Andre Tan Updated (With Page Number)

SURGERY NOTES Adapted from Andre Tan

1

1.

TRAUMA & PERIOPERATIVE CARE

1. 2. 3. 4. 5. 6. 7. 8.

ADVANCED TRAUMA LIFE SUPPORT ABDOMINAL TRAUMA CARDIOTHORACIC TRAUMA NEUROSURGICAL TRAUMA MUSCULOSKELETAL TRAUMA POST-OPERATIVE COMPLICATIONS SHOCK PERIOPERATIVE CARE

2.

LUMPS & BUMPS

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

HERNIA SCROTAL SWELLINGS APPROACH TO LUMPS & BUMPS LIPOMA SEBACEOUS CYST GANGLION BASAL CELL CARCINOMA SQUAMOUS CELL CARCINOMA MALIGNANT MELANOMA NEUROFIBROMA DERMOID CYST SEBORRHOEIC KERATOSIS HAEMANGIOMA PYOGENIC GRANULOMA PAPILLOMA KERATOCANTHOMA KELOID (HYPERTROPHIC SCAR) KAPOSI’S  SARCOMA FIBROSARCOMA PYODERMA GANGRENOSUM RADIOTHERAPY MARKS

5. 4 7 8 10 13 14 18 21

6.

SURGICAL INSTRUMENTS & PROCEDURES

1. 2. 3. 4. 5.

DRAINS 64 CENTRAL VENOUS PRESSURE LINE 65 NASOGASTRIC TUBE 67 TRACHEOSTOMY 68 SENGSTAKEN-BLAKEMORE TUBE (MINNESOTA TUBE) 70 71 URINARY CATHETERISATION 72 CHEST TUBE

4.

ABDOMINAL SURGICAL EMERGENCIES

1. 2. 3.

APPROACH TO ABDOMINAL PAIN APPROACH TO ABDOMINAL MASSES INTESTINAL OBSTRUCTION (& MECKEL’S   DIVERTICULUM) ISCHAEMIC BOWEL ACUTE APPENDICITIS

4. 5.

1. 2. 3. 4.

28 34 37 40 41 42 44 46 48 52 54 55 56 58 59 60 60 61 61 62 63

3.

6. 7.

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

APPROACH TO BLEEDING LOWER GIT COLORECTAL CANCER STOMAS DIVERTICULAR DISEASE INFLAMMATORY  BOWEL  DISEASE  (CROHN’S   DISEASE, ULCERATIVE COLITIS)

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 1. 2. 3.

2

APPROACH TO BLEEDING UPPER GIT VARICEAL BLEEDING PEPTIC ULCER DISEASE GASTRIC CANCER

1. 2. 3. 4. 5.

9.

86 86 87 91 96 100 101

UPPER GIT

LOWER GIT & COLORECTAL DISEASES

1. 2. 3.

76 82 84

ANATOMY OF THE OESOPHAGUS PHYSIOLOGY OF SWALLOWING APPROACH TO DYSPHAGIA OESOPHAGEAL CANCER GASTRO-OESOPHAGEAL REFLUX DISEASE BARRETT’S  OESOPHAGUS ACHALASIA

7.

8.

74 75

OESOPHAGEAL DISEASES

102 105 108 112

116 118 130 134 137

ANAL & PERIANAL DISORDERS HAEMORRHOIDS ANAL FISTULA ANAL FISSURES

140 142 144

LIVER DISEASES ANATOMY OF THE LIVER CAUSES OF HEPATOMEGALY CAUSES FOR A LIVER NODULE ON IMAGING HEPATOCELLULAR CARCINOMA LIVER METASTASES LIVER HAEMANGIOMA SIMPLE LIVER CYSTS HEPATIC ABSCESS (PYOGENIC / AMOEBIC) ASCITES

145 145 145 146 152 152 153 153 154

PANCREATIC DISEASES ACUTE PANCREATITIS CHRONIC PANCREATITIS PANCREATIC CANCER

155 161 162

11. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 12. 1. 2. 3. 4. 5. 6. 7. 13. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

BILIARY TRACT DISEASES CAUSES OF JAUNDICE APPROACH TO OBSTRUCTIVE JAUNDICE GALLSTONE DISEASE ACUTE CHOLECYSTITIS GALLBLADDER CANCER CHOLEDOCHOLITHIASIS CHOLANGITIS MIRIZZI’S  SYNDROME RECURRENT PYOGENIC CHOLANGITIS CHOLANGIOCARCINOMA

14. 1. 2. 3. 4. 5. 6.

182 182 183 188 189 195 195

4. 5.

ANATOMY OF THE THYROID GLAND APPROACH TO THYROID PROBLEMS APPROACH TO THE SOLITARY THYROID NODULE THYROID CANCERS SURGERY IN BENIGN THYROID DISEASE

16.

PERIPHERAL ARTERIAL DISEASES

15. 1. 2. 3.

1. 2. 3.

NECK MASSES ANATOMY OF THE NECK THYROGLOSSAL CYST DERMOID CYST PLUNGING RANULA BRANCHIAL CYST/FISTULA CHEMODECTOMA PHARYNGEAL POUCH CYSTIC HYGROMA CERVICAL RIB NEUROMA/SCHWANNOMA CERVICAL LYMPHADENOPATHY

203 ANATOMY OF THE PAROTID GLAND ANATOMY OF THE SUBMANDIBULAR GLAND 203 203 ANATOMY OF THE SUBLINGUAL GLAND APPROACH TO SALIVARY GLAND SWELLINGS 204 205 SIALOLITHIASIS 206 SALIVARY GLAND TUMOURS

166 167 169 173 175 175 176 178 178 180

BREAST DISEASES ANATOMY OF THE BREAST PRESENTATION OF BREAST DISEASES APPROACH TO A BREAST LUMP APPROACH TO NIPPLE DISCHARGE BREAST CANCER PAGET’S  DISEASE  OF  THE  NIPPLE GYNAECOMASTIA

SALIVARY GLAND SWELLINGS

196 197 197 197 198 199 199 200 200 200 201

ANATOMY OF THE LOWER LIMB ARTERIES ACUTE LIMB ISCHAEMIA CHRONIC LIMB ISCHAEMIA

17.

ABDOMINAL AORTIC ANEURYSM

18.

PERIPHERAL VENOUS DISEASES

1. 2. 3. 4. 19. 1. 2. 3. 4. 5. 6. 7.

3

THYROID DISEASES

ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB CHRONIC VENOUS INSUFFICIENCY VARICOSE VEINS VENOUS ULCERS

208 209 211 212 215

216 217 222 228

230 232 233 236

UROLOGICAL DISEASES APPROACH TO HAEMATURIA RENAL CELL CARCINOMA BLADDER TRANSITIONAL CELL CARCINOMA UROLITHIASIS APPROACH TO ACUTE RETENTION OF URINE BENIGN PROSTATIC HYPERPLASIA PROSTATIC CANCER

238 241 244 246 249 252 256

1.

TRAUMA & PERIOPERATIVE CARE

1.

ADVANCED TRAUMA LIFE SUPPORT Approach: Primary survey and resuscitation with adjuncts Re-evaluation of the patient Secondary survey with adjuncts Post-resuscitation monitoring and re-evaluation Optimise for transfer and definitive care

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 PRIMARY SURVEY – ABCDE 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 / modified jaw thrust (protect C-spine!) Remove any FBs in the mouth if possible Oro/nasopharyngeal airway Definitive airway – endotracheal tube, cricothyroidotomy, tracheostomy

BREATHING

Assessment of breathing 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

CIRCULATION

Assessment of organ perfusion Level of consciousness Skin colour and temperature (cold, mottled, clammy), capillary refill Pulse rate and character (weak, thread) – all major pulses Blood pressure Classes of haemorrhagic shock - gradual transition from one stage to the next I II III Bld loss : Amt (ml) 30 20-30 5-15 AnxiousMental state Sl anxious Mild anxiety confused Crystalloid + Fluid replacement Crystalloid Crystalloid blood

IV >2000 >40 >140 Critical Prolonged >35 Oliguric-anuric Confusedlethargic Blood

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

4

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

Glasgow coma scale Eye (E4) Spontaneous opening Opens to voice Opens to pain No response

4 3 2 1

Verbal (V5) Oriented speech Confused Inappropriate Incomprehensible No verbal response

Motor (M6) 5 4 3 2 1

Obeys Purposeful Withdraws Flexion response Extension response No response GCS: > 13 (minor); 8-13 (moderate); < 8 (severe)

6 5 4 3 2 1

AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive Pupillary reactivity Call for neurosurgical consult as indicated EXPOSURE

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

ADJUNCTS

Monitoring Vital signs – BP, pulse rate, saturation (pulse oximeter) ECG monitoring Arterial blood gas Diagnostic tools Screening X-ray films (trauma series): CXR, AP pelvis, lateral C-spine Focused abdominal sonography in trauma (FAST) Diagnostic peritoneal lavage Urinary catheter Functions: decompress bladder, measurement of urinary output Caution in urethral injury: blood at urethral meatus, perineal ecchymosis/haematoma, high-riding prostate Gastric catheter (orogastric or nasogastric) Function: decompress stomach, look at aspirate (bloody? bilious?) Caution in base of skull fracture: CSF otorrhoea/rhinorrhoea, periorbital ecchymosis, mid-face instability (grab the incisors and rock), haemotympanum insert orogastric tube instead of nasogastric

SECONDARY SURVEY When to do secondary survey:

AMPLE HISTORY

Primary survey and resuscitation completed ABCDEs reassessed Vital functions returning to normal i.e. no need for active resuscitation at the moment

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

5

COMPLETE HEAD-TOTOE EXAMINATION

Head Complete neurological examination GCS or AVPU assessment Comprehensive examination of eyes and ears for base of skull fractures Caution: unconscious patient; periorbital oedema; occluded auditory canal Maxillofacial Bony crepitus/deformity, palpable deformity Comprehensive oral/dental examination Caution: potential airway obstruction in maxillofacial injury; cribriform plate # with CSF rhinorrhoea do not insert nasogastric tube Cervical spine Palpate for tenderness, any step deformity Complete neurological examination C-spine imaging Caution: Injury above clavicles; altered consciousness (cannot assess accurately); other severe, painful injury (distracts from cervical spine pain) Neck (soft tissues) Blunt versus penetrating injuries Airway obstruction, hoarseness Crepitus (subcutaneous emphysema), haematoma, stridor, bruit Caution: delayed s/s of airway obstruction that progressively develop; occult injuries Chest Inspect, palpate, percuss, auscultate Re-evaluate frequently Look at CXR Caution: missed injury; increase in chest tube drainage Abdomen Inspect, palpate, percuss, auscultate Abrasions and ecchymosis – “seat-belt  sign” Lower rib fractures liver and spleen injury Re-evaluate frequently Special studies: FAST, DPL (diagnostic peritoneal lavage), CT scan Caution: hollow viscus and retroperitoneal injuries; excessive pelvic manipulation Perineum Contusions, haematomas, lacerations Urethral blood DRE: Sphincter tone, high-riding prostate, pelvic #; rectal wall integrity; blood Vaginal examination: blood, lacerations Musculoskeletal – extremities Contusion, deformity Pain, Perfusion, Neurovascular status X-rays as appropriate Caution: potential blood loss is high in certain injuries (e.g. pelvic fracture, femoral shaft fracture); missed fractures; soft-tissue or ligamentous injuries; examine  patient’s  back

ADJUNCTS & SPECIAL

As required according to suspicion, but should not delay transfer

DX TESTS

FREQUENT REEVALUATION

Have a high index of suspicion for injuries to avoid missing them Frequent re-evaluation & continuous monitoring rapidly recognise when pt is deteriorating

PAIN MX

Intravenous analgesia as appropriate

6

2.

ABDOMINAL TRAUMA

TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA Solid organ injury: spleen, liver – bleeding (may be quite massive) Hollow viscus injury with rupture Vascular injury with bleeding INDICATIONS FOR IMMEDIATE LAPAROTOMY 1) Evisceration, stab wounds with implement in-situ, gunshot wounds traversing abdominal cavity 2) Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation 3) Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising haemodynamics 4) Obvious signs of peritoneal irritation 5) Rectal exam reveals fresh blood 6) Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries excluded as source of bleeding) 7) X-ray evidence of pneumoperitoneum or diaphragmatic rupture INVESTIGATIONS FOCUSED ABDOMINAL SONOGRAPHY IN TRAUMA (FAST) Ultrasonographic evaluation of 4 windows: Pericardial, R upper quadrant, L upper quadrant, Pelvis CT SCAN Only suitable for stable patient as quite long time involved in imaging with only patient in the room pt can collapse DIAGNOSTIC PERITONEAL LAVAGE (DPL) Involves making a cut in the infraumbilical region and inserting a catheter into the peritoneal cavity, aspirate, then instillation of saline and re-aspiration

If patient is stable: FAST and/or CT scan If patient is unstable: FAST and/or DPL 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 + for bacteria in effluent

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

Contraindications Absolute indication for laparotomy 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 cxs (haematoma, infx); 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

7

3.

CARDIOTHORACIC TRAUMA

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

Clinical features Chest trauma and hypotension Beck’s  triad (hypotension, muffled heart sounds, distended neck veins) – only in 50% of cases as hypovolaemia may prevent neck vein distension; muffled heart sounds 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 = alternation of QRS complex amplitude or axis between beats.

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

8

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

PNEUMOTHORAX (TENSION/ OPEN)

Tension pneumothorax = develops when air is trapped in the pleural cavity under positive pressure, displacing mediastinal structures and compromising cardiopulmonary function It is a clinical diagnosis (CXR will only delay treatment, and may cause death) – signs of pneumothorax, hypotension, neck vein distension, severe respiratory distress Decreased venous return caused by compression of the relatively thin walls of the atria impairs cardiac function. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. It is most evident in trauma patients who may be hypovolemic with reduced venous blood return to the heart. Immediate needle thoracotomy in second intercostal space in mid-clavicular line Followed by chest tube insertion Open pneumothorax occurs in a large chest wall defect with equilibration between intrathoracic and  atmospheric  pressure,  producing  a  “sucking  chest  wound”. Cover defect with a sterile dressing, taping it down on 3 sides to produce a flutter-valve effect, letting air out of the pleural cavity but not back in Insert chest tube (not through the wound)

9

4.

NEUROSURGICAL TRAUMA

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

Contusion Intracranial haemorrhage

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 Small haematoma 13)

Most common Indications for admission:

Moderate head injury (GCS 8 - 13)

All will be CT-scanned at ED NES will operate if any indication to do so In ward: as per mild head injury

Persistent headache and/or vomiting CSF leak Neurological deficit Skull fracture History of loss of consciousness Amnesia In ward: NBM, IV drip (no dextrose saline!), no sedation, monitor GCS If pt deteriorates CT scan Exclude metabolic causes (e.g. hypoglycaemia) Do septic workup (exclude sepsis)

11

Severe head injury

Must scan to look for reversible causes of raised ICP but stabilise patient first Medical methods to lower ICP Raise head of bed (improves venous drainage but could pressure of blood to the head) Intubate and hyperventilate (the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic -- hence it is no longer widely used. Furthermore, the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation, which could cause the vessels to rapidly dilate if carbon-dioxide levels were returned to normal too quickly) IV mannitol: create a hypertonic solution within the blood to draw water out of the neurons. This helps to reduce the fluid within intracranial space, however prolonged administration may lead to increase in ICP (must catheterise patient also; do not give if patient is unstable) Screen for other life-threatening injuries (likely to be multi-trauma patient) Achieve haemodynamic stability Check for long bone fractures FAST for bleeding into abdominal cavity ABG to detect acidosis Keep monitoring patient and re-investigate where appropriate Operate if reversible cause found Craniectomy (i.e. bone flap not replaced) or craniotomy (bone flap replaced after blood evacuated) [Burrhole usually not big enough to drain an acute bleed] Evacuate clot Insert endoventricular drain (EVD) if there is hydrocephalus Total sedation after operation, ward in ICU Prevents patient from struggling which will raise ICP

Depressed skull fracture

Can leave alone unless depression is greater than the thickness of the skull bone

Compound depressed fracture

There is through-and-through skin laceration over the fracture Always explore to ensure underlying dura is intact, and repair if dura is torn (since meningitis can occur with a torn dura)

12

5.

MUSCULOSKELETAL TRAUMA

GENERAL POINTS Extremity trauma tends not to be life-threatening But occult blood loss can occur in large volumes esp in certain injuries – pelvic # (up to 3L), femoral shaft # (2L) Need to have high level of suspicion and treat with urgency Look out for any tachycardia, early signs of shock Prepare to resuscitate patient ASSESSMENT OF THE EXTREMITY Perfusion: colour, pulses, skin temperature, capillary refill Viability of the limb Neurological assessment Wounds – open or closed injury; abrasion over a fracture is considered open fracture Soft tissue assessment Deformity Abnormal joint mobility – ligamentous injury around joint; in knee, highly likely that popliteal artery is injured as well THE PULSELESS EXTREMITY

Things to consider Is pulselessness due to shock? Arterial or venous compromise? Is there compartment syndrome (pulselessness is a very late sign) Any pre-existing vascular disease? Physical examination Any limb deformity (can result in kinking of vessels)? Any joint instability (dislocation of a joint can result in intimal tear in the major vessel running across it, with thrombosis and occlusion)? Skin colour/temperature Post-reduction tibial pulse in knee dislocation – if still absent, do an urgent angiogram!

SOFT TISSUE INJURIES

Types Open: laceration, abrasion Crushing Degloving: open or closed Closed Wound care Swabs of the wounds for culture and sensitivity IV antibiotic prophylaxis Tetanus toxoid cover Photograph wound (to prevent re-opening of wound by every doctor that comes to see pt) Betadine (povidone-iodine) dressing In OT: generous debridement, irrigation (within 4-8 hours, especially in open fractures), fracture stabilisation (internal or external fixation depending on Gustilo classification) Leave wound OPEN

MANAGEMENT OF FRACTURES

Recognise fracture and/or dislocation Complete neurovascular examination of the limb involved before reduction Appropriate X-rays (at least 2 planes) Analgesia Correction of deformity Temporary immobilisation – backslab, malleable splint Neurovascular examination; examine for compartment syndrome Circulation chart

13

OPEN FRACTURES Definition: communication between the # or fracture haematoma and the external environment Gustilo-Andersen classification Type I 1cm AND no extensive soft tissue damage, avulsions or flaps Type IIIA Extensive soft tissue damage, avulsions or flaps but adequate soft tissue coverage of bone OR High-energy trauma cause regardless of size of wound Type IIIB Extensive soft tissue loss with periosteal stripping and exposure of bone. Massive contamination common. Type IIIC Arterial injury requiring repair Management of open fractures Stabilise patient first Pain relief and analgesia Cover the wound with moist gauze Temporary immobilisation and splinting IV broad spectrum antibiotics Appropriate X-rays Nil by mouth Pre-op investigations: FBC, U/E/Cr, PT/PTT, GXM, ECG, CXR Arrange for emergency operation Angiogram if needed Surgery involves Generous debridement of the wound with irrigation to decrease bacterial load Treat any soft-tissue injuries Stabilise fracture – usually using external fixator 6.

POST OPERATIVE COMPLICATIONS

General or specific? Immediate, early or late? Local or systemic? IMMEDIATE (20mmHg) ECG CXR (Exclude Ddx – pneumothorax, pneumonia, heart failure, tumour, rib #, pleural effusion, collapse) Pulmonary angiogram (gold standard) Pain relieve – use opioids with caution (resp depression) Fluid resus & inotropic support if haemodynamically unstable Anticoagulation: IV heparin 5000U bolus OR subcut fraxiparine (0.4ml 65kg) Convert to oral warfarin later Thrombolysis: intra pulm arterial urokinase for 12-24hrs Surgical: complete IV ligation or partial caval interruption

NEUROGENIC SHOCK

SEPTIC SHOCK (SIRS + source of sepsis + shock)

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 IV methyl Prednisolone 30 mg/kg over 15mins, followed by 5.4mg/kg/h for nxt 23 hrs Indications – non-penetrating spinal cord injury & w/in 8 hrs of injury Contraindications: 38 or 90bpm RR > 20 breaths/min OR PaCO212000/mm3, 10% immature forms

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

19

Empirical Abx: Immunocompetent w/o obvious source Immunocompromised w/o obvious source Gram-positive (burns, FB / lines present) Anaerobic source (intraabdo, biliary, female genital tract, aspiration pneumonia) ANAPHYLACTIC SHOCK

3rd gen cephalosporin (IV ceftriaxone 1g) OR Quinolones (ciprofloxacin 200mg) Anti-pseudomonal ABx (IV ceftazidime 1g) OR Quinolone PLUS aminoglycoside (Gentamicin 80mg) IV cefazolin 2g IV vancomycin 1g (if IVDA, indwelling cath, pen allergy) IV metronidazole 500mg + ceftriazone 1g + IV gentamicin 80mg

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 Adrenaline Normotensive – 0.01ml/kg (max 0.5ml) 1:1000 dilution SC/IM Hypotensive – 0.1ml/kg (max 5ml) 1:10,000 dilution IV over 5 mins Glucagon Indications: failure of adrenaline Rx OR if adrenaline is contraindicated e.g. IHD, severe HPT, pregnancy, -blocker use 0.5-1.0mg IV/IM. Can be repeated once after 30mins Antihistamines Diphenhydramine 25mg IM/IV Chlorpheniramine 10mg IM/IV Promethazine 25mg IM/IV Cimetidine For persistent symptoms unresponsive to above Rx 200-400mg IV bolus Nebulised For persistent bronchospasm bronchodilator Salbutamol 2:2 q20-30mins Corticosteroids Hydrocortisone 200-300mg IV bolus, q 6hr

20

8.

PERIOPERATIVE CARE

INPUT / OUTPUT Normal daily intake

Normal daily output

Water Diet Metbolism

2300 ml 200ml

Urine Skin loss

1400ml (min obligatory volume = 400ml) 500ml (obligatory diffusion & vaporisation) Sweating in pyrexia / heat can cause several litres extra loss per day

Lung loss Faecal loss

500ml (obligatory) 100ml

Sodium Diet 150 mmol/day (range 50 – 300 mmol)

Stool Skin transpiration Urine

5 mmol/day 5 mmol/day (in absence of sweating) 140 mmol/day (can fall to 15 mmol/day)

Stool Skin Urine

10 mmol/day (obligatory) < 5 mmol/day 85 mmol/day (rarely falls below 60 mmol/day)

Potassium Diet 100 mmol/day (range 50 – 200 mmol)

DAILY GASTROINTESTINAL SECRETIONS & ELECTROLYTE COMPOSITION Secretion

Volume (L)

Na (mmol/L)

K (mmol/L)

Cl (mmol/L)

HCO3 (mmol/L)

Saliva

1 – 1.5

20 – 80

10 – 20

20 – 40

20 – 160

Gastric juice

1 – 2.5

20 – 100

5 – 10

120 – 160

Nil

Bile

Up to 1

150 – 250

5 – 10

40 – 60

20 – 60

Pancreatic juice

1–2

120

5 – 10

10 – 60

80 – 120

Small bowel secretions

2–3

140

5

Variable

Variable

(up to 40 in inflammatory diarrhoea)

(succus entericus)

DAILY REQUIREMENTS Fluid 100 ml/kg/day Na

2

mmol/kg/day

K

1-2

mmol/kg/day

PARKLAND’S FORMULA FOR BURNS 2-4 ml / kg (body wt) / % (BSA of burn)

DAILY CALORIC REQUIREMENTS 2000 – 2500 kcal/day

Divide total volume into 2 halves Infuse 1st half in 1st 8h Infuse the rest in next 16h Start time = time of burn injury Fluid  of  choice  =  Hartmann’s  solution

CALORIC CONTENTS Glucose: 4 kcal/g Protein 4 kcal/g Fats: 9 kcal/g Alcohol: 7 kcal/g

21

FLUIDS / MAINTENANCE Body composition Total body water = 55% body weight Extracellular fluid = 20% body weight Blood volume = 7% body weight Acute blood loss required to produce shock = 25-30% of blood volume Basal requirements Children have higher water content (higher metabolic rate, greater surface area to body weight ratio)

Deficits Thirsty: Tachycardia: Hypotensive:

Ongoing/ anticipated losses

1.5L deficit 3L deficit 6L deficit

Insensible losses o Every 100kcal burned = 30ml loss through skin o Losses 10% for every deg of fever > 37°C Sweat GIT Urine (normal = 0.5 – 1 ml/kg/hr) Blood Respirators

Holliday-Segar method: 1st 10 kg – 100 ml/kg/day (5ml /kg/hr) 2nd 10 kg – 50 ml/kg/day (2ml /kg/hr) > 20 kg – 20 ml/kg/day (1ml /kg/hr)

Components of regularly used IV fluids 0.9% NaCl/ Normal saline (NS) 9g Na in 1L / 154 mmol Na & Cl (isotonic) Dextrose 5% (D5W)

50g glucose in 1L (200kcal; 1g glucose = 4kcal) (isotonic)

Dextrose 5% in 0.9% NaCl (D5NS)

50g glucose + 9g Na in 1L (hypertonic)

Hartmann’s  solution  /  Ringer’s  lactate

Na Cl K Ca Lactate

131 mmol/L 111 mmol/L 5 mmol/L 2 mmol/L 29 mmol/L

Amount of required (KCl) infused in divided doses over 24h Premixed IV fluids are generally available with 20 or 40 mmol of KCl per 500ml or 1000ml infusion bags If concentrations of KCl > 40 mmol in 500ml are required, they should be given via infusion in the ICU with cardiac monitoring Added K is not usually required in the 1st 24-48h after surgery because K is released from damaged cells

Sample daily IV fluid regimen 1L NS + 20 mmol KCl + 1L D5W + 20 mmol KCl + 1L D5W + 20 mmol KCL (each bag given over 8 h) Total: 154 mmol Na + 60 mmol K

HCT

From loss of pure plasma (burns/pancreatitis/peritonitis): 1 point = 100ml loss of fluid From loss of isotonic extracellular fluid (GIT): 1 point = 500 ml loss of fluid From loss of pure water (evaporation from lungs): no change CHOICE OF FLUID REPLACEMENT If pt losing blood blood transfusion Diarrhoea / vomiting crystalloids Burns pt (losing protein) colloids

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CVP MONITORING Swan-Ganz/ pulmonary artery catheter

Pressure in RA Pressure in PA Pulmonary capillary wedge pressure (indirect estimate of LA pressure) Normal CVP = 5 – 10 mmHg Useful in evaluating blood volume status when fluids are administered during hypotensive shock Administer fluids at a rate that maintains CVP at 12 – 15 mmHg (cardiac output optimal) Ohm’s  Law: 𝐶𝑂 =  

𝑀𝐴𝑃 − 𝐶𝑉𝑃   × 80 𝑆𝑉𝑅

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

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ACID BASE & ELECTROLYTES Metabolic Acidosis

pH < 7.35

[HCO3] < 20 mmol/L

Respiratory Acidosis

pH < 7.35

PCO2 > 45 mmHg

Metabolic Alkalosis

pH > 7.45

[HCO3] > 24 mmol/L

Respiratory Alkalosis

pH > 7.45

PCO2 < 35 mmHg

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

[HCO3] 1 mmol/L =

PCO2 1.2 mmHg

Expected PCO2 = (1.5 x [HCO3]) + 8 mmHg PCO2 < expected concurrent respi alkalosis PCO2 > expected concurrent respi acideosis Calculate change in anion gap ( AG) AG + [HCO3] = normal [HCO3] HAGMA AG + [HCO3] > normal [HCO3] concurrent metabolic alkalosis AG + [HCO3] < normal [HCO3] concurrent NAGMA

Metabolic Alkalosis

[HCO3] 1 mmol/L =

PCO2 0.7 mmHg

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

Respiratory Acidosis

Acute: PCO2 1 mmHg = [HCO3] 0.1 mmol/L Chronic: PCO2 1 mmHg = [HCO3] 0.4 mmol/L

Respiratory Alkalosis

Acute: PCO2 1 mmHg = [HCO3] 0.2 mmol/L Chronic: PCO2 1mmHg = [HCO3] 0.4 mmol/L

Acute: [HCO3] 1-2 mmol/L for every PCO2 by 10 mmHg Chronic: [HCO3] 4-5 mmol/L for every PCO2 by 10 mmHg

If pH normal, check for balanced acid base disorder: [HCO3] < 20

PCO2 < 35

Metabolic acidosis + Respiratory alkalosis

[HCO3] > 24

PCO2 > 45

Metabolic alkalosis + Respiratory acidosis

[HCO3] & PCO2 normal

AG > 11

HAGMA + metabolic alkalosis

[HCO3] & PCO2 normal

AG normal

Normal (unlikely NAGMA + metabolic alkalosis)

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Hyponatremia

Hypernatremia

Signs

Confusion Seizures Cardiac failure Muscle weakness Nausea, anorexia

Thirst Dehydration Confusion Coma Seizures

Causes

Diuretics (esp thiazides) Water excess Diarrhoea / vomiting Intestinal fistula Cardiac failure / Renal failure SIADH Addison’s  disease

Fluid loss w/o water replacement (esp burns) Saline excess Diabetes Insipidus DKA Conn’s  syndrome

Treatment

Rehydration with appropriate sodiumcontaining IV fluids Diuretics for cardiac failure Fluid restriction to 1L per day

Encourage oral intake IV fluids with low sodium content

Hypokalemia Signs

Cardiac arrhythmias Muscle weakness Hypotonia (& GI motility Muscle cramps Tetany

Hyperkalemia Cardiac arrhythmias Sudden death paralytic ileus)

Causes

Diarrhoea / vomiting Intestinal fistula Diuretics Renal tubular failure Cushing’s  /  exogenous  steroids  /  ACTH Conn’s  syndrome   Metabolic alkalosis

Treatment

Oral potassium supplements KCl added to IV fluids

Sampling artefact (haemolysis) Drugs (ACEI, spironolactone, suxamethonium) Digoxin poisoning Massive blood transfusion KCl excess Burns Rhabdomyolysis Tumour lysis Renal failure Addison’s  disease Metabolic acidosis 1. Calcium gluconate 10% (50-100ml) 2. Insulin 20 units + 250ml 25% dextrose over 4-6 hrs 3. Diuretics 4. 2 adrenergic agonists 5. Sodium bicarbonate (50 – 100ml) 6. Resin (polystyrene sulfonate sodium) (every g exchanges 3 mmol of Na for K) 7. Hemodialysis (definitive)

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NUTRITION Nutritional support should be considered for: BMI < 18.5 Unintentional weight loss > 10% BW within last 3 – 6 months BMI < 20 and unintentional weight loss > 5% within last 3 – 6 months Poor oral intake for > 5 days Poor absorptive capacity, high nutrient losses, increased catabolic rate REFEEDING SYNDROME Gastric emptying one of the last aspects of gut function to recover after an operation/major insult Risk factors: low BMI, duration of reduced intake, degree of weight loss, electrolyte abnormalities Feeding should be introduced gradually over 48 – 72 hours (Safe to start feeding at 50% of estimated protein and calorie requirements and build up to full requirements over a 24 – 48 hour period.) ENTERAL FEEDING Start at 20ml/h x 6h, then increase by 20-30ml/h and repeat. Indications: Proximal small intestine intact & functional Stimulation of secretory function does not worsen the condition being treated (e.g. small bowel fistula) Contraindications: Complete small bowel obstruction Inadequately treated shock states (risk of intestinal ischemia) Severe diarrhoea (slow rate of feeding) Proximal small intestinal fistula Severe pancreatitis Routes: Nasogastric tube feeding Nasojejunal or nasoduodenal feeding (when gastric emptying is a problem) Tube enterostomy Percutaneous endoscopic gastrostomy Complications: infection at PEG site, blockage/extrusion/removal, peritonitis, aspiration pneumonia Complications of enteral feeding: Fistulation Wound infection Peritonitis Displacement & catheter migration Blockage of tube Aspiration pneumonia Feed intolerance Diarrhoea Types of Oral Feeds: Ensure (protein 9g /serving) Ensure Plus (highly concentrated in calories 1.5 cal/ml & protein 13 g/serving) Glucerna (for DM pts carbohydrates, modified fat) Pulmocare (for COPD pts high calorie, low carb to help CO2 production) Novasource Renal (for renal pts low protein & nitrogen content)

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TOTAL PARENTERAL NUTRITION Provision of all nutritional requirements by the intravenous route alone Due to high osmolality of the mixture, TPN must be given into a central vein TPN orders: 24 hr feeding volume 2500ml, rate 100ml/hr 5 days a week: kcal from carbohydrate 2500, kcal from fat 0 2 days a week: kcal from carbohydrate 2000, kcal from fat 500

Indications: Critical illness: where enteral feeding is not established within 5 days Obstruction of GIT: proximal small bowel obstruction not immediately relieved Short bowel syndrome: o Temporary (before adaptation) in < 3m of functional small intestine o Permanent in < 1m of functional small intestine Proximal intestinal fistula: facilitate fistula closure Refractory  inflammatory  disease  of  the  GIT  (e.g.  Crohn’s,  UC) Inability to use the GIT: pancreatitis with pseudocysts/abscess where enteral nutrition is not tolerated Complications: Catheter-related o Mechanical: blockage, central vein thrombosis, migration, fracture, dislodgement o Infective: exit-site infection, line sepsis, infective endocarditis Metabolic o Hyperglycaemia o Deranged liver function: biliary stasis, enzyme induction from amino acid imbalance and excessive calorie administration, fat deposition in liver o Hypoglycaemia (too rapid cessation of glucose infusion) o Hypertriglyceridemia o Hyperchloraemic acidosis

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2.

LUMPS & BUMPS

1. HERNIA Hernia = a protrusion of an organ through an opening in the wall of the cavity in which it is normally contained Lifetime risk = 2-10% Causes of abdominal wall weakness - Congenital – normal (due to piercing structures), or patent processus vaginalis - Acquired – trauma, surgical incision or disease Consist of 3 parts: - Sac: pouch of peritoneum (neck & body) - Coverings of sac: layers of abdominal wall - Contents Types: 1) 2) 3) 4) 5)

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

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

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INGUINAL HERNIA: indirect or direct; Indirect inguinal hernia: - Most common; 65% - Congenital; patent processus vaginalis + weakened fascia at deep ring - Hernial sac enters the inguinal canal with the spermatic cord via the deep ring, then emerges from the superficial ring & descends into the scrotum - ♂ > ♀,  R>  L,  20%  are  bilateral,  children>adults Direct inguinal hernia: - Bulges directly ant though a weakened fascia Hesselbach’s triangle, post to the inguinal canal (med to inferior epigastric art) Hesselbach’s  ∆:  inf.  Epigastric  art.,  rectus  abd,  inguinal  ligament

-

Hernia sac is not with the spermatic cord Rare  in  ♀,  usually  occur  bilaterally in  ♂  with   weak abdominal muscles and comorbid  conditions  causing  ↑  intra-abdominal pressure

Clinical differences between indirect and direct inguinal hernia Indirect Hernia

Direct Hernia

Neck lies lateral to inferior epigastric artery, out  of  Hasselbach’s  triangle

Neck lies medial to inferior epigastric artery, within  Hasselbach’s  triangle

Reduces upwards, laterally and backwards

Reduces upwards and straight backwards

Controlled after reduction by pressure over the deep ring

Controlled after reduction by pressure over the superficial ring

May descend down the scrotum

Does not descend down the scrotum

May cause strangulation at superficial ring (narrow)

Rarely causes strangulation due to wide hernia neck

Does not readily reduce on lying down

Readily reduces on lying down

More common in young adults and infants

More common in old men

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Anatomy of inguinal canal -

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

Boundaries: Ant. wall: aponeurosis of the external oblique (reinforced in lat. third by internal oblique) Post. wall: transversalis fascia (reinforced in med. third by conjoint tendon) Roof: arching fibres of the int. oblique & transversus abdominis before they merge as conjoint tendon Floor: inguinal ligament and lacunar ligament medially Contents: Ilioinguinal nerve (L1): supplies skin over root of penis & upper part of scrotum or skin over mons pubis & labia majora ♀:  round  ligament  of  the  uterus   from uterus to labia majora ♂:  transmits  spermatic  cord  from   abdomen to testes Anatomy of the spermatic cord Coverings: 3 concentric layers of fascia Internal spermatic fascia: derived from transversalis fascia Cremasteric fascia & muscle: derived from internal oblique External spermatic fascia: derived from external oblique Contents: 3 Arteries: Testicular artery Artery to the vas deferens Cremasteric artery 3 Nerves: Nerve to cremaster Autonomic nerves (T10) Genital br of genitofemoral nerve 3 Others: Vas deferens Pampiform venous plexus Lymphatics

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Complications Reducible  →  Irreducible  /  Incarcerated  →  Obstructed  →  Strangulated - Irreducible/ Incarcerated hernia: contents of hernial sac cannot be replaced into abdomen - Obstructed: loop of bowel trapped in hernial sac such that its lumen, but not blood supply, is obstructed (no ischaemia not unduly tender, but with IO) - Stangulated: blood supply to trapped bowel is cut off, bowel is dead or dying; 6hrs to gangrene. (acutely tender with s/s of IO;;  exception:  Richter’s  hernia:  segment  of  bowel  is  trapped  &  ischaemic  but  lumen  is  patent no IO) Management Non-surgical: Raised intraabdominal pressure o Weight loss, change jobs, avoid heavy lifting o Treat medical conditions causing chronic cough, chronic constipation Truss: for compression of reducible hernia at deep ring (poor pickup rate) If obstructed/strangulated: NBM, IV drip, NG tube on suction, IV ABx Surgical: Hernioplasty/ Herniorraphy with mesh repair (open or laparoscopic) o Immediately if suspect incarceration to prevent any bowel perforation Principles: reduce bowel, ±excise hernia sac, reinforce posterior wall o Lichtenstein tension-free mesh repair (lightweight, polypropylene mesh insertion & suture) o Shouldice repair (non-mesh technique: 2 continuous back & forth sutures with permanent suture material) Complications o 2o to GA: AMI, CVA o Immediate to early 1. ARU 2. Bruising , bleeding (testicular, cremasteric, artery to vas deferens, inferior epigastric, femoral arteries) 3. Injury to surrounding structures pain, parasthesia, impotence: spermatic cord (vas deferens, testicular artery), round ligament, ilioinguinal nerve, nerve to cremaster o Early 1. Infection of wound/ mesh 2. Haematoma (10%; no cough impulse, non-reducible, hard) 3. Wound dehiscence 4. pain o Late 1. Chronic post-op pain 2. Recurrence of hernia ( Firm > Tense > Soft 6. Mobility Ulcers: - Fully mobile in all directions? Base: granulation tissue, slough, fascia, muscle, bone - Fixed and immobile? Edge: sloping (healing), punched out, undermined, - Mobile only in certain directions? rolled (BCC), everted (SCC) 7. Relations to surrounding tissues Discharge: serous, sanguinous, haemoserous, purulent - Move lump in 2 perpendicular planes o Attached to skin? muscle / tendon / bone? o If appears to be attached to muscle: Ask patient to tense muscle; Reassess mobility in the 2 planes Intramuscular or below the muscle, it will disappear. Above the muscle it will be more prominent. Fixed to muscle, it will become less mobile. 8. Fluctuant? (for small / medium lumps) - Paget’s  sign:  Rest  2  fingers  on  opposite  sides  of  lump,  press  down  on  middle  of  lump +ve: Feel fingers moving apart 9.

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

Request – “I  would  like  to  complete  my  examination  by…” Examine the draining LNs If sebaceous cyst / lipoma “Looking  for  other  lumps  elsewhere” Ganglion “Looking  for  other  lumps  elsewhere” + “Asking  for  hand  dominance” + “Taking  an  occupational  history”

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Symptoms and signs

Diagnostic significance

1. Lump in or on the skin Size, shape and surface features Revealed by inspection-is the lesion smooth-surfaced, irregular, exophytic (i.e. projecting out of the surface)?

Epidermal lesions such as warts usually have a surface abnormality but deeper lesions are usually covered by normal epidermis. A punctum suggests the abnormality arises from an epidermal appendage, e.g. epidermal (sebaceous) cyst

Depth within the skin Superficial and deep attachments. Which tissue is the swellingderived from?

Tends to reflect the layer from which lesion is derived and therefore the range of differential diagnosis (i.e. epidermis, dermis, hypodermis or deeper)

Character of the margin Discreteness, tethering to surrounding tissues, three-dimensional shape

A regular shaped, discrete lesion is most likely cystic or encapsulated (e.g. benign tumour). Deep tethering implies origin from deeper structures (e.g. ganglion). Immobility of overlying epidermis suggests a lesion derived from skin appendage (e.g. epidermal cyst)

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

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

Pulsatility

Pulsatility is usually transmitted from an underlying artery which may simply be tortuous or may be abnormal (e.g. aneurysm or arteriovenous fistula)

Emptying and refilling

Vascular lesions (e.g. venous malformations or haemangiomas) empty or blanch on pressure and then refill

Transilluminability

Lesions filled with clear fluid such as cysts 'light up' when transilluminated

Temperature

Excessive warmth implies acute inflammation, e.g. pilonidal abscess

2. Pain, tenderness and discomfort

These symptoms often indicate acute inflammation. Pain also develops if a noninflammatory lesion becomes inflamed or infected (e.g. inflamed epidermal cyst). Malignant lesions are usually painless

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3. Ulceration (i.e. loss of epidermal integrity with an inflamed base formed by dermis or deeper tissues)

Malignant lesions and keratoacanthomas tend to ulcerate as a result of central necrosis. Surface breakdown also occurs in arterial or venous insufficiency (e.g. ischaemic leg ulcers), chronic infection (e.g. TB or tropical ulcers) or trauma, particularly in an insensate foot

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

Malignant ulcers expand inexorably (though often slowly), but may go through cycles of breakdown and healing (often with bleeding)

4. Colour and pigmentation Normal colour

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

Red or purple

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

Deeply pigmented

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

5. Rapidly developing lesion

Keratoacanthoma, warts and pyogenic granuloma may all develop rapidly and eventually regress spontaneously. When fully developed, these conditions may be difficult to distinguish from malignancy. Spontaneous regression marks the lesion as benign

6. Multiple, recurrent and spreading lesions

In certain rare syndromes, multiple similar lesions develop over a period. Examples include neurofibromatosis and recurrent lipomata in Dercum's disease. Prolonged or intense sun exposure predisposes a large area of skin to malignant change. Viral warts may appear in crops. Malignant melanoma may spread diffusely (superficial spreading melanoma) or produce satellite lesions via dermal lymphatics

7. Site of the lesion

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

8. Age when lesion noticed Congenital vascular abnormalities such as strawberry naevus or port-wine stain may be present at birth. Benign pigmented naevi (moles) may be detectable at birth, but only begin to enlarge and darken after the age of 2

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4. LIPOMA Inspection o Can be single, often multiple o Usually at neck, trunk o Hemispherical – may appear lobulated o Scars Implies recurrent lipoma Palpation o Smooth or lobulated on firm pressure – bulging between strands of fibrous tissue) o Soft / firm (depending on nature of fat) o Well defined edges (may not be regular; series of curves corresponding to each lobule o Pseudo-fluctuance if large – lipomas are not liquid; but fat maybe more liquid o Mobile in all directions (if subcutaneous) o Positive slip sign; No transilluminance / thrill o Usually in the subcutaneous tissue. [check attachment skin & muscle] “Mr.  X  is  a  young  Chinese  gentleman…” “On  inspection,  there  is  a  hemispherical lump over the right scapula” “It  measures  10 by 8 cm” “There  are  no scars, punctum, ulceration, or discharge seen, nor any overlying or surrounding skin changes” “On  palpation, the overlying skin is not warm, it is non-tender” “The  surface  is  lobulated, and its margins are not well-defined” “The  consistency  is  soft, and it is fluctuant” “The  lump  is  not attached to  the  overlying  skin” “It  is  mobile in all directions with a positive slip sign” “It  is  not transilluminable” “I  would  like  to  complete  my  examination  by  looking for other similar lumps” “My  provisional  diagnosis  is  a  lipoma” “My  differential  diagnosis  is:  large  sebaceous  cyst” Background Information Definition: Benign tumour consisting of mature fat cells (distended with fat from over-activity) o Malignant change does not occur o Liposarcomas arise de novo; occur in older age (deeper tissues – retroperitoneal, deep tissues of thigh, subscapular) Liposarcoma classification 1. Well-differentiated 2. Myxoid, round cell (poorly differentiated myxoid) 3. Pleomorphic liposarcoma Clinical features o Can occur at all ages (not common in children) o Slow-growing, never regress o May be multiple: lipomatosis (multiple continuous lipomata) Occur in buttocks / neck Can cause distortion of subcutaneous tissues. Treatment o Non-surgical – watch & wait o Surgical – If patient wants it removed (Pain / peripheral neuropathy – Dercum’s  disease,  Cosmesis) Can be removed under LA Nuchal lipomas (back of the neck): extremely fibrous septae: difficult to excise If close to joint: LA may not be possible (may communicate with joint) Variants of lipomas / syndromes associated with lipomas o Adiposis dolorosa (Dercum’s disease) Multiple painful lipomas in limbs, sometimes trunk Associated with peripheral neuropathy Angiolipomas: prominent vascular component o Hibernomas: brown fat cells o Cowden’s  disease – associated with: Thyroid cancers Lipomas Palmoplantar keratoses Multiple facial papules Oral papillomatoses o Bannayan-Zonana syndrome – rare AD dz: lipomas with macrocephaly and haemangiomas, intestinal polyps

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5. 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

“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”

Palpation Normal Temperature, non-tender (unless inflamed) Smooth surface Well-defined margins (lies in subcutaneous fat) Tense consistency, may stretch overlying skin ( plastic deformation) Non fluctuant, not transilluminable Attached to skin, not attached to deeper structures, mobile in all directions

“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

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

Inflamed Cyst

Treatment o Non-surgical: leave alone (if small, asymptomatic). o Surgical Complete excision of cyst and contents under LA. Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the lines of Langers. If at the angle of jaw, be careful of the facial nerve during operation. Damage to zygomatic branch can cause eye ulceration. If lump is increasing in size, what to exclude? - Malignancies: BCC, Malignant melanoma. Cock’s peculiar tumour (complication) o Proliferating trichilemmal cysts that can grow to large size, ulcerate may become infected, open, granulating & edematous Boggy, painful, discharging swelling solitary, 90% occur in scalp o often mistaken for SCC scalp; Angry, malignant-looking (malignant transformation rare) Heaping up of granulation tissue from the lining of the cyst burst through skin, giving everted appearance regional lymphadenopathy may be present Gardner’s  syndrome (If multiple lumps found) o Genetic disorder associated with: Multiple osteomata of skull & epidermal cysts Adenomatous polyposis of large bowel & CRCs Desmoid tumours Thyroid cancers

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6. GANGLION Inspection Single; may have ovelying scar [recurrent mass] Hemispherical, flattened, Near joint capsules, tendon sheaths (90% on wrist, hand – ventral / dorsal) Variable (0.5 – 6 cm) Palpation Normal temperature, non-tender Smooth surface with Well-defined margins May be multilocular Soft & fluctuant if large > firm consistency if small Weakly transilluminant. (gelatinous material) Mobility: o Should assess mobility in 2 perpendicular planes, then with underlying muscles tensed (less mobile when tensed) o Not attached to overlying skin (mobile over it) o Attached to fibrous structures of origin [to joint capsule, tendon sheath, intramuscular septum, fixed when tensed] Reducibility: may slip between deep structures when pressed (appears falsely reduce into joint) Request Other similar lumps Ask which hand is dominant (may affect management) Occupation “Mr.  X  is  a  young  Chinese  gentleman,  who  is  alert  and  comfortable…” “On  inspection, there is a single hemispherical lump on the dorsum of the left wrist” “It  measures  3 by 2 cm” “There  are  no scars, ulcerations, or discharge  seen,  nor  any  overlying  or  surrounding  skin  changes” “On  palpation, the overlying skin is not warm. It is non-tender” “The  surface  is  smooth, with clearly-defined margins” “The  consistency  is  soft, and it is fluctuant” “The  lump  is  not attached to  the  overlying  skin” “It  appears  to  be  attached to underlying muscle,  as  it  is  mobile  horizontally  but  not  longitudinally” “It  is  transilluminant”   “I  would  like  to  complete  my  examination  by…” “Looking  for  other  similar  lumps” “Asking  Mr.  X  for  his  hand dominance” “Taking  an  occupational  history” “My  provisional  diagnosis  is  a  ganglion” My differential is a 1. Bursa 2. Cystic protrusions of synovial cavity of arthritic joints 3. Benign giant cell tumours of flexor shealth (These 2 are normally soft in consistency. Ganglion is more tense.)

Background Information Definition:

Cystic myxomatous degeneration related to synovial lined cavity [joint capsule or tendon sheath] Origin controversial: pockets of synovium communicating with joint, tendon sheath / degeneration of mucoid fibrous tissue

Site: o 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

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

Bursae (soft) Cystic protrusion of synovial cavity in OA (joint will be abnormal) Benign giant cell tumours of flexor shealth (Pigmented VilloNodular Synovitis) Lipoma Sebaceous cyst Non-surgical Watch & wait, usually may disappear after a few months. Aspiration + 3/52 of immobilisation (successful in 30-50%). High chance of recurrence 6-12/12 later. Surgical Complete excision to include neck of ganglion at site of origin. Along the lines of Langers. Complications 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 o o Treatment o o o o

SqCC

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

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

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Acquired

o

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)

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

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

Bowen’s disease (SqCC in situ)

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

Solar (actinic) keratosis (SqCC in situ)

o o o o o

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

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9. MALIGNANT MELANOMA “Mr.  X  is  a  middle  aged  Chinese  gentleman…” “On  inspection, there is a single flat-looking lesions over the right foot” “It  measures  2 by 4 cm” “It  is  variegated  in  appearance,  and  exhibits  red,  white,  and  black  discolouration” “The  margins  are  clearly-defined and irregular” “There  are  no  scars,  nor  any  surrounding  pigmentation,  erythema,  or  ulceration,  bleeding,  or  discharge” “On  palpation, the overlying lesion is palpable. It is not warm. It is non-tender” “The  surface  is  smooth, and its consistency is firm” “The  lump  is  attached to  the  skin,  and  moves  with  it  over  deeper  structures” “My  provisional  diagnosis  is  malignant  melanoma” “My  differential  diagnoses  are:  BCC,  pigmented  naevus” “I  would  like  to  complete  my  examination  by…” “Examining  for  regional  lymphadenopathy” “Take  a  history  for:  cardinal  symptoms  of  malignant  change,  and  any  predisposing  factors” Inspection Usually single (may have satellite lesions around primary lesion) Site: Limbs, head & neck, trunk, subungual, mucocutaneous junction, mouth, anus Any colour: pale pink, brown, black, purple (rich blood supply) Clearly defined but irregular May ulcerate, discharge May have surrounding halo: brown (pigment), pink (inflammation) Types: o Superficial spreading melanoma (70%): Legs of women and backs of men Red, white, blue in colour Irregular edge o Nodular type melanoma (15-30%): On trunk Polyploidal and raised Smooth surface with irregular edge Frequently ulcerated o Lentigo maligna melanoma: On face or dorsum of hands & forearms Underlying lesion is flat, brown-black with irregular outline Malignant area is thicker and darker o Acral lentiginous melanoma: More common in Asians and Blacks On hairless skin: subungual area, palms, soles Irregular area of brown/ balck pigmentation o Others: amelanotic melanoma, intra-cranial melanoma, retinal melanoma “Beware  of  the  man  with  the  glass  eye  and  hepatomegaly” Palpation Normal Temperature, Non-tender Surface o If small: smooth epithelium o If ulcerates: covered with crust (blood + serum) o If bleeding, / infected: wet, soft, boggy Firm consistency (small satellite nodules feel hard) Mobile, moves with skin over deeper structures Request Palpation for regional lymphadenopathy Palpation for other subcutaneous nodules (lying along course of draining lymphatics)

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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 I Epidermis only II Invades papillary dermis III Fills papillary dermis IV Invades reticular dermis V Subcutaneous tissue invasion

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

Breslow’s thickness (different in absolute depth of invasion, LN involvement) Breslow Thickness 10-Year Survival < 0.76 mm 92% < 3 mm 50% < 4 mm 30% LN Involvement < 40% (8 yr) Also: Beahrs and Myer’s system Prognosis generally poor – above 3 types of staging, or other indicators of poor prognosis: a. Elderly b. Male c. Lesions on trunk d. Ulceration e. Depigmentation, amelanotic f. Aneuploidy, high mitotic index Treatment Prevention (VERY IMPORTANT): a. Avoidance of causative factors Surgical excision with wide margins down to deep fascia a. Main lesion: i. < 0.76 mm: excise with 1 cm margin ii. 0.76 – 1.0 mm: excise with 2 cm margin iii. > 1.0 mm: excise with 3 cm margin b. Nodal spread: i. If clinical suspicion, biopsy or FNAC of lymph nodes ii. If palpable: therapeutic block dissection Palliation / adjuvant for distant metastases a. Intralesional BCG therapy b. Immunotherapy: vaccines (raises anti-melanoma response), monoclonal antibody, cytokine interferon therapy

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Superficial Spreading

Nodular

Lentigo Maligna

Acral Lentiginous

70%

15-30%

–

Rare

♂:  Back ♀:  Legs

Trunk

Face; Dorsum of hand / forearm

Hairless skin (palms, soles, subungual area)

Red, white, blue (varying pigmentation)

Most often black

Brown / black

Brown / black

Edge

Irregular

Regular outline

Irregular

Irregular

Shape

Palpable, but thin

Thick, polypoid, raised

Flat

Flat

Surface

-

Smooth

-

-

% Site Colour

Remarks

-

•  Frequently  ulcerated,   bleeding

Pictures

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

•  Rare  type •  Often  misdiagnosed  as   haematoma, paronychia

10. NEUROFIBROMA “Mr.  X  is  a  young  Chinese  gentleman…” “On  inspection, there are two spherical, pedunculated masses on the  back” “One  measures    2 cm, and the other 0.5 cm in diameter” They are pink in colour, with well-defined  margins” “There  are  no  scars,  sinuses,  ulceration,  or  discharge  seen,  nor  any  surrounding  skin  changes” “On  palpation, they are not warm and non-tender” “Their  surfaces  are  smooth, and are firm,  and  rubbery” “They  are  attached  to  the  skin,  and  are  mobile  over  the  deeper  tissue  layers” “My  provisional  diagnosis  is  neurofibromata” “I  would  like  to  complete  my  examination  by…” "Looking for other similar  lesions” “Looking  for  manifestations  of  neurofibromatosis” “Examining  the  cranial  nerves” Inspection Often multiple Anywhere in skin, subcutaneous tissues, e.g. forearm Spherical / Pedunculated / Fusiform (long axes lie along length of limb) Rarely more than few cm Comment on any café-au-lait spots Palpation normal temp., Non-tender Smooth, Well-defined Soft/ fleshy, rubbery consistency Non-fluctuant If in subcutaneous tissue: mobile within it Move most freely perpendicular to course of nerve Request Look for other similar lesions & other manifestations of NF-1: café-au-lait spots, axillary freckling, lisch nodules, optic glioma Measure the BP (HPT 2o to phaeochromocytoma, CoA, RAS) Examination of cranial nerve VII & VIII (acoustic neuroma) Background Information Sporadic Neurofibroma Benign tumour containing mixture of elements from peripheral nerves: o Neural (ectodermal) o Fibrous (mesodermal) Often multiple History o Any age (but usually adult) o Symptoms: usually cause no discomfort, rarely disfiguring o If related to nerve trunk, may be tender Patient may get tingling sensations in distribution of nerve Histology o Schwann cells: appear as bundles of elongated wavy spindle cells o Collagen fibrils, myxoid material o Often not encapsulated (unlike neurilemmomas) Complications of Neurofibroma o Pressure effects: spinal cord, nerve root compression o Deafness: involvement of VIII o Neurofibrosarcoma (only in NF-1): 5-13 % o Intra-abdominal effects: obstruction, chronic GI bleeding o Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis Treatment (single neurofibroma) o Non-surgical: leave alone if asymptomatic, patient agreeable o Surgical: indicated only if malignancy suspected Local re-growth common (cannot be surgically detached from underlying nerve)

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Neurofibromatosis I (Von  Recklinhausen’s  disease) (Refer to paediatrics notes – neurocutaneous syndromes) AD, neurocutaneous syndrome; chr 17 Characterised by pigmentary changes, tumours, and skeletal, vascular dysplasias o Fibroma  ≥2 NF  or  ≥1  plexiform  NF o Iiris harmatomas (Lisch Nodules) o Bone: dysplasia, pseudoarthrosis o Relatives o Optic glioma o Macules >6; >15mm post-pubertal o Axillary freckling Neurofibromata of all sizes (few mm to large subcutaneous nodules), related differently to skin o Within skin o Tethered to skin o Pedunculated Plexiform Neurofibroma (elephantiasis neurofibromatosis) Very rare Excessive overgrowth of neural tissue in subcutaneous layers, giving tissue swollen oedematous appearance o Often mistaken for lymphoedema, but lymphatic drainage is normal Can result in severe deformity: diffuse enlargement of peripheral nerve with skin involvement

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11. DERMOID CYST “Ms.  X  is  a  young  Chinese  girl…” “On  inspection, there is a single ovoid lump just above the lateral edge of the left eyebrow” “It  measures  3 by 2 cm” “There  are  no  scars,  ulceration,  or  discharge  seen,  nor  any  overlying  or  surrounding  skin  changes)” “On  palpation, the overlying skin is not warm. It is non-tender.” “The  surface  is  smooth, with clearly-defined margins” “The  consistency  is  firm, and it is fluctuant” “The  lump  is  not  attached to the overlying skin nor underlying tissues.” “It  is  fully mobile in  all  directions.” “My  provisional  diagnosis  is  a  congenital dermoid cyst” “My  differentials  are:  sebaceous  cyst,  lipoma”   Inspection Usually single Ovoid / spherical Site: o Congenital, 1-2 cm usually Along lines of fusion of ophthalmic & maxillary facial processes Inner & outer ends of upper eyebrow o Acquired, 0.5-1 cm usually Beneath skin likely to be injured e.g. fingers Scars often present Palpation Not warm, maybe tender if infected Smooth surface, Well-defined margins Consistency o Congenital: Soft (not tense / hard) o Acquired: Hard & tense (sometimes stony hard) Fluctuant (if large) Mobile over deeper tissues o Deep to skin, in subcutaneous tissue i. Congenital: Not attached to skin or underlying structures ii. Acquired: may be tethered to scar Background Information A dermoid cyst is a cyst deep to the skin, lined by skin 2 different methods of formation: o Congenital: Accident during antenatal development o Acquired: Implantation of skin into subcutaneous tissue by injury Clinical features Congenital (suspect if in child, young adult) o Formed intra-utero, when skin dermatomes fuse o Occur at any point in mid-line, common in neck / face / nose Particularly along lines of fusion of ophthalmic & maxillary facial processes Also: inner & outer ends of upper eyebrow o May be seen at birth o Distends a few years later, becomes obvious; few symptoms other than cosmetic problems o Rarely infected Acquired – Implantation dermoid (suspect if in adult – Browse pg 60) o Develop when piece of skin survives after being forcibly implanted into subcutaneous tissue Often by injury: cut, stab, etc. o Symptoms Small, tense lump Painful and tender (in areas subjected to repeated trauma) Local effects (e.g. problems with grip / touch if on finger) Also rarely infected o Differentials Sebaceous cyst (look for old injury, presence of scar near cyst: more likely dermoid) Treatment Congenital o Surgical treatment; complete excision o Full extent should first be established with X-ray / CT Midline cysts may communicate with CSF; must exclude bony defect Acquired o Complete excision of cyst

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12. SEBORRHOEIC KERATOSIS

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

“Mr.  X  is  an elderly  Chinese  gentleman…” “On  inspection, there is a single ovoid lesion lump on the back” “It  measures  1 by 2 cm” “The  margins  are  well-defined,  and  it  appears  to  be  slightly  raised  above  the  skin”   “There  are  no  scars,  ulceration,  or  discharge  seen,  nor  any  surrounding  skin  changes” “On  palpation, the overlying skin is not warm. It is non-tender” “The  surface is rough and greasy; the consistency is firm” “The  lump  arises from the skin” “My  provisional  diagnosis  is  seborrhoeic  keratosis” “My  differential  diagnosis  is:  pigmented  naevus,  melanoma” “I  would  like  to  complete  my  examination  by…” “Looking  for  similar  lesions  elsewhere” Inspection Often multiple Any part of skin; most found on back & face Round / oval Light  brown  →  black “stuck  on  appearance”;;  appears  warty Varying size; Few mm to 2-3 cm Distinct margins Palpation No warmth, no tenderness Rough surface (sometimes papilliferous) More firm than surrounding skin Attached to skin Special tests o May be picked off gently – reveals patch of pale-pink skin, 1-2 surface capillaries (bleed slightly) (DON’T  DO  THIS  IN  EXAM) Request to look for similar lesions elsewhere Background Information Benign outgrowth of basal layer of epidermis o Raised above the level of normal epidermis Microscopy: o Hyperkeratosis (thickening of keratin layer) o Acanthosis (thickening of prickle cell layer) o Hyperplasia of variably pigmented basaloid cells Clinical features Occur in both sexes More common in elderly people Begin as a patch, o increases in area, size over months / years o May not increase in thickeness o May suddenly fall off: leave pale-pink patch of skin Complications: o May become disfiguring, catch on clothes o May get infected (may imitate SCC, pyogenic granuloma) o Seldom bleeds (may cause it to change colour to brown) Leser-Trelat sign: Sudden onset of multiple seborrhoeic keratoses may imply visceral malignancy Treatment Non-surgical o Can be left alone as it is benign Surgical – for cosmetic reasons, etc. o Superficial shaving (lies above level of normal epidermis) o Cautery

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13. HAEMANGIOMA Background Information Vascular malformations o Types

o

Features

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

Develop as abnormal proliferation of embryonic vascular network Hamartomas May ulcerate, induce hyperkeratosis in overlying stratum corneum Many forms of cutaneous haemangiomata: (see table) o Strawberry naevus (cavernous haemangioma) o Port-wine stain (naevus vinosus) o Spider naevus o Campbell de Morgan spot Strawberry Naevus

Port-Wine Stain

Spider Naevi

Cambell de Morgan Spot

Head & Neck (can be anywhere)

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

Upper torso, head and neck (drainage of SVC)

Trunk (bilat) – upper > lower Occasionally on limbs

Number

May be multiple

Usually single

Usually multiple

Usually multiple

Colour

Bright red / dark red

Purple-red

Bright red

Dark red / deep purple

Inspection Site

Size

Variable; 1-10 cm

Variable

Variable; few mm

1-3 mm

Edge

Well-defined

Well-defined

–

Well-defined

Shape

Sessile  →  pedunculated as they grow larger

Variable

Variable

Circular, may be raised

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

Palpation Surface

Soft

–

–

–

Mobility

Mobile

–

–

–

Relations

Confined to skin

–

–

–

Compressible: pressure squeezes mass, leaves it collapsed: slowly refills Not pulsatile

–

Compressible, fade completely

–

Infants (congenital)

Infants (congenital)

–

Middle-age  →  elderly

♂  =  ♀

–

–

Consistency

Special Tests

Background Information Age Gender

–

Symptoms

•  Cosmesis •  May  ulcerate,  bleed  on trauma

•  Cosmesis •  Bleeding  may  occur

Pressure

•  Collapses  on  pressure

•  Diminishes  colour  but  doesn’t   revert to normal

•  Branches  fade  when  arteriole   compressed

•  Fade  slightly

Regress spontaneously (few months – 3 years)

•  Extensive, intradermal •  Present  from  birth,  does  not   change in size •  Sturge-Weber syndrome: facial PWS with corresponding haemangioma in brain – contralateral focal fits •  Found  in  limbs  when  a/w   Klippel-Tranaunay Syndrome

•  Form  of  telangiectasia •  Dilated  skin  arteriole  feeding   small branches (leaving radially) •  Increase  in  number   •  Associated  with  pregnancy,   chronic liver disease (> 5) – request for abdominal examination

•  Formed  by  collection  of  dilated   capillaries fed by single / small cluster of arterioles •  Have  appearance  of  drops  of   sealing wax •  No  clinical  significance

Remarks

–

Pictures

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•  Cosmesis •  Non-tender

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

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14. PYOGENIC GRANULOMA “Mr.  X  is  a  young  Chinese  gentleman…” “On  inspection, there is a single hemispherical lump  over  the  thenar  eminence  of  the  right  hand” “It  measures  about  0.8    cm  in  diameter,  with  clearly-defined  margins” “It  is  bright  red  in  colour,  with  surrouding  erythema” “There  are  no  scars,  sinuses,  ulceration,  active  bleeding  or  discharge  seen” “I would like to proceed on to palpation” “On  palpation, it is not warm. It is slightly tender” “The  surface  is  smooth. The consistency is soft and fleshy” “The  lump  is  confined to  the  skin” “My  provisional  diagnosis  is  pyogenic  granuloma” “My  differential  diagnoses  are  SCC,  non-pigmented  melanma” “I  would  like  to  complete  my  examination  by…” o “Asking  Mr.  X  for  any  previous  injuries  to  the  hand” o “Asking  him  how  rapidly  the  lump  has  been  growing” Inspection Single; usu < 1 cm, bright red o May be blood-encrusted or Ulceration Hemispherical; may be sessile / pedunculated Likely sites to be injured, e.g. hands, face Bright red; long-standing lesions may be skin-coloured May have sinuses, associated serous / purulent discharge, Erythema / cellulitis Palpation – request to palpate: may bleed easily May be slightly tender o May bleed easily on palpation Well-defined edges Soft, fleshy consistency Confined to skin Slightly compressible (vascular origin) Request Take history for previous injury Rate of growth of lump? (rapid growth in few days) Background Information – Neither pyogenic nor a granuloma! Rapidly-growing capillary haemangioma, usually less then 1 cm Occur commonly after injury: o Small capillary loops develop in healing wound, form granulation tissue o When capillary loops grow too vigorously, form protruding mass, epithelisation o Mass form called pyogenic granuloma (surface often ulcerated, infected) Clinical features Uncommon in children May have history of minor injury, chronic infection (e.g. paronychia) Rapidly-growing lump on skin, Bleeds easily, discharges serous / purulent fluid o Bleeding, pain stops once lump epithelises Once nodule is completely covered, begins to shrink (rarely disappears completely) Treatment Surgical o 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

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15. PAPILLOMA

(skin tags / fibroepithelial polyps)

“Mr.  X  is  a  young  Chinese  gentleman…” “On  inspection, there is a (single) (hemispherical) lump on the (dorsum of the forearm)” “It  measures  3 by 2 cm. “The surface is papilliferous – there  is  no  ulceration  or  discharge  seen,  nor  any  surrounding  skin  changes.” “On  palpation, the skin is not warm. It is non-tender. The  consistency  is  soft.” “The  lump  is  attached to  the  skin” “My  provisional  diagnosis  is:  papilloma” “My  differential  diagnosis  is:  viral  wart” “I  would  like  to  complete  my  examination  by…looking  for  similar  lumps,  asking  for  associated  conditions” Inspection Single / multiple Variable: from raised plaque to pedunculated polyp Site: Neck, trunk, face, anus (anywhere on skin) Variable Flesh-coloured Palpation Not warm, non-tender Variable: smooth to papilliferous Soft, not compressible Arises from skin Request Similar lumps elsewhere Ask for associated conditions: pregnancy, diabetes, intestinal polyposis Background Information An overgrowth of all layers of the skin with central vascular core Not a neoplasm, but a hamartoma (skin tag is a more accurate term) Increasingly common with age – may be congenital Clinical features Catches on cloths, rubs against other body parts May resemble carcinoma if granulation is excessive Complications: o May become red, swollen, and ulcerate o May become infarcted if injured o May be infected (contains all skin components – sebaceous glands, etc.) Treatment Excision – diathermy, scissors o Bleeding from central vascular core controlled using single suture / diathermy

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16. KERATOCANTHOMA

(adenoma sebaceum, molluscum pseudo-carcinomatosum)

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

17. KELOID (HYPERTROPHIC SCAR) Healing by primary intention – 3 stages: o Tissue defect filled by blood / fibrin o Replacement by collagen and fibrous tissue o Organisation of fibrous tissue to maximise wound strength Most surgical scars have thin lines, but tissue response may be excessive: hypertrophic / keloid scar Wounds prone to hypertrophic / keloid scar o Infection o Trauma o Burns o Tension o Susceptible areas: across flexion areas, earlobes, chest, neck, shoulder Hypertrophic scar o any age – common 8-20  years,  ♂=♀,  all  races o Excessive amount of fibrous tissue, but confined to scar (between skin edges) o Located across flexor surfaces, skin creases o Common, especially if infection / excessive tension o Only enlarge for 2-3 months, then regress spontaneuosly o Do not recur if excised and causative factor eliminated Keloid scar o puberty  to  30  years,  ♀>♂,  black,  hispanic  more  likely o Hypertrophy and overgrowth extend beyond original wound o Located at earlobes, chin, neck, shoulder, chest o Due to local release of fibroblast growth factors o Continue to enlarge 6-12/12 after initial injury o May be tender, unsightly o Will recur unless special measures taken Treatment (recurrence can be as high as 55%) o Non-surgical: mechanical pressure therapy – topical silicone gel sheets (day and night for 1 year), Intralesional steroid, LA injections: e.g. triamcinolone with lignocaine o Surgical: revision of scar by direct suturing, skin grafting (avoid excessive tension)

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

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

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20. PYODERMA GANGRENOSUM Inspect Ulcer with a necrotis base Irregular bluish red overhanging edges a/w surrounding erythematous plaques with pustules Request to examine for evidence of inflammatory bowel disease, RA Backgound information more common in males pyoderma gangrenosum is associated with: o IBD o RA o Myeloproliferative disorders: PRV, myeloma o Autoimmune hepatitis Differential diagnosis: o Autoimmune: rheumatoid vasculitis o Infectious: tertiary syphilis, amoebiasis o Iatrogenic: warfarin necrosis o Others:  Behcet’s  disease Treatment: o Non-surgical: treat underlying condition, saline cleansing, high dose oral or intralesional steroids. KIV cyclosporine & antibiotics o Surgical: serial allograft followed by autologous skin graft or muscle flap coverage when necessary

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21. RADIOTHERAPY MARKS Vital points on examination: Of the underlying disease: o Cachexia, o masectomy scar/ wide excision scar suggest breast cancer o obvious skin cancer, o clubbing & other signs of chest disease suggest lung cancer o suprapubic mass suggest pelvic tumour o neck swellings with cranial nerve palsies head and neck tumour of the radiotherapy: o site of radiation o shape: usually well defined borders o features of active RT: Indian ink marks, skin markings Erythema, desquamation o Features of previous RT: Telangiectasia, hyperpigmentation Complications of radiotherapy: o Depends of site o Look for future cancers: Haematogenous malignancy Thyroid cancers Breast cancers Background information High energy X-rays interact with tissue to release electrons that cause local damage to DNA in adjacent cells via oxygen dependent mechanism. o Damage is usually irreparable, and normal cells have greater ability to repopulate than tumour cells in this setting o If reparable, manifests as chromosomal abnormalities Radiotherapy affects cells with: o Rapid turnover: Skin (epidermal layers), small intestine, bone marrow stem cells o Limited replicative ability: spinal cord, gonads Complications: o Early:

o

Late:

General: malaise, fatigue, LOA, N/V Skin changes & temporary hair loss 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

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3.

SURGICAL INSTRUMENTS & PROCEDURES

1. DRAINS FUNCTIONS OF DRAINS Drains are inserted to: Evacuate collections of pus, blood or fluids (e.g. lymph) Drain potential collections

COMPLICATIONS Infection Bleeding Tissue damage- by mechanical pressure or suction Drain failure - blocked/slipped/kinked Incisional hernia - occurs when drain inserted through incision wound site- create a separate incision site for drain!

Rationale: Drainage of fluid removes further fluid collections Allow early detection of anastomotic leaks/ haemorrhage Leave tract for potential collections to drain after removal

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

Active

Active drains require suction. Jackson-Pratt Drain, Redivac Drain, T-tube Have expandable chambers to create low-pressure suction Used when small – mod amts of drainage are expected or when a passive drainage system won't provide adequate drainage Tubing of the low-pressure active drainage system is placed through a separate puncture wound or the tube may exit the edge of the surgical wound If the tubing isn't sutured in place, it could become dislodged If a portion of the tube is pulled outside the skin, an air leak will cause the chamber to fill with air & it won't drain properly.

Corrugated drain, Yeates drain, Penrose drain Drain fluid collects in gauze pad or stoma bag Easier to drain infected collections Closed

Passive

Consist of tubes draining into a bag or bottle They include chest and abdominal drains The risk of infection is reduced

Passive drains rely on gravity. Passive drains have no suction, rely on gravity Works by differential pressure betw body cavities and the exterior Used when a mod – large amt of drainage is expected

CARE AND PREVENTION OF COMPLICATIONS OF TUBES: Prevent Infection- maintain meticulous skin care and aseptic technique around the insertion site Prevent blockage of the drain- do not allow bottles to fill up Prevent slippage by securing drain carefully to skin; refix as required Never hold a drainage collection device higher than the tube insertion site to prevent the drainage from flowing backward into the patient Note amount of drainage daily REMOVAL OF DRAINS A drain is removed as soon as it is no longer required. The following are general guidelines: Drains put in to cover perioperative bleeding and haematoma formation, can come out after 24— 48 hours. Where a drain has been put in to drain an infection (abscess), remove it when fever settles or when there is evidence of complete drainage.

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2. CENTRAL VENOUS PRESSURE LINE INDICATIONS 1. Vascular access 2. Total parenteral nutrition 3. Infusion of irritant drugs 4. Measurement of CVP 5. Cardiac catheterization 6. Pulmonary artery catheterization 7. Transvenous cardiac pacing.

CONTRAINDICATIONS: 1. Do not insert into an infected area. 2. Avoid infraclavicular approach to subclavian vein if patient has apical emphysema or bullae. 3. Avoid internal jugular vein if carotid aneurysm present on the same side. 4. Bleeding diatheses 5. Septicaemia 6. Hypercoagulable states

ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE: 1. 2. 3. 4.

Internal jugular vein Subclavian vein Femoral vein External jugular vein

CANNULATION OF THE INTERNAL JUGULAR VEIN The internal jugular vein (IJV) is accessible, so cannulation of this vein is associated with a lower complication rate than with other approaches. Hence, it is the vessel of choice for central venous cannulation. Anatomy of the IJV The vein originates at the jugular foramen and runs down the neck, to terminate behind the sternoclavicular joint, where it joins the subclavian vein. It lies alongside the carotid artery and vagus nerve within the carotid sheath. The vein is initially posterior to, then lateral and then anterolateral to the carotid artery during its descent in the neck. The vein lies most superficially in the upper part of the neck. Relations of the IJV Anterior: Internal carotid artery and vagus nerve. Posterior: C1, sympathetic chain, dome of the pleura. On the left side, the IJV lies anterior to the thoracic duct. Medial: Carotid arteries, cranial nerves IX-XII Technique of IJV cannulation Place the patient in a supine position, at least 15 degrees head-down to distend the neck veins and to reduce the risk of air embolism. Turn the head away from the venepuncture site. Cleanse the skin and drape the area. Sterile gloves and a gown should be worn to avoid catheter-related sepsis. Procedure 1. Use local anaesthetic to numb the venepuncture site. 2. Introduce the large calibre needle, attached to an empty 10 ml syringe. 3. Surface mark the internal jugular vein at the centre of the triangle formed by the two lower heads of the sternocleidomastoid muscle and the clavicle. Palpate the carotid artery and ensure that the needle enters the skin lateral to the artery. 4. Direct the needle caudally, parallel to the sagittal plane, aiming towards the ipsilateral nipple. 5. While needle is advanced, maintain gentle aspiration. 6. When vein is entered, flush of blood appears in the syringe. Now, cannulate the vein via the Seldinger technique (below). 7. Remove syringe, holding needle firmly in place. Occlude needle to prevent air embolism or bleeding. 8. Advance guide wire, J-shaped end first, into the vessel through the needle. 9. Hold guide wire in place and remove needle. Maintain a firm grip on the guide wire at all times. 10. Use a dilator to enlarge the hole in the vein. Remove the dilator. 11. Thread tip of catheter into the vein through the guidewire. Grasp the catheter near the skin and advance it into the vein with a slight twisting motion. 12. Advance catheter into final indwelling position. Hold catheter and REMOVE GUIDEWIRE. 13. Check lumen placement by aspirating through all the pigtails and flushing with saline next. 14. Suture the catheter to the skin to keep it in place. 15. Apply dressing according to hospital protocol. 16. The catheter tip should lie in the superior vena cava above the pericardial reflection. 17. Perform check chest X-ray to confirm position and exclude pneumothorax. Complications 1. Pneumothorax/haemothorax 2. Air embolism - ensure head-down position. 3. Arrhythmias – This  happens  if  cathether  “irritates”  the  heart.  Avoid  passing  guidewire  too  far,  cardiac  monitoring during insertion. 4. Carotid artery puncture/cannulation - palpate artery and ensure needle is lateral to it, or use ultrasound-guided placement, transduce needle before dilating and passing central line into vessel, or remove syringe from needle and ensure blood is venous. 5. Chylothorax- Avoid cannulating the vein on the left side as the thoracic duct lies there. 6. Catheter-related sepsis

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CANNULATION OF THE SUBCLAVIAN VEIN The subclavian vein (SVC) may be preferred for central venous access if 1. Patient has a cervical spine injury 2. Line is for long-term use e.g. dialysis, feeding. This site may be more comfortable for the patient. Anatomy of the SCV The SCV is the continuation of the axillary vein and originates at the lateral border of the first rib. The SCV passes over the first rib anterior to the subclavian artery, to join with the internal jugular vein at the medial end of the clavicle. The external jugular vein joins the SCV at the midpoint of the clavicle. Technique 1. Place the patient in a supine position, head-down. 2. Turn the head to the contralateral side (if C-spine injury excluded). 3. Adopt full asepsis. 4. Introduce a needle attached to a 10 ml syringe. 5. Surface mark the subclavian vein 1 cm below the junction of the middle and medial thirds of the clavicle. Direct the needle medially, slightly cephalad, and posteriorly behind the clavicle toward the suprasternal notch. 6. Slowly advance needle while gently withdrawing plunger. 7. When a free flow of blood appears, follow the Seldinger approach, as detailed previously. 8. The catheter tip should lie in the superior vena cava above the pericardial reflection. 9. Perform check chest X-ray to confirm position and exclude pneumothorax.

Complications As listed for internal jugular venous cannulation. The risk of pneumothorax is far greater with this technique. Damage to the subclavian artery may occur; direct pressure cannot be applied to prevent bleeding. Ensure that a chest X-ray is ordered, to identify the position of the line and to exclude pneumothorax.

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3. NASOGASTRIC TUBE INDICATIONS [4] 1. Diagnostic 2.

Decompresssion

a) b)

bleeding from the upper gastrointestinal tract, haematemesis pentagastrin studies (rarely done now)

Therapeutic

a) b) c)

intestinal obstruction pyloric stenosis haematemesis, esp in pts at risk of hepatic encephalopathy

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

Preventive: d) therapeutic and prophylactic decompression after major abdominal surgery e) prevention of further soilage after gastric perforation f) prevention of anastomotic rupture after gastric surgery g) prevention of obstruction of the operative field by air in the stomach 3.

Nutrition

a) b)

patients with dysphagia comatose or weak patients

4.

Lavage

a) b)

poisoning gastrointestinal bleeding

The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric tube insertion. PRE-PROCEDURE 1. Gather equipment. 2. Don non-sterile gloves. 3. Explain the procedure to the patient and show equipment. 4. If possible, sit patient upright with head forward for optimal neck/stomach alignment. Otherwise, prop the patient up at 45 °. 5. Deflate the endotracheal tube or tracheostomy cuff 6. Determine the size of the nasogastric tube required (usually 14 – 16FG). If aspirating, use as large a tube as possible to reduce the risk of blocking during use or the formation of a false passage during introduction; if feeding, a smaller tube may be used (eg. 8FG) because it is more comfortable in the long term. PROCEDURE 1. Estimate the length of the tube to be inserted: from the bridge of the nose to the tragus of the ear to the point halfway between the xiphisternum and the navel. Mark the measured length with a marker or note the distance. 2. Examine nostrils for deformity/obstructions (eg. choanal stenosis) to determine best side for insertion. Select the largest nostril for insertion. 3. Lubricate tube with water. The nose may be lubricated with lignocaine gel. 4. Introduce the tube through the nostril horizontally in, passing the tube along the floor of the nose. Resistance may be felt as tip reaches the nasopharynx, which is the most uncomfortable part of the procedure. In the operation theatre, when the patient is under general anaesthesia, the  McGill’s  forceps  may  be  used  to  guide  the  tube  down. 5. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated) and advance the tube as the patient swallows. Swallowing of small sips of water may enhance passage of tube into esophagus. If patient is uncooperative, bend his head to elicit a swallowing reflex. 6. Continue to advance the tube down the oesophagus. There should not be resistance. If resistance is met, rotate the tube slowly with downward advancement towards the closer ear. Do not force the tube down against resistance as this may form a false passage. 7. Withdraw the tube immediately if changes occur in the patient's respiratory status, if the tube coils in the mouth, or if the patient begins to cough or turns pretty colours. 8. Advance the tube until mark is reached (approximately 40cm). Stop. 9. Check for correct placement by attaching a syringe to the free end of the tube and aspirating a sample of gastric contents to test with litmus, auscultating the epigastrium while injecting air through the tube, or obtaining an x-ray to verify placement before instilling any feedings/medications or if you have concerns about the placement of the tube. 10. Secure the tube with adhesive tape. 11. Re-inflate the endotracheal tube or tracheostomy cuff if necessary. 12. If for suction, remove the syringe from the free end of the tube; connect to suction; set machine on type of suction and pressure as prescribed. 13. Document the reason for the tube insertion, type & size of tube, the nature and amount of aspirate, the type of suction and pressure setting if for suction, the nature and amount of drainage, and the effectiveness of the intervention. PROBLEMS AND COMPLICATIONS [5] 1. a) b) c) d) e)

Technical insertion into the trachea choking. coiling & reentry into oesophagus (rare). trauma to the nose and the pharynx. dislodgement perforation of the pharynx and oesophagus

2. a) b) c) d) e)

Gastrointestinal Gastric erosions Pressure necrosis of pharynx, oesophagus or the external nares. Varices: traumatic haemorrhage GERD Oesophageal erosions strictures

3. a) b)

Lung complications decreased ventilation aspiration pneumonia

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4.

Loss of fluids & electrolytes, especially sodium, potassium, chloride and hydrogen ions.

5.

Dry mouth and parotitis due to fluid loss and mouth breathing.

4. TRACHEOSTOMY INDICATIONS FOR TRACHEOSTOMY 1. Maintenance of airway patency. 2. Protection of the airway from aspiration. 3. Application of positive pressure to the airway. 4. Delivery of high oxygen concentrations. 5. Facilitation of secretion clearance. RELATIVE CONTRAINDICATIONS 1. Evidence of infection in the soft tissues of the neck at the prospective surgical site. 2. Medically uncorrectable bleeding diatheses. 3. Gross distortion of the neck anatomy due to hematoma, tumour, thyromegaly, high innominate artery or scarring from previous neck surgery. 4. Documented or clinically suspected tracheomalacia. 5. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water. 6. Patient obesity with short neck that obscures neck landmarks. 7. Patient age younger than 15 years. TYPES OF TRACHEOTOMY 1. Temporary: Portex (cuffed). 2. Permanent: Consist of inner and outer tubes made of stainless steel. Tracheostomy is more useful in the elective setting compared to endotracheal intubation because: 1. Better tolerated. 2. Avoids risk of laryngeal stenosis 3. Avoids risk of endotracheal obstruction. PROCEDURE 1.

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

2.

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

3.

Identify anatomical landmarks (thyroid cartilage, cricoid cartilage).

4.

Administer local anaethesia.

5.

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

6.

Dissect through the subcutaneous layers and platysma.

7.

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

8.

Visualise the thyroid isthmus and retract isthmus.

9.

Retract cricoid cartilage upwards wth cricoid hook.

10. Incise the trachea between the 2nd and 3rd tracheal rings, making an inverted U-flap incision. 11. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks. 12. Suction of blood and secretions in the lumen. 13. Insert the tracheostomy tube. 14. Remove the obturator and insert the inner cannula. 15. Dress wound and secure to the neck using sutures and adhesive tape.

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COMPLICATIONS During Procedure 1. Bleeding if damage to the innominate or inferior thyroid artery. 2. Damage to surrounding structures, eg esophagus, recurrent laryngeal nerve, brachiocephalic vein. 3. Pneumothorax. Pneumomediastinum. Immediate post-op 1. Surgical emphysema (refers to the condition that causes air to be trapped under the skin). Subcutaneous emphysema. 2. Obstruction, eg clot, mucus. 3. Bleeding. 4. Dislodgment. Late post-op 1. Infection . 2. Obstruction, eg dislodgment of tube, crust formation from secretions. 3. Tracheal stenosis. 4. Tracheomalacia. 5. Tracheo-esophageal fistula. Wound breakdown 6. Scarring. POST-OP CARE 1. Position patient in a propped up position. 2. Prevent obstruction by suction, saline irrigation, mucolytic agents (mucomyst, guaifenesin) and humidified air. 3. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday. 4. Unlock the metal tube every night so that the patient can cough it out if it becomes obstructed.

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5. SENGSTAKEN-BLAKEMORE TUBE (MINNESOTA TUBE) INDICATIONS Oesophageal varices CONTRAINDICATIONS 1. Base of skull fracture 2. Oesophageal tear 3. Severe facial injury PROCEDURE - Keep SBT in fridge to make it stiff. 1.

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

2.

Sit the patient upright or at 45 degrees.

3.

Apply local anaesthesia (lignocaine nasal spray).

4.

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

5.

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

6.

Check that the tube is in the stomach by: (i) aspirating fluid and testing it with litmus, (ii) auscultating the epigastrium while injecting air, or (iii) doing an X-ray.

7.

Traction.

8.

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

9.

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

10. Check the oesophageal balloon pressure hourly and release 5mins hourly. 11. Release oeophageal balloon after 24hrs. 12. Release gastric balloon after 48hrs. 13. The tube should not be used for more than 72hrs. COMPLICATIONS 1. Aspiration pneumonia 2. Respiratory obstruction 3. Oesophageal ulceration and rupture 4. Rebleeding 5. Gastric varices not controlled

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6. URINARY CATHETERISATION INDICATIONS FOR SHORT-TERM CATHETERISATION 1. 2. 3. 4. 5.

6.

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

INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION 1. Refractory bladder outlet obstruction. 2. Chronic retention of urine, eg. neurogenic bladder. 3. Incontinence, e.g.  in  palliative  care  of  terminally  ill  or  patient’s  preference. CONTRAINDICATIONS 1. Presence of urethral injury, as manifested by: a) blood from the meatus, b) scrotal haematoma, c) pelvic fracture, or d) high-riding prostate, elicited from a genital and digital rectal examination. (alternative: suprapubic drainage) 2. Urinary tract infection, as an indwelling catheter causes difficulty in treatment. PROCEDURE 1. Gather equipment. 2. Explain  procedure  to  the  patient.  Maximize  patient’s  privacy.  Have  a  chaperone  if  performing the procedure on a member of the opposite sex. 3. Assist patient into supine position with legs spread and feet together. 4. Open the catheterization kit and catheter. 5. Prepare sterile field. Don the sterile gloves from the kit. 6. Test the balloon at the tip of the catheter. 7. Generously coat the distal portion (2 - 5cm) of the catheter with lubricant. 8. Using the non-dominant hand to come in contact with the patient and the dominant hand to use items from the kit (recall that once your hand comes in contact with the patient, it is no longer sterile and cannot be used to obtain items from the kit), cleanse the peri-urethral mucosa with antiseptic-drenched swabs held by forceps. Cleanse anterior to posterior, inner to outer, one swipe per swab, discard away from sterile field. a) Male: Hold the penis and retract the foreskin. Swab the penis and surrounding area, making sure to cleanse beneath the foreskin. b) Female: Retract the labia majora. Swab the perineum. 9. Apply sterile drape. 10. Installation of local anaesthesia. a) Male: (i) Smear lignocaine gel around the meatus and apply the gel gently into urethra. (ii) Massage gel carefully down the urethra to sphincter, squeezing the meatus shut (iii) Wait for for 5 minutes (alternatively, with less anaesthetic effect, smear gel over the catheter tip). b) Female: (i) Apply lignocaine gel to urethra or catheter tip. 11. In the male, lift the penis to a position perpendicular to patient's body and apply light upward traction (with non-dominant hand); in the female, expose the external urethral orifice. 12. Gently insert tip of catheter into the meatus using forceps until 1 to 2 inches beyond where urine is noted to drain into kidney dish. If no urine appears although the catheter seems to be in the right place, flush with sterile saline as the lumen may be blocked with gel. If this is still unsuccessful, withdraw and reinsert. 13. Inflate balloon, using correct amount of sterile saline (usually 20 – 30mls but check actual balloon size). This process should be painless. If patient feels pain, deflate balloon immediately and reposition catheter. 14. Gently pull catheter until inflation balloon is snug against bladder neck. 15. Connect catheter to drainage system. 16. Secure catheter to abdomen or thigh, without tension on tubing. 17. Place drainage bag below level of bladder. 18. Evaluate catheter function and amount, color, odour and quality of urine. 19. Remove gloves. Dispose equipment appropriately. Wash hands. 20. Document size of catheter inserted, amount of water in balloon, patient's response to procedure and assessment of urine. COMPLICATIONS 1. Infection, which may lead to stone formation. 2. Stricture formation due either to faulty technique or an irritant material used in the catheter. 3. Creation of a false passage due to wrong technique of insertion. 4. Occasionally, irritation of the bladder may cause severe bladder spasms.

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7. CHEST TUBE Chest tubes are inserted to drain blood, fluid, or air and allow full expansion of the lungs. The tube is placed between the ribs and into the space pleural space. The area where the tube will be inserted is anesthetized locally. The patient may also be sedated. The chest tube is inserted through an incision between the ribs into the chest and is connected to a bottle or canister that contains sterile water (underwater seal). Suction is attached to the system to encourage drainage. A suture and adhesive tape is used to keep the tube in place. The chest tube usually remains in place until the X-rays show that all the blood, fluid, or air has drained from the chest and the lung has fully re-expanded. When the chest tube is no longer needed, it can be easily removed, usually without the need for medications to sedate or numb the patient. Antibiotics may be used to prevent or treat infection. INDICATIONS 1. Pneumothorax. 2. Hemothorax. 3. Drainage of pleural effusion. 4. Chylothorax 5. Drainage of empyema/lung abcesses 6. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center CONTRAINDICATIONS 1. Infection over insertion site 2. Uncontrolled bleeding diathesis/coagulopathy MATERIALS 1. Iodine & alcohol swabs for skin prep 2. Sterile drapes & gloves 3. Scalpel blade & handle 4. Clamp 5. Silk suture 6. Needle holder 7. Petrolatum-impregnated gauze 8. Sterile gauze 9. Tape 10. Suction apparatus (Pleuravac)/underwater seal apparatus 11. Chest tube (size 32 to 40 Fr, depending on clinical setting) 12. 1% lignocaine with epinephrine, 10 cc syringe, 25- & 22-g needles PRE-PROCEDURE PATIENT EDUCATION 1. Obtain informed consent 2. Inform the patient of the possibility of major complications and their treatment 3. Explain the major steps of the procedure, and necessity for repeated chest radiographs PROCEDURE 1. Determine the site of insertion. Locate the triangle of safety; bounded by the lateral border of the pectoris major, 5th or 6th intercostal space, imaginary vertical line between the anterior and mid axillary lines. 2. Surgically prepare and drape the chest at the predetermined site of the tube insertion. 3. Locally anaesthetized the skin and rib periosteum. 4. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect through the subcutaneous tissues, just over the top of the rib. 5. Puncture the parietal pleura with the tip of a clamp and put a gloved finger into the incision to avoid injury to other organs and to clear any adhesions, clots, etc. 6. Clamp the proximal end of the chest tube and advance the tube into the pleural space to the desired length. 7. Look for fogging of the chest tube with expiration or listen to air movement. 8. Connect the end of the chest tube to an underwater seal apparatus. 9. Suture the tube in place. 10. Apply a dressing and tape the tube to the chest. 11. Do a chest X ray 12. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as necessary.

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COMPLICATIONS Damage to structures: 1. Laceration or puncture of the intrathoracic and/or abdominal organs, all of which can be prevented by using the finger technique before inserting the chest tube. 2. Damage to the intercostals nerve, artery or vein. 3. Subcutaneous emphysema, usually at tube site. Equipment: 4. Incorrect intrathoracic or extrathoracic tube position. 5. Chest tube kinking, clogging or dislodging from the chest wall or disconnection from the underwater seal apparatus. 6. Anaphylactic or allergic reaction to surgical preparation or anaesthesia. Failure: 7. Introduction of pleural infection. 8. Persistent pneumothorax 9. Recurrence of pneumothorax upon removal of the chest tube. 10. Lungs fail to expand due to plugged bronchus; bronchoscopy required. Recovery from the chest tube insertion and removal is usually complete, with only a small scar. The patient will stay in the hospital until the chest tube is removed. While the chest tube is in place, the nursing staff will carefully check for possible air leaks, breathing difficulties, and need for additional oxygen. Frequent deep breathing and coughing is necessary to help re-expand the lung, assist with drainage, and prevent normal fluids from collecting in the lungs.

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4.

ABDOMINAL SURGICAL EMERGENCIES

1. APPROACH TO ABDOMINAL PAIN RHC Thoracic Pneumonia Pleural effusion Biliary Cholangitis Cholecystitis Gallstone disease

Epigastric

Hepatic Hepatitis (viral, autoimm etc) Hepatomegaly Abscess Others Subphrenic abscess Pancreatitis PUD Appendicitis

Rt Loin Biliary (see RUQ) Urological Infection Pyelonephritis Abscess Others PKD Renal cyst Angiomyolipoma Infarction

Others Pancreatitis

Gastrointestinal Oesophagitis GERD PUD Gastric outlet obstructn CA stomach

Thoracic Pneumonia Pleural effusion MI Gastrointestinal PUD Diverticulitis Mesenteric ischaemia

Periumbilical

Obstruction Hydronephrosis Nephrolithiasis Ureteral obstruction CA

Thoracic MI Pericarditis Aortic aneurysm

LHC

RCC TCC renal pelvis Bladder ca (ureteral obstructn)

Gastrointestinal Appendicitis (early) I/O Mesenteric ischaemia Colitis IBD

Others Aortic Aneurysm Pancreatitis

Others Subphrenic abscess Splenomegaly Pancreatitis

Lt Loin Splenic disease Urological (see Rt Loin)

Others Appendicitis RIF Gastrointestinal Appendicitis Terminal ileitis Meckel’s   diverticulitis Mesenteric ischaemia Mesenteric adenitis IBD Colitis Colorectal CA Hernia

O&G Ovarian cyst Ovarian torsion Ectopic pregnancy PID Orthopaedics (See LIF)

Hypogastric Gastrointestinal Colorectal CA

O&G Ectopic pregnancy Abortion PID Uterine rupture Fibroid complications Adenomyosis Endometriosis

Urological ARU Bladder calculi Cystitis / UTI

LIF Orthopaedics Infection Septic hip arthritis TB hip Degeneration OA hip Inflammation RA hip Ankylosing spondylitis Reiter’s  syndrome Inflitration 1o bone tumour (hip) Metastasis to hip Destruction # - NOF, pubic rami Radiation Back pathologies (referred pain) Paediatric ortho conditions Transient synovitis Perthes’  dz SCFE

Gastrointestinal Diverticulitis IBD Colitis Colorectal CA Hernia O&G (see RLQ)

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2. APPROACH TO ABDOMINAL MASSES RHC Liver

Gallbladder Pancreatic/periamp ullary ca Acute cholecystitis Hydrops Empyema Mirizzi syndrome

Massive Cancer: HCC Metastases Myeloprolftve dz Alcoholic liver dz Rt ht failure/ tricuspid regurg

Ascending colon Cancer Diverticular mass/abscess Faeces

Moderate Above causes Lymphoprolftve dz Haemochromatosis Amyloidosis

Epigastrium Liver (see RHC)

Stomach Cancer Distension (GOO)

Pancreas Pseudocyst Tumour

Aorta Aortic aneurysm

Transverse colon Cancer Diverticular mass/abscess Faeces

Retroperitoneal lNpathy Lymphoma Teratoma Other malignancies

Right adrenal gland

Mild Above causes Infxns: Viral – Hep, IMS Bacterial – abscess Parasitic – hydatid cyst, amoebic abscess Biliary obstruction Cirrhosis

Right kidney (see Rt lumbar)

Right Lumbar Right Kidney Hydro/pyonephrosis Cancer – RCC Polycystic dz Single cyst Amyloidosis Tuberous sclerosis, VHL

Umbilical

Right adrenal gland

Liver (see RHC)

Liver (see RHC)

Stomach(see Epigastrium)

Ascending colon mass Cancer Diverticular mass/abscess Faeces

Pancreas (see Epigastrium) Aorta Aortic Aneurysm

Small intestine Obstruction

Spleen Massive Infxns CML Myelofibrosis

O&G Ovarian cyst/tumour Fibroids

Orthopaedics Chondroma/sarcom a of ilium Bony metastasis

Vascular: Iliac artery aneurysm Iliac lymphadenitis

Urogenital: Transplanted kidney Bladder diverticulum Ectopic or undescended testis

Descending colon Cancer Diverticular mass/abscess Faeces

Moderate Above causes Portal hypt Lymphoprolftve dz (lymphoma, CLL) H’lytic  anaemia   (thal, HS) Storage dz (Gaucher’s)

Left kidney (see Rt lumbar) Left adrenal gland

Mild Above causes Infxns: Viral hep, IMS, Endocarditis Autoimmune – SLE, RA, PAN Myeloprolftve dz – PRV, essential thrombocytopaenia Infiltratn – sarcoid, amyloid Left Lumbar Spleen (see LHC)

Descending colon Cancer Diverticular mass/abscess Faeces

Left kidney (see right lumbar)

Hypogastrium

Gastrointestinal Appendiceal mass/abscess TB gut Ca caecum Distended caecum (due to distal obstruction) Crohn’s  dz  (terminal   ileitis)

Stomach

Retroperitoneal lNpathy Lymphoma Teratoma Other malignancies

Mesenteric cyst

RIF

LHC

Bladder Acute retention of urine Chronic retention of urine

Uterus Gravid uterus Fibroids Tumour Ovary Cyst Tumour

Anal/rectal mass Cancer

Skin & Msk: Psoas abscess

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LIF Gastrointestinal Diverticular mass/abscess Ca colon/sigmoid Crohn’s  dz  (terminal   ileitis) Faeces Similar causes as RIF mass

3. INTESTINAL  OBSTRUCTION  (&  MECKEL’S  DIVERTICULUM) Causes of IO 1.

Mechanical Intraluminal Impacted stool Gallstone  ‘ileus’             Foreign body Bezoars (phyto-, tricho-)

2.

Mural Tumours Diverticular stricture Intussusception Crohn’s  strictures             RT strictures

Extraluminal Adhesions (post-op,  Crohn’s) Herniae Volvulus Lymph node compression Superior mesenteric artery syndrome

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

Ogilvie pseudo-obstruction in a septic elderly patient. Note the massive dilatation of the colon, especially the right colon and cecum Others: intestinal atresia

Small bowel IO 1) Adhesions 2) Herniae 3) Ileocecal tumour 4) Intussussception

Large bowel IO 1) Cancer 2) Post-diverticulitis stricuture 3) Sigmoid volvulus Rarely adhesions ( F, Adenocarcinoma more common in West whereas SCC more in East - Increasing incidence with age - Decreasing incidence overall, increasing in distal oes RISK FACTORS SCC (70%) Modifiable 1. Smoking (100X) 2. Alcohol (2X) 3. Caustic injury [middle 1/3] 4. Diet: Hot drinks, preserved foods (nitrosamines), betel nuts; vitamin / mineral def (selenium, vit E, beta-carotene) Non1. Achalasia (2-8%) modifiable 2. PV synd (10%) [upper 1/3] 3. Tylosis (AD disorder with keratosis of palms and soles) 4. Oes. diverticulum 5. Irradiation

Adenocarcinoma (30%) 1. Smoking (10X) 2. Obesity GERD

Barrett’s

Barrett’s (30-40X, 1% per year) [distal 1/3]

PATHOLOGY - 70% squamous cell carcinoma, 30% adenocarcinoma - SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lower third and gastro-oesophageal junction (related  to  reflux  and  Barrett’s  oesophagus) - Overall: 10% of cancers occur in the upper third, 60% in the middle third, 30% in the lower third - Three growth patterns: Fungating (60%) Ulcerative (25%) Infiltrative (15%) - Tumour spread: direct extension into surrounding structures, vascular invasion, lymphatic spread - Common sites of metastases: liver, lung, bone STAGING AJCC 7th edition 2010 SCC and adenocarcinoma are staged separately Subclassification of nodal (N) status according to the number of regional nodes containing metastases Reclassification of tumors at the gastroesophageal junction (GEJ) and/ or the proximal 5 cm of the stomach that extend into the GEJ or esophagus Reassignment of stage groupings using T, N, M categories as well as histologic grade of differentiation (G), and for SCCs, tumor location Redefining of Tis (carcinoma in situ) as high-grade dysplasia Subclassification of T4 disease based upon potential resectability of adjacent involved organs or structures T

N M

Tis T1a T1b T2 T3 T4a T4b N1 N2 N3 M1

High-grade dysplasia Tumour invading lamina propria or muscularis mucosa Tumour invading submucosa but does not breach submucosa Tumour invades the muscularis propria Tumour invades adventitia Resectable tumor invading pleura, pericardium, or diaphragm Unresectable tumor invading other adjacent structures 1-2 Regional node involvement 3-6 7 or more Distant metastases

Stage

T

N

M

Grade

Tumor location

Histologic grade (G)

0

is

0

0

1, X

Any

GX

I (A/B)

1-3

0

0

1-3

Any/ lower (Ib)

Grade cannot be assessed—stage grouping as G1

II (A/B)

2/3

0-1

0

2/3

Upp mid/ lower

G1/2/3/4

Well/Mod/Poorly/Un differentiated

III (A-C)

1-4a

0-3

0

Any

Any

IV

any

any

1

Any

Any

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PRESENTATION Usually of insidious onset, with earliest symptoms being non-specific  e.g.  retrosternal  discomfort,  “indigestion”,  and  most  patients   already have advanced disease when they are diagnosed – 75% have lymph node involvement at time of diagnosis. – 50% of patients have unresectable cancer on presentation Asymptomatic  from  screening  of  Barrett’s  oes  patients  (early  detection) 1. 2. 3.

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

1+2+3 = CA oes until proven otherwise Pain develops late and is usually due to extra-oesophageal involvement Complications 4. 5. 6. 7.

Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult) Vocal cord paralysis (left - due to its longer course through the aortopulmonary window > right) Aspiration pneumonia Tracheo-oesophageal or broncho-oesophageal fistula

INVESTIGATIONS – 4 OBJECTIVES (A) Diagnosis 1.

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

2.

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

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

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ii. Distant 1. Chest X-ray - Mets o Presence of any lung metastases o Pleural and/or pericardial effusion - Cx o Aspiration pneumonia o Tracheal deviation or extrinsic compression of tracheobronchial system o Widened superior mediastinum in an upper oesophagus tumour o Raised hemidiaphragm with phrenic nerve involvement 2. CT scan (as above) 3. PET scan / CT PET - Distant N, M. - Expensive ($2000!) - Used for patients deemed fit for operation. 4. Bone scan for bony metastases Staging laparoscopy not done! (C)Complications 1. Full blood count –

Low Hb (anaemia from chronic blood loss) High TW (aspiration pneumonia)

2. Urea, electrolytes, creatinine a. electrolyte disturbances from vomiting, poor intake; b. raised Cr & urea in dehydration (Cr will be raised more than urea if patient has prerenal failure from dehydration) 3. Liver function tests – low albumin with nutritional deprivation, liver mets (rare) 4. CXR (as above) Predictors of poor outcome: Sig LOW, Low albumin. (D) Pre-op (operation requires thoracotomy) 1. Lung function test eg. Spirometry a. In view of single lung ventilation during operation b. Risk of COPD – Smoking is impt RF for CA oes (esp SCC) FEV1??, FVC > 1.25L?? 2. 2DE (in view of major op) – ideal EF>40% 3. PT/PTT, GXM 4. Usual: FBC, UECr

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TREATMENT Principles - Three modalities available – surgery, chemotherapy, radiotherapy – used singly or in combination - Aims of treatment: Curative or palliative (50%) - Surgical treatment is usually performed with curative intention, but can also achieve good long-term palliation of symptoms - Choice of treatment depends on several patient factors: age, co-morbidities, nutritional state, life expectancy, and prognosis Surgery - Curative in early lesions and part of multimodal therapy in more advanced stages - Resection should not be done in patients with distant metastases or contraindications to surgery 1. Endoluminal surgery – for early lesions (Tis, T1a); no attempt to remove any LNs (usually no LN involvement) i. Endoscopic mucosal resection (EMR) – Cx: bleeding, perf (may be prevented with sufficient saline injection to raise the mucosa containing the lesion), stricture ii. Mucosal ablation using photodynamic therapy , Nd-YAG laser, or argon plasma coagulation 2. Oesophagectomy (i) Ivor-Lewis / Lewis Tanner Two-stage procedure involving gastric mobilisation (first stage, done through upper midline abdominal incision), oesophagectomy and gastro-oesophageal anastomosis in the chest (second stage, through right thoracotomy incision) (ii) Trans-hiatal Done via two incisions – one in the abdomen and one in the neck Blunt oesophagectomy, gastric mobilisation, and gastro-oesophageal anastomosis in the neck Less morbidity than Ivor-Lewis as the chest is not opened, but controversial (iii) Tri-incisional (McKeown approach) Three incisions – abdominal, chest, and also left neck incision for gastro-oesophageal anastomosis in the neck Performed with two-field lymphadenectomy (upper abdominal and mediastinal) No difference in survival between trans-hiatal and I-L modalities; the stage of the cancer when the operation is performed is a greater factor influencing survival Radical en-bloc dissections not shown to improve survival Oesophagectomies have high mortality (5-10%) and morbidity (25%) rates, thus patients have to be carefully selected in order to maximise survival benefit from surgery Complications Dependent on extent of surgery and incisions used - Intraoperatively, injury to lung, thoracic duct, RLN can occur - Respiratory complications higher in thoracotomies – atelectasis, pneumonia - Anastomotic leak and resultant mediastinitis (for chest anastomosis) most feared - Anastomotic stricturing can also occur - Reflux can result in the long term due to loss of the LES 3. Palliative debulking for obstructive symptoms Radiotherapy - Usually given in combination with chemotherapy - Primary treatment for poor-risk patients Palliation for unresectable lesions with obstructive symptoms, pain and bleeding - SCCs are radiosensitive - Modalities: External beam radiation or brachytherapy - Obstructive symptoms may worsen temporarily after radiotherapy due to oedema - Complications: tracheo-oesophageal fistula, stricture

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Chemotherapy - Current regimen: 5-Fluorouracil and cisplatin - Addition of chemotherapy to external beam radiation for unresectable cancers shown to have improved survival compared to EBRT alone - Chemotherapy given preoperatively and postoperatively improves survival Overall curative treatment Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection), oesophagectomy, and postoperative adjuvant chemoradiotherapy for responsive tumours Palliative treatment 1. Ablation o Endoscopic laser fulguration (high frequency electric current) o Photodynamic therapy is a new treatment option - use of drugs that are absorbed by cancer cells; when exposed to a special light, the drugs become active and destroy the cancer cells o Radiofrequency o Cryotherapy 2. Surgical debulking 3. Bypass surgery rarely done nowadays 4. Stenting to maintain lumen patency and occlude fistulas – endoscopic / radiological? o Cx: metallic Perf (friable tumor) Bleeding Risk of GERD, aspiration lifelong PPI Feeding in oesophageal obstruction - Feeding via oropharyngeal route is preferred unless the passage is obstructed or it is unsafe for the patient to feed via that route (i.e. risk of aspiration) o If still able to pass NG tube around tumour feed via NG (but also consider complications with long-term NG placement e.g. erosions around nasal area, sinusitis); o consider PEG placement for long-term feeding if able to get scope around tumour - If unable to pass tube or scope around tumour, o consider open gastrostomy o Total parenteral nutrition is another option but has more complications, more costly o Relief of obstruction via various techniques as listed above help to enable oral feeding, but most techniques are not long-lasting and dysphagia will return with tumour growth PROGNOSIS - 80% mortality at 1 year, overall 5-year survival other races PATHOPHYSIOLOGY - Lower oesophageal sphincter is a physiological sphincter with various mechanisms that help to prevent reflux - Some physiological reflux occurs that is rapidly cleared by peristaltic movements in the oesophagus - GORD results from various pathophysiological factors (loss of the normal protective mechanisms, or the mechanisms are overwhelmed) singly or in combination: I. Motor failure of oesophagus with loss of peristalsis II. Loss of LES function – decreased tone, hiatal hernia, iatrogenic injury III. Increased intra-abdominal pressure – obesity, tight garments, large meal IV. Delayed gastric emptying

- Acid incites inflammation in lower oesophagus – extent of inflammation increases with increasing duration of contact with acid - Chronic inflammation results in  complications  of  GORD:  oesophagitis,  stricture,  Barrett’s  oesophagus CAUSES/RISK FACTORS - Motility disorder of oesophagus e.g. scleroderma Malfunction of LES Hiatal hernia (loss of normal LES mechanisms) Drugs that cause smooth muscle relaxation e.g. calcium channel blockers, sedatives, beta agonists, anticholinergics, etc. Coffee and smoking also cause LES relaxation. - Chronically increased intra-abdominal pressure – pregnancy, chronic cough, obesity, constipation, etc - Eating habits – lying down after a heavy meal Any cause of decreased gastric emptying PRESENTATION - Heartburn: retrosternal pyrosis (=burning sensation in upp abdo) - Acid brash/Regurgitation: reflux of sour gastric juices into back of mouth i.e. regurgitation o These symptoms occur usu after food, particularly a heavy meal, and are aggravated by lying flat (posturally related) - Other symptoms: globus (feeling of a lump at the throat), water brash (hypersalivation in response to reflux) Chest pain (can mimic anginal pain with radiation to neck, jaw, arm), nausea high false positive - Complications o Long-standing disease can lead to dysphagia due to stricture formation; dysphagia can also result from an underlying oesophageal motility disorder; odynophagia suggests oesophagitis with ulceration o Reflux can also lead to pulmonary symptoms: chronic cough, chest infections (aspiration)

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COMPLICATIONS 1. Pain and spasm 2. Stricture 3. Shortening of oesophagus 4. Dysmotility 5. Haemorrhage (occult > frank) 6. Ulceration 7. Barrett’s  oesophagus  (see  below) 8. Schatzki’s  ring  (constrictive  ring  at  the  squamocolumnar junction composed of mucosa and submucosa) 9. Malignancy  (adenocarcinoma  arising  from  Barrett’s  oesophagus) DIAGNOSIS 1. History!! is important as most patients with reflux are seen in the primary setting with no facilities for detailed investigation - Exclude cardiac cause of chest pain, and exclude malignant cause of dysphagia - GerdQ questionnaire 2. Oesophageal pH probe - Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probe especially if oesophagitis is not seen on OGD - Antimony probe (24hr) most commonly used; alternative is the Bravo capsule (a wireless capsule that is temporarily attached to the oesophageal wall, 48hr) - The probe is placed 5cm above the manometrically-determined upper limit of the LES (for the wired probe), or 6cm above the endoscopically-determined squamocolumnar junction (for the wireless capsule) - Diagnosis based on the percentage of time in 24hrs the pH reading is below 4 (positive if >5.5%) - Can have false negative consider repeat test. Either one positive is diagnostic. 3. Oesophagogastroduodenoscopy - Cannot actually diagnose reflux (poor correlation btw oesophagitis and reflux). Therefore, selective usage. - Uses: o Dx: Rule out gastric malignancy/ other conditions mimicking symptoms (in areas with high prevalence of gastric CA) o Cx: Can visualise and grade oesophagitis if present, and take biopsy specimens for confirmation (see below) o Ax: May see a hiatal hernia which is associated with reflux (though not all patients with hiatus hernia will have reflux) 4. Barium swallow and follow-through - Not of much value in diagnosing reflux - Ax: Can detect motility disorders that cause reflux, - Cx: oesophageal ulceration and stricturing resulting from reflux - Can sometimes see reflux of barium contrast into oesophagus 5. Manometry - No value in reflux except for detecting motility disorder (tro achalasia! – will be much aggravated by surgical Tx of reflux) GRADING OF OESOPHAGITIS

1. Savary-Miller classification Grade I: Grade II: Grade III: Grade IV: Grade V:

One or more supravestibular non-confluent reddish spots, with or without exudates Erosive and exudative lesions, may be confluent but not circumferential Circumferential erosions covered by haemorrhagic and pseudomembranous exudate Presence of chronic complications such as deep ulcers, stenosis, stricture Barrett’s  metaplasia

2. Los Angeles classification

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

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TREATMENT Lifestyle 1. Diet and eating habits Avoid coffee, chocolate, fatty foods, or anything that worsens symptoms Do not eat 2 hours prior to sleeping Walk after eating Avoid excessive eating; eat small meals 2. Avoid drugs that relax LES e.g. anticholinergics, muscle relaxants, etc. 3. Weight reduction if obese 4. Elevate head of bed 5. Smoking and alcohol intake cessation Medication 1. Acid suppression therapy: PPI (best! switch  ard  if  patient  doesn’t  respond  to  one,  rather  than  increasing  dosing  frequency)  or   H2-receptor antagonists May require LT tx. If patient stops PPI and symptoms recur, restart PPI first, no need to reinvestigate. 2. Prokinetics to increase LES pressure e.g. domperidone (anti-dopaminergic), metoclopramide (anti-dopaminergic + antiserotoninergic) Surgical - Indications: Failure of medical therapy (or incomplete resolution of symptoms) Oesophagitis with frank ulceration or stricture Complications of reflux oesophagitis – respiratory  complications,  Barrett’s  oesophagus Severe symptoms or progressive disease Compliance problems - patient does not want to be on medication for life (despite good results) - Goal of surgery: Increase pressure at the gastro-oesophageal junction but not so much that it prevents food from entering the stomach (too tight dysphagia) - Surgery versus conservative treatment Surgery has higher rates of cure and better long-term results?? / results not longstanding? No need to adhere to strict lifestyle and diet change as well as long-term medication Disadvantage of surgery is the associated morbidity and mortality

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- Fundoplication (mainstay of surgical therapy) Can be done via open surgery or laparoscopic surgery (most laparoscopic now) a. Nissen fundoplication is the most commonly done – a 360 degree (total) wrap of the fundus around the gastrooesophageal junction b. Partial fundoplications can also be done in patients where oesophageal motility is poor or the oesophagus is foreshortened; anterior 90 degrees, anterior 180 deg, and posterior 270 deg fundoplications are various options available - Complications of surgery 1. Perforation – most feared complication, may result in mediastinitis if not promptly detected and repaired intraoperatively 2. Excessively tight wrap resulting in dysphagia 3. Excessively loose or short wrap – reflux recurs (failure of treatment) 4. “Slipped-Nissen”  body of the stomach intussuscepts through the fundoplication, creating an hourglass deformity whereby the stomach resides both above and below the wrap; usually due to a foreshortened oesophagus unrecognised in the first operation. Causes severe reflux as pouch above the wrap traps food and serves as reservoir. 5. “Gas  bloat  syndrome”  – patient experiences difficulty burping gas that is swallowed (gas accumulation) - Outcome of surgery 80-90% Excellent to good (no symptoms, no medications and lifestyle changes required) 10-15% Satisfactory (some residual symptoms) 20 - Patient’s  conscious  level  – confused? (shock) - Compare current vitals with vitals in ambulance, ED – is there a worsening trend? - Urine output: renal perfusion indicates cardiac output

2. General inspection

- Pallor - Cold clammy peripheries impending shock - Stigmata of chronic liver disease

3. Peripheries

- Cold clammy peripheries - LN (mets)

impending shock

4. Abdomen

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

5. Digital rectal examination

- Malaena or frank blood - tumor deposits / rectal mass

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

-

2. Adjuncts - NG tube if patient is having haematemesis – prevents aspiration, allows gastric lavage prior to OGD (DO NOT insert if suspect varices) - Catheterisation – monitor I/O balance esp in elderly or when large amount of fluid resuscitation required, or anticipating surgery - Intubate if: 1) massive uncontrolled active hematemesis 2) signs of decompensation eg. obtunded 3. Early medications - IV omeprazole 80mg bolus --> 8mg/hr infusion X 3/7 stomach pH and stabilises clot formation regimen to prevent rebleed (normal Tx dose 40mg bd) - If suspecting varices – IV somatostatin/octreotide, IV antibiotics - Stop antiplatelets, anticoagulants, NSAIDS 4. Close monitoring - Monitor for: SHOCK ( HR, BP, - HD with hourly para if Elderly with many comorbidities Hypotension

urine output,

confusion & lethargy)

5. Emergency oesophagogastroduodenoscopy

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

- Repeat OGD with greater detail if it is normal the 1st time. Exclude haemoptysis & bleeding from nasopharynx Look for Mallory weiss tear and posterior wall D1 bleeding ulcer (gastroduodenal artery) Obscure overt bleed: OGD normal Colonoscopy normal Small bowel imaging: a) Capsule endoscopy b) Tagged RBC c) CT enterography CT mesenteric angio anytime when patient becomes unstable.

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2. VARICEAL BLEEDING PATHOPHYSIOLOGY A result of portal hypertension (i.e. portal venous pressure >20 cmH2O or >12 mmHg – normal = 7-14 cmH2O / 5-10 mmHg) MANAGEMENT OF VARICES can be divided into three categories: 1. Acute bleeding 2. Prophylaxis 3. Chronic management

WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT - Previous history of variceal bleed - Chronic alcohol intake - Jaundice or stigmata of chronic liver disease - Profuse hematemesis

I. ACUTE BLEEDING – MANAGEMENT 1. Resuscitate - Airway, breathing, circulation - If patient appears well, look for early signs of shock – tachycardia, postural hypotension - Look at hydration status 2. Assess mental state - If patient has altered mental state (encephalopathy)

need to protect airway (may require intubation)

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

portal pressure

4. Management of severe bleeding: Sengstaken-Blakemore tube - If hypotensive and bleeding is ongoing, may require use of Sengstaken-Blakemore tube for up to 48hr (if unable to ligate) - Protect airway before inserting tube. - Inflate gastric balloon and pull upwards against cardioesophageal junction (balloon will press on perforator veins entering oesophagus from stomach, and thus decrease oesophageal variceal bleeding); oesophageal balloon is not inflated nowadays 5. IV somatostatin or S/C Octreotide (Not given in ulcer bleed) - Mode of action: splanchnic vasoconstrictor which portal blood flow and hence portal pressures - Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow

variceal bleeding

6. Acid suppression - Increasing intragastric pH increases clot stability, aids haemostasis - Agents available: omeprazole (Losec), esomeprazole (Nexium), pantoprazole, etc. 7. Antibiotics - Not given in ulcer bleed - Risk of sepsis in patients with CLD and bleeding - Studies have shown that cover with broad spectrum Abx (Gram neg cover) - Ceftriaxone, Ciproflox 1g/day - Preferably started before endoscopy (procedures increase bacteraemia)

infectious cx, mortality, and also risk of recurrent bleed

8. Emergency endoscopy - Purpose: confirm diagnosis and institute management - Needs to be done emergently (on admission) as soon as patient is stabilised since bleeding can be torrential and life-threatening - Intervene if ESRF present or active bleed (not electively) - Banding/Ligation is the best modality for oesophageal variceal bleeding (sclerotherapy a/w higher morbidity e.g. mucosal ulceration) - Gastric varices are usually too large to be banded, sclerotherapy/ Glue (Histoacryl) used instead – risk of embolism from histoacryl 9. Observation - Keep patient in ICU! - NBM 2-3/7 - Continue antibiotics and omeprazole - Continue somatostatin up to the point where haemostasis is achieved or 5 days (exact ideal duration not well studied) - Antiencephalopathy Tx: Lactulose + Cipro (clear gut to prevent absorption of NH3) - Anticipate complications: (a) encephalopathy – fleet and lactulose, treat hypokalaemia from vomiting (b) aspiration – protect airway; ?benefit of gastric decompression using NG tube (c) risks of procedure – OGD-related risks 10. Management of possible precipitants - NSAIDs; Hepatic vein thrombosis

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

Insert Sengstaken-Blakemore tube up to 48hr (only temporary) If rebleed after 48hr of SBT: consider surgery

repeat endoscopy 10-12 hours later

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

C. Shunt surgery Portocaval shunts (portal vein to IVC) – side-to-side, end-to-side Mesocaval shunts (sup mesenteric vein to IVC) Proximal splenorenal shunt (splenectomy with end-toside anastomosis of portal side of splenic vein to left renal vein) Distal splenorenal shunt (Warren-Zeppa shunt – splenic vein divided, splenic side anastomosed end-toside to left renal vein)

A. Normal liver with normal blood flow. B. End to side spelnorenal shunt. C. End to side portacaval shunt. D. Mesocaval H-graft shunt

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

Splenectomy Proximal gastric devascularisation Selective vagotomy Pyloroplasty Oesophageal devascularisation Oesophageal transection

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II. PROPHYLAXIS OF VARICEAL BLEEDING SECONDARY = Band ligation + Non-selective beta-blockers - Best option is combination propranolol unless CI: decrease size and prevent rebleeding 3 weekly ligation until completely obliterated PRIMARY = Non-selective beta-blockers (oesophageal varices with no previous history of variceal hemorrhage) In pts with small varices with no risk of bleeding, the use of propranolol is of questionable benefit – repeat OGD to monitor varices. cardiac  output  by  β1 blockade  and  splanchnic  blood  flow  by  blocking  vasodilating  β2 receptors at splanchnic vasculature - The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%, to be continued indefinitely - The dose: determined by a 20% decrease in baseline resting HR / decrease in HR to 55 bpm / dev adverse effects - If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives - Band ligation/ Sclerotherapy: not used as primary prevention. as effective as treatment with propranolol Predictors of variceal haemorrhage: [SRCPS] 1 Site: varices at the GE junction have the thinnest coat of supporting tissue and are at highest risk of rupture and bleeding 2 Size: F1: Small straight varices F2: Enlarged tortuous varices that occupy less than one-third of the lumen F3: Large coil-shaped varices that occupy more than one-third of the lumen 3 Child’s  score – patients  with  higher  Child’s  score  have  higher  risk 4 Red signs: (ESRH)

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

5 Previous variceal haemorrhage: 70% of patients will have further variceal bleeds after an index bleed (risk highest in first 48 hours after first bleed) 30% rebleed within 6 weeks; 30% rebleed after 6 weeks III. CHRONIC MANAGEMENT - Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapy and subsequent endoscopic monitoring and repeated ligation/sclerotherapy as required to completely ablate varices) - If patient bleeds again failed ablation consider surgery (as above – shunts, or Sugiura) - LT propanolol + PPI - Refer to Hepato for liver disease http://www.heart-intl.net/HEART/011507/PortalHypertension.htm

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3. PEPTIC ULCER DISEASE EPIDEMIOLOGY - Incidence about 100 per 100,000 per year - 68% of patients are over 60 years of age - Overall mortality 7-10%, unchanged for last 20yrs – mostly due to ulcer bleeding esp in elderly with significant comorbidities MAIN AETIOLOGICAL FACTORS H. pylori - 60% of population are positive for H. pylori by age 21 - About 10-20% of infected patients develop an ulcer - Accounts for 90-95% of duodenal ulcers, and 50% of gastric ulcers NSAIDs - Accounts for most of the rest of ulcer disease not caused by H. pylori - 30% of patients on NSAIDs will get an ulcer, of which 20% (6% overall) will have a clinically significant ulcer i.e. symptomatic, bleeding Other factors - Cigarette smoking - Alcohol - Steroids and anticoagulants do not increase the risk of ulcer formation, but increase the risk of bleeding in an existent ulcer PATHOGENESIS - An imbalance between mucosal protective mechanisms against acid, and aggressive forces that damage the gastric mucosa - 2 Aggressive forces: gastric activity and pepsin activity - 5 Protective mechanisms: mucus secretion, bicarbonate secretion into mucus, robust mucosal blood flow to remove protons, epithelial regenerative capacity, prostaglandin secretion by mucosa to maintain blood flow - H. pylori causes a local inflammatory reaction and secretes enzymes that break down the gastric mucosal barrier, and also enhances gastric acid secretion and decreases bicarbonate production - NSAIDs impair mucosal prostaglandin production (through non-selective COX inhibition) prostaglandins are important for mucosal bicarbonate and mucin production and inhibiting gastric acid secretion, as well as maintaining mucosal blood flow PRESENTATION 1. Incidentally detected on OGD 2. Symptoms of dyspepsia (a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom (b) Dysmotility-like dyspepsia: non-painful discomfort in upper abdo, a/w upper abdo fullness, early satiety, bloating, belching, nausea (c) Unspecified dyspepsia - Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a duodenal ulcer 3. Bleed - As above, presenting with haematemesis (coffee-grounds vomitus) or malaena 4. Perforation - Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements - Board-like rigidity, guarding will be present on examination (signs of peritonism) - Erect CXR will show air under diaphragm ENDOSCOPY (OGD) - The most important and valuable investigation - Roles of endoscopy: (a)

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

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(b) Prognostication of bleeding risk (in UBGIT) Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH) Forrest grade 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 Adherent clot must flush and remove clot --> grade ulcer again

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

Classical bleeding BV: posterior-D1 (gastroduodenal art) Tx: Only pigmented spot can leave alone, the rest must intervene! (c) Endotherapy (in UBGIT) 1. Injection with adrenaline (1:10,000 dilute to 10ml - continue with N/S if need more) or absolute alcohol – tamponade effect is the most effective. Also vasoconstriction for adrenaline. Inject around ulcer (4 quadrants). Cx: perforation, bleeding, necrosis, arrhythmia. 2. Coagulation (Heater probe = thermal / Argon plasma) 3. Haemostatic clipping (endoclip) Principle: Dual modality better than single (as less risk of recurrent bleed and mortality) --> Usually Injection + Clip/Heater probe No study proves superiority of either therapy. Failed OGD hemostasis (after 1hr) a) Surgery is mainstay b) Transcatheter embolisation a. ind: failed surgery, rebleed post-Sx (usually GDA), not fit for Sx b. identify bleeding vessel and embolise with i. Mechanical (non-absorbable coil eg. Titanium) ii. Chemical (gel foam): can recannulise again in 2/52 c. Sandwich technique: embolise both prox and distal ends of vessel as bleeding can occur both ways. Post-endotherapy: Monitor for rebleed = drop in Hb (not malaena / vomit blood clots as these are expected. Changes in vitals may be too late.) Diet individualised: usually NBM 1-2/7, 3/7 if worrisome, 2years) 1. Failure to heal after 3 months of conservative therapy 2. Dysplasia or carcinoma 3. Recurrence 4. Perforation, persistent bleeding Surgery 1. Bleed = a. Ulcerectomy (if patient unstable, old, unfit) b. Antiulcer surgery (if patient stable, can tolerate) 2. Perforation = a. Omental patch repair + Bx (small 2cm or suspect malignancy) (parietal peritoneum, jejunum serosa, stomach local flap) 3. Definitive antiulcer surgery = Gastrectomy a. Partial gastrec if distal ulcer b. Proximal ½ ulcers may require total gastrec Can be used in emergency bleed if patient stable, but considered antiulcer Sx as parietal cell mass and antrum (contains gastrin containing cells) are removed. Bancroft’s  closure (for severe inflammation/scarring that prevents dissection around pylorus. Remove all antral mucosa to prevent marginal ulcers) If prepyloric ulcer, can treat similar to duodenal ulcer

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4. GASTRIC CANCER EPIDEMIOLOGY - Fourth most common cancer in males, sixth most common in females in Singapore - Female to male ratio 2:1 - Incidence 10-18 per 100,000 per year - Incidence increases steeply after 50 years old RISK FACTORS 1. Environmental - Diet: preserved foods (nitrosamines), smoked foods, polycyclic hydrocarbons - Smoking - Alcohol - Occupational exposure: asbestos, heavy metals, rubber - Low socioeconomic status 2. Genetic - Blood type A - HNPCC – Lynch syndrome II - P53 mutation - Germline mutation of e-cadherin - Family history of gastric cancer PRECURSOR CONDITIONS 1. Partial gastrectomy for benign disease with Bilroth II reconstruction - Usually occurs >15 years after surgery - Due to chronic exposure of gastric mucosa to biliary, pancreatic and intestinal secretions at the anastomotic zone 2. Gastric polyps - Highest risk in inflammatory polyps: 75-90% - 10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology - Also increased risk of adenocarcinoma elsewhere in the stomach 3. Chronic atrophic gastritis - Hypertrophic gastritis (Menetrier’s  disease) – inflammatory disease of gastric epithelium, up to 10% risk of malignant change - Pernicious anaemia – autoantibodies to parietal cells with achlorhydria, 2-10% risk of gastric cancer 4. Peptic ulcer disease - 35 years old should cause concern COMPLICATIONS -

Bleeding Gastric outlet obstruction Perforation Malnutrition

vomiting (dehydration, hypokalaemic metabolic alkalosis, aspiration ± pneumonia)

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INVESTIGATIONS Diagnosis OGD –visualisation and biopsy (ulcer with heaped-up edges) Staging investigations 1. CXR/ CT thorax– lung mets 2. Endoscopic ultrasound – gold standard for T staging and good for N staging 3. CT abdo pelvis – good for T, N & M staging 4. Staging laparoscopy prior to operation – picks up small peritoneal metastases that are occult on CT scanning (up to 1/5 of patients) upstage of disease Complications 5. FBC – low Hb 6. U/E/Cr – if vomiting, low potassium, low chloride, alkalosis 7. LFTs – albumin as a marker of nutritional status (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 fx preserved) Total gastrectomy is the resection of choice for proximal tumours (fundus, cardia, body) as well as diffuse-type tumours and cardio-oesophageal junction tumours - Reconstruction Bilroth I (end-to-end gastroduodenostomy) – rarely done (diff to mobilise duodenum to anastomose with residual stomach) Bilroth II/ Poly-A (gastrojejunostomy) – no protection against biliary reflux into stomach Roux-en-Y – to prevent biliary reflux; but involves 2 anastomoses, higher chance of leak Oesophagojejunostomy (after total gastrectomy)

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Complications of gastrectomy: Early 1. Bleeding 2. Infection 3. Anastomotic leak 4. Injury to surrounding structures eg. pancreas Late 1.

Early satiety

2.

Retained antrum syndrome a. Not enough antrum removed

acidity in residual stomach, with formation of marginal ulcers on the jejunal side of the anastomosis

3.

Intestinal hurry a. Inadequate reservoir function leads to poor digestion

4.

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

5.

Biliary/intestinal reflux into stomach a. Leads to symptoms of dyspepsia

6.

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

7.

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

may have phytobezoar (veg fibre bezoar) formation

decreased iron absorption in terminal ileum

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

-

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

CHEMOTHERAPY/RADIOTHERAPY Adjuvant therapy 5-fluorouracil with chemotherapy 5-fluorouracil with epirubicin for advanced disease Neoadjuvant therapy - 5-FU and cisplatin can be used to downstage unresectable, locally advanced disease with a significant increase in resectability (61% - For resectable disease: preoperative 5-FU, cisplatin, doxorubicin, methotrexate, followed by intraperitoneal 5-FU improved resection rates, response rates, median survival PALLIATIVE THERAPY - For palliation of symptoms such as pain, bleeding, obstruction 1. 2. 3. 4.

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)

PROGNOSIS -

Stage I Stage II Stage III Stage IV

90% 5-year survival 70% 40% 0%

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79%)

7.

LOWER GIT & COLORECTAL DISEASES

1. APPROACH TO BLEEDING LOWER GIT 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

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PHYSICAL EXAMINATION 1. 2. 3.

4. 5.

6.

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

ACUTE MANAGEMENT Resuscitation o Supplemental oxygen, insert 2 large-bore IV cannula with fast infusion of crystalloids (N/S 500ml over ½hr) o Infuse colloids if ongoing blood loss while waiting for whole blood (GXM) o Catheterise and monitor urine output, insert NGT on suction to detect UBGIT o Continuous vital signs monitoring & I/O charting ± CVP & stool chart o ECG + cardiac enzymes to detect possible AMI o Take blood for investigations - FBC: low Hb level (repeat FBC 2-3 hours later or when necessary) – packed cell transfusion 4 pint PCT: give FFP to prevent over-dilution of clotting factors - UECr: hydration status, any acute renal failure from shock, electrolyte imbalance – replace - PT/PTT: must correct coagulopathy before trying to stop bleeding – fresh frozen plasma - LFT: exclude bleeding varices - ABG: may have metabolic acidosis in shock due to organ ischaemia – IV bicarb, dialysis if severe - GXM 4 pints Identify source & stop bleeding o Arrange urgent colonoscopy (patient must be stabilised before procedure) - Diagnostic: identify cancer, diverticulosis, angiodysplasia, areas of inflammation & bleeding - Therapeutic: clip, diathermize, or inject adrenaline/ sclerosant into bleeding vessel o Double contrast barium enema: good for picking up diverticulum which may be missed on scope o Mesenteric angiogram or CT mesenteric angiogram - More precise; can cannulate all 3 main trunks & their branches - Diagnostic: shows  blush  in  active  bleeding,  shows  ↓  perfusion  of  ischaemic  bowel - Therapeutic (not for CT): embolisation/sclerotherapy for angiodysplasia, beware of causing bowel ischaemia (use foam medium) o Capsule Endoscopy: - for stable patients with suspected SI bleed & unable to swallow - takes 36hrs to read the results, but unable to localise the site & intervene o double balloon enteroscope: - only for suspected proximal SI - able to do therapeutic manoeuvres o Labelled RBC isotope scan under gamma camera - For intermittent, occult bleeds not detectable on mesenteric angiogram - Not for urgent setting; can take up to 24 hours! o Laparotomy with saline lavage if massive on going bleed, recurrent bleeding - On table scope to transilluminate bowel & identify bleeding source - On table angiogram - Oversewing of bleeding vessel, partial/total colectomy as last resort

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2. COLORECTAL CANCER EPIDEMIOLOGY COMMONEST CANCER IN SINGAPORE Prevalence in Singapore: 6% (Commonest cancer in M, number 2 cancer in F) Peak incidence at 60-70 years of age (increase with age) Increasing incidence through the years. Chinese more prevalent. PATHOLOGY - Almost all tumours are adenocarcinomas - 90% of tumours are sporadic - 8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and 1% with familial adenomatous polyposis (APC) - 1% arise in association with long-standing ulcerative colitis (>10 years)

CRC Sporadic (90%) APC pathway (80%)

DNA mismatch repair (15%)

Inherited (10%)

HNPCC (8%)

FAP (1%)

UC > 10yrs (1%)

PATHOGENESIS There are 2 pathways for cancer development in the colorectal mucosa: 1. APC pathway (adenoma-carcinoma sequence) - Accounts for 80% of sporadic colorectal carcinomas - Characterised by chromosomal instability - Stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes: Loss of the APC suppressor gene on 5q21 (congenitally absent in patients with familial adenomatous polyposis – APC) is the earliest event in adenoma formation detected using Protein truncation test APC is required to break down beta-catenin; with the loss of APC, beta-catenin accumulates and activates various genes in the nucleus (such as MYC and cyclin D1) which promote cell proliferation K-RAS (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering mitotic signals and prevent apoptosis Loss of tumour suppressor gene at 18q21 Loss of p53 late in carcinogenesis -

The molecular evolution of colon cancer through this pathway occurs through a series of morphologically identifiable stages: localised epithelial proliferation small adenoma large, more dysplastic adenoma carcinoma in-situ invasive cancer

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

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MORPHOLOGY 1. Scirrhous  /  annular  “apple-core”  lesions  (most  common)  - more common in the left colon 2. Polypoid – more common in the right colon as there is more space to grow 3. Ulcerated 4. Nodular SPREAD 1. Intramural –Transmural (along bowel wall. Seldom >2cm spread) or Intraluminal 2. Direct extension into surrounding tissues e.g. small bowel, ovary, ureters, bladder 3. Lymphatic 4. Haematogenous – to liver, lungs, bone, brain 5. Transcoelomic – direct seeding: through entire thickness peritoneal cavity spread thru peritoneal fluid. Late stage > T4. RISK FACTORS Non-modifiable (4)

1. Age >50 years 2. Genetic predisposition (a)

(b)

(c)

(d)

Personal history of CRCs in the first 5 years after resection of a primary CRC, i. Metachronous CRC: occurs at a rate of 3-5%, ii. Metachronous adenomas: rate of 25-40% (Metachronous = primary tumors occurring more than 6 months apart) Family history of CRCs 1 first-degree relative with CRC: increases risk of CRC 1.7X, 2 1st-degree relatives with CRC, or if the relative had CRC 1.7X FHx of colonic adenoma same significance as CRC?? Polyposis syndromes near 100% risk of cancer formation: i. FAP and its variants ii. Gardner’s  syndrome:  multiple  osteomas  in  mandible/skull/  long  bones,  sebaceous  cyst,  desmoid  tumor iii. Turcot’s  syndrome:  glioblastoma  multiforme other polyposis syndromes such as Peutz-Jegher’s,  Cronkhite-Canada have a small increased malignant potential HNPCC (AD) – more common than FAP, accounting for 8% of cancers.

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

4. Adenomatous polyps - Increased risk if there is a personal history of large (>1cm) adenomatous polyps, and polyps with tubulovillous or villous histology, particularly if multiple (3-6X increased risk) - Small (/- 1cm tumors Double-contrast barium enema (barium + air) - Classically can see an apple core lesion with barium enema - Not adequate for diagnostic purposes, may miss small lesions & distal lesions - Need to insert a rigid sigmoidoscope 10-15cm to instil air & contrast II. STAGING All CRCs (a) CT scan of the abdomen and pelvis for colon tumours - Local T staging & invasion into bladder, ureter, uterus - Staging of regional and no-regional lymph node involvement - Metastases to the liver, obvious peritoneal seeding, omental kinking, - Look for ascites, hydroureter/ hydronephrosis, intestinal obstruction (b) CXR + CT scan of the chest (c) Bone scan if symptomatic (more for Ca breast, lung, prostate, thyroid) (d) CT brain if symptomatic Rectal tumors (below peritoneal reflection): (e) Endoscopic ultrasound / transrectal ultrasound (for rectal tumour) - Very good for T staging to determine depth of involvement: locally  advanced  CA  (≥T3)  requires  neoadjuvant chemoRT - Can also assess local lymph node status (f) MRI of the tumour - Superior to CT for delineating fat planes in T staging especially in rectal cancer - Circumferential resection margin (CRM) refers to the fascia propria - High risk tumors for recurrence: CRM < 2mm, T3/4 (+/- bulky T2) Neoadjuvant ChemoRT III. COMPLICATIONS Basic laboratory investigations: (a) FBC for low Hb, together with iron studies (b) UECr: fluid and electrolyte abnormalities from vomiting (eg. in IO), or 3rd space losses (intraluminal); creatinine may be elevated (prerenal failure) and hence risk of contrast nephropathy (c) LFT for derangements caused by metastasis (occur late) – raised bilirubin, ALP (first to be raised) (d) PT/PTT, GXM for surgery (e) Carcinoembryonic antigen level (CEA) - A tumour marker for colorectal carcinoma (glycoprotein synthesised by foetal intestinal tissue) - >90% of CRC produce CEA, Raised levels: 70% CRC, 10-20% lung/ BrCA - Measured pre-operatively as a baseline level – if the CEA is raised pre-op and falls to within normal range post-op, it is likely tumour has been totally removed. Usually, normal values 6wks post-op? - Follow-up after surgery with CEA levels to detect tumour recurrence - Causes of false positive raised CEA: smoking, pregnancy, bronchitis, cholangitis and cancers of the stomach, lung, breast, pancreas, cervix, bladder and kidney Imaging (f) Erect and supine AXR to look for intestinal obstruction (usually large bowel closed loop obstruction) and caecal distension; near perforation (g) Erect CXR in perforated tumour to detect air under diaphragm (h) ECG :anaesthesia assessment

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TNM STAGING

DUKE’S STAGING (SURGICAL AND HISTOLOGICAL FINDINGS)

Stg

Description

A

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

75%

5yr surv

B

Invades past muscularis propria into extrarectal/ extracolic tissue, no LN

55%

C

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

C1:40% C2:20%

D

Distant mets/ extensive local mets such that surgically incurable

Poor unless mets are resectable

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TREATMENT SURGERY Aim: eradicate tumor with clear margins and LN drainage Pre-operative measures - Bowel prep Modification of diet – 3 days low residue diet (reduce frequence and volume of stools – low fibre, reduce food that increase bowel activity), NBM day before operation Bowel clearance with polyethylene glycol. CI obstruction? - Prophylactic antibiotics (max at first incision) ampi/ genta/ metronidazole at induction of anesthesia Principles of surgery for colonic carcinomas - En-bloc resection of tumour with adequate margins For colonic tumours, a margin of 5 cm proximally and distally is adequate While segmental resection is sufficient for primary tumour removal, a wider resection is often required to achieve sufficient lymphadenectomy Adequate clearance of the draining lymphatics involves excision of the vascular arcades supplying the segment of involved colon back to their origin (from the SMA or IMA) as lymphatics follow the arteries generally - Obstructed left sided carcinoma No difference shown for doing a staged procedure (i.e. tumour removed with proximal end of colon brought out as a colostomy) as compared to creating a primary anastomosis On-table bowel decompression ( irrigation) for clearance of faecal material Segmental colectomy for the tumour with intraoperative decompression is comparable to subtotal/total colectomy without decompression with regard to bowel function and rates of complications - Site of anastomosis: SB more reliable blood supply so SB-LB >>> LB-LB - Site of surgery for colonic carcinoma Marginal artery of Drummond = Artery formed by the anastomosis between the ileocolic artery, middle colic artery, right and left colic arteries and sigmoidal artery. It is a continuous vessel running along the inner perimeter of the large intestine in the mesentery as part of the vascular arcade that connects the SMA and IMA, from the ileocolic junction to the rectum. This artery is almost always present and its absence should be considered a variant.

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Tumour Site Caecum / Ascending colon

Surgery Right hemicolectomy

Hepatic flexure / transverse colon near hepatic flexure

Extended right hemicolectomy (B)

Mid-transverse colon

Transverse colectomy (C)

Transverse colon near splenic flexure

Left segmental colectomy (D)

Descending colon

Left hemicolectomy

Sigmoid colon

Sigmoid colectomy = High anterior resection

Structures Involved (Excision of structures + Division of vessels) Excision of caecum + ascending colon Ileocolic artery Right colic artery Right branch of the middle colic artery

Excision of caecum, ascending colon and proximal transverse colon Ileocolic artery Right colic artery Middle colic artery (at its origin)

Excision of transverse colon Middle colic artery

Excision of distal transverse colon and proximal descending colon Left branch of middle colic artery Left colic artery

Excision of descending colon Left colic artery Left branch of middle colic artery Inferior mesenteric vessels

Excision of sigmoid colon with variable length of upper rectum & distal descending colon Inferior mesenteric vessels

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High AR: margin above peritoneal reflection

16cm Upper 1/3 12cm: usually where peritoneal reflection sits Middle 1/3

Low AR: margin below peritoneal reflection

8cm Lower 1/3

Ultra low AR: anastomosis to the upper end of the anal canal

4cm Anal canal: 2-4cm

Anterior resection = Resection of IMA at its pedicle (with parts of the colon where it supplies – Sigmoid and Rectum) Not descending colon as the LMCA can extend its supply to it. I/O cases: SB-LB anastomosis better than LB-LB anastomosis - Because SB has more abundant and predictable blood supply - Dilated LB prox to obstruction will be edematous not suitable for anastomosis never do a left hemicolectomy (do right hemicolectomy/extended hemicolectomy) Principles of surgery for rectal carcinomas - En-bloc resection with adequate margins For rectal tumours a margin of 5 cm proximally and 2 cm distally is adequate (as it has been found that lymphatic spread of rectal tumours is predominantly in the proximal direction) Radial margins are also important as there is a zone of downward spread within the mesorectum (peritoneal investment of the upper rectum; just anterior to the sacrum) - Sphincter-sparing versus loss of sphincter The anal sphincter can be spared if the distal margin is >1-2cm above the level of the sphincter complex, usually taken to be at the level of the dentate line (which is 5cm above the anal verge) i.e. distal margin of the tumour must be >7cm from the anal verge Sphincter-sparing low anterior resection (below the peritoneal reflection); ultra low AR if just above the anal sphincter Sphincter-sacrificing surgery abdominoperineal resection (entire anus & sphincter complex is dissected, creation of an end colostomy) - Reconstruction Formation of a straight coloanal anastomosis in anterior resections is a/w poor function due to the lack of reservoir function 1. Creation of a colonic J-pouch using the proximal end of colon (the end of the colon is folded back on itself to form a J, and the two limbs opened and stitched together to form a pouch, the apex of the J being anastomosed to the anus) is associated with improved post-operative function 2. Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal colon is cut longitudinally but sewn transversely, widening the diameter at that segment to form a small pouch), done when there is difficulty creating the colonic J-pouch

- Mesorectal excision Proximal rectal tumours – 5cm distal margin of mesorectal excision Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the tumour Lower rectum tumours – total mesorectal excision required (complete excision of the intact visceral mesorectal tissue to the level of the levators)

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- Extended resections For locally advanced, adherent tumours (T4), multivisceral resection of organs involved (pelvic exenteration) is associated with improved local control and overall survival compared with standard resection, though high morbidity of 25-50% is associated Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease - Stoma creation A defunctioning loop ileostomy (or loop colostomy) is usually created during an low AR as the manipulation of the colon deep within the pelvic cavity causes increased risk of an anastomotic leak & also poorer blood supply to anastomosis A defunctioning stoma does not protect against anastomotic leak, but mitigates against disastrous complications of faecal peritonitis should a leak occur Closed in 2-6/12 after check with gastrograffin reveals no leak - Neoadjuvant chemoradiotherapy for rectal tumours Neoadjuvant RT with 5-fluorouracil can downstage tumour significantly ability to preserve sphincter, ability to resect previously unresectable tumour, reduce local recurrence Good evidence for ≥T3  tumours,  CRM risk of RT (esp. that pt becomes too ill to be operated on) Not possible for colon carcinomas due to risk of small bowel radiation if given above peritoneal reflection Done before Sx as ChemoRT requires blood supply to work (disrupted during Sx) - Surgical treatment according to stage Stage of disease

Treatment

T1

Involvement of submucosa, but no penetration 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

Invasion of other organs or involvement of free peritoneal cavity

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 II. Hereditary Non-Polyposis Colorectal CA (HNPCC) - Divided into Lynch syndrome I or Lynch syndrome II based on clinical features - Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure) - Tumours tend to arise from polyps which are commonly flat, with villous histology - Resultant tumour is often poorly differentiated - Lynch syndrome type II is associated with increased risk of cancer elsewhere, most commonly endometrial cancer, and also ovarian, gastric, small bowel, hepatobiliary, and renal pelvis/ureter cancers o Offer a THBSO with total colectomy if CRC detected - Diagnosis is based on the Amsterdam criteria – see above - Surveillance – 1-3yrly colonoscopy starting at 20 years old III. Ulcerative colitis - Screening – yearly colonoscopy starting after 10 years of UC

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3. STOMAS Stoma: opening of a luminal organ into the external environment Indications 1. For input: feeding (Percutaneous endoscopic gastrostomy) 2. For output: decompression/ lavage, defunctioning/ diversion, draining/ exteriorization (urine, faeces) Nursing intervention - Stoma nurse to perform counselling & discuss best site for stoma placement Stoma siting - Over the rectus sheath decreases the risk of prolapse, - Away from the surgical incision risk of wound contamination and infection - Away from skin creases or bony prominences stoma wafer can be flush with the skin (any gaps between skin and wafer leakage of fluid skin excoriation & infx) - Away from old surgical scars risk of hernia - Sited for easy accessibilty i.e. not under a large fold of abdominal fat - Intra-operatively, avoid tension over the stoma to marked site causes vascularity of the stoma stoma necrosis Types of stomas Permanent (end colostomy) - When patient or surgeon factors are against reversal of stoma (relative) - When no distal bowel remaining (absolute) After abdomino-perineal resection for Low rectal/ anal tumor After Panproctocolectomy without ileal pouch anal anastomosis Temporary - Decompression – relief of bowel obstruction causing proximal dilatation - Defunctioning – to reduce effects of anastomotic leak Esp. after low anterior resection, where risk of anastomotic leakage is high 2o to poor blood supply to anastomotic site Usually loop ileostomies or colostomies with 2 openings (ileostomies usually on the right side, colostomies in the epigastric/hypochondriac [transverse colostomy] or left side) - To rest an inflamed distal portion e.g.  acute  Crohn’s Colostomy (vs ileostomy) ?usually flushed with skin,  (vs  protrudes  3cm  ‘spout’,  as  ileal  contents  are  corrosive,  to  prevent  contact  with  skin) firm brown faceal output (vs watery greenish ilieal output) larger diameter of stoma (vs smaller diameter in ileostomy) Stoma Complications Early - Necrosis of terminal bowel (stoma appears dusky (grey black); check by intubating with a glass tube into the stoma to look at colour of mucosa) refashion stoma - Obstruction (fecal impaction explore with finger, enema / secondary to adhesion – more in ileostomy) - Leakage skin erosion, parastomal infection resite - Bleeding - Stoma diarrhoea (high output) correct water & electrolyte imbalance (hypoK), add anti-motility agent to thicken output (loperamide +/- codeine) http://www.wjgnet.com/1007-9327/7/741.asp Late - Prolapse of bowel refashion/refresh - Parastomal hernia (+ve cough impulse) refashion - Stenosis (unable to pass finger through) refashion - Retraction refashion - Fistulae - Skin excoriation - Psychological problems

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End colostomy

This procedure is most commonly performed to manage carcinoma of the lower rectum or anus, diverticular disease, and rare cases of faecal incontinence that do not respond to medical mx. For example, a very low rectal cancer will require resection of the rectum and anus (abdominoperineal excision of rectum). The remaining descending and sigmoid colon is mobilised and the cut end brought to the abdominal surface at an opening about 2 cm across. This is usually sited in the left iliac fossa.

Abdominoperineal excision of the rectum

If the anus, rectum, and a portion of the lower colon have not been removed, as in Hartmann's procedure, two outcomes are possible. In the first, the distal, non-functioning part of the colon and the rectum can be stapled or sewn closed and left inside the abdomen as a rectal stump. The proximal colon is then taken out as an end colostomy. Because the rectum has not been removed, the urge to have a bowel movement may occur. Mucus and some old stool, if present, will be passed. If the colostomy is temporary, a second operation is needed to reconnect the two ends.

Hartmann's procedure

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

Loop colostomy

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

End ileostomy

When the entire colon, rectum, and anus must be removed (panproctocolectomy) an end ileostomy must be employed. This occurs most commonly in severe ulcerative colitis but also in familial polyposis and some cases of colorectal cancer (for example, hereditary non-polyposis colorectal cancer). The ileum is resected just short of its junction with the caecum, and 6-7 cm of the small bowel is brought through the abdominal wall, usually in the right iliac fossa. It is everted to form a spout and then sutured to the bowel wall to protect the skin from the irritating content of the ileal fluid. After a panproctocolectomy the ileostomy is permanent. Temporary end ileostomy is often used after an emergency subtotal colectomy, which leaves part of the sigmoid colon and rectum left in place; for acute ulcerative colitis; acute ischaemic bowel; or neoplastic obstruction of the sigmoid .

Loop ileostomy

This type of stoma allows for defunctioning of an obstructed colon (in cancer), defunctioning of a distal anastomosis (after resection and primary anastomosis either as an emergency or after radiotherapy), or defunctioning of the anus (in incontinence or perineal involvement in Crohn's disease). Loop ileostomy has largely replaced loop colostomy because it is easier to site, less bulky, and easier to surgically close. A loop ileostomy has two openings, and most are temporary.

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End-loop ileostomy

This less commonly performed procedure is used when an end ileostomy cannot be fashioned safely because the patient is obese or because of unfavourable mesenteric anatomy. The formation of this stoma is similar to a loop ileostomy, but the efferent limb is short and blind ended. On inspection at the bedside this type of stoma is indistiguishable from a loop ileostomy.

Double barrel stoma

When the caecum is removed, the surgeon might create a double barrel stoma. In essence, this is an end ileostomy (small bowel) and a mucous fistula (the remaining colon) sited beside each other. On examination this will look almost identical to a loop ileostomy, however, closer inspection will show two separate stomas.

Urostomy

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

Stoma bags Stoma bags are of two main types. Single piece systems stick straight on to the patient's skin.

Two piece systems have a separate base (a flange) that sticks to the skin, and the bag attaches to this. This enables the bag to be changed wo removing the flange.

Some bags have a second opening at the bottom to allow emptying. These are most useful in the period immediately after operation and in patients who have had ileostomy, who need to drain their bag regularly. Closed bags are used when the faeces are well formed and are usually only changed once or twice a day. Most patients with a stoma will use an opaque bag, but in the period immediately after operation a transparent bag is used to observe the new stoma for complications such as persistent oedema or necrosis. Modern stoma bags are fitted with a carbon or charcoal flatus filter that allows gas to escape to prevent the bag from ballooning or detaching and neutralises odour. Complications Functional problems, such as skin excoriation and stoma noises, are the most common complications and are usually managed by the stoma nurse. Patients with stoma admitted to hospital with increased or decreased output should be appropriately managed to exclude any abdominal emergency, with particular emphasis on careful history taking to establish the normal bowel pattern, and attention to fluid balance. Most structural problems, such as stoma prolapse, retraction, and parastomal hernia formation can be managed conservatively with modified bags and specialised belts. Only about 10% of patients with these complications will require further surgery. Patients should be alert to any change in colour of their stoma. Stomal oedema is normal for several days after surgery, but if the mucosa becomes dusky or necrotic the surgeon should be contacted promptly.

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Question

Answer

Stoma

Where is the stoma?

Left iliac fossa

Most likely a colostomy

Right iliac fossa

Most likely an ileostomy

Flush with skin

Most likely a colostomy

Raised spout

Ileostomy; less commonly a urostomy

One

End colostomy; end ileostomy; urostomy

Two (adjacent)—efferent limb may be difficult to see

Loop colostomy; loop ileostomy; end-loop ileostomy

Two (separate stomas)

Most likely end colostomy with a mucous fistula; double barrel stoma; rarely bowel stoma and urostomy

Fully formed stool

Colostomy

Semisolid or liquid stool

Most likely ileostomy; colostomy

Urine

Urostomy

Mucus

Mucous fistula

How does the bowel lie in relation to the external skin?

How many lumens are present?

What are the contents of the stoma bag (don't be afraid to feel it)?

Examining a patient with an abdominal stoma and bag

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4. DIVERTICULAR DISEASE PATHOLOGY – acquired herniation of colonic mucosa through muscular wall, with a covering of colonic serosa TERMS - Diverticulosis coli – presence of acquired pseudodiverticula - Diverticular disease – symptomatic diverticulosis coli - Diverticulitis – inflammation of diverticula EPIDEMIOLOGY - Increases with age; up to 25% in >70YO (2-5% are 4 units of PCT c. Previous bleed

Indications for elective operation

1. Stricture 2. Fistula 3. Recurrent attacks – occurs in 30% of patients after 1st episode. a/w higher mortality & complication rates 4. Young patientss 70%) & to drink lots of fluid, weight reduction and exercise Recurrent diverticulitis after surgical treatment - incidence ranging from 1% to 10%. - In general, the progression of diverticular disease in the remaining colon is approximately 15%. - Important factors to be considered in terms of surgery are the adequacy of resection, meaning the degree of proximal resection and level of distal anastomosis. The use of the rectum as the distal margin decreases the rate of recurrence. - Care also must be taken to exclude other components of differential diagnosis, especially irritable bowel syndrome, inflammatory bowel disease, and ischemic colitis.

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

Bowel involvement Location

Crohn’s

Ulcerative colitis

Can affect entire GIT anywhere from mouth to anus, but usually affecting the terminal ileum

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

40% terminal ileum 30% small intestine 30% colon 3% anorectal (usu. spared)

40% rectum alone 40% left colon 20% total colitis Backwash ileitis (10%) – 30cm of ileum affected due to incompetent ileocecal valve causing reflux of noxious inflammatory mediators

Continuity

Not continuous, with skip lesions

Longitudinal mucosal continuity

Complications

Strictures, fistulae, sinuses, malnutrition (SB involve), SB obstruction, toxic dilatation, CRC

These complications absent. Massive PR bleed, toxic megacolon, venous thrombosis, CRC ++

Histopathology

Macroscopic: bowel is thick-walled & nodular (cobblestone appearance) with creeping fat, mesenteric thickening & deep linear ulcers Microscopic: transmural involvement, non-caseating granulomas (pathognomonic, but only present in 2/3)

Macroscopic: granular appearance of mucosa , loss of vascular markings, pseudopolyps interspersed with areas of shallow ulceration Microscopic: only mucosal & submucosal involvement, ulcers, crypt abscesses - Muscularis propria & serosa may be affected in fulminant disease

Risk of carcinoma

Slight increased risk of colorectal Ca, increased risk of small bowel lymphoma

Substantially higher risk of CRC 2% at 10 years 8% at 20 years (15% if pan colitis) 18% at 30 years Much higher risk with concomitant PSC

Associated Ab

ASCA: anti-saccharomyces cerevisiae antibodies

p-ANCA: perinuclear antineutrophil cytoplastic ab

Severity

Harvey Bradshaw severity index

Modified Truelove & Witts severity index (Mild, moderate, severe, fulminant)

Epidemiology Bimodal distribution: affects young in the 2nd & 3rd decades of life, with second onset in the 5th & 6th decades of life Equal gender predominance Higher prevalence amongst Ashkenazi Jews & in cooler climates e.g. Scandinavia, UK, Germany, northern USA Genetic association History GIT: abdominal pain, diarrhea, N/V, bloating, distension, bloody stools with mucous & pus Crohn’s  fistula:  colovesical fistula or coloovarian fistula: faeces in urine/ pneumaturia, faeces per vaginal/ PID Non-specific systemic: LOW, LOA, fever, fatigue, symptoms of anemia, chronic malnutrition Specific extra-intestinal manifestations Physical examination: usually normal +/- extra-intestinal manifestations Acute severe: fever, tachycardia, tender/distended abdomen. Nutritional deficits. Extraintestinal: clubbing, oral ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis/episcleritis/iritis, arthritis/sacroilitis/AS, fatty liver. Differential diagnoses 1) Gastroenteritis: exclude with stool microscopy & culture + C.diff toxin Bacterial: E. coli, Campylobacter, Salmonella, Shigella, C. difficile Parasitic: E. histolytica Viral: rotavirus 2) Other infective causes: diverticulitis, colorectal TB 3) Ischaemic colitis 4) Bleeding diverticulosis 5) Colorectal carcinoma

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CROHN’S DISEASE P/E: RIF mass, perianal enlarged skin tags/ fistula/ abscesses, anal stricture Investigations: supportive (see UC) & diagnostic Diagnostic (mainly at terminal ileum) Contrast radiographic studies: assess location & extent of disease, look for strictures & fistulae o Barium studies: small bowel series & enema (cobblestone) o CT scan with oral & IV contrast Endoscopy: look for typical features o Colonoscopy with tissue biopsy (non-caseating granulomas) o OGD: upper GIT involvement o Endoanal U/S (EUS): identify fistula tracts Management Medical (principle treatment) o Nutritional support e.g. TPN (may also aid closure of fistulae) o Pharmacological Corticosteroids for acute exacerbation of disease, but not for long term use 1st line: 5-ASA or 5-aminosalicylic acid (sulfasalazine, mesalazine) induce & maintain remission of disease: oral, rectal suppository or enema (up to splenic flexure) 2nd line: immunosuppressive agents e.g. azathioprine, 6-MP, MTX, Tacrolimus & cyclosporine when 1st line agents ineffective o Cyclosporin and Tacrolimus are nephrotoxic avoid LT Biologics = created by biologic processes, rather than being chemically synthesized. - Ind: for steroid resistant - Remicade (infliximab) = TNF blocker - ACT 1 and ACT 2 (Acute ulcerative Colitis Treatment) trials showed that 44-45% of patients treated with infliximab for a year maintained a response to the medication, cf 21% on placebo - Pretreatment: rule out TB, hepatitis first (as tx can cause reactivation) - Require close surveillance for SE (blood disorders, infections, lymphoma & solid tissue cancers, hepatotoxicity, drug-induced lupus, demyelinating disorders) Surgical o Principles Avoid surgery until absolutely necessary (80% require surgery within 20 years of onset) & when indicated perform bowel preserving surgery as repeated bowel resections can lead to short gut syndrome o Indications : Disease refractory to medical therapy (common) Serious complications of medical therapy Severe bleeding, perforation Intestinal obstruction due to strictures o

Fistulae Abscesses Toxic megacolon Malignancy

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

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ULCERATIVE COLITIS Extra-intestinal manifestations (20% of patients) Joints (most common) o Transient asymmetrical polyarthritis: mirrors course of colitis & is cured by colectomy o Ankylosing spondylitis o Isolated sacroiliitis Liver o PSC  (5%):  fibrous  structuring  of  entire  biliary  tree:  ↑  ALP,  MRCP,  ERCP,  liver  biopsy.  Tx:  stenting, transplant o Hepatic failure over 5-10 years independent of course of colitis o ↑  risk  of  cholangiocarcinoma  &  ↑↑↑  risk  of  colorectal  carcinoma Eye o Iritis, episcleritis, anterior uvetitis. Tx: topical and/or oral corticosteroids Skin o Pyoderma gangrenosum: deep ulceration with violaceous border that overhangs ulcer bed, usually affecting LL o Erythema nodosum: poorly defined, tender, erythematous nodules tt do not ulcerate/ suppurate, usu on the shin o Tx: corticosteroids, will improve slowly following colectomy Investigations Supportive (looking for complications & assessing severity of disease) Blood tests o FBC: anemia, leukocytosis & thrombocytosis indicate more severe disease o UECr: hypokalemia & dehydration in prolonged diarrhoea o LFT: hypoalbuminemia due to poor nutritional intake o CRP, ESR: markers of severity o Autoantibody assay: p-ANCA  ↑  in  UC,  ASCA  ↑  in  CD Radiological o AXR to evaluate colonic caliber (>6 cm is abnormal) o CXR to rule out perforation (risk of perforation in acute disease) Diagnostic (mainly at rectum) Endoscopy: look for typical features o Flexible sigmoidoscopy with tissue biopsy: bleeding may occur with contact with scope. Never do barium enema during a severe acute attack or as a diagnostic test?? Management Medical:  similar  to  Crohn’s  disease o Mild: PO pred + Mesalazine. If distal dz: Pred retention enema/ steroid foam. If no improve after 2/52 mod. o Mod: PO pred (40mg/d x1/52 30mg/d x 1/52 20mg/d x 4/52) + 5-ASA + steroid enema BD. If no improve after 2/52 severe. o Severe: IV Hydrocort400mg/d + rectal steroid. If improve in 5/7 PO pred + 5-ASA. If CRP >45/ >6 stools per day ciclosporin/infliximab/Sx. Surgical (25% eventually require surgery) o Indications : 1. Disease refractory to medical therapy with severe & extensive colitis (most common) 2. Serious complications of medical therapy 3. Severe bleeding 4. Perforation 5. Toxic megacolon (colon > 6cm): most common cause of death - Involvement of the muscularis propria in the most severe cases can lead to damage to the nerve plexus, resulting in colonic dysmotility, dilation, and eventual infarction and gangrene 6. Malignancy o Procedure (laparoscopic or open) Acute setting (uncontrolled bleeding, perf, toxic megacolon, fulminant attack): total colectomy with end ileostomy: diseased rectum left in-situ with resection & IPAA at later date when patient has regained health & steroids have been withdrawn (as rectum is extraperitoneum organ and dissection/resection takes a long time). Foley catheter used to decompress rectum for 3-4 days IPAA (ileo-pouch anal anastamosis): standard of care for patients with UC who ultimately require colectomy. Avoid necessity  for  long  term  stoma.  Crohn’s  disease  remains  an  absolute  contraindication  as  overall  failure  rates   approach 50% Alternative: Total proctocolectomy with end ileostomy o Complications: o Mortality 2-7%, 50% if perforation o Pouchitis: Tx with Abx (metronidazole + ciproflox X 2/52) + immunosupp.

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8.

ANAL & PERIANAL DISORDERS

1. HAEMORRHOIDS Anal cushions.They are clusters of vascular tissue (eg, arterioles, venules, arteriolarvenular connections), smooth muscle (eg, Treitz muscle), and connective tissue lined by the normal epithelium of the anal canal. External hemorrhoids develop from ectoderm Internal hemorrhoids develop from endoderm

covered by squamous epithelium columnar epithelium of anal mucosa.

External hemorrhoids are innervated by cutaneous nerves that supply the perianal area. These nerves include the pudendal nerve and the sacral plexus. Internal hemorrhoids are not supplied by somatic sensory nerves and therefore cannot cause pain - internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids. Internal hemorrhoids can also cause acute pain when incarcerated and strangulated Internal hemorrhoids drain through the superior rectal vein into the portal system. External hemorrhoids drain through the inferior rectal vein into the inferior vena cava. Rich anastomoses exist between these 2 and the middle rectal vein, connecting the portal and systemic circulations. Causes: 1. Decreased venous return / increase intra abd pressure: preg, constipation (low fibre diet) 2. Portal hypertension and anorectal varices 3. Increase rectal vein pressure: obesity, prolonged sitting

straining

The most common presentation of hemorrhoids is rectal bleeding, pain, pruritus, or prolapse. Painless fresh PR bleeding after defecation: coating / dripping, not mixed with stools Most symptoms arise from enlarged internal hemorrhoids. Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation. External hemorrhoids cause symptoms in 2 ways. Acute thrombosis: usually related to a specific event, such as physical exertion, straining with constipation, a bout of diarrhea, or a change in diet. Pain results from rapid distention of innervated skin by the clot and surrounding edema. The pain lasts 7-14 days and resolves with resolution of the thrombosis Occasionally erode the overlying skin and cause bleeding External hemorrhoids: not true hemorrhoids, but rather painful thrombosed veins arising distal to the dentate line Internal hemorrhoids: those arising proximal to the dentate line, usually painless unless prolapsed & strangulated Complications:

thrombosis, infection, prolapse

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Classification & Treatment Grade 1

Conservative: Lifestyle modifications Meds (Daflon) – improves venous tone

Hemorrhoid protrudes into the anal canal but does not prolapse outside the anus, hyperaemia of mucosa

Grade 2

Surgery: Rubber band ligation Injection sclerotherapy (phenol emoilent oil)

Hemorrhoid protrudes through the anus during straining or evacuation but returns spontaneously

Grade 3

Surgery: Haemorrhoidectomy Staple Excision

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

Grade 4 Hemorrhoid remains prolapsed outside the anus

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2. ANAL FISTULA Anal fistulae are abnormal communications, hollow tracts lined with granulation tissue connecting the primary opening inside the anal canal to a secondary opening in the perineal skin. They are usually associated with anorectal abscesses (obstruction of ducts infection). Conditions associated with multiple anal fistulas: 1. Crohn’s  disease 2. TB 3. Actinomycosis 4. Hydra-adenitis suppurativa GOODSALL’S LAW

Posterior ½: (All fistula tracts with external openings within 3 cm of the anal verge and posterior to a line drawn through the ischial spines)

Curvilinear Internal opening in posterior midline (at level of dentate line) Anterior ½: Straight tracts Tracts closer to anal verge = simpler, shorter Tracts further away = transphincteric, long, high tracts

INVESTIGATIONS Endoanal U/S (H2O2 aided for hyperechoic effect) – to view course of fistula tract MRI – able to visualise entire pelvis, beyond the sphincter complex CT/fistulography (in emergency situation) – for complex fistulas / unusual anatomy

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CRYPTOGLANDULAR THEORY OF PARKS / PARKS CLASSIFICATION Type

Diagram

Intersphincteric

Management Fistulotomy Division of the internal sphincter alone usu does not compromise fetal continence Base of the wound is curetted and left open to heal by secondary intention

The common course is via internal sphincter to the intersphincteric space and then to the perineum. 70% of all anal fistulae Other possible tracts include no perineal opening, high blind tract, and high tract to lower rectum or pelvis. Transsphincteric

Low: Fistulotomy On pts who have good pre-op anal sphincter function

The common course is low via internal & external sphincters into the ischiorectal fossa and then to the perineum. 25% of all anal fistulae Other possible tracts include high tract with perineal opening and high blind tract

High / anterior fistulae in women: (Higher risk for post-fistulotomy incontinence)

Conservative approach

Suprasphincteric

1.

Cutting seton Reactive suture / elastic placed through the fistula tract Tightening of seton tie sequentially until it cuts through the fistula tract

2. 3.

Partial fistulectomy & endoanal flap Injection of fibrin glue

Cutting setons Endorectal advancement flap

The common course is via intersphincteric space superiorly to above puborectalis muscle into ischiorectal fossa and then to perineum. 5% of all anal fistulae Other possible tracts include high blind tract (ie, palpable through rectal wall above dentate line). a/w drainage of ischiorectal abscess

Sphincter reconstruction

Extrasphincteric

Endorectal advancement flap Laparotomy & resection of involved intestinal segment and curettage of fistula tract (for those fistulae from more proximal sections of the colon)

The common course is from perianal skin through levator ani muscles to the rectal wall completely outside the sphincter mechanism. 1% of all anal fistulae Not related to sphincter complex a/w  Crohn’s,  CA,  recurrent  fistulas

Fistulotomy (for simple, short tracts) – cut & lay open tract Fistulectomy – core along tract & remove tract entirely Seton – for complex, long, high tracts

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4. ANAL FISSURES

An anal fissure is a painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. Most will heal because of good blood supply (within 1 day / 2 days) If  they  don’t  heal:  usu  due  to  spasm  of  internal  sphincter  muscle Features of a chronic anal fissure: 1. Boat shaped 2. Punched out 3. Exposing internal sphincter 4. Sentinel skin tag 5. Hypertrophic anal papilla MANAGEMENT Definitive for chronic anal fissure Internal anal sphincterotomy (but do not cut through muscle – irreversible) Medical sphincterotomy (reversible): GTN paste, botulinum toxoid injections

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9.

LIVER DISEASES

1.

ANATOMY OF THE LIVER The liver is divided into two lobes, right and left The anatomical division of the liver lobes is demarcated by the falciform ligament The functional division (more practical in surgery) is demarcated by the plane of the gallbladder and inferior vena cava (also by the plane in which the middle hepatic vein runs) impt for reading CT scans and in surgery The liver can be further divided into 8 functional segments (Couinaud segments) that each have their own vascular inflow, outflow, and biliary drainage, independent of the other segments

Segments divided by 1 transverse plane and 3 sagittal planes The transverse plane is at the level of the main branches of the portal vein (divides liver into upper half and lower half) The sagittal planes are formed by the three main hepatic veins (right, middle and left) Segment I is the caudate lobe Segments II to VIII are named clockwise, while facing the patient, starting from the upper right corner (i.e. the upper left segment of liver) Segment IV can be further divided into IVa and IVb, where IVa is the superior and IVb is the inferior subsegment The liver has two blood supplies – portal vein (formed from the joining of the splenic vein and superior mesenteric vein) and hepatic artery (a branch of the coeliac trunk) Drainage is via the 3 hepatic veins into the inferior vena cava 2.

CAUSES OF HEPATOMEGALY Vascular: RHF, TR, Budd-Chiari syndrome Infective: viral (hepatitis viruses, EBV, CMV, HIV), bacteria (pygenic abscess, TB), parasite( amoebiasis, hydatid cyst, malaria) Metabolic:  fatty  liver,  haemochromatosis,  amyloidosis,  wilson’s  disease Tumour: see below

3.

CAUSES FOR A LIVER NODULE ON IMAGING

Benign

Cyst Haemangioma

Malignant

Adenoma Fibronodular hyperplasia Secondary Primary

-

Single Multiple – familial (polycystic) or non-familial Small Big

Colorectal, stomach, pancreas, breast, urogenital tract, lung Hepatocellular carcinoma (or hepatoblastoma in children) Cholangiocarcinoma (only 10% intrahepatic) – presents like HCC except no background of cirrhosis

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4. HEPATOCELLULAR CARCINOMA EPIDEMIOLOGY -

Annual incidence in Singapore is 18/100,000 in males, and 4.6/100,000 in females 3rd most cancer among males, overall 4th most common cancer Men: female = 3:1 Peak age of onset: 30-40 years old 1o liver cancers are mainly HCCs (85%), with a small proportion of intrahepatic cholangiocarcinoma (6%)

AETIOLOGY AND RISK FACTORS 1. Hepatitis B infection (high HBV DNA load, HBeAg positivity increase the risk) – 100X normal population 2. Hepatitis C infection 3. Cirrhosis (of which cirrhosis resulting from hep B, hep C and haemochromatosis are associated with the highest risk): 20-30years following initial insult - Others:  Aflatoxin  ingestion,  α-1- antitrypsin deficiency, haemochromatosis, PBC, anabolic steroids, schistosomiasis Non-cirrhotic HCC – 5% in west, 40% in Asians PATHOLOGY Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular damage with high cellular regeneration, which leads to rates of genetic mutation in the cells and accumulation of these mutations leading to carcinoma formation - Two histological subtypes: Nonfibrolamellar – associated with HBV and cirrhosis Fibrolamellar – associated with younger patients, more common in females, no association with hep B or cirrhosis, AFP usually normal, 70% resectable, good prognosis - Metastasises to lymph nodes, bones, lungs and adrenals (more common in intrahepatic lesions >5cm) -

PRESENTATION HCC is frequently diagnosed late in its course because of the absence of pathognomonic symptoms and the liver's large functional reserve. 1. Asymptomatic - During screening (ultrasound) for chronic hepatitis B carrier - Investigations for liver cirrhosis (esp with rising AFP levels) - Incidentally found on imaging of the abdomen 2. Local signs & symptoms 1. Upper abdominal pain - 2o to a. hemorrhage internally capsular distension or externally b. necrosis c. infection 2. Early satiety/ vomiting (likely 2o to compression) 3. Pyrexia (central tumour necrosis) 4. Hepatomegaly 5. Constitutional: LOW, LOA, malaise 6. Budd-Chiari syndrome: occlusion of hepatic, intrahepatic or portal vein causing portal HTN & congestive hepatopathy 7. Jaundice (5-10%) a. Cholestatic (conjugated): invasion/ compression of intrahepatic ducts or extrahepatic compression by metastatic LN b. Hepatic (unconjugated): a/w pre-existing cirrhosis or acute flair of chronic hepatitis 3. Tumour rupture (15% remains after 15 minutes, the patient cannot tolerate major liver resection (>3 segments removed) - CT volumetry: residual liver function calculated with a CT liver scan via a computer program - If  patient  has  cirrhosis,  assess  the  Child’s  status   only Child’s A and good Child’s B can be considered for resection Child-Pugh classification of CLD/ cirrhosis 1) Prognosis 2) Strength of medical treatment 3) Necessity of liver transplant Child’s 1 year survival % 2 year survival % Disease status Treatment in concomitant HCC

Points Albumin (g/L) Bilirubin  (μmoles/L) Coagulopathy = PT Distension (ascites) Encephalopathy A(5-6) 100 85 Well compensated disease Resection of up to 4 segments

1 >35 < 35 2.20 Severe/refractory Grade III-IV

C( 10-15) 45 35 Decompensated liver dz, consider transplant Consider transplant

4. Residual liver function post-operatively (at least 20%) - Dependent on tumour size and how much of the liver it takes up, because tumour is non-functional - A large tumour taking up most of the liver segments being resected translates to smaller amount of functional liver tissue being resected, while a small tumour means that more functional tissue is removed with the same resection margins 5. Degree of portal hypertension (= hepatic vein pressure grad >10mmHg) - Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has decreased increased resistance to flow - Detected during hepatic vein catheterization. Not necessary if clinically sig portal hpt: varices, ascites requiring diuretic therapy, plt75% 5-year survival if followed) (a) Single tumour 5cm or smaller, or 3 or less tumours none larger than 3cm (b) No evidence of gross vascular invasion (c) No regional nodal or distant metastasis - Problems with availability of donor organ – the disease might have progressed past being suitable for transplant by the time donor organ is available Possibility of “bridging therapy” (radiofrequency ablation) to shrink disease & slow progression until donor liver available - In hepatitis B carriers, there is a risk for reinfection of the donor liver (high risk factors are HBeAg positivity, high HBV DNA levels) – can be aggressively treated with anti-viral drugs 2 months before transplant and anti-HBV immunoglobulin long-term after transplant PALLIATIVE THERAPY 1. Loco-regional ablation (a) Radiofrequency ablation (RFA) – best results for locoregional strategies (b) Percutaneous ethanol injection – ethanol kills HCC cells but more painful (c) Cryotherapy 2. Intra-arterial therapy (a) Transarterial chemoembolisation (TACE) (b) Transarterial embolisation (TAE) (c) Selective Intrahepatic Radiation – Yttrium-90 radioactive beads 3. Systemic therapy – limited results; Sorafenib imporves median survival by 3/12

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SCREENING FOR CHRONIC HEPATITIS CARRIERS - Target pop: Hep B / C carriers, Cirrhosis, FHx of HCC, Patients on transplant waiting list (transplant priority if HCC dev, detect HCC tt exceeds transplant guidelines) - Combination of 6/12 to yearly Ultrasound + AFP levels - US is operator dependent & may miss certain areas of the liver where imaging is difficult, but it is not associated with radiation exposure. (sensitivity 65-80%, specificity 90%) Features suggestive of HCC include poorly-defined margins and coarse, irregular internal echoes. Small tumors are often hypoechoic. As the tumor grows, the echo pattern tends to become isoechoic or hyperechoic, indistinguishable from surrounding liver. Added benefit of assessing patency of the hepatic blood supply and the presence of vascular invasion by the tumor. - AFP is also not a perfect screening test as 20% of HCC will not have raised AFP - Thus the combination of ultrasound and AFP can increase the sensitivity and specificity of screening

- Frequency of screening is controversial, but should be increased in patients at increased risk – HbeAg positivity, high HBV DNA levels Frequency determined by tumor growth rate, not by the degree of risk. - Important as it detects smaller and resectable HCCs increasing survival from 26 to 88/52 - Screen family for chronic hepatitis B carrier status especially if there is a family history! – e.g. mother had hep B/HCC, sibling has hep B, etc - Alternatives: des gamma carboxy prothrombin (DGCP aka PIVKA II) – potential marker of portal vein invasion by tumor

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5. LIVER METASTASES - Still more common than primary liver tumour for malignancy occurring in the liver - Primaries: Colorectal, gastric, pancreatic, urogenital, breast, lung PRESENTATION DEPENDS ON SITE OF METASTASIS Mets to liver parenchyma - Incidentally found on follow up (for cancer) - Hard mass - Heaviness - Pain from rupture

Mets to porta hepatis LN - 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 usu hypovascular compared to hypervascular HCC; spread via portal vein) - Increasing contrast uptake on portal venous and delayed phases ROLE OF SURGERY -

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

6. LIVER HAEMANGIOMA EPIDEMIOLOGY - Prevalence 0.4-20% - Female to male ratio 3:1 PATHOGENESIS - Vascular malformation that enlarges by ectasia, congenital in origin PRESENTATION 1. Usually small and asymptomatic, found incidentally 2. Mass effects compressing on surrounding organs 3. Pain from liver capsule stretch 4. Rupture (3cm – open drainage or percutaneous aspiration

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Percutaneous aspiration - 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

Open drainage - 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

9. ASCITES Vital signs on examination: o Abdominal distension o Flank dullness shifting dullness fluid thrill o Peripheral stigmata of chronic liver disease and portal HPT o Other signs of fluid overload: LL, sacral oedema, bibasal crepitations o Signs of malignancy Background information Causes of ascites: Transudate (30g/L) 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 sx (TIPSS, peritoneovenous shunt [silastic catheter], Denver shunt when with a subcutaneous pump]

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10.

PANCREATIC DISEASES

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

CAUSES (I GET SMASHED)

Infx: mumps, VZV

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

Drugs: Alc, Steriods, SAND Idiopathic (up to 10%) Gallstones most common: >90% combined Metabolic: hyperlipidemia, hypercalcemia Ethanol Autoimmune: SLE, PAN Trauma – penetrating > blunt trauma Steroids Neoplastic: Ca head of pancreas Mumps and other infx (VZV, Coxsackie, EBV, measles, echovirus, ascaris, Congenital: CFs, Pancreas divisum mycoplasma, salmonella, campylobacter, MTB) 7. Autoimmune – SLE, PAN 8. Scorpion toxin Severe), hypothermia 9. Hypercalcaemia, HyperTG (>1000 mg/dL, T1 and TV 10. ERCP (4%) - aggressive preintervention intravenous hydration to prevent 11. Drug-induced usually mild (SAND: Sulphonamides/ azathioprine/ NSAIDs/ diuretics, HCTZ, metronidazole, nitrofurantoin, procainamide, chemo (esp asparaginase, cisplatin), cimetidine, diphenoxylate, estrogen) 12. Rare causes: Cystic fibrosis, cancer of the head of the pancreas, pancreas divisum (failure of the dorsal and ventral pancreatic ducts to fuse during embryogenesis), Sphincter of Oddi dysfunction

Gallstone: usu very small stones due to edema at the ampulla as stone passes into duod (no stone in 80% suggesting stone passage)

increases pancreatic duct pressure

The disease develops in pts whose alcohol ingestion is habitual over 5-15 years. Alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis. Occasionally, however, pancreatitis can develop in a patient with a weekend binging habit. PATHOPHYSIOLOGY - The initiating event may be anything that injures the acinar cell and impairs the secretion of zymogen granules Gallstones: obstruction of the pancreatic duct causing interstitial oedema which impairs blood flow to the pancreatic cells ischaemic cellular injury predisposition to enzyme activation It is believed alcohol itself results in injury to pancreatic cells through generation of free radicals during its metabolism, and may sensitise the pancreas to injury by other agents - The final common pathway inappropriate activation of proenzymes stored within zymogen granules in the pancreatic cell (trypsin activates most of the proenzymes secreted by the pancreas when they are secreted into the duodenum) - The activated lytic enzymes destroy the pancreatic acinar cells macrophages themselves secrete pro-inflammatory cytokines

release of potent cytokines that attract neutrophils and

- 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

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PRESENTATION - Symptoms (generally non-specific): Abdominal pain (most consistent, in >90% of patients) – constant epigastric pain, classically radiating to the back (in 50%), maximal intensity within several hours of onset; usually occurs after a heavy meal; alleviated by sitting up & leaning forward, worse on movement Nausea, vomiting, Anorexia Also rule out other causes: Gastric causes: PUD Perforated viscus (mainly on examination: look for peritonism) AMI, DKA or even a lower lobe pneumonia Hepatitis or GB / CBD disease Ask for causes of pancreatitis: Gallstone disease: biliary colic, symptoms of cholecytitis/ CBD stone/ cholangitis Recent alcohol abuse or chronic alcohol abuse Recent blunt trauma or ERCP done PHx or hyperlipidemia, hypercalcemia, autoimmune disease (SLE, PAN) Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling) Recent drug history: steroids, NSAIDs, diuretics - Signs (also non-specific) Tachycardia, low grade fever, low BP, toxic looking, jaundiced? Epigastric tenderness, signs of peritonism (130/min, Hypotension 50 - Presence  of  Gray  Turner’s/Cullen’s  sign - Oliguria 55 yrs >16x109/dL >11.2mmol/L >600U/L >120U/L

- Pancreatic or peripancreatic necrosis - A/w organ failure or local Cx - Any 1 of the following Ranson’s  3 or more APACHE II 8 or more (within 1st 48hr) Organ failure (RT, CVS, Renal, BGIT) Local Cx (pancreatic necrosis, abscess, pseudocyst)

Within 48 hours of admission 1. Fall in Hct >10% 2. Rise in urea >0.9mmol/L 3. Calcium 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 III. Glasgow/ Imrie score- PANCREAS 1. PaO2 55yrs 3. Neutrophil/WBC >15x109/dL 4. Calcium 16mmol/L 6. Enzymes LDH >600U/L AST >100/L 7. Albumin 10mmol/L

>3 criteria

severe

- Preferred  over  Ranson’s  scoring  in  certain  centres - combine with CRP IV. C-reactive peptide - As a single prognostic marker; 210mg/dL at 48 hours, the pancreatitis is more likely to be severe - No relevance >3/7 of onset as other confounding factors come into the picture - Combination of Glasgow score and CRP improves overall prognostic value V.  Balthazar’s  CT  severity  index  (consider  a  CT  AP  @  ~  3/7  from onset) - Grades severity of disease according to CT findings detects  h’ge  &  necrosis - Not very useful as CT is not usually done in the 1/52 in local context, and disease is still evolving (CT findings lag behind) in the early stages 1. A - Normal 2. B - Enlargement 3. C - Peripancreatic inflammation 4. D - Single fluid collection 5. E - Multiple fluid collections: 50% chance of developing an infection and a 15% chance of dying

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COURSE OF DISEASE - 75%: mild course of disease; recover unless comorbidities cause deterioration -------Deterioration from mild to severe very rapid!------ 20-25%: severe outcome (Acute necrotizing pancreatitis 15%) 1/3 of these patients will ultimately die - Overall mortality rate 8mm (impt to identify dilated INTRAhepatic ducts as it indicates that (a) obstruction is more severe (b) PTC is a possible option if ERCP fails) ii. Gallstone disease / Cholecystitis: GB stones or sludge, thickened GB wall, pericholecystic fluid, fat stranding iii. Complications of gallstones: iv. Liver consistency (fatty or cirrhotic) b. Disadv: i. Unable to detect malignancy well ii. Unable to detect distal CBD stones well iii. Sensitivity reduced with fat patient habitus iv. Operator dependent CTAP: a. Indications i. Suspected perf oratedGB (view air ard GB in lung window) ii. Rule out malignant etiology b. Adv i. Preferred if there is a suspicion of malignancy (Ca pancreas or periampulary cancer) define the tumour (T) better & stage at the same time (N & M) ii. Logistics (can be done earlier esp cholangitic patient to plan for early intervention) CXR a. ARDS in cholangitis b. Pleural effusion

MANAGEMENT The patient is managed as for the causative aetiology (see relevant sections)

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3. GALLSTONE DISEASE DEFINITION Gallstone is a generic term for any kind of stone (cholesterol, pigment) in any part of the biliary system (gallbladder, cystic duct, hepatic duct, common bile duct, etc) EPIDEMIOLOGY - Exact incidence in Singapore not known - In the West: overall 10-15%; 20% in women and 10% in men - Consistent 2:1 female to male ratio, 1:1 in elderly - Typical  picture  (the  5  F’s):  Fat, female, forty, fertile, flatulent – refers to cholesterol stones but no longer applies. NORMAL PHYSIOLOGY OF BILE - Normal bile contains bile salts (primary and secondary), phospholipids, cholesterol, protein, and bilirubin - Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol (in micelles, vesicles) - a/w simple refined sugar in diet STONE COMPOSITION AND PATHOPHYSIOLOGY 1. Cholesterol: cholesterol - hard and faceted 2. Black: mostly calcium salts and bilirubin - soft stones and crumble easily 3. Brown: calcium salts, bilirubin, and more cholesterol than black pigment stones Cholesterol stones - More common in older (peak at 40-50 years) but increasing in younger - Developed countries – 22% of SG population (18% with signs and symptoms) - M=F - From disruption in the solubility equilibrium of bile. 1. Increased cholesterol secretion in bile old Obesity, rapid weight loss Hyperlipidaemia Increased oestrogens: female, pregnancy, exogenous administration 2. Decreased emptying of the gallbladder Gallbladder malignancy is an important cause to exclude Gallbladder stasis: Truncal vagotomy, Spinal cord injury Pregnancy Fasting, TPN Pigment stones - bilirubin - More common in younger patients, developing countries a)

b)

Black pigment stones: a. increased secretion of bilirubin into bile (e.g. chronic HAEMOLYSIS, - most commonly G6PD-def, CIRRHOSIS, chronic liver disease, TPN), b. decreased bilirubin solubilisers, and gallbladder stasis Brown stones: = RPC!!! Form in the biliary ducts due to infection with bacterial degradation of biliary lipids (hydrolyse conjugate bilirubin to free form), the degradation products of which then precipitate as calcium bilirubinate. Increasing in incidence due to influx of foreign workers.

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

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CLINICAL COURSE Asymptomatic

Leave alone

- 80-95% of patients - Risk of symptom occurrence = 1 to 2% per year greatest risk in first 5 years of diagnosis – 10% at 5 yrs, 15% at 10 yrs, 18% at 15-20 yrs 7-10% mod, 3-5% severe; the rest minor symptoms majority do not require removal of the stones or the gallbladder = expectant mx (Risks of Sx > Risks of doing nth) - Role of surgery: [3] (a) Suspicious / high risk of MALIGNANCY (causing gallbladder stasis stones) eg. susp gallbladder mass, gallbladder polyp, porcelain gallbladder prophylactic surgery (b) IMMUNOCOMPROMISED presentation is abnormal & difficult to detect (c) Patients with CHRONIC HAEMOLYTIC DISEASE (e.g. sickle cell anaemia, thalassaemia) – as high as 50-60% will develop symptomatic disease in their lifetime Symptomatic sequlae 1. Biliary colic (15%) - Location: epigastric (70%) or RHC pain - Radiation: inferior angle of the right scapula, tip of right shoulder or interscapular - Character: NOT a true colic: Waxing-waning in character but rarely have any pain-free intervals between waves of pain (Basal pain is due to inflm of ductal epithelium & proximal distension) - CBD is not muscular, so absence of biliary colic, but a constant pain with OJ 2o to obstruction - Duration: minutes to 2 hours, often resolves spontaneously (if >6hrs, susp complication eg. cholecystitis) - Trigger: meals – binge-eating, fried oily foods, dehydration - Associated: N/V (patient gets better after vomiting), bloating, abdominal distension Biliary  colic  is  a  “herald”  symptom  that  indicates  risk  of  further  sequelae. 2. Infection

i. Acute / Chronic cholecystitis ii. Cholangitis iii. Pancreatitis

3. Gallstone dyspepsia: (non-ulcer dyspepsia) fatty food intolerance, dyspepsia and flatulence not due to other causes Complications 4. Choledocholithiasis with obstructive jaundice 5. Mirizzi syndrome with obstructive jaundice (see below) 6. Mucocoele of the gallbladder / Hydrops / Empyema of Gallbladder (see below) 7. Fistulation and gallstone ileus (see below) 8. Porcelain gallbladder: due to calcium salts ppt in GB wall. Calcium secreted into lumen of hydropic GB 9. Gallbladder CA

‘limey’  bile.

INVESTIGATIONS FOR GALLSTONE DISEASE Plain abdominal X-ray - Pickup rate for gallstones is less than 10% since most stones are radiolucent 1. Ultrasound of the hepatobiliary system - Investigation of choice for gallstones - >92% sensitivity, 99% specificity - Even more sensitive than CT scan for stones since CT may miss small stones due to the spacing of the cuts taken - Features of stone on ultrasound: strong echogeneic rim around the stone, with posterior acoustic shadowing - Bile should appear as black patch in gallbladder; if not homogeneous sludge

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2. CT scan - Usually not done to diagnose stones (as mentioned above) a) DDx: Usually done in symptomatic patient where it is uncertain what is the cause of symptoms possible causes as well (liver/pancreatic) b) Cx: detect complications of gallstones

looking for other

3. Magnetic resonance cholangiopancreatography (MRCP) - MRCP is not the same as MRI liver/pancreas – only selected cuts taken in order to reconstruct the biliary tree without contrast only T2 images, resolution is not as good as MRI - Comparable to ERCP, and also minimally invasive preferred to ERCP if patient does not require any therapeutic intervention that ERCP provides 4. Endoscopic retrograde cholangiopancreatography (ERCP) - Will definitely involve cholangiogram - The largest value of ERCP lies in its therapeutic potential 1. Stone removal (using balloon catheter, or Dormia basket) 2. Sphincterotomy (in order to relieve obstruction or facilitate removal of stone) 3. Stenting - High level of complications Overall risk is 10-15% a. Pancreatitis in 1-3%: i. Due to inflammation from a) injection of contrast (increased p) and b) edema when removing stone ii. Increased risk in: younger, F, prev post-ERCP pancreatitis, cannulation/ injection of pancreatic duct, sphincter of Oddi dysfunction b. Haemorrhage 2-3%: esp sphincterotomy c. Cholangitis 1-2% d. Perforation into bile duct, duodenum 0.1% (esp if sphincterotomy): (OGD 0.01% ie 1 in 10000– ERCP slightly higher since it uses side viewing scope) e. Failed ERCP f. Over sedation (hypotension, resp depression, N/V) Also: Cholecystitis, Contrast related reaction (allergy to iodine) rare - Before doing ERCP, need to assess the benefits and risks, and select patients carefully 5. Percutaneous transhepatic cholangiography (PTC) /biliary drainage (PTBD) - PTC involves a tube being inserted under radiologic guidance into one of the biliary ducts (must be dilated duct) - Rarely done now; main indications: 1) Diagnostic: high obstruction not well visualised in ERCP; prev surgery with altered anatomy (eg gastrectomy) 2) Therapeutic: obstructed system that cannot be drained from below; - Mostly for therapeutic rather than diagnostic purposes - Complications: bleeding (esp in biliary obs pts due to coagulopathy sec to decreased Vit K abs); leakage of bile when tube is removed 6. HIDA scan - No longer used commonly, except in biliary atresia 5 criteria for a normal cholangiopancreatogram (a) (b) (c) (d) (e)

Normal intrahepatic ducts No filling defects Smooth common bile duct No stricture/narrowing of the common bile duct Good and free flow of contrast into duodenum

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

Cholecystectomy is the only way to treat gallbladder stones that are symptomatic (esp if cxs arise Open or laparoscopic ( preferred) Adv of Lap: shorter hospital stay, less pain, less complications post-operatively Risks of Lap: Conversion to open - up to 5% Due to abnormal anatomy; difficult or complicated dissection; iatrogenic injury. Conversion rate is higher if there is ongoing infection e.g. cholecystitis – up to 1 in 3 to 1 in 4 Injury to surroundings: bowel & biliary structures e.g. CBD Haemorrhage Infection Spilled bile peritonitis, sepsis

high risk of 2nd attack)

Non-Surgical - Non- surgical means of stone treatment Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around to dampen waves; good results only for cholesterol stones. Expensive. Bile salt therapy necessary following lithotripsy todissolve gallstone fragments. CI: more than 3 stones, large/calcified stones, non-functioning GB, Cx of gallstones Medical Tx in radiolucent gallstones, 1000, pancreatitis!), 5. LFT (mild transaminitis)/ UECr (dehydration) 6. CXR, KUB: Radioopaque gallstones, aerobilia (due to fistula). Exclude lower lobe pneumonia, perf viscus, abnormal right hemidiaph/thorax. 7. PFO: PT/PTT, ECG MANAGEMENT A) Conservative -

Resuscitate the patient, senior to r/v if pt systemically unwell Septic workup NBM and intravenous fluids Analgesia Empirical intravenous antibiotics – IV ceftriaxone (1g bd) and metronidazole (500mg tds) Bed rest Careful monitoring for signs of failure (peritonism, non-resolving fever/pain)

Cholecysitits usu resolves with medical management (60%), but inflammation may progress complications, including peritonitis. - Definitive treatment – laparoscopic (better success if within 72hrs of symptom onset) cholecystectomy B) Timing of cholecystectomy - Dependent on several factors: Severity of illness Response to resuscitation and antibiotic therapy Logistical considerations (availability of OT, surgeon etc) - Possibilities available: i. Emergency (immediate; in very sick patients who are not doing well/ not responding to treatment) ii. Early (within few days of onset – ideally within 5 days) iii.Delayed/interval (after 6-8 weeks)

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

Delayed 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 / acute pancreatitis during the time (20%)

Early surgery has been found to be more beneficial (

mortality, total duration of dz, length of hosp stay, cost)

Gallstone disease in elderly more severe - higher rate of complications - extremely high mortality for emergency cholecystectomy - Acute cholecystitis: timely diagnosis, early stabilization, semiurgent cholecystectomy C) Cholecystostomy (fastest way) - In moribund patients who are not fit for surgery / early surgery is difficult due to extensive inflammation - Can be done under LA, or more commonly under radiologic guidance (percutaneous) - Drains the gallbladder and alleviates the inflammation (resolves acute episode) better outcomes - Can be followed by cholecystectomy 4-6 wks later COMPLICATIONS OF ACUTE CHOLECYSTITIS 1. Hydrops/ Mucocele - Cystic duct obstruction leads to a tense gallbladder filled with mucus (slow distension from continuous mucus secretion) - May lead to gallbladder wall necrosis if pressure exceeds capillary bld pressure 2. Empyema - Gallbladder is filled with pus due to bacterial infection of the stagnant bile (cystic duct being obstructed by a stone) - Patient is usually toxic, requiring urgent surgery 3. Gangrene and perforation – rare due to rich blood supply from hepatic and cystic arteries - Localised perforation abscess that is confined by the omentum (new mass) - Free perforation generalised peritonitis and sepsis sudden generalised abdo pain

emergency laparotomy

4. Cholecystenteric fistula - Most commonly occurs in duodenum, then colon, and stomach; after repeated attacks of cholecystitis - Usually asymptomatic - On AXR, aerobilia is seen in 40% of cases - Symptomatic fistulas (malabsorption and steatorrhoea) should be treated with cholecystectomy and fistula closure 5. Gallstone ileus - Stones causing cholecystenteric fistula pass into the enteric lumen causing intermittent bouts of small bowel obstruction - Accounts for 1-2% of IO overall - Ppt: unexplained gradual onset of SB obstruction - Small stones (2.5cm and migrated into gut impact at terminal ileum (commonest), duod, sigmoid colon - Mortality is 10-15%, mostly in elderly patients in whom gallstone ileus is more common - Ix: AXR, Barium follow through - Tx: Small bowel enterotomy proximal to the point of obstruction is usually required to remove the stone (Immediate cholecystectomy not warranted as 60years, with DM - Causes: 2° cardiovascular pulmonary complications (older), uncontrolled sepsis with peritonitis and intraabdominal abscess ACALCULOUS CHOLECYSTITIS - Occurs in very ill patients with prolonged stay in ICU – prolonged fasting, poor nutrition, labile blood pressure, sepsis - Poor nutrition leads to biliary stasis, while dehydration and hypotension leads to formation of viscous bile and gallbladder ischaemia may get infected cholecystitis - Treatment involves emergent cholecystectomy / percutaneous cholecystostomy to control acute disease followed by cholecystectomy

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bile

5. GALLBLADDER CANCER -

-

uncommon, increasing in China and North India RF - F:M=2:1, obesity, chronic cholecystitis/ cholelithiasis Mostly adenocarcinoma, small percentage SCC Signs and symptoms Early: mimic gallstone inflammation (RHC pain) Late: biliary and stomach obstruction (jaundice, vomiting, LOA, LOW) Mostly incidental histo finding after cholecystectomy Related to gallstones building up (95%) porcelain gallbladder Commonly spreads to liver, bile ducts, duodenum, stomach Treatment: cholecystectomy + liver resection and LN dissection +/- chemoRT Palliative: Endoscopic stent to biliary tree and stomach Prognosis: poor (most die by 1 year after surgery)

6. CHOLEDOCHOLITHIASIS PRESENTATION - Obstructive jaundice – tea-coloured urine, pale stools - Biliary colic - If infection sets in cholangitis (see below) BLOODS - FBC (check TW for any rise suggestive of infection) - Amylase (CBD stone may cause pancreatitis) - LFTs (raised bilirubin – direct; ALP raised more than transaminases – also high if LT due to liver damage) ULTRASOUND - Gallstones in gallbladder - Gallstone in CBD (50% missed, esp in distal CBD) - Dilated CBD (normally 10mm is abnormal In older patients, post-cholecystectomy, or patients on long-term opiates, the CBD may be larger, up to 11-12mm in size MANAGEMENT - If unsure of presence of stone less invasive investigation such as MRCP, EUS - If likelihood of CBD stone is high ERCP with stone removal ERCP successful ERCP failed

Plan for lap cholecystectomy If patient is well and can tolerate another ERCP, try again (+ stent in between to drain bile) Operative removal – Open CBD exploration – Lap CBD exploration

- If no facilities to do ERCP: open or laparoscopic cholecystectomy with CBD exploration When to do operative removal of stones (i.e. not suitable for ERCP) - Stone >25mm, Intrahepatic stone, Large number of stones, Impacted stone - Dual pathology, Tortuous duct, Previous Bilroth II (unsuitable anatomy for ERCP)

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7. CHOLANGITIS PRESENTATION - Classically Charcot’s triad: RHC pain, fever, jaundice (only 50-70% of patients have the classic triad) - Reynold’s pentad:  Charcot’s  triad  plus  mental  obtundation  and  shock - A surgical emergency! (mention in exams!) PATHOLOGY - Usually results from obstruction to the biliary system with infection of stagnant bile - Most common cause is choledocholithiasis (60%); Consider benign strictures (instrumentation), malignancy (pancreatic, biliary), foreign body (prev instrumentation), PSC, choledochocysts, Mirrizi’s,  hemobilia,  biliary  enteric  anastomosis - Common causative organisms are gram negative bacteria and anaerobes – Klebsiella, E. coli, Enterobacter, Enterococcus - Small proportion (elderly, prev biliary surgery) – anaerobes (bacteriodes, clostridium), developing world – parasites (Clonorchis sinensis, Ascaris lumbricoides) COMPLICATIONS - sepsis - electrolyte abnormality (dehydration) - infection - coagulopathy (Vit K) MANAGEMENT 1. Resuscitation – “In view of cholangitis being a surgical emergency, I will like to resuscitate the patient who may be in septic shock”.Anticipate  rapid  deterioration. - Inform seniors - Obtain good intravenous access and fluid resuscitate as appropriate - Take bloods for investigations – cultures especially - Close monitoring of vitals in HD/ICU Hrly para + SpO2 Keep MAP > 65mmHg (or to inform doctors if SBP0.5mg/kg/hr) CVP line insertion if patient has shock unresponsive to fluid resuscitation (keep 10-12mmHg) 2. Antibiotics (after blood c/s) - IV ceftriaxone (2g STAT + OM) & metronidazole (500mg STAT + Q8h); imipenem if pt in shock - 7 – 10 days 3. Investigate for cause - ultrasound (preferred if suspecting stones) vs CT (for non-stone cause) etc as above 4. Biliary DECOMPRESSION +/- definitive treatment - Biliary decompression and definitive treatment can be combined or separate - Timing usually deferred until 24-48h after admission when pt is stable/improved w Abx Emergency if deteriorating / Abx not improving infection (15%) - ERCP a) Decompression commonly performed using ERCP Decompression is the primary objective – endoscopic sphincterotomy + stenting/external drainage (nasobiliary drain: bile duct to nose for continuous drainage) Success rate 90% b) If cause of obstruction can be treated in the same setting (e.g. stones to be removed) then treat the cause also - Other methods to decompress: percutaneous transhepatic drainage (esp if neoplastic obstruction) operative decompression 5. Definitive treatment = Cholecystectomy +/- CBDE - Definitive treatment dependent on: Medical condition of patient Success of biliary decompression Logistical considerations

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- Choices for definitive treatment: (a) Open cholecystectomy with CBD exploration (b) Laparoscopic cholecystectomy (if CBD exploration is to be performed, need to convert to open – lap CBDE not done in Singapore must mention during consent taking) CBD EXPLORATION - Cholangiogram or choledochoscopy is performed 1. Cholangiogram involves injection of dye – can image higher ducts 2. Choledochoscopy involves using a scope to visualise the large biliary ducts – cannot image higher ducts, thus not as sensitive, but can be used to remove stones visualised in the duct Choice of imaging depends on site of obstruction and the cause - Removal of stones 1. Manual removal with stone-grasping forceps 2. Flushing out stones 3. Dredging stones out using balloon catheter or Dormia basket 4. Lithotripsy - Consider use of biliary stent or T-tube after removal of stone(s) If there is a lot of instrumentation of the biliary system during the operation, one should anticipate swelling and oedema of the biliary system resulting in post-operative obstruction and buildup of bile higher risk of biliary leakage (a) Stent – removed later by endoscopy (b) T-tube (usually inserted after CBD-E) A T-shaped tube with its horizontal limb placed in the CBD and the vertical limb leading out to drain bile Adv i. Functions  as  a  “pressure  release  valve”  as  most  of  the  bile  will  flow  through  the  horizontal limb of the tube into the distal part of the CBD; only when there is obstruction to flow will bile be diverted out through the vertical limb ii. Allows for post-op cholangiogram (at POD 9-10) before removal 1. free flow of contrast into duodenum, 2. no residual stones, 3. no free leak of contrast into peritoneum If all normal release anchoring stitch & exert gentle traction on tube; tube should slip out easily, if not, call for help If stones are present leave tube in for 4-6 weeks to form a fibrous tract allows for instrumentation of tract with a scope to remove the stones BILIARY BYPASS (UNCOMMON) - Consider biliary bypass if there are 1. multiple stones, 2. the CBD is more than 2cm in diameter, or 3. there are strictures (since the CBD has been chronically dilated, quite unlikely that it will function normally even after removal of the obstruction) Mostly replaced by endoscopic stenting. Cholecystojejunostomy preferred over Roux-en-Y choledochojejunostomy.

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8. MIRIZZI’S  SYNDROME PATHOLOGY - Gallstone  in  the  Hartmann’s  pouch  compressing  the  common  hepatic  resulting  in  obstructive  jaundice - Compression effect is not just physical (the stone) but also contributed by the surrounding inflammation - One  of  the  caveats  to  Courvoisier’s  law GRADING Type I - No fistula present Type IA - Presence of the cystic duct Type IB - Obliteration of the cystic duct Types II-IV - Fistula present Type II - Defect smaller than 33% of the CBD diameter Type III - Defect 33-66% of the CBD diameter Type IV - Defect larger than 66% of the CBD diameter

MANAGEMENT - Grade 1: attempt laproscopic cholecystectomy - Grades 2-4: open cholecystectomy with CBD exploration

9. RECURRENT PYOGENIC CHOLANGITIS BACKGROUND Cholangiohepatitis, or recurrent pyogenic cholangitis (RPC), is characterized by: 1. Recurrent bacterial cholangitis 2. Intrahepatic pigment stones 3. Intrahepatic biliary obstruction. PATHOPHYSIOLOGY epithelial damage predispose to seeding of coliforms Helminthic infxn (eg Ascaris lumbricoides, Clonorchis sinensis) repeated portal bacteraemia cascade of events (biliary stasis, into biliary system via bacterial translocation recurrent cholangitis obstruction, stone formation) deficiency of enzymes calcium bilirubinate pigment stones formation recurrent biliary obstruction Malnutrition recurrent cholangitis HISTORY: - A history of recurrent attacks of cholangitis – typical hx: 1-2 episodes of fevers, jaundice, and RUQ abdominal pain per year Hx of prev biliary surgery, endoscopic procedures, or percutaneous biliary drainage procedures. - Complications of pyogenic cholangitis cirrhosis with portal hypertension cholangiocarcinoma

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PHYSICAL EXAMINATION No specific physical findings are evident in RPC. Dx based on history. DIFFERENTIALS Primary Sclerosing Cholangitis INVESTIGATIONS For diagnosis For Complications Bloods - FBC - LFT with ALP>ALT, AST - Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and vitamin K deficiency) Impt to exclude – correct with parenteral Vit K before invasive procedures - Blood C/S: bacteremia – results help guide antibiotic choice. - Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present. Radiology - U/S HBS segmental biliary dilatation hepatolithiasis liver abscesses helps determine choice of supplemental axial imaging techniques. - ERCP or PTC – imaging modality of choice for delineating the biliary tree. - CT scan centrally dilated bile ducts with peripheral tapering bile duct stones pyogenic liver abscesses. TREATMENT PRINCIPLES: - Treat current infection - Biliary drainage - Management of other complications e.g. dehydration etc Surgical - Usual surgical approach includes: Initial biliary decompression – ERCP sphincterotomy / stent placement Definitive biliary drainage procedure – e.g. Roux-en-Y choledochojejunostomy PROGNOSIS - Death occurs in approximately 15-20% of patients over 5-6 years.

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10. CHOLANGIOCARCINOMA SITE - Intrahepatic/peripheral 10% - Distal 25% - Perihilar 65% (Altemeier-Klatskin tumour) Bismuth classification i. Type I: below confluence of hepatic ducts ii. Type II: tumour reaching confluence iii. Type IIIA/B: involving common hepatic duct and either right or left hepatic duct iv. Type IV: multicentric or involving confluence and both hepatic ducts ASSOCIATIONS - Related to chronic cholestasis: Primary sclerosing cholangitis / Ulcerative colitis Parasitic infection – Clonorchis sinensis, Opisthorchis viverrini Hepatolithiasis Recurrent pyogenic cholangitis - Bile duct adenoma - Choledochal cyst (20-25% in Type 1) Caroli’s  disease  =  congenital  cystic  dilatation  (multifocal  segmental  dilatation  of  large  intrahepatic  bile  ducts) - Thorotrast exposure (radioactive Xray contrast) - Instrumentation PRESENTATION -

Painless jaundice (painful if there is cholangitis) Acholic stools Pruritus Advanced signs and symptoms: Abdominal pain Fatigue, malaise Weight loss Hepatomegaly

DIAGNOSIS U/S detects biliary dilatation but not useful for ductal lesions. - CA 19-9  >100μl/ml  (good  sensitivity  of  89%,  specificity  86%) - Contrast CT - PTC: when biliary obstruction from distal end. 2 functions: 1) roadmapping for surgery; 2) drainage of obstructed system if ERCP cannot drain - ERCP: can obtain brushings for cytology, less bile leak than PTC - Selective celiac angiography: aid in determination of surgical resectability by identifying tumor involvement with adjacent blood vessels CURATIVE TREATMENT - Surgery is the only chance of long-term cure - Only 25% of tumours are resectable - Contraindications to surgery Bilateral or multifocal intrahepatic disease (2nd order biliary radicles in both hepatic lobes) Invasion of portal vein trunk or hepatic artery Bilateral involvement of hepatic arterial or portal venous branches Unilateral hepatic vascular invasion with contralateral ductal spread Distant metastases

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PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) - Intrahepatic: 35-45% - Distal 35-45% - Perihilar 10-30% (worse prognosis due to early lymphatic spread) PALLIATION - Endoscopic/percutaneous transhepatic biliary stenting - Bilateral drainage for hilar cholangiocarcinoma - If after opening up and finding that tumour is not resectable, can perform surgical bypass

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12.

BREAST DISEASES

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

- Lymphatic drainage: 1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes 1. 40-50 nodes in 5 groups: Anterior, posterior, medial, lateral, apical 2. Drains into supraclavicular and jugular nodes Anatomic/ Surgical division into levels I, II and III by the pectoralis minor muscle: Level I: lateral to pectoralis minor – usu e first LN where BrCA spreads to Level II: posterior to pectoralis minor Level III: medial to pectoralis minor, extending up to apex of axilla 2. Internal mammary nodes--20% of drainage from the ipsilateral breast upper and lower inner quadrants About 4 nodes per side, with one node in each of the first three interspaces and one in the fifth or sixth interspace 3. Interpectoral (Rotter’s  nodes)  – between pec major and pec minor muscles

2. PRESENTATION OF BREAST DISEASES 1. Lump (painful vs painless) 2. Pain (cyclical vs non-cyclical) [ 3. Nipple changes or discharge

more likely benign]

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3. APPROACH TO A BREAST LUMP DIFFERENTIALS (AGE DEPENDENT) Painless lump Elderly: (post-menopausal) 1. Carcinoma Younger: 2. Cyst 3. Fibroadenoma - can get cyclical pain (swell with the rest of  the  breast  cos  it’s  breast  tissue) 4. Area of fibroadenosis (nodularity)

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

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

May not be painful if pt has received treatment / some infx.

Cyst, fibroadenosis and carcinoma can be painful/ painless. HISTORY 1. History of lump - Site of the lump? - Single or multiple? – multiple: fibroadenoma / cysts / fibroadenosis. - When & Why was it first noticed? (Pain, self-examination, etc)? - Painful or painless? - Overlying skin changes noted: Erythema, warmth Dimpling: shortening of Cooper’s  ligaments  due  to  tumor  pressure? Any general asymmetry of the breasts noticed? Discharge – ind CA invasion - Duration since first noticed – long duration unlikely CA - Any increase in size from first noticed to now? - Any changes in the nipple e.g. retraction - Nipple discharge? If present, what is the colour and consistency? - Any other lumps elsewhere – other breast? Axilla? Neck? - Has the lump been treated before? RF – to sieve out ppl carrying BrCA gene, ID high risk patient (to continue f/u even if lump benign) 2. Oestrogen exposure history Increased risk: - Age of menarche (early 55YO increased risk) - Use of HRT (>1yr) – cumulative risk with duration of therapy and/or Oestrogen based OCP (not proven) ‘Confers  protective  effect’: - How many full term pregnancies? (nulliparity increased risk) - Age at which first child was born (>30 years old) - Whether patient breastfed her children, and if so, for how long 3. Other risk factors for cancer A. STRONGEST RF: Family history of cancers* in paternal (BRCA2) and maternal side (BRCA 1&2), especially if cancer occurs in: a. first degree relative below the age of 40, in bilateral breasts b. >/= 2 relatives with Breast CA around 50yo *Includes breast, ovarian, prostate and CRC. Lifetime risk in gene carrier – 80%. B. Previous breast disease: a. Treated cancer b. Previous biopsy showing atypical ductal hyperplasia or LCIS C. Exposure to ionising radiation (esp. RT for previous breast disease) D. Daily Alcohol intake, especially before age of 30 (link has been shown) 4. Systemic review - LOA, LOW (constitutional) - Fever (infective cause) - Bone pain, SOB, headache (metastasis)

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PHYSICAL EXAMINATION Preliminaries (HELP) - Hi: Introduce yourself & ask for permission to examine the breast Always have a chaperone to accompany you if you are male - Expose patient adequately from the waist up with exposure of axillae - Lighting: good - Position the patient at 45o or sitting position if a bed is not available Inspection

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

- General appearance - Patient’s  hands  relaxed  at  her  sides  – look for: any asymmetry in the breast contours, any obvious skin changes peau  d’orange  –infiltration of malignant cells into lymphatics causing edema (not compression), erythema, puckering any scars of previous operation or procedure e.g. punch biopsy - Look for nipple changes (7  D’s):   Discolouration Depression (retraction) Destruction Discharge Deviation (Duplication – unlikely) Displacement - Manouvres: 1. Ask patient to raise her arms (to see the axilla and underside of breasts, and accentuate any tethering to skin dimpling) 2. Ask the patient to contract the pectoralis major (push her hands against her hips) may reveal a previously unnoticeable lump if tethered to both skin and muscle 3. Press arms down & lean forward the rest of the breast will flop fwd but not the CA that is attached to underlying muscle Palpation - Patient should be lying down at 45 degrees to the horizontal with her hand tucked behind her head – this splays the breast out so it can be palpated properly - Start with the normal side first! - Ask for any pain before starting to palpate - Use one hand to retract and stabilise the breast and palpate with the other - Palpate in a systematic manner e.g. quadrant by quadrant from centre outwards - Examine the entire breast including the axillary tail - When the lump is located, check with the patient whether this is the same lump - Characterise the lump: Site (which quadrant) “I  feel  a  lump  in  the  upper outer quadrant of the Right breast. This Size lump is NOT WARM, and NON-TENDER, is hemispherical with Shape (hemispherical/ oval) poorly defined edges, measuring ___X___CM. It is firm in Surface (smooth or nodular/irregular) consistency with a irregularsurface and is NOT FLUCTUANT. Consistency (soft, firm, or hard) It is NOT FIXED to  the  SKIN  ………….(ask  her  to  contract  the  pect   Tender or non-tender maj)….  ………….And  NOT FIXED to  the    underlying  muscle” Warmth of overlying skin Fluctuance Margins (regular and smooth, or irregular and ill-defined) 1. Fixation to the skin – try to pick up the skin above the lump 2. Fixation to underlying muscle – Move lump in 2 perpendicular directions. Then ask patient to press her hands against her hips to contract the pectoralis major muscle, then try to move the lump in 2 perpendicular directions. (no need to do if already attached to chest wall) - Continue to examine carefully for other lumps - Ask patient if she can show you the discharge by expressing it herself (NEVER squeeze the nipple yourself!) If patient cannot do it, then ask the chaperone to help / squeeze yourself by milking the breast from outside in (ideally with patient sitting forward)

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Axillary lymph nodes -

Palpate the normal side first Rest the pt’s  right forearm on your right forearm and use your left hand to palpate the right axilla (vice versa for the left side) Palpate gently, slowly, and systematically, covering the major groups of nodes: anterior, posterior, medial, lateral, and apical If any lymph nodes are found to be enlarged, note the number of lymph nodes, their site, size, tenderness, consistency (firm, hard, matted), mobility

To complete the examination -

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

FINDINGS FOR THE COMMON BREAST LUMPS Type of lump Cyst Nodularity Fibroadenoma Cancer

Age 3055 2055 1525 35+

Pain Occ

Surface Smooth

Consistency Soft to hard

Mobility Not fixed

Occ

Indistinct

Not fixed

No

Smooth, bosselated Irregular

Mixed, fluctuant Rubbery Stony hard

May be tethered or fixed

No

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Very mobile

INVESTIGATIONS “The  evaluation  of  a  breast  lump  is  via  the  TRIPLE ASSESSMENT – (i)  Clinical  examination;;  (ii)  Imaging;;  and  (iii)  Histology.”

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

Imaging 1. Mammography: always cf Prev MMG (alert if any CHANGE) - Most sensitive of the proven breast imaging modalities (Gold std) - Purposes: Dx Screen the rest of the Breast helps to plan treatment (possibility of breast conserving Sx) Screen contralateral breast (in case B/L BrCA – rare) Baseline for future f/u for contralateral breast (Br CA is RF for CA development) - Usually performed in asymptomatic older women (>35YO) [breast tissue in younger women is denser; more difficult to pick up abnormalities], but 5/mm2 cluster - Sole feature of 33% of cancers detected on mammography - Causes: A. DCIS, B. invasive cancer, C. fibrocystic disease, D. papilloma - Features of malignancy: 1. pleomorphic microcals, heterogeneous appearance; segmental 2. closely grouped or arranged in a linear pattern (ductal distribution), 3. underlying density - Features of Benign microcals:  punctate,  “tea-cup”  appearance (c) Spiculated mass or stellate lesionwith poor outline or comet sign - 95% of spiculated masses on mammography are due to malignancy - Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance of it being malignant - Causes: A. Invasive cancer, Comet sign: enhancing lesion with a tail (directed towards nipple). B. radial scar (benign), Indicates early DCIS. DDx – prev Bx / Sx to that area. C. fat necrosis, D. abscess, etc (d) Architectural distortion (of the contour), tent sign , nipple changes - Look at the axilla on the MLO view for any enlarged lymph nodes BI-RADS (Breast Imaging Reporting and Data System) classification Category 0: Need additional imaging evaluation Category 1: Negative (nothing to comment on, 0.05% risk still present) Category 2: Benign Category 3: Probably benign, short-term follow-up suggested (1yr after stopping breastfeeding) 3. Is the discharge worrisome? - Unilateral or bilateral (unilateral more worrisome) - Discharge from multiple ducts or single duct (single duct more worrisome) - Nature of discharge (bloody more worrisome) - Age of the patient (more worrisome in older patient >60) 4. Is it troubling the patient? PHYSICAL EXAMINATION (as described above) INVESTIGATION 1. Discharge for cytology to detect malignant cells 2. Mammography/ US of both breasts to detect any underlying malignancy 3. Histology of biopsied lesion if found on imaging 4. Ductography, ductoscope & biopsy MANAGEMENT - If malignancy found, manage malignancy - Excision for intraductal papilloma (microdocholectomy, total ductal excision, hookwire locailised excision) – scarring may affect other ducts too - Antibiotics for mastitis/abscess + incision and drainage for abscess - Conservative management for most other pathologies unless discharge persists and is troubling patient microdochectomy of offending duct

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

Invasive

Ductal

DCIS = malignant - 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 malignant - Good prognosis if treated - Tx similar to IDC

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

Lobular

LCIS = RF - From terminal duct lobular unit (like DCIS) - Do not distort lobular architecture - Usually presents with a lump, seldom detected by mammo as rarely microcal. - 60-80% multicentric and bilateral - Not premalignant, but a marker for increased risk of invasive disease in both breasts (7-10x increased risk) - If ca develops, will be IDC usually, occurs >15 years after diagnosis - Usually proceed with excision biopsy.

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

Others

Specialised 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 - No histo features of inflammation - Very poor prognosis, rapidly fatal

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swelling

SPREAD - Local: skin & subcut tissues, underlying ribs and muscle (chest wall) - Lymphatics: axillary, internal mammary LNs, supraclavicular LNs - Haematogenous: lungs, liver, brain, bone, adrenals, ovaries PRESENTATION - Asymptomatic: detected on mammographic screening - Local: - Self-detected lump in the breast (>1/3 of patients) - Nipple change: distortion, destruction, retraction, deviation, discharge, eczema - Overlying  skin  changes  e.g.  peau  d’orange,  tethering   (means  mass  is   still mobile but overlying skin will be indented when moving the lump), fixation (means the mass is not mobile), even fungating ulcer - Other lumps in axilla - Pain is uncommon. - Constitutional: LOW, LOA - Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone, brain, adrenals) DIAGNOSIS – BY TRIPLE ASSESSMENT (see above) STAGING - Triple assessment can help divide it into: - DCIS or early Breast Cancer (BC) (at most with small mobile axillary LNs) - locally advanced BC (matted LNs, skin and rib involvement) o continue to stage to look for metastasis in advanced BC - Staging Investigations: (i) CXR (for lung metastases; look for isolated hyperdensity) (ii) U/S HBS (iii) Bone scan (iv) LFT (raised ALP) + Hepatitis screen (may flare up with chemoTx) (v) CT or MRI brain – if patient symptomatic (vi) CT thorax , abdomen (for liver and adrenal metastasis) – in locally advanced BrCA T stage

N stage

Tis: Carcinoma in-situ, Paget’s  with  no  tumour

M stage

N1: Mobile ipsilat axillary nodes

T1: 5cm T4:

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

Stage 0

Stage I

Stage II

Tis

T1N0

T2N0, T3N0 T0N1, T1N1, T2N1

Stage III *skin, rib inv., matted LNs T3 N1 T0N2, T1N2, T2N2, T3N2 Any T, N3 T4, any N

DCIS Early Breast cancer Aaaaa – Stage Xb (e.g. IIb, IIIb) 5 yr Survival Stage I: Stage II: Stage III: Stage IV:

90% 60% 30% 10%

(70% in 10 yrs) (40-50%) (20-30%) (10mm; /= T2 (5cm) - Not required for DCIS (theoretically cancer cells are confined to the breast) if diagnosed on excision biopsy / wide excision. Recommended if diagnosed on Core biopsy (sampling error). - Complications: see below - Sentinel lymph node (SLN) biopsy (SLN) is a new standard of care Only in Early CA (/= 4 LN +ve - Targeted at Breast with or without internal mammary, infra/supraclavicular LN (Axillary LN are tackled during Surgery) - CI: pregnancy, previous RT, patient choice - Regimen consists of 25 to 30 cycles in total, 1 cycle per day from Mon - Fri over 5-6/52 until max dose (no repeat RT for recurrences) - Cx: radiation injury (e.g. pneumonitis, skin changes), risk of cancers 1 in 2000 in 20yrs 2. Palliative - Brain mets - Bone mets to painful areas / impending fractures Chemotherapy (polyCT with 3 drugs is better; 4-6cycles, each over 1/12) - Main purpose: eliminate micrometastasis! 1. Neoadjuvant (a) Given in Locally advanced breast cancer (stage III) to shrink the tumour before surgical resection (b) To shrink tumors before breast conserving Sx - 20% achieve complete clinical response (cCR) i.e. tumour is no longer palpable further 20% will achieve complete pathological response (cPR) i.e. no more tumour cells = good prognosis - Place clip into tumour before neoadjuvant therapy to guide surgery in case tumour  “disappears”;;  operate  according  to preop staging - Cx: as for CT drug, e.g. mouth ulcers, N/V, hair loss, immunosuppression (main disadvantage pre-op) 2. Adjuvant - Start 3/52 after surgery; given in stage III / LABC (LN+ve) & in some early breast cancers depending on stage (see below) - Premenopausal patients tend to have better response to chemotherapy than hormonal therapy (vice versa for postmenopausal patients) - Main active agents: anthracyclines (e.g. doxorubicin, epirubicin) and the taxanes (e.g. paclitaxel, docetaxel) - Common regimens: AC (anthracycline, cyclophosphamide), FAC (5-FU, anthracycline, cyclophosphamide), CMF (cyclophos, methotrexate, 5-FU) 3. Palliative - Anthracyclines and taxanes are the mainstay - Helps to reduce load of disease to alleviate symptoms, increase survival Hormonal therapy (a)

Used in adjuvant setting to eradicate micrometasis (likewise with CT & TT) For ER/PR +ve will have 90% response Preferred for postmenopausal women as response to hormonal therapy is better May render patient postmenopausal for better response to HT via medical ablation with LHRH-a or surgical oopherectomy Mostly used as adjuvant therapy but can also be used as palliative treatment & preventive treatment in high risk patients - Also reduces risk in contralateral breast Selective oestrogen receptor modulators (SERMs): Tamoxifen - 50% reduction in recurrence, 25% reduction in mortality - taken daily for 5 years - CI: PHx of CVA/DVT, immobile patients - Side effects: 1. menopausal symptoms (hot flushes, etc), 2. endometrial cancer (0.1% per year), 3. deep vein thrombosis

(b) Aromatase inhibitors: Lanastrazole, letrozole, exemestase - Inhibit peripheral conversion of testosterone and androstenedione to oestradiol (still present in post-menopausal women) - Only suitable for post-menopausal patients as use of these agents will cause overactivity of the HPA axis in premenopausal women - Side effects: 1. musculoskeletal pain, 2. osteoporosis! Targeted therapy - Herceptin (trastuzumab) - targets Her-2-neu a.k.a. C-erbB2 receptor (an epidermal growth factor receptor [EGFR] that is overexpressed in 18-20% of cancers) - Used in C-erbB2 positive tumours, early or late stage - Her-2-neu indicates worse prognosis Herceptin improves prog to normal - Side effects of Herceptin: 1. cardiomyopathy & CCF 2. pulmonary toxicity, 3. infusion reactions, 4. febrile neutropaenia - Avastin (or bevacizumab, targets vascular endothelial growth factor [VEGF] receptor, used in advanced cancer); - Lapatinib (targets Her-1 and Her-2, used in advanced cancers)

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TREATMENT BY TUMOUR STAGE Tumour can be divided into 1. in-situ cancer, early BC, locally advanced BC 2. Advanced BC palliative intention

curative intention

1. DCIS - Same Tx as invasive carcinoma: WE vs SM - Sentinel LN biopsy if DCIS not very certain (ie diagnosed on Core biopsy) - ± hormonal therapy (only if WE) to reduce recurrence at surgical site; tamoxifen reduces overall breast cancer risk by 50% in both breast not adjuvant therapy 2. Early breast cancer (stage 1 &2) - T2 or less (20mm, N stage >1

11mm < T < 20mm, N=0

T 5cm or skin/chest wall involvement), N2 or N3 (fixed lymph node involvement or supraclavicular node involvement) - Surgical resection dependent on size of tumour and resectability (if tumour is too large, the skin defect will be very large inoperable) - Systemic therapy: Neoadjuvant chemo to (1) downstage inoperable tumour (in addition, it helps by predicting the tumour response to chemotherapy before resection) and (2) eliminate micrometastasis Adjuvant therapy after resection – CT & HT (depends on the histology etc after surgery, ie does patient still require adj tx) Usually not done if patient has completed the course of chemo during neoadjuvant. 4. Advanced breast cancer (stage 4) - aim for dz control - Distant metastases: treat symptoms and prevent potential problems - Minimal locoregional therapy except for palliative purposes (new study shows that removing primary in metastatic BrCA confers survival benefit) - Systemic therapy is the mainstay of treatment – CT, HT or TT (to prevent worsening of mets) - Mets specific: 1. Bone: RT to painful areas, Fixation/RT to impending fractures, Decompression if cord compression Treat hypercalcemia from mets 2. Brain: RT 3. Pleural: drain effusion 4. Liver (usually liver failure > obstructive jaundice) FOLLOW-UP - symptoms + P/E - 3-monthly for first 2 years - 6-monthly for the next 3 years (i.e. third to fifth years) - Yearly for another 5 years (to tenth year) - MMG: same breast 1yr postop; then 2-yrly bilateral mammo for life (previous BC is a strong Risk factor for future Breast cancer) - CEA and CA15-3 are used in some centres for trending

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BREAST SCREENING Normal risk, asymptomatic

40-49 YO 50-64 YO >65 YO

Annual mammogram Biannual mammogram (by invitation) Optional 2 yrly mammogram

Increased risk

Start screening 5 yrs before onset of breast dz in youngest family member

HRT therapy

40-49 YO 50-65 YO

Monthly BSE 6 mthly CBE & U/S breast Annual mammography

Annual mammogram Biannual mammogram up to 5 yrs after cessation of HRT

6. PAGET’S  DISEASE  OF  THE  NIPPLE - Presents as erythema and eczematous change of the nipple (not the areola) with crusting exudates, may develop into erosions and ulcerations - Often associated with intraductal carcinoma (DCIS) or invasive carcinoma just beneath the nipple - Malignant cells invade across the epithelial-epidermal junction and enter the epidermis of the nipple, breaking the normal epidermal barrier thus allowing fluid to be extruded onto the nipple - Examination and investigations should be targeted towards detecting an underlying tumour – may find a palpable mass and/or mammographic abnormalities - Punch biopsy of the nipple may be required - Prognosis  of  the  underlying  cancer  is  not  altered  by  the  presence  of  Paget’s  disease  of  the  nipple - Treatment should be planned according to the underlying cancer if found - If no palpable mass or mammographic abnormality is detected, wide excision is an adequate treatment

7. GYNAECOMASTIA - Causes: - Physiological: puberty (maybe painful) - Drugs: Recreational drugs Cimetidine (H2 blockers) Digosin Spironolactone Antimicrobials (Isoniazid, ketoconazole) - Endocrine disorders: Thyroid disorders Acromegaly Hypogonadism  (testicular  atrophy,  Klinefelters’  syndrome) - Malignancy: testicular tumours, lymphomas - Chronic liver disease: cirrhosis - Investigation: - TFT, testosterone/ LH - LFT,  α-FP, ß-HCG - Treatment - Conservative management - Surgical excision

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13.

NECK MASSES

1. ANATOMY OF THE NECK - The neck is composed of two triangles on each side – anterior and posterior triangles - The anterior triangle is bounded by the lower border of the mandible superiorly, the midline anteriorly, and the anterior border of the sternocleidomastoid posteriorly - The posterior triangle is bounded by the posterior border of the sternocleidomastoid anteriorly, the anterior border of the trapezius posteriorly, and the clavicle inferiorly

- Masses in the neck can be subdivided according to the triangle they occur in as there are pathologies peculiar to each triangle - Locations: (i) Midline (ii) Anterior triangle (iii) Posterior triangle - In general, enlarged lymph nodes are the most common cause of a lump in the neck, regardless of location MASSES BY LOCATION Midline (5) 1. Submental lymph node 2. Thyroglossal cyst 3. Thyroid nodule in the isthmus 4. Sublingual dermoid cyst 5. Plunging ranula (retention cyst of the sublingual) 6. Rarely, hyoid pathology e.g. bursa

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

Anterior triangle 1. Lymph node – along anterior border of sternocleidomastoid (levels II, III, IV) 2. Thyroid nodule 3. Submandibular gland mass (see later section on Salivary gland swellings) 4. Branchial cyst + fistula 5. Chemodectoma (carotid body tumour) 6. Carotid aneurysm 7. Pharyngeal pouch 8. Laryngocoele (rare; an air-filled, compressible structure seen in glass-blowers) Posterior triangle 1. Lymph node (mainly) – level V and supraclavicular lymph node groups 2. Cystic hygroma 3. Cervical rib 4. Brachial plexus neuroma/schwannoma

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2.

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

3.

DERMOID CYST Pathology: Can be congenital or acquired. (i) Congenital – developmental inclusion of epidermis along lines of fusion of skin dermatomes (seen in younger patients, present since birth). Locations include: o medial and lateral ends of the eyebrows (internal and external angular dermoid cysts) o midline of the nose (nasal dermoid cysts) o midline of the neck and trunk (ii) Acquired – due to forced inclusion of skin into subcutaneous tissue following an injury, usually on fingers. Seen in older patients, no previous history of mass, history of trauma to area (may have associated scar). Histology: Cyst lined by epidermis, with evidence of adnexal structures such as hair follicles, sebaceous glands and sweat glands. Features: Small non-tender mobile subcutaneous lump, may be fluctuant, skin-coloured or bluish. Management - Imaging investigations (e.g. XR, U/S, CT) are important especially for cysts on the skull as they can communicate with cerebrospinal fluid. - Complete surgical excision of the cyst.

4.

PLUNGING RANULA Pathology: A pseudocyst associated with the sublingual glands and submandibular ducts. Ranulas (frog mouth) can be congenital or acquired after oral trauma. Typically appears as a blue-grey dome-like swelling beneath the tongue. A large ranula can present as a neck mass if it extends through the mylohyoid musculature of the floor of the mouth – termed  a  “plunging”  ranula. Treatment: - Complete resection if possible, often in continuity with assoc sublingual gland (but often difficult due to close association with the lingual nerve and submandibular duct). - If complete resection not possible, marsupialisation (de-roofing the cyst so that it opens into the floor of the mouth) and suturing of the pseudocyst wall to the oral mucosa may be effective. Incomplete removal leads to recurrence.

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5. BRANCHIAL CYST/FISTULA Epidemiology: Affects both sexes equally, usually in young adults in their 20s. Pathology: A branchial cyst is thought to develop because of failure of fusion of the embryonic second and third branchial arches. It is lined by squamous epithelium. Features: - Occurs anterior to the upper or middle third of the sternocleidomastoid muscle. - Smooth firm swelling that is ovoid in shape, with its long axis running downwards and forwards. - May be fluctuant, usually not transilluminable (due to desquamated epithelial cell contents). - Look for fistula in this area – a branchial fistula will run between tonsillar fossa and the anterior neck, passing between the external and internal carotid arteries. - Fine needle aspiration of the cyst will yield opalescent fluid with cholesterol crystals under microscopy. - May be complicated by recurrent infections – purulent discharge, fixation to surrounding structures. Management: - If fistula present, perform fistulogram to delineate course. - Surgical excision of the cyst where possible. (perc drainage rarely permanently successful) If fistula/sinus present,  inject  Bonney’s  blue  dye  into  tract  prior  to  surgery  to  allow  accurate  surgical  excision. - Treatment of infection with antibiotics. - Complications: cyst recurrence; chronic discharging sinus.

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6. CHEMODECTOMA Pathology: A chemodectoma is a tumour of the paraganglion cells (paraganglionoma) of the carotid body located at the bifurcation of the common carotid artery (into the internal and external carotids). They are usually benign, but locally invasive; the risk of malignancy is 10%, with metastasis to local lymph nodes (no histopathological features for malignancy, thus malignant nature can only be diagnosed by presence of metastasis). Features: - Solid, firm mass at the level of the hyoid bone (where the bifurcation is) – be gentle during palpation as pressure on the carotid body can cause vasovagal syncope. - Mass is pulsatile but not expansile, due to transmitted pulsation from carotids. - Due to close association with carotid arteries, lump can be moved side to side but not up and down. - May be bilateral. Differentials: - Main differential is carotid artery aneurysm - Aneurysm can occur at any level but carotid body tumour occurs at the level of the hyoid bone. - If suspecting aneurysm, (a) listen for bruit, look for (b) signs   of   Horner’s   syndrome, (c) examine the rest of the peripheral vascular system. Investigation: - DO NOT PERFORM FNA - Angiography (gold standard) – shows a hypervascular mass displacing the bifurcation. May also show vessel compromise by tumour invasion, and undetected synchronous tumours. - CT and/or MRI can be used to delineate tumour anatomy in relation to surrounding structures; CT reveals homogenous mass with intense enhancement following IV contrast administration. Treatment: - Surgical excision with pre-operative embolisation (reduces bleeding and complications, and facilitates resection); any enlarged ipsilateral lymph nodes are also removed due to the small possibility of malignancy - Radiotherapy is an effective alternative for patients who are unfit for surgery or whose tumours are too large.

7. PHARYNGEAL POUCH Pathology: A herniation of the pharyngeal mucosa (pulsion diverticulum) through its muscular coat at the weakest point – Killian’s   dehiscence – between the cricopharyngeus muscle and the lower inferior constrictor muscles. Features - Occurs in older patients - A cystic swelling low down in the anterior triangle, usually on the left - Squelching sound on deep palpation - Patient complains of o halitosis, o regurgitation of undigested food with coughing o dysphagia in the neck, o hoarseness, o weight loss - Complications: aspiration pneumonia; diverticular neoplasm ( CA o Growth pattern / rate of growth: last few days = infx / inflammatory / haemorrhage into cyst last few months = CA - Constitutional symptoms o Fever, malaise, arthralgia, myalgia (viral prodrome); o Night sweats, low-grade fever (TB, B symptoms of lymphoma); o Loss of appetite, loss of weight (chronic infection, malignancy) - Local symptoms – intra-oral diseases e.g. tooth decay, oral/tongue ulcer, tonsillitis. Use of dentures. - Past medical history – cancer, TB (contact? Diagnosed? treated or untreated?) - Social history: travel and contact history, sexual history for HIV, ORAL SEX PHYSICAL EXAMINATION Inspection - SITE - Size, shape, surface: erythema, discharging sinus (multiple lymph node enlargement with discharging sinuses can be TB or actinomycosis; sulphur granules seen in actinomycosis) “Is  there  any  pain?  I  am  going  to  feel  the  lump,  if  any  pain,  let  me  know” Palpate from behind, one side at a time – start at submental, then submandibular, preauricular, postauricular, along anterior border of sternocleidomastoid, supraclavicular, posterior triangle, lastly occipital. Use pulps of the fingers in a gentle rolling movement. - Tenderness to palpation - Consistency – hard, matted nodes are more suspicious for malignancy - Fixation to overlying skin or underlying structures Potential drainage sites: - Upper LN (5) : MOUTH!!, face, scalp, thyroid, salivary glands - Lateral LN: thyroid - Lower LN: UL, Breast, Lungs, Abdomen (if Virchows), Oesophagus - Susp lymphoma (3): axilla,parotid, inguinal + liver/spleen To complete the examination: - Formal ear, nose, throat examination especially looking at the post-nasal space for nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged cervical lymph nodes) - Full respiratory and abdominal examination especially if supraclavicular lymph node found - Examination of the thyroid gland - Examination of lymphoreticular system – other lymph node groups, liver, spleen - Breast examination in female patient INVESTIGATIONS - Fine needle aspiration o Able to definitively diagnose CA and TB. (still the possibility of false positive and false negative results) o Only lymphoma requires excision Bx to diagnose (to be done after FNAC) o Do not do excision Bx first as it can compromise resection later if LN mets is from H&N CA, because LN mets counted as locally advanced dz (still resectable). - Radio: CT, ultrasound (esp thyroid), MRI (mainly CA as pre-op w/u) to assess nature of lump, extent, other enlarged nodes that are not clinically palpable, and can be used to visualise primary tumour if present - Panendoscopy: to look for synchronous tumors as smoking/alc affect squamous cells o Nose – airway: nasolaryngoscopy, bronscopy o Mouth – CE junction: OGD MANAGEMENT - According to FNAC results - Malignant – work up for primary if present (e.g. squamous cell carcinoma – look for oral cavity, skin, ENT, lung malignancy; adenocarcinoma – look for breast, GI tract malignancy) and treat as appropriate - Infective/Inflammatory – treat underlying condition

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14. 1.

SALIVARY GLAND SWELLINGS ANATOMY OF THE PAROTID GLAND

- Surrounded by tough fibrous capsule – the parotid sheath (thus mumps is painful as the gland swells within a tight envelope) - Sandwiched between the posterior border of the ramus of the mandible and the mastoid process - Important structures that pass through the gland in order from lateral to medial: (i) Facial nerve and its branches (ii) Retromandibular vein (formed as the maxillary veins drain into the superficial temporal vein) (iii) External carotid artery (branching into its two terminal branches, the superficial temporal and maxillary arteries) - Nerve supply: (i) Parasympathetic secretomotor supply from auriculotemporal nerve carrying postganglionic fibres from the otic ganglion (preganglionic fibres from inferior salivary nucleus); (ii) Somatic sensory supply of the gland from auriculotemporal nerve; sensory supply of the capsule from the great auricular nerve. - Parotid duct (of Stensen) runs 5cm across the masseter (surface marking: along the line joining the intertragic notch to the midpoint of the philtrum), drains into the mouth opposite to the upper second molar tooth - Histology: predominantly serous acini, many ducts (other glands have few ducts) 2.

ANATOMY OF THE SUBMANDIBULAR GLAND

- Consists of a large superficial part & a small deep part that are continuous with one another around the free posterior border of the mylohyoid - The deep part of the gland is closely associated with the lingual nerve (with the attached submandibular ganglion) above it, and the hypoglossal nerve and submandibular duct below it – surgery may injure these nerves - Nerve supply: parasympathetic secretomotor supply from lingual nerve carrying postganglionic fibres from the submandibular ganglion (preganglionic fibres in superior salivary nucleus) - Submandibular duct (of Wharton) arises from the superficial part of the gland, runs forwards deep to mylohyoid and drains into the oral cavity at the sublingual papilla just adjacent to the frenulum - Histology: mixed serous and mucous acini, few ducts 3.

ANATOMY OF THE SUBLINGUAL GLAND -

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

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4. APPROACH TO SALIVARY GLAND SWELLINGS HISTORY - About the lump: onset, duration, progress, associated symptoms e.g. pain o If pain is present, is it precipitated by food ingestion? (suggestive of sialolithiasis) o Intermittent swelling a/w food (inflammatory) - Symptoms of infection e.g. fever, malaise; if considering mumps, ask about testicular pain and swelling (orchitis), abdominal pain (pancreatitis) - Any noticed asymmetry of the face – incomplete closure of the eye on one side, drooping corner of the mouth, drooling - Does the patient have symptoms of Sjogren: xerostomia (e.g. cannot eat a piece of biscuit or bread without water), xerophthalmia - History of connective tissue disease e.g. rheumatoid arthritis, SLE PHYSICAL EXAMINATION Inspect - Put yourself at the level  of  the  patient’s  face and look from front for any asymmetry with an obvious mass on one side o parotid mass is located between the angle of the jaw and the ear, and lifts the earlobe if large; o submandibular mass is located just under the mandible - Look for scars – parotidectomy scar runs anteriorly to the ear, below the earlobe and around posteriorly before looping forward again under the jaw - Look for fistula/sinus - Look  at  the  patient’s  face  for  asymmetry (facial nerve palsy) “Is  there  any  pain?  I  am  going  to  feel  the  lump,  if any  pain,  let  me  know” Palpate from behind - Palpate the obviously enlarged gland: - Check for warmth of overlying skin, tenderness, consistency, surface, margins - Fixation to underlying structures – for parotid, ask pt to clench the teeth to contract the masseter, then try to move the gland - Fixation to overlying skin - Palpate the contralateral gland for any swelling - Palpate for cervical lymphadenopathy Other tests 1. Examination of the duct openings: Using a torch and a tongue depressor, examine opposite the second upper molar tooth (opening of the parotid duct), and under the tongue (opening of the submandibular duct) Look for (1) red inflamed opening, (2) discharge-purulent, (3) visible stone. For the parotid duct, can palpate the duct along the masseter for stone, and look for discharge inside the mouth while palpating 2. Tonsillar fossa: enlargement of deep lobe of the parotid (in retropharyngeal space) pushes tonsils and archs aside see asymmetry of the arches 3. Palpate the gland openings for stones. 4. Bimanual palpation of the submandibular gland 5. Facial nerve examination Suspicious features of malignancy: 1. Facial nerve involvement 2. LN involvement 3. Skin involvement: eg Hyperaemic hot skin over lump 1+2+3 = CA until proven otherwise -

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

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CAUSES OF SWELLING OF THE PAROTID Parenchymal swelling

Neoplasia

Stones Infection/ Inflammation Autoimmune Infiltration Systemic disease: bilateral Nonparenchymal swelling

Benign - pleomorphic adenoma - Warthin’s  (10% bilateral) Malignant tumours Lymphoma and leukaemia: bilateral Sialolithasis Mumps: bilateral Acute sialadenitis Chronic recurrent sialadenitis HIV Sjogren’s  syndrome:  bilateral Sarcoidosis: bilateral Alcoholic liver disease Diabetes mellitus Pancreatitis Acromegaly Malnutrition

(MADMAP) Lymph node Facial neuroma Temporal artery aneurysm Skin and soft tissue swellings e.g. sebaceous cyst, lipoma

INVESTIGATIONS - FNAC: malign vs benign - CT: confirm salivary gland (vs LN) o esp parotid – multiple swelling likely LN (DDx Warthin)

5. SIALOLITHIASIS Epidemiology - Stones of the salivary gland that may be impacted within the gland itself or in the duct. - Usually occurs in males more than females, and between the ages of 30 and 60. - 80% occur in the submandibular gland (due to its higher mucus and calcium content with a long duct, and slow flow of the saliva against gravity); 10% occur in the parotid, 7% sublingual. - Most submandibular gland stones occur in the duct, while 50% of parotid stones occur in the gland itself. - 80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the floor of the mouth, and 60% of parotid stones are radio-opaque. Presentation - Complete obstruction Acute pain & swelling of the gland involved at meal times, rapid onset within minutes of starting to eat, resolves about an hour after the meal. - Partial obstruction Occasional symptomatic episodes interspersed by asymptomatic periods of days-weeks, chronically enlarged mass in submandibular region - Cx: sialadenitis, and even abscess formation worsening of symptoms of pain and redness; systemic symptoms such as fever, chills; purulent discharge from duct opening - Stone may be palpable along the duct or at the opening of the duct Investigations - CT scan (Noncontrast) – can pick up almost all stones when fine cuts are requested - Plain X-rays can pick up radio-opaque stones - Sialogram (rarely done as it is invasive and technically demanding; CT is better. Contraindicated in acute sialadenitis and contrast allergy.) Management - General measures: o Good hydration, good oral hygiene, soft diet, avoid sour food (increase salivation) o Massage of the gland, milking the duct, application of moist hot towel o Lifestyle changes: activities that exacerbate the pain eg. Blowing instruments o Analgesia – NSAIDs such as ibuprofen - If sialadenitis present: o Antibiotics– usually to cover Staph and Strept e.g. Augmentin o Refer specialist treatment if symptoms persist for several days, or sialadenitis persists despite antibiotic therapy - Surgical removal o Transoral removal of stones for submandibular duct stones (50% can be removed thus), less for parotid duct stones o If stones cannot be removed via transoral surgery or is intraglandular, partial gland resection can be performed - Other options: Lithotripsy, wire basket removal, sialoendoscopy

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6. SALIVARY GLAND TUMOURS Epidemiology: (80% rule for parotid) - 80% occur in the parotid, of which 80% are benign (80% of the benign tumours are pleomorphic adenomas) - 10% occur in the submandibular, of which 60% are benign (95% pleomorphic adenoma) - 15% occur in minor salivary glands, of which 50% are benign (all benign tumours are pleomorphic adenomas) - 0.3% occur in sublingual glands, of which all are malignant Pathology Adenomas (benign) Pleomorphic adenoma Warthin’s  tumour

Epithelial Carcinomas (malignant) Adenoid cystic ca Pleomorphic adenoca Mucoepidermoid ca Acinic cell ca Adenoca Squamous cell ca Undifferentiated

Non-epithelial Haemangioma Lymphangioma Neurofibroma Neurilemmoma Lipoma Sarcoma Malignant lymphoma

PLEOMORPHIC ADENOMA Epidemiology: - Most common benign tumour - 85% occur in the parotid gland - Equal sex ratio, occurs in younger patients (50 years) - Related to cigarette smoking Histology: Consists of cleftlike or cystic spaces lined by two-tiered epithelium, containing mucin, surrounded by a stroma of well-developed lymphoid tissue with germinal centres. Features: - Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail (inferior) - Invariably benign with no risk of malignant change - 10% bilateral (check contralateral side) Diagnosis by clinical, FNA + MRI Treatment - Can be left alone if  absolutely  certain  that  the  entire  mass  is  composed  of  only  Warthin’s  tumour  cells,  since  there  is  no  malignant  potential - Superficial parotidectomy if causing trouble to patient

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MALIGNANT TUMOURS Tumor grade Nerve involvement Most common malignancies 1. Mucoepidermoid (34%) - most common malignant tumour in the parotid. Younger patients. 2. Adenoid cystic carcinomas (22%) – most common in the submandibular, sublingual and minor salivary glands. Equal sex ratio, can occur in any salivary gland, in older patients (usually >60 yrs). Tends to spread along nerves. 3. Malignant pleomorphic adenoma o Usually occurs in pre-existing pleomorphic adenoma, rarely de novo o Worst prognosis of any salivary gland tumour o 30-70% recurrence and metastasis rate TREATMENT OF SALIVARY GLAND CANCERS Parotid: - Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be grafted with great auricular nerve) - Radical neck dissection if neck nodes positive - Postoperative radiotherapy If localised in superficial lobe - Superficial parotidectomy only (if sufficient margin) - + RT (in higher grade tumor / adenoid cystic – cos may have spread to nerves) Submandibular: - Radical excision of gland with lymphatic clearance of submandibular triangle - Radical neck dissection if neck nodes positive - Postoperative radiotherapy COMPLICATIONS OF PAROTIDECTOMY Immediate (within 24 hrs) 1. Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to the submandibular gland, damage to the hypoglossal and/or lingual nerves can occur intraoperatively) 2. Reactionary haemorrhage: early post-op bleeding due to displacement of a clot in a BV / slippage of a ligature Early (1 to 30 days) 1. Wound infection 2. Skin flap necrosis 3. Temporary facial weakness (neuropraxia of facial nerve) 4. Salivary fistula 5. Division of great auricular nerve loss of sensation over pinna 6. Trismus (inability to open mouth due to spasm of masseter) Late (more than 30 days) 1. Wound dimple, cosmetic problems 2. Hyperaesthesia of local skin 3. Frey’s  syndrome (gustatory sweating syndrome / auriculotemporal syndrome) a. Increased sweating and redness of facial skin when eating b. Auriculotemp nerve: symp branches (sweat glands of the scalp), parasympathetic branches (parotid gland secretion) c. due to reinnervation of divided sympathetic nerves to the facial skin sweat glands by fibres of the secretomotor branch of the auriculotemporal nerve

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15.

THYROID DISEASES

1. ANATOMY OF THE THYROID GLAND

Structure: 2 lateral lobes joined by an isthmus that lies in front of the 2nd, 3rd and 4th tracheal rings. Strap muscles of the neck lie superficial to the thyroid gland. Nerves and vessels: Superior thyroid artery (from external carotid) Inferior thyroid artery (from thyrocervical trunk, a branch of the first part of the subclavian artery). External laryngeal nerve – supplies the cricothyroid muscle which controls pitch of voice; runs close to superior thyroid artery. Recurrently laryngeal nerve – supplies all the other intrinsic muscles of the larynx (except for cricothyroid) and runs close to the branches of the inferior thyroid. The nerve runs behind the pretracheal fascia and so will not be damaged if the fascia is not breached during operation. Important to visualise nerve and avoid damaging it! Embryonic origin: Thyroglossal tract from foramen caecum of the tongue (in the midline, at the junction between anterior two-thirds and posterior one-third of the tongue) descends close to the hyoid bone expansion of the caudal end of the tract forms the thyroid gland. Parathyroid glands: 2 superior and 2 inferior glands that lie behind the lateral lobes. Level VI lymph nodes – first nodes that a thyroid malignancy spreads to; they lie in the tracheo-oesophageal groove and are not palpable.

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2. APPROACH TO THYROID PROBLEMS 1. Problem with configuration/anatomy (i) Solitary thyroid nodule (most common in exam) (ii) Multinodular goitre (iii) Diffuse enlargement 2. Problem with function (usually hyperfunctioning) (i) Graves’  disease (ii) Toxic adenoma (iii) Toxic multinodular goitre (iv) Hashimoto’s  disease AIMS OF ASSESSMENT IN THYROID NODULE/ENLARGEMENT: - Exclude cancer! - Address issues of thyroid function - Look for any complications e.g. compression (of airway, oesophagus, rarely nerve) - Cosmesis – is patient bothered by lump? HISTORY-TAKING About the LUMP - Onset (gradual or sudden), duration - Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth; ddx includes haemorrhage into necrotic nodule or cyst, subacute thyroiditis) - Any pain – bleeding into cyst can result in sudden increase in size and pain; rarely pain can occur in anaplastic carcinoma and thyroiditis - Compressive symptoms: difficulty swallowing, difficulty breathing, hoarseness of voice (benign pathologies almost never compress the recurrent laryngeal nerve) - Cosmetic effects About THYROID FUNCTION Hyperthyroid 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

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

About RISK FACTORS - History of autoimmune disease e.g.  type  I  DM,  SLE,  RA,  pernicious  anaemia  (associations  with  Graves  and  Hashimoto’s) - History of cancer elsewhere – metastatic disease to thyroid; lymphoma; papillary cancer is associated with familial polyposis syndromes ask about GI polyps/ca - History of thyroid disease – long-standing MNG can progress to lymphoma - Occupational history – any exposure to radiation (papillary cancer risk) - Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2, AD inheritance), ~5% of papillary cancers About previous TREATMENT for any thyroid disease - Medications given e.g. propylthiouracil, carbimazole, propranolol – for how long, efficacy, side effects - Radioactive iodine treatment – what was the result? Is the patient receiving replacement? - Surgery – what kind of surgery, any complications? - Follow-up – what investigations done?

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PHYSICAL EXAMINATION A. THYROID GLAND GREET PATIENT, ASK FOR PERMISSION to examine (and listen to the voice – is it hoarse?) POSITION PATIENT – on a chair with space behind the chair for you to stand. INSPECT FROM THE FRONT 1. Any swelling? Where is it? (if unable to see, ask patient to swallow) 2. Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a skin crease)? Sinuses? 3. Any skin changes over the mass? 4. Check if mass moves on swallowing by asking patient to take a sip of water – “Please  take  a  sip  of  water  and  hold  it  in  your   mouth,  do  not  swallow  until  I  tell  you  to.” 5. Check if mass moves on protruding the tongue – “Please  open  your  jaw  slightly.  Now,  without  moving  your  jaw,  please  stick   your  tongue  out  and  back  in  again.” NB. A thyroid lump moves only on swallowing; a thyroglossal cyst will move on both swallowing & protrusion of the tongue. 6. Check for plethora of face, distended neck veins – may be due to compressive nature of mass (but rarely seen). PALPATE FROM BEHIND – one side at a time, the opposite hand stabilises the gland. Ask for pain before palpating! 1. Characteristics of lump: site (anterior triangle), size (discrete nodule or multinodular enlargement or diffuse enlargement?), consistency (soft, cystic, hard, multinodular?), mobility (fixed to skin? Fixed to underlying structures?), tenderness. 2. Check swallowing while palpating to confirm mass moves on swallowing. 3. Check tongue protrusion. 4. Palpate lymph nodes PALPATE TRACHEA from in front for tracheal deviation. PERCUSS – any retrosternal extension? AUSCULTATE – bruit in Graves’ OFFER to do Pemberton’s sign to check for thoracic inlet obstruction; check thyroid status; ask patient about compressive symptoms. B. THYROID STATUS HANDS (get patient to stretch arms out in front of him, palms down) 1. Feel palms – warm sweaty palms 2. Nails – thyroid acropachy, onycholysis (both  seen  in  Graves’) 3. Feel pulse – tachycardia, atrial fibrillation (AF  more  in  toxic  MNG  than  Graves’) 4. Fine postural tremor – accentuate by placing a sheet of paper on the hands 5. Palms up – palmar erythema FACE 1. Expression – staring, unblinking (hyperthyroid); lethargic, apathetic (hypothyroid) 2. Complexion – dry,  ‘peaches-and-cream’  complexion,  loss  of  outer  third  of  eyebrows  (hypothyroid) 3. Eyes - Lid retraction (can see sclera between upper limbus of iris and upper eyelid) - Exophthalmos (sclera between lower limbus and lower eyelid) - Chemosis (oedema and erythema of conjunctiva) - Ophthalmoplegia (restriction of eye movements; ask about diplopia!) - Lid lag (eyelid lags behind eye when patient follows your finger downwards) - Proptosis (look  from  above  patient’s  head  – eye visible over supraorbital ridge) NEUROMUSCULAR 1. Proximal myopathy (Graves’) 2. Reflexes – slow to relax in hypothyroidism 3. Legs for pretibial non-pitting oedema (Graves’  or  hypothyroid)

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3.

APPROACH TO THE SOLITARY THYROID NODULE Prevalence:

About 4-8% of population in US have palpable thyroid nodules; prevalence in Singapore not known.

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

Clinical features suspicious of malignancy: 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 - 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 that can cause bilateral vocal cord palsy

take extra care not to injure opposite recurrent laryngeal nerve as

MANAGEMENT OF BENIGN NODULE - Soft, small, round nodule with benign FNAC results, non-functional, not causing any symptoms - A lump >4cm has a greater risk for malignancy

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can follow-up and monitor for

in size

4. THYROID CANCERS Differentiated thyroid carcinoma Proportion Age F:M ratio

Medullary carcinoma

Anaplastic carcinoma

Lymphoma

10%

7%

3%

5%

25-40 years

40-50 years

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

60-70 years

>50 years

3:1

3:1

1:1

3:2

2:1

Papillary carcinoma

Follicular carcinoma

75%

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

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

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

- 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

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

Chemotherapy and/or radiotherapy depending on type of lymphoma

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

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 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) 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 Disadvantages of TT: - Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism - Very low incidence of cancer recurrence in residual thyroid – microfoci probably not clinically significant - Limited thyroidectomy may spare patient from having to be on lifelong thyroid hormone replacement Risk stratification helps to guide the extent of surgical resection in differentiated thyroid cancer according to  the  patient’s  disease. Lymph node clearance -

Tracheo-oesophageal groove (level VI) node clearance usually done Radical neck dissection or modified radical neck if: (i) Tracheo-oesophageal groove nodes histologically positive for cancer (ii) Clinically positive nodes in the neck – palpable or enlarged on ultrasound

Radical neck dissection The removal, en-bloc, of the entire ipsilateral lymphatic structures of the neck, from the mandible superiorly to the clavicle inferiorly, from the infrahyoid muscles medially to the anterior border of the trapezius laterally - Classic radical neck dissection (Crile’s) – internal jugular vein, sternocleido-mastoid muscle, and accessory nerve are resected. Structures not resected: carotid arteries, vagus nerve, hypoglossal nerve, brachial plexus, phrenic nerve - Modified radical neck (i) Type I: one of the three structures not removed, usually accessory nerve (ii) Type II: two of the structures not removed – accessory and IJV (iii) Type III: all of the three structures not removed (iv) Extended radical neck dissection: resection of lymph nodes and/or structures not included in the classic neck dissection - Complications of radical neck dissection: (i) Injury to nerves – vagus  (vocal  cord  paralysis),  cervical  sympathetic  chain  (Horner’s),  mandibular  branch  of  facial (lower lip weakness) (ii) Haematoma bring back to OT to find source of bleeding and stop it (iii) Salivary fistula (usually when pt has received RT to the neck, and if the upper GI tract was opened during the surgery) – infection can result (iv) Wound infection – risk factors: previous irradiation, if upper aerodigestive tract is opened during surgery with salivary contamination, salivary fistula (v) Carotid blowout – risk factors: infection, irradiation resus, apply constant pressure all the way to the OT! (vi) Poor healing – usually in irradiated skin; weakest point is the junction of the trifurcate incision -

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

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5.

SURGERY IN BENIGN THYROID DISEASE Indications for surgery: 1. Cannot be treated medically - failed medical therapy or unsuitable for medical tx 2. Cancer 3. Compression on neighbouring structures 4. Cosmesis 5. Compliance/cost problems – with long-term medical therapy (but patient may still require long-term therapy after op if he/she becomes hypothyroid or is still hyperthyroid) 6. Child-bearing (not a very strong indication since medical therapy can still be given, but not RAI) Types of surgery available: 1. Hemithyroidectomy – removal of one lobe of the gland, including the isthmus and the pyramidal lobe; usually for suspicious thyroid nodules 2. Total thyroidectomy – entire gland removed completely; usually done in MNG 3. Subtotal thyroidectomy - Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides - Harley-Dunhill subtotal thyroidectomy – leave a thumb-sized amount on one side with removal of the rest of the gland Total versus subtotal thyroidectomy (for hyperfunctioning thyroid disease) - Result of total thyroidectomy is always hypothyroidism, thus the patient will require life-long thyroid replacement and follow-up problems with compliance, cost, inconvenience - Results of subtotal thyroidectomy (at 5 years): o 60-70% euthyroid (do not require medication but still have to be followed up closely) o 16-20% hypothyroid (usually becomes evident within 1 year of surgery) o 8-10% hyperthyroid (percentage increases proportionately with time failure of surgical therapy) Difficulty in managing post-operatively and in the long term as patients need close monitoring (better off to just replace everyone after TT?), but weigh this against the benefits of not requiring any medication (for which there is a good chance) Complications of thyroid surgery: (Mostly  H’s,  one  I  and  one  T) IMMEDIATE ( Leg muscles (toe mvmts produced by leg muscles detect late) Can assess viability of muscle by making a cut – viable muscle will be shiny and twitches in response to flicking, while dead muscle will be dull and will not twitch - Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites in the muscle -

P/E Search for sources of embolisation: - Cardiac: AF, murmur (MDM), prosthetic click - Non-cardiac: AAA? Bruit?

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DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE (IMPT AS THE MANAGEMENT IS DIFFERENT) Embolic Thrombotic Identifiable source Present – AF, recent AMI Less common Claudication hx Negative Positive Physical findings Contralat pulses present Contralat pulses diminished White limb (no blood) Dusky limb (collaterals still supplying limb) Angiography Minimal atherosclerosis, Diffuse atherosclerosis, sharp cut-off, few collaterals irregular cut-off, well-developed collaterals CLASSIFICATION OF SEVERITY (SVS/ISCVS) Three categories: viable, threatened and non-viable (i) Viable: No immediate threat of tissue loss (ii) Threatened: Salvageable if revascularised promptly (iii) Non-viable: Limb cannot be salvaged and has to be amputated, no emergency to operate. Patient may require revascularisation to allow lower amputation or help the amputation to heal Severity depends on: - capability of existing collaterals to carry blood around occlusion - location of obs relative to no. of axial arteries (pop=1, fem=2, tib=3) - extent of obs: larger lose more collaterals - duration Pain Capillary refill Motor deficit Sensory deficit Arterial Doppler Venous Doppler Treatment

Viable Mild Intact None None Audible Audible Urgent work-up

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

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

ACUTE MANAGEMENT 1. DOPPLER U/S: viable vs threatened vs non-viable + level of obstruction 2. EARLY ANTICOAGULATION - Important to start anticoagulation with heparin if the suspicion of acute limb ischaemia is high, to avoid clot propogation - Give IV heparin bolus 3000-5000 units - Follow with IV heparin infusion at 1000 units/hour - Ideal PTT is 2 to 2.5 times normal 3. ANALGESIA 4. MEASURES TO IMPROVE EXISTING PERFUSION - Keep foot dependent - Avoid pressure to heel, extremes of temp - Max tissue oxygenation (O2 supp) - Correct hypotension 5. TREAT OTHER ASSOCIATED CONDITIONS (CHF, AF) INVESTIGATIONS -

Pre-operative investigations FBC, U/E/Cr, PT/PTT, GXM CXR and ECG if patient is older than 40 yrs old If suspecting an AMI with mural thrombus, do cardiac enzymes Biochemical abnormalities (muscle necrosis): K, CK, lactic acidosis

- ANGIOGRAM Can be done in pts with viable limb; in pts with threatened limb there is no time for angiogram may do on-table angiography High clinical probability of embolism does not need angiography Useful in 1. confirming an occlusion, 2. cause – thrombotic or embolic 3. pinpointing the level of occlusion and the anatomy DEFINITIVE TREATMENT OPTIONS Surgical - Embolectomy - Endarterectomy - Bypass grafting - Fasciotomy - Primary amputation

Endovascular - Thrombolysis - Angioplasty - Stenting

In general, embolectomy is done for embolic occlusion, while thrombolysis is done for thrombotic occlusion. Embolectomy - Can be done under LA but still require anaesthetist to monitor patient as he may be quite sick (e.g. AMI), and hyperkalaemia with cardiac arrhythmia can occur after reperfusion - Involves clamping of the involved artery and making an arterotomy - A Fogarty balloon catheter is inserted into artery until distal to the clot, then balloon is inflated to trawl clot out of the artery - Check for forward-bleeding and back-bleeding of the vessel (i.e. free spontaneous flow from proximal and distal ends of the artery when unclamped) - Flush with heparinised saline - Check foot – warm foot with good pulse indicates reperfusion - Important to monitor ECG for any arrhythmias! - Closure of arterotomy with meticulous haemostasis as patient is on heparin - Post-op: patient monitored in high-dependency; look out for reperfusion injury The reperfused muscles become oedematous (due to ROS tt injure cells), ing pressure in the compartments of the leg, like compartment syndrome Patient complains of calf pain Unable to dorsiflex ankle as the anterior compartment is affected first Requires three compartment fasciotomy to release pressure - Need to convert to full warfarin anticoagulation, uptitrating dose until INR 2-2.5 before stopping heparin (pt at risk of further embolic events) discharge patient to anticoagulation clinic for follow-up with warfarin advice

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Catheter directed thrombolysis - Angiogram done before thrombolysis to locate occlusion - Thrombolysis catheter inserted into the clot, and the thrombolytic agent is infused (Streptokinase, Urokinase, tPA) - Patient will be in high-dependency with thrombolytic infusion for 6 hours (~1000-4000 units per minute) - After 6 hrs, redo angiogram to check for residual clot; if some clot remains, adjust catheter into clot and infuse for 6 more hrs - After complete lysis of the clot, can do angioplasty - Takes much longer than embolectomy - Thrombolysis may be preferred for embolism in a diseased artery, since it may be difficult to trawl out the clot in a diffusely stenosed vessel – the clot may get caught on a proximal stenosed segment - CI Absolute 1. CVA within past 2 months 2. Active bleeding / recent BGIT past 10 days 3. Intracranial trauma/ neuroSx past 3 months Relative 1. CPR past 10 days 2. Major Sx / trauma past 10 days 3. Uncontrolled HTN Results: - Embolectomy has a 20% mortality, almost full success rate - Thrombolysis has a 10% mortality, only 35% successful DDx: - Acute DVT: Phlegmasia cerulean dolens = painful blue edema - Blue toe syndrome: atheroembolism from AAA or more proximal - Purple toe syndrome: Cx of warfarin therapy - Venous insufficiency - Venous occlusion - Acrocyanosis

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3. CHRONIC LIMB ISCHAEMIA Chronic limb ischaemia can be divided into critical and non-critical limb ischaemia, and non-critical ischaemia further subdivided into that which causes symptoms (usually claudication) and that which is asymptomatic. Most common cause is atherosclerosis with gradually developing diffuse stenosis of the peripheral arteries resulting in diminished blood supply to the lower limb (imbalance between supply and demand). Multiple collaterals form to bypass the obstructed vessels as a compensatory mechanism. Progression:

CRITICAL LIMB ISCHAEMIA Critical limb ischaemia is defined as decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present more than two weeks after the acute event (the converse of the definition of acute limb ischaemia). FEATURES: 1. Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks +/- Tissue loss (Gangrene or ulcers over the toes or feet) 2. Objective indication of poor vascular supply to the lower limbs (a) Ankle brachial pressure index 0.9 (can be more than 1.0 as ankle pressures tend to be higher than brachial; ABPI between 0.5 - 0.9 – occlusion, often associated with claudication ABPI 1.25, suggests non-compressible calcified vessel esp seen in DM patients do Toe pressure index instead (every value minus 0.2) - Accuracy of the index ABPI below 0.9 has 95% sensitivity and 100% specificity for detecting angiogram-positive peripheral arterial disease and is associated with >50% stenosis in one or more major vessels - Exercise treadmill testing Measure ABPI before and after patient exercises on a treadmill If the ABPI falls by >0.2 claudication 2. Arterial Duplex ultrasound - Non-invasive test, good alternative to angiogram - Duplex (means 2 modalities) = 2D ultrasound plus Doppler ultrasound (measures flow and waveforms) - Normal arterial flow waveform should be triphasic (rapid antegrade flow reaching a peak during systole, transient reversal of flow during early diastole, and slow antegrade flow during late diastole.); biphasic & monophasic waves are abnormal - Distal to stenosis: rate of rise is delayed, the amplitude decreased, and the transient flow reversal in early diastole is lost - A twofold increase in peak systolic velocity compared with the velocity in an adjacent segment of the artery usually signifies a stenosis of 50% or more - Can define anatomy of occlusions and also look for relatively  good  arteries  distally  for  “landing  zone”  of  bypass  graft

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3. Angiogram (arteriogram) - Invasive and associated with risks of 1. bleeding from arterial puncture, 2. dissection 3. damage to artery with worsening ischaemia - Usually only done if planning intervention e.g. angioplasty, stenting - Preparing for angiogram: Take informed consent from patient Ask about contrast allergy, asthma, renal disease, metformin Investigations: FBC (platelets impt), PT/PTT, UECr - Angiogram with digital subtraction – the images of the underlying bone are removed so as to better visualise the arteries (if the bones are visible, then it is a normal angiogram, without digital subtraction) 4. Basic laboratory investigation - FBC, UECr, PT/PTT, septic workup: bld c/s, wound c/s ASSESSMENT OF SEVERITY The  three  L’s  of  peripheral  arterial  disease: (i) Life – does disease threaten life (e.g. sepsis; other cxs of atherosclerosis e.g. stroke, AMI;) or will intervention cause risks (ii) Limb – will patient lose the limb (iii) Lifestyle – is the lifestyle of the patient severely handicapped, does it require intervention Fontaine system Stage I: Asymptomatic Stage IIa: Mild claudication Stage IIb: Moderate to severe claudication Stage III: Ischaemic rest pain Stage IV: Ulceration or gangrene (A) TREATMENT OF CLAUDICATION – BASED ON QOL Conservative Mainstay for all cases of claudicants, esp. foot and calf claudicants - RF control Assessment and treatment to optimise control of CVS risk factors– cardiologist Antiplatelets [e.g. aspirin] and statins (target lipid levels are much lower) Smoking cessation – not shown to be useful - Exercise training to stimulate collateral formation symptoms get better Exercise at least half to one hour every day Walk until pain comes, rest 2-3 minutes, walk again Keep a walk diary recording daily claudication distance in paces Supervised exercise 3X/wk helps. Advice to exercise alone does not. - Patient educaton: Teach patient to go to ED if symptoms of critical ischaemia arises Podiatrist to teach foot care - Medications Craxilen and Cilasterzol shown to increase claud dist - Ex. Use of Vasteral (methoxyphylline) is controversial - Monitor regularly with measurement of ABPI Intervention (endovascular or surgical) At least 6 months of conservative treatment first; mainly for aortoiliac disease Monitor claudication distance & ABPI – usually intervene if claudication distance 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 CVS 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 veins below the tourniquet are dilated when pt stands up, then the incompetent perforator is below level of the tourniquet - Repeat the test, placing the tourniquet at different sites: (i) Mid thigh (just below the Hunterian perforator) (ii) Below the knee (iii) Mid-calf - The incompetent perforator is located between just above the level where the tourniquet prevents dilation of the veins in the limb on standing -

[The alternative is the triple tourniquet test, where three tourniquets are tied with the patient lying down and then released from the bottom up to locate the site of insufficiency] TRENDELENBURG TEST - The SFJ is occluded (landmark is 2.5 cm below and lateral to the pubic tubercle) with the patient lying down - Get the patient to stand while holding the SFJ occluded - If varicosities do not fill up, the SFJ is the site of incompetence; if they fill up, there are other sites of incompetence (the SFJ may or may not be incompetent) PERTHES’ TEST (Test of deep venous obstruction) - Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe and then relax - In a person with normal deep venous drainage and competent venous valves in the communicating veins the superficial veins should drain into the deep veins - Positive test: patient will complain of pain and stop after ard 20 times because of increased swelling as blood cannot drain out through the deep veins

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Completing the examination - Auscultate over the varicosities for any bruit (indicate arteriovenous malformation) - Examine the abdomen for any mass that may be causing the varicosities Use of a handheld Doppler probe to detect incompetence 1. 2. 3. 4.

Doppler probe is placed along groin crease over SFJ (caution in obese ppl whose groin crease are lower) with patient standing Look for arterial signal then move medially SFJ 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 a prolonged sound – a second whoosh >0.5s indicates reflux of blood i.e. there is valvular incompetence of SFJ (90% accurate prediction) Can also perform test over popliteal fossa for SPJ but less accurate as the junction is variable. Therefore, you may be getting signals from the deep perforators instead. INVESTIGATIONS Venous duplex ultrasound - Indications: 1. Recurrent varicose veins 2. Complications of CVI: History of superficial thromobophlebitis 3. Skin manifestations of CVI: Venous eczema, Haemosiderin staining, Venous ulceration , Lipodermatosclerosis, 4. Everyone with varicosities to exclude subclinical DVT - Ask for (a) SFJ and SPJ reflux, (b) perforator, deep venous incompetency (c) DVT screen - Can delineate deep and superficial venous systems and locate sites of incompetence - Exclude presence of deep vein thrombosis – stripping is contraindicated MANAGEMENT Conservative 1. Lifestyle changes - Decrease amount of time spent standing - If due to job, change job or ask for change to position to stand & walking less 2. Graduated compression stockings, usually grade II ensure good pulses 3. Medications e.g. Daflon (only symptomatic, like painkillers) Surgical – the only definitive treatment Indications: 1. Cosmesis – large unsightly varicosities 2. Symptoms – pain, discomfort 3. Complications – signs of chronic venous insufficiency, venous ulceration Contraindications: 1. Infected ulcers. (slow healing ulcers that are not infected can still operate as it may improve the ulcer) 2. DVT: can rescan after medical treatment. If DVT resolves, can opt for selective stripping. 3. Thrombotic tendencies: patient may dev DVT in the future. Available modalities: 1. High tie with great saphenous vein stripping, and stab avulsion of varicosities 2. Ultrasound-guided foam sclerotherapy 3. Endovenous laser therapy (burns vein from within) 20% recurrence: due to large number of perforators left over even after stripping.

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4. VENOUS ULCERS CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY 1. Obstruction to venous flow – thrombosis 2. Incompetent valves – varicose veins, deep vein reflux (post-DVT) 3. Muscle pump failure – stroke, neuromuscular disease INVESTIGATIONS 1. Exclude infection of the ulcer and other complications - FBC for raised total white count - Swabs of the ulcer for Gram stain and cultures - X-ray of the area to exclude underlying gas, bone involvement 2. Venous duplex to map out venous system 3. Check for peripheral arterial disease by doing ABPI 4. Biopsy if  cannot  exclude  malignant  transformation  (Marjolin’s  ulcer) MANAGEMENT Conservative 1. 4 layer compression stockings (change 2X/week if ulcer, 1X/wk if no ulcer) (a) Non-adherent wound dressing over ulcer (e.g. Menolin) followed by wool bandage – most impt layer to protect ulcer (b) Crepe bandage (c) Blue-line bandage (Elset) (d) Adhesive bandage (Coban) Aim: ankle pressure around 30mmHg (can vary according to needs) Nowadays, 2 layer stockings are used too – can achieve the same ankle pressure but not as effective as it loses pressure more quickly so less consistent pressure. 2. Stockings: Once healed (cannot use with ulcer/wound), compression stockings should be fitted and continued for life 3. Symptomatic: Analgesia 4. Antibiotics if infected 5. Lifestyle (a) Warn patient to avoid trauma to affected area (b) Encourage rest and elevate leg Surgical If ulcer fails to heal: - First, exclude malignancy or other causes of ulcer (biopsy) - Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue - Venous surgery for the underlying pathology

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UROLOGICAL DISEASES

1. APPROACH TO HAEMATURIA DEFINITION: - >3 RBC / hpf. - DDx: haemoglobinuria, myoglobinuria, pseudohaematuria (menstruation), meds causing discoloration (eg rifampicin, phenytoin) CAUSES PreRenal

Renal

Postrenal

Drugs

Analgesics (NSAIDs) Anticoagulants Cytotoxic/immunosuppressive agents (eg cyclophosphamide) OCP Penicillin Quinine Warfarin Systemic Bleeding diathesis Sickle cell disease Metabolic Hypercalciuria Hyperuricosuriia Vascular AV malformations Renal artery disease – thromboembolism, dissecting aneurysms, malignant hypertension Renal vein thrombosis Vasculitis HSP PAN Wegener granulomatosis Glomerular Post-strep GN Post-infectious GN IgA nephropathy Lupus nephritis Other GNs TubuloPolycystic kidney disease interstitial Nephrolithiasis dz Malignancy – RCC, metastatic Pyelonephritis Renal cysts Infxns of ureter, bladder, prostate, urethra – eg schistosomiasis, TB etc Cancers of ureter, bladder (TCC), prostate, urethra Nephrolithiasis

HISTORY Post-renal Causes 1. Which part of urine stream is blood stained? - Beginning – urethra distal to UG diaphragm - End – bladder neck or prostate - Throughout – upper urinary tract or upper bladder 2. Painful vs painless haematuria Painful - UTI - Pyelonephritis - Tumour - Hydronephrosis - Renal cysts - Ureteric stone / clot - Bladder outflow obstruction (e.g. BPH, strictures)

Painless - Malignancy – TCC, RCC, Prostate - Drugs - GN - Bleeding diathesis - ITP / HSP - Infections – malaria, schistosomiasis - Exercise  (jogger’s  hematuria)

3. Severity - Clots - S/S of anemia

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4. Frequency + dysuria + haematuria - DDx: nephrolithiasis (colicky), malignancy, UTI (women & children), bladder outflow obstruction (men e.g. BPH – vascular prostate may bleed) 5. Other urological symptoms - Storage problem – frequency, urgency, nocturia, incontinence - Voiding problem – strangury, hesitancy, dribbling, incomplete emptying etc - Others – polyuria, oliguria, urethral discharge Pre-renal & Renal Causes 6. Associated fever – pyelonephritis, malaria 7. Screen for pre-renal causes LOW / bone pain / sickness 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), HTN, urolithiasis

Other necessary history 1. Infection - Fever, travel and contact history 2. Sorethroat - Post-strep/infective GN, IgA nephropathy 3. Autoimmune - Fever, rash, joint pain, oedema 4. Malignancy - LOW, bone pain, neuro deficits, SOB, liver function 5. PMHx - Renal dz, systemic dz (DM HPT Bleeding sickle cell) 6. Drug history / Hx of radiation 7. Family history – PKD, renal dz, Sickle cell, HPT PHYSICAL EXAMINATION 1. Check  patient’s  vitals- stable? 2. Conjunctival pallor 3. Abdomen – renal/bladder mass, palpable bladder (clot causing retention) 4. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension of tumour into renal vein, blocking the testicular vein where it drains into the left renal vein) 5. External genitalia – blood from urethra 6. Digital rectal examination – prostate enlargement (BPH versus cancer) INVESTIGATIONS URINE 1. Urine dipstick - Causes of false-positive for blood: haemoglobinuria, beetroot, drugs (rifampicin), metabolic (alkaptonuria, porphyria) 2. UFEME (normal (all below 5): RBC 3-5, WBC 2-5, EC 5 WBC per hpf), organisms - Casts nephritis

infection

3. Urine cytology for malignant cells - useful for: - High grade urothelial carcinoma (LG hardly shed cells) - Carcinoma in situ (imaging cannot see) 4. Urine phase contrast - RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source, while isomorphic RBCs suggest postrenal source (ureter, bladder, etc) 5. Urine culture and sensitivity

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BLOOD 6. Full blood count - How low is the Hb? - Elevated TW – infection 7. Urea, electrolytes and creatinine - Any renal impairment and electrolyte abn (renal or pre-renal dz more likely) 8. PT/PTT - Anycoagulopathy 9. GXM!!! IMAGING (HEMATURIA – IMAGE ENTIRE URINARY SYSTEM) Upper tract: imaging, lower tract: cystoscopy 10. Plain KUB - Margins: Superiorly needs to be above upper pole of the right kidney (T12), inferiorly needs to show pubic symphysis - Stones, size of kidney 11. Ultrasound of the kidneys - Renal size - Presence of any hydronephrosis, hydroureters - Renal stones 12. Intravenous urogram (IVU) - Look for 1. Distortion of renal OUTLINE and pelvic calyces by RCC, may have specks of calcification 2. Contrast UPTAKE: present or not (no contrast in obstruction / non-functioning), equal and symmetrical uptake 3. Configuration of the kidneys eg. Horseshoe kidneys 4. Stones (filling defect, proximal dilatation, decreased distal passage of contrast) + hydroureter and/or hydronephrosis 5. Filling defect in bladder due to TCC 6. Increased residual volume in bladder after micturition due to BPH - Intravenous contrast used to delineate anatomy of the kidneys and urinary system - Various phases: (i) Control film – plain KUB (ii) Tomogram – zoom into kidneys before contrast (iii) Nephrogram phase (1 min after contrast) – contrast fills kidney parenchyma so kidneys become more visible measure size, outline (iv) Pyelogram phase (3-5 min) – contrast fills calyces & pelvis, can detect dilated calyces/pelvis (hydronephrosis), any filling defects (v) Release film (abdominal binder which was placed to slow the flow of contrast into the bladder is released) – shows ureters, any hydroureter, filling defects (vi) Cystogram - any filling defects, abnormal appearance of the bladder (fir-tree appearance in neurogenic bladder) (vii) Post-micturition – any residual urine in bladder after voiding - Contraindicated in: (a) Contrast allergy (b) Renal impairment (Cr >200) (c) Patients on metformin (can cause lactic acidosis; patients need to stop metformin 2 days before and after study) (d) Patients with asthma (given steroids for 3 days before study) (e) Pregnancy: ask LMP 13. CT urogram / IVP - Non-contrast phase (stones) Nephrogram (tumors) Delayed phase - Adv: Ability to see renal parenchyma tumors (IVU only sees outline) - Disadv: Radiation ++ (3 CT scans) 14. Cystoscopy - Detection of bladder tumour (IVU may not pick up small tumours 50% of cases - When tumour has grown large enough, dull flank pain and palpable mass may result Classical triad of RCC: flank pain, painless haematuria, palpable renal mass (indicates late stage disease) 2. Complications 1. May have fever a/w night sweats, LOA, LOW, malaise 2. Polycythaemia occurs in 1-5% (due to increased erythropoietin) 3. For left renal tumour, extension of tumour into left renal vein can cause a left varicocoele as the left testicular vein becomes occluded 4. Extension into IVC can cause (a) lower limb oedema, (b) ascites, (c) liver dysfunction, (d) pulmonary embolism 5. Paraneoplastic syndromes are uncommon – Cushing’s,  hypercalcaemia,  hypertension 3. Metastasis - Symptoms of metastases – lungs, liver, bones, brain, lymph nodes

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INVESTIGATIONS DIAGNOSTIC 1.

Imaging – CT and/or ultrasound - Presumptive diagnosis is made on imaging – a renal parenchymal mass with (a) thickened irregular walls and (b) enhancement after contrast injection suggests malignancy

2.

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

STAGING 1.

CT scan of the abdomen - Perinephric invasion, adjacent organ invasion - Extension into renal vein, IVC - Lymph node enlargement - Liver metastases

2.

CT scan of the chest - For lung metastases

Also, Bone scan - Only done if patient complains of bone pain and/or alkaline phosphatase is raised MRI of abdomen and heart - Superior to CT for evaluation of IVC and right atrium involvement T1

Tumour 90% 5 year survival >75% >60% 60 years old) - 4:1 male predominance PATHOLOGY - TCC is the most common tumour of the bladder (>90%) Thought to arise due to exposure to carcinogenic substances in the urine urothelial cancers think FIELD CHANGE effect, thus urothelial tumours often occur multifocally Screen ENTIRE urothelium every f/u Papillary in nature (more differentiated) - Adenocarcinoma (1%, arises from remnant of the urachus in the dome of the bladder), - SCC (T2

Grading is also important T1 15% becomes invasive T1G3 75-80% invasive

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thus used for staging

MANAGEMENT DEPENDENT ON STAGE SUPERFICIAL TUMOUR - Primary treatment is TURBT of the tumour - Intravesical therapy BCG – 1 instillation per week for 6 weeks Mitomycin C – single instillation within 24hrs of TURBT, or weekly/monthly treatments for up to 2 years Indicated in patients with high risk of tumour recurrence or tumour progression: 1. high grade, 2. multiple primary sites, 3. multiple recurrences, 4. tumour size >3cm, 5. primary or coexisting carcinoma in-situ, 6. prostatic urethral involvement - Follow-up: Urine cytology with cystoscopy 3-monthly for 1 year 6-monthly for next 4 years Yearly thereafter IVU every 2 years MUSCLE-INVASIVE0 - Radical cystectomy with urinary diversion Radical cystoprostatectomy with pelvic lymphadenectomy in male Anterior exenteration with pelvic lymphadenectomy in female (Cx: perineal hernia) Ways of diverting urine output o Ileal conduit (a segment of ileum with ureters attached, as a stoma; not continent) o Neobladder construction using ileum (only if urethra not removed; continent, better quality of life) o Cutaneous ureterostomy (use ureters to create stoma, but easily stenosed due to small calibre; not continent) o Stoma with pouch construction under abdominal wall (not continent) - Radiotherapy (not as good as surgery) METASTATIC Chemotherapy

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4. UROLITHIASIS STONE COMPOSITION - Calcium oxalate or calcium phosphate stones – 75% - Magnesium ammonium phosphate (struvite = MAP) stones – 15% - Uric acid and cystine stones – 10% - Can occur at any level in the urinary tract, but most commonly in the kidney PATHOLOGY - Most  important  cause  of  stone  formation  is  increased  urine  concentration  of  the  stone’s  constituents,  such  that  they  exceed  their solubility precipitate as stones E.g. hypercalciuria with or without hypercalcaemia, hyperuricuria - Urinary tract infections– struvite stones form in Proteus vulgaris infections ( splits urea into ammonium), generating alkaline urine Bacteria can also form nidi for the formation of any kind of stone PRESENTATION DEPENDS ON SITE Renal stones - Most often asymptomatic unless the stone gets lodged in the pelviureteric junction causing hydronephrosis and subsequent infection pyonephrosis - Vague flank pain may occur. Bleeding? Ureteric stones - Even small stones can cause severe symptoms as the ureter is narrow (a) Classically ureteric colic pain – severe, intermittent loin-to-groin pain (b) Haematuria – gross or microscopic (c) Irritative symptoms – frequency, urgency (d) Can cause upper urinary tract infection Pyonephrosis! (infected purulent urine in an obstructed collecting system) fever with C&R, pain, can be very ill (sepsis) Management: - Broad spec Abx eg. Ceftriaxone - DECOMPRESSION using PCN or URS with stenting (no need to remove stone in same setting) Loin pain DDx: MSK (diff to differentiate) Bladder stones - May be asymptomatic (a) Can cause irritative urinary symptoms – frequency, urgency (b) Haematuria (c) If infection is present – dysuria, fever, etc PHYSICAL EXAMINATION - In ureteric colic, symptoms are often out of proportion to signs – no guarding, rebound, etc - If the patient has pyelonephritis, renal punch may be positive (DDx spinal pain by pressing on the spine) - Otherwise unremarkable examination

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INVESTIGATIONS Diagnosis 1.

2. 3.

KUB - May be able to see radio-opaque stone (90% of renal stones are radio-opaque) - False neg: too small. False positive: Phlebolith (perfectly round, sometimes with lucent centre. Found in pelvis near ureters), stools - K: Look at kidney size, any renal stones - U: Trace path of ureter along tips of transverse processes, across sacroiliac joint, in front of bifurcation of common iliac arteries and medially into bladder at ischial tuberosity, looking for ureteric stones - B: Look for bladder stones Intravenous urogram - Can also help to visualise a stone - Can show dilated urinary system secondary to stone obstruction – hydroureter and/or hydronephrosis Ultrasound of kidney or bladder - Features of stone: echogeneic rim, posterior acoustic shadowing

Complications 4. 5. 6.

Urine tests – dipstick, UFEME, urine culture/sensitivity - Haematuria - Pyuria, micro-organisms (UTI) Intravenous urogram - as above MAG-3 renogram - If pyelonephritis present due to stone obstruction, it is valuable to measure the renal function using the MAG-3 renogram - The renogram gives the differential function of each kidney – in normal individuals the function should be approximately 50% on each side (out of 100% for both kidneys combined) - If one kidney has less than 15% of total renal function, it is not worth salvaging the kidney

TREATMENT CONSERVATIVE Stones smaller than 5mm can be treated conservatively as 60% will be passed out; only treat if they (a) do not pass out after 4 to 6 weeks, and/or (b) cause symptoms (a) Treatment of any urinary tract infection (b) If underlying disease present that causes increased urinary concentration of stone components e.g. hypercalcaemia disease if possible (c) Diet: High fluid intake Low salt intake Restriction of red meat, dairy produce, refined sugars Increase citrus fruit intake SURGICAL INTERVENTION Indications: - S/S: Constant pain - Cx: Obstructs urine flow Causes urinary tract infection Damages renal tissue or causes significant bleeding Increase in size - Unlikely to resolve with conservative Tx: Does not pass after one month Too large to pass spontaneously

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treat

Types of treatment available: [from top to bottom] 1.

Percutaneous nephrolithotomy (PCNL) - Done for renal stones that are too large for ESWL to disintegrate - CI : uncorrected bleeding diathesis, patients unfit for GA

2.

Extracorporeal shock wave lithotripsy (ESWL) - Calcium oxalate, uric acid and struvite stones fragment easily, but calcium phosphate and cystine do not - Used for stones below 2cm in size - Used for renal stones and upper ureter stones – not so good for lower system due to difficulty in access - CI: (a) pregnancy, (b) untreated UTI, (c) untreated bleeding diathesis, (d) Total obstruction ( need stone-urine interface for it to work) (e) distal obstruction that cannot be bypassed with a stent (f) ESRF (no urine to flush stones down) - Cx: (a) Bleeding (capsular hematoma) (b) Sepsis (if stone is infected) (c) Injuries to surr tissues

3.

Ureterorenoscopy with lithotripsy (URS + LL) (usually laser lithotripsy, can also be done by pneumatic drill, electrohydraulic means) - For stones along the ureter - Retrograde pyelogram to see the stone?

4.

Cystolitholapaxy (stone crushing) for bladder stone

Open surgery (pyelolithotomy or ureterolithotomy) – rarely done; only if failed other management strategies, altered anatomy, performing open surgery for another reason anyway, non-functioning kidney Adjuncts: Double-J stent (or DJ stent) – inserted to stent the urinary system when - worried that stone fragments after ESWL may cause obstruction e.g. when ESWL used for treatment of a large stone; or if system is obstructed to begin with, may want to stent to ensure good drainage after surgery - to prevent stricturing Summary of treatment modalities (ESWL: any level of ureter) Location Renal: 2cm

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

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

Upper 1cm

< 5mm 5-10mm > 10mm

Conservative management unless symptomatic/persistent ESWL URS with lithotripsy

Mid/Distal ureter: 5mm

< 5mm > 5mm

Bladder: multiple

< 30mm > 30mm

Conservative management unless symptomatic/persistent URS with lithotripsy ESWL Cystolitholapaxy Open cystolithotomy (also if there are multiple stones)

ureter:

3cm/

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5. APPROACH TO ACUTE RETENTION OF URINE CAUSES: BPH, FAECES, ANTICHOL, UTI, STRICTURE, STONES Mechanical

Extraluminal (5)

Intramural 54)

Intraluminal (3) Nonmechanical

Cord disease/ injury neurogenic bladder Neuropathy Drugs (4A) Others (3P)

Prostate enlargement (benign/malignant/prostatitis) – BPH is the commonest cause! Faecal impaction Pelvic tumour, ovarian cyst, fibroid Pregnancy, retroverted gravid uterus UV prolapsed Tumour of the bladder neck (TCC) Urethritis (UTI) Urethral stricture from STD, prev instrumentation Phimosis Urethral trauma/rupture Stones Blood clot (clot retention in haematuria) Foreign body Cord compression, cauda equina Multiple sclerosis Tabes dorsalis (Tertiary syphilis) Diabetic autonomic neuropathy Anticholinergics (cough medicine, Overactive bladder Tx), antihistamines, anti-depressants, alcohol Prolonged immobility Post-anaesthesia Pain

HISTORY 1. Confirm Dx (Symptoms of ARU) [3] - Sudden inability to pass urine - Suprapubic pain (unlike chronic retention of urine which is painless) – severe! - Suprapubic distension 2. Precipitating factors: (if present, higher the chances of retaining bladder abilities after Tx with TURP) [4] (a) UTI: dysuria, frequency, urgency, nocturia, haematuria (b) Constipation (c) Drugs e.g. cough mixture, antihistamines (d) Immobility 3. History suggestive of aetiology: - Previous history of obstructive symptoms BPH - Previous history of ureteric colic pain or stones - Previous urethral instrumentation or STD stricture - Gross painless haematuria recently TCC, bladder stone, blood clot - Recent trauma to urethra - Inguinotesticular pain, urethral burning, dribbling Prostatitis - Lower limb weakness/paralysis, bowel incontinence, back trauma, history of spinal disease e.g. PID, spinal stenosis neurogenic bladder - Constitutional symptoms: LOW, LOA, malaise (any tumour in general) 4. Complications: [3] - Infection – symptoms of UTI - Stone disease (if in the bladder, usually asymptomatic) - Renal failure (more likely in chronic retention) – vomiting, lethargy, drowsiness

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PHYSICAL EXAMINATION - General condition Vitals (fever) sallow appearance, scratch marks, pedal oedema, etc (uraemia) - Abdomen Palpable bladder – tense, dull, rounded, tender, pressure chronic retention) Other pelvic masses – fibroid, gravid uterus, ovarian cyst Faecal loading Bilateral enlarged kidneys (hydronephrosis)

desire to micturate (large bladder up to umb suggests b/g of

- External genitalia: narrow maetus, tight foreskin - Digital rectal examination Any saddle anaesthesia (buttock and perineum – ind cauda equina) Anal tone Prostate enlargement (>2FB) – firm and smooth? Or hard, craggy, irregular, rectal mucosa not mobile? Tender? (prostatitis) Stool impaction - Neurological examination LMN paralysis of the lower limbs? Any sensory level present? IMMEDIATE MANAGEMENT – PROMPT BLADDER DECOMPRESSION - 1st choice: URETHRAL CATHETERISATION (14F) (CI!!: S/S of urethral injury – (a) blood at urethral meatus, (b) high-riding prostate – more relevant in the trauma setting) If cannot pass into bladder: a) enlarged prostate use thicker catheter (stiffer, easier to pass through) b) urethral stricture (clue: catheter is stuck quite proximally along the penile urethra / PHx of instrumentation/STD) smaller gauge catheter Do not push too hard – may cause false passage creation if the obstruction is due to a stricture - If urethral catheterisation fails suprapubic catheterisation Requires distended bladder which pushes the surrounding bowel loops away so that risk of bowel injury is lower: Method: Local anaesthetic injected 2 fingerbreadths above pubic symphysis Small incision made in the skin and fascia, and trocar inserted When a gush of urine is seen, the suprapubic catheter is inserted and secured INVESTIGATIONS 1.

2.

Bloods/Urine a. Urine dipstick, UFEME and culture/sensitivity (UTI, hematuria) b. UECr: raised creatinine (renal impairment secondary to obstructive nephropathy) c. FBC: raised TW (infection) – not usually done Imaging 1) KUB for stones, faecal loading 2) U/S bladder: (1) stones, (2) tumour, (3) prostate volume, (4) intravesical protrusion of prostate 3) U/S kidney, ureters: hydronephrosis, hydroureters (obstructive complication)

PSA - to be done 4-6/52 later (as ARU can cause raised PSA) - PSA velocity (rate of rise), free/total PSA, PSA density (= PSA/prostate volume) - >/= 2 readings 2/52 apart - Causes of raised PSA i. ii. iii. iv. v.

cancer BPH [usually 11days ARU

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TREATMENT 1.

Treat reversible causes - Stop drugs that may have precipitated ARU - Relieve constipation with fleet enema, lactulose, senna etc - Treat any urinary tract infection if present

2.

Monitor for complications (a) Post-obstructive diuresis = diuresis that persists after decompression of bladder Urine output >200ml/hr for 2 hours or more Due to tubular damage from chronic obstruction of drainage of the pelvicalyceal system, resulting in transient impairment of concentrating function. Usually seen in CRU, representing appropriate attempt to get rid of excess fluid in the body during period of obstruction. Can result in hypotension and electrolyte abnormalities (hyponatraemia, hypokalaemia, hypovolaemia) close monitoring of urine output and fluid/electrolyte status with appropriate replacement and resuscitation (b) Haemorrhage ex-vacuo (transient hematuria) Bladder mucosal disruption with sudden emptying of greatly distended bladder Usually self-limiting, rarely clinically significant drain urine in 500-750ml aliquots, with 15-20min intervals between each (c) Hypotension secondary to vasovagal response or relief of pelvic venous congestion

3.

Trial-off catheter - Take  off  catheter  and  watch  patient’s  output,  as  well  as  perform bladder scan to measure bladder volume - If patient cannot pass urine and bladder volume >400ml re-catheterise - When patient passes urine, can perform 1) uroflow to investigate severity of outlet obstruction, and also do 2) bladder scan post-micturition to check residual volume

Failed Trial of void: after how long can try TOC? 1. Long term catheterization 2. Clean intermittent catheterization: a. Adv: improved rate of spontaneous voiding (pt can PU in btw), decrease UTI 3. TURP (if sec to BPH): refer to indications 1 and 2 are done while waiting for medical therapy to work. Urinary obstruction + Fever

Admit! (Uro emergency)

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6. BENIGN PROSTATIC HYPERPLASIA EPIDEMIOLOGY - Very common problem in men - Frequency rises with age after the age of 30, reaching 90% in men older than 80 PATHOLOGY - Results from proliferation of both the epithelial and stromal components of the prostate with resultant enlargement of the gland - Commonly occurs in the central zone of the prostate 1) Major stimulus: dihydrotestosterone (produced from testosterone by 5-alpha reductase) 2) Age-related increases in oestrogen levels may also contribute to BPH by increasing the expression of dihydrotestosterone receptors on prostatic parenchymal cells - Chronic obstruction leads to hypertrophy of the detrusor muscle and trabeculation of the bladder mucosa as the bladder tries to empty against increased resistance PRESENTATION (APPROACH TO OBSTRUCTIVE UROPATHY) - Lower urinary tract symptoms (LUTS): Obstructive Hesitancy Straining to pass urine (strangury) Weak stream Prolonged micturition Terminal dribbling Feeling of incomplete voiding Double voiding (pis-en-deux) Obstructive S/S predominate.

Irritative [FUNI] Frequency Urgency Nocturia Urge incontinence Dysuria Irritative S/S significant for Cx of urine retention: UTI, stones

- Haematuria (UTI or rupture of enlarged veins) - Fever (UTI - pyelonephritis from ascending infection) - Rule out other DDx (refer ARU): Stricture/ bladder neck contractures: previous instrumentation or STDs causing urethritis/ post- TURP Drug causes: codeine (cough mixture), BB, anti-cholingerics, TCAs Chronic constipation Ca bladder neck/ Ca Prostate: LOW, LOA, bone pain, haematuria Neurogenic bladder - 6 COMPLICATIONS of an obstructive uropathy: a) Acute urinary retention (previous admissions and IDC) b) UTI: irritative symptoms, haematuria c) Stones: irritative symptoms, haematuria d) Hydronephrosis, pyelonephrosis: loin pain, fever Renal impairment: polyuria/ anuria. e) Overflow incontinence 2o to Chronic urinary retention with high post-void residual volume in the bladder f) Hernia sec to chronic straining - Other aspects of history: Social history (effect on lifestyle)

252

253

PHYSICAL EXAMINATION Inspection - Vitals: BP for HPT? (CRF) Fever? (UTI) Urine output? (CRF) - Already on IDC? (ARU) Diapers? (incontinence) Hematuria? (UTI, stones) - Sallow? Anaemia? (of CRF/ underlying malignancy) Cachexia (CA) - Hernia repair scar? (hernia) Palpation - Check for hernias - Abdominoperineal masses (fecal loading, masses to compress) - Any ballotable kidneys? (Hydronephrosis, Pyelonephritis) - Renal punch? (Pyelonephritis) - Palpable tender bladder in (ARU) non-tender (CRU) - Pedal/ sacral oedema (CRF) - Bony tenderness (tumor) Confirm diagnosis and R/O DDx: - DRE impacted stools prostate (benign): 1. smooth enlarged 2. median sulcus, 3. rubbery, 4. non-tender, 5. mobile mucosa INVESTIGATIONS Blood - FBC: anaemia, raised WBC - UECr: dehydration, raised creatinine renal impairment due to chronic obstruction - UFEME, cytology, urine c/s: for UTI and screen for cancer - PSA (done 4-6/52 later to avoid false +ves): normal 100ml, bladder stone, measure intravesical prostatic protrusion (IPP) - Cystoscopy to rule out stones, strictures/ bladder neck obstruction or cancer, - Uroflowmetry to confirm obstruction to urinary outflow (IMPT!!) 1. normal bell shaped curve, saw tooth appearance 2. Volume voided (>100ml to be valid): too low (falsely low peak flow rate), too high (falsely long duration, increase RU) 3. Normal peak flow rate (Qmax) > 15ml/sec 4. Residual urine 0 in young males, can accept up to 50ml in elderly

A) BOO with normal detrusor muscle: max flow rate 10ml/sec, prolonged flow. B) BOO with abdo straining: intermittent flow, peak flow rate may be normal or high, especially if outlet resistance is reduced

- ± urodynamic studies, TRUS with biopsy TRO prostate cancer if PSA >10

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COMPLICATIONS -

Acute/chronic urinary retention Bladder stones & Recurrent UTI Gross haematuria (after excluding other causes) Renal impairment secondary to outflow obstruction Co-existence of prostate cancer

MANAGEMENT - Divided into watchful waiting, medical management, and surgical management - Objectives of treatment: Rapid and sustained relief of symptoms, prevent long-term  complications,  improve  patient’s  quality  of  life I. Watchful waiting - Suitable for patients with minimal symptoms, no complications and normal invx - Monitor  patient’s  symptoms  and  clinical  course  annually II. Medical treatment 1. Alpha blockers (Prazosin, Terazosin, Doxazosin, Alfuzosin) - dynamic - Treatment of symptoms (blocking  the  α-1 adrenergic receptors in the bladder neck, prostate and urethra – relaxing the area) - Result in decreased outflow resistance and decreased bladder instability - SEs: include postural hypotension, dizziness, lethargy, lightheadedness 2. 5-alpha reductase inhibitors (Finasteride, Dutasteride) – static -

Treats the disease (not just symptoms) by inhibiting conversion of testosterone to dihydrotestosterone by 5-alpha reductase

-

Proven to decrease need for surgery and acute retention rates Only effective after 6 /12 (counsel the patient!), and in prostates >40g Most common side-effect is Sexual dysfunction. Warn patient about Gynaecomastia (1%) and stop med when they notice it developing. Hair growth. Ex: $3/pill. Combi therapy better than monotherapy.

-

III. Surgery Types Transurethral resection of prostate (TURP)is the gold standard Transurethral incision of the prostate (TUIP): decision made during TURP when the prostate does not appear to be enlarged cuts around the bladder neck area to open it up. Adv: 50% chance of Retrograde ejaculation Laser prostectomy is promising (pending long term results) Other techniques do not show good results: stenting, cryoablation, etc.

prostate size

make small

Indications: 1. Failed medical treatment 2. Significant Complications (4): Refractory urinary retention, Recurrent UTI, Bladder calculi, Obstructive uropathy 3. Recurrent gross haematuria Aim: to widen bladder neck Complications of TURP: bold = must mention during consent taking 1. 2. 3. 4. 5.

6.

Bleeding, infection, risk of GA/ spinal analgesia Local injury causing incontinence (1%), stricture / bladder neck stenosis Perforation of the urethra or bladder dome can form fistula Retrograde ejaculation (100%) impotence: (incompetent bladder neck). Always check if pt is planning to have children! TUR syndrome (10ng/ml: biopsy recommended as >50% of patients will have prostate cancer - 4-10ng/ml: biopsy advised, though only 20% will have prostate cancer -