Andre Tan's Surgical Notes

CONTENTS I

TRAUMA (MULTI-SPECIALTY APPROACH)

Page 2

II

APPROACH TO ABDOMINAL PAIN

10

III

APPROACH TO ABDOMINAL MASSES

11

IV

OESOPHAGEAL DISEASES

12

For the M.B.B.S.

V

UPPER BLEEDING GIT AND ITS CAUSES

21

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

Surgery Notes

TRAUMA (MULTI-SPECIALTY APPROACH)

ADVANCED TRAUMA LIFE SUPPORT ALGORITHM MAIN PRINCIPLES: - Treat greatest threat to life first - Definitive diagnosis is less important - Time is important – the ―golden hour‖ after trauma is when 30% of trauma deaths occur, and are preventable by ATLS APPROACH 1. Primary survey and Resuscitation with adjuncts 2. Re-evaluation of the patient 3. Secondary survey with adjuncts 4. Post-resuscitation monitoring and re-evaluation 5. Optimise for transfer and definitive care PRIMARY SURVEY – ABCDE 1. AIRWAY Assessment of airway patency

-

Is patient alert, can patient speak? Gurgling, stridor Maxillofacial injuries Laryngeal injuries Caution: C-spine injury

Establishing patent airway

-

Chin-lift or modified jaw thrust (protect C-spine) Remove any foreign objects in the mouth where possible Oro/nasopharyngeal airway Definitive airway – endotracheal tube, cricothyroidotomy, tracheostomy

2. BREATHING Assessment of breathing

-

2

Look, listen, feel: chest rise, breath sounds – rhythm and equality bilaterally Rate of respiration Effort of respiration Colour of patient Percuss chest Look for chest deformities e.g. flail chest

Management of breathing

-

Supplemental oxygen Ventilate as required if patient requires assistance with breathing Needle thoracotomy for tension pneumothorax, followed by chest tube Occlusive dressing for open pneumothorax

3. CIRCULATION Assessment of organ perfusion

-

Level of consciousness Skin colour and temperature, capillary refill Pulse rate and character – all major pulses Blood pressure

Classes of haemorrhagic shock Bld loss Amt (ml) Percentage Ht rate BP Cap refill Resp rate Ur output (ml/h) Mental state Fluid replacement

I

II

III

IV

120 Decreased Prolonged 30-40 5-15 Anxiousconfused Crystalloid + blood

>2000 >40 >140 Decreased Prolonged >35 Oliguric-anuric Confusedlethargic Blood

Management

- Sources of bleeding  apply direct pressure or pressure on proximal pressure point - Be suspicious about occult bleeding e.g. intraperitoneal, retroperitoneal (pelvic fracture), soft tissue (long bone fracture) - Venous access – large bore, proximal veins - Restore circulatory volume with rapid crystalloid infusion – Ringer‘s lactate - Blood transfusion if not responsive to fluids or response is transient - Reassess frequently

3 SECONDARY SURVEY

4. DISABILITY - Glasgow coma scale Eye Spontaneous opening Opens to voice Opens to pain No response

When to do secondary survey 4 3 2 1

Verbal Oriented speech Confused Inappropriate Incomprehensible No verbal response

5 4 3 2 1

Motor Obeys Purposeful Withdraws Flexion response Extension response No response

6 5 4 3 2 1

GCS: 14-15 (minor); 8-13 (moderate); 3-7 (severe) - AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive - Pupillary reactivity

- Primary survey and resuscitation completed - ABCDEs reassessed - Vital functions returning to normal i.e. no need for active resuscitation at the moment 1. AMPLE HISTORY - Allergy - Medications - Past history - Last meal - Events leading to injury, Environment in which trauma occurred 2. COMPLETE HEAD-TO-TOE EXAMINATION

- Call for neurosurgical consult as indicated

Head

-

5. EXPOSURE - Remove all clothes - Check everywhere for injuries (log-roll to look at the back) - Prevent hypothermia

Complete neurological examination GCS or AVPU assessment Comprehensive examination of eyes and ears for base of skull fractures Caution: unconscious patient; periorbital oedema; occluded auditory canal

Maxillofacial

-

6. ADJUNCTS TO PRIMARY SURVEY Monitoring

- Vital signs – BP, pulse rate, saturation (pulse oximeter) - ECG monitoring - Arterial blood gas

Cervical spine

Diagnostic tools

-

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

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

Bony crepitus/deformity Palpable deformity Comprehensive oral/dental examination Caution: potential airway obstruction in maxillofacial injury; cribriform plate fracture with CSF rhinorrhoea  do not insert nasogastric tube

perineal

Gastric catheter (orogastric or nasogastric)

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

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

Neck (soft tissues)

-

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

Chest

-

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

Abdomen

-

Inspect, palpate, percuss, auscultate Abrasions and ecchymosis – ―seat-belt sign‖ Lower rib fractures  liver and spleen injury Re-evaluate frequently Special studies: FAST, DPL, CT scan Caution: hollow viscus and retroperitoneal injuries; excessive pelvic manipulation

Perineum

- Contusions, haematomas, lacerations - Urethral blood - DRE: Sphincter tone, high-riding prostate, pelvic fracture (may feel fragments of bone); rectal wall integrity; blood - Vaginal examination: blood, lacerations Musculoskeletal – extremities

-

Contusion, deformity Pain Perfusion Peripheral neurovascular status X-rays as appropriate Caution: potential blood loss is high in certain injuries (e.g. pelvic fracture, femoral shaft fracture); missed fractures; soft-tissue or ligamentous injuries; examine patient‘s back

3. ADJUNCTS AND SPECIAL DIAGNOSTIC TESTS - As required according to suspicion, but should not delay transfer 4. FREQUENT RE-EVALUATION - Have a high index of suspicion for injuries to avoid missing them - Frequent re-evaluation and continuous monitoring  rapidly recognise when patient is deteriorating 5. PAIN MANAGEMENT - Intravenous analgesia as appropriate

4

ABDOMINAL TRAUMA TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA - Solid organ injury: spleen, liver – bleeding (may be quite massive) - Hollow viscus injury with rupture - Vascular injury with bleeding INDICATIONS FOR IMMEDIATE LAPAROTOMY - Evisceration, stab wounds with implement in-situ, gunshot wounds traversing abdominal cavity - Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation - Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising haemodynamics - Obvious signs of peritoneal irritation - Rectal exam reveals fresh blood - Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries excluded as source of bleeding) - X-ray evidence of pneumoperitoneum or diaphragmatic rupture INVESTIGATIONS - If patient is stable: FAST and/or CT scan - If patient is unstable: FAST and/or DPL FOCUSED ABDOMINAL SONOGRAPHY IN TRAUMA (FAST) - Ultrasonographic evaluation of four windows: Pericardial, right upper quadrant, left upper quadrant, pelvis - Advantages

   

Portable Can be done quickly in 5ml) or obvious bowel contents aspirated  Lavage fluid seen to exit from chest drain or urinary catheter  RBC >100,000 per mm3, WBC >500, Gram stain positive for bacteria in effluent - Indications:

 Any unstable patient with suspicion of abdominal trauma or where clinical exam is difficult or equivocal  Unexplained hypotension in multiple trauma  Patient requiring immediate surgery for extra-abdominal injuries - Contraindications

    

Absolute indication for laparotomy already exists Previous abdominal surgery or infections Gravid uterus Morbid obesity Coagulopathy

- Advantages

 Can promptly reveal or exclude the presence of intraperitoneal haemorrhage  Valuable in discovery of potentially lethal bowel perforation - Disadvantages

 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

CARDIOTHORACIC TRAUMA There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving: cardiac tamponade, airway obstruction, flail chest, haemothorax, and pneumothorax. CARDIAC TAMPONADE - High index of suspicion required - Clinical features

 Chest trauma and hypotension  Beck‘s triad (hypotension, muffled heart sounds, distended neck veins) – only seen in 50% of cases as hypovolaemia may prevent neck vein distension; muffled heart sounds are least reliable  Pulseless electrical activity  Kussmaul‘s signs (increased neck distension during inspiration, pulsus paradoxus) - Diagnostic clues

 Enlarged cardiac shadow in CXR (globular heart – very rarely seen)  Small ECG voltages, electrical alternans (uncommon)  Pericardial fluid demonstrated on FAST or 2D-echo - definitive - Management

 Aggressive fluid resuscitation – helps maintain cardiac output and buys time  Pericardiocentesis: ECG lead-guided or 2D-echo guided AIRWAY OBSTRUCTION - Chin lift or jaw thrust - Remove any foreign body manually, suction blood/secretions - Definitive airway – ETT, cricothyroidotomy, tracheostomy FLAIL CHEST - When 2 or more ribs are fractured at 2 points forming a flail segment that moves paradoxically with breathing - Results in hypoxaemia mainly due to underlying pulmonary contusion, contributed to by pain with restricted chest wall movement - Management: ensure adequate oxygenation and ventilation; judicious fluid therapy (avoid fluid overload); adequate intravenous analgesia - Consider mechanical ventilation in high risk patients: shock, severe head injury, previous pulmonary disease, fracture of >8 ribs, age > 65, >3 associated injuries

HAEMOTHORAX - Chest tube insertion in the triangle of safety (bound by the lateral border of the pectoralis major medially, a line just anterior to the mid-axillary line laterally, and the upper border of the fifth rib inferiorly) - Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot - If blood >1500mls  massive haemothorax, call urgent cardiothoracic consult

(b) Subdural haemorrhage  Crescent shaped haematoma under the dura (between the dura and the arachnoid)  More severe than EDH (usually due to nature of injury that causes SDH to occur – associated with higher impact, thus brain has other injuries)  Pathology: underlying brain damage in addition to expanding SOL  Removal of blood does not solve underlying brain damage  poorer results

PNEUMOTHORAX (OPEN/TENSION) - Tension pneumothorax is a clinical diagnosis (CXR will only delay treatment, and may cause death) – signs of pneumothorax, hypotension, neck vein distension, severe respiratory distress - Immediate needle thoracotomy in second intercostal space in mid-clavicular line - Followed by chest tube insertion

(c) Traumatic subarachnoid haemorrhage  Usually only small amount of blood  conservative treatment sufficient (d) Intraparenchymal haemorrhage  Any shape, size, location  If large haematoma, will require evacuation 4. Diffuse axonal injury

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

- Global injury of axons - Arises from injury that causes rotational and shearing forces (high impact injury) – rapid acceleration and deceleration of brain in the intracranial cavity against relatively fixed points of attachment at the falx and tentorium - 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 AIM in management of head injuries is the prevention of secondary brain injury (from hypotension, hypoxaemia, increased ICP etc) since neuronal death is irreversible. PATHOLOGIES:

(a) Hypoxic (cellular)  Decreased blood supply (oxygenation)  loss of function of Na-K pump as ATP decreases  increased intracellular sodium  cellular swelling (b) Interstitial  Breakdown of blood-brain barrier  proteins enter interstitial space  oedema

1. Concussion

- Physiological dysfunction without anatomical or radiological abnormality - (Physiological dysfunction is the first step towards cell death, but is reversible if no further insult occurs) - Usually recovers in 2-3 hours 2. Contusion

- Small haematoma 7=1c) Nonregional lymph node involvement Other distant metastases

Stage 0 I IIA IIB III IVA IVB

T

N

M

is 1 2/3 1/2 3 4 any any

0 0 0 1 1 any any any

0 0 0 0 0 0 1a 1b

PRESENTATION Usually of insidious onset, with earliest symptoms being non-specific e.g. retrosternal discomfort, ―indigestion‖, and most patients already have advanced disease when they are diagnosed – 75% have lymph node involvement at time of diagnosis. 1. Dysphagia - Present in 80% of patients – most common presentation - Pain develops late and is usually due to extra-oesophageal involvement 2. Weight loss 3. Regurgitation 4. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult) 5. Vocal cord paralysis (left more than right) 6. Aspiration pneumonia 7. Tracheo-oesophageal or broncho-oesophageal fistula INVESTIGATIONS Diagnosis

1. Barium swallow - 92% accuracy in showing mucosal irregularity and annular constrictions but not able to diagnose malignancy with confidence 2. Oesophagogastroduodenoscopy - Allows biopsy of the lesion  confirmatory histological diagnosis 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 - Presence of any lung metastases - Aspiration pneumonia - Pleural and/or pericardial effusion - Tracheal deviation or extrinsic compression of tracheobronchial system - Widened superior mediastinum in an upper oesophagus tumour - Raised hemidiaphragm with phrenic nerve involvement 3. CT scan or MRI of the thorax with extension to include liver and adrenals - Can be used for T, N, and M staging 4. Bronchoscopy - Exclude bronchial involvement especially in tumours involving upper two-thirds of oesophagus 5. Bone scan for bony metastases 6. Laryngoscope to assess for vocal cord paralysis Supportive

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

16

- Endoluminal surgery – for early lesions; no attempt to remove any LNs (usually no LN involvement) - Oesophagectomy (i) Ivor-Lewis Two-stage procedure involving gastric mobilisation (first stage, done through upper midline abdominal incision), oesophagectomy and gastro-oesophageal anastomosis in the chest (second stage, through right thoracotomy incision) (ii)

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

(iii) Tri-incisional Three incisions – abdominal, chest, and also left neck incision for gastrooesophageal anastomosis in the neck  Performed with two-field lymphadenectomy (upper abdominal and mediastinal)  No difference in survival between trans-hiatal and I-L modalities; the stage of the cancer when the operation is performed is a greater factor influencing survival  Radical en-bloc dissections not shown to improve survival  Oesophagectomies have high mortality (5%) 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

17 Chemotherapy

GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD)

- 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

EPIDEMIOLOGY Incidence in Singapore not known Increasing prevalence, more common in males than females

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 12 mmHg – normal should be 7-14 cmH2O or 5-10 mmHg) WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT - Previous history of variceal bleed - Chronic alcohol intake - Jaundice or stigmata of chronic liver disease MANAGEMENT OF VARICES can be divided into three categories: 1. Acute bleeding 2. Prophylaxis 3. Chronic management I. ACUTE BLEEDING – MANAGEMENT 1. Resuscitate

- Airway, breathing, circulation - If patient appears well, look for early signs of shock – tachycardia, postural hypotension - Look at hydration status 2. Assess mental state

- If patient has altered mental state (encephalopathy)  need to protect airway (may require intubation) 3. Vascular access, fluids/blood resuscitation, and blood investigations

4. Emergency oesophagogastroduodenoscopy

- Indications:  Shock (resuscitated)  Ongoing BGIT  Suspected variceal bleed - Role of endoscopy  Diagnostic: confirm UBGIT & identify source of bleeding,  Therapeutic: injection of ulcer, ligation/sclerotherapy for varices - Repeat OGD with greater detail if it is normal the 1st time.  Exclude haemoptysis & bleeding from nasopharynx  Look for Mallory weiss tear and posterior wall duodenal bleeding ulcer

22

-

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

4. Management of severe bleeding

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

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)

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

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

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

11. Management of possible precipitants

- NSAIDs; Hepatic vein thrombosis

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

PEPTIC ULCER DISEASE

1. Incidentally detected on OGD 2. Symptoms of dyspepsia

EPIDEMIOLOGY - Incidence about 100 per 100,000 per year - 68% of patients are over 60 years of age - Overall mortality is 7-10%, unchanged for last 2 decades – mostly due to ulcer bleeding especially in elderly with significant comorbidities MAIN AETIOLOGICAL FACTORS H. pylori

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

- Accounts for most of the rest of ulcer disease not caused by H. pylori - 30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a clinically significant ulcer i.e. symptomatic, bleeding Other factors

- Cigarette smoking - Alcohol - Steroids and anticoagulants do not increase the risk of ulcer formation, but increase the risk of bleeding in an existent ulcer PATHOGENESIS - An imbalance between mucosal protective mechanisms against acid, and aggressive forces that damage the gastric mucosa - Aggressive forces: gastric activity and pepsin activity - 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

(a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom (b) Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen, associated with upper abdominal fullness, early satiety, bloating, belching, nausea (c) Unspecified dyspepsia - Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a duodenal ulcer 3. Bleed

- As above, presenting with haematemesis (coffee-grounds vomitus) or malaena 4. Perforation

- Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements - Board-like rigidity, guarding will be present on examination (signs of peritonism) - Erect CXR will show air under diaphragm ENDOSCOPY (OGD) - The most important and valuable investigation - Roles of endoscopy: (a) Diagnosis

   

Confirmation of ulcer disease Location of ulcer Biopsy to rule out malignancy (usually 6 bites) Biopsy of antral tissue for CLO (Campylobacter-like organism) test for H. pylori

25 (b) Prognostication of bleeding risk (in UBGIT)

 Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH)

SURGICAL MANAGEMENT DUODENAL ULCER

Forrest grade 1a Spurting (arterial) 1b Non-spurting, ooze (venous) 2a Non-bleeding ulcer with visible vessel 2b Non-bleeding ulcer with adherent clot 2c Ulcer with haematin-covered base (flat spot) 3 Ulcer with clean base

Bleeding risk 90% 20% 40% 20% 10% 5%

(c) Endotherapy (in UBGIT)

   

Injection with adrenaline (1:10,000) or absolute alcohol Thermal coagulation (heater probe) Haemostatic clipping (endoclip) Argon plasma coagulation

CONSERVATIVE MANAGEMENT 1. Gastroprotection

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

Indications for surgery:

1. Persistent bleeding (e.g. erosion of a posterior duodenal ulcer into gastroduodenal artery) 2. Perforation 3. Gastric outlet obstruction (patient presents with vomiting of undigested food not long after meal, succussion splash, air-fluid levels on AXR; characteristic electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria) 4. Failure of medical management (ulcer does not heal) Surgery:

1. Oversewing the bleeding vessel 2. Vagotomy with gastric drainage procedures - Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric secretion; parietal cells also become less responsive to histamine and gastrin, and vagal stimulus for gastrin release is abolished - Vagotomy can be truncal, selective, or highly selective - Drainage procedures usually done with vagotomy as gastric emptying is decreased with denervation  gastrojejunostomy or pyloroplasty 3. Antrectomy with truncal vagotomy 4. Gastrectomy 5. Omental patch repair is sufficient for small perforated ulcer Perforated ulcer: IV fluids, IV antibiotics, PPI, surgery (patch repair)

2. H. pylori eradication

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

1. 2. 3. 4.

Failure to heal after 3 months of conservative therapy Dysplasia or carcinoma Recurrence Perforation, persistent bleeding

Surgery

1. Oversewing the bleeding vessel 2. Gastrectomy 3. If prepyloric ulcer, can treat similar to duodenal ulcer

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 - Female to male ratio 2:1 - Incidence 10-18 per 100,000 per year - Incidence increases steeply after 50 years old RISK FACTORS 1. Environmental

-

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

2. Genetic

-

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

PRECURSOR CONDITIONS 1. Partial gastrectomy for benign disease with Bilroth II reconstruction

- Usually occurs >15 years after surgery - Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal secretions at the anastomotic zone 2. Gastric polyps

- Highest risk in inflammatory polyps: 75-90% - 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology - Also increased risk of adenocarcinoma elsewhere in the stomach 3. Chronic atrophic gastritis

- Hypertrophic gastritis (Menetrier‘s disease) – inflammatory disease of gastric epithelium, up to 10% risk of malignant change - Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10% risk of gastric cancer 4. Peptic ulcer disease

- 35 years old should cause concern COMPLICATIONS - Bleeding - Gastric outlet obstruction  vomiting (dehydration, hypokalaemic metabolic alkalosis, aspiration ± pneumonia) - Perforation - Malnutrition INVESTIGATIONS Diagnosis  OGD –visualisation and biopsy (ulcer with heaped-up edges) Staging investigations

1. 2. 3. 4.

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

Supportive investigations

5. FBC – low Hb 6. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis 7. LFTs – albumin as a marker of nutritional status (alb15 regional LN involved

CURATIVE TREATMENT SURGERY Principles of surgery:

- Wide resection of the tumour to negative margins (at least 6cm margins) - En-bloc excision of regional lymph nodes - Choice between total gastrectomy and subtotal gastrectomy  Subtotal gastrectomy leaves a small portion of proximal stomach – easier to anastomose to jejunum than oesophagus since oesophagus does not have serosa (higher risk of leak)  Subtotal gastrectomy is associated with less morbidity, better functional outcome (some residual reservoir function preserved)  Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia, body) as well as diffuse-type tumours and cardio-oesophageal junction tumours - Reconstruction  Bilroth I (end-to-end gastroduodenostomy) – rarely done as it is difficult to mobilise duodenum up to anastomose with residual stomach  Bilroth II/Polya (gastrojejunostomy) – no protection against biliary reflux into stomach  Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higher chance of leak  Oesophagojejunostomy (after total gastrectomy) Complications of gastrectomy: Early

1. Bleeding 2. Infection 3. Anastomotic leak

Late



Early satiety



Retained antrum syndrome - Not enough antrum removed leads to increased acidity in residual stomach, with formation of marginal ulcers on the jejunal side of the anastomosis



Intestinal hurry - Inadequate reservoir function leads to poor digestion  may have phytobezoar formation

PALLIATIVE THERAPY - For palliation of symptoms such as pain, bleeding, obstruction - Endoscopic laser ablation for obstruction - Embolisation for bleeding - Surgical options: subtotal gastrectomy (6-15% mortality), total gastrectomy (20-40%), gastrojejunostomy for obstruction - External beam radiotherapy for pain, low-level ongoing bleeding (not for heavy bleeding as it takes weeks to cause fibrosis)



Dumping syndromes - Early dumping syndrome: due to increased osmotic load in bowel occurring half to one hour after meal, resulting in flushing, palpitations, dizziness, nausea; treat by eating small frequent meals with low carbo and high protein/fat - Late dumping syndrome: reactive hyperinsulinaemia with hypoglycaemia; treat by eating more carbohydrates

PROGNOSIS - Stage I 90% 5-year survival - Stage II 70% - Stage III 40% - 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

COLORECTAL CARCINOMA EPIDEMIOLOGY Commonest cancer in Singapore men, number 2 cancer in Singapore women Peak incidence at 60-70 years of age PATHOLOGY - Almost all tumours are adenocarcinomas - 90% of tumours are sporadic - 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and 1% in association with familial adenomatous polyposis (APC) - 1% arise in association with long-standing ulcerative colitis (>10 years) PATHOGENESIS There are 2 pathways for cancer development in the colorectal mucosa: 1. APC pathway (adenoma-carcinoma sequence)

- Accounts for 80% of sporadic colorectal carcinomas - Characterised by chromosomal instability - Stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes:  Loss of the APC suppressor gene on 5q21 (congenitally absent in patients with familial adenomatous polyposis – APC) is the earliest event in adenoma formation  APC is required to break down beta-catenin; with the loss of APC, betacatenin accumulates and activates various genes in the nucleus (such as MYC and cyclin D1) which promote cell proliferation  K-RAS (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering mitotic signals and prevent apoptosis  Loss of tumour suppressor gene at 18q21  Loss of p53 late in carcinogenesis - The molecular evolution of colon cancer through this pathway occurs through a series of morphologically identifiable stages: localised epithelial proliferation  small adenoma  large, more dysplastic adenoma  carcinoma in-situ  invasive cancer

2. Defects in DNA mismatch repair

- Involved in 10-15% of sporadic cases - Like the APC pathway, there is accumulation of mutations, but due to a different mechanism, and without clearly identifiable morphologic correlates i.e. no adenomas - Due to mutations in one of the five DNA repair genes (MSH2, MSH6, MLH1, PMS1, PMS2) of which MSH2 and MLH1 are the most commonly involved in sporadic colorectal carcinomas - Loss of DNA mismatch repair results in microsatellite instability which affects coding or promoter regions of genes involved in cell growth such as the BAX gene and the type II TGF-β receptor - Tumours that arise from this pathway have a better prognosis than tumours that arise from the APC pathway SITE: - 25% in caecum and ascending colon, - 25% in transverse colon, - 25% in descending colon and proximal sigmoid, - 25% in distal sigmoid and rectum - Most are left-sided though there is an increasing incidence of right-sided tumours MORPHOLOGY 1. Polypoid – more common in the right colon as there is more space to grow 2. Scirrhous – annular ―apple-core‖ lesions, more common in the left colon 3. Ulcerated 4. Nodular

SPREAD 1. Intramural – along bowel wall or Intraluminal 2. Direct extension into surrounding tissues e.g. small bowel, ovary 3. Lymphatic 4. Haematogenous – to liver, lungs 5. Transcoelomic

RISK FACTORS

HISTORY

1. Age >50 years

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

2. Environmental factors

- Diet: high in red meat, preserved foods (nitrosamines), low in fibre, vitamins, minerals - NSAIDs may be protective against CRC



Local:  Change in bowel habits/ PR bleed  Frequency:>3x/day=diarrhoea; 1-2cm above the level of the sphincter complex, usually taken to be at the level of the dentate line (which is 5cm above the anal verge) i.e. distal margin of the tumour must be >7cm from the anal verge  Sphincter-sparing  low anterior resection (below the peritoneal reflection); ultra low AR if just above the anal sphincter  Sphincter-sacrificing surgery abdominoperineal resection (entire anus and sphincter complex is dissected, with the creation of an end colostomy)

- Reconstruction  Formation of a straight coloanal anastomosis in anterior resections is associated with poor function due to the lack of reservoir function  Creation of a colonic J-pouch using the proximal end of colon (the end of the colon is folded back on itself to form a J, and the two limbs opened and stitched together to form a pouch, the apex of the J being anastomosed to the anus) is associated with improved post-operative function  Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal colon is cut longitudinally but sewn transversely, widening the diameter at that segment to form a small pouch), done when there is difficulty creating the colonic J-pouch - Mesorectal excision  Proximal rectal tumours – 5cm distal margin of mesorectal excision  Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the tumour  Lower rectum tumours – total mesorectal excision required (complete excision of the intact visceral mesorectal tissue to the level of the levators) - Extended resections  For locally advanced, adherent tumours (T4), multivisceral resection of organs involved (pelvic exenteration) is associated with improved local control and overall survival compared with standard resection, though high morbidity of 2550% is associated  Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease - Stoma creation  A defunctioning loop ileostomy (or loop colostomy) is usually created during an low AR as the manipulation of the colon deep within the pelvic cavity causes increased risk of an anastomotic leak & also poorer blood supply to anastomosis  A defunctioning stoma does not protect against anastomotic leak, but mitigates against disastrous complications of faecal peritonitis should a leak occur  Closed in 2-6/12 after check with gastrograffin reveals no leak - Neoadjuvant chemoradiotherapy for rectal tumours  Neoadjuvant RT with 5-fluorouracil can downstage tumour significantly  ability to preserve sphincter, ability to resect previously unresectable tumour, reduce local recurrence  Good evidence for ≥T3 tumours: benefits > risk of RT (esp. that pt becomes too ill to be operated on)



Not possible for colon carcinomas due to risk of small bowel radiation if given above peritoneal reflection

- Surgical treatment according to stage Stage of disease

Treatment

T1

Involvement of submucosa, but no penetration through muscularis propria

Local excision (AR or APR)

T2

Invasion into, but not penetration through, muscularis propria

a) Local excision + adjuvant Chemo/RT OR b) radical resection

T3

Penetration through muscularis propria into subserosa (if present), or pericolic fat, but not into peritoneal cavity or other organs

Neoadjuvant chemo / RT before radical resection

T4

Surgery for metastases

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

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

RADIOTHERAPY - Role as neoadjuvant therapy in rectal cancer to downstage tumour - Post-operative adjuvant therapy in stage II or III rectal cancer

Invasion of other organs or involvement of free peritoneal cavity CHEMOTHERAPY Adjuvant therapy

Operative complications Immediate (100 adenomatous polyps all over colon; polyps take 5-6 yrs to turn malignant 50% patients will have polyps by 16yrs; 90% will have colorectal CA by 45yrs

- Other sites for polyps: stomach, duodenum - Extraintestinal manifestations  Skin: Epidermoid cysts, Lipoma  Bone: Osteoma of skull/ mandible, Dental abnormalities  Eye: Congenital hypertrophy of retinal pigment epithelium (CHRPE)  Other tumours:  Desmoid tumours (intra-abdominal tumours, treated with CT, RT or HT.)  Thyroid cancer (follicular or papillary type)  Periampullary CA - Diagnosis  Colonoscopy showing >100 polyps  Genetic testing - Surveillance  Yearly colonoscopy for at-risk family members from 12y onwards  5 yearly OGD for surveillance of Periampullary Cancer.

 



Genetic testing of at-risk family members Affected members should undergo prophylactic proctocolectomy with ileal pouch anal anastomosis (IPAA – involves folding loops of ileum back on themselves and stitching or stapling them together to form a reservoir pouch which is them anastomosed to the anus) at ~ 20 YO Subtotal colectomy is an option if the rectum is relatively spared of polyps

PATHOGENESIS 1. Increased intraluminal pressure

- Associated with lack of dietary fibre 2. Degenerative changes in colonic wall

- Usually at point of entry of terminal arterial branches where serosa is weakest - Associated with weakening of collagen structure with age

Hereditary Non-Polyposis Colorectal CA (HNPCC)

PRESENTATIONS

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

1. Acute diverticulitis

- Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure) - Tumours tend to arise from polyps which are commonly flat, with villous histology - Resultant tumour is often poorly differentiated - Lynch syndrome type II is associated with increased risk of cancer elsewhere, most

commonly endometrial cancer, and also ovarian, gastric, small bowel, hepatobiliary, and renal pelvis/ureter cancers o Offer a THBSO with total colectomy if CRC detected - Diagnosis is based on the Amsterdam criteria – see above - Surveillance – 1-3yrly colonoscopy starting at 20 years old Ulcerative colitis - Screening – yearly colonoscopy starting after 10 years of UC

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

- Symptoms: LLQ pain, N/V, Constipation / diarrhoea - Signs: Low grade fever, Tender palpable mass - Investigation:  WBC 2. Chronic diverticulitis

- Recurrent LIF pain - Irregular bowel habit - Passage of mucus PR 3. Complicated diverticulitis

a. b. c. d. e.

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

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

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

Stage 1

Pericolonic / Mesenteric abscess

Stage 2

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

Stage 3 Stage 4

Pelvic / retroperitoneal abscess Purulent peritonitis Faecal peritonitis

36

- ABx, NBM, IV fluids - Consider 1 stage surgery after acute episode – resection of affected bowel segment with primary anastomosis - Percutaneous drainage - Elective 1 stage surgery - 2 stage operation – Hartmann‘s procedure (partial colectomy + diverting end colostomy & rectal stump formation) + secondary re-anastomosis 3 months later

Note: current controversy of management for stage 3: haartman‟s vs segmental resection with primary anastomosis with or without defunctioning ileostomy

37 Presentation

Clinical features

Investigations

Differentials

Management

Acute Diverticulitis

- LIF pain – colicky, progressing to constant, relieved by defecation - LIF tenderness - Palpable LIF mass - Nausea - Pyrexia - Increase pulse rate

-

FBC – leucocytosis, ↑ ESR Erect CXR to rule out perforation AXR – ileus, air-fluid level w/in an abscess Barium enema CT scan w triple contrast  Contrast: IV for vascular lesions, oral for small bowels, enema for large bowels  Features – diverticula elsewhere, confirm colitis (mesenteric fat infiltration, concentric bowel thickening) but only suggest diverticulitis, pelvic abscess, free gas, extravasated contrast  Cannot tell if inflm is due to diverticula - Laparoscopy – if diagnosis is in doubt - Avoid colonoscopy as risk of perforation is high

- See Ddx to RIF/LIF pain - GI: appendicitis, colitis, GE, IBS, IBD, mesenteric ischaemia/ adenitis, Ca colorectal - Uro: UTI, stones, cancer, cyst/ Angiomyolipoma, hydronephrosis - Obgyn: PID, torsion of cyst/ ovary, endometriosis, ectopic pregnancy - #: #, infx, inflm,

Conservative - Bed rest - NBM, IV fluid - Broad-spectrum antibiotics – augmentin or metronidazole or ciprofloxacin - Antispasmodics

- Recurrent LIF pain - Irregular bowel habits – constipation & bouts of diarrhoea - Passage of mucus PR - Ruled out cancer, IBD, ureteric colic, Msk pain etc.

- Rigid sigmoidoscopy – oedematous mucosa & rigidity of rectosigmoid junction - Flexible sigmoidoscopy – diverticular orifices - Barium enema – ‗saw-tooth‘ appearance, diverticula, strictures - Colonoscopy – exclude differentials (i.e. Ca colon)

Generalised peritonitis / perforation

- Acute onset abdominal pain – severe & continuous - Abdominal guarding & rigidity - Vomiting - Tachycardia - Pyrexia

- FBC – ↑ TW, ↑Hb (dehydration) - U/E/Cr – dehydration & ARF - CXR – free gas under diaphragm

- CA colon – may coexist. Hard to differentiate – therefore, ALWAYS exclude CA colon e.g. histology after bowel resection - Ischaemic colitis - Radiation colitis - Colonic endometriosis - Other causes of peritonitis – perforated PUD/ appendicitis/ bowel/ ectopic pregnancy, ishaemic bowel, acute pancreatitis, ruptured AA/ hepatoma, torsion of testis/ ovary, pyonephrosis

Pericolic abscess

-

- FBC – ↑ TW - CT – differentiate between inflammatory phlegmon & pericolic abscess

Persistent inflammatory mass

- LIF pain, tenderness & palpable mass - Fever - Malaise

Chronic Diverticulitis Not a common clinical entity

Small bowel I/O

May follow acute diverticulitis LIF tenderness & guarding LIF mass – may be detected on DRE Swinging fever

After acute phase has settled - Ba enema &/or Colonoscopy – confirm dx & exclude CA colon Role of surgery: see behind Conservative – see above Surgical Indications: - Severe / recurrent attacks - Possible CA colon - Segmental resection of affected colon + anastomosis Mgmt as for acute abdomen - Resuscitate - Surgical  Peritoneal toilet  Resection of affected segment  End sigmoid colostomy (Hartmann‘s procedure) - CT/US guided percutaneous aspiration - Surgery – evacuation of pus ± resection of affected segment

- Usually temporary, due to attachment of enteric loop against area of acute diverticulitis - Surgery if does not resolve

Presentation

Clinical features

Investigations

Differentials

Management

Large bowel I/O

- PHx of recurrent acute diverticulitis or irregular bowel habit - Colicky abdominal pain, constipation & abdo distension

- AXR – dilated bowels proximal to stenosis - Water soluble contrast enema

- CA colon

- NBM, Drip & suck - Surgery – Resection ± primary anastomosis

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

- Invx as for LGIT bleed – resus, invesigations + colonoscopy & angiography (both diagnostic AND therapeutic value) - ± on-table enteroscopy if required - ± tagged RBC scan (not as sensitive compared to angiogram)

-

- Resuscitate & correct coagulopathy - Colonoscopic management: adrenaline injection, endoclips on bleeding vessel, heat coagulation - Radiologic embolisation of site of bleeding with temp foam material via angiography - Surgery – segmental resection; total colectomy if unable to localise bleed

Vesicocolic fistula

- PHx of chronic diverticulitis & UTI - Hx of dysuria, freq, haematuria, pneumaturia, faecaluria

-

- Other causes of fistula – CA colon, CA bladder, Crohn‘s disease, post-irradiation necrosis

UFEME & urine c/s: confirm UTI and organisms Cystoscopy – cystitis Sigmoidoscopy – usually normal KUB – air in bladder Barium enema – diseased diverticular bowel segment

Anorectal bleed Angiodysplasia Ischaemic colitis Colorectal CA Colitis (inflm or infx) UBGIT Coagulopathy

- Surgery – Resection of affected colon + anastomosis + closure of bladder fistula opening

Outcomes: well or derteriorate requiring surgery, recurrent episodes, stricture & subacute IO (offer surgery) Indications for emergency operation

1. 2. 3. 4. 5.

Sepsis from abscess or faecal peritonitis Perforation Diverticulitis not responding to conservative management Obstruction with pending perforation – need to rule out cancer at the same time 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. 2. 3. 4. 5.

Stricture Fistula Recurrent attacks – occurs in 30% of patients after 1st episode. a/w higher mortality & complication rates Young patientss 15% remains after 15 minutes, the patient cannot tolerate major liver resection (>3 segments removed) - CT volumetry: residual liver function calculated with a CT liver scan via a computer programe - If patient has cirrhosis, assess the Child‘s status  only Child’s A and good Child’s B can be considered for resection Child-Pugh classification of CLD/cirrhosis 1) Prognosis 2) Strength of medical treatment 3) Necessity of liver transplant Points 1 Albumin (g/L) >35 Bilirubin (μmoles/L) < 35 Coagulopathy 10mmHg) - Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has decreased  increased resistance to flow 6. Location of tumour - Has to be located in a suitable location for resection

PALLIATIVE THERAPY Loco-regional ablation

(a) Radiofrequency ablation (RFA) – best results for locoregional strategies (b) Percutaneous ethanol injection (c) Cryotherapy Intra-arterial therapy

2 28-35 35-50 1.70- 2.20 Slight - mod Grade I – II

B(7-9) 80 60 Significant functional compromise Maximum resection of 2 segments

3 50 >2.20 Severe/refractory Grade III-IV C( 10-15) 45 35 Decompensated liver disease, consider transplant Consider transplant

(a) Transarterial chemoembolisation (TACE) (b) Transarterial embolisation (TAE) (c) Selective Intrahepatic Radiation – Yttrium-90 radioactive beads Systemic therapy – limited results; Sorafenib imporves median survival by 3/12

SCREENING FOR CHRONIC HEPATITIS CARRIERS - Combination of 6/12 to yearly ultrasound with AFP levels - US is operator dependent & may miss certain areas of the liver where imaging is difficult, but it is not associated with radiation exposure - AFP is also not a perfect screening test as 20% of HCC will not have raised AFP - Thus the combination of ultrasound and AFP can increase the sensitivity and specificity of screening - Frequency of screening is controversial, but should be increased in patients at increased risk – HbeAg positivity, high HBV DNA levels - 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 - Still more common than primary liver tumour for malignancy occurring in the liver - Primaries: Colorectal, gastric, pancreatic, urogenital, breast, lung PRESENTATION DEPENDS ON SITE OF METASTASIS Mets to liver parenchyma

Mets to porta hepatis LN

- Incidentally found on follow up (for cancer) - Hard mass - Heaviness - Pain from rupture

- Symptoms of obstructive jaundice  Yellow sclera  Tea-coloured urine  Pale stools

P/E

- Hard, irregular nodular hepatomeg - Jaundice is a late sign

- Jaundice early, progressive - Hepatomegaly may not be present

Invx

- Both obstructive and transaminitis picture

- Obstructive picture in early stages

Hx

TRIPHASIC CT - 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 ROLE OF SURGERY - Promising results with colorectal and neuroendocrine metastases if isolated resectable metastatic disease – 5-yr survival >50% - Increasing role in urogenital, breast mets - Poor results for stomach, oesophageal mets - Palliation for symptoms in neuroendocrine metastases

LIVER HAEMANGIOMA EPIDEMIOLOGY - Prevalence 0.4-20% - Female to male ratio 3:1 PATHOGENESIS - Vascular malformation that enlarges by ectasia, congenital in origin

PRESENTATION 1. Usually small and asymptomatic, found incidentally 2. Mass effects compressing on surrounding organs 3. Pain from liver capsule stretch 4. Rupture (3cm – open drainage or percutaneous aspiration

PYOGENIC ABSCESS - More common than amoebic abscess locally - Causative organisms: Klebsiella pneumoniae, Enterococcus, Enterobacter, E. coli, Staph aureus - Routes of infection:

(a) Ascending infection from biliary system (ascending cholangitis) (b) Intra-abdominal source through portal vein – acute appendicitis, diverticulitis, IBD, pancreatitis, pelvic abscess (c) Contiguous spread – from gallbladder empyema (d) Haematogenous spread in sepsis e.g. infective endocarditis (e) External inoculation – iatrogenic, traumatic

Percutaneous aspiration

Open drainage

- Minimally invasive, performed under radiologic guidance - Can be done under LA - Longer stay for patient as drainage tube stays in patient for a longer time - May require multiple attempts if unable to completely drain pus - Contraindications:  Ascites (pus can leak into peritoneal cavity)  Uncorrected coagulopathy  Proximity to vital structures

-

- Presentation: RHC pain (capsular stretch) with Spiking fever with chills, rigors. 50% of patients have jaundice, and one-third have hepatomegaly - Investigations:

Laboratory:  FBC, U/E/Cr, hepatitis markers  Blood cultures, Melioidosis & amoebic serology/ PCR, Stool ova, cysts and parasites  Tumour markers: AFP, CA 19-9, CEA (may resemble infected tumour on imaging)  If any aspiration done, aspirates for cytology, stains & c/s Imaging:  US HBS or CT scan (to exclude liver tumour, KIV endoscopy to rule out GI malignancy)  Findings: Irregular lesion with central area of necrosis, air-fluid levels, may be multiloculated. Rim-enhancing appearance on triphasic CT scan. - Treatment

1. Resuscitate if necessary 2. Close monitoring of vitals with strict IO charting

44

Invasive procedure, done under GA Shorter hospital stay Single procedure Not dependent on location Indications:  Concomitant pathology requiring surgery e.g. gall stones  Multiple abscesses or multiloculated abscess  Immunocompromised patient  Failed percutaneous drainage (tube blocked, or pt not getting better)  Ascites  Ruptured abscess

AMOEBIC ABSCESS - Causative organism: Entamoeba histolytica (infects the gut, forming ulcers in the colon, then spreads to the liver through the portal vein) - Transmission is faecal-oral - Presentation

   

Usually single abscess No sepsis, jaundice Hepatomegaly often present Complications: rupture into pleural/peritoneal spaces

- Treatment:  Metronidazole (very responsive)  Aspiration if amoebic serology inconclusive; pregnancy (metronidazole contraindicated); suspicion of secondary infection; severe symptoms from distension or fever; impending rupture

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 pancreatic cells  ischaemic cellular injury  predisposition to enzyme activation

ACUTE PANCREATITIS DEFINITION An acute inflammatory process of the pancreas with variable involvement of regional tissues or remote organ systems EPIDEMIOLOGY - Incidence is difficult to measure accurately (not all diagnosed). - ~ 7-10% presenting with abdominal pain acute pancreatitis Trauma: blunt trauma, ERCP, gall stones

CAUSES (I GET SMASHED) Infx: mumps, VZV 1. Idiopathic Drugs: EthanolSteriods, NSAIDS, 2. Gallstones 3. Ethanol diuretics, sulphnamides 4. Trauma Metabolic: hyperlipidemia, hypercalcemia 5. Steroids Autoimmune: SLE, PAN 6. Mumps and other infections (VZV also) Neoplastic: Ca head of pancreas 7. Autoimmune – SLE, PAN 8. Scorpion toxin Congenital: CFs, Pancreas divisum 9. Hypercalcaemia, hypertriglyceridaemia, hypothermia 10. ERCP 11. Drugs (SAND: Sulphonamides, azathioprine, NSAIDs, diuretics) 12. Rare causes: Cystic fibrosis, cancer of the head of the pancreas, severe blunt trauma, pancreas divisum Gallstones and alcohol are the most common causes (>90% of acute pancreatitis) PATHOPHYSIOLOGY - The final common pathway of pancreatitis involves inappropriate activation of proenzymes stored within zymogen granules in the pancreatic cell – trypsin is implicated in this mechanism as it activates most of the proenzymes secreted by the pancreas when they are secreted into the duodenum - The activated lytic enzymes destroy the pancreatic acinar cells resulting in release of potent cytokines that attract neutrophils and macrophages, which themselves secrete pro-inflammatory cytokines - The cytokine cascade amplifies the local inflammatory response and also results in a systemic inflammatory response [2 of 4: T>38 / 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

- The mechanisms in which alcohol cause pancreatitis are not known, though it is believed alcohol itself results in injury to pancreatic cells through generation of free radicals during its metabolism, and may sensitise the pancreas to injury by other agents ATLANTA CLASSIFICATION (FOR SEVERITY) Mild acute pancreatitis

- Interstitial oedema - Minimal organ dysfunction - Uneventful recovery

Severe acute pancreatitis (any 1)

- Pancreatic or peripancreatic necrosis - Associated with organ failure - May be a/w local complications

PRESENTATION - Symptoms (generally non-specific):  Abdominal pain (most consistent, in >90% of patients) – constant epigastric pain, classically radiating to the back (in 50%), maximal intensity within several hours of onset; usually occurs after a heavy meal; alleviated by sitting up & leaning forward, worse on movement  Nausea, vomiting, Anorexia - Also rule out other causes:  Gastric causes: PUD  Perforated viscus (mainly on examination: look for peritonism)  AMI, DKA or even a lower lobe pneumonia  Hepatitis or GB / CBD disease - Ask for causes of pancreatitis:  Gall stone disease: biliary colic, symptoms of cholecytitis/ CBD stone/ cholangitis  Recent alcohol abuse or chronic alcohol abuse  Recent blunt trauma or ERCP done  PHx or hyperlipidemia, hypercalcemia, autoimmune disease (SLE, PAN)  Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling)  Recent drug history: steroids, NSAIDs, diuretics

- Signs (also non-specific)  Tachycardia, low grade fever, low BP, toxic looking, jaundiced?  Epigastric tenderness or signs of peritonism (130/min, Hypotension 50 Presence of Gray Turner‘s/Cullen‘s sign Oliguria 55 yrs >16x109/dL >11.2mmol/L >600U/L >120U/L

Within 48 hours of admission 1. 2. 3. 4. 5. 6.

Fall in Hct Rise in urea Calcium PaO2 Base excess Neg fluid balance

>10% >0.9mmol/L 6L

- Ranson‘s criteria prognosticates mortality according to score - Any patient with a score of 3 and above is considered to have severe pancreatitis - Mortality: 6 90% - Shortfalls of Ranson‘s:  validated for alcoholic pancreatitis only revised Ranson‘s score was created for gallstone pancreatitis,  difficult to tell aetiology in acute setting & cumbersome to wait for 48 hours, and difficult to assess for negative fluid balance

IV. C-reactive peptide

-

As a single prognostic marker; 210mg/dL at 48 hours, the pancreatitis is more likely to be severe No relevance >3/7 of onset as other confounding factors come into the picture Combination of Glasgow score and CRP improves overall prognostic value

V. Balthazar’s CT severity index (consider a CT AP @ ~ 3/7 from onset)

- Grades severity of disease according to CT findings detects h‟ge & necrosis - Not very useful as CT is not usually done in the 1/52 in local context, and disease is still evolving (CT findings lag behind) in the early stages COURSE OF DISEASE - 75%: mild course of disease; recover unless comorbidities cause deterioration - 20-25%: severe outcome  1/3 of these patients will ultimately die - Overall mortality rate 15x109/dL 16mmol/L >600U/L >100/L 10mmol/L

2. NBM (bowel rest) and IV fluid replacement

>3 criteria  severe

- Preferred over Ranson‘s scoring in certain centres

- May include gastric decompression with NGT if there is persistent vomiting, significant gastroparesis, or intestinal obstruction (ileus) - Acid suppression does not change course of disease, but protects against stress ulcer formation; octetride has no benefit (thought to reduce pancreatic secretions) - Fast patients for at least 2/7 until more stable - May start oral feeding early with fluids in mild pancreatitis if tolerated - Prolonged NBM results in poorer recovery due to nutritional debilitation – think about NJ feeding, or open jejunostomy creation early in patients with severe pancreatitis; if not tolerable, then consider TPN

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) - Use opioid analgesics (tramadol, pethidine) other than morphine (causes increased tone of sphincter of Oddi) 4. Treatment of fluid and electrolyte abnormalities hypocalcaemia, hypoglycemia 5. Antibiotics

- Either prophylactic or therapeutic  Not shown to have any benefit in mild pancreatitis - Prophylactic in severe acute pancreatitis to prevent infection of necrosis (infection will occur in 40-70% of patients with necrosis and increases the mortality rate from 12 to 33%)  Carbapenem (only imipenem has been shown to prevent sepsis) - Therapeutic in cholangitis (coexisting with Gallstone disease or a s complication of pancreatitis) & infection of pancreatic necrosis/ pseudocyst - Duration: 14-28 days 6. Support for organ failure

o o o

Ventilate with PEEP if hypoxemic (e.g. ARDS) Dialysis & CVP monitoring if in ARF Fluid resuscitation & inotropes if Hypotensive

MONITORING FOR COMPLICATIONS AND TREATING Local complications:

- Acute fluid collections  Due to increased vascular permeability; 70-80% resolve spontaneously - Pseudocyst  Persistent fluid collection (enzymes, blood, necrotic tissue) walled off by fibrosis and not an epithelium-lined surface (after 4 weeks)  Presents as Gastric outlet obstruction, infx, peritonitis, h‘ge (erosion of splenic vessels), Persistently raised amylase despite resolution of pancreatitis  50% resolve spontaneously - Abscess  Infection of fluid collection (not necrosis) - Pancreatic necrosis  Areas of no contrast uptake on CT with intravenous contrast - Infected necrosis  Gas bubbles on CT scan  Positive bacterial culture on CT, U/S guided FNA

48

Systemic complications

o o o o o

Peritoneal sepsis Pancreatic ascites (massive accumulation of pancreatic fluid in peritoneum) Intra-abdominal haemorrhage (erosion of splenic vessels) Multiple organ failure (ARDS, acute renal failure, hypovolaemic shock, DIVC) Hypocalcaemia, hyper/ hypoglycaemia

Intervention for local complications

- ERCP - No benefit in mild biliary pancreatitis - Indications:  Severe pancreatitis  Evidence of ductal stones  Cholangitis  No response to treatment within 48 hours - ERCP should be done within first 48-72 hours for maximum benefit - CT-guided aspiration of pancreatic necrosis  Can help differentiate between sterile and infected necrosis  Consider surgery if patient doing poorly - Necrosectomy for infected necrosis  Some kind of lavage and drainage procedure is done after necrosectomy to decrease infective load - Role of surgery  Infected necrotic pancreas (mortality 100% without operation)  Sterile necrotic pancreas (necrosectomy)  Delay surgery till as late as possible for demarcation of necrotic areas (repeated surgeries required)  Diagnostic uncertainty  Complications e.g. intra-abdominal haemorrhage - Pseudocyst  Operate if larger than 6cm and persisting for more than 6 weeks as the chance of spontaneous resolution is low and risk of complications (infection, haemorrhage, rupture) is high  Surgery can be open, laparoscopic, endoscopic or percutaneous (radiologically guided)  Endoscopic – internal drainage via a cystogastrostomy, cystoduodenostomy or cystojejunostomy

49 MANAGEMENT OF AETIOLOGY & PREVENTION OF RECURRENCE Avoid alcohol, stop all offending medication & control hyperlipidemia Cholecystectomy for biliary pancreatitis

-

18-21% of patients with biliary pancreatitis will have another episode Among these, 25-65% will develop the 2nd episode within 30 days of the initial one done in the same admission for pts with mild pancreatitis In patients with severe pancreatitis, there is reluctance to do the surgery early, as the patient may develop complications that require surgical intervention – better to do all surgery in the same operation instead of opening the patient twice

PRESENTATION May be asymptomatic, picked up on imaging for some other purpose Pancreatic head or periampullary

Pancreatic body/tail

- Obstructive jaundice (painless obstructive jaundice with palpable GB) + cholangitis - Duodenal obstruction - Bleeding upper GIT (haematemesis and/or malaena) - Malaise, weight loss, anorexia, nausea

Late presentation - Coeliac and mesenteric plexus invasion – dull constant pain in the epigastrium radiating to the back - Malaise, weight loss, anorexia, nausea - Exocrine insufficiency with duct obstruction  steatorrhoea, malabsorption - Metastatic symptoms: ascites, bone pain, CNS symptoms, dyspnoea - Paraneoplastic syndromes – migratory thrombophlebitis in 6%

PANCREATIC CANCER EPIDEMIOLOGY - Incidence about 3-5 per 100,000 per year in each gender - Eighth cause of cancer death in Singapore - 1.7:1 male to female ratio - Very poor prognosis – median survival for unresectable disease is 6 months (80% of patients have unresectable disease at presentation); overall 5-year survival indirect; Normal 3:7); raised ALP and GGT more than AST and ALT (obstructive picture) 4. Amylase 5. PT/PTT – any prolonged PT from vitamin K malabsorption, liver dysfunction 6. Tumour markers – CA 19-9, CEA (cholangioca and pancreatic ca) 7. Blood c/s if febrile and jaundiced Imaging

- Ultrasound versus CT  US findings: GB stones or sludge, thickened GB wall, pericholecystic fluid, duct dilation, liver consistency (fatty or cirrhotic)  Both useful in demonstrating dilated biliary system and site of obstruction as well as the cause of obstruction  Ultrasound is sufficient if malignancy is unlikely but unable to detect distal CBD stones well, but CT is preferred if there is a suspicion of malignancy (Ca pancreas or periampulary cancer)  define the tumour (T) better & stage at the same time (N & M) MANAGEMENT The patient is managed as for the causative aetiology (see relevant sections)

GALLSTONE DISEASE DEFINITION Gallstone is a generic term for any kind of stone (cholesterol, pigment) in any part of the biliary system (gallbladder, cystic duct, hepatic duct, common bile duct, etc) EPIDEMIOLOGY - Exact incidence in Singapore not known - In the West: overall 10-15%; 20% in women and 10% in men - Consistent 2:1 female to male ratio - Typical picture (the F‘s): Fat, female, forty, fertile, flatulent

52

NORMAL PHYSIOLOGY OF BILE - Normal bile contains bile salts (primary and secondary), phospholipids, cholesterol, protein, and bilirubin - Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol STONE COMPOSITION AND PATHOPHYSIOLOGY Cholesterol stones

-

More common in older patients (peak at 40-50 years) Cholesterol stones are hard and faceted Cholesterol stones results from disruption in the solubility equilibrium of bile Risk factors for cholesterol stones formation: 1. Increased cholesterol secretion in bile  Obesity  Hyperlipidaemia  Increased oestrogens: female, pregnancy, exogenous administration 2. Decreased emptying of the gallbladder  Gallbladder malignancy is an important cause to exclude  Truncal vagotomy  Spinal cord injury

Pigment stones

-

More common in younger patients Pigment stones are soft stones and crumble easily 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 gallbladder stasis - Brown stones are composed of calcium salts, bilirubin, and more cholesterol than black pigment stones; they form in the biliary ducts due to infection with bacterial degradation of biliary lipids, the degradation products of which then precipitate Biliary sludge

-

Microlithiasis suspended in bile; a milieu that predisposes to stone formation Can be visualised on the ultrasound scan as layering in the biliary tree Sludge is a pre-stone condition, but not all sludge becomes stones 20% of biliary sludge will disappear, 60% recur, and 10% form stones

53 CLINICAL COURSE

INVESTIGATIONS FOR GALLSTONE DISEASE

Asymptomatic

1. Plain abdominal X-ray

- 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

- 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)

Symptomatic sequlae

Basal pain is due to inflm of ductal epithelium & proximal distension.

1. Biliary colic - 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

- 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 (PTBD)

- PTC involves a tube being inserted into the liver under radiologic guidance into one of the biliary ducts (must be dilated duct) - Rarely done now; main indications: 1) high obstruction not well visualised in ERCP; 2) therapeutic purpose of drainage for an obstructed system that cannot be drained from below - Mostly for therapeutic rather than diagnostic purposes - Complications: bleeding; leakage of bile when tube is removed 7. HIDA scan

- No longer used commonly, except in biliary atresia 5 criteria for a normal cholangiopancreatogram (a) Normal intrahepatic ducts (b) No filling defects (c) Smooth common bile duct (d) No stricture/narrowing of the common bile duct (e) Good and free flow of contrast into duodenum TREATMENT Asymptomatic

- No surgery required unless patient has indications for surgery (see above) - Expectant management and close follow-up - Counsel patient about symptoms – biliary colic, acute cholecystitis, obstructive jaundice, etc Symptomatic

- Cholecystectomy is the only way to treat gallbladder stones that are symptomatic - Can be open or laparoscopic – laparoscopic is preferred as it is associated with shorter hospital stay, less pain, less complications post-operatively - Risks of laparoscopic cholecystectomy  Conversion to open operation up to 5% (due to abnormal anatomy; difficult or complicated dissection; iatrogenic injury); conversion rate is higher if there is ongoing infection e.g. cholecystitis – up to 1 in 3 to 1 in 4  Injury to surroundings: bowel & biliary structures e.g. CBD  Spilled bile  peritonitis, sepsis  Haemorrhage  Infection

54

- Non- surgical means of stone treatment  Chemodissolution  Liver diet  Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around to dampen waves; good results only for cholesterol stones   All not shown to work for long-term

ACUTE CHOLECYSTITIS PATHOPHYSIOLOGY - Gallstone gets stuck in the cystic duct causing obstruction of biliary flow - Gallbladder becomes distended and inflamed PRESENTATION - Constant, severe RHC pain (less commonly epigastric) - Radiates to the inferior angle of the scapula - 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 empyema - LFTs usually normal; no jaundice ULTRASOUND FEATURES OF ACUTE CHOLECYSTITIS - Presence of gallstones in biliary system - Contracted gallbladder (from chronic gallstone disease) - Pericholecystic fluid (oedema of gallbladder wall) - Sonographic Murphy‘s positive - (Fat stranding around gallbladder not seen on ultrasound but on CT) MANAGEMENT - Resuscitate the patient - Septic workup - Bowel rest and intravenous fluids - Analgesia - Empirical intravenous antibiotics – IV ceftriaxone and metronidazole - Definitive treatment – laparoscopic cholecystectomy

55 Timing of cholecystectomy

- Dependent on several factors:  Severity of illness  Response to resuscitation and antibiotic therapy  Logistical considerations (availability of OT, surgeon etc)

3. Gangrene and perforation

- Possibilities available: i. Emergency (immediate; in very sick patients who are not doing well/not responding to treatment) ii. Early (within few days of onset) iii. Delayed/interval (after 6-8 weeks)

4. Cholecystenteric fistula

Early

Delayed

Advantages - Everything done in one admission - Easier to operate as the gallbladder is oedematous

Advantages - Lower risks - Better laparoscopic success

Disadvantages - Ongoing inflammation  higher risk of bleeding - Higher risk of injuring some other structure due to difficulty in visualisation - Higher conversion rate to open chole - Increased risks of post-op infection

Disadvantages - Fibrosis  difficulty mobilising gallbladder - Need for another admission - Chance of recurrence during the time

- Localised perforation  abscess that is confined by the omentum - Free perforation  generalised peritonitis and sepsis, requiring emergency laparotomy - Most commonly occurs in duodenum, then colon, and stomach; after repeated attacks of cholecystitis - Usually asymptomatic - On AXR, aerobilia is seen in 40% of cases - Symptomatic fistulas should be treated with cholecystectomy and fistula closure 5. Gallstone ileus

- Stones causing cholecystenteric fistula pass into the enteric lumen causing intermittent bouts of small bowel obstruction - Accounts for 1-2% of IO overall - Most common site of obstruction is terminal ileum - Small stones (100μl/ml (good sensitivity of 89%, specificity 86%) - Contrast CT - PTC (2 functions: 1) roadmapping for surgery; 2) drainage of obstructed system if ERCP cannot drain) CURATIVE TREATMENT - Surgery is the only chance of long-term cure - Only 25% of tumours are resectable - Contraindications to surgery  Bilateral or multifocal intrahepatic disease  Invasion of portal vein trunk or hepatic artery  Bilateral involvement of hepatic arterial or portal venous branches  Unilateral hepatic vascular invasion with contralateral ductal spread  Distant metastases PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) - Intrahepatic: 35-45% - Distal 35-45% - Perihilar 10-30% (worse prognosis due to early lymphatic spread) PALLIATION - Endoscopic/percutaneous transhepatic biliary stenting - Bilateral drainage for hilar cholangiocarcinoma - If after opening up and finding that tumour is not resectable, can perform surgical bypass

RECURRENT PYOGENIC CHOLANGITIS BACKGROUND Cholangiohepatitis, or recurrent pyogenic cholangitis (RPC), is characterized by: - Recurrent bacterial cholangitis - Intrahepatic pigment stones - Intrahepatic biliary obstruction. PATHOPHYSIOLOGY Helminthic infxn (eg Ascaris lumbricoides, Clonorchis sinensis)  epithelial damage  predispose to seeding of coliforms into biliary system  stone formation  recurrent cholangitis HISTORY: - A history of recurrent attacks of cholangitis – typical hx:  1-2 episodes of fevers, jaundice, and RUQ abdominal pain per year  Hx of prev biliary surgery, endoscopic procedures, or percutaneous biliary drainage procedures. - Complications of pyogenic cholangitis  cirrhosis with portal hypertension  cholangiocarcinoma PHYSICAL EXAMINATION No specific physical findings are evident in RPC. Dx based on history. DIFFERENTIALS Primary Sclerosing Cholangitis INVESTIGATIONS For diagnosis For Complications Bloods

- FBC - LFT with ALP>ALT, AST - Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and vitamin K deficiency)  Impt to exclude – correct with parenteral Vit K before invasive procedures - Blood C/S: bacteremia – results help guide antibiotic choice. - Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present.

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

ANATOMY - The breast is a modified sweat gland that lies in the subcutaneous tissue of the anterior chest wall between the superficial and deep layers of the superficial fascia - The base of each breast extends from the lateral border of the sternum to the midaxillary line, from the second to the sixth rib - The axillary tail pierces the deep fascia and enters the axilla - Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts that open separately on the nipple - Fibrous septa (Cooper‟s ligaments) interdigitate the mammary parenchyma and extend from the posterior capsule of the breast to the superficial layer of fascia within the dermis, and provide structural support to the breast (involvement of these ligaments by malignancy causes dimpling of the overlying skin)

2. Internal mammary nodes--20% of drainage from the ipsilateral breast  Account for about– upper and lower inner quadrants  About 4 nodes per side, with one node in each of the first three interspaces and one in the fifth or sixth interspace 3. Interpectoral (Rotter‘s nodes) – between pec major and pec minor muscles

PRESENTATION OF BREAST DISEASE 1. Lump (painful vs painless) 2. Pain (cyclical vs non-cyclical) [ more likely benign] 3. Nipple changes or discharge

APPROACH TO BREAST LUMP DIFFERENTIALS (AGE DEPENDENT) Painless lump

Painful lump

Elderly: 1. Carcinoma

1. 2. 3. 4. 5. 6. 7.

Younger: 2. Cyst 3. Fibroadenoma 4. Area of fibroadenosis (nodularity)

Area of fibroadenosis Cyst Abscess (usually in lactating women) Fat necrosis (minor trauma) Periductal mastitis Galactocoele (lactating women) Carcinoma (rare; ~10% & advanced)

HISTORY 1. History of lump

- Lymphatic drainage: 1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes 1. 40-50 nodes in 5 groups: Anterior, posterior, medial, lateral, apical 2. Drains into supraclavicular and jugular nodes Anatomic/ Surgical division into levels I, II and III by the pectoralis minor muscle: Level I: lateral to pectoralis minor Level II: posterior to pectoralis minor Level III: medial to pectoralis minor, extending up to apex of axilla

60

-

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,  Dimpling (more prominent hair follicles 2o to dermal oedema from blocked lymphatics)  Swelling?  Any general asymmetry of the breasts noticed? Duration since first noticed Any increase in size from first noticed to now? Any changes in the nipple e.g. retraction Nipple discharge? If present, what is the colour and consistency? Any other lumps elsewhere – other breast? Axilla? Neck?

61 - 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

2. Oestrogen exposure history

Increased risk: - Age of menarche (early 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

Palpation

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

Check list: - Breast - Nipple - SC LN - Spinal Tap - Lung effusion - Hepatomegaly

Inspection

- General appearance - Patient‘s hands relaxed at her sides – look for:  any asymmetry in the breast contours,  any obvious skin changes (peau d‘orange, 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)

- 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, and NON-TENDER, is hemispherical with  Tender or non-tender poorly defined edges, measuring  Warmth of overlying skin ___X___CM. It is firm in consistency with a  Size 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)  Fixation to the skin – try to pick up the skin above the lump  Fixation to underlying muscle – ask patient to press her hands against her hips to contract the pectoralis major muscle, then try to move the lump in 2 perpendicular directions, then ask patient to relax and try to move the lump again - Continue to examine carefully for other lumps (multiple lumps are unlikely malignant, usually fibroadenoma or fibroadenosis) - 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: anterior, posterior, medial, lateral, and apical - If any lymph nodes are found to be enlarged, note the number of lymph nodes, their site, size, tenderness, consistency (firm, hard, matted), mobility To complete the examination

-

Examine the the supraclavicular LNs & cervical LNs Examine the lungs for any pleural effusion Percuss the spine for bony tenderness Examine the abdomen looking for hepatomegaly

FINDINGS FOR THE COMMON BREAST LUMPS Type of lump Cyst Nodularity

Age

Pain

Surface

Consistency

Mobility

30-55 20-55

Occ Occ

Smooth Indistinct

Not fixed Not fixed

Fibroadenoma Cancer

15-25 35+

No No

Smooth, bosselated Irregular

Soft to hard Mixed, fluctuant Rubbery Stony hard

Very mobile May be tethered or fixed

(c) Spiculated mass or stellate lesionwith poor outline or comet sign - 95% of spiculated masses on mammography are due to malignancy - Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance of it being malignant - Causes: Invasive cancer, radial scar (benign), fat necrosis, abscess, etc (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 – (i) Clinical examination; (ii) Imaging; and (iii) Histology.” Imaging

All 3 must be concordant for benign to have >99% specificity to r/o malignancy

1. Mammography - Most sensitive of the proven breast imaging modalities - Usually performed in asymptomatic older women (>40YO) [breast tissue in younger women is denser; more difficult to pick up abnormalities], but >35YO in symptomatic women - Normally, 2 views are done: 70%  craniocaudal (CC)  right /Left  70% tumours in lateral quadrant (upper)  mediolateral oblique (MLO)  captures the tail  right/ left  80% tumours in oblique milky way 80%

- Additional specialised views: magnification and coned compression; done on request to help magnify areas of abnormality or help visualise breast better

62

- Abnormal features: (a) Neo-density or asymmetric density (look for bilateral synchronous ca; satellite lesion) (b) Microcalcifications (0.5mm  macrocalcifications; >5/mm2  cluster - Sole feature of 33% of cancers detected on mammography - Causes: DCIS, invasive cancer, fibrocystic disease, papilloma - Features of malignancy:  pleomorphic microcals,  heterogeneous appearance; segmental  closely grouped or arranged in a linear pattern (ductal distribution),  underlying density - Features of Benign microcals: punctate, ―tea-cup‖ appearance

BI-RADS (Breast Imaging Reporting and Data System) classification Category 0: Need additional imaging evaluation Category 1: Negative (nothing to comment on, 0.05% risk still present) Category 2: Benign Category 3: Probably benign, short-term follow-up suggested (1yr after stopping breastfeeding) 3. Is the discharge worrisome?

-

Unilateral or bilateral (unilateral more worrisome) Discharge from multiple ducts or single duct (single duct more worrisome) Nature of discharge (bloody more worrisome) Age of the patient (more worrisome in older patient >60)

4. Is it troubling the patient?

PHYSICAL EXAMINATION (as described above) INVESTIGATION 1. Discharge for cytology to detect malignant cells 2. Mammography/ US of both breasts to detect any underlying malignancy 3. Histology of biopsied lesion if found on imaging 4. Ductography, ductoscope & biopsy MANAGEMENT - If malignancy found, manage malignancy - Excision for intraductal papilloma (microdocholectomy, total ductal excision, hookwire locailised excision) - Antibiotics for mastitis/abscess + incision and drainage for abscess - Conservative management for most other pathologies unless discharge persists and is troubling patient  microdochectomy of offending duct

Lobular

BREAST CANCER EPIDEMIOLOGY - Most common cancer in females in Singapore: - Age-standardised incidence 55 per 100,000 in 2002; incidence is half that of the West - Bimodal age distribution: 45-55YO & older (>75YO) - Gender ratio is about 100-150 female :1 male RISK FACTORS 1. Age (increases with increasing age with two peaks as mentioned) 2. Genetic: - Family history: maternal & paternal (breast or ovarian cancer, especially if in first degree relative, young onset 55YO - Oral contraceptive usage (pure oestrogen type) - HRT (>5yrs, small increase in risk; reduced when stopped) 4. Previous breast disease: - Previous breast cancer (10X) - Previous biopsy with atypical ductal hyperplasia or LCIS (7-10X) 5. Ionising radiation to breast (previous RT) 6. Alcohol consumption (daily) PATHOLOGY (WHO classification: epithelial and non-epithelial tumours.) - Non-epithelial tumours arise from supporting stroma (e.g. angiosarcoma, malignant phyllodes tumour, primary sarcomas) and are very uncommon - Epithelial tumours arise from cells lining the ducts or lobules, and can be further divided into invasive and non-invasive based on invasion of the basement membrane Ductal

Non-invasive

Invasive

DCIS

IDC

-

- 70-80% of invasive breast cancer - Includes all cancers that cannot be subclassified into a specialised type  ―no special type‖ - Poorer prognosis than a carcinoma of specialised type - 2/3 express ER/PR, - 1/3 overexpress C-erbB2

From terminal duct lobular unit, Cause distortion of lobules, Do not invade BM Non-palpable, detected microcals 35% multicentric, occult invasive ca in 10-20% - Progress to ca within 10 yrs, ~30% risk; considered pre-malignant - Good prognosis if treated

64

Others

LCIS

ILC

- From terminal duct lobular unit (like DCIS) - Do not distort lobular architecture - Usually non-palpable & not detected by mammo, incidentally detected - 60-80% multicentric and bilateral - Not premalignant, but a marker for increased risk of invasive disease in both breasts (7-10x increased risk) - If ca develops, will be IDC usually, occurs >15 years after diagnosis

- 5-10% of invasive cancers - 10-20% multicentric and/or bilat - Cells morphologically similar to cells of LCIS: monomorphic, bland round nuclei - Cells invade individually into stroma (due to loss of E-cadherin, a cell-adhesion molecule) - Similar prognosis to IDC

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

Inflammatory carcinoma - Presents as erythematous. enlarged, swollen breast w/o palpable mass - Histologically not specialised - Diffuse invasion of breast parenchyma by ca cells blocking numerous dermal lymphatic spaces  swelling - No histo features of inflammation - Very poor prognosis, rapidly fatal

SPREAD - Local: skin & subcut tissues, underlying ribs and muscle (chest wall) - Lymphatics: axillary, internal mammary LNs, supraclavicular LNs - Haematogenous: lungs, liver, brain, bone, adrenals, ovaries PRESENTATION - Asymptomatic: detected on mammographic screening - Local: - Self-detected lump in the breast (>1/3 of patients) - Nipple change: distortion, destruction, retraction, deviation, discharge, eczema - Overlying skin changes e.g. peau d‘orange, tethering (means mass is still mobile but overlying skin will be indented when moving the lump), fixation (means the mass is not mobile), even fungating ulcer - Other lumps in axilla - Pain is uncommon. - Constitutional: LOW, LOA - Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone, brain, adrenals)

65 DIAGNOSIS – BY TRIPLE ASSESSMENT (see above)

PROGNOSIS Prognostic factors:

STAGING - Triple assessment can help divide it into:

-

DCIS or early Breast Cancer (BC) (at most with small mobile axillary LNs) locally advanced BC (matted LNs, skin and rib involvement) o  continue to stage to look for metastasis in advanced BC

- Staging Investigations:

(i) CXR or CT thorax (for lung metastases; look for isolated hyperdensity) (ii) LFT (raised ALP) or US HBS or CT abdomen (for liver and adrenal metastasis) (iii) Bone scan (iv) CT or MRI brain T stage Tis: Carcinoma in-situ, Paget‘s with no tumour

N stage N1: Mobile ipsilat axillary nodes

M stage M1: distant mets

T1: 10mm; 5cm

Surgery

T4: T4a – Chest wall involvmt T4b – Skin involvmt T4c – Both 4a and 4b T4d – Inflammatory ca

Stage 0 Tis

DCIS

Stage I

Stage II

T1N0

T2N0, T3N0 T0N1, T1N1, T2N1

Early

Breast cancer

Stage III *skin, rib inv., matted LNs

Stage IV

T3 N1 T0N2, T1N2, T2N2, T3N2 Any T, N3 T4, any N Locally advanced BC

M1 Adv. BC

Aaaaa – Stage Xb (e.g. IIb, IIIb) Survival

Stage I: Stage II: Stage III: Stage IV:

90% 60% 30% 10%

(70% in 10 yrs)  95% with adjuvant Rx (40-50%)  76% with adjuvant Rx (20-30%)  50% with adjuvant Rx (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

APPROACH TO THYROID PROBLEMS – 2 MAIN TYPES 1. Problem with configuration/anatomy

(i) (ii) (iii)

-

Solitary thyroid nodule (most common in exam) Multinodular goitre Diffuse enlargement

2. Problem with function (usually hyperfunctioning)

(i) (ii) (iii) (iv)

Graves‘ disease Toxic adenoma Toxic multinodular goitre Hashimoto‘s disease

-

HISTORY-TAKING Onset (gradual or sudden), duration Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth; ddx includes haemorrhage into necrotic nodule or cyst, subacute thyroiditis) Any pain – bleeding into cyst can result in sudden increase in size and pain; rarely pain can occur in anaplastic carcinoma and thyroiditis Compressive symptoms: difficulty swallowing, difficulty breathing, hoarseness of voice (benign pathologies almost never compress the recurrent laryngeal nerve) Cosmetic effects

-

About THYROID FUNCTION Hyperthyroid Weight loss despite increased appetite Heat intolerance Increased sweating Proximal myopathy (Graves’) Diarrhoea, frequent bowel movement Tachycardia, atrial fibrillation Oligomenorrhoea, amenorrhoea Nervousness; easily irritable; emotional lability; insomnia Fine tremor

78

-

Medications given e.g. propylthiouracil, carbimazole, propranolol – for how long, efficacy, side effects Radioactive iodine treatment – what was the result? Is the patient receiving replacement? Surgery – what kind of surgery, any complications? Follow-up – what investigations done?

PHYSICAL EXAMINATION

About the LUMP

-

-

History of autoimmune disease e.g. type I DM, SLE, RA, pernicious anaemia (associations with Graves and Hashimoto‘s) History of cancer elsewhere – metastatic disease to thyroid; lymphoma; papillary cancer is associated with familial polyposis syndromes  ask about GI polyps/ca History of thyroid disease – long-standing MNG can progress to lymphoma Occupational history – any exposure to radiation (papillary cancer risk) Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2, AD inheritance), ~5% of papillary cancers

About previous TREATMENT for any thyroid disease

AIMS OF ASSESSMENT IN THYROID NODULE/ENLARGEMENT: - Exclude cancer! - Address issues of thyroid function - Look for any complications e.g. compression (of airway, oesophagus, rarely nerve) - Cosmesis – is patient bothered by lump?

-

-

Hypothyroid Decreased appetite, weight gain, lethargy Cold intolerance Dry skin, loss of outer third of eyebrows Muscle fatigue Constipation Bradycardia Menorrhagia Slow thought, speech and action; depression; dementia Carpal tunnel syndrome symptoms

A. THYROID GLAND

GREET PATIENT, ASK FOR PERMISSION to examine (and listen to the voice – is it hoarse?) POSITION PATIENT – on a chair with space behind the chair for you to stand. INSPECT FROM THE FRONT 1. Any swelling? Where is it? 2. Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a skin crease)? Sinuses? 3. Any skin changes over the mass? 4. Check if mass moves on swallowing by asking patient to take a sip of water – ―Please take a sip of water and hold it in your mouth, do not swallow until I tell you to.‖ 5. Check if mass moves on protruding the tongue – ―Please open your jaw slightly. Now, without moving your jaw, please stick your tongue out and back in again.‖ NB. A thyroid swelling moves only on swallowing; a thyroglossal cyst will move on both swallowing and protrusion of the tongue. 6. Check for plethora of face, distended neck veins – may be due to compressive nature of mass (but rarely seen).

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.

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!



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

Embryonic origin:

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)

the tracheo-oesophageal groove and are not palpable.

NEUROMUSCULAR 1. Proximal myopathy (Graves‘) 2. Reflexes – slow to relax in hypothyroidism 3. Legs for pretibial non-pitting oedema (Graves‘ or hypothyroid)

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

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. 2. 3. 4.

Cancer (only 10-20% of nodules is malignant, but need to exclude!) Follicular adenoma Cyst (simple, colloid, or haemorrhagic) Dominant nodule of a multinodular goitre

Clinical features suspicious of malignancy:

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

1. FINE NEEDLE ASPIRATION CYTOLOGY - The most important investigation modality! - 90-95% sensitivity and specificity - 4 possible results: (i) Benign (thyroiditis, dominant nodule of MNG) (ii) Malignant (papillary, medullary, anaplastic, mets) (iii) Suspicious (follicular, Hurthle cell change in follicular lesion) (iv) Inadequate  repeat FNAC - Can be both therapeutic and diagnostic for cyst – chocolate-brown fluid aspirated; feel lump after aspiration to check for resolution - Cannot differentiate follicular adenoma from follicular carcinoma as the mark of malignant disease is capsular invasion – can only tell from a histological specimen of the nodule - Procedure: inject local anaesthetic in area, insert 20-22G needle and apply suction while fanning needle in region of nodule, release suction before pulling out needle, expel contents onto slide, then fix - Best to have experienced cytologist on hand to view slides and re-do FNAC if the sample is inadequate 2. ULTRASOUND OF THYROID - Advantages: (i) Objective measurement of nodule (ii) Detection of subclinical nodule/screening – of value in papillary carcinoma since multicentric disease occurs in 15% (iii) Detection of lymph node enlargement (especially level VI nodes) (iv) Can define consistency of nodule – solid, cystic, or complex

80

- Suspicious sonographic features: (i) Microcalcifications (in psammoma bodies  papillary cancer) (ii) Indistinct margins (iii) Sonolucent halo around lesion (iv) Hypoechoeic or anechoeic lesion – carcinoma is almost never hyperechoeic (v) Increased intranodular vascularity - Ultrasound still does not provide as good diagnostic value as FNAC 3. THYROID FUNCTION TEST - Easy to perform, establish baseline, detect any abnormal function - No real diagnostic value 4. RADIO-ISOTOPE SCAN - Hot nodule: only 1% malignant; but cold nodule: 10-20% malignant - But not very useful diagnostically 5. BASELINE TUMOUR MARKERS (IF SUSPECTED OR CONFIRMED MALIGNANCY) - For differentiated thyroid cancer: thyroglobulin - For medullary thyroid cancer: calcitonin, carcinoembryonic antigen (CEA) 6. CT SCAN OR MRI - Not routine in thyroid nodular study - Uses: (i) Evaluating invasion of surrounding structures (ii) Retrosternal extension (iii) Lymph node involvement - Care to be taken with CT as contrast contains iodine and will affect post-op radioactive iodine body scan once given - MRI has same functions as CT but higher cost 7. ENT EXAMINATION OF VOCAL CORDS - In the rare occasion that there is pre-existing vocal cord palsy on one side  take extra care not to injure opposite recurrent laryngeal nerve as that can cause bilateral vocal cord palsy Management of benign nodule:

-

Soft, small, round nodule with benign FNAC results, non-functional, not causing any symptoms  can follow-up and monitor any increase in size A lump >4cm has a greater risk for malignancy

81 PART III: THYROID CANCERS Differentiated thyroid carcinoma Papillary carcinoma Follicular carcinoma

Medullary carcinoma

Anaplastic carcinoma

Lymphoma

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 - Polyposis syndromes (FAP, Gardner‘s, etc) - Positive family history in 5%

- Follicular adenoma is NOT a risk factor - Iodine deficiency may be associated

- Significant family history in the familial type – MEN2 (AD, complete penetrance, associated with parathyroid adenoma and phaeochromocytoma – see notes below)

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

- History of lymphoma or MALT elsewhere - Hashimoto’s thyroiditis (60X increased risk)

Pathological features

- Characteristic Orphan Annie nuclei, nuclear pseudoinclusions - Papillary architecture with psammoma bodies - Tall cell variant (nuclear features of papillary ca within follicular lesion) behaves like papillary ca, has worse prognosis

- Follicular structures similar to normal thyroid - Diagnosis of cancer made on evidence of capsular or vascular invasion by tumour cells (vs follicular adenoma) - Hurthle cell variant – worse prognosis

- Arise from parafollicular C cells (which produce calcitonin) - Distinctive deposits of acellular amyloid material – altered calcitonin collections - Multicentric C-cell hyperplasia may be seen in familial cases

- Small blue round cells that are highly anaplastic – may resemble lymphoma

- FNAC may suggest lymphoma but definitive diagnosis requires trucut or excision biopsy - Almost always nonHodgkin’s of B-cell type

Clinical features

-

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

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

- Large bulky mass involving neck structures – locally advanced - Aggressive growth - Multiple metastases probably present at presentation

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

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

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

Palliative therapy for compressive effects - Chemotherapy to shrink tumour - Surgical debulking - Tracheostomy

Chemotherapy and/or radiotherapy depending on type of lymphoma

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

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

Median survival 40, presence of metastases, extrathyroid invasion, size>4cm (more details on risk stratification below) Treatment

TSH suppression – give L-thyroxine to suppress TSH levels to 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

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, sternocleidomastoid 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

PART IV: SURGERY IN BENIGN THYROID DISEASE

A group of inherited diseases resulting in proliferative lesions (hyperplasia, adenomas, carcinomas) of multiple endocrine organs.

Indications for surgery:

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

1. 2. 3. 4. 5.

Cannot be treated medically - failed medical therapy or unsuitable for medical tx Cancer Compression on neighbouring structures Cosmesis Compliance/cost problems – with long-term medical therapy (but patient may still require long-term therapy after op if he/she becomes hypothyroid or is still hyperthyroid) 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)

IMMEDIATE (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 1.3, suggests non-compressible calcified vessel)  ABPI between 0.5 - 0.9 – occlusion, often associated with claudication  ABPI 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

ASSESSMENT OF SEVERITY The three L’s of peripheral arterial disease:

Life – does disease threaten life (e.g. sepsis; other complications of atherosclerosis e.g. stroke, AMI;) or will intervention cause risks (ii) Limb – will patient lose the limb (iii) Lifestyle – is the lifestyle of the patient severely handicapped, does it require intervention (i)

Fontaine system

Stage I: Asymptomatic Stage IIa: Mild claudication Stage IIb: Moderate to severe claudication Stage III: Ischaemic rest pain Stage IV: Ulceration or gangrene TREATMENT OF CLAUDICATION Conservative

- Mainstay for all cases of claudicants, esp. foot and calf claudicants - Smoking cessation - Exercise training to stimulate collateral formation  symptoms get better  Exercise at least half to one hour every day  Walk until pain comes, rest 2-3 minutes, walk again  Keep a walk diary recording daily claudication distance in paces - Podiatrist to teach foot care - Assessment and treatment to optimise control of CVS risk factors– cardiologist Patient educaton: Teach patient to go to ED if symptoms of critical ischaemia arises - Antiplatelets [e.g. aspirin] and statins (target lipid levels are much lower) - Use of Vasteral (methoxyphylline) is controversial - Monitor regularly with measurement of ABPI -



Intervention (endovascular or surgical)

- At least 6 months of conservative treatment first; mainly for aortoiliac disease - Monitor claudication distance and ABPI – intervene if deteriorating despite conservative management - Confirm disease outline with CT angiogram or angiogram - If parameters improve but then plateau, discuss with patient about whether he can accept the level of symptoms, and the risks of intervention  weigh risks against benefits - Usually do angioplasty rather than bypass as it is less invasive, though may not be as effective in treating the symptoms

92

1. Angioplasty  Stenting usually not done for lower limbs except in aortoiliacs (since stent needs to be placed in a vessel which is relatively fixed and won‘t be kinked/bent by movement)  Angioplasty only effective for focal stenotic lesions and better for large vessels  Problem with angioplasty is that it is not long-lasting – restenosis can occur  New method: subintimal angioplasty – if lumen is so occluded that guide wire cannot pass through, the guidewire is threaded into the subintimal space to create a dissection around the occluded segment, and this space is then angioplastied to create a channel parallel to the actual lumen for blood to flow through 2. Bypass grafting  Consider bypass when lesions cannot be treated by angioplasty i.e. lesion extends for long distance through the vessel and/or no lumen for guide wire to pass through (complete occlusion)  Needs a good ―landing zone‖ for graft distally – if vessel is diffusely diseased, difficult to perform bypass TREATMENT OF CRITICAL LIMB ISCHAEMIA -

Need to revascularise – either angioplasty or bypass grafting

AMPUTATION Indications (3 D’s)

1. Dead: Necrotic tissue 2. Dangerous: Gangrene, ascending sepsis 3. Damn nuisance: Non-functional limb; bad smell; pain; constant need to dress wound - Level of amputation depends on vascularity of the limb and the indication (e.g. if infected, need to amputate above level of infection) - As far as possible try to preserve function of the lower limb - May require revascularisation interventions before amputation to ensure good healing, or to enable lower amputation - Do not simply amputate without ensuring good vascular supply to the surgical site, otherwise the wound will not heal

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 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 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

- Auscultate over the varicosities for any bruit (indicate arteriovenous malformation) - Examine the abdomen for any mass that may be causing the varicosities Use of a handheld Doppler probe to detect incompetence

- Doppler probe is placed in the popliteal fossa over small saphenous vein - 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 reflux of blood i.e. there is valvular incompetence INVESTIGATIONS Venous duplex ultrasound

- Indications:  Recurrent varicose veins  History of superficial thromobophlebitis or DVT  Complications of CVI: Venous eczema, Haemosiderin staining, Venous ulceration , Lipodermatosclerosis, - Ask for SFJ and SPJ reflux, perforator, deep venous incompetency & DVT screen - Can delineate deep and superficial venous systems and locate sites of incompetence - Exclude presence of deep vein thrombosis – stripping is contraindicated MANAGEMENT Conservative

1. Lifestyle changes - Decrease amount of time spent standing - If due to job, change job or ask for change to position to stand & walking less 2. Graduated compression stockings, usually grade II  ensure good pulses 3. Medications e.g. Daflon Surgical

Indications: 1. Cosmesis – large unsightly varicosities 2. Symptoms – pain, discomfort 3. Complications – signs of chronic venous insufficiency, venous ulceration Available modalities: 1. High tie with great saphenous vein stripping, and stab avulsion of varicosities 2. Ultrasound-guided foam sclerotherapy 3. Endovenous laser therapy (burns vein from within)

98

VENOUS ULCERS CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY 1. Obstruction to venous flow – thrombosis 2. Incompetent valves – varicose veins, deep vein reflux (post-DVT) 3. Muscle pump failure – stroke, neuromuscular disease INVESTIGATIONS 1. Exclude infection of the ulcer and other complications - FBC for raised total white count - Swabs of the ulcer for Gram stain and cultures - X-ray of the area to exclude underlying gas, bone involvement 2. Venous duplex to map out venous system 3. Check for peripheral arterial disease by doing ABPI 4. Biopsy if cannot exclude malignant transformation (Marjolin‘s ulcer) MANAGEMENT: Conservative

1. 4 layer compression stockings (change once per week) (a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool bandage (b) Crepe bandage (c) Blue-line bandage (Elset) (d) Adhesive bandage (Coban) 2. Analgesia 3. Antibiotics if infected 4. Warn patient to avoid trauma to affected area 5. Encourage rest and elevate leg 6. Once healed, compression stockings should be fitted and continued for life Surgical

- If ulcer fails to heal - First, exclude malignancy or other causes of ulcer (biopsy) - Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue - Venous surgery for the underlying pathology

99 UROLOGICAL DISEASES

HISTORY Post-renal Causes

APPROACH TO HAEMATURIA DEFINITION: - >3 RBC / hpf. - DDx: haemoglobinuria, myoglobinuria, pseudohaematuria (menstruating women), medications causing discoloration of urine (eg rifampicin, phenytoin) CAUSES Drugs PreRenal

Renal

Analgesics (NSAIDs) Anticoagulants Cytotoxic/immunosuppressive agents (eg cyclophosphamide) OCP Penicillin Quinine Warfarin

2. Painful vs painless haematuria Painful - Tumour - Hydronephrosis - Renal cysts - Ureteric stone / clot - Pyelonephritis - UTI - Bladder outflow obstruction (e.g. BPH, strictures)

Painless - Malignancy – RCC, TCC, Prostate - Drugs - GN - Bleeding diathesis - ITP / HSP - Infections – malaria, schistosomiasis - Exercise

Systemic

 Bleeding diathesis  Sickle cell disease

Metabolic

 Hypercalciuria  Hyperuricosuriia

3. Frequency + dysuria + haematuria - DDx: nephrolithiasis (colicky), malignancy, UTI (women & children), bladder outflow obstruction (men e.g. BPH)

Vascular

 AV malformations  Renal artery disease – thromboembolism, dissecting aneurysms, malignant hypertension  Renal vein thrombosis

4. Other urological symptoms - Storage problem – frequency, urgency, nocturia, incontinence - Voiding problem – strangury, hesitancy, dribbling, incomplete emptying etc - Others – polyuria, oliguria, urethral discharge

Vasculitis

 HSP  PAN  Wegener granulomatosis

Pre-renal & Renal Causes

Glomerular

Tubulointerstitial dz

Postrenal

      

1. Which part of urine stream is blood stained? - Beginning – urethra distal to UG diaphragm - End – bladder neck or prostate - Throughout – upper urinary tract or upper bladder

    

Post-strep GN Post-infectious GN IgA nephropathy Lupus nephritis Other GNs

    

Polycystic kidney disease Nephrolithiasis Malignancy – RCC, metastatic Pyelonephritis Renal cysts

 Infxns of ureter, bladder, prostate, urethra – eg schistosomiasis, TB etc  Cancers of ureter, bladder (TCC), prostate, urethra  Nephrolithiasis

5. Associated fever – pyelonephritis, malaria 6. Screen for pre-renal causes LOW / bone pain / sickness Rash, arthritis, arthralgia, myalgia, fever, oedema Sore throat, skin infxns, URTI Ongoing URTI or GE Iatrogenic Travel history PMHx Family history

Malignancies, TB, systemic illnesses Autoimmune causes, vasculitis Post-strep / post-infective GN IgA nephropathy Drug causes, radiotherapy Schistosomiasis, malaria Renal disease, HPT, diabetic nephropathy, bleeding diathesis, sickle cell dz PKD, sickle cell disease, renal dzes (eg Alport syndrome – ask for deafness), hypt, urolithiasis

Other necessary history

1. 2. 3. 4. 5.

Infection - Fever, travel and contact history Sorethroat - Post-strep/infective GN, IgA nephropathy Autoimmune - Fever, rash, joint pain, oedema Malignancy - LOW, bone pain, neuro deficits, SOB, liver function PMHx - Renal dz, - systemic dz (DM HPT Bleeding sickle cell) 6. Drug history / Hx of radiation 7. Family history – PKD, renal dz, Sickle cell, HPT PHYSICAL EXAMINATION 1. Check patient‘s vitals- stable? 2. Conjunctival pallor 3. Abdomen – renal mass, palpable bladder/bladder mass 4. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension of tumour into renal vein, blocking the testicular vein where it drains into the left renal vein) 5. Digital rectal examination – prostate enlargement (BPH versus cancer) INVESTIGATIONS 1. Urine dipstick

- Causes of false-positive for blood: haemoglobinuria, beetroot, drugs (rifampicin), metabolic (alkaptonuria, porphyria) 2. UFEME

- Confirm presence of red blood cells - Casts  nephritis - Elevated WBC (pyuria is >5 WBC per hpf), organisms  infection 3. Urine cytology for malignant cells 4. Urine phase contrast

- RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source, while isomorphic RBCs suggest post-renal source (ureter, bladder, etc) 5. Urine culture and sensitivity 6. Full blood count

- How low is the Hb? - Elevated TW – infection 7. Urea, electrolytes and creatinine

- Any renal impairment and electrolyte abn (renal or pre-renal dz more likely)

100

8. Plain KUB

- Stones, size of kidney 9. Ultrasound of the kidneys

- Renal size - Presence of any hydronephrosis - Renal stones 10. Intravenous urogram (IVU) – see below for more details

- Distortion of renal outline and pelvic calyces by RCC, may have specks of calcification - Stones (filling defect, proximal dilatation, decreased distal passage of contrast) + hydroureter and/or hydronephrosis - Filling defect in bladder due to TCC - Increased residual volume in bladder after micturition due to BPH 11. Cystoscopy

- Detection of bladder tumour (IVU may not pick up small tumours 200) (c) Patients on metformin (can cause lactic acidosis; patients need to stop metformin 2 days before and after study) (d) Patients with asthma (given steroids for 3 days before study)

101 RENAL CELL CARCINOMA INVESTIGATIONS EPIDEMIOLOGY - 3% of adult malignancy - Most frequent occurring solid lesion within kidney - 2:1 male predominance - Peak incidence 60-70 years PATHOLOGY - Most common primary renal tumour (80-85% of all tumours of the kidney) - Arise from the renal tubular epithelium - Three cell types: clear cell carcinoma (70-80%), papillary renal cell carcinoma (1015%), and chromophobe renal cell carcinoma (5%) - Other renal tumours: TCC of renal pelvis, Wilms‘ tumour, lymphoma RISK FACTORS - Smoking - Exposure to cadmium - Family history  von-Hippel Lindau syndrome due to mutation of the VHL gene on chromosome 3p25 (associated with CNS haemangioblastomas (usually cerebellar), bilateral multicentric retinal angiomas, phaeochromocytomas, etc)  clear cell carcinomas  Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene on chromosome 7q31  multifocal bilateral papillary carcinomas - Acquired polycystic kidney disease (secondary to chronic dialysis) PRESENTATION - Initially asymptomatic (may be detected incidentally) - Painless gross haematuria is the most common presenting symptom – >50% of cases - When tumour has grown large enough, dull flank pain and palpable mass may result  Classical triad of RCC: flank pain, painless haematuria, palpable renal mass (indicates late stage disease) - May have fever a/w night sweats, LOA, LOW, malaise - Polycythaemia occurs in 1-5% (due to increased erythropoietin) - For left renal tumour, extension of tumour into left renal vein can cause a left varicocoele as the left testicular vein becomes occluded - 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

DIAGNOSTIC 1. Imaging – CT and/or ultrasound

- Presumptive diagnosis is made on imaging – a renal parenchymal mass with thickened irregular walls and enhancement after contrast injection suggests malignancy 2. Pathological diagnosis

- Needle biopsy usually not done for resectable lesions due to fears of tumour seeding - In these resectable lesions, a partial or total nephrectomy is often performed, and provides the tissue diagnosis post-operatively - In tumours with metastatic disease on presentation, biopsy of the metastatic site may be easier STAGING 1. CT scan of the abdomen

-

Perinephric invasion, adjacent organ invasion Extension into renal vein, IVC Lymph node enlargement Liver metastases

2. CT scan of the chest

- For lung metastases 3. Bone scan

- Only done if patient complains of bone pain and/or alkaline phosphatase is raised 4. MRI of abdomen and heart

- Superior to CT for evaluation of IVC and right atrium involvement T1

Tumour 60 years old) - 4:1 male predominance

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  nephronsaving 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

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 (90% 5 year survival 75-90% 60-70% T2 MANAGEMENT DEPENDENT ON STAGE SUPERFICIAL TUMOUR - Primary treatment is TURBT of the tumour - Intravesical therapy indicated in patients with high risk of tumour recurrence or tumour progression (high grade, multiple primary sites, multiple recurrences, tumour size >3cm, primary or coexisting carcinoma in-situ, prostatic urethral involvement)  BCG – 1 instillation per week for 6 weeks  Mitomycin C – single instillation within 24hrs of TURBT, or weekly/monthly treatments for up to 2 years - Follow-up:  3-monthly cystoscopy for 1 year  6-monthly cystoscopy for next 4 years  Yearly cystoscopy thereafter  IVU every 2 years

Urine cytology with every cystoscopy

MUSCLE-INVASIVE - Radical cystectomy  Radical cystoprostatectomy with pelvic lymphadenectomy in male  Anterior exenteration with pelvic lymphadenectomy in female  Ways of diverting urine output o Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due to small calibre; not continent)

o o

Ileal conduit (a segment of ileum with ureters attached, as a stoma; not continent) Neobladder construction using ileum (only if urethra not removed; continent, better quality of life) Stoma with pouch construction under abdominal wall (not continent)

- Radiotherapy (not as good as surgery)

UROLITHIASIS STONE COMPOSITION - Calcium oxalate or calcium phosphate stones – 75% - Magnesium ammonium phosphate (struvite) stones – 15% - Uric acid and cystine stones – 10% 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 stone‘s constituents, such that they exceed their solubility  precipitate as stones - E.g. hypercalciuria with or without hypercalcaemia, hyperuricuria - Urinary tract infections can also cause stone formation – struvite stones form in Proteus vulgaris infections as this organism splits urea into ammonium, generating alkaline urine - Bacteria can also form nidi for the formation of any kind of stone PRESENTATION DEPENDS ON SITE Renal stones

- Most often asymptomatic unless the stone gets lodged in the pelviureteric junction causing hydronephrosis and subsequent infection  pyonephrosis - Vague flank pain may occur Ureteric stones

-

Even small stones can cause severe symptoms as the ureter is narrow Classically ureteric colic pain – severe, intermittent loin-to-groin pain Haematuria – gross or microscopic Irritative symptoms – frequency, urgency Can cause upper urinary tract infection  fever, pain

Bladder stones

-

May be asymptomatic Can cause irritative urinary symptoms – frequency, urgency Haematuria If infection is present – dysuria, fever, etc

PHYSICAL EXAMINATION - In ureteric colic, symptoms are often out of proportion to signs – no guarding, rebound, etc - If the patient has pyelonephritis, renal punch may be positive - Otherwise unremarkable examination

-

High fluid intake Low salt intake Restriction of red meat, dairy produce, refined sugars Increase citrus fruit intake

SURGICAL INTERVENTION INVESTIGATIONS

Indications:

1. Urine tests – dipstick, UFEME, urine culture/sensitivity

-

- Haematuria - Pyuria, micro-organisms (UTI) 2. KUB

- May be able to see radio-opaque stone (90% of renal stones are radio-opaque) - Look at kidney size, any renal stones - Trace path of ureter along tips of transverse processes, across sacroiliac joint, and medially into bladder, looking for ureteric stones - Look for bladder stones 3. Intravenous urogram

- Can also help to visualise a stone - Can show dilated urinary system secondary to stone obstruction – hydroureter and/or hydronephrosis 4. Ultrasound of kidney or bladder

- Features of stone: echogeneic rim, posterior acoustic shadowing 5. MAG-3 renogram

- If pyelonephritis present due to stone obstruction, it is valuable to measure the renal function using the MAG-3 renogram - The renogram gives the differential function of each kidney – in normal individuals the function should be approximately 50% on each side (out of 100% for both kidneys combined) - If one kidney has less than 15% of total renal function, it is not worth salvaging the kidney TREATMENT CONSERVATIVE Stones smaller than 5mm can be treated conservatively as 60% will be passed out; only treat if they do not pass out after 4 to 6 weeks, and/or cause symptoms - Treatment of any urinary tract infection - If underlying disease present that causes increased urinary concentration of stone components e.g. hypercalcaemia  treat disease if possible

104

Constant pain Does not pass after one month Too large to pass spontaneously Obstructs urine flow Causes urinary tract infection Damages renal tissue or causes significant bleeding Increase in size

Types of treatment available:

1. Percutaneous nephrolithotomy (PCNL) - Done for renal stones that are too large for ESWL to disintegrate - Contraindicated in uncorrected bleeding diathesis, patients unfit for GA 2. Extracorporeal shock wave lithotripsy (ESWL) - Calcium oxalate, uric acid and struvite stones fragment easily, but calcium phosphate and cystine do not - Used for stones below 10mm in size - Used for renal stones and upper ureter stones – not so good for lower system due to difficulty in access - Contraindicated in pregnancy, untreated UTI, untreated bleeding diathesis, distal obstruction that cannot be bypassed with a stent 3. Ureteroscopy with lithotripsy (usually laser lithotripsy, can also be done by pneumatic drill, electrohydraulic means) - For stones along the ureter 4. Cystolitholapaxy for bladder stone 5. Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed other management strategies, altered anatomy, performing open surgery for another reason anyway, non-functioning kidney Adjuncts:

- Double-J stent (or DJ stent) – inserted to stent the urinary system when worried that stone fragments after ESWL may cause obstruction e.g. when ESWL used for treatment of a large stone; or if system is obstructed to begin with, may want to stent to ensure good drainage after surgery

105 Summary of treatment modalities

Location Renal

Size < 5mm 5-10mm 10-20mm > 20mm

Treatment Conservative management unless symptomatic/persistent ESWL Either ESWL or PCNL PCNL

Upper ureter

< 5mm 5-10mm > 10mm

Conservative management unless symptomatic/persistent ESWL URS with lithotripsy

Middle ureter/ Distal ureter

< 5mm > 5mm

Conservative management unless symptomatic/persistent URS with lithotripsy

Bladder

< 30mm > 30mm

Cystolitholapaxy Open cystolithotomy (also if there are multiple stones)

HISTORY Symptoms of ARU:

- Inability to pass urine - Suprapubic distension with pain (unlike chronic retention of urine which is painless) Precipitating factors:

- Symptoms of urinary tract infection: dysuria, frequency, urgency, nocturia, haematuria - Constipation - Drugs e.g. cough mixture, antihistamines - Immobility History suggestive of aetiology:

APPROACH TO ACUTE RETENTION OF URINE

- Previous history of obstructive symptoms e.g. poor stream, hesitancy, terminal dribbling etc  BPH - 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 - Constitutional symptoms: LOW, LOA, malaise (any tumour in general)

CAUSES

Complications:

Mechanical

Extraluminal

Intramural

Intraluminal

Nonmechanical

Cord disease/ injury Neuropathy Drugs Others

Prostate enlargement (benign/malignant) Faecal impaction Pelvic tumour Pregnancy UV prolapse Tumour of the bladder neck (TCC) Urethritis (UTI) Urethral stricture from STD, prev instrumentation Stones Blood clot (clot retention in haematuria) Foreign body Cord compression Multiple sclerosis Tabes dorsalis Diabetic autonomic neuropathy Anticholinergics (cough medicine), antihistamines, anti-depressants, alcohol Prolonged immobility Post-anaesthesia Pain

- Infection – symptoms of UTI - Stone disease (if in the bladder, usually asymptomatic) - Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness PHYSICAL EXAMINATION - General condition – sallow appearance, scratch marks, pedal oedema, etc (uraemia) - Abdomen  Palpable bladder – tender  Other pelvic masses – fibroid, gravid uterus, ovarian cyst  Faecal loading  Bilateral enlarged kidneys (hydronephrosis) - Digital rectal examination  Any saddle anaesthesia  Anal tone  Prostate enlargement – firm and smooth? Or hard, craggy, irregular, rectal mucosa not mobile?  Stool impaction - Neurological examination  LMN paralysis of the lower limbs?  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 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 Hesitancy Straining to pass urine (strangury) Weak stream Prolonged micturition Terminal dribbling Feeling of incomplete voiding Double voiding (pis-en-deux)

Irritative Frequency Urgency Nocturia Dysuria Urge incontinence

- Haematuria (UTI or rupture of enlarged veins) - Ask about the complications of an obstructive uropathy):  Acute urinary retention (previous admissions and IDC)  UTI, Stones: irritative symptoms, haematuria  Hydronephrosis, pyelonephrosis, renal impairment: loin pain, fever, polyuria/ anuria. Overflow incontinence 2o to Chronic urinary retention with high post-void residual volume in the bladder 



- Try to Rule out other differentials:  Stricture/ bladder neck contractures: previous instrumentation or STDs causing urethritis/ post- TURP  Drug causes: codeine (cough mixture), BB, anti-cholingerics, TCAs  Chronic constipation  Ca bladder neck/ Ca Prostate: LOW, LOA, bone pain, haematuria  Neurogenic bladder - Other aspects of history: Social history (effect on lifestyle) PHYSICAL EXAMINATION - Already on IDC? Urine output? Anaemia (of CRF/ underlying malignancy) - Vitals: BP for HPT? - Any ballotable kidneys? Check for hernias (chronic straining) - Palpable tender bladder in ARU (non-tender in chronic retention) - DRE for impacted stools & prostate: smooth enlarged, median sulcus, rubbery, nontender, mobile mucosa INVESTIGATIONS Blood - FBC: anaemia, raised WBC - UECr: dehydration, raised creatinine  renal impairment due to chronic obstruction - UFEME, cytology, urine c/s: for UTI and screen for cancer - PSA (done in interval periods to avoid false +ves): normal 100ml, bladder stone, measure intravesical prostatic protrusion (IPP) - Cystoscopy to rule out stones, strictures/ bladder neck obstruction or cancer, - Uroflowmetry to confirm obstruction to urinary outflow (normal peak flow rate > 15ml/sec, normal bell shaped curve, saw tooth appearance, Residual urine 10 PROBLEMS - Acute/chronic urinary retention, complicated by Bladder stones & Recurrent UTI - Gross haematuria (after excluding other causes) - Renal impairment secondary to outflow obstruction - Co-existence of prostate cancer MANAGEMENT - Divided into watchful waiting, medical management, and surgical management - Objectives of treatment: Rapid and sustained relief of symptoms, prevent long-term complications, improve patient‘s quality of life I. Watchful waiting

- Suitable for patients with minimal symptoms, no complications and normal invx - Monitor patient‘s symptoms and clinical course annually II. Medical treatment

1. Alpha blockers (Prazosin, Terazosin, Doxazosin, Alfuzosin) - Treatment of symptoms (blocking the α-1 adrenergic receptors in the bladder neck, prostate and urethra) - Result in decreased outflow resistance and decreased bladder instability - SEs: include postural hypotension, dizziness 2. 5-alpha reductase inhibitors (Finasteride, Dutasteride) - Treats the disease (not just the symptoms) by inhibiting the conversion of testosterone to dihydrotestosterone by 5-alpha reductase  reduced prostate size - Proven to decrease need for surgery and acute retention rates - Only effective after 6 /12 (counsel the patient!), and in prostates >40g - Most common side-effect is sexual dysfunction & hair growth III. Surgery

Types - Transurethral resection of prostate (TURP)is the gold standard - Laser prostectomy is promising (pending long term results) - Other techniques do not show good results: stenting, cryoablation, etc.

Indications: - Failed medical treatment - Significant Complications: Refractory urinary retention Recurrent UTI, Bladder calculi, Obstructive uropathy - Recurrent gross haematuria Complications of surgery (TURP) Early 1. Bleeding, infection, risk of GA 2. Local injury causing incontinence, stricture/ bladder neck stenosis 3. Perforation of the urethra or bladder dome 4. TUR syndrome - Symptoms: Nausea, vomiting, confusion, hypertension, visual disturbance, giddiness, seizure - Hyponatraemia due to constant irrigation during TURP (glycine used for irrigation – cannot use N/S, as ionic solutions make diathermy non-functional) - Irrigation fluid is hypotonic, thus water enters open vasculature during surgery - Risk increases with prolonged operation and increased pressure of irrigation, thus op is kept to shorter than one hour, and irrigation pressures 100 is highly suggestive) - Local symptoms: obstructive LUTS, bladder outlet obstruction; (uncommon as most cancers arise in peripheral zones) haematuria, haematospermia, new onset ED - Metastatic symptoms – lower back pain (from Batson‘s venous plexus) PHYSICAL EXAMINATION - DRE: Asymmetric area of induration, or frank hard irregular nodule - Percuss spine for any bone pain DIAGNOSIS 1. PSA level

- >10ng/ml: biopsy recommended as >50% of patients will have prostate cancer - 4-10ng/ml: biopsy advised, though only 20% will have prostate cancer - ♀, R> L, 20% are bilateral, children>adults

Direct inguinal hernia: - Bulges directly anterior though a weakened fascia Hesselbach‘s triangle, posterior to the inguinal canal (medial to the inferior epigastric artery)  Hesselbach‘s ∆: inf. Epigastric art., rectus abd, inguinal ligament - Hernia sac is not with the spermatic cord - Rare in ♀, usually occur bilaterally in ♂ with weak abdominal muscles and comorbid conditions causing ↑ intra-abdominal pressure

Anatomy of the spermatic cord Coverings: 3 concentric layers of fascia  Internal spermatic fascia: derived from transversalis fascia  Cremasteric fascia & muscle: derived from internal oblique  External spermatic fascia: derived from external oblique Contents:  3 Arteries: testicular artery, artery to the vas deferens, cremasteric artery  3 Nerves: nerve to cremaster, autonomic nerves (T10), genital br of genitofemoral nerve  3 Others: Vas deferens, pampiform venous plexus, lymphatics

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

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Recurrence of hernia ( Firm > Tense > Soft overlying skin, and it is non-pulsitile.” 6. Mobility “It (appears to be attached to - Fully mobile in all directions? underlying muscle, as it is mobile - Fixed and immobile? horizontally but not longitudinally)” - Mobile only in certain directions? 7. Relations to surrounding tissues - Move lump in 2 perpendicular planes o Attached to skin? muscle / tendon / bone? o If appears to be attached to muscle:  Ask patient to tense muscle; Reassess mobility in the 2 planes  Intramuscular or below the muscle, it will disappear.  Above the muscle it will be more prominent.  Fixed to muscle, it will become less mobile. 8. Fluctuant? (for small / medium lumps) - Paget‘s sign: Rest 2 fingers on opposite sides of lump, press down on middle of lump +ve: Feel fingers moving apart

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9. Special tests - Transillumination [only for large lumps; Use pen torch on one side] - Pulsatility (only for some sites, e.g. Neck, abdomen) - Place finger on opposite sides of lump o Expansile: fingers pushed apart o Transmitted: Fingers pushed in same direction (usually upwards) - Slip sign – if lipoma is suspected - Tends to slip away from the examining finger on gentle pressure - Compressibility / reducibility [if AVM, haemangioma, hernia suspected] - Compressible: Disappears on pressure, reappears on release (AVM) - Reducible: Disappears on pressure, reappears with opposing force (hernia) - Auscultation – only for certain sites / lesions (e.g. neck, abdomen, etc.) Request – “I would like to complete my examination by…”  Examine the draining LNs  If sebaceous cyst / lipoma  “Looking for other lumps elsewhere”  Ganglion  “Looking for other lumps elsewhere”  “Asking for hand dominance”  “Taking an occupational history” S: site, size, shape, scars, skin changes, surface E: edge, expansility/ pulsatility C: colour, consistency, compressibility T: tenderness, temperature, transillumability O: others [fluctuance, fulid thrill] R: reducability, relationship to each other For ulcers: Add into inspection: - Base: granulation tissue, slough, fascia, muscle, bone - Edge: sloping (healing), punched out, undermined, rolled (BCC), everted (SqCC) - Discharge: serous, sanguinous, haemoserous, purulent

125 LIPOMA Inspection o Can be single, often multiple o Usually at neck, trunk o Hemispherical – may appear lobulated o Scars  Implies recurrent lipoma Palpation o Smooth or lobulated on firm pressure – bulging between strands of fibrous tissue) o Soft / firm (depending on nature of fat) o Well defined edges (may not be regular; series of curves corresponding to each lobule o Pseudo-fluctuance if large – lipomas are not liquid; but fat maybe more liquid o Mobile in all directions (if subcutaneous) o Positive slip sign; No transilluminance / thrill o Usually in the subcutaneous tissue. [check attachment skin & muscle] “Mr. X is a young Chinese gentleman…” “On inspection, there is a hemispherical lump over the right scapula” “It measures 10 by 8 cm” “There are no scars, punctum, ulceration, or discharge seen, nor any overlying or surrounding skin changes” “On palpation, the overlying skin is not warm, it is non-tender” “The surface is lobulated, and its margins are not well-defined” “The consistency is soft, and it is fluctuant” “The lump is not attached to the overlying skin” “It is mobile in all directions with a positive slip sign” “It is not transilluminable” “I would like to complete my examination by looking for other similar lumps” “My provisional diagnosis is a lipoma” ―My differential diagnosis is: large sebaceous cyst”

Background Information  Definition: Benign tumour consisting of mature fat cells (distended with fat from over-activity) o Malignant change does not occur o Liposarcomas arise de novo; occur in older age-group (deeper tissues – retroperitoneal, deep tissues of the thigh, subscapular)  Liposarcoma classification 1. Well-differentiated

2. Myxoid, round cell (poorly differentiated myxoid) 3. Pleomorphic liposarcoma  Clinical features o Can occur at all ages (not common in children) o Slow-growing, never regress o May be multiple: lipomatosis (multiple continuous lipomata)  Occur in buttocks / neck  Can cause distortion of subcutaneous tissues.  Treatment o Non-surgical – watch & wait o Surgical – If patient wants it removed (Pain / peripheral neuropathy – Dercum‘s disease, Cosmesis)  Can be removed under LA  Nuchal lipomas (back of the neck): extremely fibrous septae: difficult to excise  If close to joint: LA may not be possible (may communicate with joint)  Variants of lipomas / syndromes associated with lipomas o Adiposis dolorosa (Dercum’s disease)  Multiple painful lipomas in limbs, sometimes trunk  Associated with peripheral neuropathy  Angiolipomas: prominent vascular component o Hibernomas: brown fat cells o Cowden‘s disease – associated with:  Thyroid cancers  Lipomas  Palmoplantar keratoses  Multiple facial papules  Oral papillomatoses o Bannayan-Zonana syndrome – rare AD dz: lipomas with macrocephaly and haemangiomas, intestinal polyps

SEBACEOUS CYST Inspection  Usually solitary (can be multiple)  Hemispherical  Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles)  Variable size ; few mm to 4-5 cm  May have bluish discolouration  Punctum in apex: in 50%  May exhibit plastic deformation on palpation Palpation  Normal Temperature, non-tender (unless inflamed)  Smooth surface  Well-defined margins (lies in subcutaneous fat)  Tense Consistency, may stretch overlying skin & exhibit plastic deformation  Non fluctuant, not transilluminable  Attached to skin, Not attached to deeper structures, Usually mobile in all directions “Mr. X is a young Chinese gentleman…” “On inspection, there is a single hemispherical lump in the middle of the forehead just above the eyebrows” “It measures 1 by 1 cm in diameter” “There is a visible punctum over the lump” “There are no scars, sinuses, ulceration, or discharge seen, nor any overlying or surrounding skin changes” “On palpation, the overlying skin is not warm. It is non-tender.” “The surface is smooth, with clearly-defined margins” “The consistency is firm, and it is non-fluctuant” “The lump is attached to the overlying skin” “It is mobile in all directions” “Slip sign is negative” “I would like to complete my examination by…” “Looking for other lumps elsewhere” “My provisional diagnosis is a sebaceous cyst” My differentials are: Lipoma Dermoid cyst Inflamed Cyst

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Background Information  Sometimes considered to be similar to epidermoid cyst o More accurate terminology: pilar / trichilemmal cysts  2 histological types: o Epidermal cyst: from infundibular portions of hair follicles o Trichilemmal cyst: from hair follicle epithelium (most common on scalp), frequently multiple (AD inheritance)  Arise from infundibular parts of hair follicles  Definition: Distension of sebaceous glands with sebum from blockage of opening  Clinical features o Occur in all age groups, rarely present before adolescence o Slow growing,– may appear suddenly at adolescence o May become infected: acutely painful, sudden increase in size o May spontaneously discharge contents through punctum, regress  Point of fixation & discharge along a hair follicle  Point gets pulled inwards on enlargement of the mass – creates punctum  Sebaceous horn may form from hardening of slow discharge from wide punctum  Sebum slowly exudes, dries and hardens into conical spike  Sebum usually washed away – horn results only if overlying skin not washed  Can be pulled out of skin  Treatment: excision / curettage along with base + histological assessment  Complications 1. Infection (±discharge) 2. Ulceration 3. Calcification (trichilemmal cyst) (may lead to cyst hardening) 4. Sebaceous horn formation, [hardening of a slow discharge of sebum from a large, central punctum.] 5. Malignant change  Treatment o Non-surgical: leave alone (if small, asymptomatic). o Surgical  Complete excision of cyst and contents under LA.  Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the lines of Langers.  If at the angle of jaw, be careful of the facial nerve during operation. Damage to zygomatic branch can cause eye ulceration.

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

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 Differentials o Bursae (soft) o Cystic protrusion of synovial cavity in OA (joint will be abnormal) o Benign giant cell tumours of flexor shealth (Pigmented VilloNodular Synovitis) o Lipoma o Sebaceous cyst  Treatment o Non-surgical  Watch & wait, usually may disappear after a few months.  Aspiration + 3/52 of immobilisation (successful in 30-50%). High chance of recurrence 6-12/12 later. o Surgical  Complete excision to include neck of ganglion at site of origin. Along the lines of Langers.  Complications of surgery  Wound complications: Scar, haematoma, infection  Recurrence females o Grow very slowly; months / years typically o May spread radially – leaving central scar o Persistent nodule / ulcer with central scab (repeatedly falls off, reforms) o May have itch / pain o If neglected: deep infected ulcer

 Macroscopic appearances: o Above the skin:  Nodular  Nodulo-ulcerative / Deeply eroding ulcer (―rodent ulcer‖)  Cystic o Not raised above the skin:  Pigmented  Geographical / cicatricial / ―bush-fire‖ (advancing edge, healing centre)  Sclerosing (flat / depressed tumour, ill-defined edge)  Superficial (erythematous scaly patches)  Microscopic features o Most commonly islands and nests of basaloid cells in dermis o High mitotic rates, peripheral palisading o (islands arranged radially with long axes in // alignment)  Origin of various appearances: o Tumour always starts as a nodule o When central epithelium dies, ulcer develops (nodulo-ulcerative)  Edge rolled – raised up and rounded (but not everted) (may be only clue to diagnosis) o If centre of tumour does not necrose / ulcerate: nodule enlarges → cystic appearance  Not really cystic: solid and non-fluctuant o If pigmented brown by excess melanin: pigmented BCC o Geographical appearance:  When nodule first ulcerates, rolled edge is circular  Shape becomes irregular as malignant cells spread  As ulcer heals: irregular, raised edge around flat white scar – ―bush-fire‖ BCC  Differentials o SqCC  Especially if ulcerated  But if rolled edge: more likely BCC o Keratoacanthoma (adenoma sebaceum, molluscum carcinomatosum)  But scar will be deep (see below) o If pigmented: malignant melanoma (rare in Singapore)

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 Treatment o o o o

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

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

“Mr. X is an elderly Chinese gentleman…” “On inspection, there is a single irregular ulcer on the dorsum of the right hand, proximal to the 1st & 2nd MCP joints” “It measures 1.5 by 1.5 cm. The edge of the ulcer is well-defined, red and heaped up.” “The base of the ulcer is shallow and contains red granulation tissue.” “There are no scars, or discharge seen, nor any surrounding skin changes.” “On palpation, the surrounding skin is not warm. It is non-tender” “The edges are firm” “The lump arises from the skin” “It is fixed and immobile” “My provisional diagnosis is squamous cell carcinoma” “My differentials are…” o Benign: Keratoacanthoma, infected seborrhoeic wart, solar acanthosis, pyogenic granuloma o Malignant: BCC, malignant melanoma, solar keratosis “I would like to complete my examination by…” “Examining the local lymph nodes for lymphadenopathy” “Taking a history looking for sites of metastases” “Examining the abdomen and lungs for signs of metastases” Background Information  Carcinoma of the cells of the epidermis forming superficial keratinous squamous layer  Local invasion inyo epidermis, dermis, adjacent tissues, & lymphatic spread to LNs  Microscopy: o Tongues of tumours cells spreading in all directions o ―Epithelial pearls‖ – nest of squamous epithelium, cells are arranged in concentric circles surrounding a central focus of acellular keratin  Clinical features o Incidence increases with age (usually elderly male) o Predisposition:  Congenital:  Xeroderma pigmentosum (AD, failure of DNA transcription)  Acquired  Envn: sunlight, Irradiation, Chemicals  Pre-existing lesions: Solar keratosis, Bowen‘s disease  Chronic ulcers: old burns, chronic venous ulcers  Immunosuppresion (post-transplant, HIV)

Usually has been growing for 1 – 2 months before being noticed  Begins as small nodules on skin  As enlargement occurs, centre necroses, sloughs  Nodule turns into ulcer  Ulcer initially circular with prominent everted edges  Subsequently enlarges & changes to any shape  Bleeding (more common with SCC than BCC)  Discharge  Pain (invasion of deep structures)  Lymphadenopathy  Complications o Infection o Bleeding (massive / fatal if erosion into large vessel) o

 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

 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 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  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)

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Bowen‘s disease

Solar / Actinic Keratosis

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

“Mr. X is a middle aged Chinese gentleman…” “On inspection, there is a single flat-looking lesions over the right foot” “It measures 2 by 4 cm” “It is variegated in appearance, and exhibits red, white, and black discolouration” “The margins are clearly-defined and irregular” “There are no scars, nor any surrounding pigmentation, erythema, or ulceration, bleeding, or discharge” “On palpation, the overlying lesion is palpable. It is not warm. It is non-tender” “The surface is smooth, and its consistency is firm” “The lump is attached to the skin, and moves with it over deeper structures” “My provisional diagnosis is malignant melanoma” “My differential diagnoses are: BCC, pigmented naevus” “I would like to complete my examination by…” “Examining for regional lymphadenopathy” “Take a history for: cardinal symptoms of malignant change, and any predisposing factors” Background information 4 commonest types of malignant melanoma  Superficial spreading melanoma (70%)  Nodular melanoma (15 - 30%)  Lentigo maligna melanoma  Acral lentigous melanoma Microscopic features  Consists of loose nests of melanocytes in basal cell layer:  Invade epidermis (leading to destruction, ulceration) & deeper into dermis, subcutaneous fat Clinical Features  Very rare before puberty (usually > 20 years old)  Equally in both sexes (but distribution different – see below)  > 25% arise de novo o Change in surface, size, colour, Halo, satellite nodules o Ulceration, bleeding o Itch, No pain o Lymphadenopathy  Symptoms of distant metastases: LOW, SOB, jaundice o Lymphatogenouly to: regional LN o haematogenously to: Lungs [pleural effusion], Liver [hepatomegaly], Brain [focal neurological signs] & Skin and subcutaneous tissues

Predisposing Factors  Congenital / non-modifiable o Light skinned race o Xeroderma pigmentosum o Dysplastic naevus syndrome (B-K mole, FAMM syndrome) – 100% risk if 2 family members affected o Large congenital naevi o FHx in 1st degree relatives (1.5X risk)  Acquired / modifiable o Sunlight exposure o Pre-existing skin lesions  Lentigo  > 20 benign pigmented naevi (3 x risk) o Previous melanoma (3.5 x risk) Features of pigmented skin lesion suspicious of malignancy 1. Asymmetry 2. Bleeding & ulceration (late) 3. Change in: colour, size, shape, surface, number (early) a. Surface: i. Loss of normal surface markings (e.g. skin creases) around lesion ii. Skin may become rough / scaly iii. Itchy with pale-pink halo (inflammation) b. Size: i. Growth of newly-formed / long-standing mole ii. Increase in edge, width, thickness c. Colour: i. Becoming darker ii. Halo of brown discolouration in skin around the lesion iii. Patchy colour change (black, to blue-purple  ↑ vascularity) iv. Occasionally colourless: no melanin production d. Number: i. Satellite nodules of tumour around the lesion ii. Enlarged inguinal, axillary lymph nodes 4. Diameter >6mm 5. Elevation (flat plaque → nodule)

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Request  Examine draining lymph nodes  Take a history for: o Cardinal symptoms of malignant change in a mole  Rapid increase in size  Itching  Bleeding  Change in colour / shape / thickness o Predisposing factors Differentials  Benign o Moles (pigmented naevus – ↑ melanocytes, ↑ melanin) o Freckles (normal number of melanocytes, ↑ melanin from each) o Lentigo (↑ melanocytes, normal amount of melanin from each) o Pigmented seborrhoeic keratoses o Dermatofibroma o Thrombosed haemangioma  Malignant o Pigmented BCC Staging by depth of invasion Clark’s levels of invasion Level Extent of Tumour 5-Year Survival Epidermis only 98% I Invades papillary dermis 96% II Fills papillary dermis 94% III Invades reticular dermis 78% IV Subcutaneous tissue invasion 44% V Breslow’s thickness (different in absolute depth of invasion, LN involvement) Breslow Thickness 10-Year Survival 92% < 0.76 mm 50% < 3 mm 30% < 4 mm < 40% (8-yr) LN Involvement  Also: Beahrs and Myer’s system

135  Prognosis prognosis: a. b. c. d. e. f.

generally poor – above 3 types of staging, or other indicators of poor Elderly Male Lesions on trunk Ulceration Depigmentation, amelanotic Aneuploidy, high mitotic index

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

% Site

Colour Edge Shape Surface

Remarks

Pictures

Superficial Spreading 70% ♂: Back ♀: Legs Red, white, blue (varying pigmentation) Irregular Palpable, but thin -

-

Nodular

Lentigo Maligna

Acral Lentigous

15-30%

–

Trunk

Face; Dorsum of hand / forearm

Rare Hairless skin (palms, soles, subungual area)

Most often black

Brown / black

Brown / black

Regular outline Thick, polypoid, raised Smooth

Irregular

Irregular

Flat

Flat

• Frequently ulcerated, bleeding

• Arises from patch of Hutchinson‘s Lentigo • Malignant area usually thicker, darker • Area seldom ulcerates

-

• Rare type • Often misdiagnosed as haematoma, paronychia

NEUROFIBROMA Inspection  Often multiple  Anywhere in skin, subcutaneous tissues, e.g. forearm  Spherical / Pedunculated / Fusiform (long axes lie along length of limb)  Rarely more than few cm  comment on any café-au-lait spots Palpation  normal temp., Non-tender  Smooth, Well-defined  Soft/ fleshy, rubbery consistency  Non-fluctuant  If in subcutaneous tissue: mobile within it  Move most freely perpendicular to course of nerve Request  Look for other similar lesions & other manifestations of NF-1: café-au-lait spots, axillary freckling, lisch nodules, optic glioma  Measure the BP (HPT 2o to phaeochromocytoma, CoA, RAS)  Examination of cranial nerve VII & VIII (acoustic neuroma)

“Mr. X is a young Chinese gentleman…” “On inspection, there are two spherical, pedunculated masses on the back” “One measures 2 cm, and the other 0.5 cm in diameter” They are pink in colour, with well-defined margins” “There are no scars, sinuses, ulceration, or discharge seen, nor any surrounding skin changes” “On palpation, they are not warm and non-tender” “Their surfaces are smooth, and are firm, and rubbery” “They are attached to the skin, and are mobile over the deeper tissue layers” “My provisional diagnosis is neurofibromata” “I would like to complete my examination by…”  "Looking for other similar lesions”  “Looking for manifestations of neurofibromatosis”  “Examining the cranial nerves”

136

Background Information Sporadic Neurofibroma  Benign tumour containing mixture of elements from peripheral nerves: o Neural (ectodermal) o Fibrous (mesodermal)  Often multiple  History o Any age (but usually adult) o Symptoms: usually cause no discomfort, rarely disfiguring o If related to nerve trunk, may be tender  Patient may get tingling sensations in distribution of nerve  Histology o Schwann cells: appear as bundles of elongated wavy spindle cells o Collagen fibrils, myxoid material o Often not encapsulated (unlike neurilemmomas)  Complications of Neurofibroma o Pressure effects: spinal cord, nerve root compression o Deafness: involvement of VIII o Neurofibrosarcoma (only in NF-1): 5-13 % o Intra-abdominal effects: obstruction, chronic GI bleeding o Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis  Treatment (single neurofibroma) o Non-surgical: leave alone if asymptomatic, patient agreeable o Surgical: indicated only if malignancy suspected  Local re-growth common (cannot be surgically detached from underlying nerve) Neurofibromatosis I (Von Recklinhausen‘s disease) (Refer to paediatrics notes – neurocutaneous syndromes)  AD, neurocutaneous syndrome; chr 17  Characterised by pigmentary changes, tumours, and skeletal, vascular dysplasias o Fibroma ≥2 NF or ≥1 plexiform NF o Iiris harmatomas (Lisch Nodules) o Bone: dysplasia, pseudoarthrosis o Relatives o Optic glioma o Macules >6; >15mm post-pubertal o Axillary freckling  Neurofibromata of all sizes (few mm to large subcutaneous nodules), related differently to skin o Within skin o Tethered to skin o Pedunculated

137 Plexiform Neurofibroma (elephantiasis neurofibromatosis)  Very rare  Excessive overgrowth of neural tissue in subcutaneous layers, giving tissue swollen oedematous appearance o Often mistaken for lymphoedema, but lymphatic drainage is normal  Can result in severe deformity: diffuse enlargement of peripheral nerve with skin involvement

DERMOID CYST Inspection  Usually single  Ovoid / spherical  Site: o Congenital, 1-2 cm usually  Along lines of fusion of ophthalmic & maxillary facial processes  Inner & outer ends of upper eyebrow o Acquired, 0.5-1 cm usually  Beneath skin likely to be injured e.g. fingers  Scars often present Palpation  Not warm, maybe tender if infected  Smooth surface, Well-defined margins  Consistency o Congenital: Soft (not tense / hard) o Acquired: Hard & tense (sometimes stony hard)  Fluctuant (if large)  Mobile over deeper tissues o Deep to skin, in subcutaneous tissue i. Congenital: Not attached to skin or underlying structures ii. Acquired: may be tethered to scar

“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  A dermoid cyst is a cyst deep to the skin, lined by skin  2 different methods of formation: o Congenital: Accident during antenatal development o Acquired: Implantation of skin into subcutaneous tissue by injury Clinical features  Congenital (suspect if in child, young adult) o Formed intra-utero, when skin dermatomes fuse o Occur at any point in mid-line, common in neck / face / nose  Particularly along lines of fusion of ophthalmic & maxillary facial processes  Also: inner & outer ends of upper eyebrow o May be seen at birth o Distends a few years later, becomes obvious; few symptoms other than cosmetic problems o Rarely infected  Acquired – Implantation dermoid (suspect if in adult – Browse pg 60) o Develop when piece of skin survives after being forcibly implanted into subcutaneous tissue  Often by injury: cut, stab, etc. o Symptoms  Small, tense lump  Painful and tender (in areas subjected to repeated trauma)  Local effects (e.g. problems with grip / touch if on finger)  Also rarely infected o Differentials  Sebaceous cyst (look for old injury, presence of scar near cyst: more likely dermoid) Treatment  Congenital o Surgical treatment; complete excision o Full extent should first be established with X-ray / CT  Midline cysts may communicate with CSF; must exclude bony defect  Acquired o Complete excision of cyst

138

SEBORRHOEIC KERATOSIS (Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma) Inspection  Often multiple  Any part of skin; most found on back & face  Round / oval  Light brown → black  ―stuck on appearance‖; appears warty  Varying size; Few mm to 2-3 cm  Distinct margins Palpation  No warmth, no tenderness  Rough surface (sometimes papilliferous)  More firm than surrounding skin  Attached to skin  Special tests o May be picked off gently – reveals patch of pale-pink skin, 1-2 surface capillaries (bleed slightly) (DON‘T DO THIS IN EXAM) Request to look for similar lesions elsewhere “Mr. X is an elderly Chinese gentleman…” “On inspection, there is a single ovoid lesion lump on the back” “It measures 1 by 2 cm” “The margins are well-defined, and it appears to be slightly raised above the skin” “There are no scars, ulceration, or discharge seen, nor any surrounding skin changes” “On palpation, the overlying skin is not warm. It is non-tender” “The surface is rough and greasy; the consistency is firm” “The lump arises from the skin” “My provisional diagnosis is seborrhoeic keratosis” “My differential diagnosis is: pigmented naevus, melanoma” “I would like to complete my examination by…”  “Looking for similar lesions elsewhere”

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

HAEMANGIOMA Background Information  Vascular malformations o Types  Capillary: ⅔ of cases, include the cutaneous haemangiomata, telangiectasias  Predominantly venous: venous angioma  Deeper levels of subcutaneous tissue, may extend into muscle / joint  May have distended veins over the surface of the mass  Empty with pressure, may have bruit  Predominantly lymphatic: lymphangioma circumscriptum o Features  Develop as abnormal proliferation of embryonic vascular network  Hamartomas  May ulcerate, induce hyperkeratosis in overlying stratum corneum  Many forms of cutaneous haemangiomata: (see table) o Strawberry naevus (cavernous haemangioma) o Port-wine stain (naevus vinosus) o Spider naevus o Campbell de Morgan spot Strawberry Naevus

Cambell de Morgan Spot

Port-Wine Stain

Spider Naevi

Lips, face, mucous membranes of mouth, shoulders, neck, buttock

Upper torso, head and neck (drainage of SVC)

Usually single

Usually multiple

Purple-red

Bright red

Variable

Variable; few mm

1-3 mm

Well-defined

–

Well-defined

Variable

Variable

Circular, may be raised

Inspection

Site

Head & Neck (can be anywhere)

Number

May be multiple

Colour Size Edge Shape

Bright red / dark red Variable; 1-10 cm Well-defined Sessile → pedunculated as they grow larger

Trunk (both sides) – upper > lower Occasionally on limbs Usually multiple Dark red / deep purple

Skin Changes

May have small areas of ulceration with scabs

May have dilated subcutaneous veins around lesion

–

–

• Irregular • Covered with smooth, pitted epithelium

Smooth

–

Smooth

• Soft

–

–

–

Mobile

–

–

–

Confined to skin

–

–

–

corresponding haemangioma in brain – contralateral focal fits • Found in limbs when a/w KlippelTranaunay Syndrome

Palpation Surface Consiste ncy Mobility Relation s

• Compressible: pressure squeezes mass, Special leaves it Tests collapsed: slowly refills • Not pulsatile Background Information Strawberry Naevus Infants Age (congenital) Gender

♂=♀

Sympto ms

• Cosmesis • May ulcerate, bleed if traumatised

Pressur e

• Collapses on pressure

Remark s

140

• Regress spontaneously (few months – 3 years)

• Associated with pregnancy, chronic liver disease (> 5) – request for abdominal examination

drops of sealing wax • No clinical significance

Pictures –

• Compressible, fade completely

Port-Wine Stain

Spider Naevi

Infants (congenital)

–

–

–

• Cosmesis • Bleeding may occur • Diminishes colour but doesn‘t revert to normal • Extensive intradermal haemangioma • Present from birth, does not change in size • Sturge-Weber syndrome: facial PWS with

– • Branches fade when arteriole compressed • Form of telangiectasia • Dilated skin arteriole feeding small branches (leaving it radially) • Increase in number

–

Cambell de Morgan Spot Middle-age → elderly – • Cosmesis • Non-tender • Fade slightly • Formed by collection of dilated capillaries fed by single / small cluster of arterioles • Have appearance of

Also  Telangiectasias o Dilatation of normal capillaries o Can be secondary to irradiation o Can be part of hereditary haemorrhagic telangiectasia (Osler-RenduWeber syndrome)  Autosomal dominant disease  Overt and occult haemorrhage can present as haematuria, haematemesis, melaena, epistaxis, iron-deficiency anaemia  Vin rosé patch o Congenital intradermal vascular abnormality o Mild dilatation of vessels in sub-papillary dermal plexus o Can occur anywhere, gives skin pale-pink colour o Associated with other vascular abnormalities (e.g. haemangiomata, AV fistulae, lymphoedema) o Usually not disfiguring

141 PYOGENIC GRANULOMA Inspection  Single; usu < 1 cm, bright red o May be blood-encrusted or Ulceration  Hemispherical; may be sessile / pedunculated  Likely sites to be injured, e.g. hands, face  Bright red; long-standing lesions may be skin-coloured  May have sinuses, associated serous / purulent discharge, Erythema / cellulitis Palpation – request to palpate: may bleed easily  May be slightly tender o May bleed easily on palpation  Well-defined edges  Soft, fleshy consistency  Confined to skin  Slightly compressible (vascular origin) Request  Take history for previous injury  Rate of growth of lump? (rapid growth in few days) “Mr. X is a young Chinese gentleman…” “On inspection, there is a single hemispherical lump over the thenar eminence of the right hand” “It measures about 0.8 cm in diameter, with clearly-defined margins” “It is bright red in colour, with surrouding erythema” “There are no scars, sinuses, ulceration, active bleeding or discharge seen” “I would like to proceed on to palpation” “On palpation, it is not warm. It is slightly tender” “The surface is smooth. The consistency is soft and fleshy” “The lump is confined to the skin” “My provisional diagnosis is pyogenic granuloma” “My differential diagnoses are SCC, non-pigmented melanma” “I would like to complete my examination by…” o ―Asking Mr. X for any previous injuries to the hand‖ o ―Asking him how rapidly the lump has been growing‖

Background Information – Neither pyogenic nor a granuloma!  Rapidly-growing capillary haemangioma, usually less then 1 cm  Occur commonly after injury: o Small capillary loops develop in healing wound, form granulation tissue o When capillary loops grow too vigorously, form protruding mass, epithelisation o Mass form called pyogenic granuloma (surface often ulcerated, infected) Clinical features  Uncommon in children  May have history of minor injury, chronic infection (e.g. paronychia)  Rapidly-growing lump on skin,  Bleeds easily, discharges serous / purulent fluid o Bleeding, pain stops once lump epithelises  Once nodule is completely covered, begins to shrink (rarely disappears completely) Treatment  Surgical o o

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

PAPILLOMA (skin tags / fibroepithelial polyps) Inspection  Single / multiple  Variable: from raised plaque to pedunculated polyp  Site: Neck, trunk, face, anus (anywhere on skin)  Variable  Flesh-coloured Palpation  Not warm, non-tender  Variable: smooth to papilliferous  Soft, not compressible  Arises from skin Request  Similar lumps elsewhere  Ask for associated conditions: pregnancy, diabetes, intestinal polyposis

“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

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

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

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

143 KERATOACANTHOMA (adenoma sebaceum, molluscum pseudo-carcinomatosum) Inspection  Often found on face  Usually solitary;1 – 2 cm in diameter  Hemispherical or conical, with central crater  Normal skin colour Palpation  Firm and rubbery (central core is hard)  Confined to skin, freely mobile over subcutaneous tissues Background information  Benign overgrowth of hair follicle cells with a central plug of keratin  Occur in adults  complain of rapidly-growing lump in skin  Not painful, but can be unsightly  Takes 2 – 4 weeks to grow, regresses in 2 – 3 months o Central slough appears, o surrounding skin retracts to form puckered scar  Cause is unknown (may be self-limiting benign neoplasm or post-viral infection)  Treatment: o Conservative if asymptomatic o Surgical excision of lesion with histology to r/o SqCC

KELOID / HYPERTROPHIC SCAR  Healing by primary intention – 3 stages: o Tissue defect filled by blood / fibrin o Replacement by collagen and fibrous tissue o Organisation of fibrous tissue to maximise wound strength  Most surgical scars have thin lines, but tissue response may be excessive: hypertrophic / keloid scar  Wounds prone to hypertrophic / keloid scar o Infection o Trauma o Burns o Tension o Susceptible areas: across flexion areas, earlobes, chest, neck, shoulder

 Hypertrophic scar o any age – common 8-20 years, ♂=♀, all races o Excessive amount of fibrous tissue, but confined to scar (between skin edges) o Located across flexor surfaces, skin creases o Common, especially if infection / excessive tension o Only enlarge for 2-3 months, then regress spontaneuosly o Do not recur if excised and causative factor eliminated  Keloid scar o puberty to 30 years, ♀>♂, black, hispanic more likely o Hypertrophy and overgrowth extend beyond original wound o Located at earlobes, chin, neck, shoulder, chest o Due to local release of fibroblast growth factors o Continue to enlarge 6-12/12 after initial injury o May be tender, unsightly o Will recur unless special measures taken  Treatment (recurrence can be as high as 55%) o Non-surgical: mechanical pressure therapy – topical silicone gel sheets (day and night for 1 year), Intralesional steroid, LA injections: e.g. triamcinolone with lignocaine o Surgical: revision of scar by direct suturing, skin grafting (avoid excessive tension)

KAPOSI’S SARCOMA

FIBROSARCOMA

Inspection  Purple papules and plaques  Solitary, but usually multiple  Site: limbs, mouth, tip of nose/ palate or anywhere on the skin or mucosa

Inspection  Single; Usually limbs (but can be anywhere)  Spherical or hemispherical  If large, vascular: may make skin shiny & pink  May have o Sinuses & Discharge o Ulceration o Erythema / cellulitis

Request to take a history of previous transplantation or current underlying immunocompromise. Background information  Derived from capillary endothelial cells or from fibrous tisse  Linked to HHV-8  Types: o Classic Kaposi‘s Sarcoma  Confined to skin of lower limbs of elderly Jews  Not fatal o AIDS associated Kaposi‘s Sarcoma  AIDS defining; Found in 1/3 of AIDS patients  1/3 develops a 2nd malignancy e.g. leukaemia/ lymphoma o Endemic (African) Kaposi‘s Sarcoma  Aggressive and invasive fatal tumour  Good response to chemotherapy o Transplation- associated Kaposi‘s Sarcoma  Following high dose immunosuppressive therapy  Often regress when treatment is ended Treatment  Conservative if asymptomatic. Start anti-retrovirals if HIV +ve  Surgical: local radiotherapy amd chemotherapy (IFN- alpha, doxorubicin, intralesional vinblastine)

144

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

145 PYODERMA GANGRENOSUM

RADIOTHERAPY MARKS

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

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

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

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

o



146

  Late:    

Bone marrow suppresion, esp. if to long bone and pelvis GI: diarrhea

Skin changes Heart: IHD Lung: pneumonitis, pulmonary fibrosis Bld vssl: radiation arteritis, esp to carotids  necrosis, distal ischaemia and vssl rupture  CNS: spinal cord myelopathy  Uro: bladder fibrosis, Renal impairment (depletion of tubular cells)  Abdo: IO 2o to strictures & adhesions,  Genital: infertility  Endocrine: hypothyroidism  Eye: cataracts  Increase incidence of future cancers:  Haematogenous malignancy, e.g. leukemia  Solid tumours: Thyroid cancers  Breast cancers Minimalising of side effects of radiotherapy: o Lead shields to eyes, gonads and thyroid o Dose fractionation (to allow recovery of normal cells) o Prior chemotherapy (increase sensitivity of tumour cells) o Regional hypothermia o Radiolabelled antibody to deliver local radiation to tumour

ASCITES Vital signs on examination: o Abdominal distension o Flank dullness  shifting dullness  fluid thrill o Peripheral stigmata of chronic liver disease and portal HPT o Other signs of fluid overload: LL, sacral oedema, bibasal crepitations o Signs of malignancy Background information  Causes of ascites: Transudate (30g/L) Cirrhosis Malignancy Infective causes: TB Chylous ascites



Role of peritoneal tap: o diagnostic and therapeutic  Send fluid for FEME, protein, microbiology, cytology  Relieve of discomfort & diaphragm splinting from distension o Indications:  Failed medical treatment  symptomatic o perform under aseptic technique, LA, US guidance  may insert a pigtail catheter via seldinger technique  open drain into stoma bag



Treatment of ascites: o Conservative: low salt diet, diuresis o Peritoneal tap o Surgical: shunt surgery (TIPSS, peritoneovenous shunt [silastic catheter], Denver shunt when with a subcutaneous pump]

147 SHOCK

Definition – inadequate tissue and organ perfusion leading to a hypoperfusion state & eventual cellular hypoxia and its attendant sequelae. S/S: Hypotension, urine output, tachycardia, diaphoresis, AMS

Management General Mx  Airway  Breathing  Circulation 

Types of Shock Types Causes

S/S

Invxs

‗White‘ shock Hypovolaemic Cardiogenic Haemorrhage Burns Ruptured ectopic pregnancy Severe GE Acute pancreatitis Pallor Cold clammy skin peri vas   Hct (late)

Neurogenic

Septic

AMI Dysrhythmia

Spinal injury

Infxns

Pallor Cold clammy skin peri vas 

Warm skin N/ heart rate Neuro deficit

Fever, rigors Warm skin

‗Red‘ shock Anaphylactic Monitoring

Fever, rigors Warm skin

Cardiac FBC enzymes Bld C/S ECG Also, Obstructive Shock due to tension pneumothorax, cardiac tamponade or pulmonary embolism

    

Maintain airway – consider intubation if necessary 100% O2 via non-rebreather mask 2 large bore (14-16G) cannulae  Inotropic support o IV dopamine 5-10g/kg/min o IV dobutamine 5-10g/kg/min (esp for cardiogenic shock) o IV norepinephrine 5-20g/kg/min (esp for septic shock) Pulse oximetry ECG BP Heart rate Urine output – catheterize patient

Hypovolaemic Shock Invxs  FBC - Hct in acute alcoholic binge due to diuresis. Hct is an Inaccurate marker of bld loss acutely.  GXM 6 units  U/E/Cr  Troponin T & Cardiac enzymes  Coagulation profile with DIVC screen (PT/PTT, pltlet, Ddimer)  ABG – metab acidosis, lactate, base deficits are poor Px factors  UPT - ?ectopic pregnancy? Ask for LMP  Examine abdomen for pulsatile AAA  1 L crystalloid fast infusion w/in 1 hr Fluid Rx  Assess response  Subsequent colloid or whole blood infusion  Used to guide fluid Rx, esp in CCF patients  CVP line

Cardiogenic Shock ECG Trop T & cardiac enzymes



Manage accordingly – refer acute coronary syndrome & ACLS notes

Neurogenic Shock Hx/PE    Immobilize Invxs  

Fluid Rx  IV methyl prednisolone

       

Disposition



Trauma – site, mechanism, force Neuro exam, DRE – document initial neurological deficits Immobilize spine in neutral position C-spine X-ray (AP & lat) – ensure visualization up to C7/T1 junction  Swimmer‘s view (visualize C7/T1 jn) & open mouth view (visualize C1/2 injury) Thoracic & lumbar spine X-ray (AP & lat)  CT scan  MRI later Titrate fluid resus with urine output  vasopressors if BP does not respond to fluid challenge 30 mg/kg over 15mins, followed by 5.4mg/kg/h for nxt 23 hrs Indications – non-penetrating spinal cord injury & w/in 8 hrs of injury Contraindications o 20mmHg)  ECG (may be normal)

148

o o o

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non-specific ST depression & T wave inversion Sinus tachycardia Right heart strain  Right axis deviation  Transient RBBB  T wave inversion in V1-3  P pulmonale  S1Q3T3 o Exclude DDxes – MI, pericarditis CXR (may be normal) o Westermark sign – oligaemic lung fields o Pul infarcts – wedge shape opacities w apex pointing towards the hilum o Atelectasis o Pleural effusions o Raised diaphragm o Consolidation o ‗Plump‘ pul. arteries o Exclude DDxes – pneumothorax, pneumonia, L heart failure, tumour, rib #, massive pleural effusion, lobar collapse  Spiral CT, Echo, MRI, lung scintigraphy, pulmonary angiogram (gold std)

Rx  Pain relieve – use Opioids with caution  Fluid Rx & inotropic support if haemodynamically unstable  Anticoagulation Rx: o IV heparin 5000U bolus or SC fraxiparine (0.4ml if 65kg) o Convert to Oral warfarin later   Thrombolysis o Intra pul. arterial urokinase fro 12-24 hrs  Surgical o Complete IVC ligation or partial caval interruption Septic Shock (SIRS + source of sepsis + shock) SIRS =  2 of the following present: o Temp >38 or 90bpm o RR > 20 breaths/min OR PaCO212000/mm3, 10% immature forms

149 Hx / PE Invx

Fluid Rx  Inotropic support Empirical ABx

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Identify site of infxn – UTI (indwelling cathether), gallbladder dz, peritonitis, pneumonia, appendicitis, immunocompromised state  FBC -  TW  U/E/Cr  DIVC screen – PT/PTT, pltlet, fibrinogen, D-dimer  Bld C/S (2 different sites)  Capillary bld glucose  ABG  CXR – pneumonia, ARDS  ECG  Urine dipstick – UTI  Urine C/S  Rapid infusion 1-2L crystalloids   CVP line insertion  if no response to fluid Rx  Noradrenaline (drug of choice) - 1g/kg/min OR  Dopamin 5-20g/kg/min Immunocompetent w/o  3rd gen cephalosporin (IV obvious source ceftriaxone 1g) OR  Quinolones (ciprofloxacin 200mg) Immunocompromised w/o  Anti-pseudomonal ABx (IV obvious source ceftazidime 1g) OR  Quinolone  PLUS aminoglycoside (Gentamicin 80mg) Gram-positive (burns, FB /  IV cefazolin 2g lines present)  IV vancomycin 1g if hx of IVDA, indwelling cath. Or penicillin allergy Anaerobic source (intra IV metronidazole 500mg + abdo, biliary, female genital ceftriazone 1g + IV gentamicin tract, aspiration pneumonia) 80mg

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



Anaphylactoid rxn – resembles anaphylactic rxn, but due to direct histamine release from mast cells w/o need for prior sensitization

Common causes  Drugs – penicililns & NSAIDS commonest, aspirin, TCM, sulpha drugs  Food – shellfish, egg white, peanuts  Venoms – bees, wasps, hornets  Environment – dust, pollen  Infections – EBV, HBV, coxsackie virus, parasites Stop Pptant  Stop administration of suspected agent / flick out insect stinger with tongue blade  Gastric lavage & activated charcoal if drug was ingested Airway  Prepare for intubation or cricothyroidectomy – ENT/Anaesthesia consult Fluid Rx  2L Hartman‘s or N/S bolus Drug Rx  Normotensive – 0.01ml/kg (max 0.5ml) Adrenaline 1:1000 dilution SC/IM  Hypotensive – 0.1ml/kg (max 5ml) 1:10,000 dilution IV over 5 mins  Indications: failure of adrenaline Rx OR if Glucagon adrenaline is contraindicated eg IHD, severe HPT, pregnancy, -blocker use  0.5-1.0mg IV/IM. Can be repeated once after 30mins Antihistamines  Diphenhydramine 25mg IM/IV  Chlorpheniramine 10mg IM/IV  Promethazine 25mg IM/IV  For persistent symptoms unresponsive to Cimetidine above Rx  200-400mg IV bolus  for persistent bronchospasm Nebulised bronchodilator  Salbutamol 2:2 q20-30mins Corticosteroids  Hydrocortisone 200-300mg IV bolus, q 6hr

150

151 CAUSES of LOWER GIT BLEEDING

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1) Colon    

2) 3) 4) 5)

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

-





HISTORY (if patient is stable) 1) Nature of bleeding  Haematochezia - Mixed with or coating stool - Torrential or drops, any clots? – Brisk upper GI bleed can present as haematochezia - Bright red (lower) or darker red (higher) - Any mucous  Malaena - Altered blood, indicates bleeding from upper GIT above ligament of Treitz (duodeno-jejunal junction) - Ask for history as per UBGIT 2) Aetiological clues  Exclude upper GIT cause - Any malaena, hematemesis, coffee grounds vomitus - History of PUD, gastritis, varices, Ca stomach, Mallory-Weiss tear, risk factors for each  Bleeding diverticulosis/angiodysplasia - Usually torrential bleeding that stops spontaneously; altered clots - History of previous bleeding episodes  Colorectal carcinoma - Constitutional symptoms: LOW, LOA, fatigue - Change in bowel habits, tenesmus - Symptoms of anaemia (chronic occult bleed) - Previous history/family history of GIT or ovarian cancer

Colitis Infective: any fever/chills/rigors, night sweats, N/V, diarrhoea, pain, recent travel/contact history, eating seafood, previous TB exposure or infection, BCG vaccination status - Inflammatory: ask about history of UC or Crohn‘s, joint, liver, eye & skin manifestations - Ischaemic: ask about atherosclerotic risk factors, previous AMI, stroke Hemorrhoids - bleeding to passing motion, blood coating stool, pain - Any mass noticed at anus - History of constipation, hard stools, low fibre diet, chronic straining, recent pregnancy Coagulopathy - Any history of bleeding disorders, easily bleeding, petechiae

3) Complications  Symptoms of anemia (may be only presentation!): SOB, postural giddiness, palpitations, chest pain, ↓ effort tolerance, fatigue, syncope  Symptoms of dehydration & shock: extreme thirst, confusion, pallor, ↓ urine output  May have complication of AMI if old patient with history of IHD PHYSICAL EXAMINATION 1. Vitals: - HR, supine & postural BP –stable? urine output (if catheter in-situ), - Any fever? 2. General inspection: - pallor, - confusion? 3. Peripheries: - signs of dehydration e.g. capillary refill, dry tongue. - Any supraclavicular lymph nodes? - Any skin manifestations of inflammatory bowel disease? - Stigmata of CLD? 4. Abdomen: - Scars? Any palpable masses 5. DRE: - any anal fissures or prolapsed hemorrhoids seen, - any masses felt, - any fresh blood or malaena 6. Offer proctoscopy to look for internal haemorrhoids

ACUTE MANAGEMENT Resuscitation o Supplemental oxygen, insert 2 large-bore IV cannula with fast infusion of crystalloids (N/S 500ml over ½hr) o Infuse colloids if ongoing blood loss while waiting for whole blood (GXM) o Catheterise and monitor urine output, insert NGT on suction to detect UBGIT o Continuous vital signs monitoring & I/O charting ± CVP & stool chart o ECG + cardiac enzymes to detect possible AMI o Take blood for investigations - FBC: low Hb level (repeat FBC 2-3 hours later or when necessary) – packed cell transfusion  4 pint PCT: give FFP to prevent over-dilution of clotting factors - UECr: hydration status, any acute renal failure from shock, electrolyte imbalance – replace - PT/PTT: must correct coagulopathy before trying to stop bleeding – fresh frozen plasma - LFT: exclude bleeding varices - ABG: may have metabolic acidosis in shock due to organ ischaemia – IV bicarb, dialysis if severe - GXM 4 pints Identify source & stop bleeding o Arrange urgent colonoscopy (patient must be stabilised before procedure) - Diagnostic: identify cancer, diverticulosis, angiodysplasia, areas of inflammation & bleeding - Therapeutic: clip, diathermize, or inject adrenaline/ sclerosant into bleeding vessel o Double contrast barium enema: good for picking up diverticulum which may be missed on scope o Mesenteric angiogram or CT mesenteric angiogram - More precise; can cannulate all 3 main trunks & their branches - Diagnostic: shows blush in active bleeding, shows ↓ perfusion of ischaemic bowel - Therapeutic (not for CT): embolisation/sclerotherapy for angiodysplasia, beware of causing bowel ischaemia (use foam medium) o Capsule Endoscopy: - for stable patients with suspected SI bleed & unable to swallow - takes 36hrs to read the results, but unable to localise the site & intervene o double balloon enteroscope: - only for suspected proximal SI - able to do therapeutic manoeuvres

152

o o

Labelled RBC isotope scan under gamma camera - For intermittent, occult bleeds not detectable on mesenteric angiogram - Not for urgent setting; can take up to 24 hours! Laparotomy with saline lavage if massive on going bleed, recurrent bleeding - On table scope to transilluminate bowel & identify bleeding source - On table angiogram - Oversewing of bleeding vessel, partial/total colectomy as last resort

HEMORRHOIDS  External hemorrhoids: not true hemorrhoids, but rather painful thrombosed veins arising distal to the dentate line  Internal hemorrhoids: those arising proximal to the dentate line, usually painless unless prolapsed & strangulated Banov grading of internal hemorrhoids Grade Description I The hemorrhoids do not prolapse II Hemorrhoids prolapse on BO but spontaneously reduce III Hemorrhoids prolapse on BO & must be manually reduced IV Hemorrhoids are prolapsed and cannot be reduced

Treatment Rubber band ligation

Staple hemorrhoidectomy Excision (due to high reccurence)

INFLAMMATORY BOWEL DISEASE

Bowel involvement

Location

Continuity Complications

Crohn’s Can affect entire GIT anywhere from mouth to anus, but usually affecting the terminal ileum  40% terminal ileum  30% small intestine  30% colon  3% anorectal (usu. spared) Not continuous, with skip lesions Strictures, fistulae, sinuses, malnutrition (SB involvement)

Ulcerative colitis Usually begins in the rectum and can extend proximally to affect entire colon   

40% rectum alone 40% left colon 20% total colitis

Longitudinal mucosal continuity These complications absent

153 Histopathology

Risk of carcinoma

Associated antibodies Severity

Macoscopic: bowel is thickwalled & nodular (cobblestone appearance) with creeping fat, mesenteric thickening & deep linear ulcers Microscopic: transmural involvement, non-caseating granulomas (pathognomonic, but only present in 2/3) Slight increased risk of colorectal Ca, increased risk of small bowel lymphoma

ASCA: anti-saccharomyces cerevisiae antibodies Harvey Bradshaw severity index

Macroscopic: granular appearance of mucosa , loss of vascular markings, pseudopolyps interspersed with areas of shallow ulceration Microscopic: only mucosal & submucosal involvement, crypt abscesses - Muscularis propria & serosa may be affected in fulminant disease Substantially higher risk of colorectal Ca  2% at 10 years  8% at 20 years  18% at 30 years  Much higher risk with concomitant PSC p-ANCA: perinuclear antineutrophil cytoplastic antibodies Modified Truelove & Witts severity index (Mild, moderate, severe, fulminant)

Epidemiology  Bimodal distribution: affects young in the 2nd & 3rd decades of life, with second onset in the 5th & 6th decades of life  Equal gender predominance  Higher prevalence amongst Ashkenazi Jews & in cooler climates e.g. Scandinavia, UK, Germany, northern USA  Genetic association History  GIT: abdominal pain, diarrhea, N/V, bloating, distention, bloody stools with mucous & pus  Crohn‘s fistula: colovesical fistula or coloovarian fistula: faeces in urine/ pneumaturia, faeces per vaginal/ PID  Non-specific systemic: LOW, LOA, fever, fatigue, symptoms of anemia, chronic malnutrition  Specific extra-intestinal manifestations Physical examination: usually normal +/- extra-intestinal manifestations

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

CROHN’S DISEASE P/E: RIF mass, enlarged skin tags, anal stricture Investigations: supportive (see UC) & diagnostic Diagnostic  Contrast radiographic studies: assess location & extent of disease, look for strictures & fistulae o Barium studies: small bowel series & enema o CT scan with oral & IV contrast 

Endoscopy: look for typical features o Colonosopy with tissue biopsy (non-caseating granulomas) o OGD: upper GIT involvement o Endoanal U/S: identify fistula tracts Management  Medical (principle treatment) o Nutritional support e.g. TPN (may also aid closure of fistulae) o Pharmacological  Corticosteroids for acute exacerbation of disease, but not for long term use  1st line: sulfasalazine, mesalazine (5-ASA or 5-aminosalicylic acid) induce & maintain remission of disease: oral, rectal suppository or enema (up to splenic flexure)  2nd line: immunosuppressive agents e.g. azathioprine, 6-MP, MTX & cyclosporine when 1st line agents ineffective  Biologics: Remicade (infliximab), a TNF blocker - Require close surveillance for SE (blood disorders, infections, lymphoma & solid tissue cancers, hepatotoxicity, drug-induced lupus, demyelinating disorders)



Surgical o Principles  Avoid surgery until absolutely necessary (80% require surgery within 20 years of onset) & when indicated perform bowel preserving surgery as repeated bowel resections can lead to short gut syndrome o Indications :    

Disease refractory to medical therapy Serious complications of medical therapy Severe bleeding, perforation Intestinal obstruction due to strictures

   

o

Procedure (laparoscopic or open)  CT abdomen for pre-operative percutaneous drainage of abcesses (↓ inflammation & risk of sepsis)  Small bowel: (bowel preservation is key) - Short segment disease: stricturoplasty - Long segment disease: long stricturoplasty or resection - Fistula: resect diseased bowel & repair involved organ  Large bowel: - Total colectomy + ileorectal anastamosis (if rectum spared) or proctocolectomy + end ileostomy (if rectum affected) - Segmental colectomy only in selected cases as high recurrence rate  Perianal disease: - Setons, fistulotomy, proctectomy in severe disease

Fistulae Abscesses Toxic megacolon Malignancy

ULCERATIVE COLITIS Extra-intestinal manifestations (20% of patients)  Joints (most common) o Transient asymmetrical polyarthritis: mirrors course of colitis & is cured by colectomy o Ankylosing spondylitis o Isolated sacroiliitis  Liver o PSC (5%): fibrous structuring of entire biliary tree: ↑ ALP, MRCP, ERCP, liver biopsy. Tx: stenting, transplant o Hepatic failure over 5-10 years independent of course of colitis o ↑ risk of cholangiocarcinoma & ↑↑↑ risk of colorectal carcinoma  Eye o Iritis, episcleritis, anterior uvetitis. Tx: topical and/or oral corticosteroids  Skin

154

o o

Pyoderma gangrenosum: deep ulceration with violaceous border that overhangs ulcer bed, usually affecting LL Erythema nodosum: poorly defined, tender, erythematous nodules that do not ulcerate or suppurate, usually on the shin Tx: corticosteroids, will improve slowly following colectomy

o Investigations Supportive (looking for complications & assessing severity of disease)  Blood tests o FBC: anemia, leukocytosis & thrombocytosis indicate more severe disease o UECr: hypokalemia & dehydration in prolonged diarrhoea o LFT: hypoalbuminemia due to poor nutritional intake o CRP, ESR: markers of severity o Autoantibody assay: p-ANCA ↑ in UC, ASCA ↑ in CD  Radiological o AXR to evaluate colonic caliber (>6 cm is abnormal) o CXR to rule out perforation (risk of perforation in acute disease) Diagnostic  Endoscopy: look for typical features o Flexible sigmoidoscopy with tissue biopsy: bleeding may occur with contact with scope Management  Medical: similar to Crohn‘s disease  Surgical (25% eventually require surgery) o Indications : o Disease refractory to medical therapy with severe & extensive colitis o Serious complications of medical therapy o Severe bleeding o Perforation o Toxic megacolon (colon > 6cm) o Malignancy o Procedure (laparoscopic or open)  Acute setting: total colectomy with end ileostomy: diseased rectum left in-situ with resection & IPAA at later date when patient has regained health & steroids have been withdrawn. Foley catheter used to decompress rectum for 3-4 days  IPAA (ileo-pouch anal anastamosis): standard of care for patients with UC who ultimately require colectomy. Avoid necessity for long term stoma. Crohn‘s disease remains an absolute contradindication as overall failure rates approach 50%  Total proctocolectomy with end ileostomy

155 Causes of Jaundice

o o o o o o o

Pre-hepatic Urine/stools normal May have symptoms of anemia Unconjugated hyperbilirubinemia ↑ LDH, ↓ haptoglobin PBF Direct Coomb‘s test for autoimmune hemolytic anemia Stool OCP (ova, cysts, parasites) malaria

Hemolytic anemias: 1) Inherited  Thalassemia  G6DP  Spherocytosis  Sickle-cell anemia 2) Acquired  Infective: malaria  Autoimmune: SLE, Evan‘s syndrome  Hemolytic uremic syndrome (hemolytic anemia, ARF & thrombocytopaenia)

o o o o o o

o o o

Hepatic Mixed signs; urine may be dark with normal stools Variable liver biochemistry ↑ ALT, AST disproportionate to ALP, GGT ↓ Albumin, prolonged INR (cirrhosis) AFP: exclude complication of malignancy Viral hepatitis serology  Acute: Anti-HBc IgM, Anti-HAV IgM  Chronic: HBsAg, anti-HCV, HCV RNA Autoimmune screen  ANA, anti-dsDNA, AMA Metabolic screen  Caeruloplasmin, 24 hour urine copper Do abdominal U/S: surface nodularity & ↑ echogenicity in cirrhosis, also look for signs of portal HTN (splenomegaly & ascites)

1) Infective  Acute viral hepatitis (HBV, HAV)  EBV, CMV  TB 2) Liver cirrhosis/chronic liver disease  Alcoholic liver disease  Chronic viral hepatitis (HBV, HCV)  Metabolic (Wilson‘s, hematochromatosis)  Infiltrative (Sarcoidosis, amyloidosis) 3) Hepatotoxic drugs  Alcohol, paracetamol, TCM, isoniazid, augmentin, MTX, phenytoin, corticosteroids 4) Autoimmune hepatitis  SLE 5) Inherited ↓/absent activity of UGT (unconjugated hyperbilirubinemia)  Gilbert‘s syndrome  Crigler Najjar 1 & 2 6) Inherited impaired biliary excretion (conjugated hyperbilirubinemia)  Dubin-Johnson syndrome  Rotor syndrome

o o o o

Cholestatic Tea-colored urine, pale stools, intense pruritis Conjugated hyperbilirubinemia ↑ ALP, GGT disproportionate to ALT, AST Do abdominal U/S  If ducts dilated (>8mm), do ERCP/MRCP/PTC  If ducts not dilated, further serologic testing: AMA (M2-IgG most specific for PBC), p-ANCA (PSC), ANA & anti-SMA. Consider ERCP, liver biopsy

1) Intraluminal  Gallstones (painful)  Parasites: Ascaris lumbricoides, schistosomiasis 2) Mural  Biliary strictures post ERCP  Biliary strictures from gallstones, chronic pancreatitis  PBC (intrahepatic bile ducts): middle aged ♀  PSC (intra & extrahepatic): ♂ with IBD esp. UC  Cholangitis (Charcot‘s triad)  Choledochal cyst (type I-V)  Distal cholangiocarcinoma 3) Extraluminal  Ca head of pancreas (painless, w distended GB)  Other peri-ampullary Ca (cholangio, dudeno, ampullary)  Mirrizi‘s syndrome (chronic cholecystitis) 4) Others:  Biliary atresia  Drug-induced: paracetamol, penicillins, corticosteroids

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

Causes of IO 1. Mechanical Intraluminal -Impacted stool -Gallstone ‗ileus‘ -Foreign body -Bezoars (phytotricho-)

Mural -Tumours -Diverticular stricture -Intussusception -Crohn‘s strictures - RT strictures

PHYSICAL EXAMINATION  Vitals: Is patient stable? Any fever? (sepsis) Hypotension, tachycardia? (dehydration) Extraluminal - Adhesions (post-op, Crohn‘s) - Herniae - Volvulus - Lymph node compression - Superior mesenteric artery syndrome



General inspection: Abdominal distension? Cachexia? Confusion?



Peripheries: Look for signs of dehydration e.g. capillary refill, dry tongue Palpate lymph nodes



Abdomen:  Any distension?  Scars from previous abdominal surgery?  Visible peristalsis? – severe obstruction  Any signs of peritonitis: guarding, rebound tenderness, or soft and NT  Any masses, herniae  Bowel sounds:  Initially hyperactive, later may be sluggish or absent  Tinkling BS: small bowel obstruction  Succussion splash + epigastric tenderness: gastric outlet obstruction



DRE: any masses felt, any stools?

2. Functional (give rise to megacolon) - Paralytic ileus (post-op, sepsis, ischaemic, metabolic, hypothyroidism, opiateinduced) - Hirschsprung‘s disease: absent ganglia in Auerbach‘s plexus - Ogilvie syndrome : in severely ill patients Others: intestinal atresia Small bowel IO 1) Adhesions 2) Herniae 3) Ileocecal tumour 4) Intussussception

Large bowel IO 1) Cancer 2) Post-diverticulitis stricuture 3) Sigmoid volvulus

HISTORY 4 cardinal symptoms 1. Pain: - Usually colicky, 4-5 days duration - Complete obstruction: constant, sharp pain - Volvulus: sudden, severe pain 2. Vomiting: ask if projectile, bilious, or fecal stained 3. Abdominal distention 4. Constipation - Ask about normal BO frequency - Complete obstipation: cannot even pass flatus Other pertinent history - Symptoms of GIT bleed, infection - Previous surgeries - Underlying GIT disorders - Recent change in bowel habit - Risk factors for ischaemic bowel: atherosclerotic RH, heart disease, previous stroke - Suspicion of malignancy: LOW, LOA, previous Ca, FH of Ca

ACUTE MANAGEMENT o Resuscitate if necessary, monitor vitals - Urinary catheter: monitor output o NBM: rest bowel + IV drip o NG tube on constant suction o Correct acidosis, replace K+ as guided by investigations o Start broad spectrum ABx [IO affects normal translocation of bacterial flora] o Rule out surgical emergencies (history/physical examination/investigations) 1. Obstructed abdominal hernia 2. Volvulus (sigmoid, caecal, stomach) 3. Closed-loop obstruction (competent ileocecal valve) 4. Ischaemic bowel with bowel necrosis 5. Perforation/peritonitis INVESTIGATIONS Bloods Assess complications  FBC: any infection, anemia  UECr : any dehydration due to: - Intra-luminal 3rd space loss (damaged enterocytes unable to reabsorb) - Vomiting (also assess K+ loss: can perpetuate paralytic ileus)





ABG - Acidosis from bowel ischaemia - Alkalosis due to vomiting (more for pyloric stenosis in children) Pre-operative  GXM 4 pints of blood, PT/PTT  Cardiac enzymes x2 sets (+ ECG) Imaging Assess complications  Erect CXR : air under diaphragm, any aspiration pneumonia  AXR: Rigler‘s Sign (obvious bowel wall due to extra-luminal air) Diagnostic  AXR - Erect: air fluid levels (>6) - Supine: look for small or large bowel dilatation on radiograph  Duodenum: C-shaped  Jejunum/proximal ileum: centrally located, stack of coins appearance (plicae circulares)  Distal ileum: plicae circulares disappears, lead-pipe appearance  Colon: incomplete bands (haustrations due to presence of teniae coli) - Sigmoid volvulus? Coffee bean + parrot‘s beak sign - Closed loop obstruction? Distal lesion with v. distended cecum (thinnest wall; up to 12cm), ileum not dilated - Bowel ischaemia with necrosis? Gas in bowel wall (pneumatosis intestinalis) due to gas gangrene - Gas present in rectum? No: complete obstruction (may require KUB film)  Barium enema - Gastrografin preferable if risk of perforation; risk of barium peritonitis - Upper GI barium studies contraindicated  Colonoscopy done without bowel prep (not necessary, and also contraindicated, in IO)  CT colonography DEFINITIVE MANAGEMENT (Depends on cause) 1) Obstructed abdominal hernia  Herniorrhapy 2) Sigmoid volvulus  Ryle‘s tube decompression: - Gown up - Put end of Ryle‘s tube in a bottle submerged in water - Insert lubricated Ryle‘s tube into anus

158

3)

4)

5)

6)

7)

Flexible sigmoidoscopic decompression with sigmoid colectomy & formation of double barrel colostomy (Paul-Mikulicz procedure) with future re-anastamosis  Sigmoidopexy: fix sigmoid to posterior abdominal wall (rarely done as high risk of recurrence)  Caecal volvulus: resection & re-anastamosis  Gastric volvulus: gastropexy Closed loop obstruction (if due to distal tumour)  Resect bowel, primary anastamosis with proximal defunctioning colostomy  Hartmann‘s/Paul-Mikulicz procedure if bowel is too inflamed/oedematous to anastamose (high risk of leakage) Ischaemic bowel  Bowel ischaemia alone can cause paralytic ileus, usually occurring in the splenic flexure (watershed area receiving blood from the most distal arterial branches)  Supportive management e.g. NBM, drip & suck, antibiotics while waiting for collaterals to re-supply bowel, re-establish peristalsis  Surgical intervention if bowel is non-viable e.g. gangrenous or necrotic o Will have relook laprotomy in 2-3/7 to ensure good resection of bowel margins Perforation (usually in caecum as it is thin walled)  Occurs due to ischaemia of stretched out bowel wall; >12cm dilated  Emergency laparotomy: resect lesion & perforated bowel with generous peritoneal lavage  If lesion e.g. tumour is proximal enough to the cecum, can do extended right hemi-colectomy  If lesion is distal, may require total-colectomy with ileo-rectal anastamosis  Continue antibiotics following surgery Intussusception  Children: usually due to hypertrophic Peyer‘s patches. Administer barium enema: watch intussception reduce on fluoroscopy  Elderly: usually leading point present (polyp, Ca). Barium enema unlikely to work, or if works recurrence rate is high, therefore surgery is 1st line treatment Post-op paralytic ileus (>3 days post-op)  Supportive management: drip & suck, wait for peristalsis to restart  Oral gastrografin: hyperosmotic, causes intraluminal osmosis , can reestablish peristalsis  Prokinetic agents: erythromycin, metaclopromide, cisapride

159 ACUTE APPENDICITIS

HISTORY - Classic: LOA with periumbilical pain which radiates to the RIF, followed by nausea & vomiting - N/V almost always occurs after pain, if it precedes pain, exclude IO - May have diarrhoea or constipation - Inflamed appendix near bladder/ureter may cause irritative voiding symptoms & haematuria PHYSICAL EXAMINATION - RIF (McBurney‘s point) tenderness on percussion, rebound tenderness, rigidity & guarding - RIF mass may be palpable - LIF tenderness in patients with situs inversus or lengthy appendix extending to the LIF -

Cough sign: RIF pain on coughing (localized peritonitis) Rovsing sign: RIF pain with palpation of the LIF Obturator sign: RIF pain with internal rotation of a flexed right hip Psoas sign: RIF pain with hyperextension of the right hip

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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

INVESTIGATIONS Blood: FBC, UECr, CRP, Blood culture, PT/PTT, GXM Urine: UFEME (may have pyuria & haematuria) Imaging: Erect CXR, CTAP, abdominal U/S

MANAGEMENT - NBM, IV drip, IV antibiotics, correct electrolyte imbalance - Symptomatic relief: anti-emetics & analgesia -

Definitive treatment: appendicectomy (open or laparoscopic)

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Conservative treatment for appendiceal mass: Oschner Sherren regime  Omentum naturally wraps around inflamed appendix, containing inflammatory process  Symptomatic treatment as well as antibiotics, monitor patient as well as size of mass  When mass has reduced in size, patient is stable, do surgery (less inflammation: easier)  Exceptions: very young or very old patients, or patients with suspected appendicular abscess (require incision & drainage of pus)

MECKEL’S DIVERTICULUM

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

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

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

160

MANAGEMENT - NBM, IV drip, correct electrolyte imbalance -

IO: NG tube on constant suction, supine AXR

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PR bleed: PCT if necessary, gastric lavage to exclude UBGIT, OGD & colonoscopy

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Definitive treatment: surgery (open or laparoscopic)  Wide base: wedge ileal resection with anastamosis  Narrow base: resection of the diverticulum

161 POST-OP COMPLICATIONS

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