3. Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%), gastrojejunostomy for obstruction
4. External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy bleeding as it takes weeks to cause fibrosis)

PROGNOSIS

- Stage I 90% 5-year survival

- Stage II 70%
- Stage III 40%
- Stage IV 0%

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7. LOWER GIT & COLORECTAL DISEASES

1. APPROACH TO BLEEDING LOWER GIT

1) Colon
Bleeding diverticulosis
Angiodysplasia
Colorectal carcinoma, polyps
Colitis
- Infective (gastroenteritis, diverticulitis, colorectal TB)
- Inflammatory  (UC  &  Crohn’s)
- Ischaemic
2) Ileum:  Meckel’s  diverticulum  - usually dark red blood
3) Anorectal junction: hemorrhoids
4) Anus: anal fissure
5) Massive Upper GIT bleeding, e.g. bleeding DU

HISTORY (if patient is stable)

1) Nature of bleeding
Haematochezia
- Mixed with or coating stool
- Torrential or drops, any clots? – Brisk upper GI bleed can present as haematochezia
- Bright red (lower) or darker red (higher)
- Any mucous
Malaena
- Altered blood, indicates bleeding from upper GIT above ligament of Treitz (duodeno-jejunal junction)
- Ask for history as per UBGIT

2) Aetiological clues
Exclude upper GIT cause
- Any malaena, hematemesis, coffee grounds vomitus
- History of PUD, gastritis, varices, Ca stomach, Mallory-Weiss tear, risk factors for each
Bleeding diverticulosis/angiodysplasia
- Usually torrential bleeding that stops spontaneously; altered clots
- History of previous bleeding episodes
Colorectal carcinoma
- Constitutional symptoms: LOW, LOA, fatigue
- Change in bowel habits, tenesmus
- Symptoms of anaemia (chronic occult bleed)
- Previous history/family history of GIT or ovarian cancer
Colitis
- Infective: any fever/chills/rigors, night sweats, N/V, diarrhoea, pain, recent travel/contact history, eating
seafood, previous TB exposure or infection, BCG vaccination status
- Inflammatory: ask about history  of  UC  or  Crohn’s,  joint,  liver,  eye  &  skin  manifestations
- Ischaemic: ask about atherosclerotic risk factors, previous AMI, stroke
Hemorrhoids
- bleeding to passing motion, blood coating stool, pain
- Any mass noticed at anus
- History of constipation, hard stools, low fibre diet, chronic straining, recent pregnancy
Coagulopathy
- Any history of bleeding disorders, easily bleeding, petechiae

3) Complications
Symptoms of anemia (may be only presentation!): SOB, postural giddiness, palpitations, chest pain, ↓  effort  tolerance,  
fatigue, syncope
Symptoms  of  dehydration  &  shock:  extreme  thirst,  confusion,  pallor,  ↓  urine  output
May have complication of AMI if old patient with history of IHD

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PHYSICAL EXAMINATION

1. Vitals:
- HR, supine & postural BP –stable? urine output (if catheter in-situ),
- Any fever?
2. General inspection:
- pallor,
- confusion?
3. Peripheries:
- signs of dehydration e.g. capillary refill, dry tongue.
- Any supraclavicular lymph nodes?
- Any skin manifestations of inflammatory bowel disease?
- Stigmata of CLD?
4. Abdomen:
- Scars? Any palpable masses
5. DRE:
- any anal fissures or prolapsed hemorrhoids seen,
- any masses felt,
- any fresh blood or malaena
6. Offer proctoscopy to look for internal haemorrhoids

ACUTE MANAGEMENT

Resuscitation
o Supplemental oxygen, insert 2 large-bore IV cannula with fast infusion of crystalloids (N/S 500ml over ½hr)
o Infuse colloids if ongoing blood loss while waiting for whole blood (GXM)
o Catheterise and monitor urine output, insert NGT on suction to detect UBGIT
o Continuous vital signs monitoring & I/O charting ± CVP & stool chart
o ECG + cardiac enzymes to detect possible AMI
o Take blood for investigations
- FBC: low Hb level (repeat FBC 2-3 hours later or when necessary) – packed cell transfusion
4 pint PCT: give FFP to prevent over-dilution of clotting factors
- UECr: hydration status, any acute renal failure from shock, electrolyte imbalance – replace
- PT/PTT: must correct coagulopathy before trying to stop bleeding – fresh frozen plasma
- LFT: exclude bleeding varices
- ABG: may have metabolic acidosis in shock due to organ ischaemia – IV bicarb, dialysis if severe
- GXM 4 pints

Identify source & stop bleeding

o Arrange urgent colonoscopy (patient must be stabilised before procedure)
- Diagnostic: identify cancer, diverticulosis, angiodysplasia, areas of inflammation & bleeding
- Therapeutic: clip, diathermize, or inject adrenaline/ sclerosant into bleeding vessel
o Double contrast barium enema: good for picking up diverticulum which may be missed on scope
o Mesenteric angiogram or CT mesenteric angiogram
- More precise; can cannulate all 3 main trunks & their branches
- Diagnostic: shows  blush  in  active  bleeding,  shows  ↓  perfusion  of  ischaemic  bowel
- Therapeutic (not for CT): embolisation/sclerotherapy for angiodysplasia, beware of causing bowel ischaemia
(use foam medium)
o Capsule Endoscopy:
- for stable patients with suspected SI bleed & unable to swallow
- takes 36hrs to read the results, but unable to localise the site & intervene
o double balloon enteroscope:
- only for suspected proximal SI
- able to do therapeutic manoeuvres
o Labelled RBC isotope scan under gamma camera
- For intermittent, occult bleeds not detectable on mesenteric angiogram
- Not for urgent setting; can take up to 24 hours!
o Laparotomy with saline lavage if massive on going bleed, recurrent bleeding
- On table scope to transilluminate bowel & identify bleeding source
- On table angiogram
- Oversewing of bleeding vessel, partial/total colectomy as last resort

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2. COLORECTAL CANCER

EPIDEMIOLOGY
COMMONEST CANCER IN SINGAPORE
Prevalence in Singapore: 6% (Commonest cancer in M, number 2 cancer in F)
Peak incidence at 60-70 years of age (increase with age)
Increasing incidence through the years.
Chinese more prevalent.

PATHOLOGY
- Almost all tumours are adenocarcinomas
- 90% of tumours are sporadic
- 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and 1% with familial adenomatous polyposis (APC)
- 1% arise in association with long-standing ulcerative colitis (>10 years)

CRC

Sporadic (90%) Inherited (10%)

APC pathway DNA mismatch

(80%) repair (15%) HNPCC (8%) FAP (1%) UC > 10yrs (1%)

PATHOGENESIS

There are 2 pathways for cancer development in the colorectal mucosa:

1. APC pathway (adenoma-carcinoma sequence)

- Accounts for 80% of sporadic colorectal carcinomas

- Characterised by chromosomal instability
- Stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes:

Loss of the APC suppressor gene on 5q21 (congenitally absent in patients with familial adenomatous polyposis – APC) is the
earliest event in adenoma formation detected using Protein truncation test
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
K-RAS (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering mitotic signals
and prevent apoptosis
Loss of tumour suppressor gene at 18q21
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, more dysplastic adenoma carcinoma in-situ invasive cancer

2. Defects in DNA mismatch repair

- Involved in 10-15% of sporadic cases

- Like the APC pathway, there is 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
- 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-β  receptor
- Tumours that arise from this pathway have a better prognosis than tumours that arise from the APC pathway

SITE

Rectosigmoid Caecum + Ascending colon the rest

- 25% in caecum and ascending colon,
- 25% in transverse colon,
- 25% in descending colon and proximal sigmoid,
- 25% in distal sigmoid and rectum
Most are left-sided though there is an increasing incidence of right-sided tumours

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MORPHOLOGY

1. Scirrhous  /  annular  “apple-core”  lesions  (most  common)  - more common in the left colon
2. Polypoid – more common in the right colon as there is more space to grow
3. Ulcerated
4. Nodular

SPREAD

1. Intramural –Transmural (along bowel wall. Seldom >2cm spread) or Intraluminal

2. Direct extension into surrounding tissues e.g. small bowel, ovary, ureters, bladder
3. Lymphatic
4. Haematogenous – to liver, lungs, bone, brain
5. Transcoelomic – direct seeding: through entire thickness peritoneal cavity spread thru peritoneal fluid. Late stage > T4.

RISK FACTORS

Non-modifiable (4)

1. Age >50 years

2. Genetic predisposition

(a) Personal history of CRCs

in the first 5 years after resection of a primary CRC,
i. Metachronous CRC: occurs at a rate of 3-5%,
ii. Metachronous adenomas: rate of 25-40%
(Metachronous = primary tumors occurring more than 6 months apart)
(b) Family history of CRCs
1 first-degree relative with CRC: increases risk of CRC 1.7X,
2 1st-degree relatives with CRC, or if the relative had CRC <55YO: risk > 1.7X
FHx of colonic adenoma same significance as CRC??
(c) Polyposis syndromes
near 100% risk of cancer formation:
i. FAP and its variants
ii. Gardner’s  syndrome:  multiple  osteomas  in  mandible/skull/  long  bones,  sebaceous  cyst,  desmoid  tumor
iii. Turcot’s  syndrome:  glioblastoma  multiforme
other polyposis syndromes such as Peutz-Jegher’s,  Cronkhite-Canada have a small increased malignant potential

(d) HNPCC (AD) – more common than FAP, accounting for 8% of cancers.

3. Ulcerative colitis

- Increased risk after 10 years of disease if the patient has pancolitis; after 15-20 years if the patient has disease limited to the left colon

4. Adenomatous polyps

- Increased risk if there is a personal history of large (>1cm) adenomatous polyps, and polyps with tubulovillous or villous histology,
particularly if multiple (3-6X increased risk)
- Small (<1cm) tubular polyps do not have increased risk

Modifiable

5. Environmental factors

- Diet:
i. high in red meat, preserved foods (nitrosamines)
ii. high in refined sugar/fat potentially toxic oxidative byproducts by bac degradation
iii. low in fibre decrease stool bulk high fecal retention toxic products in contact with colonic mucosa for longer periods
iv. low in vitamins ACE, minerals lack antioxidants
- Alcohol, smoking
- NSAIDs may be protective against CRC

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HISTORY

A) Presentation

- Asymptomatic: detection during screening (e.g. Ulcerative colitis)

- Symptomatic:

Local:
Right sided 1. Iron deficiency / MCHC anemia – less Fe stores in the body cf folate & B12, so Fe depleted first
(OCCULT 2. Right sided abdo mass
present late) 3. Abdo pain
NO obstruction as stools more liquid and colon more spacious.
Left sided 1. Change in bowel habits (Progressive constipation, alternating constipation and diarrhoea)
(due to MASS 2. Spurious diarrhoea (due to bacteria degradation of prox stools gassy explosive diarrhoea)
EFFECT) 3. Decrease in stool calibre
4. PR bleed (Mixed in stool? / Separate from stool?)
5. I/O
6. Tenesmus = constant intense desire to defaecate. may be painful. defaecation nothing/ small amt of
mucus and loose faeces (due to SOL in lumen/wall of rectum)
7. Mucoid stools (suggests polypoid masses)
Consitutional: LOW, LOA, malaise
Complications:
1. Perforation : Symptoms of peritonism (rigid, guarding, rebound)
2. Intestinal obstruction (4): abdominal distension, abdominal colick pain, vomiting, absolute constipation
3. Haemorrhage
4. Symptoms of fistula, e.g. faecuria/ pneumaturia/ recurrent UTI (colovesical fistula)
5. Involvement of surrounding structures: eg. Rectosigmoid CA: pain, bladder, ureter hydroureter/hydronephrosis, GU
organs (but usually no S/S as uterus wall very thick)
6. Symptoms of infection: abscesses, peritonitis
7. Iron deficiency anaemia (6): fatigue, SOB, CP, palpitations, decreased ET, postural giddiness
Metastasis:
bone pain/ #, LL weakness with loss of sensation, bowel and urinary continence
RHC discomfort (parenchymal involvement most common), jaundice
SOB (pleural effusion most common), decrease ET, orthopnoea
morning headache
Stool Changes
B) Strong-risk factors - Bloody diarrhoea – ddx:
IBD
1. Positive Family history Infective e.g. amoeba, TB, hookworm,
- 1 or more 1st deg relative with CC at age <40 Antibiotic Associated Colitis (C. difficile)
- 2 or more 1st/2nd deg same side relative with CC at any age - Haematochezia = passage of FRESH blood
- Personal or family history of breast, ovarian cancer per anus, usually in or with stools – ddx:
Diverticulitis
2. FAP history / FHx Angiodysplasia (AVM, common in old)
- Diagnosis: Colonoscopy Hemorrhoids
- Can also do Protein truncation test for APC gene mutation Massive upper GI
3. HNPCC: Amsterdam II Criteria – [3, 2, 2, 1] It takes about 14 hours for blood to be broken down within
- ≥3  family  members  from  the  same  side  with HNPCC related cancer, the intestinal lumen; therefore if transit time is less than 14
one of whom is a 1st deg relative of the other 2 hours the patient will have hematochezia, and if greater
(At least 2 of which must be 1st-degree relatives) than 14 hours the patient will exhibit melena. One often-
HNPCC related: stated rule of thumb is that melena only occurs if the
source of bleeding is above the ligament of Treitz.
Colorectal carcinoma,
Endometrial carcinoma,
other related cancers: small bowel, TCC of the upper urinary tract, stomach, ovarian, brain (Turcot syndrome) and
sebaceous gland adenomas or keratoacanthomas (Muir-Torre syndrome).
- 2 successive generations
- ≥1  of  the  HNPCC  related  cancers  must  occur  prior  to  age  50
- FAP is excluded

4. History of adenomatous polyps

Family history alone = high-risk; FAP / HNPCC = very high-risk

Other risk factors

- Low fibre diet, Red meat
- Obesity
- Ulcerative colitis >10 years

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SCREENING

- Screening has been shown to improve survival!

- Why CRC is suitable for screening
1. Prevalent and lethal disease
2. Precursor can be detected early (long asymptomatic period)
3. Early detection makes a difference (can institute treatment)
4. Safe, effective, feasible test available
- 2 categories
i. CA prevention test = detect POLYPS and cancer
superior to (ii) as POLYPECTOMY PROVEN TO PREVENT CANCER
Colonoscopy is the only test.
ii. CA detection test = detect cancer only
Faecal immunochemical testing (more sensitive than FOBT) shown to be the best test.
- Colonoscopy normal Repeat in <10 year intervals

PHYSICAL EXAM

1. Abdominal mass
2. Mass on DRE: (rectal mass)
a. hard, non-tender, polypoid, irregular, contact bleeding
b. distance from anal verge >7cm (internal anal sphincter)
3. Complications, Metastases
- Cachexia
- Pallor at nail beds and conjunctiva (anaemia)
- Jaundice, hepatomegaly (irregular surface & nodular edge)
- Cervical lymphadenopathy – Virchow’s  node  
- Bone tenderness, consolidation or effusion, AMS

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INVESTIGATIONS

Aims: Diagnose, Stage the cancer & Investigate for complications of cancer

I. DIAGNOSIS

Colonoscopy – first-line investigation(diagnostic & therapeutic)

- Ensure good bowel preparation
- Visualise lesion: size and location of lesion
- Take biopsies of the lesion
- Enables detection of synchronous lesions (primary tumors occurring less than 6 months apart) – synchronous polyps in 30%,
synchronous cancer in 3-5%.Therefore, do not do a sigmoidoscopy only.
- Enables therapeutic procedures e.g. polypectomy, stenting of obstructed colon
CT colonography a.k.a virtual colonoscopy
- Next best to colonoscopy: needs IV contrast, air and contrast enema
- Detects >/- 1cm tumors
Double-contrast barium enema (barium + air)
- Classically can see an apple core lesion with barium enema
- Not adequate for diagnostic purposes, may miss small lesions & distal lesions
- Need to insert a rigid sigmoidoscope 10-15cm to instil air & contrast

II. STAGING

All CRCs
(a) CT scan of the abdomen and pelvis for colon tumours
- Local T staging & invasion into bladder, ureter, uterus
- Staging of regional and no-regional lymph node involvement
- Metastases to the liver, obvious peritoneal seeding, omental kinking,
- Look for ascites, hydroureter/ hydronephrosis, intestinal obstruction
(b) CXR + CT scan of the chest
(c) Bone scan if symptomatic (more for Ca breast, lung, prostate, thyroid)
(d) CT brain if symptomatic

Rectal tumors (below peritoneal reflection):

(e) Endoscopic ultrasound / transrectal ultrasound (for rectal tumour)
- Very good for T staging to determine depth of involvement: locally  advanced  CA  (≥T3)  requires  neoadjuvant chemoRT
- Can also assess local lymph node status
(f) MRI of the tumour
- Superior to CT for delineating fat planes in T staging especially in rectal cancer
- Circumferential resection margin (CRM) refers to the fascia propria
- High risk tumors for recurrence: CRM < 2mm, T3/4 (+/- bulky T2)
Neoadjuvant ChemoRT

III. COMPLICATIONS

Basic laboratory investigations:

(a) FBC for low Hb, together with iron studies
(b) UECr: fluid and electrolyte abnormalities from vomiting (eg. in IO), or 3rd space losses (intraluminal); creatinine may be elevated (prerenal
failure) and hence risk of contrast nephropathy
(c) LFT for derangements caused by metastasis (occur late) – raised bilirubin, ALP (first to be raised)
(d) PT/PTT, GXM for surgery
(e) Carcinoembryonic antigen level (CEA)
- A tumour marker for colorectal carcinoma (glycoprotein synthesised by foetal intestinal tissue)
- >90% of CRC produce CEA, Raised levels: 70% CRC, 10-20% lung/ BrCA
- Measured pre-operatively as a baseline level – if the CEA is raised pre-op and falls to within normal range post-op, it is likely tumour
has been totally removed.
Usually, normal values 6wks post-op?
- Follow-up after surgery with CEA levels to detect tumour recurrence
- Causes of false positive raised CEA: smoking, pregnancy, bronchitis, cholangitis and cancers of the stomach, lung, breast, pancreas,
cervix, bladder and kidney

Imaging
(f) Erect and supine AXR to look for intestinal obstruction (usually large bowel closed loop obstruction) and caecal distension; near perforation
(g) Erect CXR in perforated tumour to detect air under diaphragm
(h) ECG :anaesthesia assessment

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TNM STAGING

DUKE’S STAGING (SURGICAL AND HISTOLOGICAL FINDINGS)

Stg Description 5yr surv

A Tumor confined to bowel wall with no extension into extrarectal/ extracolic tissue, no LN mets 75%
B Invades past muscularis propria into extrarectal/ extracolic tissue, no LN 55%
C LN mets present
C1: only nearby nodes involved (paracolic LNs) C1:40%
C2: continuous string of LN involved up to proximal resection C2:20%
(LN at base of mesentery)
D Distant mets/ extensive local mets such that surgically incurable Poor unless mets are resectable

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TREATMENT

SURGERY

Aim: eradicate tumor with clear margins and LN drainage

Pre-operative measures

- Bowel prep
Modification of diet – 3 days low residue diet (reduce frequence and volume of stools – low fibre, reduce food that increase
bowel activity), NBM day before operation
Bowel clearance with polyethylene glycol. CI obstruction?
- Prophylactic antibiotics (max at first incision)
ampi/ genta/ metronidazole at induction of anesthesia

Principles of surgery for colonic carcinomas

- En-bloc resection of tumour with adequate margins

For colonic tumours, a margin of 5 cm proximally and distally is adequate

While segmental resection is sufficient for primary tumour removal, a wider resection is often required to
achieve sufficient lymphadenectomy
Adequate clearance of the draining lymphatics involves excision of the vascular arcades supplying the segment of involved
colon back to their origin (from the SMA or IMA) as lymphatics follow the arteries generally

- Obstructed left sided carcinoma

No difference shown for doing a staged procedure (i.e. tumour removed with proximal end of colon brought out as a
colostomy) as compared to creating a primary anastomosis
On-table bowel decompression ( irrigation) for clearance of faecal material
Segmental colectomy for the tumour with intraoperative decompression is comparable to subtotal/total colectomy without
decompression with regard to bowel function and rates of complications

- Site of anastomosis: SB more reliable blood supply so SB-LB >>> LB-LB

- Site of surgery for colonic carcinoma

Marginal artery of Drummond

= Artery formed by the anastomosis between the
ileocolic artery, middle colic artery, right and left
colic arteries and sigmoidal artery. It is a continuous
vessel running along the inner perimeter of the large
intestine in the mesentery as part of the vascular
arcade that connects the SMA and IMA, from the
ileocolic junction to the rectum. This artery is almost
always present and its absence should be
considered a variant.

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 Tumour Site Surgery Structures Involved (Excision of structures + Division of vessels)
Caecum / Right hemicolectomy Excision of caecum + ascending colon
Ascending colon Ileocolic artery
Right colic artery
Right branch of the middle colic artery

Hepatic flexure / Extended right hemicolectomy (B) Excision of caecum, ascending colon and proximal transverse colon
transverse colon near Ileocolic artery
hepatic flexure Right colic artery
Middle colic artery (at its origin)

Mid-transverse colon Transverse colectomy (C) Excision of transverse colon

Middle colic artery

Transverse colon Left segmental colectomy (D) Excision of distal transverse colon and proximal descending colon
near splenic flexure Left branch of middle colic artery
Left colic artery

Descending colon Left hemicolectomy Excision of descending colon

Left colic artery
Left branch of middle colic artery
Inferior mesenteric vessels

Sigmoid colon Sigmoid colectomy Excision of sigmoid colon

= High anterior resection with variable length of upper rectum & distal descending colon
Inferior mesenteric vessels

125
 16cm High AR:
margin above
peritoneal
Upper 1/3 reflection

12cm: usually where

peritoneal reflection sits

Middle 1/3
Low AR: margin
below peritoneal
8cm reflection
Lower 1/3
Ultra low AR:
4cm anastomosis to
the upper end of
Anal canal: the anal canal
2-4cm

Anterior resection = Resection of IMA at its pedicle (with parts of the colon where it supplies – Sigmoid and Rectum)
Not descending colon as the LMCA can extend its supply to it.

I/O cases: SB-LB anastomosis better than LB-LB anastomosis

- Because SB has more abundant and predictable blood supply
- Dilated LB prox to obstruction will be edematous not suitable for anastomosis
- never do a left hemicolectomy (do right hemicolectomy/extended hemicolectomy)

Principles of surgery for rectal carcinomas

- En-bloc resection with adequate margins

For rectal tumours a margin of 5 cm proximally and 2 cm distally is adequate (as it has been found that lymphatic spread of rectal tumours
is predominantly in the proximal direction)
Radial margins are also important as there is a zone of downward spread within the mesorectum (peritoneal investment of the upper
rectum; just anterior to the sacrum)

- Sphincter-sparing versus loss of sphincter

The anal sphincter can be spared if the distal margin is >1-2cm above the level of the sphincter complex, usually taken to be at the level of
the dentate line (which is 5cm above the anal verge) i.e. distal margin of the tumour must be >7cm from the anal verge
Sphincter-sparing low anterior resection (below the peritoneal reflection); ultra low AR if just above the anal sphincter
Sphincter-sacrificing surgery abdominoperineal resection (entire anus & sphincter complex is dissected, creation of an end colostomy)

- Reconstruction

Formation of a straight coloanal anastomosis in anterior resections is a/w poor function due to the lack of reservoir function

1. Creation of a colonic J-pouch using the proximal end of

colon (the end of the colon is folded back on itself to form a
J, and the two limbs opened and stitched together to form a
pouch, the apex of the J being anastomosed to the anus) is
associated with improved post-operative function

2. Coloplasty is another alternative that is equivalent to

colonic J-pouch (the distal colon is cut longitudinally but
sewn transversely, widening the diameter at that segment to
form a small pouch), done when there is difficulty creating
the colonic J-pouch

- Mesorectal excision

Proximal rectal tumours – 5cm distal margin of mesorectal excision

Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the tumour
Lower rectum tumours – total mesorectal excision required (complete excision of the intact visceral mesorectal tissue to the level of the
levators)

126
- Extended resections

For locally advanced, adherent tumours (T4), multivisceral resection of organs involved (pelvic exenteration) is associated with improved
local control and overall survival compared with standard resection, though high morbidity of 25-50% is associated
Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease

- Stoma creation

A defunctioning loop ileostomy (or loop colostomy) is usually created during an low AR as the manipulation of the colon deep within the
pelvic cavity causes increased risk of an anastomotic leak & also poorer blood supply to anastomosis
A defunctioning stoma does not protect against anastomotic leak, but mitigates against disastrous complications of faecal peritonitis
should a leak occur
Closed in 2-6/12 after check with gastrograffin reveals no leak

- Neoadjuvant chemoradiotherapy for rectal tumours

Neoadjuvant RT with 5-fluorouracil can downstage tumour significantly ability to preserve sphincter, ability to resect previously
unresectable tumour, reduce local recurrence
Good evidence for ≥T3  tumours,  CRM<2mm: benefits > risk of RT (esp. that pt becomes too ill to be operated on)
Not possible for colon carcinomas due to risk of small bowel radiation if given above peritoneal reflection
Done before Sx as ChemoRT requires blood supply to work (disrupted during Sx)

- Surgical treatment according to stage

Stage of disease Treatment

T1 Involvement of submucosa, but no penetration Local excision (AR or APR)
through muscularis propria
T2 Invasion into, but not penetration through, a) Local excision + adjuvant Chemo/RT
muscularis propria OR
b) radical resection
T3 Penetration through muscularis propria into Neoadjuvant chemo / RT before radical
subserosa (if present), or pericolic fat, but not resection
into peritoneal cavity or other organs
T4 Invasion of other organs or involvement of free
peritoneal cavity

Operative complications

Immediate (<24h) Damage to other organs e.g. ureters

Early (<30 days)
Late (>30 days)
Wound infection
Bleeding
Abscess
Anastomosis breakdown/leak faecal peritonitis
Early stoma complications
Diarrhoea
Impotence (damage of pelvic nerves)
Adhesions (I/O)
Anastomotic stricture
Late stoma complications

Surgery for palliation

- Resection of primary for palliation of symptoms such as bleeding, perforation, obstruction or pain
- Resection of asymptomatic primary is controversial, but may confer survival benefit in a select group of patients where metastatic tumour
burden is restricted to one side? and liver involvement is not extensive

Surgery for metastases

- Isolated liver metastases (synchronous or metachronous) may be resected with survival benefit; neoadjuvant chemotherapy can be given to
downstage the metastases if they are initially resectable
- Lung metastases usually indicate systemic dissemination of disease, but in the rare setting that there is an isolated lung secondary, resection
can provide survival benefit

Surgery for recurrence

- Loco-regional recurrence, if detected early with adequate resection, can confer survival benefit

127
RADIOTHERAPY
- Role as neoadjuvant therapy in rectal cancer to downstage tumour (in T3/T4)
- Post-operative adjuvant therapy in stage II or III rectal cancer

CHEMOTHERAPY

Adjuvant therapy

- Colon cancer: 5-FU + folinic acid (leucovorin) for 6 months, or 5-FU  +  levamisole  for  12  months  in  Duke’s  C  cancer  (node  
positive);;  not  recommended  in  Duke’s  B  or  less
- Rectal cancer: post-operative adjuvant therapy in combination with radiotherapy in stage II or III disease (5-FU based regimen
used)

Palliative therapy

- 5-FU in combination with folinic acid is first-line therapy

- Alternatives for first-line therapy: Raltitrexed when 5-FU is not tolerated; capecitabine or UFT (uracil combined with tegafur)
plus folinic acid

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 (recommended frequency not known)

128
ASSOCIATED CONDITIONS

I. Familial adenomatous polyposis (FAP)

- 1 in 10,000, autosomal dominant inheritance

- Germline mutation of APC gene on 5q21
- >100 adenomatous polyps all over colon; polyps take 5-6 yrs to turn malignant
- 50% patients will have polyps by 16yrs; 90% will have colorectal CA by 45yrs

- Other sites for polyps: stomach, duodenum

- Extraintestinal manifestations
Skin: Epidermoid cysts, Lipoma
Bone: Osteoma of skull/ mandible, Dental abnormalities
Eye: Congenital hypertrophy of retinal pigment epithelium (CHRPE)
Other tumours:
Desmoid tumours (intra-abdominal tumours, treated with CT, RT or HT.)
Thyroid cancer (follicular or papillary type)
Periampullary CA

- Diagnosis
Colonoscopy showing >100 polyps
Genetic testing

- Surveillance
Yearly colonoscopy for at-risk family members from 12y onwards
5 yearly OGD for surveillance of Periampullary Cancer.
Genetic testing of at-risk family members
Affected members should undergo prophylactic proctocolectomy with ileal pouch anal anastomosis (IPAA – involves folding
loops of ileum back on themselves and stitching or stapling them together to form a reservoir pouch which is them
anastomosed to the anus) at ~ 20 YO

Subtotal colectomy is an option if the rectum is relatively spared of polyps

II. Hereditary Non-Polyposis Colorectal CA (HNPCC)

- Divided into Lynch syndrome I or Lynch syndrome II based on clinical features

- Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure)

- Tumours tend to arise from polyps which are commonly flat, with villous histology
- Resultant tumour is often poorly differentiated

- Lynch syndrome type II is associated with increased risk of cancer elsewhere, most commonly endometrial cancer, and also
ovarian, gastric, small bowel, hepatobiliary, and renal pelvis/ureter cancers
o Offer a THBSO with total colectomy if CRC detected

- Diagnosis is based on the Amsterdam criteria – see above

- Surveillance – 1-3yrly colonoscopy starting at 20 years old

III. Ulcerative colitis

- Screening – yearly colonoscopy starting after 10 years of UC

129
3. STOMAS

Stoma: opening of a luminal organ into the external environment

Indications
1. For input: feeding (Percutaneous endoscopic gastrostomy)
2. For output: decompression/ lavage, defunctioning/ diversion, draining/ exteriorization (urine, faeces)

Nursing intervention
- Stoma nurse to perform counselling & discuss best site for stoma placement

Stoma siting

- Over the rectus sheath decreases the risk of prolapse,

- Away from the surgical incision risk of wound contamination and infection
- Away from skin creases or bony prominences stoma wafer can be flush with the skin (any gaps between skin and wafer
leakage of fluid skin excoriation & infx)
- Away from old surgical scars risk of hernia
- Sited for easy accessibilty i.e. not under a large fold of abdominal fat
- Intra-operatively, avoid tension over the stoma to marked site causes vascularity of the stoma stoma necrosis

Types of stomas

Permanent (end colostomy)

- When patient or surgeon factors are against reversal of stoma (relative)
- When no distal bowel remaining (absolute)
After abdomino-perineal resection for Low rectal/ anal tumor
After Panproctocolectomy without ileal pouch anal anastomosis

Temporary
- Decompression – relief of bowel obstruction causing proximal dilatation
- Defunctioning – to reduce effects of anastomotic leak
Esp. after low anterior resection, where risk of anastomotic leakage is high 2o to poor blood supply to anastomotic site
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  Crohn’s

Colostomy (vs ileostomy)

?usually flushed with skin,  (vs  protrudes  3cm  ‘spout’,  as  ileal  contents  are  corrosive,  to  prevent  contact  with  skin)
firm brown faceal output (vs watery greenish ilieal output)
larger diameter of stoma (vs smaller diameter in ileostomy)

Stoma Complications

Early
- Necrosis of terminal bowel (stoma appears dusky (grey black); check by intubating with a glass tube into the stoma to look
at colour of mucosa) refashion stoma
- Obstruction (fecal impaction explore with finger, enema / secondary to adhesion – more in ileostomy)
- Leakage skin erosion, parastomal infection resite
- Bleeding
- Stoma diarrhoea (high output) correct water & electrolyte imbalance (hypoK), add anti-motility agent to thicken output
(loperamide +/- codeine)
http://www.wjgnet.com/1007-9327/7/741.asp

Late
- Prolapse of bowel refashion/refresh
- Parastomal hernia (+ve cough impulse) refashion
- Stenosis (unable to pass finger through) refashion
- Retraction refashion
- Fistulae
- Skin excoriation
- Psychological problems

130
End colostomy This procedure is most commonly performed to manage carcinoma of the lower rectum or anus,
diverticular disease, and rare cases of faecal incontinence that do not respond to medical mx.

For example, a very low rectal cancer will require resection of the rectum and anus
(abdominoperineal excision of rectum). The remaining descending and sigmoid colon is mobilised
and the cut end brought to the abdominal surface at an opening about 2 cm across.

This is usually sited in the left iliac fossa.

Abdominoperineal excision of the rectum If the anus, rectum, and a portion of the lower colon have not been removed, as in Hartmann's
procedure, two outcomes are possible. In the first, the distal, non-functioning part of the colon and
the rectum can be stapled or sewn closed and left inside the abdomen as a rectal stump. The
proximal colon is then taken out as an end colostomy.

Because the rectum has not been removed, the urge to have a bowel movement may occur.
Mucus and some old stool, if present, will be passed.

If the colostomy is temporary, a second operation is needed to reconnect the two ends.

Hartmann's procedure Less commonly, two separate stomas may be created.

One stoma is the exit of the functioning part of the colon through which stool and gas pass.
The second stoma opens into the non-functioning portion of the colon and rectum and is called a
mucous fistula. The second stoma is usually small, flat, pink-red in colour, and moist, and it
produces only mucus.

Loop colostomy A loop colostomy was traditionally created to defunction an inflamed sigmoid in diverticular
disease or to defunction a distal anastomosis.It has largely been replaced by loop ileostomy.
A loop of colon is brought to the surface of the body and may be supported on a rod, which is
removed after about five days. The bowel wall is partially cut to produce two openings—of an
afferent limb and an efferent limb. The opening of the afferent limb leads to the functioning part of
the colon, through which stool and gas pass out. The opening of the efferent limb leads into the
non-functioning part of the colon. The stoma site was usually high on the abdomen above the
waistline because the transverse colon was commonly used.

Currently, loop colostomies are more often fashioned from the sigmoid colon to defunction the
rectum (for example, in cancer) or anus (for example, in incontinence).
A loop colostomy may be temporary or permanent.
End ileostomy When the entire colon, rectum, and anus must be removed (panproctocolectomy) an end
ileostomy must be employed. This occurs most commonly in severe ulcerative colitis but also in
familial polyposis and some cases of colorectal cancer (for example, hereditary non-polyposis
colorectal cancer).

The ileum is resected just short of its junction with the caecum, and 6-7 cm of the small bowel is
brought through the abdominal wall, usually in the right iliac fossa. It is everted to form a spout
and then sutured to the bowel wall to protect the skin from the irritating content of the ileal fluid.

After a panproctocolectomy the ileostomy is permanent. Temporary end ileostomy is often used
after an emergency subtotal colectomy, which leaves part of the sigmoid colon and rectum left in
place; for acute ulcerative colitis; acute ischaemic bowel; or neoplastic obstruction of the sigmoid .
Loop ileostomy This type of stoma allows for defunctioning of an obstructed colon (in cancer), defunctioning of a
distal anastomosis (after resection and primary anastomosis either as an emergency or after
radiotherapy), or defunctioning of the anus (in incontinence or perineal involvement in Crohn's
disease). Loop ileostomy has largely replaced loop colostomy because it is easier to site, less
bulky, and easier to surgically close. A loop ileostomy has two openings, and most are temporary.

131
End-loop ileostomy This less commonly performed procedure is used when an end ileostomy cannot be fashioned
safely because the patient is obese or because of unfavourable mesenteric anatomy. The
formation of this stoma is similar to a loop ileostomy, but the efferent limb is short and blind
ended. On inspection at the bedside this type of stoma is indistiguishable from a loop ileostomy.
Double barrel stoma When the caecum is removed, the surgeon might create a double barrel stoma. In essence, this is
an end ileostomy (small bowel) and a mucous fistula (the remaining colon) sited beside each
other. On examination this will look almost identical to a loop ileostomy, however, closer
inspection will show two separate stomas.
Urostomy This is a general term for the surgical diversion of the urinary tract. The main reasons for a
urostomy are cancer of the bladder, neuropathic bladder, and resistant urinary incontinence.

The bladder is usually removed, but this may depend on the underlying condition. Formation of an
ileal conduit is the most common procedure, which constitutes isolation of a segment of ileum.
One end of the ileum is closed and the two ureters are anastomosed to it. Finally, the open end of
ileum is brought out onto the skin as an everted spout and will look similar to an end ileostomy.
Urine drains almost constantly from the kidneys through the ureters and ileal conduit into a bag.

Stoma bags

Stoma bags are of two main types.

Single piece systems stick straight on to the patient's skin. Two piece systems have a separate base (a flange) that
sticks to the skin, and the bag attaches to this. This
enables the bag to be changed wo removing the flange.

Some bags have a second opening at the bottom to allow emptying. These are most useful in the period immediately after operation
and in patients who have had ileostomy, who need to drain their bag regularly. Closed bags are used when the faeces are well
formed and are usually only changed once or twice a day. Most patients with a stoma will use an opaque bag, but in the period
immediately after operation a transparent bag is used to observe the new stoma for complications such as persistent oedema or
necrosis. Modern stoma bags are fitted with a carbon or charcoal flatus filter that allows gas to escape to prevent the bag from
ballooning or detaching and neutralises odour.

Complications

Functional problems, such as skin excoriation and stoma noises, are the most common complications and are usually managed by
the stoma nurse. Patients with stoma admitted to hospital with increased or decreased output should be appropriately managed to
exclude any abdominal emergency, with particular emphasis on careful history taking to establish the normal bowel pattern, and
attention to fluid balance.

Most structural problems, such as stoma prolapse, retraction, and parastomal hernia formation can be managed conservatively with
modified bags and specialised belts. Only about 10% of patients with these complications will require further surgery. Patients should
be alert to any change in colour of their stoma. Stomal oedema is normal for several days after surgery, but if the mucosa becomes
dusky or necrotic the surgeon should be contacted promptly.

132
Question Answer Stoma

Where is the stoma? Left iliac fossa Most likely a colostomy

Right iliac fossa Most likely an ileostomy

How does the bowel lie in relation to Flush with skin Most likely a colostomy
the external skin?
Raised spout Ileostomy; less commonly a urostomy

How many lumens are present? One End colostomy; end ileostomy; urostomy

Two (adjacent)—efferent limb Loop colostomy; loop ileostomy; end-loop ileostomy

may be difficult to see

Two (separate stomas) Most likely end colostomy with a mucous fistula; double
barrel stoma; rarely bowel stoma and urostomy

What are the contents of the stoma Fully formed stool Colostomy
bag (don't be afraid to feel it)?
Semisolid or liquid stool Most likely ileostomy; colostomy

Urine Urostomy

Mucus Mucous fistula

Examining a patient with an abdominal stoma and bag

133
4. DIVERTICULAR DISEASE

PATHOLOGY – acquired herniation of colonic mucosa through muscular wall, with a covering of colonic serosa

TERMS
- Diverticulosis coli – presence of acquired pseudodiverticula
- Diverticular disease – symptomatic diverticulosis coli
- Diverticulitis – inflammation of diverticula

EPIDEMIOLOGY
- Increases with age; up to 25% in >70YO (2-5% are <40YO, more in obese M)
- Majority are asymptomatic; 10-30% are symptomatic
- Risk factors – dietary fibre & genetics
- Site
o majority are in the sigmoid colon, right sided are thought to be genetic;
o Asians: 40% right, 60% left, Caucasians: 20% right, 80% left
o not in rectum as taeni coli has fused

PATHOGENESIS

1. Increased intraluminal pressure

- Associated with lack of dietary fibre
2. Degenerative changes in colonic wall
- Usually at point of entry of terminal arterial branches where serosa is weakest
- Associated with weakening of collagen structure with age

PRESENTATIONS - depends on location of the affected diverticulum, the severity of the inflammatory process, and presence of complications

1. Acute diverticulitis
- Symptoms: LLQ pain, N/V, Constipation / diarrhoea, flatulence/bloating
- Signs: Low grade fever, Tender palpable mass
- Investigation: WBC

2. Chronic diverticulitis
- Recurrent LIF pain
- Irregular bowel habit
- Passage of mucus PR

3. Complicated diverticulitis (dangerous)

a. Perforation
b. Paracolic abscess / inflammatory mass – 2o to localized perforation
c. Bowel obstruction – 2o to stricture or adherence to a diverticular mass
d. LGIT haemorrhage – ulcerated vessel @ neck of diverticulum; torrential
e. Fistula formation (commonest: colovesical fistula) – 2o to pericolic abscess discharging, operation or drainage of pericolic abscess. May
present with urinary symptoms. Others – colo-cutaneous, colo-uterine, colo-enteric, colo-vaginal

Elderly and patients on steroids may have no sign even in severe diverticulitis.
There is an increased rate of free perforation (43% vs. 14% in immunocompetent patients), increased need for surgery (58% vs. 33%), and
increased postoperative mortality (39% vs. 2%).

STAGING
- Hinchey classification of complicated acute diverticulitis – need for surgery is reflected by degree of infective complications

Stage 1 Pericolonic / Mesenteric - ABx, NBM, IV fluids

abscess (small) - Consider 1 stage surgery after acute episode – resection of affected bowel
segment with primary anastomosis
Stage 2 Pelvic / retroperitoneal - Percutaneous drainage
abscess (large) - Elective 1 stage surgery
Stage 3 Purulent peritonitis - 2 stage operation – Hartmann’s  procedure  (partial  colectomy  +  diverting  end  
(fm perf diverticulitis) colostomy & rectal stump formation) + secondary re-anastomosis 3 months later
Stage 4 Faecal peritonitis
(fm ruptured diverticula)

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.
Note: current controversy  of  management  for  stage  3:  hartmann’s  vs  segmental  resection  with  primary  anastomosis  with  or  without  defunctioning  ileostomy
In the absence of complications and systemic signs and symptoms, patients with mild abdominal tenderness may be treated conservatively.
Conservative treatment typically includes dietary modification and oral or IV antibiotics. This has been shown to be successful in 70% to 100% of patients.

134
Presentation Clinical features
Acute Diverticulitis - LIF pain – colicky,
progressing to constant,
relieved by defecation
- LIF tenderness
- Palpable LIF mass
- Nausea
- Urinary symptoms
- Pyrexia
- Increase pulse rate
Chronic Diverticulitis - Recurrent LIF pain
- Irregular bowel habits –
Not a common constipation & bouts of
clinical entity diarrhoea
- Passage of mucus PR
- Ruled out cancer, IBD,
ureteric colic, Msk pain etc.
Generalised peritonitis - Acute onset abdominal
/ perforation pain – severe & continuous
- Abdominal guarding &
rigidity
- Vomiting
- Tachycardia
- Pyrexia
Pericolic abscess - May follow acute
diverticulitis
- LIF tenderness & guarding
- LIF mass – may be
detected on DRE
- Swinging fever
Persistent - LIF pain, tenderness &
inflammatory mass palpable mass
- Fever
- Malaise
Small bowel I/O
Large bowel I/O - PHx of recurrent acute
diverticulitis or irregular
bowel habit
- Colicky abdominal pain,
constipation & abdo
distension
Hemorrhage - Usually in the elderly who
have higher density of
sigmoid diverticula
- Massive bleed (altered
blood ± clots; not melena)
usually right-sided
- Colicky pain as blood is
irritative & causes spasm
Vesicocolic fistula - PHx of chronic diverticulitis
& UTI
- Hx of dysuria, freq,
haematuria, pneumaturia,
faecaluria
Investigations
- FBC – leucocytosis, ↑ ESR
- Erect CXR to rule out perforation
- AXR – ileus, air-fluid level w/in an
abscess
- CT scan w triple contrast (choice)
Severity, complication, clinical
staging
Water soluble contrast: IV for
vascular lesions, oral for small
bowels, enema for large bowels
Features – diverticula elsewhere,
confirm colitis (mesenteric fat
infiltration, concentric bowel
thickening) but only suggest
diverticulitis, pelvic abscess, free
gas, extravasated contrast
Cannot tell if inflm is due to
diverticula
Better than intraluminal
examinations as bulk of inflm is
extraluminal
- Laparoscopy – if diagnosis is in doubt
- Barium enema – CI as barium may
leak out into abdo cavity
- Avoid colonoscopy as risk of
perforation is high (by air insufflations
or instruments) + worsens diverticulitis
- Rigid sigmoidoscopy – oedematous
mucosa & rigidity of rectosigmoid jx
- Flexible sigmoidoscopy – diverticular
orifices
- Barium enema – ‘saw-tooth’   bowel resection
appearance, diverticula, strictures
- Colonoscopy – exclude differentials
(i.e. Ca colon)
- FBC – ↑  TW,  ↑Hb  (dehydration)
- U/E/Cr – dehydration & ARF
- CXR – free gas under diaphragm
- FBC – ↑  TW
- CT – differentiate between
inflammatory phlegmon (spreading
diffuse inflammation with pus/purulent
exudates) & pericolic abscess
- AXR – dilated bowels prox to stenosis
- Water soluble contrast enema
- Invx as for LGIT bleed – resus,
investigations + colonoscopy &
angiography (both diagnostic AND
therapeutic value)
- ± on-table enteroscopy if required
- ± tagged RBC scan (not as sensitive
compared to angiogram): RBC tagged
with radioisotope
- UFEME & urine c/s: confirm UTI and
organisms (polymicrobial as opposed
to  sterile  pyuria  in  ‘UTI  from  adj   disease, post-irradiation
diverticulitis’)
- Cystoscopy – cystitis
- KUB – air in bladder
- Barium enema – diverticular bowel
segment
- Sigmoidoscopy – usually normal
135
Differentials
Can dev anywhere in GIT. See
Ddx to RIF/LIF pain
- GI: colitis, GE, IBS, IBD,
mesenteric ischaemia/
adenitis, Ca colorectal
- Right colon/redundant (extra
bend in descending colon)
sigmoid colon: appendicitis
- Transverse colon: PUD,
pancreatitis, cholecystitis
- Inflm adj to UT: UTI, stones,
cancer, cyst/
Angiomyolipoma,
hydronephrosis
- Lower quad pain in F
(Obgyn): PID, torsion of
cyst/ ovary, endometriosis,
ectopic pregnancy
- Retroperitoneal perf (leg
pain): thigh abscess, leg
emphysema
- #, infx, inflm,
- CA colon – may coexist.
Hard to differentiate –
therefore, ALWAYS exclude
CA colon e.g. histology after
- Ischaemic colitis
- Radiation colitis
- Colonic endometriosis
- Other causes of peritonitis –
perforated PUD/ appendicitis/
bowel/ ectopic pregnancy,
ishaemic bowel, acute
pancreatitis, ruptured AA/
hepatoma, torsion of testis/
ovary, pyonephrosis
- CA colon
- Anorectal bleed
- Angiodysplasia
- Ischaemic colitis
- Colorectal CA
- Colitis (inflm or infx)
- UBGIT
- Coagulopathy
- Other causes of fistula – CA
colon,  CA  bladder,  Crohn’s   colon + anastomosis + closure of
necrosis
Management
Conservative
- Bed rest
- NBM, IV fluid
- Broad-spectrum antibiotics –
augmentin or metronidazole or
ciprofloxacin
- Antispasmodics
After acute phase settled (4-6 wks)
- Colonoscopy – confirm dx &
exclude CA colon and/ or
- Barium enema is inferior to
colonoscopy in terms of image
quality and is usually only
performed if the patient has
strictures or an excessively
tortuous sigmoid colon where
colonoscopy is difficult or
dangerous
Role of surgery: see below
Conservative – see above
Surgical
Indications:
- Severe / recurrent attacks
- Possible CA colon
Stage: Segmental resection of
affected colon + anastomosis
Mgmt as for acute abdomen
- Resuscitate
- Surgical
Peritoneal toilet
Hartmann’s  procedure  
(Resection of affected
segment
+ End sigmoid colostomy)
- CT/ US guided percutaneous
aspiration
- Surgery – evacuation of pus ±
resection of affected segment
- Usually temporary, due to
attachment of enteric loop against
area of acute diverticulitis
- Surgery if does not resolve
- NBM, Drip & suck
- Surgery – Resection ± primary
anastomosis
- Resuscitate & correct
coagulopathy
- Colonoscopic management:
adrenaline injection, endoclips on
bleeding vessel, heat coagulation
- Radiologic embolisation of site
of bleeding with temp foam
material via angiography
- Surgery – segmental resection;
total colectomy if unable to
localise bleed
- Surgery – Resection of affected
bladder fistula opening
 Outcomes: well or deteriorate requiring surgery, recurrent episodes, stricture & subacute IO (offer surgery)

Indications for 1. Sepsis from abscess or faecal peritonitis

emergency operation
2. Perforation
3. Diverticulitis not responding to conservative management
4. Obstruction with pending perforation – need to rule out cancer at the same time
5. Emergency bleed (controversial clamping both side & look for active bleed into
segment segmental resection)
a. Haemodynamically unstable with failure of embolization
b. Need > 4 units of PCT
c. Previous bleed

Indications for elective 1. Stricture

operation 2. Fistula
3. Recurrent attacks – occurs in 30% of patients after 1st episode. a/w higher mortality &
complication rates
4. Young patientss <40YO – high recurrence rates
5. Immunocompromised patients (e.g. renal transplant) – may not show S/S of acute attack or
complications

Advice to patients:
- 70% of patients will not have recurrence after first attack (after first attack, 1/3 will have second. out of whom 1/3 will have 3 rd)
- Advise high fibre diet (prevents recurrence in >70%) & to drink lots of fluid, weight reduction and exercise

Recurrent diverticulitis after surgical treatment

- incidence ranging from 1% to 10%.
- In general, the progression of diverticular disease in the remaining colon is approximately 15%.
- Important factors to be considered in terms of surgery are the adequacy of resection, meaning the degree of proximal resection and
level of distal anastomosis. The use of the rectum as the distal margin decreases the rate of recurrence.
- Care also must be taken to exclude other components of differential diagnosis, especially irritable bowel syndrome, inflammatory
bowel disease, and ischemic colitis.

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5. INFLAMMATORY  BOWEL  DISEASE  (CROHN’S  DISEASE,  ULCERATIVE  COLITIS)

Crohn’s Ulcerative colitis

Bowel Can affect entire GIT anywhere from mouth to anus, Usually begins in the rectum and can extend
involvement but usually affecting the terminal ileum proximally to affect entire colon
Location 40% terminal ileum 40% rectum alone
30% small intestine 40% left colon
30% colon 20% total colitis
3% anorectal (usu. spared) Backwash ileitis (10%) – 30cm of ileum affected
due to incompetent ileocecal valve causing reflux
of noxious inflammatory mediators
Continuity Not continuous, with skip lesions Longitudinal mucosal continuity
Complications Strictures, fistulae, sinuses, malnutrition (SB involve), These complications absent.
SB obstruction, toxic dilatation, CRC Massive PR bleed, toxic megacolon, venous
thrombosis, CRC ++
Histopathology Macroscopic: bowel is thick-walled & nodular Macroscopic: granular appearance of mucosa , loss of
(cobblestone appearance) with creeping fat, vascular markings, pseudopolyps interspersed with
mesenteric thickening & deep linear ulcers areas of shallow ulceration
Microscopic: transmural involvement, non-caseating Microscopic: only mucosal & submucosal involvement,
granulomas (pathognomonic, but only present in 2/3) ulcers, crypt abscesses
- Muscularis propria & serosa may be affected in
fulminant disease
Risk of Slight increased risk of colorectal Ca, increased risk of Substantially higher risk of CRC
carcinoma small bowel lymphoma 2% at 10 years
8% at 20 years (15% if pan colitis)
18% at 30 years
Much higher risk with concomitant PSC
Associated Ab ASCA: anti-saccharomyces cerevisiae antibodies p-ANCA: perinuclear antineutrophil cytoplastic ab
Severity Harvey Bradshaw severity index Modified Truelove & Witts severity index
(Mild, moderate, severe, fulminant)

Epidemiology
Bimodal distribution: affects young in the 2nd & 3rd decades
of life, with second onset in the 5th & 6th decades of life
Equal gender predominance
Higher prevalence amongst Ashkenazi Jews & in cooler
climates e.g. Scandinavia, UK, Germany, northern USA
Genetic association

History
GIT: abdominal pain, diarrhea, N/V, bloating, distension,
bloody stools with mucous & pus
Crohn’s  fistula:  colovesical fistula or coloovarian fistula:
faeces in urine/ pneumaturia, faeces per vaginal/ PID
Non-specific systemic: LOW, LOA, fever, fatigue, symptoms
of anemia, chronic malnutrition
Specific extra-intestinal manifestations

Physical examination: usually normal +/- extra-intestinal manifestations

Acute severe: fever, tachycardia, tender/distended abdomen.

Nutritional deficits.
Extraintestinal: clubbing, oral ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis/episcleritis/iritis, arthritis/sacroilitis/AS, fatty liver.

Differential diagnoses
1) Gastroenteritis: exclude with stool microscopy & culture + C.diff toxin
- Bacterial: E. coli, Campylobacter, Salmonella, Shigella, C. difficile
- Parasitic: E. histolytica
- Viral: rotavirus
2) Other infective causes: diverticulitis, colorectal TB
3) Ischaemic colitis
4) Bleeding diverticulosis
5) Colorectal carcinoma
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CROHN’S DISEASE

P/E: RIF mass, perianal enlarged skin tags/ fistula/ abscesses, anal stricture

Investigations: supportive (see UC) & diagnostic

Diagnostic (mainly at terminal ileum)

Contrast radiographic studies: assess location & extent of disease, look for strictures & fistulae
o Barium studies: small bowel series & enema (cobblestone)
o CT scan with oral & IV contrast
Endoscopy: look for typical features
o Colonoscopy with tissue biopsy (non-caseating granulomas)
o OGD: upper GIT involvement
o Endoanal U/S (EUS): identify fistula tracts

Management

Medical (principle treatment)

o Nutritional support e.g. TPN (may also aid closure of fistulae)
o Pharmacological
Corticosteroids for acute exacerbation of disease, but not for long term use
1st line: 5-ASA or 5-aminosalicylic acid (sulfasalazine, mesalazine) induce & maintain remission of disease:
oral, rectal suppository or enema (up to splenic flexure)
2nd line: immunosuppressive agents e.g. azathioprine, 6-MP, MTX, Tacrolimus & cyclosporine when 1st line
agents ineffective
o Cyclosporin and Tacrolimus are nephrotoxic avoid LT
Biologics = created by biologic processes, rather than being chemically synthesized.
- Ind: for steroid resistant
- Remicade (infliximab) = TNF blocker
- ACT 1 and ACT 2 (Acute ulcerative Colitis Treatment) trials showed that 44-45% of patients treated
with infliximab for a year maintained a response to the medication, cf 21% on placebo
- Pretreatment: rule out TB, hepatitis first (as tx can cause reactivation)
- Require close surveillance for SE (blood disorders, infections, lymphoma & solid tissue cancers,
hepatotoxicity, drug-induced lupus, demyelinating disorders)
Surgical
o Principles
Avoid surgery until absolutely necessary (80% require surgery within 20 years of onset) & when indicated
perform bowel preserving surgery as repeated bowel resections can lead to short gut syndrome
o Indications :
Disease refractory to medical therapy (common) Fistulae
Serious complications of medical therapy Abscesses
Severe bleeding, perforation Toxic megacolon
Intestinal obstruction due to strictures Malignancy
o Procedure (laparoscopic or open)
CT abdomen for pre-operative percutaneous drainage of  abscesses  (↓  inflammation  &  risk  of  sepsis)
Small bowel: (bowel preservation is key)
- Short segment disease: stricturoplasty
- Long segment disease: long stricturoplasty or resection
- Fistula: resect diseased bowel & repair involved organ
Large bowel:
- Total colectomy + ileorectal anastamosis (if rectum spared) or proctocolectomy + end ileostomy (if
rectum affected)
- Segmental colectomy only in selected cases as high recurrence rate
Perianal disease:
- Setons, fistulotomy, proctectomy in severe disease

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ULCERATIVE COLITIS

Extra-intestinal manifestations (20% of patients)

Joints (most common)
o Transient asymmetrical polyarthritis: mirrors course of colitis & is cured by colectomy
o Ankylosing spondylitis
o Isolated sacroiliitis
Liver
o PSC  (5%):  fibrous  structuring  of  entire  biliary  tree:  ↑  ALP,  MRCP,  ERCP,  liver  biopsy.  Tx:  stenting, transplant
o Hepatic failure over 5-10 years independent of course of colitis
o ↑  risk  of  cholangiocarcinoma  &  ↑↑↑  risk  of  colorectal  carcinoma
Eye
o Iritis, episcleritis, anterior uvetitis. Tx: topical and/or oral corticosteroids
Skin
o Pyoderma gangrenosum: deep ulceration with violaceous border that overhangs ulcer bed, usually affecting LL
o Erythema nodosum: poorly defined, tender, erythematous nodules tt do not ulcerate/ suppurate, usu on the shin
o Tx: corticosteroids, will improve slowly following colectomy

Investigations
Supportive (looking for complications & assessing severity of disease)
Blood tests
o FBC: anemia, leukocytosis & thrombocytosis indicate more severe disease
o UECr: hypokalemia & dehydration in prolonged diarrhoea
o LFT: hypoalbuminemia due to poor nutritional intake
o CRP, ESR: markers of severity
o Autoantibody assay: p-ANCA  ↑  in  UC,  ASCA  ↑  in  CD
Radiological
o AXR to evaluate colonic caliber (>6 cm is abnormal)
o CXR to rule out perforation (risk of perforation in acute disease)
Diagnostic (mainly at rectum)
Endoscopy: look for typical features
o Flexible sigmoidoscopy with tissue biopsy: bleeding may occur with contact with scope.
Never do barium enema during a severe acute attack or as a diagnostic test??

Management
Medical:  similar  to  Crohn’s  disease
o Mild: PO pred + Mesalazine. If distal dz: Pred retention enema/ steroid foam.
If no improve after 2/52 mod.
o Mod: PO pred (40mg/d x1/52 30mg/d x 1/52 20mg/d x 4/52) + 5-ASA + steroid enema BD.
If no improve after 2/52 severe.
o Severe: IV Hydrocort400mg/d + rectal steroid.
If improve in 5/7 PO pred + 5-ASA. If CRP >45/ >6 stools per day ciclosporin/infliximab/Sx.
Surgical (25% eventually require surgery)
o Indications :
1. Disease refractory to medical therapy with severe & extensive colitis (most common)
2. Serious complications of medical therapy
3. Severe bleeding
4. Perforation
5. Toxic megacolon (colon > 6cm): most common cause of death - Involvement of the muscularis propria in the most
severe cases can lead to damage to the nerve plexus, resulting in colonic dysmotility, dilation, and eventual
infarction and gangrene
6. Malignancy
o Procedure (laparoscopic or open)
Acute setting (uncontrolled bleeding, perf, toxic megacolon, fulminant attack): total colectomy with end ileostomy:
diseased rectum left in-situ with resection & IPAA at later date when patient has regained health & steroids have
been withdrawn (as rectum is extraperitoneum organ and dissection/resection takes a long time). Foley catheter
used to decompress rectum for 3-4 days
IPAA (ileo-pouch anal anastamosis): standard of care for patients with UC who ultimately require colectomy. Avoid
necessity  for  long  term  stoma.  Crohn’s  disease  remains  an  absolute  contraindication  as  overall  failure  rates  
approach 50%
Alternative: Total proctocolectomy with end ileostomy
o Complications:
o Mortality 2-7%, 50% if perforation
o Pouchitis: Tx with Abx (metronidazole + ciproflox X 2/52) + immunosupp.

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8. ANAL & PERIANAL DISORDERS

1. HAEMORRHOIDS

Anal cushions.They are clusters of vascular tissue (eg, arterioles, venules, arteriolar-
venular connections), smooth muscle (eg, Treitz muscle), and connective tissue lined by
the normal epithelium of the anal canal.

External hemorrhoids develop from ectoderm covered by squamous epithelium

Internal hemorrhoids develop from endoderm columnar epithelium of anal mucosa.

External hemorrhoids are innervated by cutaneous nerves that supply the perianal area.
These nerves include the pudendal nerve and the sacral plexus.

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

Internal hemorrhoids drain through the superior rectal vein into the portal system.
External hemorrhoids drain through the inferior rectal vein into the inferior vena cava.
Rich anastomoses exist between these 2 and the middle rectal vein, connecting the portal and systemic circulations.

Causes:
1. Decreased venous return / increase intra abd pressure: preg, constipation (low fibre diet) straining
2. Portal hypertension and anorectal varices
3. Increase rectal vein pressure: obesity, prolonged sitting

The most common presentation of hemorrhoids is rectal bleeding, pain, pruritus, or prolapse.
Painless fresh PR bleeding after defecation: coating / dripping, not mixed with stools

Most symptoms arise from enlarged internal hemorrhoids.

Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to
stretching of the suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal mucosa
is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the
arteriovenous anastomoses.
Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation.

External hemorrhoids cause symptoms in 2 ways.

Acute thrombosis: usually related to a specific event, such as physical exertion, straining with constipation, a bout of diarrhea,
or a change in diet. Pain results from rapid distention of innervated skin by the clot and surrounding edema. The pain lasts 7-14
days and resolves with resolution of the thrombosis
Occasionally erode the overlying skin and cause bleeding

External hemorrhoids: not true hemorrhoids, but rather painful thrombosed veins arising distal to the dentate line
Internal hemorrhoids: those arising proximal to the dentate line, usually painless unless prolapsed & strangulated

Complications: thrombosis, infection, prolapse

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Classification & Treatment

Grade 1 Conservative:
Lifestyle modifications
Hemorrhoid protrudes into the anal canal Meds (Daflon) – improves venous tone
but does not prolapse outside the anus,
hyperaemia of mucosa

Grade 2 Surgery:
Rubber band ligation
Hemorrhoid protrudes through the anus Injection sclerotherapy (phenol emoilent oil)
during straining or evacuation but returns
spontaneously

Grade 3 Surgery: Haemorrhoidectomy

Staple
Hemorrhoid protrudes through the anus Excision
during straining or evacuation but needs
to be manually returned to position

Grade 4

Hemorrhoid remains prolapsed outside

the anus

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2. ANAL FISTULA

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. Crohn’s  disease
2. TB
3. Actinomycosis
4. Hydra-adenitis suppurativa

GOODSALL’S LAW
Posterior ½:
(All fistula tracts with external openings within 3 cm of the anal
verge and posterior to a line drawn through the ischial spines)
Curvilinear
Internal opening in posterior midline (at level of
dentate line)

Anterior ½:
Straight tracts

Tracts closer to anal verge = simpler, shorter

Tracts further away = transphincteric, long, high tracts

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

142
CRYPTOGLANDULAR THEORY OF PARKS / PARKS CLASSIFICATION

Type Diagram Management

Intersphincteric Fistulotomy
Division of the internal sphincter
The common course is via internal alone usu does not compromise
sphincter to the intersphincteric space fetal continence
and then to the perineum. Base of the wound is curetted and
70% of all anal fistulae left open to heal by secondary
Other possible tracts include no perineal intention
opening, high blind tract, and high tract
to lower rectum or pelvis.

Transsphincteric Low:
Fistulotomy
The common course is low via internal On pts who have good pre-op anal
& external sphincters into the sphincter function
ischiorectal fossa and then to the
perineum.
25% of all anal fistulae
High / anterior fistulae in women:
Other possible tracts include high tract
(Higher risk for post-fistulotomy incontinence)
with perineal opening and high blind
Conservative approach
tract
1. Cutting seton
Reactive suture / elastic placed
through the fistula tract
Tightening of seton tie sequentially
until it cuts through the fistula tract

2. Partial fistulectomy & endoanal flap

3. Injection of fibrin glue

Suprasphincteric Cutting setons

The common course is via Endorectal advancement flap

intersphincteric space superiorly to
above puborectalis muscle into Sphincter reconstruction
ischiorectal fossa and then to perineum.
5% of all anal fistulae
Other possible tracts include high blind
tract (ie, palpable through rectal wall
above dentate line).
a/w drainage of ischiorectal abscess
Extrasphincteric Endorectal advancement flap

The common course is from perianal Laparotomy & resection of involved

skin through levator ani muscles to the intestinal segment and curettage of fistula
rectal wall completely outside the tract (for those fistulae from more
sphincter mechanism. proximal sections of the colon)
1% of all anal fistulae
Not related to sphincter complex
a/w  Crohn’s,  CA,  recurrent  fistulas

Fistulotomy (for simple, short tracts) – cut & lay open tract
Fistulectomy – core along tract & remove tract entirely
Seton – for complex, long, high tracts

143
4. ANAL FISSURES

An anal fissure is 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  don’t  heal:  usu  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

Definitive for chronic anal fissure Internal anal sphincterotomy

(but do not cut through muscle – irreversible)

Medical sphincterotomy (reversible): GTN paste, botulinum toxoid injections

144
9. LIVER DISEASES

1. ANATOMY OF THE LIVER

The liver is divided into two lobes, right and left

The anatomical division of the liver lobes is demarcated
by the falciform ligament
The functional division (more practical in surgery) is
demarcated by the plane of the gallbladder and inferior
vena cava (also by the plane in which the middle hepatic
vein runs) impt for reading CT scans and in surgery

The liver can be further divided into 8 functional segments

(Couinaud segments) that each have their own vascular inflow,
outflow, and biliary drainage, independent of the other segments

Segments divided by 1 transverse plane and 3 sagittal planes

The transverse plane is at the level of the main branches of

the portal vein (divides liver into upper half and lower half)

The sagittal planes are formed by the three main hepatic

veins (right, middle and left)

Segment I is the caudate lobe

Segments II to VIII are named clockwise, while facing the
patient, starting from the upper right corner (i.e. the upper left
segment of liver)

Segment IV can be further divided into IVa and IVb, where

IVa is the superior and IVb is the inferior subsegment

The liver has two blood supplies – portal vein (formed from
the joining of the splenic vein and superior mesenteric vein)
and hepatic artery (a branch of the coeliac trunk)

Drainage is via the 3 hepatic veins into the inferior vena cava

2. CAUSES OF HEPATOMEGALY

Vascular: RHF, TR, Budd-Chiari syndrome

Infective: viral (hepatitis viruses, EBV, CMV, HIV), bacteria (pygenic abscess, TB), parasite( amoebiasis, hydatid cyst, malaria)
Metabolic:  fatty  liver,  haemochromatosis,  amyloidosis,  wilson’s  disease
Tumour: see below

3. CAUSES FOR A LIVER NODULE ON IMAGING

Benign Cyst - Single

- Multiple – familial (polycystic) or non-familial
Haemangioma - Small
- Big
Adenoma
Fibronodular
hyperplasia
Malignant Secondary Colorectal, stomach, pancreas, breast, urogenital tract, lung
Primary Hepatocellular carcinoma (or hepatoblastoma in children)
Cholangiocarcinoma (only 10% intrahepatic) – presents like
HCC except no background of cirrhosis

145
4. HEPATOCELLULAR CARCINOMA

EPIDEMIOLOGY

- Annual incidence in Singapore is 18/100,000 in males, and 4.6/100,000 in females

- 3rd most cancer among males, overall 4th most common cancer
- Men: female = 3:1
- Peak age of onset: 30-40 years old
- 1o liver cancers are mainly HCCs (85%), with a small proportion of intrahepatic cholangiocarcinoma (6%)

AETIOLOGY AND RISK FACTORS

1. Hepatitis B infection (high HBV DNA load, HBeAg positivity increase the risk) – 100X normal population
2. Hepatitis C infection
3. Cirrhosis (of which cirrhosis resulting from hep B, hep C and haemochromatosis are associated with the highest risk): 20-30years following
initial insult
- Others:  Aflatoxin  ingestion,  α-1- antitrypsin deficiency, haemochromatosis, PBC, anabolic steroids, schistosomiasis
Non-cirrhotic HCC – 5% in west, 40% in Asians

PATHOLOGY

- Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular damage with high cellular regeneration, which leads to
rates of genetic mutation in the cells and accumulation of these mutations leading to carcinoma formation
- Two histological subtypes:
Nonfibrolamellar – associated with HBV and cirrhosis
Fibrolamellar – associated with younger patients, more common in females, no association with hep B or cirrhosis, AFP usually normal,
70% resectable, good prognosis
- Metastasises to lymph nodes, bones, lungs and adrenals (more common in intrahepatic lesions >5cm)

PRESENTATION

HCC is frequently diagnosed late in its course because of the absence of pathognomonic symptoms and the liver's large functional reserve.

1. Asymptomatic
- During screening (ultrasound) for chronic hepatitis B carrier
- Investigations for liver cirrhosis (esp with rising AFP levels)
- Incidentally found on imaging of the abdomen

2. Local signs & symptoms

1. Upper abdominal pain - 2o to
a. hemorrhage internally capsular distension or externally
b. necrosis
c. infection
2. Early satiety/ vomiting (likely 2o to compression)
3. Pyrexia (central tumour necrosis)
4. Hepatomegaly
5. Constitutional: LOW, LOA, malaise
6. Budd-Chiari syndrome: occlusion of hepatic, intrahepatic or portal vein causing portal HTN & congestive hepatopathy
7. Jaundice (5-10%)
a. Cholestatic (conjugated): invasion/ compression of intrahepatic ducts or extrahepatic compression by metastatic LN
b. Hepatic (unconjugated): a/w pre-existing cirrhosis or acute flair of chronic hepatitis

3. Tumour rupture (<3%)

- Severe abdominal pain (peritonism), pallor with shock [ddx: ruptured AAA]
50% mortality; Rx with transarterial embolization (TAE); reports of peritoneal seeding in survivors
- US +ve for peritoneal fluid, DPL +ve for blood

4. Liver decompensation (on top of underlying cirrhosis)

- Worsening liver function (encephalopathy, jaundice, pruritis, coagulopathy, oedema) suspect HCC when there is decompensation
of liver cirrhosis
- Worsening portal hypertension: Ascites, LL oedema, haematemesis & melena 2o to bleeding varices (COJ & gastric)
- Hepatorenal syndrome in late stages of liver failure

Stages of Hepatic Encephalopathy

Stage 1 Sleep-wake cycle inversion
Stage 2 Lethargy, personality change, asterixis, ataxia
Stage 3 Confusion, acalculia, paranoia, agitation, Babinski, clonus
Stage 4 Coma

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5. Metastases (low incidence in HCC, mortality rarely from mets)
- Bone pain, Dyspnoea

6. Paraneoplastic syndromes
1. Hypoglycaemia (due to high metabolic demands of tumour, <5% secrete IGF symptomatic hypogly),
2. Erythrocytosis (tumour produces erythropoietin, but most pts are anemic),
3. Hypercalcaemia (osteolytic lesions, tumor secretes PTH-rel protein)
4. Watery diarrhoea (related to secretion of peptides that cause intestinal secretion eg. gastrin. can be severe & intractable)
5. Cutaneous features (eg dermatomyositis, pemphigus foliaceus)

Complications from hepatocellular carcinoma are those of hepatic failure; death occurs from cachexia, variceal bleeding, or (rarely) tumor
rupture and bleeding into the peritoneum.

INVESTIGATIONS

Basic laboratory investigation:

o FBC (low Hb from BGIT, raised TW in SBP, low Plt)
o UECr (dehydration, 3rd spacing of fluids, use of diuretics for ascites, r/o nephropathy for contrast imaging)
o LFT (low albumin, high bilirubin, raised ALP, nonspecific transaminitis)
o AFP (Normal <5; WHO criteria >400; diagnostic & trending; note false +ve: pregnancy, infants, cirrhosis, hepatitis, teratoma,
other CA esp gastric) - Serum levels of AFP do not correlate well with other clinical features of HCC, such as size, stage,
or prognosis. Can be normal in up to 40% of small HCC.
Alternatives: des-gamma-carboxy prothrombin, tumor associated enzymes of GGT etc.
o Hepatitis markers (look for carrier status or chronic infection)
o PT/PTT (raised PT)
Imaging:
o Triphasic CT scan (see below)

DIAGNOSIS

Biopsy is usu not performed due to risk of tumour seeding (1-2% risk) along the needle track – may render the patient unsuitable for transplant!
Diagnosis is based on clinical, biochemical and radiological tests

WHO criteria for HCC:

(a) Risk factors for HCC e.g. hep B/C carrier
(b) Characteristic CT findings (of a hypervascular lesion)
(c) Raised AFP (>400)

1. Alpha-foetoprotein (AFP): elevated in 80%

2. Triphasic CT scan [gold standard investigation]

- CT liver scan at three different times after IV contrast:

(a) Arterial phase –contrast fills arteries: aorta (& HCC, bleeds) lights up, IVC and portal vein are dark
(b) Portal venous phase (most CT scans taken at this phase) – contrast enters portal system so portal vein is as bright as the aorta
(c) Delayed phase – contrast drains out, so none of the vessels in the liver are lighted up
- Characteristic feature of HCC is enhancement in the arterial phase (have a rich hepatic arterial supply) with rapid contrast washout
in the portal venous phase (hypodense)
Haemangioma: capsular enhancement in delayed phase
Metastasis: enchancement in portal venous phase
- In a patient with hepatitis B/C and raised AFP, a liver lesion on imaging should be considered HCC until proven otherwise
- CT can also look for nodal involvement, and metastases to the adrenals

3. Dynamic MRI scan of the liver

- Adjunct investigation done when CT findings are equivocal

- Images liver in greater detail without need for contrast, can be used to exclude benign conditions

4. Hepatic angiogram with lipiodol and post-lipiodol CT scan

- Lipiodol will be retained in HCC even after many days as the HCC does not contain Kupffer cells to ingest lipiodol
- Hepatic angiogram may reveal abnormal blood vessels within the HCC
- CT scan of the liver weeks after lipiodol ingestion will pick up the areas of tumour (where the pre-lipiodol CT may not have
demonstrated the tumour clearly)
- Not commonly used given the need for intraarterial injection

5. If indicated, investigations to look for GI primary

- CEA, CA 19-9, endoscopy

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STAGING (looking for metastases)

1. CXR, CT thorax: lung

2. CT abdopelvis: liver and adrenals, peritoneum and LNs
3. Bone scan if clinically indicated: bone

Different staging systems:

- TNM
- Okuda
- Barcelona-clinic-liver-cancer (BCLC)

In BCLC, staging depends on extent of liver disease, symptoms, liver function, vascular invasion and extrahepatic spread.

1. Very early HCC is currently very difficult to diagnose confidently prior to surgical ablation. In these lesions the absence of
microvascular invasion and dissemination offers the highest likelihood of cure and thus, in Child–Pugh A, patients may theoretically
achieve a 5-year survival of almost 100%.
2. Early stage disease includes patients with preserved liver function (Child–Pugh A and B) with solitary HCC or up to 3 nodules </=3
cm in size. These patients can be effectively treated by resection, liver transplantation or percutaneous ablation with possibility of
long term cure, with 5-year survival figures ranging from 50% to 75%.
3. The intermediate stage consists of Child–Pugh A and B patients with large/multifocal HCC who do not have cancer related symptoms
and do not have macrovascular invasion or extrahepatic spread. Their survival at 3 years without therapy may reach 50%. These are
the optimal candidates for transarterial chemoembolization.
4. Patients who present with cancer symptoms and/or with vascular invasion or extrahepatic spread comprise the advanced stage.
They have a shorter life expectancy (50% survival at 1 year) and are candidates to enter therapeutic trials with new agents
5. Patients with extensive tumor involvement leading to severe deterioration of their physical capacity [WHO performance status>2]
and/or major impairment of liver function (Child–Pugh C), are considered end stage. Their median survival is less than 3 months.

ECOG performance status grades:

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TREATMENT

SURGERY (ACHIEVE TUMOUR REMOVAL WITH GOOD LIVER FUNCTION)

- Only about 10-20% of patients with HCC will have disease amenable to surgery
- The only curative treatment for HCC is surgical removal of the tumour
- 2 surgical possibilities:
(a) Resection of tumour (partial hepatectomy)
(b) Liver transplantation

Factors affecting resectability:

1. Stage of disease

- Metastatic disease is not suitable for resection

- Multicentric disease affecting both lobes is a contraindication to hepatectomy

2. General fitness for operation

3. Liver function pre-operatively

- Cirrhotic patients have higher risk of post-operative mortality (4-14%) compared to non-cirrhotic patients (0-4%) due to
complications such as liver failure, bleeding and infection
- Use of indocyanin green (ICG) – the percentage of ICG remaining in the liver after 15 minutes indicates the level of liver
function. If >15% remains after 15 minutes, the patient cannot tolerate major liver resection (>3 segments removed)
- CT volumetry: residual liver function calculated with a CT liver scan via a computer program
- If  patient  has  cirrhosis,  assess  the  Child’s  status   only Child’s A and good Child’s B can be considered for resection

Child-Pugh classification Points 1 2 3

of CLD/ cirrhosis Albumin (g/L) >35 28-35 <28
1) Prognosis
Bilirubin  (μmoles/L) < 35 35-50 >50
2) Strength of
Coagulopathy = PT <1.70 1.70- 2.20 >2.20
medical treatment
Distension (ascites) None Slight - mod Severe/refractory
3) Necessity of liver
transplant Encephalopathy None Grade I – II Grade III-IV

Child’s A(5-6) B(7-9) C( 10-15)

1 year survival % 100 80 45
2 year survival % 85 60 35
Well compensated Significant functional Decompensated liver
Disease status
disease compromise dz, consider transplant
Treatment in Resection of up to 4 Maximum resection of 2 Consider transplant
concomitant HCC segments segments

4. Residual liver function post-operatively (at least 20%)

- Dependent on tumour size and how much of the liver it takes up, because tumour is non-functional
- A large tumour taking up most of the liver segments being resected translates to smaller amount of functional liver tissue
being resected, while a small tumour means that more functional tissue is removed with the same resection margins

5. Degree of portal hypertension (= hepatic vein pressure grad >10mmHg)

- Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has
decreased increased resistance to flow
- Detected during hepatic vein catheterization. Not necessary if clinically sig portal hpt: varices, ascites requiring diuretic
therapy, plt<100000 a/w splenomeg.
- Studies have shown that a normal bilirubin concentration, and the absence of clinically significant portal hypertension are
the best predictors of excellent outcomes after surgery, with almost no risk for postoperative liver failure.

6. Location of tumour

- Has to be located in a suitable location for resection

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a) Hepatectomy

- Problem in patients with cirrhosis is that there is already a “field-change” effect in the liver, thus a new tumour can still
develop in the remnant liver. 75% of HCC are multifocal on diagnosis.
- Requires a fine balance between adequate resection margins and preservation of sufficient functional liver to prevent
liver failure
- Good immediate and short-term results, but not long term (<30% 5-year survival)
- >70% tumor recurrence at 5 years due to dissemination and de novo tumors (eg occurrence of new 1° in the cirrhotic liver)
- Most powerful predictors of recurrence: Microvascular invasion and/or more than one tumors (This suggests that the majority
of recurrences are due to dissemination from the 1° tumor and not metachronous tumors developing in a liver with cirrhosis)
- No effective adjuvant therapy to reduce recurrence rate.
- Solitary recurrence might benefit from repeat resection, but in most patients recurrence after primary resection will be
multifocal because of intra-hepatic dissemination from the primary tumor
- only those patients in whom recurrence is due to de novo oncogenesis can be expected to benefit from salvage
transplantation or repeated resection

b) Transplantation

- Milan criteria for transplantation (>75% 5-year survival if followed)

(a) Single tumour 5cm or smaller, or 3 or less tumours none larger than 3cm
(b) No evidence of gross vascular invasion
(c) No regional nodal or distant metastasis

- Problems with availability of donor organ – the disease might have progressed past being suitable for transplant by the time
donor organ is available
Possibility of “bridging therapy” (radiofrequency ablation) to shrink disease & slow progression until donor liver available
- In hepatitis B carriers, there is a risk for reinfection of the donor liver (high risk factors are HBeAg positivity, high HBV DNA
levels) – can be aggressively treated with anti-viral drugs 2 months before transplant and anti-HBV immunoglobulin long-term
after transplant

PALLIATIVE THERAPY

1. Loco-regional ablation

(a) Radiofrequency ablation (RFA) – best results for locoregional strategies

(b) Percutaneous ethanol injection – ethanol kills HCC cells but more painful
(c) Cryotherapy

2. Intra-arterial therapy

(a) Transarterial chemoembolisation (TACE)

(b) Transarterial embolisation (TAE)
(c) Selective Intrahepatic Radiation – Yttrium-90 radioactive beads

3. Systemic therapy – limited results; Sorafenib imporves median survival by 3/12

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SCREENING FOR CHRONIC HEPATITIS CARRIERS

- Target pop: Hep B / C carriers, Cirrhosis, FHx of HCC, Patients on transplant waiting list (transplant priority if HCC dev, detect
HCC tt exceeds transplant guidelines)
- Combination of 6/12 to yearly Ultrasound + AFP levels

- US is operator dependent & may miss certain areas of the liver where imaging is difficult, but it is not associated with
radiation exposure. (sensitivity 65-80%, specificity 90%)
Features suggestive of HCC include poorly-defined margins and coarse, irregular internal echoes. Small tumors are often
hypoechoic. As the tumor grows, the echo pattern tends to become isoechoic or hyperechoic, indistinguishable from
surrounding liver. Added benefit of assessing patency of the hepatic blood supply and the presence of vascular invasion by
the tumor.
- AFP is also not a perfect screening test as 20% of HCC will not have raised AFP
- Thus the combination of ultrasound and AFP can increase the sensitivity and specificity of screening

- Frequency of screening is controversial, but should be increased in patients at increased risk – HbeAg positivity, high HBV
DNA levels
Frequency determined by tumor growth rate, not by the degree of risk.
- Important as it detects smaller and resectable HCCs increasing survival from 26 to 88/52

- Screen family for chronic hepatitis B carrier status especially if there is a family history! – e.g. mother had hep B/HCC, sibling
has hep B, etc
- Alternatives: des gamma carboxy prothrombin (DGCP aka PIVKA II) – potential marker of portal vein invasion by tumor

151
5. LIVER METASTASES

- Still more common than primary liver tumour for malignancy occurring in the liver
- Primaries: Colorectal, gastric, pancreatic, urogenital, breast, lung

PRESENTATION DEPENDS ON SITE OF METASTASIS

Mets to liver parenchyma Mets to porta hepatis LN

Hx - Incidentally found on follow up (for - Symptoms of obstructive jaundice
cancer) Yellow sclera
- Hard mass Tea-coloured urine
- Heaviness Pale stools
- Pain from rupture

P/E - Hard, irregular nodular hepatomeg - Jaundice early, progressive

- Jaundice is a late sign - Hepatomegaly may not be present

Invx - Both obstructive and transaminitis - Obstructive picture in early stages

picture

TRIPHASIC CT

- Hypodense on arterial phase (as metastases are usu hypovascular compared to hypervascular HCC; spread via portal vein)
- Increasing contrast uptake on portal venous and delayed phases

ROLE OF SURGERY

- Promising results with colorectal and neuroendocrine metastases if isolated resectable metastatic disease – 5-yr survival >50%
- Increasing role in urogenital, breast mets
- Poor results for stomach, oesophageal mets
- Palliation for symptoms in neuroendocrine metastases

6. LIVER HAEMANGIOMA

EPIDEMIOLOGY
- Prevalence 0.4-20%
- Female to male ratio 3:1

PATHOGENESIS
- Vascular malformation that enlarges by ectasia, congenital in origin

PRESENTATION
1. Usually small and asymptomatic, found incidentally
2. Mass effects compressing on surrounding organs
3. Pain from liver capsule stretch
4. Rupture (<1%)
5. Kassabach-Merritt syndrome for large haemangiomas – consumptive coagulopathy, thrombocytopaenia
6. Heart failure from large arteriovenous shunt

DIAGNOSIS
- Radiological
Characteristic features on triphasic CT – slow enhancement of the rims on arterial and portal venous phase, brightest in the
delayed phase
- DO NOT BIOPSY

TREATMENT
- Only for symptomatic or complicated lesions
- Possible role for prophylactic surgery in large, lateral, inferior lesions since there is higher risk for rupture

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7. SIMPLE LIVER CYSTS

EPIDEMIOLOGY
- 50% of cysts are single
- Prevalence 1-3%
- 9:1 female predominance for symptomatic cysts

PATHOGENESIS
- Congenital malformation when an aberrant bile duct loses communication with the rest of the biliary tree and becomes progressively dilated
(fluid within the cyst is not bilious)
- No solid component and not septated (mixed cysts with septations are suggestive of malignancy)
- [Cysts that communicate with the biliary system are called choledochal cysts]

PRESENTATION – WITH COMPLICATIONS

- Torsion
- Bleeding & Rupture
- Mass effect; Compression of IVC; Cholestasis due to compression of CBD; Portal hypertension
- Fistulation into duodenum
- Malignant change (rare)
TREATMENT (IF SYMPTOMATIC)
- Aspiration
- Ethanol sclerotherapy (painful)
- Fenestration (open or laparoscopic)
- Excision/resection

8. HEPATIC ABSCESS (PYOGENIC / AMOEBIC)

PYOGENIC ABSCESS

- More common than amoebic abscess locally

- Causative organisms: Klebsiella pneumoniae, Enterococcus, Enterobacter, E. coli, Staph aureus

- Routes of infection:

(a) Ascending infection from biliary system (ascending cholangitis)

(b) Intra-abdominal source through portal vein – acute appendicitis, diverticulitis, IBD, pancreatitis, pelvic abscess
(c) Contiguous spread – from gallbladder empyema
(d) Haematogenous spread in sepsis e.g. infective endocarditis
(e) External inoculation – iatrogenic, traumatic

- Presentation: RHC pain (capsular stretch) with Spiking fever with chills, rigors. 50% of patients have jaundice, and one-third have
hepatomegaly

- Investigations:

Laboratory:
FBC, U/E/Cr, hepatitis markers
Blood cultures, Melioidosis & amoebic serology/ PCR, Stool ova, cysts and parasites
Tumour markers: AFP, CA 19-9, CEA (may resemble infected tumour on imaging)
If any aspiration done, aspirates for cytology, stains & c/s

Imaging:
US HBS or CT scan (to exclude liver tumour, KIV endoscopy to rule out GI malignancy)
Findings: Irregular lesion with central area of necrosis, air-fluid levels, may be multiloculated. Rim-enhancing appearance on triphasic CT
scan.

- Treatment

1. Resuscitate if necessary
2. Close monitoring of vitals with strict IO charting
3. Antibiotics via PICC

Empirical antibiotics – Ampicillin/Gentamicin/Metronidazole

Change to definitive antibiotics when blood c/s results return
Total duration of 6 /52 – 1st 2/52 IV, next 4/52 PO

4. Drainage
Drainage if >3cm – open drainage or percutaneous aspiration

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 Percutaneous aspiration Open drainage
- Minimally invasive, performed under - Invasive procedure, done under GA
radiologic guidance - Shorter hospital stay
- Can be done under LA - Single procedure
- Longer stay for patient as drainage tube - Not dependent on location
stays in patient for a longer time - Indications:
- May require multiple attempts if unable to Concomitant pathology requiring surgery
completely drain pus e.g. gall stones
- Contraindications: Multiple abscesses or multiloculated
Ascites (pus can leak into peritoneal abscess
cavity) Immunocompromised patient
Uncorrected coagulopathy Failed percutaneous drainage (tube
Proximity to vital structures blocked, or pt not getting better)
Ascites
Ruptured abscess

AMOEBIC ABSCESS

- Causative organism: Entamoeba histolytica (infects the gut, forming ulcers in the colon, then spreads to the liver through the portal vein)
- Transmission is faecal-oral

- Presentation
Usually single abscess
No sepsis, jaundice
Hepatomegaly often present
Complications: rupture into pleural/peritoneal spaces

- Treatment:
Metronidazole (very responsive)
Aspiration if amoebic serology inconclusive; pregnancy (metronidazole contraindicated); suspicion of secondary infection; severe
symptoms from distension or fever; impending rupture

9. ASCITES

Vital signs on examination:

o Abdominal distension
o Flank dullness shifting dullness fluid thrill
o Peripheral stigmata of chronic liver disease and portal HPT
o Other signs of fluid overload: LL, sacral oedema, bibasal crepitations
o Signs of malignancy

Background information
Causes of ascites:
Transudate (<30g/L protein) Exudative (>30g/L)
Cardiac: CCF, RHF, TR, constrictive pericarditis Cirrhosis
Abdo: CLD Malignancy
Renal: ESRF, nephrotic syndrome Infective causes: TB
GIT: protein losing enteropathy Chylous ascites

Role of peritoneal tap:

o diagnostic and therapeutic
Send fluid for FEME, protein, microbiology, cytology
Relieve of discomfort & diaphragm splinting from distension
o Indications:
Failed medical treatment
symptomatic
o perform under aseptic technique, LA, US guidance
may insert a pigtail catheter via seldinger technique
open drain into stoma bag

Treatment of ascites:
o Conservative: low salt diet, diuresis
o Peritoneal tap
o Surgical: shunt sx (TIPSS, peritoneovenous shunt [silastic catheter], Denver shunt when with a subcutaneous pump]

154
10. PANCREATIC DISEASES

1. ACUTE PANCREATITIS

DEFINITION

An acute inflammatory process of the pancreas with variable involvement of regional tissues or remote organ systems

EPIDEMIOLOGY

- Incidence is difficult to measure accurately (not all diagnosed).

- ~ 7-10% presenting with abdominal pain acute pancreatitis
Trauma: blunt trauma, ERCP, gall stones
CAUSES (I GET SMASHED)
Infx: mumps, VZV
1. Idiopathic (up to 10%) Drugs: Alc, Steriods, SAND
2. Gallstones most common: >90% combined Metabolic: hyperlipidemia, hypercalcemia
3. Ethanol
4. Trauma – penetrating > blunt trauma Autoimmune: SLE, PAN
5. Steroids Neoplastic: Ca head of pancreas
6. Mumps and other infx (VZV, Coxsackie, EBV, measles, echovirus, ascaris, Congenital: CFs, Pancreas divisum
mycoplasma, salmonella, campylobacter, MTB)
7. Autoimmune – SLE, PAN
8. Scorpion toxin
9. Hypercalcaemia, HyperTG (>1000 mg/dL, T1 and TV Severe), hypothermia
10. ERCP (4%) - aggressive preintervention intravenous hydration to prevent
11. Drug-induced usually mild (SAND: Sulphonamides/ azathioprine/ NSAIDs/ diuretics, HCTZ, metronidazole, nitrofurantoin,
procainamide, chemo (esp asparaginase, cisplatin), cimetidine, diphenoxylate, estrogen)
12. Rare causes: Cystic fibrosis, cancer of the head of the pancreas, pancreas divisum (failure of the dorsal and ventral pancreatic
ducts to fuse during embryogenesis), Sphincter of Oddi dysfunction

Gallstone: usu very small stones due to edema at the ampulla as stone passes into duod increases pancreatic duct pressure
(no stone in 80% suggesting stone passage)

The disease develops in pts whose alcohol ingestion is habitual over 5-15 years. Alcoholics are usually admitted with an acute
exacerbation of chronic pancreatitis. Occasionally, however, pancreatitis can develop in a patient with a weekend binging habit.

PATHOPHYSIOLOGY

- The initiating event may be anything that injures the acinar cell and impairs the secretion of zymogen granules
Gallstones: obstruction of the pancreatic duct causing interstitial oedema which impairs blood flow to the
pancreatic cells ischaemic cellular injury predisposition to enzyme activation
It is believed alcohol itself results in injury to pancreatic cells through generation of free radicals during its metabolism,
and may sensitise the pancreas to injury by other agents

- The final common pathway inappropriate activation of proenzymes stored within zymogen granules in the pancreatic
cell (trypsin activates most of the proenzymes secreted by the pancreas when they are secreted into the duodenum)

- The activated lytic enzymes destroy the pancreatic acinar cells release of potent cytokines that attract neutrophils and
macrophages themselves secrete pro-inflammatory cytokines

- The cytokine cascade amplifies the local inflammatory response and also results in a systemic inflammatory response
[2 of 4: T>38 / <36, HR> 100, RR>20 or TW>15], may progress to sepsis (if source of infection is found) severe sepsis with
1 organ dysfunction septic shock MODS

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PRESENTATION

- Symptoms (generally non-specific):

Abdominal pain (most consistent, in >90% of patients) – constant epigastric pain, classically radiating to the back
(in 50%), maximal intensity within several hours of onset; usually occurs after a heavy meal; alleviated by sitting up
& leaning forward, worse on movement
Nausea, vomiting, Anorexia

Also rule out other causes:

Gastric causes: PUD
Perforated viscus (mainly on examination: look for peritonism)
AMI, DKA or even a lower lobe pneumonia
Hepatitis or GB / CBD disease

Ask for causes of pancreatitis:

Gallstone disease: biliary colic, symptoms of cholecytitis/ CBD stone/ cholangitis
Recent alcohol abuse or chronic alcohol abuse
Recent blunt trauma or ERCP done
PHx or hyperlipidemia, hypercalcemia, autoimmune disease (SLE, PAN)
Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling)
Recent drug history: steroids, NSAIDs, diuretics

- Signs (also non-specific)

Tachycardia, low grade fever, low BP, toxic looking, jaundiced?

Epigastric tenderness, signs of peritonism (<1/3 of patients)
May have a palpable mass (pseudocyst, pancreatic phlegmon)
Abdominal distension ± ascites with diminished or no bowel sounds (ileus)
Ecchymoses (usually not present): flank (Grey-Turner’s   sign)   or   umbilical   (Cullen’s)   suggest   severe haemorrhagic
pancreatitis associated with profound fluid loss (third-spacing)

Organ failure
Ask for urine output
Offer to auscultate the lungs for any effusion or ARDS (creps, reduced air entry)

MANAGEMENT STRATEGY

Diagnosis

Severity stratification

Assess for aetiology

Supportive Monitor for Treat aetiology

treatment complications (reverse / control)

Manage Prevent future

complications recurrence

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INVESTIGATIONS

DIAGNOSTIC (CLINICAL + BIOCHEMICAL DIAGNOSIS)

1. Serum amylase
- raised within 12 hours of onset, usually more than 1000 or 3 times normal
- High sensitivity and moderate specificity (specificity increased when cut-off taken at 3 times normal upper limit)
- Returns to normal level 48 to 72 hours after onset – not useful in late diagnosis

2. Serum lipase
- Rises within 8 hours of onset of symptoms and returns to normal after 7-10 days, also 3 times normal
- Thus more useful in late diagnosis of acute pancreatitis

3. Urinary diastase
- Similar function to serum lipase, used when serum amylase is equivocally raised or normal
- elevated for even longer period after onset

Other causes of elevated serum amylase:

GI sources - PUD, IO, perforation, Ischaemic bowel (amylase in the thousands), Cholecystitis, cholangitis
Non-GI sources - Ectopic pregnancy
- Impaired clearance due to chronic renal failure
- Kidney stone
- Salivary gland injury or inflammation (rare)
- Macroamylasaemia

PROGNOSTIC / SUPPORTIVE / LOOKING FOR AETIOLOGY

Imaging

4. Ultrasound [1st investigation]

- Preferred over CT scan
- Good for visualising biliary tree and picking up gallstones (can intervene!)
Dilated CBD ERCP to remove gallstones/Bx tumor
Not dilated MRCP (susp parenchymal disease)
- Pancreas may be diffusely enlarged and hypoechoeic – often difficult to visualise due to overlying bowel gas

5. Erect CXR & AXR

- Erect CXR may show no air under the diaphragm, pleural
effusion, elevated hemidiaphragm, pulmonary infiltrates;
complete whiteout (ARDS)
- AXR may show the “sentinel loop sign” (dilated proximal
jejunal loop near the pancreas) or “colon cut-off sign”
(distended colon from ascending to mid-transverse with no
air distally) due to functional spasm of the bowel around the
pancreas resulting from inflammation
- presence of calcifications within the pancreas may indicate
chronic pancreatitis

6. CT AbdoPelvis
1. Only if considering other pathologies eg. CA in elderly (CT may worsen pancreatitis)
2. At ~72hrs of known case of pancreatitis: detect fluid collections; necrosis (IV contrast needs to be given ) Balthazar for severity

Laboratory

Severity/ Cx: 1. FBC (TW for Ranson, Glasgow; haematocrit for Ranson)
2. U/E/Cr (urea for Ranson and Glasgow; electrolyte imbalances, dehydration)
3. Glucose (for Ranson and Glasgow)
4. LFTs (AST for Ranson and Glasgow; albumin for Glasgow; obstructive picture in gallstone pancreatitis)
5. CRP
6. Lactate dehydrogenase (for Ranson and Glasgow)
7. ABG (PaO2 for Ranson and Glasgow; base excess for Ranson)
Etiologies: 8. Ca/Mg/PO4 with albumin (hypercalcaemia – aetiology)
9. Fasting lipids (hyperlipidaemia – aetiology)
10. ECG & cardiac enzymes (rule out AMI as a cause of epigastric pain)

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SEVERITY STRATIFICATION (RANSON, GLASGOW, APACHE II)

I. Danger signs in the first few hours

- Encephalopathy
- Hypoxaemia
- Tachycardia >130/min, Hypotension <90mmHg, Haematocrit >50
- Presence  of  Gray  Turner’s/Cullen’s  sign
- Oliguria <50mls/hr, Azotemia (serum urea)

ATLANTA CLASSIFICATION (FOR SEVERITY)

Mild acute pancreatitis Severe acute pancreatitis (15-25%)

- Interstitial oedema - Pancreatic or peripancreatic necrosis

- Minimal organ - A/w organ failure or local Cx
dysfunction - Any 1 of the following
- Uneventful recovery Ranson’s  3 or more
APACHE II 8 or more (within 1st 48hr)
Organ failure (RT, CVS, Renal, BGIT)
Local Cx (pancreatic necrosis, abscess, pseudocyst)

II. Ranson criteria

Present at admission Within 48 hours of admission
1. Age >55 yrs 1. Fall in Hct >10%
2. White cell count >16x109/dL 2. Rise in urea >0.9mmol/L
3. Fasting bld gluc >11.2mmol/L 3. Calcium <2mmol/L
4. LDH >600U/L 4. PaO2 <60mmHg
5. AST >120U/L 5. Base excess >4mmol/L
6. Neg fluid balance >6L

- Ranson’s  criteria  prognosticates  mortality  according  to  score

- Any patient with a score of 3 and above is considered to have severe pancreatitis
- Mortality: <3 0.9%
3-4 15%
5-6 50%
>6 90%
- Shortfalls  of  Ranson’s:
validated for alcoholic pancreatitis only revised  Ranson’s  score  was  created  for  gallstone  pancreatitis,  
difficult to tell aetiology in acute setting & cumbersome to wait for 48 hours, and difficult to assess for negative fluid balance

III. Glasgow/ Imrie score- PANCREAS

1. PaO2 <60mmHg
2. Age >55yrs
3. Neutrophil/WBC >15x109/dL
4. Calcium <2mmol/L
5. Renal (urea) >16mmol/L
6. Enzymes LDH >600U/L
AST >100/L
7. Albumin <32g/L
8. Sugar (Glucose ) >10mmol/L >3 criteria severe

- Preferred  over  Ranson’s  scoring  in  certain  centres

- combine with CRP

IV. C-reactive peptide

- As a single prognostic marker; <100 is unlikely severe
- If CRP is >210mg/dL at 48 hours, the pancreatitis is more likely to be severe
- No relevance >3/7 of onset as other confounding factors come into the picture
- Combination of Glasgow score and CRP improves overall prognostic value

V.  Balthazar’s  CT  severity  index  (consider  a  CT  AP  @  ~  3/7  from onset)
- Grades severity of disease according to CT findings detects  h’ge  &  necrosis
- Not very useful as CT is not usually done in the 1/52 in local context, and disease is still evolving (CT findings lag behind) in the early stages
1. A - Normal
2. B - Enlargement
3. C - Peripancreatic inflammation
4. D - Single fluid collection
5. E - Multiple fluid collections: 50% chance of developing an infection and a 15% chance of dying

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COURSE OF DISEASE

- 75%: mild course of disease; recover unless comorbidities cause deterioration

-------Deterioration from mild to severe very rapid!------
- 20-25%: severe outcome (Acute necrotizing pancreatitis 15%) 1/3 of these patients will ultimately die

- Overall mortality rate <10%. Death is bimodally distributed:

(a) Early
Within 1/52; due to severe organ failure, SIRS
Very little can be done in terms of treatment
(b) Late
Most common cause is INFECTION with resultant sepsis
Multi-organ failure can be the course of death

SUPPORTIVE TREATMENT

1. Resuscitate if needed

2. Monitoring

- In general ward if mild pancreatitis; HD/ICU monitoring if severe (≥3)

- Monitor vitals [SpO2, BP, HR, Temp.], urine output & CVP

3. NBM (bowel rest) and IV fluid replacement

- Fast patients for at least 2/7 until more stable

- Fluid resuscitate with crystalloids
- May include gastric decompression with NGT if there is persistent vomiting, significant gastroparesis, or intestinal
obstruction (ileus)
- May start oral feeding early with fluids in mild pancreatitis if tolerated
Prolonged NBM results in poorer recovery due to nutritional debilitation – think about NJ feeding, or open jejunostomy
creation early in patients with severe pancreatitis; if not tolerable, then consider TPN
- Acid suppression does not change course of disease, but protects against stress ulcer formation; octetride has no
benefit (thought to reduce pancreatic secretions)

4. Analgesia

- Do not give NSAIDs as they can worsen pancreatitis & cause renal failure (since there is already decreased renal
perfusion in acute pancreatitis)
- Use opioid analgesics (tramadol, pethidine)
NOT morphine (causes increased tone of sphincter of Oddi)

5. Treatment of fluid and electrolyte abnormalities hypocalcaemia, hypoglycemia

6. Antibiotics

- Either prophylactic or therapeutic

Not shown to have any benefit in mild pancreatitis
a) Prophylactic in severe acute pancreatitis to prevent infection of necrosis
infection will occur in 40-70% of patients with necrosis and increases the mortality rate from 12 to 33%
Carbapenem (only imipenem has been shown to prevent sepsis, imipenem and quinolones have better penetration
into pancreatic tissues)
b)Therapeutic in cholangitis (coexisting with Gallstone disease or as complication of pancreatitis) & infection of
pancreatic necrosis/ pseudocyst
- Duration: 14-28 days

7. Support for organ failure

o Ventilate with PEEP if hypoxemic (e.g. ARDS)
o Dialysis & CVP monitoring if in ARF
o Fluid resuscitation & inotropes if Hypotensive

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MONITORING FOR COMPLICATIONS AND TREATING

Local complications:

- Acute fluid collections

Due to increased vascular permeability; 70-80% resolve spontaneously
- Pseudocyst
Persistent fluid collection (enzymes, blood, necrotic tissue) walled off by fibrosis and not an epithelium-lined surface (after 4
weeks)
Presents  as  1.  Gastric  outlet  obstruction,  2.  infx,  3.  peritonitis,  4.    h’ge  (erosion  of  splenic  vessels),  Persistently raised
amylase despite resolution of pancreatitis
50% resolve spontaneously
- Abscess
Infection of fluid collection (not necrosis)
- Pancreatic necrosis
Areas of no contrast uptake on CT with intravenous contrast
- Infected necrosis
Gas bubbles on CT scan
Positive bacterial culture on CT, U/S guided FNA
accts for much of the morbidity and mortality - Infections occurring early (<3 weeks) in the course of the illness appear to be
associated with a higher mortality rate
Often polymicrobial and involve both aerobic and anaerobic bacteria – GIT org: Escherichia coli, Klebsiella spp,
Enterobacter spp, Proteus spp, Pseudomonas aeruginosa, Bacteroides spp, and Clostridium spp, and the enterococci
- Chronic pancreatitis, exocrine insufficiency & endocrine insufficiency

Systemic complications
o Peritoneal sepsis
o Pancreatic ascites (massive accumulation of pancreatic fluid in peritoneum)
o Intra-abdominal haemorrhage (erosion of splenic vessels)
o Multiple organ failure (ARDS, acute renal failure, hypovolaemic shock, DIVC)
o Hypocalcaemia, hyper/ hypoglycaemia

Intervention for local complications

- ERCP
- No benefit in mild biliary pancreatitis
- Indications:
Severe pancreatitis
Evidence of ductal stones
Cholangitis
No response to treatment within 48 hours
- ERCP should be done within first 48-72 hours for maximum benefit

- CT-guided aspiration of pancreatic necrosis

Can help differentiate between sterile and infected necrosis
Consider surgery if patient doing poorly

- Necrosectomy for infected necrosis

Some kind of lavage and drainage procedure is done after necrosectomy to decrease infective load

- Role of surgery
Infected necrotic pancreas (mortality 100% without operation)
Sterile necrotic pancreas (necrosectomy)
Delay surgery till as late as possible for demarcation of necrotic areas (repeated surgeries required)
Diagnostic uncertainty
Complications e.g. intra-abdominal haemorrhage

- Pseudocyst
Operate if larger than 6cm and persisting for more than 6 weeks as the chance of spontaneous resolution is low and risk
of complications (infection, haemorrhage, rupture) is high
Surgery can be open, laparoscopic, endoscopic or percutaneous (radiologically guided)
Endoscopic – internal drainage via a cystogastrostomy, cystoduodenostomy or cystojejunostomy

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 MANAGEMENT OF AETIOLOGY & PREVENTION OF RECURRENCE

Avoid alcohol, stop all offending medication & control hyperlipidemia

Cholecystectomy for biliary pancreatitis

- 18-21% of patients with biliary pancreatitis will have another episode
- Among these, 25-65% will develop the 2nd episode within 30 days of the initial one
- done in the same admission for pts with mild pancreatitis
- In patients with severe pancreatitis, there is reluctance to do the surgery early, as the patient may develop complications that
require surgical intervention – better to do all surgery in the same operation instead of opening the patient twice

13. CHRONIC PANCREATITIS

Chronic, irreversible architectural disruption of the pancreas resulting in chronic epigastric pain and pancreatic insufficiency

Causes: NOT GALLSTONES!

- Alcholism – 80%
- strictures (congenital, acquired),
- trauma,
- genetic (North Indians)
- Smoking
- CRF
- Hypercalcemia

Presentation:
a) Pain (85%) – mostly episodic, some have persistent relentless pain
b) Diarrhoea (15%)
c) LOW (sec to anorexia, malabsorption)
d) Newly diagnosed DM (30%)
e) Steatorrhea (late)

Complications:
Local complications: persistent pseudocyst, fistulae, ascites
Chronic pain
Pancreatic insufficiency
o Type I DM
o Steatorrhoea, vitamin deficiency, malnutrition
Pancreatic cancer

INVESTIGATIONS

a) Dx:
a. MRCP (choice!): chain of lakes appearance of pancreatic duct (strictures and cystic dilatations)
b. AXR: calcification
c. EUS
b) Baseline function
a. Secretin injection check for pure pancreatic juice (gold std but invasive)
b. Faecal pancreatic elastase
c) Complications: MRCP (pseudocyst, duodenal stenosis, portal vein thrombosis)

Outline of management
Treat underlying cause (stop alcohol, relieve ductal stricture)
Control blood sugar with insulin
Pancreatic enzyme supplements
Pain relief

Role of surgery
Persistent local complications: pseudocyst, fistulae, local obstruction secondary to fibrosis (CBD, duodenum)
Pain relief (pancreatectomy, coeliac plexus block, thoracic splanchnicectomy)
Relief of pancreatic duct obstruction
o Puestow procedure: side to side pancreatico-jejunostomy

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14. PANCREATIC CANCER

EPIDEMIOLOGY
- Incidence about 3-5 per 100,000 per year in each gender
- Eighth cause of cancer death in Singapore
- 1.7:1 male to female ratio, increase with age
- Very poor prognosis – median survival for unresectable disease is 6 months (80% of patients have unresectable disease at
presentation); overall 5-year survival <3%

ASSOCIATIONS
- Cigarette smoking (most clearly established – 2-5X increased risk)
- Industrial carcinogens – benzidine, betanaphthylamine (dye)
- Diabetes mellitus
- Chronic pancreatitis
- Genetic factors (mutations in K-ras gene, p16 gene)
- Familial cancer syndromes e.g. Peutz-Jeghers (Hereditary intestinal polyposis syndrome, AD, hyperpigmented macules in lips
and oral mucoas), HNPCC, MEN, FAMMM (familial atypical mole multiple melanoma syndrome)
- Lower socioeconomic class

PATHOLOGY
- Most common histology is ductal adenocarcinoma (90% of tumours)
- Anatomic distribution: 75% in the head, 20% in the body, 5% in the tail
- Distinct category of tumours collectively called periampullary tumour (30%):

Malignant cells arise from one of a few cells:

(a) Duodenal epithelium (best outcome out of all three)
(b) Biliary ductular epithelium
(c) Ampullary ductular epithelium

The periampullary tumours have better tumour biology than pancreatic adenoca
smaller size, better diff, low nodal stage, margins neg, less vascular invasion
Different TNM staging
90% resectability, median survival after Sx is 38mth

Prognosis is also better as they present earlier with obstructive jaundice

PRESENTATION
May be asymptomatic, picked up on imaging for some other purpose

Pancreatic head or periampullary Pancreatic body/tail

- OBSTRUCTIVE JAUNDICE Late presentation

Painless obstructive jaundice with
palpable  GB  (Courvoisier’s  sign)
+ Cholangitis
- Duodenal obstruction (vomit)
- Bleeding upper GIT (haematemesis
and/or malaena)
- Malaise, LOW!, anorexia, nausea
- Endocrine: Diabetes mellitus
- Coeliac and mesenteric plexus invasion – dull constant (incessant and
boring) PAIN in the epigastrium radiating to the back, relieves with
bending fwd
- Malaise, weight loss, anorexia, nausea
- Exocrine insufficiency with duct obstruction
steatorrhoea, malabsorption
- Metastatic symptoms: ascites, bone pain, CNS symptoms, dyspnoea
- Paraneoplastic syndromes – migratory thrombophlebitis in 6%

Also
- Recurrent venous thrombosis
- Acute pancreatitis
- Depression

162
 localized areas of reticulated erythema and hyperpigmentation due
to chronic and repeated exposure to heat: regular application of
heat to the same painful part over a period of at least a few weeks
suggests that the pain is severe and consistent.

IMMEDIATE MANAGEMENT
- Treat any life-threatening complications such as cholangitis, pancreatitis, bleeding

INVESTIGATIONS

DIAGNOSTIC

1. CA 19-9
- Not a screening test for pancreatic cancer as it can be false positive
- Can act as a prognostic marker: high CA 19-9 levels usu associated with unresectable disease with poorer prognosis
- Can be used as a marker for tumour recurrence during post-op follow-up

2. CT scan (MAIN)
- Better sensitivity (85-90%) and equal specificity (90-95%) in diagnosing pancreatic cancer
- 1. Mass lesion within pancreas,
2. Both bile & pancreatic duct dilatation in head of pancreas tumours (double duct sign)
3. GB distension
4. Staging: Extra-pancreatic spread (Involvement of regional LNs, liver metastases, ascites)

3. MRI pancreas with MRCP – MRI pancreas is not superior to CT scan (Diagnosis and staging)
MRCP is useful in delineating biliary system anatomy especially if the system is not obstructed
and there are no therapeutic indications for ERCP (since there are considerable risks with ERCP)

4. ERCP with stenting to relieve obstruction (in cholangitis)

5. Endoscopic ultrasound + FNA biopsy

- Dx: FNA with EUS guidance preferred to transcutaneous biopsy (less risk of tumour seeding)
- Staging: tumour and nodal involvement

The most difficult clinical situation in which to diagnose pancreatic carcinoma is in the patient with underlying chronic pancreatitis. All of the
above imaging studies may show abnormalities that may not help to differentiate between pancreatic carcinoma and chronic pancreatitis. Even
tumor markers can be elevated in patients with chronic pancreatitis. Often combine multiple imaging modalities, close clinical follow-up, serial
imaging studies, and, occasionally, empiric resection, to diagnose an underlying pancreatic carcinoma

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STAGING [LIVER, LUNGS, PERITONEUM, BONE]

1. CT/MRI of the abdomen – T, N stage; metastasis to the liver

2. Endoscopic ultrasound – T, N stage

3. Lungs – CXR + CT thorax

4. Bones – bone scan when suspicion is high

5. Staging laparoscopy – for peritoneal metastases, just before definitive operation for a resectable tumour (since CT/MRI may
miss small peritoneal deposits in ard 25%) if no peritoneal disease found, continue with surgery, otherwise, close up and
abort surgery

TREATMENT

SURGERY

Curative resection
- Improves chances of survival
- Only about 15-20% of patients will have resectable disease at presentation – usu in periampullary / head of pancreas tumours
- However, recurrence rates after surgery are high – 5 year survival only 10 to 30%
- Recent trials: improved survival with adjuvant chemo (5-FU + Folinic acid or gemcitabine)

- Resectable disease:
No metastases (lung, liver, bone, peritoneum)
Patent superior mesenteric vein and portal vein – no longer absolute CI
Definable tissue plane between tumour and superior mesenteric artery as well as coeliac axis

Whipple’s operation
Pancreaticoduodenectomy for head of pancreas or periampullary tumour
Usually preceded by a staging laparoscopy to confirm absence of peritoneal metastases
Removal of the head of the pancreas, duodenum, proximal 15cm of jejunum, common bile duct, gallbladder, distal part of
the stomach and LN removal (impt prog factor)
Common hepatic duct and pancreas are then anastomosed to the jejunum, 45-60cm proximal to the gastrojejunostomy

164
- Complications  of  Whipple’s  operation
Mortality rate is 2-7%, with a morbidity rate of up to 20-30% (mostly mild complications)
Intraoperative/early complications
General:
(a) Injury to other organs – liver, kidney, bowel
(b) Bleeding
(c) Infection abscess, sepsis
Specific:
(d) Pancreatitis
(e) Pancreatic anastomotic leak (5-20%)
(f) Biliary anastomotic breakdown
(g) Fistulation, pseudocyst formation may occur due to anastomotic leaks
Late
Surgical:
(a) Gastric stasis with or without pylorus-preserving  Whipple’s  (25%)  – NG decompression, longer hosp stay
(b) Diarrhoea resulting from autonomic nerve injury during lymph node dissection LOW
(c) Dumping syndrome: increased gastric emptying (from antrectomy) causing Nutritional deficiency
Functional:
(d) Long-term exocrine insufficiency resulting in malabsorption and steatorrhoea
(e) Endocrine insufficiency DM

Pylorus-preserving pancreaticoduodenectomy (PPPD)

- comparable operation time, blood loss, hospital stay, mortality, morbidity, and incidence of delayed gastric emptying.
- The overall long-term and disease-free survival was comparable in both groups.
- Both surgical procedures are equally effective for the treatment of pancreatic and periampullary carcinoma

Palliative surgery

Surgical bypass of obstruction

- Triple bypass involving anastomosis between [all to jejunum]

(a) Stomach and jejunum (gastrojejunostomy)
(b) Biliary system and jejunum (choledocho-/hepatico-/cholecysto-jejunostomy)
(c) Jejunum and jejunum, to prevent reflux of food into biliary tree – essentially a Roux-en-Y loop (jejunojejunostomy)

NON-SURGICAL PALLIATIVE MEASURES

1. Endoscopic stenting
- Stenting of obstructed biliary duct
- Stenting of obstructed duodenum

2. Coeliac plexus block for pain

3. Palliative chemotherapy/radiotherapy/chemoradiotherapy
- Not shown to provide good outcomes

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11. BILIARY TRACT DISEASES

1. CAUSES OF JAUNDICE

Pre-hepatic Hepatic Cholestatic

o Urine/stools normal
o May have symptoms of anemia
o Unconjugated hyperbilirubinemia
o ↑  LDH,  ↓  haptoglobin
o PBF
o Direct  Coomb’s  test  for  autoimmune   o
hemolytic anemia
o Stool OCP (ova, cysts, parasites) malaria
o Mixed signs; urine may be dark with
normal stools
o Variable liver biochemistry
o ↑  ALT  AST  disproportionate to ALP GGT
o ↓  Albumin,  prolonged  INR  (cirrhosis)
AFP: exclude complication of malignancy
o Viral hepatitis serology
Acute: Anti-HBc IgM, Anti-HAV IgM
Chronic: HBsAg, anti-HCV, HCV RNA
o Autoimmune screen
ANA, anti-dsDNA, AMA
o Metabolic screen
Caeruloplasmin, 24hr urine copper
o Abdo U/S:  surface  nodularity  &  ↑  
echogenicity in cirrhosis, signs of portal
HTN (splenomegaly, ascites)
o Tea-colored urine, pale stools, pruritis
o Conjugated hyperbilirubinemia
o ↑  ALP,  GGT  disproportionate  to  ALT,  AST
o Do abdominal U/S
If ducts dilated (>8mm), do
ERCP/MRCP/PTC
If ducts not dilated, further
serologic testing: AMA (M2-IgG
most specific for PBC), p-ANCA
(PSC), ANA & anti-SMA.
Consider ERCP, liver biopsy

Hemolytic anemias:
1) Inherited 1) Infective 1) Intraluminal
Thalassemia Acute viral hepatitis (HBV, HAV) Gallstones (painful)
G6DP EBV, CMV Parasites: Ascaris lumbricoides,
Spherocytosis TB schistosomiasis
Sickle-cell anemia 2) Liver cirrhosis/chronic liver disease 2) Mural
2) Acquired Alcoholic liver disease Biliary strictures post ERCP
Infective: malaria Chronic viral hepatitis (HBV, HCV) Biliary strictures from gallstones,
Autoimmune:  SLE,  Evan’s   Metabolic  (Wilson’s,   chronic pancreatitis
syndrome hematochromatosis) PBC (intrahepatic bile ducts):
Hemolytic uremic syndrome Infiltrative (Sarcoidosis, middle  aged    ♀
(hemolytic anemia, ARF & amyloidosis) PSC (intra & extrahepatic):  ♂  
thrombocytopaenia) 3) Hepatotoxic drugs with IBD esp. UC
Alcohol, paracetamol, TCM, Cholangitis  (Charcot’s  triad)  
isoniazid, augmentin, MTX, Choledochal cyst (type I-V)
phenytoin, corticosteroids Distal cholangiocarcinoma
4) Autoimmune hepatitis 3) Extraluminal
SLE Ca head of pancreas (painless, w
5) Inherited  ↓/absent  activity of UGT distended GB)
(unconjugated hyperbilirubinemia) Other peri-ampullary Ca
Gilbert’s  syndrome (cholangio, dudeno, ampullary)
Crigler Najjar 1 & 2 Mirrizi’s  syndrome  (chronic
6) Inherited impaired biliary excretion cholecystitis)
(conjugated hyperbilirubinemia) 4) Others:
Dubin-Johnson syndrome Biliary atresia
Rotor syndrome Drug-induced: paracetamol,
penicillins, corticosteroids

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2. APPROACH TO OBSTRUCTIVE JAUNDICE

CAUSES (POSTHEPATIC JAUNDICE)

Benign
Intraluminal - Gallstones
- Parasitic infections (recurrent pyogenic cholangitis)

Benign
- Post-instrumentation strictures (ERCP, operation)
- Strictures from other causes (gallstones, chronic pancreatitis)
- Benign papillary fibrosis: prev gallstone passage (can give post cholecystectomy pain, acute pancreatitis)
Mural - Primary sclerosing cholangitis
- Choledochal cyst

Malignant
- Cholangiocarcinoma (distal)
Benign
- Mirizzi syndrome
- Pancreatitis: secondary bile duct compression from edema
Extramural
Malignant
- Head of pancreas cancer
- Periampullary cancer
- Metastases to the porta hepatis

Obstructive jaundice Commonest causes of jaundice

Painless: CA HOP, Cholangiocarcinoma, Periamp CA 1. Gallstone
Painful: Stone, Stricture, Hepatic causes 2. Tumor
3. Hepatitis

HISTORY

1. Confirm obstructive jaundice

- Confirm jaundice – pt’s  sclera  are  yellow (carotenemia does not result in scleral icterus or elevation of the bilirubin level)
- Establish obstructive jaundice – tea-coloured urine, pale stools
- Exclude pre-hepatic and hepatic jaundice (more importantly hepatic jaundice since it can also cause tea-coloured urine)
Symptoms suggestive of viral hepatitis: prodrome of fever, malaise, arthralgia, myalgia, nausea/vomiting, etc.
Risk factors for viral hepatitis: travel history, ingestion of seafood, family history of hepatitis (esp mother, siblings), blood transfusions,
drug abuse/needle sharing, needlestick injuries, sexual contact
Alcohol intake: shown to affect bile acid uptake and secretion, resulting in cholestasis. Chronic alcohol use may result in fatty liver
(steatosis), hepatitis, and cirrhosis
Drug history: any TCM intake recently, any new medications taken
History of chronic liver disease

2. Aetiology – benign or malignant

- Recurrent spikes of similar jaundice that resolve on their own with time suggest benign obstruction e.g. stones, strictures
- A young patient with painful jaundice usually benign cause
- Previous history of gallstone disease or biliary colic symptoms
- Previous history of surgery to the biliary tract or ERCP
- Malignancy is suggested if the patient is old, jaundice is of new onset and progressively worsening, and there is no associated pain (i.e.
painless progressive jaundice)
- Constitutional symptoms: loss of appetite, loss of weight, malaise
- Metastatic symptoms: bone pain, neck lump, dyspnoea, etc
- Pain is a late symptom of pancreatic CA & tends to be constant and relentless compared to biliary colic which subsides after few hours

3. Complications

- Symptoms of cholangitis: fever, chills, rigors with RHC pain and jaundice
- Pancreatitis (gallstone as cause): abdominal pain radiating to the back with N/V
- Pruritus as a result of bile salt retention
- Decompensation: encephalopathy, hepatic fetor, worsening ascites
- Fat malabsorption: steatorrhoea, fat-soluble vitamin deficiency (A, D, E, K) – especially coagulopathy (very unlikely in acute setting)

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PHYSICAL EXAMINATION

1. Vitals: Is patient haemodynamically stable? Any fever?

2. General inspection: Jaundice. Pallor? Any abdominal distension, leg swelling?
3. Peripheries: Stigmata of chronic liver disease? Scratch marks? Conjunctival pallor?
4. Abdomen
- Any scars of abdominal surgery?
- Generalised distension? Ascites could be due to:
1. malnutrition (low albumin)
2. peritoneal malignancy
3. obstruction of portal vein by cancer
- Hepatomegaly? (Could be due to metastatic disease, or primary liver pathology)
- Enlarged gallbladder?  (Courvoisier’s  law  – if the gallbladder is palpable with painless obstructive jaundice, cause is unlikely stones)
- Splenomegaly? (Portal hypertension – think prehepatic, hepatic, posthepatic)
5. DRE: Pale stools?
6. Cervical and supraclavicular lymph nodes
7. Bony tenderness
8. Respiratory examination

INVESTIGATIONS (guided by clinical suspicion after Hx and P/E)

Bloods

Firstly to confirm obstructive jaundice:

1. LFT – classical obstructive picture = bilirubin raised (+/- direct>indirect; Normal 3:7) + raised ALP (and GGT - only ordered if Dx is ambiguous,
not routine) more than AST and ALT **Classical picture more often seen in CA than gallstone disease.

Secondly to confirm inflammation/infection:

2. FBC – any infection (impt as some pts haven mounted ferbrile response), anaemia (correct before ERCP)

Followed by the rest:

3. U/E/Cr: dehydration, Cr level for suitability of CT imaging!!
4. Amylase: concomitant pancreatitis
5. PT/PTT – any prolonged PT from vitamin K malabsorption, liver dysfunction (to be CORRECTED before procedures like ERCP can be done)
6. Tumour markers – CA 19-9, CEA (cholangioca and pancreatic ca)
7. Blood c/s if febrile and jaundiced (TRO HBS sepsis)
8. GXM – in case of op (eg. cholecystectomy)

Imaging
(Ultrasound versus CT - Both useful in demonstrating dilated biliary system as well as site & cause of obstruction)

1. U/S HBS: best for imaging stones

a. US findings:
i. Choledocholithiasis: Duct dilation>8mm
(impt to identify dilated INTRAhepatic ducts as it indicates that (a) obstruction is more severe (b) PTC is a
possible option if ERCP fails)
ii. Gallstone disease / Cholecystitis: GB stones or sludge, thickened GB wall, pericholecystic fluid, fat stranding
iii. Complications of gallstones:
iv. Liver consistency (fatty or cirrhotic)
b. Disadv:
i. Unable to detect malignancy well
ii. Unable to detect distal CBD stones well
iii. Sensitivity reduced with fat patient habitus
iv. Operator dependent
2. CTAP:
a. Indications
i. Suspected perf oratedGB (view air ard GB in lung window)
ii. Rule out malignant etiology
b. Adv
i. Preferred if there is a suspicion of malignancy (Ca pancreas or periampulary cancer) define the tumour (T)
better & stage at the same time (N & M)
ii. Logistics (can be done earlier esp cholangitic patient to plan for early intervention)
3. CXR
a. ARDS in cholangitis
b. Pleural effusion

MANAGEMENT
The patient is managed as for the causative aetiology (see relevant sections)

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3. GALLSTONE DISEASE

DEFINITION
Gallstone is a generic term for any kind of stone (cholesterol, pigment) in any part of the biliary system (gallbladder, cystic duct,
hepatic duct, common bile duct, etc)

EPIDEMIOLOGY
- Exact incidence in Singapore not known
- In the West: overall 10-15%; 20% in women and 10% in men
- Consistent 2:1 female to male ratio, 1:1 in elderly
- Typical  picture  (the  5  F’s):  Fat, female, forty, fertile, flatulent – refers to cholesterol stones but no longer applies.

NORMAL PHYSIOLOGY OF BILE

- Normal bile contains bile salts (primary and secondary), phospholipids, cholesterol, protein, and bilirubin
- Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol (in micelles, vesicles)
- a/w simple refined sugar in diet

STONE COMPOSITION AND PATHOPHYSIOLOGY

1. Cholesterol: cholesterol - hard and faceted
2. Black: mostly calcium salts and bilirubin - soft stones and crumble easily
3. Brown: calcium salts, bilirubin, and more cholesterol than black pigment stones

Cholesterol stones
- More common in older (peak at 40-50 years) but increasing in younger
- Developed countries – 22% of SG population (18% with signs and symptoms)
- M=F
- From disruption in the solubility equilibrium of bile.

1. Increased cholesterol secretion in bile

old
Obesity, rapid weight loss
Hyperlipidaemia
Increased oestrogens: female, pregnancy, exogenous administration

2. Decreased emptying of the gallbladder

Gallbladder malignancy is an important cause to exclude
Gallbladder stasis: Truncal vagotomy, Spinal cord injury
Pregnancy
Fasting, TPN

Pigment stones - bilirubin

- More common in younger patients, developing countries

a) Black pigment stones:

a. increased secretion of bilirubin into bile (e.g. chronic HAEMOLYSIS, - most commonly G6PD-def, CIRRHOSIS,
chronic liver disease, TPN),
b. decreased bilirubin solubilisers, and gallbladder stasis
b) Brown stones: = RPC!!!
Form in the biliary ducts due to infection with bacterial degradation of biliary lipids (hydrolyse conjugate bilirubin to free
form), the degradation products of which then precipitate as calcium bilirubinate.
Increasing in incidence due to influx of foreign workers.

Mixed
- Majority

Biliary sludge
- Microlithiasis suspended in bile; a milieu that predisposes to stone formation
- Can be visualised on the ultrasound scan as layering in the biliary tree
- Sludge is a pre-stone condition, but not all sludge becomes stones
- 20% of biliary sludge will disappear, 60% recur, and 10% form stones

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CLINICAL COURSE

Asymptomatic Leave alone

- 80-95% of patients
- Risk of symptom occurrence = 1 to 2% per year
greatest risk in first 5 years of diagnosis – 10% at 5 yrs, 15% at 10 yrs, 18% at 15-20 yrs
7-10% mod, 3-5% severe; the rest minor symptoms
majority do not require removal of the stones or the gallbladder = expectant mx (Risks of Sx > Risks of doing nth)
- Role of surgery: [3]
(a) Suspicious / high risk of MALIGNANCY (causing gallbladder stasis stones) eg. susp gallbladder mass, gallbladder
polyp, porcelain gallbladder prophylactic surgery
(b) IMMUNOCOMPROMISED presentation is abnormal & difficult to detect
(c) Patients with CHRONIC HAEMOLYTIC DISEASE (e.g. sickle cell anaemia, thalassaemia) – as high as 50-60% will
develop symptomatic disease in their lifetime

Symptomatic sequlae

1. Biliary colic (15%)

- Location: epigastric (70%) or RHC pain
- Radiation: inferior angle of the right scapula, tip of right shoulder or interscapular
- Character:
NOT a true colic: Waxing-waning in character but rarely have any pain-free intervals between waves of pain (Basal
pain is due to inflm of ductal epithelium & proximal distension) - CBD is not muscular, so absence of biliary colic, but a
constant pain with OJ 2o to obstruction
- Duration:
minutes to 2 hours,
often resolves spontaneously (if >6hrs, susp complication eg. cholecystitis)
- Trigger:
meals – binge-eating, fried oily foods,
dehydration
- Associated: N/V (patient gets better after vomiting), bloating, abdominal distension
Biliary  colic  is  a  “herald”  symptom  that  indicates  risk  of  further  sequelae.

2. Infection
i. Acute / Chronic cholecystitis
ii. Cholangitis
iii. Pancreatitis

3. Gallstone dyspepsia: (non-ulcer dyspepsia) fatty food intolerance, dyspepsia and flatulence not due to other causes

Complications

4. Choledocholithiasis with obstructive jaundice

5. Mirizzi syndrome with obstructive jaundice (see below)
6. Mucocoele of the gallbladder / Hydrops / Empyema of Gallbladder (see below)
7. Fistulation and gallstone ileus (see below)
8. Porcelain gallbladder: due to calcium salts ppt in GB wall. Calcium secreted into lumen of hydropic GB ‘limey’  bile.
9. Gallbladder CA

INVESTIGATIONS FOR GALLSTONE DISEASE

Plain abdominal X-ray

- Pickup rate for gallstones is less than 10% since most stones are radiolucent

1. Ultrasound of the hepatobiliary system

- Investigation of choice for gallstones
- >92% sensitivity, 99% specificity
- Even more sensitive than CT scan for stones since CT may miss small stones due to the spacing of the cuts taken
- Features of stone on ultrasound: strong echogeneic rim around the stone, with posterior acoustic shadowing
- Bile should appear as black patch in gallbladder; if not homogeneous sludge

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2. CT scan

- Usually not done to diagnose stones (as mentioned above)

a) DDx: Usually done in symptomatic patient where it is uncertain what is the cause of symptoms looking for other
possible causes as well (liver/pancreatic)
b) Cx: detect complications of gallstones

3. Magnetic resonance cholangiopancreatography (MRCP)

- MRCP is not the same as MRI liver/pancreas –

only selected cuts taken in order to reconstruct the biliary tree
without contrast
only T2 images,
resolution is not as good as MRI
- Comparable to ERCP, and also minimally invasive preferred to ERCP if patient does not require any therapeutic
intervention that ERCP provides

4. Endoscopic retrograde cholangiopancreatography (ERCP)

- Will definitely involve cholangiogram

- The largest value of ERCP lies in its therapeutic potential
1. Stone removal (using balloon catheter, or Dormia basket)
2. Sphincterotomy (in order to relieve obstruction or facilitate removal of stone)
3. Stenting
- High level of complications Overall risk is 10-15%
a. Pancreatitis in 1-3%:
i. Due to inflammation from a) injection of contrast (increased p) and b) edema when removing stone
ii. Increased risk in: younger, F, prev post-ERCP pancreatitis, cannulation/ injection of pancreatic duct,
sphincter of Oddi dysfunction
b. Haemorrhage 2-3%: esp sphincterotomy
c. Cholangitis 1-2%
d. Perforation into bile duct, duodenum 0.1% (esp if sphincterotomy): (OGD 0.01% ie 1 in 10000– ERCP slightly
higher since it uses side viewing scope)
e. Failed ERCP
f. Over sedation (hypotension, resp depression, N/V)
Also: Cholecystitis, Contrast related reaction (allergy to iodine) rare
- Before doing ERCP, need to assess the benefits and risks, and select patients carefully

5. Percutaneous transhepatic cholangiography (PTC) /biliary drainage (PTBD)

- PTC involves a tube being inserted under radiologic guidance into one of the biliary ducts (must be dilated duct)
- Rarely done now; main indications:
1) Diagnostic: high obstruction not well visualised in ERCP; prev surgery with altered anatomy (eg gastrectomy)
2) Therapeutic: obstructed system that cannot be drained from below;
- Mostly for therapeutic rather than diagnostic purposes
- Complications: bleeding (esp in biliary obs pts due to coagulopathy sec to decreased Vit K abs); leakage of bile when
tube is removed

6. HIDA scan

- No longer used commonly, except in biliary atresia

5 criteria for a normal cholangiopancreatogram

(a) Normal intrahepatic ducts

(b) No filling defects
(c) Smooth common bile duct
(d) No stricture/narrowing of the common bile duct
(e) Good and free flow of contrast into duodenum

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TREATMENT

Asymptomatic

- No surgery required unless patient has indications for surgery (see above)
- Expectant management and close follow-up
- Counsel patient about symptoms – biliary colic, acute cholecystitis, obstructive jaundice, etc

Symptomatic

Surgical = Cholecystectomy

- Cholecystectomy is the only way to treat gallbladder stones that are symptomatic (esp if cxs arise high risk of 2nd attack)
- Open or laparoscopic ( preferred)
- Adv of Lap: shorter hospital stay, less pain, less complications post-operatively
- Risks of Lap:
Conversion to open - up to 5%
Due to abnormal anatomy; difficult or complicated dissection; iatrogenic injury.
Conversion rate is higher if there is ongoing infection e.g. cholecystitis – up to 1 in 3 to 1 in 4
Injury to surroundings: bowel & biliary structures e.g. CBD
Haemorrhage
Infection
Spilled bile peritonitis, sepsis

Non-Surgical

- Non- surgical means of stone treatment

Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around to dampen waves; good results only for
cholesterol stones. Expensive. Bile salt therapy necessary following lithotripsy todissolve gallstone fragments.
CI: more than 3 stones, large/calcified stones, non-functioning GB, Cx of gallstones
Medical Tx in radiolucent gallstones, <15mm, mod obesity, no/mild symptoms. (success in 75% who fulfil this criteria)
Chemodissolution: LT oral bile acid ursodeoxycholic/ chenodeoxycholic acid (thought to reduce hepatic synthesis of
cholesterol and reduce chol secretion)
9 mths intensive followed by lifelong maintenance.
Toxicity and S/E, high cost.
Liver diet: mod carbo, low fat and cholesterol, high fibre

All therapeutic regimens retaining the GB have 50% recurrence of stones aft 5yrs (no LT benefit)

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4. ACUTE CHOLECYSTITIS

PATHOPHYSIOLOGY
- Gallstone gets stuck in the cystic duct causing obstruction of biliary flow
- Gallbladder becomes distended and inflamed
- 50% of cultures are sterile (infection occurs eventually. In elderly, DM severe with gas-forming organisms causing emphysematous
cholecystitis)

PRESENTATION

- Constant, severe RHC pain (less commonly epigastric)

- Radiates to the inferior angle of the scapula, interscapular
- Associated with nausea, vomiting
- Tachycardia, Low grade fever (chills uncommon), Dehydration
- RHC  tenderness  with  guarding  found  on  clinical  examination;;  Murphy’s  sign  positive  (increased  rigidity  on  inspiration)
- Gallbladder may be palpable (30%) – omentum wrapping around GB; worst case scenario is empyema
- Jaundice  <  10%:  due  to  Mirrizi’s  or  passage  of  stones  into  CBD  (15%  have  CBD  stones)

INVESTIGATIONS

1. ULTRASOUND FEATURES OF ACUTE CHOLECYSTITIS

a) Presence of gallstones in biliary system
b) Contracted gallbladder (from chronic gallstone disease)
c) Pericholecystic fluid (oedema of gallbladder wall)
d) Thickened GB wall
e) Sonographic  Murphy’s  positive

2. CT AP
Fat stranding around gallbladder not seen on ultrasound but on CT
Exclude complications (empyema, perforation)
3. FBC: leukocytosis (except elderly) – if severe, indicates complications
4. Amylase (can be raised mildly, if >1000, pancreatitis!),
5. LFT (mild transaminitis)/ UECr (dehydration)
6. CXR, KUB:
Radioopaque gallstones, aerobilia (due to fistula).
Exclude lower lobe pneumonia, perf viscus, abnormal right hemidiaph/thorax.
7. PFO: PT/PTT, ECG

MANAGEMENT

A) Conservative

- Resuscitate the patient, senior to r/v if pt systemically unwell

- Septic workup
- NBM and intravenous fluids
- Analgesia
- Empirical intravenous antibiotics – IV ceftriaxone (1g bd) and metronidazole (500mg tds)
- Bed rest
- Careful monitoring for signs of failure (peritonism, non-resolving fever/pain)

Cholecysitits usu resolves with medical management (60%), but inflammation may progress complications, including peritonitis.
- Definitive treatment – laparoscopic (better success if within 72hrs of symptom onset) cholecystectomy

B) Timing of cholecystectomy

- Dependent on several factors:

Severity of illness
Response to resuscitation and antibiotic therapy
Logistical considerations (availability of OT, surgeon etc)

- Possibilities available:
i. Emergency (immediate; in very sick patients who are not doing well/ not responding to treatment)
ii. Early (within few days of onset – ideally within 5 days)
iii.Delayed/interval (after 6-8 weeks)

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 Early Delayed
Advantages Advantages
- Everything done in one admission - Lower risks
- Easier to operate as the gallbladder is oedematous - Better laparoscopic success

Disadvantages
- Ongoing inflammation higher risk of bleeding Disadvantages
- Higher risk of injuring some other structure due to difficulty in - Fibrosis difficulty mobilising gallbladder
visualisation - Need for another admission
- Higher conversion rate to open chole - Chance of recurrence / acute pancreatitis during the time
- Increased risks of post-op infection (20%)

Early surgery has been found to be more beneficial ( mortality, total duration of dz, length of hosp stay, cost)

Gallstone disease in elderly more severe

- higher rate of complications
- extremely high mortality for emergency cholecystectomy
- Acute cholecystitis: timely diagnosis, early stabilization, semiurgent cholecystectomy

C) Cholecystostomy (fastest way)

- In moribund patients who are not fit for surgery / early surgery is difficult due to extensive inflammation
- Can be done under LA, or more commonly under radiologic guidance (percutaneous)
- Drains the gallbladder and alleviates the inflammation (resolves acute episode) better outcomes
- Can be followed by cholecystectomy 4-6 wks later

COMPLICATIONS OF ACUTE CHOLECYSTITIS

1. Hydrops/ Mucocele
- Cystic duct obstruction leads to a tense gallbladder filled with mucus (slow distension from continuous mucus secretion)
- May lead to gallbladder wall necrosis if pressure exceeds capillary bld pressure

2. Empyema
- Gallbladder is filled with pus due to bacterial infection of the stagnant bile (cystic duct being obstructed by a stone)
- Patient is usually toxic, requiring urgent surgery

3. Gangrene and perforation – rare due to rich blood supply from hepatic and cystic arteries
- Localised perforation abscess that is confined by the omentum (new mass)
- Free perforation generalised peritonitis and sepsis sudden generalised abdo pain emergency laparotomy

4. Cholecystenteric fistula
- Most commonly occurs in duodenum, then colon, and stomach; after repeated attacks of cholecystitis
- Usually asymptomatic
- On AXR, aerobilia is seen in 40% of cases
- Symptomatic fistulas (malabsorption and steatorrhoea) should be treated with cholecystectomy and fistula closure

5. Gallstone ileus
- Stones causing cholecystenteric fistula pass into the enteric lumen causing intermittent bouts of small bowel obstruction
- Accounts for 1-2% of IO overall
- Ppt: unexplained gradual onset of SB obstruction
- Small stones (<2-3cm) usually pass spontaneously without problems
- If >2.5cm and migrated into gut impact at terminal ileum (commonest), duod, sigmoid colon
- Mortality is 10-15%, mostly in elderly patients in whom gallstone ileus is more common
- Ix: AXR, Barium follow through
- Tx: Small bowel enterotomy proximal to the point of obstruction is usually required to remove the stone (Immediate cholecystectomy
not warranted as <4% of patients will have further symptoms)

PROGNOSIS

- 5% mortality
- Nearly all >60years, with DM
- Causes: 2° cardiovascular pulmonary complications (older), uncontrolled sepsis with peritonitis and intraabdominal abscess

ACALCULOUS CHOLECYSTITIS

- Occurs in very ill patients with prolonged stay in ICU – prolonged fasting, poor nutrition, labile blood pressure, sepsis
- Poor nutrition leads to biliary stasis, while dehydration and hypotension leads to formation of viscous bile and gallbladder ischaemia bile
may get infected cholecystitis
- Treatment involves emergent cholecystectomy / percutaneous cholecystostomy to control acute disease followed by cholecystectomy

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5. GALLBLADDER CANCER

- uncommon, increasing in China and North India

- RF - F:M=2:1, obesity, chronic cholecystitis/ cholelithiasis
- Mostly adenocarcinoma, small percentage SCC
- Signs and symptoms
Early: mimic gallstone inflammation (RHC pain)
Late: biliary and stomach obstruction (jaundice, vomiting, LOA, LOW)
Mostly incidental histo finding after cholecystectomy
- Related to gallstones building up (95%) porcelain gallbladder
- Commonly spreads to liver, bile ducts, duodenum, stomach
- Treatment: cholecystectomy + liver resection and LN dissection +/- chemoRT
- Palliative: Endoscopic stent to biliary tree and stomach
- Prognosis: poor (most die by 1 year after surgery)

6. CHOLEDOCHOLITHIASIS

PRESENTATION
- Obstructive jaundice – tea-coloured urine, pale stools
- Biliary colic
- If infection sets in cholangitis (see below)

BLOODS
- FBC (check TW for any rise suggestive of infection)
- Amylase (CBD stone may cause pancreatitis)
- LFTs (raised bilirubin – direct; ALP raised more than transaminases – also high if LT due to liver damage)

ULTRASOUND
- Gallstones in gallbladder
- Gallstone in CBD (50% missed, esp in distal CBD)
- Dilated CBD (normally <8-9mm)
>10mm is abnormal
In older patients, post-cholecystectomy, or patients on long-term opiates, the CBD may be larger, up to 11-12mm in size

MANAGEMENT
- If unsure of presence of stone less invasive investigation such as MRCP, EUS
- If likelihood of CBD stone is high ERCP with stone removal

ERCP successful Plan for lap cholecystectomy

ERCP failed If patient is well and can tolerate another ERCP, try again (+ stent
in between to drain bile)

Operative removal – Open CBD exploration

– Lap CBD exploration

- If no facilities to do ERCP: open or laparoscopic cholecystectomy with CBD exploration

When to do operative removal of stones (i.e. not suitable for ERCP)

- Stone >25mm, Intrahepatic stone, Large number of stones, Impacted stone
- Dual pathology, Tortuous duct, Previous Bilroth II (unsuitable anatomy for ERCP)

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7. CHOLANGITIS

PRESENTATION
- Classically Charcot’s triad: RHC pain, fever, jaundice (only 50-70% of patients have the classic triad)
- Reynold’s pentad:  Charcot’s  triad  plus  mental  obtundation  and  shock
- A surgical emergency! (mention in exams!)

PATHOLOGY
- Usually results from obstruction to the biliary system with infection of stagnant bile
- Most common cause is choledocholithiasis (60%);
Consider benign strictures (instrumentation), malignancy (pancreatic, biliary), foreign body (prev instrumentation), PSC,
choledochocysts, Mirrizi’s,  hemobilia,  biliary  enteric  anastomosis
- Common causative organisms are gram negative bacteria and anaerobes – Klebsiella, E. coli, Enterobacter, Enterococcus
- Small proportion (elderly, prev biliary surgery) – anaerobes (bacteriodes, clostridium), developing world – parasites (Clonorchis
sinensis, Ascaris lumbricoides)

COMPLICATIONS
- sepsis
- electrolyte abnormality (dehydration)
- infection
- coagulopathy (Vit K)

MANAGEMENT

1. Resuscitation – “In view of cholangitis being a surgical emergency, I will like to resuscitate the patient who may be in septic
shock”.Anticipate  rapid  deterioration.
- Inform seniors
- Obtain good intravenous access and fluid resuscitate as appropriate
- Take bloods for investigations – cultures especially
- Close monitoring of vitals in HD/ICU
Hrly para + SpO2 Keep MAP > 65mmHg (or to inform doctors if SBP<100mmHg)
Catheterise and watch urine output (hrly urine output) – hepatorenal! (keep >0.5mg/kg/hr)
CVP line insertion if patient has shock unresponsive to fluid resuscitation (keep 10-12mmHg)

2. Antibiotics (after blood c/s)

- IV ceftriaxone (2g STAT + OM) & metronidazole (500mg STAT + Q8h); imipenem if pt in shock
- 7 – 10 days

3. Investigate for cause

- ultrasound (preferred if suspecting stones) vs CT (for non-stone cause) etc as above

4. Biliary DECOMPRESSION +/- definitive treatment

- Biliary decompression and definitive treatment can be combined or separate
- Timing
usually deferred until 24-48h after admission when pt is stable/improved w Abx
Emergency if deteriorating / Abx not improving infection (15%)
- ERCP
a) Decompression commonly performed using ERCP
Decompression is the primary objective
– endoscopic sphincterotomy + stenting/external drainage (nasobiliary drain: bile duct to nose for continuous
drainage)
Success rate 90%
b) If cause of obstruction can be treated in the same setting (e.g. stones to be removed) then treat the cause also
- Other methods to decompress:
percutaneous transhepatic drainage (esp if neoplastic obstruction)
operative decompression

5. Definitive treatment = Cholecystectomy +/- CBDE

- Definitive treatment dependent on:
Medical condition of patient
Success of biliary decompression
Logistical considerations

176
 - Choices for definitive treatment:
(a) Open cholecystectomy with CBD exploration
(b) Laparoscopic cholecystectomy (if CBD exploration is to be performed, need to convert to open – lap CBDE not done
in Singapore must mention during consent taking)

CBD EXPLORATION

- Cholangiogram or choledochoscopy is performed

1. Cholangiogram involves injection of dye – can image higher ducts
2. Choledochoscopy involves using a scope to visualise the large biliary ducts – cannot image higher ducts, thus not as
sensitive, but can be used to remove stones visualised in the duct
Choice of imaging depends on site of obstruction and the cause

- Removal of stones
1. Manual removal with stone-grasping forceps
2. Flushing out stones
3. Dredging stones out using balloon catheter or Dormia basket
4. Lithotripsy

- Consider use of biliary stent or T-tube after removal of stone(s)

If there is a lot of instrumentation of the biliary system during the operation, one should anticipate swelling and oedema of the
biliary system resulting in post-operative obstruction and buildup of bile higher risk of biliary leakage

(a) Stent – removed later by endoscopy

(b) T-tube (usually inserted after CBD-E)
A T-shaped tube with its horizontal limb placed in the CBD and the vertical limb leading out to drain bile
Adv
i. Functions  as  a  “pressure  release  valve”  as  most  of  the  bile  will  flow  through  the  horizontal limb of the
tube into the distal part of the CBD; only when there is obstruction to flow will bile be diverted out
through the vertical limb
ii. Allows for post-op cholangiogram (at POD 9-10) before removal
1. free flow of contrast into duodenum,
2. no residual stones,
3. no free leak of contrast into peritoneum
If all normal release anchoring stitch & exert gentle traction on tube; tube should slip out easily, if not, call for help
If stones are present leave tube in for 4-6 weeks to form a fibrous tract allows for instrumentation of tract with a
scope to remove the stones

BILIARY BYPASS (UNCOMMON)

- Consider biliary bypass if there are

1. multiple stones,
2. the CBD is more than 2cm in diameter, or
3. there are strictures
(since the CBD has been chronically dilated, quite unlikely that it will function normally even after removal of the obstruction)
Mostly replaced by endoscopic stenting.
Cholecystojejunostomy preferred over Roux-en-Y choledochojejunostomy.

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8. MIRIZZI’S  SYNDROME

PATHOLOGY
- Gallstone  in  the  Hartmann’s  pouch  compressing  the  common  hepatic  resulting  in  obstructive  jaundice
- Compression effect is not just physical (the stone) but also contributed by the surrounding inflammation
- One  of  the  caveats  to  Courvoisier’s  law

GRADING

Type I - No fistula present

Type IA - Presence of the cystic duct
Type IB - Obliteration of the cystic duct

Types II-IV - Fistula present

Type II - Defect smaller than 33% of the CBD diameter
Type III - Defect 33-66% of the CBD diameter
Type IV - Defect larger than 66% of the CBD diameter

MANAGEMENT
- Grade 1: attempt laproscopic cholecystectomy
- Grades 2-4: open cholecystectomy with CBD exploration

9. RECURRENT PYOGENIC CHOLANGITIS

BACKGROUND
Cholangiohepatitis, or recurrent pyogenic cholangitis (RPC), is characterized by:
1. Recurrent bacterial cholangitis
2. Intrahepatic pigment stones
3. Intrahepatic biliary obstruction.

PATHOPHYSIOLOGY
Helminthic infxn (eg Ascaris lumbricoides, Clonorchis sinensis) epithelial damage predispose to seeding of coliforms
into biliary system via bacterial translocation repeated portal bacteraemia cascade of events (biliary stasis,
obstruction, stone formation) recurrent cholangitis
Malnutrition deficiency of enzymes calcium bilirubinate pigment stones formation recurrent biliary obstruction
recurrent cholangitis

HISTORY:
- A history of recurrent attacks of cholangitis – typical hx:
1-2 episodes of fevers, jaundice, and RUQ abdominal pain per year
Hx of prev biliary surgery, endoscopic procedures, or percutaneous biliary drainage procedures.
- Complications of pyogenic cholangitis
cirrhosis with portal hypertension
cholangiocarcinoma

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PHYSICAL EXAMINATION
No specific physical findings are evident in RPC. Dx based on history.

DIFFERENTIALS
Primary Sclerosing Cholangitis

INVESTIGATIONS

For diagnosis
For Complications

Bloods
- FBC
- LFT with ALP>ALT, AST
- Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and vitamin K deficiency)
Impt to exclude – correct with parenteral Vit K before invasive procedures
- Blood C/S: bacteremia – results help guide antibiotic choice.
- Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present.

Radiology

- U/S HBS
segmental biliary dilatation
hepatolithiasis
liver abscesses
helps determine choice of supplemental axial imaging techniques.

- ERCP or PTC – imaging modality of choice for delineating the biliary tree.

- CT scan
centrally dilated bile ducts with peripheral tapering
bile duct stones
pyogenic liver abscesses.

TREATMENT PRINCIPLES:
- Treat current infection
- Biliary drainage
- Management of other complications e.g. dehydration etc

Surgical
- Usual surgical approach includes:
Initial biliary decompression – ERCP sphincterotomy / stent placement
Definitive biliary drainage procedure – e.g. Roux-en-Y choledochojejunostomy

PROGNOSIS
- Death occurs in approximately 15-20% of patients over 5-6 years.

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10. CHOLANGIOCARCINOMA

SITE

- Intrahepatic/peripheral 10%
- Distal 25%
- Perihilar 65% (Altemeier-Klatskin tumour)

Bismuth classification
i. Type I: below confluence of hepatic ducts
ii. Type II: tumour reaching confluence
iii. Type IIIA/B: involving common hepatic duct and either right or left hepatic duct
iv. Type IV: multicentric or involving confluence and both hepatic ducts

ASSOCIATIONS

- Related to chronic cholestasis:

Primary sclerosing cholangitis / Ulcerative colitis
Parasitic infection – Clonorchis sinensis, Opisthorchis viverrini
Hepatolithiasis
Recurrent pyogenic cholangitis
- Bile duct adenoma
- Choledochal cyst (20-25% in Type 1)
Caroli’s  disease  =  congenital  cystic  dilatation  (multifocal  segmental  dilatation  of  large  intrahepatic  bile  ducts)
- Thorotrast exposure (radioactive Xray contrast)
- Instrumentation

PRESENTATION

- Painless jaundice (painful if there is cholangitis)

- Acholic stools
- Pruritus
- Advanced signs and symptoms:
Abdominal pain
Fatigue, malaise
Weight loss
Hepatomegaly

DIAGNOSIS

U/S detects biliary dilatation but not useful for ductal lesions.
- CA 19-9  >100μl/ml  (good  sensitivity  of  89%,  specificity  86%)
- Contrast CT
- PTC: when biliary obstruction from distal end. 2 functions: 1) roadmapping for surgery; 2) drainage of obstructed system if
ERCP cannot drain
- ERCP: can obtain brushings for cytology, less bile leak than PTC
- Selective celiac angiography: aid in determination of surgical resectability by identifying tumor involvement with adjacent blood
vessels

CURATIVE TREATMENT

- Surgery is the only chance of long-term cure

- Only 25% of tumours are resectable
- Contraindications to surgery
Bilateral or multifocal intrahepatic disease (2nd order biliary radicles in both hepatic lobes)
Invasion of portal vein trunk or hepatic artery
Bilateral involvement of hepatic arterial or portal venous branches
Unilateral hepatic vascular invasion with contralateral ductal spread
Distant metastases

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PROGNOSIS FOR RESECTABLE DISEASE (5-year survival)

- Intrahepatic: 35-45%
- Distal 35-45%
- Perihilar 10-30% (worse prognosis due to early lymphatic spread)

PALLIATION

- Endoscopic/percutaneous transhepatic biliary stenting

- Bilateral drainage for hilar cholangiocarcinoma
- If after opening up and finding that tumour is not resectable, can perform surgical bypass

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12. BREAST DISEASES

1. ANATOMY OF THE BREAST

- The breast is a modified sweat gland that lies in the subcutaneous tissue of the anterior chest wall between the 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
- Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts that open separately on the nipple
- Fibrous septa (Cooper’s  ligaments) interdigitate the mammary parenchyma and extend from the posterior capsule of the breast
to the superficial layer of fascia within the dermis, and provide structural support to the breast (involvement of these ligaments
by malignancy causes dimpling of the overlying skin)

- Lymphatic drainage:

1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes

1. 40-50 nodes in 5 groups: Anterior, posterior, medial, lateral, apical
2. Drains into supraclavicular and jugular nodes

Anatomic/ Surgical division into levels I, II and III by the pectoralis minor muscle:
Level I: lateral to pectoralis minor – usu e first LN where BrCA spreads to
Level II: posterior to pectoralis minor
Level III: medial to pectoralis minor, extending up to apex of axilla

2. Internal mammary nodes--20% of drainage from the ipsilateral breast

upper and lower inner quadrants
About 4 nodes per side, with one node in each of the first three interspaces and one in the fifth or sixth
interspace

3. Interpectoral (Rotter’s  nodes)  – between pec major and pec minor muscles

2. PRESENTATION OF BREAST DISEASES

1. Lump (painful vs painless)

2. Pain (cyclical vs non-cyclical) [ more likely benign]
3. Nipple changes or discharge

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3. APPROACH TO A BREAST LUMP

DIFFERENTIALS (AGE DEPENDENT)

Painless lump Painful lump
Elderly: (post-menopausal) 1. Area of fibroadenosis
1. Carcinoma 2. Cyst
3. Abscess (usually in lactating women)
Younger: 4. Fat necrosis (minor trauma)
2. Cyst 5. Periductal mastitis
3. Fibroadenoma - can get cyclical pain (swell with the rest 6. Galactocoele (lactating women)
of  the  breast  cos  it’s  breast  tissue) 7. Carcinoma (rare; ~10% & advanced)
4. Area of fibroadenosis (nodularity)
May not be painful if pt has received treatment / some infx.
Cyst, fibroadenosis and carcinoma can be painful/ painless.

HISTORY

1. History of lump
- Site of the lump?
- Single or multiple? – multiple: fibroadenoma / cysts / fibroadenosis.
- When & Why was it first noticed? (Pain, self-examination, etc)?
- Painful or painless?
- Overlying skin changes noted:
Erythema, warmth
Dimpling: shortening of Cooper’s  ligaments  due  to  tumor  pressure?
Any general asymmetry of the breasts noticed?
Discharge – ind CA invasion
- Duration since first noticed – long duration unlikely CA
- Any increase in size from first noticed to now?
- Any changes in the nipple e.g. retraction
- Nipple discharge? If present, what is the colour and consistency?
- Any other lumps elsewhere – other breast? Axilla? Neck?
- Has the lump been treated before?
RF – to sieve out ppl carrying BrCA gene, ID high risk patient (to continue f/u even if lump benign)

2. Oestrogen exposure history

Increased risk:
- Age of menarche (early <12YO increased risk)
- Age of menopause if applicable? (>55YO increased risk)
- Use of HRT (>1yr) – cumulative risk with duration of therapy and/or Oestrogen based OCP (not proven)
‘Confers  protective  effect’:
- How many full term pregnancies? (nulliparity increased risk)
- Age at which first child was born (>30 years old)
- Whether patient breastfed her children, and if so, for how long

3. Other risk factors for cancer

A. STRONGEST RF:
Family history of cancers* in paternal (BRCA2) and maternal side (BRCA 1&2), especially if cancer occurs in:
a. first degree relative below the age of 40, in bilateral breasts
b. >/= 2 relatives with Breast CA around 50yo
*Includes breast, ovarian, prostate and CRC.
Lifetime risk in gene carrier – 80%.
B. Previous breast disease:
a. Treated cancer
b. Previous biopsy showing atypical ductal hyperplasia or LCIS
C. Exposure to ionising radiation (esp. RT for previous breast disease)
D. Daily Alcohol intake, especially before age of 30 (link has been shown)

4. Systemic review
- LOA, LOW (constitutional)
- Fever (infective cause)
- Bone pain, SOB, headache (metastasis)

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PHYSICAL EXAMINATION

Preliminaries (HELP)

- Hi: Introduce yourself & ask for permission to examine the breast Check list:
Always have a chaperone to accompany you if you are male - Breast
- Expose patient adequately from the waist up with exposure of axillae - Nipple
- SC LN
- Lighting: good
- Spinal Tap
- Position the patient at 45o or sitting position if a bed is not available - Lung effusion
- Hepatomegaly
Inspection

- General appearance
- Patient’s  hands  relaxed  at  her  sides  – look for:
any asymmetry in the breast contours,
any obvious skin changes
peau  d’orange  –infiltration of malignant cells into lymphatics causing edema (not compression),
erythema,
puckering
any scars of previous operation or procedure e.g. punch biopsy
- Look for nipple changes (7  D’s):  
Discolouration Depression (retraction) Destruction
Discharge Deviation (Duplication – unlikely)
Displacement
- Manouvres:
1. Ask patient to raise her arms (to see the axilla and underside of breasts, and accentuate any tethering to skin dimpling)
2. 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
3. Press arms down & lean forward the rest of the breast will flop fwd but not the CA that is attached to underlying muscle

Palpation

- Patient should be lying down at 45 degrees to the horizontal with her hand tucked behind her head – this splays the breast out
so it can be palpated properly
- Start with the normal side first!
- Ask for any pain before starting to palpate
- Use one hand to retract and stabilise the breast and palpate with the other
- Palpate in a systematic manner e.g. quadrant by quadrant from centre outwards
- Examine the entire breast including the axillary tail
- When the lump is located, check with the patient whether this is the same lump

- Characterise the lump:

Site (which quadrant)
Size “I  feel  a  lump  in  the  upper outer quadrant of the Right breast. This
lump is NOT WARM, and NON-TENDER, is hemispherical with
Shape (hemispherical/ oval)
poorly defined edges, measuring ___X___CM. It is firm in
Surface (smooth or nodular/irregular) consistency with a irregularsurface and is NOT FLUCTUANT.
Consistency (soft, firm, or hard) It is NOT FIXED to  the  SKIN  ………….(ask  her  to  contract  the  pect  
Tender or non-tender maj)….  ………….And  NOT FIXED to  the    underlying  muscle”
Warmth of overlying skin
Fluctuance
Margins (regular and smooth, or irregular and ill-defined)

1. Fixation to the skin – try to pick up the skin above the lump
2. Fixation to underlying muscle – Move lump in 2 perpendicular directions. Then ask patient to press her hands against
her hips to contract the pectoralis major muscle, then try to move the lump in 2 perpendicular directions. (no need to do if
already attached to chest wall)

- Continue to examine carefully for other lumps

- Ask patient if she can show you the discharge by expressing it herself (NEVER squeeze the nipple yourself!)
If patient cannot do it, then ask the chaperone to help / squeeze yourself by milking the breast from outside in (ideally with
patient sitting forward)

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Axillary lymph nodes

- Palpate the normal side first

- Rest the pt’s  right forearm on your right forearm and use your left hand to palpate the right axilla (vice versa for the left side)
- Palpate gently, slowly, and systematically, covering the major groups of nodes: anterior, posterior, medial, lateral, and apical
- If any lymph nodes are found to be enlarged, note the number of lymph nodes, their site, size, tenderness, consistency (firm,
hard, matted), mobility

To complete the examination

- Examine the the supraclavicular LNs & cervical LNs

- Examine the lungs for any pleural effusion
- Percuss the spine for bony tenderness
- Examine the abdomen looking for hepatomegaly

FINDINGS FOR THE COMMON BREAST LUMPS

Type of lump Age Pain Surface Consistency Mobility

Cyst 30- Occ Smooth Soft to hard Not fixed
55
Nodularity 20- Occ Indistinct Mixed, Not fixed
55 fluctuant
Fibroadenoma 15- No Smooth, Rubbery Very mobile
25 bosselated
Cancer 35+ No Irregular Stony hard May be tethered
or fixed

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INVESTIGATIONS

“The  evaluation  of  a  breast  lump  is  via  the  TRIPLE ASSESSMENT All 3 must be concordant for benign to
– (i)  Clinical  examination;;  (ii)  Imaging;;  and  (iii)  Histology.” have >99% specificity to r/o malignancy

Imaging

1. Mammography: always cf Prev MMG (alert if any CHANGE)

- Most sensitive of the proven breast imaging modalities (Gold std)
- Purposes:
Dx
Screen the rest of the Breast helps to plan treatment (possibility of breast conserving Sx)
Screen contralateral breast (in case B/L BrCA – rare)
Baseline for future f/u for contralateral breast (Br CA is RF for CA development)
- Usually performed in asymptomatic older women (>35YO) [breast tissue in younger women is denser; more difficult to
pick up abnormalities], but <35YO in symptomatic women
- Normally, 2 views are done:
craniocaudal (CC)
right /Left 70%
70% tumours in lateral quadrant (upper)
mediolateral oblique (MLO)
captures the tail
right/ left
80% tumours in oblique milky way

- Additional specialised views: magnification and coned compression; done on request to

help magnify areas of abnormality or help visualise breast better
80%
- Abnormal features:
(a) Neo-density or asymmetric density (look for bilateral synchronous ca; satellite lesion)
(b) Microcalcifications (<0.5mm in size)
- If calcifications >0.5mm macrocalcifications; >5/mm2 cluster
- Sole feature of 33% of cancers detected on mammography
- Causes:
A. DCIS,
B. invasive cancer,
C. fibrocystic disease,
D. papilloma
- Features of malignancy:
1. pleomorphic microcals, heterogeneous appearance; segmental
2. closely grouped or arranged in a linear pattern (ductal distribution),
3. underlying density
- Features of Benign microcals:  punctate,  “tea-cup”  appearance
(c) Spiculated mass or stellate lesionwith poor outline or comet sign
- 95% of spiculated masses on mammography are due to malignancy
- Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance of
it being malignant
- Causes:
A. Invasive cancer, Comet sign: enhancing lesion with a tail (directed towards nipple).
B. radial scar (benign), Indicates early DCIS. DDx – prev Bx / Sx to that area.
C. fat necrosis,
D. abscess, etc
(d) Architectural distortion (of the contour), tent sign , nipple changes
- Look at the axilla on the MLO view for any enlarged lymph nodes

BI-RADS (Breast Imaging Reporting and Data System) classification

Category 0: Need additional imaging evaluation
Category 1: Negative (nothing to comment on, 0.05% risk still present)
Category 2: Benign
Category 3: Probably benign, short-term follow-up suggested (<0.2% risk)
Category 4: Suspicious, biopsy should be considered (25-74% risk)
Category 5: Highly suggestive of malignancy (75-99% risk)
Category 6: Known malignancy

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2. Ultrasound
- Usually used as the 1st investigation in young patients (<35 years old) or pregnant, lactating patients – as mammogram has radiation
(small amount); not the gold standard for screening
- Used when there is a breast lump:
A.Guide procedures e.g. Biopsy, drainage of abscess, aspiration of cyst
B.Evaluates consistency (solid vs cystic) &margins
C. Problems with Mammogram
Localisation of lesion seen in only one mammographic projection
Evaluation of a palpable mass with a negative mammogram
Evaluation in mammographically-difficult areas e.g. chest wall, axilla
- Pitalls:
Operator dependent, non-standardised techniques, poor resolution,
Unable to detect most microcalcifications
- Features of malignancy:
1. Markedly hypoechoeic with + thick echogenic halo
2. Irregular edges; Destruction of surrounding structures
3. Hypoechoeic shadowing; Posterior acoustic shadowing
4. Taller than it is wide (fir-tree appearance; invasion of fascia)
5. High central vascularity – Doppler to evaluate BV
6. Microcalcification (if large number)

3. MRI of the breast

- Expensive, but Good soft tissue definition without radiation (>90% sensitivity)
- Useful for pre-menopausal women with dense breast
- Look for contour, enhancement, washout kinetics (how fast/ whether dye stays)
- Indications:
1. Pre screening: Screening in high risk patient (BrAC gene +: yearly MMG and MRI surveillance)
2. Post screening
a. Occult lesions: Axillary LAD but Mammogram & US -ve
b. Suspicion of multifocal or bilateral malignancy (esp ILC)
3. Pre treatment: When planning for breast conservation surgery
4. Post treatment: Assessment of response to neoadjuvant chemotherapy

Histology

- Options available:
(a) Fine needle aspiration cytology
(b) Core biopsy (Trucut/ mammotome)
(c) Incisional biopsy – remove part of lump (usually not done now except Frozen section intra-op)
(d) Excisional biopsy – remove entire lump
(c) and (d) GA, larger wound.

- Mostly a choice between FNAC and core biopsy

FNAC is less invasive, less painful, smaller wound (23G needle), does not require any local anaesthetic, cheap, repeatable.
But only cells are obtained with no histology cannot differentiate between in-situ cancer and invasive cancer, requires skilled
cytopathologist
If FNAC shows malignant cells, do frozen section intraop before proceeding with surgery (recommended).

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.
But can obtain tissue specimen, can stain for ER/PR status better diagnostic value

Should  have  ‘tissue  diagnosis’  if  you  are  subjecting  patient  to  cancer  treatment!
- Guided by clinical palpation or radiologic guidance[ more accurate, not 100%]
US guidance
Stereotactic guidance (stereotactic mammotome) – stereotactic = Xray from 2 angles, mammotome = vacuum-assisted biopsy device
(able to sample larger tissue volumes)

MANAGEMENT

- If triple assessment suggests a benign lump (i.e. all 3 are concordant), follow up with physical examination for 1 year (q3-6mths) to ensure
the lump is stable or regresses
- If all 3 concordant for malignancy further staging and treatment
- If 1 or 2 of 3 aspects suggest malignancy further workup, excisional Bx?

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4. APPROACH TO NIPPLE DISCHARGE

CAUSES

Colour of discharge Cause

Red or pink (blood + serum) Ductal papilloma (benign)
Ductal carcinoma
Clear yellow (serous) Ductal papilloma
Duct ectasia (= periductal mastitis)
Cyst
Ductal carcinoma
Green, brown, black (cell debris) Duct ectasia
Purulent, foul-smelling Mastitis/abscess
Thin, white fluid (milk) Galactorrhoea/lactation

HISTORY

1. Is the discharge true?

- Exclude other conditions may mimick e.g.  eczema,  Paget’s,  etc

2. Is the discharge significant?

- Spontaneous or only on pressing (spontaneous is sig)
- Intermittent or persistent (persistent is sig)
- Relation to breastfeeding (significant if >1yr after stopping breastfeeding)

3. Is the discharge worrisome?

- Unilateral or bilateral (unilateral more worrisome)
- Discharge from multiple ducts or single duct (single duct more worrisome)
- Nature of discharge (bloody more worrisome)
- Age of the patient (more worrisome in older patient >60)

4. Is it troubling the patient?

PHYSICAL EXAMINATION (as described above)

INVESTIGATION

1. Discharge for cytology to detect malignant cells

2. Mammography/ US of both breasts to detect any underlying malignancy
3. Histology of biopsied lesion if found on imaging
4. Ductography, ductoscope & biopsy

MANAGEMENT

- If malignancy found, manage malignancy

- Excision for intraductal papilloma (microdocholectomy, total ductal excision, hookwire locailised excision) – scarring may affect
other ducts too
- 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

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5. BREAST CANCER

EPIDEMIOLOGY
- Most common cancer in females in Singapore:
- Age-standardised incidence 55 per 100,000 in 2002; incidence is half that of the West
- Bimodal age distribution: 45-55YO & older (>75YO)
- Gender ratio is about 100-150 female :1 male

RISK FACTORS

1. Age (increases with increasing age with two peaks as mentioned)

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

PATHOLOGY (WHO classification: epithelial and non-epithelial tumours.)

- Non-epithelial tumours arise from supporting stroma (e.g. angiosarcoma, malignant phyllodes tumour, primary sarcomas); very uncommon
- Epithelial tumours arise from cells lining the ducts or lobules, and can be further divided into invasive and non-invasive based on invasion of
the basement membrane

Non-invasive Invasive
Ductal DCIS = malignant IDC
- From terminal duct lobular unit, - 70-80% of invasive breast cancer
- Cause distortion of lobules, - Includes all cancers that cannot be subclassified into a
- Do not invade BM specialised type “no  special  type”
- Non-palpable, detected microcals - Poorer prognosis than a carcinoma of specialised type
- 35% multicentric, occult invasive ca in 10-20% - 2/3 express ER/PR,
- Progress to CA within 10 yrs ~30% risk; considered - 1/3 overexpress C-erbB2
malignant
- Good prognosis if treated
- Tx similar to IDC
Lobular LCIS = RF ILC
- From terminal duct lobular unit (like DCIS) - 5-10% of invasive cancers
- Do not distort lobular architecture - 10-20% multicentric and/or bilat
- Usually presents with a lump, seldom detected by - Cells morphologically similar to cells of LCIS:
mammo as rarely microcal. monomorphic, bland round nuclei
- 60-80% multicentric and bilateral - Cells invade individually into stroma (due to loss of E-
- Not premalignant, but a marker for increased risk of cadherin, a cell-adhesion molecule)
invasive disease in both breasts (7-10x increased risk) - Similar prognosis to IDC
- If ca develops, will be IDC usually, occurs >15 years
after diagnosis
- Usually proceed with excision biopsy.
Others Specialised types
- Medullary, colloid (mucinous), tubular, papillary
- Better prognosis than IDC

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

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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

PRESENTATION

- Asymptomatic: detected on mammographic screening

- Local:
- Self-detected lump in the breast (>1/3 of patients)
- Nipple change: distortion, destruction, retraction, deviation, discharge, eczema
- Overlying  skin  changes  e.g.  peau  d’orange,  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
- Other lumps in axilla
- Pain is uncommon.
- Constitutional: LOW, LOA
- Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone, brain, adrenals)

DIAGNOSIS – BY TRIPLE ASSESSMENT (see above)

STAGING

- Triple assessment can help divide it into:

- DCIS or early Breast Cancer (BC) (at most with small mobile axillary LNs)
- locally advanced BC (matted LNs, skin and rib involvement)
o continue to stage to look for metastasis in advanced BC
- Staging Investigations:
(i) CXR (for lung metastases; look for isolated hyperdensity)
(ii) U/S HBS
(iii) Bone scan
(iv) LFT (raised ALP) + Hepatitis screen (may flare up with chemoTx)
(v) CT or MRI brain – if patient symptomatic
(vi) CT thorax , abdomen (for liver and adrenal metastasis) – in locally advanced BrCA

T stage N stage M stage

Tis: Carcinoma in-situ,
Paget’s  with  no  tumour N1: Mobile ipsilat axillary nodes M1: distant mets

T1: <2cm N2: Fixed/matted ipsilat axillary nodes

T1a – 0.1 to 0.5 cm
T1b – 0.5 to 1.0 cm N3: N3a – Ipsilat infraclav nodes
T1c – 1.0 to 2.0 cm N3b – Ipsilat int mammary nodes
N3c – Ipsilat supraclav nodes
T2: 2 to 5 cm

T3: >5cm

T4: T4a – Chest wall involvmt

T4b – Skin involvmt
T4c – Both 4a and 4b
T4d – Inflammatory ca

Stage 0 Stage I Stage II Stage III Stage IV

*skin, rib inv., matted LNs
Tis T1N0 T2N0, T3N0 T3 N1 M1
T0N1, T1N1, T2N1 T0N2, T1N2, T2N2, T3N2
Any T, N3
T4, any N

DCIS Early Breast cancer Locally advanced BC Advanced BC

Aaaaa – Stage Xb (e.g. IIb, IIIb)

5 yr Survival
Stage I: 90% (70% in 10 yrs) 95% with adjuvant Rx
Stage II: 60% (40-50%) 76% with adjuvant Rx
Stage III: 30% (20-30%) 50% with adjuvant Rx
Stage IV: 10% (<2%)

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PROGNOSIS

Prognostic factors: - to predict RECURRENCE rate to decide on the SYSTEMIC TREATMENT

1. Patient factors - ability to tolerate chemo

- Age (younger patient higher chance of recurrence, progress of disease)
- Comorbidities
- +/- Social support

2. Tumor factors
- Stage of disease – tumour size, lymph node involvement [Major prognostic factor]
- Grade of tumour
- Lymphovascular invasion

3. Predictive factors (predict response to a Tx):

- C-erbB2/Her-2 positivity indicates more aggressive tumour worse
- 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.

Recurrence score: to identify people who will recur

using gene typing

THERAPEUTIC OPTIONS

Options can be divided into aims of control (with either curative of palliative intent):

(a) Locoregional control: Aim of adjuvant therapy:

Surgery (WEAC vs SMAC) 1. Prevent local recurrence
Radiotherapy a. RT
(b) Systemic control: (size >10mm; <70YO) b. ± CT, HT, TT
Chemotherapy 2. Eradicate micrometastasis
Hormonal therapy a. CT, HT, TT
b. ± RT
Targeted therapy
Reduces recurrence by 1/3; but if recurs
have poor prognosis
Surgery

1. Preparing for operation:

- Anaesthesia workup and necessary imaging. Mark out the site

- Psychological counselling, consent taking, discuss breast reconstruction

2. Wide excision (breast-conserving surgery; standard of care)

- Removal of tumour with clear margins, while achieving good cosmetic result
- Criteria: [Nodal status does not influence decision for WE or SM]
1. Only 1 tumour, not multicentric/ multiple DCIS/ LCIS (multifocal) unless same quadrant
2. No metastatic disease
3. Appropriate tumour size-to-breast ratio (to achieve good cosmetic result) - not about T staging anymore
4. Previously conserved breast
5. Patient must agree to post-operative radiotherapy (daily RT in hosp)
6. No CI to RT
a. not PREGNANT (the only absolute CI)
b. No CTD –underlying inflammation may get worse
c. No previous RT to the chest
- Results: 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)
- Higher risk in younger patients as cancer tends to be more aggressive

191
2. Simple mastectomy (if any CI to Wide excision)
Other forms of mastectomy (modified
- Removal of breast tissue, nipple-areolar complex, and overlying skin raical, radical or extended radical
- Ind mastectomy) are not performed anymore.
1. CI to wide excision
2. Patient prefers to remove entire breast
3. Need to remove nipple (WE cannot give good cosmesis)
- Lower rates of local recurrence; similar long term prognosis as WE (Italian trial)
- If done for DCIS, dont need to give adjuvant therapy

3. Axillary clearance

- Purpose of removal: NODAL STAGING (for prognostication) - does not confer survival benefit
- Routinely be done in (1) Clinically palpable LN / detected on US (2) BrCA >/= T2 (5cm)
- Not required for DCIS (theoretically cancer cells are confined to the breast) if diagnosed on excision biopsy / wide
excision. Recommended if diagnosed on Core biopsy (sampling error).
- Complications: see below
- Sentinel lymph node (SLN) biopsy (SLN) is a new standard of care
Only in Early CA (</= 5cm)
Principle: the sentinel lymph node, being the first lymph node draining the breast, 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 as well
o Solitary internal mammary LAD is rare
Use of blue dye (isosulphan blue, methylene blue) or radioactive isotope (Tc-99 sulphur colloid or colloidal albumin)
injected in the area of the breast just before surgery concentrates in the first lymph node (sentinel node) that drains
the breast after 5mins
During the op, look for the SLN by colour, or using a Geiger-Muller counter to detect the node with highest
radioactivity. Send node for frozen section (FS)
If -ve do not clear axilla; if +ve, perform axillary clearance
False –ve rate of SLN Bx <5%; false –ve rate of FS ~ 33% if so, re-explore if histology +ve and do AC
No difference in axillary recurrence between AC vs SLN biopsy

4. Palliative surgery

- Palliative mastectomy for symptoms (bleeding, fungating, infected tumour) - 'toilet mastectomy'
- Surgery at other sites:
Fixation of pathological fractures,
decompression of spinal cord compression,
surgical excision of brain metastases

5. Breast reconstruction

- Safe, can be done during breast surgery or at a later time

- No delay in subsequent treatment and no increase in rates of relapse
- Cx: abnormal sensation of breast, unable to breastfeed
- Options:
(i) Prosthesis – 6 wks post-op
(ii) Muscle flap from rectus abdominis or latissimus dorsi

Complications of surgery

Early Haemorrhage (POD1)

Wound Infection (POD3)
Seroma formation (accumulation of serum) in 50%
Flap ischemia
Late 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 vs staphstrep
- Shoulder stiffness – require physiotherapy
- Intercostobrachial nerve transection – numbness over inner aspect of arm.

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 Radiotherapy

1. Adjuvant: to decrease local recurrence rate

- (a) Usually done 6/52 after WE
- (b) High risk of local recurrence: >/= 5cm OR >/= 4 LN +ve
- Targeted at Breast with or without internal mammary, infra/supraclavicular LN (Axillary LN are tackled during Surgery)
- CI: pregnancy, previous RT, patient choice
- 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)
- Cx: radiation injury (e.g. pneumonitis, skin changes), risk of cancers 1 in 2000 in 20yrs

2. Palliative
- Brain mets
- Bone mets to painful areas / impending fractures

Chemotherapy (polyCT with 3 drugs is better; 4-6cycles, each over 1/12) - Main purpose: eliminate micrometastasis!

1. Neoadjuvant
(a) Given in Locally advanced breast cancer (stage III) to shrink the tumour before surgical resection
(b) To shrink tumors before breast conserving Sx
- 20% achieve complete clinical response (cCR) i.e. tumour is no longer palpable
further 20% will achieve complete pathological response (cPR) i.e. no more tumour cells = good prognosis
- Place clip into tumour before neoadjuvant therapy to guide surgery in case tumour  “disappears”;;  operate  according  to preop staging
- Cx: as for CT drug, e.g. mouth ulcers, N/V, hair loss, immunosuppression (main disadvantage pre-op)

2. Adjuvant
- Start 3/52 after surgery; given in stage III / LABC (LN+ve) & in some early breast cancers depending on stage (see below)
- 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: AC (anthracycline, cyclophosphamide), FAC (5-FU, anthracycline, cyclophosphamide), CMF (cyclophos,
methotrexate, 5-FU)

3. Palliative
- Anthracyclines and taxanes are the mainstay
- Helps to reduce load of disease to alleviate symptoms, increase survival

Hormonal therapy

- Used in adjuvant setting to eradicate micrometasis (likewise with CT & TT)

- For ER/PR +ve will have 90% response
- Preferred for postmenopausal women as response to hormonal therapy is better
- May render patient postmenopausal for better response to HT via medical ablation with LHRH-a or surgical oopherectomy
- Mostly used as adjuvant therapy but can also be used as palliative treatment & preventive treatment in high risk patients
- Also reduces risk in contralateral breast

(a) Selective oestrogen receptor modulators (SERMs): Tamoxifen

- 50% reduction in recurrence, 25% reduction in mortality
- taken daily for 5 years
- CI: PHx of CVA/DVT, immobile patients
- Side effects: 1. menopausal symptoms (hot flushes, etc),
2. endometrial cancer (0.1% per year),
3. deep vein thrombosis

(b) Aromatase inhibitors: Lanastrazole, letrozole, exemestase

- 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: 1. musculoskeletal pain,
2. 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: 1. cardiomyopathy & CCF
2. pulmonary toxicity,
3. infusion reactions,
4. febrile neutropaenia
- Avastin (or bevacizumab, targets vascular endothelial growth factor [VEGF] receptor, used in advanced cancer);
- Lapatinib (targets Her-1 and Her-2, used in advanced cancers)

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TREATMENT BY TUMOUR STAGE

Tumour can be divided into

1. in-situ cancer, early BC, locally advanced BC curative intention
2. Advanced BC palliative intention

1. DCIS
- Same Tx as invasive carcinoma: WE vs SM
- Sentinel LN biopsy if DCIS not very certain (ie diagnosed on Core biopsy)
- ± hormonal therapy (only if WE) to reduce recurrence at surgical site; tamoxifen reduces overall breast cancer risk by
50% in both breast not adjuvant therapy

2. Early breast cancer (stage 1 &2)

- T2 or less (<5cm), N1 or less (no nodes or non-fixed nodes)
- Locoregional therapy: SMAC, or WEAC with postop RT
- Adjuvant therapy
Purpose of adjuvant therapy is to destroy systemic micrometastases
Likelihood of patient having micromets is deduced from T and N stage (major prognostic factors):

Chemo Intermediate No chemo

T >20mm, N stage 11mm < T < 20mm, N=0 T <10mm, N=0

>1
Look at histological grade
(minor prognostic factor); if
high grade chemo

Adjuvant therapy: CT if tolerable and/or HT if ER/PR +ve

In general: In premenopausal pt chemotherapy + hormonal
In postmenopausal pt hormonal + chemotherapy

3. Locally advanced breast cancer (stage 3)

- T3 or T4 (tumour >5cm or skin/chest wall involvement), N2 or N3 (fixed lymph node involvement or supraclavicular node
involvement)
- Surgical resection dependent on size of tumour and resectability (if tumour is too large, the skin defect will be very large
inoperable)
- Systemic therapy:
Neoadjuvant chemo to (1) downstage inoperable tumour (in addition, it helps by predicting the tumour response to
chemotherapy before resection) and (2) eliminate micrometastasis
Adjuvant therapy after resection – CT & HT (depends on the histology etc after surgery, ie does patient still require
adj tx) Usually not done if patient has completed the course of chemo during neoadjuvant.

4. Advanced breast cancer (stage 4) - aim for dz control

- Distant metastases: treat symptoms and prevent potential problems
- Minimal locoregional therapy except for palliative purposes (new study shows that removing primary in metastatic BrCA
confers survival benefit)
- Systemic therapy is the mainstay of treatment – CT, HT or TT (to prevent worsening of mets)
- Mets specific:
1. Bone: RT to painful areas, Fixation/RT to impending fractures, Decompression if cord compression
Treat hypercalcemia from mets
2. Brain: RT
3. Pleural: drain effusion
4. Liver (usually liver failure > obstructive jaundice)

FOLLOW-UP
- symptoms + P/E
- 3-monthly for first 2 years
- 6-monthly for the next 3 years (i.e. third to fifth years)
- Yearly for another 5 years (to tenth year)
- MMG: same breast 1yr postop; then 2-yrly bilateral mammo for life (previous BC is a strong Risk factor for future Breast cancer)
- CEA and CA15-3 are used in some centres for trending

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 BREAST SCREENING

Normal risk, 40-49 YO Annual mammogram

asymptomatic 50-64 YO Biannual mammogram (by invitation)
>65 YO Optional 2 yrly mammogram

Increased risk Start screening 5 yrs before Monthly BSE

onset of breast dz in youngest 6 mthly CBE & U/S breast
family member Annual mammography

HRT therapy 40-49 YO Annual mammogram

50-65 YO Biannual mammogram up to 5 yrs after cessation of HRT

6. PAGET’S  DISEASE  OF  THE  NIPPLE

- Presents as erythema and eczematous change of the nipple (not the areola) with crusting exudates, may develop into erosions
and ulcerations
- Often associated with intraductal carcinoma (DCIS) or invasive carcinoma just beneath the nipple
- Malignant cells invade across the epithelial-epidermal junction and enter the epidermis of the nipple, breaking the normal
epidermal barrier thus allowing fluid to be extruded onto the nipple
- Examination and investigations should be targeted towards detecting an underlying tumour – may find a palpable mass and/or
mammographic abnormalities
- Punch biopsy of the nipple may be required
- Prognosis  of  the  underlying  cancer  is  not  altered  by  the  presence  of  Paget’s  disease  of  the  nipple
- Treatment should be planned according to the underlying cancer if found
- If no palpable mass or mammographic abnormality is detected, wide excision is an adequate treatment

7. GYNAECOMASTIA

- Causes:
- Physiological: puberty (maybe painful)
- Drugs:
Recreational drugs
Cimetidine (H2 blockers)
Digosin
Spironolactone
Antimicrobials (Isoniazid, ketoconazole)
- Endocrine disorders:
Thyroid disorders
Acromegaly
Hypogonadism  (testicular  atrophy,  Klinefelters’  syndrome)
- Malignancy: testicular tumours, lymphomas
- Chronic liver disease: cirrhosis

- Investigation:
- TFT, testosterone/ LH
- LFT,  α-FP, ß-HCG

- Treatment
- Conservative management
- Surgical excision

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13. NECK MASSES

1. 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

- Masses in the neck can be subdivided according to the triangle they occur in as there are pathologies peculiar to each triangle
- Locations: (i) Midline
(ii) Anterior triangle
(iii) Posterior triangle
- In general, enlarged lymph nodes are the most common cause of a lump in the neck, regardless of location

MASSES BY LOCATION

Midline (5)
Approach:
1. Submental lymph node
2. Thyroglossal cyst - Does it move with swallowing – divides the thyroglossal cyst and
3. Thyroid nodule in the isthmus thyroid nodule from the other causes
4. Sublingual dermoid cyst - If it moves with swallowing, does it move with tongue protrusion –
5. Plunging ranula (retention cyst of the sublingual) thyroglossal cyst moves with protrusion but a thyroid nodule does not
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 glass-blowers)

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

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2. 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.
75% are in the midline while 25% are slightly to the left or right.
Usually asymptomatic but may become infected.

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!)

3. DERMOID CYST

Pathology:
Can be congenital or acquired.
(i) 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
(ii) 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).

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.

4. PLUNGING RANULA

Pathology:
A pseudocyst associated with the
sublingual glands and submandibular ducts.
Ranulas (frog mouth) can be congenital or
acquired after oral trauma.

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.

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5. BRANCHIAL CYST/FISTULA

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

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  Bonney’s  blue  dye  into  tract  prior  to  surgery  to  allow  accurate  surgical  excision.
- Treatment of infection with antibiotics.
- Complications: cyst recurrence; chronic discharging sinus.

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6. CHEMODECTOMA

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).

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   Horner’s   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.

Treatment:
- Surgical excision with pre-operative embolisation (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.

7. PHARYNGEAL POUCH

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

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)

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8. CYSTIC HYGROMA

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:
- 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

9. CERVICAL RIB

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
- Adson’s   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
- Diagnosis by CXR

10. 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  Tinnel’s  positive  – tap on the mass for any paraesthesia occurring in distribution of the nerve
- DO NOT PERFORM FNA – excruciatingly painful

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11. CERVICAL LYMPHADENOPATHY

There are six levels of lymph nodes in the neck, and different structures drain to different groups of nodes:
Level 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)

CAUSES:
1. Cancer (3): SCC, NPC, Adenocarcinoma
2. Lymphoma
3. TB

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

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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

PHYSICAL EXAMINATION

Inspection
- 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”
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.

- Tenderness to palpation
- Consistency – hard, matted nodes are more suspicious for malignancy
- 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

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)

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, bronscopy
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

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14. SALIVARY GLAND SWELLINGS

1. 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:
(i) Facial nerve and its branches
(ii) Retromandibular vein (formed as the maxillary veins drain into the superficial temporal vein)
(iii) External carotid artery (branching into its two terminal branches, the superficial temporal and maxillary arteries)
- Nerve supply:
(i) Parasympathetic secretomotor supply from auriculotemporal nerve carrying postganglionic fibres from the otic ganglion (preganglionic
fibres from inferior salivary nucleus);
(ii) 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)

2. ANATOMY OF THE SUBMANDIBULAR GLAND

- 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

3. 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

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4. APPROACH TO SALIVARY GLAND SWELLINGS

HISTORY

- About the lump: onset, duration, progress, associated symptoms e.g. pain
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  patient’s  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, and lifts the earlobe if large;
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  patient’s  face  for  asymmetry (facial nerve palsy)

“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 of overlying skin, 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

Other tests

1. Examination of the duct openings:

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)
Look for (1) red inflamed opening, (2) discharge-purulent, (3) visible stone.
For the parotid duct, can palpate the duct along the masseter for stone, and look for discharge inside the
mouth while palpating
2. Tonsillar fossa: enlargement of deep lobe of the parotid (in retropharyngeal space) pushes tonsils and archs aside see
asymmetry of the arches
3. Palpate the gland openings for stones.
4. Bimanual palpation of the submandibular gland
5. 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

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

204
 CAUSES OF SWELLING OF THE PAROTID

Parenchymal Neoplasia Benign

swelling - pleomorphic adenoma
- Warthin’s  (10% bilateral)
Malignant tumours
Lymphoma and leukaemia: bilateral
Stones Sialolithasis
Infection/ Mumps: bilateral
Inflammation Acute sialadenitis
Chronic recurrent sialadenitis
HIV
Autoimmune Sjogren’s  syndrome:  bilateral
Infiltration Sarcoidosis: bilateral
Systemic Alcoholic liver disease
disease: Diabetes mellitus
bilateral Pancreatitis
Acromegaly
(MADMAP) Malnutrition
Non- Lymph node
parenchymal Facial neuroma
swelling Temporal artery aneurysm
Skin and soft tissue swellings e.g. sebaceous cyst, lipoma

INVESTIGATIONS

- FNAC: malign vs benign

- CT: confirm salivary gland (vs LN)
o esp parotid – multiple swelling likely LN (DDx Warthin)

5. 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
radio-opaque.

Presentation
- Complete obstruction
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
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

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.)

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

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6. SALIVARY GLAND TUMOURS

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
Epithelial Non-epithelial
Adenomas (benign) Carcinomas (malignant)
Pleomorphic adenoma Adenoid cystic ca Haemangioma
Warthin’s  tumour Pleomorphic adenoca Lymphangioma
Mucoepidermoid ca Neurofibroma
Acinic cell ca Neurilemmoma
Adenoca Lipoma
Squamous cell ca Sarcoma
Undifferentiated Malignant lymphoma

PLEOMORPHIC ADENOMA

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  Warthin’s)
- 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

WARTHIN’S  TUMOUR AKA PAPILLARY CYSTADENOMA LYMPHOMATOSUM / ADENOLYMPHOMA

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

Histology:
Consists of cleftlike 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  Warthin’s  tumour  cells,  since  there  is  no  malignant  potential
- Superficial parotidectomy if causing trouble to patient

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MALIGNANT TUMOURS

Tumor grade
Nerve involvement

Most common malignancies

1. Mucoepidermoid (34%) - most common malignant tumour in the parotid. Younger patients.
2. 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.
3. 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

TREATMENT OF SALIVARY GLAND CANCERS

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 – cos may have spread to nerves)

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)

1. 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)
2. Reactionary haemorrhage: early post-op bleeding due to displacement of a clot in a BV / slippage of a ligature

Early (1 to 30 days)

1. Wound infection
2. Skin flap necrosis
3. Temporary facial weakness (neuropraxia of facial nerve)
4. Salivary fistula
5. Division of great auricular nerve loss of sensation over pinna
6. Trismus (inability to open mouth due to spasm of masseter)

Late (more than 30 days)

1. Wound dimple, cosmetic problems

2. Hyperaesthesia of local skin
3. Frey’s  syndrome (gustatory sweating syndrome / auriculotemporal syndrome)
a. Increased sweating and redness of facial skin when eating
b. Auriculotemp nerve: symp branches (sweat glands of the scalp), parasympathetic branches (parotid gland secretion)
c. due to reinnervation of divided sympathetic nerves to the facial skin sweat glands by fibres of the secretomotor branch
of the auriculotemporal nerve

207
15. THYROID DISEASES

1. ANATOMY OF THE THYROID GLAND

Structure:
2 lateral lobes joined by an isthmus that lies in front of the 2nd, 3rd and 4th tracheal rings.
Strap muscles of the neck lie superficial to the thyroid gland.

Nerves and vessels:

Superior thyroid artery (from external carotid)
Inferior thyroid artery (from thyrocervical trunk, a branch of the first part of the subclavian artery).
External laryngeal nerve – supplies the cricothyroid muscle which controls pitch of voice; runs close to superior thyroid artery.
Recurrently laryngeal nerve – supplies all the other intrinsic muscles of the larynx (except for cricothyroid) and runs close to
the branches of the inferior thyroid. The nerve runs behind the pretracheal fascia and so will not be damaged if the fascia is
not breached during operation. Important to visualise nerve and avoid damaging it!

Embryonic origin:
Thyroglossal tract from foramen caecum of the tongue (in the midline, at the junction between anterior two-thirds and posterior
one-third of the tongue) descends close to the hyoid bone expansion of the caudal end of the tract forms the thyroid gland.

Parathyroid glands: 2 superior and 2 inferior glands that lie behind the lateral lobes.

Level VI lymph nodes – first nodes that a thyroid malignancy spreads to; they lie in the tracheo-oesophageal groove and are not
palpable.

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2. APPROACH TO THYROID PROBLEMS

1. Problem with configuration/anatomy

(i) Solitary thyroid nodule (most common in exam)
(ii) Multinodular goitre
(iii) Diffuse enlargement

2. Problem with function (usually hyperfunctioning)

(i) Graves’  disease
(ii) Toxic adenoma
(iii) Toxic multinodular goitre
(iv) Hashimoto’s  disease

AIMS OF ASSESSMENT IN THYROID NODULE/ENLARGEMENT:

- Exclude cancer!
- Address issues of thyroid function
- Look for any complications e.g. compression (of airway, oesophagus, rarely nerve)
- Cosmesis – is patient bothered by lump?

HISTORY-TAKING

About the LUMP

- Onset (gradual or sudden), duration
- Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth; ddx includes haemorrhage into
necrotic nodule or cyst, subacute thyroiditis)
- Any pain – bleeding into cyst can result in sudden increase in size and pain; rarely pain can occur in anaplastic carcinoma and
thyroiditis
- Compressive symptoms: difficulty swallowing, difficulty breathing, hoarseness of voice (benign pathologies almost never
compress the recurrent laryngeal nerve)
- Cosmetic effects

About THYROID FUNCTION

Hyperthyroid Hypothyroid
Weight loss despite increased appetite Decreased appetite, weight gain, lethargy
Heat intolerance Cold intolerance
Increased sweating Dry skin, loss of outer third of eyebrows
Proximal  myopathy  (Graves’) Muscle fatigue
Diarrhoea, frequent bowel movement Constipation
Tachycardia, atrial fibrillation Bradycardia
Oligomenorrhoea, amenorrhoea Menorrhagia
Nervousness; easily irritable; emotional Slow thought, speech and action;
lability; insomnia depression; dementia
Fine tremor Carpal tunnel syndrome symptoms

About RISK FACTORS

- History of autoimmune disease e.g.  type  I  DM,  SLE,  RA,  pernicious  anaemia  (associations  with  Graves  and  Hashimoto’s)
- History of cancer elsewhere – metastatic disease to thyroid; lymphoma; papillary cancer is associated with familial polyposis
syndromes ask about GI polyps/ca
- History of thyroid disease – long-standing MNG can progress to lymphoma
- Occupational history – any exposure to radiation (papillary cancer risk)
- Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2, AD inheritance), ~5% of papillary cancers

About previous TREATMENT for any thyroid disease

- Medications given e.g. propylthiouracil, carbimazole, propranolol – for how long, efficacy, side effects
- Radioactive iodine treatment – what was the result? Is the patient receiving replacement?
- Surgery – what kind of surgery, any complications?
- Follow-up – what investigations done?

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PHYSICAL EXAMINATION

A. THYROID GLAND

GREET PATIENT, ASK FOR PERMISSION to examine (and listen to the voice – is it hoarse?)
POSITION PATIENT – on a chair with space behind the chair for you to stand.

INSPECT FROM THE FRONT

1. Any swelling? Where is it? (if unable to see, ask patient to swallow)
2. Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a skin crease)? Sinuses?
3. Any skin changes over the mass?
4. Check if mass moves on swallowing by asking patient to take a sip of water – “Please  take  a  sip  of  water  and  hold  it  in  your  
mouth,  do  not  swallow  until  I  tell  you  to.”
5. Check if mass moves on protruding the tongue – “Please  open  your  jaw  slightly.  Now,  without  moving  your  jaw,  please  stick  
your  tongue  out  and  back  in  again.”
NB. A thyroid lump moves only on swallowing; a thyroglossal cyst will move on both swallowing & protrusion of the tongue.
6. Check for plethora of face, distended neck veins – may be due to compressive nature of mass (but rarely seen).

PALPATE FROM BEHIND – one side at a time, the opposite hand stabilises the gland.
Ask for pain before palpating!

1. Characteristics of lump: site (anterior triangle), size (discrete nodule or multinodular enlargement or diffuse enlargement?),
consistency (soft, cystic, hard, multinodular?), mobility (fixed to skin? Fixed to underlying structures?), tenderness.
2. Check swallowing while palpating to confirm mass moves on swallowing.
3. Check tongue protrusion.
4. Palpate lymph nodes

PALPATE TRACHEA from in front for tracheal deviation.

PERCUSS – any retrosternal extension?
AUSCULTATE – bruit in Graves’

OFFER to do Pemberton’s sign to check for thoracic inlet obstruction; check thyroid status; ask patient about compressive
symptoms.

B. THYROID STATUS

HANDS (get patient to stretch arms out in front of him, palms down)

1. Feel palms – warm sweaty palms

2. Nails – thyroid acropachy, onycholysis (both  seen  in  Graves’)
3. Feel pulse – tachycardia, atrial fibrillation (AF  more  in  toxic  MNG  than  Graves’)
4. Fine postural tremor – accentuate by placing a sheet of paper on the hands
5. Palms up – palmar erythema

FACE

1. Expression – staring, unblinking (hyperthyroid); lethargic, apathetic (hypothyroid)

2. Complexion – dry,  ‘peaches-and-cream’  complexion,  loss  of  outer  third  of  eyebrows  (hypothyroid)
3. Eyes
- Lid retraction (can see sclera between upper limbus of iris and upper eyelid)
- Exophthalmos (sclera between lower limbus and lower eyelid)
- Chemosis (oedema and erythema of conjunctiva)
- Ophthalmoplegia (restriction of eye movements; ask about diplopia!)
- Lid lag (eyelid lags behind eye when patient follows your finger downwards)
- Proptosis (look  from  above  patient’s  head  – eye visible over supraorbital ridge)

NEUROMUSCULAR

1. Proximal myopathy (Graves’)

2. Reflexes – slow to relax in hypothyroidism
3. Legs for pretibial non-pitting oedema (Graves’  or  hypothyroid)

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3. APPROACH TO THE SOLITARY THYROID NODULE

Prevalence: About 4-8% of population in US have palpable thyroid nodules; prevalence in Singapore not known.

Differential diagnoses: Clinical features suspicious of malignancy:

1. Cancer (only 10-20% of nodules is malignant,
but need to exclude!)
2. Follicular adenoma
3. Cyst (simple, colloid, or haemorrhagic)
4. Dominant nodule of a multinodular goitre
1. Male gender (thyroid nodules less common in male but more likely to be malignant)
2. Age <15yrs or >60yrs (majority of nodules occurs in 3rd to 6th decades – likely benign)
3. History of head and neck radiation or thyroiditis
4. Family history of  thyroid  cancer  (or  MEN2,  Gardner’s  syndrome,  FAP)
5. Rapidly enlarging nodule
6. Hard, single nodule and/or nodules fixed to surrounding structures
7. Hoarseness (i.e. recurrent laryngeal nerve invasion)
8. Cervical lymphadenopathy
9. Other symptoms of invasion e.g. haemoptysis, stridor, dysphagia

INVESTIGATIONS

1. FINE NEEDLE ASPIRATION CYTOLOGY - The most important investigation modality!

- 90-95% sensitivity and specificity
- 4 possible results:
(i) Benign (thyroiditis, dominant nodule of MNG)
(ii) Malignant (papillary, medullary, anaplastic, mets)
(iii) Suspicious (follicular, Hurthle cell change in follicular lesion)
(iv) Inadequate repeat FNAC
- Can be both therapeutic and diagnostic for cyst – chocolate-brown fluid aspirated; feel lump after aspiration to check for resolution
- Cannot differentiate follicular adenoma from follicular carcinoma as the mark of malignant disease is capsular invasion – can only tell from a
histological specimen of the nodule
- Procedure: inject local anaesthetic in area, insert 20-22G needle and apply suction while fanning needle in region of nodule, release suction
before pulling out needle, expel contents onto slide, then fix
- Best to have experienced cytologist on hand to view slides and re-do FNAC if the sample is inadequate

2. ULTRASOUND OF THYROID
- Advantages:
(i) Objective measurement of nodule
(ii) Detection of subclinical nodule/screening – of value in papillary carcinoma since multicentric disease occurs in 15%
(iii) Detection of lymph node enlargement (especially level VI nodes)
(iv) Can define consistency of nodule – solid, cystic, or complex
- Suspicious sonographic features:
(i) Microcalcifications (in psammoma bodies papillary cancer)
(ii) Indistinct margins
(iii) Sonolucent halo around lesion
(iv) Hypoechoeic or anechoeic lesion – carcinoma is almost never hyperechoeic
(v) Increased intranodular vascularity
- Ultrasound still does not provide as good diagnostic value as FNAC

3. THYROID FUNCTION TEST

- Easy to perform, establish baseline, detect any abnormal function
- No real diagnostic value

4. RADIO-ISOTOPE SCAN
- Hot nodule: only 1% malignant; but cold nodule: 10-20% malignant
- But not very useful diagnostically

5. BASELINE TUMOUR MARKERS (IF SUSPECTED OR CONFIRMED MALIGNANCY)

- For differentiated thyroid cancer: thyroglobulin
- For medullary thyroid cancer: calcitonin, carcinoembryonic antigen (CEA)

6. CT SCAN OR MRI
- Not routine in thyroid nodular study
- Uses: (i) Evaluating invasion of surrounding structures
(ii) Retrosternal extension
(iii) Lymph node involvement
- Care to be taken with CT as contrast contains iodine and will affect post-op radioactive iodine body scan once given
- MRI has same functions as CT but higher cost

7. ENT EXAMINATION OF VOCAL CORDS

- In the rare occasion that there is pre-existing vocal cord palsy on one side take extra care not to injure opposite recurrent laryngeal nerve as
that can cause bilateral vocal cord palsy

MANAGEMENT OF BENIGN NODULE

- Soft, small, round nodule with benign FNAC results, non-functional, not causing any symptoms can follow-up and monitor for in size
- A lump >4cm has a greater risk for malignancy

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4. THYROID CANCERS

Differentiated thyroid carcinoma Anaplastic

Medullary carcinoma Lymphoma
Papillary carcinoma Follicular carcinoma carcinoma
Proportion 75% 10% 7% 3% 5%
Age >50 yrs for sporadic type;
25-40 years 40-50 years 60-70 years >50 years
20-30 years for familial
F:M ratio 3:1 3:1 1:1 3:2 2:1
Risk factors - Radiation exposure - Follicular adenoma - Significant family history in the - Longstanding - History of
- Polyposis is NOT a risk factor familial type – MEN2 (AD, goitre lymphoma
syndromes (FAP, - Iodine deficiency complete penetrance, associated - History of or MALT
Gardner’s,  etc) may be associated with parathyroid adenoma and previous elsewhere
- Positive family phaeochromocytoma – see notes differentiated - Hashimoto’s
history in 5% below) thyroid ca thyroiditis
(30% of (60X
anaplastic ca) increased
risk)
Pathological - Characteristic - Follicular structures - Arise from parafollicular C cells - Small blue - FNAC may
features Orphan Annie similar to normal (which produce calcitonin) round cells suggest
nuclei, nuclear thyroid - Distinctive deposits of acellular that are highly lymphoma
pseudoinclusions - Diagnosis of cancer amyloid material – altered anaplastic – but definitive
- Papillary made on evidence calcitonin collections may resemble diagnosis
architecture with of capsular or - Multicentric C-cell hyperplasia may lymphoma requires
psammoma bodies vascular invasion be seen in familial cases trucut or
- Tall cell variant by tumour cells (vs excision
(nuclear features of follicular adenoma) biopsy
papillary ca within - Hurthle cell variant – - Almost
follicular lesion) worse prognosis always non-
behaves like Hodgkin’s of
papillary ca, has B-cell type
worse prognosis
Clinical - Slow-growing - Solitary - Sporadic cases usually solitary, - Large bulky - Usually
features tumour - Haematologic worse prognosis mass involving presents as
- Spread by spread to bone, - Familial cases all multicentric, neck rapidly
lymphatics lung, liver, brain better prognosis structures – enlarging
- 30-50% multicentric - LN involvement in - Aggressive growth; spread via locally goitre with
- LN involvement in 10% (rare) local, lymphatic, haematological advanced compressive
80% of disease at routes - Aggressive symptoms
diagnosis (level VI - 95% produce calcitonin, 80% growth - 60-80%
first) produce CEA - Multiple aggressive
- Very good prognosis - Unilat LN involved in 60-80%, metastases and 30%
- Poor prognostic factors (AMES): Age>40, contralat LN in 40% probably more
presence of metastases, extra-thyroid invasion, - Always exclude MEN2 – serum present at indolent
size>4cm (more details on risk stratification below) calcium, 24hr urinary presentation
catecholamines
Treatment Surgical resection Surgical resection Palliative therapy for Chemotherapy
- Hemithyroidectomy for selected low-risk patients - Aggressive resection – total compressive effects and/or
(see below) thyroidectomy with level VI node - Chemotherapy radiotherapy
- Total thyroidectomy for the majority clearance to shrink depending on type
- LN clearance: tracheo-oesophageal nodes - Sampling of cervical and tumour of lymphoma
cleared, and neck dissection if neck nodes are mediastinal nodes and modified - Surgical
positive dissection where positive debulking
- For suspicious lesion – hemithyroidectomy with - Tracheostomy
histology, KIV TT No good adjuvant therapy

Adjuvant therapy Follow-up

- Radioactive iodine at ablative levels to ablate - Thyroxine replacement (not for
remnant thyroid and any cancer tissue (only for TSH suppression but to maintain
total thyroidectomy) euthyroid state)
- External radiotherapy (only shown to have good - Serum calcitonin and CEA six
results in pts with locally advanced follicular ca) mths after surgery (if normal,
considered cured – 5% 5yr
TSH suppression – give L-thyroxine to suppress recurrence)
TSH levels to <0.005U/L - High calcitonin – screen for
residual or metastatic disease,
Follow-up treat surgically, with RT or chemo
- Check TSH levels as appropriate
- 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, 60-70% Median survival Dependent on
50% in high-risk pts <6mths histo, stage,
Slightly worse for follicular ca treatment, etc.

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RISK STRATIFICATION:
- Risk factors can be divided into patient factors and disease factors

- Patient factors: Age – >45 years old is high risk; Gender – male is high risk

- Tumour factors:
Size – nodule >4cm has higher risk
Histology – tall cell variant of papillary ca and Hurthle cell variant of follicular ca are considered unfavourable
Extrathyroidal extension into surrounding structures – worse
Lymph node or distant metastases – worse

- Various score systems have been formulated to stratify risk:

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:

(i) Low risk – low risk patient and low risk disease (i.e. no high risk features)
(ii) Intermediate risk – low risk patient with high risk disease, or high risk patient with low risk disease
(iii) 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%

TOTAL THYROIDECTOMY VERSUS HEMITHYROIDECTOMY

Advantages of TT:
- Evidence for microfoci of disease and multicentricity of cancer – removal of the entire thyroid decreases risk of recurrence
- Ability to use adjuvant radioiodine to ablate any residual cancer tissue after surgery
- Ability to use radioiodine to detect recurrent disease (normal thyroid picks up iodine better than cancer cells, thus the presence of the thyroid
gland will decrease the ability of RAI to pick up recurrent cancer) and as treatment for recurrence
- Ability to use serum thyroglobulin as a cancer marker for recurrence

Disadvantages of TT:
- Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism
- Very low incidence of cancer recurrence in residual thyroid – microfoci probably not clinically significant
- Limited thyroidectomy may spare patient from having to be on lifelong thyroid hormone replacement

Risk stratification helps to guide the extent of surgical resection in differentiated thyroid cancer according to  the  patient’s  disease.

Lymph node clearance

- Tracheo-oesophageal groove (level VI) node clearance usually done

- Radical neck dissection or modified radical neck if:
(i) Tracheo-oesophageal groove nodes histologically positive for cancer
(ii) 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 (Crile’s) – internal jugular vein, sternocleido-mastoid muscle, and accessory nerve are resected.
Structures not resected: carotid arteries, vagus nerve, hypoglossal nerve, brachial plexus, phrenic nerve
- Modified radical neck
(i) Type I: one of the three structures not removed, usually accessory nerve
(ii) Type II: two of the structures not removed – accessory and IJV
(iii) Type III: all of the three structures not removed
(iv) Extended radical neck dissection: resection of lymph nodes and/or structures not included in the classic neck dissection
- Complications of radical neck dissection:
(i) Injury to nerves – vagus  (vocal  cord  paralysis),  cervical  sympathetic  chain  (Horner’s),  mandibular  branch  of  facial (lower lip weakness)
(ii) Haematoma bring back to OT to find source of bleeding and stop it
(iii) 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
(iv) Wound infection – risk factors: previous irradiation, if upper aerodigestive tract is opened during surgery with salivary contamination,
salivary fistula
(v) Carotid blowout – risk factors: infection, irradiation resus, apply constant pressure all the way to the OT!
(vi) Poor healing – usually in irradiated skin; weakest point is the junction of the trifurcate incision

213
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  P’s:  
Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands
Pancreas (>40%) – aggressive metastatic tumours (e.g. gastrinoma, insulinoma), leading cause of death in MEN 1 patients
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:

1. MEN 2a (Sipple syndrome)

Medullary carcinoma of the thyroid (almost all)
Phaeochromocytoma (50%, of which less than 10% are malignant)
Parathyroid hyperplasia and hyperparathyroidism (30%)

2. MEN 2b (William syndrome)

Thyroid and adrenal involvement like MEN 2a, but no hyperparathyroidism
Neurocutaneous manifestations: ganglioneuromas on oral mucosa, lips eyelids
Other features: Marfanoid habitus, SCFE, delayed puberty

214
5. SURGERY IN BENIGN THYROID DISEASE

Indications for surgery:

1. Cannot be treated medically - failed medical therapy or unsuitable for medical tx
2. Cancer
3. Compression on neighbouring structures
4. Cosmesis
5. 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)
6. Child-bearing (not a very strong indication since medical therapy can still be given, but not RAI)

Types of surgery available:

1. Hemithyroidectomy – removal of one lobe of the gland, including the isthmus and the pyramidal lobe; usually for suspicious thyroid nodules
2. Total thyroidectomy – entire gland removed completely; usually done in MNG
3. Subtotal thyroidectomy
- Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides
- 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)

Complications of thyroid surgery: (Mostly  H’s,  one  I  and  one  T)

IMMEDIATE (<24HRS)

1. Haemorrhage with haematoma formation

- Haematoma forms in the paratracheal region, mostly below the strap muscles compression of airway if not released (patient can die!)
- Cut the subcuticular stitches and also the stitches holding the strap muscles opposed to let the blood drain out

2. Hoarseness or airway compromise from recurrent laryngeal nerve injury

- Risk of nerve injury is <1%
- Unilateral nerve injury for hemithyroidectomy, bilateral nerve injury for total or subtotal thyroidectomy
- If bilateral nerve palsy resulting in compromised airway, will require tracheostomy

3. Hyperthyroidism
- Resection of gland can release large amounts of stored thyroid hormone into bloodstream
- May result in thyroid storm (see Management of thyroid storm)

4. Tracheomalacia
- Floppiness of trachea resulting from chronic compression e.g. by large goitre
- Requires intubation to secure airway

INTERMEDIATE (1 DAY TO 1 MTH)

1. Infection

2. Hypoparathyroidism leading to hypocalcaemia

- 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 post-operatively – POD 1,3,5
- Ask patient for any symptoms and look for signs of hypocalcaemia – paraesthesia around the mouth, difficulty breathing, carpopedal spasm,
Chvostek’s  sign (spasm of the facial muscles on tapping the facial nerve), Trousseau’s  sign (carpopedal spasm on inflating BP cuff over arm)
- Dangerous as it can cause laryngeal spasm and airway compromise
- Check serum calcium together with albumin to get corrected calcium!

Measured serum calcium + 0.02 (40 – Albumin)

- Replacement: 5mmol/6h if symptoms mild, 10ml of 10% calcium gluconate over 30 minutes if severe
- Hypocalcaemia  may  also  occur  due  to  “hungry  bone  syndrome”  after  thyroidectomy  in  long-standing thyrotoxicosis

LATE (MORE THAN 30 DAYS)

1. Hypothyroidism
2. Hyperthyroidism (failed treatment)
3. Permanent hypoparathyroidism
4. Hypertrophic scarring or keloid formation – ask patient if he/she has keloids

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16. PERIPHERAL ARTERIAL DISEASES

1. ANATOMY OF THE 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
- The profunda femoris supplies compartments of the thigh via 2 main branches, the medial & lateral circumflex femoral arteries
- 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
-
- 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)
- 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

PAD is a very powerful predictor of CVD/CAD, and mortality.

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2. ACUTE LIMB ISCHAEMIA

Acute limb ischemia is 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).

The decrease in perfusion is usually due to sudden occlusion of a feeding arterial vessel, and this may be in a setting of already
narrowed vessel lumen (acute on chronic ischaemia) or in a normal lumen.

CAUSES

1. Arterial embolism

- Most common cause of acute limb ischaemia (60-80% of the time)

- The most likely source of embolus is the heart (80%), of which 70% is due to atrial fibrillation, 20% to AMI with left
ventricular mural thrombus, and a small proportion to prosthetic heart valves
- Non-cardiac emboli arise from other arteries where there are atherosclerotic plaques or an aneurysm (the embolic
material may be thrombus or part of a plaque, but atheroemboli are less likely to cause complete arterial occlusion)
- Most common sites where emboli lodge:
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
Arm (about 20% of emboli)
- Emboli usually cause lower limb ischaemia mostly
- After emboli obstructs the vessel, thrombus can propagate distally (due to stasis of blood) and proximally (due to
turbulence  of  incoming  blood  hitting  embolus)  by  derangements  in  the  Virchow’s  triad

2. Acute thrombosis

- Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel)

- Less common cause of acute limb ischaemia
- When thrombotic occlusion of a vessel does occur, the resulting ischaemia is usually less severe than in an embolic
occlusion, because collaterals have had time to form around the chronically stenosed vessel
- Other less common causes of acute thrombosis include the arteritides (usually affecting medium-sized arteries), ergotism,
and hypercoagulable states (notably antiphospholipid syndrome).

3. Arterial trauma

- Increasing incidence of acute arterial occlusion due to endovascular diagnostic or interventional procedures
- Trauma can cause development of an arteriovenous fistula that shunts blood away from the limb
- Fracture or dislocations can stretch an artery and cause an intimal tear while the media and adventitia layers are intact
(because they contain elastin and can stretch) a thrombus forms at the site of the tear where underlying thrombogenic
collagen is exposed
- Compartment syndrome can result from trauma as well

4. Dissecting aortic aneurysm

- As blood dissects between the intima and media of the aorta, it can cause occlusion of the aortic branches at their origins

PATHOPHYSIOLOGY

In order of sensitivity to ischaemia, the tissues affected are nerves (most sensitive), muscle, skin, and bone (least sensitive); thus
early signs of ischaemia involve pain and numbness, and muscle paralysis as well as skin changes occur later. The lower limb
can survive about 6 to 8 hours in an ischaemic state before injury becomes irreversible.

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PRESENTATION

The classic 6 P’s of acute limb ischaemia: Pain, Paraesthesia, Pallor, Pulselessness, Paralysis, Perishingly cold

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

- 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
Black: gangrene
- The disclouration 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, but still possible
- 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 and twitches in response to flicking, while dead
muscle will be dull and will not twitch
- Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites in the muscle

P/E

Search for sources of embolisation:

- Cardiac: AF, murmur (MDM), prosthetic click
- Non-cardiac: AAA? Bruit?

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DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE (IMPT AS THE MANAGEMENT IS DIFFERENT)
-
Embolic Thrombotic
Identifiable source Present – AF, recent AMI Less common
Claudication hx Negative Positive
Physical findings Contralat pulses present Contralat pulses diminished
White limb (no blood) Dusky limb (collaterals still
supplying limb)
Angiography Minimal atherosclerosis, Diffuse atherosclerosis,
sharp cut-off, few collaterals irregular cut-off, well-developed
collaterals

CLASSIFICATION OF SEVERITY (SVS/ISCVS)

Three categories: viable, threatened and non-viable

(i) Viable: No immediate threat of tissue loss
(ii) Threatened: Salvageable if revascularised promptly
(iii) 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
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

Viable Threatened Non-viable

Pain Mild Severe (rest pain) Variable (anaesthesia)
Capillary refill Intact Delayed Absent (fixed stain)
Motor deficit None Partial Complete
Sensory deficit None Partial Complete
Arterial Doppler Audible Inaudible Inaudible
Venous Doppler Audible Audible Inaudible
Treatment Urgent work-up Emergency Amputation
surgery

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ACUTE MANAGEMENT

1. DOPPLER U/S: viable vs threatened vs non-viable + level of obstruction

2. EARLY ANTICOAGULATION
- Important to start anticoagulation with heparin if the suspicion of acute limb ischaemia is high, to avoid clot propogation
- Give IV heparin bolus 3000-5000 units
- Follow with IV heparin infusion at 1000 units/hour
- Ideal PTT is 2 to 2.5 times normal
3. ANALGESIA
4. MEASURES TO IMPROVE EXISTING PERFUSION
- Keep foot dependent
- Avoid pressure to heel, extremes of temp
- Max tissue oxygenation (O2 supp)
- Correct hypotension
5. TREAT OTHER ASSOCIATED CONDITIONS (CHF, AF)

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

DEFINITIVE TREATMENT OPTIONS

Surgical Endovascular
- Embolectomy - Thrombolysis
- Endarterectomy - Angioplasty
- Bypass grafting - Stenting
- Fasciotomy
- Primary amputation
In general, embolectomy is done for embolic occlusion, while thrombolysis is done for thrombotic occlusion.

Embolectomy
- Can be done under LA but still require anaesthetist to monitor patient as he may be quite sick (e.g. AMI), and hyperkalaemia
with cardiac arrhythmia can occur after reperfusion
- Involves clamping of the involved artery and making an arterotomy
- A Fogarty balloon catheter is inserted into artery until distal to the clot, then balloon is inflated to trawl clot out of the artery
- Check for forward-bleeding and back-bleeding of the vessel (i.e. free spontaneous flow from proximal and distal ends of the
artery when unclamped)
- Flush with heparinised saline
- Check foot – warm foot with good pulse indicates reperfusion
- Important to monitor ECG for any arrhythmias!
- Closure of arterotomy with meticulous haemostasis as patient is on heparin
- Post-op: patient monitored in high-dependency; look out for reperfusion injury
The reperfused muscles become oedematous (due to ROS tt injure cells), ing pressure in the compartments of the leg,
like compartment syndrome
Patient complains of calf pain
Unable to dorsiflex ankle as the anterior compartment is affected first
Requires three compartment fasciotomy to release pressure
- Need to convert to full warfarin anticoagulation, uptitrating dose until INR 2-2.5 before stopping heparin (pt at risk of further
embolic events) discharge patient to anticoagulation clinic for follow-up with warfarin advice

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Catheter directed thrombolysis
- Angiogram done before thrombolysis to locate occlusion
- Thrombolysis catheter inserted into the clot, and the thrombolytic agent is infused (Streptokinase, Urokinase, tPA)
- Patient will be in high-dependency with thrombolytic infusion for 6 hours (~1000-4000 units per minute)
- After 6 hrs, redo angiogram to check for residual clot; if some clot remains, adjust catheter into clot and infuse for 6 more hrs
- After complete lysis of the clot, can do angioplasty
- Takes much longer than embolectomy
- Thrombolysis may be preferred for embolism in a diseased artery, since it may be difficult to trawl out the clot in a diffusely
stenosed vessel – the clot may get caught on a proximal stenosed segment
- CI
Absolute
1. CVA within past 2 months
2. Active bleeding / recent BGIT past 10 days
3. Intracranial trauma/ neuroSx past 3 months
Relative
1. CPR past 10 days
2. Major Sx / trauma past 10 days
3. Uncontrolled HTN

Results:
- Embolectomy has a 20% mortality, almost full success rate
- Thrombolysis has a 10% mortality, only 35% successful

DDx:
- Acute DVT: Phlegmasia cerulean dolens = painful blue edema
- Blue toe syndrome: atheroembolism from AAA or more proximal
- Purple toe syndrome: Cx of warfarin therapy
- Venous insufficiency
- Venous occlusion
- Acrocyanosis

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3. CHRONIC LIMB ISCHAEMIA

Chronic limb ischaemia can be divided into critical and non-critical limb ischaemia, and non-critical ischaemia further subdivided into that
which causes symptoms (usually claudication) and that which is asymptomatic.

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.

Progression:

CRITICAL LIMB ISCHAEMIA

Critical limb ischaemia is defined as 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 more than two weeks after the acute event (the converse of the definition of
acute limb ischaemia).

FEATURES:

1. Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks
+/- Tissue loss (Gangrene or ulcers over the toes or feet)

2. 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

I. 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

II. Ischaemic ulcers (most are neuroarteropathic 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

III. 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
- Either dry or wet:
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.

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NON-CRITICAL LIMB ISCHAEMIA WITH CLAUDICATION

Intermittent claudication is defined as a reproducible discomfort of a defined group of muscles that is induced by exercise and relieved with rest.
Usually described as the patient as a cramping, aching pain in the muscle group on exertion such as walking, and alleviated on stopping (patient does
not have to sit down for pain to go away) – “shop  window  to  shop  window”.

- 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 Buerger’s)
- Thigh claudication common femoral artery or aortoiliac disease

- LeRiche’s syndrome arises from occlusion of the aortoiliacs, and is composed of a classical tetrad of buttock claudication, impotence in men,
absent femoral pulses (and distal pulses), and occasionally presence of aortoiliac bruits.
- Determine  “claudication distance”  – within a short period of time it is usu fairly constant, but can shorten as the disease progresses
- Need to differentiate the various causes: vascular vs neurogenic vs musculoskeletal

CAUSES OF VASCULAR CLAUDICATION

- Mainly an atherosclerotic disease; pain is due to acidosis & buildup of metabolites
- Other  less  common  causes:  ergot  toxicity,  Takayasu’s  arteritis,  Buerger’s  disease  (thromboangiitis  obliterans),  vasospasm

DDX NEUROGENIC CLAUDICATION!!!

Vascular intermittent claudication needs to be differentiated from neurogenic claudication (can also present as pain in the lower limb on exertion)
The characteristic of neurogenic claudication is “park  bench  to  park  bench”
1. patient has to sit down and flex the spine to relieve the pain (pain results from compression of the cord and spinal nerves in spinal stenosis;
extension of the spine further narrows the spinal canal while flexion widens it)
2. “Claudication  distance”  of  neurogenic claudication is more variable
3. Pulses will be absent/diminished in vascular but not in neurogenic claudication
4. Parasthesia is common in neurogenic claudication

TAKING A HISTORY OF CHRONIC LIMB ISCHAEMIA

1. Claudication = muscular pain, reproducible, incr 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  LeRiche’s
- 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

2. 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)

3. 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

4. Risk  factors  (“Arteropath”)

- 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

5. Drug history
- Aspirin and statin intake – commonly prescribed for vasculopath
- Any allergies to contrast (for angiography)
- Ergots

6. Social history
- Premorbid function and current function
- Social support and home condition (need to climb stairs?)

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PHYSICAL EXAMINATION

Examine  the  patient’s  lower  limbs  in  a  warm  room,  exposed  optimally  (from  the  thighs  to  the  feet,  wearing  underwear).  
Patient is supine with the bed flat.

Look

1. Colour of the lower limb

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

Feel

1. Warmth of the skin

- Use  the  dorsum  of  the  fingers  of  both  hands  to  simultaneously  run  up  the  patient’s  feet  to  the  shins  and  thighs  bilaterally
- Compare the temperature on both sides (note if one side is cooler)
- If one limb feels cool, feel for the level where the skin becomes warm
2. Capillary refill
- Press hard on a toe for a few seconds, then release
- Normal capillary refill should be 2 seconds or less
- If a toe is blue, check for blanchability (fixed staining = dead toe)
3. Palpating the ulcer if present
- Any surrounding tenderness (infection)
- Bogginess of surrounding tissue (may have abscess formation)
- See if any discharge from the ulcer when palpating
4. Pulses – compare both legs. Check regularity of pulses.
- Feel the distal pulses and work your way proximally
- Posterior tibial pulse: one-third of the way down a line joining the medial malleolus to the heel
- 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
- 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]
- Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior superior iliac spine (mid-inguinal point),
just below the inguinal ligament
- Abdominal aorta

Grading of pulses: 2+ normal; 1+ diminished (but may be normal for popliteal); negative if not felt

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Move

1. Buerger’s  test
- Lift both legs together to compare
- Holding the heel of the foot, with the pt’s  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 Buerger’s angle
Normal  lower  limb  can  be  raised  to  90  degrees  without  turning  white;;  if  the  Buerger’s  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  you’re  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)

INVESTIGATIONS

1. Ankle-brachial pressure index

- How the ankle-brachial pressure index is done

Lie patient supine (so that ankle pulse will not increase sec to dependency)
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
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
The ankle pressure to be used for each leg is the higher of the two taken
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

Normal ABPI is > 0.9 (can be more than 1.0 as ankle pressures tend to be higher than brachial;
ABPI between 0.5 - 0.9 – occlusion, often associated with claudication
ABPI <0.5: Critical ischaemia Rest pain
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

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

Measure ABPI before and after patient exercises on a treadmill
If the ABPI falls by >0.2 claudication

2. 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

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3. Angiogram (arteriogram)

- Invasive and associated with risks of

1. bleeding from arterial puncture,
2. dissection
3. damage to artery with worsening ischaemia
- Usually only done if planning intervention e.g. angioplasty, stenting
- Preparing for angiogram:
Take informed consent from patient
Ask about contrast allergy, asthma, renal disease, metformin
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)

4. Basic laboratory investigation

- FBC, UECr, PT/PTT, septic workup: bld c/s, wound c/s

ASSESSMENT OF SEVERITY

The  three  L’s  of  peripheral  arterial  disease:

(i) Life – does disease threaten life (e.g. sepsis; other cxs of atherosclerosis e.g. stroke, AMI;) or will intervention cause risks
(ii) Limb – will patient lose the limb
(iii) Lifestyle – is the lifestyle of the patient severely handicapped, does it require intervention

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

(A) TREATMENT OF CLAUDICATION – BASED ON QOL

Conservative
Mainstay for all cases of claudicants, esp. foot and calf claudicants

- RF control
Assessment and treatment to optimise control of CVS risk factors– cardiologist
Antiplatelets [e.g. aspirin] and statins (target lipid levels are much lower)
Smoking cessation – not shown to be useful
- Exercise training to stimulate collateral formation symptoms get better
Exercise at least half to one hour every day
Walk until pain comes, rest 2-3 minutes, walk again
Keep a walk diary recording daily claudication distance in paces
Supervised exercise 3X/wk helps. Advice to exercise alone does not.
- Patient educaton:
Teach patient to go to ED if symptoms of critical ischaemia arises
Podiatrist to teach foot care
- Medications
Craxilen and Cilasterzol shown to increase claud dist - Ex.
Use of Vasteral (methoxyphylline) is controversial
- Monitor regularly with measurement of ABPI

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 weigh risks against benefits
- Usually do angioplasty rather than bypass as it is less invasive, though may not be as effective in treating the symptoms

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 1. Angioplasty
1. Stenting usually not done for lower limbs except in aortoiliacs (since stent needs to be placed in a vessel which is
relatively  fixed  and  won’t  be  kinked/bent  by  movement)  – not true: can even stent foot arteries!
2. 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
3. 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

2. Bypass grafting
Consider bypass when lesions cannot be treated by angioplasty i.e. lesion extends for long distance through the vessel
and/or no lumen for guide wire to pass through (complete occlusion)
Needs  a  good  “landing  zone”  for  graft  distally  – if vessel is diffusely diseased, difficult to perform bypass

(B) TREATMENT OF CRITICAL LIMB ISCHAEMIA

- Need to revascularise – either angioplasty or bypass grafting

(C) AMPUTATION

Indications  (3  D’s)

1. Dead: Necrotic tissue
2. Dangerous: Gangrene, ascending sepsis
3. Damn nuisance: Non-functional limb; bad smell; pain; constant need to dress wound

- Level of amputation depends on

vascularity of the limb (palpable pop pulse: BKA)
indication (e.g. if infected, need to amputate above level of infection)

- As far as possible try to preserve function of the lower limb

- May require revascularisation interventions before amputation to ensure good healing, or to enable lower amputation
- Do not simply amputate without ensuring good va
- scular supply to the surgical site, otherwise the wound will not heal

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17. ABDOMINAL AORTIC ANEURYSM

EPIDEMIOLOGY

More common in men than in women (4:1 ratio)

Predominantly in older patients (>60 years old)
Other risk factors: smoking, hypertension, strong family history (Marfan, Ehler-Danlos)

PATHOLOGY

- An aneurysm is a localised abnormal dilatation of a blood vessel wall or the heart

- True aneurysms are bound by all layers of the blood vessel wall, while a false aneurysm is a breach in the blood vessel wall
leading to an extravascular haematoma that freely communicates with the intravascular space
- Atherosclerosis is the most common aetiological factor – plaque formation results in destruction of the tunica media (and the
elastin fibres in it) arterial wall thinning and loss of elastic recoil dilatation
- Other causes: cystic medial degeneration (in Marfan), trauma, infection (mycotic)
- Location: 95% of cases are infrarenal, may extend to involve common iliac arteries, rarely beyond. 5% are juxtarenal, thoracic
or both
- Size: 3 to 15 cm (normal aorta is 2cm in diameter)
- Shape: Usually fusiform – long dilated segment (versus saccular which is spherical)
- Often contains mural thrombus due to turbulence and stasis

RISK OF RUPTURE

- Small aneurysms <5cm have a 2-3% chance of rupture per year, while aneurysm larger than 5.5 cm will have a 10% risk of
rupture per year
75% of aneurysms 7cm or larger will rupture in 5 years

PRESENTATION

- Asymptomatic (Most commonly; found incidentally during imaging)

- Rupture: intense abdominal pain radiating to the back, becomes rapidly hypotensive and goes into shock (Most feared
presentation)
- Trash feet: distal Thromboembolism gangrene of feet
- Local compression on neighbouring structures e.g. ureter
- Obstruction of branches from aorta e.g. iliac, renal, mesenteric, vertebral
- Also ask for vascular risk factors (DM, smoking, HPT, hyperlipidemia, previous CVA, IHD), AAA risk factors (smoking, HPT,
Marfan’s/  Ehler-Danlos) & GA risk factors (any heart, lung or kidney diseases)

PHYSICAL EXAMINATION

- Ensure vitals stable

- Visible pulsation over abdomen
- Pulsations and mass in epigastric region felt on deep palpation
- Mass is expansile – when fingers of both hands are placed at the edges on either side of the mass, the fingers are pushed
upwards and outwards
- Auscultate for bruit over the mass
- Check the other arteries – femoral, popliteal – for any aneurysm, and listen for bruits
- Look at the lower limbs for any gangrene, infection, etc

DIFFERENTIAL DIAGNOSIS OF UPPER ABDOMINAL PAIN WITH SHOCK

- Pale: ruptured AAA, ruptured hepatoma, BGIT, ruptured spleen in trauma, mesenteric bleed
- Not pale: sepsis, pancreatitis, perforated viscus, AMI , pyonephrosis

INVESTIGATIONS

Imaging: CT AbdoPelvis
Other investigations: FBC, UECr, PT/PTT, GXM for 4 units, ECG & CXR

MANAGEMENT

Dependent upon clinical context: asymptomatic, symptomatic, or ruptured?

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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

1. Stabilise patient – resuscitation with fluid and blood products

Do not intubate as neuromuscular blocking agents will reduce tamponade effect, worsening haemorrhage
2. Call for vascular surgeon
3. Bring to OT for open repair – quickly isolate the aorta and clamp it proximally
can be clamped for about 30 minutes without significant visceral ischaemia
AAA is incised, the surrounding haematoma and mural thrombus within the AAA are cleared out
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
o Mortality rate of repair operation in this setting is about 50%
4. 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:
(a) Aneurysm > 5.5 cm in largest diameter [risk of surgery outweighs that of AAA]
(b) Increase in diameter of more than 1cm per year
(c) Symptomatic aneurysm – back pain, tenderness on palpation, distal embolism, ruptured/leaking aneurysm
- Patient’s  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%

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

1. Acute myocardial infarction – most patients already have atherosclerotic disease of coronary vessels and are at risk of AMI
(responsible for 50-60% of mortality)
2. Stroke (due to hypotension or embolism)
3. Renal insufficiency
4. Colon ischaemia – occurs in 2-6%
5. Trash foot – embolism of thrombus from the aneurysm
6. Infection of graft
7. Spinal cord ischaemia (quite uncommon)
8. Haemorrhage

Late

1. Aortoenteric fisula – frank PR bleeding, torrential

2. Late infection of prosthetic graft material
3. 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

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18. PERIPHERAL VENOUS DISEASES

1. ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB

- The venous drainage of the lower limb is divided into a deep venous system and a superficial venous system separated by the
deep fascia of the lower limb
- The deep venous system is composed of veins corresponding to the arterial supply e.g. anterior and posterior tibial veins,
popliteal vein, femoral vein
- The superficial venous system is composed of two major veins, the great saphenous vein and the small saphenous vein

- Course of the great saphenous vein:

Arises from the medial end of the dorsal venous arch of the foot
Passes anterior to the medial malleolus
Runs up the leg posteriorly to pass behind the medial surface of the knee
Then runs anteriorly and laterally up the thigh
Pierces the cribriform fascia at the saphenofemoral junction to drain into the femoral vein

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- Course of the small saphenous vein:
Arises from the lateral end of the dorsal venous arch of the foot
Passes posterior to the lateral malleolus
Runs up the midline of the calf
Pierces the deep fascia over the popliteal fossa to drain into the popliteal vein

- The superficial system and the deep system communicate through communicating veins that contain valves which allow only
one-way flow of blood from the superficial vein into the deep vein
(Foot perforators allow bi-directional flow directed by muscle movements)

- Locations of the communicating veins:

a. Saphenofemoral junction (great saphenous drains into femoral vein): located 2.5 cm below and lateral to the pubic
tubercle
[HDB]
b. Hunterian perforator: mid-thigh
c. Dodd’s  perforator:  distal  thigh
d. Boyd’s  perforator:  knee
e. Calf perforators: at 5, 10, and 15 cm above the medial malleolus

- Physiology of venous drainage:

Main mechanism is the calf muscle pump:

Contraction of the calf muscles compresses large venous sinuses in the muscles, squeezing the blood into the popliteal vein
and back to the heart

(The deep veins have many valves to prevent backflow, so blood only flows towards the heart)

During calf muscle relaxation, the intramuscular veins open and suck blood in from the superficial system through the
communicating veins, thus draining the superficial veins

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2. CHRONIC VENOUS INSUFFICIENCY

Chronic venous insufficiency develops when there is venous hypertension, which can result from:

1. Obstruction to venous flow e.g. tumour compression in the pelvis, pregnancy, deep vein thrombosis
2. Dysfunction of venous valves e.g. varicose veins
3. Failure of the “venous pump” – dependent on adequate muscle contraction (stroke, muscular weakness can cause failure) as
well as competent venous valves

MANIFESTATIONS OF CHRONIC VENOUS INSUFFICIENCY: [4]

1. Venous dilatations[4]

(a) Telangiectasias (spider veins or venous stars – intradermal veins)

15 % of men and 25 % of women in the general population.In the classification of veins, telangiectasias are
classified as type I veins. Spider veins are amenable to laser therapy and sclerotherapy.
(b) Reticular veins (slightly larger intermediate veins)
also known as blue veins and intradermal varices. In the classification of veins, reticular veins are
considered type III veins.
(c) Varicosities (visible, dilated tortuous superficial veins; formed by main tributaries of the saphenous veins
because these do not have a strong coat of smooth muscle in their walls, unlike the saphenous veins; they are more
superficial and not bound down to the deep fascia)
Trunk varicosities – along main trunk of LSV/SSV.
(d) Corona phlebectactica (a network of small dilated venules beneath the lateral and/or medial
malleolus with severe venous hypertension)

2. Oedema – pitting: The hallmark of CVI; present in all but the earliest stages
Unilateral oedema worsened by dependency (worse at the end of the day) and better with recumbency

3. Skin changes[5]

(a) Hyperpigmentation over medial lower third of the leg (gaiter area) – extravasation with haemosiderin deposits
(b) Atrophie blanche – hypopigmented scars of healed venous ulcers (avascular and fibrotic skin)
(c) Venous stasis eczema – pruritic, weeping, scaling, with erosions and crusting
(d) Lipodermatosclerosis (fats and skin hardening) – a fibrosing panniculitis of the subcutaneous tissue that results in a
firm area of tender, hyperpigmented skin that is fixed to subcutaneous tissue.
Results from severe venous hypertension hemosiderin deposits at fats inflammation chronic inflammation
Starts in the gaiter area and extends circumferentially to surround the leg
If  severe  can  result  in  an  “inverted  champagne  bottle”  appearance  of  the  leg  with  brawny  oedema  above  and  below  
the area of lipodermatosclerosis
(e) Cellulitis

4. Venous ulcer formation

- Typical location is over the medial malleolus

- Shallow, flat ulcer with sloping edges; base may be sloughy or granulating, usually quite moist-looking
- Surrounding skin will show signs of CVI
- In long-standing ulcer SCC can develop (Marjolin’s  ulcer) – If ulcer
1. enlarges,
2. becomes painful
3. malodorous,
4. edge becomes thickened or raised,
5. inguinal lymph nodes are enlarged

SYMPTOMS
1. asymptomatic
2. leg fullness / swelling
3. heaviness,
4. non-specific pain: aching discomfort, dull, shooting
5. nocturnal leg cramps,
6. itch (40%)
7. bursting pain upon standing.

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 CEAP CLASSIFICATION OF CHRONIC VENOUS INSUFFICIENCY

3. VARICOSE VEINS

Varicose veins are dilated, tortuous veins of the superficial venous system (secondary to incompetent leg valves
resulting in reflux).
Primary varicose veins: cause is unknown (may be related to posture and components and structure of the vein wall)
GENETIC! (20% risk in gen pop, 50% 1 parent, 80% both parents)
Secondary varicose veins:
1. destruction of the valves by thrombosis (DVT most common secondary cause),
2. proximal venous obstruction,
3. increase in flow and pressure caused by an arteriovenous fistula,
4. pelvic masses – compress on deep veins

PATHOPHYSIOLOGY
- Inherent weakness in the vein wall, leading to dilation and separation of valve cusps so they become incompetent
- This may be aggravated by obstruction to venous return (as above)

RISK FACTORS (NOT CAUSES!) - in already predisposed people

- Age
- Parity
- Occupation – requiring long periods of standing
- Weight
- Posture – crossing legs all the time
- Increased abdominal pressure – constipation, chronic cough, etc
- Family history: 1 parent (50% risk, both parents (up to 80% risk)

HISTORY
Asymptomatic
Symptomatic: local (non specific pain, swelling, itching, heavy legs)
Complications :
1. ulceration +/- cancer
2. thrombophlebitis (= thrombosis inflammation, chemical rather than infective. commonly mistaken as cellulitis)
3. bleeding,
4. hyperpigmentation,
5. eczema,
6. infection (due to dependent oedema)
Risk factors: Ask for Past history of DVT & thrombophlebitis, obstetrics history, family history

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EXAMINATION

Examine patient STANDING with adequate exposure of the lower limbs

Inspection (look all around the limb!)

1. Presence of signs of chronic venous insufficiency (as above)

- Oedema
- Skin changes, stasis eczema, lipodermatosclerosis (feels like leather, v tight)
- Venous ulcers from pressure necrosis from insude
2. Look at course of great saphenous vein and short saphenous vein for varicosities
3. Look at the inguinal region for any saphena varix

Palpate

1. Feel any dilated varicosities: Direct tenderness that  can  account  for  patient’s  pain  symptoms  
(if  patient’s  varicosities  are  not tender, warn patient that ankle/calf pain may not go away after surgery as the pain may not
be directly from the veins)
2. Palpate along the course of the saphenous veins and their tributaries to feel any varicosities and for tenderness (may be
more palpable especially in fat legs)
3. Palpate the inguinal region for a saphena varix (compressible lump that refills when released)
4. Do the cough test to feel for reflux at the saphenofemoral junction (2.5 cm below and lateral to the pubic tubercle)
5. Percussion (tap test) – test for valvular incompetence (not a very valuable test) – Ensure good distance between both hands
first, to cover valves in between.
Positive if the distal hand can feel the wave of blood flowing retrogradely after tapping the proximal varicosities (normal: tap
bottom, feel thrill on top)
6. Feel the peripheral pulses!!! of Lower limb to exclude any ischaemia as the management will involve compression of limbs
(ABI >0.8)

Special tests

TOURNIQUET TEST

- Lie the patient down and empty the varicosities & tie a tourniquet just below the SFJ
- Ask the patient to stand up
- Look for filling up of the varicosities above and below the tourniquet
- If the veins dilate above but not below the tourniquet, this indicates that the perforators below the level of the tourniquet are not
incompetent and that the SFJ is incompetent confirm this by releasing the tourniquet and watching the veins dilate
- If veins below the tourniquet are dilated when pt stands up, then the incompetent perforator is below level of the tourniquet
- Repeat the test, placing the tourniquet at different sites:
(i) Mid thigh (just below the Hunterian perforator)
(ii) Below the knee
(iii) Mid-calf
- The incompetent perforator is located between just above the level where the tourniquet prevents dilation of the veins in the
limb on standing

[The alternative is the triple tourniquet test, where three tourniquets are tied with the patient lying down and then released from
the bottom up to locate the site of insufficiency]

TRENDELENBURG TEST

- The SFJ is occluded (landmark is 2.5 cm below and lateral to the pubic tubercle) with the patient lying down
- Get the patient to stand while holding the SFJ occluded
- If varicosities do not fill up, the SFJ is the site of incompetence; if they fill up, there are other sites of incompetence (the SFJ
may or may not be incompetent)

PERTHES’ TEST (Test of deep venous obstruction)

- Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe and then relax
- In a person with normal deep venous drainage and competent venous valves in the communicating veins the superficial veins
should drain into the deep veins
- Positive test: patient will complain of pain and stop after ard 20 times because of increased swelling as blood cannot drain out
through the deep veins

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Completing the examination

- Auscultate over the varicosities for any bruit (indicate arteriovenous malformation)
- Examine the abdomen for any mass that may be causing the varicosities

Use of a handheld Doppler probe to detect incompetence

1. Doppler probe is placed along groin crease over SFJ (caution in obese ppl whose groin crease are lower) with patient standing
2. Look for arterial signal then move medially SFJ
3. Squeeze the calf to empty the veins – should hear a whoosh as blood flows through the small saphenous vein
4. When the calf is relaxed there should not be a prolonged sound – a second whoosh >0.5s indicates reflux of blood i.e. there is
valvular incompetence of SFJ (90% accurate prediction)
Can also perform test over popliteal fossa for SPJ but less accurate as the junction is variable. Therefore, you may be getting
signals from the deep perforators instead.

INVESTIGATIONS

Venous duplex ultrasound

- Indications:
1. Recurrent varicose veins
2. Complications of CVI: History of superficial thromobophlebitis
3. Skin manifestations of CVI: Venous eczema, Haemosiderin staining, Venous ulceration , Lipodermatosclerosis,
4. Everyone with varicosities to exclude subclinical DVT

- Ask for
(a) SFJ and SPJ reflux,
(b) perforator, deep venous incompetency
(c) DVT screen
- Can delineate deep and superficial venous systems and locate sites of incompetence

- Exclude presence of deep vein thrombosis – stripping is contraindicated

MANAGEMENT

Conservative

1. Lifestyle changes
- Decrease amount of time spent standing
- If due to job, change job or ask for change to position to stand & walking less
2. Graduated compression stockings, usually grade II ensure good pulses
3. Medications e.g. Daflon (only symptomatic, like painkillers)

Surgical – the only definitive treatment

Indications:
1. Cosmesis – large unsightly varicosities
2. Symptoms – pain, discomfort
3. Complications – signs of chronic venous insufficiency, venous ulceration

Contraindications:
1. Infected ulcers. (slow healing ulcers that are not infected can still operate as it may improve the ulcer)
2. DVT: can rescan after medical treatment. If DVT resolves, can opt for selective stripping.
3. Thrombotic tendencies: patient may dev DVT in the future.

Available modalities:
1. High tie with great saphenous vein stripping, and stab avulsion of varicosities
2. Ultrasound-guided foam sclerotherapy
3. Endovenous laser therapy (burns vein from within)

20% recurrence: due to large number of perforators left over even after stripping.

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4. VENOUS ULCERS

CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY

1. Obstruction to venous flow – thrombosis

2. Incompetent valves – varicose veins, deep vein reflux (post-DVT)
3. Muscle pump failure – stroke, neuromuscular disease

INVESTIGATIONS

1. Exclude infection of the ulcer and other complications

- FBC for raised total white count
- Swabs of the ulcer for Gram stain and cultures
- X-ray of the area to exclude underlying gas, bone involvement

2. Venous duplex to map out venous system

3. Check for peripheral arterial disease by doing ABPI

4. Biopsy if  cannot  exclude  malignant  transformation  (Marjolin’s  ulcer)

MANAGEMENT

Conservative

1. 4 layer compression stockings (change 2X/week if ulcer, 1X/wk if no ulcer)

(a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool bandage – most impt layer to protect ulcer
(b) Crepe bandage
(c) Blue-line bandage (Elset)
(d) Adhesive bandage (Coban)
Aim: ankle pressure around 30mmHg (can vary according to needs)
Nowadays, 2 layer stockings are used too – can achieve the same ankle pressure but not as effective as it loses pressure more
quickly so less consistent pressure.

2. Stockings: Once healed (cannot use with ulcer/wound), compression stockings should be fitted and continued for life
3. Symptomatic: Analgesia
4. Antibiotics if infected

5. Lifestyle
(a) Warn patient to avoid trauma to affected area
(b) Encourage rest and elevate leg

Surgical

If ulcer fails to heal:

- First, exclude malignancy or other causes of ulcer (biopsy)
- Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue
- Venous surgery for the underlying pathology

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237
19. UROLOGICAL DISEASES

1. APPROACH TO HAEMATURIA

DEFINITION:
- >3 RBC / hpf.
- DDx: haemoglobinuria, myoglobinuria, pseudohaematuria (menstruation), meds causing discoloration (eg rifampicin, phenytoin)

CAUSES
Pre- Drugs Analgesics (NSAIDs)
Renal Anticoagulants
Cytotoxic/immunosuppressive agents (eg cyclophosphamide)
OCP
Penicillin
Quinine
Warfarin
Systemic Bleeding diathesis
Sickle cell disease
Metabolic Hypercalciuria
Hyperuricosuriia
Vascular AV malformations
Renal artery disease – thromboembolism, dissecting aneurysms, malignant
hypertension
Renal vein thrombosis
Renal Vasculitis HSP
PAN
Wegener granulomatosis
Glomerular Post-strep GN
Post-infectious GN
IgA nephropathy
Lupus nephritis
Other GNs
Tubulo- Polycystic kidney disease
interstitial Nephrolithiasis
dz Malignancy – RCC, metastatic
Pyelonephritis
Renal cysts
Post- Infxns of ureter, bladder, prostate, urethra – eg schistosomiasis, TB etc
renal Cancers of ureter, bladder (TCC), prostate, urethra
Nephrolithiasis

HISTORY

Post-renal Causes

1. Which part of urine stream is blood stained?

- Beginning – urethra distal to UG diaphragm
- End – bladder neck or prostate
- Throughout – upper urinary tract or upper bladder

2. Painful vs painless haematuria

Painful Painless
- UTI - Malignancy – TCC, RCC, Prostate
- Pyelonephritis - Drugs
- Tumour - GN
- Hydronephrosis - Bleeding diathesis
- Renal cysts - ITP / HSP
- Ureteric stone / clot - Infections – malaria, schistosomiasis
- Bladder outflow obstruction (e.g. BPH, - Exercise  (jogger’s  hematuria)
strictures)

3. Severity
- Clots
- S/S of anemia

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4. Frequency + dysuria + haematuria
- DDx: nephrolithiasis (colicky), malignancy, UTI (women & children), bladder outflow obstruction (men e.g. BPH – vascular
prostate may bleed)

5. Other urological symptoms

- Storage problem – frequency, urgency, nocturia, incontinence
- Voiding problem – strangury, hesitancy, dribbling, incomplete emptying etc
- Others – polyuria, oliguria, urethral discharge

Pre-renal & Renal Causes

6. Associated fever – pyelonephritis, malaria

7. Screen for pre-renal causes
LOW / bone pain / sickness Malignancies, TB, systemic illnesses
Rash, arthritis, arthralgia, myalgia, fever, oedema Autoimmune causes, vasculitis
Sore throat, skin infxns, URTI Post-strep / post-infective GN
Ongoing URTI or GE IgA nephropathy
Iatrogenic Drug causes, radiotherapy
Travel history Schistosomiasis, malaria
PMHx Renal disease, HPT, diabetic nephropathy, bleeding diathesis, sickle cell dz
Family history PKD, sickle cell disease, renal dzes (eg Alport syndrome – ask for
deafness), HTN, urolithiasis

Other necessary history

1. Infection - Fever, travel and contact history
2. Sorethroat - Post-strep/infective GN, IgA nephropathy
3. Autoimmune - Fever, rash, joint pain, oedema
4. Malignancy - LOW, bone pain, neuro deficits, SOB, liver function
5. PMHx - Renal dz, systemic dz (DM HPT Bleeding sickle cell)
6. Drug history / Hx of radiation
7. Family history – PKD, renal dz, Sickle cell, HPT

PHYSICAL EXAMINATION

1. Check  patient’s  vitals- stable?

2. Conjunctival pallor
3. Abdomen – renal/bladder mass, palpable bladder (clot causing retention)
4. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension of tumour into renal vein, blocking the
testicular vein where it drains into the left renal vein)
5. External genitalia – blood from urethra
6. Digital rectal examination – prostate enlargement (BPH versus cancer)

INVESTIGATIONS

URINE

1. Urine dipstick
- Causes of false-positive for blood: haemoglobinuria, beetroot, drugs (rifampicin), metabolic (alkaptonuria, porphyria)

2. UFEME (normal (all below 5): RBC 3-5, WBC 2-5, EC <5)
- Confirm presence of red blood cells
- Elevated WBC (pyuria is >5 WBC per hpf), organisms infection
- Casts nephritis

3. Urine cytology for malignant cells - useful for:

- High grade urothelial carcinoma (LG hardly shed cells)
- Carcinoma in situ (imaging cannot see)

4. Urine phase contrast

- RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source, while isomorphic RBCs suggest post-
renal source (ureter, bladder, etc)
5. Urine culture and sensitivity

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BLOOD

6. Full blood count

- How low is the Hb?
- Elevated TW – infection
7. Urea, electrolytes and creatinine
- Any renal impairment and electrolyte abn (renal or pre-renal dz more likely)
8. PT/PTT
- Anycoagulopathy
9. GXM!!!

IMAGING (HEMATURIA – IMAGE ENTIRE URINARY SYSTEM)

Upper tract: imaging, lower tract: cystoscopy

10. Plain KUB

- Margins: Superiorly needs to be above upper pole of the right kidney (T12), inferiorly needs to show pubic symphysis
- Stones, size of kidney

11. Ultrasound of the kidneys

- Renal size
- Presence of any hydronephrosis, hydroureters
- Renal stones

12. Intravenous urogram (IVU)

- Look for
1. Distortion of renal OUTLINE and pelvic calyces by RCC, may have specks of calcification
2. Contrast UPTAKE: present or not (no contrast in obstruction / non-functioning), equal and symmetrical uptake
3. Configuration of the kidneys eg. Horseshoe kidneys
4. Stones (filling defect, proximal dilatation, decreased distal passage of contrast) + hydroureter and/or hydronephrosis
5. Filling defect in bladder due to TCC
6. Increased residual volume in bladder after micturition due to BPH

- Intravenous contrast used to delineate anatomy of the kidneys and urinary system
- Various phases:
(i) Control film – plain KUB
(ii) Tomogram – zoom into kidneys before contrast
(iii) Nephrogram phase (1 min after contrast) – contrast fills kidney parenchyma so kidneys become more visible
measure size, outline
(iv) Pyelogram phase (3-5 min) – contrast fills calyces & pelvis, can detect dilated calyces/pelvis (hydronephrosis), any
filling defects
(v) Release film (abdominal binder which was placed to slow the flow of contrast into the bladder is released) – shows
ureters, any hydroureter, filling defects
(vi) Cystogram - any filling defects, abnormal appearance of the bladder (fir-tree appearance in neurogenic bladder)
(vii) Post-micturition – any residual urine in bladder after voiding

- Contraindicated in:
(a) Contrast allergy
(b) Renal impairment (Cr >200)
(c) Patients on metformin (can cause lactic acidosis; patients need to stop metformin 2 days before and after study)
(d) Patients with asthma (given steroids for 3 days before study)
(e) Pregnancy: ask LMP

13. CT urogram / IVP

- Non-contrast phase (stones) Nephrogram (tumors) Delayed phase
- Adv: Ability to see renal parenchyma tumors (IVU only sees outline)
- Disadv: Radiation ++ (3 CT scans)

14. Cystoscopy
- Detection of bladder tumour (IVU may not pick up small tumours <1cm)
- Biopsy can be taken at the same time

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2. RENAL CELL CARCINOMA

EPIDEMIOLOGY
- 3% of adult malignancy
- Most frequent occurring solid lesion within kidney
- 2:1 male predominance
- Peak incidence 60-70 years

PATHOLOGY
- Most common primary renal tumour (80-85% of all tumours of the kidney)
- Arise from the renal tubular epithelium
- Three cell types:
1. clear cell carcinoma (70-80%),
2. papillary renal cell carcinoma (10-15%),
3. chromophobe renal cell carcinoma (5%)

Other  renal  tumours:  TCC  of  renal  pelvis,  Wilms’  tumour,  lymphoma

RISK FACTORS
- Smoking
- Exposure to cadmium (industrial)
- Family history
von-Hippel Lindau syndrome clear cell carcinomas
Due to mutation of the VHL gene on chromosome 3p25 resulting in abnormal growth of BV ie. angiomas
(associated with CNS haemangioblastomas (usually cerebellar), bilateral multicentric retinal angiomas,
phaeochromocytomas, etc)
Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene on chromosome 7q31 multifocal bilateral
papillary carcinomas
- Acquired polycystic kidney disease (secondary to chronic dialysis)

PRESENTATION

- Initially asymptomatic (may be detected incidentally)

1. Local S/S
- Painless gross haematuria is the most common – >50% of cases
- When tumour has grown large enough, dull flank pain and palpable mass may result
Classical triad of RCC: flank pain, painless haematuria, palpable renal mass (indicates late stage disease)

2. Complications
1. May have fever a/w night sweats, LOA, LOW, malaise
2. Polycythaemia occurs in 1-5% (due to increased erythropoietin)
3. For left renal tumour, extension of tumour into left renal vein can cause a left varicocoele as the left testicular vein
becomes occluded
4. Extension into IVC can cause (a) lower limb oedema, (b) ascites, (c) liver dysfunction, (d) pulmonary embolism
5. Paraneoplastic syndromes are uncommon – Cushing’s,  hypercalcaemia,  hypertension

3. Metastasis
- Symptoms of metastases – lungs, liver, bones, brain, lymph nodes

241
INVESTIGATIONS

DIAGNOSTIC

1. Imaging – CT and/or ultrasound

- Presumptive diagnosis is made on imaging – a renal parenchymal mass with
(a) thickened irregular walls and
(b) enhancement after contrast injection suggests malignancy

2. Pathological diagnosis
- Needle biopsy usually not done for resectable lesions due to fears of tumour seeding
- In these resectable lesions, a partial or total nephrectomy is often performed, and provides the tissue diagnosis post-
operatively
- In tumours with metastatic disease on presentation, biopsy of the metastatic site may be easier

STAGING

1. CT scan of the abdomen

- Perinephric invasion, adjacent organ invasion
- Extension into renal vein, IVC
- Lymph node enlargement
- Liver metastases

2. CT scan of the chest

- For lung metastases

Also,
Bone scan
- Only done if patient complains of bone pain and/or alkaline phosphatase is raised
MRI of abdomen and heart
- Superior to CT for evaluation of IVC and right atrium involvement

T1 Tumour <7cm, limited to the kidney

T1a: tumour <4cm
T1b: tumour >4cm but <7cm

T2 Tumour >7cm, limited to the kidney

T3 Tumour extends into major veins or invades adrenal gland or perinephric tissues, but not
beyond  Gerota’s  fascia

T4 Tumour invades beyond Gerota’s fascia

Fuhrman grading prognosis (not tx)

- size and shape of nucleus
- no and size of nucleoli
- chromatin clumping
I (best) IV (worst)

Prognosis
Stage I (T1N0): >90% 5 year survival
Stage II (T2N0): >75%
Stage III (T3N0/N1): >60%
Metastatic disease: <10%

242
TREATMENT

A. RESECTABLE TUMOURS

Surgery + Adj chemo + Surveillance after resection to detect relapse early

- Laparoscopic versus open methods

- Retroperitoneal versus transperitoneal approach

1. Partial nephrectomy (T1a)

- spares part of the kidney that is not involved nephron-saving

2. Total nephrectomy (T1b)

- entire kidney removed

3. Radical nephrectomy (T2 and beyond)

- entire  kidney  together  with  Gerota’s  fascia
- In T3 disease, aim for radical nephrectomy and removal of structures affected e.g. adrenal gland

Patients who cannot undergo resection

- Most small tumours grow slowly and do not become symptomatic or metastasise – reasonable to manage conservatively
with periodic re-evaluation
- Alternatives: radiofrequency ablation, cryotherapy of lesions

B. ADVANCED TUMOURS

Immunotherapy
- High dose interleukin-2 – associated with good results in patients whose tumours respond to treatment, as treatment can induce
long-term remissions without relapse. However, associated with high toxicity and often not tolerable
- Cytoreductive nephrectomy performed prior to starting immunotherapy can improve survival

Molecular targeted therapy: Sorafenib, Bevacizumab

1. Sorafenib – an inhibitor of tyrosine kinase blocks intracellular domain of the vascular endothelial growth factor (VEGF) receptor
2. Bevacizumab – monoclonal antibody against VEGF

243
3. BLADDER TRANSITIONAL CELL CARCINOMA

EPIDEMIOLOGY
- Ninth most common cancer in Singaporean males
- Increasing incidence with age (80% diagnosed in patient >60 years old)
- 4:1 male predominance

PATHOLOGY
- TCC is the most common tumour of the bladder (>90%)
Thought to arise due to exposure to carcinogenic substances in the urine urothelial cancers think FIELD
CHANGE effect, thus urothelial tumours often occur multifocally
Screen ENTIRE urothelium every f/u
Papillary in nature (more differentiated)
- Adenocarcinoma (1%, arises from remnant of the urachus in the dome of the bladder),
- SCC (<5%, due to chronic irritation e.g. long term indwelling catheter or untreated bladder stone)

RISK FACTORS
- Cigarette smoking (Urothelial CA!) – ask secondary smoking
- Industrial chemicals – naphthylamine, aniline-containing dyes, etc
- Occupational (hairdressers – exposure to hair dyes)
- Chronic cystitis (SCC)
Schistosomiasis
Radiation (pelvic)
Chemotherapy (cyclophosphamide)
- Analgesic abuse (phenacetin)

PRESENTATION

- Haematuria most common (90%) – typically gross, painless, intermittent, occurring throughout the stream
- LUTS
– irritative symptoms suggestive of carcinoma in-situ,
- obstructive symptoms: indicate a tumour at the bladder neck or prostatic urethra
- Pain – in locally advanced or metastatic tumour
(a) flank pain due to urinary obstruction,
(b) suprapubic pain due to local invasion,
(c) bone pain due to metastasis
- Constitutional symptoms – LOW, LOA, fatigue

DIAGNOSIS

1. Urine cytology for malignant cells (not very sensitive but very specific)
2. Cystoscopy with cell brushings and biopsy
3. IVU or CT urogram to detect SYNCHRONOUS LESIONS (3% chance of proximal tumour)

STAGING

1. CT abdo/pelvis for T, N and M staging

2. Transurethral resection of bladder tumour (TURBT) with histopathology – can reach the muscular layer thus used for staging

Ta Superficial, does not involve lamina propria

Tis Carcinoma in-situ:  “flat  tumour”
T1 Superficial, involves lamina propria (up to muscularis propria)
T2a Superficial involvement of muscularis propria – up to inner half of muscle
T2b Deep involvement of muscularis propria – up to outer half of muscle
T3a Microscopic extension outside bladder (from TURBT specimen)
T3b Macroscopic extension outside bladder
T4a Invasion of prostate, vagina, uterus
T4b Invasion of lateral pelvic walls, abdominal wall

Generally can be divided into 2 main groups: Grading is also important

(a) Superficial tumour (70-80% of patients) – Ta, Tis, T1 T1 15% becomes invasive
(b) Muscle-invasive tumour (20-30%) – >T2 T1G3 75-80% invasive

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MANAGEMENT DEPENDENT ON STAGE

SUPERFICIAL TUMOUR

- Primary treatment is TURBT of the tumour

- Intravesical therapy

BCG – 1 instillation per week for 6 weeks

Mitomycin C – single instillation within 24hrs of TURBT, or weekly/monthly treatments for up to 2 years
Indicated in patients with high risk of tumour recurrence or tumour progression:
1. high grade,
2. multiple primary sites,
3. multiple recurrences,
4. tumour size >3cm,
5. primary or coexisting carcinoma in-situ,
6. prostatic urethral involvement

- Follow-up:

Urine cytology with cystoscopy

3-monthly for 1 year
6-monthly for next 4 years
Yearly thereafter

IVU every 2 years

MUSCLE-INVASIVE0
- Radical cystectomy with urinary diversion
Radical cystoprostatectomy with pelvic lymphadenectomy in male
Anterior exenteration with pelvic lymphadenectomy in female (Cx: perineal hernia)

Ways of diverting urine output

o Ileal conduit (a segment of ileum with ureters attached, as a stoma; not continent)
o Neobladder construction using ileum (only if urethra not removed; continent, better quality of life)
o Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due to small calibre; not continent)
o Stoma with pouch construction under abdominal wall (not continent)

- Radiotherapy (not as good as surgery)

METASTATIC
Chemotherapy

245
4. UROLITHIASIS

STONE COMPOSITION
- Calcium oxalate or calcium phosphate stones – 75%
- Magnesium ammonium phosphate (struvite = MAP) stones – 15%
- Uric acid and cystine stones – 10%
- Can occur at any level in the urinary tract, but most commonly in the kidney

PATHOLOGY
- Most  important  cause  of  stone  formation  is  increased  urine  concentration  of  the  stone’s  constituents,  such  that  they  exceed  their
solubility precipitate as stones
E.g. hypercalciuria with or without hypercalcaemia, hyperuricuria
- Urinary tract infections–
struvite stones form in Proteus vulgaris infections ( splits urea into ammonium), generating alkaline urine
Bacteria can also form nidi for the formation of any kind of stone

PRESENTATION DEPENDS ON SITE

Renal stones
- Most often asymptomatic unless the stone gets lodged in the pelviureteric junction causing hydronephrosis and subsequent
infection pyonephrosis
- Vague flank pain may occur. Bleeding?

Ureteric stones
- Even small stones can cause severe symptoms as the ureter is narrow
(a) Classically ureteric colic pain – severe, intermittent loin-to-groin pain
(b) Haematuria – gross or microscopic
(c) Irritative symptoms – frequency, urgency
(d) Can cause upper urinary tract infection Pyonephrosis!
(infected purulent urine in an obstructed collecting system)
fever with C&R, pain, can be very ill (sepsis)
Management:
- Broad spec Abx eg. Ceftriaxone
- DECOMPRESSION using PCN or URS with stenting (no need to remove stone in same setting)
Loin pain DDx: MSK (diff to differentiate)

Bladder stones
- May be asymptomatic
(a) Can cause irritative urinary symptoms – frequency, urgency
(b) Haematuria
(c) If infection is present – dysuria, fever, etc

PHYSICAL EXAMINATION

- In ureteric colic, symptoms are often out of proportion to signs – no guarding, rebound, etc
- If the patient has pyelonephritis, renal punch may be positive (DDx spinal pain by pressing on the spine)
- Otherwise unremarkable examination

246
INVESTIGATIONS

Diagnosis

1. KUB
- May be able to see radio-opaque stone (90% of renal stones are radio-opaque)
- False neg: too small. False positive: Phlebolith (perfectly round, sometimes with lucent centre. Found in pelvis near ureters),
stools
- K: Look at kidney size, any renal stones
- U: Trace path of ureter along tips of transverse processes, across sacroiliac joint, in front of bifurcation of common iliac
arteries and medially into bladder at ischial tuberosity, looking for ureteric stones
- B: Look for bladder stones
2. Intravenous urogram
- Can also help to visualise a stone
- Can show dilated urinary system secondary to stone obstruction – hydroureter and/or hydronephrosis
3. Ultrasound of kidney or bladder
- Features of stone: echogeneic rim, posterior acoustic shadowing

Complications

4. Urine tests – dipstick, UFEME, urine culture/sensitivity

- Haematuria
- Pyuria, micro-organisms (UTI)
5. Intravenous urogram
- as above
6. MAG-3 renogram
- If pyelonephritis present due to stone obstruction, it is valuable to measure the renal function using the MAG-3 renogram
- The renogram gives the differential function of each kidney – in normal individuals the function should be approximately 50%
on each side (out of 100% for both kidneys combined)
- If one kidney has less than 15% of total renal function, it is not worth salvaging the kidney

TREATMENT

CONSERVATIVE

Stones smaller than 5mm can be treated conservatively as 60% will be passed out; only treat if they (a) do not pass out after 4 to 6
weeks, and/or (b) cause symptoms

(a) Treatment of any urinary tract infection

(b) If underlying disease present that causes increased urinary concentration of stone components e.g. hypercalcaemia treat
disease if possible
(c) Diet:
High fluid intake
Low salt intake
Restriction of red meat, dairy produce, refined sugars
Increase citrus fruit intake

SURGICAL INTERVENTION

Indications:
- S/S: Constant pain
- Cx:
Obstructs urine flow
Causes urinary tract infection
Damages renal tissue or causes significant bleeding
Increase in size
- Unlikely to resolve with conservative Tx:
Does not pass after one month
Too large to pass spontaneously

247
Types of treatment available: [from top to bottom]

1. Percutaneous nephrolithotomy (PCNL)

- Done for renal stones that are too large for ESWL to disintegrate
- CI : uncorrected bleeding diathesis, patients unfit for GA

2. Extracorporeal shock wave lithotripsy (ESWL)

- Calcium oxalate, uric acid and struvite stones fragment easily, but calcium phosphate and cystine do not
- Used for stones below 2cm in size
- Used for renal stones and upper ureter stones – not so good for lower system due to difficulty in access
- CI:
(a) pregnancy,
(b) untreated UTI,
(c) untreated bleeding diathesis,
(d) Total obstruction ( need stone-urine interface for it to work)
(e) distal obstruction that cannot be bypassed with a stent
(f) ESRF (no urine to flush stones down)
- Cx:
(a) Bleeding (capsular hematoma)
(b) Sepsis (if stone is infected)
(c) Injuries to surr tissues

3. Ureterorenoscopy with lithotripsy (URS + LL) (usually laser lithotripsy, can also be done by pneumatic drill, electrohydraulic
means)
- For stones along the ureter
- Retrograde pyelogram to see the stone?

4. Cystolitholapaxy (stone crushing) for bladder stone

Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed other management strategies, altered anatomy,
performing open surgery for another reason anyway, non-functioning kidney

Adjuncts:
Double-J stent (or DJ stent) – inserted to stent the urinary system when
- worried that stone fragments after ESWL may cause obstruction e.g. when ESWL used for treatment of a large stone; or if system
is obstructed to begin with, may want to stent to ensure good drainage after surgery
- to prevent stricturing

Summary of treatment modalities (ESWL: any level of ureter)

Location Size Treatment

Renal: 2cm < 5mm Conservative management unless symptomatic/persistent
5-10mm ESWL
10-20mm Either ESWL or PCNL
> 20mm PCNL

Upper ureter: < 5mm Conservative management unless symptomatic/persistent

1cm 5-10mm ESWL
> 10mm URS with lithotripsy

Mid/Distal < 5mm Conservative management unless symptomatic/persistent

ureter: 5mm > 5mm URS with lithotripsy
ESWL
Bladder: 3cm/ < 30mm Cystolitholapaxy
multiple > 30mm Open cystolithotomy (also if there are multiple stones)

248
5. APPROACH TO ACUTE RETENTION OF URINE

CAUSES: BPH, FAECES, ANTICHOL, UTI, STRICTURE, STONES

Mechanical Extraluminal (5) Prostate enlargement (benign/malignant/prostatitis) – BPH is the commonest cause!
Faecal impaction
Pelvic tumour, ovarian cyst, fibroid
Pregnancy, retroverted gravid uterus
UV prolapsed
Intramural 54) Tumour of the bladder neck (TCC)
Urethritis (UTI)
Urethral stricture from STD, prev instrumentation
Phimosis
Urethral trauma/rupture
Intraluminal (3) Stones
Blood clot (clot retention in haematuria)
Foreign body
Non- Cord disease/ Cord compression, cauda equina
mechanical injury Multiple sclerosis
neurogenic Tabes dorsalis (Tertiary syphilis)
bladder
Neuropathy Diabetic autonomic neuropathy
Drugs (4A) Anticholinergics (cough medicine, Overactive bladder Tx), antihistamines, anti-depressants, alcohol
Others (3P) Prolonged immobility
Post-anaesthesia
Pain

HISTORY

1. Confirm Dx (Symptoms of ARU) [3]

- Sudden inability to pass urine
- Suprapubic pain (unlike chronic retention of urine which is painless) – severe!
- Suprapubic distension

2. Precipitating factors: (if present, higher the chances of retaining bladder abilities after Tx with TURP) [4]
(a) UTI: dysuria, frequency, urgency, nocturia, haematuria
(b) Constipation
(c) Drugs e.g. cough mixture, antihistamines
(d) Immobility

3. History suggestive of aetiology:

- Previous history of obstructive symptoms BPH
- Previous history of ureteric colic pain or stones
- Previous urethral instrumentation or STD stricture
- Gross painless haematuria recently TCC, bladder stone, blood clot
- Recent trauma to urethra
- Inguinotesticular pain, urethral burning, dribbling Prostatitis
- Lower limb weakness/paralysis, bowel incontinence, back trauma, history of spinal disease e.g. PID, spinal stenosis
neurogenic bladder
- Constitutional symptoms: LOW, LOA, malaise (any tumour in general)

4. Complications: [3]
- Infection – symptoms of UTI
- Stone disease (if in the bladder, usually asymptomatic)
- Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness

249
PHYSICAL EXAMINATION

- General condition
Vitals (fever)
sallow appearance, scratch marks, pedal oedema, etc (uraemia)

- Abdomen
Palpable bladder – tense, dull, rounded, tender, pressure desire to micturate (large bladder up to umb suggests b/g of
chronic retention)
Other pelvic masses – fibroid, gravid uterus, ovarian cyst
Faecal loading
Bilateral enlarged kidneys (hydronephrosis)

- External genitalia: narrow maetus, tight foreskin

- Digital rectal examination
Any saddle anaesthesia (buttock and perineum – ind cauda equina)
Anal tone
Prostate enlargement (>2FB) – firm and smooth? Or hard, craggy, irregular, rectal mucosa not mobile? Tender? (prostatitis)
Stool impaction

- Neurological examination
LMN paralysis of the lower limbs?
Any sensory level present?

IMMEDIATE MANAGEMENT – PROMPT BLADDER DECOMPRESSION

- 1st choice: URETHRAL CATHETERISATION (14F)

(CI!!: S/S of urethral injury – (a) blood at urethral meatus, (b) high-riding prostate – more relevant in the trauma setting)

If cannot pass into bladder:

a) enlarged prostate use thicker catheter (stiffer, easier to pass through)
b) urethral stricture (clue: catheter is stuck quite proximally along the penile urethra / PHx of instrumentation/STD)
smaller gauge catheter
Do not push too hard – may cause false passage creation if the obstruction is due to a stricture

- If urethral catheterisation fails suprapubic catheterisation

Requires distended bladder which pushes the surrounding bowel loops away so that risk of bowel injury is lower:
Method:
Local anaesthetic injected 2 fingerbreadths above pubic symphysis
Small incision made in the skin and fascia, and trocar inserted
When a gush of urine is seen, the suprapubic catheter is inserted and secured

INVESTIGATIONS

1. Bloods/Urine
a. Urine dipstick, UFEME and culture/sensitivity (UTI, hematuria)
b. UECr: raised creatinine (renal impairment secondary to obstructive nephropathy)
c. FBC: raised TW (infection) – not usually done
2. Imaging
1) KUB for stones, faecal loading
2) U/S bladder: (1) stones, (2) tumour, (3) prostate volume, (4) intravesical protrusion of prostate
3) U/S kidney, ureters: hydronephrosis, hydroureters (obstructive complication)

PSA
- to be done 4-6/52 later (as ARU can cause raised PSA)
- PSA velocity (rate of rise), free/total PSA, PSA density (= PSA/prostate volume)
- >/= 2 readings 2/52 apart
- Causes of raised PSA
i. cancer
ii. BPH [usually <40]
iii. prostatitis
iv. instrumentation /catheterization >11days
v. ARU

250
TREATMENT

1. Treat reversible causes

- Stop drugs that may have precipitated ARU
- Relieve constipation with fleet enema, lactulose, senna etc
- Treat any urinary tract infection if present

2. Monitor for complications

(a) Post-obstructive diuresis = diuresis that persists after decompression of bladder

Urine output >200ml/hr for 2 hours or more
Due to tubular damage from chronic obstruction of drainage of the pelvicalyceal system, resulting in transient
impairment of concentrating function. Usually seen in CRU, representing appropriate attempt to get rid of excess fluid
in the body during period of obstruction.
Can result in hypotension and electrolyte abnormalities (hyponatraemia, hypokalaemia, hypovolaemia)
close monitoring of urine output and fluid/electrolyte status with appropriate replacement and resuscitation
(b) Haemorrhage ex-vacuo (transient hematuria)
Bladder mucosal disruption with sudden emptying of greatly distended bladder
Usually self-limiting, rarely clinically significant
drain urine in 500-750ml aliquots, with 15-20min intervals between each
(c) Hypotension
secondary to vasovagal response or relief of pelvic venous congestion

3. Trial-off catheter
- Take  off  catheter  and  watch  patient’s  output,  as  well  as  perform bladder scan to measure bladder volume
- If patient cannot pass urine and bladder volume >400ml re-catheterise
- When patient passes urine, can perform
1) uroflow to investigate severity of outlet obstruction, and also do
2) bladder scan post-micturition to check residual volume

Failed Trial of void: after how long can try TOC?

1. Long term catheterization
2. Clean intermittent catheterization:
a. Adv: improved rate of spontaneous voiding (pt can PU in btw), decrease UTI
3. TURP (if sec to BPH): refer to indications

1 and 2 are done while waiting for medical therapy to work.

Urinary obstruction + Fever Admit! (Uro emergency)

251
6. BENIGN PROSTATIC HYPERPLASIA

EPIDEMIOLOGY
- Very common problem in men
- Frequency rises with age after the age of 30, reaching 90% in men older than 80

PATHOLOGY
- Results from proliferation of both the epithelial and stromal components of the prostate with resultant enlargement of the gland
- Commonly occurs in the central zone of the prostate
1) Major stimulus: dihydrotestosterone (produced from testosterone by 5-alpha reductase)
2) Age-related increases in oestrogen levels may also contribute to BPH by increasing the expression of dihydrotestosterone
receptors on prostatic parenchymal cells
- Chronic obstruction leads to hypertrophy of the detrusor muscle and trabeculation of the bladder mucosa as the bladder tries to
empty against increased resistance

PRESENTATION (APPROACH TO OBSTRUCTIVE UROPATHY)

- Lower urinary tract symptoms (LUTS):

Obstructive Irritative [FUNI]
Hesitancy Frequency
Straining to pass urine (strangury) Urgency
Weak stream Nocturia
Prolonged micturition Urge incontinence
Terminal dribbling Dysuria
Feeling of incomplete voiding
Double voiding (pis-en-deux)
Irritative S/S significant for Cx of urine
Obstructive S/S predominate. retention: UTI, stones

- Haematuria (UTI or rupture of enlarged veins)

- Fever (UTI - pyelonephritis from ascending infection)
- Rule out other DDx (refer ARU):
Stricture/ bladder neck contractures: previous instrumentation or STDs causing urethritis/ post- TURP
Drug causes: codeine (cough mixture), BB, anti-cholingerics, TCAs
Chronic constipation
Ca bladder neck/ Ca Prostate: LOW, LOA, bone pain, haematuria
Neurogenic bladder

- 6 COMPLICATIONS of an obstructive uropathy:

a) Acute urinary retention (previous admissions and IDC)
b) UTI: irritative symptoms, haematuria
c) Stones: irritative symptoms, haematuria
d) Hydronephrosis, pyelonephrosis: loin pain, fever Renal impairment: polyuria/ anuria.
e) Overflow incontinence 2o to Chronic urinary retention with high post-void residual volume in the bladder
f) Hernia sec to chronic straining

- Other aspects of history: Social history (effect on lifestyle)

252
253
PHYSICAL EXAMINATION

Inspection
- Vitals: BP for HPT? (CRF) Fever? (UTI) Urine output? (CRF)
- Already on IDC? (ARU) Diapers? (incontinence) Hematuria? (UTI, stones)
- Sallow? Anaemia? (of CRF/ underlying malignancy) Cachexia (CA)
- Hernia repair scar? (hernia)

Palpation
- Check for hernias
- Abdominoperineal masses (fecal loading, masses to compress)
- Any ballotable kidneys? (Hydronephrosis, Pyelonephritis)
- Renal punch? (Pyelonephritis)
- Palpable tender bladder in (ARU) non-tender (CRU)
- Pedal/ sacral oedema (CRF)
- Bony tenderness (tumor)

Confirm diagnosis and R/O DDx:

- DRE
impacted stools
prostate (benign):
1. smooth enlarged
2. median sulcus,
3. rubbery,
4. non-tender,
5. mobile mucosa

INVESTIGATIONS

Blood
- FBC: anaemia, raised WBC
- UECr: dehydration, raised creatinine renal impairment due to chronic obstruction
- UFEME, cytology, urine c/s: for UTI and screen for cancer
- PSA (done 4-6/52 later to avoid false +ves): normal <4

Imaging
- KUB for bladder stone
- US kidney – hydronephrosis
- US bladder – post-void residual volume >100ml, bladder stone, measure intravesical prostatic protrusion (IPP)
- Cystoscopy to rule out stones, strictures/ bladder neck obstruction or cancer,
- Uroflowmetry to confirm obstruction to urinary outflow (IMPT!!)
1. normal bell shaped curve, saw tooth appearance
2. Volume voided (>100ml to be valid): too low (falsely low peak flow rate), too high (falsely long duration, increase RU)
3. Normal peak flow rate (Qmax) > 15ml/sec
4. Residual urine 0 in young males, can accept up to 50ml in elderly

A) BOO with normal detrusor muscle: max flow rate

10ml/sec, prolonged flow. B) BOO with abdo straining:
intermittent flow, peak flow rate may be normal or high,
especially if outlet resistance is reduced

- ± urodynamic studies, TRUS with biopsy TRO prostate cancer if PSA >10

254
COMPLICATIONS

- Acute/chronic urinary retention Bladder stones & Recurrent UTI

- Gross haematuria (after excluding other causes)
- Renal impairment secondary to outflow obstruction
- Co-existence of prostate cancer

MANAGEMENT

- Divided into watchful waiting, medical management, and surgical management

- Objectives of treatment: Rapid and sustained relief of symptoms, prevent long-term  complications,  improve  patient’s  quality  of  life

I. Watchful waiting
- Suitable for patients with minimal symptoms, no complications and normal invx
- Monitor  patient’s  symptoms  and  clinical  course  annually

II. Medical treatment

1. Alpha blockers (Prazosin, Terazosin, Doxazosin, Alfuzosin) - dynamic
- Treatment of symptoms (blocking  the  α-1 adrenergic receptors in the bladder neck, prostate and urethra – relaxing the area)
- Result in decreased outflow resistance and decreased bladder instability
- SEs: include postural hypotension, dizziness, lethargy, lightheadedness
2. 5-alpha reductase inhibitors (Finasteride, Dutasteride) – static
- Treats the disease (not just symptoms) by inhibiting conversion of testosterone to dihydrotestosterone by 5-alpha reductase prostate size
- Proven to decrease need for surgery and acute retention rates
- Only effective after 6 /12 (counsel the patient!), and in prostates >40g
- Most common side-effect is Sexual dysfunction. Warn patient about Gynaecomastia (1%) and stop med when they notice it
developing. Hair growth.
- Ex: $3/pill. Combi therapy better than monotherapy.

III. Surgery
Types
- Transurethral resection of prostate (TURP)is the gold standard
- Transurethral incision of the prostate (TUIP): decision made during TURP when the prostate does not appear to be enlarged make small
cuts around the bladder neck area to open it up.
Adv: 50% chance of Retrograde ejaculation
- Laser prostectomy is promising (pending long term results)
- Other techniques do not show good results: stenting, cryoablation, etc.

Indications:
1. Failed medical treatment
2. Significant Complications (4): Refractory urinary retention, Recurrent UTI, Bladder calculi, Obstructive uropathy
3. Recurrent gross haematuria
Aim: to widen bladder neck

Complications of TURP: bold = must mention during consent taking

1. Bleeding, infection, risk of GA/ spinal analgesia

2. Local injury causing incontinence (1%), stricture / bladder neck stenosis
3. Perforation of the urethra or bladder dome can form fistula
4. Retrograde ejaculation (100%) impotence: (incompetent bladder neck). Always check if pt is planning to have children!
5. TUR syndrome (<1%) = hyponatremia
- Symptoms: Nausea, vomiting, confusion, hypertension, visual disturbance, giddiness, seizure
- Hyponatraemia due to constant irrigation during TURP (glycine used for irrigation – cannot use N/S, as ionic solutions make
diathermy non-functional)
- Irrigation fluid is hypotonic, thus water enters open vasculature during surgery
- Risk with prolonged operation & pressure of irrigation, thus op is kept to < 1 hour, and irrigation pressures <60mmHg
- Patient  usually  given  spinal  anaesthesia  during  TURP  so  the  surgeon  can  assess  the  patient’s  mental status during the operation
- Now uncommon as new technology allows isotonic irrigation
6. Failure of procedure: S/S recur

Caution: Must rule out Neurogenic bladder / Detrusor hypotonia before TURP!!
Do Urodynamic studies
1. Insert narrow catheter with pressure gauge at the end into
a. Bladder: intravesical pressure
b. Rectum: intraabdominal pressure
Detrusor pressure = a – b
2. Fill up bladder: look for detrusor contractions
3. Cough when erect: stress incontinence
4. Void: detrusor pressure should be sufficient, good flow (Qmax)

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7. PROSTATIC CANCER

EPIDEMIOLOGY
- Prostate Cancer is the 6th commonest cancer among men in Singapore.
- 5th common cancer in Singapore
- Peak incidence between 65 and 75 years of age

PATHOLOGY
- Adenocarcinoma
- Arise in the outer parts of the prostate 70-80% of the time and are thus palpable on digital rectal examination

RISK FACTORS
- Hormonal – growth of tumour can be inhibited by orchidectomy or administration of oestrogens
- Genetic – racial variations in onset and prevalence, family history
- Environmental – industrial chemical exposure, diet containing high animal fat

PRESENTATION

- Asymptomatic (mostly): incidentally picked up on DRE or due to elevated prostate-specific antigen (PSA) level (>100 is highly
suggestive)
- Local symptoms: obstructive LUTS, bladder outlet obstruction; (uncommon as most cancers arise in peripheral zones) haematuria,
haematospermia, new onset erectile dysfunction
- Metastatic symptoms – lower back pain (from Batson’s  venous  plexus)

PHYSICAL EXAMINATION

- DRE: Asymmetric area of induration, or frank hard irregular nodule

- Percuss spine for any bone pain

Staging (TNM staging)

T1: non-palpable lesions

o 1a: diagnosed on TURP (Gleason score <7, <5% involvement)
o 1b: diagnosed on TURP (Gleason score >7, >5% involvement)
o 1c: diagnosed with PSA screening and TRUS biopsy
T2: confined to prostate
o 2a: confined to 1 lobe
o 2b: both lobes of prostate involved
T3: extra-prostatic spread (beyond prostatic capsule)
T4: prostate stuck down to pelvic structures

Gleason score for prostate Ca is based on its microscopic appearance.

Higher scores means more aggressive lesion and worse prognosis.

DIAGNOSIS

1. Transrectal ultrasound (TRUS) with biopsy- gold standard

- Histology of prostate carcinoma is graded by the Gleason score looking at glandular architecture at low magnification
2. PSA level
- >10ng/ml: biopsy recommended as >50% of patients will have prostate cancer
- 4-10ng/ml: biopsy advised, though only 20% will have prostate cancer
- <4ng/ml: majority will have negative biopsies, and yet there is a significant proportion of men with prostate cancer with PSA
<4ng/ml biopsy if the rate of rise of PSA is >0.75ng/ml per year

STAGING

1. Clinical examination (palpable tumour T2)

2. TRUS biopsy for staging purpose
3. CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal status (regional, non-regional)
4. Bone scan for metastasis

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TREATMENT

LOCALISED DISEASE (T1/2, NO N/M) AND <75YEARS OLD

1. Radical prostatectomy
- Open, laparoscopic or robot-assisted
- Open – retropubic or perineal approaches

2. Radiotherapy
- External beam radiotherapy (EBRT) or Brachytherapy

LOCALLY ADVANCED DISEASE (T3/4)

1. Radiotherapy with androgen ablation

METASTATIC DISEASE
1. Androgen ablation
A. Castration (decrease Testosterone by 90-95%)
a. Surgical orchidectomy
b. Medical – LHRH agonist (luteinizing hormone releasing hormone)
i. 7-10 days: hormone flare (raised testosterone)
ii. After: pituitary stops signaling testicles castration level testosterone
B. Anti-androgen
a. Non-steroidal e.g. Flutamide
b. Steroidal – cyproterone acetate
C. Combined androgen blockade (A + B)
D. Oestrogen therapy (diethylstilbestrol)
a. binds Testosterone-R at hypothalamus decrease LHRH
b. S/E: CVS

HORMONAL REFRACTORY PROSTATIC CANCER

- 2 consecutive PSA rises no less than 2 wks apart and/or documented dz progression based on clinical/radiological findings in pts
with castrate levels of testosterone
- Management:
1. Secondary hormonal manipulation
Glucocorticoids – prednisone, dexamethasone, hydrocortisone
Progesterone – megestrol acetate
Adrenal suppressives – ketoconazole, aminoglutethimide
2. Chemotherapy (relieves pain from bone mets + slow dz progression)
Docetaxel + Prednisone (gold standard)
Mitoxantrone + Prednisone

Watchful waiting is possible in elderly (>75yo).

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