CONTENTS

Page
I TRAUMA (MULTI-SPECIALTY APPROACH) 2
II APPROACH TO ABDOMINAL PAIN 10
III APPROACH TO ABDOMINAL MASSES 11
Surgery Notes IV OESOPHAGEAL DISEASES 12
V UPPER BLEEDING GIT AND ITS CAUSES 21
For the M.B.B.S.
VI COLORECTAL DISEASES 19

By Andre Tan VII LIVER DISEASES 39

VIII PANCREATIC DISEASES 45
IX BILIARY TRACT DISEASES 51
X BREAST DISEASES 59
XI HEAD AND NECK MASSES 69
XII SALIVARY GLAND SWELLINGS 74
XIII THYROID DISEASES 78
XIV PERIPHERAL ARTERIAL DISEASE 85
XV ABDOMINAL AORTIC ANEURYSM 93
XVI PERIPHERAL VENOUS DISEASE 95
XVII UROLOGICAL DISEASES 99
XVIII SURGICAL INSTRUMENTS 110
XIX IMPORTANT LUMPS & BUMPS AND OTHERS 119
TRAUMA (MULTI-SPECIALTY APPROACH) Management of breathing
- Supplemental oxygen
- Ventilate as required if patient requires assistance with breathing
ADVANCED TRAUMA LIFE SUPPORT ALGORITHM
- Needle thoracotomy for tension pneumothorax, followed by chest tube
MAIN PRINCIPLES: - Occlusive dressing for open pneumothorax
- Treat greatest threat to life first
- Definitive diagnosis is less important 3. CIRCULATION
- Time is important – the ―golden hour‖ after trauma is when 30% of trauma deaths Assessment of organ perfusion
occur, and are preventable by ATLS - Level of consciousness
- Skin colour and temperature, capillary refill
- Pulse rate and character – all major pulses
APPROACH
- Blood pressure
1. Primary survey and Resuscitation with adjuncts
2. Re-evaluation of the patient Classes of haemorrhagic shock
3. Secondary survey with adjuncts I II III IV
4. Post-resuscitation monitoring and re-evaluation Bld loss
5. Optimise for transfer and definitive care Amt (ml) <750 750-1500 1500-2000 >2000
Percentage <15 15-30 30-40 >40
Ht rate <100 >100 >120 >140
PRIMARY SURVEY – ABCDE BP Normal Normal Decreased Decreased
Cap refill Normal Prolonged Prolonged Prolonged
1. AIRWAY Resp rate 14-20 20-30 30-40 >35
Assessment of airway patency Ur output (ml/h) >30 20-30 5-15 Oliguric-anuric
- Is patient alert, can patient speak? Mental state Sl anxious Mild anxiety Anxious- Confused-
- Gurgling, stridor confused lethargic
- Maxillofacial injuries Fluid Crystalloid Crystalloid Crystalloid + Blood
replacement blood
- Laryngeal injuries
- Caution: C-spine injury
Establishing patent airway Management
- Chin-lift or modified jaw thrust (protect C-spine) - Sources of bleeding  apply direct pressure or pressure on proximal pressure
- Remove any foreign objects in the mouth where possible point
- Oro/nasopharyngeal airway - Be suspicious about occult bleeding e.g. intraperitoneal, retroperitoneal (pelvic
- Definitive airway – endotracheal tube, cricothyroidotomy, tracheostomy fracture), soft tissue (long bone fracture)
- Venous access – large bore, proximal veins
2. BREATHING - Restore circulatory volume with rapid crystalloid infusion – Ringer‘s lactate
Assessment of breathing - Blood transfusion if not responsive to fluids or response is transient
- Look, listen, feel: chest rise, breath sounds – rhythm and equality bilaterally - Reassess frequently
- Rate of respiration
- Effort of respiration
- Colour of patient
- Percuss chest
- Look for chest deformities e.g. flail chest

2
3
4. DISABILITY SECONDARY SURVEY
- Glasgow coma scale When to do secondary survey
Eye Verbal Motor - Primary survey and resuscitation completed
Spontaneous opening 4 Oriented speech 5 Obeys 6 - ABCDEs reassessed
Opens to voice 3 Confused 4 Purposeful 5 - Vital functions returning to normal i.e. no need for active resuscitation at the moment
Opens to pain 2 Inappropriate 3 Withdraws 4
No response 1 Incomprehensible 2 Flexion response 3
No verbal response 1 Extension response 2 1. AMPLE HISTORY
No response 1 - Allergy
- Medications
GCS: 14-15 (minor); 8-13 (moderate); 3-7 (severe) - Past history
- Last meal
- AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive - Events leading to injury, Environment in which trauma occurred
- Pupillary reactivity
2. COMPLETE HEAD-TO-TOE EXAMINATION
- Call for neurosurgical consult as indicated
Head
- Complete neurological examination
5. EXPOSURE
- GCS or AVPU assessment
- Remove all clothes - Comprehensive examination of eyes and ears for base of skull fractures
- Check everywhere for injuries (log-roll to look at the back) - Caution: unconscious patient; periorbital oedema; occluded auditory canal
- Prevent hypothermia
Maxillofacial
6. ADJUNCTS TO PRIMARY SURVEY - Bony crepitus/deformity
Monitoring - Palpable deformity
- Vital signs – BP, pulse rate, saturation (pulse oximeter) - Comprehensive oral/dental examination
- ECG monitoring - Caution: potential airway obstruction in maxillofacial injury; cribriform plate
- Arterial blood gas fracture with CSF rhinorrhoea  do not insert nasogastric tube

Diagnostic tools Cervical spine

- Screening X-ray films (trauma series): CXR, AP pelvis, lateral C-spine - Palpate for tenderness, any step deformity
- Focused abdominal sonography in trauma (FAST) - Complete neurological examination
- Diagnostic peritoneal lavage - C-spine imaging
- Caution: Injury above clavicles; altered consciousness (cannot assess
Urinary catheter accurately); other severe, painful injury (distracts from cervical spine pain)
- Functions: decompress bladder, measurement of urinary output
- Caution in urethral injury: blood at urethral meatus, perineal Neck (soft tissues)
ecchymosis/haematoma, high-riding prostate - Blunt versus penetrating injuries
- Airway obstruction, hoarseness
Gastric catheter (orogastric or nasogastric) - Crepitus (subcutaneous emphysema), haematoma, stridor, bruit
- Function: decompress stomach, look at aspirate (bloody? bilious?) - Caution: delayed symptoms and signs of airway obstruction that progressively
- Caution in base of skull fracture: CSF otorrhoea/rhinorrhoea, periorbital develop; occult injuries
ecchymosis, mid-face instability (grab the incisors and rock), haemotympanum
 insert orogastric tube instead of nasogastric
 Chest ABDOMINAL TRAUMA
- Inspect, palpate, percuss, auscultate
- Re-evaluate frequently TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA
- Look at CXR - Solid organ injury: spleen, liver – bleeding (may be quite massive)
- Caution: missed injury; increase in chest tube drainage - Hollow viscus injury with rupture
- Vascular injury with bleeding
Abdomen
- Inspect, palpate, percuss, auscultate
- Abrasions and ecchymosis – ―seat-belt sign‖ INDICATIONS FOR IMMEDIATE LAPAROTOMY
- Lower rib fractures  liver and spleen injury - Evisceration, stab wounds with implement in-situ, gunshot wounds traversing
- Re-evaluate frequently abdominal cavity
- Special studies: FAST, DPL, CT scan - Any penetrating injury to the abdomen with haemodynamic instability or peritoneal
- Caution: hollow viscus and retroperitoneal injuries; excessive pelvic irritation
manipulation - Obvious or strongly suspected intra-abdominal injury with shock or difficulty in
stabilising haemodynamics
Perineum - Obvious signs of peritoneal irritation
- Contusions, haematomas, lacerations - Rectal exam reveals fresh blood
- Urethral blood - Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries
- DRE: Sphincter tone, high-riding prostate, pelvic fracture (may feel fragments of excluded as source of bleeding)
bone); rectal wall integrity; blood - X-ray evidence of pneumoperitoneum or diaphragmatic rupture
- Vaginal examination: blood, lacerations
Musculoskeletal – extremities INVESTIGATIONS
- Contusion, deformity - If patient is stable: FAST and/or CT scan
- Pain - If patient is unstable: FAST and/or DPL
- Perfusion
- Peripheral neurovascular status FOCUSED ABDOMINAL SONOGRAPHY IN TRAUMA (FAST)
- X-rays as appropriate
- Caution: potential blood loss is high in certain injuries (e.g. pelvic fracture, - Ultrasonographic evaluation of four windows: Pericardial, right upper quadrant, left
femoral shaft fracture); missed fractures; soft-tissue or ligamentous injuries; upper quadrant, pelvis
examine patient‘s back - Advantages
 Portable
3. ADJUNCTS AND SPECIAL DIAGNOSTIC TESTS  Can be done quickly in <5min
- As required according to suspicion, but should not delay transfer  Can be used for serial examination
 Does not require contrast, no radiation risk
4. FREQUENT RE-EVALUATION - Disadvantages
- Have a high index of suspicion for injuries to avoid missing them  Does not image solid parenchymal damage, retroperitoneum, diaphragmatic
- Frequent re-evaluation and continuous monitoring  rapidly recognise when defects or bowel injury
patient is deteriorating  Compromised in uncooperative, agitated patient, obesity, substantial bowel gas,
subcutaneous air
5. PAIN MANAGEMENT  Less sensitive, more operator-dependent than DPL and cannot distinguish blood
- Intravenous analgesia as appropriate from ascites
 Intermediate results require follow-up attempts or alternative diagnostic tests

4
5
CT SCAN CARDIOTHORACIC TRAUMA
- Only suitable for stable patient as quite long time involved in imaging with only
patient in the room  can collapse There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving:
cardiac tamponade, airway obstruction, flail chest, haemothorax, and pneumothorax.
- Advantages
 Able to precisely locate intra-abdominal lesions preoperatively
 Able to evaluate retroperitoneum CARDIAC TAMPONADE
 Able to identify injuries that can be managed non-operatively - High index of suspicion required
 Not invasive - Clinical features
- Disadvantages  Chest trauma and hypotension
 Expensive  Beck‘s triad (hypotension, muffled heart sounds, distended neck veins) – only
 Time required to transport patient seen in 50% of cases as hypovolaemia may prevent neck vein distension; muffled
 Use of contrast heart sounds are least reliable
 Pulseless electrical activity
 Kussmaul‘s signs (increased neck distension during inspiration, pulsus paradoxus)
DIAGNOSTIC PERITONEAL LAVAGE (DPL)
- Involves making a cut in the infraumbilical region and inserting a catheter into the - Diagnostic clues
peritoneal cavity, aspirate, then instillation of saline and re-aspiration  Enlarged cardiac shadow in CXR (globular heart – very rarely seen)
 Small ECG voltages, electrical alternans (uncommon)
- Positive DPL  Pericardial fluid demonstrated on FAST or 2D-echo - definitive
 Frank blood (>5ml) or obvious bowel contents aspirated
 Lavage fluid seen to exit from chest drain or urinary catheter - Management
 RBC >100,000 per mm3, WBC >500, Gram stain positive for bacteria in effluent  Aggressive fluid resuscitation – helps maintain cardiac output and buys time
 Pericardiocentesis: ECG lead-guided or 2D-echo guided
- Indications:
 Any unstable patient with suspicion of abdominal trauma or where clinical exam
is difficult or equivocal AIRWAY OBSTRUCTION
 Unexplained hypotension in multiple trauma - Chin lift or jaw thrust
 Patient requiring immediate surgery for extra-abdominal injuries - Remove any foreign body manually, suction blood/secretions
- Definitive airway – ETT, cricothyroidotomy, tracheostomy
- Contraindications
 Absolute indication for laparotomy already exists
 Previous abdominal surgery or infections FLAIL CHEST
 Gravid uterus - When 2 or more ribs are fractured at 2 points forming a flail segment that moves
 Morbid obesity paradoxically with breathing
 Coagulopathy - Results in hypoxaemia mainly due to underlying pulmonary contusion, contributed to
by pain with restricted chest wall movement
- Advantages
 Can promptly reveal or exclude the presence of intraperitoneal haemorrhage - Management: ensure adequate oxygenation and ventilation; judicious fluid therapy
 Valuable in discovery of potentially lethal bowel perforation (avoid fluid overload); adequate intravenous analgesia
- Consider mechanical ventilation in high risk patients: shock, severe head injury,
- Disadvantages previous pulmonary disease, fracture of >8 ribs, age > 65, >3 associated injuries
 Morbidity involved – wound complications (haematoma, infection);
intraperitoneal injury
 False negative rate of 2% when there is failure to recover lavage fluid, early
hollow viscus injury, diaphragmatic injuries, injuries to retroperitoneal structures
HAEMOTHORAX (b) Subdural haemorrhage
- Chest tube insertion in the triangle of safety (bound by the lateral border of the  Crescent shaped haematoma under the dura (between the dura and the
pectoralis major medially, a line just anterior to the mid-axillary line laterally, and the arachnoid)
upper border of the fifth rib inferiorly)  More severe than EDH (usually due to nature of injury that causes SDH to
- Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot occur – associated with higher impact, thus brain has other injuries)
- If blood >1500mls  massive haemothorax, call urgent cardiothoracic consult  Pathology: underlying brain damage in addition to expanding SOL
 Removal of blood does not solve underlying brain damage  poorer results
PNEUMOTHORAX (OPEN/TENSION) (c) Traumatic subarachnoid haemorrhage
- Tension pneumothorax is a clinical diagnosis (CXR will only delay treatment, and  Usually only small amount of blood  conservative treatment sufficient
may cause death) – signs of pneumothorax, hypotension, neck vein distension, severe (d) Intraparenchymal haemorrhage
respiratory distress  Any shape, size, location
- Immediate needle thoracotomy in second intercostal space in mid-clavicular line  If large haematoma, will require evacuation
- Followed by chest tube insertion
4. Diffuse axonal injury
- Open pneumothorax occurs in a large chest wall defect with equilibration between - Global injury of axons
intrathoracic and atmospheric pressure, producing a ―sucking chest wound‖ - Arises from injury that causes rotational and shearing forces (high impact
- Cover defect with a sterile dressing, taping it down on 3 sides to produce a flutter- injury) – rapid acceleration and deceleration of brain in the intracranial cavity
valve effect, letting air out of the pleural cavity but not back in against relatively fixed points of attachment at the falx and tentorium
- Insert chest tube (not through the wound) - Maximal effects at corpus callosum and brainstem
- If severe, will see punctate haemorrhages at the grey-white border
5. Cerebral oedema (2 types)
NEUROSURGICAL TRAUMA (a) Hypoxic (cellular)
 Decreased blood supply (oxygenation)  loss of function of Na-K pump as
AIM in management of head injuries is the prevention of secondary brain injury (from ATP decreases  increased intracellular sodium  cellular swelling
hypotension, hypoxaemia, increased ICP etc) since neuronal death is irreversible.
(b) Interstitial
 Breakdown of blood-brain barrier  proteins enter interstitial space 
PATHOLOGIES: oedema
1. Concussion
- Physiological dysfunction without anatomical or radiological abnormality
- (Physiological dysfunction is the first step towards cell death, but is reversible if PATHOPHYSIOLOGY
no further insult occurs) 1. Monroe-Kellie doctrine
- Usually recovers in 2-3 hours - Intracranial cavity is of fixed volume and its contents (brain, CSF, blood) are
relatively incompressible
2. Contusion - Thus increase in intracranial volume  raised ICP
- Small haematoma <1cm
Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure
3. Intracranial haemorrhage
(a) Extradural haemorrhage - Compensatory mechanisms:
 Lens-shaped haematoma outside the dura (between skull and dura) (a) Hyperventilation  vasoconstriction of cerebral vessels due to increased
 Pathology: expanding space-occupying lesion partial pressure of carbon dioxide  decrease in blood volume
 20% of patients with EDH are alert and well; underlying brain is minimally (b) CSF pushed into spinal canal (but limited volume available)
damaged, thus drainage gives good results - Removal of any reversible cause of raised ICP will improve cerebral perfusion
6
7
2. Fixed dilated pupil
- Constrictor fibres to the pupil run in the oculomotor nerve, which exits the 3. Moderate head injury
brainstem at the upper midbrain – nerve fibres lie just under the tentorium - All will be CT-scanned at ED  NES will operate if any indication to do so
- Uncus of the temporal lobe sits on the tentorium - In ward: as per mild head injury
- In raised ICP, the uncus herniates over the edge of the tentorium,
compressing the fibres of the oculomotor nerve just below 4. Severe head injury
- Thus a fixed dilated pupil occurs on the side of the compression due to - Must scan to look for reversible causes of raised ICP but stabilise patient first
unoppressed sympathetic supply (dilates the pupil)
- Medical methods to lower ICP
3. Cushing’s reflex (a) Intubate and hyperventilate
- A triad of: (b) IV mannitol (must catheterise patient also; do not give if patient is unstable)
(a) Raised ICP - Screen for other life-threatening injuries (likely to be multi-trauma patient)
(b) Hypertension - Achieve haemodynamic stability
(c) Bradycardia (a) Check for long bone fractures
- From Monroe-Kellie doctrine, an increase in mean arterial pressure helps to (b) FAST for bleeding into abdominal cavity
maintain cerebral perfusion pressure when ICP is raised (c) ABG to detect acidosis
- Increase in mean arterial pressure achieved by sympathetic overdrive: (d) Keep monitoring patient and re-investigate where appropriate
(a) Increased heart rate - Operate if reversible cause found
(b) Increased contractility (a) Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced
(c) Increased vasoconstriction – increased total peripheral resistance after blood evacuated) [Burrhole usually not big enough to drain an acute
(a) and (b) increase cardiac output  increased BP; (c) increases BP bleed]
- Baroreceptors detect abnormally raised blood pressure and try to decrease it  (b) Evacuate clot
heart rate falls (c) Insert endoventricular drain (EVD) if there is hydrocephalus
- Total sedation after operation, ward in ICU
MANAGEMENT  Prevents patient from struggling which will raise ICP
1. Assessment
- 3 important parameters: ABCs, GCS, pupil size 5. Depressed skull fracture
- Glasgow coma scale (see above) – Minor head injury: 14-15; moderate injury: 8- - Can leave alone unless depression is greater than the thickness of the skull bone
13; severe injury: 3-7
6. Compound depressed fracture
2. Minor head injury - There is through-and-through skin laceration over the fracture
- Most common - Always explore to ensure underlying dura is intact, and repair if dura is torn
- Indications for admission: (since meningitis can occur with a torn dura)
 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 patient deteriorates  CT scan, exclude metabolic causes (e.g. hypoglyc), do
septic workup (exclude sepsis)
MUSCULOSKELETAL TRAUMA Wound care
- Swabs of the wounds for culture and sensitivity
GENERAL POINTS - IV antibiotic prophylaxis
- Extremity trauma tends not to be life-threatening - Tetanus toxoid cover
- But occult blood loss can occur in large volumes especially in certain types of - Photograph wound (to prevent re-opening of wound by every doctor that comes to
injuries – pelvic fracture (up to 3L), femoral shaft fracture (up to 2L) see patient)
- Need to have high level of suspicion and treat with urgency - Betadine dressing
- Look out for any tachycardia, early signs of shock - In OT: generous debridement, irrigation (within 4-8 hours, especially in open
- Prepare to resuscitate patient fractures), fracture stabilisation (internal or external fixation depending on Gustilo
classification)
- Leave wound OPEN
ASSESSMENT OF THE EXTREMITY
- Perfusion: colour, pulses, skin temperature, capillary refill
- Deformity MANAGEMENT OF FRACTURES
- Wounds – open or closed injury; abrasion over a fracture is considered open fracture - Recognise fracture and/or dislocation
- Soft tissue assessment - Complete neurovascular examination of the limb involved before reduction
- Abnormal joint mobility – ligamentous injury around the joint; if in the knee, highly - Appropriate X-rays (at least 2 planes)
likely that the popliteal artery is injured as well - Analgesia
- Neurological assessment - Correction of deformity
- Viability of the limb - Temporary immobilisation – backslab, malleable splint
- Neurovascular examination; examine for compartment syndrome
- Circulation chart
THE PULSELESS EXTREMITY
Things to consider
- Is pulselessness due to shock? OPEN FRACTURES
- Arterial or venous compromise? Definition: there is communication between the fracture or fracture haematoma and the
- Is there compartment syndrome (pulselessness is a very late sign) external environment
- Any pre-existing vascular disease?
Gustilo-Andersen classification
Physical examination
Type I  <1cm AND clean
- Any limb deformity (can result in kinking of vessels)?
- Any joint instability (dislocation of a joint can result in intimal tear in the major Type II  >1cm AND no extensive soft tissue damage, avulsions or flaps
vessel running across it, with thrombosis and occlusion)? Type IIIA  Extensive soft tissue damage, avulsions or flaps but adequate soft
- Skin colour/temperature tissue coverage of bone OR
- Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent  High-energy trauma cause irregardless of size of wound
angiogram!
Type IIIB  Extensive soft tissue loss with periosteal stripping and exposure of
bone.
SOFT TISSUE INJURIES
 Massive contamination common
Types
- Open: laceration, abrasion Type IIIC  Arterial injury requiring repair
- Crushing
- Degloving: open or closed
- Closed

8
9
- Grade I
 Low velocity injury, prognosis similar to closed fracture
 Treat with ORIF within 6 hours
- Grade II
 Moderate velocity, more trauma
- Grade IIIA
 Skin graft usually possible
- Grade IIIB
 Skin graft alone often not adequate
 Local and free flaps will be necessary
 Secondary bone procedures
- Grade IIIC
 Neurovascular injuries present in addition to musculoskeletal injuries

Management of open fractures

- Recognise an open fracture
- 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:
(a) Generous debridement of the wound with irrigation to decrease bacterial load
(b) Treat any soft-tissue injuries
(c) Stabilise fracture – usually using external fixator
ABDOMINAL PAIN
RHC Epigastric LHC
Thoracic Hepatic Thoracic Others Thoracic Others
 Pneumonia  Hepatitis (viral, autoimm etc)  MI  Pancreatitis  Pneumonia  Subphrenic abscess
 Pleural effusion  Hepatomegaly  Pericarditis  Pleural effusion  Splenomegaly
 Abscess  Aortic aneurysm  MI  Pancreatitis
Biliary
 Cholangitis Others Gastrointestinal Gastrointestinal
 Cholecystitis  Subphrenic abscess  Oesophagitis  PUD
 Gallstone disease  Pancreatitis  GERD  Diverticulitis
 PUD  PUD  Mesenteric ischaemia
 Appendicitis  Gastric outlet obstructn
 CA stomach

Rt Loin Periumbilical Lt Loin

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

RIF Hypogastric LIF

Gastrointestinal O&G Gastrointestinal O&G Orthopaedics
 Appendicitis  Ovarian cyst  Colorectal CA  Ectopic pregnancy Infection Paediatric ortho conditions
 Terminal ileitis  Ovarian torsion  Abortion  Septic hip arthritis  Transient synovitis
 Meckel‘s diverticulitis  Ectopic pregnancy Urological  PID  TB hip  Perthes‘ dz
 Mesenteric ischaemia  PID  ARU  Uterine rupture Degeneration  SCFE
 Mesenteric adenitis  Bladder calculi  Fibroid complications  OA hip
 IBD Orthopaedics (See LIF)  Cystitis / UTI  Adenomyosis Gastrointestinal
Inflammation
 Colitis  Endometriosis  Diverticulitis
 RA hip
 Colorectal CA  IBD
 Ankylosing spondylitis
 Hernia  Colitis
 Reiter‘s syndrome
 Colorectal CA
Inflitration  Hernia
 1o bone tumour (hip)
 Metastasis to hip O&G (see RLQ)
Destruction
 # - NOF, pubic rami
Radiation
 Back pathologies (referred
pain)

10
11
ABDOMINAL MASS
RHC Epigastrium LHC
Liver Gallbladder Liver (see RHC) Stomach Spleen Stomach
Massive  Pancreatic/periampullary ca  Cancer Massive
 Cancer: HCC  Acute cholecystitis Pancreas  Distension (GOO)  Infxns Descending colon
Metastases  Hydrops  Pseudocyst  CML  Cancer
Myeloprolftve dz  Empyema  Tumour Aorta  Myelofibrosis  Diverticular mass/abscess
 Alcoholic liver dz  Mirizzi syndrome  Aortic aneurysm  Faeces
Moderate
 Rt ht failure/tricuspid regurg Transverse colon
 Above causes
Ascending colon  Cancer Retroperitoneal lNpathy Left kidney(see Rt lumbar)
Moderate  Portal hypt
 Cancer  Diverticular mass/abscess  Lymphoma
 Above causes  Lymphoprolftve dz
 Diverticular mass/abscess  Faeces  Teratoma Left adrenal gland
 Lymphoprolftve dz (lymphoma, CLL)
 Faeces  Other malignancies
 Haemochromatosis  H‘lytic anaemia (thal, HS)
 Amyloidosis  Storage dz (Gaucher‘s)
Right adrenal gland
Mild Mild
 Above causes Right kidney(see Rt lumbar)  Above causes
 Infxns: Viral – Hep, IMS  Infxns: Viral hep, IMS
Bacterial – abscess Endocarditis
Parasitic – hydatid  Autoimm – SLE, RA, PAN
cyst, amoebic abscss  Myeloprolftve dz – PRV,
 Biliary obstruction essential thrombocytopaenia
 Cirrhosis  Infiltratn – sarcoid, amyloid

Right Lumbar Umbilical Left Lumbar

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

RIF Hypogastrium LIF

Gastrointestinal O&G Bladder Uterus Gastrointestinal
 Appendiceal mass/abscess  Ovarian cyst/tumour  Acute retention of urine  Gravid uterus  Diverticular mass/abscess
 TB gut  Fibroids  Chronic retention of urine  Fibroids  Ca colon/sigmoid
 Ca caecum Urogenital:  Tumour  Crohn‘s dz (terminal ileitis)
 Distended caecum (due to  Transplanted kidney Anal/rectal mass  Faeces
distal obstruction)  Bladder diverticulum  Cancer Ovary
 Crohn‘s dz (terminal ileitis)  Ectopic or undesc testis  Cyst Similar causes as RIF mass
Vascular:  Tumour
Orthopaedics  Iliac artery aneurysm
 Chondroma/sarcoma of ilium  Iliac lymphadenitis
 Bony metastasis Skin & Msk:
 Psoas abscess
OESOPHAGEAL DISEASES - Pharyngeal muscles contract to propel food bolus past the relaxed cricopharyngeus
into the oesophagus
ANATOMY - Once in the oesophagus, involuntary contractions of the muscularis propria form
- Oesophagus is a muscular tube that is 25cm (10 inches) long peristaltic waves to propel food bolus into stomach
- Starts at the cricoid cartilage (C6 vertebra) from the oropharynx and continues into
the stomach at the level of T10
APPROACH TO DYSPHAGIA
- Upper oesophageal sphincter is formed by cricopharyngeus muscle
- Lower sphincter is not an anatomical sphincter, but physiological: CAUSES OF DYSPHAGIA
(i) Increased tone of the muscularis propria at the lower oesophageal sphincter - Dysphagia can be divided into oropharyngeal and oesophageal dysphagia
(ii) Fibres of the right diaphragmatic crus loop around the cardio-oesophageal - In each anatomic region the dysphagia can be caused by neuromuscular dysfunction
junction and ontract during coughing, sneezing etc when intra-abdominal (impaired physiology of swallowing) or mechanical obstruction to the lumen
pressure increases, thus preventing reflux
Oropharyngeal Oesophageal
(iii) Angle of His where the oesophagus joins the stomach – acts as a valve Neuromuscular diseases Neuromuscular diseases
(iv) Intra-abdominal pressure being higher than intra-thoracic pressure Stroke Achalasia
- 3 narrow points along the course of the oesophagus Parkinson’s disease Spastic motor disorders
Brain stem tumours Diffuse oesophageal spasm
(i) Cricopharyngeus muscle (15cm from incisor teeth) Hypertensive lower oesophageal sphincter
Degenerative conditions e.g. ALS, MS
(ii) Carina where the left bronchus crosses the oesophagus (27cm from incisors) Peripheral neuropathy Nutcracker oesophagus
(iii) Where the oesophagus passes through the diaphragm (40cm from incisors) Myasthaenia gravis Scleroderma
Myopathies e.g. myotonic dystrophy
- Structure: mucosa, submucosa, muscularis propria, adventitia (no peritoneal lining
except for a short segment of intra-abdominal oesophagus) Obstructive lesions Obstructive lesions
Muscularis propria is composed of striated muscle in the upper one-third, striated and Tumours Intrinsic structural lesions
smooth muscle in the middle third, and smooth muscle in the lower third Inflammatory masses e.g. abscess Tumours
Oesophageal webs Strictures: Peptic (reflux oesophagitis)
- Blood supply (roughly divided into thirds): Inferior thyroid artery to upper third, Pharyngeal pouch (Zenker‘s divert) Radiation
oesophageal branches of the aorta to the middle third, oesophageal branches of left Anterior mediastinal mass Chemical (caustic ingestion)
gastric artery to lower third Medication
- Venous return also divided into thirds: Brachiocephalic veins (upper), azygos veins Lower oesophageal rings (Schatzki‘s ring)
Oesophageal webs (Plummer-Vinson)
(middle), left gastric vein (lower) --- a portosystemic anastomosis exists at the lower
Foreign bodies
oesophagus thus leading to formation of varices in portal hypertension
Extrinsic structural lesions
Vascular compression (enlarged aorta or
PHYSIOLOGY OF SWALLOWING
left atrium)
- Process of mastication forms a food bolus on the dorsum of the tongue Mediastinal masses – retrosternal thyroid,
- The tongue then contracts upwards and backwards pushing the food bolus against the lymphadenopathy
hard palate
Others
- Soft palate elevates (contraction of palatoglossus) to close off nasopharynx Oesophagitis: Reflux
- Further elevation of tongue pushes food bolus into oropharynx Infectious (candida, herpes)
Radiation-induced
- As the base of the tongue is elevated posterior, the epiglottis falls back; at the same
Medication-induced
time, the pharyngeal muscles contract to bring the posterior surface of the larynx Chemical-induced (alcohol)
upwards to make the laryngeal inlet smaller  closed off by the epiglottis
12
13
HISTORY: - Medication history
1. Is there odynophagia (pain associated with difficulty swallowing)? - Symptoms of systemic disease e.g. stroke (focal neurological deficits),
- Signifies some form of oesophagitis: infectious (candida, herpes), post-radiation, scleroderma (telangiectasia, sclerodactyly, calcinosis, Raynaud‘s), Parkinson‘s
chemical-induced (usually alcohol), reflux oesophagitis
5. Systemic review
- Oesophageal spasm
- Loss of weight occurs in cancer and achalasia, but of much later onset in
- Scleroderma
achalasia compared to cancer
- Pain occurs late in achalasia and oesophageal cancer (not painful from the start)
- Symptoms of anaemia (bleeding from tumour, or as part of Plummer-Vinson
2. Differentiating oropharyngeal from oesophageal dypshagia syndrome)
- Symptoms of aspiration pneumonia – fever, cough, shortness of breath
(i) Oropharyngeal
- Presenting complaint is usually of difficulty in initiating swallowing
6. Tumour spread
- May be associated with choking, coughing, nasal regurgitation - Hoarseness (recurrent laryngeal nerve)
- Voice may sound nasal (bulbar palsy) - Fever, cough and haemoptysis (tracheo-oesophageal fistula)
- Cause of oropharyngeal dysphagia is usually neuromuscular rather than - Haematemesis (invasion into aorta)
mechanical; stroke is the most common cause - Neck lump (lymph node)
(ii) Oesophageal
- Presenting complaint is that of food “getting stuck” in the throat or chest PHYSICAL EXAMINATION
- Patient‘s localisation of the symptom often does not correspond to actual site
of pathology 1. General condition
- Can be due to either neuromuscular dysfunction or mechanical obstruction - Vitals: the patient may be hypovolaemic from vomiting/decreased intake
- Nutrition: presence of cachexia
3. Differentiating mechanical obstruction from neuromuscular dysfunction - Conjunctival pallor: bleeding from tumour, oesophagitis ulcerations, or
(i) Mechanical associated with P-V syndrome
- Patient complains of more difficulty swallowing solids than fluids - Scleral icterus: metastases to liver
- May have regurgitation of undigested food - Dehydration (mucous membranes, skin turgor, etc)
- Recent onset dysphagia that is progressively worsening, with loss of weight
2. Disease
 high suspicion of oesophageal cancer
- Presence of cervical lymph nodes (esp Virchow‘s node)
- Intermittent symptoms are suggestive of webs, rings
- Scars/marks over the chest and abdomen suggesting previous surgery, radiation
(ii) Neuromuscular - Palpable mass in abdomen (not likely)
- Patient complains of more trouble swallowing fluids than solids - Hepatomegaly
- Dysphagia more long-standing, slowly progressive - Ascites
- Intermittent symptoms suggestive of diffuse oesophageal spasm, nutcracker - PR examination for malaena
oesophagus
- May have history of stroke, neuromuscular disease 3. Complications of disease
- Signs of pneumonia: patient febrile, may be toxic, lung crepitations, decreased
4. History of predisposing conditions air entry usually over right lower lobe
- Reflux symptoms e.g. retrosternal burning pain (heartburn), sour fluid reflux into
mouth (acid brash), excessive salivation (water brash), postural aggravation on 4. Treatment
lying down - Tube feeding through NG tube, gastrostomy/jejunostomy – if aspirates seen,
- Caustic chemical ingestion in the past what is the colour?
- Smoking, chronic alcohol intake - Total parenteral nutrition
- Radiation to the chest
MANAGEMENT
1. Stabilise patient
- Resuscitate if patient is haemodynamically unstable
- IV fluids (correct fluid deficits and also any electrolyte derangements)
- 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
- Keep NBM if patient cannot tolerate even fluids
- Treat any aspiration pneumonia – NBM, IV antibiotics
2. Investigate for underlying cause and treat it
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) or 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

INVESTIGATIONS Supportive
1. Blood investigations:
Diagnostic
- Full blood count – Low Hb (anaemia from chronic blood loss)
1. Barium swallow
High TW (aspiration pneumonia)
- Advantage of barium swallow is that it is less invasive than OGD, especially - Urea, electrolytes, creatinine – electrolyte disturbances from vomiting, poor
when suspecting webs, diverticula in the oesophagus where OGD may cause intake; raised creat and urea in dehydration (creat will be raised more than urea if
perforation; however if patient is at high risk of aspiration, barium swallow is patient has prerenal failure from dehydration)
dangerous.
- Liver function tests – low albumin with nutritional deprivation
- Visualisation of obstructive lesions:
o Shouldering of a stricture (benign strictures form a smoother contour 2. CXR
whereas malignant strictures form a more right-angled contour) - Consolidation (aspiration pneumonia)
o Bird‟s beak sign of achalasia
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)

Achalasia Benign stricture Carcinoma

- Visualisation of pharyngeal pouch or oesophageal diverticulum
- Diffuse oesophageal spasm gives a corkscrew appearance

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)
14
15
CANCER OF THE OESOPHAGUS STAGING
T Tis High-grade dysplasia/carcinoma in-situ
Stage T N M
EPIDEMIOLOGY T1a Tumour invading lamina propria or
muscularis mucosa 0 is 0 0
- Third most common gastrointestinal tract cancer in Singapore
- Male predominance T1b Tumour invading submucosa but does I 1 0 0
- Increasing incidence with age not breach submucosa IIA 2/3 0 0
T2 Tumour invades the muscularis propria IIB 1/2 1 0
T3 Tumour invades adventitia
RISK FACTORS T4 Invasion of surrounding structures
III 3 1 0
- Smoking (100x increased risk for SCC, 10x for adenocarcinoma) 4 any 0
N N1 Regional node involvement (1-3 nodes
- Alcohol (2x increased risk) involved =1a; 4-7=1b; >7=1c) IVA any any 1a
- Obesity (related to reflux, increases adenocarcinoma incidence) M M1a Nonregional lymph node involvement IVB any any 1b
M1b Other distant metastases
- Diet: Hot beverages, preserved foods (nitrosamines), betel nuts; vitamin and mineral
deficiencies (selenium, vitamin E, beta-carotene)
PRESENTATION
- Tylosis (autosomal dominant disorder with keratosis of palms and soles
Usually of insidious onset, with earliest symptoms being non-specific e.g. retrosternal
- Barrett‘s oesophagus (intestinal metaplasia of oesophageal mucosa due to reflux; discomfort, ―indigestion‖, and most patients already have advanced disease when they
increased risk of cancer due to metaplasia-dysplasia-carcinoma sequence; risk is 30- are diagnosed – 75% have lymph node involvement at time of diagnosis.
40x higher than in individual without Barrett‘s, and is about 1% per year)
1. Dysphagia
- Achalasia (2-8% incidence of SCC) - Present in 80% of patients – most common presentation
- Caustic injury (ca occurs at site of scar/stricture, mostly middle third of oesophagus) - Pain develops late and is usually due to extra-oesophageal involvement
- Plummer-Vinson (or Paterson-Brown-Kelly) syndrome – Post-cricoid oesophageal 2. Weight loss
web and iron deficiency anaemia. (10% develop cancer in upper third of oesophagus) 3. Regurgitation
4. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult)
PATHOLOGY 5. Vocal cord paralysis (left more than right)
- 70% squamous cell carcinoma, 30% adenocarcinoma 6. Aspiration pneumonia
- SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lower 7. Tracheo-oesophageal or broncho-oesophageal fistula
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 INVESTIGATIONS
lower third
Diagnosis
- Three growth patterns: 1. Barium swallow
 Fungating (60%) - 92% accuracy in showing mucosal irregularity and annular constrictions but not
 Ulcerative (25%) able to diagnose malignancy with confidence
 Infiltrative (15%)
- Tumour spread: direct extension into surrounding structures, vascular invasion, 2. Oesophagogastroduodenoscopy
lymphatic spread - Allows biopsy of the lesion  confirmatory histological diagnosis
- Common sites of metastases: liver, lung, bone Staging
1. Endoscopic ultrasound
- If endoscope can pass around the lesion, the EUS is good for T staging, and also
to identify enlarged regional lymph nodes
2. Chest X-ray - Endoluminal surgery – for early lesions; no attempt to remove any LNs (usually no
- Presence of any lung metastases LN involvement)
- Aspiration pneumonia
- Pleural and/or pericardial effusion - Oesophagectomy
- Tracheal deviation or extrinsic compression of tracheobronchial system (i) Ivor-Lewis
- Widened superior mediastinum in an upper oesophagus tumour Two-stage procedure involving gastric mobilisation (first stage, done through
- Raised hemidiaphragm with phrenic nerve involvement upper midline abdominal incision), oesophagectomy and gastro-oesophageal
anastomosis in the chest (second stage, through right thoracotomy incision)
3. CT scan or MRI of the thorax with extension to include liver and adrenals
- Can be used for T, N, and M staging (ii) Trans-hiatal
Done via two incisions – one in the abdomen and one in the neck
4. Bronchoscopy Blunt oesophagectomy, gastric mobilisation, and gastro-oesophageal
- Exclude bronchial involvement especially in tumours involving upper two-thirds anastomosis in the neck
of oesophagus Less morbidity than Ivor-Lewis as the chest is not opened, but controversial

5. Bone scan for bony metastases (iii) Tri-incisional

Three incisions – abdominal, chest, and also left neck incision for gastro-
6. Laryngoscope to assess for vocal cord paralysis oesophageal anastomosis in the neck

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

1. Full blood count – Low Hb (anaemia from chronic blood loss)
High TW (aspiration pneumonia)
2. 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)
3. Liver function tests – low albumin with nutritional deprivation
TREATMENT
Principles
- Three modalities available – surgery, chemotherapy, radiotherapy – used singly or in
combination
- Aims of treatment: Curative or palliative (50% of patients have unresectable cancer
on presentation)
- 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 of cancer
Surgery
- Curative in early lesions (in-situ, T1a) and part of multimodal therapy in more
advanced stages
- Resection should not be done in patients with distant metastases or contraindications
to surgery
 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%) and morbidity (25%) rates, thus
patients have to be carefully selected in order to maximise survival benefit from
surgery
 Complications of surgery 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
- Reflux can result in the long term due to loss of the LES
- Anastomotic stricturing can also occur
- 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

16
17
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
- Surgical debulking
- Bypass surgery rarely done nowadays
- Endoscopic laser fulguration to relieve obstruction
- Photodynamic therapy is a new treatment option
- Stenting to maintain lumen patency
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)
- 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); consider PEG placement for long-term feeding if able to get scope around
tumour
- If unable to pass tube or scope around tumour, consider open gastrostomy
- Total parenteral nutrition is another option but has more complications, more costly
- 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%
GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)
EPIDEMIOLOGY
Incidence in Singapore not known
Increasing prevalence, more common in males than females
PATHOPHYSIOLOGY
- Lower oesophageal sphincter is a physiological sphincter with various mechanisms
that help to prevent reflux (see above, Anatomy of the oesophagus)
- 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:
 Loss of LES function – decreased tone, hiatal hernia, iatrogenic injury
 Delayed gastric emptying
 Increased intra-abdominal pressure – obesity, tight garments, large meal
 Motor failure of oesophagus with loss of peristalsis
- Acid incites inflammation in the 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
- Malfunction of LES
- Motility disorder of oesophagus e.g. scleroderma
- Hiatal hernia (loss of normal LES mechanisms)
- Chronically increased intra-abdominal pressure – pregnancy, chronic cough, obesity,
constipation, etc
- Drugs that cause smooth muscle relaxation e.g. calcium channel blockers, sedatives,
beta agonists, anticholinergics, etc. Coffee and smoking also cause LES relaxation.
- Eating habits – lying down after a heavy meal
- Any cause of decreased gastric emptying
PRESENTATION
- Heartburn: retrosternal pyrosis
- Acid brash: reflux of sour gastric juices into back of mouth i.e. regurgitation
- These symptoms occur usually after food, particularly a heavy meal, and are
aggravated by lying flat (posturally related)
- 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
- Reflux can also lead to pulmonary symptoms: chronic cough, chest infections
(aspiration)
- Other symptoms: globus (feeling of a lump at the throat), chest pain (can mimic
anginal pain with radiation to neck, jaw, arm), nausea, water brash (hypersalivation in
response to reflux)
- Can detect motility disorders that cause reflux, and also pick up 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

COMPLICATIONS GRADING OF OESOPHAGITIS

1. Pain and spasm
1. Savary-Miller classification
2. Stricture
Grade I: One or more supravestibular non-confluent reddish spots, with or
3. Haemorrhage (occult more common than frank)
without exudates
4. Shortening of oesophagus
Grade II: Erosive and exudative lesions, may be confluent but not circumferential
5. Ulceration Grade III: Circumferential erosions covered by haemorrhagic and
6. Barrett‘s oesophagus (see below) pseudomembranous exudate
7. Dysmotility Grade IV: Presence of chronic complications such as deep ulcers, stenosis, or
8. Schatzki‘s ring (constrictive ring at the squamocolumnar junction composed of scarring with Barrett‘s metaplasia
mucosa and submucosa)
9. Malignancy (adenocarcinoma arising from Barrett‘s oesophagus) 2. Los Angeles classification
Grade A: one or more mucosal breaks, each <5cm in length
DIAGNOSIS Grade B: at least one mucosal break >5cm long, but not between the tops of
adjacent mucosal folds
1. History is important as most patients with reflux are seen in the primary setting Grade C: at least one mucosal break that is continuous between the tops of adjacent
with no facilities for detailed investigation mucosal folds, but which is not circumferential
- Exclude cardiac cause of chest pain, and exclude malignant cause of dysphagia Grade D: mucosal break that involves at least three-quarters of the luminal
2. Oesophagogastroduodenoscopy circumference
- Cannot actually diagnose reflux - Relevance of classification schemes: subjective and dependent on assessment by the
- Can visualise and grade oesophagitis if present, and take biopsy specimens for endoscopist; also, due to the multitude of classification schemes available, just
confirmation (see below) mentioning a grade may not have any meaning if the actual abnormalities are not
- May see a hiatal hernia which is associated with reflux (though not all patients described
with hiatus hernia will have reflux)
TREATMENT
3. Oesophageal pH probe
- Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probe Lifestyle
especially if oesophagitis is not seen on OGD 1. Diet and eating habits
- Antimony probe most commonly used; alternative is the Bravo capsule (a  Avoid coffee, chocolate, fatty foods, or anything that worsens symptoms
wireless capsule that is temporarily attached to the oesophageal wall)  Do not eat 2 hours prior to sleeping
 Walk after eating
- The probe is placed 5cm above the manometrically-determined upper limit of the  Avoid excessive eating; eat small meals
LES (for the wired probe), or 6cm above the endoscopically-determined
squamocolumnar junction (for the wireless capsule) 2. Avoid drugs that relax LES e.g. anticholinergics, muscle relaxants, etc.
- Diagnosis based on the percentage of time in 24hrs the pH reading is below 4 3. Weight reduction if obese
4. Elevate head of bed
4. Barium swallow and follow-through 5. Smoking and alcohol intake cessation
- Not of much value in diagnosing reflux
18
19
Medication
1. Acid suppression therapy: proton pump inhibitors or H2-receptor antagonists
2. Prokinetics to increase LES pressure e.g. domperidone, metoclopramide
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
 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
- Fundoplication is the mainstay of surgical therapy
 Can be done via open surgery or laparoscopic surgery (most laparoscopic now)
 Nissen fundoplication is the most commonly done – a 360 degree (total) wrap of
the fundus around the gastro-oesophageal junction
 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
 Perforation of the oesophagus – most feared complication, may result in
mediastinitis if not promptly detected and repaired intraoperatively
 Excessively tight wrap resulting in dysphagia
 Excessively loose or short wrap – reflux recurs (failure of treatment)
 ―Slipped-Nissen‖ occurs when the wrap slides down, the GE junction retracts
into the chest, and the stomach is partitioned; usually due to a foreshortened
oesophagus unrecognised in the first operation
 ―Gas bloat syndrome‖ – patient experiences difficulty burping gas that is
swallowed
- 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
 Dilatation (variety of means available – balloon, dilators, etc)
 Treatment of underlying reflux
 If resistant to dilatation  resection and reconstruction
BARRETT’S OESOPHAGUS
Features
- Intestinal metaplasia of the oesophageal epithelial lining (stratified squamous
epithelium converted to mucus-secreting columnar epithelium with goblet cells)
- Associated with long-term reflux – an adaptation mechanism where intestinal
epithelium withstands exposure to acidic reflux better than oesophageal epithelium
- Diagnosed on endoscopy and histology:
 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
- Short segment Barrett‘s is defined as the squamocolumnar junction being <3cm
above the gastro-oesophageal junction, while in long segment Barrett‘s the distance
between the two junctions is >3cm.
- Long segment Barrett‘s is 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, 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
- 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 (q3mths for at least one year) to detect cancer
development
3. Treatment of high-grade dysplasia
- Endoscopic therapies to ablate the dysplastic tissue e.g. photodynamic therapy,
laser therapy, argon plasma coagulation  will not remove all dysplastic cells
thus potential for malignancy still remains
- Oesophagectomy is the only definitive treatment to remove all dysplasia, but is
associated with high morbidity and mortality (worth it?)
- Possibility of endoscopic mucosal resection as a treatment modality (research
still undergoing)
20
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
- Aetiology unknown
- 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:
 Injection of botulinum toxin (problem is that it is not long lasting and only used
in patients not fit for surgery)
 Pneumatic balloon dilatation (about 65% of patients improve, 40% response rate
at 5 years)
- Surgical treatment
 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 helps prevent this
21
UPPER BLEEDING GIT AND ITS CAUSES 3. Aetiological clues
Gastric ulcer/gastritis/erosions
APPROACH TO BLEEDING UPPER GIT - Any history of dyspepsia, gastric ulcer (any OGD done in the past showing these
problems? On any ―gastric‖ medications?)
CAUSES - Any drugs that may predispose – NSAIDs, antiplatelets, steroids, anticoagulants,
1. Peptic ulcer disease (bleeding peptic ulcer) TCM
2. Gastritis, gastric erosions, duodenitis Varices
3. Gastric malignancy - Any history of chronic liver disease
4. Gastro-oesophageal varices Mallory-Weiss tear
5. Mallory-Weiss tear - Binge-drinking with subsequent severe retching and vomiting leading to
6. Rare causes: AV malformation (Dieulafoy lesion), aortoenteric fistula haemetemesis
7. Bleeding from other sources: Haemoptysis, nasopharyngeal bleeding
Malignancy
- Recent constitutional symptoms e.g. LOA, LOW, malaise
HISTORY (if patient is stable)
- Early satiety
1. Nature of bleeding - Dyspepsia
Haematemesis
4. Complications
- Can be fresh red blood as in variceal bleeding, Mallory-Weiss tear, AV
- Symptoms of anaemia: postural giddiness, shortness of breath, lethargy,
malformation
decreased effort tolerance, palpitations, chest pain
- Coffee grounds vomitus is altered blood (due to gastric acid) and can come from
- AMI  esp. if it‘s an old patient with previous history of IHD
gastric ulcer, gastritis/erosions, or variceal blood that has entered the stomach
Malaena 5. Comorbidities
- Altered blood; malaena indicates bleeding from the upper GIT i.e. above the - Elderly patient (>60)  high risk
ligament of Treitz - Other comorbidities: liver disease, renal disease, IHD  high risk
- Different types of malaena:
(a) Fresh malaena – jet black with sheen, tarry, non-particulate (almost liquid PHYSICAL EXAMINATION
in consistency)
1. Vitals!
(b) Stale malaena – black-grey, dull, mixed with normal stool, occasionally
- Blood pressure, heart rate stable? Any postural hypotension? (Tachycardia is an
particulate
early sign of shock)
(c) Iron stool – greenish hue on rubbing between gloved fingers, particulate. - Patient‘s conscious level – confused?
- If gloved finger is stirred in a cup of water, malaena will ―dissolve‖ completely - Compare current vitals with vitals in ambulance, ED – is there a worsening trend?
with no sedimentation and turn the water black, but iron stool will sedimentate
and turn the water green 2. General inspection
- Pallor
Frank PR bleeding - Cold clammy peripheries  impending shock
- Very brisk upper GI bleed can present as frank PR bleeding as blood passes - Stigmata of chronic liver disease
down so fast it doesn‘t get altered
3. Abdomen
2. Amount of blood - Any tenderness (not very helpful)
- If patient is having haematemesis, ask how much blood  Cup? Bowl?
4. Digital rectal examination
- Malaena or frank blood
IMMEDIATE MANAGEMENT VARICEAL BLEEDING
1. Resuscitation
PATHOPHYSIOLOGY
- Protect airway, supplemental oxygen, 2 large-bore IV cannula in antecubital
fossa A result of portal hypertension (i.e. portal venous pressure >20 cmH2O or >12 mmHg –
normal should be 7-14 cmH2O or 5-10 mmHg)
- Take blood for investigations: FBC, U/E/Cr, PT/PTT, LFT, GXM 4 pints
- ECG to detect any acute myocardial ischaemia/infarction
- 1 pint N/S over half to one hour if patient is in shock, followed by more fluids if WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT
necessary (be wary in patients with renal failure, heart failure) - Previous history of variceal bleed
- Packed cells if Hb is less than 10, to keep Hb above 10g/dL - Chronic alcohol intake
- Jaundice or stigmata of chronic liver disease
- May consider platelets if patient is on antiplatelet medication (qualitative defect
in platelets)
- FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K) MANAGEMENT OF VARICES can be divided into three categories:
1. Acute bleeding
2. Adjuncts 2. Prophylaxis
- NG tube if patient is having haematemesis – prevents aspiration, allows gastric 3. Chronic management
lavage prior to OGD (DO NOT insert if suspecting varices)
- Catheterisation – monitor input/output balance especially in elderly patient or I. ACUTE BLEEDING – MANAGEMENT
when large amount of fluid resuscitation required, or anticipating surgery
1. Resuscitate
- IV omeprazole 80mg bolus (increases stomach pH and stabilises clot formation) - Airway, breathing, circulation
- If suspecting varices – IV somatostatin/octreotide, IV antibiotics, vitamin K - If patient appears well, look for early signs of shock – tachycardia, postural
hypotension
3. Close monitoring - Look at hydration status
- Monitor for:
 Increase in heart rate 2. Assess mental state
 Decrease in BP - If patient has altered mental state (encephalopathy)  need to protect airway
 Decrease in urine output (may require intubation)
 Increasing confusion and lethargy
3. Vascular access, fluids/blood resuscitation, and blood investigations
4. Emergency oesophagogastroduodenoscopy - 2 large-bore IV cannula in proximal veins (cubital, EJV, IJV)
- Indications: - Send bloods – GXM 4 pints, FBC, U/E/Cr, LFT, PT/PTT
 Shock (resuscitated) - Infuse fluids
 Ongoing BGIT - Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9, as
 Suspected variceal bleed enthusiastic transfusion can increase portal pressure and cause more bleeding
- Role of endoscopy 4. Management of severe bleeding
 Diagnostic: confirm UBGIT & identify source of bleeding, - If patient is hypotensive and bleeding is still continuing – may require use of
 Therapeutic: injection of ulcer, ligation/sclerotherapy for varices Sengstaken-Blakemore tube for up to 48hr
- Protect airway before inserting tube.
- Repeat OGD with greater detail if it is normal the 1st time. - Inflate gastric balloon and pull upwards against cardioesophageal junction
 Exclude haemoptysis & bleeding from nasopharynx (balloon will press on perforator veins entering oesophagus from stomach, and
 Look for Mallory weiss tear and posterior wall duodenal bleeding ulcer thus decrease oesophageal variceal bleeding); oesophageal balloon is not inflated
nowadays

22
23
5. IV somatostatin/octreotide
- Not given in ulcer bleed; mode of action is as a splanchnic vasoconstrictor which
decreases portal blood flow and hence portal pressures  decreased 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, esomeprazole, pantoprazole, etc.
7. Antibiotics
- Not given in ulcer bleed
- Studies have shown that cover with broad spectrum antibiotics (with Gram neg
cover) decreases infectious complications, possibly mortality, and also risk of
recurrent bleed
- Preferably started before endoscopy (procedures increase bacteraemia)
8. Endoscopy
- Purpose: confirm diagnosis and institute management
- Needs to be done emergently (on that night of admission) as soon as patient is
stabilised since bleeding can be torrential and life-threatening
- Banding is the best modality for stopping oesophageal variceal bleeding
(sclerotherapy is associated with higher morbidity e.g. mucosal ulceration)
- Gastric varices are usually too large to be banded, sclerotherapy used instead
9. Observation
- Continue antibiotics and omeprazole
- Continue somatostatin up to the point where haemostasis is achieved or 5 days
(exact ideal duration not well studied)
- 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. Secondary prophylaxis
- Best option is combination of band ligation and non-selective beta-blockers e.g.
propranolol unless propranolol is contraindicated
11. Management of possible precipitants
- NSAIDs; Hepatic vein thrombosis
If bleeding is not remediable by endoscopic intervention:
- Insert Sengstaken-Blakemore tube (only temporary) and repeat endoscopy 10-12
hours later
- Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt
(TIPSS) if in good Child‘s score to avoid ppt. encephalopathy
- Shunt surgery
 Portocaval shunts (joining portal vein to IVC) – side-to-side, end-to-side
 Mesocaval shunts (joining superior 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 and splenic
side anastomosed end-to-side to left renal vein)
- Sugiura procedure (last resort): splenectomy, proximal gastric devascularisation,
selective vagotomy, pyloroplasty, oesophageal devascularisation, oesophageal
transection
II. PRIMARY PROPHYLAXIS OF VARICEAL BLEEDING
Use of non-selective beta-blocker e.g. propranolol can be used to prevent development
of varices in patients without varices, and can decrease the size of and prevent bleeding
from varices in patients who already have them. In patients with small varices with no
risk of bleeding, the use of propranolol is of questionable benefit – repeat OGD to
monitor varices.
Predictors of variceal haemorrhage:
1 Site: varices at the gastro-oesophageal 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
30% rebleed within 6 weeks (risk highest in first 48 hours after first bleed); 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)
- 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
PEPTIC ULCER DISEASE
2. Symptoms of dyspepsia
EPIDEMIOLOGY (a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom
- Incidence about 100 per 100,000 per year (b) Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen,
- 68% of patients are over 60 years of age associated with upper abdominal fullness, early satiety, bloating, belching,
- Overall mortality is 7-10%, unchanged for last 2 decades – mostly due to ulcer nausea
bleeding especially in elderly with significant comorbidities (c) Unspecified dyspepsia
- Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a
MAIN AETIOLOGICAL FACTORS duodenal ulcer
H. pylori 3. Bleed
- 60% of population are positive for H. pylori by age 21 - As above, presenting with haematemesis (coffee-grounds vomitus) or malaena
- About 10-20% of infected patients develop an ulcer
- Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers 4. Perforation
- Patient presents with sudden generalised abdominal pain that is aggravated by
NSAIDs even the slightest movements
- Accounts for most of the rest of ulcer disease not caused by H. pylori - Board-like rigidity, guarding will be present on examination (signs of peritonism)
- 30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a clinically - Erect CXR will show air under diaphragm
significant ulcer i.e. symptomatic, bleeding
Other factors ENDOSCOPY (OGD)
- Cigarette smoking - The most important and valuable investigation
- Alcohol
- Steroids and anticoagulants do not increase the risk of ulcer formation, but increase - Roles of endoscopy:
the risk of bleeding in an existent ulcer (a) Diagnosis
 Confirmation of ulcer disease
PATHOGENESIS  Location of ulcer
- An imbalance between mucosal protective mechanisms against acid, and aggressive  Biopsy to rule out malignancy (usually 6 bites)
forces that damage the gastric mucosa  Biopsy of antral tissue for CLO (Campylobacter-like organism) test for H.
- Aggressive forces: gastric activity and pepsin activity pylori
- 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

24
25
(b) Prognostication of bleeding risk (in UBGIT) SURGICAL MANAGEMENT
 Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH)
DUODENAL ULCER
Forrest grade Bleeding risk Indications for surgery:
1a Spurting (arterial) 90% 1. Persistent bleeding (e.g. erosion of a posterior duodenal ulcer into gastroduodenal
1b Non-spurting, ooze (venous) 20% artery)
2a Non-bleeding ulcer with visible vessel 40% 2. Perforation
2b Non-bleeding ulcer with adherent clot 20%
2c Ulcer with haematin-covered base (flat spot) 10% 3. Gastric outlet obstruction (patient presents with vomiting of undigested food not
3 Ulcer with clean base 5% long after meal, succussion splash, air-fluid levels on AXR; characteristic
electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with
paradoxical aciduria)
(c) Endotherapy (in UBGIT)
 Injection with adrenaline (1:10,000) or absolute alcohol 4. Failure of medical management (ulcer does not heal)
 Thermal coagulation (heater probe) Surgery:
 Haemostatic clipping (endoclip) 1. Oversewing the bleeding vessel
 Argon plasma coagulation 2. Vagotomy with gastric drainage procedures
- Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric
CONSERVATIVE MANAGEMENT secretion; parietal cells also become less responsive to histamine and gastrin, and
vagal stimulus for gastrin release is abolished
1. Gastroprotection
- Vagotomy can be truncal, selective, or highly selective
(a) Standard dose proton pump inhibitor - Drainage procedures usually done with vagotomy as gastric emptying is
 20mg OM decreased with denervation  gastrojejunostomy or pyloroplasty
 Promotes ulcer healing even with ongoing NSAID use
3. Antrectomy with truncal vagotomy
(b) Double dose famotidine
4. Gastrectomy
 40mg BD
 Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs 5. Omental patch repair is sufficient for small perforated ulcer
are stopped; ulcers will not heal with ongoing NSAID therapy Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)
2. H. pylori eradication
 First line triple therapy: omeprazole 20mg BD, amoxicillin 1g BD, GASTRIC ULCER
clarithromycin 500mg BD for 7 days Indications for surgery
 In penicillin-allergic patients, substitute amoxicillin with metronidazole 400mg 1. Failure to heal after 3 months of conservative therapy
BD 2. Dysplasia or carcinoma
 Document eradication by endoscopy with CLO test, urea breath test or stool 3. Recurrence
serology testing 4. Perforation, persistent bleeding
 Treatment failure occurs in up to 20% - treat with quadruple therapy: colloidal Surgery
bismuth subcitrate 120mg QDS, tetracycline 500mg QDS, metronidazole 400mg 1. Oversewing the bleeding vessel
BD, omeprazole 20mg BD for 7 days 2. Gastrectomy
3. If prepyloric ulcer, can treat similar to duodenal ulcer
Re-scope in 6 weeks to document ulcer healing
If ulcer still present, biopsy ulcer again (exclude malignancy for gastric ulcer) and also
do antral biopsy for CLO test (to confirm eradication of H. pylori)
GASTRIC CARCINOMA 5. H. pylori infection
- 3-6X increased risk of gastric cancer
EPIDEMIOLOGY
- Fourth most common cancer in males, sixth most common in females in Singapore HISTOLOGY
- Female to male ratio 2:1
- Incidence 10-18 per 100,000 per year Adenocarcinomas
- Incidence increases steeply after 50 years old - Make up 90-95% of stomach tumours
- Lauren classification:
RISK FACTORS (a) Intestinal type (most common overall) – occurs in high risk population, distal
1. Environmental third of the stomach, in older men; associated with erbB2 and erbB3 receptor
- Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons stimulation
- Smoking (b) Diffuse type – occurs in low risk population, proximal third and cardio-
- Alcohol oesophageal junction, in younger and female patients; more aggressive, present
- Occupational exposure: asbestos, heavy metals, rubber later, worse prognosis; associated with K-sam oncogene
- Low socioeconomic status - Early gastric cancer
2. Genetic  Confined to mucosa and submucosa
- Blood type A  Good survival and prognosis regardless of size, lymph node status, histological
- HNPCC – Lynch syndrome II grade
- P53 mutation
Non-adenocarcinoma
- Germline mutation of e-cadherin
- Family history of gastric cancer - Make up less than 10% of stomach tumours
- Types: SCC, neuroendocrine tumour, leiomyosarcoma, GIST, primary gastric non-
Hodgkin‘s lymphoma (MALT, linitis plastica)
PRECURSOR CONDITIONS
1. Partial gastrectomy for benign disease with Bilroth II reconstruction
- Usually occurs >15 years after surgery MORPHOLOGY
- Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal Borrmann’s classification:
secretions at the anastomotic zone - Type I (3%): Nonulcerated, polypoid, growing intraluminally
2. Gastric polyps - Type II (18%): Ulcerated, circumscribed with sharp margins
- Highest risk in inflammatory polyps: 75-90% - Type III (16%): Ulcerated, margin not sharply circumscribed
- 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those - Type IV (63%): Diffuse, infiltrating, may be ulcerated; may diffuse entire stomach
with villous histology (linitis plastica)
- Also increased risk of adenocarcinoma elsewhere in the stomach
3. Chronic atrophic gastritis LOCATION
- Hypertrophic gastritis (Menetrier‘s disease) – inflammatory disease of gastric - 30% in pyloric channel or antrum
epithelium, up to 10% risk of malignant change - 20% in body
- Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10% - 37% in cardia
risk of gastric cancer
- 12% in entire stomach
4. Peptic ulcer disease
- <1% risk of malignant change

26
27
SPREAD Supportive investigations
- Direct extension to neighbouring organs 5. FBC – low Hb
- Lymphatic spread 6. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis
(a) Regional nodes 7. LFTs – albumin as a marker of nutritional status (alb<35 is poor); liver mets
(b) Supraclavicular nodes (Virchow‘s node)
(c) Umbilical (Sister Joseph‘s node) STAGING
- Haematogenous spread – liver, lung, bone, brain
Tis Carcinoma in situ N0 No regional LN
- Peritoneal seeding to omentum, parietal peritoneum, ovaries (Krukenberg‘s tumour), Tumour limited to mucosa and submucosa 1-6 regional LN involved
T1 N1
or cul-de-sac (Blumer‘s shelf) Tumour invades muscularis mucosa 7-15 regional LN involved
T2 N2
T3 Tumour penetrates serosa N3 >15 regional LN involved
PRESENTATION T4 Tumour invades adjacent structures
1. Asymptomatic: from histology of
Very non-specific symptoms and signs: ulcer biopsy
- Abdominal pain 60% 2. symptomatic: non specific CURATIVE TREATMENT
- Weight loss 50% abdominal pain, early satiety, N/V,
- Nausea/vomiting 40% LOW, LOA SURGERY
- Anaemia 40% 3. Complications: s/s of anaemia, s/s Principles of surgery:
- Palpable mass 30% of UBGIT, s/s of GOO, s/s of
- Haematemesis/malaena 25% - Wide resection of the tumour to negative margins (at least 6cm margins)
metastasis, peritonism (perforation) - En-bloc excision of regional lymph nodes
- Early satiety 17%
- Metastatic symptoms late (bony tenderness, neurological deficits, etc) - Choice between total gastrectomy and subtotal gastrectomy
 Subtotal gastrectomy leaves a small portion of proximal stomach – easier to
 New onset dyspepsia at age>35 years old should cause concern anastomose to jejunum than oesophagus since oesophagus does not have serosa
(higher risk of leak)
COMPLICATIONS  Subtotal gastrectomy is associated with less morbidity, better functional outcome
(some residual reservoir function preserved)
- Bleeding
 Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia,
- Gastric outlet obstruction  vomiting (dehydration, hypokalaemic metabolic
body) as well as diffuse-type tumours and cardio-oesophageal junction tumours
alkalosis, aspiration ± pneumonia)
- Perforation - Reconstruction
- Malnutrition  Bilroth I (end-to-end gastroduodenostomy) – rarely done as it is difficult to
mobilise duodenum up to anastomose with residual stomach
INVESTIGATIONS  Bilroth II/Polya (gastrojejunostomy) – no protection against biliary reflux into
stomach
Diagnosis  Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higher
 OGD –visualisation and biopsy (ulcer with heaped-up edges) chance of leak
Staging investigations  Oesophagojejunostomy (after total gastrectomy)
1. CXR/ CT thorax– lung mets
2. Endoscopic ultrasound – gold standard for T staging and good for N staging Complications of gastrectomy:
3. CT abdo pelvis – good for T, N & M staging Early
4. Staging laparoscopy prior to operation – picks up small peritoneal metastases that 1. Bleeding
are occult on CT scanning (up to 1/5 of patients)  upstage of disease 2. Infection
3. Anastomotic leak
Late
 Early satiety PALLIATIVE THERAPY
- For palliation of symptoms such as pain, bleeding, obstruction
 Retained antrum syndrome
- Endoscopic laser ablation for obstruction
- Not enough antrum removed leads to increased acidity in residual stomach, with
- Embolisation for bleeding
formation of marginal ulcers on the jejunal side of the anastomosis
- Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%),
 Intestinal hurry gastrojejunostomy for obstruction
- Inadequate reservoir function leads to poor digestion  may have phytobezoar - External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy
formation bleeding as it takes weeks to cause fibrosis)
 Dumping syndromes
- Early dumping syndrome: due to increased osmotic load in bowel occurring PROGNOSIS
half to one hour after meal, resulting in flushing, palpitations, dizziness, nausea; - Stage I 90% 5-year survival
treat by eating small frequent meals with low carbo and high protein/fat - Stage II 70%
- Late dumping syndrome: reactive hyperinsulinaemia with hypoglycaemia; treat - Stage III 40%
by eating more carbohydrates - Stage IV 0%
 Biliary/intestinal reflux into stomach
- Leads to symptoms of dyspepsia
 Afferent limb syndrome
- Occurs in Bilroth II/Polya reconstruction
- Mechanical obstruction of the afferent jejunal loop due to kinking, anastomotic
narrowing, or adhesions  postprandial epigastric pain with non-bilious
vomiting
- Can be decreased by doing Roux-en-Y surgery (but may still occur)
 Nutritional deficiency
- Iron deficiency – mixed picture
(a) Loss of intrinsic factor  B12 deficiency
(b) Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid  decreased
iron absorption in terminal ileum
- Need to supplement with B12 injections and iron supplements

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

28
29
COLORECTAL DISEASES 2. Defects in DNA mismatch repair
- Involved in 10-15% of sporadic cases
COLORECTAL CARCINOMA - Like the APC pathway, there is accumulation of mutations, but due to a different
mechanism, and without clearly identifiable morphologic correlates i.e. no
EPIDEMIOLOGY adenomas
Commonest cancer in Singapore men, number 2 cancer in Singapore women - Due to mutations in one of the five DNA repair genes (MSH2, MSH6, MLH1,
Peak incidence at 60-70 years of age PMS1, PMS2) of which MSH2 and MLH1 are the most commonly involved in
sporadic colorectal carcinomas
PATHOLOGY - Loss of DNA mismatch repair results in microsatellite instability which affects
- Almost all tumours are adenocarcinomas coding or promoter regions of genes involved in cell growth such as the BAX
- 90% of tumours are sporadic gene and the type II TGF-β receptor
- 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and - Tumours that arise from this pathway have a better prognosis than tumours that
1% in association with familial adenomatous polyposis (APC) arise from the APC pathway
- 1% arise in association with long-standing ulcerative colitis (>10 years)
SITE:
PATHOGENESIS - 25% in caecum and ascending colon,
There are 2 pathways for cancer development in the colorectal mucosa: - 25% in transverse colon,
- 25% in descending colon and proximal sigmoid,
1. APC pathway (adenoma-carcinoma sequence) - 25% in distal sigmoid and rectum
- Accounts for 80% of sporadic colorectal carcinomas - Most are left-sided though there is an increasing incidence of right-sided tumours
- Characterised by chromosomal instability
- Stepwise accumulation of mutations in a series of oncogenes and tumour MORPHOLOGY
suppressor genes: 1. Polypoid – more common in the right colon as there is more space to grow
 Loss of the APC suppressor gene on 5q21 (congenitally absent in patients 2. Scirrhous – annular ―apple-core‖ lesions, more common in the left colon
with familial adenomatous polyposis – APC) is the earliest event in adenoma 3. Ulcerated
formation 4. Nodular
 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 SPREAD
that causes the RAS to keep delivering mitotic signals and prevent apoptosis 1. Intramural – along bowel wall or Intraluminal
 Loss of tumour suppressor gene at 18q21 2. Direct extension into surrounding tissues e.g. small bowel, ovary
 Loss of p53 late in carcinogenesis 3. Lymphatic
4. Haematogenous – to liver, lungs
- The molecular evolution of colon cancer through this pathway occurs through a
series of morphologically identifiable stages: localised epithelial proliferation  5. Transcoelomic
small adenoma  large, more dysplastic adenoma  carcinoma in-situ 
invasive cancer
RISK FACTORS HISTORY
1. Age >50 years A)Presentation
- Asymptomatic: detection during screening (e.g. Ulcerative colitis)
2. Environmental factors
- Symptomatic:
- Diet: high in red meat, preserved foods (nitrosamines), low in fibre, vitamins,  Local:
minerals
 Change in bowel habits/ PR bleed
- NSAIDs may be protective against CRC  Frequency:>3x/day=diarrhoea; <2x/week=constipation
 Progressive constipation
3. Genetic predisposition  spurious diarrhoea (alternating constipation & diarrhoea)
(a) Personal history of CRCs  mucoid stools
 Metachronous colorectal cancers occur at a rate of 3-5% in the first  Associated secretions
five years after resection of a primary CRC, while metachronous  Blood
adenomas occur at a rate of 25-40% o Mixed in stool?
(b) Family history of CRCs o Separate from stool?
 1 first-degree relative with CRC increases risk of CRC 1.7X,  Mucus
 Risk is further increased if there are 2 1st-degree relatives with CRC,  Consistency – pellet, normal, soft, watery
or if the relative had CRC <55YO  Colour – black, clay, brown
 Anyone with a 1st degree relative diagnosed with CRC <45YO, or two  Effort – tenesmus (suggest a rectal pathology)
1st or 2nd degree relatives from the same side of the family with CRC at
any age, should be screened starting at age 45, or 10 years earlier than  Consitutional: LOW, LOA, malaise
the youngest cancer in the family
(c) Polyposis syndromes Stool Changes
 FAP and its variants, Gardner‘s and Turcot‘s syndromes: near 100% - Bloody diarrhoea – ddx:
risk of cancer formation;  IBD
 other polyposis syndromes such as Peutz-Jegher‘s, Cronkhite-Canada  Infective e.g. amoeba, TB, hookworm, Antibiotic Associated Colitis (C.
have a small increased malignant potential difficile)
(d) HNPCC – more common than FAP, accounting for 8% of cancers - Haematochezia – ddx:
 Diverticulitis
4. Ulcerative colitis  Angiodysplasia (AVM, common in old)
- Increased risk after 10 years of disease if the patient has pancolitis; after 15-20  Hemorrhoids
years if the patient has disease limited to the left colon  Massive upper GI

Note: Site of CA
5. Adenomatous polyps - Ascending: anaemia from occult bleeds, no obstructive symptoms usually
- Increased risk if there is a personal history of large (>1cm )adenomatous polyps, - Lower down: I/O, bleed, tenesmus
and polyps with tubulovillous or villous histology, particularly if multiple (3-6X
increased risk)  Complications:
- Small (<1cm) tubular polyps do not have increased risk  Haemorrhage
 Symptoms of infection: abscesses, peritonitis
 Symptoms of fistula, e.g. faecuria/ pneumaturia/ recurrent UTI
(colovesical fistula)

30
31
 Iron deficiency anaemia: fatigue, SOB, CP, decreased ET, INVESTIGATIONS
palpitations, postural giddiness, Aims: Diagnose, Stage the cancer & Investigate for complications of cancer
 Intestinal obstruction: abdominal distension, abdominal colick pain,
vomiting, absolute constipation I. DIAGNOSIS
 Symptoms of peritonism: perforation
 Colonoscopy – first-line investigation(diagnostic & therapeutic)
 Symptoms of metastasis: bone pain/ #, SOB, LL weakness with loss
- Ensure good bowel preparation
or bowel and urinary continence, RHC discomfort
- Visualise lesion: size and location of lesion
B) Strong-risk factors - Take biopsies of the lesion
- Enables detection of synchronous lesions – synchronous polyps in 30%,
Positive Family history synchronous cancer in 3-5% ( do not do a sigmiodoscopy)
- 1 or more 1st deg relative with CC at age <40
- Enables therapeutic procedures e.g. polypectomy, stenting of obstructed colon
- 2 or more 1st/2nd deg same side relative with CC at any age
 CT colonography
- Personal or family history of breast, ovarian cancer
- Next best to colonoscopy: needs IV contrast, air and contrast enema
FAP history  Double-contrast barium enema (barium + air)
- Classically can see an apple core lesion with barium enema
Amsterdam Criteria for Hereditary Non-Polyposis Colorectal Ca (HNPCC) – - Not adequate for diagnostic purposes, may miss small lesions & distal lesions
[3, 2, 1] - Need to insert a rigid sigmiodoscope 10-15cm to instil air & contrast
- ≥3 family members from the same side with CRC or HNPCC related cancer,
 one of which is a 1st deg relative of the other 2 (At least 2 of which must
be 1st-degree relatives) II. STAGING
- 2 successive generations (a) CT scan of the abdomen and pelvis for colon tumours
- 1 of the CC must occur prior to age 50 - Local T staging & invasion into bladder, ureter, uterus
- FAP is excluded - Staging of regional and no-regional lymph note involvement
- Metastases to the liver, obvious peritoneal seeding, omental kinking,
 Family history alone = high-risk; FAP / HNPCC = very high-risk
- Look for ascites, hydroureter/ hydronephrosis, intestinal obstruction
Other risk factors (b) Endoscopic ultrasound or transrectal ultrasound for rectal tumour
- Low fibre diet, Red meat - Very good for T staging to determine depth of involvement by tumour
- Obesity - Can also assess local lymph node status
- Ulcerative colitis >10 years
(c) MRI of the tumour
PHYSICAL EXAM - Superior to CT for delineating fat planes in T staging especially in rectal cancer
1. Abdominal mass (d) CXR + CT scan of the chest
2. Mass on DRE: (rectal mass) (e) Bone scan if appropriate (more for Ca breast, lung, prostate, thyroid)
a. hard, non-tender, polypoid, irregular, contact bleeding
b. distance from anal verge >7cm (internal anal sphincter) III. COMPLICATIONS
3. Complications, Metastases Basic laboratory investigations:
- Cachexia (a) FBC for low Hb, together with iron studies
- Pallor at nail beds and conjunctiva (anaemia) (b) UECr: fluid and electrolyte abnormatlities from vomiting, or 3rd space losses
- Jaundice, hepatomegaly (irregular surface & nodular edge) (intraluminal); creatinine may be elevated and hence risk of contrast nephropathy
- Cervical lymphadenopathy – Virchow‘s node (c) LFT for derangements caused by metastasis (occur late) – raised bilirubin, ALP
- Bone tenderness, consolidation or effusion, AMS (d) PT/PTT, GXM for surgery
(e) Carcinoembryonic antigen level (CEA) Principles of surgery for colonic carcinomas
- A tumour marker for colorectal carcinoma – >90% of tumours produce CEA - En-bloc resection of tumour with adequate margins
- Measured pre-operatively as a baseline level – if the CEA is raised pre-op and
 For colonic tumours, a margin of 5 cm proximally and distally is adequate
falls to within normal range post-op, it is likely tumour has been totally removed  While segmental resection is sufficient for primary tumour removal, a wider
- Follow-up after surgery with CEA levels to detect tumour recurrence
resection is often required to achieve sufficient lymphadenectomy
- Causes of false positive raised CEA: smoking, pregnancy, bronchitis, cholangitis
and cancers of the stomach, lung, breast, pancreas, cervix, bladder and kidney  Adequate clearance of the draining lymphatics involves excision of the vascular
arcades supplying the segment of involved colon back to their origin (from the
Imaging SMA or IMA) as lymphatics follow the arteries generally
(f) Erect and supine AXR to look for intestinal obstruction (usually large bowel closed - Obstructed left sided carcinoma
loop obstruction) and caecal distension; near perforation
 No difference shown for doing a staged procedure (i.e. tumour removed with
(g) Erect CXR in perforated tumour to detect air under diaphragm
proximal end of colon brought out as a colostomy) as compared to creating a
(h) ECG :anaesthesia assessment
primary anastomosis
 On-table bowel decompression ( irrigation) for clearance of faecal material
DUKE’S STAGING (SURGICAL AND HISTOLOGICAL FINDINGS)
 Segmental colectomy for the tumour with intraoperative decompression is
Stg Description 5yr surv comparable to subtotal/total colectomy without decompression with regard to
A Tumor confined to bowel wall with no extension into extrarectal/ 75% bowel function and rates of complications
extracolic tissue, no LN mets
- Site of surgery for colonic carcinoma
B Invades past muscularis propria into extrarectal/ extracolic tissue, 55%
no LN
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

TREATMENT

SURGERY
Pre-operative measures
- Bowel prep
 Modification of diet – 3 days low residue diet, NBM day before operation)
 Bowel clearance with polyethylene glycol
- Prophylactic antibiotics
 ampi/ genta/ metronidazole at induction of anesthesia

32
33
Tumour site Surgery Structures involved - Reconstruction
- Caecum Right - Excision of caecum and ascending colon  Formation of a straight coloanal anastomosis in anterior resections is associated
- Ascending colon hemicolectomy - Division of ileocolic and right colic arteries, and with poor function due to the lack of reservoir function
the right branch of the middle colic artery
- Hepatic flexure Extended right - Excision of caecum, ascending colon, and  Creation of a colonic J-pouch using the proximal end of colon (the end of the
- Transverse colon hemicolectomy proximal transverse colon colon is folded back on itself to form a J, and the two limbs opened and stitched
near the hepatic - Division of ileocolic and right colic arteries, and together to form a pouch, the apex of the J being anastomosed to the anus) is
flexure the middle colic artery at its origin associated with improved post-operative function
- Mid-transverse Transverse - Excision of transverse colon  Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal
colon colectomy - Division of middle colic artery colon is cut longitudinally but sewn transversely, widening the diameter at that
- Transverse colon Left segmental - Excision of distal transverse colon and proximal segment to form a small pouch), done when there is difficulty creating the
near splenic colectomy descending colon colonic J-pouch
flexure - Division of supplying vessels – left branch of
middle colic artery, left colic artery - Mesorectal excision
- Descending colon Left - Excision of descending colon
 Proximal rectal tumours – 5cm distal margin of mesorectal excision
hemicolectomy - Division of left colic and inferior mesenteric
arteries  Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the
- Sigmoid colon Sigmoid - Excision of sigmoid colon tumour
colectomy - Division of inferior mesenteric artery and/or  Lower rectum tumours – total mesorectal excision required (complete excision
High anterior sigmoid branches of the intact visceral mesorectal tissue to the level of the levators)
resection - High AR is above the peritoneal reflection
- Extended resections
 For locally advanced, adherent tumours (T4), multivisceral resection of organs
Principles of surgery for rectal carcinomas involved (pelvic exenteration) is associated with improved local control and
overall survival compared with standard resection, though high morbidity of 25-
- En-bloc resection with adequate margins 50% is associated
 For rectal tumours a margin of 5 cm proximally and 2 cm distally is adequate (as
 Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease
it has been found that lymphatic spread of rectal tumours is predominantly in the
proximal direction) - Stoma creation
 Radial margins are also important as there is a zone of downward spread within  A defunctioning loop ileostomy (or loop colostomy) is usually created during an
the mesorectum (peritoneal investment of the upper rectum; just anterior to the low AR as the manipulation of the colon deep within the pelvic cavity causes
sacrum) increased risk of an anastomotic leak & also poorer blood supply to anastomosis
- Sphincter-sparing versus loss of sphincter  A defunctioning stoma does not protect against anastomotic leak, but mitigates
against disastrous complications of faecal peritonitis should a leak occur
 The anal sphincter can be spared if the distal margin is >1-2cm above the level
 Closed in 2-6/12 after check with gastrograffin reveals no leak
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 - Neoadjuvant chemoradiotherapy for rectal tumours
>7cm from the anal verge
 Neoadjuvant RT with 5-fluorouracil can downstage tumour significantly 
 Sphincter-sparing  low anterior resection (below the peritoneal reflection); ability to preserve sphincter, ability to resect previously unresectable tumour,
ultra low AR if just above the anal sphincter reduce local recurrence
 Sphincter-sacrificing surgery abdominoperineal resection (entire anus and  Good evidence for ≥T3 tumours: benefits > risk of RT (esp. that pt becomes too
sphincter complex is dissected, with the creation of an end colostomy) ill to be operated on)
  Not possible for colon carcinomas due to risk of small bowel radiation if given Surgery for metastases
above peritoneal reflection - Isolated liver metastases (synchronous or metachronous) may be resected with
survival benefit; neoadjuvant chemotherapy can be given to downstage the
- Surgical treatment according to stage metastases if they are initially resectable
Stage of disease Treatment - Lung metastases usually indicate systemic dissemination of disease, but in the rare
T1 Involvement of submucosa, but no Local excision (AR or APR) setting that there is an isolated lung secondary, resection can provide survival benefit
penetration through muscularis propria
Surgery for recurrence
T2 Invasion into, but not penetration a) Local excision + adjuvant - Loco-regional recurrence, if detected early with adequate resection, can confer
through, muscularis propria Chemo/RT OR survival benefit
b) radical resection
T3 Penetration through muscularis propria Neoadjuvant chemo / RT before
into subserosa (if present), or pericolic radical resection RADIOTHERAPY
fat, but not into peritoneal cavity or - Role as neoadjuvant therapy in rectal cancer to downstage tumour
other organs - Post-operative adjuvant therapy in stage II or III rectal cancer
T4 Invasion of other organs or
involvement of free peritoneal cavity
CHEMOTHERAPY
Adjuvant therapy
Operative complications - Colon cancer: 5-FU + folinic acid (leucovorin) for 6 months, or 5-FU + levamisole
Immediate (<24h) Damage to other organs e.g. ureters for 12 months in Duke‘s C cancer (node positive); not recommended in Duke‘s B or
less
Early (<30 days) Wound infection
- Rectal cancer: post-operative adjuvant therapy in combination with radiotherapy in
Bleeding
stage II or III disease (5-FU based regimen used)
Abscess
Anastomosis breakdown/leak  faecal peritonitis
Early stoma complications Palliative therapy
Late (>30 days) Diarrhoea - 5-FU in combination with folinic acid is first-line therapy
Impotence (damage of pelvic nerves) - Alternatives for first-line therapy: Raltitrexed when 5-FU is not tolerated;
Adhesions (I/O) capecitabine or UFT (uracil combined with tegafur) plus folinic acid
Anastomotic stricture
Late stoma complications
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
Surgery for palliation - Yearly colonoscopy
- Resection of primary for palliation of symptoms such as bleeding, perforation, - CXR and liver ultrasound to detect metastases (recommended frequency not known)
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
34
35
STOMA PRINCIPLES Stoma Complications
Stoma: opening of a luminal organ into the external environment Early
Indications - Necrosis of terminal bowel (stoma appears dusky; check by intubating with a glass
1. For input: feeding (Percutaneous endoscopic gastrostomy)
tube into the stoma to look at colour of mucosa)  refashion stoma
2. For output: decompression/ lavage, defunctioning/ diversion, draining/
exteriorization (urine, faeces) - Obstruction e.g. fecal impaction  explore with finger, enema
- Leakage  skin erosion, parastomal infection  resite
Nursing intervention - Bleeding
- Stoma nurse to perform counselling & discuss best site for stoma placement - Stoma diarrhoea (high output)  correct water & electrolyte imbalance, add anti-
motility agent
Stoma siting Late
- Over the rectus sheath  decreases the risk of prolapse, - Prolapse of bowel  refashion
- Away from the surgical incision  risk of wound contamination and infection - Parastomal hernia (+ve cough impulse) refashion
- Away from skin creases or bony prominences stoma wafer can be flush with the - Stenosis (unable to pass finger through) refashion
skin (any gaps between skin and wafer  leakage of fluid skin excoriation & infx) - Retraction  refashion
- Away from old surgical scars  risk of hernia - Skin excoriation
- Sited for easy accessibilty i.e. not under a large fold of abdominal fat - Psychological problems
- Intra-operatively, avoid tension over the stoma to marked site  causes decreased
vascularity of the stoma  stoma necrosis ASSOCIATED CONDITIONS
Types of stomas I. Familial adenomatous polyposis (FAP)
Permanent (end colostomy)
- When patient or surgeon factors - 1 in 10,000, autosomal dominant inheritance
are against reversal of stoma (relative) - Germline mutation of APC gene on 5q21
- When no distal bowel remaining (absolute) - >100 adenomatous polyps all over colon; polyps take 5-6 yrs to turn malignant
 After abdomino-perineal resection for Low rectal/ anal tumor - 50% patients will have polyps by 16yrs; 90% will have colorectal CA by 45yrs
 After Panproctocolectomy without ileal pouch anal anastomosis - Other sites for polyps: stomach, duodenum
Temporary
- Extraintestinal manifestations
- Decompression – relief of bowel obstruction causing proximal dilatation
 Skin: Epidermoid cysts, Lipoma
- Defunctioning – to reduce effects of anastomotic leak
 Bone: Osteoma of skull/ mandible, Dental abnormalities
 Esp. after low anterior resection, where risk of anastomotic leakage is high 2o to
 Eye: Congenital hypertrophy of retinal pigment epithelium (CHRPE)
poor blood supply to anastomotic site
 Other tumours:
 Usually loop ileostomies or colostomies with 2 openings (ileostomies usually on
 Desmoid tumours (intra-abdominal tumours, treated with CT, RT or HT.)
the right side, colostomies in the epigastric/hypochondriac [transverse colostomy]
 Thyroid cancer (follicular or papillary type)
or left side)
 Periampullary CA
- To rest an inflamed distal portion e.g. acute Crohn‘s
- Diagnosis
Colostomy (vs ileostomy)  Colonoscopy showing >100 polyps
 usually flushed with skin, (vs protrudes 3cm „spout‟, as ileal contents are  Genetic testing
corrosive, to prevent contact with skin)
 firm brown faceal output (vs watery greenish ilieal output) - Surveillance
 larger diameter of stoma (vs smaller diameter in ileostomy)  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 PATHOGENESIS
 Affected members should undergo prophylactic proctocolectomy with ileal 1. Increased intraluminal pressure
pouch anal anastomosis (IPAA – involves folding loops of ileum back on - Associated with lack of dietary fibre
themselves and stitching or stapling them together to form a reservoir pouch 2. Degenerative changes in colonic wall
which is them anastomosed to the anus) at ~ 20 YO - Usually at point of entry of terminal arterial branches where serosa is weakest
 Subtotal colectomy is an option if the rectum is relatively spared of polyps - Associated with weakening of collagen structure with age

Hereditary Non-Polyposis Colorectal CA (HNPCC) PRESENTATIONS

- Divided into Lynch syndrome I or Lynch syndrome II based on clinical features 1. Acute diverticulitis
- Symptoms: LLQ pain, N/V, Constipation / diarrhoea
- Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure) - Signs: Low grade fever, Tender palpable mass
- Tumours tend to arise from polyps which are commonly flat, with villous histology - Investigation:  WBC
- Resultant tumour is often poorly differentiated
2. Chronic diverticulitis
- Lynch syndrome type II is associated with increased risk of cancer elsewhere, most - Recurrent LIF pain
commonly endometrial cancer, and also ovarian, gastric, small bowel, hepatobiliary, - Irregular bowel habit
and renal pelvis/ureter cancers - Passage of mucus PR
o Offer a THBSO with total colectomy if CRC detected 3. Complicated diverticulitis
- Diagnosis is based on the Amsterdam criteria – see above a. Perforation
- Surveillance – 1-3yrly colonoscopy starting at 20 years old b. Paracolic abscess / inflammatory mass – 2o to localized perforation
c. Bowel obstruction – 2o to structure or adherence to a diverticular mass
d. LGIT haemorrhage – ulcerated vessel @ neck of diverticulum; torrential
Ulcerative colitis
e. Fistula formation (commonest: colovesical fistula) – 2o to pericolic abscess
- Screening – yearly colonoscopy starting after 10 years of UC discharging, operation or drainage of pericolic abscess. May present with
urinary symptoms. Others – colo-cutaneous, colo-uterine, colo-enteric, colo-
DIVERTICULAR DISEASE vaginal

PATHOLOGY – acquired herniation of colonic mucosa through muscular wall, with a STAGING
covering of colonic serosa - Hinchey classification of acute diverticulitis – need for surgery is reflected by degree
of infective complications
TERMS Stage 1 Pericolonic / - ABx, NBM, IV fluids
- Diverticulosis coli – presence of acquired pseudodiverticula Mesenteric abscess - Consider 1 stage surgery after acute episode –
- Diverticular disease – symptomatic diverticulosis coli resection of affected bowel segment with primary
anastomosis
- Diverticulitis – inflammation of diverticula
Stage 2 Pelvic / retroperitoneal - Percutaneous drainage
abscess - Elective 1 stage surgery
EPIDEMIOLOGY Stage 3 Purulent peritonitis - 2 stage operation – Hartmann‘s procedure (partial
- Increases with age; up to 25% in >70YO Stage 4 Faecal peritonitis colectomy + diverting end colostomy & rectal
- Majority are asymptomatic; 10-30% are symptomatic stump formation) + secondary re-anastomosis 3
- Risk factors – dietary fibre & genetics months later
- Site – majority are in the sigmoid colon (right sided are thought to be genetic; in Note: current controversy of management for stage 3: haartman‟s vs segmental
Asians; left sided are more in Caucasians; not in rectum as taeni coli has fused) resection with primary anastomosis with or without defunctioning ileostomy

36
37
Presentation Clinical features Investigations Differentials Management
Acute - LIF pain – colicky, progressing to - FBC – leucocytosis, ↑ ESR - See Ddx to RIF/LIF pain Conservative
Diverticulitis constant, relieved by defecation - Erect CXR to rule out perforation - GI: appendicitis, colitis, GE, - Bed rest
- LIF tenderness - AXR – ileus, air-fluid level w/in an abscess IBS, IBD, mesenteric - NBM, IV fluid
- Palpable LIF mass - Barium enema ischaemia/ adenitis, Ca - Broad-spectrum antibiotics –
- Nausea - CT scan w triple contrast colorectal augmentin or metronidazole or
- Pyrexia  Contrast: IV for vascular lesions, oral for small - Uro: UTI, stones, cancer, ciprofloxacin
- Increase pulse rate bowels, enema for large bowels cyst/ Angiomyolipoma, - Antispasmodics
 Features – diverticula elsewhere, confirm colitis hydronephrosis
(mesenteric fat infiltration, concentric bowel - Obgyn: PID, torsion of cyst/ After acute phase has settled
thickening) but only suggest diverticulitis, pelvic ovary, endometriosis, - Ba enema &/or Colonoscopy –
abscess, free gas, extravasated contrast ectopic pregnancy confirm dx & exclude CA colon
 Cannot tell if inflm is due to diverticula - #: #, infx, inflm,
- Laparoscopy – if diagnosis is in doubt Role of surgery: see behind
- Avoid colonoscopy as risk of perforation is high

Chronic - Recurrent LIF pain - Rigid sigmoidoscopy – oedematous mucosa & - CA colon – may coexist. Conservative – see above
Diverticulitis - Irregular bowel habits – constipation rigidity of rectosigmoid junction Hard to differentiate –
Surgical
& bouts of diarrhoea - Flexible sigmoidoscopy – diverticular orifices therefore, ALWAYS
Indications:
Not a - Passage of mucus PR - Barium enema – ‗saw-tooth‘ appearance, exclude CA colon e.g.
- Severe / recurrent attacks
common - Ruled out cancer, IBD, ureteric colic, diverticula, strictures histology after bowel
- Possible CA colon
clinical entity Msk pain etc. - Colonoscopy – exclude differentials (i.e. Ca colon) resection
- Segmental resection of affected
- Ischaemic colitis
colon + anastomosis
- Radiation colitis
- Colonic endometriosis
Generalised - Acute onset abdominal pain – severe - FBC – ↑ TW, ↑Hb (dehydration) - Other causes of peritonitis – Mgmt as for acute abdomen
peritonitis / & continuous - U/E/Cr – dehydration & ARF perforated PUD/ - Resuscitate
perforation - Abdominal guarding & rigidity - CXR – free gas under diaphragm appendicitis/ bowel/ ectopic - Surgical
- Vomiting pregnancy, ishaemic bowel,  Peritoneal toilet
- Tachycardia acute pancreatitis, ruptured  Resection of affected segment
- Pyrexia AA/ hepatoma, torsion of  End sigmoid colostomy
testis/ ovary, pyonephrosis (Hartmann‘s procedure)

Pericolic - May follow acute diverticulitis - FBC – ↑ TW - CT/US guided percutaneous

abscess - LIF tenderness & guarding - CT – differentiate between inflammatory phlegmon aspiration
- LIF mass – may be detected on DRE & pericolic abscess - Surgery – evacuation of pus ±
- Swinging fever resection of affected segment

Persistent - LIF pain, tenderness & palpable mass

inflammatory - Fever
mass - Malaise

Small bowel - Usually temporary, due to

I/O attachment of enteric loop against
area of acute diverticulitis
- Surgery if does not resolve
Presentation Clinical features
Large bowel - PHx of recurrent acute diverticulitis
I/O 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 - PHx of chronic diverticulitis & UTI
fistula - Hx of dysuria, freq, haematuria,
pneumaturia, faecaluria
Outcomes: well or derteriorate requiring surgery, recurrent episodes, stricture & subacute IO (offer surgery)
Investigations Differentials Management
- AXR – dilated bowels proximal to stenosis - CA colon - NBM, Drip & suck
- Water soluble contrast enema - Surgery – Resection ± primary
anastomosis
- Invx as for LGIT bleed – resus, invesigations + - Anorectal bleed - Resuscitate & correct coagulopathy
colonoscopy & angiography (both diagnostic AND - Angiodysplasia - Colonoscopic management:
therapeutic value) - Ischaemic colitis adrenaline injection, endoclips on
- ± on-table enteroscopy if required - Colorectal CA bleeding vessel, heat coagulation
- ± tagged RBC scan (not as sensitive compared to - Colitis (inflm or infx) - Radiologic embolisation of site of
angiogram) - UBGIT bleeding with temp foam material
- Coagulopathy via angiography
- Surgery – segmental resection;
total colectomy if unable to localise
bleed
- UFEME & urine c/s: confirm UTI and organisms - Other causes of fistula – CA - Surgery – Resection of affected
- Cystoscopy – cystitis colon, CA bladder, Crohn‘s colon + anastomosis + closure of
- Sigmoidoscopy – usually normal disease, post-irradiation bladder fistula opening
- KUB – air in bladder necrosis
- Barium enema – diseased diverticular bowel
segment

Indications for emergency operation 1. Sepsis from abscess or faecal peritonitis

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 operation 1. Stricture

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
- Advise high fibre diet & to drink lots of fluid

38
39
SURGICAL LIVER PROBLEMS
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)  important for reading CT scans and in surgery
- 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) – see picture
- Segment IV can be further divided into IVa and IVb, where IVa is the superior
subsegment 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 three hepatic veins into the inferior vena cava
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

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
- 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
- The segments are divided by one transverse plane and three sagittal planes
- The transverse plane is at the level of the main branches of the portal vein, and
divides the liver into an upper half and a lower half
- The sagittal planes are formed by the three main hepatic veins (right, middle and
left)
HEPATOCELLULAR CARCINOMA - Budd-Chiari syndrome: occlusion of the hepatic, intrahepatic or portal vein
causing portal hypertension & congestive hepatopathy
EPIDEMIOLOGY - Jaundice (5-10%)
- Annual incidence in Singapore is 18/100,000 in males, and 4.6/100,000 in females  Cholestatic: invasion/compression of intrahepatic ducts or extrahepatic
compression by metastatic LN
- 3rd most cancer among males, overall 4th most common cancer
 Hepatic: a/w pre-existing cirrhosis or acute flair of chronic hepatitis
- Men: female = 3:1
- Peak age of onset: 30-40 years old 3. Tumour rupture (<3%)
- 1o liver cancers are mainly HCCs (85%), with a small proportion of intrahepatic - Severe abdominal pain (peritonism), pallor with shock [ddx: ruptured AAA]
cholangiocarcinoma (6%)  50% mortality; Rx with TAE; reports of peritoneal seeding in survivors
- US +ve for peritoneal fluid, DPL +ve for blood
AETIOLOGY AND RISK FACTORS
- Hepatitis B infection (high HBV DNA load, HBeAg positivity increase the risk) 4. Liver decompensation (on top of underlying cirrhosis)
- Hepatitis C infection - Worsening liver function (encephalopathy, jaundice, pruritis, coagulopathy,
oedema)  suspect HCC when there is decompensation of liver cirrhosis
- Cirrhosis (of which cirrhosis resulting from hep B, hep C and haemochromatosis are
- Worsening portal hypertension: Ascites, LL oedema, haematemesis & melena 2o
associated with the highest risk)
to bleeding varices (COJ & gastric)
- Others: Aflatoxin ingestion, α-1- antitrypsin deficiency, haemochromatosis, PBC, - Hepatorenal syndrome in late stages of liver failure
anabolic steroids, schistosomiasis)
Stages of Hepatic Encephalopathy
PATHOLOGY Stage 1 Sleep-wake cycle inversion
- Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular Stage 2 Lethargy, personality change, asterixis, ataxia
damage with high cellular regeneration, which leads to increased rates of genetic Stage 3 Confusion, acalculia, paranoia, agitation, Babinski, clonus
mutation in the cells and accumulation of these mutations leading to carcinoma Stage 4 Coma
formation
5. Metastases (low incidence in HCC, mortality rarely from mets)
- Two histological subtypes:
- Bone pain, Dyspnoea
 Nonfibrolamellar – associated with HBV and cirrhosis
 Fibrolamellar – associated with younger patients, more common in females, no 6. Paraneoplastic syndromes
association with hep B or cirrhosis, 70% resectable, good prognosis  Hypoglycaemia (high metabolic demands of tumour),
- Metastasises to lymph nodes, bones, lungs and adrenals  Erythrocytosis (tumour produces erythropoietin),
 Hypercalcaemia, watery diarrhoea, etc.
PRESENTATION
1. Asymptomatic
- During screening (ultrasound) for chronic hepatitis B carrier
INVESTIGATIONS
- Investigations for liver cirrhosis
 Basic laboratory investigation:
- Incidentally found on imaging of the abdomen
o FBC (low Hb from BGIT, raised TW in SBP)
2. Local signs & symptoms o UECr (dehydration, 3rd spacing of fluids, use of diuretics for ascites,
- Upper abdominal pain (2o to capsular distension) r/o nephropathy for contrast imaging)
- Early satiety/ vomiting (likely 2o to compression) o LFT (low albumin, high bilirubin, raised ALP)
- Pyrexia (central tumour necrosis) o AFP (Normal <5; WHO criteria >400; diagnostic & trending; note
- Hepatomegaly false +ve: pregnancy, infants, cirrhosis, hepatitis, teratoma)
- Constitutional: LOW, LOA, malaise o Hepatitis markers (look for carrier status or chronic infection)

40
41
 Imaging:
o Triphasic CT scan (see below)
DIAGNOSIS
Biopsy is usually not performed due to risk of tumour seeding (1-2% risk) along the
needle track – 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, 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)
5. If indicated, investigations to look for GI primary
- CEA, CA 19-9, endoscopy
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
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
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
- 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)
due to occurrence of new primaries in the cirrhotic liver
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” such as radiofrequency ablation to shrink
disease and prevent progression until donor liver is 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
Factors affecting resectability: 4. Residual liver function post-operatively (at least 20%)
1. Stage of disease - Dependent on tumour size and how much of the liver it takes up, because tumour
- Metastatic disease is not suitable for resection is non-functional
- Multicentric disease affecting both lobes is a contraindication to hepatectomy - 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
2. General fitness for operation means that more functional tissue is removed with the same resection margins
3. Liver function pre-operatively 5. Degree of portal hypertension (>10mmHg)
- Cirrhotic patients have higher risk of post-operative mortality (4-14%) compared - Resection of the liver results in worsened portal hypertension since the effective
to non-cirrhotic patients (0-4%) due to complications such as liver failure, portal venous capillary bed has decreased  increased resistance to flow
bleeding and infection
6. Location of tumour
- 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 - Has to be located in a suitable location for resection
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 programe PALLIATIVE THERAPY
- If patient has cirrhosis, assess the Child‘s status  only Child’s A and good Loco-regional ablation
Child’s B can be considered for resection (a) Radiofrequency ablation (RFA) – best results for locoregional strategies
(b) Percutaneous ethanol injection
Child-Pugh classification of CLD/cirrhosis (c) Cryotherapy
1) Prognosis Intra-arterial therapy
2) Strength of medical treatment (a) Transarterial chemoembolisation (TACE)
3) Necessity of liver transplant
(b) Transarterial embolisation (TAE)
Points 1 2 3
Albumin (g/L) >35 28-35 <28 (c) Selective Intrahepatic Radiation – Yttrium-90 radioactive beads
Bilirubin (μmoles/L) < 35 35-50 >50 Systemic therapy – limited results; Sorafenib imporves median survival by 3/12
Coagulopathy <1.70 1.70- 2.20 >2.20
Distension (ascites) None Slight - mod Severe/refractory
Encephalopathy None Grade I – II Grade III-IV SCREENING FOR CHRONIC HEPATITIS CARRIERS
- Combination of 6/12 to yearly ultrasound with AFP levels
Child‘s A(5-6) B(7-9) C( 10-15) - US is operator dependent & may miss certain areas of the liver where imaging is
1 year survival % 100 80 45 difficult, but it is not associated with radiation exposure
2 year survival % 85 60 35 - AFP is also not a perfect screening test as 20% of HCC will not have raised AFP
Disease status Well Significant Decompensated liver - Thus the combination of ultrasound and AFP can increase the sensitivity and
compensated functional disease, consider specificity of screening
disease compromise transplant - Frequency of screening is controversial, but should be increased in patients at
Treatment in Resection of up Maximum resection Consider transplant increased risk – HbeAg positivity, high HBV DNA levels
concomitant HCC to 4 segments of 2 segments - 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

42
43
LIVER METASTASES PRESENTATION
1. Usually small and asymptomatic, found incidentally
- Still more common than primary liver tumour for malignancy occurring in the liver 2. Mass effects compressing on surrounding organs
- Primaries: Colorectal, gastric, pancreatic, urogenital, breast, lung 3. Pain from liver capsule stretch
4. Rupture (<1%)
PRESENTATION DEPENDS ON SITE OF METASTASIS 5. Kassabach-Merritt syndrome for large haemangiomas – consumptive coagulopathy,
thrombocytopaenia
Mets to liver parenchyma Mets to porta hepatis LN 6. Heart failure from large arteriovenous shunt
Hx - Incidentally found on follow up - Symptoms of obstructive jaundice
(for cancer)  Yellow sclera DIAGNOSIS
- Hard mass  Tea-coloured urine - Radiological
- Heaviness  Pale stools Characteristic features on triphasic CT – slow enhancement of the rims on arterial
- Pain from rupture and portal venous phase, brightest in the delayed phase
P/E - Hard, irregular nodular hepatomeg - Jaundice early, progressive - DO NOT BIOPSY
- Jaundice is a late sign - Hepatomegaly may not be present
Invx - Both obstructive and transaminitis - Obstructive picture in early stages TREATMENT
picture - Only for symptomatic or complicated lesions
TRIPHASIC CT - Possible role for prophylactic surgery in large, lateral, inferior lesions since there is
higher risk for rupture
- Hypodense on arterial phase (as metastases are usually hypovascular compared to
hypervascular HCC; spread via portal vein)
- Increasing contrast uptake on portal venous and delayed phases SIMPLE LIVER CYSTS
EPIDEMIOLOGY
ROLE OF SURGERY - 50% of cysts are single
- Promising results with colorectal and neuroendocrine metastases if isolated - Prevalence 1-3%
resectable metastatic disease – 5-yr survival >50% - 9:1 female predominance for symptomatic cysts
- Increasing role in urogenital, breast mets
- Poor results for stomach, oesophageal mets PATHOGENESIS
- Palliation for symptoms in neuroendocrine metastases - 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)
LIVER HAEMANGIOMA - [Cysts that communicate with the biliary system are called choledochal cysts]

EPIDEMIOLOGY PRESENTATION – WITH COMPLICATIONS

- Prevalence 0.4-20% - Torsion
- Female to male ratio 3:1 - Bleeding & Rupture
- Mass effect; Compression of IVC; Cholestasis due to compression of CBD; Portal
PATHOGENESIS hypertension
- Vascular malformation that enlarges by ectasia, congenital in origin - Fistulation into duodenum
- Malignant change (rare)
TREATMENT (IF SYMPTOMATIC) 3. Antibiotics via PICC
- Aspiration  Empirical antibiotics – Ampicillin/Gentamicin/Metronidazole
- Ethanol sclerotherapy (painful)  Change to definitive antibiotics when blood c/s results return
- Fenestration (open or laparoscopic)
 Total duration of 6 /52 – 1st 2/52 IV, next 4/52 PO
- Excision/resection
4. Drainage
Drainage if >3cm – open drainage or percutaneous aspiration
HEPATIC ABSCESS (PYOGENIC OR AMOEBIC)
Percutaneous aspiration Open drainage
PYOGENIC ABSCESS
- Minimally invasive, performed under - Invasive procedure, done under GA
- More common than amoebic abscess locally radiologic guidance - Shorter hospital stay
- Causative organisms: Klebsiella pneumoniae, Enterococcus, Enterobacter, E. coli, - Can be done under LA - Single procedure
Staph aureus - Longer stay for patient as drainage - Not dependent on location
tube stays in patient for a longer time - Indications:
- Routes of infection: - May require multiple attempts if  Concomitant pathology requiring
(a) Ascending infection from biliary system (ascending cholangitis) unable to completely drain pus surgery e.g. gall stones
(b) Intra-abdominal source through portal vein – acute appendicitis, diverticulitis, - Contraindications:  Multiple abscesses or
IBD, pancreatitis, pelvic abscess  Ascites (pus can leak into multiloculated abscess
(c) Contiguous spread – from gallbladder empyema peritoneal cavity)  Immunocompromised patient
 Uncorrected coagulopathy  Failed percutaneous drainage (tube
(d) Haematogenous spread in sepsis e.g. infective endocarditis
 Proximity to vital structures blocked, or pt not getting better)
(e) External inoculation – iatrogenic, traumatic  Ascites
 Ruptured abscess
- Presentation: RHC pain (capsular stretch) with Spiking fever with chills, rigors.
50% of patients have jaundice, and one-third have hepatomegaly
AMOEBIC ABSCESS
- Investigations:
Laboratory: - Causative organism: Entamoeba histolytica (infects the gut, forming ulcers in the
 FBC, U/E/Cr, hepatitis markers colon, then spreads to the liver through the portal vein)
 Blood cultures, Melioidosis & amoebic serology/ PCR, Stool ova, cysts and
parasites - Transmission is faecal-oral
 Tumour markers: AFP, CA 19-9, CEA (may resemble infected tumour on
imaging) - Presentation
 Usually single abscess
 If any aspiration done, aspirates for cytology, stains & c/s
 No sepsis, jaundice
Imaging:
 Hepatomegaly often present
 US HBS or CT scan (to exclude liver tumour, KIV endoscopy to rule out GI
 Complications: rupture into pleural/peritoneal spaces
malignancy)
 Findings: Irregular lesion with central area of necrosis, air-fluid levels, may be
- Treatment:
multiloculated. Rim-enhancing appearance on triphasic CT scan.
 Metronidazole (very responsive)
 Aspiration if amoebic serology inconclusive; pregnancy (metronidazole
- Treatment
contraindicated); suspicion of secondary infection; severe symptoms from
1. Resuscitate if necessary distension or fever; impending rupture
2. Close monitoring of vitals with strict IO charting

44
45
PANCREATIC DISEASES - Gallstones are thought to cause acute pancreatitis due to obstruction of the
pancreatic duct causing interstitial oedema which impairs blood flow to the
ACUTE PANCREATITIS pancreatic cells  ischaemic cellular injury  predisposition to enzyme activation
- The mechanisms in which alcohol cause pancreatitis are not known, though it is
DEFINITION
believed alcohol itself results in injury to pancreatic cells through generation of free
An acute inflammatory process of the pancreas with variable involvement of regional radicals during its metabolism, and may sensitise the pancreas to injury by other
tissues or remote organ systems agents

EPIDEMIOLOGY
- Incidence is difficult to measure accurately (not all diagnosed). ATLANTA CLASSIFICATION (FOR SEVERITY)
- ~ 7-10% presenting with abdominal pain acute pancreatitis Mild acute pancreatitis Severe acute pancreatitis (any 1)
Trauma: blunt trauma, ERCP, gall stones - Interstitial oedema - Pancreatic or peripancreatic necrosis
CAUSES (I GET SMASHED) - Minimal organ dysfunction - Associated with organ failure
Infx: mumps, VZV - May be a/w local complications
1. Idiopathic - Uneventful recovery
2. Gallstones Drugs: EthanolSteriods, NSAIDS,
3. Ethanol diuretics, sulphnamides
4. Trauma Metabolic: hyperlipidemia, hypercalcemia PRESENTATION
5. Steroids
Autoimmune: SLE, PAN - Symptoms (generally non-specific):
6. Mumps and other infections (VZV also)
7. Autoimmune – SLE, PAN Neoplastic: Ca head of pancreas  Abdominal pain (most consistent, in >90% of patients) – constant
8. Scorpion toxin epigastric pain, classically radiating to the back (in 50%), maximal
Congenital: CFs, Pancreas divisum
9. Hypercalcaemia, hypertriglyceridaemia, hypothermia intensity within several hours of onset; usually occurs after a heavy meal;
10. ERCP alleviated by sitting up & leaning forward, worse on movement
11. Drugs (SAND: Sulphonamides, azathioprine, NSAIDs, diuretics)  Nausea, vomiting, Anorexia
12. Rare causes: Cystic fibrosis, cancer of the head of the pancreas, severe blunt trauma,
pancreas divisum - Also rule out other causes:
 Gastric causes: PUD
Gallstones and alcohol are the most common causes (>90% of acute pancreatitis)
 Perforated viscus (mainly on examination: look for peritonism)
 AMI, DKA or even a lower lobe pneumonia
PATHOPHYSIOLOGY  Hepatitis or GB / CBD disease
- The final common pathway of pancreatitis involves inappropriate activation of
proenzymes stored within zymogen granules in the pancreatic cell – trypsin is - Ask for causes of pancreatitis:
implicated in this mechanism as it activates most of the proenzymes secreted by the  Gall stone disease: biliary colic, symptoms of cholecytitis/ CBD stone/
pancreas when they are secreted into the duodenum cholangitis
 Recent alcohol abuse or chronic alcohol abuse
- The activated lytic enzymes destroy the pancreatic acinar cells resulting in release of  Recent blunt trauma or ERCP done
potent cytokines that attract neutrophils and macrophages, which themselves secrete  PHx or hyperlipidemia, hypercalcemia, autoimmune disease (SLE, PAN)
pro-inflammatory cytokines  Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling)
- The cytokine cascade amplifies the local inflammatory response and also results in  Recent drug history: steroids, NSAIDs, diuretics
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
- Signs (also non-specific) 3. Urinary diastase
 Tachycardia, low grade fever, low BP, toxic looking, jaundiced? - Similar function to serum lipase, used when serum amylase is equivocally raised
 Epigastric tenderness or signs of peritonism (<1/3 of patients) or normal
Other causes of elevated serum amylase:
 May have a palpable mass (pseudocyst, pancreatic phlegmon)
 Abdominal distension ± ascites with diminished or no bowel sounds (ileus) GI sources - PUD, IO, perforation, Ischaemic bowel (amylase in the
thousands), Cholecystitis, cholangitis
 Ecchymoses (usually not present): flank (Grey-Turner‘s sign) or umbilical
Non-GI - Kidney stone
(Cullen‘s) suggest severe haemorrhagic pancreatitis associated with profound
sources - Ectopic pregnancy
fluid loss (third-spacing)
- Salivary gland injury or inflammation
- Macroamylasaemia
 Ask for urine output
- Impaired clearance due to chronic renal failure
 Offer to auscultate the lungs for any effusion or ARDS (creps, reduced air entry)
PROGNOSTIC / SUPPORTIVE / LOOKING FOR AETIOLOGY
MANAGEMENT STRATEGY Imaging
4. Erect CXR & AXR
Diagnosis - 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
Severity stratification pancreas) or “colon cut-off sign” (distended colon from ascending to mid-
Assess for aetiology transverse with no air distally) –due to functional spasm of the bowel around the
pancreas resulting from inflammation
5. Ultrasound
- Preferred over CT scan
Supportive Monitor for Treat aetiology - Good for visualising biliary tree and picking up gallstones
treatment complications (reverse / control) - Pancreas may be diffusely enlarged and hypoechoeic – often difficult to
visualise due to overlying bowel gas
6. CT AbdoPelvis
Manage Prevent future - Only if considering other pathologies (CT may worsen pancreatitis)
complications recurrence - At ~72hrs of known case of pancreatitis: detect fluid collections; necrosis (IV
contrast needs to be given )

INVESTIGATIONS Laboratory
1. FBC (TW for Ranson, Glasgow; haematocrit for Ranson)
DIAGNOSTIC 2. U/E/Cr (urea for Ranson and Glasgow; electrolyte imbalances, dehydration)
1. Serum amylase 3. Glucose (for Ranson and Glasgow)
4. LFTs (AST for Ranson and Glasgow; albumin for Glasgow; obstructive picture in
- raised within 12 hours of onset, usually more than 1000 or 3 times normal
gallstone pancreatitis)
- High sensitivity and moderate specificity (specificity increased when cut-off
5. Lactate dehydrogenase (for Ranson and Glasgow)
taken at 3 times normal upper limit)
- Returns to normal level 48 to 72 hours after onset – not useful in late diagnosis 6. ABG (PaO2 for Ranson and Glasgow; base excess for Ranson)
2. Serum lipase
7. Ca/Mg/PO4 with albumin (hypercalcaemia – aetiology)
8. Fasting lipids (hyperlipidaemia – aetiology)
- Rises within 8 hours of onset of symptoms and returns to normal after 7-10 days
9. ECG & cardiac enzymes (rule out AMI as a cause of epigastric pain)
- Thus more useful in late diagnosis of acute pancreatitis
46
47
SEVERITY STRATIFICATION (RANSON, GLASGOW, APACHE II) IV. C-reactive peptide
- As a single prognostic marker; <100 is unlikely severe
I. Danger signs in the first few hours - If CRP is >210mg/dL at 48 hours, the pancreatitis is more likely to be severe
- Encephalopathy - No relevance >3/7 of onset as other confounding factors come into the picture
- Hypoxaemia, - Combination of Glasgow score and CRP improves overall prognostic value
- Tachycardia >130/min, Hypotension <90mmHg, Haematocrit >50
- Presence of Gray Turner‘s/Cullen‘s sign V. Balthazar’s CT severity index (consider a CT AP @ ~ 3/7 from onset)
- Oliguria <50mls/hr, Azotemia
- 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
II. Ranson’s criteria
still evolving (CT findings lag behind) in the early stages
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 COURSE OF DISEASE
3. Fasting bld gluc >11.2mmol/L 3. Calcium <2mmol/L
4. LDH >600U/L 4. PaO2 <60mmHg - 75%: mild course of disease; recover unless comorbidities cause deterioration
5. AST >120U/L 5. Base excess >4mmol/L - 20-25%: severe outcome  1/3 of these patients will ultimately die
6. Neg fluid balance >6L
- Overall mortality rate <10%
- Ranson‘s criteria prognosticates mortality according to score
- Death is bimodally distributed:
- Any patient with a score of 3 and above is considered to have severe pancreatitis
- Mortality: <3 0.9% (a) Early
3-4 15%  Within 1/52; due to severe organ failure, SIRS
5-6 50%  Very little can be done in terms of treatment
>6 90% (b) Late
- Shortfalls of Ranson‘s:  Most common cause is infection with resultant sepsis
 validated for alcoholic pancreatitis only revised Ranson‘s score was created  Multi-organ failure can be the course of death
for gallstone pancreatitis,
 difficult to tell aetiology in acute setting & cumbersome to wait for 48 hours, and
difficult to assess for negative fluid balance SUPPORTIVE TREATMENT
1. Monitoring (after resuscitating)
- In general ward if mild pancreatitis; HD/ICU monitoring if severe (≥3)
III. Glasgow/Imrie score- PANCREAS - Fluid resuscitate with crystalliods
1. PaO2 <60mmHg - Monitor vitals [SpO2, BP, HR, Temp.], urine output & CVP
2. Age >55yrs
3. Neutrophil/WBC >15x109/dL 2. NBM (bowel rest) and IV fluid replacement
4. Calcium <2mmol/L - May include gastric decompression with NGT if there is persistent vomiting,
5. Renal (urea) >16mmol/L significant gastroparesis, or intestinal obstruction (ileus)
6. Enzymes LDH >600U/L - Acid suppression does not change course of disease, but protects against stress
AST >100/L ulcer formation; octetride has no benefit (thought to reduce pancreatic secretions)
7. Albumin <32g/L - Fast patients for at least 2/7 until more stable
8. Sugar (Glucose ) >10mmol/L >3 criteria  severe - May start oral feeding early with fluids in mild pancreatitis if tolerated
- Prolonged NBM results in poorer recovery due to nutritional debilitation – think
- Preferred over Ranson‘s scoring in certain centres about NJ feeding, or open jejunostomy creation early in patients with severe
pancreatitis; if not tolerable, then consider TPN
3. Analgesia - Chronic pancreatitis, exocrine insufficiency & endocrine insufficiency
- Do not give NSAIDs as they can worsen pancreatitis & cause renal failure (since
there is already decreased renal perfusion in acute pancreatitis) Systemic complications
- Use opioid analgesics (tramadol, pethidine) other than morphine (causes o Peritoneal sepsis
increased tone of sphincter of Oddi) o Pancreatic ascites (massive accumulation of pancreatic fluid in peritoneum)
o Intra-abdominal haemorrhage (erosion of splenic vessels)
4. Treatment of fluid and electrolyte abnormalities hypocalcaemia, o Multiple organ failure (ARDS, acute renal failure, hypovolaemic shock, DIVC)
hypoglycemia o Hypocalcaemia, hyper/ hypoglycaemia
5. Antibiotics
Intervention for local complications
- Either prophylactic or therapeutic
 Not shown to have any benefit in mild pancreatitis - ERCP
- Prophylactic in severe acute pancreatitis to prevent infection of necrosis - No benefit in mild biliary pancreatitis
(infection will occur in 40-70% of patients with necrosis and increases the - Indications:
mortality rate from 12 to 33%)  Severe pancreatitis
 Carbapenem (only imipenem has been shown to prevent sepsis)  Evidence of ductal stones
- Therapeutic in cholangitis (coexisting with Gallstone disease or a s  Cholangitis
complication of pancreatitis) & infection of pancreatic necrosis/ pseudocyst  No response to treatment within 48 hours
- Duration: 14-28 days - ERCP should be done within first 48-72 hours for maximum benefit
6. Support for organ failure - CT-guided aspiration of pancreatic necrosis
o Ventilate with PEEP if hypoxemic (e.g. ARDS)  Can help differentiate between sterile and infected necrosis
o Dialysis & CVP monitoring if in ARF  Consider surgery if patient doing poorly
o Fluid resuscitation & inotropes if Hypotensive
- Necrosectomy for infected necrosis
 Some kind of lavage and drainage procedure is done after necrosectomy to
MONITORING FOR COMPLICATIONS AND TREATING decrease infective load
Local complications: - Role of surgery
- Acute fluid collections  Infected necrotic pancreas (mortality 100% without operation)
 Due to increased vascular permeability; 70-80% resolve spontaneously  Sterile necrotic pancreas (necrosectomy)
- Pseudocyst  Delay surgery till as late as possible for demarcation of necrotic areas
 Persistent fluid collection (enzymes, blood, necrotic tissue) walled off by fibrosis (repeated surgeries required)
and not an epithelium-lined surface (after 4 weeks)  Diagnostic uncertainty
 Presents as Gastric outlet obstruction, infx, peritonitis, h‘ge (erosion of splenic  Complications e.g. intra-abdominal haemorrhage
vessels), Persistently raised amylase despite resolution of pancreatitis
 50% resolve spontaneously - Pseudocyst
- Abscess  Operate if larger than 6cm and persisting for more than 6 weeks as the chance
 Infection of fluid collection (not necrosis) of spontaneous resolution is low and risk of complications (infection,
- Pancreatic necrosis haemorrhage, rupture) is high
 Areas of no contrast uptake on CT with intravenous contrast  Surgery can be open, laparoscopic, endoscopic or percutaneous
- Infected necrosis (radiologically guided)
 Gas bubbles on CT scan  Endoscopic – internal drainage via a cystogastrostomy,
 Positive bacterial culture on CT, U/S guided FNA cystoduodenostomy or cystojejunostomy

48
49
MANAGEMENT OF AETIOLOGY & PREVENTION OF RECURRENCE PRESENTATION
Avoid alcohol, stop all offending medication & control hyperlipidemia May be asymptomatic, picked up on imaging for some other purpose
Pancreatic head or periampullary Pancreatic body/tail
Cholecystectomy for biliary pancreatitis
- Obstructive jaundice (painless Late presentation
- 18-21% of patients with biliary pancreatitis will have another episode obstructive jaundice with palpable - Coeliac and mesenteric plexus
- Among these, 25-65% will develop the 2nd episode within 30 days of the initial one GB) + cholangitis invasion – dull constant pain in the
- done in the same admission for pts with mild pancreatitis epigastrium radiating to the back
- Duodenal obstruction
- In patients with severe pancreatitis, there is reluctance to do the surgery early, as the - Malaise, weight loss, anorexia, nausea
- Bleeding upper GIT (haematemesis
patient may develop complications that require surgical intervention – better to do all
and/or malaena) - Exocrine insufficiency with duct
surgery in the same operation instead of opening the patient twice
- Malaise, weight loss, anorexia, nausea obstruction  steatorrhoea,
malabsorption
PANCREATIC CANCER
- Metastatic symptoms: ascites, bone
EPIDEMIOLOGY pain, CNS symptoms, dyspnoea
- Incidence about 3-5 per 100,000 per year in each gender - Paraneoplastic syndromes – migratory
- Eighth cause of cancer death in Singapore thrombophlebitis in 6%
- 1.7:1 male to female ratio
- Very poor prognosis – median survival for unresectable disease is 6 months (80% of
patients have unresectable disease at presentation); overall 5-year survival <3% IMMEDIATE MANAGEMENT
- Treat any life-threatening complications such as cholangitis, pancreatitis, bleeding
ASSOCIATIONS
- Cigarette smoking (most clearly established – 2-5X increased risk) INVESTIGATIONS
- Industrial carcinogens – benzidine, betanaphthylamine
DIAGNOSTIC
- Lower socioeconomic class
1. CA 19-9
- Diabetes mellitus
- Not a screening test for pancreatic cancer as it can be false positive
- Chronic pancreatitis
- Can act as a prognostic marker: high CA 19-9 levels usually associated with
- Genetic factors (mutations in K-ras gene, p16 gene) unresectable disease with poorer prognosis
- Familial cancer syndromes e.g. Peutz-Jeghers - Can be used as a marker for tumour recurrence during post-op follow-up

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:
 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
 Prognosis is also better as they present earlier with obstructive jaundice
2. CT scan
- Better sensitivity (85-90%) and equal specificity (90-95%) in diagnosing
pancreatic cancer
- Features: Mass lesion within pancreas, bile and pancreatic duct dilatation in head
of pancreas tumours (double duct sign)
- Any evidence of extra-pancreatic spread: Involvement of regional lymph nodes,
liver metastases, ascites
3. MRI pancreas with MRCP – MRI pancreas is not superior to CT scan; 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) - Complications of Whipple‘s operation
 Mortality rate is 2-7%, with a morbidity rate of up to 20-30% (mostly mild
5. Endoscopic ultrasound + FNA biopsy
complications)
- Can be used to stage tumour and nodal involvement
- FNA with EUS guidance is preferred to transcutaneous biopsy as there is less  Intraoperative/early complications
risk of tumour seeding (a) Injury to other organs – liver, kidney, bowel
(b) Bleeding
STAGING (c) Infection  sepsis
1. CT/MRI of the abdomen – T, N stage; metastasis to the liver (d) Pancreatitis
2. Endoscopic ultrasound – T, N stage (e) Pancreatic anastomotic leak (5-20%)
(f) Biliary anastomotic breakdown
3. Lungs – CXR + CT thorax (g) Fistulation, pseudocyst formation may occur due to anastomotic leaks
4. Bones – bone scan when suspicion is high
 Late
5. Staging laparoscopy – for peritoneal metastases, just before definitive operation (a) Long-term exocrine insufficiency resulting in malabsorption and
for a resectable tumour (since CT/MRI may miss small peritoneal deposits)  if no steatorrhoea
peritoneal disease found, continue with surgery, otherwise, close up and abort (b) Gastric stasis with pylorus-preserving Whipple‘s
surgery (c) Diarrhoea resulting from autonomic nerve injury during lymph node
dissection
TREATMENT (d) Endocrine insufficiency  DM
SURGERY
Palliative surgery
Curative resection
- Improves chances of survival Surgical bypass of obstruction
- However, recurrence rates after surgery are high – 5 year survival only 10 to 30% - Triple bypass involving anastomosis between
- Only about 15-20% of patients will have resectable disease at presentation – usually (a) Stomach and jejunum (gastrojejunostomy)
in periampullary or head of pancreas tumours; tumours of the body and tail present (b) Biliary system and jejunum (choledocho-/hepatico-/cholecysto-jejunostomy)
too late to be resectable (c) Jejunum and jejunum, to prevent reflux of food into biliary tree – essentially a
- Resectable disease: Roux-en-Y loop (jejunojejunostomy)
 No metastases (lung, liver, bone, peritoneum)
 Patent superior mesenteric vein and portal vein NON-SURGICAL PALLIATIVE MEASURES
 Definable tissue plane between tumour and superior mesenteric artery as well as 1. Endoscopic stenting
coeliac axis - Stenting of obstructed biliary duct
- Stenting of obstructed duodenum
- Whipple‘s operation
 Pancreaticoduodenectomy for head of pancreas or periampullary tumour 2. Coeliac plexus block for pain
 Usually preceded by a staging laparoscopy to confirm absence of peritoneal 3. Palliative chemotherapy/radiotherapy/chemoradiotherapy
metastases - Not shown to provide good outcomes
 Removal of the head of the pancreas, duodenum, proximal 15cm of jejunum,
common bile duct, gallbladder, and distal part of the stomach
 Common hepatic duct and pancreas are then anastomosed to the jejunum, 45-
60cm proximal to the gastrojejunostomy

50
51
DISEASES OF THE BILIARY SYSTEM 2. Aetiology – benign or malignant
- Recurrent spikes of similar jaundice that resolve on their own with time suggest
APPROACH TO OBSTRUCTIVE JAUNDICE benign obstruction e.g. stones, strictures
- A young patient with painful jaundice  usually benign cause
CAUSES - Previous history of gallstone disease or biliary colic symptoms
Intraluminal Benign - Previous history of surgery to the biliary tract or ERCP
- Gallstones - Malignancy is suggested if the patient is old, jaundice is of new onset and
- Parasitic infections (recurrent pyogenic cholangitis) progressively worsening, and there is no associated pain (i.e. painless
Mural Benign progressive jaundice)
- Post-instrumentation strictures (ERCP, operation) - Constitutional symptoms: loss of appetite, loss of weight, malaise
- Strictures from other causes (gallstones, chronic pancreatitis) - Metastatic symptoms: bone pain, neck lump, dyspnoea, etc
- Primary sclerosing cholangitis - Pain is a late symptom of pancreatic cancer and tends to be constant and
- Choledochal cyst relentless compared to biliary colic which subsides after a few hours
Malignant 3. Complications
- Cholangiocarcinoma (distal)
- Symptoms of cholangitis: fever, chills, rigors with RHC pain and jaundice
Extramural Benign - Fat malabsorption: steatorrhoea, fat-soluble vitamin deficiency (A, D, E, K) –
- Mirizzi syndrome especially coagulopathy (very unlikely in acute setting)
Malignant - Liver decompensation: encephalopathy, hepatic fetor, worsening ascites
- Head of pancreas cancer - Pruritus as a result of bile salt retention
- Periampullary cancer - Pancreatitis (gallstone as cause): abdominal pain radiating to the back with N/V
- Metastases to the porta hepatis
PHYSICAL EXAMINATION
HISTORY 1. Vitals: Is patient haemodynamically stable? Any fever?
2. General inspection: Jaundice. Pallor? Any abdominal distension, leg swelling?
1. Confirm obstructive jaundice 3. Peripheries: Stigmata of chronic liver disease? Scratch marks? Conjunctival pallor?
- Confirm jaundice – patient‘s sclera are yellow 4. Abdomen
- Establish obstructive jaundice – tea-coloured urine, pale stools - Any scars of abdominal surgery?
- Exclude pre-hepatic and hepatic jaundice (more importantly hepatic jaundice - Generalised distension? (ascites could be due to malnutrition, peritoneal
since it can also cause tea-coloured urine) malignancy, or obstruction of portal vein by cancer)
 Symptoms suggestive of viral hepatitis: prodrome of fever, malaise, - Hepatomegaly? (Could be due to metastatic disease, or primary liver pathology)
arthralgia, myalgia, nausea/vomiting, etc. - Enlarged gallbladder? (Recall Courvoisier‘s law – if the gallbladder is palpable
 Risk factors for viral hepatitis: travel history, ingestion of seafood, family in a person with painless obstructive jaundice, the cause is unlikely to be stones)
history of hepatitis (esp mother, siblings), blood transfusions, drug - Splenomegaly? (Portal hypertension – think prehepatic, hepatic, posthepatic)
abuse/needle sharing, needlestick injuries, sexual contact
5. DRE: Pale stools?
 Alcohol intake
 Drug history: any TCM intake recently, any new medications taken 6. Cervical and supraclavicular lymph nodes
 History of chronic liver disease 7. Bony tenderness
8. Respiratory examination
INVESTIGATIONS (guided by clinical suspicion after Hx and P/E) NORMAL PHYSIOLOGY OF BILE
- Normal bile contains bile salts (primary and secondary), phospholipids, cholesterol,
Bloods
protein, and bilirubin
1. FBC – any infection, anaemia
- Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol
2. U/E/Cr
3. LFT – bilirubin raised (direct>indirect; Normal 3:7); raised ALP and GGT more STONE COMPOSITION AND PATHOPHYSIOLOGY
than AST and ALT (obstructive picture)
4. Amylase Cholesterol stones
5. PT/PTT – any prolonged PT from vitamin K malabsorption, liver dysfunction - More common in older patients (peak at 40-50 years)
6. Tumour markers – CA 19-9, CEA (cholangioca and pancreatic ca) - Cholesterol stones are hard and faceted
7. Blood c/s if febrile and jaundiced - Cholesterol stones results from disruption in the solubility equilibrium of bile
- Risk factors for cholesterol stones formation:
Imaging
- Ultrasound versus CT 1. Increased cholesterol secretion in bile
 Obesity
 US findings: GB stones or sludge, thickened GB wall, pericholecystic fluid, duct
 Hyperlipidaemia
dilation, liver consistency (fatty or cirrhotic)
 Increased oestrogens: female, pregnancy, exogenous administration
 Both useful in demonstrating dilated biliary system and site of obstruction as
well as the cause of obstruction 2. Decreased emptying of the gallbladder
 Gallbladder malignancy is an important cause to exclude
 Ultrasound is sufficient if malignancy is unlikely but unable to detect distal CBD
 Truncal vagotomy
stones well, but CT is preferred if there is a suspicion of malignancy (Ca
 Spinal cord injury
pancreas or periampulary cancer)  define the tumour (T) better & stage at the
same time (N & M)
Pigment stones
- More common in younger patients
MANAGEMENT
- Pigment stones are soft stones and crumble easily
The patient is managed as for the causative aetiology (see relevant sections)
- Can be divided into black pigment stones and brown pigment stones
- Black pigment stones are composed of mostly calcium salts and bilirubin –
predisposing factors include increased secretion of bilirubin into bile (e.g. chronic
haemolysis, chronic liver disease, TPN), decreased bilirubin solubilisers, and
GALLSTONE DISEASE gallbladder stasis
DEFINITION - Brown stones are composed of calcium salts, bilirubin, and more cholesterol than
Gallstone is a generic term for any kind of stone (cholesterol, pigment) in any part of black pigment stones; they form in the biliary ducts due to infection with bacterial
the biliary system (gallbladder, cystic duct, hepatic duct, common bile duct, etc) degradation of biliary lipids, the degradation products of which then precipitate

Biliary sludge
EPIDEMIOLOGY
- Microlithiasis suspended in bile; a milieu that predisposes to stone formation
- Exact incidence in Singapore not known
- Can be visualised on the ultrasound scan as layering in the biliary tree
- In the West: overall 10-15%; 20% in women and 10% in men
- Sludge is a pre-stone condition, but not all sludge becomes stones
- Consistent 2:1 female to male ratio
- 20% of biliary sludge will disappear, 60% recur, and 10% form stones
- Typical picture (the F‘s): Fat, female, forty, fertile, flatulent

52
53
CLINICAL COURSE
Asymptomatic
- 80-95% of patients will have asymptomatic gallstones
- Risk of symptom occurrence is 1 to 2% per year, of which the greatest risk is
within the first 5 years of diagnosis – 10% at 5 yrs, 15% at 10 yrs, 18% at 15-20 yrs
- Of those who develop symptoms, 7-10% will have moderate symptoms, and 3-5%
severe; the rest will have minor symptoms
- Thus the majority of patients do not require removal of the stones or the
gallbladder  expectant management
- Role of surgery in the asymptomatic patient:
(a) Predisposing cause for gallbladder stasis that should be surgically treated e.g.
gallbladder mass suspicious of malignancy, or in patients with high risk of
malignancy (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
Basal pain is due to inflm of ductal epithelium
1. Biliary colic & proximal distension.
- Typically epigastric or RHC pain
- Radiation to the inferior angle of the right scapula, or tip of right shoulder
- Waxing-waning in character but rarely have any pain-free intervals between
waves of pain (unlike ureteric colic where pain resolves completely in between)
- Often triggered by meals – binge-eating, fried oily foods, dehydration
- Lasts for minutes to hours, often resolves spontaneously
- Associated with N/V (patient gets better after vomiting), bloating, abdominal
distension
- Biliary colic is a ―herald‖ symptom that indicates risk of further sequelae
2. Acute cholecystitis (see below)
3. Mirizzi syndrome with obstructive jaundice (see below)
4. Mucocoele of the gallbladder or hydrops or Empyema of Gallbladder (see below)
5. Choledocholithiasis with obstructive jaundice (CBD is not muscular, so absence of
biliary colic, but a constant pain with OJ 2o to obstruction)
6. Cholangitis and septic sequelae (see below)
7. Acute pancreatitis (see above)
8. Fistulation and passage into gut resulting in gallstone ileus – subacute IO
INVESTIGATIONS FOR GALLSTONE DISEASE
1. Plain abdominal X-ray
- Pickup rate for gallstones is less than 10% since most stones are radiolucent
2. Ultrasound of the hepatobiliary system
- Investigation of choice for gallstones
- 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
3. CT scan
- Usually not done to diagnose stones (as mentioned above)
- Usually done in symptomatic patient where it is uncertain what is the cause of
symptoms  looking for other possible causes as well
4. Magnetic resonance cholangiopancreatography (MRCP)
- MRCP is not the same as MRI liver/pancreas – only selected cuts taken in order
to reconstruct the biliary tree & is without contrast  only T2 images, so the
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
5. Endoscopic retrograde cholangiopancreatography (ERCP)
- The largest value of ERCP lies in its therapeutic potential
 Stone removal (using balloon catheter, or Dormia basket)
 Sphincterotomy (in order to relieve obstruction or facilitate removal of stone)
 Stenting
- High level of complications
 Pancreatitis in 2-3%
 Cholangitis 1-2%, haemorrhage 2-3%
 Perforation into bile duct, duodenum 0.5-1%
 Overall risk of complications is 10-15%
- Before doing ERCP, need to assess the benefits and risks, and select patients
carefully
6. Percutaneous transhepatic cholangiography (PTC) /biliary drainage - Non- surgical means of stone treatment
(PTBD)  Chemodissolution
- PTC involves a tube being inserted into the liver under radiologic guidance into  Liver diet
one of the biliary ducts (must be dilated duct)  Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around
- Rarely done now; main indications: 1) high obstruction not well visualised in to dampen waves; good results only for cholesterol stones
ERCP; 2) therapeutic purpose of drainage for an obstructed system that cannot   All not shown to work for long-term
be drained from below
- Mostly for therapeutic rather than diagnostic purposes
- Complications: bleeding; leakage of bile when tube is removed
ACUTE CHOLECYSTITIS
7. HIDA scan
- No longer used commonly, except in biliary atresia PATHOPHYSIOLOGY
- Gallstone gets stuck in the cystic duct causing obstruction of biliary flow
5 criteria for a normal cholangiopancreatogram - Gallbladder becomes distended and inflamed
(a) Normal intrahepatic ducts
(b) No filling defects PRESENTATION
(c) Smooth common bile duct - Constant, severe RHC pain (less commonly epigastric)
(d) No stricture/narrowing of the common bile duct - Radiates to the inferior angle of the scapula
(e) Good and free flow of contrast into duodenum - Associated with fever, nausea, vomiting
- RHC tenderness with guarding found on clinical examination; Murphy‘s sign positive
- Gallbladder may be palpable – omentum wrapping around GB; worst case scenario is
TREATMENT empyema
Asymptomatic - LFTs usually normal; no jaundice
- No surgery required unless patient has indications for surgery (see above)
- Expectant management and close follow-up ULTRASOUND FEATURES OF ACUTE CHOLECYSTITIS
- Counsel patient about symptoms – biliary colic, acute cholecystitis, obstructive - Presence of gallstones in biliary system
jaundice, etc - Contracted gallbladder (from chronic gallstone disease)
- Pericholecystic fluid (oedema of gallbladder wall)
Symptomatic
- Sonographic Murphy‘s positive
- Cholecystectomy is the only way to treat gallbladder stones that are symptomatic
- (Fat stranding around gallbladder not seen on ultrasound but on CT)
- Can be open or laparoscopic – laparoscopic is preferred as it is associated with
shorter hospital stay, less pain, less complications post-operatively
MANAGEMENT
- Risks of laparoscopic cholecystectomy
- Resuscitate the patient
 Conversion to open operation up to 5% (due to abnormal anatomy; difficult or
complicated dissection; iatrogenic injury); conversion rate is higher if there is - Septic workup
ongoing infection e.g. cholecystitis – up to 1 in 3 to 1 in 4 - Bowel rest and intravenous fluids
 Injury to surroundings: bowel & biliary structures e.g. CBD - Analgesia
 Spilled bile  peritonitis, sepsis
 Haemorrhage - Empirical intravenous antibiotics – IV ceftriaxone and metronidazole
 Infection - Definitive treatment – laparoscopic cholecystectomy

54
55
Timing of cholecystectomy
- Dependent on several factors: 3. Gangrene and perforation
 Severity of illness - Localised perforation  abscess that is confined by the omentum
 Response to resuscitation and antibiotic therapy - Free perforation  generalised peritonitis and sepsis, requiring emergency
 Logistical considerations (availability of OT, surgeon etc) laparotomy
- Possibilities available: 4. Cholecystenteric fistula
i. Emergency (immediate; in very sick patients who are not doing well/not - Most commonly occurs in duodenum, then colon, and stomach; after repeated
responding to treatment) attacks of cholecystitis
ii. Early (within few days of onset) - Usually asymptomatic
iii. Delayed/interval (after 6-8 weeks) - On AXR, aerobilia is seen in 40% of cases
Early Delayed - Symptomatic fistulas should be treated with cholecystectomy and fistula closure
Advantages Advantages
- Everything done in one admission - Lower risks 5. Gallstone ileus
- Easier to operate as the gallbladder is - Better laparoscopic success - Stones causing cholecystenteric fistula pass into the enteric lumen causing
oedematous intermittent bouts of small bowel obstruction
- Accounts for 1-2% of IO overall
Disadvantages Disadvantages - Most common site of obstruction is terminal ileum
- Ongoing inflammation  higher risk - Fibrosis  difficulty mobilising - Small stones (<2-3cm) usually pass spontaneously without problems
of bleeding gallbladder - Mortality is 10-15%, mostly in elderly patients in whom gallstone ileus is more
- Higher risk of injuring some other - Need for another admission common
structure due to difficulty in - Chance of recurrence during the time
- Small bowel enterotomy proximal to the point of obstruction is usually required
visualisation
to remove the stone
- Higher conversion rate to open chole
- Increased risks of post-op infection - Immediate cholecystectomy not warranted as <4% of patients will have further
symptoms
 Early surgery has been found to be more beneficial than delayed surgery

Cholecystostomy ACALCULOUS CHOLECYSTITIS

- In moribund patients who are not fit for surgery
- Can be done under LA, or more commonly under radiologic guidance (percutaneous)
- Drains the gallbladder and alleviates the inflammation  better outcomes
COMPLICATIONS OF ACUTE CHOLECYSTITIS
1. Hydrops
- Cystic duct obstruction leads to a tense gallbladder filled with mucus
- May lead to gallbladder wall necrosis if pressure exceeds capillary bld pressure
- 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

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
CHOLEDOCHOLITHIASIS CHOLANGITIS
PRESENTATION PRESENTATION
- Obstructive jaundice – tea-coloured urine, pale stools - Classically Charcot’s triad: RHC pain, fever, jaundice (only 50-70% of patients
- Biliary colic have the classic triad)
- If infection sets in  cholangitis (see below) - Reynold’s pentad: Charcot‘s triad plus mental obtundation and shock
- A surgical emergency!
BLOODS
- FBC (check TW for any rise suggestive of infection) PATHOLOGY
- Amylase (CBD stone may cause pancreatitis) - Usually results from obstruction to the biliary system with infection of stagnant bile
- LFTs (raised bilirubin – direct; ALP raised more than transaminases) - Most common cause is choledocholithiasis (60%); also consider benign strictures and
malignancy (pancreatic, biliary)
- Common causative organisms are gram negative bacteria and anaerobes – Klebsiella,
ULTRASOUND
E. coli, Enterobacter, Enterococcus
- Gallstones in gallbladder
- Gallstone in CBD MANAGEMENT
- Dilated CBD (normally <8-9mm)
 >10mm is abnormal 1. Resuscitation
 In older patients, post-cholecystectomy, or patients on long-term opiates, the - Anticipate rapid deterioration
- Obtain good intravenous access and fluid resuscitate as appropriate
CBD may be larger, up to 11-12mm in size
- Take bloods for investigations – cultures especially
- Close monitoring of vitals in HD/ICU
MANAGEMENT - Catheterise and watch urine output
- If unsure of presence of stone  less invasive investigation such as MRCP, EUS - CVP line insertion if patient has shock unresponsive to fluid resuscitation
- If likelihood of CBD stone is high  ERCP with stone removal
2. Antibiotics
ERCP successful Plan for lap cholecystectomy - IV ceftriaxone and metronidazole; imipenem if the patient is in shock
ERCP failed If patient is well and can tolerate another ERCP, try again
(+ stent in between to drain bile) 3. Biliary decompression and definitive treatment
- Biliary decompression and definitive treatment can be combined or separate
Operative removal – Open CBD exploration
– Lap CBD exploration - Investigate for cause of obstruction – ultrasound or CT (depending on what
facilities are available; ultrasound is preferred if suspecting stones)
- If no facilities to do ERCP: open or laparoscopic cholecystectomy with CBD
exploration - Decompression commonly performed using ERCP
 Decompression is the primary objective – stenting or external drainage
When to do operative removal of stones (i.e. not suitable for ERCP) (nasobiliary drain)
- Stone >25mm  If cause of obstruction can be treated in the same setting (e.g. stones to be
- Intrahepatic stone removed) then treat the cause also
- Large number of stones  Success rate 90%
- Impacted stone
- Dual pathology - Definitive treatment dependent on:
- Tortuous duct  Medical condition of patient
- Previous Bilroth II (unsuitable anatomy for ERCP)  Success of biliary decompression
 Logistical considerations
56
57
- Choices for definitive treatment: MIRIZZI’S SYNDROME
(a) Open cholecystectomy with CBD exploration
(b) Laparoscopic cholecystectomy PATHOLOGY
(c) Laparoscopic cholecystectomy with CBD exploration - Gallstone in the Hartmann‘s pouch compressing the common hepatic resulting in
obstructive jaundice
CBD EXPLORATION - Compression effect is not just physical (the stone) but also contributed by the
surrounding inflammation
- Cholangiogram or choledochoscopy is performed
- One of the caveats to Courvoisier‘s law
 Cholangiogram involves injection of dye – can image higher ducts
 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 GRADING
stones visualised in the duct - Grade I: No fistula; extrinsic compression on CHD
 Choice of imaging depends on site of obstruction and the cause - Grade II: Fistulation into common bile duct with the fistula <1/3 diameter of the
CHD
- Removal of stones - Grade III: Fistula 1/3 to 2/3 diameter of CHD
 Manual removal with stone-grasping forceps - Grade IV: Fistula >2/3 diameter of CHD
 Flushing out stones
 Dredging stones out using balloon catheter or Dormia basket MANAGEMENT
 Lithotripsy - Grade 1: attempt laproscopic cholecystectomy
- Grades 2-4: open cholecystectomy with CBD exploration
- 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 CHOLANGIOCARCINOMA
should anticipate swelling and oedema of the biliary system resulting in post-
operative obstruction and buildup of bile  higher risk of biliary leakage SITE
- Intrahepatic/peripheral 10%
(a) Stent – removed later by endoscopy
- Distal 25%
(b) T-tube (usually inserted after CBD-E) - Perihilar 65% (Altemeier-Klatskin tumour)
 A T-shaped tube with its horizontal limb placed in the CBD and the vertical
Bismuth classification
limb leading out to drain bile
i. Type I: below confluence of hepatic ducts
 Functions as a ―pressure release valve‖ as most of the bile will flow through ii. Type II: tumour reaching confluence
the horizontal limb of the tube into the distal part of the CBD; only when iii. Type IIIA/B: involving common hepatic duct and either right or left hepatic duct
there is obstruction to flow will bile be diverted out through the vertical limb iv. Type IV: multicentric or involving confluence and both hepatic ducts
 Allows for post-op cholangiogram to check for remaining stones (at POD 9-
10) before removal – free flow of contrast into duodenum, no residual stones,
ASSOCIATIONS
and no free leak of contrast into peritoneum
- Related to chronic cholestasis:
 If all normal  release anchoring stitch and exert gentle traction on the tube;  Primary sclerosing cholangitis / Ulcerative colitis
the tube should slip out easily, if not, call for help  Hepatolithiasis
 If stones are present  leave tube in for 4-6 weeks to form a fibrous tract   Parasitic infection – Clonorchis sinensis, Opisthorchis viverrini
allows for instrumentation of tract with a scope to remove the stones  Caroli‘s disease (multifocal segmental dilatation of large intrahepatic bile ducts)
- Consider biliary bypass if there are multiple stones, the CBD is more than 2cm in - Bile duct adenoma
diameter, or there are strictures (since the CBD has been chronically dilated, quite - Choledochal cyst
unlikely that it will function normally even after removal of the obstruction)
- Thorotrast exposure
PRESENTATION RECURRENT PYOGENIC CHOLANGITIS
- Painless jaundice (painful if there is cholangitis)
- Acholic stools BACKGROUND
- Pruritus Cholangiohepatitis, or recurrent pyogenic cholangitis (RPC), is characterized by:
- Advanced signs and symptoms: - Recurrent bacterial cholangitis
 Abdominal pain - Intrahepatic pigment stones
 Fatigue, malaise - Intrahepatic biliary obstruction.
 Weight loss
 Hepatomegaly PATHOPHYSIOLOGY
Helminthic infxn (eg Ascaris lumbricoides, Clonorchis sinensis)  epithelial damage
DIAGNOSIS  predispose to seeding of coliforms into biliary system  stone formation 
- CA 19-9 >100μl/ml (good sensitivity of 89%, specificity 86%) recurrent cholangitis
- Contrast CT
- PTC (2 functions: 1) roadmapping for surgery; 2) drainage of obstructed system if HISTORY:
ERCP cannot drain) - A history of recurrent attacks of cholangitis – typical hx:
 1-2 episodes of fevers, jaundice, and RUQ abdominal pain per year
CURATIVE TREATMENT  Hx of prev biliary surgery, endoscopic procedures, or percutaneous biliary
- Surgery is the only chance of long-term cure drainage procedures.
- Only 25% of tumours are resectable - Complications of pyogenic cholangitis
- Contraindications to surgery  cirrhosis with portal hypertension
 Bilateral or multifocal intrahepatic disease  cholangiocarcinoma
 Invasion of portal vein trunk or hepatic artery
 Bilateral involvement of hepatic arterial or portal venous branches PHYSICAL EXAMINATION
 Unilateral hepatic vascular invasion with contralateral ductal spread No specific physical findings are evident in RPC. Dx based on history.
 Distant metastases
DIFFERENTIALS
PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) Primary Sclerosing Cholangitis
- Intrahepatic: 35-45%
- Distal 35-45% INVESTIGATIONS
- Perihilar 10-30% (worse prognosis due to early lymphatic spread)
For diagnosis
For Complications
PALLIATION
- Endoscopic/percutaneous transhepatic biliary stenting Bloods
- Bilateral drainage for hilar cholangiocarcinoma - FBC
- If after opening up and finding that tumour is not resectable, can perform surgical - LFT with ALP>ALT, AST
bypass - 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.

58
59
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.
DISEASES OF THE BREAST 2. Internal mammary nodes--20% of drainage from the ipsilateral breast
 Account for about– upper and lower inner quadrants
ANATOMY  About 4 nodes per side, with one node in each of the first three
- The breast is a modified sweat gland that lies in the subcutaneous tissue of the interspaces and one in the fifth or sixth interspace
anterior chest wall between the superficial and deep layers of the superficial fascia 3. Interpectoral (Rotter‘s nodes) – between pec major and pec minor muscles
- 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 PRESENTATION OF BREAST DISEASE
- The axillary tail pierces the deep fascia and enters the axilla 1. Lump (painful vs painless)
- Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts 2. Pain (cyclical vs non-cyclical) [ more likely benign]
that open separately on the nipple 3. Nipple changes or discharge
- 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
APPROACH TO BREAST LUMP
the dermis, and provide structural support to the breast (involvement of these DIFFERENTIALS (AGE DEPENDENT)
ligaments by malignancy causes dimpling of the overlying skin)
Painless lump Painful lump
Elderly: 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 6. Galactocoele (lactating women)
4. Area of fibroadenosis (nodularity) 7. Carcinoma (rare; ~10% & advanced)

HISTORY
1. History of lump
- Site of the lump?
- Single or multiple?
- When & Why was it first noticed? (Pain, self-examination, etc)?
- Painful or painless?
- Overlying skin changes noted:
 Erythema, warmth,
- Lymphatic drainage:  Dimpling (more prominent hair follicles 2o to dermal oedema from blocked
1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes lymphatics)
1. 40-50 nodes in 5 groups: Anterior, posterior, medial, lateral, apical  Swelling?
2. Drains into supraclavicular and jugular nodes  Any general asymmetry of the breasts noticed?
- Duration since first noticed
Anatomic/ Surgical division into levels I, II and III by the pectoralis minor muscle: - Any increase in size from first noticed to now?
Level I: lateral to pectoralis minor - Any changes in the nipple e.g. retraction
Level II: posterior to pectoralis minor - Nipple discharge? If present, what is the colour and consistency?
Level III: medial to pectoralis minor, extending up to apex of axilla - Any other lumps elsewhere – other breast? Axilla? Neck?

60
61
2. Oestrogen exposure history
Increased risk:
- Age of menarche (early <12YO  increased risk)
- Age of menopause if applicable? (>55YO increased risk)
- Use of HRT (>5yrs) and/or Oestrogen based OCP?
Protective factors:
- How many children? (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
- Family history of breast cancer or ovarian cancer in paternal (BRCA2) and
maternal side (BRCA 1&2), especially if cancer occurs in:
 first degree relative below the age of 40,
 in bilateral breasts
- Previous breast disease:
 Treated cancer
 Previous biopsy showing atypical ductal hyperplasia or LCIS
- Exposure to ionising radiation (esp. RT for previous breast disease)
- Daily Alcohol intake, especially before age of 30 (link has been shown)
4. Systemic review
- LOA, LOW (constitutional)
- Fever (infective cause)
- Bone pain, SOB (metastasis)
PHYSICAL EXAMINATION
Preliminaries (HELP)
- Hi: Introduce yourself & ask for permission to examine the breast
 Always have a chaperone to accompany you if you are male
- Expose patient adequately from the waist up with exposure of axillae
- Lighting: good
- Position the patient at 45o or sitting position if a bed is not available
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, erythema, puckering)
 any scars of previous operation or procedure e.g. punch biopsy
- Ask patient to raise her arms (to accentuate any tethering to the skin  dimpling)
- Ask the patient to contract the pectoralis major (push her hands against her hips) 
may reveal a previously unnoticeable lump
- Look for nipple changes (7 D‘s):
 Discolouration  Depression (retraction)  Destruction
 Discharge  Deviation  (Duplication – unlikely)
 Displacement
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: “I feel a lump in the upper outer quadrant of
 Site (which quadrant) the Right breast. This lump is NOT WARM,
 Tender or non-tender and NON-TENDER, is hemispherical with
poorly defined edges, measuring
 Warmth of overlying skin
 Size ___X___CM. It is firm in consistency with a
irregularsurface and is NOT FLUCTUANT.
 Shape (hemispherical/ oval)
It is NOT FIXED to the SKIN ………….(ask
 Surface (smooth or nodular/irregular) her to contract the pect maj)…. ………….And
 Consistency (soft, firm, or hard) NOT FIXED to the underlying muscle”
 Fluctuance
 Margins (regular and smooth, or irregular and ill-defined)
Check list:
 Fixation to the skin – try to pick up the skin above the lump
- Breast  Fixation to underlying muscle – ask patient to press her hands against her hips
- Nipple to contract the pectoralis major muscle, then try to move the lump in 2
- SC LN perpendicular directions, then ask patient to relax and try to move the lump again
- Spinal Tap
- Lung effusion - Continue to examine carefully for other lumps (multiple lumps are unlikely
malignant, usually fibroadenoma or fibroadenosis)
- Hepatomegaly
- 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
Axillary lymph nodes
- Palpate the normal side first
- Rest the patient‘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: - Abnormal features:
anterior, posterior, medial, lateral, and apical (a) Neo-density or asymmetric density (look for bilateral synchronous ca;
- If any lymph nodes are found to be enlarged, note the number of lymph nodes, their satellite lesion)
site, size, tenderness, consistency (firm, hard, matted), mobility (b) Microcalcifications (<0.5mm in size)
- If calcifications >0.5mm  macrocalcifications; >5/mm2  cluster
To complete the examination - Sole feature of 33% of cancers detected on mammography
- Examine the the supraclavicular LNs & cervical LNs - Causes: DCIS, invasive cancer, fibrocystic disease, papilloma
- Examine the lungs for any pleural effusion - Features of malignancy:
- Percuss the spine for bony tenderness  pleomorphic microcals,
- Examine the abdomen looking for hepatomegaly  heterogeneous appearance; segmental
 closely grouped or arranged in a linear pattern (ductal distribution),
FINDINGS FOR THE COMMON BREAST LUMPS  underlying density
- Features of Benign microcals: punctate, ―tea-cup‖ appearance
Type of lump Age Pain Surface Consistency Mobility
Cyst 30-55 Occ Smooth Soft to hard Not fixed (c) Spiculated mass or stellate lesionwith poor outline or comet sign
Nodularity 20-55 Occ Indistinct Mixed, Not fixed - 95% of spiculated masses on mammography are due to malignancy
fluctuant - Stellate lesion is a localised distortion of the breast parenchyma without
Fibroadenoma 15-25 No Smooth, bosselated Rubbery Very mobile perceptible mass lesion – high chance of it being malignant
Cancer 35+ No Irregular Stony hard May be tethered - Causes: Invasive cancer, radial scar (benign), fat necrosis, abscess, etc
or fixed (d) Architectural disortion (of the contour), tent sign , nipple changes
- Look at the axilla on the MLO view for any enlarged lymph nodes
INVESTIGATIONS
“The evaluation of a breast lump is via the TRIPLE ASSESSMENT All 3 must be
– (i) Clinical examination; (ii) Imaging; and (iii) Histology.” concordant for BI-RADS (Breast Imaging Reporting and Data System) classification
benign to have Category 0: Need additional imaging evaluation
Imaging >99% specificity Category 1: Negative (nothing to comment on, 0.05% risk still present)
1. Mammography to r/o malignancy Category 2: Benign
- Most sensitive of the proven breast imaging modalities Category 3: Probably benign, short-term follow-up suggested (<0.2% risk)
- Usually performed in asymptomatic older women (>40YO) [breast tissue in Category 4: Suspicious, biopsy should be considered (25-74% risk)
younger women is denser; more difficult to pick up abnormalities], but >35YO Category 5: Highly suggestive of malignancy (75-99% risk)
in symptomatic women Category 6: Known malignancy
- Normally, 2 views are done: 70%
 craniocaudal (CC) 2. Ultrasound
 right /Left - Usually used as the 1st investigation in young patients (<35 years old) or
 70% tumours in lateral quadrant (upper) pregnant, lactating patients; not the gold standard for screening
 mediolateral oblique (MLO) - Uses:
 captures the tail  Guide procedures e.g. Biopsy, drainage of abscess, aspiration of cyst
 right/ left  Evaluates consistency (solid vs cystic) &margins
 80% tumours in oblique milky way
80%  Localisation of lesion seen in only one mammographic projection
 Evaluation of a palpable mass with a negative mammogram
- Additional specialised views: magnification and coned compression; done on
request to help magnify areas of abnormality or help visualise breast better  Evaluation in mammographically-difficult areas e.g. chest wall, axilla

62
63
- Pitalls: APPROACH TO NIPPLE DISCHARGE
 Operator dependent, non-standardised techniques, poor resolution,
CAUSES
 Unable to detect most microcalcifications
- Features of malignancy: Colour of discharge Cause
 Markedly hypoechoeic with + thick echogenic halo Red or pink (blood + serum) Ductal papilloma
 Irregular edges; Destruction of surrounding structures Ductal carcinoma
 Hypoechoeic shadowing; Posterior acoustic shadowing Clear yellow (serous) Ductal papilloma
 Taller than it is wide (fir-tree appearance; invasion of fascia) Duct ectasia (= periductal mastitis)
 High central vascularity Cyst
Ductal carcinoma
3. MRI of the breast Green, brown, black (cell debris) Duct ectasia
- Expensive, but Good soft tissue definition without radiation (>90% sensitivity) Purulent, foul-smelling Mastitis/abscess
- Indications: Thin, white fluid (milk) Galactorrhoea/lactation
 Occult lesions: Axillary LAD but Mammogram & US -ve
 Suspicion of multifocal or bilateral malignancy (esp ILC) HISTORY:
 Assessment of response to neoadjuvant chemotherapy 1. Is the discharge true?
 When planning for breast conservation surgery - Exclude other conditions may mimick e.g. eczema, Paget‘s, etc
 Screening in high risk patient 2. Is the discharge significant?
- Spontaneous or only on pressing (spontaneous is sig)
Histology - Intermittent or persistent (persistent is sig)
- Options available: - Relation to breastfeeding (significant if >1yr after stopping breastfeeding)
(a) Fine needle aspiration cytology 3. Is the discharge worrisome?
(b) Core biopsy (Trucut/ mammotome) - Unilateral or bilateral (unilateral more worrisome)
(c) Incisional or Excisional biopsy - Discharge from multiple ducts or single duct (single duct more worrisome)
- Mostly a choice between FNAC and core biopsy - Nature of discharge (bloody more worrisome)
 FNAC is less invasive, less painful, smaller wound, does not require any local - Age of the patient (more worrisome in older patient >60)
anaesthetic, but only cells are obtained with no histology  cannot differentiate 4. Is it troubling the patient?
between in-situ cancer and invasive cancer, requires skilled cytopathologist
 Core biopsy is more invasive, requires local anaesthetic, will result in a larger PHYSICAL EXAMINATION (as described above)
wound, more painful, risk of complications higher (because biopsy needle is a
spring-loaded firing mechanism, improper angling may result in puncture of the INVESTIGATION
1. Discharge for cytology to detect malignant cells
lung or heart), but can obtain tissue specimen, can stain for ER/PR status  better
2. Mammography/ US of both breasts to detect any underlying malignancy
diagnostic value
3. Histology of biopsied lesion if found on imaging
- Guided by clinical palpation or radiologic guidance[ more accurate, not 100%] 4. Ductography, ductoscope & biopsy
 US or Stereotactic guidance (stereotactic mammotome)
MANAGEMENT
MANAGEMENT - If malignancy found, manage malignancy
- Excision for intraductal papilloma (microdocholectomy, total ductal excision,
- If triple assessment suggests a benign lump (i.e. all 3 are concordant), follow up with
hookwire locailised excision)
physical examination for 1 year (q3-6mths) to ensure the lump is stable or regresses
- Antibiotics for mastitis/abscess + incision and drainage for abscess
- If all 3 concordant for malignancy  further staging and treatment - Conservative management for most other pathologies unless discharge persists and is
- If 1 or 2 of 3 aspects suggest malignancy  further workup,  excisional Bx? troubling patient  microdochectomy of offending duct
BREAST CANCER Lobular LCIS ILC
EPIDEMIOLOGY - From terminal duct lobular unit - 5-10% of invasive cancers
- Most common cancer in females in Singapore: (like DCIS) - 10-20% multicentric and/or bilat
- Age-standardised incidence 55 per 100,000 in 2002; incidence is half that of the West - Do not distort lobular architecture - Cells morphologically similar to
- Bimodal age distribution: 45-55YO & older (>75YO) - Usually non-palpable & not cells of LCIS: monomorphic, bland
- Gender ratio is about 100-150 female :1 male detected by mammo, incidentally round nuclei
detected - Cells invade individually into
- 60-80% multicentric and bilateral stroma (due to loss of E-cadherin, a
RISK FACTORS - Not premalignant, but a marker for cell-adhesion molecule)
1. Age (increases with increasing age with two peaks as mentioned) increased risk of invasive disease in - Similar prognosis to IDC
2. Genetic: both breasts (7-10x increased risk)
- Family history: maternal & paternal (breast or ovarian cancer, especially if in - If ca develops, will be IDC usually,
first degree relative, young onset <40 YO, bilateral cancer in relative affected) occurs >15 years after diagnosis
- Known BRCA1 (on 17q; maternal side) or BRCA2 (both sides),
- Li-Fraumeni syndrome involving p53 mutation) Others Specialised types
- Medullary, colloid (mucinous), tubular, papillary
3. High oestrogen exposure:
- Better prognosis than IDC
- early menarche <12YO, nulliparity, late childbearing at >30YO, late menopause
>55YO Inflammatory carcinoma
- Oral contraceptive usage (pure oestrogen type) - Presents as erythematous. enlarged, swollen breast w/o palpable mass
- HRT (>5yrs, small increase in risk; reduced when stopped) - Histologically not specialised
4. Previous breast disease: - Diffuse invasion of breast parenchyma by ca cells blocking numerous
- Previous breast cancer (10X) dermal lymphatic spaces  swelling
- Previous biopsy with atypical ductal hyperplasia or LCIS (7-10X) - No histo features of inflammation
5. Ionising radiation to breast (previous RT) - Very poor prognosis, rapidly fatal
6. Alcohol consumption (daily) SPREAD
- Local: skin & subcut tissues, underlying ribs and muscle (chest wall)
PATHOLOGY (WHO classification: epithelial and non-epithelial tumours.) - Lymphatics: axillary, internal mammary LNs, supraclavicular LNs
- Non-epithelial tumours arise from supporting stroma (e.g. angiosarcoma, malignant - Haematogenous: lungs, liver, brain, bone, adrenals, ovaries
phyllodes tumour, primary sarcomas) and are very uncommon
- Epithelial tumours arise from cells lining the ducts or lobules, and can be further PRESENTATION
divided into invasive and non-invasive based on invasion of the basement membrane - Asymptomatic: detected on mammographic screening
Non-invasive Invasive - Local:
- Self-detected lump in the breast (>1/3 of patients)
Ductal DCIS IDC
- Nipple change: distortion, destruction, retraction, deviation, discharge, eczema
- From terminal duct lobular unit, - 70-80% of invasive breast cancer
- Cause distortion of lobules, - Includes all cancers that cannot be - Overlying skin changes e.g. peau d‘orange, tethering (means mass is still mobile
- Do not invade BM subclassified into a specialised type but overlying skin will be indented when moving the lump), fixation (means the
- Non-palpable, detected microcals  ―no special type‖ mass is not mobile), even fungating ulcer
- 35% multicentric, occult invasive - Poorer prognosis than a carcinoma - Other lumps in axilla
ca in 10-20% of specialised type - Pain is uncommon.
- Progress to ca within 10 yrs, ~30% - 2/3 express ER/PR, - Constitutional: LOW, LOA
risk; considered pre-malignant - 1/3 overexpress C-erbB2 - Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone, brain, adrenals)
- Good prognosis if treated

64
65
DIAGNOSIS – BY TRIPLE ASSESSMENT (see above) PROGNOSIS
Prognostic factors:
STAGING - Stage of disease – tumour size, lymph node involvement [Major prognostic factor]
- Triple assessment can help divide it into: - Histological grade of tumour
- DCIS or early Breast Cancer (BC) (at most with small mobile axillary LNs) - Lymphovascular invasion
- locally advanced BC (matted LNs, skin and rib involvement)
- Age (younger patient  higher chance of recurrence, progress of disease)
o  continue to stage to look for metastasis in advanced BC
- C-erbB2/Her-2 positivity indicates more aggressive tumour  worse
- Staging Investigations: - ER/PR positivity is good – more of a ―predictive factor‖ because it predicts 90%
(i) CXR or CT thorax (for lung metastases; look for isolated hyperdensity) response to treatment with tamoxifen; also means tumour is less undifferentiated
(ii) LFT (raised ALP) or US HBS or CT abdomen (for liver and adrenal metastasis) - p53 mutation
(iii) Bone scan
(iv) CT or MRI brain THERAPEUTIC OPTIONS
T stage N stage M stage Options can be divided into aims of control (with eiter curative of palliative intent):
Tis: Carcinoma in-situ, Paget‘s N1: Mobile ipsilat axillary nodes M1: distant mets (a) Locoregional control: Aim of adjuvant therapy:
with no tumour N2: Fixed/matted ipsilat axillary nodes Surgery (WEAC vs SMAC) 1. Prevent local recurrence
T1: <2cm Radiotherapy a. RT
N3: N3a – Ipsilat infraclav nodes
T1a – 0.1 to 0.5 cm N3b – Ipsilat int mammary nodes (b) Systemic control: (size >10mm; <70YO) b. ± CT, HT, TT
T1b – 0.5 to 1.0 cm N3c – Ipsilat supraclav nodes Chemotherapy 2. Eradicate micrometastasis
T1c – 1.0 to 2.0 cm
Hormonal therapy a. CT, HT, TT
T2: 2 to 5 cm Targeted therapy b. ± RT
T3: >5cm  Reduces recurrence by 1/3; but
T4: T4a – Chest wall involvmt Surgery if recurs have poor prognosis
T4b – Skin involvmt 1. Preparing for operation:
T4c – Both 4a and 4b - Anaesthesia workup and necessary imaging. Mark out the site
T4d – Inflammatory ca - Psychological counselling, consent taking, discuss breast reconstruction
2. Wide excision (breast-conserving surgery; standard of care)
Stage 0 Stage I Stage II Stage III Stage IV - Removal of tumour with clear margins, while achieving good cosmetic result
Tis *skin, rib inv., matted LNs
- Criteria: [Nodal status does not influence decision for WE or SM]
T1N0 T2N0, T3N0
 ≤T2: Tumour <5cm in size, no skin or chest wall involvement
T0N1, T1N1, T2N1 T3 N1
 Only 1 tumour, not multicentric/ multiple DCIS/ LCIS unless same quadrant
T0N2, T1N2, T2N2, T3N2
Any T, N3
 No metastatic disease
T4, any N  Appropriate tumour size-to-breast ratio (to achieve good cosmetic result)
M1  Patient must agree to post-operative radiotherapy
DCIS Early Breast cancer Locally advanced BC Adv. BC - Results: overall survival at 25 years for WEAC comparable to SMAC, with
Aaaaa – Stage Xb (e.g. IIb, IIIb) Slightly higher local recurrence rates (for WEAC: 1% per year, 4% in 5 years)
Survival Other forms of - Higher risk in younger patients as cancer tends to be more aggressive
Stage I: 90% (70% in 10 yrs)  95% with adjuvant Rx mastectomy (modified
Stage II: 60% (40-50%)  76% with adjuvant Rx raical, radical or extended 2. Simple mastectomy (if any CI to Wide excision)
Stage III: 30% (20-30%)  50% with adjuvant Rx radical mastectomy) are - Removal of breast tissue, nipple-areolar complex, and overlying skin
Stage IV: 10% (<2%) not performed anymore. - Lower rates of local recurrence; similar long term prognosis as WE (Italian trail)

3. Axillary clearance
- Performed for all invasive carcinoma (WEAC or SMAC)
- Not required for DCIS (theoretically cancer cells are confined to the breast)
- Complications: see below
- Sentinel lymph node (SLN) biopsy (SLN) is a new standard of care
 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)
- 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
(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
66
Late Cosmetic deformity
Complications of Axillary Clearance:
- Lymphoedema – RT 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.
Radiotherapy
1. Adjuvant
- Usually done 6/52 after WEAC, LN +ve after SMAC, or in high risk patients
- Targeted at breast with or without 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 Monday to
Friday over 5-6/52 until maximum dose (no repeat RT for recurrences)
- Cx: radiation injury (e.g. pneumonitis, skin changes), risk of cancers 1 in 2000 in
20yrs
2. Palliative
Chemotherapy (polyCT with 3 drugs is better; 4-6cycles, each over 1/12)
1. Neoadjuvant
- Given in LABC (stage III) to shrink the tumour before surgical resection
- 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
- Need to place a clip into the tumour before starting neoadjuvant therapy to guide
surgery in case the tumour ―disappears‖; operate according preop staging
- Cx: as for CT drug, e.g. mouth ulcers, N/V, hair loss, immunosuppression
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 (and 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
67
Hormonal therapy TREATMENT BY TUMOUR STAGE
- Used in adjuvant setting to eradicate micrometasis (likewise with CT & TT) Tumour can be divided into
- For ER/PR +ve  will have 90% response 1. in-situ cancer, early BC, locally advanced BC  curative intention
- Preferred for postmenopausal women as response to hormonal therapy is better 2. Advanced BC  palliative intention
- May render patient postmenopausal for better response to HT via medical ablation
with LHRH-a or surgical oopherectomy 1. DCIS
- Mostly used as adjuvant therapy but can also be used as palliative treatment & - WE only (without AC n or adjuvant therapy)
preventive treatment in high risk patients - ± hormonal therapy to reduce recurrence at surgical site; tamoxifen reduces
- Also reduces risk in contralateral breast overall breast cancer risk by 50% in both breast  not adjuvant therapy
Classes 2. Early breast cancer (stage 1 &2)
(a) Selective oestrogen receptor modulators (SERMs): Tamoxifen - T2 or less (<5cm), N1 or less (no nodes or non-fixed nodes)
- 50% reduction in recurrence, 25% reduction in mortality - Locoregional therapy: SMAC, or WEAC with postop RT
- taken daily for 5 years - Adjuvant therapy
- Side effects:  Purpose of adjuvant therapy is to destroy systemic micrometastases
1. menopausal symptoms (hot flushes, etc),  Likelihood of patient having micromets is deduced from T and N stage (major
2. endometrial cancer (0.1% per year), prognostic factors):
3. deep vein thrombosis Chemo Intermediate No chemo
(b) Aromatase inhibitors: Lanastrazole, letrozole, exemestase T >20mm, N stage >1 11mm < T < 20mm, N=0 T <10mm, N=0
- Inhibit peripheral conversion of testosterone and androstenedione to oestradiol Look at histological grade
- Only suitable for post-menopausal patients as use of these agents will cause (minor prognostic factor); if
overactivity of the HPA axis in premenopausal women high grade  chemo
- Side effects:
1. musculoskeletal pain,
 Adjuvant therapy: CT if tolerable and/or HT if ER/PR +ve
2. osteoporosis  In general: In premenopausal pt  chemotherapy + hormonal
In postmenopausal pt  hormonal + chemotherapy
Targeted therapy
- Herceptin (trastuzumab) 3. Locally advanced breast cancer (stage 3)
- targets Her-2-neu a.k.a. C-erbB2 receptor (a type of epidermal growth factor - T3 or T4 (tumour >5cm or skin/chest wall involvement), N2 or N3 (fixed lymph
receptor [EGFR] that is overexpressed in 18-20% of cancers) node involvement or supraclavicular node involvement)
- Used in C-erbB2 positive tumours, early or late stage - Surgical resection dependent on size of tumour and resectability (if tumour is too
- Side effects of Herceptin: large, the skin defect will be very large  inoperable)
1. cardiomyopathy & CCF - Systemic therapy:
2. pulmonary toxicity,  Neoadjuvant therapy to downstage inoperable tumour (in addition, it helps by
3. infusion reactions, predicting the tumour response to chemotherapy before resection)
4. febrile neutropaenia  Adjuvant therapy after resection – CT & HT (as above)
- Avastin (or bevacizumab, targets vascular endothelial growth factor [VEGF] receptor,
4. Advanced breast cancer (stage 4)
used in advanced cancer); - Distant metastases
- Lapatinib (targets Her-1 and Her-2, used in advanced cancers) - Minimal locoregional therapy except for palliative purposes
- Systemic therapy is the mainstay of treatment – CT, HT or TT
FOLLOW-UP GYNAECOMASTIA
- 3-monthly for first 2 years - Causes
- 6-monthly for the next 3 years (i.e. third to fifth years) - Physiological: puberty (maybe painful)
- Yearly for another 5 years (to tenth year) - Drugs:
- At each visit – ask about symptoms and do clinical examination  Recreational drugs
- Repeat mammo of same breast 1yr postop; then 2-yrly bilateral mammo for life:  Cimetidine (H2 blockers)
previous BC is a strong Risk factor for future Breast cancer  Digosin
 Spironolactone
BREAST SCREENING  Antimicrobials (Isoniazid, ketoconazole)
- Endocrine disorders:
Normal risk, 40-49 YO  Annual mammogram  Thyroid disorders
asymptomatic 50-64 YO  Biannual mammogram (by invitation)  Acromegaly
>65 YO  Optional 2 yrly mammogram  Hypogonadism (testicular atrophy, Klinefelters‘ syndrome)
- Malignancy: testicular tumours, lymphomas
Increased risk Start screening 5 yrs before  Monthly BSE - Chronic liver disease: cirrhosis
onset of breast dz in  6 mthly CBE & U/S breast - Investigation:
youngest family member  Annual mammography - TFT, testosterone/ LH
- LFT, α-FP, ß-HCG
HRT therapy 40-49 YO Annual mammogram - Treatment
50-65 YO Biannual mammogram up to 5 yrs after cessation of - Conservative management
HRT - Surgical excision

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

68
69
APPROACH TO NECK MASSES MASSES BY LOCATION
Midline
NECK MASSES 1. Submental lymph node
2. Thyroglossal cyst
ANATOMY 3. Thyroid nodule in the isthmus
- The neck is composed of two triangles on each side – anterior and posterior 4. Sublingual dermoid cyst
triangles 5. Plunging ranula (retention cyst of the sublingual)
- The anterior triangle is bounded by the lower border of the mandible superiorly, the 6. Rarely, hyoid pathology e.g. bursa
midline anteriorly, and the anterior border of the sternocleidomastoid posteriorly
- The posterior triangle is bounded by the posterior border of the sternocleidomastoid Anterior triangle
anteriorly, the anterior border of the trapezius posteriorly, and the clavicle inferiorly 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 – level V and supraclavicular lymph node groups
2. Cystic hygroma
3. Cervical rib
4. Brachial plexus neuroma/schwannoma

CAUSES OF MIDLINE MASS

Approach:
- Does it move with swallowing – divides the thyroglossal cyst and thyroid nodule
from the other causes
- If it moves with swallowing, does it move with tongue protrusion – thyroglossal cyst
moves with protrusion but a thyroid nodule does not

- Masses in the neck region can be subdivided according to the triangle they occur in Thyroglossal cyst
as there are pathologies peculiar to each triangle Epidemiology:
- Locations: (i) Midline Equal in males and females. Occurs mostly in children and adolescents but up to one-
(ii) Anterior triangle third occur in patients older than 20 years.
(iii) Posterior triangle
Pathology:
- In general, enlarged lymph nodes are the most common cause of a lump in the neck, A cystic expansion of the remnant thyroglossal tract (the embryological origin of the
regardless of location (see section on Lymph node enlargement) thyroid gland 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 with sinus formation and
seropurulent discharge (occurs with incision or rupture of cyst)
Histology:
Cyst with columnar or squamous epithelial lining which may be ciliated. The cyst may
also contain thyroid and lymphoid tissue. If malignancy occurs (carcinoma of the
thyroglossal duct), it is usually a papillary carcinoma (~90%).
Treatment:
Sistrunk procedure – resection of the cyst and mid-portion of the hyoid bone in
continuity and resection of a core of tissue from the hyoid upwards towards the foramen
caecum.
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.
70
Plunging ranula
Pathology:
A pseudocyst associated with the sublingual glands and submandibular ducts. Ranulas
can be congenital or acquired after oral trauma. 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 the associated sublingual
gland (but often difficult due to close association with the lingual nerve and
submandibular duct).
- If complete resection not possible, marsupialisation and suturing of the pseudocyst
wall to the oral mucosa may be effective.
CAUSES OF ANTERIOR TRIANGLE MASS
Branchial cyst and/or 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. 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.
71
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.
- If suspecting aneurysm, listen for bruit, look for signs of Horner‘s syndrome,
examine the rest of the peripheral vascular system.
Differentials and investigation:
- Main differential is carotid artery aneurysm; aneurysm can occur at any level but
carotid body tumour occurs at the level of the hyoid bone.
- DO NOT PERFORM FNA
- 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.
- Angiography is the gold standard investigation – shows a hypervascular mass
displacing the bifurcation. May also show vessel compromise by tumour invasion,
and undetected synchronous tumours.
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.
Pharyngeal pouch (also called Zenker’s diverticulum)
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 halitosis, regurgitation of undigested food with coughing and
dysphagia in the neck, hoarseness, weight loss
- Complications: chest infection (due to aspiration); 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)
CAUSES OF POSTERIOR TRIANGLE MASS
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
- Lobulated 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: CERVICAL LYMPHADENOPATHY
- Radiological investigations e.g. CXR, CT to delineate extent of cyst
- Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful) ANATOMY:
- Surgical excision – partial (to alleviate symptoms) or complete

Cervical rib
Features:
- Usually more symptoms than signs as it causes thoracic outlet syndrome
- 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

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
Levels
distribution of the nerve
There are six levels of lymph nodes in the neck, and different structures drain to
- DO NOT PERFORM FNA – excruciatingly painful
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

72
73
Drainage: PHYSICAL EXAMINATION
- Oral cavity and oropharynx  levels I – III Inspection
- Thyroid and larynx  levels II – VI - Location
- Nasopharynx  II – V (usually upper neck – level II and high level V) - Any overlying skin changes e.g. erythema, discharging sinus (multiple lymph node
enlargement with discharging sinuses can be TB or actinomycosis; sulphur granules
CAUSES: seen in actinomycosis)
Can be divided into three main groups: infective, inflammatory, and neoplastic
Palpate from behind, one side at a time – start at submental, then submandibular,
Infective Viral
preauricular, postauricular, along anterior border of sternocleidomastoid,
Epstein-Barr virus, cytomegalovirus (infectious mononucleosis); HIV
supraclavicular, posterior triangle, lastly occipital. Use pulps of the fingers in a gentle
Bacteria
rolling movement.
Streptococcus, Staphylococcus, Klebsiella (from intraoral pathology
e.g. dental abscess, tonsillitis) - Tenderness to palpation
Tuberculosis - Consistency – hard, matted nodes are more suspicious for malignancy
Parasitic - Fixation to overlying skin or underlying structures
Toxoplasma
To complete the examination:
Fungi
Actinomycosis - Complete examination of the face and scalp for any primary site of infection or
neoplasia
Neoplastic Metastatic Head and neck primary
Nasopharyngeal carcinoma - Formal ear, nose, throat examination especially looking at the post-nasal space for
Oral cavity, oropharynx, larynx, hypopharynx, nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged
thyroid, etc. cervical lymph nodes)
Other primary sites (4B‘s) - Examination of the thyroid gland
Bowel (stomach, colon), breast, bronchus (lung), - Examination of lymphoreticular system – other lymph node groups, liver, spleen
balls (testicular) - Full respiratory and abdominal examination especially if supraclavicular lymph node
Primary - lymphoma found
Inflammatory SLE - Breast examination in female patient
Kikuchi‘s (necrotising lymphadenitis occurring in young females,
presenting as painful cervical lymphadenopathy) INVESTIGATIONS:
Sarcoidosis - Fine needle aspiration provides most definitive results (though there is still the
possibility of false positive and false negative results)
HISTORY - Radiological investigation e.g. ultrasound, CT – to assess nature of lump, extent,
- The lump itself – onset, duration, rate of growth, any pain, associated symptoms, other enlarged nodes that are not clinically palpable, and can be used to visualise
lumps elsewhere primary tumour if present
- Constitutional symptoms
o Fever, malaise, arthralgia, myalgia (viral prodrome); MANAGEMENT:
o Night sweats, low-grade fever (TB, B symptoms of lymphoma); - According to FNAC results
o Loss of appetite, loss of weight (chronic infection, malignancy) - Malignant – work up for primary if present (e.g. squamous cell carcinoma – look for
- Local symptoms – intra-oral diseases e.g. tooth decay, oral/tongue ulcer, tonsillitis oral cavity, skin, ENT, lung malignancy; adenocarcinoma – look for breast, GI tract
- Past medical history – cancer, TB (contact? Diagnosed? treated or untreated?) malignancy) and treat as appropriate
- Social history: travel and contact history, sexual history for HIV - Infective/Inflammatory – treat underlying condition
SALIVARY GLAND SWELLINGS
ANATOMY:
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
74
- Histology: predominantly serous acini, many ducts (other glands have few ducts)
Submandibular gland
- Consists of a large superficial part and 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
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
75
HISTORY - Palpate the gland openings for stones.
- About the lump: onset, duration, progress, associated symptoms e.g. pain - Bimanual palpation of the submandibular gland
- If pain is present, is it precipitated by food ingestion? (suggestive of sialolithiasis) - Facial nerve examination
- Symptoms of infection e.g. fever, malaise; if considering mumps, ask about testicular
pain and swelling (orchitis), abdominal pain (pancreatitis) Suspicious features of malignancy:
- Any noticed asymmetry of the face – incomplete closure of the eye on one side, - Hyperaemic hot skin over lump
drooping corner of the mouth, drooling - Pain
- Fixation to underlying structures or skin
- Does the patient have symptoms of xerostomia (e.g. cannot eat a piece of biscuit or
bread without water), xerophthalmia - Hard consistency
- Irregular surface or ill-defined border
- History of connective tissue disease e.g. rheumatoid arthritis, SLE - Facial nerve involvement

PHYSICAL EXAMINATION CAUSES OF SWELLING OF THE PAROTID

Inspect
- Put yourself at the level of the patient‘s face and look from front for any asymmetry
Parenchymal Neoplasia Benign e.g. pleomorphic adenoma, Warthin‘s
swelling Malignant tumours
with an obvious mass on one side – parotid mass is located between the angle of the
jaw and the ear, and lifts the earlobe if large; submandibular mass is located just Lymphoma and leukaemia*
under the mandible Stones Sialolithasis
Infection/ Mumps*
- Look for scars – parotidectomy scar runs anteriorly to the ear, below the earlobe and
Inflammation Acute sialadenitis
around posteriorly before looping forward again under the jaw
Chronic recurrent sialadenitis
- Look for fistula/sinus HIV
- Look at the patient‘s face for asymmetry (facial nerve palsy) Autoimmune Sjogren‘s syndrome*
Infiltration Sarcoidosis*
Palpate from behind Systemic Alcoholic liver disease
- Ask patient about any pain before starting to palpate disease* Diabetes mellitus
- Palpate the obviously enlarged gland, and always remember to also palpate the Pancreatitis
contralateral gland for any swelling Acromegaly
- Check for warmth of overlying skin, tenderness, consistency, surface, margins Malnutrition
- Fixation to underlying structures – for parotid, ask patient to clench the teeth to Non- Lymph node
contract the masseter, then try to move the gland parenchymal Facial neuroma
swelling Temporal artery aneurysm
- Fixation to overlying skin
Skin and soft tissue swellings e.g. sebaceous cyst, lipoma
- Palpate for cervical lymphadenopathy * are conditions in which parotid swelling is bilateral
Other tests
- Examination of the duct openings:
o Using a torch and a tongue depressor, examine opposite the second upper molar
tooth for the opening of the parotid duct, and under the tongue for the opening of
the submandibular duct.
o Look for red inflamed duct opening, discharge (purulent), or any visible stone.
o For the parotid duct, can palpate the duct along the masseter for stone, and look
for discharge inside the mouth while palpating.
SIALOLITHIASIS - Surgical removal
o Transoral removal of stones for submandibular duct stones (50% can be removed
Epidemiology thus), less for parotid duct stones
- Stones of the salivary gland that may be impacted within the gland itself or in the o If stones cannot be removed via transoral surgery or is intraglandular, partial
duct. gland resection can be performed
- Usually occurs in males more than females, and between the ages of 30 and 60. - Other options: Lithotripsy, wire basket removal, sialoendoscopy
- 80% of salivary stones 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. SALIVARY GLAND TUMOURS
- Most submandibular gland stones occur in the duct, while 50% of parotid stones Epidemiology:
occur in the gland itself. - 80% occur in the parotid, of which 80% are benign (80% of the benign tumours are
- 80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the pleomorphic adenomas)
floor of the mouth, and 60% of parotid stones are radio-opaque. - 10% occur in the submandibular, of which 60% are benign (95% pleomorphic
adenoma)
Presentation - 15% occur in minor salivary glands, of which 50% are benign (all benign tumours are
- Complete obstruction pleomorphic adenomas)
Acute pain and swelling of the gland involved at meal times, rapid onset within - 0.3% occur in sublingual glands, of which all are malignant
minutes of starting to eat, resolves about an hour after the meal.
Pathology
- Partial obstruction
Occasional symptomatic episodes interspersed by asymptomatic periods of days to Epithelial Non-epithelial
weeks, chronically enlarged mass in the submandibular region Adenomas (benign) Carcinomas (malignant)
Pleomorphic adenoma Adenoid cystic ca Haemangioma
- Can result in sialadenitis, and even abscess formation  worsening of symptoms of
Warthin‘s tumour Pleomorphic adenoca Lymphangioma
pain and redness; systemic symptoms such as fever, chills; purulent discharge from
Mucoepidermoid ca Neurofibroma
duct opening
Acinic cell ca Neurilemmoma
- Stone may be palpable along the duct or at the opening of the duct Adenoca Lipoma
Squamous cell ca Sarcoma
Investigations Undifferentiated Malignant lymphoma
- Noncontrast CT scan – can pick up almost all stones when fine cuts are requested
- Plain X-rays can pick up radio-opaque stones
Pleomorphic adenoma
- Sialogram (rarely done today as it is invasive and technically demanding, and CT is
better. Contraindicated in acute sialadenitis and contrast allergy.) Epidemiology:
- Most common benign tumour
Management - 85% occur in the parotid gland
- General measures: - Equal sex ratio, occurs in younger patients less than 50 years old
o Good hydration, soft diet, good oral hygiene
o Massage of the gland, milking the duct, application of moist hot towel Histology:
Very heterogeneous appearance, containing epithelial cells surrounded by loose stroma
o Analgesia – NSAIDs such as ibuprofen
with islands of chondromyxoid (mesenchymal components), and interspersed islands of
o Antibiotics if patient has sialadenitis – usually antibiotics to cover Staph and
myoepithelial cells. The tumour appears to be encapsulated, but histology shows
Strept e.g. Augmentin
multiple sites of capsular penetration by tumour cells.
o Refer specialist treatment if symptoms persist for several days, or sialadenitis
persists despite antibiotic therapy

76
77
Features: Mucoepidermoid ca is the most common malignant tumour in the parotid, while
- Slow-growing, painless swelling occurring in the lower pole of the parotid adenoid cystic ca is the most common in the submandibular, sublingual and minor
- Irregular and lobulated surface, texture of cartilage (slightly harder than Warthin‘s) salivary glands
- Does not invade or metastasise
- Chance of malignant transformation if left for 10-15 years (1-6% risk) Malignant pleomorphic adenoma
- If not completely excised, can recur (recurrence rate of 2%) - Usually occurs in pre-existing pleomorphic adenoma, rarely de novo
- Worst prognosis of any salivary gland tumour
Diagnosis by clinical, FNAC, + MRI - 30-70% recurrence and metastasis rate
Treatment – surgical excision
- Parotid: Superficial parotidectomy for superficial tumour; if tumour is deep or large, Treatment of salivary gland cancers
total parotidectomy with preservation of the facial nerve Parotid:
- Submandibular: Total gland excision together with adjacent connective tissue, - Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be
sparing lingual and hypoglossal nerves grafted with great auricular nerve)
- Radical neck dissection if neck nodes positive
- Postoperative radiotherapy
Warthin’s tumour
Epidemiology: Submandibular:
- Only occurs in the parotid gland (10% of parotid tumours) - Radical excision of gland with lymphatic clearance of submandibular triangle
- More common in males than females (4:1) - Radical neck dissection if neck nodes positive
- Occurs in older patients (>50 years) - Postoperative radiotherapy
- Related to cigarette smoking
COMPLICATIONS OF PAROTIDECTOMY
Histology:
Also called papillary cystadenoma lymphomatosum or just adenolymphoma. Consists Immediate (within 24 hrs)
of cleftlike or cystic spaces lined by two-tiered epithelium, containing mucin, 1. Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to
surrounded by a stroma of well-developed lymphoid tissue with germinal centres. the submandibular gland, damage to the hypoglossal and/or lingual nerves can
occur intraoperatively)
Features: 2. Reactionary haemorrhage
- Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail
- Invariably benign with no risk of malignant change Early (1 to 30 days)
1. Wound infection
Diagnosis by clinical, FNA + MRI
2. Skin flap necrosis
Treatment 3. Temporary facial weakness (neuropraxia of facial nerve)
- Can be left alone if absolutely certain that the entire mass is composed of only 4. Salivary fistula
Warthin‘s tumour cells, since there is no malignant potential 5. Division of great auricular nerve  loss of sensation over pinna
- Superficial parotidectomy if causing trouble to patient 6. Trismus (inability to open mouth due to spasm of masseter)

Late (more than 30 days)

Malignant tumours
Most common malignancies are mucoepidermoid (34%) and adenoid cystic carcinomas
(22%) – equal sex ratio, can occur in any salivary gland, in older patients (usually >60
yrs)
1. Wound dimple, cosmetic problems
2. Hyperaesthesia of local skin
3. Frey‟s syndrome – increased sweating and redness of facial skin when eating, due
to reinnervation of divided sympathetic nerves to the facial skin by fibres of the
secretomotor branch of the auriculotemporal nerve
THE THYROID GLAND About RISK FACTORS
- History of autoimmune disease e.g. type I DM, SLE, RA, pernicious anaemia
APPROACH TO THYROID PROBLEMS – 2 MAIN TYPES (associations with Graves and Hashimoto‘s)
1. Problem with configuration/anatomy - History of cancer elsewhere – metastatic disease to thyroid; lymphoma; papillary
(i) Solitary thyroid nodule (most common in exam) cancer is associated with familial polyposis syndromes  ask about GI polyps/ca
(ii) Multinodular goitre - History of thyroid disease – long-standing MNG can progress to lymphoma
(iii) Diffuse enlargement
- Occupational history – any exposure to radiation (papillary cancer risk)
2. Problem with function (usually hyperfunctioning) - Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2,
(i) Graves‘ disease AD inheritance), ~5% of papillary cancers
(ii) Toxic adenoma
(iii) Toxic multinodular goitre About previous TREATMENT for any thyroid disease
(iv) Hashimoto‘s disease - Medications given e.g. propylthiouracil, carbimazole, propranolol – for how long,
AIMS OF ASSESSMENT IN THYROID NODULE/ENLARGEMENT: efficacy, side effects
- Exclude cancer! - Radioactive iodine treatment – what was the result? Is the patient receiving
- Address issues of thyroid function replacement?
- Look for any complications e.g. compression (of airway, oesophagus, rarely nerve) - Surgery – what kind of surgery, any complications?
- Cosmesis – is patient bothered by lump? - Follow-up – what investigations done?

HISTORY-TAKING PHYSICAL EXAMINATION

About the LUMP
- Onset (gradual or sudden), duration A. THYROID GLAND
- Size (Diffuse or one side predominant? Any sudden increase in size? – malignant GREET PATIENT, ASK FOR PERMISSION to examine (and listen to the voice – is it hoarse?)
growth; ddx includes haemorrhage into necrotic nodule or cyst, subacute thyroiditis)
POSITION PATIENT – on a chair with space behind the chair for you to stand.
- Any pain – bleeding into cyst can result in sudden increase in size and pain; rarely
pain can occur in anaplastic carcinoma and thyroiditis INSPECT FROM THE FRONT
- Compressive symptoms: difficulty swallowing, difficulty breathing, hoarseness of 1. Any swelling? Where is it?
voice (benign pathologies almost never compress the recurrent laryngeal nerve)
2. Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a
- Cosmetic effects skin crease)? Sinuses?
3. Any skin changes over the mass?
About THYROID FUNCTION
Hyperthyroid Hypothyroid 4. Check if mass moves on swallowing by asking patient to take a sip of water –
Weight loss despite increased appetite Decreased appetite, weight gain, lethargy ―Please take a sip of water and hold it in your mouth, do not swallow until I tell you
Heat intolerance Cold intolerance to.‖
Increased sweating Dry skin, loss of outer third of eyebrows 5. Check if mass moves on protruding the tongue – ―Please open your jaw slightly.
Proximal myopathy (Graves’) Muscle fatigue Now, without moving your jaw, please stick your tongue out and back in again.‖
Diarrhoea, frequent bowel movement Constipation NB. A thyroid swelling moves only on swallowing; a thyroglossal cyst will move
Tachycardia, atrial fibrillation Bradycardia on both swallowing and protrusion of the tongue.
Oligomenorrhoea, amenorrhoea Menorrhagia
Nervousness; easily irritable; emotional Slow thought, speech and action; 6. Check for plethora of face, distended neck veins – may be due to compressive
lability; insomnia depression; dementia nature of mass (but rarely seen).
Fine tremor Carpal tunnel syndrome symptoms
78
79
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)
PROBLEMS WITH GLAND CONFIGURATION
PART I: RELEVANT ANATOMY
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.
PART II: APPROACH TO THE SOLITARY THYROID NODULE
Prevalence:
About 4-8% of population in US have palpable thyroid nodules; prevalence in
Singapore not known.
History and physical examination – as above
Differential diagnoses:
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
Clinical features suspicious of malignancy: - Suspicious sonographic features:
1. Male gender (thyroid nodules less common in male but more likely to be malignant) (i) Microcalcifications (in psammoma bodies  papillary cancer)
2. Age <15yrs or >60yrs (majority of nodules occurs in 3rd to 6th decades – likely (ii) Indistinct margins
benign) (iii) Sonolucent halo around lesion
3. History of head and neck radiation or thyroiditis (iv) Hypoechoeic or anechoeic lesion – carcinoma is almost never
4. Family history of thyroid cancer (or MEN2, Gardner‘s syndrome, FAP) hyperechoeic
5. Rapidly enlarging nodule (v) Increased intranodular vascularity
6. Hard, single nodule and/or nodules fixed to surrounding structures - Ultrasound still does not provide as good diagnostic value as FNAC
7. Hoarseness (i.e. recurrent laryngeal nerve invasion)
3. THYROID FUNCTION TEST
8. Cervical lymphadenopathy - Easy to perform, establish baseline, detect any abnormal function
9. Other symptoms of invasion e.g. haemoptysis, stridor, dysphagia - No real diagnostic value

Investigations: 4. RADIO-ISOTOPE SCAN

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
80
- 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 any increase in size
- A lump >4cm has a greater risk for malignancy
81
PART III: THYROID CANCERS
Differentiated thyroid carcinoma
Medullary carcinoma Anaplastic carcinoma Lymphoma
Papillary carcinoma Follicular carcinoma
Proportion 75% 10% 7% 3% 5%
Age 25-40 years 40-50 years >50 years for sporadic type; 20-30 years for familial 60-70 years >50 years
F:M ratio 3:1 3:1 1:1 3:2 2:1
Risk factors - Radiation exposure - Follicular adenoma is NOT a risk - Significant family history in the familial type – - Longstanding goitre - History of lymphoma or
- Polyposis syndromes (FAP, factor MEN2 (AD, complete penetrance, associated with - History of previous MALT elsewhere
Gardner‘s, etc) - Iodine deficiency may be parathyroid adenoma and phaeochromocytoma – see differentiated thyroid ca - Hashimoto’s thyroiditis
- Positive family history in 5% associated notes below) (30% of anaplastic ca) (60X increased risk)
Pathological - Characteristic Orphan Annie - Follicular structures similar to - Arise from parafollicular C cells (which produce - Small blue round cells - FNAC may suggest
features nuclei, nuclear pseudoinclusions normal thyroid calcitonin) that are highly lymphoma but definitive
- Papillary architecture with - Diagnosis of cancer made on - Distinctive deposits of acellular amyloid material – anaplastic – may diagnosis requires trucut
psammoma bodies evidence of capsular or vascular altered calcitonin collections resemble lymphoma or excision biopsy
- Tall cell variant (nuclear features invasion by tumour cells (vs - Multicentric C-cell hyperplasia may be seen in - Almost always non-
of papillary ca within follicular follicular adenoma) familial cases Hodgkin’s of B-cell
lesion) behaves like papillary ca, - Hurthle cell variant – worse type
has worse prognosis prognosis
Clinical - Slow-growing tumour - Solitary - Sporadic cases usually solitary, worse prognosis - Large bulky mass - Usually presents as
features - Spread by lymphatics - Haematologic spread to bone, - Familial cases all multicentric, better prognosis involving neck rapidly enlarging goitre
- 30-50% multicentric lung, liver, brain - Aggressive growth; spread via local, lymphatic, structures – locally with compressive
- LN involvement in 80% of disease - LN involvement in 10% (rare) haematological routes advanced symptoms
at diagnosis (level VI first) - 95% produce calcitonin, 80% produce CEA - Aggressive growth - 60-80% aggressive and
- Very good prognosis - Unilat LN involved in 60-80%, contralat LN in 40% - Multiple metastases 30% more indolent
- Poor prognostic factors (AMES): Age>40, presence of metastases, extra- - Always exclude MEN2 – serum calcium, 24hr probably present at
thyroid invasion, size>4cm (more details on risk stratification below) urinary catecholamines presentation

Treatment Surgical resection Surgical resection Palliative therapy for Chemotherapy and/or
- Hemithyroidectomy for selected low-risk patients (see below) - Aggressive resection – total thyroidectomy with compressive effects radiotherapy depending
- Total thyroidectomy for the majority level VI node clearance - Chemotherapy to shrink on type of lymphoma
- LN clearance: tracheo-oesophageal nodes cleared, and neck dissection if - Sampling of cervical and mediastinal nodes and tumour
neck nodes are positive modified dissection where positive - Surgical debulking
- For suspicious lesion – hemithyroidectomy with histology, KIV TT - Tracheostomy
No good adjuvant therapy
Adjuvant therapy Follow-up
- Radioactive iodine at ablative levels to ablate remnant thyroid and any
- Thyroxine replacement (not for TSH suppression but
cancer tissue (only for total thyroidectomy)
to maintain euthyroid state)
- External radiotherapy (only shown to have good results in pts with locally
- Serum calcitonin and CEA six mths after surgery (if
advanced follicular ca)
normal, considered cured – 5% 5yr recurrence)
TSH suppression – give L-thyroxine to suppress TSH levels to <0.005U/L - High calcitonin – screen for residual or metastatic
disease, treat surgically, with RT or chemo as
Follow-up
appropriate
- Check TSH levels
- Thyroglobulin as a tumour marker of recurrence
- Radioactive iodine scan to detect recurrence, followed by ablation
5yr survival 95% in low-risk pts, 88% in intermediate-risk pts, 50% in high-risk pts 60-70% Median survival <6mths Dependent on histo, stage,
Slightly worse for follicular ca treatment, etc.
Differentiated thyroid cancer
- Papillary and follicular cancers are considered differentiated thyroid cancer (as
opposed to anaplastic – undifferentiated – thyroid cancer)
- Prognosis is excellent
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
82
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
Thus, 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
83
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
PART IV: 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 only 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) LATE (MORE THAN 30 DAYS)
IMMEDIATE (<24HRS) 1. Hypothyroidism
1. Haemorrhage with haematoma formation 2. Hyperthyroidism (failed treatment)
- Haematoma forms in the paratracheal region, mostly below the strap muscles  3. Permanent hypoparathyroidism
can result in compression of airway if not released (patient can die!)
- Cut the subcuticular stitches and also the stitches holding the strap muscles 4. Hypertrophic scarring or keloid formation – ask patient if he/she has keloids
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 hypocalcaemia
- 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 blood pressure 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
84
85
PERIPHERAL ARTERIAL DISEASE
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 the compartments of the thigh via two main branches,
the medial and 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
FORMS OF PERIPHERAL ARTERIAL DISEASE
Peripheral arterial disease
Acute Chronic
Critical Non-critical.
Asymptomatic Claudicants.
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
86
4. Dissecting aortic aneurysm
- As the 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.
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
Pallor
- Assess skin colour, temperature, 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:
 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
87
Pulselessness EARLY ANTICOAGULATION
- If able to feel one good pulse (PT or DP), quite unlikely that the limb is ischaemic, - Important to start anticoagulation with heparin if the suspicion of acute limb
but still possible ischaemia is high
- If unable to feel, assess with a handheld Doppler the arterial and venous flow in the - Give IV heparin bolus 3000-5000 units
limb – there can still be flow without a palpable pulse - Follow with IV heparin infusion at 1000 units/hour
- Also feel the pulses on the other limbs – gives a clue as to whether the cause is - Ideal PTT is 2 to 2.5 times normal
embolic or thrombotic (see below)
INVESTIGATIONS
Paralysis
- Pre-operative investigations
- Total paralysis occurs late and usually indicates that the limb is non-viable
- Can assess viability of muscle by making a cut – viable muscle will be shiny and - FBC, U/E/Cr, PT/PTT, GXM
twitches in response to flicking, while dead muscle will be dull and will not twitch - CXR and ECG if patient is older than 40 yrs old
- Dangerous to save dead muscle as reperfusion can cause circulation of toxic - If suspecting an AMI with mural thrombus, do cardiac enzymes
metabolites in the muscle - Angiogram can be done in patients with viable limb, but in patients with threatened
limb there is no time for angiogram  may do on-table angiography
CLASSIFICATION OF SEVERITY (SVS/ISCVS) [Angiography is useful in confirming an occlusion, the cause – thrombotic or
Three categories: viable, threatened and non-viable embolic – and also pinpointing the level of occlusion and the anatomy]
(i) Viable: No immediate threat of tissue loss
(ii) Threatened: Salvageable if revascularised promptly DEFINITIVE TREATMENT OPTIONS
(iii) Non-viable: Limb cannot be salvaged and has to be amputated, no emergency to
Surgical Endovascular
operate. Patient may require revascularisation to allow lower amputation or help
- Embolectomy - Thrombolysis
the amputation to heal
- Endarterectomy - Angioplasty
Viable Threatened Non-viable - Bypass grafting - Stenting
Pain Mild Severe Variable - Fasciotomy
Capillary refill Intact Delayed Absent (fixed stain) - Primary amputation
Motor deficit None Partial Complete
Sensory deficit None Partial Complete In general, embolectomy is done for embolic occlusion, while thrombolysis is done for
Arterial Doppler Audible Inaudible Inaudible thrombotic occlusion.
Venous Doppler Audible Audible Inaudible
Treatment Urgent work-up Emergency surgery Amputation 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
DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE
reperfusion
Embolic Thrombotic - Involves clamping of the involved artery and making an arterotomy
Identifiable source Present – AF, recent AMI Less common
Claudication hx Negative Positive - A Fogarty balloon catheter is inserted into the artery until distal to the clot, then the
Physical findings Contralat pulses present Contralat pulses diminished balloon is inflated to trawl the clot out of the artery
White limb (no blood) Dusky limb (collaterals still - Check for forward-bleeding and back-bleeding of the vessel (i.e. free spontaneous
supplying limb) flow from proximal and distal ends of the artery when unclamped)
Angiography Minimal atherosclerosis, Diffuse atherosclerosis, - Flush with heparinised saline
sharp cut-off, few collaterals irregular cut-off, well-
developed collaterals - 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, increasing 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 (patient at risk of further embolic events)
- Discharge patient to anticoagulation clinic for follow-up with warfarin advice
Thrombolysis
- Angiogram done before thrombolysis to locate occlusion
- Thrombolysis catheter inserted into the clot, and the thrombolytic agent is infused
- Patient will be in high-dependency with thrombolytic infusion for 6 hours (~1000-
4000 units per minute)
- After 6 hours, redo angiogram to check for residual clot; if some clot remains, adjust
catheter into the clot and infuse for 6 more hours
- 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
Results:
- Embolectomy has a 20% mortality, almost full success rate
- Thrombolysis has a 10% mortality, only 35% successful
88
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
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
AND/OR
2. Gangrene or ulcers over the toes or feet
AND
3. Objective indication of poor vascular supply to the lower limbs
(a) Ankle brachial pressure index <0.5
(b) 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
- 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
- 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)
89
- Usually deep, dry, punctate (unlike venous ulcers that tend to be superficial, moist,
diffuse)
- May become infected resulting in cellulitis, even abscess formation, 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 – moist, swollen, frequently blistered. Often occurs in diabetics with
decreased sensation and unrecognised trauma, requiring an emergency surgical
debridement or amputation.
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 and 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.
- Important to determine the ―claudication distance‖ – within a short period of time
the distance is usually 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
NEUROGENIC CLAUDICATION
- Vascular intermittent claudication needs to be differentiated from neurogenic
claudication which can also present as pain in the lower limb on exertion
- The characteristic of neurogenic claudication is “park bench to park bench” where
the 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)
- ―Claudication distance‖ of neurogenic claudication is more variable
- Pulses will be absent/diminished in vascular but not in neurogenic claudication
- Parasthesia is common in neurogenic claudication
TAKING A HISTORY OF CHRONIC LIMB ISCHAEMIA
1. Claudication
- Which part of the lower limb does the pain occur in
- 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, increasing areas of
lower limb affected, pain on less exertion, development of 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 more than 2
weeks, 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  Neuropathic ulcers form at areas such as the ball of the foot and the heel
feeling in the toe involved? Any sensory changes in the other normal toes, foot, - Size, shape
limb?
- Edges (punched out – arterial; sloping – venous)
- Any systemic signs of infection – fever, chills, rigors, malaise
- Base
4. Risk factors (“Arteropath”)  Depth of the ulcer (can see underlying tendon? Down to bone?)
- Diabetes mellitus – take a full diabetic history including other complications  Appearance of the base – Necrotic? Granulating (beefy-red)? Sloughy?
- Hyperlipidaemia  Any discharge – pus, blood?
- Heart disease
- Surrounding skin
- Stroke
 Erythema (cellulitis) – there may be an underlying abscess (confirm on
- Smoking (very strong RF; 3-6X risk of claudication, higher than the risk for IHD)
palpation)
- Family history
 Blistering, purplish colour (possibility of necrotising fasciitis)
5. Drug history
5. Presence of gangrene
- Aspirin intake
- Wet (infected) or dry (not infected)
- Any allergies to contrast (for angiography)
- Extent of gangrene (level of demarcation)
- Ergots
6. (If the patient has diabetes, may see deformities – Charcot‘s joint)
6. Social history
- Premorbid function and current function Feel
- Social support and home condition (need to climb stairs?)
1. Warmth of the skin
- Use the dorsum of the fingers of both hands to simultaneously run up the
PHYSICAL EXAMINATION patient‘s feet to the shins and thighs bilaterally
Examine the patient‘s lower limbs in a warm room, with the patient exposed optimally - Compare the temperature on both sides (note if one side is cooler)
(from the thighs to the feet, wearing underwear). Patient is supine with the bed flat. - If one limb feels cool, feel for the level where the skin becomes warm
2. Capillary refill
Look - Press hard on a toe for a few seconds, then release
1. Colour of the lower limb - Normal capillary refill should be 2 seconds or less
- White (pallor); pink (normal); blue/dusky (cyanosed); mottled - If a toe is blue, check for blanchability (fixed staining = dead toe)
2. Trophic changes 3. Palpating the ulcer if present
- Loss of hair - Any surrounding tenderness (infection)
- Dry, shiny skin - Bogginess of surrounding tissue (may have abscess formation)
- Nail changes - See if any discharge from the ulcer when palpating
- Wasting
4. Pulses
3. Presence of any diabetic dermopathy - Feel the distal pulses and work your way proximally
4. Presence of ulcer - Posterior tibial pulse: one-third of the way down a line joining the medial
- Look carefully at the entire lower limb, including the heels (ask patient to flex at malleolus to the heel
the knee so you can look at the heel) and between the toes - Dorsalis pedis pulse: one third of the way down a line joining the midpoint of
- Site of the ulcer the two malleoli to the cleft between the first and second toes
 Venous ulcers form at the medial malleolus - Popliteal pulse: Ask patient to bend the knee ~60-90 degrees, then palpate
 Arterial ulcers are more distal, usually between the toes, and at pressure deeply in the popliteal fossa with the fingers of one hand pressing the fingers of
points such as the lateral malleolus; the other [If the pulse is very well felt, suspect a popliteal aneurysm]
90
91
- Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior
superior iliac spine (mid-inguinal point), just below the inguinal ligament
- Grading of pulses: 2+ is normal; 1+ is diminished (but may be normal for
popliteal); negative if not felt  label on a stick-figure diagram
Move
1. Buerger‘s test
- Do one side at a time
- Holding the heel of the foot, with the patient‘s lower limb straightened, slowly
lift the entire lower limb, 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 20 degrees, this indicates severe ischaemia
- There may be venous guttering of the lower limb at this angle as well
- 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)
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
 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; if >1.3, suggests non-compressible calcified vessel)
 ABPI between 0.5 - 0.9 – occlusion, often associated with claudication
 ABPI <0.5: Critical ischaemia Rest pain
- 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 two modalities) = 2D ultrasound (like the normal kind) plus
Doppler ultrasound (measures flow and waveforms)
- Normal arterial flow waveform should be triphasic; biphasic and monophasic
waves are abnormal
- Can define anatomy of occlusions and also look for relatively good arteries
distally for ―landing zone‖ of bypass graft
3. Angiogram (arteriogram)
- Invasive and associated with risks of bleeding from arterial puncture,
dissection/damage to artery with worsening ischaemia
- Usually only done if planning intervention e.g. angioplasty, stenting
- Preparing for angiogram:
 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
 1. Angioplasty
ASSESSMENT OF SEVERITY  Stenting usually not done for lower limbs except in aortoiliacs (since stent
The three L’s of peripheral arterial disease: needs to be placed in a vessel which is relatively fixed and won‘t be
(i) Life – does disease threaten life (e.g. sepsis; other complications of atherosclerosis kinked/bent by movement)
e.g. stroke, AMI;) or will intervention cause risks  Angioplasty only effective for focal stenotic lesions and better for large
(ii) Limb – will patient lose the limb vessels
(iii) Lifestyle – is the lifestyle of the patient severely handicapped, does it require  Problem with angioplasty is that it is not long-lasting – restenosis can occur
intervention  New method: subintimal angioplasty – if lumen is so occluded that guide
wire cannot pass through, the guidewire is threaded into the subintimal space
Fontaine system
to create a dissection around the occluded segment, and this space is then
Stage I: Asymptomatic
angioplastied to create a channel parallel to the actual lumen for blood to
Stage IIa: Mild claudication
flow through
Stage IIb: Moderate to severe claudication
Stage III: Ischaemic rest pain
2. Bypass grafting
Stage IV: Ulceration or gangrene
 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
TREATMENT OF CLAUDICATION to pass through (complete occlusion)
Conservative  Needs a good ―landing zone‖ for graft distally – if vessel is diffusely
- Mainstay for all cases of claudicants, esp. foot and calf claudicants diseased, difficult to perform bypass
- Smoking cessation
- Exercise training to stimulate collateral formation  symptoms get better TREATMENT OF CRITICAL LIMB ISCHAEMIA
 Exercise at least half to one hour every day
 Walk until pain comes, rest 2-3 minutes, walk again - Need to revascularise – either angioplasty or bypass grafting
 Keep a walk diary recording daily claudication distance in paces
- Podiatrist to teach foot care AMPUTATION
- Assessment and treatment to optimise control of CVS risk factors– cardiologist Indications (3 D’s)
- Patient educaton: Teach patient to go to ED if symptoms of critical ischaemia arises 1. Dead: Necrotic tissue
- Antiplatelets [e.g. aspirin] and statins (target lipid levels are much lower) 2. Dangerous: Gangrene, ascending sepsis


- Use of Vasteral (methoxyphylline) is controversial 3. Damn nuisance: Non-functional limb; bad smell; pain; constant need to dress
wound
- Monitor regularly with measurement of ABPI
- Level of amputation depends on vascularity of the limb and the indication (e.g. if
Intervention (endovascular or surgical) infected, need to amputate above level of infection)
- At least 6 months of conservative treatment first; mainly for aortoiliac disease - As far as possible try to preserve function of the lower limb
- Monitor claudication distance and ABPI – intervene if deteriorating despite
- May require revascularisation interventions before amputation to ensure good healing,
conservative management
or to enable lower amputation
- Confirm disease outline with CT angiogram or angiogram
- If parameters improve but then plateau, discuss with patient about whether he can - Do not simply amputate without ensuring good vascular supply to the surgical site,
accept the level of symptoms, and the risks of intervention  weigh risks against otherwise the wound will not heal
benefits
- Usually do angioplasty rather than bypass as it is less invasive, though may not be as
effective in treating the symptoms
92
93
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?
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 Post operative investigations:
reduced by giving frusemide or mannitol pre-operatively before anaesthesia  FBC: Hb and plt (blood loss and consumptive coagulopathy)
induction  UECr: renal insufficiency or contrast nephropathy
 KUB: check position of stent
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 cardiovascular 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 the stent (ensure that stent has 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
94
95
PERIPHERAL VENOUS DISEASE - Course of the great saphenous vein:
 Arises from the medial end of the dorsal venous arch of the foot
ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB  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

- 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

- Locations of the communicating veins:

 Saphenofemoral junction (great saphenous drains into femoral vein): located 2.5
cm below and lateral to the pubic tubercle
 Hunterian perforator: mid-thigh
 Dodd‘s perforator: distal thigh
 Boyd‘s perforator: knee
 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
- The venous drainage of the lower limb is divided into a deep venous system and a superficial veins
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
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. 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 enlarges,
becomes painful and malodorous, edge becomes thickened or raised, if inguinal
lymph nodes are enlarged
These manifestations can be asymptomatic or associated with symptoms of leg fullness,
aching discomfort, heaviness, nocturnal leg cramps, or bursting pain upon standing.

1. Venous dilatations
(a) Telangiectasias (spider veins or venous stars – intradermal veins) CEAP CLASSIFICATION OF CHRONIC VENOUS INSUFFICIENCY
(b) Reticular veins (slightly larger intermediate 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)
(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
(a) Hyperpigmentation of the skin over medial lower third of the leg (gaiter
area) – due to 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 – a fibrosing panniculitis of the subcutaneous tissue that
results in a firm area of tender, indurated, hyperpigmented skin that is fixed to VARICOSE VEINS
subcutaneous tissue. Varicose veins are dilated, tortuous veins of the superficial venous system.
 Results from severe venous hypertension  Primary varicose veins: where the cause is unknown (may be related to posture
 Starts in the gaiter area and extends circumferentially to surround the leg and components and structure of the vein wall),
 If severe can result in an ―inverted champagne bottle‖ appearance of the  Secondary varicose veins: from proximal venous obstruction, destruction of the
leg with brawny oedema above and below the area of lipodermatosclerosis valves by thrombosis or an increase in flow and pressure caused by an
(e) Cellulitis arteriovenous fistula.

96
97
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
- Age
- Parity
- Occupation – requiring long periods of standing
- Weight
- Posture – crossing legs all the time
- Increased abdominal pressure – constipation, chronic cough, etc
- Pelvic tumour or other lesion compressing on the deep veins
- Family history: 1 parent (50% risk, both parents (up to 80% risk)
HISTORY
 Asymptomatic
 Symptomatic: local (non specific pain, swelling, itching, heavy legs)
 Complications : thrombophlebitis, bleeding, hyperpigmentation, eczema, ulceration
 Ask for Past history of DVT & thrombophlebitis, obstetrics history, family history
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
- 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
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) –
positive if the distal hand can feel the wave of blood flowing retrogradely after
tapping the proximal varcosities
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 the veins below the tourniquet are dilated when the patient stands up, then the
incompetent perforator is below the 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
- 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
- If the patient‘s varicosities remain enlarged then he or she has obstructed deep
venous drainage or incompetent valves in the communicating veins
Completing the examination VENOUS ULCERS
- Auscultate over the varicosities for any bruit (indicate arteriovenous malformation)
- Examine the abdomen for any mass that may be causing the varicosities CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY
1. Obstruction to venous flow – thrombosis
Use of a handheld Doppler probe to detect incompetence
2. Incompetent valves – varicose veins, deep vein reflux (post-DVT)
- Doppler probe is placed in the popliteal fossa over small saphenous vein
3. Muscle pump failure – stroke, neuromuscular disease
- Squeeze the calf to empty the veins – should hear a whoosh as blood flows through
the small saphenous vein
- When the calf is relaxed there should not be any sound – a second whoosh indicates INVESTIGATIONS
reflux of blood i.e. there is valvular incompetence 1. Exclude infection of the ulcer and other complications
- FBC for raised total white count
INVESTIGATIONS - Swabs of the ulcer for Gram stain and cultures
Venous duplex ultrasound - X-ray of the area to exclude underlying gas, bone involvement
- Indications: 2. Venous duplex to map out venous system
 Recurrent varicose veins 3. Check for peripheral arterial disease by doing ABPI
 History of superficial thromobophlebitis or DVT 4. Biopsy if cannot exclude malignant transformation (Marjolin‘s ulcer)
 Complications of CVI: Venous eczema, Haemosiderin staining, Venous
ulceration , Lipodermatosclerosis,
- Ask for SFJ and SPJ reflux, perforator, deep venous incompetency & DVT screen MANAGEMENT:
- Can delineate deep and superficial venous systems and locate sites of incompetence Conservative
- Exclude presence of deep vein thrombosis – stripping is contraindicated 1. 4 layer compression stockings (change once per week)
(a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool
bandage
MANAGEMENT
(b) Crepe bandage
Conservative (c) Blue-line bandage (Elset)
1. Lifestyle changes (d) Adhesive bandage (Coban)
- Decrease amount of time spent standing
- If due to job, change job or ask for change to position to stand & walking less 2. Analgesia
2. Graduated compression stockings, usually grade II  ensure good pulses 3. Antibiotics if infected
3. Medications e.g. Daflon 4. Warn patient to avoid trauma to affected area
5. Encourage rest and elevate leg
Surgical 6. Once healed, compression stockings should be fitted and continued for life
Indications:
1. Cosmesis – large unsightly varicosities Surgical
2. Symptoms – pain, discomfort - If ulcer fails to heal
3. Complications – signs of chronic venous insufficiency, venous ulceration - First, exclude malignancy or other causes of ulcer (biopsy)
Available modalities: - Split skin graft can be considered with excision of dead skin and graft attached to
1. High tie with great saphenous vein stripping, and stab avulsion of varicosities healthy granulation tissue
2. Ultrasound-guided foam sclerotherapy - Venous surgery for the underlying pathology
3. Endovenous laser therapy (burns vein from within)

98
99
UROLOGICAL DISEASES HISTORY
Post-renal Causes
APPROACH TO HAEMATURIA 1. Which part of urine stream is blood stained?
DEFINITION: - Beginning – urethra distal to UG diaphragm
- End – bladder neck or prostate
- >3 RBC / hpf.
- Throughout – upper urinary tract or upper bladder
- DDx: haemoglobinuria, myoglobinuria, pseudohaematuria (menstruating women),
medications causing discoloration of urine (eg rifampicin, phenytoin) 2. Painful vs painless haematuria
Painful Painless
CAUSES - Tumour - Malignancy – RCC, TCC, Prostate
Pre- Drugs  Analgesics (NSAIDs) - Hydronephrosis - Drugs
Renal  Anticoagulants - Renal cysts - GN
 Cytotoxic/immunosuppressive agents (eg cyclophosphamide) - Ureteric stone / clot - Bleeding diathesis
 OCP - Pyelonephritis - ITP / HSP
 Penicillin - UTI - Infections – malaria, schistosomiasis
 Quinine - Bladder outflow obstruction (e.g. - Exercise
 Warfarin
BPH, strictures)
Systemic  Bleeding diathesis
 Sickle cell disease 3. Frequency + dysuria + haematuria
Metabolic  Hypercalciuria - DDx: nephrolithiasis (colicky), malignancy, UTI (women & children), bladder
 Hyperuricosuriia outflow obstruction (men e.g. BPH)
Vascular  AV malformations 4. Other urological symptoms
 Renal artery disease – thromboembolism, dissecting aneurysms, - Storage problem – frequency, urgency, nocturia, incontinence
malignant hypertension - Voiding problem – strangury, hesitancy, dribbling, incomplete emptying etc
 Renal vein thrombosis - Others – polyuria, oliguria, urethral discharge
Renal Vasculitis  HSP
 PAN Pre-renal & Renal Causes
 Wegener granulomatosis 5. Associated fever – pyelonephritis, malaria
Glomerular  Post-strep GN 6. Screen for pre-renal causes
 Post-infectious GN
 IgA nephropathy LOW / bone pain / sickness Malignancies, TB, systemic illnesses
 Lupus nephritis Rash, arthritis, arthralgia, Autoimmune causes, vasculitis
 Other GNs myalgia, fever, oedema
Sore throat, skin infxns, URTI Post-strep / post-infective GN
Tubulo-  Polycystic kidney disease
 Nephrolithiasis Ongoing URTI or GE IgA nephropathy
interstitial
 Malignancy – RCC, metastatic Iatrogenic Drug causes, radiotherapy
dz
 Pyelonephritis Travel history Schistosomiasis, malaria
 Renal cysts PMHx Renal disease, HPT, diabetic nephropathy,
bleeding diathesis, sickle cell dz
Post-  Infxns of ureter, bladder, prostate, urethra – eg schistosomiasis, TB etc
Family history PKD, sickle cell disease, renal dzes (eg
renal  Cancers of ureter, bladder (TCC), prostate, urethra Alport syndrome – ask for deafness), hypt,
 Nephrolithiasis urolithiasis
Other necessary history 8. Plain KUB
1. Infection - Fever, travel and contact history - Stones, size of kidney
2. Sorethroat - Post-strep/infective GN, IgA nephropathy
9. Ultrasound of the kidneys
3. Autoimmune - Fever, rash, joint pain, oedema - Renal size
4. Malignancy - LOW, bone pain, neuro deficits, SOB, liver function - Presence of any hydronephrosis
5. PMHx - Renal dz, - Renal stones
- systemic dz (DM HPT Bleeding sickle cell)
6. Drug history / Hx of radiation 10. Intravenous urogram (IVU) – see below for more details
- Distortion of renal outline and pelvic calyces by RCC, may have specks of
7. Family history – PKD, renal dz, Sickle cell, HPT
calcification
- Stones (filling defect, proximal dilatation, decreased distal passage of contrast) +
PHYSICAL EXAMINATION hydroureter and/or hydronephrosis
1. Check patient‘s vitals- stable? - Filling defect in bladder due to TCC
2. Conjunctival pallor - Increased residual volume in bladder after micturition due to BPH
3. Abdomen – renal mass, palpable bladder/bladder mass 11. Cystoscopy
4. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension - Detection of bladder tumour (IVU may not pick up small tumours <1cm)
of tumour into renal vein, blocking the testicular vein where it drains into the left - Biopsy can be taken at the same time
renal vein)
5. Digital rectal examination – prostate enlargement (BPH versus cancer) KUB FILM
- Margins: Superiorly needs to be above the upper pole of the right kidney (T12),
inferiorly needs to show the pubic symphysis
INVESTIGATIONS
1. Urine dipstick INTRAVENOUS UROGRAM
- Causes of false-positive for blood: haemoglobinuria, beetroot, drugs (rifampicin), - Intravenous contrast used to delineate anatomy of the kidneys and urinary system
metabolic (alkaptonuria, porphyria)
- Various phases:
2. UFEME (i) Control film – plain KUB
- Confirm presence of red blood cells (ii) Nephrogram phase (taken 1 minute after contrast given) – contrast fills
- Casts  nephritis kidney parenchyma so the kidneys become more visible, can measure size
- Elevated WBC (pyuria is >5 WBC per hpf), organisms  infection (iii) Pyelogram phase (3-5 minutes) – contrast fills calyces and pelvis, can
3. Urine cytology for malignant cells detect dilated calyces/pelvis (hydronephrosis), any filling defects
(iv) Release film (abdominal binder which was placed to slow the flow of
4. Urine phase contrast contrast into the bladder is released) – shows ureters, any hydroureter,
- RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source, filling defects; bladder – any filling defects, abnormal appearance of the
while isomorphic RBCs suggest post-renal source (ureter, bladder, etc) bladder (fir-tree appearance in neurogenic bladder)
5. Urine culture and sensitivity (v) Post-micturition – any residual urine in bladder after voiding
6. Full blood count - Contraindicated in:
- How low is the Hb? (a) Contrast allergy
- Elevated TW – infection (b) Renal impairment (Cr >200)
(c) Patients on metformin (can cause lactic acidosis; patients need to stop
7. Urea, electrolytes and creatinine metformin 2 days before and after study)
- Any renal impairment and electrolyte abn (renal or pre-renal dz more likely) (d) Patients with asthma (given steroids for 3 days before study)

100
101
RENAL CELL CARCINOMA
INVESTIGATIONS
EPIDEMIOLOGY
- 3% of adult malignancy DIAGNOSTIC
- Most frequent occurring solid lesion within kidney 1. Imaging – CT and/or ultrasound
- 2:1 male predominance - Presumptive diagnosis is made on imaging – a renal parenchymal mass with
- Peak incidence 60-70 years thickened irregular walls and enhancement after contrast injection suggests
malignancy
PATHOLOGY 2. Pathological diagnosis
- Most common primary renal tumour (80-85% of all tumours of the kidney) - Needle biopsy usually not done for resectable lesions due to fears of tumour
- Arise from the renal tubular epithelium seeding
- Three cell types: clear cell carcinoma (70-80%), papillary renal cell carcinoma (10- - In these resectable lesions, a partial or total nephrectomy is often performed, and
15%), and chromophobe renal cell carcinoma (5%) provides the tissue diagnosis post-operatively
- Other renal tumours: TCC of renal pelvis, Wilms‘ tumour, lymphoma - In tumours with metastatic disease on presentation, biopsy of the metastatic site
may be easier
RISK FACTORS
STAGING
- Smoking
1. CT scan of the abdomen
- Exposure to cadmium
- Perinephric invasion, adjacent organ invasion
- Family history
- Extension into renal vein, IVC
 von-Hippel Lindau syndrome due to mutation of the VHL gene on chromosome
- Lymph node enlargement
3p25 (associated with CNS haemangioblastomas (usually cerebellar), bilateral
- Liver metastases
multicentric retinal angiomas, phaeochromocytomas, etc)  clear cell
carcinomas 2. CT scan of the chest
 Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene - For lung metastases
on chromosome 7q31  multifocal bilateral papillary carcinomas
3. Bone scan
- Acquired polycystic kidney disease (secondary to chronic dialysis)
- Only done if patient complains of bone pain and/or alkaline phosphatase is raised

PRESENTATION 4. MRI of abdomen and heart

- Initially asymptomatic (may be detected incidentally) - Superior to CT for evaluation of IVC and right atrium involvement
- Painless gross haematuria is the most common presenting symptom – >50% of cases
T1 Tumour <7cm, limited to the kidney
- When tumour has grown large enough, dull flank pain and palpable mass may result
T1a: tumour <4cm
 Classical triad of RCC: flank pain, painless haematuria, palpable renal mass
T1b: tumour >4cm but <7cm
(indicates late stage disease)
- May have fever a/w night sweats, LOA, LOW, malaise T2 Tumour >7cm, limited to the kidney
- Polycythaemia occurs in 1-5% (due to increased erythropoietin) T3 Tumour extends into major veins or invades adrenal gland or perinephric
- For left renal tumour, extension of tumour into left renal vein can cause a left tissues, but not beyond Gerota‘s fascia
varicocoele as the left testicular vein becomes occluded T4 Tumour invades beyond Gerota‘s fascia
- Extension into IVC can cause lower limb oedema, ascites, liver dysfunction,
pulmonary embolism
- Symptoms of metastases – lungs, liver, bones, brain, lymph nodes
- Paraneoplastic syndromes are uncommon – Cushing‘s, hypercalcaemia, hypertension
TREATMENT
RESECTABLE TUMOURS
Surgery
- Laparoscopic versus open methods
- Retroperitoneal versus transperitoneal approach
1. Partial nephrectomy
- Done in T1a disease – spares part of the kidney that is not involved  nephron-
saving
2. Total nephrectomy
- Done in T1b disease – entire kidney removed
3. Radical nephrectomy
- Done in T2 disease – entire kidney together with Gerota‘s fascia
- In T3 disease, aim for radical nephrectomy and removal of structures affected e.g.
adrenal gland
Adjuvant chemotherapy
Surveillance after resection to detect relapse early
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
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 – an inhibitor of tyrosine kinase  blocks intracellular domain of the
vascular endothelial growth factor (VEGF) receptor
- Bevacizumab – monoclonal antibody against VEGF
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  field
change effect, thus urothelial tumours often occur multifocally
- Other types of bladder tumours: 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
- Industrial chemicals – naphthylamine, aniline-containing dyes, etc
- Cigarette smoking
- Occupational (hairdressers – exposure to hair dyes)
- Analgesic abuse (phenacetin)
- Chronic cystitis
- Schistosomiasis
- Radiation (pelvic)
- Chemotherapy (cyclophosphamide)
PRESENTATION
- Haematuria is the most common presenting symptom (90%) – typically gross,
painless, intermittent, occurring throughout the stream
- LUTS – irritative symptoms (frequency, dysuria, urgency) suggestive of carcinoma
in-situ, while obstructive symptoms (decreased stream, intermittent voiding, feeling
of incomplete voiding, strangury) indicate a tumour at the bladder neck or prostatic
urethra
- Pain – in locally advanced or metastatic tumour  flank pain due to urinary
obstruction, suprapubic pain due to local invasion, bone pain due to metastasis
- Constitutional symptoms – LOW, LOA, fatigue

Prognosis DIAGNOSIS
Stage I (T1N0): >90% 5 year survival 1. Urine cytology for malignant cells
Stage II (T2N0): 75-90% 2. Cystoscopy with cell brushings and biopsy
Stage III (T3N0/N1): 60-70% 3. IVU or CT urogram to detect synchronous lesions (3% chance of proximal tumour)
Metastatic disease: <10%

102
103
STAGING o Ileal conduit (a segment of ileum with ureters attached, as a stoma; not
1. CT abdo/pelvis for T, N and M staging continent)
2. Transurethral resection of bladder tumour (TURBT) with histopathology o Neobladder construction using ileum (only if urethra not removed; continent,
better quality of life)
Ta Superficial, does not involve lamina propria o Stoma with pouch construction under abdominal wall (not continent)
Tis Carcinoma in-situ: ―flat tumour‖
T1 Superficial, involves lamina propria (up to muscularis propria) - Radiotherapy (not as good as surgery)
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) UROLITHIASIS
T3b Macroscopic extension outside bladder
STONE COMPOSITION
T4a Invasion of prostate, vagina, uterus
- Calcium oxalate or calcium phosphate stones – 75%
T4b Invasion of lateral pelvic walls, abdominal wall
- Magnesium ammonium phosphate (struvite) stones – 15%
Generally can be divided into 2 main groups: - Uric acid and cystine stones – 10%
(a) Superficial tumour (70-80% of patients) – Ta, Tis, T1
(b) Muscle-invasive tumour (20-30%) – >T2 PATHOLOGY
- Can occur at any level in the urinary tract, but most commonly in the kidney
- Most important cause of stone formation is increased urine concentration of the
MANAGEMENT DEPENDENT ON STAGE
stone‘s constituents, such that they exceed their solubility  precipitate as stones
SUPERFICIAL TUMOUR - E.g. hypercalciuria with or without hypercalcaemia, hyperuricuria
- Primary treatment is TURBT of the tumour - Urinary tract infections can also cause stone formation – struvite stones form in
Proteus vulgaris infections as this organism splits urea into ammonium, generating
- Intravesical therapy indicated in patients with high risk of tumour recurrence or alkaline urine
tumour progression (high grade, multiple primary sites, multiple recurrences, tumour - Bacteria can also form nidi for the formation of any kind of stone
size >3cm, primary or coexisting carcinoma in-situ, prostatic urethral involvement)
 BCG – 1 instillation per week for 6 weeks
PRESENTATION DEPENDS ON SITE
 Mitomycin C – single instillation within 24hrs of TURBT, or weekly/monthly
treatments for up to 2 years Renal stones
- Most often asymptomatic unless the stone gets lodged in the pelviureteric junction
- Follow-up: causing hydronephrosis and subsequent infection  pyonephrosis
 3-monthly cystoscopy for 1 year - Vague flank pain may occur
 6-monthly cystoscopy for next 4 years Urine cytology with every cystoscopy
 Yearly cystoscopy thereafter Ureteric stones
- Even small stones can cause severe symptoms as the ureter is narrow
 IVU every 2 years
- Classically ureteric colic pain – severe, intermittent loin-to-groin pain
- Haematuria – gross or microscopic
MUSCLE-INVASIVE - Irritative symptoms – frequency, urgency
- Radical cystectomy - Can cause upper urinary tract infection  fever, pain
 Radical cystoprostatectomy with pelvic lymphadenectomy in male
 Anterior exenteration with pelvic lymphadenectomy in female Bladder stones
- May be asymptomatic
 Ways of diverting urine output
- Can cause irritative urinary symptoms – frequency, urgency
o Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due
- Haematuria
to small calibre; not continent)
- If infection is present – dysuria, fever, etc
PHYSICAL EXAMINATION - High fluid intake
- In ureteric colic, symptoms are often out of proportion to signs – no guarding, - Low salt intake
rebound, etc - Restriction of red meat, dairy produce, refined sugars
- If the patient has pyelonephritis, renal punch may be positive - Increase citrus fruit intake
- Otherwise unremarkable examination
SURGICAL INTERVENTION
INVESTIGATIONS Indications:
- Constant pain
1. Urine tests – dipstick, UFEME, urine culture/sensitivity
- Haematuria - Does not pass after one month
- Pyuria, micro-organisms (UTI) - Too large to pass spontaneously
- Obstructs urine flow
2. KUB - Causes urinary tract infection
- May be able to see radio-opaque stone (90% of renal stones are radio-opaque) - Damages renal tissue or causes significant bleeding
- Look at kidney size, any renal stones - Increase in size
- Trace path of ureter along tips of transverse processes, across sacroiliac joint,
and medially into bladder, looking for ureteric stones Types of treatment available:
- Look for bladder stones 1. Percutaneous nephrolithotomy (PCNL)
- Done for renal stones that are too large for ESWL to disintegrate
3. Intravenous urogram - Contraindicated in uncorrected bleeding diathesis, patients unfit for GA
- Can also help to visualise a stone 2. Extracorporeal shock wave lithotripsy (ESWL)
- Can show dilated urinary system secondary to stone obstruction – hydroureter - Calcium oxalate, uric acid and struvite stones fragment easily, but calcium
and/or hydronephrosis phosphate and cystine do not
4. Ultrasound of kidney or bladder - Used for stones below 10mm in size
- Features of stone: echogeneic rim, posterior acoustic shadowing - Used for renal stones and upper ureter stones – not so good for lower system due
to difficulty in access
5. MAG-3 renogram - Contraindicated in pregnancy, untreated UTI, untreated bleeding diathesis, distal
- If pyelonephritis present due to stone obstruction, it is valuable to measure the obstruction that cannot be bypassed with a stent
renal function using the MAG-3 renogram 3. Ureteroscopy with lithotripsy (usually laser lithotripsy, can also be done by
- The renogram gives the differential function of each kidney – in normal pneumatic drill, electrohydraulic means)
individuals the function should be approximately 50% on each side (out of 100% - For stones along the ureter
for both kidneys combined)
- If one kidney has less than 15% of total renal function, it is not worth salvaging 4. Cystolitholapaxy for bladder stone
the kidney 5. Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed
other management strategies, altered anatomy, performing open surgery for another
TREATMENT reason anyway, non-functioning kidney
CONSERVATIVE Adjuncts:
Stones smaller than 5mm can be treated conservatively as 60% will be passed out; only - Double-J stent (or DJ stent) – inserted to stent the urinary system when worried that
treat if they do not pass out after 4 to 6 weeks, and/or cause symptoms stone fragments after ESWL may cause obstruction e.g. when ESWL used for
- Treatment of any urinary tract infection treatment of a large stone; or if system is obstructed to begin with, may want to stent
- If underlying disease present that causes increased urinary concentration of stone to ensure good drainage after surgery
components e.g. hypercalcaemia  treat disease if possible

104
105
Summary of treatment modalities HISTORY
Location Size Treatment Symptoms of ARU:
Renal < 5mm Conservative management unless symptomatic/persistent - Inability to pass urine
5-10mm ESWL - Suprapubic distension with pain (unlike chronic retention of urine which is painless)
10-20mm Either ESWL or PCNL Precipitating factors:
> 20mm PCNL - Symptoms of urinary tract infection: dysuria, frequency, urgency, nocturia,
Upper ureter < 5mm Conservative management unless symptomatic/persistent haematuria
5-10mm ESWL - Constipation
> 10mm URS with lithotripsy - Drugs e.g. cough mixture, antihistamines
- Immobility
Middle ureter/ < 5mm Conservative management unless symptomatic/persistent
Distal ureter > 5mm URS with lithotripsy History suggestive of aetiology:
- Previous history of obstructive symptoms e.g. poor stream, hesitancy, terminal
Bladder < 30mm Cystolitholapaxy dribbling etc  BPH
> 30mm Open cystolithotomy (also if there are multiple stones) - Previous history of ureteric colic pain or stones
- Previous urethral instrumentation or STD  stricture
- Gross painless haematuria recently  TCC, bladder stone
- Lower limb weakness/paralysis, bowel incontinence, back trauma, history of spinal
disease e.g. PID, spinal stenosis  neurogenic bladder
APPROACH TO ACUTE RETENTION OF URINE - Constitutional symptoms: LOW, LOA, malaise (any tumour in general)

CAUSES Complications:
- Infection – symptoms of UTI
Mechanical Extraluminal Prostate enlargement (benign/malignant) - Stone disease (if in the bladder, usually asymptomatic)
Faecal impaction - Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness
Pelvic tumour
Pregnancy
UV prolapse PHYSICAL EXAMINATION
Intramural Tumour of the bladder neck (TCC) - General condition – sallow appearance, scratch marks, pedal oedema, etc (uraemia)
Urethritis (UTI) - Abdomen
Urethral stricture from STD, prev instrumentation  Palpable bladder – tender
Intraluminal Stones  Other pelvic masses – fibroid, gravid uterus, ovarian cyst
Blood clot (clot retention in haematuria)  Faecal loading
Foreign body  Bilateral enlarged kidneys (hydronephrosis)
Non- Cord disease/ Cord compression - Digital rectal examination
mechanical injury Multiple sclerosis  Any saddle anaesthesia
Tabes dorsalis  Anal tone
Neuropathy Diabetic autonomic neuropathy  Prostate enlargement – firm and smooth? Or hard, craggy, irregular, rectal
Drugs Anticholinergics (cough medicine), antihistamines, mucosa not mobile?
anti-depressants, alcohol  Stool impaction
Others Prolonged immobility - Neurological examination
Post-anaesthesia  LMN paralysis of the lower limbs?
Pain  Any sensory level present?
IMMEDIATE MANAGEMENT – CATHETERISATION
- Try urethral catheterisation first (impt: urethral catheterisation contraindicated if
patient has signs suggestive of urethral injury – blood at urethral meatus, high-riding
prostate – more relevant in the trauma setting)
 If urethral catheterization cannot pass into bladder, there are two possibilities: 1)
enlarged prostate; and 2) urethral stricture
 For enlarged prostate, try again with a thicker catheter (stiffer, easier to pass
through)
 For stricture (when you feel the catheter is stuck quite proximally along the
penile urethra, it is more likely to be a stricture), try a 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, perform suprapubic catheterisation
 Requires distended bladder which pushes the surrounding bowel loops away so
that risk of bowel injury is lower
 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 (FOR CAUSES)
1. Full blood count for raised TW (infection)
2. Urea, electrolytes and creatinine for raised creatinine (renal impairment secondary
to obstructive nephropathy)
3. Urine dipstick, UFEME and culture/sensitivity for infection
4. PSA – keeping in mind causes of raised PSA (cancer, BPH [usually <40], prostatitis,
instrumentation >11days)
5. KUB for stones, faecal loading
6. Ultrasound of the bladder for stones, tumour, intravesical protrusion of prostate
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. Anticipate complications
(a) Post-obstructive diuresis
 Urine output >200ml/hr for 2 hours or more
106
 Due to tubular damage from obstruction of drainage of the pelvicalyceal
system, resulting in transient impairment of concentrating function
 Can result in hypotension and electrolyte abnormalities (hyponatraemia,
hypokalaemia, hypovolaemia)
 Requires close monitoring of urine output and fluid/electrolyte status with
appropriate replacement and resuscitation
(b) Haemorrhage ex-vacuo
 Bladder mucosal disruption with sudden emptying of greatly distended
bladder
 Usually self-limiting
3. Trial-off catheter
- Take off catheter and watch patient‘s output, as well as perform bladder scan to
measure bladder volume
- When patient passes urine, can perform uroflow to investigate severity of outlet
obstruction, and also do bladder scan post-micturition to check residual volume
- If patient cannot pass urine and bladder volume >400ml  re-catheterise
BENIGN PROSTATIC HYPERPLASIA (BPH)
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
- Major stimulus: dihydrotestosterone (produced from testosterone by 5-alpha
reductase)
- 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
- Lower urinary tract symptoms (LUTS): obstructive (predominate) >> irritative
symptoms (obstruction of the prostatic urethra)
 Irritative symptoms significant for complications of urine retention: UTI, stones
107
Obstructive Irritative - US kidney and bladder – hydronephrosis, post-void residual volume >100ml, bladder
Hesitancy Frequency stone, measure intravesical prostatic protrusion (IPP)
Straining to pass urine (strangury) Urgency - Cystoscopy to rule out stones, strictures/ bladder neck obstruction or cancer,
Weak stream Nocturia - Uroflowmetry to confirm obstruction to urinary outflow (normal peak flow rate >
Prolonged micturition Dysuria 15ml/sec, normal bell shaped curve, saw tooth appearance, Residual urine <100ml in
Terminal dribbling Urge incontinence elderly; 0 in young males)
Feeling of incomplete voiding - ± urodynamic studies, TRUS with biopsy TRO prostate cancer if PSA >10
Double voiding (pis-en-deux)
- Haematuria (UTI or rupture of enlarged veins) PROBLEMS
- Ask about the complications of an obstructive uropathy): - Acute/chronic urinary retention, complicated by Bladder stones & Recurrent UTI
 Acute urinary retention (previous admissions and IDC) - Gross haematuria (after excluding other causes)
 UTI, Stones: irritative symptoms, haematuria - Renal impairment secondary to outflow obstruction
 Hydronephrosis, pyelonephrosis, renal impairment: loin pain, fever, - Co-existence of prostate cancer
polyuria/ anuria.
 Overflow incontinence 2o to Chronic urinary retention with high post-void MANAGEMENT
residual volume in the bladder

- Divided into watchful waiting, medical management, and surgical management
- Try to Rule out other differentials: - Objectives of treatment: Rapid and sustained relief of symptoms, prevent long-term
 Stricture/ bladder neck contractures: previous instrumentation or STDs complications, improve patient‘s quality of life
causing urethritis/ post- TURP
 Drug causes: codeine (cough mixture), BB, anti-cholingerics, TCAs I. Watchful waiting
 Chronic constipation - Suitable for patients with minimal symptoms, no complications and normal invx
 Ca bladder neck/ Ca Prostate: LOW, LOA, bone pain, haematuria - Monitor patient‘s symptoms and clinical course annually
 Neurogenic bladder
II. Medical treatment
- Other aspects of history: Social history (effect on lifestyle)
1. Alpha blockers (Prazosin, Terazosin, Doxazosin, Alfuzosin)
- Treatment of symptoms (blocking the α-1 adrenergic receptors in the bladder
PHYSICAL EXAMINATION neck, prostate and urethra)
- Already on IDC? Urine output? Anaemia (of CRF/ underlying malignancy) - Result in decreased outflow resistance and decreased bladder instability
- Vitals: BP for HPT? - SEs: include postural hypotension, dizziness
- Any ballotable kidneys? Check for hernias (chronic straining) 2. 5-alpha reductase inhibitors (Finasteride, Dutasteride)
- Palpable tender bladder in ARU (non-tender in chronic retention) - Treats the disease (not just the symptoms) by inhibiting the conversion of
- DRE for impacted stools & prostate: smooth enlarged, median sulcus, rubbery, non- testosterone to dihydrotestosterone by 5-alpha reductase  reduced prostate size
tender, mobile mucosa - Proven to decrease need for surgery and acute retention rates
- Only effective after 6 /12 (counsel the patient!), and in prostates >40g
INVESTIGATIONS - Most common side-effect is sexual dysfunction & hair growth
Blood
- FBC: anaemia, raised WBC III. Surgery
- UECr: dehydration, raised creatinine  renal impairment due to chronic obstruction Types
- UFEME, cytology, urine c/s: for UTI and screen for cancer - Transurethral resection of prostate (TURP)is the gold standard
- PSA (done in interval periods to avoid false +ves): normal <4 - Laser prostectomy is promising (pending long term results)
Imaging - Other techniques do not show good results: stenting, cryoablation, etc.
- KUB for bladder stone
Indications: PRESENTATION
- Failed medical treatment - Asymptomatic (mostly): incidentally picked up on DRE or due to elevated prostate-
- Significant Complications: Refractory urinary retention Recurrent UTI, Bladder specific antigen (PSA) level (>100 is highly suggestive)
calculi, Obstructive uropathy - Local symptoms: obstructive LUTS, bladder outlet obstruction; (uncommon as most
- Recurrent gross haematuria cancers arise in peripheral zones) haematuria, haematospermia, new onset ED
Complications of surgery (TURP) - Metastatic symptoms – lower back pain (from Batson‘s venous plexus)
Early
1. Bleeding, infection, risk of GA PHYSICAL EXAMINATION
2. Local injury causing incontinence, stricture/ bladder neck stenosis - DRE: Asymmetric area of induration, or frank hard irregular nodule
3. Perforation of the urethra or bladder dome - Percuss spine for any bone pain
4. TUR syndrome
- Symptoms: Nausea, vomiting, confusion, hypertension, visual disturbance, DIAGNOSIS
giddiness, seizure
1. PSA level
- Hyponatraemia due to constant irrigation during TURP (glycine used for - >10ng/ml: biopsy recommended as >50% of patients will have prostate cancer
irrigation – cannot use N/S, as ionic solutions make diathermy non-functional) - 4-10ng/ml: biopsy advised, though only 20% will have prostate cancer
- Irrigation fluid is hypotonic, thus water enters open vasculature during surgery - <4ng/ml: majority will have negative biopsies, and yet there is a significant
- Risk increases with prolonged operation and increased pressure of irrigation, proportion of men with prostate cancer with PSA <4ng/ml  biopsy if the rate
thus op is kept to shorter than one hour, and irrigation pressures <60mmHg of rise of PSA is >0.75ng/ml per year
- Patient usually given spinal anaesthesia during TURP so the surgeon can assess
the patient‘s mental status during the operation 2. Transrectal ultrasound (TRUS) with biopsy
- Now uncommon as new technology allows isotonic irrigation - Histology of prostate carcinoma is graded by the Gleason score looking at
glandular architecture at low magnification
Late
1. Retrograde ejaculation (10%)
STAGING
2. Impotence (5%)
1. Clinical examination (palpable tumour  T2)
PROSTATIC CANCER 2. TRUS biopsy for staging purpose
3. CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal
EPIDEMIOLOGY status (regional, non-regional)
- Prostate Cancer is the 6th commonest cancer among men in Singapore. 4. Bone scan for metastasis
- 5th common cancer in Singapore
- Peak incidence between 65 and 75 years of age Staging (TNM staging)
PATHOLOGY  T1: non-palpable lesions
- Adenocarcinoma o 1a: diagnosed on TURP (Gleason score <7, <5% involvement)
- Arise in the outer parts of the prostate 70-80% of the time and are thus palpable on o 1b: diagnosed on TURP (Gleason score >7, >5% involvement)
digital rectal examination o 1c: diagnosed with PSA screening and TRUS biopsy
 T2: confined to prostate
RISK FACTORS o 2a: confined to 1 lobe
- Hormonal – growth of tumour can be inhibited by orchidectomy or administration of o 2b: both lobes of prostate involved
oestrogens  T3: extra-prostatic spread
- Genetic – racial variations in onset and prevalence, family history  T4: prostate stuck down to pelvic structures
- Environmental – industrial chemical exposure, diet containing high animal fat

108
109
Gleason score for prostate Ca is based on its microscopic appearance. Higher scores
means more aggressive lesion and worse prognosis.

TREATMENT
LOCALISED DISEASE (T1/2)
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
- Castration
 Surgical orchidectomy
 Medical – LHRH agonist
- Anti-androgen
 Non-steroidal e.g. Flutamide
 Steroidal – cyproterone acetate
- Combined androgen blockade
- Oestrogen therapy (diethylstilbestrol)

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
 Docetaxel + Prednisone (gold standard)
 Mitoxantrone + Prednisone
SURGICAL INSTRUMENTS - Used when small to moderate amounts of drainage are expected or when a passive
drainage system won't provide adequate drainage
- active drainage systems have a clear graduated scale by which you can see the
DRAINS
type and amount of drainage and determine when to empty the drainage chamber
FUNCTIONS OF DRAINS - Tubing of the low-pressure active drainage system is placed through a separate
Drains are inserted to: puncture wound or the tube may exit the edge of the surgical wound
- Evacuate collections of pus, blood or other fluids (e.g. lymph) - If the tubing isn't sutured in place, it could become dislodged when you change
- Drain potential collections dressings or reposition the patient, so be careful. If a portion of the tube is pulled
outside his skin, an air leak will cause the collection chamber to rapidly fill with
Rationale: air and the system won't drain properly.
- Drainage of fluid removes further fluid collections
- May allow the early detection of anastomotic leaks or haemorrhage Passive drains
- Passive drains have no suction, rely on gravity
- Leave a tract for potential collections to drain following removal
- Function by the differential pressure between body cavities and the exterior
- Used when a moderate to large amount of drainage is expected
COMPLICATIONS:
1. Infection
2. Bleeding CARE AND PREVENTION OF COMPLICATIONS OF TUBES:
- Prevent Infection- maintain meticulous skin care and aseptic technique around the
3. Tissue damage- by mechanical pressure or suction
4. Drain failure- blocked/slipped/kinked insertion site
- Prevent blockage of the drain- do not allow bottles to fill up
5. Incisional hernia- occurs when drain inserted through incision wound site- create a
- Prevent slippage by securing drain carefully to skin; refix as required
separate incision site for drain!
- Never hold a drainage collection device higher than the tube insertion site to prevent
the drainage from flowing backward into the patient
TYPES OF DRAINS - Note amount of drainage daily
- Drains classified as:
 Open or closed
 Active or passive
REMOVAL OF DRAINS
- Active drains require suction. Passive drains rely on gravity.
A drain is removed as soon as it is no longer required. The following are general
- Drains are often made from inert silastic material
guidelines:
- They induce minimal tissue reaction
1. Drains put in to cover perioperative bleeding and haematoma formation, can come
- Red rubber drains induce an intense tissue reaction allowing a tract to form
out after 24— 48 hours.
- In some situations this may be useful (e.g. biliary t-tube)
2. Where a drain has been put in to drain an infected site e.g. abscess, remove it when
the fever settles or when there is evidence of complete drainage.
Open drains
- Corrugated drain, Yeates drain, Penrose drain
- Drain fluid collects in gauze pad or stoma bag
- Easier to drain infected collections
Closed drains
- Consist of tubes draining into a bag or bottle
- They include chest and abdominal drains
- The risk of infection is reduced
Active drains
- Jackson-Pratt Drain, Redivac Drain, T-tube
- Have expandable chambers to create low-pressure suction

110
111
CENTRAL VENOUS PRESSURE LINE INSERTION Technique of IJV cannulation
Place the patient in a supine position, at least 15 degrees head-down to distend the neck
INDICATIONS veins and to reduce the risk of air embolism. Turn the head away from the venepuncture
1. Vascular access site. Cleanse the skin and drape the area. Sterile gloves and a gown should be worn to
2. Total parenteral nutrition avoid catheter-related sepsis.
3. Infusion of irritant drugs
4. Measurement of central venous pressure Procedure
5. Cardiac catheterization 1. Use local anaesthetic to numb the venepuncture site.
6. Pulmonary artery catheterization 2. Introduce the large calibre needle, attached to an empty 10 ml syringe.
7. Transvenous cardiac pacing. 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
CONTRAINDICATIONS: carotid artery and ensure that the needle enters the skin lateral to the artery.
1. Do not insert into an infected area. 4. Direct the needle caudally, parallel to the sagittal plane, aiming towards the
2. Avoid infraclavicular approach to subclavian vein if patient has apical emphysema ipsilateral nipple.
or bullae. 5. While needle is advanced, maintain gentle aspiration.
3. Avoid internal jugular vein if carotid aneurysm present on the same side.
4. Bleeding diatheses 6. When vein is entered, flush of blood appears in the syringe. Now, cannulate the
5. Septicaemia vein via the Seldinger technique as described below.
6. Hypercoagulable states 7. Remove syringe, holding needle firmly in place. Occlude needle to prevent air
embolism or bleeding.
ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE: 8. Advance guide wire, J-shaped end first, into the vessel through the needle.
1. Internal jugular vein 9. Hold guide wire in place and remove needle. Maintain a firm grip on the guide wire
2. Subclavian vein at all times.
3. Femoral vein 10. Use a dilator to enlarge the hole in the vein. Remove the dilator.
4. External jugular vein 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.
CANNULATION OF THE INTERNAL JUGULAR VEIN 12. Advance catheter into final indwelling position. Hold catheter and REMOVE
The internal jugular vein (IJV) is accessible, so cannulation of this vein is associated GUIDEWIRE.
with a lower complication rate than with other approaches. Hence, it is the vessel of 13. Check lumen placement by aspirating through all the pigtails and flushing with
choice for central venous cannulation. saline next.
Anatomy of the IJV 14. Suture the catheter to the skin to keep it in place.
The vein originates at the jugular foramen and runs down the neck, to terminate 15. Apply dressing according to hospital protocol.
behind the sternoclavicular joint, where it joins the subclavian vein. It lies alongside 16. The catheter tip should lie in the superior vena cava above the pericardial reflection.
the carotid artery and vagus nerve within the carotid sheath. The vein is initially Perform check chest X-ray to confirm position and exclude pneumothorax.
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. Complications
1. Pneumothorax/haemothorax
Relations of the IJV 2. Air embolism - ensure head-down position.
Anterior: Internal carotid artery and vagus nerve. 3. Arrhythmias – This happens if cathether ―irritates‖ the heart. Avoid passing
Posterior: C1, sympathetic chain, dome of the pleura. On the left side, the IJV lies guidewire too far, observe rhythm on cardiac monitor during insertion.
anterior to the thoracic duct.
Medial: Carotid arteries, cranial nerves IX-XII
4. Carotid artery puncture/cannulation - palpate artery and ensure needle is lateral to it, NASOGASTRIC TUBE
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. INDICATIONS
5. Chylothorax- Avoid cannulating the vein on the left side as the thoracic duct lies 1. Diagnostic
there. a) bleeding from the upper gastrointestinal tract, haematemesis
6. Catheter-related sepsis b) pentagastrin studies (rarely done now)
2. Decompresssion
CANNULATION OF THE SUBCLAVIAN VEIN a) intestinal obstruction
The subclavian vein (SVC) may be preferred for central venous access if b) pyloric stenosis
1. Patient has a cervical spine injury c) haematemesis, particularly in patients at risk of hepatic encephalopathy
2. Line is for long-term use e.g. dialysis, feeding. This site may be more comfortable d) therapeutic and prophylactic decompression after major abdominal surgery
for the patient. e) prevention of further soilage after gastric perforation
f) prevention of anastomotic rupture after gastric surgery
Anatomy of the SCV g) prevention of obstruction of the operative field by air in the stomach
The SCV is the continuation of the axillary vein and originates at the lateral border of 3. Nutrition
the first rib. The SCV passes over the first rib anterior to the subclavian artery, to join a) patients with dysphagia
with the internal jugular vein at the medial end of the clavicle. The external jugular b) comatose or weak patients
vein joins the SCV at the midpoint of the clavicle. 4. Lavage
Technique a) poisoning
1. Place the patient in a supine position, head-down. b) gastrointestinal bleeding
2. Turn the head to the contralateral side (if C-spine injury excluded).
3. Adopt full asepsis. CONTRAINDICATIONS
4. Introduce a needle attached to a 10 ml syringe. 1. Base of skull fracture
5. Surface mark the subclavian vein 1 cm below the junction of the middle and medial 2. Oesophageal tear
thirds of the clavicle. Direct the needle medially, slightly cephalad, and posteriorly 3. Severe facial injury
behind the clavicle toward the suprasternal notch.
6. Slowly advance the needle while gently withdrawing the plunger. The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric
7. When a free flow of blood appears, follow the Seldinger approach, as detailed tube insertion.
previously.
8. The catheter tip should lie in the superior vena cava above the pericardial reflection. PRE-PROCEDURE
Perform check chest X-ray to confirm position and exclude pneumothorax. 1. Gather equipment.
2. Don non-sterile gloves.
Complications 3. Explain the procedure to the patient and show equipment.
As listed for internal jugular venous cannulation. The risk of pneumothorax is far 4. If possible, sit patient upright for optimal neck/stomach alignment with the head
greater with this technique. Damage to the subclavian artery may occur; direct pressure forward. Otherwise, prop the patient up at 45 degrees.
cannot be applied to prevent bleeding. 5. Deflate the endotracheal tube or tracheostomy cuff
Ensure that a chest X-ray is ordered, to identify the position of the line and to exclude 6. Determine the size of the nasogastric tube required (usually 14 – 16FG). If
pneumothorax. 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.

112
113
PROCEDURE PROBLEMS AND COMPLICATIONS
1. Estimate the length of the tube to be inserted: from the bridge of the nose to the 1. Technical
tragus of the ear to the point halfway between the xiphisternum and the navel. Mark a) insertion into the trachea, resulting in choking.
the Mark measured length with a marker or note the distance. b) coiling and reentry into the oesophagus (rare).
2. Examine nostrils for deformity/obstructions (eg. choanal stenosis) to determine best c) trauma to the nose and the pharynx.
side for insertion. Select the largest nostril for inserting the tube. d) dislodgement
e) perforation of the pharynx and oesophagus.
3. Lubricate tube with water. The nose may be lubricated with lignocaine gel.
2. Lung complications
4. Introduce the tube through the nostril, passing the tube along the floor of the nose. a) decreased ventilation
Resistance may be felt as tip reaches the nasopharynx, which is the most b) aspiration pneumonia
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. 3. Loss of fluids and electrolytes, especially sodium, potassium, chloride
and hydrogen ions.
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 4. Dry mouth and parotitis due to fluid loss and mouth breathing.
may enhance passage of tube into esophagus. If patient is uncooperative, bend his 5. Gastrointestinal
head to elicit a swallowing reflex. a) gastric erosions
6. Continue to advance the tube down the oesophagus. There should not be resistance. b) pressure necrosis of the pharynx, oesophagus or the external nares.
If resistance is met, rotate the tube slowly with downward advancement towards the c) traumatic haemorrhage of varices.
closer ear. Do not force the tube down against resistance as this may form a false d) gastroesophageal reflux due to functional incompetence of the lower
passage. oesophageal sphincter.
e) erosions of the oesophagus leading to strictures.
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.
TRACHEOSTOMY 8. Visualise the thyroid isthmus and retract isthmus.
9. Retract cricoid cartilage upwards wth cricoid hook.
INDICATIONS FOR TRACHEOSTOMY
1. Maintenance of airway patency. 10. Incise the trachea between the 2nd and 3rd tracheal rings, making an inverted U-flap
2. Protection of the airway from aspiration. incision.
3. Application of positive pressure to the airway. 11. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks.
4. Facilitation of secretion clearance. 12. Suction of blood and secretions in the lumen.
5. Delivery of high oxygen concentrations. 13. Insert the tracheostomy tube.
14. Remove the obturator and insert the inner cannula.
RELATIVE CONTRAINDICATIONS
15. Dress wound and secure to the neck using sutures and adhesive tape.
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 COMPLICATIONS
innominate artery or scarring from previous neck surgery. During Procedure
4. Documented or clinically suspected tracheomalacia. 1. Bleeding if damage to the innominate or inferior thyroid artery.
5. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water. 2. Damage to surrounding structures, eg esophagus, recurrent laryngeal nerve,
6. Patient obesity with short neck that obscures neck landmarks. brachiocephalic vein.
7. Patient age younger than 15 years. 3. Pneumothorax.
4. Pneumomediastinum.
TYPES OF TRACHEOTOMY Immediate post-op
1. Temporary: Portex (cuffed). 1. Surgical emphysema.
2. Permanent: Consist of inner and outer tubes made of stainless steel. 2. Obstruction, eg clot, mucus.
3. Bleeding.
Tracheostomy is more useful in the elective setting compared to endotracheal intubation
4. Dislodgment.
because:
5. Subcutaneous emphysema.
1. Better tolerated.
2. Avoids risk of laryngeal stenosis Late post-op
3. Avoids risk of endotracheal obstruction. 1. Infection .
2. Obstruction, eg dislodgment of tube, crust formation from secretions.
PROCEDURE 3. Tracheo-esophageal fistula.
1. Position the patient. Place rolled towel under the patient‘s neck to hyperextend the 4. Tracheal stenosis.
neck for better exposure. 5. Wound breakdown.
2. Clean and drape. Clean the skin of the neck from the chin to the suprasternal notch 6. Scarring.
and laterally to the base of the neck and clavicles. Drape field. 7. Tracheomalacia.
3. Identify anatomical landmarks (thyroid cartilage, cricoid cartilage).
POST-OP CARE
4. Administer local anaethesia. 1. Position patient in a propped up position.
5. Incise skin. In the emergency setting, make a vertical incision 3cm from cricoid 2. Prevent obstruction by suction, saline irrigation, mucolytic agents (mucomyst,
cartilage downwards. In the elective setting, make a tranverse incision 4cm wide, guaifenesin) and humidified air.
3cm above the suprasternal notch. 3. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday.
6. Dissect through the subcutaneous layers and platysma. 4. Unlock the metal tube every night so that the patient can cough it out if it becomes
7. Identify the communicating branch of the anterior jugular vein, clamp and ligate the obstructed.
artery (ignore this in an emergency).
114
115
SENGSTAKEN-BLAKEMORE TUBE (OR MINNESOTA TUBE) URINARY CATHETERISATION

INDICATIONS INDICATIONS FOR SHORT-TERM CATHETERISATION

Oesophageal varices 1. Relief of acute retention of urine, e.g. benign prostatic hypertrophy, bladder
outflow obstruction.
CONTRAINDICATIONS 2. Bladder washout, e.g. blood clots causing acute retention of urine.
1. Base of skull fracture
2. Oesophageal tear 3. Cystourethrogram.
3. Severe facial injury 4. Administration of intra-vesical drugs.
5. As an adjunctive measure pre/post-operatively
PROCEDURE a) Pre-operatively:
1. Measure the length of the tube. Test balloons. Test patency of the tube. (i) to drain the bladder so as to improve access to the pelvis in urologic or
2. Sit the patient upright or at 45 degrees. pelvic surgery.
3. Apply local anaesthesia (lignocaine nasal spray). (ii) to allow accurate measurement of urine output in major surgery.
4. Lubricate and insert the tube through the nose, asking the patient to swallow or b) Post-operatively:
drink water to aid in smoother passage of the tube through the pharynx and (i) to relieve acute urinary retention because post –op pain results in failure
oesophagus. of the sphincter to relax.
5. Inflate the gastric balloon slowly with 100-150ml saline. 6. Urinary output monitoring, e.g. in patient with hypovolaemic shock or the
6. Check that the tube is in the stomach by: critically ill.
(i) aspirating fluid and testing it with litmus,
(ii) auscultating the epigastrium while injecting air, or INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION
(iii) doing an X-ray. 1. Refractory bladder outlet obstruction.
7. Traction. 2. Chronic retention of urine, eg. neurogenic bladder.
8. Inflate the oesophageal balloon to 35 – 45mmHg: use the Y-connector piece with 3. Incontinence, e.g. in palliative care of terminally ill or patient‘s preference.
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 CONTRAINDICATIONS
Minnesota tube, use the additional lumen provided (with the additional lumen for 1. Presence of urethral injury, as manifested by:
aspirating fluid in the oesophagus, the Minnesota tube decreases the likelihood of a) blood from the meatus,
aspiration pneumonia occurring). b) scrotal haematoma,
c) pelvic fracture, or
10. Check the oesophageal balloon pressure hourly and release 5mins hourly.
d) high-riding prostate, elicited from a genital and digital rectal examination.
11. Release oeophageal balloon after 24hrs. (alternative: suprapubic drainage)
12. Release gastric balloon after 48hrs.
2. Urinary tract infection, as an indwelling catheter causes difficulty in treatment.
13. The tube should not be used for more than 72hrs.
PROCEDURE
COMPLICATIONS 1. Gather equipment.
1. Aspiration pneumonia
2. Respiratory obstruction 2. Explain procedure to the patient. Maximize patient‘s privacy. Have a chaperone if
3. Oesophageal ulceration and rupture performing the procedure on a member of the opposite sex.
4. Rebleeding 3. Assist patient into supine position with legs spread and feet together.
5. Gastric varices not controlled 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 swab 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.
116
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.
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
117
MATERIALS COMPLICATIONS
1. Iodine & alcohol swabs for skin prep 1. Laceration or puncture of the intrathoracic and/or abdominal organs, all of which
2. Sterile drapes & gloves can be prevented by using the finger technique before inserting the chest tube.
3. Scalpel blade & handle 2. Introduction of pleural infection.
4. Clamp 3. Damage to the intercostals nerve, artery or vein.
5. Silk suture
6. Needle holder 4. Incorrect intrathoracic or extrathoracic tube position.
7. Petrolatum-impregnated gauze 5. Chest tube kinking, clogging or dislodging from the chest wall or disconnection
8. Sterile gauze from the underwater seal apparatus.
9. Tape 6. Persistent pneumothorax
10. Suction apparatus (Pleuravac)/underwater seal apparatus 7. Subcutaneous emphysema, usually at tube site.
11. Chest tube (size 32 to 40 Fr, depending on clinical setting) 8. Recurrence of pneumothorax upon removal of the chest tube.
12. 1% lignocaine with epinephrine, 10 cc syringe, 25- & 22-g needles
9. Lungs fail to expand due to plugged bronchus; bronchoscopy required.
10. Anaphylactic or allergic reaction to surgical preparation or anaesthesia.
PRE-PROCEDURE PATIENT EDUCATION
1. Obtain informed consent
2. Inform the patient of the possibility of major complications and their treatment Recovery from the chest tube insertion and removal is usually complete, with only a
3. Explain the major steps of the procedure, and necessity for repeated chest small scar. The patient will stay in the hospital until the chest tube is removed. While
radiographs 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
PROCEDURE normal fluids from collecting in the lungs.
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.
118
119
IMPORTANT LUMPS AND BUMPS Clinical differences between indirect and direct inguinal hernia
Indirect Hernia Direct Hernia
HERNIA Neck lies lateral to inferior epigastric Neck lies medial to inferior epigastric
 Hernia = a protrusion of an organ through an opening in the wall of the cavity in which it artery, out of Hasselbach‘s triangle artery, within Hasselbach‘s triangle
is normally contained Reduces upwards, laterally and backwards Reduces upwards and straight backwards
 Lifetime risk = 2-10% Controlled after reduction by pressure Controlled after reduction by pressure
 Causes of abdominal wall weakness over the deep ring over the superficial ring
- Congenital – normal (due to piercing structures), or patent processus vaginalis May descend down the scrotum Does not descend down the scrotum
- Acquired – trauma, surgical incision or disease May cause strangulation at superficial ring Rarely causes strangulation due to wide
 Consist of 3 parts: (narrow) hernia neck
- Sac: pouch of peritoneum (neck & body) Does not readily reduce on lying down Readily reduces on lying down
- Coverings of sac: layers of abdominal wall More common in young adults and infants More common in old men
- Contents
Types: Anatomy of inguinal canal
1) Inguinal (96%)  indirect (85%), direct (15%) or pantaloon (direct & indirect) - 4 to 6 cm long oblique passage above the inguinal ligament, from the deep to
2) Femoral (4%) & Richter‘s hernia (knuckle of bowel wall is strangulated but superficial rings.
lumen is patent) - Deep inguinal ring lies in the midpoint of the inguinal ligament & is formed
3) Incisional, Parastomal from a defect in the transversalis fascia.
4) Umbilical, Epigastric (herniation of extra-peritoneal fat) - Superficial ring is a triangular defect in the aponeurosis of the external oblique.
5) Rare types: Spigelian (herniation of linea semilunaris: lat. border of rectus), Boundaries:
Obturator, Lumbar, Gluteal, Internal, Sliding (herniation of posterior peritoneum  Ant. wall: aponeurosis of the external oblique (reinforced in lat. third by
with underlying retroperitoneal structures: caecum, sigmoid, bladder) internal oblique)
 Post. wall: transversalis fascia (reinforced in med. third by conjoint tendon)
PHYSICAL EXAMINTION (common signs)  Roof: arching fibres of the int. oblique & transversus abdominis before they
- Location: all occur at congenital or acquitted weak spots in the abdominal wall merge as conjoint tendon
- Reducibility: on direct pressure or lying down  Floor: inguinal ligament and lacunar ligament medially
- Expansile cough impulse Contents:
 Ilioinguinal nerve (L1): supplies skin over root of penis & upper part of
INGUINAL HERNIA: indirect or direct;
scrotum or skin over mons pubis & labia majora
Indirect inguinal hernia:
 ♀: transmits round ligament of the uterus from uterus to labia majora
- Most common; 65%
- Congenital; patent processus vaginalis + weakened fascia at deep ring  ♂: transmits spermatic cord from abdomen to testes
- Hernial sac enters the inguinal canal with the spermatic cord via the deep ring, then
emerges from the superficial ring & descends into the scrotum Anatomy of the spermatic cord
- ♂>♀, R> L, 20% are bilateral, children>adults Coverings: 3 concentric layers of fascia
 Internal spermatic fascia: derived from transversalis fascia
Direct inguinal hernia:  Cremasteric fascia & muscle: derived from internal oblique
- Bulges directly anterior though a weakened fascia Hesselbach‘s triangle, posterior  External spermatic fascia: derived from external oblique
to the inguinal canal (medial to the inferior epigastric artery) Contents:
 Hesselbach‘s ∆: inf. Epigastric art., rectus abd, inguinal ligament  3 Arteries: testicular artery, artery to the vas deferens, cremasteric artery
- Hernia sac is not with the spermatic cord  3 Nerves: nerve to cremaster, autonomic nerves (T10), genital br of
- Rare in ♀, usually occur bilaterally in ♂ with weak abdominal muscles and genitofemoral nerve
comorbid conditions causing ↑ intra-abdominal pressure  3 Others: Vas deferens, pampiform venous plexus, lymphatics
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:
 Weight loss, change jobs/, avoid heavy lifting, Truss: for compression of
reducible hernia at deep ring (poor pickup rate)
 Treat medical conditions causing chronic cough, chronic constipation
 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 boewl 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
- ARU
- Bruising , bleeding (testicular, cremasteric, @ to vas deferens,
inferior epigastric, femoral arteries)
- Injury to surrounding structures pain, parasthesia, impotence:
spermatic cord (vas deferens, testicular artery), round ligament,
ilioinguinal nerve, nerve to cremaster
o Early
- Infection of wound/ mesh
- Haematoma (10%; no cough impulse, non-reducible, hard)
- Wound dehiscence
- pain
o Late
- Chronic post-op pain
120
- Recurrence of hernia (<0.5%; incomplete dissection, poor tissue,
too early mobilization, uncontrolled co-morbidities)
- 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
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
- Inspect as per a lump: (if unable to see, ask the patient)
o Is lump above or below the inguinal ligament? Any scrotal lump?
o Use a ruler to measure the dimensions of the lump
o Any skin changes? Previous scars (look hard)?
- Palpate:
o Define the inguinal ligament (ASIS to pubic tubercle, lat to pubic
symphysis, down frim umbilicus)
 show the lump is above it
o Lump: consistency (soft, fluctuant), size, temperate, any tenderness?
o Scrotum: Cannot get above lump; feel for testis to rule out
undescended testis
o for expansile cough impulse (bilaterally)
Lay the patient supine
- Get patient to reduce the lump himself
- Locate the deep ring (2cm above the midpoint of inguinal ligament)
- Keep pressure on deep ring, ask patient to sit up & support his pelvis, then
swing over the bed and stand
- Cough when standing: if remains reduced – indirect hernia, 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:
1) Abdominal exam: for scars, masses, ascites, ARU, constipation, signs of IO
2) DRE for BPH, impacted stools
3) Respiratory exam for COPD
4) Ask patient for history of heavy lifting
121
Differential diagnosis INCISIONAL HERNIA
- Femoral hernia - Extrusion of the peritoneum and abdominal contents through a weak scar or
- Inguinal LN wound on the abdominal wall
- Hydrocele of the cord (boys), or canal of Nuck (girls) - Physical examination similar, just add:
- Saphenous varix: [bluish-tinge, disappears on lying supine, also has positive o lifting head off the bed to exacerbate hernia
cough impulse] o palpate to determine the size of defect
- Undescended testes - Similar complications as any hernia
- Lipoma of the cord - Risk factors:
o Pre-op: age, immunocompromised, obese/ distended abdomen,
FEMORAL HERNIA Malignancy,
- Uncommon, but more common in females o Intra-Op: poor technique of wound closure, placement of drains
- Rarely put up for exams as it is operated quickly; o Post-op: wound haematoma, wound infx, early mobilization, post-op
- Femoral hernia is a marble shaped lump below the inguinal ligament and coughing
medial to femoral pulse - Treatment options:
o usually irreducible; narrow neck  risk of strangulation is high o Not every patient should undergo repair due to high risk of wound
o Usually does not have a cough impulse haematoma, infection, dehiscence and recurrent hernia
- DDx: o Conservative:
o Skin/ soft tissue: cyst, lipoma - Offer corset or truss
o Vascular masses: saphena varix, femoral aneurysm, inguinal LAD - Weight loss and control the risk factors leading to
o Hernia: inguinal hernia, obturator hernia o Surgical:
o Other: psoas bursa, ectopic testis - Offer if complications of hernia are present
- Control CVS & resp. disease; encourage pre-op wt loss
Differences between an inguinal and a femoral hernia - Principles: dissect the sac and close the defect using mesh
Inguinal Hernia Femoral Hernia overlapping
Appear through superficial ring above and Appears through femoral canal below and
medial to pubic tubercle lateral to pubic tubercle UMBILICAL HERNIA/ PARAUMBILICAL HERNIA
Usually reducible Usually not reducible - Uncommon b4 40YO; may grow to large size.
Expansile cough impulse usually present Expansile cough impulse usually absent - Cause: defect through the linea alba 2o to stretching the fibers
Low risk of strangulation High risk of strangulation o Pregnancy, ascites, cyst, fibroids, distention
- Issues of concern:
Anatomy of the femoral canal o Narrow Neck of hernia sac  higher risk of strangulation/ infarction
- The femoral sheath is the downward protrusion of fascia containing the femoral o Fistula formation with discharge of contents may occur
vessels and lymphatics below the inguinal ligament. - Management:
- The medial compartment of the sheath constitutes the femoral canal, which o Conservative: treat medcial co-morbidities.
carries the lymphatics. o Surgical: Mayo‘s Vest over pants operation
- 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
APPROACH TO SCROTAL SWELLINGS EXAMINATION OF THE SCROTUM
- ― Examine this gentleman‘s scrotum:‖
ANSWER 4 QUESTIONS: - Always examine him STANDING!
1. Can you get above the swelling? Inspect
2. Can you identify the testis and the epididymis? - inspect the groin and scrotum: scars and swelling
3. Is the swelling transilluminable? - groin incisions are usually oblique; scrotal incisions are usually in the median
4. Is the swelling tender? raphe
Palpate
- ask for any pain; when palpate, look at patient for tenderness
Cannot Cough impulse Hernia
get
- palpate one testes at a time
Reducible
above - if palpated any swelling:
Testis palpable
swelling  Is it tender?
Opaque
 Can you get above the swelling?
No cough impulse Infantile hydrocoele  Can you identify the epididymis and testis  lump is separate
Not reducible or part of them?
Testis not palpable  Is it transilluminable?
Transilluminable Offer to:
- Transilluminate the swelling if it is likely at hydrocele
Can get Testis not definable Opaque Non tender Chronic haematocoele - Continue the examine the groin if it is a inguinoscrotal hernia
above from epididymis Gumma - Examine the abdomen
swelling Tumour
HYDROCELE
Tender Torsion - Points from examination:
Epididymo-orchitis o Very swollen scrotum; uniformly enlarged
Acute haematocoele o Cannot define testis well; no separable from testis
o Maybe firm, tense or lax
Transilluminable Hydrocoele o Maybe transilluminable if acute (less in chronic hydrocele)
o Can get above the mass; the superficial ring is distinct
Testis definable Opaque Non-tender Tumour
from epididymis swelling of testis - Definition of hydrocele:
o Excess accumulation of fluid in processus vaginalis (fold of
peritoneum as testis descends; usually patent for fluid to accumulate)
Non-tender TB epididymis
swelling of
- Types of 1o hydrocele:
epididymis
o Vaginal hydrocele:
 Only in tunica vaginalis & does not extend into the cord
Tender Epididymoorchitis o Hydrocele of the cord
 Mass around the cord; attached distally to the testis
Transilluminable Cyst of epididymis  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

122
123
- Types of 2o hydrocele VARICOCELE
o From testicular tumours - Best noticed on palpating the standing patient
o From torsion - Points from examination:
o From trauma o Mass is separate from testis; can get above it
o From orchitis (any inflm) o Feels like a bag of worms; +ve cough impulse
- Treatment options: o Not transilluminable
o Conservative: - Definition:
 Watch & wait or Aspiration [tend to reccumulate] o Dilated, tortuous pampiniform plexus
 Must exclude a 2o cause o 98% on Left side: left vein is more vertical, connects to left renal vein,
o Surgical: longer than right one, often lacks a terminal valve
 Lord‘s plication of the sac - Causes:
 Jaboulay‘s operation to evert the sac o Idiopathic in younger males around puberty
o In older men with retroperitoneal disease: RCC
TESTICULAR TUMOUR
- Points from examination: - Treatment options:
o Inseparable form the testis; can get above i o Conservative: risk of infertility
o Hard, nodular, irregular, non tender o Surgical:
o Not transilluminable (but maybe a/w hydrocele)  Transfemoral radiological embolization with coil or sclerosant
- DDx:  Excise the surrounding veins via high retroperitoneum,
o Chronic infection with scarring inguinal or laprascopic approach
o Long standing hydrocele with calcification,
- Classiccation: TESTICULAR TORSION (Surgical emergency)
o Mostly seminomas or teratomas - Clinical features:
 Seminomas: 30-40YO, normal tumour markers, Rx with RT o Children/ teenagers
to paraaortic nodes and CT according to staging o acute abdomen (T10 inervation) & acute scrotum a/w vomiting
 Teratomas: 20-30YO, AFP/ BHCG raised in 90%, Rx with CT o swollen and tender scrotum, testis is high in scrotum; pain worsen by
o Others: embryonal carcinoma, choriocarcinoma, yolk sac tumour, lifting testis up
Leydig cell tumours (10% malignant ; a/w gynaecomastia), Sertoli cell o Previous attacks of self limitng pain; ppt by trauma, cycling, straining,
tumour (a/w gynaecomastia), Lymphoma (look for lymphoma coitus
elsewhere; poor prognosis) - DDx:
- Treatment: o Epididymitis
o Staging, excision of whole testis with combination chemotherapy o Torsion of testicular appendage (pea coloured lump through scrotum)
o Strangulated inguinoscrotal hernia
EPIDIDYMAL CYST - Cause:
- Points from examination: o Maldescended testis hanging like a bell clapper within tunica vaginalis
o Small mass separate from testis; can get above it - Treatment:
o Firm; maybe loculated; transilluminable if large cyst o Emergency exporation if Doppler US –ve for flow or clinical suspicion
- Often multiple in the head of epididymis  Untwisting (lateral) of affected testis and orchidoplexy of both
- May occur as a complication of vasectomy (spermatoceles) testis to scrotum
- Treatment:  Warm up with warm pad to see reperfusion or check with
o Conservative [mainstay] dopler after untwisting [4 hours before ischaemia]
o Surgical: if painful, very large or frequent recurrences. Complicated by  If dead, excise and replace with prosthesis
operative damage and fibrosis of epididymis  subfertility
APPROACH TO LUMPS AND BUMPS 9. Special tests
Permission: Introduce yourself - Transillumination [only for large lumps; Use pen torch on one side]
Position: Ensure patient (and you) are comfortable - Pulsatility (only for some sites, e.g. Neck, abdomen)
Exposure: Expose area to be examined fully - Place finger on opposite sides of lump
(Remember: Compare with other side if applicable) o Expansile: fingers pushed apart
o Transmitted: Fingers pushed in same direction (usually upwards)
“Mr. X is a young Chinese
Inspection - Slip sign – if lipoma is suspected
gentleman…”
1. Number: solitary / multiple - Tends to slip away from the examining finger on gentle pressure
“On inspection, there is a (single)
2. Site: take reference from bony points - Compressibility / reducibility [if AVM, haemangioma, hernia suspected]
(hemispherical) lump on the (dorsum of
3. Shape / Symmetry: - Compressible: Disappears on pressure, reappears on release (AVM)
the forearm)”
- Hemispherical, Round, Exophytic - Reducible: Disappears on pressure, reappears with opposing force (hernia)
“It measures <take out ruler> ( x by x
4. Size - Auscultation – only for certain sites / lesions (e.g. neck, abdomen, etc.)
cm)”
5. Scars
“There are (? scars, sinuses, ulceration,
6. Colour & skin changes?
or discharge seen, nor overlying or
i. Sinuses, discharge Request – “I would like to complete my examination by…”
surrounding skin changes)”
ii. Ulceration  Examine the draining LNs
iii. Erythema / cellulitis  If sebaceous cyst / lipoma
“Is the lump tender?”  “Looking for other lumps elsewhere”
 Ganglion
Palpation (Ask patient: Is area painful?) “On palpation, the overlying skin is  “Looking for other lumps elsewhere”
1. Overlying skin temperature (not) found to be warm. It is (non-  “Asking for hand dominance”
2. Tenderness tender)”  “Taking an occupational history”
3. Surface: “The surface is (smooth), with clearly-
- Smooth/ Irregular/ Rough defined margins”
“The consistency is firm, and it is (non- S: site, size, shape, scars, skin changes, surface
4. Margins clearly defined? E: edge, expansility/ pulsatility
5. Consistency fluctuant)”
“The lump is (not) attached to the C: colour, consistency, compressibility
- Hard > Firm > Tense > Soft
overlying skin, and it is non-pulsitile.” T: tenderness, temperature, transillumability
6. Mobility O: others [fluctuance, fulid thrill]
- Fully mobile in all directions? “It (appears to be attached to
underlying muscle, as it is mobile R: reducability, relationship to each other
- Fixed and immobile?
- Mobile only in certain directions? horizontally but not longitudinally)”
7. Relations to surrounding tissues For ulcers:
- Move lump in 2 perpendicular planes Add into inspection:
o Attached to skin? muscle / tendon / bone? - Base: granulation tissue, slough, fascia, muscle, bone
o If appears to be attached to muscle: - Edge: sloping (healing), punched out, undermined, rolled (BCC), everted (SqCC)
 Ask patient to tense muscle; Reassess mobility in the 2 planes - Discharge: serous, sanguinous, haemoserous, purulent
 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

124
125
LIPOMA 2. Myxoid, round cell (poorly differentiated myxoid)
Inspection 3. Pleomorphic liposarcoma
o Can be single, often multiple  Clinical features
o Usually at neck, trunk o Can occur at all ages (not common in children)
o Hemispherical – may appear lobulated o Slow-growing, never regress
o Scars  Implies recurrent lipoma o May be multiple: lipomatosis (multiple continuous lipomata)
 Occur in buttocks / neck
Palpation  Can cause distortion of subcutaneous tissues.
o Smooth or lobulated on firm pressure – bulging between strands of fibrous  Treatment
tissue) o Non-surgical – watch & wait
o Soft / firm (depending on nature of fat) o Surgical – If patient wants it removed (Pain / peripheral neuropathy –
o Well defined edges (may not be regular; series of curves corresponding to each Dercum‘s disease, Cosmesis)
lobule  Can be removed under LA
o Pseudo-fluctuance if large – lipomas are not liquid; but fat maybe more liquid  Nuchal lipomas (back of the neck): extremely fibrous septae:
o Mobile in all directions (if subcutaneous) difficult to excise
o Positive slip sign; No transilluminance / thrill  If close to joint: LA may not be possible (may communicate with
o Usually in the subcutaneous tissue. [check attachment skin & muscle] joint)
 Variants of lipomas / syndromes associated with lipomas
“Mr. X is a young Chinese gentleman…” o Adiposis dolorosa (Dercum’s disease)
“On inspection, there is a hemispherical lump over the right scapula”  Multiple painful lipomas in limbs, sometimes trunk
“It measures 10 by 8 cm”  Associated with peripheral neuropathy
“There are no scars, punctum, ulceration, or discharge seen, nor any overlying or  Angiolipomas: prominent vascular component
surrounding skin changes” o Hibernomas: brown fat cells
“On palpation, the overlying skin is not warm, it is non-tender” o Cowden‘s disease – associated with:
“The surface is lobulated, and its margins are not well-defined”  Thyroid cancers
“The consistency is soft, and it is fluctuant”  Lipomas
“The lump is not attached to the overlying skin”  Palmoplantar keratoses
“It is mobile in all directions with a positive slip sign”  Multiple facial papules
“It is not transilluminable”  Oral papillomatoses
“I would like to complete my examination by looking for other similar lumps” o Bannayan-Zonana syndrome – rare AD dz: lipomas with macrocephaly and
“My provisional diagnosis is a lipoma” haemangiomas, intestinal polyps
―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-group (deeper tissues –
retroperitoneal, deep tissues of the thigh, subscapular)
 Liposarcoma classification
1. Well-differentiated
SEBACEOUS CYST Background Information
Inspection  Sometimes considered to be similar to epidermoid cyst
 Usually solitary (can be multiple) o More accurate terminology: pilar / trichilemmal cysts
 Hemispherical  2 histological types:
 Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles) o Epidermal cyst: from infundibular portions of hair follicles
 Variable size ; few mm to 4-5 cm o Trichilemmal cyst: from hair follicle epithelium (most common on scalp),
 May have bluish discolouration frequently multiple (AD inheritance)
 Punctum in apex: in 50%  Arise from infundibular parts of hair follicles
 Definition: Distension of sebaceous glands with sebum from blockage of opening
 May exhibit plastic deformation on palpation
 Clinical features
o Occur in all age groups, rarely present before adolescence
Palpation
o Slow growing,– may appear suddenly at adolescence
 Normal Temperature, non-tender (unless inflamed)
o May become infected: acutely painful, sudden increase in size
 Smooth surface o May spontaneously discharge contents through punctum, regress
 Well-defined margins (lies in subcutaneous fat)  Point of fixation & discharge along a hair follicle
 Tense Consistency, may stretch overlying skin & exhibit plastic deformation  Point gets pulled inwards on enlargement of the mass – creates
 Non fluctuant, not transilluminable punctum
 Attached to skin, Not attached to deeper structures, Usually mobile in all  Sebaceous horn may form from hardening of slow discharge from
directions wide punctum
 Sebum slowly exudes, dries and hardens into conical
“Mr. X is a young Chinese gentleman…” spike
“On inspection, there is a single hemispherical lump in the middle of the forehead  Sebum usually washed away – horn results only if
just above the eyebrows” overlying skin not washed
“It measures 1 by 1 cm in diameter”  Can be pulled out of skin
“There is a visible punctum over the lump”  Treatment: excision / curettage along with base +
“There are no scars, sinuses, ulceration, or discharge seen, nor any overlying or histological assessment
surrounding skin changes”  Complications
1. Infection (±discharge)
“On palpation, the overlying skin is not warm. It is non-tender.” 2. Ulceration
“The surface is smooth, with clearly-defined margins” 3. Calcification (trichilemmal cyst) (may lead to cyst hardening)
“The consistency is firm, and it is non-fluctuant” 4. Sebaceous horn formation, [hardening of a slow discharge of
“The lump is attached to the overlying skin” sebum from a large, central punctum.]
“It is mobile in all directions” 5. Malignant change
“Slip sign is negative”
“I would like to complete my examination by…”  Treatment
“Looking for other lumps elsewhere” o Non-surgical: leave alone (if small, asymptomatic).
“My provisional diagnosis is a sebaceous cyst” o Surgical
My differentials are:  Complete excision of cyst and contents under LA.
Lipoma  Prevention of recurrence: by removal of elliptical portion of skin
Dermoid cyst containing punctum along the lines of Langers.
 If at the angle of jaw, be careful of the facial nerve during
Inflamed operation. Damage to zygomatic branch can cause eye ulceration.
Cyst
126
127
 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
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 again with
underlying muscles tensed, and should be 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, becomes fixes 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…”  Differentials
“On inspection, there is a single hemispherical lump on the dorsum of the left o Bursae (soft)
wrist” o Cystic protrusion of synovial cavity in OA (joint will be abnormal)
“It measures 3 by 2 cm” o Benign giant cell tumours of flexor shealth (Pigmented VilloNodular
“There are no scars, ulcerations, or discharge seen, nor any overlying or Synovitis)
surrounding skin changes” o Lipoma
“On palpation, the overlying skin is not warm. It is non-tender” o Sebaceous cyst
“The surface is smooth, with clearly-defined margins”  Treatment
“The consistency is soft, and it is fluctuant” o Non-surgical
“The lump is not attached to the overlying skin”  Watch & wait, usually may disappear after a few months.
“It appears to be attached to underlying muscle, as it is mobile horizontally but not  Aspiration + 3/52 of immobilisation (successful in 30-50%).
longitudinally” High chance of recurrence 6-12/12 later.
“It is transilluminant” o Surgical
“I would like to complete my examination by…”  Complete excision to include neck of ganglion at site of
“Looking for other similar lumps” origin. Along the lines of Langers.
“Asking Mr. X for his hand dominance”  Complications of surgery
“Taking an occupational history”  Wound complications: Scar, haematoma, infection
“My provisional diagnosis is a ganglion”  Recurrence <10%
My differential is a  Damage to adjacent neurovascular structures.
1. Bursa  Stiffness & Contractures
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] Its origin is controversial: seen as pockets of synovium
communicating with joint, tendon shealth or degeneration of mucoid fibrous tissue,
 Site:
o Can occur anywhere in body; 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
 Clinical features
o Majority between 20 and 60 years (rare in children)
o Grow slowly over months / years
o Non painful

128
129
BASAL CELL CARCINOMA “Mr. X is an elderly Chinese gentleman…”
– “Examine this gentleman‟s face” “On inspection, there is a single hemispherical lump just above alar of the nose”
(If the other side of the face, etc. needs to be inspected, ask the patient to turn his head – “It measures 2 by 2 cm”
avoid moving around the patient) “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
Inspection telangiectasia are seen over the lump”
 Single (often multiple) “There are no visible scars, ulceration, or discharge seen, nor any other overlying
 Commonly found on the face, (above line drawn from angle of mouth to earlobe) or surrounding skin changes”
 Hair-bearing, sun-exposed skin (especially around the eye) “On palpation, the overlying skin is not warm. It is non-tender.”
 Lesions raised above the skin: “The surface is smooth”
o Nodular/ nodulo-ulcerated type (most common): “The consistency is firm”
 Pearly, rolled edges [smooth, glistening, slightly transparent] “The lump arises from the skin”
 May be pigmented, with telangiectasia over the lump “It is freely mobile over the underlying tissues”
 May have central ulceration; erode facial structures if advanced “My provisional diagnosis is basal cell carcinoma”
o Cystic: large cystic nodule “My differentials include SqCC, keratoacanthoma”
 Lesions not raised: “I would like to complete my examination by…”
o Pigmented: contains melanin; confused with malignant melanoma Examining for cervical lymphadenopathy (although very rare in BCC)
o Sclerosing: flat or depressed with ill defined edges; maybe ulcerated
o Bush-fire / Cicatricial: multiple superficial erythematous lesions with pale Background Information
atrophic areas  Locally invasive carcinoma of basal layer of the epidermis
o Superficial: erythematous scaly patches  Does not metastasize, but can infiltrate adjacent tissues
 Base:  Common in sun-exposed skin
o May be covered with coat of dried serum & epithelial cells  Pre-disposing factors
o If deep: may expose deeper tissues (bone, muscle, etc.), covered with poor- o Congenital (rare)
quality granulation tissue  Xeroderma pigmentosum (familial, associated with failure of
o On face: may erode deep into facial structures DNA transcription)
 Gorlin‘s syndrome (rare autosomal dominant cancer)
Palpation (Important to palpate for mobility: fixation and deep local invasion) o Acquired
 Normal temperature, may be painful / itchy  Sunlight (especially UV light; UV-B range)
 Firm / solid consistency  Carcinogens (smoking, arsenic)
 should be mobile over underlying structures, confined to skin  Previous RT
o If fixed, immobile  deeper invasion  Malignant transformation in previous skin lesions (e.g. naevus
 Regional LAD (metastases are extremely rare, to rule out SCC) sebaceous)
 Clinical features
Ask about pre-disposing factors 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:  Treatment
o Above the skin: o Raised above skin: excision with 0.5 cm margin (maximum)
 Nodular o Not raised above skin: wider margin of excision, especially if at inner
 Nodulo-ulcerative / Deeply eroding ulcer (―rodent ulcer‖) acanthus of eye, nasolabial fold, nasal floor, ear
 Cystic  Frozen section may be needed to ensure adequate excision
o Not raised above the skin: o Alternative:
 Pigmented  RT
 Geographical / cicatricial / ―bush-fire‖ (advancing edge, o Eyes, ears, nasolabial fold lesions: Moh’s chemosurgery
healing centre)  Staged chemosurgery, histological assessment of margins &
 Sclerosing (flat / depressed tumour, ill-defined edge) electrodessication
 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)

130
131
SQUAMOUS CELL CARCINOMA “Mr. X is an elderly Chinese gentleman…”
“On inspection, there is a single irregular ulcer on the dorsum of the right
Inspection hand, proximal to the 1st & 2nd MCP joints”
 Single (may be multiple) “It measures 1.5 by 1.5 cm. The edge of the ulcer is well-defined, red and
 More common on sun-exposed skin – head, neck, arms, hands, trunk heaped up.”
 may be of considerable size (> 1 cm) “The base of the ulcer is shallow and contains red granulation tissue.”
 Round nodule or Circular ulcer or Irregular/ exophytic/ fungating mass “There are no scars, or discharge seen, nor any surrounding skin changes.”
 Well defined edges: “On palpation, the surrounding skin is not warm. It is non-tender”
o everted (excessive growth raises it above skin) “The edges are firm”
o dark, red-brown colour (very vascular) “The lump arises from the skin”
 May have central ulceration, Base: “It is fixed and immobile”
o Necrotic tumour; may be covered with coagulated blood / serum “My provisional diagnosis is squamous cell carcinoma”
o Granulation tissue: tends to be pale, unhealthy “My differentials are…”
o Deep tissues may be exposed o Benign: Keratoacanthoma, infected seborrhoeic wart, solar acanthosis,
o Depth: variable (may be very deep; especially in soft tissue) pyogenic granuloma
o Can be copious, bloody, purulent, foul-smelling discharge o Malignant: BCC, malignant melanoma, solar keratosis
 Surrounding tissue may be oedematous, thickened “I would like to complete my examination by…”
“Examining the local lymph nodes for lymphadenopathy”
Palpation “Taking a history looking for sites of metastases”
 normal temperature, not tender “Examining the abdomen and lungs for signs of metastases”
 usually mobile
o If immobile: invasion into deep structures Background Information
 Carcinoma of the cells of the epidermis forming superficial keratinous squamous
Request for: layer
 Examination of local lymph nodes (5% at time of presentation)  Local invasion inyo epidermis, dermis, adjacent tissues, & lymphatic spread to LNs
o Often enlarged (but may not contain tumour even if enlarged – can be from  Microscopy:
infection) o Tongues of tumours cells spreading in all directions
 Examination for sites of metastases o ―Epithelial pearls‖ – nest of squamous epithelium, cells are arranged in
o Respiratory: lung (pleural effusion) concentric circles surrounding a central focus of acellular keratin
o Abdominal: liver (hepatomegaly)
 Take a history looking for predisposing factors (see below)
 Clinical features
o Incidence increases with age (usually elderly male)
o Predisposition:
 Congenital:
 Xeroderma pigmentosum (AD, failure of DNA
transcription)
 Acquired
 Envn: sunlight, Irradiation, Chemicals
 Pre-existing lesions: Solar keratosis, Bowen‘s disease
 Chronic ulcers: old burns, chronic venous ulcers
 Immunosuppresion (post-transplant, HIV)
 oUsually 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 & Marjolin‘s Ulcer
electrodessication
 Solar (actinic) keratosis (SqCC in situ)
o Multiple yellow-grey to brown scaly tumour
 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 atypic only
(vs atypia in whole epidermis in SqCC)
o Treatment:
 Non-surgical: cryotherapy, topical chemotherapy (5-FU)
 Surgical: curettage of affected skin
Solar / Actinic Keratosis

Lesions Associated with SqCC

 Marjolin’s ulcer
o SqCC arising in long-standing benign ulcer / scar
 Commonest ulcer: venous ulcer
 Commonest scar: burns
o Very similar in appearance to classic SqCC, but may not be so florid

 Bowen’s disease (SqCC in situ)

o Very slowly growing, may progress to SqCC
o red, scaly irregular plaque on the trunk Bowen‘s disease
 if on the penis, vulva or oral cavity = erythroplasia of
Queyrat
o Intraepidermal carcinoma
 a/w visceral malignancies in 5-7 yrs time esp if area of skin
has not been exposed to the sun
o HPV has been found in some lesions
o Microscopically
 Epidermis
 Atypical keratinocytes
 Basal layer is intact
o Treatment: excision (SqCC will grow eventually)
132
133
MALIGNANT MELANOMA “Mr. X is a middle aged Chinese gentleman…”
Inspection “On inspection, there is a single flat-looking lesions over the right foot”
 Usually single (may have satellite lesions around primary lesion) “It measures 2 by 4 cm”
 Site: Limbs, head & neck, trunk, subungual, mucocutaneous junction, mouth, anus “It is variegated in appearance, and exhibits red, white, and black discolouration”
 Any colour: pale pink, brown, black, purple (rich blood supply) “The margins are clearly-defined and irregular”
 Clearly defined but irregular “There are no scars, nor any surrounding pigmentation, erythema, or ulceration,
 May ulcerate, discharge bleeding, or discharge”
 May have surrounding halo: brown (pigment), pink (inflammation) “On palpation, the overlying lesion is palpable. It is not warm. It is non-tender”
 Types: “The surface is smooth, and its consistency is firm”
o Superficial spreading melanoma (70%): “The lump is attached to the skin, and moves with it over deeper structures”
 Legs of women and backs of men “My provisional diagnosis is malignant melanoma”
 Red, white, blue in colour “My differential diagnoses are: BCC, pigmented naevus”
 Irregular edge “I would like to complete my examination by…”
o Nodular type melanoma (15-30%): “Examining for regional lymphadenopathy”
 On trunk “Take a history for: cardinal symptoms of malignant change, and any
 Polyploidal and raised predisposing factors”
 Smooth surface with irregular edge
 Frequently ulcerated Background information
o Lentigo maligna melanoma: 4 commonest types of malignant melanoma
 On face or dorsum of hands & forearms  Superficial spreading melanoma (70%)
 Underlying lesion is flat, brown-black with irregular outline  Nodular melanoma (15 - 30%)
 Malignant area is thicker and darker  Lentigo maligna melanoma
o Acral lentiginous melanoma:  Acral lentigous melanoma
 More common in Asians and Blacks
 On hairless skin: subungual area, palms, soles Microscopic features
 Irregular area of brown/ balck pigmentation  Consists of loose nests of melanocytes in basal cell layer:
o Others: amelanotic melanoma, intra-cranial melanoma, retinal melanoma  Invade epidermis (leading to destruction, ulceration) & deeper into dermis,
 “Beware of the man with the glass eye and hepatomegaly” subcutaneous fat

Palpation Clinical Features

 Normal Temperature, Non-tender  Very rare before puberty (usually > 20 years old)
 Surface  Equally in both sexes (but distribution different – see below)
o If small: smooth epithelium  > 25% arise de novo
o If ulcerates: covered with crust (blood + serum) o Change in surface, size, colour, Halo, satellite nodules
o If bleeding, / infected: wet, soft, boggy o Ulceration, bleeding
 Firm consistency (small satellite nodules feel hard) o Itch, No pain
 Mobile, moves with skin over deeper structures o Lymphadenopathy
 Symptoms of distant metastases: LOW, SOB, jaundice
Request o Lymphatogenouly to: regional LN
 Palpation for regional lymphadenopathy o haematogenously to: Lungs [pleural effusion], Liver [hepatomegaly], Brain
 Palpation for other subcutaneous nodules (lying along course of draining [focal neurological signs] & Skin and subcutaneous tissues
lymphatics)
Predisposing Factors Request
 Congenital / non-modifiable  Examine draining lymph nodes
o Light skinned race  Take a history for:
o Xeroderma pigmentosum o Cardinal symptoms of malignant change in a mole
o Dysplastic naevus syndrome (B-K mole, FAMM syndrome) – 100% risk  Rapid increase in size
if 2 family members affected  Itching
o Large congenital naevi  Bleeding
o FHx in 1st degree relatives (1.5X risk)  Change in colour / shape / thickness
 Acquired / modifiable o Predisposing factors
o Sunlight exposure
o Pre-existing skin lesions Differentials
 Lentigo  Benign
 > 20 benign pigmented naevi (3 x risk) o Moles (pigmented naevus – ↑ melanocytes, ↑ melanin)
o Previous melanoma (3.5 x risk) o Freckles (normal number of melanocytes, ↑ melanin from each)
o Lentigo (↑ melanocytes, normal amount of melanin from each)
Features of pigmented skin lesion suspicious of malignancy o Pigmented seborrhoeic keratoses
1. Asymmetry o Dermatofibroma
2. Bleeding & ulceration (late) o Thrombosed haemangioma
3. Change in: colour, size, shape, surface, number (early)  Malignant
a. Surface: o Pigmented BCC
i. Loss of normal surface markings (e.g. skin creases) around lesion
ii. Skin may become rough / scaly Staging by depth of invasion
iii. Itchy with pale-pink halo (inflammation) Clark’s levels of invasion
b. Size: Level Extent of Tumour 5-Year Survival
i. Growth of newly-formed / long-standing mole I Epidermis only 98%
ii. Increase in edge, width, thickness II Invades papillary dermis 96%
c. Colour: III Fills papillary dermis 94%
i. Becoming darker IV Invades reticular dermis 78%
ii. Halo of brown discolouration in skin around the lesion V Subcutaneous tissue invasion 44%
iii. Patchy colour change (black, to blue-purple  ↑ vascularity) Breslow’s thickness (different in absolute depth of invasion, LN involvement)
iv. Occasionally colourless: no melanin production Breslow Thickness 10-Year Survival
d. Number: < 0.76 mm 92%
i. Satellite nodules of tumour around the lesion < 3 mm 50%
ii. Enlarged inguinal, axillary lymph nodes
< 4 mm 30%
4. Diameter >6mm
LN Involvement < 40% (8-yr)
5. Elevation (flat plaque → nodule)
 Also: Beahrs and Myer’s system

134
135
 Prognosis generally poor – above 3 types of staging, or other indicators of poor Superficial
Nodular Lentigo Maligna Acral Lentigous
prognosis: Spreading
a. Elderly % 70% 15-30% – Rare
b. Male
Hairless skin
c. Lesions on trunk ♂: Back Face; Dorsum of
Site Trunk (palms, soles,
d. Ulceration ♀: Legs hand / forearm
e. Depigmentation, amelanotic subungual area)
f. Aneuploidy, high mitotic index Red, white,
Colour blue (varying Most often black Brown / black Brown / black
Treatment pigmentation)
 Prevention (VERY IMPORTANT): Edge Irregular Regular outline Irregular Irregular
a. Avoidance of causative factors Palpable, but Thick, polypoid,
 Surgical excision with wide margins down to deep fascia Shape Flat Flat
thin raised
a. Main lesion:
Surface - Smooth - -
i. < 0.76 mm: excise with 1 cm margin
ii. 0.76 – 1.0 mm: excise with 2 cm margin • Arises from
iii. > 1.0 mm: excise with 3 cm margin patch of
b. Nodal spread: Hutchinson‘s • Rare type
i. If clinical suspicion, biopsy or FNAC of lymph nodes • Frequently Lentigo • Often
ii. If palpable: therapeutic block dissection Remarks - ulcerated, • Malignant area misdiagnosed as
 Palliation / adjuvant for distant metastases bleeding usually thicker, haematoma,
a. Intralesional BCG therapy darker paronychia
b. Immunotherapy: vaccines (raises anti-melanoma response), • Area seldom
monoclonal antibody, cytokine interferon therapy ulcerates
Pictures
NEUROFIBROMA Background Information
Inspection Sporadic Neurofibroma
 Often multiple  Benign tumour containing mixture of elements from peripheral nerves:
 Anywhere in skin, subcutaneous tissues, e.g. forearm o Neural (ectodermal)
 Spherical / Pedunculated / Fusiform (long axes lie along length of limb) o Fibrous (mesodermal)
 Rarely more than few cm  Often multiple
 comment on any café-au-lait spots  History
o Any age (but usually adult)
Palpation o Symptoms: usually cause no discomfort, rarely disfiguring
 normal temp., Non-tender o If related to nerve trunk, may be tender
 Patient may get tingling sensations in distribution of nerve
 Smooth, Well-defined
 Histology
 Soft/ fleshy, rubbery consistency
o Schwann cells: appear as bundles of elongated wavy spindle cells
 Non-fluctuant o Collagen fibrils, myxoid material
 If in subcutaneous tissue: mobile within it o Often not encapsulated (unlike neurilemmomas)
 Move most freely perpendicular to course of nerve  Complications of Neurofibroma
o Pressure effects: spinal cord, nerve root compression
Request o Deafness: involvement of VIII
 Look for other similar lesions & other manifestations of NF-1: café-au-lait spots, o Neurofibrosarcoma (only in NF-1): 5-13 %
axillary freckling, lisch nodules, optic glioma o Intra-abdominal effects: obstruction, chronic GI bleeding
 Measure the BP (HPT 2o to phaeochromocytoma, CoA, RAS) o Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis
 Examination of cranial nerve VII & VIII (acoustic neuroma)  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)

Neurofibromatosis I (Von Recklinhausen‘s disease)

(Refer to paediatrics notes – neurocutaneous syndromes)
 AD, neurocutaneous syndrome; chr 17
“Mr. X is a young Chinese gentleman…”  Characterised by pigmentary changes, tumours, and skeletal, vascular dysplasias
“On inspection, there are two spherical, pedunculated masses on the back” o Fibroma ≥2 NF or ≥1 plexiform NF
“One measures 2 cm, and the other 0.5 cm in diameter” o Iiris harmatomas (Lisch Nodules)
They are pink in colour, with well-defined margins” o Bone: dysplasia, pseudoarthrosis
“There are no scars, sinuses, ulceration, or discharge seen, nor any surrounding o Relatives
skin changes” o Optic glioma
“On palpation, they are not warm and non-tender” o Macules >6; >15mm post-pubertal
“Their surfaces are smooth, and are firm, and rubbery” o Axillary freckling
“They are attached to the skin, and are mobile over the deeper tissue layers”  Neurofibromata of all sizes (few mm to large subcutaneous nodules), related
“My provisional diagnosis is neurofibromata” differently to skin
“I would like to complete my examination by…” o Within skin
 "Looking for other similar lesions” o Tethered to skin
 “Looking for manifestations of neurofibromatosis” o Pedunculated
 “Examining the cranial nerves”
136
137
Plexiform Neurofibroma (elephantiasis neurofibromatosis) DERMOID CYST
 Very rare Inspection
 Excessive overgrowth of neural tissue in subcutaneous layers, giving tissue swollen  Usually single
oedematous appearance  Ovoid / spherical
o Often mistaken for lymphoedema, but lymphatic drainage is normal  Site:
 Can result in severe deformity: diffuse enlargement of peripheral nerve with skin o Congenital, 1-2 cm usually
involvement  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

“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”
Background Information SEBORRHOEIC KERATOSIS
 A dermoid cyst is a cyst deep to the skin, lined by skin (Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma)
 2 different methods of formation: Inspection
o Congenital: Accident during antenatal development  Often multiple
o Acquired: Implantation of skin into subcutaneous tissue by injury  Any part of skin; most found on back & face
Clinical features  Round / oval
 Congenital (suspect if in child, young adult)  Light brown → black
o Formed intra-utero, when skin dermatomes fuse  ―stuck on appearance‖; appears warty
o Occur at any point in mid-line, common in neck / face / nose  Varying size; Few mm to 2-3 cm
 Particularly along lines of fusion of ophthalmic & maxillary  Distinct margins
facial processes
 Also: inner & outer ends of upper eyebrow
Palpation
o May be seen at birth
 No warmth, no tenderness
o Distends a few years later, becomes obvious; few symptoms other than
 Rough surface (sometimes papilliferous)
cosmetic problems
o Rarely infected  More firm than surrounding skin
 Acquired – Implantation dermoid (suspect if in adult – Browse pg 60)  Attached to skin
o Develop when piece of skin survives after being forcibly implanted  Special tests
into subcutaneous tissue o May be picked off gently – reveals patch of pale-pink skin, 1-2 surface
 Often by injury: cut, stab, etc. capillaries (bleed slightly)
o Symptoms (DON‘T DO THIS IN EXAM)
 Small, tense lump
 Painful and tender (in areas subjected to repeated trauma) Request to look for similar lesions elsewhere
 Local effects (e.g. problems with grip / touch if on finger)
 Also rarely infected “Mr. X is an elderly Chinese gentleman…”
o Differentials “On inspection, there is a single ovoid lesion lump on the back”
 Sebaceous cyst (look for old injury, presence of scar near cyst: “It measures 1 by 2 cm”
more likely dermoid) “The margins are well-defined, and it appears to be slightly raised above the skin”
Treatment “There are no scars, ulceration, or discharge seen, nor any surrounding skin
 Congenital changes”
o Surgical treatment; complete excision “On palpation, the overlying skin is not warm. It is non-tender”
o Full extent should first be established with X-ray / CT “The surface is rough and greasy; the consistency is firm”
 Midline cysts may communicate with CSF; must exclude “The lump arises from the skin”
bony defect “My provisional diagnosis is seborrhoeic keratosis”
 Acquired “My differential diagnosis is: pigmented naevus, melanoma”
o Complete excision of cyst “I would like to complete my examination by…”
 “Looking for similar lesions elsewhere”

138
139
Background Information HAEMANGIOMA
 Benign outgrowth of basal layer of epidermis Background Information
o Raised above the level of normal epidermis  Vascular malformations
 Microscopy: o Types
o Hyperkeratosis (thickening of keratin layer)  Capillary: ⅔ of cases, include the cutaneous haemangiomata,
o Acanthosis (thickening of prickle cell layer) telangiectasias
o Hyperplasia of variably pigmented basaloid cells  Predominantly venous: venous angioma
 Deeper levels of subcutaneous tissue, may extend into
Clinical features muscle / joint
 Occur in both sexes  May have distended veins over the surface of the
 More common in elderly people mass
 Begin as a patch,  Empty with pressure, may have bruit
o increases in area, size over months / years  Predominantly lymphatic: lymphangioma circumscriptum
o May not increase in thickeness o Features
o May suddenly fall off: leave pale-pink patch of skin  Develop as abnormal proliferation of embryonic vascular
 Complications: network
o May become disfiguring, catch on clothes  Hamartomas
o May get infected (may imitate SCC, pyogenic granuloma)  May ulcerate, induce hyperkeratosis in overlying stratum
o Seldom bleeds (may cause it to change colour to brown) corneum
 Leser-Trelat sign: Sudden onset of multiple seborrhoeic keratoses may imply  Many forms of cutaneous haemangiomata: (see table)
visceral malignancy o Strawberry naevus (cavernous haemangioma)
o Port-wine stain (naevus vinosus)
Treatment o Spider naevus
 Non-surgical o Campbell de Morgan spot
o Can be left alone as it is benign
 Surgical – for cosmetic reasons, etc. Strawberry Cambell de
o Superficial shaving (lies above level of normal epidermis) Port-Wine Stain Spider Naevi
Naevus Morgan Spot
o Cautery Inspection
Lips, face, Trunk (both
Upper torso, head
Head & Neck mucous sides) – upper >
and neck
Site (can be membranes of lower
(drainage of
anywhere) mouth, shoulders, Occasionally on
SVC)
neck, buttock limbs
Usually
Number May be multiple Usually single Usually multiple
multiple
Bright red / dark Dark red / deep
Colour Purple-red Bright red
red purple
Variable; 1-10
Size Variable Variable; few mm 1-3 mm
cm
Edge Well-defined Well-defined – Well-defined
Sessile →
Circular, may
Shape pedunculated as Variable Variable
be raised
they grow larger
 May have small May have dilated corresponding • Associated with drops of sealing
Skin areas of subcutaneous haemangioma in pregnancy, wax
– –
Changes ulceration with veins around brain – chronic liver • No clinical
scabs lesion contralateral focal disease (> 5) – significance
Palpation fits request for
• Irregular • Found in limbs abdominal
• Covered with when a/w examination
Surface Smooth – Smooth Klippel-
smooth, pitted
epithelium Tranaunay
Consiste Syndrome
• Soft – – –
ncy
Mobility Mobile – – –
Relation
Confined to skin – – –
s
• Compressible: Pictures
pressure
squeezes mass,
Special • Compressible,
leaves it – –
Tests fade completely
collapsed:
slowly refills
• Not pulsatile
Background Information Also
Strawberry Cambell de  Telangiectasias
Port-Wine Stain Spider Naevi o Dilatation of normal capillaries
Naevus Morgan Spot
Infants Infants Middle-age → o Can be secondary to irradiation
Age – o Can be part of hereditary haemorrhagic telangiectasia (Osler-Rendu-
(congenital) (congenital) elderly
Weber syndrome)
Gender ♂=♀ – – –
 Autosomal dominant disease
• Cosmesis  Overt and occult haemorrhage can present as haematuria,
• Cosmesis
Sympto • May ulcerate, • Cosmesis
• Bleeding may – haematemesis, melaena, epistaxis, iron-deficiency anaemia
ms bleed if • Non-tender
occur  Vin rosé patch
traumatised
o Congenital intradermal vascular abnormality
• Diminishes • Branches fade
Pressur • Collapses on o Mild dilatation of vessels in sub-papillary dermal plexus
colour but doesn‘t when arteriole • Fade slightly
e pressure
revert to normal compressed
o Can occur anywhere, gives skin pale-pink colour
• Extensive • Form of • Formed by
o Associated with other vascular abnormalities (e.g. haemangiomata, AV
intradermal telangiectasia collection of fistulae, lymphoedema)
haemangioma • Dilated skin dilated o Usually not disfiguring
• Regress
• Present from arteriole feeding capillaries fed
Remark spontaneously
birth, does not small branches by single / small
s (few months – 3
change in size (leaving it cluster of
years)
• Sturge-Weber radially) arterioles
syndrome: facial • Increase in • Have
PWS with number appearance of

140
141
PYOGENIC GRANULOMA Background Information – Neither pyogenic nor a granuloma!
Inspection  Rapidly-growing capillary haemangioma, usually less then 1 cm
 Single; usu < 1 cm, bright red  Occur commonly after injury:
o May be blood-encrusted or Ulceration o Small capillary loops develop in healing wound, form granulation
 Hemispherical; may be sessile / pedunculated tissue
 Likely sites to be injured, e.g. hands, face o When capillary loops grow too vigorously, form protruding mass,
 Bright red; long-standing lesions may be skin-coloured epithelisation
 May have sinuses, associated serous / purulent discharge, Erythema / cellulitis o Mass form called pyogenic granuloma (surface often ulcerated,
infected)
Palpation – request to palpate: may bleed easily Clinical features
 May be slightly tender  Uncommon in children
o May bleed easily on palpation  May have history of minor injury, chronic infection (e.g. paronychia)
 Rapidly-growing lump on skin,
 Well-defined edges
 Bleeds easily, discharges serous / purulent fluid
 Soft, fleshy consistency
o Bleeding, pain stops once lump epithelises
 Confined to skin
 Once nodule is completely covered, begins to shrink (rarely disappears completely)
 Slightly compressible (vascular origin)
Treatment
Request  Surgical
 Take history for previous injury oCurettage with diathermy of the base
 Rate of growth of lump? (rapid growth in few days) oComplete excision biopsy
 (if recurrent; malignancy e.g. amelanotic melanoma has to be
“Mr. X is a young Chinese gentleman…” excluded)
“On inspection, there is a single hemispherical lump over the thenar eminence of  Non-surgical
the right hand” o Regression is uncommon: surgical treatment best option
“It measures about 0.8 cm in diameter, with clearly-defined margins” o Silver nitrate cautery is possible
“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‖
PAPILLOMA (skin tags / fibroepithelial polyps) Background Information
Inspection  An overgrowth of all layers of the skin with central vascular core
 Single / multiple  Not a neoplasm, but a hamartoma (skin tag is a more accurate term)
 Variable: from raised plaque to pedunculated polyp  Increasingly common with age – may be congenital
 Site: Neck, trunk, face, anus (anywhere on skin)
 Variable
 Flesh-coloured Clinical features
 Catches on cloths, rubs against other body parts
Palpation  May resemble carcinoma if granulation is excessive
 Not warm, non-tender  Complications:
o May become red, swollen, and ulcerate
 Variable: smooth to papilliferous
o May become infarcted if injured
 Soft, not compressible
o May be infected (contains all skin components – sebaceous glands, etc.)
 Arises from skin

Request
Treatment
 Similar lumps elsewhere  Excision – diathermy, scissors
 Ask for associated conditions: pregnancy, diabetes, intestinal polyposis o Bleeding from central vascular core controlled using single suture /
diathermy

“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”

142
143
KERATOACANTHOMA (adenoma sebaceum, molluscum pseudo-carcinomatosum)  Hypertrophic scar
Inspection o any age – common 8-20 years, ♂=♀, all races
 Often found on face o Excessive amount of fibrous tissue, but confined to scar (between skin
 Usually solitary;1 – 2 cm in diameter edges)
 Hemispherical or conical, with central crater o Located across flexor surfaces, skin creases
 Normal skin colour o Common, especially if infection / excessive tension
o Only enlarge for 2-3 months, then regress spontaneuosly
Palpation o Do not recur if excised and causative factor eliminated
 Firm and rubbery (central core is hard)
 Confined to skin, freely mobile over subcutaneous tissues  Keloid scar
o puberty to 30 years, ♀>♂, black, hispanic more likely
Background information o Hypertrophy and overgrowth extend beyond original wound
 Benign overgrowth of hair follicle cells with a central plug of keratin o Located at earlobes, chin, neck, shoulder, chest
 Occur in adults o Due to local release of fibroblast growth factors
 complain of rapidly-growing lump in skin o Continue to enlarge 6-12/12 after initial injury
 Not painful, but can be unsightly o May be tender, unsightly
 Takes 2 – 4 weeks to grow, regresses in 2 – 3 months o Will recur unless special measures taken
o Central slough appears,
o surrounding skin retracts to form puckered scar  Treatment (recurrence can be as high as 55%)
 Cause is unknown (may be self-limiting benign neoplasm or post-viral infection) o Non-surgical: mechanical pressure therapy – topical silicone gel sheets
 Treatment: (day and night for 1 year), Intralesional steroid, LA injections: e.g.
o Conservative if asymptomatic triamcinolone with lignocaine
o Surgical excision of lesion with histology to r/o SqCC o Surgical: revision of scar by direct suturing, skin grafting (avoid excessive
tension)

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
KAPOSI’S SARCOMA FIBROSARCOMA

Inspection Inspection
 Purple papules and plaques  Single; Usually limbs (but can be anywhere)
 Solitary, but usually multiple  Spherical or hemispherical
 Site: limbs, mouth, tip of nose/ palate or anywhere on the skin or mucosa  If large, vascular: may make skin shiny & pink
 May have
Request to take a history of previous transplantation or current underlying o Sinuses & Discharge
immunocompromise. o Ulceration
o Erythema / cellulitis
Background information
 Derived from capillary endothelial cells or from fibrous tisse Palpation
 Linked to HHV-8  Usually feel warmer (abnormal blood supply)
 Types:  May be tender
o Classic Kaposi‘s Sarcoma  Smooth surface (may be bosselated – covered with knobs)
 Confined to skin of lower limbs of elderly Jews  Well-defined margins (indistinct if fast-growing, invasive)
 Not fatal  Firm / hard consistency (rarely stony hard; do not ossify)
o AIDS associated Kaposi‘s Sarcoma  Usually fixed
 AIDS defining; Found in 1/3 of AIDS patients  May pulsate, have audible bruit, palpable thrill (may be very vascular)
 1/3 develops a 2nd malignancy e.g. leukaemia/ lymphoma
o Endemic (African) Kaposi‘s Sarcoma Request to test for distal neurological status (for invasion of nerve)
 Aggressive and invasive fatal tumour
 Good response to chemotherapy Background Information
o Transplation- associated Kaposi‘s Sarcoma  Fibrosarcoma is one of the commonest mesodermal soft tissue malignant tumours
 Following high dose immunosuppressive therapy o Pure benign fibroma is very rare
 Often regress when treatment is ended  History
o More common in elderly (but can occur any age)
Treatment o Common complaints
 Conservative if asymptomatic. Start anti-retrovirals if HIV +ve  Growth: disfigurement, interference with ROM
 Surgical: local radiotherapy amd chemotherapy (IFN- alpha, doxorubicin,  Pain
intralesional vinblastine)  Weakness (infiltration of other structures)
 General debility
 Prognosis: generally good

144
145
PYODERMA GANGRENOSUM RADIOTHERAPY MARKS

Inspect Vital points on examination:

 Ulcer with a necrotis base  Of the underlying disease:
 Irregular bluish red overhanging edges o Cachexia,
 a/w surrounding erythematous plaques with pustules o masectomy scar/ wide excision scar  suggest breast cancer
o obvious skin cancer,
Request to examine for evidence of inflammatory bowel disease, RA o clubbing & other signs of chest disease  suggest lung cancer
o suprapubic mass  suggest pelvic tumour
Backgound information o neck swellings with cranial nerve palsies  head and neck tumour
 more common in males  of the radiotherapy:
 pyoderma gangrenosum is associated with: o site of radiation
o IBD o shape: usually well defined borders
o RA o features of active RT:
o Myeloproliferative disorders: PRV, myeloma  Indian ink marks, skin markings
o Autoimmune hepatitis  Erythema, desquamation
 Differential diagnosis: o Features of previous RT:
o Autoimmune: rheumatoid vasculitis  Telangiectasia, hyperpigmentation
o Infectious: tertiary syphilis, amoebiasis  Complications of radiotherapy:
o Iatrogenic: warfarin necrosis o Depends of site
o Others: Behcet‘s disease o Look for future cancers:
 Treatment:  Haematogenous malignancy
o Non-surgical: treat underlying condition, saline cleansing, high dose oral or  Thyroid cancers
intralesional steroids. KIV cyclosporine & antibiotics  Breast cancers
o Surgical: serial allograft followed by autologous skin graft or muscle flap
coverage when necessary
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 ASCITES
 GI: diarrhea Vital signs on examination:
o Late: o Abdominal distension
 Skin changes o Flank dullness  shifting dullness  fluid thrill
 Heart: IHD o Peripheral stigmata of chronic liver disease and portal HPT
 Lung: pneumonitis, pulmonary fibrosis o Other signs of fluid overload: LL, sacral oedema, bibasal crepitations
 Bld vssl: radiation arteritis, esp to carotids  necrosis, distal o Signs of malignancy
ischaemia and vssl rupture
 CNS: spinal cord myelopathy Background information
 Uro: bladder fibrosis, Renal impairment (depletion of tubular  Causes of ascites:
cells) Transudate (<30g/L protein) Exudative (>30g/L)
 Abdo: IO 2o to strictures & adhesions, Cardiac: CCF, RHF, TR, constrictive Cirrhosis
 Genital: infertility pericarditis
 Endocrine: hypothyroidism Abdo: CLD Malignancy
 Eye: cataracts Renal: ESRF, nephrotic syndrome Infective causes: TB
 Increase incidence of future cancers: GIT: protein losing enteropathy Chylous ascites
 Haematogenous malignancy, e.g. leukemia
 Solid tumours: Thyroid cancers  Role of peritoneal tap:
 Breast cancers o diagnostic and therapeutic
 Minimalising of side effects of radiotherapy:  Send fluid for FEME, protein, microbiology, cytology
o Lead shields to eyes, gonads and thyroid  Relieve of discomfort & diaphragm splinting from distension
o Dose fractionation (to allow recovery of normal cells) o Indications:
o Prior chemotherapy (increase sensitivity of tumour cells)  Failed medical treatment
o Regional hypothermia  symptomatic
o Radiolabelled antibody to deliver local radiation to tumour 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 surgery (TIPSS, peritoneovenous shunt [silastic catheter],
Denver shunt when with a subcutaneous pump]

146
147
SHOCK Management
General Mx
Definition – inadequate tissue and organ perfusion leading to a hypoperfusion state & Airway  Maintain airway – consider intubation if necessary
eventual cellular hypoxia and its attendant sequelae. Breathing  100% O2 via non-rebreather mask
Circulation  2 large bore (14-16G) cannulae
S/S: Hypotension, urine output, tachycardia, diaphoresis, AMS   Inotropic support
o IV dopamine 5-10g/kg/min
Types of Shock o IV dobutamine 5-10g/kg/min (esp for cardiogenic
‗White‘ shock ‗Red‘ shock shock)
Types Hypovolaemic Cardiogenic Neurogenic Septic Anaphylactic o IV norepinephrine 5-20g/kg/min (esp for septic
shock)
Causes Haemorrhage AMI Spinal Infxns Monitoring  Pulse oximetry
Burns Dysrhythmia injury  ECG
Ruptured  BP
ectopic  Heart rate
pregnancy  Urine output – catheterize patient
Severe GE
Acute
pancreatitis
Hypovolaemic Shock
S/S Pallor Pallor Warm skin Fever, Fever, rigors Invxs  FBC - Hct in acute alcoholic binge due to diuresis. Hct is an
Cold clammy Cold clammy N/ heart rigors Warm skin
Inaccurate marker of bld loss acutely.
skin skin rate Warm
 GXM 6 units
peri vas  peri vas  Neuro skin
 U/E/Cr
deficit  Troponin T & Cardiac enzymes
 Coagulation profile with DIVC screen (PT/PTT, pltlet, D-
Invxs  Hct (late) Cardiac FBC dimer)
enzymes Bld C/S  ABG – metab acidosis, lactate, base deficits are poor Px
ECG factors
Also, Obstructive Shock due to tension pneumothorax, cardiac tamponade or pulmonary  UPT - ?ectopic pregnancy? Ask for LMP
embolism  Examine abdomen for pulsatile AAA
Fluid Rx  1 L crystalloid fast infusion w/in 1 hr
 Assess response
 Subsequent colloid or whole blood infusion
 CVP line  Used to guide fluid Rx, esp in CCF patients

Cardiogenic Shock
ECG  Manage accordingly – refer acute coronary
Trop T & cardiac syndrome & ACLS notes
enzymes
Neurogenic Shock o non-specific ST depression & T wave inversion
Hx/PE  Trauma – site, mechanism, force o Sinus tachycardia
 Neuro exam, DRE – document initial neurological deficits o Right heart strain
Immobilize  Immobilize spine in neutral position  Right axis deviation
Invxs  C-spine X-ray (AP & lat) – ensure visualization up to C7/T1  Transient RBBB
junction  T wave inversion in V1-3
  Swimmer‘s view (visualize C7/T1 jn) & open mouth view  P pulmonale
(visualize C1/2 injury)  S1Q3T3
 Thoracic & lumbar spine X-ray (AP & lat) o Exclude DDxes – MI, pericarditis
  CT scan  CXR (may be normal)
o Westermark sign – oligaemic lung fields
  MRI later
o Pul infarcts – wedge shape opacities w apex
Fluid Rx  Titrate fluid resus with urine output pointing towards the hilum
  vasopressors if BP does not respond to fluid challenge o Atelectasis
 IV methyl  30 mg/kg over 15mins, followed by 5.4mg/kg/h for nxt 23 hrs o Pleural effusions
prednisolone  Indications – non-penetrating spinal cord injury & w/in 8 hrs of o Raised diaphragm
injury o Consolidation
 Contraindications o ‗Plump‘ pul. arteries
o <13YO o Exclude DDxes – pneumothorax, pneumonia, L
o pregnancy heart failure, tumour, rib #, massive pleural
o mild injury of the cauda equina / nerve root effusion, lobar collapse
o abdominal trauma present   Spiral CT, Echo, MRI, lung scintigraphy, pulmonary
o major life-threatening morbidity angiogram (gold std)
Disposition  Refer Ortho / NeuroSx
Rx
 Pain relieve – use Opioids with caution
 Fluid Rx & inotropic support if haemodynamically unstable
Obstructive Shock  Anticoagulation Rx:
Tension  Decompression: insert 14G cannula over 2nd intercostals space o IV heparin 5000U bolus or SC fraxiparine (0.4ml
Pneumothorax in mid-clav. Line if <50kg; 0.5ml if 50-65kg; 0.6ml if >65kg)
Cardiac  IV fluid bolus 500ml N/S o Convert to Oral warfarin later
tamponade   IV dopamine infusion 5g/kg/min   Thrombolysis
 Prepare for pericardiocentesis o Intra pul. arterial urokinase fro 12-24 hrs
Pul Embolism Invx  Surgical
 FBC o Complete IVC ligation or partial caval interruption
 GXM 6 units
 U/E/Cr Septic Shock (SIRS + source of sepsis + shock)
 DIVC screen (D-dimer) SIRS =  2 of the following present:
 ABG o Temp >38 or <36oC
o  PaO2 & N/ PaCO2 o HR > 90bpm
o widened alveolo-arterial P02 gradient (AaPO2 o RR > 20 breaths/min OR PaCO2<32mmHg
>20mmHg) o WCC>12000/mm3, <4000/mm3,or >10% immature forms
 ECG (may be normal)
148
149
Hx / PE  Identify site of infxn – UTI (indwelling cathether), gallbladder dz,  Anaphylactoid rxn – resembles anaphylactic rxn, but due to direct histamine
peritonitis, pneumonia, appendicitis, immunocompromised state release from mast cells w/o need for prior sensitization
Invx  FBC -  TW
 U/E/Cr Common causes
 DIVC screen – PT/PTT, pltlet, fibrinogen, D-dimer  Drugs – penicililns & NSAIDS commonest, aspirin, TCM, sulpha drugs
 Bld C/S (2 different sites)  Food – shellfish, egg white, peanuts
 Capillary bld glucose  Venoms – bees, wasps, hornets
 ABG  Environment – dust, pollen
 CXR – pneumonia, ARDS  Infections – EBV, HBV, coxsackie virus, parasites
 ECG Stop Pptant  Stop administration of suspected agent / flick out insect stinger
 Urine dipstick – UTI with tongue blade
 Urine C/S  Gastric lavage & activated charcoal if drug was ingested
Fluid Rx  Rapid infusion 1-2L crystalloids Airway  Prepare for intubation or cricothyroidectomy – ENT/Anaesthesia
  CVP line insertion consult
 Inotropic  if no response to fluid Rx Fluid Rx  2L Hartman‘s or N/S bolus
support  Noradrenaline (drug of choice) - 1g/kg/min OR Drug Rx Adrenaline  Normotensive – 0.01ml/kg (max 0.5ml)
 Dopamin 5-20g/kg/min 1:1000 dilution SC/IM
Empirical Immunocompetent w/o  3rd gen cephalosporin (IV  Hypotensive – 0.1ml/kg (max 5ml) 1:10,000
ABx obvious source ceftriaxone 1g) OR dilution IV over 5 mins
 Quinolones (ciprofloxacin Glucagon  Indications: failure of adrenaline Rx OR if
200mg) adrenaline is contraindicated eg IHD, severe
Immunocompromised w/o  Anti-pseudomonal ABx (IV HPT, pregnancy, -blocker use
obvious source ceftazidime 1g) OR  0.5-1.0mg IV/IM. Can be repeated once after
 Quinolone 30mins
 PLUS aminoglycoside Antihistamines  Diphenhydramine 25mg IM/IV
(Gentamicin 80mg)  Chlorpheniramine 10mg IM/IV
Gram-positive (burns, FB /  IV cefazolin 2g  Promethazine 25mg IM/IV
lines present)  IV vancomycin 1g if hx of Cimetidine  For persistent symptoms unresponsive to
IVDA, indwelling cath. Or above Rx
penicillin allergy  200-400mg IV bolus
Anaerobic source (intra-  IV metronidazole 500mg + Nebulised  for persistent bronchospasm
abdo, biliary, female genital ceftriazone 1g + IV gentamicin bronchodilator  Salbutamol 2:2 q20-30mins
tract, aspiration pneumonia) 80mg Corticosteroids  Hydrocortisone 200-300mg IV bolus, q 6hr

Anaphylactic Shock
Definitions
 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
150
151
CAUSES of LOWER GIT BLEEDING  Colitis
1) Colon -
Infective: any fever/chills/rigors, night sweats, N/V, diarrhoea,
 Bleeding diverticulosis pain, recent travel/contact history, eating seafood, previous TB
 Angiodysplasia exposure or infection, BCG vaccination status
 Colorectal carcinoma, polyps - Inflammatory: ask about history of UC or Crohn‘s, joint, liver,
 Colitis eye & skin manifestations
- Infective (gastroenteritis, diverticulitis, colorectal TB) - Ischaemic: ask about atherosclerotic risk factors, previous AMI,
- Inflammatory (UC & Crohn‘s) stroke
- Ischaemic  Hemorrhoids
2) Ileum: Meckel‘s diverticulum - usually dark red blood - bleeding to passing motion, blood coating stool, pain
3) Anorectal junction: hemorrhoids - Any mass noticed at anus
4) Anus: anal fissure - History of constipation, hard stools, low fibre diet, chronic
5) Massive Upper GIT bleeding, e.g. bleeding DU straining, recent pregnancy
 Coagulopathy
- Any history of bleeding disorders, easily bleeding, petechiae

3) Complications
HISTORY (if patient is stable)  Symptoms of anemia (may be only presentation!): SOB, postural giddiness,
1) Nature of bleeding palpitations, chest pain, ↓ effort tolerance, fatigue, syncope
 Haematochezia  Symptoms of dehydration & shock: extreme thirst, confusion, pallor, ↓ urine
- Mixed with or coating stool output
- Torrential or drops, any clots? – Brisk upper GI bleed can present  May have complication of AMI if old patient with history of IHD
as haematochezia
- Bright red (lower) or darker red (higher) PHYSICAL EXAMINATION
- Any mucous 1. Vitals:
 Malaena - HR, supine & postural BP –stable? urine output (if catheter in-situ),
- Altered blood, indicates bleeding from upper GIT above - Any fever?
ligament of Treitz (duodeno-jejunal junction) 2. General inspection:
- Ask for history as per UBGIT - pallor,
- confusion?
2) Aetiological clues 3. Peripheries:
 Exclude upper GIT cause - signs of dehydration e.g. capillary refill, dry tongue.
- Any malaena, hematemesis, coffee grounds vomitus - Any supraclavicular lymph nodes?
- History of PUD, gastritis, varices, Ca stomach, Mallory-Weiss - Any skin manifestations of inflammatory bowel disease?
tear, risk factors for each - Stigmata of CLD?
 Bleeding diverticulosis/angiodysplasia 4. Abdomen:
- Usually torrential bleeding that stops spontaneously; altered clots - Scars? Any palpable masses
- History of previous bleeding episodes 5. DRE:
 Colorectal carcinoma - any anal fissures or prolapsed hemorrhoids seen,
- Constitutional symptoms: LOW, LOA, fatigue - any masses felt,
- Change in bowel habits, tenesmus - any fresh blood or malaena
- Symptoms of anaemia (chronic occult bleed) 6. Offer proctoscopy to look for internal haemorrhoids
- Previous history/family history of GIT or ovarian cancer
ACUTE MANAGEMENT o Labelled RBC isotope scan under gamma camera
Resuscitation - For intermittent, occult bleeds not detectable on mesenteric angiogram
o Supplemental oxygen, insert 2 large-bore IV cannula with fast infusion of - Not for urgent setting; can take up to 24 hours!
crystalloids (N/S 500ml over ½hr) o Laparotomy with saline lavage if massive on going bleed, recurrent bleeding
o Infuse colloids if ongoing blood loss while waiting for whole blood (GXM) - On table scope to transilluminate bowel & identify bleeding source
o Catheterise and monitor urine output, insert NGT on suction to detect UBGIT - On table angiogram
o Continuous vital signs monitoring & I/O charting ± CVP & stool chart - Oversewing of bleeding vessel, partial/total colectomy as last resort
o ECG + cardiac enzymes to detect possible AMI
o Take blood for investigations HEMORRHOIDS
- FBC: low Hb level (repeat FBC 2-3 hours later or when necessary) –  External hemorrhoids: not true hemorrhoids, but rather painful thrombosed
packed cell transfusion veins arising distal to the dentate line
 4 pint PCT: give FFP to prevent over-dilution of clotting  Internal hemorrhoids: those arising proximal to the dentate line, usually
factors painless unless prolapsed & strangulated
- UECr: hydration status, any acute renal failure from shock, electrolyte
imbalance – replace Banov grading of internal hemorrhoids
- PT/PTT: must correct coagulopathy before trying to stop bleeding – Grade Description Treatment
fresh frozen plasma I The hemorrhoids do not prolapse Rubber band ligation
- LFT: exclude bleeding varices II Hemorrhoids prolapse on BO but
- ABG: may have metabolic acidosis in shock due to organ ischaemia – spontaneously reduce
IV bicarb, dialysis if severe III Hemorrhoids prolapse on BO & must be Staple hemorrhoidectomy
- GXM 4 pints manually reduced
IV Hemorrhoids are prolapsed and cannot be Excision (due to high
Identify source & stop bleeding reduced reccurence)
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 INFLAMMATORY BOWEL DISEASE
bleeding vessel Crohn’s Ulcerative colitis
o Double contrast barium enema: good for picking up diverticulum which may be Bowel Can affect entire GIT Usually begins in the rectum and can
missed on scope involvement anywhere from mouth to extend proximally to affect entire
o Mesenteric angiogram or CT mesenteric angiogram anus, but usually affecting colon
- More precise; can cannulate all 3 main trunks & their branches the terminal ileum
- Diagnostic: shows blush in active bleeding, shows ↓ perfusion of
Location  40% terminal ileum  40% rectum alone
ischaemic bowel
- Therapeutic (not for CT): embolisation/sclerotherapy for  30% small intestine  40% left colon
angiodysplasia, beware of causing bowel ischaemia (use foam medium)  30% colon  20% total colitis
o Capsule Endoscopy:  3% anorectal (usu.
- for stable patients with suspected SI bleed & unable to swallow spared)
- takes 36hrs to read the results, but unable to localise the site & Continuity Not continuous, with skip Longitudinal mucosal continuity
intervene lesions
o double balloon enteroscope: Complications Strictures, fistulae, sinuses, These complications absent
- only for suspected proximal SI malnutrition (SB
- able to do therapeutic manoeuvres involvement)

152
153
Histopathology Macoscopic: bowel is thick- Macroscopic: granular appearance of Differential diagnoses
walled & nodular mucosa , loss of vascular markings, 1) Gastroenteritis: exclude with stool microscopy & culture
(cobblestone appearance) pseudopolyps interspersed with areas - Bacterial: E. coli, Campylobacter, Salmonella, Shigella, C. difficile
with creeping fat, mesenteric of shallow ulceration - Parasitic: E. histolytica
thickening & deep linear Microscopic: only mucosal & - Viral: rotavirus
ulcers submucosal involvement, crypt 2) Other infective causes: diverticulitis, colorectal TB
Microscopic: transmural abscesses 3) Ischaemic colitis
involvement, non-caseating - Muscularis propria & serosa may be 4) Bleeding diverticulosis
granulomas (pathognomonic, affected in fulminant disease 5) Colorectal carcinoma
but only present in 2/3)
Risk of Slight increased risk of Substantially higher risk of colorectal
carcinoma colorectal Ca, increased risk Ca
of small bowel lymphoma  2% at 10 years CROHN’S DISEASE
 8% at 20 years
 18% at 30 years P/E: RIF mass, enlarged skin tags, anal stricture
 Much higher risk with
concomitant PSC Investigations: supportive (see UC) & diagnostic
Associated ASCA: anti-saccharomyces p-ANCA: perinuclear antineutrophil
antibodies cerevisiae antibodies cytoplastic antibodies Diagnostic
Severity Harvey Bradshaw severity Modified Truelove & Witts severity  Contrast radiographic studies: assess location & extent of disease, look for
index index strictures & fistulae
(Mild, moderate, severe, fulminant) o Barium studies: small bowel series & enema
o CT scan with oral & IV contrast
Epidemiology
 Bimodal distribution: affects young in the 2nd & 3rd decades of life, with second  Endoscopy: look for typical features
onset in the 5th & 6th decades of life o Colonosopy with tissue biopsy (non-caseating granulomas)
o OGD: upper GIT involvement
 Equal gender predominance
o Endoanal U/S: identify fistula tracts
 Higher prevalence amongst Ashkenazi Jews & in cooler climates e.g.
Management
Scandinavia, UK, Germany, northern USA
 Medical (principle treatment)
 Genetic association
o Nutritional support e.g. TPN (may also aid closure of fistulae)
o Pharmacological
History
 Corticosteroids for acute exacerbation of disease, but not for long
 GIT: abdominal pain, diarrhea, N/V, bloating, distention, bloody stools with term use
mucous & pus  1st line: sulfasalazine, mesalazine (5-ASA or 5-aminosalicylic acid)
 Crohn‘s fistula: colovesical fistula or coloovarian fistula: faeces in urine/ induce & maintain remission of disease: oral, rectal suppository or
pneumaturia, faeces per vaginal/ PID enema (up to splenic flexure)
 Non-specific systemic: LOW, LOA, fever, fatigue, symptoms of anemia,  2nd line: immunosuppressive agents e.g. azathioprine, 6-MP, MTX
chronic malnutrition & cyclosporine when 1st line agents ineffective
 Specific extra-intestinal manifestations  Biologics: Remicade (infliximab), a TNF blocker
- Require close surveillance for SE (blood disorders,
Physical examination: usually normal +/- extra-intestinal manifestations infections, lymphoma & solid tissue cancers, hepatotoxicity,
drug-induced lupus, demyelinating disorders)
  Surgical o Pyoderma gangrenosum: deep ulceration with violaceous border that
o Principles overhangs ulcer bed, usually affecting LL
 Avoid surgery until absolutely necessary (80% require surgery o Erythema nodosum: poorly defined, tender, erythematous nodules that
within 20 years of onset) & when indicated perform bowel do not ulcerate or suppurate, usually on the shin
preserving surgery as repeated bowel resections can lead to short o Tx: corticosteroids, will improve slowly following colectomy
gut syndrome Investigations
o Indications : Supportive (looking for complications & assessing severity of disease)
 Blood tests
 Disease refractory to medical therapy  Fistulae
o FBC: anemia, leukocytosis & thrombocytosis indicate more severe
 Serious complications of medical therapy  Abscesses
disease
 Severe bleeding, perforation  Toxic megacolon
o UECr: hypokalemia & dehydration in prolonged diarrhoea
 Intestinal obstruction due to strictures  Malignancy
o LFT: hypoalbuminemia due to poor nutritional intake
o Procedure (laparoscopic or open) o CRP, ESR: markers of severity
 CT abdomen for pre-operative percutaneous drainage of abcesses (↓ o Autoantibody assay: p-ANCA ↑ in UC, ASCA ↑ in CD
inflammation & risk of sepsis)  Radiological
 Small bowel: (bowel preservation is key) o AXR to evaluate colonic caliber (>6 cm is abnormal)
- Short segment disease: stricturoplasty o CXR to rule out perforation (risk of perforation in acute disease)
- Long segment disease: long stricturoplasty or resection Diagnostic
- Fistula: resect diseased bowel & repair involved organ  Endoscopy: look for typical features
 Large bowel: o Flexible sigmoidoscopy with tissue biopsy: bleeding may occur with
- Total colectomy + ileorectal anastamosis (if rectum spared) contact with scope
or proctocolectomy + end ileostomy (if rectum affected) Management
- Segmental colectomy only in selected cases as high  Medical: similar to Crohn‘s disease
recurrence rate  Surgical (25% eventually require surgery)
 Perianal disease: o Indications :
- Setons, fistulotomy, proctectomy in severe disease o Disease refractory to medical therapy with severe & extensive
colitis
ULCERATIVE COLITIS o Serious complications of medical therapy
Extra-intestinal manifestations (20% of patients) o Severe bleeding
 Joints (most common) o Perforation
o Transient asymmetrical polyarthritis: mirrors course of colitis & is o Toxic megacolon (colon > 6cm)
cured by colectomy o Malignancy
o Ankylosing spondylitis o Procedure (laparoscopic or open)
o Isolated sacroiliitis  Acute setting: total colectomy with end ileostomy: diseased rectum
 Liver left in-situ with resection & IPAA at later date when patient has
o PSC (5%): fibrous structuring of entire biliary tree: ↑ ALP, MRCP, regained health & steroids have been withdrawn. Foley catheter
ERCP, liver biopsy. Tx: stenting, transplant used to decompress rectum for 3-4 days
o Hepatic failure over 5-10 years independent of course of colitis  IPAA (ileo-pouch anal anastamosis): standard of care for patients
o ↑ risk of cholangiocarcinoma & ↑↑↑ risk of colorectal carcinoma with UC who ultimately require colectomy. Avoid necessity for
 Eye long term stoma. Crohn‘s disease remains an absolute
o Iritis, episcleritis, anterior uvetitis. Tx: topical and/or oral contradindication as overall failure rates approach 50%
corticosteroids  Total proctocolectomy with end ileostomy
 Skin
154
155
Causes of Jaundice

Pre-hepatic Hepatic Cholestatic

o Urine/stools normal o Mixed signs; urine may be dark with normal stools o Tea-colored urine, pale stools, intense pruritis
o May have symptoms of anemia o Variable liver biochemistry o Conjugated hyperbilirubinemia
o Unconjugated hyperbilirubinemia o ↑ ALT, AST disproportionate to ALP, GGT o ↑ ALP, GGT disproportionate to ALT, AST
o ↑ LDH, ↓ haptoglobin o ↓ Albumin, prolonged INR (cirrhosis) o Do abdominal U/S
o PBF o AFP: exclude complication of malignancy  If ducts dilated (>8mm), do ERCP/MRCP/PTC
o Direct Coomb‘s test for autoimmune o Viral hepatitis serology  If ducts not dilated, further serologic testing:
hemolytic anemia  Acute: Anti-HBc IgM, Anti-HAV IgM AMA (M2-IgG most specific for PBC), p-ANCA
o Stool OCP (ova, cysts, parasites) malaria  Chronic: HBsAg, anti-HCV, HCV RNA (PSC), ANA & anti-SMA. Consider ERCP, liver
biopsy
Hemolytic anemias: o Autoimmune screen
1) Inherited  ANA, anti-dsDNA, AMA
 Thalassemia o Metabolic screen 1) Intraluminal
 G6DP  Caeruloplasmin, 24 hour urine copper  Gallstones (painful)
 Spherocytosis o Do abdominal U/S: surface nodularity & ↑ echogenicity in  Parasites: Ascaris lumbricoides, schistosomiasis
 Sickle-cell anemia cirrhosis, also look for signs of portal HTN (splenomegaly & 2) Mural
2) Acquired ascites)  Biliary strictures post ERCP
 Infective: malaria  Biliary strictures from gallstones, chronic
 Autoimmune: SLE, Evan‘s syndrome 1) Infective pancreatitis
 Hemolytic uremic syndrome (hemolytic  Acute viral hepatitis (HBV, HAV)  PBC (intrahepatic bile ducts): middle aged ♀
anemia, ARF & thrombocytopaenia)  EBV, CMV  PSC (intra & extrahepatic): ♂ with IBD esp. UC
 TB  Cholangitis (Charcot‘s triad)
2) Liver cirrhosis/chronic liver disease  Choledochal cyst (type I-V)
 Alcoholic liver disease  Distal cholangiocarcinoma
 Chronic viral hepatitis (HBV, HCV) 3) Extraluminal
 Metabolic (Wilson‘s, hematochromatosis)  Ca head of pancreas (painless, w distended GB)
 Infiltrative (Sarcoidosis, amyloidosis)  Other peri-ampullary Ca (cholangio, dudeno,
3) Hepatotoxic drugs ampullary)
 Alcohol, paracetamol, TCM, isoniazid, augmentin,  Mirrizi‘s syndrome (chronic cholecystitis)
MTX, phenytoin, corticosteroids 4) Others:
4) Autoimmune hepatitis  Biliary atresia
 SLE  Drug-induced: paracetamol, penicillins,
5) Inherited ↓/absent activity of UGT (unconjugated corticosteroids
hyperbilirubinemia)
 Gilbert‘s syndrome
 Crigler Najjar 1 & 2
6) Inherited impaired biliary excretion (conjugated
hyperbilirubinemia)
 Dubin-Johnson syndrome
 Rotor syndrome
CHRONIC PANCREATITIS
Chronic, irreversible architectural disruption of the pancreas resulting in chronic
epigastric pain and pancreatic insufficiency
 MRCP: chain of lakes appearance of pancreatic duct (strictures and cystic
dilatations)

Causes:
- Alcholism,
- strictures (congenital, acquired),
- trauma,
- genetic (North Indians)

Complications:
 Local complications: persistent pseudocyst, fistulae, ascites
 Chronic pain
 Pancreatic insufficiency
o Type I DM
o Steatorrhoea, vitamin deficiency, malnutrition
 Pancreatic cancer

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

156
157
INTESTINAL OBSTRUCTION PHYSICAL EXAMINATION
Causes of IO  Vitals: Is patient stable? Any fever? (sepsis) Hypotension, tachycardia?
1. Mechanical (dehydration)
Intraluminal Mural Extraluminal
-Impacted stool -Tumours - Adhesions (post-op, Crohn‘s)  General inspection: Abdominal distension? Cachexia? Confusion?
-Gallstone ‗ileus‘ -Diverticular stricture - Herniae
-Foreign body -Intussusception - Volvulus  Peripheries: Look for signs of dehydration e.g. capillary refill, dry tongue
-Bezoars (phyto- -Crohn‘s strictures - Lymph node compression Palpate lymph nodes
tricho-) - RT strictures - Superior mesenteric artery syndrome
 Abdomen:
2. Functional (give rise to megacolon)  Any distension?
- Paralytic ileus (post-op, sepsis, ischaemic, metabolic, hypothyroidism, opiate-  Scars from previous abdominal surgery?
induced)  Visible peristalsis? – severe obstruction
- Hirschsprung‘s disease: absent ganglia in Auerbach‘s plexus  Any signs of peritonitis: guarding, rebound tenderness, or soft and NT
- Ogilvie syndrome : in severely ill patients  Any masses, herniae
 Bowel sounds:
Others: intestinal atresia  Initially hyperactive, later may be sluggish or absent
 Tinkling BS: small bowel obstruction
Small bowel IO Large bowel IO  Succussion splash + epigastric tenderness: gastric outlet obstruction
1) Adhesions 1) Cancer
2) Herniae 2) Post-diverticulitis stricuture  DRE: any masses felt, any stools?
3) Ileocecal tumour 3) Sigmoid volvulus
4) Intussussception ACUTE MANAGEMENT
o Resuscitate if necessary, monitor vitals
HISTORY - Urinary catheter: monitor output
4 cardinal symptoms o NBM: rest bowel + IV drip
1. Pain: o NG tube on constant suction
- Usually colicky, 4-5 days duration o Correct acidosis, replace K+ as guided by investigations
- Complete obstruction: constant, sharp pain o Start broad spectrum ABx [IO affects normal translocation of bacterial flora]
- Volvulus: sudden, severe pain o Rule out surgical emergencies (history/physical examination/investigations)
2. Vomiting: ask if projectile, bilious, or fecal stained 1. Obstructed abdominal hernia
3. Abdominal distention 2. Volvulus (sigmoid, caecal, stomach)
4. Constipation 3. Closed-loop obstruction (competent ileocecal valve)
- Ask about normal BO frequency 4. Ischaemic bowel with bowel necrosis
- Complete obstipation: cannot even pass flatus 5. Perforation/peritonitis
Other pertinent history
- Symptoms of GIT bleed, infection INVESTIGATIONS
- Previous surgeries Bloods
- Underlying GIT disorders Assess complications
- Recent change in bowel habit  FBC: any infection, anemia
- Risk factors for ischaemic bowel: atherosclerotic RH, heart disease, previous  UECr : any dehydration due to:
stroke - Intra-luminal 3rd space loss (damaged enterocytes unable to reabsorb)
- Suspicion of malignancy: LOW, LOA, previous Ca, FH of Ca - Vomiting (also assess K+ loss: can perpetuate paralytic ileus)
  ABG  Flexible sigmoidoscopic decompression with sigmoid colectomy &
- Acidosis from bowel ischaemia formation of double barrel colostomy (Paul-Mikulicz procedure) with future
- Alkalosis due to vomiting (more for pyloric stenosis in children) re-anastamosis
Pre-operative  Sigmoidopexy: fix sigmoid to posterior abdominal wall (rarely done as high
 GXM 4 pints of blood, PT/PTT risk of recurrence)
 Cardiac enzymes x2 sets (+ ECG)  Caecal volvulus: resection & re-anastamosis
 Gastric volvulus: gastropexy
Imaging 3) Closed loop obstruction (if due to distal tumour)
Assess complications  Resect bowel, primary anastamosis with proximal defunctioning colostomy
 Erect CXR : air under diaphragm, any aspiration pneumonia  Hartmann‘s/Paul-Mikulicz procedure if bowel is too inflamed/oedematous to
 AXR: Rigler‘s Sign (obvious bowel wall due to extra-luminal air) anastamose (high risk of leakage)
Diagnostic 4) Ischaemic bowel
 AXR  Bowel ischaemia alone can cause paralytic ileus, usually occurring in the
- Erect: air fluid levels (>6) splenic flexure (watershed area receiving blood from the most distal arterial
- Supine: look for small or large bowel dilatation on radiograph branches)
 Duodenum: C-shaped  Supportive management e.g. NBM, drip & suck, antibiotics while waiting
 Jejunum/proximal ileum: centrally located, stack of coins for collaterals to re-supply bowel, re-establish peristalsis
appearance (plicae circulares)  Surgical intervention if bowel is non-viable e.g. gangrenous or necrotic
 Distal ileum: plicae circulares disappears, lead-pipe appearance o Will have relook laprotomy in 2-3/7 to ensure good resection of
 Colon: incomplete bands (haustrations due to presence of teniae coli) bowel margins
- Sigmoid volvulus? Coffee bean + parrot‘s beak sign
5) Perforation (usually in caecum as it is thin walled)
- Closed loop obstruction? Distal lesion with v. distended cecum (thinnest
 Occurs due to ischaemia of stretched out bowel wall; >12cm dilated
wall; up to 12cm), ileum not dilated
 Emergency laparotomy: resect lesion & perforated bowel with generous
- Bowel ischaemia with necrosis? Gas in bowel wall (pneumatosis
peritoneal lavage
intestinalis) due to gas gangrene
 If lesion e.g. tumour is proximal enough to the cecum, can do extended right
- Gas present in rectum? No: complete obstruction (may require KUB film)
hemi-colectomy
 Barium enema  If lesion is distal, may require total-colectomy with ileo-rectal anastamosis
- Gastrografin preferable if risk of perforation; risk of barium  Continue antibiotics following surgery
peritonitis
- Upper GI barium studies contraindicated 6) Intussusception
 Colonoscopy done without bowel prep (not necessary, and also contraindicated,  Children: usually due to hypertrophic Peyer‘s patches. Administer barium
in IO) enema: watch intussception reduce on fluoroscopy
 CT colonography  Elderly: usually leading point present (polyp, Ca). Barium enema unlikely to
work, or if works recurrence rate is high, therefore surgery is 1st line
DEFINITIVE MANAGEMENT (Depends on cause) treatment
1) Obstructed abdominal hernia 7) Post-op paralytic ileus (>3 days post-op)
 Herniorrhapy  Supportive management: drip & suck, wait for peristalsis to restart
 Oral gastrografin: hyperosmotic, causes intraluminal osmosis , can re-
2) Sigmoid volvulus
 Ryle‘s tube decompression: establish peristalsis
- Gown up  Prokinetic agents: erythromycin, metaclopromide, cisapride
- Put end of Ryle‘s tube in a bottle submerged in water
- Insert lubricated Ryle‘s tube into anus

158
159
ACUTE APPENDICITIS INVESTIGATIONS
Blood: FBC, UECr, CRP, Blood culture, PT/PTT, GXM
HISTORY Urine: UFEME (may have pyuria & haematuria)
- Classic: LOA with periumbilical pain which radiates to the RIF, followed by Imaging: Erect CXR, CTAP, abdominal U/S
nausea & vomiting
- N/V almost always occurs after pain, if it precedes pain, exclude IO
- May have diarrhoea or constipation MANAGEMENT
- Inflamed appendix near bladder/ureter may cause irritative voiding symptoms - NBM, IV drip, IV antibiotics, correct electrolyte imbalance
& haematuria - Symptomatic relief: anti-emetics & analgesia
PHYSICAL EXAMINATION - Definitive treatment: appendicectomy (open or laparoscopic)
- RIF (McBurney‘s point) tenderness on percussion, rebound tenderness, rigidity
& guarding - Conservative treatment for appendiceal mass: Oschner Sherren regime
- RIF mass may be palpable  Omentum naturally wraps around inflamed appendix, containing
- LIF tenderness in patients with situs inversus or lengthy appendix extending to inflammatory process
the LIF  Symptomatic treatment as well as antibiotics, monitor patient as well
as size of mass
- Cough sign: RIF pain on coughing (localized peritonitis)  When mass has reduced in size, patient is stable, do surgery (less
- Rovsing sign: RIF pain with palpation of the LIF inflammation: easier)
- Obturator sign: RIF pain with internal rotation of a flexed right hip  Exceptions: very young or very old patients, or patients with suspected
- Psoas sign: RIF pain with hyperextension of the right hip appendicular abscess (require incision & drainage of pus)

- Infants/children may present with inflamed hemiscrotum due to migration of

pus through patent processus vaginalis – often mistaken for acute testicular
torsion

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) Ischaemic colitis
5) Colon cancer
MECKEL’S DIVERTICULUM MANAGEMENT
- NBM, IV drip, correct electrolyte imbalance
RULE OF 2s
- Like the appendix, Meckel‘s diverticulum is a true congenital diverticulum, a - IO: NG tube on constant suction, supine AXR
vestigial remnant of the vitelline duct
- 2 inches in length, 2cm wide, 2 feet from ileocaecal valve - PR bleed: PCT if necessary, gastric lavage to exclude UBGIT, OGD &
- Occurs in 2% of the population, ♂>♀ in the ratio of 2:1 colonoscopy
- Usually asymptomatic but if often presents at age 2 if symptomatic
- 2 types of ectopic tissue - Definitive treatment: surgery (open or laparoscopic)
 Pancreatic (6%)  Wide base: wedge ileal resection with anastamosis
 Gastric (60%) – gastric acid secretion can produce inflammation, peptic  Narrow base: resection of the diverticulum
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

160
161
POST-OP COMPLICATIONS  Incisional hernia
General or specific? o 10-15% of abdominal wounds
Immediate, early or late? o Usu. asymptomatic, but if painful, consider strangulation
Local or systemic? (uncommon due to wide neck)
o RF: Obesity, poor muscle tone (old age), (increased intra-
IMMEDIATE (<1 hour post-op) abdominal pressure (chronic cough, straining from constipation),
1) Local wound infection, multiple use of same incision site
 Damage to surrounding structures o Surgical repair of hernia if strangulated or if enlarging
 Primary haemorrhage  Bowel obstruction due to adhesions
o Either starting during surgery or following postoperative increase  Fistula formation
in blood pressure  Secondary haemorrhage: often as a result of infection
o Replace blood loss and may require return to theatre to re- 2) Systemic
explore wound  Fever: wind (atelectasis), water (UTI), walking (DVT/PE), wound (infxn),
2) Systemic wonder drug (drug fever)
 Basal atelectasis (collapse of alveoli):  Infections (day 3-5): phlebitis, pneumonia, UTI, abscesses (subphrenic,
o ↑ bronchial secretions post-op pelvic)
o Patient does not breath deeply due to pain  Acute confusion: exclude dehydration & sepsis
o Tx: chest physiotherapy, incentive spirometry  DVT & PE (day 5-7)
 Shock: due to blood loss, or inadequate fluid replacement peri-operatively
 AMI, pulmonary embolism
POST-OP HAEMORRHAGE
EARLY (first 24-48 hours post-op)
1) Local Early post-op haemorrhage:
 Pain, hemorrhage  Consumptive coagulopathy – if large volumes of blood transfused
2) Systemic  Pre-op anticoagulation
 Atelectasis, shock, AMI, PE  Unrecognized bleeding diathesis
 Nausea & vomiting, analgesia/anaesthesia induced  Damage to blood vessels/vascular organs
 Acute confusion: dehydration or sepsis Management
 FBC: check platelets
LATE (between 48 hours to 1 month post-op)  PT/PTT
1) Local  GXM & order blood
 Post-op paralytic ileus  Give protamine if heparin was used
 Wound or anastomotic dehiscence  Give FFP / platelet concentrates if clotting screen abnormal
o Occurs around Day 7 – 10
 Consider surgical re-exploration
o Heralded by serosanguinous exudate
o Analgesia, sterile wound dressing, fluid resuscitation, resuture
Late post-op haemorrhage:
under GA in OT
 Occurs several days after surgery
o Mortality up to 30%
 Usually due to infection damaging vessels at the operation site
 Post-op wound infection
o Usually within 1st week
Management
o Pain, redness, swelling, discharge, usually due to skin
staphylococci  Treat infection and consider exploratory surgery
POOR WOUND HEALING  Classic triad of PE: chest pain, dyspnoea, haemoptysis (poor sensitivity/
specificity)
Factors which predispose to poor wound healing: o Others: seizures, syncope, new onset atrial fibrillation etc

Patient factors: Physical Examination

 Poor blood supply  Homan‘s sign: passive dorsiflexion of the ankle produced sharp pain in calf
 Malnutrition (DON‘T DO: risk of clot propagation)
 Vitamin deficiency
 Immunosuppressive therapy Investigations:
 Long term steroids  Duplex ultrasound to detect DVT
 Radiotherapy  Chest x-ray: usually normal (classical findings listed below are rarely seen)
 Co-morbid conditions e.g. DM, HIV o Atelectasis, pleural effusion, raised hemi-diaphragm
o Westermark sign: dilatation of the pulmonary vessels proximal to
Surgeon factors: the embolism, with collapse of the distal vessels
 Suturing under tension o Hampton hump: late sign, wedged shaped infiltrate with apex
 Did not observe aseptic technique towards the hilum
 CT pulmonary angiogram (gold standard)
Wound factors: o Look for filling defects in pulmonary artery
 Wound infection  V/Q perfusion scan: no longer done
 Poor wound care o Inhale radioactive isotope, do CXR to assess ventilation of lungs
o IV contrast, do CXR again to assess perfusion of lungs
o Look for areas of ventilation without perfusion (V/Q mismatch)
Approach to Post Operative DVT/ PE o Correlate with clinical findings, calculate probability of PE
 ECG:
DVT in deep calf veins: 5-10% risk of PE o May have normal ECG with sinus tachycardia
DVT in iliofemoral veins: 50-60% risk of PE o Signs of right heart strain
- Right axis deviation: S waves in lead I
Risk Factors (Virchow’s Triad): - Right ventricular hypertrophy: tall R waves in V1, deep
 Alterations in blood flow (stasis) S waves in V6
o Prolonged bed rest, pregnancy (IVC compression) - Right atrial hypertrophy: peaked P waves
 Vascular endothelial injury - RBBB
o Trauma, pelvic/ vascular surgery, intravenous drug use - Classic S1Q3T3: S wave in I, Q wave in III, T inversion
 Alterations in blood constituents (hypercoagulable state) in III (rarely seen)
o Congenital: protein C/ protein S deficiency, Factor V Leiden mutation,  D-dimer: poor sensitivity and specificity in ruling in/ ruling out DVT or
anti-phospholipid syndrome, homocysteinuria pulmonary embolism
o Acquired: liver disease, cancer (production of pro-thrombotic factors),
oral contraceptive use

Presentation Prophylaxis/Treatment
 Post-operative fever (typically day 5-7)
 Lower limb pain & swelling, discolouration: may not be at site of clot  Non-pharmacological

162
163
o Use of inflatable calf compressors intra-operatively in patients  Intra-venous thrombolytics if not contraindicated
undergoing long operations  Surgical/ catheter embolectomy
o Early ambulation post surgery
o Use of thromboembolic deterrent(TED) stockings/ intermittent
pneumatic leg compression
 Pharmacological Well’s Criteria: A set of criteria to determine the pretest probability of DVT
o Unfractionated heparin or LMW heparin – acute setting Clinical feature Score
- Heparin Active cancer (treatment ongoing or within the previous 6 months or 1
 Potentiates effect of anti-thrombin III, inactivates palliative)
thrombin (PTT ↑) Paralysis, paresis, or recent plaster immobilization of the lower extremities 1
 Onset: immediate for IV, 30 minutes subcutaneously Recently bedridden for more than 3 days or major surgery, within 4 weeks 1
 Efficacy monitored using aPTT Localized tenderness along the distribution of the deep venous system 1
 Antidote: protamine sulphate Entire leg swollen 1
 Side effects: thrombocytopaenia Calf swelling by more than 3 cm when compared to the asymptomatic leg 1
- LMW heparin (Clexane) (measured below tibial tuberosity)
 Potentiates effect of anti-factor 10a (not reflected by PTT) Pitting edema (greater in the symptomatic leg) 1
 Onset: immediate for IV, Collateral superficial veins (nonvaricose) 1
 More predictable dose-effect relationship Alternative diagnosis as likely or more likely than that of deep venous -2
 Reversibility by protamine sulphate limited thrombosis
o Warfarin – long term (8-9 months, or until clot dissolves)
 Vitamin K antagonist, inhibits hepatic synthesis of High Probability: ≥ 3 Moderate Probability 1 or 2 Low Probability ≤0
vitamin K dependent clotting 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
o IVC filter (permanent or temporary: remove after 2 weeks of anti-
coagulation)
- 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