SURGERY NOTESAdapted 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) <750 750-1500 1500-2000 % 15-30 30-40 <15 Ht rate <100 >100 >120 BP Normal Normal/min low Decreased Cap refill Normal Prolonged Prolonged Resp rate 14-20 20-30 30-40 Ur output (ml/h) >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 pelvic #. missed fractures. rectal wall integrity. stridor. percuss.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. palpable deformity Comprehensive oral/dental examination Caution: potential airway obstruction in maxillofacial injury. any step deformity Complete neurological examination C-spine imaging Caution: Injury above clavicles. deformity Pain. painful injury (distracts from cervical spine pain) Neck (soft tissues) Blunt versus penetrating injuries Airway obstruction. Neurovascular status X-rays as appropriate Caution: potential blood loss is high in certain injuries (e. soft-tissue or ligamentous injuries. CT scan Caution: hollow viscus and retroperitoneal injuries. cribriform plate # with CSF rhinorrhoea do not insert nasogastric tube Cervical spine Palpate for tenderness. blood Vaginal examination: blood. examine patient’s back ADJUNCTS & SPECIAL As required according to suspicion. excessive pelvic manipulation Perineum Contusions. femoral shaft fracture). lacerations Musculoskeletal – extremities Contusion. haematoma. 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 . hoarseness Crepitus (subcutaneous emphysema). occult injuries Chest Inspect. Perfusion. pelvic fracture.g. altered consciousness (cannot assess accurately). auscultate Abrasions and ecchymosis – “seat-belt sign” Lower rib fractures liver and spleen injury Re-evaluate frequently Special studies: FAST. percuss. palpate. bruit Caution: delayed s/s of airway obstruction that progressively develop. DPL (diagnostic peritoneal lavage). periorbital oedema. increase in chest tube drainage Abdomen Inspect. auscultate Re-evaluate frequently Look at CXR Caution: missed injury. palpate. high-riding prostate. occluded auditory canal Maxillofacial Bony crepitus/deformity. lacerations Urethral blood DRE: Sphincter tone. other severe. haematomas. diaphragmatic defects or bowel injury Compromised in uncooperative. agitated patient. ABDOMINAL TRAUMA TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA Solid organ injury: spleen. 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.2. 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 <5min Can be used for serial examination Does not require contrast. R upper quadrant. WBC >500. L upper quadrant. obesity. diaphragmatic injuries. aspirate. intraperitoneal injury False negative rate of 2% when there is failure to recover lavage fluid. 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. more operator-dependent. 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. cannot distinguish blood from ascites Intermediate results require follow-up attempts or alternative diagnostic tests Disadvantages Expensive Time required to transport patient Use of contrast Frank blood (>5ml) or obvious bowel contents aspirated Lavage fluid seen to exit from chest drain or urinary catheter RBC >100. subcutaneous air Less sensitive. early hollow viscus injury. infx). 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.000 per mm3. retroperitoneum. injuries to retroperitoneal structures 7 . substantial bowel gas. no radiation risk Advantages Able to precisely locate intra-abdominal lesions preoperatively Able to evaluate retroperitoneum Able to identify injuries that can be managed non-operatively Not invasive Positive DPL: Disadvantages Does not image solid parenchymal damage. muffled heart sounds. slowly withdraw the needle until the pattern returns to normal. CARDIAC TAMPONADE High index of suspicion required Clinical features Chest trauma and hypotension Beck’s triad (hypotension. distended neck veins) – only in 50% of cases as hypovolaemia may prevent neck vein distension. flail chest. pulsus paradoxus) Diagnostic clues Enlarged cardiac shadow in CXR (globular heart – very rarely seen) Small ECG voltages.3. If the ECG waveform shows an injury pattern (ST segment elevation). and pneumothorax. haemothorax. Pericardial fluid demonstrated on FAST or 2D-echo . electrical alternans = alternation of QRS complex amplitude or axis between beats. as this change in waveform suggests that the spinal needle is in direct contact with the myocardium) 8 . muffled heart sounds least reliable Pulseless electrical activity Kussmaul’s signs (increased neck distension during inspiration. airway obstruction. CARDIOTHORACIC TRAUMA There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving: cardiac tamponade.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. It is most evident in trauma patients who may be hypovolemic with reduced venous blood return to the heart. fracture of >8 ribs. cricothyroidotomy. Cover defect with a sterile dressing. Results in hypoxaemia mainly due to underlying pulmonary contusion. previous pulmonary disease. tracheostomy FLAIL CHEST When 2 or more ribs are fractured at 2 points forming a flail segment that moves paradoxically with breathing. >3 associated injuries HAEMOTHORAX Chest tube insertion in the triangle of safety (bound by the lateral border of the pectoralis major medially. producing a “sucking chest wound”. taping it down on 3 sides to produce a flutter-valve effect.AIRWAY OBSTRUCTION Chin lift or jaw thrust Remove any foreign body manually. letting air out of the pleural cavity but not back in Insert chest tube (not through the wound) 9 . judicious fluid therapy (avoid fluid overload). contributed to by pain with restricted chest wall movement. age > 65. Management: Ensure adequate oxygenation and ventilation. severe respiratory distress Decreased venous return caused by compression of the relatively thin walls of the atria impairs cardiac function. neck vein distension. hypotension. 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. adequate intravenous analgesia Consider mechanical ventilation in high risk patients: shock. severe head injury. displacing mediastinal structures and compromising cardiopulmonary function It is a clinical diagnosis (CXR will only delay treatment. 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. and may cause death) – signs of pneumothorax. The inferior vena cava is thought to be the first to kink and restrict blood flow back to the heart. suction blood/secretions Definitive airway – ETT. a line just anterior to the mid-axillary line laterally. call urgent cardiothoracic consult PNEUMOTHORAX (TENSION/ OPEN) Tension pneumothorax = develops when air is trapped in the pleural cavity under positive pressure. and pre-retinal hemorrhages) Pathology: underlying brain damage in addition to expanding SOL Removal of blood does not solve brain damage poorer results Star shaped appearance (cisterns) Usually only small amount of blood conservative tx sufficient Any shape. will require evacuation Global injury of axons Arises from injury that causes rotational and shearing forces (high impact injury) – rapid acceleration and deceleration of brain in the intracranial cavity against relatively fixed points of attachment at the falx and tentorium (e. when rapidly changing velocities within the skull may stretch and tear small bridging veins Generally result from shearing injuries due to various rotational or linear forces (e. location If large haematoma. size. in which similar shearing forces classically cause intra.g. will see punctate haemorrhages at the grey-white border Hypoxic / Cytotoxic (cellular) Decreased blood supply (oxygenation) loss of function of Na-K pump as ATP decreases intracellular sodium cellular swelling Conventionally thought to be resistant to any known medical treatment Interstitial Impaired absorption of CSF increases in transependymal CSF flow acute hydrocephalus Also not responsive to steroid administration. shaken baby syndrome) Maximal effects at corpus callosum and brainstem One of the major causes of unconsciousness and persistent vegetative state after head trauma If severe. thus drainage gives good results Crescent shaped haematoma under the dura (between dura & arachnoid) More severe than EDH (usu due to nature of injury that causes SDH to occur – associated with higher impact. falls. RTA. assaults. and inflammatory conditions This edema subtype is responsive to both steroid administration and osmotherapy 10 increased . shaken baby syndrome. and its response to osmotherapy is debatable Vasogenic Breakdown of blood-brain barrier proteins enter interstitial space oedema Seen in TBI. but is reversible if no further insult occurs) Usually recovers in 2-3 hours Small haematoma <1cm Extradural haemorrhage Subdural haemorrhage Traumatic subarachnoid haemorrhage Intraparenchymal haemorrhage Diffuse axonal injury Cerebral oedema (3 types) Lens-shaped haematoma outside the dura (between skull & dura) Pathology: expanding space-occupying lesion 20% of patients with EDH are alert and well. neoplasms. increased ICP etc) since neuronal death is irreversible. thus brain has other injuries) Most often caused by head injury.4.g. underlying brain is minimally damaged. hypoxaemia. NEUROSURGICAL TRAUMA AIM: prevention of secondary brain injury (from hypotension. PATHOLOGIES Concussion Contusion Intracranial haemorrhage Physiological dysfunction without anatomical or radiological abnormality (Physiological dysfunction is the first step towards cell death. the uncus herniates over the edge of the tentorium. blood) are enclosed in a rigid space whose total volume tends to remain constant increase in the volume of one component will elevate pressure and decrease the volume of one of the other elements Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure Compensatory mechanisms: Hyperventilation vasoconstriction of cerebral vessels due to pCO2 CSF pushed into spinal canal (but limited volume available) Removal of any reversible cause of raised ICP will improve cerebral perfusion Fixed dilated pupil Cushing’s reflex blood volume Constrictor fibres to the pupil run in the oculomotor nerve. compressing the fibres of the oculomotor nerve just below Thus a fixed dilated pupil occurs on the side of the compression due to unopposed sympathetic supply (dilates the pupil) A triad of: Widened pulse pressure (HTN) Irregular breathing (Cheyne-Stokes breathing) Bradycardia From Monroe-Kellie doctrine.PATHOPHYSIOLOGY MonroeKellie doctrine The CNS & its contents (brain. monitor GCS If pt deteriorates CT scan Exclude metabolic causes (e. CSF. Increase in mean arterial pressure achieved by sympathetic overdrive: a) Increased heart rate b) Increased contractility c) Increased vasoconstriction – increased total peripheral resistance (a) and (b) increase cardiac output increased BP. GCS. IV drip (no dextrose saline!).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.g. pupil size Minor head injury (GCS >13) Most common Indications for admission: Moderate head injury (GCS 8 . MAP maintains cerebral perfusion pressure when ICP is raised. hypoglycaemia) Do septic workup (exclude sepsis) 11 . (c) increases BP Baroreceptors detect abnormally raised BP and try to decrease it by triggering a parasympathetic response via vagus nerve + Direct distortion of vagus nerve due to raised ICP heart rate Distortion and/or increased pressure of brainstem (controls involuntary breathing) irregular breathing and/or apnoea MANAGEMENT Assessment 3 important parameters: ABCs. no sedation. which exits the brainstem at the upper midbrain – nerve fibres lie just under the tentorium Uncus of the temporal lobe sits on the tentorium In raised ICP. 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.e. 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.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. This helps to reduce the fluid within intracranial space. however prolonged administration may lead to increase in ICP (must catheterise patient also. 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. Furthermore. the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation. and repair if dura is torn (since meningitis can occur with a torn dura) 12 . 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. do an urgent angiogram! SOFT TISSUE INJURIES Types Open: laceration. capillary refill Viability of the limb Neurological assessment Wounds – open or closed injury. 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. femoral shaft # (2L) Need to have high level of suspicion and treat with urgency Look out for any tachycardia. examine for compartment syndrome Circulation chart 13 . early signs of shock Prepare to resuscitate patient ASSESSMENT OF THE EXTREMITY Perfusion: colour. 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. skin temperature. abrasion over a fracture is considered open fracture Soft tissue assessment Deformity Abnormal joint mobility – ligamentous injury around joint. pulses. in knee. 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. with thrombosis and occlusion)? Skin colour/temperature Post-reduction tibial pulse in knee dislocation – if still absent.5. especially in open fractures). 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). malleable splint Neurovascular examination. ECG. early or late? Local or systemic? IMMEDIATE (<1 hour post-op) Local Damage to surrounding structures Primary haemorrhage (either starting during surgery or following post-op in BP) Replace blood loss and may require return to theatre to re-explore wound Systemic Basal atelectasis (collapse of alveoli): bronchial secretions post-op & patient does not breathe deeply due to pain Tx: chest physiotherapy. AMI. GXM. avulsions or flaps Type IIIA Extensive soft tissue damage. pulmonary embolism EARLY (first 24-48 hours post-op) Local Pain. hemorrhage Systemic Atelectasis (commonest cause of mild pyrexia in first 48hr) Shock.OPEN FRACTURES Definition: communication between the # or fracture haematoma and the external environment Gustilo-Andersen classification Type I <1cm AND clean Type II >1cm AND no extensive soft tissue damage. 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. Massive contamination common. incentive spirometry Shock: due to blood loss. 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. PT/PTT. or inadequate fluid replacement peri-operatively AMI. U/E/Cr. POST OPERATIVE COMPLICATIONS General or specific? Immediate. 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. PE Nausea & vomiting (analgesia/anaesthesia induced) Acute confusion: dehydration or sepsis (post-op confusion seen in 40%) 14 . Water (UTI). multiple use of same incision site Tx: Surgical repair of hernia if strangulated or if enlarging Bowel obstruction due to adhesions Fistula formation Secondary haemorrhage: often as a result of infection (usu 1-2wk post-op) Systemic Fever: Wind (atelectasis). fluid resuscitation. but if painful.LATE (between 48 hours to 1 month post-op) Local Post-op paralytic ileus Wound or anastomotic dehiscence (POD 7 – 10) Serosanguinous exudate Tx: Analgesia.g. Wonder drug (drug fever) Infections (day 3-5): phlebitis. pneumonia. straining from constipation). resuture under GA in OT Mortality up to 30% Post-op wound infection (usu within 1st week post-op) Pain. DM. usually due to skin staphylococci Incisional hernia 10-15% of abdominal wounds Usu asymptomatic. HIV Wound factors Wound infection Poor wound care 15 Surgeon factors Suturing under tension Did not observe aseptic technique . pelvic) Acute confusion: exclude dehydration & sepsis DVT & PE (day 5-7) POST-OP HAEMORRHAGE EARLY Consumptive coagulopathy – if large volumes of blood transfused Pre-op anticoagulation Unrecognized bleeding diathesis Damage to blood vessels/vascular organs Management FBC (plt). GXM & order blood Give protamine if heparin was used Give FFP / platelet concentrates if clotting screen abnormal Consider surgical re-exploration LATE Occurs several days after surgery Usually due to infection damaging vessels at the operation site Management Treat infection and consider exploratory surgery POOR WOUND HEALING Patient factors Poor blood supply Malnutrition Vitamin deficiency Immunosuppressive therapy Long term steroids Radiotherapy Co-morbidities e. (increased intra-abdominal pressure (chronic cough. redness. abscesses (subphrenic. wound infection. Walking (DVT/PE). UTI. Wound (infxn). consider strangulation (uncommon due to wide neck) RF: Obesity. sterile wound dressing. PT/PTT. poor muscle tone (old age). discharge. swelling. pregnancy (IVC compression) Trauma. deep S waves in V6 Right atrial hypertrophy: peaked P waves RBBB Classic S1Q3T3: S wave in I. pleural effusion. with collapse of the distal vessels (oligemia) Hampton hump: late sign. T inversion in III (rarely seen) D-dimer: poor sensitivity & specificity in ruling in/ out DVT or pulmonary embolism 16 . pelvic/ vascular surgery. antiphospholipid syndrome. intravenous drug use Congenital: protein C/ protein S deficiency. calculate probability of PE ECG May have normal ECG with sinus tachycardia Signs of right heart strain Right axis deviation: S waves in lead I Right ventricular hypertrophy: tall R waves in V1. tender. homocysteinuria/homocysteinemia Acquired: liver disease. dyspnoea. syncope. erythema Pitting oedema Homan’s sign: passive dorsiflexion of the ankle with knees flexed (DON’T DO: risk of clot propagation/ dislodging) Investigations sharp pain in calf Duplex ultrasound to detect DVT Chest x-ray: usually normal (classical findings listed below are rarely seen) Atelectasis. do CXR to assess ventilation of lungs IV contrast. new onset atrial fibrillation etc Physical Examination Mild fever Calf warmth. raised hemi-diaphragm Westermark sign: dilatation of the pulmonary vessels proximal to the embolism. Factor V Leiden mutation. Q wave in III. do CXR again to assess perfusion of lungs Look for areas of ventilation without perfusion (V/Q mismatch) Correlate with clinical findings. OCP use Presentation Post-operative fever (typically day 5-7) Lower limb pain & swelling. haemoptysis (poor sensitivity/specificity) Others: seizures. wedged shaped infiltrate with apex towards the hilum CT pulmonary angiogram (gold standard) Look for filling defects in pulmonary artery V/Q perfusion scan: no longer done Inhale radioactive isotope. cancer (production of pro-thrombotic factors). swelling.DVT/PE Affects 25-50% of surgical patients DVT in deep calf veins: 5-10% risk of PE DVT in iliofemoral veins: 50-60% risk of PE Risk Factors Virchow’s Triad 1) Alterations to flow 2) Endothelial injury 3) Hypercoagulable state Prolonged bed rest. discolouration: may not be at site of clot Classic triad of PE: chest pain. .0 to 3. X) Onset: 2 to 4 days (start by overlapping with heparin for 4 days) Efficacy monitored using PT/INR (target INR: 2. inactivates thrombin (PTT Onset: immediate for IV. intubation. inhibits synthesis of Vit K dependent factors (II. within 4 weeks Localized tenderness along the distribution of the deep venous system Entire leg swollen Calf swelling by more than 3 cm when compared to the asymptomatic leg (measured below tibial tuberosity) Pitting edema (greater in the symptomatic leg) Collateral superficial veins (nonvaricose) Alternative diagnosis as likely or more likely than that of deep venous thrombosis High Probability: ≥ 3 – treat as susp DVT and perform compression U/S Moderate Probability 1 or 2 – treat as susp DVT and perform compression U/S Low Probability ≤0 – D-dimer test 17 Score 1 1 1 1 1 1 1 1 -2 . paresis. VII. FFP SE: haemorrhage.Prophylaxis/ Treatment Non-pharmacological Use of inflatable calf pumps intra-operatively in patients undergoing long operations Early ambulation post surgery Thromboembolic deterrent (TED) stockings/ intermittent pneumatic leg compression Pharmacological Unfractionated heparin or LMW heparin – acute setting Unfractionated heparin Potentiates effect of anti-thrombin III. mechanical ventilation Initiate anti-coagulation Intra-venous thrombolytics if not contraindicated Surgical/ catheter embolectomy Well’s Criteria A set of criteria to determine the pretest probability of DVT Clinical feature Active cancer (treatment ongoing or within the previous 6 months or palliative) Paralysis.0) Antidote: vitamin K. 30 mins subcutaneously Efficacy monitored using aPTT Antidote: protamine sulphate Side effects: thrombocytopaenia ) LMW heparin (Clexane) Potentiates effect of anti-factor 10a (not reflected by PTT) Onset: immediate for IV More predictable dose-effect relationship Reversibility by protamine sulphate limited Warfarin – long term (8-9 months.g. or recent plaster immobilization of the lower extremities Recently bedridden for more than 3 days or major surgery. skin necrosis (in patients with protein C/S deficiency) Surgical IVC filter (permanent or temporary: remove after 2 weeks of anti-coagulation) Indications: History of recurrent DVT/PE Free floating thombus seen on duplex scan Patient not suitable for anti-coagulation e. up to 7 days post-op Allergy to anti-coagulation Treatment of Pulmonary Embolism Supplemental oxygen. hepatitis. or until clot dissolves) Vitamin K antagonist. IX. urine output. rigors Warm skin Fever.7. tachycardia. AMS cellular hypoxia TYPES OF SHOCK Types Hypovolaemic Causes S/S Invxs Cardiogenic Haemorrhage Burns Ruptured ectopic pregnancy Severe GE Acute pancreatitis AMI Dysrhythmia Pallor Cold clammy skin peri vas Pallor Cold clammy skin peri vas Hct (late) Neurogenic Spinal injury Obstructive Tension pneumothorax Cardiac tamponade Pulmonary embolism Warm skin N/ heart rate Neuro deficit Cardiac enzymes ECG Septic Anaphylactic Infxns Fever. rigors Warm skin FBC Bld C/S GENERAL MANAGEMENT AIRWAY Maintain airway – consider intubation if necessary BREATHING 100% O2 via non-rebreather mask CIRCULATION 2 large bore (14-16G) cannulae Inotropic support IV dopamine 5-10 g/kg/min IV dobutamine 5-10 g/kg/min (esp for cardiogenic shock) IV norepinephrine 5-20 g/kg/min (esp for septic shock) MONITORING Pulse oximetry ECG BP Heart rate Urine output – catheterize patient SPECIFIC MANAGEMENT HYPOVOLAEMIC SHOCK FBC – Hct (but inaccurate marker of acute blood loss . lactate. Trop T & cardiac enzymes Manage accordingly to cause – refer Emed book 18 .Hct in alcoholic binge from dieresis) GXM 6 units U/E/Cr Trop T (Cardiac enzymes) Coagulation profile with DIVC screen (PT/PTT. SHOCK Shock = inadequate tissue & organ perfusion to meet metabolic demands S/S: BP. diaphoresis. base deficits = poor prognostic factor UPT – r/o ectopic pregnancy (ask for LMP) Examine the abdomen for any pulsatile AAA Fluid resus: 1L crystalloid fast infusion over 1 hr Assess response Subsequent colloid or whole blood infusion CVP line insertion – to guide fluid resus CARDIOGENIC SHOCK ECG. D-dimer) ABG – metabolic acidosis. 4mg/kg/h for nxt 23 hrs Indications – non-penetrating spinal cord injury & w/in 8 hrs of injury Contraindications: <13YO Pregnancy Mild injury of the cauda equina / nerve root Abdominal trauma present Major life-threatening morbidity Refer Ortho / NeuroSx SIRS = 2 of the following present: Temp >38 or <36oC HR > 90bpm RR > 20 breaths/min OR PaCO2<32mmHg WCC>12000/mm3. pneumonia. GXM x 6 units. immunocompromised state FBC. pleural effusion. D-dimer). 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 . D-dimer ABG: PaO2 & N/ PaCO2. mechanism. gallbladder dz. U/E/Cr. U/E/Cr.4ml <50kg.5ml 50-65 kg. 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.OBSTRUCTIVE SHOCK Tension Pneumothorax Decompression: insert 14G cannula over 2nd intercostals space in mid-clavicular line Cardiac Tamponade IV fluid bolus 500ml N/S IV dopamine infusion 5 g/kg/min Prepare for pericardiocentesis Pulmonary Embolism FBC. DIVC screen (PT/PTT. fibrinogen. CXR. ABG. widened alveolo-arterial PO2 gradient (AaPO2 >20mmHg) ECG CXR (Exclude Ddx – pneumothorax. <4000/mm3. 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. 0.or >10% immature forms Identify site of infxn – UTI (indwelling cathether). followed by 5. rib #. 0. force Neuro exam. peritonitis.6ml >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. pneumonia. ECG. appendicitis. tumour. blood C/S. heart failure. Non-pruritic. severe HPT.000 dilution IV over 5 mins Glucagon Indications: failure of adrenaline Rx OR if adrenaline is contraindicated e. 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. egg white.1ml/kg (max 5ml) 1:10. peanuts Venoms – bees. FB / lines present) Anaerobic source (intraabdo. coxsackie virus. HBV. 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. pollen Infections – EBV. -blocker use 0.Empirical Abx: Immunocompetent w/o obvious source Immunocompromised w/o obvious source Gram-positive (burns. May be a/w numbness & pain Anaphylaxis – severe systemic allergic rxn to an Ag.g. q 6hr 20 . female genital tract. indwelling cath.0mg IV/IM. Ppt by abrupt release of chemical mediators in a previously sensitized patient Anaphylactoid rxn – resembles anaphylactic rxn. TCM. but due to direct histamine release from mast cells w/o need for prior sensitization Common causes Drugs – penicililns & NSAIDS commonest. aspirin. hornets Environment – dust.01ml/kg (max 0.5ml) 1:1000 dilution SC/IM Hypotensive – 0. pregnancy. 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. IHD. biliary. 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.5-1. wasps. sulpha drugs Food – shellfish. 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 . 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 – 2.8. greater surface area to body weight ratio) Deficits Thirsty: Tachycardia: Hypotensive: Ongoing/ anticipated losses 1.5 – 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. 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 22 .9% NaCl/ Normal saline (NS) 9g Na in 1L / 154 mmol Na & Cl (isotonic) Dextrose 5% (D5W) 50g glucose in 1L (200kcal.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.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.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. 1g glucose = 4kcal) (isotonic) Dextrose 5% in 0. the more O2 damage to the lungs) PEEP = positive end expiratory pressure (opens alveoli that would otherwise collapse in expiration) o Normal: 3 – 5 cmH2O (physiologic PEEP) o Therapeutic PEEP can go up to 10 – 35 cmH2O (but too high impedes venous return to the heart) Atelectasis = V/Q mismatch (shunt) 23 . the higher it is .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%. 45 [HCO3] > 24 mmol/L Respiratory Alkalosis pH > 7.5 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 1.35 [HCO3] < 20 mmol/L Respiratory Acidosis pH < 7.2 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 0.45 PCO2 < 35 mmHg Anion gap = [Na] – [Cl] – [HCO3] Normal = 3-11 mmol/L Hypoalbuminemia: anion gap in 2.2 mmol/L Chronic: PCO2 1mmHg = [HCO3] 0.35 PCO2 > 45 mmHg Metabolic Alkalosis pH > 7.6 x [HCO3 – 24]) + 40 mmHg PCO2 < expected concurrent respi alkalosis PCO2 > expected concurrent respi acidosis Respiratory Acidosis Acute: PCO2 1 mmHg = [HCO3] 0.7 mmHg Expected PCO2 = (0.4 mmol/L Respiratory Alkalosis Acute: PCO2 1 mmHg = [HCO3] 0.1 mmol/L Chronic: PCO2 1 mmHg = [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) 24 .ACID BASE & ELECTROLYTES Metabolic Acidosis pH < 7. Hyponatremia Hypernatremia Signs Confusion Seizures Cardiac failure Muscle weakness Nausea. Insulin 20 units + 250ml 25% dextrose over 4-6 hrs 3. Resin (polystyrene sulfonate sodium) (every g exchanges 3 mmol of Na for K) 7. suxamethonium) Digoxin poisoning Massive blood transfusion KCl excess Burns Rhabdomyolysis Tumour lysis Renal failure Addison’s disease Metabolic acidosis 1. Diuretics 4. 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. Calcium gluconate 10% (50-100ml) 2. spironolactone. 2 adrenergic agonists 5. Hemodialysis (definitive) 25 . Sodium bicarbonate (50 – 100ml) 6. NUTRITION Nutritional support should be considered for: BMI < 18. modified fat) Pulmocare (for COPD pts high calorie. 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. 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. high nutrient losses. peritonitis. then increase by 20-30ml/h and repeat.) ENTERAL FEEDING Start at 20ml/h x 6h. duration of reduced intake. degree of weight loss.5 cal/ml & protein 13 g/serving) Glucerna (for DM pts carbohydrates. Indications: Proximal small intestine intact & functional Stimulation of secretory function does not worsen the condition being treated (e. 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.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. 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.g. low carb to help CO2 production) Novasource Renal (for renal pts low protein & nitrogen content) 26 . blockage/extrusion/removal. enzyme induction from amino acid imbalance and excessive calorie administration. TPN must be given into a central vein TPN orders: 24 hr feeding volume 2500ml. Crohn’s. central vein thrombosis. 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. kcal from fat 0 2 days a week: kcal from carbohydrate 2000. line sepsis.g. UC) Inability to use the GIT: pancreatitis with pseudocysts/abscess where enteral nutrition is not tolerated Complications: Catheter-related o Mechanical: blockage. rate 100ml/hr 5 days a week: kcal from carbohydrate 2500. fat deposition in liver o Hypoglycaemia (too rapid cessation of glucose infusion) o Hypertriglyceridemia o Hyperchloraemic acidosis 27 . migration. infective endocarditis Metabolic o Hyperglycaemia o Deranged liver function: biliary stasis.TOTAL PARENTERAL NUTRITION Provision of all nutritional requirements by the intravenous route alone Due to high osmolality of the mixture. fracture. dislodgement o Infective: exit-site infection. Parastomal Umbilical. Lumbar. LUMPS & BUMPS 1.Coverings of sac: layers of abdominal wall . 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 .Sac: pouch of peritoneum (neck & body) . Obturator. border of rectus).Location: all occur at congenital or acquired weak spots in the abdominal wall .2. sigmoid. Gluteal.Expansile cough impulse 28 . Epigastric (herniation of extra-peritoneal fat) Rare types: Spigelian (herniation of linea semilunaris: lat.Acquired – trauma.Reducibility: on direct pressure or lying down . Sliding (herniation of posterior peritoneum with underlying retroperitoneal structures: caecum. direct (15%) or pantaloon (direct & indirect) Femoral (4%) & Richter’s hernia (knuckle of bowel wall is strangulated but lumen is patent) Incisional. or patent processus vaginalis . Internal. surgical incision or disease Consist of 3 parts: .Contents Types: 1) 2) 3) 4) 5) Inguinal (96%) indirect (85%). bladder) PHYSICAL EXAMINTION (common signs) .Congenital – normal (due to piercing structures). out of Hasselbach’s triangle Neck lies medial to inferior epigastric artery. R> L.Most common. then emerges from the superficial ring & descends into the scrotum . 20% are bilateral. laterally and backwards Reduces upwards and straight backwards Controlled after reduction by pressure over the deep ring Controlled after reduction by pressure over the superficial ring May descend down the scrotum Does not descend down the scrotum May cause strangulation at superficial ring (narrow) Rarely causes strangulation due to wide hernia neck Does not readily reduce on lying down Readily reduces on lying down More common in young adults and infants More common in old men 29 . patent processus vaginalis + weakened fascia at deep ring . 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.. rectus abd. 65% .Hernial sac enters the inguinal canal with the spermatic cord via the deep ring. post to the inguinal canal (med to inferior epigastric art) Hesselbach’s ∆: inf.Bulges directly ant though a weakened fascia Hesselbach’s triangle. children>adults Direct inguinal hernia: . inguinal ligament - Hernia sac is not with the spermatic cord Rare in ♀.INGUINAL HERNIA: indirect or direct. Epigastric art.♂ > ♀. within Hasselbach’s triangle Reduces upwards. Indirect inguinal hernia: .Congenital. oblique & transversus abdominis before they merge as conjoint tendon Floor: inguinal ligament and lacunar ligament medially Contents: Ilioinguinal nerve (L1): supplies skin over root of penis & upper part of scrotum or skin over mons pubis & labia majora ♀: round ligament of the uterus from uterus to labia majora ♂: transmits spermatic cord from abdomen to testes Anatomy of the spermatic cord Coverings: 3 concentric layers of fascia Internal spermatic fascia: derived from transversalis fascia Cremasteric fascia & muscle: derived from internal oblique External spermatic fascia: derived from external oblique Contents: 3 Arteries: Testicular artery Artery to the vas deferens Cremasteric artery 3 Nerves: Nerve to cremaster Autonomic nerves (T10) Genital br of genitofemoral nerve 3 Others: Vas deferens Pampiform venous plexus Lymphatics 30 . Deep inguinal ring lies in the midpoint of the inguinal LIGAMENT & is formed from a defect in the transversalis fascia.Anatomy of inguinal canal - 4 to 6 cm long oblique passage above the inguinal ligament. from the deep to superficial rings. third by conjoint tendon) Roof: arching fibres of the int. Superficial ring is a triangular defect in the aponeurosis of the external oblique. wall: transversalis fascia (reinforced in med. wall: aponeurosis of the external oblique (reinforced in lat. third by internal oblique) Post. Boundaries: Ant. ilioinguinal nerve. Recurrence of hernia (<0. round ligament. no cough impulse. cremasteric.Irreducible/ Incarcerated hernia: contents of hernial sac cannot be replaced into abdomen . parasthesia. Haematoma (10%. Injury to surrounding structures pain.5%. chronic constipation Truss: for compression of reducible hernia at deep ring (poor pickup rate) If obstructed/strangulated: NBM. but not blood supply. but able to bathe immediately o Abx cover??? 31 . testicular artery). too early mobilization. non-reducible. artery to vas deferens. Ischaemic orchitis & Testicular atrophy from testicular artery damage or from pampiniform plexus thrombosis Post. bleeding (testicular.Complications Reducible → Irreducible / Incarcerated → Obstructed → Strangulated . ARU 2. ±excise hernia sac. inferior epigastric. femoral arteries) 3. IV ABx Surgical: Hernioplasty/ Herniorraphy with mesh repair (open or laparoscopic) o Immediately if suspect incarceration to prevent any bowel perforation Principles: reduce bowel. is obstructed (no ischaemia not unduly tender. uncontrolled comorbidities) 3. NG tube on suction. 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. IV drip. Wound dehiscence 4. Chronic post-op pain 2. Bruising . hard) 3. nerve to cremaster o Early 1. 6hrs to gangrene. poor tissue. reinforce posterior wall o Lichtenstein tension-free mesh repair (lightweight.Obstructed: loop of bowel trapped in hernial sac such that its lumen. impotence: spermatic cord (vas deferens. (acutely tender with s/s of IO. bowel is dead or dying.operation monitoring: o Work leave for 6/52 with avoiding of heavy lifting o Treat any medical conditions to avoid coughing. but with 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. Infection of wound/ mesh 2. avoid heavy lifting o Treat medical conditions causing chronic cough. constipation o Early mobilization from D10 o Keep area clean and wash carefully. incomplete dissection. CVA o Immediate to early 1.Stangulated: blood supply to trapped bowel is cut off. change jobs. pain o Late 1. IO 2) DRE for BPH. Is lump above or below the inguinal ligament? Any scrotal lump? 2. cannot separate from testis 2. Recurrent. chronic constipation Also 4Cs: cirrhosis. could you reduce the lump for me? o Reducible: The point of reduction is “above and medial to the pubic tubercle” (superficial ring) o Incarcerated: The patient is unable to reduce the lump. increase intraperitoneal fluid . Bilateral (2 types of lap: TEP. is there any pain over the groin area? I am going to feel the lump. young. Complications a) Obstructed/ Strangulated b) Spontaneous rupture c) Involved in peritoneal diseases 4. Can get above the lump? 2. ask patient to sit up & support his pelvis. scrotal hematoma. ischemic orchitis EXAMINATION OF AN INGUINAL HERNIA “Please examine this patient’s groin” Don gloves. any tenderness? 4. then swing over the bed and stand With patient standing: Sir. fluctuant). Post-op complications a) Immediate: bruise. Locate the Deep inguinal ring: [vice versa for right side] o Left hand define pt’s pubic tubercle: from umbilicus down pubic symp. raised intraabdominal pressure 5. cannot get above lump 3. disappears on lying supine. catheter (dialysis) 3. TAP) c) Conservative only if: small. Any skin changes? Previous scars (look hard)? 4. could you turn head and cough? o if remains reduced – indirect hernia. I notice a groin / inguinoscrotal lump. easily reducible.Indirect: M. BPH. wound hematoma. introduce yourself and explain your intention. to the left 1st bony prominence o Right hand define the ASIS o Left hand to the midpoint of inguinal ligament 2cm above Keep pressure on deep ring. right. temperature. examine both sides Mr X is a ___ who appears comfortable at rest. pain b) Later: mesh infection. could you turn head and cough again? Feel for Palpable cough impulse (bilaterally?) Sir. Groin vs Inguinoscrotal a) groin cough impulse b) inguinoscrotal 1. cough impulse (may not be present in a large one) 2. (supposing you’re standing on patient’s LEFT) Reduce the hernia if patient has not done so. also has positive cough impulse] Undescended testes Lipoma of the cord 32 . cancer. Squat down and examine! Inspect as per a lump: (if unable to see. Risk factors: Increased intra-abdo pressure: chronic cough. direct hernia 6. ARU. nerve injury. Any lump on the other side? 5.APPROACH TO AN INGUINAL HERNIA 1. ARU. ascites. direct hernia.Direct: M. constipation. Lay the patient supine. impacted stools 3) Respiratory exam for COPD 4) Ask patient for history of heavy lifting Differential diagnosis: Femoral hernia Inguinal LN Hydrocele of the cord (boys). recurrence (10% /10years). masses. Abdominal distension / visible abdo mass? Sir. o if not. 2. Estimate the dimensions of the lump 3. then expose the patient STAND patient up. (poor accuracy) Remove pressure & watch movement of hernia: slide obliquely (indirect) or project forward (direct) Percuss & ascultate for bowel sounds Examine other side Offer: 1) Abdo exam: scars. Patient profile . Treatment: a) OPEN hernia repair!!! b) Lap only if 1. Lump: consistency (soft. could you turn head and cough? Look for Visible cough impulse (seen in large inguinoscrotal hernias) Sir. size. old. ask the patient) 1. Sir. or canal of Nuck (girls) Saphenous varix: [bluish-tinge. Palpate: 1. Can feel testis? 3. heart failure. The superior opening of the femoral canal is known as the femoral ring. ectopic testis Differences between an inguinal and a femoral hernia Inguinal Hernia Appear through superficial ring above & medial to pubic tubercle Usually reducible Expansile cough impulse usually present Low risk of strangulation Femoral Hernia Appears through femoral canal below & lateral to pubic tubercle Usually not reducible Expansile cough impulse usually absent High risk of strangulation Anatomy of the femoral canal The femoral sheath is the downward protrusion of fascia containing the femoral vessels & lymphatics below inguinal lig. infection. wound infx. The medial compartment of the sheath constitutes the femoral canal. obese/ distended abdomen. cyst. inguinal LAD o Hernia: inguinal hernia. Malignancy. distention Issues of concern: o Narrow Neck of hernia sac higher risk of strangulation/ infarction o Fistula formation with discharge of contents may occur Management: o Conservative: treat medcial co-morbidities. disease. o Intra-Op: poor technique of wound closure. post-op coughing Treatment options: o Not all should undergo repair due to high risk of wound haematoma. immunocompromised. early mobilization. Femoral hernia is a marble shaped lump below the inguinal ligament and medial to femoral pulse o usually irreducible. which carries the lymphatics. just add: o lifting head off the bed to exacerbate hernia o palpate to determine the size of defect Similar complications as any hernia Risk factors: o Pre-op: age. lipoma o Vascular masses: saphena varix. femoral aneurysm. Boundaries of the femoral ring: Anterior: inguinal ligament Posterior: iliopectineal ligament and superior ramus of pubis Medial: lacunar ligament Lateral: femoral vein INCISIONAL HERNIA Extrusion of the peritoneum and abdominal contents through a weak scar or wound on the abdominal wall Physical examination similar. o Surgical: Mayo’s Vest over pants operation 33 . fibroids. dehiscence and recurrent hernia o Conservative: Offer corset or truss Weight loss and control the risk factors leading to o Surgical: Offer if complications of hernia are present Control CVS & resp. obturator hernia o Other: psoas bursa. placement of drains o Post-op: wound haematoma.FEMORAL HERNIA Uncommon. may grow to large size. ascites. but more common in females Rarely put up for exams as it is operated quickly. narrow neck risk of strangulation is high o Usually does not have a cough impulse DDx: o Skin/ soft tissue: cyst. Cause: defect through the linea alba 2o to stretching the fibers o Pregnancy. encourage pre-op wt loss Principles: dissect the sac and close the defect using mesh overlapping UMBILICAL HERNIA/ PARAUMBILICAL HERNIA Uncommon b4 40YO. when palpate.Transilluminate the swelling if it is likely at hydrocele .Continue the examine the groin if it is a inguinoscrotal hernia . Can you identify the testis and the epididymis? 3. Is the swelling tender? Cannot get above swelling Cough impulse Reducible Testis palpable Opaque Hernia No cough impulse Not reducible Testis not palpable Transilluminable Can get above swelling Testis not definable from epididymis Infantile hydrocoele Non tender Chronic haematocoele Gumma Tumour Tender Torsion Epididymo-orchitis Acute haematocoele Opaque Transilluminable Testis definable from epididymis Opaque Hydrocoele Non-tender swelling of testis Tumour Non-tender swelling of epididymis TB epididymis Tender Epididymoorchitis Transilluminable Cyst of epididymis EXAMINATION OF THE SCROTUM Inspect Palpate - “ Examine this gentleman’s scrotum:” Always examine him STANDING! inspect the groin and scrotum: scars and swelling groin incisions are usually oblique.2.Examine the abdomen 34 lump is separate or part of them? . scrotal incisions are usually in the median raphe ask for any pain. Can you get above the swelling? 2. Is the swelling transilluminable? 4. look at patient for tenderness palpate one testes at a time if palpated any swelling: Is it tender? Can you get above the swelling? Can you identify the epididymis and testis Is it transilluminable? Offer to: . SCROTAL SWELLINGS ANSWER 4 QUESTIONS: 1. May occur as a complication of vasectomy (spermatoceles) . yolk sac tumour. uniformly enlarged o Cannot define testis well. Complicated by operative damage and fibrosis of epididymis subfertility 35 . non tender o Not transilluminable (but maybe a/w hydrocele) . the superficial ring is distinct - Definition of hydrocele: o Excess accumulation of fluid in processus vaginalis (fold of peritoneum as testis descends. no separable from testis o Maybe firm. normal tumour markers.DDx: o Chronic infection with scarring o Long standing hydrocele with calcification. . can get above i o Hard. nodular. poor prognosis) .Points from examination: o Very swollen scrotum.Treatment: o Conservative [mainstay] o Surgical: if painful. usually patent for fluid to accumulate) - Types of 1o hydrocele: o Vaginal hydrocele: Only in tunica vaginalis & does not extend into the cord o Hydrocele of the cord Mass around the cord. excision of whole testis with combination chemotherapy EPIDIDYMAL CYST . AFP/ BHCG raised in 90%. choriocarcinoma. attached distally to the testis Difficult to distinguish from irreducible inguinoscrotal hernia May extend up and beyond o Congenital hydrocele: patent processus vaginalis filled with peritoneal fluid o Infantile hydrocele: hydrocele of cord and congenital hydrocele Types of 2o hydrocele o From testicular tumours o From torsion o From trauma o From orchitis (any inflm) Treatment options: o Conservative: Watch & wait or Aspiration [tend to reccumulate] Must exclude a 2o cause o Surgical: Lord’s plication of the sac Jaboulay’s operation to evert the sac - - TESTICULAR TUMOUR . maybe loculated. Leydig cell tumours (10% malignant . can get above it o Firm. transilluminable if large cyst .Points from examination: o Inseparable form the testis.Classiccation: o Mostly seminomas or teratomas Seminomas: 30-40YO.Points from examination: o Small mass separate from testis.Treatment: o Staging. Lymphoma (look for lymphoma elsewhere.Often multiple in the head of epididymis . Rx with CT o Others: embryonal carcinoma. very large or frequent recurrences. Sertoli cell tumour (a/w gynaecomastia). a/w gynaecomastia). tense or lax o Maybe transilluminable if acute (less in chronic hydrocele) o Can get above the mass. irregular. Rx with RT to paraaortic nodes and CT according to staging Teratomas: 20-30YO.HYDROCELE . DDx: o Epididymitis o Torsion of testicular appendage (pea coloured lump through scrotum) o Strangulated inguinoscrotal hernia .VARICOCELE . straining. cycling.Best noticed on palpating the standing patient . coitus . pain worsen by lifting testis up o Previous attacks of self limitng pain. connects to left renal vein. can get above it o Feels like a bag of worms.Causes: o Idiopathic in younger males around puberty o In older men with retroperitoneal disease: RCC - Treatment options: o Conservative: risk of infertility o Surgical: Transfemoral radiological embolization with coil or sclerosant Excise the surrounding veins via high retroperitoneum. longer than right one. ppt by trauma.Definition: o Dilated. often lacks a terminal valve . inguinal or laprascopic approach TESTICULAR TORSION (Surgical emergency) . excise and replace with prosthesis 36 . +ve cough impulse o Not transilluminable . tortuous pampiniform plexus o 98% on Left side: left vein is more vertical. testis is high in scrotum.Clinical features: o Children/ teenagers o acute abdomen (T10 inervation) & acute scrotum a/w vomiting o swollen and tender scrotum.Points from examination: o Mass is separate from testis.Cause: o Maldescended testis hanging like a bell clapper within tunica vaginalis .Treatment: o Emergency exporation if Doppler US –ve for flow or clinical suspicion Untwisting (lateral) of affected testis and orchidoplexy of both testis to scrotum Warm up with warm pad to see reperfusion or check with doppler after untwisting [4h before ischaemia] If dead. surface 2. temperature. fulid thrill] 5. Exophytic 4. fascia. there is a (single) (hemispherical) lump on the (dorsum of the forearm)” “It measures <take out ruler> ( x by x cm)” “There are (? scars. slough. Site: take reference from bony points 3. Consistency R: reducability.Slip sign – if lipoma is suspected . e. size.Pulsatility (only for some sites. muscle. It is (non-tender)” “The surface is (smooth). Reassess mobility in the 2 planes Intramuscular or below the muscle.Reducible: Disappears on pressure. reappears on release (AVM) .Auscultation – only for certain sites / lesions (e. the overlying skin is (not) found to be warm. neck. ulceration. it will disappear. skin changes. Margins clearly defined? O: others [fluctuance. purulent . Fluctuant? (for small / medium lumps) . Round.Tends to slip away from the examining finger on gentle pressure .Fixed and immobile? Edge: sloping (healing). Ulceration c.Paget’s sign: Rest 2 fingers on opposite sides of lump. relationship to each other .Mobile only in certain directions? rolled (BCC). Overlying skin temperature S: site. Surface: C: colour. hernia suspected] . compressibility .Fully mobile in all directions? Base: granulation tissue. Above the muscle it will be more prominent.Transillumination [only for large lumps. expansility/ pulsatility 3. Use pen torch on one side] . Relations to surrounding tissues Discharge: serous.” “It (appears to be attached to underlying muscle.g. and it is (non-fluctuant)” “The lump is (not) attached to the overlying skin. nor overlying or surrounding skin changes)” Inspection 1. Sinuses. Number: solitary / multiple 2. punched out. 8. X is a young Chinese gentleman…” “On inspection. haemangioma.Place finger on opposite sides of lump o Expansile: fingers pushed apart o Transmitted: Fingers pushed in same direction (usually upwards) . shape. Tenderness E: edge. etc. discharge b. and it is non-pulsitile.Compressibility / reducibility [if AVM.Compressible: Disappears on pressure. Neck.Hard > Firm > Tense > Soft 6. Colour & skin changes? a. or discharge seen. Shape / Symmetry: .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. Erythema / cellulitis “Is the lump tender?” “On palpation. sanguinous. haemoserous.) Request – “I would like to complete my examination by…” Examine the draining LNs If sebaceous cyst / lipoma “Looking for other lumps elsewhere” Ganglion “Looking for other lumps elsewhere” + “Asking for hand dominance” + “Taking an occupational history” 37 . abdomen. transillumability 4. it will become less mobile. as it is mobile horizontally but not longitudinally)” Palpation (Ask patient: Is area painful?) 1. Scars 6.Hemispherical. Size 5. abdomen) . Fixed to muscle. APPROACH TO LUMPS & BUMPS Permission: Introduce yourself Position: Ensure patient (and you) are comfortable Exposure: Expose area to be examined fully (Remember: Compare with other side if applicable) “Mr. everted (SCC) 7. Special tests . with clearly-defined margins” “The consistency is firm. consistency. .3. scars. press down on middle of lump +ve: Feel fingers moving apart 9.Smooth/ Irregular/ Rough T: tenderness. undermined. bone . reappears with opposing force (hernia) .g. Mobility Ulcers: . sinuses. gouty tophi) or consist of bone (e. pilonidal abscess 2. exostoses) Pulsatility Pulsatility is usually transmitted from an underlying artery which may simply be tortuous or may be abnormal (e. Bony-hard lesions are either mineralised (e.e. exophytic (i.g. e.g. discrete lesion is most likely cystic or encapsulated (e.g.g. epidermal (sebaceous) cyst Depth within the skin Superficial and deep attachments.g. hypodermis or deeper) Character of the margin Discreteness. Immobility of overlying epidermis suggests a lesion derived from skin appendage (e. irregular. e. epidermal cyst) Consistency Soft.epidermal cysts).g. shape and surface features Revealed by inspection-is the lesion smooth-surfaced. inflamed epidermal cyst). Malignant lesions are usually painless 38 .Symptoms and signs Diagnostic significance 1. Malignant lesions tend to be hard and irregular ('indurated') with an ill-defined margin due to invasion of surrounding tissue. Pain. benign tumour). hard. ganglion). Lump in or on the skin Size.g. small ganglion). projecting out of the surface)? Epidermal lesions such as warts usually have a surface abnormality but deeper lesions are usually covered by normal epidermis.g.g. rubbery Soft lesions are usually lipomas or fluid-filled cysts. or the cyst is tense (e. Deep tethering implies origin from deeper structures (e. tenderness and discomfort These symptoms often indicate acute inflammation. A punctum suggests the abnormality arises from an epidermal appendage. epidermis. aneurysm or arteriovenous fistula) Emptying and refilling Vascular lesions (e.g. three-dimensional shape A regular shaped. 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.g. 'indurated'. Pain also develops if a noninflammatory lesion becomes inflamed or infected (e. Which tissue is the swellingderived from? Tends to reflect the layer from which lesion is derived and therefore the range of differential diagnosis (i. tethering to surrounding tissues.e. firm. Most cysts are fluctuant unless filled by semi-solid material (e. dermis.g. are nearly always pigmented. TB or tropical ulcers) or trauma. warts and pyogenic granuloma may all develop rapidly and eventually regress spontaneously. 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. Benign pigmented naevi (moles) may be detectable at birth. pilonidal sinus. whereas venous disorders such as port-wine stain are darker. Colour and pigmentation Normal colour If a lesion is covered by normal-coloured skin then the lesion must lie deeply in the skin (e. Rapidly developing lesion Keratoacanthoma. Rarely. Examples include neurofibromatosis and recurrent lipomata in Dercum's disease. Vascular lesions blanch on pressure and must be distinguished from purpura which does not Deeply pigmented Benign naevi (moles) and their malignant counterpart. epidermal cyst) or deep to the skin (e. particularly in an insensate foot Character of the ulcer margin Benign ulcers-the margin is only slightly raised by inflammatory oedema. recurrent and spreading lesions In certain rare syndromes. Prolonged or intense sun exposure predisposes a large area of skin to malignant change.g. the centre of which eventually becomes necrotic and breaks down. but may go through cycles of breakdown and healing (often with bleeding) 4. Malignant melanoma may spread diffusely (superficial spreading melanoma) or produce satellite lesions via dermal lymphatics 7. which is most common in inflammatory conditions like furuncles. papillomata or seborrhoeic keratoses may become pigmented secondarily.g. chronic infection (e. solar keratoses or basal cell carcinomas of hands and face) 8. ganglion) Red or purple Redness implies increased arterial vascularity. malignant melanomas. Age when lesion noticed Congenital vascular abnormalities such as strawberry naevus or port-wine stain may be present at birth. Multiple. Spontaneous regression marks the lesion as benign 6. The margin is typically elevated 'rolled' and indurated by tumour growth and invasion Behaviour of the ulcer Malignant ulcers expand inexorably (though often slowly). Viral warts may appear in crops.g. Other lesions such as warts. Vascular abnormalities which contain a high proportion of arterial blood such as Campbell de Morgan spots or strawberry naevi are also red. external angular dermoid or multiple pilar cysts of the scalp) or because of exposure to sun (e.g. Site of the lesion Some skin lesions arise much more commonly in certain areas of the body.3. malignant melanomas may be non-pigmented (amelanotic). The reason may be anatomical (e. The base lies below the level of normal skin Malignant ulcers-these begin as a solid mass of proliferating epidermal cells. Ulceration (i. these conditions may be difficult to distinguish from malignancy. When fully developed. New darkening of a pigmented lesion should be viewed with suspicion as it may indicated malignant change 5.e. Hairy pigmented moles are almost never malignant. but only begin to enlarge and darken after the age of 2 39 . ischaemic leg ulcers). multiple similar lesions develop over a period.g.g. Surface breakdown also occurs in arterial or venous insufficiency (e. 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. occur in older age (deeper tissues – retroperitoneal. or discharge seen. No transilluminance / thrill o Usually in the subcutaneous tissue. never regress o May be multiple: lipomatosis (multiple continuous lipomata) Occur in buttocks / neck Can cause distortion of subcutaneous tissues. the overlying skin is not warm. Treatment o Non-surgical – watch & wait o Surgical – If patient wants it removed (Pain / peripheral neuropathy – Dercum’s disease. [check attachment skin & muscle] “Mr. series of curves corresponding to each lobule o Pseudo-fluctuance if large – lipomas are not liquid. nor any overlying or surrounding skin changes” “On palpation. LIPOMA Inspection o Can be single. Well-differentiated 2. there is a hemispherical lump over the right scapula” “It measures 10 by 8 cm” “There are no scars. and its margins are not well-defined” “The consistency is soft.4. Pleomorphic liposarcoma Clinical features o Can occur at all ages (not common in children) o Slow-growing. often multiple o Usually at neck. round cell (poorly differentiated myxoid) 3. subscapular) Liposarcoma classification 1. intestinal polyps 40 . deep tissues of thigh. X is a young Chinese gentleman…” “On inspection. ulceration. 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. 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. but fat maybe more liquid o Mobile in all directions (if subcutaneous) o Positive slip sign. 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. Myxoid. it is non-tender” “The surface is lobulated. punctum. malignant-looking (malignant transformation rare) Heaping up of granulation tissue from the lining of the cyst burst through skin. discharging swelling solitary. 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. open. sudden increase in size o May spontaneously discharge contents through punctum. sinuses. not attached to deeper structures.Malignancies: BCC. X is a young Chinese gentleman…” “On inspection. may stretch overlying skin ( plastic deformation) Non fluctuant. 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. nor any overlying or surrounding skin changes” Palpation Normal Temperature. Angry. what to exclude? . Malignant melanoma. mobile in all directions “On palpation. Malignant change Inflamed Cyst Treatment o Non-surgical: leave alone (if small. with clearly-defined margins” “The consistency is firm. giving everted appearance regional lymphadenopathy may be present Gardner’s syndrome (If multiple lumps found) o Genetic disorder associated with: Multiple osteomata of skull & epidermal cysts Adenomatous polyposis of large bowel & CRCs Desmoid tumours Thyroid cancers 41 . the overlying skin is not warm.– may appear suddenly at adolescence o May become infected: acutely painful. granulating & edematous Boggy. be careful of the facial nerve during operation. not transilluminable Attached to skin. Sebaceous horn formation. Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the lines of Langers. 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). central punctum.] 5. [hardening of a slow discharge of sebum from a large. 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. ulceration. back. If at the angle of jaw. or discharge seen. o Surgical Complete excision of cyst and contents under LA. Ulceration 3. ulcerate may become infected. asymptomatic). If lump is increasing in size. Infection (±discharge) 2. rarely present before adolescence o Slow growing. 90% occur in scalp o often mistaken for SCC scalp. Cock’s peculiar tumour (complication) o Proliferating trichilemmal cysts that can grow to large size.5. non-tender (unless inflamed) Smooth surface Well-defined margins (lies in subcutaneous fat) Tense consistency. shoulders (none on palms / soles) Variable size . scalp. Calcification (trichilemmal cyst) (may lead to cyst hardening) 4. 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. neck. Damage to zygomatic branch can cause eye ulceration. painful. few mm to 4-5 cm May have bluish discolouration Punctum in apex: in 50% May exhibit plastic deformation on palpation “Mr. It is non-tender. SEBACEOUS CYST Inspection Usually solitary (can be multiple) Hemispherical Site: face.” “The surface is smooth. trunk. 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.g. hand – ventral / dorsal) Variable (0. tendon sheath / degeneration of mucoid fibrous tissue Site: o o Can occur anywhere in body Common in areas of fibrous tissue (e. there is a single hemispherical lump on the dorsum of the left wrist” “It measures 3 by 2 cm” “There are no scars.5 – 6 cm) Palpation Normal temperature. flattened. X is a young Chinese gentleman. Ganglion is more tense. tendon sheaths (90% on wrist. nor any overlying or surrounding skin changes” “On palpation. the overlying skin is not warm. with clearly-defined margins” “The consistency is soft. who is alert and comfortable…” “On inspection. Benign giant cell tumours of flexor shealth (These 2 are normally soft in consistency. intramuscular septum. 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. 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. Simple 2. tendon sheath. GANGLION Inspection Single. (gelatinous material) Mobility: o Should assess mobility in 2 perpendicular planes. 3. ulcerations. Interosseous 42 . non-tender Smooth surface with Well-defined margins May be multilocular Soft & fluctuant if large > firm consistency if small Weakly transilluminant. X for his hand dominance” “Taking an occupational history” “My provisional diagnosis is a ganglion” My differential is a 1. Bursa 2. around joints. and it is fluctuant” “The lump is not attached to the overlying skin” “It appears to be attached to underlying muscle. Occult 4. It is non-tender” “The surface is smooth. or discharge seen.6. may have ovelying scar [recurrent mass] Hemispherical. esp. Near joint capsules. Cystic protrusions of synovial cavity of arthritic joints 3.) Background Information Definition: Cystic myxomatous degeneration related to synovial lined cavity [joint capsule or tendon sheath] Origin controversial: pockets of synovium communicating with joint. Dorsal > Volar wrist @ scapholunate joint) Most common soft-tissue mass in the hand Types: 1. Compound – chronic inflammation distends tendon sheath above and below the flexor retinaculum. High chance of recurrence 6-12/12 later. Along the lines of Langers.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. Aspiration + 3/52 of immobilisation (successful in 30-50%). Stiffness & Contractures 43 . Surgical Complete excision to include neck of ganglion at site of origin. Complications Wound complications: Scar. usually may disappear after a few months. haematoma. infection Recurrence <10% Damage to adjacent neurovascular structures. rolled appearance” “There is a small area of pigmentation on the periphery of the lump. sun-exposed skin (especially around the eye) Lesions raised above the skin: o Nodular/ nodulo-ulcerated type (most common): Pearly. slightly transparent] May be pigmented. immobile deeper invasion Regional LAD (metastases are extremely rare. muscle. (above line drawn from angle of mouth to earlobe) Hair-bearing. rolled edges [smooth. ask the patient to turn his head – avoid moving around the patient) “Mr.). nor any other overlying or surrounding skin changes” “On palpation. with telangiectasia over the lump May have central ulceration. confused with malignant melanoma o Sclerosing: flat or depressed with ill defined edges. X is an elderly Chinese gentleman…” “On inspection. keratoacanthoma” “I would like to complete my examination by…” Examining for cervical lymphadenopathy (although very rare in BCC) Inspection Single (often multiple) Commonly found on the face. ulceration. glistening.” “The surface is smooth” “The consistency is firm” “The lump arises from the skin” “It is freely mobile over the underlying tissues” “My provisional diagnosis is basal cell carcinoma” “My differentials include SqCC. confined to skin o If fixed. etc. the overlying skin is not warm. and fine telangiectasia are seen over the lump” “There are no visible scars. maybe ulcerated o Bush-fire / Cicatricial: multiple superficial erythematous lesions with pale atrophic areas o Superficial: erythematous scaly patches Base: o May be covered with coat of dried serum & epithelial cells o If deep: may expose deeper tissues (bone. covered with poor-quality granulation tissue o On face: may erode deep into facial structures Palpation (Important to palpate for mobility: fixation and deep local invasion) Normal temperature. erode facial structures if advanced o Cystic: large cystic nodule Lesions not raised: o Pigmented: contains melanin. It is non-tender. may be painful / itchy Firm / solid consistency should be mobile over underlying structures. with a pearly. or discharge seen.7. etc. to rule out SCC) + Ask about pre-disposing factors A = nodular B = pigmented C = sclerosing D = superficial 44 . there is a single hemispherical lump just above alar of the nose” “It measures 2 by 2 cm” “The edges of the lump are well defined. BASAL CELL CARCINOMA – “Examine this gentleman’s face” (If the other side of the face. needs to be inspected. rolled edge is circular Shape becomes irregular as malignant cells spread As ulcer heals: irregular. associated with failure of DNA transcription) Gorlin’s syndrome (rare autosomal dominant cancer) o Acquired Sunlight (especially UV light.g. healing centre) Sclerosing (flat / depressed tumour. 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. molluscum pseudo-carcinomatosum) But scar will be deep (see below) If pigmented: malignant melanoma (rare in Singapore) Raised above skin: excision with 0. nasolabial fold lesions: Moh’s chemosurgery Staged chemosurgery. UV-B range) Carcinogens (smoking. 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.Background Information Locally invasive carcinoma of basal layer of the epidermis Does not metastasize. 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. naevus sebaceous) Clinical features o In elderly people (incidence increases with age) o Rare in dark-skinned races o Males > females o Grow very slowly. months / years typically o May spread radially – leaving central scar o Persistent nodule / ulcer with central scab (repeatedly falls off.5 cm margin (maximum) Not raised above skin: wider margin of excision. ears. 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. but can infiltrate adjacent tissues Common in sun-exposed skin Pre-disposing factors o Congenital (rare) Xeroderma pigmentosum (familial. especially if at inner acanthus of eye. arsenic) Previous RT Malignant transformation in previous skin lesions (e. nasolabial fold. histological assessment of margins & electrodessication 45 . ill-defined edge) Superficial (erythematous scaly patches) Microscopic features o Most commonly islands and nests of basaloid cells in dermis o High mitotic rates. nasal floor. ear Frozen section may be needed to ensure adequate excision Alternative: RT Eyes. pyogenic granuloma o Malignant: BCC. bloody. red-brown colour (very vascular) May have central ulceration. proximal to the 1st & 2nd MCP joints” “It measures 1. purulent. dermis. thickened Palpation normal temperature. foul-smelling discharge Surrounding tissue may be oedematous. Base: o Necrotic tumour. SQUAMOUS CELL CARCINOMA “Mr.” “There are no scars. 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. or discharge seen.5 by 1. failure of DNA transcription) 46 . unhealthy o Deep tissues may be exposed o Depth: variable (may be very deep. infected seborrhoeic wart. there is a single irregular ulcer on the dorsum of the right hand.5 cm. malignant melanoma. the surrounding skin is not warm. 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.” “The base of the ulcer is shallow and contains red granulation tissue. 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. neck. red and heaped up. solar acanthosis. hands. X is an elderly Chinese gentleman…” “On inspection. 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.” “On palpation. The edge of the ulcer is well-defined. 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. nor any surrounding skin changes.8. & lymphatic spread to LNs Microscopy: o Tongues of tumours cells spreading in all directions o “Epithelial pearls” – nest of squamous epithelium. arms. especially in soft tissue) o Can be copious. may be covered with coagulated blood / serum o Granulation tissue: tends to be pale. adjacent tissues. atypical dividing cells in prickle cell layer (irregular acanthosis). Bowen’s disease Chronic ulcers: old burns. hard. basal layer atypical only (vs atypia in whole epidermis in SqCC) Treatment: Non-surgical: cryotherapy. nodal spread) o + Block dissection of regional lymph nodes (if involved) o Eyes. may progress to SqCC red. topical chemotherapy (5-FU) Surgical: curettage of affected skin 47 . scaly irregular plaque on the trunk o if on the penis. Chemicals Pre-existing lesions: Solar keratosis. focal parakeratosis. nasolabial fold lesions: Moh’s chemosurgery Staged chemosurgery. 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. but may not be so florid Bowen’s disease (SqCC in situ) Very slowly growing. centre necroses.Acquired o Envn: sunlight. ears. Irradiation. chronic venous ulcers Immunosuppresion (post-transplant. Begin with thickening of skin On sun-exposed skin of elderly patients 25% may undergo change to SqCC Microscopically: hyperkeratosis. 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. HIV) Usually has been growing for 1 – 2 months before being noticed Begins as small nodules on skin As enlargement occurs. 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. and black discolouration” “The margins are clearly-defined and irregular” “There are no scars. or discharge” “On palpation. erythema. and moves with it over deeper structures” “My provisional diagnosis is malignant melanoma” “My differential diagnoses are: BCC. discharge May have surrounding halo: brown (pigment). X is a middle aged Chinese gentleman…” “On inspection. Non-tender Surface o If small: smooth epithelium o If ulcerates: covered with crust (blood + serum) o If bleeding. MALIGNANT MELANOMA “Mr. pigmented naevus” “I would like to complete my examination by…” “Examining for regional lymphadenopathy” “Take a history for: cardinal symptoms of malignant change. white. there is a single flat-looking lesions over the right foot” “It measures 2 by 4 cm” “It is variegated in appearance. retinal melanoma “Beware of the man with the glass eye and hepatomegaly” Palpation Normal Temperature. subungual. intra-cranial melanoma. 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. black. mouth. and any predisposing factors” Inspection Usually single (may have satellite lesions around primary lesion) Site: Limbs. head & neck. and exhibits red. or ulceration.9. boggy Firm consistency (small satellite nodules feel hard) Mobile. soft. It is non-tender” “The surface is smooth. / infected: wet. 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. pink (inflammation) Types: o Superficial spreading melanoma (70%): Legs of women and backs of men Red. palms. It is not warm. brown. soles Irregular area of brown/ balck pigmentation o Others: amelanotic melanoma. mucocutaneous junction. purple (rich blood supply) Clearly defined but irregular May ulcerate. nor any surrounding pigmentation. anus Any colour: pale pink. white. bleeding. and its consistency is firm” “The lump is attached to the skin. the overlying lesion is palpable. trunk. moves with skin over deeper structures Request Palpation for regional lymphadenopathy Palpation for other subcutaneous nodules (lying along course of draining lymphatics) 48 . Halo. Occasionally colourless: no melanin production d. size. Loss of normal surface markings (e. Size: i. Increase in edge. width. Asymmetry 2. axillary lymph nodes 4.5X risk) Acquired / modifiable o Sunlight exposure o Pre-existing skin lesions Lentigo > 20 benign pigmented naevi (3 x risk) o Previous melanoma (3. 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. Elevation (flat plaque → nodule) 49 . Enlarged inguinal. SOB. bleeding o Itch. FAMM syndrome) – 100% risk if 2 family members affected o Large congenital naevi o FHx in 1st degree relatives (1. Liver [hepatomegaly]. jaundice o Lymphatogenouly to: regional LN o haematogenously to: Lungs [pleural effusion]. Satellite nodules of tumour around the lesion ii.5 x risk) Features of pigmented skin lesion suspicious of malignancy 1. ulceration) & deeper into dermis. satellite nodules o Ulceration. Becoming darker ii. Halo of brown discolouration in skin around the lesion iii. Growth of newly-formed / long-standing mole ii. Number: i. Skin may become rough / scaly iii. thickness c.30%) Lentigo maligna melanoma Acral lentigous melanoma Microscopic features Consists of loose nests of melanocytes in basal cell layer: Invade epidermis (leading to destruction. Surface: i. to blue-purple ↑ vascularity) iv. 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. Diameter >6mm 5. Itchy with pale-pink halo (inflammation) b.Background information 4 commonest types of malignant melanoma Superficial spreading melanoma (70%) Nodular melanoma (15 . shape. colour. number (early) a. No pain o Lymphadenopathy Symptoms of distant metastases: LOW.g. Patchy colour change (black. size. skin creases) around lesion ii. surface. Bleeding & ulceration (late) 3. Change in: colour. Colour: i. If clinical suspicion. < 0. If palpable: therapeutic block dissection Palliation / adjuvant for distant metastases a.76 mm: excise with 1 cm margin ii.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. Ulceration e. > 1. cytokine interferon therapy 50 . Elderly b. 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. ↑ melanin) o Freckles (normal number of melanocytes. Avoidance of causative factors Surgical excision with wide margins down to deep fascia a.76 – 1. Male c. amelanotic f.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. Main lesion: i. Aneuploidy. Depigmentation. biopsy or FNAC of lymph nodes ii. Intralesional BCG therapy b. Lesions on trunk d.0 mm: excise with 3 cm margin b. Nodal spread: i. high mitotic index Treatment Prevention (VERY IMPORTANT): a. LN involvement) Breslow Thickness 10-Year Survival < 0.0 mm: excise with 2 cm margin iii. monoclonal antibody. or other indicators of poor prognosis: a. ↑ melanin from each) o Lentigo (↑ melanocytes. Immunotherapy: vaccines (raises anti-melanoma response). 0. subungual area) Red. soles. white. polypoid.Superficial Spreading Nodular Lentigo Maligna Acral Lentiginous 70% 15-30% – Rare ♂: Back ♀: Legs Trunk Face. blue (varying pigmentation) Most often black Brown / black Brown / black Edge Irregular Regular outline Irregular Irregular Shape Palpable. Dorsum of hand / forearm Hairless skin (palms. but thin Thick. darker • Area seldom ulcerates • Rare type • Often misdiagnosed as haematoma. raised Flat Flat Surface - Smooth - - % Site Colour Remarks - • Frequently ulcerated. bleeding Pictures 51 • Arises from patch of Hutchinson’s Lentigo • Malignant area usually thicker. paronychia . and rubbery” “They are attached to the skin. there are two spherical. CoA.. patient agreeable o Surgical: indicated only if malignancy suspected Local re-growth common (cannot be surgically detached from underlying nerve) 52 . with well-defined margins” “There are no scars. they are not warm and non-tender” “Their surfaces are smooth. rarely disfiguring o If related to nerve trunk. 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. ulceration.5 cm in diameter” They are pink in colour. X is a young Chinese gentleman…” “On inspection. and the other 0. lisch nodules. myxoid material o Often not encapsulated (unlike neurilemmomas) Complications of Neurofibroma o Pressure effects: spinal cord. 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. pedunculated masses on the back” “One measures 2 cm. Well-defined Soft/ fleshy. 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. nerve root compression o Deafness: involvement of VIII o Neurofibrosarcoma (only in NF-1): 5-13 % o Intra-abdominal effects: obstruction. cystic changes. subcutaneous tissues. optic glioma Measure the BP (HPT 2o to phaeochromocytoma. axillary freckling. NEUROFIBROMA “Mr. Non-tender Smooth. e.10.g. and are firm. 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. chronic GI bleeding o Skeletal changes: kyphoscoliosis. pseudoarthrosis Treatment (single neurofibroma) o Non-surgical: leave alone if asymptomatic. sinuses. nor any surrounding skin changes” “On palpation. or discharge seen. 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. neurocutaneous syndrome. and skeletal. but lymphatic drainage is normal Can result in severe deformity: diffuse enlargement of peripheral nerve with skin involvement 53 . tumours. chr 17 Characterised by pigmentary changes. vascular dysplasias o Fibroma ≥2 NF or ≥1 plexiform NF o Iiris harmatomas (Lisch Nodules) o Bone: dysplasia. giving tissue swollen oedematous appearance o Often mistaken for lymphoedema. pseudoarthrosis o Relatives o Optic glioma o Macules >6. 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. >15mm post-pubertal o Axillary freckling Neurofibromata of all sizes (few mm to large subcutaneous nodules).Neurofibromatosis I (Von Recklinhausen’s disease) (Refer to paediatrics notes – neurocutaneous syndromes) AD. problems with grip / touch if on finger) Also rarely infected o Differentials Sebaceous cyst (look for old injury. maybe tender if infected Smooth surface. tense lump Painful and tender (in areas subjected to repeated trauma) Local effects (e. and it is fluctuant” “The lump is not attached to the overlying skin nor underlying tissues. 0. Congenital: Not attached to skin or underlying structures ii. 1-2 cm usually Along lines of fusion of ophthalmic & maxillary facial processes Inner & outer ends of upper eyebrow o Acquired.g.” “My provisional diagnosis is a congenital dermoid cyst” “My differentials are: sebaceous cyst. o Symptoms Small. lipoma” Inspection Usually single Ovoid / spherical Site: o Congenital. It is non-tender. Acquired: may be tethered to scar Background Information A dermoid cyst is a cyst deep to the skin. with clearly-defined margins” “The consistency is firm. presence of scar near cyst: more likely dermoid) Treatment Congenital o Surgical treatment. becomes obvious. fingers Scars often present Palpation Not warm.” “The surface is smooth. DERMOID CYST “Ms.5-1 cm usually Beneath skin likely to be injured e. when skin dermatomes fuse o Occur at any point in mid-line. in subcutaneous tissue i. nor any overlying or surrounding skin changes)” “On palpation. or discharge seen. young adult) o Formed intra-utero.” “It is fully mobile in all directions. ulceration. etc. the overlying skin is not warm.11. 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. 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. stab. must exclude bony defect Acquired o Complete excision of cyst 54 . 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. complete excision o Full extent should first be established with X-ray / CT Midline cysts may communicate with CSF. X is a young Chinese girl…” “On inspection.g. 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. 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. It is non-tender” “The surface is rough and greasy. ulceration. o increases in area. 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. SEBORRHOEIC KERATOSIS (Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma) “Mr. and it appears to be slightly raised above the skin” “There are no scars.12. o Superficial shaving (lies above level of normal epidermis) o Cautery 55 . melanoma” “I would like to complete my examination by…” “Looking for similar lesions elsewhere” Inspection Often multiple Any part of skin. or discharge seen. the consistency is firm” “The lump arises from the skin” “My provisional diagnosis is seborrhoeic keratosis” “My differential diagnosis is: pigmented naevus. 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. etc. Few mm to 2-3 cm Distinct margins Palpation No warmth. most found on back & face Round / oval Light brown → black “stuck on appearance”.; appears warty Varying size. nor any surrounding skin changes” “On palpation. X is an elderly Chinese gentleman…” “On inspection. the overlying skin is not warm. 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. there is a single ovoid lesion lump on the back” “It measures 1 by 2 cm” “The margins are well-defined. catch on clothes o May get infected (may imitate SCC. 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. 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 56 • Cosmesis • Non-tender . neck. may be raised Skin Changes May have small areas of ulceration with scabs May have dilated subcutaneous veins around lesion – – Irregular. may have bruit Predominantly lymphatic: lymphangioma circumscriptum Develop as abnormal proliferation of embryonic vascular network Hamartomas May ulcerate. 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. 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. few mm 1-3 mm Edge Well-defined Well-defined – Well-defined Shape Sessile → pedunculated as they grow larger Variable Variable Circular. buttock Upper torso. leaves it collapsed: slowly refills Not pulsatile – Compressible. 1-10 cm Variable Variable. 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. may extend into muscle / joint May have distended veins over the surface of the mass Empty with pressure. shoulders. mucous membranes of mouth. pitted epithelium Smooth – Smooth Palpation Surface Soft – – – Mobility Mobile – – – Relations Confined to skin – – – Compressible: pressure squeezes mass.13. HAEMANGIOMA Background Information Vascular malformations o Types o Features Capillary: ⅔ of cases. telangiectasias Predominantly venous: venous angioma Deeper levels of subcutaneous tissue. covered with smooth. face. 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. include the cutaneous haemangiomata. fade completely – Infants (congenital) Infants (congenital) – Middle-age → elderly ♂ = ♀ – – Consistency Special Tests Background Information Age Gender – Symptoms • Cosmesis • May ulcerate. epistaxis. gives skin pale-pink colour o Associated with other vascular abnormalities (e. 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. AV fistulae.g.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. melaena. haemangiomata. haematemesis. lymphoedema) o Usually not disfiguring 57 . Bleeds easily. hands. e. paronychia) Rapidly-growing lump on skin. long-standing lesions may be skin-coloured May have sinuses. pain stops once lump epithelises Once nodule is completely covered. infected) Clinical features Uncommon in children May have history of minor injury. It is slightly tender” “The surface is smooth. associated serous / purulent discharge.g. usually less then 1 cm Occur commonly after injury: o Small capillary loops develop in healing wound. X is a young Chinese gentleman…” “On inspection. it is not warm. discharges serous / purulent fluid o Bleeding. form granulation tissue o When capillary loops grow too vigorously.g.8 cm in diameter. face Bright red. may be sessile / pedunculated Likely sites to be injured. bright red o May be blood-encrusted or Ulceration Hemispherical. amelanotic melanoma has to be excluded) Non-surgical o Regression is uncommon: surgical treatment best option o Silver nitrate cautery is possible 58 . usu < 1 cm. chronic infection (e. with surrouding erythema” “There are no scars. The consistency is soft and fleshy” “The lump is confined to the skin” “My provisional diagnosis is pyogenic granuloma” “My differential diagnoses are SCC. PYOGENIC GRANULOMA “Mr. ulceration. epithelisation o Mass form called pyogenic granuloma (surface often ulcerated. begins to shrink (rarely disappears completely) Treatment Surgical o o Curettage with diathermy of the base Complete excision biopsy (if recurrent. malignancy e. X for any previous injuries to the hand” o “Asking him how rapidly the lump has been growing” Inspection Single. sinuses. with clearly-defined margins” “It is bright red in colour. there is a single hemispherical lump over the thenar eminence of the right hand” “It measures about 0. active bleeding or discharge seen” “I would like to proceed on to palpation” “On palpation.g. 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.14. form protruding mass. Erythema / cellulitis Palpation – request to palpate: may bleed easily May be slightly tender o May bleed easily on palpation Well-defined edges Soft. non-pigmented melanma” “I would like to complete my examination by…” o “Asking Mr. scissors o Bleeding from central vascular core controlled using single suture / diathermy 59 . PAPILLOMA (skin tags / fibroepithelial polyps) “Mr. X is a young Chinese gentleman…” “On inspection.) Treatment Excision – diathermy. “The surface is papilliferous – there is no ulceration or discharge seen.” “On palpation. not compressible Arises from skin Request Similar lumps elsewhere Ask for associated conditions: pregnancy. asking for associated conditions” Inspection Single / multiple Variable: from raised plaque to pedunculated polyp Site: Neck. nor any surrounding skin changes.15. non-tender Variable: smooth to papilliferous Soft. face. etc. It is non-tender. The consistency is soft. there is a (single) (hemispherical) lump on the (dorsum of the forearm)” “It measures 3 by 2 cm. but a hamartoma (skin tag is a more accurate term) Increasingly common with age – may be congenital Clinical features Catches on cloths. anus (anywhere on skin) Variable Flesh-coloured Palpation Not warm. and ulcerate o May become infarcted if injured o May be infected (contains all skin components – sebaceous glands. diabetes. rubs against other body parts May resemble carcinoma if granulation is excessive Complications: o May become red. swollen.” “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. the skin is not warm. trunk. intestinal polyposis Background Information An overgrowth of all layers of the skin with central vascular core Not a neoplasm. hispanic more likely o Hypertrophy and overgrowth extend beyond original wound o Located at earlobes. especially if infection / excessive tension o Only enlarge for 2-3 months. Intralesional steroid. molluscum pseudo-carcinomatosum) Inspection Often found on face Usually solitary.g. LA injections: e.16. KERATOCANTHOMA (adenoma sebaceum. triamcinolone with lignocaine o Surgical: revision of scar by direct suturing.1 – 2 cm in diameter Hemispherical or conical. chin. but can be unsightly Takes 2 – 4 weeks to grow. neck. chest o Due to local release of fibroblast growth factors o Continue to enlarge 6-12/12 after initial injury o May be tender. 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. 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. 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). skin grafting (avoid excessive tension) 60 . but confined to scar (between skin edges) o Located across flexor surfaces. ♂=♀. neck. chest. with central crater Normal skin colour Palpation Firm and rubbery (central core is hard) Confined to skin. regresses in 2 – 3 months o Central slough appears. earlobes. ♀>♂. then regress spontaneuosly o Do not recur if excised and causative factor eliminated Keloid scar o puberty to 30 years. black. shoulder. all races o Excessive amount of fibrous tissue. shoulder Hypertrophic scar o any age – common 8-20 years. skin creases o Common. 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. 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. leukaemia/ lymphoma o Endemic (African) Kaposi’s Sarcoma Aggressive and invasive fatal tumour Good response to chemotherapy o Transplation. 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. Found in 1/3 of AIDS patients 1/3 develops a 2nd malignancy e. but usually multiple Site: limbs. Start anti-retrovirals if HIV +ve Surgical: local radiotherapy amd chemotherapy (IFN. tip of nose/ palate or anywhere on the skin or mucosa Request to take a history of previous transplantation or current underlying immunocompromise.g. doxorubicin. intralesional vinblastine) 19. 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. FIBROSARCOMA Inspection Single. mouth. interference with ROM Pain Weakness (infiltration of other structures) General debility Prognosis: generally good 61 . invasive) Firm / hard consistency (rarely stony hard.alpha. do not ossify) Usually fixed May pulsate. Usually limbs (but can be anywhere) Spherical or hemispherical If large. KAPOSI’S SARCOMA Inspection Purple papules and plaques Solitary. have audible bruit.18.associated Kaposi’s Sarcoma Following high dose immunosuppressive therapy Often regress when treatment is ended Treatment Conservative if asymptomatic. 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. KIV cyclosporine & antibiotics o Surgical: serial allograft followed by autologous skin graft or muscle flap coverage when necessary 62 . RA Backgound information more common in males pyoderma gangrenosum is associated with: o IBD o RA o Myeloproliferative disorders: PRV. 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. myeloma o Autoimmune hepatitis Differential diagnosis: o Autoimmune: rheumatoid vasculitis o Infectious: tertiary syphilis.20. saline cleansing. amoebiasis o Iatrogenic: warfarin necrosis o Others: Behcet’s disease Treatment: o Non-surgical: treat underlying condition. high dose oral or intralesional steroids. leukemia Solid tumours: Thyroid cancers Breast cancers Minimalising of side effects of radiotherapy: o Lead shields to eyes. pulmonary fibrosis Bld vssl: radiation arteritis. manifests as chromosomal abnormalities Radiotherapy affects cells with: o Rapid turnover: Skin (epidermal layers). Renal impairment (depletion of tubular cells) Abdo: IO 2o to strictures & adhesions. LOA. 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. and normal cells have greater ability to repopulate than tumour cells in this setting o If reparable. N/V Skin changes & temporary hair loss Bone marrow suppresion. o masectomy scar/ wide excision scar suggest breast cancer o obvious skin cancer. distal ischaemia and vssl rupture CNS: spinal cord myelopathy Uro: bladder fibrosis. desquamation o Features of previous RT: Telangiectasia. esp. RADIOTHERAPY MARKS Vital points on examination: Of the underlying disease: o Cachexia. if to long bone and pelvis GI: diarrhea Skin changes Heart: IHD Lung: pneumonitis. Genital: infertility Endocrine: hypothyroidism Eye: cataracts Increase incidence of future cancers: Haematogenous malignancy. o Damage is usually irreparable. fatigue. small intestine. bone marrow stem cells o Limited replicative ability: spinal cord.21. skin markings Erythema. gonads and thyroid o Dose fractionation (to allow recovery of normal cells) o Prior chemotherapy (increase sensitivity of tumour cells) o Regional hypothermia o Radiolabelled antibody to deliver local radiation to tumour 63 . gonads Complications: o Early: o Late: General: malaise. esp to carotids necrosis. e.g. 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. by mechanical pressure or suction Drain failure . 64 . Yeates drain. blood or fluids (e.do not allow bottles to fill up Prevent slippage by securing drain carefully to skin.blocked/slipped/kinked Incisional hernia .g.g. 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. DRAINS FUNCTIONS OF DRAINS Drains are inserted to: Evacuate collections of pus.maintain meticulous skin care and aseptic technique around the insertion site Prevent blockage of the drain.3. 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. Jackson-Pratt Drain. The following are general guidelines: Drains put in to cover perioperative bleeding and haematoma formation. 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.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. SURGICAL INSTRUMENTS & PROCEDURES 1. 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. Redivac Drain. biliary t-tube) Open Active Active drains require suction. Where a drain has been put in to drain an infection (abscess). an air leak will cause the chamber to fill with air & it won't drain properly. it could become dislodged If a portion of the tube is pulled outside the skin.occurs when drain inserted through incision wound site. Corrugated drain. can come out after 24— 48 hours. remove it when fever settles or when there is evidence of complete drainage. lymph) Drain potential collections COMPLICATIONS Infection Bleeding Tissue damage. sympathetic chain.ensure head-down position. 13. 10. 5. 9. Arrhythmias – This happens if cathether “irritates” the heart. 3. Hold guide wire in place and remove needle. When vein is entered. or remove syringe from needle and ensure blood is venous. Air embolism . Procedure 1. cranial nerves IX-XII Technique of IJV cannulation Place the patient in a supine position. Catheter-related sepsis 65 . Remove syringe. 2. 17. Do not insert into an infected area. The vein is initially posterior to. into the vessel through the needle. 3. maintain gentle aspiration. to terminate behind the sternoclavicular joint. Measurement of CVP 5. 8. 14. 11. Total parenteral nutrition 3. at least 15 degrees head-down to distend the neck veins and to reduce the risk of air embolism. 3. Hypercoagulable states ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE: 1. it is the vessel of choice for central venous cannulation. Relations of the IJV Anterior: Internal carotid artery and vagus nerve. Direct the needle caudally. The vein lies most superficially in the upper part of the neck. holding needle firmly in place. Vascular access 2. Palpate the carotid artery and ensure that the needle enters the skin lateral to the artery. 2. then lateral and then anterolateral to the carotid artery during its descent in the neck. Pulmonary artery catheterization 7. attached to an empty 10 ml syringe. 4. Turn the head away from the venepuncture site. so cannulation of this vein is associated with a lower complication rate than with other approaches. 5. 6. 2. Bleeding diatheses 5. Check lumen placement by aspirating through all the pigtails and flushing with saline next. Perform check chest X-ray to confirm position and exclude pneumothorax. Internal jugular vein Subclavian vein Femoral vein External jugular vein CANNULATION OF THE INTERNAL JUGULAR VEIN The internal jugular vein (IJV) is accessible. Advance catheter into final indwelling position. 6. Sterile gloves and a gown should be worn to avoid catheter-related sepsis. transduce needle before dilating and passing central line into vessel. Medial: Carotid arteries. Occlude needle to prevent air embolism or bleeding.Avoid cannulating the vein on the left side as the thoracic duct lies there. Avoid infraclavicular approach to subclavian vein if patient has apical emphysema or bullae. Carotid artery puncture/cannulation . It lies alongside the carotid artery and vagus nerve within the carotid sheath. Advance guide wire. 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. Infusion of irritant drugs 4. dome of the pleura. Chylothorax. Hold catheter and REMOVE GUIDEWIRE. J-shaped end first. While needle is advanced. the IJV lies anterior to the thoracic duct.palpate artery and ensure needle is lateral to it. Avoid internal jugular vein if carotid aneurysm present on the same side. parallel to the sagittal plane. Maintain a firm grip on the guide wire at all times. Use local anaesthetic to numb the venepuncture site.2. 7. 16. Cardiac catheterization 6. Posterior: C1. CONTRAINDICATIONS: 1. Anatomy of the IJV The vein originates at the jugular foramen and runs down the neck. 4. Pneumothorax/haemothorax 2. 3. Suture the catheter to the skin to keep it in place. Introduce the large calibre needle. CENTRAL VENOUS PRESSURE LINE INDICATIONS 1. cannulate the vein via the Seldinger technique (below). or use ultrasound-guided placement. 12. Complications 1. aiming towards the ipsilateral nipple. Septicaemia 6. Apply dressing according to hospital protocol. Transvenous cardiac pacing. Remove the dilator. Hence. flush of blood appears in the syringe. Grasp the catheter near the skin and advance it into the vein with a slight twisting motion. Cleanse the skin and drape the area. Thread tip of catheter into the vein through the guidewire. 4. Use a dilator to enlarge the hole in the vein. cardiac monitoring during insertion. On the left side. The catheter tip should lie in the superior vena cava above the pericardial reflection. Now. 15. Avoid passing guidewire too far. 4. where it joins the subclavian vein. The SCV passes over the first rib anterior to the subclavian artery. Place the patient in a supine position. 7.CANNULATION OF THE SUBCLAVIAN VEIN The subclavian vein (SVC) may be preferred for central venous access if 1. to identify the position of the line and to exclude pneumothorax. Turn the head to the contralateral side (if C-spine injury excluded). 66 . This site may be more comfortable for the patient. Direct the needle medially. Line is for long-term use e. follow the Seldinger approach. When a free flow of blood appears. 4. 9. head-down. as detailed previously. feeding. dialysis. 2. 6. Introduce a needle attached to a 10 ml syringe. Patient has a cervical spine injury 2. The external jugular vein joins the SCV at the midpoint of the clavicle. The catheter tip should lie in the superior vena cava above the pericardial reflection. Technique 1. Damage to the subclavian artery may occur. Complications As listed for internal jugular venous cannulation. Perform check chest X-ray to confirm position and exclude pneumothorax. The risk of pneumothorax is far greater with this technique. Ensure that a chest X-ray is ordered. Adopt full asepsis.g. to join with the internal jugular vein at the medial end of the clavicle. Anatomy of the SCV The SCV is the continuation of the axillary vein and originates at the lateral border of the first rib. Slowly advance needle while gently withdrawing plunger. 5. 8. slightly cephalad. and posteriorly behind the clavicle toward the suprasternal notch. 3. direct pressure cannot be applied to prevent bleeding. Surface mark the subclavian vein 1 cm below the junction of the middle and medial thirds of the clavicle. coiling & reentry into oesophagus (rare). which is the most uncomfortable part of the procedure. a) b) c) d) e) Technical insertion into the trachea choking. Select the largest nostril for insertion. Gather equipment. trauma to the nose and the pharynx. Resistance may be felt as tip reaches the nasopharynx. 2. chloride and hydrogen ions. 6. Secure the tube with adhesive tape. oesophagus or the external nares. PROCEDURE 1. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated) and advance the tube as the patient swallows. dislodgement perforation of the pharynx and oesophagus 2. haematemesis pentagastrin studies (rarely done now) Therapeutic a) b) c) intestinal obstruction pyloric stenosis haematemesis. or if the patient begins to cough or turns pretty colours. a) b) Lung complications decreased ventilation aspiration pneumonia 67 4. connect to suction. type & size of tube. especially sodium. Determine the size of the nasogastric tube required (usually 14 – 16FG).3. If aspirating. esp in pts at risk of hepatic encephalopathy CONTRAINDICATIONS 1. remove the syringe from the free end of the tube. Decompresssion a) b) bleeding from the upper gastrointestinal tract. or obtaining an x-ray to verify placement before instilling any feedings/medications or if you have concerns about the placement of the tube. if the tube coils in the mouth. Deflate the endotracheal tube or tracheostomy cuff 6. 5. Dry mouth and parotitis due to fluid loss and mouth breathing. 9. the McGill’s forceps may be used to guide the tube down. If patient is uncooperative. Nutrition a) b) patients with dysphagia comatose or weak patients 4. PRE-PROCEDURE 1. Introduce the tube through the nostril horizontally in. 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. Document the reason for the tube insertion. sit patient upright with head forward for optimal neck/stomach alignment. 10. prop the patient up at 45 °. 5. auscultating the epigastrium while injecting air through the tube. rotate the tube slowly with downward advancement towards the closer ear. . If resistance is met. Varices: traumatic haemorrhage GERD Oesophageal erosions strictures 3. choanal stenosis) to determine best side for insertion. 8FG) because it is more comfortable in the long term. set machine on type of suction and pressure as prescribed. 5. the nature and amount of drainage. and the effectiveness of the intervention. 13. 7. Re-inflate the endotracheal tube or tracheostomy cuff if necessary. Otherwise. 12. the type of suction and pressure setting if for suction. If possible. There should not be resistance. Examine nostrils for deformity/obstructions (eg. 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. Stop. In the operation theatre. The nose may be lubricated with lignocaine gel. 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. Loss of fluids & electrolytes. Do not force the tube down against resistance as this may form a false passage. Lubricate tube with water. Swallowing of small sips of water may enhance passage of tube into esophagus. Oesophageal tear 3. Explain the procedure to the patient and show equipment. 4. Don non-sterile gloves. bend his head to elicit a swallowing reflex. a) b) c) d) e) Gastrointestinal Gastric erosions Pressure necrosis of pharynx. If for suction. Diagnostic 2. 11. PROBLEMS AND COMPLICATIONS [5] 1. 3. Advance the tube until mark is reached (approximately 40cm). Withdraw the tube immediately if changes occur in the patient's respiratory status. passing the tube along the floor of the nose. 8. Continue to advance the tube down the oesophagus. if feeding. Base of skull # 2. the nature and amount of aspirate. 4. potassium. a smaller tube may be used (eg. NASOGASTRIC TUBE INDICATIONS [4] 1. Lavage a) b) poisoning gastrointestinal bleeding The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric tube insertion. use as large a tube as possible to reduce the risk of blocking during use or the formation of a false passage during introduction. Mark the measured length with a marker or note the distance. 2. 3. when the patient is under general anaesthesia. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks. 11. 7. TYPES OF TRACHEOTOMY 1. Avoids risk of endotracheal obstruction. Drape field. 4. Place rolled towel under the patient’s neck to hyperextend the neck for better exposure. RELATIVE CONTRAINDICATIONS 1. 12.4. Delivery of high oxygen concentrations. making an inverted U-flap incision. Incise the trachea between the 2nd and 3rd tracheal rings. Incise skin. Remove the obturator and insert the inner cannula. Position the patient. 10. 3. Permanent: Consist of inner and outer tubes made of stainless steel. 2. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water. 15. 4. Patient obesity with short neck that obscures neck landmarks. Maintenance of airway patency. 3. 13. 2. 9. Administer local anaethesia. Dress wound and secure to the neck using sutures and adhesive tape. 2. Visualise the thyroid isthmus and retract isthmus. Temporary: Portex (cuffed). Identify anatomical landmarks (thyroid cartilage. Medically uncorrectable bleeding diatheses. Gross distortion of the neck anatomy due to hematoma. Identify the communicating branch of the anterior jugular vein. Clean and drape. clamp and ligate the artery (ignore this in an emergency). Retract cricoid cartilage upwards wth cricoid hook. cricoid cartilage). make a vertical incision 3cm from cricoid cartilage downwards. Clean the skin of the neck from the chin to the suprasternal notch and laterally to the base of the neck and clavicles. 2. 6. PROCEDURE 1. high innominate artery or scarring from previous neck surgery. Application of positive pressure to the airway. make a tranverse incision 4cm wide. Better tolerated. 5. 5. Protection of the airway from aspiration. thyromegaly. Dissect through the subcutaneous layers and platysma. 68 . 8. 3. Tracheostomy is more useful in the elective setting compared to endotracheal intubation because: 1. Documented or clinically suspected tracheomalacia. 3cm above the suprasternal notch. Patient age younger than 15 years. 7. 14. tumour. TRACHEOSTOMY INDICATIONS FOR TRACHEOSTOMY 1. Avoids risk of laryngeal stenosis 3. In the emergency setting. 2. Evidence of infection in the soft tissues of the neck at the prospective surgical site. 5. 4. In the elective setting. 6. Suction of blood and secretions in the lumen. Facilitation of secretion clearance. Insert the tracheostomy tube. eg clot. 2. Late post-op 1. Unlock the metal tube every night so that the patient can cough it out if it becomes obstructed. Scarring. Immediate post-op 1. eg dislodgment of tube. Obstruction. 69 . 5. Prevent obstruction by suction. 2. 3. mucus. 3. guaifenesin) and humidified air. 4. Infection . Subcutaneous emphysema. Bleeding if damage to the innominate or inferior thyroid artery. Bleeding. Wound breakdown 6. Dislodgment. Obstruction. Tracheal stenosis. recurrent laryngeal nerve. Pneumothorax. Position patient in a propped up position. Tracheo-esophageal fistula. Tracheomalacia. eg esophagus. mucolytic agents (mucomyst. crust formation from secretions. 4. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday. POST-OP CARE 1. 2. Damage to surrounding structures. Surgical emphysema (refers to the condition that causes air to be trapped under the skin). 3. 4.COMPLICATIONS During Procedure 1. 3. brachiocephalic vein. Pneumomediastinum. saline irrigation. 2. 13. or if using the Minnesota tube. Lubricate and insert the tube through the nose. Test patency of the tube. Traction. Respiratory obstruction 3. Apply local anaesthesia (lignocaine nasal spray). Rebleeding 5. Check the oesophageal balloon pressure hourly and release 5mins hourly. 1. or (iii) doing an X-ray. 2. asking the patient to swallow or drink water to aid in smoother passage of the tube through the pharynx and oesophagus. Release oeophageal balloon after 24hrs. use the additional lumen provided (with the additional lumen for aspirating fluid in the oesophagus. 8. SENGSTAKEN-BLAKEMORE TUBE (MINNESOTA TUBE) INDICATIONS Oesophageal varices CONTRAINDICATIONS 1. Severe facial injury PROCEDURE . COMPLICATIONS 1. Release gastric balloon after 48hrs. Sit the patient upright or at 45 degrees. 9. the Minnesota tube decreases the likelihood of aspiration pneumonia occurring). 12. 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. 5. Base of skull fracture 2. 10. (ii) auscultating the epigastrium while injecting air. Aspiration pneumonia 2. 7. Test balloons. 11.Keep SBT in fridge to make it stiff. Check that the tube is in the stomach by: (i) aspirating fluid and testing it with litmus.5. 4. Aspirate fluid from the oesophagus through the Ryle’s tube. Oesophageal tear 3. 6. Inflate the gastric balloon slowly with 100-150ml water. Measure the length of the tube. 3. Oesophageal ulceration and rupture 4. The tube should not be used for more than 72hrs. Gastric varices not controlled 70 . g. with less anaesthetic effect. amount of water in balloon. 13. cleanse the peri-urethral mucosa with antiseptic-drenched swabs held by forceps. 2. 71 . 19. In the male. 8. one swipe per swab. 15. INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION 1. Don the sterile gloves from the kit. Evaluate catheter function and amount. 12. Inflate balloon. Place drainage bag below level of bladder. Apply sterile drape. Cystourethrogram. If no urine appears although the catheter seems to be in the right place. 2. eg. e. b) Female: Retract the labia majora. it is no longer sterile and cannot be used to obtain items from the kit). Dispose equipment appropriately. 4. Open the catheterization kit and catheter. Maximize patient’s privacy. a) Male: Hold the penis and retract the foreskin. using correct amount of sterile saline (usually 20 – 30mls but check actual balloon size). odour and quality of urine. squeezing the meatus shut (iii) Wait for for 5 minutes (alternatively. Cleanse anterior to posterior. blood clots causing acute retention of urine. Prepare sterile field. in the female. Stricture formation due either to faulty technique or an irritant material used in the catheter. 3. benign prostatic hypertrophy. 10. This process should be painless. a) Male: (i) Smear lignocaine gel around the meatus and apply the gel gently into urethra. Gather equipment. CONTRAINDICATIONS 1. Urinary tract infection. 17. patient's response to procedure and assessment of urine. Presence of urethral injury. Have a chaperone if performing the procedure on a member of the opposite sex. 14. Refractory bladder outlet obstruction. smear gel over the catheter tip). URINARY CATHETERISATION INDICATIONS FOR SHORT-TERM CATHETERISATION 1. c) pelvic fracture. 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. 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.g. Urinary output monitoring. irritation of the bladder may cause severe bladder spasms. Generously coat the distal portion (2 . (ii) Massage gel carefully down the urethra to sphincter. 5. without tension on tubing. deflate balloon immediately and reposition catheter. Connect catheter to drainage system. 11. 18. 20. If patient feels pain. color. elicited from a genital and digital rectal examination. (ii) to allow accurate measurement of urine output in major surgery.g. lift the penis to a position perpendicular to patient's body and apply light upward traction (with non-dominant hand). in patient with hypovolaemic shock or the critically ill. Wash hands. 6. discard away from sterile field. If this is still unsuccessful. withdraw and reinsert. neurogenic bladder. (alternative: suprapubic drainage) 2. 16. 4. 3. which may lead to stone formation. 9. Installation of local anaesthesia. or d) high-riding prostate.6. b) Post-operatively: (i) to relieve acute urinary retention because post –op pain results in failure of the sphincter to relax. Bladder washout. b) scrotal haematoma. Remove gloves. 4. 3. 6.g. 2. 2. inner to outer. Relief of acute retention of urine. COMPLICATIONS 1. Explain procedure to the patient. 7. flush with sterile saline as the lumen may be blocked with gel. Swab the penis and surrounding area. bladder outflow obstruction. PROCEDURE 1. Chronic retention of urine. making sure to cleanse beneath the foreskin. as manifested by: a) blood from the meatus. 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. b) Female: (i) Apply lignocaine gel to urethra or catheter tip.5cm) of the catheter with lubricant. 3. Creation of a false passage due to wrong technique of insertion. Test the balloon at the tip of the catheter. Infection. Incontinence. 5. in palliative care of terminally ill or patient’s preference. Secure catheter to abdomen or thigh. e. Occasionally. Swab the perineum. e. expose the external urethral orifice. Assist patient into supine position with legs spread and feet together. Document size of catheter inserted. Gently pull catheter until inflation balloon is snug against bladder neck. e. Administration of intra-vesical drugs. as an indwelling catheter causes difficulty in treatment. Hemothorax. just over the top of the rib. 2. When the chest tube is no longer needed. Locate the triangle of safety. Apply a dressing and tape the tube to the chest. 4. etc. 3. clots. Clamp 5. Silk suture 6. 10. Explain the major steps of the procedure. Chest tube (size 32 to 40 Fr. 2. Suction apparatus (Pleuravac)/underwater seal apparatus 11. 4. 8. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as necessary. Inform the patient of the possibility of major complications and their treatment 3. 5th or 6th intercostal space. bounded by the lateral border of the pectoris major. Suction is attached to the system to encourage drainage. 10 cc syringe. Infection over insertion site 2. Do a chest X ray 12. imaginary vertical line between the anterior and mid axillary lines. Iodine & alcohol swabs for skin prep 2. 7. Determine the site of insertion. The tube is placed between the ribs and into the space pleural space.& 22-g needles PRE-PROCEDURE PATIENT EDUCATION 1. Connect the end of the chest tube to an underwater seal apparatus. fluid. Antibiotics may be used to prevent or treat infection. 25. 6. Suture the tube in place. Drainage of empyema/lung abcesses 6. Uncontrolled bleeding diathesis/coagulopathy MATERIALS 1. Sterile drapes & gloves 3. Locally anaesthetized the skin and rib periosteum. 9. 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. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center CONTRAINDICATIONS 1. 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). Pneumothorax. Surgically prepare and drape the chest at the predetermined site of the tube insertion. INDICATIONS 1. Look for fogging of the chest tube with expiration or listen to air movement. The area where the tube will be inserted is anesthetized locally. 1% lignocaine with epinephrine. 72 . 11. fluid. and necessity for repeated chest radiographs PROCEDURE 1. Sterile gauze 9. or air and allow full expansion of the lungs. usually without the need for medications to sedate or numb the patient. depending on clinical setting) 12. Scalpel blade & handle 4. A suture and adhesive tape is used to keep the tube in place. Drainage of pleural effusion. 5.7. The patient may also be sedated. Petrolatum-impregnated gauze 8. 3. The chest tube usually remains in place until the X-rays show that all the blood. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect through the subcutaneous tissues. Tape 10. Chylothorax 5. Needle holder 7. CHEST TUBE Chest tubes are inserted to drain blood. or air has drained from the chest and the lung has fully re-expanded. Clamp the proximal end of the chest tube and advance the tube into the pleural space to the desired length. it can be easily removed. Obtain informed consent 2. 5. bronchoscopy required. 8. usually at tube site. Frequent deep breathing and coughing is necessary to help re-expand the lung. 2. with only a small scar. and prevent normal fluids from collecting in the lungs. Incorrect intrathoracic or extrathoracic tube position. breathing difficulties. 73 . 3. artery or vein. Anaphylactic or allergic reaction to surgical preparation or anaesthesia. all of which can be prevented by using the finger technique before inserting the chest tube. Laceration or puncture of the intrathoracic and/or abdominal organs. Introduction of pleural infection. Lungs fail to expand due to plugged bronchus. and need for additional oxygen. clogging or dislodging from the chest wall or disconnection from the underwater seal apparatus. Damage to the intercostals nerve. While the chest tube is in place. the nursing staff will carefully check for possible air leaks. Recurrence of pneumothorax upon removal of the chest tube. Recovery from the chest tube insertion and removal is usually complete. Failure: 7. 6. The patient will stay in the hospital until the chest tube is removed. Persistent pneumothorax 9. 10. Chest tube kinking. Subcutaneous emphysema.COMPLICATIONS Damage to structures: 1. Equipment: 4. assist with drainage. 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) 74 . APPROACH TO ABDOMINAL PAIN RHC Thoracic Pneumonia Pleural effusion Biliary Cholangitis Cholecystitis Gallstone disease Epigastric Hepatic Hepatitis (viral.NOF. ABDOMINAL SURGICAL EMERGENCIES 1.4. 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 # . CLL) H’lytic anaemia (thal. PAN Myeloprolftve dz – PRV.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. Endocarditis Autoimmune – SLE. HS) Storage dz (Gaucher’s) Left kidney (see Rt lumbar) Left adrenal gland Mild Above causes Infxns: Viral hep. IMS Bacterial – abscess Parasitic – hydatid cyst. 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 75 LIF Gastrointestinal Diverticular mass/abscess Ca colon/sigmoid Crohn’s dz (terminal ileitis) Faeces Similar causes as RIF mass . RA. 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. 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. antacids. 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 (<1%) 76 . metabolic (hypoK/ hypoMg/ hypoNa. Post-op (most common): Physiologic ileus spontaneously resolves within 2-3 days. hypothyroidism. uraemia) 5. . Crohn’s) Herniae Volvulus Lymph node compression Superior mesenteric artery syndrome Functional (give rise to megacolon) . TCA 7. intraabd inflammation/peritonitis.Hirschsprung’s disease: absent ganglia in Auerbach’s plexus Ogilvie pseudo-obstruction in a septic elderly patient. tricho-) 2. Mechanical Intraluminal Impacted stool Gallstone ‘ileus’ Foreign body Bezoars (phyto-. Sepsis 3.Paralytic ileus = hypomobility without obstruction accumulate gas/fluids DDx mechanical/pseudo: hypo/absent BS as opposed to highpitch tinkling 1. Lap shorter duration of ileus than open. trauma (# rib/spine/HI) .Pseudoobstruction = acute marked LB distension without obstruction. Clinical picture similar to mechanical obs. ischaemic (eg bowel. biliary/renal colic. eg. Mural Tumours Diverticular stricture Intussusception Crohn’s strictures RT strictures Extraluminal Adhesions (post-op. MI) 4. Note the massive dilatation of the colon. 6.within hours. colon . stomach 1-2 days. opiate-induced. INTESTINAL OBSTRUCTION (& MECKEL’S DIVERTICULUM) Causes of IO 1.3. (Normal resumption of bowel activity after abdominal surgery follows a predictable pattern: SB . retroperitoneal hematoma 8.3-5 days) Ileus that persists for more than 3 days following surgery is termed postoperative adynamic ileus or paralytic ileus. catabolism due to poor nutrition 2. Complications: Cx of immobility. Ogilvie syndrome: in severely ill patients (large bowel peristalsis disappears in ass with retroperitoneal pathology) 50% mortality if patient progresses to necrosis and perf. after sigmoid motility returns to normal. Complete obstipation: cannot even pass flatus Other pertinent history .Closed loop: RIF bulge that is hyperresonant .Complete obstruction: constant. any impacted stools? Cx of I/O Any signs of peritonitis: guarding. 4-5 days duration . FH of Ca PHYSICAL EXAMINATION Vitals: Is patient stable? Any fever? (sepsis) Hypotension. heart disease.LB: uncommon esp if competent ileocaecal valve. infection . Sister joseph Abdomen: Dx I/O Any distension? Visible peristalsis? – severe obstruction (see browse) Bowel sounds: Mechanical: Initially hyperactive/loud resonant/ high-pitch Tinkling BS: small bowel obstruction Ileus: hypo/absent BS Succussion splash + epigastric tenderness: gastric outlet obstruction Causes of I/O SCARS from previous abdominal surgery? Any masses Any HERNIAE – inguinal + femoral (more likely strangulated) DRE: any masses felt.Symptoms of GIT bleed. tachycardia? (dehydration) General inspection: Abdominal distension? Cachexia? Confusion? Pale? Jaundice? Peripheries: Look for signs of dehydration e. esp if pt vomiting . LOA.Risk factors for ischaemic bowel: atherosclerotic RF.Volvulus: sudden.High SB: greenish blue.HISTORY Consider: Is there I/O? Is it functional or mechanical? Is the bowel strangulated? local peritoneal inflammation SB or LB obstruction? 4 cardinal symptoms 1.Underlying GIT disorders .Usually colicky (central griping pain interspersed with periods of no/little pain).SB: every 2-20min.Early in low obs.Previous surgeries!!! . Vomiting: . rigid 77 sluggish or absent . severe pain 2. capillary refill. dry tongue Palpate lymph nodes – Virchow. Abdominal distension . LB: every 30min or more . bile stained .Recent change in bowel habit . usually late symptom 3.Lower SB: brown and increasingly foul smelling (feculent = thick brown foul) .Ask about normal BO frequency .g.Suspicion of malignancy: LOW.Pyloric: watery and acid. Pain: . previous Ca. late in high obs . sharp pain . Constipation . previous stroke (see below) .SB: distension in centre of abdomen 4. projectile .Usu not seen in high obs . rebound tenderness. air under diaphragm 2. Rigler’s Sign = double wall sign (obvious bowel wall due to extra-luminal air) Blue arrows point to falciform ligament. Closed-loop obstruction (competent ileocecal valve) 4. Obstructed and strangulated abdominal hernia 2.Alkalosis due to vomiting (more for pyloric stenosis in children) ECG (+ CE X2 sets) in elderly Pre-operative GXM 4 pints of blood PT/PTT Imaging Assess complications Erect CXR : 1. stomach) 3.Intra-luminal 3rd space loss (damaged enterocytes unable to reabsorb) . aspiration pneumonia KUB/AXR: 1. 2. The red arrows demonstrate both sides of the wall of the stomach (Rigler's sign). a sign of free air.Acidosis from bowel ischaemia . Maintain airway 2. Volvulus (sigmoid. Bowel ischaemia with necrosis? Gas in bowel wall (pneumatosis intestinalis) due to gas gangrene 78 . The yellow arrow points to a skin fold. Give supplementary O2 (high flow if susp ischemia) o Monitor vitals . NG tube:aspirate stomach contents and then put on constant suction 3.ACUTE MANAGEMENT o Resuscitate if necessary 1. immediate consult with GS Reg INVESTIGATIONS Bloods Assess complications FBC: any infection. IV drip: rehydrate and correct elec imbalance o Start broad spectrum ABx [IO affects normal translocation of bacterial flora] – IV Ceftriaxone 1g + Metronidazole 500mg o Correct acidosis (ischemia). NBM: rest bowel (alone does not give adequate rest as intestine produce up to 9L of fluids per day) 2. Ischaemic bowel with bowel necrosis 5. replace K+ as guided by investigations Rule out surgical emergencies (history/physical examination/investigations) 1. Perforation/peritonitis if suspected. caecal. anemia UECr : Any dehydration due to: .Urinary catheter: monitor hourly urine output o Drip and suck 1. made visible by a large amount of free air in the peritoneal cavity.Vomiting (also assess K+ loss: can perpetuate paralytic ileus) Acute renal failure from dehydration ABG . 5cm LB. up to 12cm). distended cecum (thinnest wall. Sigmoid colectomy with primary anastomosis: Primary anastomosis is performed if the divided bowel ends are viable.Gown up . incomplete bands (haustrations due to presence of teniae coli) Gas present in rectum? No: complete obstruction (may require KUB film) . risk of barium peritonitis (100% mortality!) . lead-pipe appearance Colon: more peripheral. .Erect: air fluid levels (>6) .Gastrografin preferable if risk of perforation. peritoneal contamination is not evident. Sigmoidopexy: fix sigmoid to posterior abdominal wall (rarely done as high risk of recurrence) Other volvulus Caecal volvulus: right hemicolectomy with primary ileocolic anastomosis is the surgical procedure of choice (not endoscopic decompression as only successful in 15-20%. and also contraindicated. “stack of coins” (plicae circulares aka valvulae conniventes) Distal ileum: plicae circulares disappears. and the patient is hemodynamically stable b.Upper GI barium studies contraindicated Colonoscopy done without bowel prep (not necessary. rare to create ileostomy) Gastric volvulus: gastropexy 79 . Flexible sigmoidoscopic decompression (recur in as much ast 50%. Sigmoid colectomy & formation of double barrel colostomy (Paul-Mikulicz procedure) with future re-anastamosis d.Closed loop obstruction? Distal lesion with v.Put end of Ryle’s tube in a bottle submerged in water .Diagnostic KUB (not AXR) Dilated = 3cm SB. Ryle’s tube decompression: . The suggested interval between endoscopic decompression and definitive surgical intervention is 48-72 hours) Surgical a.Sigmoid volvulus? . Sigmoid colectomy with Hartman’s procedure (may be reversed in 3-6/12 – depends on overall clinical condition and ability to withstand another major surgery) c. Elective laparoscopic sigmoid resection and right hemicolectomy following endoscopic decompression is increasingly being described and performed to treat patients with volvulus. Note also the central cleft (white arrow) of the coffee bean.Supine (better): look for small or large bowel dilatation on radiograph Duodenum: C-shaped Jejunum/proximal ileum: centrally located. 9cm caecum (increase risk of perf) . in IO) CT colonography DEFINITIVE MANAGEMENT (Depends on cause) 1) Obstructed abdominal hernia Herniorrhapy 2) Parrot’s beak sign in sigmoid volvulus Sigmoid volvulus (refer below) Non surgical/ conservative 1. ileum not dilated Barium enema .Caecal volvulus Coffee bean sign: There is an air-fluid level (black arrows) in each segment of dilated bowel.Insert lubricated Ryle’s tube into anus 2. NBM. Supportive management: drip & suck. can do extended right hemi-colectomy If lesion is distal. therefore surgery is 1st line treatment 7) Post-op paralytic ileus (>3 days post-op) a. wait for peristalsis to restart b. cisapride 80 . Prokinetic agents: erythromycin. antibiotics while waiting for collaterals to re-supply bowel. Administer barium enema: watch intussception reduce on fluoroscopy Elderly: usually leading point present (polyp. may require total-colectomy with ileo-rectal anastamosis Continue antibiotics following surgery 6) Intussusception Children: usually due to hypertrophic Peyer’s patches.g. Oral gastrograffin: hyperosmotic. gangrenous or necrotic o Will have relook laparotomy in 2-3/7 to ensure good resection of bowel margins?? 5) Perforation (usually in caecum as it is thin walled) Occurs due to ischaemia of stretched out bowel wall. Barium enema unlikely to work. tumour is proximal enough near to the cecum.3) Closed loop obstruction (if due to distal tumour) Resect bowel + primary anastamosis with proximal defunctioning colostomy Resect bowel + Hartmann’s/Paul-Mikulicz procedure: if bowel is too inflamed/oedematous to anastamose (high risk of leakage) Palliative: colonoscopy with stenting 4) Ischaemic bowel Supportive management e. drip & suck.g. re-establish peristalsis Surgical intervention if bowel is non-viable e. Ca). causes intraluminal osmosis . >12cm dilated Emergency laparotomy: resect lesion & perforated bowel with generous peritoneal lavage If lesion e. can re-establish peristalsis c. metaclopromide. or if works recurrence rate is high.g. e. little lymphoid tissue & are self emptying 4) Others: umbilical fistula. correct electrolyte imbalance IO: NG tube on constant suction. gastric lavage to exclude UBGIT. supine AXR PR bleed: PCT if necessary.Like the appendix.Usually asymptomatic. Less prone to inflammation as most Meckel’s have wide base. colonic. OGD & colonoscopy Definitive treatment: surgery (open or laparoscopic) Wide base: wedge ileal resection with anastamosis Narrow base: resection of the diverticulum 81 . IV drip. rectal. due to peptic ulceration 3) Diverticulitis: may present exactly like acute appendicitis i.Barium studies: small bowel enteroclysis . tumour. perforation etc INVESTIGATION Blood: As per IO or lower BGIT Imaging: . intussusception.2 types of ectopic tissue Pancreatic (6%) Gastric (60%) – gastric acid secretion can produce inflammation. hepatobiliary. peptic ulceration & bleeding.2 inches in length.Occurs in 2% of the population.CT NOT helpful as hard to distinguish Meckel’s diverticulum from small bowel loops MANAGEMENT - NBM. periumbilical pain radiating to RIF. omphalomesenteric band 2) Hematochezia (most common in children): usually massive & painless. Meckel’s diverticulum is a true congenital diverticulum. 2cm wide. volvulus. 2 feet from ileocaecal valve . strictures with subsequent IO May have both types of tissue or other rarer types (jejunal. detected by gamma scan of the abdomen .Technetium-99m pertechnetate scan (investigation of choice): isotope given IV.MECKEL’S DIVERTICULUM RULE OF 2s . found incidentally during barium study or open surgery Symptomatic: 1) IO (most common presentation): strictures. a vestigial remnant of the vitelline duct . taken up by gastric mucosa.Usually asymptomatic but if often presents at age 2 if symptomatic . ♂>♀ in the ratio of 2:1 . etc) PRESENTATION . resulting in abdominal bloating. Dysarrhythmia (esp AF embolization) iii. or RIF Blood in stools Paralytic ileus. due to vasospasm and constriction) – 20-30% of acute ischemia a. hypotension. c) Finally. the abdominal pain becomes more widespread. Rapid hypovolemia shock HISTORY (typical but vague) – high index of suspicion!! Chronic Gut claudication: post prandial colicky pain (10min to 3hr after a meal) food fear LOW and malnutrition Blood in stools (as bowel begins to die) – maroon or bright red Acute Severe abdominal pain: out of proportion with examination findings: tends to be constant and central. Valvular heart disease b. MI v. Age >50 ii. tachycardia and confusion. Hypovolemia iii. CCF iv. a shock phase can develop as fluids start to leak through the damaged colon lining.4. Compression from ext sources (eg. No physical signs 3. b) A paralytic phase can follow if ischemia continues. Embolic (most lodge in SMA) – becoming less common i. PVD iv. Hypotension ii. Patients who progress to this phase are often critically ill and require intensive care. intraabdominal tumor) c. CCF iii. no further bloody stools. in which the primary symptoms are severe abdominal pain and the passage of bloody stools. in this phase. Vasoconstriction i. Radiotherapy e. Acute severe abdo pain 2. and absent bowel sounds. strangulation (from volvulus/hernia) Tissue injury can result from one of 2 mechanisms: (1) ischemic injury to the bowel or (2) reperfusion injury 2 Watershed areas: a) Marginal artery of Drummond / Griffith’s point: SMA and IMA b) Sudeck’s point: Left colic artery and Superior rectal artery Three progressive phases of ischemic colitis have been described: a) A hyperactive phase occurs first. Recent MI ii. and bowel motility decreases. the belly becomes more tender to the touch. Many patients get better and do not progress beyond this phase. Acute mesenteric ischemia (classical triad) 1. Renal failure b. This can result in shock and metabolic acidosis with dehydration. Vasculitis d. Hypovolemia v. ISCHAEMIC BOWEL RISK FACTORS Occlusive mesenteric ischemia a. Prothrombotic states – more in venous thrombosis (young) Non-occlusive (no arterial or venous abn. Poor perfusion states i. usu occurring in the splenic flexure (watershed area receiving blood from the most distal arterial branches) Diarrhoea/constipation Positive FOBT (sloughing of dead ischemia bowel) in 75% 82 . Thrombosis (Virchow’s triad) – becoming more common i. digitalis ii. MRI as sensitive as CT . ABG: Metabolic acidosis (persistant) – 50% 3. Rule out alternate diagnoses eg infx/IBD c. lateral projections show the origins of visceral branches. mesenteric vascular engagement. AT III) 5. rigid Nausea/vomiting Malaena/hematemesis Massive abdominal distension Back pain Shock Thin. a thickened bowel wall. a. Thrombosis . Intramural air/ air in portal venous system (ischemia) 4.Barium enema: stricture secondary to ischemia . a. shock. metab acidosis) a. prominent accumulation of contrast material in the bowel parenchymal. b.AXR 1. 3. portal venous gas. Urinary catheter to monitor urine output Consider NGT Antibiotics: IV Cephalosporin? and metronidazole Definitive 83 .complete lack of visualization of the SMA and its branches (as thrombosis usually starts at the prox end of SMA). Free air in abdomen (perf) .PHYSICAL EXAMINATION Initial Bowel compromise Fever. Visible light spectroscopy (analyze capillary oxygen levels). 4. ABC 2. often first sign of impending bowel infarction INVESTIGATIONS Bloods 1. ECG: AF. AP views demonstrate collateral pathways. Embolism to the SMA . Submucosal hemorrhage and edema in the colon produce a characteristic thumbprinting 2. thumbprinting and ischemia of other organs. an absence of intestinal gas. 2. Non specific findings: distended bowel. guarding. hypovolemia 4. Features: dilated arteries. Ischemic colitis has a distinctive endoscopic appearance. hypotension Peritonism – rebound. writhing in pain No peritoneal sign Auscultation may reveal a bruit Distension a late feature. Biopsies can be taken d. maintain airway and give high-flow O2 b. Raised amylase / LDH Imaging . UECr: renal failure. FBC: high Hb/ Hct (due to plasma loss/ hemoconcentration). is diagnostic MANAGEMENT Acute 1. Dilated bowel from ileus 3. PT/PTT: hypercoagulable states (if present. establish at least 1 large bore IV line and infuse fluids at maintenance rate (unless patient in shock) Monitoring (as patients are prone to extensive peritonitis.CTAP: Exclude other causes of abdominal pain Ischemic colitis: SMA or superior mesenteric vein thrombosis. ascites and air-fluid levels .filling of the proximal SMA only with a sharp cutoff of the artery Others 1. intestinal pneumatosis. performed using catheters placed through the 5 mm channel of the endoscope. STEMI Colonoscopy: procedure of choice if the diagnosis remains unclear. Tachycardia. can add Protein C/S. and dense and early venous filling Can ppt acute ischemia: ensure that the patient is well hydrated. high TW >15 in 75% 2. lack of bowel wall enhancement in contrast CT.Arteriography (limited role in diagnosis): confirm the presence and extent of occlusive disease. abdominal U/S AXR (limited use): fecalith. followed by upper respiratory infection and lower respiratory infection.While this maneuver stretches the entire peritoneal lining. INVESTIGATIONS Blood: FBC.Obstruction of appendiceal lumen Faecaliths: calcium salts & faecal debris collect around nidus of faecel material within appendix Lymphoid hyperplasia: a/w inflammatory (Crohn’s) & infective dz (GE.Pregnancy pushes appendix up right upper quadrant pain . and free air 84 .Retrocaecal right flank pain . PT/PTT. rigidity & guarding RIF mass may be palpable LIF tenderness in patients with situs inversus or lengthy appendix extending to the LIF - Cough sign: RIF pain on coughing (localized peritonitis) Rovsing sign: RIF pain with palpation of the LIF . TB. feeling of need to defaecate CAUSES . blurred right psoas. localized paralytic ileus. GXM Urine: UFEME (may have pyuria & haematuria) Imaging: Erect CXR.greater sensitivity/ accuracy/ NPV. URTI. followed by nausea & vomiting (in ½) N/V almost always occurs after pain.Pelvic appendix irritates bladder and rectum suprapubic pain.5. FB DIFFERENTIAL DIAGNOSES 1) 2) 3) 4) 5) 6) 7) 8) Mesenteric adenitis: self limiting inflammation of mesenteric LNs in RIF. it only causes pain in any location where the peritoneum is irritating the muscle. tumour. CTAP . exclude IO May have diarrhoea or constipation Inflamed appendix near bladder/ureter may cause irritative voiding symptoms & haematuria Fever (late): >39deg uncommon in first 24h but common after rupture PHYSICAL EXAMINATION - Most specific physical findings: RIF (McBurney’s point) tenderness on percussion. Obturator/ Cope sign: RIF pain with internal rotation of a flexed right hip Psoas sign: RIF pain with hyperextension of the right hip . Blood culture. a/w viral infections Meckel’s diverticulitis: inflammation of Meckel’s diverticulum (see below) Terminal ileitis: usually due to Crohn’s disease Typhilitis/caecitis Ischaemic colitis Colon cancer Appendiceal stump appendicitis Psoas abscess Most frequent misdiagnoses in Females: PID. measles) Less common causes: parasites. CRP. UECr. appendiceal gas. rebound tenderness.the inflamed appendix is retrocaecal in orientation - Atypical ppt: .Infants/children may present with inflamed hemiscrotum due to migration of pus through patent processus vaginalis – often mistaken for acute testicular torsion . followed by gastroenteritis and urinary tract infection / in Children: gastroenteritis. ACUTE APPENDICITIS HISTORY - Classic: LOA with periumbilical pain which radiates to the RIF. if it precedes pain. IMS. pain on urination. or patients with suspected appendicular abscess (require incision & drainage of pus) - - Delayed diagnosis and treatment account for much of the mortality and morbidity associated with appendicitis. monitor patient as well as size of mass When mass has reduced in size. WBC count. IV drip. If the patient's symptoms. Conservative treatment for appendiceal mass: Oschner Sherren regime Omentum naturally wraps around inflamed appendix. > 7 receive surgical consultation MANAGEMENT - NBM. with a higher frequency occurring in younger age groups (40-57%) and in patients older than 50 years (55-70%). 85 .MANTRELS Score Characteristic M = Migration of pain to the RLQ A = Anorexia N = Nausea and vomiting T = Tenderness in RLQ R = Rebound pain E = Elevated temperature L = Leukocytosis S = Shift of WBCs to the left Total Score 1 1 1 2 1 1 2 1 10 0-3 could be discharged without imaging. oral antibiotics. operative time. or complications compared with appendectomy performed within 12 hours of presentation Perforated appendix (emergent vs interval): mild symptoms and localized abscess or phlegmon on abdominopelvic computed tomography (CT) scans initially treated with IV antibiotics and percutaneous or transrectal drainage of any localized abscess. do surgery (less inflammation: easier) Exceptions: very young or very old patients. 4-6 undergo CT evaluation. in whom misdiagnosis and delayed diagnosis are common. Complications occur in 1-5% of patients with appendicitis. The rate of perforation varies from 16% to 40%. patient is stable. and fever satisfactorily resolve. correct electrolyte imbalance IV antibiotics: Preoperative antibiotics have demonstrated efficacy in decreasing postoperative wound infection rates Symptomatic relief: anti-emetics & analgesia - Definitive treatment: appendicectomy (open or laparoscopic) Urgent vs Emergent: appendectomy within 12-24 hours of presentation is not associated with an increase in hospital length of stay. and postoperative wound infections account for almost one third of the associated morbidity. advanced stages of appendicitis. Delayed (interval) appendectomy can be performed 4-8 weeks later. containing inflammatory process Symptomatic treatment as well as antibiotics. Lower sphincter is not an anatomical sphincter.Soft palate elevates (contraction of palatoglossus) to close off nasopharynx .Venous return also divided into thirds: Brachiocephalic veins (upper). oesophageal branches of left gastric artery to lower third . the epiglottis falls back.a portosystemic anastomosis exists at the lower oesophagus thus leading to formation of varices in portal hypertension 2.Upper oesophageal sphincter = cricopharyngeus muscle .Further elevation of tongue pushes food bolus into oropharynx . the pharyngeal muscles contract to bring the posterior surface of the larynx upwards to make the laryngeal inlet smaller closed off by the epiglottis .Oesophagus is a muscular tube that is 25cm (10 inches) long . left gastric vein (lower) --. ANATOMY OF THE OESOPHAGUS .Once in the oesophagus. muscularis propria. OESOPHAGEAL DISEASES 1.As the base of the tongue is elevated posterior. striated and smooth muscle in the middle third.The tongue then contracts upwards and backwards pushing the food bolus against the hard palate . adventitia (no peritoneal lining except for a short segment of intraabdominal oesophagus) very distensible Muscularis propria is composed of striated muscle in the upper one-third. involuntary contractions of the muscularis propria form peristaltic waves to propel food bolus into stomach 86 . and smooth muscle in the lower third . at the same time. oesophageal branches of the aorta to the middle third.3 narrow points along the course of the oesophagus (i) (ii) (iii) Cricopharyngeus muscle (15cm from incisor teeth) Carina where the left bronchus crosses the oesophagus (27cm from incisors) Where the oesophagus passes through the diaphragm (40cm from incisors) .Starts at the cricoid cartilage (C6 vertebra) from the oropharynx and continues into the stomach at the level of T10 .Pharyngeal muscles contract to propel food bolus past the relaxed cricopharyngeus into the oesophagus . but physiological: (i) (ii) (iii) (iv) Increased tone of the muscularis propria at the lower oesophageal sphincter Fibres of the right diaphragmatic crus loop around the cardio-oesophageal junction and contract during coughing. PHYSIOLOGY OF SWALLOWING . thus preventing reflux Angle of His where the oesophagus joins the stomach – acts as a valve Intra-abdominal pressure being higher than intrathoracic pressure .Process of mastication forms a food bolus on the dorsum of the tongue . azygos veins (middle).5. submucosa. sneezing etc when intra-abdominal pressure increases.Structure: mucosa.Blood supply (roughly divided into thirds): Inferior thyroid artery to upper third. g. MS Oesophageal Functional (Neuromuscular diseases) Achalasia Spastic motor disorders Diffuse oesophageal spasm Hypertensive lower oesophageal sphincter Nutcracker oesophagus Scleroderma Peripheral neuropathy Myasthaenia gravis Myopathies e.In each anatomic region the dysphagia can be caused by neuromuscular dysfunction (impaired physiology of swallowing) or mechanical obstruction to the lumen Oropharyngeal Functional (Neuromuscular diseases) Stroke Parkinson’s disease Brain stem tumours Degenerative conditions e. APPROACH TO DYSPHAGIA CAUSES OF DYSPHAGIA . angular stomatitis (Fe def anemia) post menopausal women genetic and nutritional factors premalignant oes/hypopharynx/oral SCC Tx: Fe supplement. herpes) Radiation-induced Medication-induced Chemical-induced (alcohol) . Oes dilatation 87 Reflux Infectious (candida.g. myotonic dystrophy Mechanical (Obstructive lesions) Tumours Inflammatory masses e. glossitis. lymphadenopathy.Dysphagia can be divided into oropharyngeal and oesophageal dysphagia . Vascular compression (enlarged aorta or left atrium) Thoracic inlet mass Kyphoscoliosis Others Oesophagitis: Plummer Vinson syndrome / Paterson Brown Kelly syndrome - Triad of dysphagia (oes web). abscess Oesophageal webs Mechanical (Obstructive lesions) Intrinsic structural lesions Tumours Strictures: Peptic (reflux oesophagitis) (MRCP) Radiation Chemical (caustic ingestion) Medication Lower oesophageal rings (Schatzki’s ring) Pharyngeal pouch (Zenker’s divert) Oesophageal webs (Plummer-Vinson) Foreign bodies Anterior mediastinal mass Extrinsic structural lesions Mediastinium – retrosternal thyroid.3. ALS.g. May be associated with choking. tetracycline. Recent onset dysphagia that is progressively worsening.Presenting complaint is usually of difficulty in initiating swallowing .Voice may sound nasal (bulbar palsy) . sclerodactyly. chronic alcohol intake Radiation to the chest Symptoms of systemic disease e. oes spasm. stroke (focal neurological deficits). nutcracker) a) Odynophagia b) Choke. retrosternal burning pain (heartburn). nasal regurgitation c) Regurgitation of undigested food d) Nasal voice 1. coughing. Differentiating mechanical obstruction from neuromuscular dysfunction (i) (ii) Mechanical 1. May have history of stroke.Patient’s localisation of the symptom often does not correspond to actual site of pathology . clindamycin. Intermittent symptoms suggestive of diffuse oesophageal spasm. post-radiation.g. nonsteroidal anti-inflammatory drugs (NSAIDs). Patient complains of more difficulty swallowing solids than fluids 2. trimethoprim-sulfamethoxazole). Dysphagia more long-standing. Raynaud’s). May have regurgitation of undigested food 3. III.Intermittent symptoms are suggestive of webs. stroke is the most common cause Oesophageal . shortness of breath esp at night . rings. cough. nutcracker oesophagus 4. and alendronate (Fosamax) Loss of weight occurs in cancer and achalasia (much later onset in achalasia compared to cancer) Smoking. with loss of weight high suspicion of oesophageal cancer . postural aggravation on lying down Caustic chemical ingestion in the past Medication history: Antibiotics (eg.Symptoms of aspiration pneumonia – fever.Symptoms of anaemia (bleeding from tumour. sour fluid reflux into mouth (acid brash). nasal regurgitation .g. Mets: Neck lump (LN).Presenting complaint is that of food “getting stuck” in the throat or chest .Locally advanced tumour: o Hoarseness (recurrent laryngeal nerve) o Thoracic spine pain (spread posteriorly to thoracic spine) o SOB (pleural effusion sec to lymphatic blockage by tumor infiltration) o Fever.Cause of oropharyngeal dysphagia is usu neuromuscular rather than mechanical. cough. doxycycline. excessive salivation (water brash). Dysphagia: II. chemical-induced (usually alcohol). herpes).Can be due to either neuromuscular dysfunction or mechanical obstruction 2. stricture) / Intermittent (webs. Differentiating oropharyngeal from oesophageal dypshagia (i) (ii) Oropharyngeal . Complications (3) . quinidine. scleroderma (CREST: telangiectasia. Is there odynophagia (pain associated with difficulty swallowing)? (a) Oesophagitis: infectious (candida. Parkinson’s 88 . emperonium bromide. Associated symptoms: Complications RF a) Difficulty initiating / Food stuck b) Solids / Liquids initially c) Progressive (CA. bone pain 5. slowly progressive 3. Patient complains of more trouble swallowing fluids than solids 2. neuromuscular disease 3. cough and haemoptysis (tracheo-oesophageal fistula) o Haematemesis (invasion into aorta massive bleed) – rare Always differentiate hematemesis from hemoptysis. jaundice. IV. calcinosis. potassium chloride. or as part of Plummer-Vinson syndrome) .HISTORY I. rings Neuromuscular 1. reflux oesophagitis (b) Oesophageal spasm (c) Scleroderma (d) Achalasia (occurs late) (e) Oesophageal cancer (occurs late) (f) Oesophageal rupture/stretching 4. History of predisposing conditions (RF) - Reflux symptoms e. IV antibiotics 2. what is the colour? . PD features. oesophagitis ulcerations.IV fluids (correct fluid deficits and also any electrolyte derangements) .Treat any aspiration pneumonia – NBM. gastrostomy/jejunostomy – if aspirates seen. Disease/Causes .Neuro examination (esp CN. General condition Vitals: the patient may be hypovolaemic from vomiting/decreased intake o Nutrition: presence of cachexia o Dehydration (mucous membranes. give slowly and carefully) . Complications of disease - Signs of pneumonia: patient febrile.Tube feeding through NG tube. Treatment .Feeding o Consider feeding with fluids if patient can tolerate it (only having problems with solid food) otherwise consider tube feeding or TPN need to correct patient’s nutritionally debilitated state o Keep NBM if patient cannot tolerate even fluids . Stabilise patient .Conjunctival pallor: bleeding from tumour.Scars/marks over the chest and abdomen suggesting previous radiation .Surgical scars MANAGEMENT 1. lung crepitations.Visualisation of obstructive lesions: o Shouldering of a stricture (benign strictures form a smoother contour whereas malignant strictures form a more right-angled contour) o Bird’s beak sign of achalasia - - Achalasia - Benign stricture Carcinoma Visualisation of pharyngeal pouch or oesophageal diverticulum Diffuse oesophageal spasm gives a corkscrew appearance 89 Cockscrew . Investigate for underlying cause and treat it INVESTIGATIONS Diagnostic 1.Resuscitate if patient is haemodynamically unstable . especially when suspecting webs.Scleral icterus: metastases to liver - 2. Barium swallow Advantage of barium swallow is that it is less invasive than OGD.Palpable mass in abdomen (not likely) . Ascites 4. myopathy) . or associated with P-V syndrome . CI in patients with difficulty initiating swallowing high risk of aspiration (therefore.Bedside swallowing test? 3. may be toxic. etc) .Total parenteral nutrition .PR examination for malaena . decreased air entry usually over right lower lobe Signs of mets: Hepatomegaly. skin turgor.PHYSICAL EXAMINATION 1.Presence of cervical lymph nodes (esp Virchow’s node) . diverticula in the oesophagus where OGD may cause perforation. poor intake.Advantage is direct visualisation of the lesion and ability to take tissue biopsy (especially useful in malignancy) . Manometry - 4. Oesophagogastroduodenoscopy (OGD) . creatinine – electrolyte disturbances from vomiting. raised creat and urea in dehydration (creat will be raised more than urea if patient has prerenal failure from dehydration) - Liver function tests – low albumin with nutritional deprivation CXR - 3. stenting the lumen. Gold standard for diagnosing achalasia: (i) Absence of peristalsis (ii) Very high pressures at the lower oesophageal sphincter (iii) Absence of relaxation at the LES on swallowing food Videofluroscopic examination of swallowing (VFES) – using barium Flexible-endoscopic examination of swallowing (FEES) - Used to assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various consistencies of food during swallowing VFES limited to cervical oesophagus (unable to exclude distal oes lesions) Supportive 1. 2. electrolytes.May also be therapeutic (stopping bleeding from a tumour.2. Blood investigations: - Full blood count – - Urea. Low Hb (anaemia from chronic blood loss) High TW (aspiration pneumonia) Consolidation (aspiration pneumonia) 24-hour pH probe monitoring - If patient complains of reflux symptoms and no signs are seen on OGD (see later section on Gastro-oesophageal reflux disease) 90 . etc) 3. 4. OESOPHAGEAL CANCER EPIDEMIOLOGY - Third most common gastrointestinal tract cancer in Singapore (1st: CRC, 2nd: gastric) - M > F, Adenocarcinoma more common in West whereas SCC more in East - Increasing incidence with age - Decreasing incidence overall, increasing in distal oes RISK FACTORS SCC (70%) 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 91 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. 92 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 93 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 94 Chemotherapy - Current regimen: 5-Fluorouracil and cisplatin - Addition of chemotherapy to external beam radiation for unresectable cancers shown to have improved survival compared to EBRT alone - Chemotherapy given preoperatively and postoperatively improves survival Overall curative treatment Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection), oesophagectomy, and postoperative adjuvant chemoradiotherapy for responsive tumours Palliative treatment 1. Ablation o Endoscopic laser fulguration (high frequency electric current) o Photodynamic therapy is a new treatment option - use of drugs that are absorbed by cancer cells; when exposed to a special light, the drugs become active and destroy the cancer cells o Radiofrequency o Cryotherapy 2. Surgical debulking 3. Bypass surgery rarely done nowadays 4. Stenting to maintain lumen patency and occlude fistulas – endoscopic / radiological? o Cx: metallic Perf (friable tumor) Bleeding Risk of GERD, aspiration lifelong PPI Feeding in oesophageal obstruction - Feeding via oropharyngeal route is preferred unless the passage is obstructed or it is unsafe for the patient to feed via that route (i.e. risk of aspiration) o If still able to pass NG tube around tumour feed via NG (but also consider complications with long-term NG placement e.g. erosions around nasal area, sinusitis); o consider PEG placement for long-term feeding if able to get scope around tumour - If unable to pass tube or scope around tumour, o consider open gastrostomy o Total parenteral nutrition is another option but has more complications, more costly o Relief of obstruction via various techniques as listed above help to enable oral feeding, but most techniques are not long-lasting and dysphagia will return with tumour growth PROGNOSIS - 80% mortality at 1 year, overall 5-year survival <10% 95 sedatives. arm).Motility disorder of oesophagus e. GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD / GERD) EPIDEMIOLOGY Incidence in Singapore not known Increasing prevalence. more common in males than females Singapore Chinese > other races PATHOPHYSIOLOGY . water brash (hypersalivation in response to reflux) Chest pain (can mimic anginal pain with radiation to neck. Loss of LES function – decreased tone. jaw. Barrett’s oesophagus CAUSES/RISK FACTORS . stricture. tight garments. beta agonists. large meal IV.Acid brash/Regurgitation: reflux of sour gastric juices into back of mouth i.g.GORD results from various pathophysiological factors (loss of the normal protective mechanisms. regurgitation o These symptoms occur usu after food.Heartburn: retrosternal pyrosis (=burning sensation in upp abdo) . calcium channel blockers. particularly a heavy meal. odynophagia suggests oesophagitis with ulceration o Reflux can also lead to pulmonary symptoms: chronic cough. Increased intra-abdominal pressure – obesity. etc .e. scleroderma Malfunction of LES Hiatal hernia (loss of normal LES mechanisms) Drugs that cause smooth muscle relaxation e. .5. or the mechanisms are overwhelmed) singly or in combination: I.Complications o Long-standing disease can lead to dysphagia due to stricture formation.Chronically increased intra-abdominal pressure – pregnancy. constipation. obesity. chest infections (aspiration) 96 . etc. iatrogenic injury III.Chronic inflammation results in complications of GORD: oesophagitis.Acid incites inflammation in lower oesophagus – extent of inflammation increases with increasing duration of contact with acid . anticholinergics.Eating habits – lying down after a heavy meal Any cause of decreased gastric emptying PRESENTATION . Motor failure of oesophagus with loss of peristalsis II.Other symptoms: globus (feeling of a lump at the throat).g. dysphagia can also result from an underlying oesophageal motility disorder. and are aggravated by lying flat (posturally related) . Delayed gastric emptying . hiatal hernia.Lower oesophageal sphincter is a physiological sphincter with various mechanisms that help to prevent reflux . chronic cough.Some physiological reflux occurs that is rapidly cleared by peristaltic movements in the oesophagus . nausea high false positive . Coffee and smoking also cause LES relaxation. Manometry .Exclude cardiac cause of chest pain. .Cx: oesophageal ulceration and stricturing resulting from reflux . Schatzki’s ring (constrictive ring at the squamocolumnar junction composed of mucosa and submucosa) 9.Ax: Can detect motility disorders that cause reflux.Relevance of classification schemes: subjective and dependent on assessment by the endoscopist. Shortening of oesophagus 4. just mentioning a grade may not have any meaning if the actual abnormalities are not described . stenosis. Malignancy (adenocarcinoma arising from Barrett’s oesophagus) DIAGNOSIS 1. Oesophageal pH probe .GerdQ questionnaire 2. 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. and exclude malignant cause of dysphagia . . alternative is the Bravo capsule (a wireless capsule that is temporarily attached to the oesophageal wall. Barium swallow and follow-through . Either one positive is diagnostic. due to the multitude of classification schemes available. also.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) .Can sometimes see reflux of barium contrast into oesophagus 5. Savary-Miller classification Grade I: Grade II: Grade III: Grade IV: Grade V: One or more supravestibular non-confluent reddish spots. Therefore.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.Diagnosis based on the percentage of time in 24hrs the pH reading is below 4 (positive if >5. Pain and spasm 2. 3. may be confluent but not circumferential Circumferential erosions covered by haemorrhagic and pseudomembranous exudate Presence of chronic complications such as deep ulcers.Cannot actually diagnose reflux (poor correlation btw oesophagitis and reflux). Oesophagogastroduodenoscopy .5%) .heartburn severity or the symptoms do not reliably predict the severity of erosive esophagitis. selective usage. Barrett’s oesophagus (see below) 8.Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probe especially if oesophagitis is not seen on OGD . stricture Barrett’s metaplasia 2. with or without exudates Erosive and exudative lesions.Not of much value in diagnosing reflux . 48hr) . older patients experience less symptoms 97 .Can have false negative consider repeat test. Stricture 3. Los Angeles classification .Antimony probe (24hr) most commonly used.No value in reflux except for detecting motility disorder (tro achalasia! – will be much aggravated by surgical Tx of reflux) GRADING OF OESOPHAGITIS 1. Ulceration 7. Haemorrhage (occult > frank) 6.COMPLICATIONS 1. History!! is important as most patients with reflux are seen in the primary setting with no facilities for detailed investigation . Dysmotility 5. anticholinergics. fatty foods. Smoking and alcohol intake cessation Medication 1. rather than increasing dosing frequency) or H2-receptor antagonists May require LT tx. chocolate. Elevate head of bed 5.patient does not want to be on medication for life (despite good results) . restart PPI first. Prokinetics to increase LES pressure e.g. Acid suppression therapy: PPI (best! switch ard if patient doesn’t respond to one. Diet and eating habits Avoid coffee.Indications: Failure of medical therapy (or incomplete resolution of symptoms) Oesophagitis with frank ulceration or stricture Complications of reflux oesophagitis – respiratory complications.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) . Avoid drugs that relax LES e.TREATMENT Lifestyle 1. Barrett’s oesophagus Severe symptoms or progressive disease Compliance problems .g. domperidone (anti-dopaminergic). etc. or anything that worsens symptoms Do not eat 2 hours prior to sleeping Walk after eating Avoid excessive eating. metoclopramide (anti-dopaminergic + antiserotoninergic) Surgical . If patient stops PPI and symptoms recur.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 98 . Weight reduction if obese 4. eat small meals 2. muscle relaxants. 2. 3. no need to reinvestigate. usually due to a foreshortened oesophagus unrecognised in the first operation. no medications and lifestyle changes required) 10-15% Satisfactory (some residual symptoms) <5% Unsatisfactory <1% Mortality 5-40% need for acid suppression therapy at 5 years due to symptoms . Nissen fundoplication is the most commonly done – a 360 degree (total) wrap of the fundus around the gastrooesophageal junction b. anterior 90 degrees. creating an hourglass deformity whereby the stomach resides both above and below the wrap.Nerve stimulation? of LES to increase tone (still under research) 99 . “Slipped-Nissen” body of the stomach intussuscepts through the fundoplication. may result in mediastinitis if not promptly detected and repaired intraoperatively 2. dilators. If resistant to dilatation resection and reconstruction Others . etc) 2.Fundoplication (mainstay of surgical therapy) Can be done via open surgery or laparoscopic surgery (most laparoscopic now) a. Dilatation (variety of means available – balloon.Management of stricture Rule out malignant cause of stricture by taking biopsy 1. Partial fundoplications can also be done in patients where oesophageal motility is poor or the oesophagus is foreshortened. anterior 180 deg. Excessively tight wrap resulting in dysphagia 3. 5.Outcome of surgery 80-90% Excellent to good (no symptoms.Complications of surgery 1.. Treatment of underlying reflux 3. Excessively loose or short wrap – reflux recurs (failure of treatment) 4. Perforation – most feared complication. Causes severe reflux as pouch above the wrap traps food and serves as reservoir. “Gas bloat syndrome” – patient experiences difficulty burping gas that is swallowed (gas accumulation) . and posterior 270 deg fundoplications are various options available . argon plasma coagulation will not remove all dysplastic cells thus potential for malignancy still remains 2. BARRETT’S OESOPHAGUS FEATURES . Oesophagectomy is the only definitive treatment to remove all dysplasia.Diagnosis: Endoscopy and histology: The squamocolumnar junction (or Z line) is visible on endoscopy as gastric and intestinal type epithelium is pink and granular in appearance.If patient has high grade dysplasia. Possibility of endoscopic mucosal resection as a treatment modality (research still undergoing) – shown to be as good as oesophagectomy with less morbidity and mortality 100 . acid suppression (PPI!). surgery etc .6.e. otherwise to undergo intensive surveillance (3 mthly for at least one year) to detect cancer development 3. but stratified squamous epithelium is smooth and pale The gastro-oesophageal junction is defined as the point where the gastric folds begin If the squamocolumnar junction is above the gastro-oesophageal junction (i. Endoscopic surveillance . the patient is diagnosed to have Barrett’s oesophagus .Not shown to decrease risk of cancer still requires surveillance?? 2. but is associated with high morbidity and mortality (worth it?) 3.Intestinal metaplasia of the oesophageal epithelial lining (stratified squamous epithelium mucus-secreting columnar epithelium with goblet cells) .Lifestyle changes. as well as higher risk of dysplasia and subsequent adenocarcinoma development than short segment Barrett’s Risk of development of adenocarcinoma is about 10-15% in 10 years MANAGEMENT 1.Complications: Short segment Barrett’s is defined as the squamocolumnar junction being <3cm above the gastro-oesophageal junction Long segment Barrett’s the distance between the two junctions is >3cm: associated with more severe reflux. Endoscopic therapies to ablate the dysplastic tissue e. photodynamic therapy. Treatment of underlying reflux .Not certain regarding benefit for surveillance if patient has Barrett’s but no dysplasia if 2 scopes in a year reveal no dysplasia.Main purpose of surveillance is to pick up dysplasia .g. laser therapy. repeat OGD once every 3 years (half-yearly 3 yearly) .Associated with long-term reflux – an adaptation mechanism where intestinal epithelium withstands exposure to acidic reflux better than oesophageal epithelium . they do not align) and biopsy of the junction shows intestinal metaplasia. Treatment of high-grade dysplasia 1. it should be treated (see below). with incomplete LES relaxation on swallowing.Mainly palliative in nature .; affects body and distal oesophagus .Non surgical treatment: Intrasphincteric injection of botulinum toxin to block the release of acetylcholine at the level of the LES (problem is that it is not long lasting and only used in patients not fit for surgery) Pneumatic balloon dilatation (A balloon is inflated at the level of the gastroesophageal junction to blindly rupture the muscle fibers while leaving the mucosa intact): about 65% of patients improve. regurgitation.Barium swallow demonstrates “bird’s beak” narrowing of distal oesophagus with proximal dilatation . Used in elderly who are not suitable for surgery/dilatation) .Adults. there is a 3% chance of developing reflux addition of fundoplication (partial wrap) helps prevent this Esophagectomy was the standard treatment in patients with achalasia and a markedly dilated or sigmoid-shaped esophagus (controversial) 101 . M:F = 1:1 . weight loss.Patients present with dysphagia.1-10% of patients develop SCC after 15-25 years of disease TREATMENT . noncholinergic. The result is a hypertensive nonrelaxed esophageal sphincter .Surgical treatment (primary Tx): Laparoscopic Heller cardiomyotomy (much like Ramstedt pyloromyotomy for pyloric stenosis) – good results with 85% symptom-free after 5 years.Aetiology unknown .Manometric studies (required for diagnosis) show abnormally high pressures at the LES. ACHALASIA FEATURES .Abnormal peristalsis secondary to absence or destruction of Auerbach’s (myenteric) plexus and failure of the LES to relax. inhibitory ganglion cells. and recurrent pulmonary infections .Lacks nonadrenergic. retrosternal chest pain.7. causing an imbalance in excitatory and inhibitory neurotransmission. 40% response rate at 5 years) Calcium channel blockers and nitrates (both decrease LES pressure but do not improve LES relaxation. and lack of progressive peristalsis (often aperistaltic) . 5L of blood in stomach before vomiting out (bleeding more than pylorus can empty) 3.Altered blood.Recent constitutional symptoms e.Very brisk upper GI bleed can present as frank PR bleeding as blood passes down so fast it doesn’t get altered 2.Elderly patient (>60) high risk (Rockall score) . anticoagulants. non-particulate (almost liquid in consistency). but iron stool will sedimentate and turn the water green Frank PR bleeding .Symptoms of anaemia: postural giddiness. mixed with normal stool. duodenitis 3.Any drugs that may predispose – NSAIDs. Mallory-Weiss tear. AV malformation . Gastro-oesophageal varices 6. shortness of breath. APPROACH TO BLEEDING UPPER GIT CAUSES Variceal vs Non-variceal! 1. Gastric malignancy 4.Previous variceal bleeds Mallory-Weiss tear .Any history of chronic liver disease . gastric ulcer (any OGD done in the past showing these problems? On any “gastric” medications?) . above the ligament of Treitz .Any history of dyspepsia. floats on water – maroon when you spread it out on gloves (b) Stale malaena – black-grey.Other comorbidities: liver disease.If gloved finger is stirred in a cup of water. Rare causes: AV malformation (Dieulafoy lesion) – most will stop bleeding spontaneously. antiplatelets. malaise . foul smelling.Binge-drinking with subsequent severe retching and vomiting leading to haemetemesis Malignancy . Aetiological clues / RF Gastric ulcer/gastritis/erosions .e.Hematemesis: easily 1. gastric erosions. if it’s an old patient with previous history of IHD effort tolerance. nasopharyngeal bleeding 9.[oes] Can be fresh red blood as in variceal bleeding. . chest pain 5. tarry. Amount of blood . LOA. LOW. Stress ulcers from burns/ instrumentation 5. ask how much blood Cup? Bowl? . occasionally particulate (c) Iron stool – greenish hue on rubbing between gloved fingers. renal failure (uraemic gastritis) HISTORY (if patient is stable) 1. Peptic ulcer disease (bleeding peptic ulcer) 2.If patient is having haematemesis.6.g.[gastric] Coffee grounds vomitus is altered blood (due to gastric acid) and can come from gastric ulcer.Dyspepsia 4. Complications . Nature of bleeding Haematemesis . UPPER GIT 1. renal disease. Systemic: coagulopathies.AMI esp. malaena indicates bleeding from the upper GIT i. particulate. palpitations. Comorbidities .Early satiety .Different types of malaena: (a) Fresh malaena – jet black with sheen. lethargy. dull. IHD high risk (Rockall score) 102 . malaena will “dissolve” completely with no sedimentation and turn the water black. . Gastritis. steroids. Bleeding from other sources: Haemoptysis. or variceal blood that has entered the stomach [oes] Malaena . TCM Varices . aortoenteric fistula 8. Mallory-Weiss tear 7. gastritis/erosions. Patient’s conscious level – confused? (shock) . or anticipating surgery . supplemental oxygen. aspiration. low plt .Malaena or frank blood . General inspection .If suspecting varices – IV somatostatin/octreotide.Blood pressure. Resuscitation ABC: Protect airway. followed by more fluids if necessary (be wary in pts with renal & heart failure) .Pallor . elec abn from vomiting) 3. LFT (Child's score . 2.Monitor for: SHOCK ( HR. U/E/Cr (dehydration . Early medications . Close monitoring . Abdomen . perforation if pt complains of pain . NSAIDS 4.Stigmata of chronic liver disease 3. Adjuncts . FBC (Hb will not drop in first 24hrs.PHYSICAL EXAMINATION 1. they are dysfunctional) .may not stop bleeding).Urine output: renal perfusion indicates cardiac output 2. allows gastric lavage prior to OGD (DO NOT insert if suspect varices) . obtunded 3.Cold clammy peripheries impending shock . Peripheries .Catheterisation – monitor I/O balance esp in elderly or when large amount of fluid resuscitation required.1 pint N/S over half to one hour if patient is in shock. heart rate stable? Any postural hypotension? (Tachycardia is an early sign of shock) Narrowing pulse pressure (ind systolic hypotension) . . 4.NG tube if patient is having haematemesis – prevents aspiration. BP. IV antibiotics . Plt ECG to detect any acute myocardial ischaemia/infarction.FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K) - 2. confusion & lethargy) 5. anticoagulants.even if plt is normal. to keep Hb above 10g/dL . PT/PTT (check and correct for coagulopathy).check if patient is on BB!! . Emergency oesophagogastroduodenoscopy 103 . Digital rectal examination .Compare current vitals with vitals in ambulance.LN (mets) impending shock 4.tumor deposits / rectal mass IMMEDIATE MANAGEMENT 1. Vitals! .Stop antiplatelets. epig mass . GXM: order in active bleed 4 pints PCT. ED – is there a worsening trend? .May consider platelets if patient is on antiplatelet meds (qualitative defect in platelets .ind etiology and outcome) .Any tenderness (not very helpful).HD with hourly para if Elderly with many comorbidities Hypotension urine output.raised Ur more than Cr.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) .do in alcoholic hx or liver disease 5.Infusion . PFO CXR: PFO.Intubate if: 1) massive uncontrolled active hematemesis 2) signs of decompensation eg. FFP.Cold clammy peripheries .Packed cells if Hb is less than 10. 2 large-bore IV cannula in antecubital fossa Bloods: 1.RR>20 .Distension (++ blood in stomach) 5. also fresh malaena) 3.Alternatively. Shock / hemodynamic instability (ensure BP is stable before OGD .requires sedation) 2.air sufflation during OGD will cause abdominal compartment syndrome --> decrease venous return --> patient may DIE splinting of the diaphragm . Injection . Varices: ligation/sclerotherapy. 104 . 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.Ensure bloods are running before OGD! . glue 2.Role of endoscopy Diagnostic: confirm UBGIT & identify source of bleeding.3 Indications: 1. Non-variceal: Clip. Suspected variceal bleed Not just low Hb as emergency scope causes more stress. . Active BGIT (esp hematemesis. scope the next available OGD (usually following day) . Biopsy (+ CLO test if ulcer) Therapeutic: 1.Repeat OGD with greater detail if it is normal the 1st time. Coag.CI: Perforation . Resuscitate .Send bloods – GXM 4 pints. IJV) .2 large-bore IV cannula in proximal veins (cubital.Continue antibiotics and omeprazole . mucosal ulceration) .Chronic alcohol intake .Infuse fluids .Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow variceal bleeding 6. U/E/Cr. Management of severe bleeding: Sengstaken-Blakemore tube . oesophageal balloon is not inflated nowadays 5.Gastric varices are usually too large to be banded. treat hypokalaemia from vomiting (b) aspiration – protect airway.Studies have shown that cover with broad spectrum Abx (Gram neg cover) .Ceftriaxone. FBC.g.Continue somatostatin up to the point where haemostasis is achieved or 5 days (exact ideal duration not well studied) .Needs to be done emergently (on admission) as soon as patient is stabilised since bleeding can be torrential and life-threatening . aids haemostasis . mortality. and thus decrease oesophageal variceal bleeding). Ciproflox 1g/day .If patient has altered mental state (encephalopathy) need to protect airway (may require intubation) 3. VARICEAL BLEEDING PATHOPHYSIOLOGY A result of portal hypertension (i. Chronic management WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT . Emergency endoscopy . enthusiastic transfusion can portal pressure 4.Look at hydration status 2. etc. ACUTE BLEEDING – MANAGEMENT 1. look for early signs of shock – tachycardia.Not given in ulcer bleed . Vascular access.Preferably started before endoscopy (procedures increase bacteraemia) infectious cx.Antiencephalopathy Tx: Lactulose + Cipro (clear gut to prevent absorption of NH3) .e.Keep patient in ICU! .Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9.2.Purpose: confirm diagnosis and institute management . may require use of Sengstaken-Blakemore tube for up to 48hr (if unable to ligate) . circulation . EJV. esomeprazole (Nexium).Anticipate complications: (a) encephalopathy – fleet and lactulose. Acid suppression . and also risk of recurrent bleed 8.Risk of sepsis in patients with CLD and bleeding .If hypotensive and bleeding is ongoing.If patient appears well. Hepatic vein thrombosis 105 . 7. postural hypotension .Agents available: omeprazole (Losec).Previous history of variceal bleed . Management of possible precipitants . Observation . ?benefit of gastric decompression using NG tube (c) risks of procedure – OGD-related risks 10. . sclerotherapy/ Glue (Histoacryl) used instead – risk of embolism from histoacryl 9. Assess mental state . 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. breathing.Profuse hematemesis I. Acute bleeding 2.NBM 2-3/7 . and blood investigations .Mode of action: splanchnic vasoconstrictor which portal blood flow and hence portal pressures .NSAIDs.Protect airway before inserting tube.Increasing intragastric pH increases clot stability. LFT. pantoprazole.Intervene if ESRF present or active bleed (not electively) . PT/PTT .Jaundice or stigmata of chronic liver disease . IV somatostatin or S/C Octreotide (Not given in ulcer bleed) .Inflate gastric balloon and pull upwards against cardioesophageal junction (balloon will press on perforator veins entering oesophagus from stomach. fluids/blood resuscitation.Airway. Prophylaxis 3. Antibiotics .Banding/Ligation is the best modality for oesophageal variceal bleeding (sclerotherapy a/w higher morbidity e. In United States. operative mortality with this procedure has exceeded 20%. encephalopathy Constant monitoring of patient. failure (blood flow in opposite direction) usually temporising procedure C. bleeding. splenic side anastomosed end-toside to left renal vein) A. thrombosis. Splenectomy Proximal gastric devascularisation Selective vagotomy Pyloroplasty Oesophageal devascularisation Oesophageal transection 106 . which inhibits future varix formation Japan cited a 5. 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. with bleeding recurring in 35% to 55% of patients. Shunt surgery Portocaval shunts (portal vein to IVC) – side-to-side.If bleeding stops. 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. End to side spelnorenal shunt.3% rate of recurrent hemorrhage. 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. home in around 1/52 Rescope before home! (ligate if rebleed) If bleeding is not remediable by endoscopic intervention: A. C. B. Normal liver with normal blood flow. to avoid as it ppt.2% operative mortality and a 6. Mesocaval H-graft shunt D. D. B. Cx: encephalopathy (increased risk with bigger shunt). End to side portacaval shunt. PROPHYLAXIS OF VARICEAL BLEEDING SECONDARY = Band ligation + Non-selective beta-blockers . the use of propranolol is of questionable benefit – repeat OGD to monitor varices.net/HEART/011507/PortalHypertension.The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%.LT propanolol + PPI . 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.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. to be continued indefinitely .II. long-acting nitrates (eg. or Sugiura) .If patient bleeds again failed ablation consider surgery (as above – shunts.Refer to Hepato for liver disease http://www.Band ligation/ Sclerotherapy: not used as primary prevention.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. isosorbide 5-mononitrate) are alternatives .heart-intl. cardiac output by β1 blockade and splanchnic blood flow by blocking vasodilating β2 receptors at splanchnic vasculature .htm 107 . 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) . Incidentally detected on OGD 2. robust mucosal blood flow to remove protons. pylori . epithelial regenerative capacity.Overall mortality 7-10%.Board-like rigidity.Accounts for 90-95% of duodenal ulcers. pylori hydrolyzes urea to ammonia. while it is relieved by food in a duodenal ulcer 3.NSAIDs impair mucosal prostaglandin production (through non-selective COX inhibition) prostaglandins are important for mucosal bicarbonate and mucin production and inhibiting gastric acid secretion. pylori: biopsy tissue is placed into a medium containing urea and an indicator such as phenol red.Steroids and anticoagulants do not increase the risk of ulcer formation. early satiety. which raises the pH of the medium. bicarbonate secretion into mucus. 108 . Bleed . of which 20% (6% overall) will have a clinically significant ulcer i.H. symptomatic.The most important and valuable investigation . pylori causes a local inflammatory reaction and secretes enzymes that break down the gastric mucosal barrier. 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. and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE).68% of patients are over 60 years of age . pylori . PEPTIC ULCER DISEASE EPIDEMIOLOGY . pylori by age 21 .Alcohol .e. a/w upper abdo fullness.An imbalance between mucosal protective mechanisms against acid.As above.Accounts for most of the rest of ulcer disease not caused by H.Incidence about 100 per 100. presenting with haematemesis (coffee-grounds vomitus) or malaena 4. prostaglandin secretion by mucosa to maintain blood flow .3. The urease produced by H. Perforation .Pain is usually worse with food in a gastric ulcer. bloating. and 50% of gastric ulcers NSAIDs . belching.60% of population are positive for H.Erect CXR will show air under diaphragm ENDOSCOPY (OGD) . and also enhances gastric acid secretion and decreases bicarbonate production . unchanged for last 20yrs – mostly due to ulcer bleeding esp in elderly with significant comorbidities MAIN AETIOLOGICAL FACTORS H. bleeding Other factors .Cigarette smoking . nausea (c) Unspecified dyspepsia .000 per year .About 10-20% of infected patients develop an ulcer .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. guarding will be present on examination (signs of peritonism) .30% of patients on NSAIDs will get an ulcer.2 Aggressive forces: gastric activity and pepsin activity . and aggressive forces that damage the gastric mucosa .Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements .5 Protective mechanisms: mucus secretion. but increase the risk of bleeding in an existent ulcer PATHOGENESIS . as well as maintaining mucosal blood flow PRESENTATION 1. Injection with adrenaline (1:10. Gastric biopsy urease test (to confirm eradication of H. 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.continue with N/S if need more) or absolute alcohol – tamponade effect is the most effective. 3/7 if worrisome. Chemical (gel foam): can recannulise again in 2/52 c. Titanium) ii.not accurate if patient on triple tx Rescope and biopsy every 6/52 until ulcer is healed resect if persistent Confirm eradication of H Pylori: Urease breath test. Re-biopsy 109 . 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. Post-endotherapy: Monitor for rebleed = drop in Hb (not malaena / vomit blood clots as these are expected. Failed OGD hemostasis (after 1hr) a) Surgery is mainstay b) Transcatheter embolisation a.000 dilute to 10ml . biopsy ulcer again 1. identify bleeding vessel and embolise with i.) Diet individualised: usually NBM 1-2/7. arrhythmia. rebleed post-Sx (usually GDA). Also vasoconstriction for adrenaline. 2. Cx: perforation. Inject around ulcer (4 quadrants). <1/7 if straight forward ulcer Re-scope the following day if you’re worried about the outcome from the first scope (notroutine) Oralise PPI after 3/7 infusion (if worrisome. the rest must intervene! (c) Endotherapy (in UBGIT) 1. pylori) . Changes in vitals may be too late. not fit for Sx b. Coagulation (Heater probe = thermal / Argon plasma) 3. can give IV bolus PPI BD) TCU 3-4/52 at clinic Re-scope in 6 weeks to document ulcer healing If ulcer still present. Histo: exclude malignancy for gastric ulcer 2. bleeding. necrosis. Sandwich technique: embolise both prox and distal ends of vessel as bleeding can occur both ways. Mechanical (non-absorbable coil eg. ind: failed surgery.(b) Prognostication of bleeding risk (in UBGIT) Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH) Forrest grade 1a Spurting (arterial) 1b Non-spurting. Duodenotomy + Oversewing/Under-running the bleeding vessel b.Usually done in elective setting for chronic duodenal ulcers . tetracycline 500mg QDS. Antiulcer Sx (>2cm or suspect malignancy) (parietal peritoneum. omeprazole 20mg BD for 7 days SURGICAL MANAGEMENT Indications for surgery for acute PUD: 1. Prev episode of shock DUODENAL ULCER Indications for surgery: ‘Patient has to BUY the op’ (more complications + duod ulcer will heal provided the high acid secretion of stomach is abolished) 1. Omental patch repair + Bx (small <2cm ulcer / patient unstable) b.Drainage procedures pyloroplasty (first) or gastrojejunostomy Usually done with vagotomy as gastric emptying is decreased with denervation. Recurrent bleeding 2.treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS. selective. ulcers will not heal with ongoing NSAID therapy 2. Failure of medical management (ulcer does not heal) Surgery: 1. amoxicillin 1g BD. metronidazole 400mg BD. Perforation Indications for surgery for chronic PUD: 1.CONSERVATIVE MANAGEMENT 1. H. Antiulcer surgery (if patient stable and known case of rebleed/perf) 2. Gastric outlet obstruction (patient presents with vomiting of undigested food not long after meal. and vagal stimulus for gastrin release is abolished . stomach local flap) 3. clarithromycin 500mg BD for 7 days In penicillin-allergic patients. Gastroprotection (a) Standard dose proton pump inhibitor 20mg OM Promotes ulcer healing even with ongoing NSAID use (b) Double dose famotidine 40mg BD Inferior to omeprazole as famotidine only promotes ulcer healing if NSAIDs are stopped. succussion splash. PPI. IV antibiotics. Persistent bleeding (e.Vagotomy can be truncal.g. urea breath test or stool serology testing Treatment failure occurs in up to 20% . Bleed = a. Bleed: Mainstay of Tx for failed OGD hemostasis (after 1hr) 2. Perforation 3. jejunum serosa. substitute amoxicillin with metronidazole 400mg BD Document eradication by endoscopy with CLO test. Perforation = a. Splitting BV difficult to clip 3. parietal cells also become less responsive to histamine and gastrin. Definitiveantiulcer surgery = Duodenectomy + Vagotomy with gastric drainage procedures . erosion of a post duodenal ulcer into GDA) 2. does not require drainage as the Nerves of latarjet that supply the pyloric sphincter are not affected) . or highly selective (selecting only those branches that appear to supply peptic cells. Pyloroplasty = incise pylorus longitudinally through mucosal layer then suture the incision transversely Perforated ulcer: IV fluids.Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric secretion. pylori eradication First line triple therapy: omeprazole 40mg BD (for 6 weeks). surgery (patch repair) 110 . characteristic electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria) 4. air-fluid levels on AXR. persistent bleeding Surgery 1. Ulcerectomy (if patient unstable. Perforation. stomach local flap) 3. Antiulcer surgery (if patient stable. unfit) b. Partial gastrec if distal ulcer b. old. Bleed = a. Antiulcer Sx (>2cm or suspect malignancy) (parietal peritoneum. can treat similar to duodenal ulcer 111 . but considered antiulcer Sx as parietal cell mass and antrum (contains gastrin containing cells) are removed. jejunum serosa. Proximal ½ ulcers may require total gastrec Can be used in emergency bleed if patient stable. Perforation = a. Dysplasia or carcinoma 3. Definitive antiulcer surgery = Gastrectomy a. Bancroft’s closure (for severe inflammation/scarring that prevents dissection around pylorus. Failure to heal after 3 months of conservative therapy 2. Omental patch repair + Bx (small <2cm ulcer / patient unstable) b. can tolerate) 2. Recurrence 4. Remove all antral mucosa to prevent marginal ulcers) If prepyloric ulcer.GASTRIC ULCER Indications for surgery ‘SELL the operation to the patient’ (risk of malignancy if >2years) 1. histological grade b) Non-adenocarcinoma . Genetic . Chronic atrophic gastritis .Types: SCC.Fourth most common cancer in males. rubber .Make up 90-95% of stomach tumours . Gastric polyps .Diet: preserved foods (nitrosamines).Make up less than 10% of stomach tumours .Alcohol .Highest risk in inflammatory polyps: 75-90% . distal third of the stomach. neuroendocrine tumour.Female to male ratio 2:1 . lymph node status.000 per year .Smoking . pancreatic and intestinal secretions at the anastomotic zone 2.4.Lauren classification: (a) Intestinal type (most common overall) – occurs in high risk population.Occupational exposure: asbestos. proximal third and cardio-oesophageal junction. GASTRIC CANCER EPIDEMIOLOGY .Family history of gastric cancer PRECURSOR CONDITIONS 1.Incidence 10-18 per 100. polycyclic hydrocarbons .Due to chronic exposure of gastric mucosa to biliary. in older men.HNPCC – Lynch syndrome II .Hypertrophic gastritis (Menetrier’s disease) – inflammatory disease of gastric epithelium. pylori infection .Early gastric cancer Confined to mucosa and submucosa Good survival and prognosis regardless of size.P53 mutation . associated with erbB2 and erbB3 receptor stimulation (b) Diffuse type – occurs in low risk population.Low socioeconomic status 2. more aggressive.Blood type A . 2-10% risk of gastric cancer 4. Environmental . leiomyosarcoma. smoked foods. worse prognosis. in younger and female patients. H.Usually occurs >15 years after surgery . GIST (gastrointestinal stromal tumor). present later. linitis plastica) – NHL in submucosa adynamic stomach N/V more than anemia 112 .<1% risk of malignant change 5.Also increased risk of adenocarcinoma elsewhere in the stomach 3.Germline mutation of e-cadherin . sixth most common in females in Singapore . Peptic ulcer disease .10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology .Pernicious anaemia – autoantibodies to parietal cells with achlorhydria. heavy metals. up to 10% risk of malignant change .Incidence increases steeply after 50 years old RISK FACTORS 1. associated with K-sam oncogene . Partial gastrectomy for benign disease with Bilroth II reconstruction .3-6X increased risk of gastric cancer HISTOLOGY a) Adenocarcinomas . primary gastric non-Hodgkin’s lymphoma (MALT. hypokalaemic metabolic alkalosis. parietal peritoneum.Abdominal pain (usu late)60% 1. s/s of GOO. . polypoid. may be ulcerated.Metastatic symptoms late (bony tenderness. brain .Palpable mass 30% .Early satiety 17% . margin not sharply circumscribed Type IV (63%): Diffuse.Lymphatic spread (a) Regional nodes (b) Supraclavicular nodes (Virchow’s node) (c) Umbilical (Sister Joseph’s node) .Peritoneal seeding to omentum. neurological deficits.Anaemia 40% 3.MORPHOLOGY Borrmann’s classification: Type I (3%): Nonulcerated. LOW. N/V. or cul-de-sac / pouch of douglas (Blumer’s shelf = shelf-like tumor of ant rectal wall DDx tuberculous peritonitis) PRESENTATION Very non-specific symptoms and signs: . aspiration ± pneumonia) 113 . infiltrating.Weight loss 50% 2. ovaries (Krukenberg’s tumour).Direct extension to neighbouring organs . etc) Asymptomatic: from histology of ulcer biopsy Symptomatic: non specific abdominal pain. lung. s/s of UBGIT.Haematogenous spread – liver. . early satiety.Haematemesis/malaena 25% . s/s of metastasis. circumscribed with sharp margins Type III (16%): Ulcerated. peritonism (perforation) New onset dyspepsia at age>35 years old should cause concern COMPLICATIONS - Bleeding Gastric outlet obstruction Perforation Malnutrition vomiting (dehydration. may diffuse entire stomach (linitis plastica) LOCATION - 37% in cardia 30% in pyloric channel or antrum 20% in body 12% in entire stomach SPREAD . bone. growing intraluminally Type II (18%): Ulcerated. . LOA Complications: s/s of anaemia.Nausea/vomiting 40% . Wide resection of the tumour to negative margins (at least 6cm margins) .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. low chloride.En-bloc excision of regional lymph nodes . 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. LFTs – albumin as a marker of nutritional status (alb<35 is poor). cardia.INVESTIGATIONS Diagnosis OGD –visualisation and biopsy (ulcer with heaped-up edges) Staging investigations 1. 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. higher chance of leak Oesophagojejunostomy (after total gastrectomy) 114 . better functional outcome (some residual reservoir fx preserved) Total gastrectomy is the resection of choice for proximal tumours (fundus. low potassium. liver mets STAGING Tis T1 T2 T3 T4 Carcinoma in situ Tumour limited to mucosa and submucosa Tumour invades muscularis mucosa Tumour penetrates serosa Tumour invades adjacent structures N0 N1 N2 N3 No regional LN 1-6 regional LN involved 7-15 regional LN involved >15 regional LN involved CURATIVE TREATMENT SURGERY Principles of surgery: . Endoscopic ultrasound – gold standard for T staging and good for N staging 3. U/E/Cr – if vomiting. N & M staging 4. FBC – low Hb 6. alkalosis 7. but involves 2 anastomoses. CT abdo pelvis – good for T. CXR/ CT thorax– lung mets 2. b. gastrojejunostomy for obstruction External beam radiotherapy for pain. Early dumping syndrome (1/2-1hr after meal): due to increased osmotic load from stomach into small intestine flushing. non-bilious vomiting c. dizzy). 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 . Nutritional deficiency a. Iron deficiency – mixed picture i. Loss of intrinsic factor B12 deficiency ii. response rates. Afferent limb syndrome a. Retained antrum syndrome a. Inadequate reservoir function leads to poor digestion 4. Early satiety 2. Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid b. Mechanical obstruction of the afferent jejunal loop due to kinking. doxorubicin. Can be decreased by doing Roux-en-Y surgery (but may still occur) 7. and pancreatitis due to transmission of high pressures back to the biliopancreatic ductal system d. Treat by eating more carbohydrates.For palliation of symptoms such as pain. palpitations. total gastrectomy (20-40%). or adhesions postprandial epigastric pain with nausea. methotrexate. 5. followed by intraperitoneal 5-FU improved resection rates. 4. 3. sweat. dizziness. locally advanced disease with a significant increase in resectability (61% . Infection 3. 2. Anastomotic leak 4. Dumping syndromes a. Biliary/intestinal reflux into stomach a. diarrhoea. 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). Late dumping syndrome (1-3hr later): reactive hyperinsulinaemia alimentary hypoglycaemia (weak. Leads to symptoms of dyspepsia 6.For resectable disease: preoperative 5-FU. ascending cholangitis.Complications of gastrectomy: Early 1. Occurs in Bilroth II/Polya reconstruction b. Injury to surrounding structures eg. hypovolemia (due to rapid entry of water into small intestine) Treat by eating small frequent meals with low carbo and high protein/fat. pancreas Late 1. one of the main causes of duodenal stump blowout in the early postoperative period and is also an etiology for postoperative obstructive jaundice. obstruction 1. median survival PALLIATIVE THERAPY . Endoscopic laser ablation for obstruction Embolisation for bleeding Surgical options: subtotal gastrectomy (6-15% mortality). Not enough antrum removed acidity in residual stomach. 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% 115 79%) . anastomotic narrowing. Intestinal hurry a. bleeding. Bleeding 2. with formation of marginal ulcers on the jejunal side of the anastomosis 3.5-FU and cisplatin can be used to downstage unresectable. cisplatin. nausea. LOWER GIT & COLORECTAL DISEASES 1. palpitations. night sweats.Mixed with or coating stool . fatigue . easily bleeding. eye & skin manifestations . altered clots .History of constipation. stroke Hemorrhoids . indicates bleeding from upper GIT above ligament of Treitz (duodeno-jejunal junction) . chronic straining.Any mucous Malaena . postural giddiness.Inflammatory: ask about history of UC or Crohn’s.Ask for history as per UBGIT 2) Aetiological clues Exclude upper GIT cause . recent travel/contact history. pallor.Ischaemic: ask about atherosclerotic risk factors. blood coating stool.7. recent pregnancy Coagulopathy .Altered blood.Any malaena.Symptoms of anaemia (chronic occult bleed) .Previous history/family history of GIT or ovarian cancer Colitis .g.Inflammatory (UC & Crohn’s) . Mallory-Weiss tear. diarrhoea.bleeding to passing motion.Change in bowel habits. pain. varices. Ca stomach. eating seafood.Constitutional symptoms: LOW.Any history of bleeding disorders. syncope Symptoms of dehydration & shock: extreme thirst.Torrential or drops. low fibre diet.Infective (gastroenteritis. confusion.Infective: any fever/chills/rigors. tenesmus . e. LOA. fatigue.History of PUD. hard stools.Any mass noticed at anus .History of previous bleeding episodes Colorectal carcinoma . N/V. colorectal TB) . previous TB exposure or infection. bleeding DU HISTORY (if patient is stable) 1) Nature of bleeding Haematochezia .Usually torrential bleeding that stops spontaneously. polyps Colitis . BCG vaccination status . chest pain. petechiae 3) Complications Symptoms of anemia (may be only presentation!): SOB. liver. joint.Bright red (lower) or darker red (higher) . previous AMI. coffee grounds vomitus .Ischaemic Ileum: Meckel’s diverticulum . ↓ effort tolerance. gastritis. diverticulitis. ↓ urine output May have complication of AMI if old patient with history of IHD 116 . any clots? – Brisk upper GI bleed can present as haematochezia . pain .usually dark red blood Anorectal junction: hemorrhoids Anus: anal fissure Massive Upper GIT bleeding. APPROACH TO BLEEDING LOWER GIT 1) Colon 2) 3) 4) 5) Bleeding diverticulosis Angiodysplasia Colorectal carcinoma. risk factors for each Bleeding diverticulosis/angiodysplasia . hematemesis. On table scope to transilluminate bowel & identify bleeding source . diathermize. capillary refill. 2. .Scars? Any palpable masses DRE: .UECr: hydration status.signs of dehydration e. . partial/total colectomy as last resort 117 .Not for urgent setting. can cannulate all 3 main trunks & their branches . areas of inflammation & bleeding . but unable to localise the site & intervene o double balloon enteroscope: .For intermittent. any acute renal failure from shock.Therapeutic (not for CT): embolisation/sclerotherapy for angiodysplasia.any masses felt.confusion? Peripheries: .Stigmata of CLD? Abdomen: . supine & postural BP –stable? urine output (if catheter in-situ). electrolyte imbalance – replace . .Any fever? General inspection: .On table angiogram .Therapeutic: clip. .able to do therapeutic manoeuvres o Labelled RBC isotope scan under gamma camera . beware of causing bowel ischaemia (use foam medium) o Capsule Endoscopy: .pallor. 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. occult bleeds not detectable on mesenteric angiogram . 6.Diagnostic: identify cancer. 3.Any skin manifestations of inflammatory bowel disease? .ABG: may have metabolic acidosis in shock due to organ ischaemia – IV bicarb.More precise.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 . . dialysis if severe .for stable patients with suspected SI bleed & unable to swallow .any anal fissures or prolapsed hemorrhoids seen.LFT: exclude bleeding varices .PT/PTT: must correct coagulopathy before trying to stop bleeding – fresh frozen plasma .GXM 4 pints Identify source & stop bleeding o Arrange urgent colonoscopy (patient must be stabilised before procedure) .only for suspected proximal SI .HR.PHYSICAL EXAMINATION 1. dry tongue.takes 36hrs to read the results. 5.any fresh blood or malaena Offer proctoscopy to look for internal haemorrhoids ACUTE MANAGEMENT Resuscitation o Supplemental oxygen. 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 .Any supraclavicular lymph nodes? . 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 . diverticulosis. can take up to 24 hours! o Laparotomy with saline lavage if massive on going bleed. recurrent bleeding . shows ↓ perfusion of ischaemic bowel .Diagnostic: shows blush in active bleeding.g. angiodysplasia.Oversewing of bleeding vessel. Vitals: . 4. 90% of tumours are sporadic .8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and 1% with familial adenomatous polyposis (APC) . MSH6. but due to a different mechanism. PMS2) of which MSH2 and MLH1 are the most commonly involved in sporadic colorectal carcinomas . MLH1.1% 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. 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.Characterised by chromosomal instability . and without clearly identifiable morphologic correlates i. APC pathway (adenoma-carcinoma sequence) .25% in distal sigmoid and rectum Most are left-sided though there is an increasing incidence of right-sided tumours 118 .2. with the loss of APC. COLORECTAL CANCER EPIDEMIOLOGY COMMONEST CANCER IN SINGAPORE Prevalence in Singapore: 6% (Commonest cancer in M. no adenomas .e.Involved in 10-15% of sporadic cases . Defects in DNA mismatch repair .25% in transverse colon.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 . there is accumulation of mutations.Almost all tumours are adenocarcinomas . PMS1.25% in descending colon and proximal sigmoid. PATHOLOGY . number 2 cancer in F) Peak incidence at 60-70 years of age (increase with age) Increasing incidence through the years. Chinese more prevalent. more dysplastic adenoma carcinoma in-situ invasive cancer 2.Due to mutations in one of the five DNA repair genes (MSH2. . .25% in caecum and ascending colon.Accounts for 80% of 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 .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.Like the APC pathway. . Intramural –Transmural (along bowel wall. and polyps with tubulovillous or villous histology. Cronkhite-Canada have a small increased malignant potential HNPCC (AD) – more common than FAP.more common in the left colon 2. lungs. small bowel. ovary. preserved foods (nitrosamines) ii. Age >50 years 2.Small (<1cm) tubular polyps do not have increased risk Modifiable 5. desmoid tumor iii. or if the relative had CRC <55YO: risk > 1.MORPHOLOGY 1.Increased risk after 10 years of disease if the patient has pancolitis.7X. Transcoelomic – direct seeding: through entire thickness peritoneal cavity spread thru peritoneal fluid. high in refined sugar/fat potentially toxic oxidative byproducts by bac degradation iii. ii. Genetic predisposition (a) (b) (c) (d) Personal history of CRCs in the first 5 years after resection of a primary CRC. particularly if multiple (3-6X increased risk) . 3. high in red meat. Nodular SPREAD 1. Adenomatous polyps . minerals lack antioxidants .NSAIDs may be protective against CRC 119 . Ulcerative colitis .Alcohol. bladder 3. accounting for 8% of cancers. Seldom >2cm spread) or Intraluminal 2.Diet: i. low in fibre decrease stool bulk high fecal retention toxic products in contact with colonic mucosa for longer periods iv.7X FHx of colonic adenoma same significance as CRC?? Polyposis syndromes near 100% risk of cancer formation: i. Environmental factors . Turcot’s syndrome: glioblastoma multiforme other polyposis syndromes such as Peutz-Jegher’s. Ulcerated 4. 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. after 15-20 years if the patient has disease limited to the left colon 4. RISK FACTORS Non-modifiable (4) 1. Scirrhous / annular “apple-core” lesions (most common) . ureters.g. Metachronous CRC: occurs at a rate of 3-5%. Polypoid – more common in the right colon as there is more space to grow 3. smoking . brain 5. Gardner’s syndrome: multiple osteomas in mandible/skull/ long bones. 2 1st-degree relatives with CRC. FAP and its variants ii. i. Direct extension into surrounding tissues e. Haematogenous – to liver. bone. sebaceous cyst. Lymphatic 4.Increased risk if there is a personal history of large (>1cm) adenomatous polyps. Late stage > T4. low in vitamins ACE. amoeba. Intestinal obstruction (4): abdominal distension. 5. e. 2. absolute constipation 3. rebound) 2. may be painful. other related cancers: small bowel. 2. Abdo pain NO obstruction as stools more liquid and colon more spacious.HISTORY A) Presentation . peritonitis 7.Ulcerative colitis >10 years 120 . 7. FAP history / FHx Angiodysplasia (AVM. decrease ET.≥3 family members from the same side with HNPCC related cancer. therefore if transit time is less than 14 . Symptoms of infection: abscesses. ovarian. TCC of the upper urinary tract. bladder. guarding. Perforation : Symptoms of peritonism (rigid. HNPCC: Amsterdam II Criteria – [3. hookworm. difficile) . Iron deficiency / MCHC anemia – less Fe stores in the body cf folate & B12. Left sided (due to MASS EFFECT) 1. usually in or with stools – ddx: Diverticulitis 2. Haemorrhage 4.FAP is excluded 4. Positive Family history Infective e.g. decreased ET.Low fibre diet. SOB. hours the patient will have hematochezia.Obesity . GU organs (but usually no S/S as uterus wall very thick) 6. Colorectal carcinoma. Iron deficiency anaemia (6): fatigue. Change in bowel habits (Progressive constipation. 1] It takes about 14 hours for blood to be broken down within the intestinal lumen. LOA. . abdominal colick pain. TB. Endometrial carcinoma. Rectosigmoid CA: pain. orthopnoea morning headache Stool Changes B) Strong-risk factors . 2. palpitations. Symptoms of fistula.Symptomatic: Local: Right sided (OCCULT present late) 1.Asymptomatic: detection during screening (e. stomach.Personal or family history of breast. Ulcerative colitis) . and if greater one of whom is a 1st deg relative of the other 2 than 14 hours the patient will exhibit melena. alternating constipation and diarrhoea) Spurious diarrhoea (due to bacteria degradation of prox stools gassy explosive diarrhoea) Decrease in stool calibre PR bleed (Mixed in stool? / Separate from stool?) I/O Tenesmus = constant intense desire to defaecate. 6. common in old) . History of adenomatous polyps Family history alone = high-risk.1 or more 1st deg relative with CC at age <40 Antibiotic Associated Colitis (C. Involvement of surrounding structures: eg. defaecation nothing/ small amt of mucus and loose faeces (due to SOL in lumen/wall of rectum) Mucoid stools (suggests polypoid masses) Consitutional: LOW.Diagnosis: Colonoscopy Hemorrhoids . FAP / HNPCC = very high-risk Other risk factors . ovarian cancer per anus.2 or more 1st/2nd deg same side relative with CC at any age . faecuria/ pneumaturia/ recurrent UTI (colovesical fistula) 5. brain (Turcot syndrome) and sebaceous gland adenomas or keratoacanthomas (Muir-Torre syndrome). Right sided abdo mass 3.≥1 of the HNPCC related cancers must occur prior to age 50 .Bloody diarrhoea – ddx: IBD 1.g. Red meat . ureter hydroureter/hydronephrosis.g. postural giddiness Metastasis: bone pain/ #. malaise Complications: 1. One often(At least 2 of which must be 1st-degree relatives) stated rule of thumb is that melena only occurs if the HNPCC related: source of bleeding is above the ligament of Treitz. . LL weakness with loss of sensation. vomiting.Haematochezia = passage of FRESH blood . 3. jaundice SOB (pleural effusion most common). so Fe depleted first 2.Can also do Protein truncation test for APC gene mutation Massive upper GI 3. 4. bowel and urinary continence RHC discomfort (parenchymal involvement most common).2 successive generations . CP. Abdominal mass 2. Prevalent and lethal disease Precursor can be detected early (long asymptomatic period) Early detection makes a difference (can institute treatment) Safe. non-tender.Why CRC is suitable for screening 1.Colonoscopy normal Repeat in <10 year intervals PHYSICAL EXAM 1. Metastases . Complications. effective.2 categories i. contact bleeding b.Bone tenderness. 3.Cachexia . polypoid. . 2.SCREENING . feasible test available . hepatomegaly (irregular surface & nodular edge) .Pallor at nail beds and conjunctiva (anaemia) . CA prevention test = detect POLYPS and cancer superior to (ii) as POLYPECTOMY PROVEN TO PREVENT CANCER Colonoscopy is the only test. ii. CA detection test = detect cancer only Faecal immunochemical testing (more sensitive than FOBT) shown to be the best test. distance from anal verge >7cm (internal anal sphincter) 3.Cervical lymphadenopathy – Virchow’s node .Jaundice. consolidation or effusion. 4. AMS 121 . hard.Screening has been shown to improve survival! . irregular. Mass on DRE: (rectal mass) a. Therefore.>90% of CRC produce CEA.Ensure good bowel preparation . or 3rd space losses (intraluminal). bladder and kidney Imaging (f) Erect and supine AXR to look for intestinal obstruction (usually large bowel closed loop obstruction) and caecal distension. obvious peritoneal seeding.Look for ascites.INVESTIGATIONS Aims: Diagnose. may miss small lesions & distal lesions .Staging of regional and no-regional lymph node involvement . ALP (first to be raised) (d) PT/PTT.Local T staging & invasion into bladder. omental kinking. .Circumferential resection margin (CRM) refers to the fascia propria . breast.bulky T2) Neoadjuvant ChemoRT III.g. Usually. polypectomy.High risk tumors for recurrence: CRM < 2mm. together with iron studies (b) UECr: fluid and electrolyte abnormalities from vomiting (eg.Very good for T staging to determine depth of involvement: locally advanced CA (≥T3) requires neoadjuvant chemoRT .A tumour marker for colorectal carcinoma (glycoprotein synthesised by foetal intestinal tissue) .Follow-up after surgery with CEA levels to detect tumour recurrence . pregnancy. uterus . DIAGNOSIS Colonoscopy – first-line investigation(diagnostic & therapeutic) .Superior to CT for delineating fat planes in T staging especially in rectal cancer .Take biopsies of the lesion . lung. STAGING All CRCs (a) CT scan of the abdomen and pelvis for colon tumours . GXM for surgery (e) Carcinoembryonic antigen level (CEA) .k.Classically can see an apple core lesion with barium enema . pancreas. it is likely tumour has been totally removed. synchronous cancer in 3-5%. COMPLICATIONS Basic laboratory investigations: (a) FBC for low Hb.Not adequate for diagnostic purposes. air and contrast enema . lung.Metastases to the liver.Detects >/. hydroureter/ hydronephrosis. cervix.Enables therapeutic procedures e. near perforation (g) Erect CXR in perforated tumour to detect air under diaphragm (h) ECG :anaesthesia assessment 122 . . cholangitis and cancers of the stomach.a virtual colonoscopy . Raised levels: 70% CRC.Can also assess local lymph node status (f) MRI of the tumour .Next best to colonoscopy: needs IV contrast. bronchitis. ureter. prostate. T3/4 (+/. normal values 6wks post-op? .Need to insert a rigid sigmoidoscope 10-15cm to instil air & contrast II. thyroid) (d) CT brain if symptomatic Rectal tumors (below peritoneal reflection): (e) Endoscopic ultrasound / transrectal ultrasound (for rectal tumour) . stenting of obstructed colon CT colonography a. creatinine may be elevated (prerenal failure) and hence risk of contrast nephropathy (c) LFT for derangements caused by metastasis (occur late) – raised bilirubin.1cm tumors Double-contrast barium enema (barium + air) . do not do a sigmoidoscopy only. 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.Enables detection of synchronous lesions (primary tumors occurring less than 6 months apart) – synchronous polyps in 30%.Visualise lesion: size and location of lesion . Stage the cancer & Investigate for complications of cancer I. intestinal obstruction (b) CXR + CT scan of the chest (c) Bone scan if symptomatic (more for Ca breast.Causes of false positive raised CEA: smoking. in IO). 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 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 123 . no LN mets 75% 5yr surv B Invades past muscularis propria into extrarectal/ extracolic tissue. Bowel prep Modification of diet – 3 days low residue diet (reduce frequence and volume of stools – low fibre. right and left colic arteries and sigmoidal artery. 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 . 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.Prophylactic antibiotics (max at first incision) ampi/ genta/ metronidazole at induction of anesthesia Principles of surgery for colonic carcinomas .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. This artery is almost always present and its absence should be considered a variant. 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 . 124 . reduce food that increase bowel activity).TREATMENT SURGERY Aim: eradicate tumor with clear margins and LN drainage Pre-operative measures .e.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.Obstructed left sided carcinoma No difference shown for doing a staged procedure (i. CI obstruction? . NBM day before operation Bowel clearance with polyethylene glycol. from the ileocolic junction to the rectum. 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 125 . e.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. 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. ultra low AR if just above the anal sphincter Sphincter-sacrificing surgery abdominoperineal resection (entire anus & sphincter complex is dissected.Mesorectal excision Proximal rectal tumours – 5cm distal margin of mesorectal excision Mid-rectal tumours – wide mesorectal excision of at least 4cm distal to the tumour Lower rectum tumours – total mesorectal excision required (complete excision of the intact visceral mesorectal tissue to the level of the levators) 126 . creation of an end colostomy) .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 . usually taken to be at the level of the dentate line (which is 5cm above the anal verge) i. just anterior to the sacrum) . I/O cases: SB-LB anastomosis better than LB-LB anastomosis .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.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.Reconstruction Formation of a straight coloanal anastomosis in anterior resections is a/w poor function due to the lack of reservoir function 1. widening the diameter at that segment to form a small pouch).Because SB has more abundant and predictable blood supply . and the two limbs opened and stitched together to form a pouch. distal margin of the tumour must be >7cm from the anal verge Sphincter-sparing low anterior resection (below the peritoneal reflection). done when there is difficulty creating the colonic J-pouch . Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal colon is cut longitudinally but sewn transversely. the apex of the J being anastomosed to the anus) is associated with improved post-operative function 2. resection can provide survival benefit Surgery for recurrence . but not penetration through.. but may confer survival benefit in a select group of patients where metastatic tumour burden is restricted to one side? and liver involvement is not extensive Surgery for metastases .Resection of asymptomatic primary is controversial. 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 chemotherapy can be given to downstage the metastases if they are initially resectable . reduce local recurrence Good evidence for ≥T3 tumours. multivisceral resection of organs involved (pelvic exenteration) is associated with improved local control and overall survival compared with standard resection. perforation. though high morbidity of 25-50% is associated Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease . or pericolic fat. ability to resect previously unresectable tumour.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.Surgical treatment according to stage Stage of disease Treatment T1 Involvement of submucosa.Neoadjuvant chemoradiotherapy for rectal tumours Neoadjuvant RT with 5-fluorouracil can downstage tumour significantly ability to preserve sphincter.Resection of primary for palliation of symptoms such as bleeding.Extended resections For locally advanced. obstruction or pain . but in the rare setting that there is an isolated lung secondary. but no penetration through muscularis propria Local excision (AR or APR) T2 Invasion into. ureters Early (<30 days) Wound infection Bleeding Abscess Anastomosis breakdown/leak Early stoma complications Late (>30 days) faecal peritonitis Diarrhoea Impotence (damage of pelvic nerves) Adhesions (I/O) Anastomotic stricture Late stoma complications Surgery for palliation . adherent tumours (T4).Loco-regional recurrence.Isolated liver metastases (synchronous or metachronous) may be resected with survival benefit. CRM<2mm: benefits > risk of RT (esp.Lung metastases usually indicate systemic dissemination of disease. 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) . can confer survival benefit 127 . 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 (<24h) Damage to other organs e.g. muscularis propria a) Local excision + adjuvant Chemo/RT OR b) radical resection T3 Penetration through muscularis propria into subserosa (if present). if detected early with adequate resection. measure CEA at each visit .Colon cancer: 5-FU + folinic acid (leucovorin) for 6 months.Follow-up visits 3-monthly for the first 2 years.Post-operative adjuvant therapy in stage II or III rectal cancer CHEMOTHERAPY Adjuvant therapy .RADIOTHERAPY .Role as neoadjuvant therapy in rectal cancer to downstage tumour (in T3/T4) .; not recommended in Duke’s B or less .5-FU in combination with folinic acid is first-line therapy .CXR and liver ultrasound to detect metastases (recommended frequency not known) 128 .Rectal cancer: post-operative adjuvant therapy in combination with radiotherapy in stage II or III disease (5-FU based regimen used) Palliative therapy . or 5-FU + levamisole for 12 months in Duke’s C cancer (node positive).Alternatives for first-line therapy: Raltitrexed when 5-FU is not tolerated.Yearly colonoscopy . capecitabine or UFT (uracil combined with tegafur) plus folinic acid FOLLOW UP . then 6-monthly for the next three years. and subsequently yearly. Resultant tumour is often poorly differentiated .Screening – yearly colonoscopy starting after 10 years of UC 129 .Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure) . and renal pelvis/ureter cancers o Offer a THBSO with total colectomy if CRC detected . treated with CT. Familial adenomatous polyposis (FAP) - 1 in 10. 90% will have colorectal CA by 45yrs .Surveillance Yearly colonoscopy for at-risk family members from 12y onwards 5 yearly OGD for surveillance of Periampullary Cancer. gastric.Diagnosis is based on the Amsterdam criteria – see above . and also ovarian.ASSOCIATED CONDITIONS I. autosomal dominant inheritance Germline mutation of APC gene on 5q21 >100 adenomatous polyps all over colon.Tumours tend to arise from polyps which are commonly flat.Surveillance – 1-3yrly colonoscopy starting at 20 years old III. polyps take 5-6 yrs to turn malignant 50% patients will have polyps by 16yrs. duodenum . with villous histology . 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. RT or HT. most commonly endometrial cancer. hepatobiliary.Other sites for polyps: stomach. Dental abnormalities Eye: Congenital hypertrophy of retinal pigment epithelium (CHRPE) Other tumours: Desmoid tumours (intra-abdominal tumours. Hereditary Non-Polyposis Colorectal CA (HNPCC) .000.Extraintestinal manifestations Skin: Epidermoid cysts. Ulcerative colitis .Lynch syndrome type II is associated with increased risk of cancer elsewhere. Lipoma Bone: Osteoma of skull/ mandible.Divided into Lynch syndrome I or Lynch syndrome II based on clinical features .Diagnosis Colonoscopy showing >100 polyps Genetic testing . small bowel.) Thyroid cancer (follicular or papillary type) Periampullary CA . g.3.Intra-operatively.Decompression – relief of bowel obstruction causing proximal dilatation .To rest an inflamed distal portion e. as ileal contents are corrosive.asp Late .When patient or surgeon factors are against reversal of stoma (relative) . add anti-motility agent to thicken output (loperamide +/.Skin excoriation .com/1007-9327/7/741. 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. faeces) Nursing intervention .Stoma nurse to perform counselling & discuss best site for stoma placement Stoma siting .Sited for easy accessibilty i.Away from the surgical incision risk of wound contamination and infection .Prolapse of bowel refashion/refresh . colostomies in the epigastric/hypochondriac [transverse colostomy] or left side) .wjgnet. draining/ exteriorization (urine. enema / secondary to adhesion – more in ileostomy) .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) .Bleeding . (vs protrudes 3cm ‘spout’.Leakage skin erosion.Psychological problems 130 .Fistulae .Away from old surgical scars risk of hernia . check by intubating with a glass tube into the stoma to look at colour of mucosa) refashion stoma .Defunctioning – to reduce effects of anastomotic leak Esp.codeine) http://www.Over the rectus sheath decreases the risk of prolapse.Stenosis (unable to pass finger through) refashion .Stoma diarrhoea (high output) correct water & electrolyte imbalance (hypoK).Obstruction (fecal impaction explore with finger. after low anterior resection. defunctioning/ diversion.Parastomal hernia (+ve cough impulse) refashion . For output: decompression/ lavage. not under a large fold of abdominal fat . parastomal infection resite . 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).When no distal bowel remaining (absolute) After abdomino-perineal resection for Low rectal/ anal tumor After Panproctocolectomy without ileal pouch anal anastomosis Temporary . . avoid tension over the stoma to marked site causes vascularity of the stoma stoma necrosis Types of stomas Permanent (end colostomy) . For input: feeding (Percutaneous endoscopic gastrostomy) 2.Retraction refashion . acute Crohn’s Colostomy (vs ileostomy) ?usually flushed with skin. STOMAS Stoma: opening of a luminal organ into the external environment Indications 1.e. Because the rectum has not been removed. the distal. in incontinence). The remaining descending and sigmoid colon is mobilised and the cut end brought to the abdominal surface at an opening about 2 cm across. less bulky. and moist. which leaves part of the sigmoid colon and rectum left in place. End ileostomy When the entire colon. and it produces only mucus. rectum. a very low rectal cancer will require resection of the rectum and anus (abdominoperineal excision of rectum). hereditary non-polyposis colorectal cancer). The opening of the afferent limb leads to the functioning part of the colon. In the first. a second operation is needed to reconnect the two ends.End colostomy This procedure is most commonly performed to manage carcinoma of the lower rectum or anus. The opening of the efferent limb leads into the non-functioning part of the colon. two outcomes are possible. This is usually sited in the left iliac fossa. usually in the right iliac fossa. and a portion of the lower colon have not been removed. A loop colostomy may be temporary or permanent. The ileum is resected just short of its junction with the caecum. One stoma is the exit of the functioning part of the colon through which stool and gas pass. defunctioning of a distal anastomosis (after resection and primary anastomosis either as an emergency or after radiotherapy). After a panproctocolectomy the ileostomy is permanent. in cancer) or anus (for example. and 6-7 cm of the small bowel is brought through the abdominal wall. Abdominoperineal excision of the rectum If the anus. as in Hartmann's procedure. loop colostomies are more often fashioned from the sigmoid colon to defunction the rectum (for example. diverticular disease. Currently. Loop colostomy A loop colostomy was traditionally created to defunction an inflamed sigmoid in diverticular disease or to defunction a distal anastomosis. through which stool and gas pass out. Temporary end ileostomy is often used after an emergency subtotal colectomy. the urge to have a bowel movement may occur. or defunctioning of the anus (in incontinence or perineal involvement in Crohn's disease). non-functioning part of the colon and the rectum can be stapled or sewn closed and left inside the abdomen as a rectal stump.It has largely been replaced by loop ileostomy. for acute ulcerative colitis. 131 . The stoma site was usually high on the abdomen above the waistline because the transverse colon was commonly used. A loop of colon is brought to the surface of the body and may be supported on a rod. The second stoma is usually small. acute ischaemic bowel. flat. if present. and anus must be removed (panproctocolectomy) an end ileostomy must be employed. rectum. The proximal colon is then taken out as an end colostomy. Mucus and some old stool. Loop ileostomy This type of stoma allows for defunctioning of an obstructed colon (in cancer). This occurs most commonly in severe ulcerative colitis but also in familial polyposis and some cases of colorectal cancer (for example. and rare cases of faecal incontinence that do not respond to medical mx. 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. A loop ileostomy has two openings. For example. and easier to surgically close. or neoplastic obstruction of the sigmoid . If the colostomy is temporary. The second stoma opens into the non-functioning portion of the colon and rectum and is called a mucous fistula. pink-red in colour. will be passed. Hartmann's procedure Less commonly. Loop ileostomy has largely replaced loop colostomy because it is easier to site. two separate stomas may be created. and most are temporary. The bowel wall is partially cut to produce two openings—of an afferent limb and an efferent limb. which is removed after about five days. such as stoma prolapse. Formation of an ileal conduit is the most common procedure. are the most common complications and are usually managed by the stoma nurse. and resistant urinary incontinence. Most structural problems. retraction. Some bags have a second opening at the bottom to allow emptying. Finally. and parastomal hernia formation can be managed conservatively with modified bags and specialised belts. Stomal oedema is normal for several days after surgery. On examination this will look almost identical to a loop ileostomy. Patients should be alert to any change in colour of their stoma. which constitutes isolation of a segment of ileum. however. Two piece systems have a separate base (a flange) that sticks to the skin. the surgeon might create a double barrel stoma. Urine drains almost constantly from the kidneys through the ureters and ileal conduit into a bag. Urostomy This is a general term for the surgical diversion of the urinary tract. One end of the ileum is closed and the two ureters are anastomosed to it. Closed bags are used when the faeces are well formed and are usually only changed once or twice a day. The formation of this stoma is similar to a loop ileostomy. These are most useful in the period immediately after operation and in patients who have had ileostomy. Patients with stoma admitted to hospital with increased or decreased output should be appropriately managed to exclude any abdominal emergency. 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. Most patients with a stoma will use an opaque bag.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. Complications Functional problems. but this may depend on the underlying condition. who need to drain their bag regularly. 132 . and the bag attaches to this. this is an end ileostomy (small bowel) and a mucous fistula (the remaining colon) sited beside each other. In essence. and attention to fluid balance. the open end of ileum is brought out onto the skin as an everted spout and will look similar to an end ileostomy. Double barrel stoma When the caecum is removed. but the efferent limb is short and blind ended. Single piece systems stick straight on to the patient's skin. 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. neuropathic bladder. with particular emphasis on careful history taking to establish the normal bowel pattern. Only about 10% of patients with these complications will require further surgery. closer inspection will show two separate stomas. This enables the bag to be changed wo removing the flange. The main reasons for a urostomy are cancer of the bladder. Stoma bags Stoma bags are of two main types. The bladder is usually removed. but if the mucosa becomes dusky or necrotic the surgeon should be contacted promptly. On inspection at the bedside this type of stoma is indistiguishable from a loop ileostomy. such as skin excoriation and stoma noises. urostomy Two (adjacent)—efferent limb may be difficult to see Loop colostomy. loop ileostomy. double barrel stoma. rarely bowel stoma and urostomy Fully formed stool Colostomy Semisolid or liquid stool Most likely ileostomy. end 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 133 . less commonly a urostomy One End colostomy. end-loop ileostomy Two (separate stomas) Most likely end colostomy with a mucous fistula.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. Note: current controversy of management for stage 3: hartmann’s vs segmental resection with primary anastomosis with or without defunctioning ileostomy In the absence of complications and systemic signs and symptoms.Site o majority are in the sigmoid colon. IV fluids .Investigation: WBC 2.ABx. colo-uterine. 14% in immunocompetent patients). torrential e. right sided are thought to be genetic. 134 . Perforation b. NBM.Irregular bowel habit .Risk factors – dietary fibre & genetics . 60% left.Elective 1 stage surgery Stage 3 Purulent peritonitis (fm perf diverticulitis) . 2%). DIVERTICULAR DISEASE PATHOLOGY – acquired herniation of colonic mucosa through muscular wall.Associated with weakening of collagen structure with age PRESENTATIONS . and increased postoperative mortality (39% vs. Bowel obstruction – 2o to stricture or adherence to a diverticular mass d. Chronic diverticulitis . LGIT haemorrhage – ulcerated vessel @ neck of diverticulum.Symptoms: LLQ pain.4. more in obese M) . 80% left o not in rectum as taeni coli has fused PATHOGENESIS 1. up to 25% in >70YO (2-5% are <40YO. Others – colo-cutaneous. Acute diverticulitis . operation or drainage of pericolic abscess.Increases with age.Usually at point of entry of terminal arterial branches where serosa is weakest . but may also predict the risk of failure of medical therapy and of secondary complications after initial conservative treatment. colo-enteric. patients with mild abdominal tenderness may be treated conservatively. 10-30% are symptomatic .Passage of mucus PR 3. o Asians: 40% right.Diverticulitis – inflammation of diverticula EPIDEMIOLOGY . May present with urinary symptoms.2 stage operation – Hartmann’s procedure (partial colectomy + diverting end colostomy & rectal stump formation) + secondary re-anastomosis 3 months later Stage 4 Faecal peritonitis (fm ruptured diverticula) Severity staging by CT scanning may allow not only the selection of patients most likely to respond to conservative treatment. and presence of complications 1. This has been shown to be successful in 70% to 100% of patients.Hinchey classification of complicated acute diverticulitis – need for surgery is reflected by degree of infective complications Stage 1 Pericolonic / Mesenteric abscess (small) .Signs: Low grade fever. flatulence/bloating . N/V. with a covering of colonic serosa TERMS .Recurrent LIF pain . Tender palpable mass . There is an increased rate of free perforation (43% vs. the severity of the inflammatory process.depends on location of the affected diverticulum. Fistula formation (commonest: colovesical fistula) – 2o to pericolic abscess discharging. colo-vaginal Elderly and patients on steroids may have no sign even in severe diverticulitis. Complicated diverticulitis (dangerous) a. Paracolic abscess / inflammatory mass – 2o to localized perforation c.Diverticulosis coli – presence of acquired pseudodiverticula . 33%). STAGING . Caucasians: 20% right.Consider 1 stage surgery after acute episode – resection of affected bowel segment with primary anastomosis Stage 2 Pelvic / retroperitoneal abscess (large) .Diverticular disease – symptomatic diverticulosis coli . increased need for surgery (58% vs.Associated with lack of dietary fibre 2. Increased intraluminal pressure . Conservative treatment typically includes dietary modification and oral or IV antibiotics.Majority are asymptomatic.Percutaneous drainage . Constipation / diarrhoea. Degenerative changes in colonic wall . ectopic pregnancy Retroperitoneal perf (leg pain): thigh abscess. cancer. ↑Hb (dehydration) U/E/Cr – dehydration & ARF CXR – free gas under diaphragm - May follow acute diverticulitis LIF tenderness & guarding LIF mass – may be detected on DRE Swinging fever - FBC – ↑ TW CT – differentiate between inflammatory phlegmon (spreading diffuse inflammation with pus/purulent exudates) & pericolic abscess - After acute phase settled (4-6 wks) . - Acute onset abdominal pain – severe & continuous Abdominal guarding & rigidity Vomiting Tachycardia Pyrexia - FBC – ↑ TW. investigations + colonoscopy & angiography (both diagnostic AND therapeutic value) ± on-table enteroscopy if required ± tagged RBC scan (not as sensitive compared to angiogram): RBC tagged with radioisotope - Anorectal bleed Angiodysplasia Ischaemic colitis Colorectal CA Colitis (inflm or infx) UBGIT Coagulopathy - Resuscitate & correct coagulopathy Colonoscopic management: adrenaline injection. Hard to differentiate – therefore.Colonoscopy – confirm dx & exclude CA colon and/ or . stones. haematuria. torsion of cyst/ ovary. ishaemic bowel. heat coagulation Radiologic embolisation of site of bleeding with temp foam material via angiography Surgery – segmental resection. CA bladder. IBD. ureteric colic. due to attachment of enteric loop against area of acute diverticulitis Surgery if does not resolve PHx of recurrent acute diverticulitis or irregular bowel habit Colicky abdominal pain. ALWAYS exclude CA colon e. Ca colon) - GI: colitis. torsion of testis/ ovary. acute pancreatitis. strictures Colonoscopy – exclude differentials (i. pancreatitis.Severe / recurrent attacks . faecaluria - - UFEME & urine c/s: confirm UTI and organisms (polymicrobial as opposed to sterile pyuria in ‘UTI from adj diverticulitis’) Cystoscopy – cystitis KUB – air in bladder Barium enema – diverticular bowel segment Sigmoidoscopy – usually normal 135 - Other causes of fistula – CA colon. Ca colorectal Right colon/redundant (extra bend in descending colon) sigmoid colon: appendicitis Transverse colon: PUD. complication.e. infx. GE. IV fluid . endoclips on bleeding vessel. Drip & suck Surgery – Resection ± primary anastomosis Usually in the elderly who have higher density of sigmoid diverticula Massive bleed (altered blood ± clots. tenderness & palpable mass Fever Malaise Small bowel I/O - Large bowel I/O - Hemorrhage - - Usually temporary. Crohn’s disease. oral for small bowels. inflm. relieved by defecation LIF tenderness Palpable LIF mass - Nausea Urinary symptoms - Pyrexia Increase pulse rate - Investigations - - Differentials FBC – leucocytosis.Presentation Acute Diverticulitis Clinical features - LIF pain – colicky. cyst/ Angiomyolipoma. constipation & abdo distension - AXR – dilated bowels prox to stenosis Water soluble contrast enema - CA colon - NBM. pelvic abscess. enema for large bowels Features – diverticula elsewhere. hydronephrosis Lower quad pain in F (Obgyn): PID. ruptured AA/ hepatoma. IBD. endometriosis.Resuscitate . Management Conservative . extravasated contrast Cannot tell if inflm is due to diverticula Better than intraluminal examinations as bulk of inflm is extraluminal Laparoscopy – if diagnosis is in doubt Can dev anywhere in GIT.NBM.Bed rest .Barium enema is inferior to colonoscopy in terms of image quality and is usually only performed if the patient has strictures or an excessively tortuous sigmoid colon where colonoscopy is difficult or dangerous Role of surgery: see below Barium enema – CI as barium may leak out into abdo cavity Avoid colonoscopy as risk of perforation is high (by air insufflations or instruments) + worsens diverticulitis Rigid sigmoidoscopy – oedematous mucosa & rigidity of rectosigmoid jx Flexible sigmoidoscopy – diverticular orifices Barium enema – ‘saw-tooth’ appearance. See Ddx to RIF/LIF pain - - - - Chronic Diverticulitis Not a common clinical entity - Generalised peritonitis / perforation - Pericolic abscess - Persistent inflammatory mass - Recurrent LIF pain Irregular bowel habits – constipation & bouts of diarrhoea Passage of mucus PR - - Ruled out cancer. cholecystitis Inflm adj to UT: UTI. air-fluid level w/in an abscess CT scan w triple contrast (choice) Severity.Broad-spectrum antibiotics – augmentin or metronidazole or ciprofloxacin . progressing to constant. leg emphysema #. IBS.Possible CA colon Stage: Segmental resection of affected colon + anastomosis - LIF pain.g. histology after bowel resection Ischaemic colitis Radiation colitis Colonic endometriosis Conservative – see above Other causes of peritonitis – perforated PUD/ appendicitis/ bowel/ ectopic pregnancy. clinical staging Water soluble contrast: IV for vascular lesions. not melena) usually right-sided Colicky pain as blood is irritative & causes spasm - Invx as for LGIT bleed – resus. total colectomy if unable to localise bleed - - Vesicocolic fistula CT/ US guided percutaneous aspiration Surgery – evacuation of pus ± resection of affected segment PHx of chronic diverticulitis & UTI Hx of dysuria. concentric bowel thickening) but only suggest diverticulitis.Antispasmodics - CA colon – may coexist.Surgical Peritoneal toilet Hartmann’s procedure (Resection of affected segment + End sigmoid colostomy) Surgical Indications: . Msk pain etc. pyonephrosis Mgmt as for acute abdomen . free gas. confirm colitis (mesenteric fat infiltration. post-irradiation necrosis - Surgery – Resection of affected colon + anastomosis + closure of bladder fistula opening . mesenteric ischaemia/ adenitis. freq. diverticula. pneumaturia. ↑ ESR Erect CXR to rule out perforation AXR – ileus. . inflammatory bowel disease. the progression of diverticular disease in the remaining colon is approximately 15%.Advise high fibre diet (prevents recurrence in >70%) & to drink lots of fluid. . Emergency bleed (controversial clamping both side & look for active bleed into segment segmental resection) a. 136 . Stricture 2. and ischemic colitis. The use of the rectum as the distal margin decreases the rate of recurrence. meaning the degree of proximal resection and level of distal anastomosis. Sepsis from abscess or faecal peritonitis 2. recurrent episodes. stricture & subacute IO (offer surgery) Indications for emergency operation 1. Immunocompromised patients (e. Recurrent attacks – occurs in 30% of patients after 1st episode. especially irritable bowel syndrome.70% of patients will not have recurrence after first attack (after first attack. Diverticulitis not responding to conservative management 4.Outcomes: well or deteriorate requiring surgery. weight reduction and exercise Recurrent diverticulitis after surgical treatment . renal transplant) – may not show S/S of acute attack or complications Advice to patients: .incidence ranging from 1% to 10%. . Haemodynamically unstable with failure of embolization b. Obstruction with pending perforation – need to rule out cancer at the same time 5.Important factors to be considered in terms of surgery are the adequacy of resection. Previous bleed Indications for elective operation 1. out of whom 1/3 will have 3 rd) . Perforation 3. Young patientss <40YO – high recurrence rates 5.g. Need > 4 units of PCT c. Fistula 3. 1/3 will have second.In general.Care also must be taken to exclude other components of differential diagnosis. a/w higher mortality & complication rates 4. pseudopolyps interspersed with areas of shallow ulceration Microscopic: only mucosal & submucosal involvement. colorectal TB 3) Ischaemic colitis 4) Bleeding diverticulosis 5) Colorectal carcinoma 137 . Campylobacter. diarrhea. fatty liver. bloody stools with mucous & pus Crohn’s fistula: colovesical fistula or coloovarian fistula: faeces in urine/ pneumaturia. Extraintestinal: clubbing. arthritis/sacroilitis/AS. non-caseating granulomas (pathognomonic.extra-intestinal manifestations Acute severe: fever. tender/distended abdomen. bloating. 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. faeces per vaginal/ PID Non-specific systemic: LOW. toxic megacolon. Shigella. C. UK. LOA. moderate. symptoms of anemia. with second onset in the 5th & 6th decades of life Equal gender predominance Higher prevalence amongst Ashkenazi Jews & in cooler climates e.Muscularis propria & serosa may be affected in fulminant disease Risk of carcinoma Slight increased risk of colorectal Ca. sinuses. pyoderma gangrenosum. ULCERATIVE COLITIS) Bowel involvement Location Crohn’s Ulcerative colitis Can affect entire GIT anywhere from mouth to anus. INFLAMMATORY BOWEL DISEASE (CROHN’S DISEASE. 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. mesenteric thickening & deep linear ulcers Microscopic: transmural involvement. coli. Nutritional deficits.g. loss of vascular markings. N/V. conjunctivitis/episcleritis/iritis. Salmonella. Scandinavia. Differential diagnoses 1) Gastroenteritis: exclude with stool microscopy & culture + C.5. severe. crypt abscesses . 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. fever. CRC These complications absent. erythema nodosum. tachycardia. Germany. difficile Parasitic: E. fistulae. but only present in 2/3) Macroscopic: granular appearance of mucosa . toxic dilatation. fulminant) Epidemiology Bimodal distribution: affects young in the 2nd & 3rd decades of life. venous thrombosis. malnutrition (SB involve). ulcers. with skip lesions Longitudinal mucosal continuity Complications Strictures. Massive PR bleed. histolytica Viral: rotavirus 2) Other infective causes: diverticulitis. oral ulcers. fatigue.diff toxin Bacterial: E. northern USA Genetic association History GIT: abdominal pain. SB obstruction. distension. CRC ++ Histopathology Macroscopic: bowel is thick-walled & nodular (cobblestone appearance) with creeping fat. chronic malnutrition Specific extra-intestinal manifestations Physical examination: usually normal +/. Remicade (infliximab) = TNF blocker . MTX. mesalazine) induce & maintain remission of disease: oral. proctectomy in severe disease 138 .Fistula: resect diseased bowel & repair involved organ Large bowel: . cf 21% on placebo . but not for long term use 1st line: 5-ASA or 5-aminosalicylic acid (sulfasalazine. TPN (may also aid closure of fistulae) o Pharmacological Corticosteroids for acute exacerbation of disease.Segmental colectomy only in selected cases as high recurrence rate Perianal 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.Short segment disease: stricturoplasty .Pretreatment: rule out TB. 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. Tacrolimus & cyclosporine when 1st line agents ineffective o Cyclosporin and Tacrolimus are nephrotoxic avoid LT Biologics = created by biologic processes.Total colectomy + ileorectal anastamosis (if rectum spared) or proctocolectomy + end ileostomy (if rectum affected) . fistulotomy. rather than being chemically synthesized. anal stricture Investigations: supportive (see UC) & diagnostic Diagnostic (mainly at terminal ileum) Contrast radiographic studies: assess location & extent of disease.Setons.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.Ind: for steroid resistant . hepatitis first (as tx can cause reactivation) .Require close surveillance for SE (blood disorders.CROHN’S DISEASE P/E: RIF mass. 6-MP.Long segment disease: long stricturoplasty or resection . lymphoma & solid tissue cancers. hepatotoxicity. 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) . . azathioprine. infections. perianal enlarged skin tags/ fistula/ abscesses. drug-induced lupus. rectal suppository or enema (up to splenic flexure) 2nd line: immunosuppressive agents e.g.g. Involvement of the muscularis propria in the most severe cases can lead to damage to the nerve plexus. 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). Serious complications of medical therapy 3. Tx: stenting. Perforation 5. If no improve after 2/52 mod. If improve in 5/7 PO pred + 5-ASA. o Severe: IV Hydrocort400mg/d + rectal steroid. resulting in colonic dysmotility. Tx: topical and/or oral corticosteroids Skin o Pyoderma gangrenosum: deep ulceration with violaceous border that overhangs ulcer bed. erythematous nodules tt do not ulcerate/ suppurate. Severe bleeding 4. usually affecting LL o Erythema nodosum: poorly defined. ERCP. episcleritis. tender. 50% if perforation o Pouchitis: Tx with Abx (metronidazole + ciproflox X 2/52) + immunosupp. MRCP. 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. anterior uvetitis. 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%. and eventual infarction and gangrene 6. perf. If CRP >45/ >6 stools per day ciclosporin/infliximab/Sx.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. toxic megacolon. o Mod: PO pred (40mg/d x1/52 30mg/d x 1/52 20mg/d x 4/52) + 5-ASA + steroid enema BD. Surgical (25% eventually require surgery) o Indications : 1. 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. will improve slowly following colectomy Investigations Supportive (looking for complications & assessing severity of disease) Blood tests o FBC: anemia. liver biopsy. Disease refractory to medical therapy with severe & extensive colitis (most common) 2. dilation. Toxic megacolon (colon > 6cm): most common cause of death . Avoid necessity for long term stoma. leukocytosis & thrombocytosis indicate more severe disease o UECr: hypokalemia & dehydration in prolonged diarrhoea o LFT: hypoalbuminemia due to poor nutritional intake o CRP. Malignancy o Procedure (laparoscopic or open) Acute setting (uncontrolled bleeding. transplant o Hepatic failure over 5-10 years independent of course of colitis o ↑ risk of cholangiocarcinoma & ↑↑↑ risk of colorectal carcinoma Eye o Iritis. ESR: markers of severity o Autoantibody assay: p-ANCA ↑ in UC. 139 . 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. If no improve after 2/52 severe. usu on the shin o Tx: corticosteroids. If distal dz: Pred retention enema/ steroid foam. 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 140 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 141 2. ANAL FISTULA Anal fistulae are abnormal communications, hollow tracts lined with granulation tissue connecting the primary opening inside the anal canal to a secondary opening in the perineal skin. They are usually associated with anorectal abscesses (obstruction of ducts infection). Conditions associated with multiple anal fistulas: 1. Crohn’s disease 2. TB 3. Actinomycosis 4. Hydra-adenitis suppurativa GOODSALL’S LAW Posterior ½: (All fistula tracts with external openings within 3 cm of the anal verge and posterior to a line drawn through the ischial spines) Curvilinear Internal opening in posterior midline (at level of dentate line) Anterior ½: Straight tracts Tracts closer to anal verge = simpler, shorter Tracts further away = transphincteric, long, high tracts INVESTIGATIONS Endoanal U/S (H2O2 aided for hyperechoic effect) – to view course of fistula tract MRI – able to visualise entire pelvis, beyond the sphincter complex CT/fistulography (in emergency situation) – for complex fistulas / unusual anatomy 142 CRYPTOGLANDULAR THEORY OF PARKS / PARKS CLASSIFICATION Type Diagram 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 143 4. ANAL FISSURES An anal fissure is a painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. Most will heal because of good blood supply (within 1 day / 2 days) If they don’t heal: usu due to spasm of internal sphincter muscle Features of a chronic anal fissure: 1. Boat shaped 2. Punched out 3. Exposing internal sphincter 4. Sentinel skin tag 5. Hypertrophic anal papilla MANAGEMENT Definitive for chronic anal fissure Internal anal sphincterotomy (but do not cut through muscle – irreversible) Medical sphincterotomy (reversible): GTN paste, botulinum toxoid injections 144 stomach. haemochromatosis. and biliary drainage. amyloidosis. EBV. 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. hydatid cyst. the upper left segment of liver) Segment IV can be further divided into IVa and IVb. wilson’s disease Tumour: see below 3. malaria) Metabolic: fatty liver. parasite( amoebiasis. HIV). breast.e. ANATOMY OF THE LIVER The liver is divided into two lobes. CMV.9. TR. Budd-Chiari syndrome Infective: viral (hepatitis viruses. lung Hepatocellular carcinoma (or hepatoblastoma in children) Cholangiocarcinoma (only 10% intrahepatic) – presents like HCC except no background of cirrhosis 145 . TB). pancreas. 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. while facing the patient. urogenital tract. CAUSES OF HEPATOMEGALY Vascular: RHF. 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. 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. starting from the upper right corner (i. middle and left) Segment I is the caudate lobe Segments II to VIII are named clockwise. bacteria (pygenic abscess. LIVER DISEASES 1. outflow. Local signs & symptoms 1. AFP usually normal. with a small proportion of intrahepatic cholangiocarcinoma (6%) AETIOLOGY AND RISK FACTORS 1. Rx with transarterial embolization (TAE). Early satiety/ vomiting (likely 2o to compression) 3.antitrypsin deficiency. Hepatitis B infection (high HBV DNA load. haematemesis & melena 2o to bleeding varices (COJ & gastric) . ataxia Stage 3 Confusion. anabolic steroids. paranoia. Hepatitis C infection 3. Cholestatic (conjugated): invasion/ compression of intrahepatic ducts or extrahepatic compression by metastatic LN b. 40% in Asians PATHOLOGY Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular damage with high cellular regeneration. malaise 6. Pyrexia (central tumour necrosis) 4. 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. good prognosis . HBeAg positivity increase the risk) – 100X normal population 2. jaundice. Budd-Chiari syndrome: occlusion of hepatic. acalculia. LL oedema. pallor with shock [ddx: ruptured AAA] 50% mortality. asterixis. α-1. Tumour rupture (<3%) . which leads to rates of genetic mutation in the cells and accumulation of these mutations leading to carcinoma formation . more common in females. Hepatic (unconjugated): a/w pre-existing cirrhosis or acute flair of chronic hepatitis 3. pruritis. DPL +ve for blood 4. Liver decompensation (on top of underlying cirrhosis) . Asymptomatic . HEPATOCELLULAR CARCINOMA EPIDEMIOLOGY - Annual incidence in Singapore is 18/100. Babinski. bones.Worsening liver function (encephalopathy.4. 1. haemochromatosis. Constitutional: LOW. schistosomiasis Non-cirrhotic HCC – 5% in west. overall 4th most common cancer Men: female = 3:1 Peak age of onset: 30-40 years old 1o liver cancers are mainly HCCs (85%).2o to a. intrahepatic or portal vein causing portal HTN & congestive hepatopathy 7. coagulopathy.Two histological subtypes: Nonfibrolamellar – associated with HBV and cirrhosis Fibrolamellar – associated with younger patients. infection 2.000 in males.Incidentally found on imaging of the abdomen 2.Metastasises to lymph nodes.Others: Aflatoxin ingestion.During screening (ultrasound) for chronic hepatitis B carrier .Worsening portal hypertension: Ascites.000 in females 3rd most cancer among males.US +ve for peritoneal fluid.Investigations for liver cirrhosis (esp with rising AFP levels) . Cirrhosis (of which cirrhosis resulting from hep B. Hepatomegaly 5. PBC. LOA. oedema) suspect HCC when there is decompensation of liver cirrhosis . Upper abdominal pain . no association with hep B or cirrhosis. agitation. personality change.6/100. clonus Stage 4 Coma 146 . hep C and haemochromatosis are associated with the highest risk): 20-30years following initial insult . reports of peritoneal seeding in survivors .Severe abdominal pain (peritonism). hemorrhage internally capsular distension or externally b. Jaundice (5-10%) a.Hepatorenal syndrome in late stages of liver failure Stages of Hepatic Encephalopathy Stage 1 Sleep-wake cycle inversion Stage 2 Lethargy. necrosis c. and 4. 70% resectable. teratoma. IVC and portal vein are dark (b) Portal venous phase (most CT scans taken at this phase) – contrast enters portal system so portal vein is as bright as the aorta (c) Delayed phase – contrast drains out. Alpha-foetoprotein (AFP): elevated in 80% 2. Cutaneous features (eg dermatomyositis. nonspecific transaminitis) o AFP (Normal <5. 2. Alternatives: des-gamma-carboxy prothrombin. investigations to look for GI primary - CEA. death occurs from cachexia. a liver lesion on imaging should be considered HCC until proven otherwise .Serum levels of AFP do not correlate well with other clinical features of HCC. such as size. tumor secretes PTH-rel protein) 4. Triphasic CT scan [gold standard investigation] CT liver scan at three different times after IV contrast: (a) Arterial phase –contrast fills arteries: aorta (& HCC. mortality rarely from mets) . Hypercalcaemia (osteolytic lesions. Dynamic MRI scan of the liver . stage. 3. 3rd spacing of fluids. cirrhosis. biochemical and radiological tests WHO criteria for HCC: (a) Risk factors for HCC e. endoscopy 147 . so none of the vessels in the liver are lighted up . bleeds) lights up.Not commonly used given the need for intraarterial injection 5. Watery diarrhoea (related to secretion of peptides that cause intestinal secretion eg.g.Adjunct investigation done when CT findings are equivocal . WHO criteria >400. or (rarely) tumor rupture and bleeding into the peritoneum.Bone pain.Characteristic feature of HCC is enhancement in the arterial phase (have a rich hepatic arterial supply) with rapid contrast washout in the portal venous phase (hypodense) Haemangioma: capsular enhancement in delayed phase Metastasis: enchancement in portal venous phase .Images liver in greater detail without need for contrast. variceal bleeding. <5% secrete IGF symptomatic hypogly). Dyspnoea 6. can be used to exclude benign conditions 4. high bilirubin. raised TW in SBP. tumor associated enzymes of GGT etc. or prognosis. use of diuretics for ascites. r/o nephropathy for contrast imaging) o LFT (low albumin. can be severe & intractable) 5. but most pts are anemic). Paraneoplastic syndromes 1. If indicated.CT scan of the liver weeks after lipiodol ingestion will pick up the areas of tumour (where the pre-lipiodol CT may not have demonstrated the tumour clearly) . raised ALP. Metastases (low incidence in HCC. Can be normal in up to 40% of small HCC. Hypoglycaemia (due to high metabolic demands of tumour. and metastases to the adrenals - 3. pemphigus foliaceus) Complications from hepatocellular carcinoma are those of hepatic failure. Hepatic angiogram with lipiodol and post-lipiodol CT scan . hep B/C carrier (b) Characteristic CT findings (of a hypervascular lesion) (c) Raised AFP (>400) 1. diagnostic & trending. infants.5. INVESTIGATIONS Basic laboratory investigation: o FBC (low Hb from BGIT. o Hepatitis markers (look for carrier status or chronic infection) o PT/PTT (raised PT) Imaging: o Triphasic CT scan (see below) DIAGNOSIS Biopsy is usu not performed due to risk of tumour seeding (1-2% risk) along the needle track – may render the patient unsuitable for transplant! Diagnosis is based on clinical.Lipiodol will be retained in HCC even after many days as the HCC does not contain Kupffer cells to ingest lipiodol . hepatitis. CA 19-9. Erythrocytosis (tumour produces erythropoietin.In a patient with hepatitis B/C and raised AFP. low Plt) o UECr (dehydration.Hepatic angiogram may reveal abnormal blood vessels within the HCC .CT can also look for nodal involvement. other CA esp gastric) . gastrin. note false +ve: pregnancy. CT thorax: lung 2. Patients who present with cancer symptoms and/or with vascular invasion or extrahepatic spread comprise the advanced stage. Early stage disease includes patients with preserved liver function (Child–Pugh A and B) with solitary HCC or up to 3 nodules </=3 cm in size. In these lesions the absence of microvascular invasion and dissemination offers the highest likelihood of cure and thus.Okuda . staging depends on extent of liver disease. 1. peritoneum and LNs 3. Bone scan if clinically indicated: bone Different staging systems: . vascular invasion and extrahepatic spread. They have a shorter life expectancy (50% survival at 1 year) and are candidates to enter therapeutic trials with new agents Patients with extensive tumor involvement leading to severe deterioration of their physical capacity [WHO performance status>2] and/or major impairment of liver function (Child–Pugh C). symptoms. patients may theoretically achieve a 5-year survival of almost 100%.STAGING (looking for metastases) 1. The intermediate stage consists of Child–Pugh A and B patients with large/multifocal HCC who do not have cancer related symptoms and do not have macrovascular invasion or extrahepatic spread. 4. Their median survival is less than 3 months. 3. liver transplantation or percutaneous ablation with possibility of long term cure. These patients can be effectively treated by resection. Their survival at 3 years without therapy may reach 50%.TNM . CT abdopelvis: liver and adrenals. liver function. 5. with 5-year survival figures ranging from 50% to 75%. in Child–Pugh A. ECOG performance status grades: 148 . CXR.Barcelona-clinic-liver-cancer (BCLC) In BCLC. Very early HCC is currently very difficult to diagnose confidently prior to surgical ablation. 2. are considered end stage. These are the optimal candidates for transarterial chemoembolization. If patient has cirrhosis.20 Slight . Residual liver function post-operatively (at least 20%) .TREATMENT SURGERY (ACHIEVE TUMOUR REMOVAL WITH GOOD LIVER FUNCTION) .70. Not necessary if clinically sig portal hpt: varices.Multicentric disease affecting both lobes is a contraindication to hepatectomy 2. General fitness for operation 3. the patient cannot tolerate major liver resection (>3 segments removed) .Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has decreased increased resistance to flow . because tumour is non-functional .Has to be located in a suitable location for resection 149 . and the absence of clinically significant portal hypertension are the best predictors of excellent outcomes after surgery.Dependent on tumour size and how much of the liver it takes up. consider transplant Consider transplant 4.Studies have shown that a normal bilirubin concentration.A large tumour taking up most of the liver segments being resected translates to smaller amount of functional liver tissue being resected.Use of indocyanin green (ICG) – the percentage of ICG remaining in the liver after 15 minutes indicates the level of liver function.2 surgical possibilities: (a) Resection of tumour (partial hepatectomy) (b) Liver transplantation Factors affecting resectability: 1. bleeding and infection . If >15% remains after 15 minutes.70 None None B(7-9) 80 60 Significant functional compromise Maximum resection of 2 segments 2 28-35 35-50 1.20 Severe/refractory Grade III-IV C( 10-15) 45 35 Decompensated liver dz. 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 <1. Degree of portal hypertension (= hepatic vein pressure grad >10mmHg) .Detected during hepatic vein catheterization.mod Grade I – II 3 <28 >50 >2.2. . 6.CT volumetry: residual liver function calculated with a CT liver scan via a computer program . while a small tumour means that more functional tissue is removed with the same resection margins 5. ascites requiring diuretic therapy.Metastatic disease is not suitable for resection . plt<100000 a/w splenomeg.Only about 10-20% of patients with HCC will have disease amenable to surgery .Cirrhotic patients have higher risk of post-operative mortality (4-14%) compared to non-cirrhotic patients (0-4%) due to complications such as liver failure. with almost no risk for postoperative liver failure.The only curative treatment for HCC is surgical removal of the tumour . Liver function pre-operatively . Stage of disease . Location of tumour . but not long term (<30% 5-year survival) . Sorafenib imporves median survival by 3/12 150 . . there is a risk for reinfection of the donor liver (high risk factors are HBeAg positivity.In hepatitis B carriers.Requires a fine balance between adequate resection margins and preservation of sufficient functional liver to prevent liver failure . .No effective adjuvant therapy to reduce recurrence rate.Solitary recurrence might benefit from repeat resection. 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. thus a new tumour can still develop in the remnant liver. 75% of HCC are multifocal on diagnosis. Intra-arterial therapy (a) Transarterial chemoembolisation (TACE) (b) Transarterial embolisation (TAE) (c) Selective Intrahepatic Radiation – Yttrium-90 radioactive beads 3.Most powerful predictors of recurrence: Microvascular invasion and/or more than one tumors (This suggests that the majority of recurrences are due to dissemination from the 1° tumor and not metachronous tumors developing in a liver with cirrhosis) .only those patients in whom recurrence is due to de novo oncogenesis can be expected to benefit from salvage transplantation or repeated resection b) Transplantation .Problem in patients with cirrhosis is that there is already a “field-change” effect in the liver.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 . or 3 or less tumours none larger than 3cm (b) No evidence of gross vascular invasion (c) No regional nodal or distant metastasis . Systemic therapy – limited results.Milan criteria for transplantation (>75% 5-year survival if followed) (a) Single tumour 5cm or smaller.Good immediate and short-term results.a) Hepatectomy . 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.>70% tumor recurrence at 5 years due to dissemination and de novo tumors (eg occurrence of new 1° in the cirrhotic liver) . but in most patients recurrence after primary resection will be multifocal because of intra-hepatic dissemination from the primary tumor . AFP is also not a perfect screening test as 20% of HCC will not have raised AFP . Added benefit of assessing patency of the hepatic blood supply and the presence of vascular invasion by the tumor.SCREENING FOR CHRONIC HEPATITIS CARRIERS . but should be increased in patients at increased risk – HbeAg positivity. As the tumor grows. high HBV DNA levels Frequency determined by tumor growth rate. (sensitivity 65-80%.Alternatives: des gamma carboxy prothrombin (DGCP aka PIVKA II) – potential marker of portal vein invasion by tumor 151 . sibling has hep B. not by the degree of risk. specificity 90%) Features suggestive of HCC include poorly-defined margins and coarse.Target pop: Hep B / C carriers.Important as it detects smaller and resectable HCCs increasing survival from 26 to 88/52 . etc . Small tumors are often hypoechoic. the echo pattern tends to become isoechoic or hyperechoic. .Frequency of screening is controversial.g. mother had hep B/HCC. but it is not associated with radiation exposure. detect HCC tt exceeds transplant guidelines) .Combination of 6/12 to yearly Ultrasound + AFP levels . .Thus the combination of ultrasound and AFP can increase the sensitivity and specificity of screening . Cirrhosis. Patients on transplant waiting list (transplant priority if HCC dev.US is operator dependent & may miss certain areas of the liver where imaging is difficult. FHx of HCC.Screen family for chronic hepatitis B carrier status especially if there is a family history! – e. indistinguishable from surrounding liver. irregular internal echoes. Primaries: Colorectal.Jaundice early. Mass effects compressing on surrounding organs 3. spread via portal vein) . progressive . brightest in the delayed phase . irregular nodular hepatomeg . Pain from liver capsule stretch 4.Both obstructive and transaminitis picture .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. gastric. thrombocytopaenia 6. inferior lesions since there is higher risk for rupture 152 .Still more common than primary liver tumour for malignancy occurring in the liver . Kassabach-Merritt syndrome for large haemangiomas – consumptive coagulopathy. congenital in origin PRESENTATION 1.4-20% .Jaundice is a late sign . oesophageal mets Palliation for symptoms in neuroendocrine metastases 6. urogenital. Heart failure from large arteriovenous shunt DIAGNOSIS .Prevalence 0. Rupture (<1%) 5. found incidentally 2.Vascular malformation that enlarges by ectasia.Hard mass .Hard.Obstructive picture in early stages Hx TRIPHASIC CT . breast. LIVER HAEMANGIOMA EPIDEMIOLOGY . breast mets Poor results for stomach. Usually small and asymptomatic. LIVER METASTASES .Female to male ratio 3:1 PATHOGENESIS .DO NOT BIOPSY TREATMENT .Radiological Characteristic features on triphasic CT – slow enhancement of the rims on arterial and portal venous phase.Symptoms of obstructive jaundice Yellow sclera Tea-coloured urine Pale stools P/E .5.Hypodense on arterial phase (as metastases are usu hypovascular compared to hypervascular HCC.Heaviness .Hepatomegaly may not be present Invx . lateral.Incidentally found on follow up (for cancer) .Possible role for prophylactic surgery in large. pancreatic.Pain from rupture Mets to porta hepatis LN .Only for symptomatic or complicated lesions . lung PRESENTATION DEPENDS ON SITE OF METASTASIS Mets to liver parenchyma . CEA (may resemble infected tumour on imaging) If any aspiration done.Torsion . Close monitoring of vitals with strict IO charting 3.[Cysts that communicate with the biliary system are called choledochal cysts] PRESENTATION – WITH COMPLICATIONS . Compression of IVC. pelvic abscess Contiguous spread – from gallbladder empyema Haematogenous spread in sepsis e.50% of cysts are single . SIMPLE LIVER CYSTS EPIDEMIOLOGY . Staph aureus . infective endocarditis External inoculation – iatrogenic. Portal hypertension .Ethanol sclerotherapy (painful) .7.Aspiration . next 4/52 PO 4. cysts and parasites Tumour markers: AFP. Enterobacter.No solid component and not septated (mixed cysts with septations are suggestive of malignancy) . HEPATIC ABSCESS (PYOGENIC / AMOEBIC) PYOGENIC ABSCESS . stains & c/s Imaging: US HBS or CT scan (to exclude liver tumour. Rim-enhancing appearance on triphasic CT scan. IBD.Routes of infection: (a) (b) (c) (d) (e) Ascending infection from biliary system (ascending cholangitis) Intra-abdominal source through portal vein – acute appendicitis. Antibiotics via PICC Empirical antibiotics – Ampicillin/Gentamicin/Metronidazole Change to definitive antibiotics when blood c/s results return Total duration of 6 /52 – 1st 2/52 IV. KIV endoscopy to rule out GI malignancy) Findings: Irregular lesion with central area of necrosis. 50% of patients have jaundice. and one-third have hepatomegaly - Investigations: Laboratory: FBC. Melioidosis & amoebic serology/ PCR.Congenital malformation when an aberrant bile duct loses communication with the rest of the biliary tree and becomes progressively dilated (fluid within the cyst is not bilious) .Fistulation into duodenum . may be multiloculated.More common than amoebic abscess locally . coli. - Treatment 1. hepatitis markers Blood cultures.Bleeding & Rupture . pancreatitis.g. air-fluid levels.Malignant change (rare) TREATMENT (IF SYMPTOMATIC) . Resuscitate if necessary 2. CA 19-9.Causative organisms: Klebsiella pneumoniae. traumatic - Presentation: RHC pain (capsular stretch) with Spiking fever with chills. Drainage Drainage if >3cm – open drainage or percutaneous aspiration 153 .Prevalence 1-3% . diverticulitis.Excision/resection 8. Stool ova. rigors. E. Enterococcus.Fenestration (open or laparoscopic) . Cholestasis due to compression of CBD.9:1 female predominance for symptomatic cysts PATHOGENESIS .Mass effect. aspirates for cytology. U/E/Cr. jaundice Hepatomegaly often present Complications: rupture into pleural/peritoneal spaces - Treatment: Metronidazole (very responsive) Aspiration if amoebic serology inconclusive. TR.Minimally invasive. peritoneovenous shunt [silastic catheter]. constrictive pericarditis Abdo: CLD Renal: ESRF. then spreads to the liver through the portal vein) Transmission is faecal-oral - Presentation Usually single abscess No sepsis. pregnancy (metronidazole contraindicated). cytology Relieve of discomfort & diaphragm splinting from distension o Indications: Failed medical treatment symptomatic o perform under aseptic technique. US guidance may insert a pigtail catheter via seldinger technique open drain into stoma bag Treatment of ascites: o Conservative: low salt diet.Indications: Concomitant pathology requiring surgery e. performed under radiologic guidance . or pt not getting better) Ascites Ruptured abscess AMOEBIC ABSCESS - Causative organism: Entamoeba histolytica (infects the gut. nephrotic syndrome GIT: protein losing enteropathy Exudative (>30g/L) Cirrhosis Malignancy Infective causes: TB Chylous ascites Role of peritoneal tap: o diagnostic and therapeutic Send fluid for FEME.Single procedure . bibasal crepitations o Signs of malignancy Background information Causes of ascites: Transudate (<30g/L protein) Cardiac: CCF. gall stones Multiple abscesses or multiloculated abscess Immunocompromised patient Failed percutaneous drainage (tube blocked.Not dependent on location .Invasive procedure. protein.Longer stay for patient as drainage tube stays in patient for a longer time . diuresis o Peritoneal tap o Surgical: shunt sx (TIPSS. sacral oedema. 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. microbiology.g.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 . LA.Percutaneous aspiration . Denver shunt when with a subcutaneous pump] 154 . severe symptoms from distension or fever. impending rupture 9. done under GA . suspicion of secondary infection.Shorter hospital stay . forming ulcers in the colon.Can be done under LA . RHF. PAN 8. 3. pancreatitis can develop in a patient with a weekend binging habit. nitrofurantoin. may progress to sepsis (if source of infection is found) severe sepsis with 1 organ dysfunction septic shock MODS 155 . diphenoxylate. pancreas divisum (failure of the dorsal and ventral pancreatic ducts to fuse during embryogenesis). ERCP. PAN Trauma – penetrating > blunt trauma Steroids Neoplastic: Ca head of pancreas Mumps and other infx (VZV. gall stones CAUSES (I GET SMASHED) Infx: mumps. SAND Idiopathic (up to 10%) Gallstones most common: >90% combined Metabolic: hyperlipidemia. echovirus. procainamide.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. hypothermia 9. 6. Scorpion toxin Severe). Hypercalcaemia. EBV. Coxsackie. 2. PANCREATIC DISEASES 1. cancer of the head of the pancreas. RR>20 or TW>15]. . HyperTG (>1000 mg/dL. 4. 5.10.aggressive preintervention intravenous hydration to prevent 11. HCTZ. Occasionally. VZV 1. Autoimmune – SLE. campylobacter. Alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis. however.The activated lytic enzymes destroy the pancreatic acinar cells macrophages themselves secrete pro-inflammatory cytokines release of potent cytokines that attract neutrophils and . hypercalcemia Ethanol Autoimmune: SLE.~ 7-10% presenting with abdominal pain acute pancreatitis Trauma: blunt trauma. metronidazole. measles. T1 and TV 10. Steriods. salmonella. HR> 100. ERCP (4%) . ascaris. Drugs: Alc. Congenital: CFs. PATHOPHYSIOLOGY . cimetidine. estrogen) 12.The cytokine cascade amplifies the local inflammatory response and also results in a systemic inflammatory response [2 of 4: T>38 / <36. 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. MTB) 7. Rare causes: Cystic fibrosis. cisplatin). Drug-induced usually mild (SAND: Sulphonamides/ azathioprine/ NSAIDs/ diuretics. chemo (esp asparaginase. and may sensitise the pancreas to injury by other agents . Pancreas divisum mycoplasma. ACUTE PANCREATITIS DEFINITION An acute inflammatory process of the pancreas with variable involvement of regional tissues or remote organ systems EPIDEMIOLOGY .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) .Incidence is difficult to measure accurately (not all diagnosed). PRESENTATION - Symptoms (generally non-specific): Abdominal pain (most consistent, in >90% of patients) – constant epigastric pain, classically radiating to the back (in 50%), maximal intensity within several hours of onset; usually occurs after a heavy meal; alleviated by sitting up & leaning forward, worse on movement Nausea, vomiting, Anorexia Also rule out other causes: Gastric causes: PUD Perforated viscus (mainly on examination: look for peritonism) AMI, DKA or even a lower lobe pneumonia Hepatitis or GB / CBD disease Ask for causes of pancreatitis: Gallstone disease: biliary colic, symptoms of cholecytitis/ CBD stone/ cholangitis Recent alcohol abuse or chronic alcohol abuse Recent blunt trauma or ERCP done PHx or hyperlipidemia, hypercalcemia, autoimmune disease (SLE, PAN) Recent symptoms of mumps (viral fever + bilateral jaw pain/swelling) Recent drug history: steroids, NSAIDs, diuretics - Signs (also non-specific) Tachycardia, low grade fever, low BP, toxic looking, jaundiced? Epigastric tenderness, signs of peritonism (<1/3 of patients) May have a palpable mass (pseudocyst, pancreatic phlegmon) Abdominal distension ± ascites with diminished or no bowel sounds (ileus) Ecchymoses (usually not present): flank (Grey-Turner’s sign) or umbilical (Cullen’s) suggest severe haemorrhagic pancreatitis associated with profound fluid loss (third-spacing) Organ failure Ask for urine output Offer to auscultate the lungs for any effusion or ARDS (creps, reduced air entry) MANAGEMENT STRATEGY Diagnosis Severity stratification Assess for aetiology Supportive treatment Monitor for complications Treat aetiology (reverse / control) Manage complications Prevent future recurrence 156 INVESTIGATIONS DIAGNOSTIC (CLINICAL + BIOCHEMICAL DIAGNOSIS) 1. Serum amylase - raised within 12 hours of onset, usually more than 1000 or 3 times normal - High sensitivity and moderate specificity (specificity increased when cut-off taken at 3 times normal upper limit) - Returns to normal level 48 to 72 hours after onset – not useful in late diagnosis 2. Serum lipase - Rises within 8 hours of onset of symptoms and returns to normal after 7-10 days, also 3 times normal - Thus more useful in late diagnosis of acute pancreatitis 3. Urinary diastase - Similar function to serum lipase, used when serum amylase is equivocally raised or normal - elevated for even longer period after onset Other causes of elevated serum amylase: GI sources Non-GI sources - PUD, IO, perforation, Ischaemic bowel (amylase in the thousands), Cholecystitis, cholangitis Ectopic pregnancy Impaired clearance due to chronic renal failure Kidney stone Salivary gland injury or inflammation (rare) Macroamylasaemia PROGNOSTIC / SUPPORTIVE / LOOKING FOR AETIOLOGY Imaging 4. Ultrasound [1st investigation] - Preferred over CT scan - Good for visualising biliary tree and picking up gallstones (can intervene!) Dilated CBD ERCP to remove gallstones/Bx tumor Not dilated MRCP (susp parenchymal disease) - Pancreas may be diffusely enlarged and hypoechoeic – often difficult to visualise due to overlying bowel gas 5. Erect CXR & AXR - Erect CXR may show no air under the diaphragm, pleural effusion, elevated hemidiaphragm, pulmonary infiltrates; complete whiteout (ARDS) - AXR may show the “sentinel loop sign” (dilated proximal jejunal loop near the pancreas) or “colon cut-off sign” (distended colon from ascending to mid-transverse with no air distally) due to functional spasm of the bowel around the pancreas resulting from inflammation - presence of calcifications within the pancreas may indicate chronic pancreatitis 6. CT AbdoPelvis 1. Only if considering other pathologies eg. CA in elderly (CT may worsen pancreatitis) 2. At ~72hrs of known case of pancreatitis: detect fluid collections; necrosis (IV contrast needs to be given ) Balthazar for severity Laboratory Severity/ Cx: Etiologies: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. FBC (TW for Ranson, Glasgow; haematocrit for Ranson) U/E/Cr (urea for Ranson and Glasgow; electrolyte imbalances, dehydration) Glucose (for Ranson and Glasgow) LFTs (AST for Ranson and Glasgow; albumin for Glasgow; obstructive picture in gallstone pancreatitis) CRP Lactate dehydrogenase (for Ranson and Glasgow) ABG (PaO2 for Ranson and Glasgow; base excess for Ranson) Ca/Mg/PO4 with albumin (hypercalcaemia – aetiology) Fasting lipids (hyperlipidaemia – aetiology) ECG & cardiac enzymes (rule out AMI as a cause of epigastric pain) 157 SEVERITY STRATIFICATION (RANSON, GLASGOW, APACHE II) I. Danger signs in the first few hours - Encephalopathy - Hypoxaemia - Tachycardia >130/min, Hypotension <90mmHg, Haematocrit >50 - Presence of Gray Turner’s/Cullen’s sign - Oliguria <50mls/hr, Azotemia (serum urea) ATLANTA CLASSIFICATION (FOR SEVERITY) Mild acute pancreatitis Severe acute pancreatitis (15-25%) - Interstitial oedema - Minimal organ dysfunction - Uneventful recovery II. Ranson criteria Present at admission 1. Age 2. White cell count 3. Fasting bld gluc 4. LDH 5. AST >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 <2mmol/L 4. PaO2 <60mmHg 5. Base excess >4mmol/L 6. Neg fluid balance >6L - Ranson’s criteria prognosticates mortality according to score - Any patient with a score of 3 and above is considered to have severe pancreatitis - Mortality: <3 0.9% 3-4 15% 5-6 50% >6 90% - Shortfalls of Ranson’s: validated for alcoholic pancreatitis only revised Ranson’s score was created for gallstone pancreatitis, difficult to tell aetiology in acute setting & cumbersome to wait for 48 hours, and difficult to assess for negative fluid balance III. Glasgow/ Imrie score- PANCREAS 1. PaO2 <60mmHg 2. Age >55yrs 3. Neutrophil/WBC >15x109/dL 4. Calcium <2mmol/L 5. Renal (urea) >16mmol/L 6. Enzymes LDH >600U/L AST >100/L 7. Albumin <32g/L 8. Sugar (Glucose ) >10mmol/L >3 criteria severe - Preferred over Ranson’s scoring in certain centres - combine with CRP IV. C-reactive peptide - As a single prognostic marker; <100 is unlikely severe - If CRP is >210mg/dL at 48 hours, the pancreatitis is more likely to be severe - No relevance >3/7 of onset as other confounding factors come into the picture - Combination of Glasgow score and CRP improves overall prognostic value V. Balthazar’s CT severity index (consider a CT AP @ ~ 3/7 from onset) - Grades severity of disease according to CT findings detects h’ge & necrosis - Not very useful as CT is not usually done in the 1/52 in local context, and disease is still evolving (CT findings lag behind) in the early stages 1. A - Normal 2. B - Enlargement 3. C - Peripancreatic inflammation 4. D - Single fluid collection 5. E - Multiple fluid collections: 50% chance of developing an infection and a 15% chance of dying 158 COURSE OF DISEASE - 75%: mild course of disease; recover unless comorbidities cause deterioration -------Deterioration from mild to severe very rapid!------ 20-25%: severe outcome (Acute necrotizing pancreatitis 15%) 1/3 of these patients will ultimately die - Overall mortality rate <10%. Death is bimodally distributed: (a) Early Within 1/52; due to severe organ failure, SIRS Very little can be done in terms of treatment (b) Late Most common cause is INFECTION with resultant sepsis Multi-organ failure can be the course of death SUPPORTIVE TREATMENT 1. Resuscitate if needed 2. Monitoring - In general ward if mild pancreatitis; HD/ICU monitoring if severe (≥3) - Monitor vitals [SpO2, BP, HR, Temp.], urine output & CVP 3. NBM (bowel rest) and IV fluid replacement - Fast patients for at least 2/7 until more stable - Fluid resuscitate with crystalloids - May include gastric decompression with NGT if there is persistent vomiting, significant gastroparesis, or intestinal obstruction (ileus) - May start oral feeding early with fluids in mild pancreatitis if tolerated Prolonged NBM results in poorer recovery due to nutritional debilitation – think about NJ feeding, or open jejunostomy creation early in patients with severe pancreatitis; if not tolerable, then consider TPN - Acid suppression does not change course of disease, but protects against stress ulcer formation; octetride has no benefit (thought to reduce pancreatic secretions) 4. Analgesia - Do not give NSAIDs as they can worsen pancreatitis & cause renal failure (since there is already decreased renal perfusion in acute pancreatitis) - Use opioid analgesics (tramadol, pethidine) NOT morphine (causes increased tone of sphincter of Oddi) 5. Treatment of fluid and electrolyte abnormalities hypocalcaemia, hypoglycemia 6. Antibiotics - Either prophylactic or therapeutic Not shown to have any benefit in mild pancreatitis a) Prophylactic in severe acute pancreatitis to prevent infection of necrosis infection will occur in 40-70% of patients with necrosis and increases the mortality rate from 12 to 33% Carbapenem (only imipenem has been shown to prevent sepsis, imipenem and quinolones have better penetration into pancreatic tissues) b)Therapeutic in cholangitis (coexisting with Gallstone disease or as complication of pancreatitis) & infection of pancreatic necrosis/ pseudocyst - Duration: 14-28 days 7. Support for organ failure o Ventilate with PEEP if hypoxemic (e.g. ARDS) o Dialysis & CVP monitoring if in ARF o Fluid resuscitation & inotropes if Hypotensive 159 MONITORING FOR COMPLICATIONS AND TREATING Local complications: - Acute fluid collections Due to increased vascular permeability; 70-80% resolve spontaneously - Pseudocyst Persistent fluid collection (enzymes, blood, necrotic tissue) walled off by fibrosis and not an epithelium-lined surface (after 4 weeks) Presents as 1. Gastric outlet obstruction, 2. infx, 3. peritonitis, 4. h’ge (erosion of splenic vessels), Persistently raised amylase despite resolution of pancreatitis 50% resolve spontaneously - Abscess Infection of fluid collection (not necrosis) - Pancreatic necrosis Areas of no contrast uptake on CT with intravenous contrast - Infected necrosis Gas bubbles on CT scan Positive bacterial culture on CT, U/S guided FNA accts for much of the morbidity and mortality - Infections occurring early (<3 weeks) in the course of the illness appear to be associated with a higher mortality rate Often polymicrobial and involve both aerobic and anaerobic bacteria – GIT org: Escherichia coli, Klebsiella spp, Enterobacter spp, Proteus spp, Pseudomonas aeruginosa, Bacteroides spp, and Clostridium spp, and the enterococci - Chronic pancreatitis, exocrine insufficiency & endocrine insufficiency Systemic complications o Peritoneal sepsis o Pancreatic ascites (massive accumulation of pancreatic fluid in peritoneum) o Intra-abdominal haemorrhage (erosion of splenic vessels) o Multiple organ failure (ARDS, acute renal failure, hypovolaemic shock, DIVC) o Hypocalcaemia, hyper/ hypoglycaemia Intervention for local complications - ERCP - No benefit in mild biliary pancreatitis - Indications: Severe pancreatitis Evidence of ductal stones Cholangitis No response to treatment within 48 hours - ERCP should be done within first 48-72 hours for maximum benefit - CT-guided aspiration of pancreatic necrosis Can help differentiate between sterile and infected necrosis Consider surgery if patient doing poorly - Necrosectomy for infected necrosis Some kind of lavage and drainage procedure is done after necrosectomy to decrease infective load - Role of surgery Infected necrotic pancreas (mortality 100% without operation) Sterile necrotic pancreas (necrosectomy) Delay surgery till as late as possible for demarcation of necrotic areas (repeated surgeries required) Diagnostic uncertainty Complications e.g. intra-abdominal haemorrhage - Pseudocyst Operate if larger than 6cm and persisting for more than 6 weeks as the chance of spontaneous resolution is low and risk of complications (infection, haemorrhage, rupture) is high Surgery can be open, laparoscopic, endoscopic or percutaneous (radiologically guided) Endoscopic – internal drainage via a cystogastrostomy, cystoduodenostomy or cystojejunostomy 160 Faecal pancreatic elastase Complications: MRCP (pseudocyst. . there is reluctance to do the surgery early. malabsorption) d) Newly diagnosed DM (30%) e) Steatorrhea (late) Complications: Local complications: persistent pseudocyst. stop all offending medication & control hyperlipidemia Cholecystectomy for biliary pancreatitis .MANAGEMENT OF AETIOLOGY & PREVENTION OF RECURRENCE Avoid alcohol. relieve ductal stricture) Control blood sugar with insulin Pancreatic enzyme supplements Pain relief Role of surgery Persistent local complications: pseudocyst. fistulae.In patients with severe pancreatitis.done in the same admission for pts with mild pancreatitis . 25-65% will develop the 2nd episode within 30 days of the initial one . AXR: calcification c. thoracic splanchnicectomy) Relief of pancreatic duct obstruction o Puestow procedure: side to side pancreatico-jejunostomy 161 . duodenal stenosis. coeliac plexus block. . duodenum) Pain relief (pancreatectomy.trauma.strictures (congenital. EUS Baseline function a. MRCP (choice!): chain of lakes appearance of pancreatic duct (strictures and cystic dilatations) b.Smoking . acquired). some have persistent relentless pain b) Diarrhoea (15%) c) LOW (sec to anorexia.18-21% of patients with biliary pancreatitis will have another episode . malnutrition Pancreatic cancer INVESTIGATIONS a) b) c) Dx: a. CHRONIC PANCREATITIS Chronic. vitamin deficiency. fistulae.Alcholism – 80% .Hypercalcemia Presentation: a) Pain (85%) – mostly episodic.Among these. ascites Chronic pain Pancreatic insufficiency o Type I DM o Steatorrhoea. local obstruction secondary to fibrosis (CBD.CRF . Secretin injection check for pure pancreatic juice (gold std but invasive) b.genetic (North Indians) . as the patient may develop complications that require surgical intervention – better to do all surgery in the same operation instead of opening the patient twice 13. irreversible architectural disruption of the pancreas resulting in chronic epigastric pain and pancreatic insufficiency Causes: NOT GALLSTONES! . portal vein thrombosis) Outline of management Treat underlying cause (stop alcohol. dyspnoea .Industrial carcinogens – benzidine. anorexia.Malaise.000 per year in each gender . bone pain. CNS symptoms. PANCREATIC CANCER EPIDEMIOLOGY . AD.Endocrine: Diabetes mellitus Late presentation .7:1 male to female ratio.Distinct category of tumours collectively called periampullary tumour (30%): Malignant cells arise from one of a few cells: (a) Duodenal epithelium (best outcome out of all three) (b) Biliary ductular epithelium (c) Ampullary ductular epithelium The periampullary tumours have better tumour biology than pancreatic adenoca smaller size. less vascular invasion Different TNM staging 90% resectability.Lower socioeconomic class PATHOLOGY . betanaphthylamine (dye) . margins neg. overall 5-year survival <3% ASSOCIATIONS . 20% in the body.Anatomic distribution: 75% in the head. malabsorption .Recurrent venous thrombosis . MEN. weight loss. FAMMM (familial atypical mole multiple melanoma syndrome) .Depression 162 .14.Bleeding upper GIT (haematemesis and/or malaena) . p16 gene) .Cigarette smoking (most clearly established – 2-5X increased risk) .Most common histology is ductal adenocarcinoma (90% of tumours) . relieves with bending fwd .Chronic pancreatitis .1. anorexia. LOW!.Familial cancer syndromes e.Diabetes mellitus . picked up on imaging for some other purpose Pancreatic head or periampullary Pancreatic body/tail . nausea . nausea .Incidence about 3-5 per 100.Very poor prognosis – median survival for unresectable disease is 6 months (80% of patients have unresectable disease at presentation). median survival after Sx is 38mth Prognosis is also better as they present earlier with obstructive jaundice PRESENTATION May be asymptomatic.Malaise. Peutz-Jeghers (Hereditary intestinal polyposis syndrome.Genetic factors (mutations in K-ras gene. HNPCC. low nodal stage. increase with age . hyperpigmented macules in lips and oral mucoas).Duodenal obstruction (vomit) .Acute pancreatitis .Metastatic symptoms: ascites.Eighth cause of cancer death in Singapore .g.Paraneoplastic syndromes – migratory thrombophlebitis in 6% Also .Exocrine insufficiency with duct obstruction steatorrhoea.Coeliac and mesenteric plexus invasion – dull constant (incessant and boring) PAIN in the epigastrium radiating to the back. better diff.OBSTRUCTIVE JAUNDICE Painless obstructive jaundice with palpable GB (Courvoisier’s sign) + Cholangitis . 5% in the tail . occasionally. MRI pancreas with MRCP – MRI pancreas is not superior to CT scan (Diagnosis and staging) MRCP is useful in delineating biliary system anatomy especially if the system is not obstructed and there are no therapeutic indications for ERCP (since there are considerable risks with ERCP) 4. to diagnose an underlying pancreatic carcinoma 163 . Endoscopic ultrasound + FNA biopsy . ERCP with stenting to relieve obstruction (in cholangitis) 5. serial imaging studies. ascites) 3. CT scan (MAIN) . Staging: Extra-pancreatic spread (Involvement of regional LNs. bleeding INVESTIGATIONS DIAGNOSTIC 1.1.Staging: tumour and nodal involvement The most difficult clinical situation in which to diagnose pancreatic carcinoma is in the patient with underlying chronic pancreatitis. Mass lesion within pancreas.Treat any life-threatening complications such as cholangitis.Can act as a prognostic marker: high CA 19-9 levels usu associated with unresectable disease with poorer prognosis . CA 19-9 . and.Dx: FNA with EUS guidance preferred to transcutaneous biopsy (less risk of tumour seeding) . liver metastases.Can be used as a marker for tumour recurrence during post-op follow-up 2. GB distension 4. empiric resection. 2. Often combine multiple imaging modalities. Both bile & pancreatic duct dilatation in head of pancreas tumours (double duct sign) 3. Even tumor markers can be elevated in patients with chronic pancreatitis. IMMEDIATE MANAGEMENT .Better sensitivity (85-90%) and equal specificity (90-95%) in diagnosing pancreatic cancer . pancreatitis.Not a screening test for pancreatic cancer as it can be false positive .localized areas of reticulated erythema and hyperpigmentation due to chronic and repeated exposure to heat: regular application of heat to the same painful part over a period of at least a few weeks suggests that the pain is severe and consistent. close clinical follow-up. All of the above imaging studies may show abnormalities that may not help to differentiate between pancreatic carcinoma and chronic pancreatitis. STAGING [LIVER. distal part of the stomach and LN removal (impt prog factor) Common hepatic duct and pancreas are then anastomosed to the jejunum. proximal 15cm of jejunum. Endoscopic ultrasound – T. PERITONEUM. close up and abort surgery TREATMENT SURGERY Curative resection . metastasis to the liver 2. liver. bone. BONE] 1. recurrence rates after surgery are high – 5 year survival only 10 to 30% . 45-60cm proximal to the gastrojejunostomy 164 . just before definitive operation for a resectable tumour (since CT/MRI may miss small peritoneal deposits in ard 25%) if no peritoneal disease found. CT/MRI of the abdomen – T. common bile duct. otherwise.Only about 15-20% of patients will have resectable disease at presentation – usu in periampullary / head of pancreas tumours . duodenum.Resectable disease: No metastases (lung.Improves chances of survival . N stage 3. Bones – bone scan when suspicion is high 5. N stage. Staging laparoscopy – for peritoneal metastases.However. peritoneum) Patent superior mesenteric vein and portal vein – no longer absolute CI Definable tissue plane between tumour and superior mesenteric artery as well as coeliac axis Whipple’s operation Pancreaticoduodenectomy for head of pancreas or periampullary tumour Usually preceded by a staging laparoscopy to confirm absence of peritoneal metastases Removal of the head of the pancreas. gallbladder.Recent trials: improved survival with adjuvant chemo (5-FU + Folinic acid or gemcitabine) . LUNGS. Lungs – CXR + CT thorax 4. continue with surgery. comparable operation time.Complications of Whipple’s operation Mortality rate is 2-7%. Palliative chemotherapy/radiotherapy/chemoradiotherapy . bowel (b) Bleeding (c) Infection abscess.. Endoscopic stenting .Stenting of obstructed biliary duct . morbidity. pseudocyst formation may occur due to anastomotic leaks Late Surgical: (a) Gastric stasis with or without pylorus-preserving Whipple’s (25%) – NG decompression. with a morbidity rate of up to 20-30% (mostly mild complications) Intraoperative/early complications General: (a) Injury to other organs – liver.Stenting of obstructed duodenum 2.The overall long-term and disease-free survival was comparable in both groups. . sepsis Specific: (d) Pancreatitis (e) Pancreatic anastomotic leak (5-20%) (f) Biliary anastomotic breakdown (g) Fistulation. to prevent reflux of food into biliary tree – essentially a Roux-en-Y loop (jejunojejunostomy) NON-SURGICAL PALLIATIVE MEASURES 1. hospital stay. kidney.Not shown to provide good outcomes 165 . and incidence of delayed gastric emptying.Triple bypass involving anastomosis between [all to jejunum] (a) Stomach and jejunum (gastrojejunostomy) (b) Biliary system and jejunum (choledocho-/hepatico-/cholecysto-jejunostomy) (c) Jejunum and jejunum. mortality.Both surgical procedures are equally effective for the treatment of pancreatic and periampullary carcinoma Palliative surgery Surgical bypass of obstruction . Coeliac plexus block for pain 3. . blood loss. longer hosp stay (b) Diarrhoea resulting from autonomic nerve injury during lymph node dissection LOW (c) Dumping syndrome: increased gastric emptying (from antrectomy) causing Nutritional deficiency Functional: (d) Long-term exocrine insufficiency resulting in malabsorption and steatorrhoea (e) Endocrine insufficiency DM Pylorus-preserving pancreaticoduodenectomy (PPPD) . pruritis Conjugated hyperbilirubinemia ↑ ALP. dudeno. anti-HCV. ↓ haptoglobin PBF Direct Coomb’s test for autoimmune hemolytic anemia Stool OCP (ova. signs of portal HTN (splenomegaly. penicillins. TCM. phenytoin. GGT disproportionate to ALT. anti-dsDNA. MTX. hematochromatosis) Infiltrative (Sarcoidosis. ANA & anti-SMA. HCV) Metabolic (Wilson’s. HAV) EBV. 24hr urine copper Abdo U/S: surface nodularity & ↑ echogenicity in cirrhosis. schistosomiasis Mural Biliary strictures post ERCP Biliary strictures from gallstones. HCV RNA Autoimmune screen ANA. BILIARY TRACT DISEASES 1. corticosteroids Autoimmune hepatitis SLE Inherited ↓/absent activity of UGT (unconjugated hyperbilirubinemia) Gilbert’s syndrome Crigler Najjar 1 & 2 Inherited impaired biliary excretion (conjugated hyperbilirubinemia) Dubin-Johnson syndrome Rotor syndrome 166 Cholestatic o o o o Tea-colored urine. ARF & thrombocytopaenia) 1) 2) 3) 4) 5) 6) Mixed signs. Consider ERCP. ascites) Infective Acute viral hepatitis (HBV. CAUSES OF JAUNDICE Pre-hepatic o o o o o o o Urine/stools normal May have symptoms of anemia Unconjugated hyperbilirubinemia ↑ LDH. further serologic testing: AMA (M2-IgG most specific for PBC). chronic pancreatitis PBC (intrahepatic bile ducts): middle aged ♀ PSC (intra & extrahepatic): ♂ with IBD esp. corticosteroids . ampullary) Mirrizi’s syndrome (chronic cholecystitis) Others: Biliary atresia Drug-induced: paracetamol. urine may be dark with normal stools Variable liver biochemistry ↑ ALT AST disproportionate to ALP GGT ↓ Albumin. augmentin. parasites) malaria Hepatic o o o o o o o o o Hemolytic anemias: 1) Inherited Thalassemia G6DP Spherocytosis Sickle-cell anemia 2) Acquired Infective: malaria Autoimmune: SLE. cysts. prolonged INR (cirrhosis) AFP: exclude complication of malignancy Viral hepatitis serology Acute: Anti-HBc IgM. CMV TB Liver cirrhosis/chronic liver disease Alcoholic liver disease Chronic viral hepatitis (HBV. do ERCP/MRCP/PTC If ducts not dilated. Anti-HAV IgM Chronic: HBsAg. AST Do abdominal U/S If ducts dilated (>8mm). UC Cholangitis (Charcot’s triad) Choledochal cyst (type I-V) Distal cholangiocarcinoma Extraluminal Ca head of pancreas (painless. paracetamol.11. w distended GB) Other peri-ampullary Ca (cholangio. isoniazid. amyloidosis) Hepatotoxic drugs Alcohol. AMA Metabolic screen Caeruloplasmin. pale stools. p-ANCA (PSC). liver biopsy 1) 2) 3) 4) Intraluminal Gallstones (painful) Parasites: Ascaris lumbricoides. Evan’s syndrome Hemolytic uremic syndrome (hemolytic anemia. etc . operation) .Decompensation: encephalopathy. siblings). worsening ascites . arthralgia. Hepatitis HISTORY 1. drug abuse/needle sharing.Symptoms of cholangitis: fever.Exclude pre-hepatic and hepatic jaundice (more importantly hepatic jaundice since it can also cause tea-coloured urine) Symptoms suggestive of viral hepatitis: prodrome of fever. hepatitis.Establish obstructive jaundice – tea-coloured urine. nausea/vomiting. etc. sexual contact Alcohol intake: shown to affect bile acid uptake and secretion.Metastases to the porta hepatis Obstructive jaundice Painless: CA HOP.Confirm jaundice – pt’s sclera are yellow (carotenemia does not result in scleral icterus or elevation of the bilirubin level) . Hepatic causes Commonest causes of jaundice 1.Cholangiocarcinoma (distal) Benign . and cirrhosis Drug history: any TCM intake recently. blood transfusions. jaundice is of new onset and progressively worsening.Mirizzi syndrome .g. malaise.Metastatic symptoms: bone pain. K) – especially coagulopathy (very unlikely in acute setting) 167 .Primary sclerosing cholangitis .Head of pancreas cancer .Benign papillary fibrosis: prev gallstone passage (can give post cholecystectomy pain. malaise .Pancreatitis (gallstone as cause): abdominal pain radiating to the back with N/V . Periamp CA Painful: Stone. E. needlestick injuries. Complications .Pancreatitis: secondary bile duct compression from edema Extramural Malignant .Post-instrumentation strictures (ERCP. Chronic alcohol use may result in fatty liver (steatosis). pale stools .2. stones. Tumor 3.Parasitic infections (recurrent pyogenic cholangitis) Benign . family history of hepatitis (esp mother.Gallstones .Pain is a late symptom of pancreatic CA & tends to be constant and relentless compared to biliary colic which subsides after few hours - 3. ingestion of seafood. Risk factors for viral hepatitis: travel history. fat-soluble vitamin deficiency (A. Stricture. hepatic fetor.Fat malabsorption: steatorrhoea. Aetiology – benign or malignant Recurrent spikes of similar jaundice that resolve on their own with time suggest benign obstruction e.Choledochal cyst Malignant . Confirm obstructive jaundice . any new medications taken History of chronic liver disease 2. myalgia.Pruritus as a result of bile salt retention . resulting in cholestasis. Cholangiocarcinoma. APPROACH TO OBSTRUCTIVE JAUNDICE CAUSES (POSTHEPATIC JAUNDICE) Intraluminal Mural Benign . D. neck lump.Strictures from other causes (gallstones. loss of weight. rigors with RHC pain and jaundice . painless progressive jaundice) . dyspnoea. Gallstone 2. chills. strictures A young patient with painful jaundice usually benign cause Previous history of gallstone disease or biliary colic symptoms Previous history of surgery to the biliary tract or ERCP Malignancy is suggested if the patient is old.Constitutional symptoms: loss of appetite. and there is no associated pain (i. acute pancreatitis) .e.Periampullary cancer . chronic pancreatitis) . Secondly to confirm inflammation/infection: 2. anaemia (correct before ERCP) Followed by the rest: 3.Both useful in demonstrating dilated biliary system as well as site & cause of obstruction) 1. Unable to detect distal CBD stones well iii. Operator dependent CTAP: a. Adv i.only ordered if Dx is ambiguous. 2. LFT – classical obstructive picture = bilirubin raised (+/.PHYSICAL EXAMINATION 1. Normal 3:7) + raised ALP (and GGT . GXM – in case of op (eg. Tumour markers – CA 19-9. leg swelling? Peripheries: Stigmata of chronic liver disease? Scratch marks? Conjunctival pallor? Abdomen . Complications of gallstones: iv. or primary liver pathology) . ARDS in cholangitis b. Rule out malignant etiology b. hepatic. Unable to detect malignancy well ii. Amylase: concomitant pancreatitis 5. Gallstone disease / Cholecystitis: GB stones or sludge. 6.Hepatomegaly? (Could be due to metastatic disease. thickened GB wall. Choledocholithiasis: Duct dilation>8mm (impt to identify dilated INTRAhepatic ducts as it indicates that (a) obstruction is more severe (b) PTC is a possible option if ERCP fails) ii. 5.Splenomegaly? (Portal hypertension – think prehepatic. posthepatic) DRE: Pale stools? Cervical and supraclavicular lymph nodes Bony tenderness Respiratory examination INVESTIGATIONS (guided by clinical suspicion after Hx and P/E) Bloods Firstly to confirm obstructive jaundice: 1. Disadv: i. Cr level for suitability of CT imaging!! 4. fat stranding iii. obstruction of portal vein by cancer .Enlarged gallbladder? (Courvoisier’s law – if the gallbladder is palpable with painless obstructive jaundice. CEA (cholangioca and pancreatic ca) 7. cause is unlikely stones) . Pleural effusion MANAGEMENT The patient is managed as for the causative aetiology (see relevant sections) 168 . US findings: i. 8. Indications i. Pallor? Any abdominal distension. Suspected perf oratedGB (view air ard GB in lung window) ii. Liver consistency (fatty or cirrhotic) b.Any scars of abdominal surgery? . peritoneal malignancy 3.Generalised distension? Ascites could be due to: 1. 2. 7. 3. PT/PTT – any prolonged PT from vitamin K malabsorption.direct>indirect. malnutrition (low albumin) 2. 3. Logistics (can be done earlier esp cholangitic patient to plan for early intervention) CXR a. liver dysfunction (to be CORRECTED before procedures like ERCP can be done) 6. 4. U/E/Cr: dehydration. U/S HBS: best for imaging stones a. Vitals: Is patient haemodynamically stable? Any fever? General inspection: Jaundice. 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. Blood c/s if febrile and jaundiced (TRO HBS sepsis) 8. FBC – any infection (impt as some pts haven mounted ferbrile response). not routine) more than AST and ALT **Classical picture more often seen in CA than gallstone disease. Sensitivity reduced with fat patient habitus iv. cholecystectomy) Imaging (Ultrasound versus CT . pericholecystic fluid. cholesterol.M=F . protein. fertile.Developed countries – 22% of SG population (18% with signs and symptoms) .g.Typical picture (the 5 F’s): Fat. Mixed .Consistent 2:1 female to male ratio. chronic HAEMOLYSIS. b. developing countries a) b) Black pigment stones: a. exogenous administration 2.Sludge is a pre-stone condition. and more cholesterol than black pigment stones Cholesterol stones . chronic liver disease.Microlithiasis suspended in bile. but not all sludge becomes stones . common bile duct. female. forty.most commonly G6PD-def. Spinal cord injury Pregnancy Fasting. 60% recur. and 10% form stones 169 .In the West: overall 10-15%. Increasing in incidence due to influx of foreign workers.soft stones and crumble easily 3. CIRRHOSIS.Exact incidence in Singapore not known . vesicles) .Can be visualised on the ultrasound scan as layering in the biliary tree . 1:1 in elderly .Normal bile contains bile salts (primary and secondary). hepatic duct.More common in younger patients. Brown: calcium salts. pregnancy.bilirubin . flatulent – refers to cholesterol stones but no longer applies. GALLSTONE DISEASE DEFINITION Gallstone is a generic term for any kind of stone (cholesterol. 20% in women and 10% in men . etc) EPIDEMIOLOGY . Cholesterol: cholesterol . 1. Decreased emptying of the gallbladder Gallbladder malignancy is an important cause to exclude Gallbladder stasis: Truncal vagotomy. cystic duct. bilirubin. Black: mostly calcium salts and bilirubin . TPN). rapid weight loss Hyperlipidaemia Increased oestrogens: female. pigment) in any part of the biliary system (gallbladder. the degradation products of which then precipitate as calcium bilirubinate. increased secretion of bilirubin into bile (e.3. phospholipids. NORMAL PHYSIOLOGY OF BILE .hard and faceted 2. a milieu that predisposes to stone formation .Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol (in micelles. 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). and bilirubin .From disruption in the solubility equilibrium of bile. . decreased bilirubin solubilisers.20% of biliary sludge will disappear.a/w simple refined sugar in diet STONE COMPOSITION AND PATHOPHYSIOLOGY 1. TPN Pigment stones .Majority Biliary sludge . Increased cholesterol secretion in bile old Obesity.More common in older (peak at 40-50 years) but increasing in younger . Risk of symptom occurrence = 1 to 2% per year greatest risk in first 5 years of diagnosis – 10% at 5 yrs. bloating. gallbladder polyp. Mirizzi syndrome with obstructive jaundice (see below) 6. Calcium secreted into lumen of hydropic GB 9.Bile should appear as black patch in gallbladder.Investigation of choice for gallstones . abdominal distension Biliary colic is a “herald” symptom that indicates risk of further sequelae. 99% specificity . cholecystitis) . Infection i. Fistulation and gallstone ileus (see below) 8. 15% at 10 yrs.CBD is not muscular.Radiation: inferior angle of the right scapula. Pancreatitis 3. Acute / Chronic cholecystitis ii. Choledocholithiasis with obstructive jaundice 5. so absence of biliary colic.Features of stone on ultrasound: strong echogeneic rim around the stone. 2. Porcelain gallbladder: due to calcium salts ppt in GB wall. tip of right shoulder or interscapular . susp gallbladder mass. dehydration . porcelain gallbladder prophylactic surgery (b) IMMUNOCOMPROMISED presentation is abnormal & difficult to detect (c) Patients with CHRONIC HAEMOLYTIC DISEASE (e.Even more sensitive than CT scan for stones since CT may miss small stones due to the spacing of the cuts taken . but a constant pain with OJ 2o to obstruction . susp complication eg. with posterior acoustic shadowing .Location: epigastric (70%) or RHC pain . often resolves spontaneously (if >6hrs.80-95% of patients . sickle cell anaemia. Gallbladder CA ‘limey’ bile. 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. fried oily foods. if not homogeneous sludge 170 .g.Associated: N/V (patient gets better after vomiting).Trigger: meals – binge-eating. Gallstone dyspepsia: (non-ulcer dyspepsia) fatty food intolerance. Ultrasound of the hepatobiliary system . dyspepsia and flatulence not due to other causes Complications 4.>92% sensitivity.CLINICAL COURSE Asymptomatic Leave alone .Pickup rate for gallstones is less than 10% since most stones are radiolucent 1. Biliary colic (15%) . thalassaemia) – as high as 50-60% will develop symptomatic disease in their lifetime Symptomatic sequlae 1. Cholangitis iii.Duration: minutes to 2 hours.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) . Mucocoele of the gallbladder / Hydrops / Empyema of Gallbladder (see below) 7. INVESTIGATIONS FOR GALLSTONE DISEASE Plain abdominal X-ray . 18% at 15-20 yrs 7-10% mod. 3-5% severe. . Due to inflammation from a) injection of contrast (increased p) and b) edema when removing stone ii. Endoscopic retrograde cholangiopancreatography (ERCP) .PTC involves a tube being inserted under radiologic guidance into one of the biliary ducts (must be dilated duct) . 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 171 . leakage of bile when tube is removed 6.01% ie 1 in 10000– ERCP slightly higher since it uses side viewing scope) e.2.Mostly for therapeutic rather than diagnostic purposes . Percutaneous transhepatic cholangiography (PTC) /biliary drainage (PTBD) .Complications: bleeding (esp in biliary obs pts due to coagulopathy sec to decreased Vit K abs). Stone removal (using balloon catheter.Will definitely involve cholangiogram . N/V) Also: Cholecystitis. need to assess the benefits and risks. main indications: 1) Diagnostic: high obstruction not well visualised in ERCP. Cholangitis 1-2% d. CT scan . Contrast related reaction (allergy to iodine) rare . resolution is not as good as MRI .Before doing ERCP. duodenum 0. Stenting . Over sedation (hypotension. prev surgery with altered anatomy (eg gastrectomy) 2) Therapeutic: obstructed system that cannot be drained from below. prev post-ERCP pancreatitis. Sphincterotomy (in order to relieve obstruction or facilitate removal of stone) 3. or Dormia basket) 2. cannulation/ injection of pancreatic duct. F.No longer used commonly. Increased risk in: younger.The largest value of ERCP lies in its therapeutic potential 1. Perforation into bile duct. resp depression. Haemorrhage 2-3%: esp sphincterotomy c. sphincter of Oddi dysfunction b. Pancreatitis in 1-3%: i.Comparable to ERCP.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. HIDA scan . Failed ERCP f. 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.High level of complications Overall risk is 10-15% a. and select patients carefully 5.1% (esp if sphincterotomy): (OGD 0. and also minimally invasive preferred to ERCP if patient does not require any therapeutic intervention that ERCP provides 4.Rarely done now. cholecystitis – up to 1 in 3 to 1 in 4 Injury to surroundings: bowel & biliary structures e.up to 5% Due to abnormal anatomy. good results only for cholesterol stones. acute cholecystitis. low fat and cholesterol.Counsel patient about symptoms – biliary colic.Expectant management and close follow-up . (success in 75% who fulfil this criteria) Chemodissolution: LT oral bile acid ursodeoxycholic/ chenodeoxycholic acid (thought to reduce hepatic synthesis of cholesterol and reduce chol secretion) 9 mths intensive followed by lifelong maintenance. <15mm.Non. Bile salt therapy necessary following lithotripsy todissolve gallstone fragments. no/mild symptoms.TREATMENT Asymptomatic . Liver diet: mod carbo.No surgery required unless patient has indications for surgery (see above) . less complications post-operatively Risks of Lap: Conversion to open . large/calcified stones. CI: more than 3 stones. CBD Haemorrhage Infection Spilled bile peritonitis. less pain. Expensive.g. 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. sepsis high risk of 2nd attack) Non-Surgical . iatrogenic injury. difficult or complicated dissection. Cx of gallstones Medical Tx in radiolucent gallstones. mod obesity. high fibre All therapeutic regimens retaining the GB have 50% recurrence of stones aft 5yrs (no LT benefit) 172 .surgical means of stone treatment Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around to dampen waves. obstructive jaundice. non-functioning GB. high cost. Toxicity and S/E.g. Conversion rate is higher if there is ongoing infection e. KUB: Radioopaque gallstones. 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. Low grade fever (chills uncommon). perforation) 3. PFO: PT/PTT. CXR.50% of cultures are sterile (infection occurs eventually.Possibilities available: i. 7. severe RHC pain (less commonly epigastric) Radiates to the inferior angle of the scapula. but inflammation may progress complications. abnormal right hemidiaph/thorax. .Definitive treatment – laparoscopic (better success if within 72hrs of symptom onset) cholecystectomy B) Timing of cholecystectomy . LFT (mild transaminitis)/ UECr (dehydration) 6. interscapular Associated with nausea. including peritonitis. in very sick patients who are not doing well/ not responding to treatment) ii. Exclude lower lobe pneumonia. FBC: leukocytosis (except elderly) – if severe.Gallbladder becomes distended and inflamed . ECG MANAGEMENT A) Conservative - Resuscitate the patient. surgeon etc) . ULTRASOUND FEATURES OF ACUTE CHOLECYSTITIS a) Presence of gallstones in biliary system b) Contracted gallbladder (from chronic gallstone disease) c) Pericholecystic fluid (oedema of gallbladder wall) d) Thickened GB wall e) Sonographic Murphy’s positive 2. 5. vomiting Tachycardia.Dependent on several factors: Severity of illness Response to resuscitation and antibiotic therapy Logistical considerations (availability of OT. Emergency (immediate.Delayed/interval (after 6-8 weeks) 173 .; Murphy’s sign positive (increased rigidity on inspiration) Gallbladder may be palpable (30%) – omentum wrapping around GB. aerobilia (due to fistula).4. if >1000. pancreatitis!). ACUTE CHOLECYSTITIS PATHOPHYSIOLOGY . perf viscus. In elderly. Dehydration RHC tenderness with guarding found on clinical examination. Early (within few days of onset – ideally within 5 days) iii. CT AP Fat stranding around gallbladder not seen on ultrasound but on CT Exclude complications (empyema. Amylase (can be raised mildly. worst case scenario is empyema Jaundice < 10%: due to Mirrizi’s or passage of stones into CBD (15% have CBD stones) INVESTIGATIONS 1.Gallstone gets stuck in the cystic duct causing obstruction of biliary flow . indicates complications 4. non-resolving fever/pain) Cholecysitits usu resolves with medical management (60%). DM cholecystitis) severe with gas-forming organisms causing emphysematous PRESENTATION - Constant. On AXR.Occurs in very ill patients with prolonged stay in ICU – prolonged fasting.Localised perforation abscess that is confined by the omentum (new mass) . requiring urgent surgery 3. Empyema . poor nutrition.Increased risks of post-op infection Disadvantages . Gallstone ileus .Nearly all >60years. Barium follow through .Fibrosis difficulty mobilising gallbladder .Cystic duct obstruction leads to a tense gallbladder filled with mucus (slow distension from continuous mucus secretion) .If >2. length of hosp stay. sigmoid colon . or more commonly under radiologic guidance (percutaneous) . total duration of dz.Higher risk of injuring some other structure due to difficulty in visualisation . Cholecystenteric fistula .5% mortality .Lower risks .Drains the gallbladder and alleviates the inflammation (resolves acute episode) better outcomes .May lead to gallbladder wall necrosis if pressure exceeds capillary bld pressure 2.Better laparoscopic success Disadvantages . cost) Gallstone disease in elderly more severe .Chance of recurrence / acute pancreatitis during the time (20%) Early surgery has been found to be more beneficial ( mortality.Can be done under LA.Stones causing cholecystenteric fistula pass into the enteric lumen causing intermittent bouts of small bowel obstruction . then colon. while dehydration and hypotension leads to formation of viscous bile and gallbladder ischaemia may get infected cholecystitis .Can be followed by cholecystectomy 4-6 wks later COMPLICATIONS OF ACUTE CHOLECYSTITIS 1. Hydrops/ Mucocele .Higher conversion rate to open chole . sepsis .Symptomatic fistulas (malabsorption and steatorrhoea) should be treated with cholecystectomy and fistula closure 5.higher rate of complications . and stomach.Early Advantages .Acute cholecystitis: timely diagnosis.Gallbladder is filled with pus due to bacterial infection of the stagnant bile (cystic duct being obstructed by a stone) .Poor nutrition leads to biliary stasis.Tx: Small bowel enterotomy proximal to the point of obstruction is usually required to remove the stone (Immediate cholecystectomy not warranted as <4% of patients will have further symptoms) PROGNOSIS . labile blood pressure.5cm and migrated into gut impact at terminal ileum (commonest).Treatment involves emergent cholecystectomy / percutaneous cholecystostomy to control acute disease followed by cholecystectomy 174 bile . uncontrolled sepsis with peritonitis and intraabdominal abscess ACALCULOUS CHOLECYSTITIS .Accounts for 1-2% of IO overall .extremely high mortality for emergency cholecystectomy . duod.Easier to operate as the gallbladder is oedematous Delayed Advantages .Free perforation generalised peritonitis and sepsis sudden generalised abdo pain emergency laparotomy 4. mostly in elderly patients in whom gallstone ileus is more common .Causes: 2° cardiovascular pulmonary complications (older). with DM .Patient is usually toxic. early stabilization.Mortality is 10-15%.Ppt: unexplained gradual onset of SB obstruction . Gangrene and perforation – rare due to rich blood supply from hepatic and cystic arteries .Ongoing inflammation higher risk of bleeding . after repeated attacks of cholecystitis .Small stones (<2-3cm) usually pass spontaneously without problems .Need for another admission . aerobilia is seen in 40% of cases .In moribund patients who are not fit for surgery / early surgery is difficult due to extensive inflammation .Most commonly occurs in duodenum.Everything done in one admission .Ix: AXR.Usually asymptomatic . semiurgent cholecystectomy C) Cholecystostomy (fastest way) . chronic cholecystitis/ cholelithiasis Mostly adenocarcinoma.Biliary colic . GALLBLADDER CANCER - - uncommon. Tortuous duct.Stone >25mm.FBC (check TW for any rise suggestive of infection) . Intrahepatic stone.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. bile ducts. not suitable for ERCP) . stomach Treatment: cholecystectomy + liver resection and LN dissection +/. pale stools . increasing in China and North India RF . EUS .If unsure of presence of stone less invasive investigation such as MRCP.chemoRT Palliative: Endoscopic stent to biliary tree and stomach Prognosis: poor (most die by 1 year after surgery) 6.Gallstones in gallbladder . or patients on long-term opiates. post-cholecystectomy. Impacted stone .Amylase (CBD stone may cause pancreatitis) . 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.If infection sets in cholangitis (see below) BLOODS . LOA. vomiting.Dilated CBD (normally <8-9mm) >10mm is abnormal In older patients.LFTs (raised bilirubin – direct.e. obesity. the CBD may be larger. CHOLEDOCHOLITHIASIS PRESENTATION .Gallstone in CBD (50% missed.F:M=2:1.Obstructive jaundice – tea-coloured urine.5. LOW) Mostly incidental histo finding after cholecystectomy Related to gallstones building up (95%) porcelain gallbladder Commonly spreads to liver. Large number of stones.Dual pathology. up to 11-12mm in size MANAGEMENT . ALP raised more than transaminases – also high if LT due to liver damage) ULTRASOUND . small percentage SCC Signs and symptoms Early: mimic gallstone inflammation (RHC pain) Late: biliary and stomach obstruction (jaundice. duodenum. esp in distal CBD) . Previous Bilroth II (unsuitable anatomy for ERCP) 175 . coli. stones to be removed) then treat the cause also .Classically Charcot’s triad: RHC pain.Take bloods for investigations – cultures especially . developing world – parasites (Clonorchis sinensis.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. Investigate for cause . I will like to resuscitate the patient who may be in septic shock”. Enterococcus .Small proportion (elderly.5mg/kg/hr) CVP line insertion if patient has shock unresponsive to fluid resuscitation (keep 10-12mmHg) 2.ultrasound (preferred if suspecting stones) vs CT (for non-stone cause) etc as above 4. choledochocysts.Most common cause is choledocholithiasis (60%). Antibiotics (after blood c/s) .Common causative organisms are gram negative bacteria and anaerobes – Klebsiella.Biliary decompression and definitive treatment can be combined or separate . PSC.infection . foreign body (prev instrumentation).sepsis .Close monitoring of vitals in HD/ICU Hrly para + SpO2 Keep MAP > 65mmHg (or to inform doctors if SBP<100mmHg) Catheterise and watch urine output (hrly urine output) – hepatorenal! (keep >0. biliary enteric anastomosis . Definitive treatment = Cholecystectomy +/.Anticipate rapid deterioration.Definitive treatment dependent on: Medical condition of patient Success of biliary decompression Logistical considerations 176 . Mirrizi’s. biliary). fever. clostridium). Resuscitation – “In view of cholangitis being a surgical emergency.IV ceftriaxone (2g STAT + OM) & metronidazole (500mg STAT + Q8h).Timing usually deferred until 24-48h after admission when pt is stable/improved w Abx Emergency if deteriorating / Abx not improving infection (15%) . CHOLANGITIS PRESENTATION .g.A surgical emergency! (mention in exams!) PATHOLOGY .Obtain good intravenous access and fluid resuscitate as appropriate . E. Ascaris lumbricoides) COMPLICATIONS . imipenem if pt in shock . hemobilia.Inform seniors . Biliary DECOMPRESSION +/.7.Usually results from obstruction to the biliary system with infection of stagnant bile . malignancy (pancreatic. Enterobacter. prev biliary surgery) – anaerobes (bacteriodes.CBDE .coagulopathy (Vit K) MANAGEMENT 1. .Other methods to decompress: percutaneous transhepatic drainage (esp if neoplastic obstruction) operative decompression 5.Reynold’s pentad: Charcot’s triad plus mental obtundation and shock . jaundice (only 50-70% of patients have the classic triad) .definitive treatment . Consider benign strictures (instrumentation).7 – 10 days 3.electrolyte abnormality (dehydration) . Cholecystojejunostomy preferred over Roux-en-Y choledochojejunostomy. there are strictures (since the CBD has been chronically dilated.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 . Flushing out stones 3. Choledochoscopy involves using a scope to visualise the large biliary ducts – cannot image higher ducts.Consider biliary bypass if there are 1. multiple stones.Removal of stones 1. 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) . Cholangiogram involves injection of dye – can image higher ducts 2. the CBD is more than 2cm in diameter. 2. Dredging stones out using balloon catheter or Dormia basket 4. no residual stones. Lithotripsy . thus not as sensitive. 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. or 3. 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. Manual removal with stone-grasping forceps 2. 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. 3. 177 . quite unlikely that it will function normally even after removal of the obstruction) Mostly replaced by endoscopic stenting. if not. but can be used to remove stones visualised in the duct Choice of imaging depends on site of obstruction and the cause . tube should slip out easily..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. no free leak of contrast into peritoneum If all normal release anchoring stitch & exert gentle traction on tube.Cholangiogram or choledochoscopy is performed 1. free flow of contrast into duodenum. 2. and RUQ abdominal pain per year Hx of prev biliary surgery. or recurrent pyogenic cholangitis (RPC). . Clonorchis sinensis) repeated portal bacteraemia cascade of events (biliary stasis.Grades 2-4: open cholecystectomy with CBD exploration 9.Complications of pyogenic cholangitis cirrhosis with portal hypertension cholangiocarcinoma 178 .8. Intrahepatic biliary obstruction. RECURRENT PYOGENIC CHOLANGITIS BACKGROUND Cholangiohepatitis.Defect 33-66% of the CBD diameter Type IV .Obliteration of the cystic duct Types II-IV . or percutaneous biliary drainage procedures.Defect larger than 66% of the CBD diameter MANAGEMENT .Grade 1: attempt laproscopic cholecystectomy .Fistula present Type II .A history of recurrent attacks of cholangitis – typical hx: 1-2 episodes of fevers. endoscopic procedures. into biliary system via bacterial translocation recurrent cholangitis obstruction.Compression effect is not just physical (the stone) but also contributed by the surrounding inflammation . stone formation) deficiency of enzymes calcium bilirubinate pigment stones formation recurrent biliary obstruction Malnutrition recurrent cholangitis HISTORY: .No fistula present Type IA . jaundice.Gallstone in the Hartmann’s pouch compressing the common hepatic resulting in obstructive jaundice . MIRIZZI’S SYNDROME PATHOLOGY . is characterized by: 1.Presence of the cystic duct Type IB .One of the caveats to Courvoisier’s law GRADING Type I . Recurrent bacterial cholangitis 2. PATHOPHYSIOLOGY epithelial damage predispose to seeding of coliforms Helminthic infxn (eg Ascaris lumbricoides.Defect smaller than 33% of the CBD diameter Type III . Intrahepatic pigment stones 3. Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and vitamin K deficiency) Impt to exclude – correct with parenteral Vit K before invasive procedures .Treat current infection .Death occurs in approximately 15-20% of patients over 5-6 years.FBC . 179 .Usual surgical approach includes: Initial biliary decompression – ERCP sphincterotomy / stent placement Definitive biliary drainage procedure – e. TREATMENT PRINCIPLES: .g. dehydration etc Surgical .U/S HBS segmental biliary dilatation hepatolithiasis liver abscesses helps determine choice of supplemental axial imaging techniques.LFT with ALP>ALT. DIFFERENTIALS Primary Sclerosing Cholangitis INVESTIGATIONS For diagnosis For Complications Bloods . Radiology . . .Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present.Blood C/S: bacteremia – results help guide antibiotic choice.g. Dx based on history. Roux-en-Y choledochojejunostomy PROGNOSIS . .CT scan centrally dilated bile ducts with peripheral tapering bile duct stones pyogenic liver abscesses.PHYSICAL EXAMINATION No specific physical findings are evident in RPC. AST .ERCP or PTC – imaging modality of choice for delineating the biliary tree.Management of other complications e.Biliary drainage . Related to chronic cholestasis: Primary sclerosing cholangitis / Ulcerative colitis Parasitic infection – Clonorchis sinensis.ERCP: can obtain brushings for cytology.CA 19-9 >100μl/ml (good sensitivity of 89%. specificity 86%) . malaise Weight loss Hepatomegaly DIAGNOSIS U/S detects biliary dilatation but not useful for ductal lesions. Opisthorchis viverrini Hepatolithiasis Recurrent pyogenic cholangitis . .Instrumentation PRESENTATION - Painless jaundice (painful if there is cholangitis) Acholic stools Pruritus Advanced signs and symptoms: Abdominal pain Fatigue.Surgery is the only chance of long-term cure .Choledochal cyst (20-25% in Type 1) Caroli’s disease = congenital cystic dilatation (multifocal segmental dilatation of large intrahepatic bile ducts) .Bile duct adenoma . Type IV: multicentric or involving confluence and both hepatic ducts ASSOCIATIONS .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 180 . Type IIIA/B: involving common hepatic duct and either right or left hepatic duct iv.Thorotrast exposure (radioactive Xray contrast) .Selective celiac angiography: aid in determination of surgical resectability by identifying tumor involvement with adjacent blood vessels CURATIVE TREATMENT . 2 functions: 1) roadmapping for surgery.Distal 25% .Perihilar 65% (Altemeier-Klatskin tumour) Bismuth classification i. 2) drainage of obstructed system if ERCP cannot drain .PTC: when biliary obstruction from distal end.Intrahepatic/peripheral 10% .Only 25% of tumours are resectable .10. Type II: tumour reaching confluence iii. CHOLANGIOCARCINOMA SITE . less bile leak than PTC .Contrast CT . Type I: below confluence of hepatic ducts ii. Distal 35-45% .Intrahepatic: 35-45% .If after opening up and finding that tumour is not resectable.Perihilar 10-30% (worse prognosis due to early lymphatic spread) PALLIATION . can perform surgical bypass 181 .Endoscopic/percutaneous transhepatic biliary stenting .PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) .Bilateral drainage for hilar cholangiocarcinoma . Nipple changes or discharge more likely benign] 182 .Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts that open separately on the nipple . Internal mammary nodes--20% of drainage from the ipsilateral breast upper and lower inner quadrants About 4 nodes per side. posterior. Drains into supraclavicular and jugular nodes Anatomic/ Surgical division into levels I. medial. Pain (cyclical vs non-cyclical) [ 3. 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.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 .Lymphatic drainage: 1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes 1. PRESENTATION OF BREAST DISEASES 1. ANATOMY OF THE BREAST . and provide structural support to the breast (involvement of these ligaments by malignancy causes dimpling of the overlying skin) . apical 2.The axillary tail pierces the deep fascia and enters the axilla . from the second to the sixth rib . Lump (painful vs painless) 2.12.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. BREAST DISEASES 1. 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. 40-50 nodes in 5 groups: Anterior. lateral. extending up to apex of axilla 2.The base of each breast extends from the lateral border of the sternum to the mid-axillary line. Any changes in the nipple e. STRONGEST RF: Family history of cancers* in paternal (BRCA2) and maternal side (BRCA 1&2). >/= 2 relatives with Breast CA around 50yo *Includes breast. 3.Age at which first child was born (>30 years old) .Has the lump been treated before? RF – to sieve out ppl carrying BrCA gene. 4. 7. first degree relative below the age of 40.Painful or painless? . etc)? .Whether patient breastfed her children. LOW (constitutional) . APPROACH TO A BREAST LUMP DIFFERENTIALS (AGE DEPENDENT) Painless lump Elderly: (post-menopausal) 1. History of lump .g. ID high risk patient (to continue f/u even if lump benign) 2. 2. 5.When & Why was it first noticed? (Pain. .Any other lumps elsewhere – other breast? Axilla? Neck? . and if so.Age of menarche (early <12YO increased risk) . especially before age of 30 (link has been shown) 4. 6.Use of HRT (>1yr) – cumulative risk with duration of therapy and/or Oestrogen based OCP (not proven) ‘Confers protective effect’: .Fever (infective cause) . what is the colour and consistency? . Area of fibroadenosis (nodularity) 1. Exposure to ionising radiation (esp. headache (metastasis) 183 . retraction . for how long 3.Age of menopause if applicable? (>55YO increased risk) .Duration since first noticed – long duration unlikely CA .3. Previous breast disease: a. especially if cancer occurs in: a.can get cyclical pain (swell with the rest of the breast cos it’s breast tissue) 4. Carcinoma Younger: 2. RT for previous breast disease) D.How many full term pregnancies? (nulliparity increased risk) .Single or multiple? – multiple: fibroadenoma / cysts / fibroadenosis.LOA. Cyst 3. ovarian.Any increase in size from first noticed to now? . B. ~10% & advanced) May not be painful if pt has received treatment / some infx. prostate and CRC. Other risk factors for cancer A. fibroadenosis and carcinoma can be painful/ painless. Treated cancer b. Previous biopsy showing atypical ductal hyperplasia or LCIS C.Site of the lump? . in bilateral breasts b. Systemic review .Overlying skin changes noted: Erythema. SOB. Oestrogen exposure history Increased risk: . Lifetime risk in gene carrier – 80%. Cyst. HISTORY 1. Daily Alcohol intake. Fibroadenoma . Painful lump Area of fibroadenosis Cyst Abscess (usually in lactating women) Fat necrosis (minor trauma) Periductal mastitis Galactocoele (lactating women) Carcinoma (rare. self-examination.Bone pain. warmth Dimpling: shortening of Cooper’s ligaments due to tumor pressure? Any general asymmetry of the breasts noticed? Discharge – ind CA invasion .Nipple discharge? If present. check with the patient whether this is the same lump .Expose patient adequately from the waist up with exposure of axillae . erythema. Fixation to underlying muscle – Move lump in 2 perpendicular directions. …………. quadrant by quadrant from centre outwards . or hard) It is NOT FIXED to the SKIN …………. and NON-TENDER.Start with the normal side first! . firm. Then ask patient to press her hands against her hips to contract the pectoralis major muscle.When the lump is located. or irregular and ill-defined) 1. and accentuate any tethering to skin dimpling) 2. then try to move the lump in 2 perpendicular directions.Spinal Tap . (no need to do if already attached to chest wall) .Breast . Ask patient to raise her arms (to see the axilla and underside of breasts. measuring ___X___CM. This Size lump is NOT WARM.Lighting: good .Look for nipple changes (7 D’s): Discolouration Depression (retraction) Destruction Discharge Deviation (Duplication – unlikely) Displacement .Nipple .Ask patient if she can show you the discharge by expressing it herself (NEVER squeeze the nipple yourself!) If patient cannot do it. any obvious skin changes peau d’orange –infiltration of malignant cells into lymphatics causing edema (not compression).Hi: Introduce yourself & ask for permission to examine the breast Always have a chaperone to accompany you if you are male . punch biopsy .Examine the entire breast including the axillary tail .(ask her to contract the pect Tender or non-tender maj)….Manouvres: 1. It is firm in Surface (smooth or nodular/irregular) consistency with a irregularsurface and is NOT FLUCTUANT. is hemispherical with Shape (hemispherical/ oval) poorly defined edges.General appearance .Use one hand to retract and stabilise the breast and palpate with the other . Fixation to the skin – try to pick up the skin above the lump 2.Hepatomegaly .Palpate in a systematic manner e.Characterise the lump: Site (which quadrant) “I feel a lump in the upper outer quadrant of the Right breast. 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.And NOT FIXED to the underlying muscle” Warmth of overlying skin Fluctuance Margins (regular and smooth.PHYSICAL EXAMINATION Preliminaries (HELP) .g.g. puckering any scars of previous operation or procedure e.Lung effusion .Position the patient at 45o or sitting position if a bed is not available Inspection Check list: .Continue to examine carefully for other lumps . Press arms down & lean forward the rest of the breast will flop fwd but not the CA that is attached to underlying muscle Palpation .Ask for any pain before starting to palpate . then ask the chaperone to help / squeeze yourself by milking the breast from outside in (ideally with patient sitting forward) 184 .Patient’s hands relaxed at her sides – look for: any asymmetry in the breast contours. Consistency (soft.SC LN .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 . and apical If any lymph nodes are found to be enlarged. size. slowly.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. note the number of lymph nodes. matted). medial. covering the major groups of nodes: anterior. and systematically. consistency (firm. 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. posterior. hard. tenderness. fluctuant Rubbery Stony hard May be tethered or fixed No 185 Very mobile . lateral. their site. bosselated Irregular Mixed. 5mm macrocalcifications. DDx – prev Bx / Sx to that area.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.Most sensitive of the proven breast imaging modalities (Gold std) .5mm in size) . abscess.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) . D.” All 3 must be concordant for benign to have >99% specificity to r/o malignancy Imaging 1. invasive cancer. Comet sign: enhancing lesion with a tail (directed towards nipple).; (ii) Imaging. done on request to help magnify areas of abnormality or help visualise breast better 80% .Causes: A.Normally. heterogeneous appearance. Indicates early DCIS.Features of Benign microcals: punctate. “tea-cup” appearance (c) Spiculated mass or stellate lesionwith poor outline or comet sign . short-term follow-up suggested (<0.05% risk still present) Category 2: Benign Category 3: Probably benign. B.Additional specialised views: magnification and coned compression. but <35YO in symptomatic women .95% of spiculated masses on mammography are due to malignancy .INVESTIGATIONS “The evaluation of a breast lump is via the TRIPLE ASSESSMENT – (i) Clinical examination. papilloma . satellite lesion) (b) Microcalcifications (<0.Features of malignancy: 1. C.Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance of it being malignant .; and (iii) Histology. closely grouped or arranged in a linear pattern (ductal distribution). D.2% risk) Category 4: Suspicious. >5/mm2 cluster . 3. underlying density . nipple changes . 0. segmental 2. B. more difficult to pick up abnormalities]. radial scar (benign). 2 views are done: craniocaudal (CC) right /Left 70% 70% tumours in lateral quadrant (upper) mediolateral oblique (MLO) captures the tail right/ left 80% tumours in oblique milky way .Sole feature of 33% of cancers detected on mammography . biopsy should be considered (25-74% risk) Category 5: Highly suggestive of malignancy (75-99% risk) Category 6: Known malignancy 186 .Causes: A. etc (d) Architectural distortion (of the contour). Mammography: always cf Prev MMG (alert if any CHANGE) .Usually performed in asymptomatic older women (>35YO) [breast tissue in younger women is denser. fat necrosis. tent sign . pleomorphic microcals. fibrocystic disease.Abnormal features: (a) Neo-density or asymmetric density (look for bilateral synchronous ca. Invasive cancer.If calcifications >0. DCIS. C. But can obtain tissue specimen.Evaluates consistency (solid vs cystic) &margins C.Expensive. Pre screening: Screening in high risk patient (BrAC gene +: yearly MMG and MRI surveillance) 2.Usually used as the 1st investigation in young patients (<35 years old) or pregnant. Suspicion of multifocal or bilateral malignancy (esp ILC) 3. chest wall.Mostly a choice between FNAC and core biopsy FNAC is less invasive. poor resolution. excisional Bx? 187 . does not require any local anaesthetic. Core biopsy is more invasive.Useful for pre-menopausal women with dense breast . But only cells are obtained with no histology cannot differentiate between in-situ cancer and invasive cancer. improper angling may result in puncture of the lung or heart). Irregular edges. larger wound.2. Hypoechoeic shadowing.If triple assessment suggests a benign lump (i. less painful.Used when there is a breast lump: A. do frozen section intraop before proceeding with surgery (recommended). mammotome = vacuum-assisted biopsy device (able to sample larger tissue volumes) MANAGEMENT . Post screening a.Guide procedures e. Taller than it is wide (fir-tree appearance. requires skilled cytopathologist If FNAC shows malignant cells. lactating patients – as mammogram has radiation (small amount). Microcalcification (if large number) 3.Guided by clinical palpation or radiologic guidance[ more accurate.Look for contour. requires local anaesthetic. repeatable. aspiration of cyst B. MRI of the breast . Posterior acoustic shadowing 4.Pitalls: Operator dependent. follow up with physical examination for 1 year (q3-6mths) to ensure the lump is stable or regresses . not the gold standard for screening . can stain for ER/PR status better diagnostic value Should have ‘tissue diagnosis’ if you are subjecting patient to cancer treatment! . more painful. Occult lesions: Axillary LAD but Mammogram & US -ve b.g. not 100%] US guidance Stereotactic guidance (stereotactic mammotome) – stereotactic = Xray from 2 angles. non-standardised techniques. but Good soft tissue definition without radiation (>90% sensitivity) . enhancement. Biopsy. axilla . Pre treatment: When planning for breast conservation surgery 4. washout kinetics (how fast/ whether dye stays) . Problems with Mammogram Localisation of lesion seen in only one mammographic projection Evaluation of a palpable mass with a negative mammogram Evaluation in mammographically-difficult areas e. Post treatment: Assessment of response to neoadjuvant chemotherapy Histology . invasion of fascia) 5.Options available: (a) Fine needle aspiration cytology (b) Core biopsy (Trucut/ mammotome) (c) Incisional biopsy – remove part of lump (usually not done now except Frozen section intra-op) (d) Excisional biopsy – remove entire lump (c) and (d) GA. Destruction of surrounding structures 3. smaller wound (23G needle).e.g.Features of malignancy: 1. risk of complications higher (because biopsy needle is a spring-loaded firing mechanism.If 1 or 2 of 3 aspects suggest malignancy further workup. High central vascularity – Doppler to evaluate BV 6. Unable to detect most microcalcifications . Markedly hypoechoeic with + thick echogenic halo 2.If all 3 concordant for malignancy further staging and treatment . will result in a larger wound (14G needle). Ultrasound .Indications: 1. cheap. drainage of abscess. . more ex as requires tissue processing. all 3 are concordant). If malignancy found.Antibiotics for mastitis/abscess + incision and drainage for abscess . etc 2.Relation to breastfeeding (significant if >1yr after stopping breastfeeding) 3.Intermittent or persistent (persistent is sig) . Is the discharge true? . Discharge for cytology to detect malignant cells 2. Is it troubling the patient? PHYSICAL EXAMINATION (as described above) INVESTIGATION 1. brown. ductoscope & biopsy MANAGEMENT .Conservative management for most other pathologies unless discharge persists and is troubling patient microdochectomy of offending duct 188 .Exclude other conditions may mimick e.Age of the patient (more worrisome in older patient >60) 4.Excision for intraductal papilloma (microdocholectomy. white fluid (milk) Cause Ductal papilloma (benign) Ductal carcinoma Ductal papilloma Duct ectasia (= periductal mastitis) Cyst Ductal carcinoma Duct ectasia Mastitis/abscess Galactorrhoea/lactation HISTORY 1. manage malignancy .Unilateral or bilateral (unilateral more worrisome) . foul-smelling Thin. hookwire locailised excision) – scarring may affect other ducts too . total ductal excision. APPROACH TO NIPPLE DISCHARGE CAUSES Colour of discharge Red or pink (blood + serum) Clear yellow (serous) Green.Spontaneous or only on pressing (spontaneous is sig) . eczema. Is the discharge significant? . Is the discharge worrisome? .4.Nature of discharge (bloody more worrisome) .Discharge from multiple ducts or single duct (single duct more worrisome) . Histology of biopsied lesion if found on imaging 4. Mammography/ US of both breasts to detect any underlying malignancy 3.g. Paget’s. black (cell debris) Purulent. Ductography. Do not distort lobular architecture .Very poor prognosis.Do not invade BM .Tx similar to IDC IDC . Genetic: . bilateral cancer in relative affected) .Li-Fraumeni syndrome involving p53 mutation) 3.10-20% multicentric and/or bilat .No histo features of inflammation . BREAST CANCER EPIDEMIOLOGY . considered malignant .5.early menarche <12YO.Non-palpable. .Family history: maternal & paternal (breast or ovarian cancer.Previous biopsy with atypical ductal hyperplasia or LCIS (7-10X) 5.g.HRT (>5yrs. incidence is half that of the West . reduced when stopped) 4. papillary . .Diffuse invasion of breast parenchyma by ca cells blocking numerous dermal lymphatic spaces .Usually proceed with excision biopsy.Progress to CA within 10 yrs ~30% risk.35% multicentric.) . small increase in risk.Histologically not specialised . seldom detected by mammo as rarely microcal. occult invasive ca in 10-20% .Good prognosis if treated .Gender ratio is about 100-150 female :1 male RISK FACTORS 1.Cells morphologically similar to cells of LCIS: monomorphic.60-80% multicentric and bilateral . tubular.Better prognosis than IDC Inflammatory carcinoma . bland round nuclei . a cell-adhesion molecule) .Most common cancer in females in Singapore: . very uncommon .Age-standardised incidence 55 per 100.000 in 2002. .Similar prognosis to IDC Others Specialised types . nulliparity. detected microcals . colloid (mucinous).Medullary. late childbearing at >30YO.Usually presents with a lump. primary sarcomas). young onset <40 YO.From terminal duct lobular unit (like DCIS) . malignant phyllodes tumour. angiosarcoma.If ca develops. enlarged.Known BRCA1 (on 17q.Cells invade individually into stroma (due to loss of Ecadherin.Previous breast cancer (10X) . will be IDC usually. late menopause >55YO . . and can be further divided into invasive and non-invasive based on invasion of the basement membrane Non-invasive Invasive Ductal DCIS = malignant . Previous breast disease: .Epithelial tumours arise from cells lining the ducts or lobules.Non-epithelial tumours arise from supporting stroma (e. High oestrogen exposure: . especially if in first degree relative. rapidly fatal 189 swelling .1/3 overexpress C-erbB2 Lobular LCIS = RF . Ionising radiation to breast (previous RT) 6.Not premalignant.Cause distortion of lobules. swollen breast w/o palpable mass .From terminal duct lobular unit. Alcohol consumption (daily) PATHOLOGY (WHO classification: epithelial and non-epithelial tumours.5-10% of invasive cancers . occurs >15 years after diagnosis .70-80% of invasive breast cancer . . maternal side) or BRCA2 (both sides).2/3 express ER/PR. ILC .Includes all cancers that cannot be subclassified into a specialised type “no special type” . Age (increases with increasing age with two peaks as mentioned) 2.Presents as erythematous. but a marker for increased risk of invasive disease in both breasts (7-10x increased risk) .Bimodal age distribution: 45-55YO & older (>75YO) .Poorer prognosis than a carcinoma of specialised type .Oral contraceptive usage (pure oestrogen type) . Asymptomatic: detected on mammographic screening .DCIS or early Breast Cancer (BC) (at most with small mobile axillary LNs) .Other lumps in axilla . T3N2 Any T.g. brain. Paget’s with no tumour M stage N1: Mobile ipsilat axillary nodes T1: <2cm T1a – 0. rib inv.Metastatic: bone pain/ #. matted LNs T3 N1 T0N2. discharge. T1N2. abdomen (for liver and adrenal metastasis) – in locally advanced BrCA T stage N stage Tis: Carcinoma in-situ. IIIb) 5 yr Survival Stage I: Stage II: Stage III: Stage IV: 90% 60% 30% 10% (70% in 10 yrs) (40-50%) (20-30%) (<2%) Locally advanced BC 95% with adjuvant Rx 76% with adjuvant Rx 50% with adjuvant Rx 190 Stage IV M1 Advanced BC . adrenals.. fixation (means the mass is not mobile). adrenals) DIAGNOSIS – BY TRIPLE ASSESSMENT (see above) STAGING . eczema .Overlying skin changes e.Local: .g.0 cm T1c – 1. skin and rib involvement) o continue to stage to look for metastasis in advanced BC .5 cm T1b – 0. supraclavicular LNs . LNs. T2N2. T3N0 T0N1.Haematogenous: lungs. SOB (metastases to lung. peau d’orange.1 to 0.SPREAD . internal mammary LNs. .Pain is uncommon. liver. bone. ovaries PRESENTATION .Nipple change: distortion. any N DCIS Early Breast cancer Aaaaa – Stage Xb (e. IIb. underlying ribs and muscle (chest wall) .Constitutional: LOW. LOA . T1N1. deviation. tethering (means mass is still mobile but overlying skin will be indented when moving the lump). destruction. N3 T4.0 to 2. even fungating ulcer .Self-detected lump in the breast (>1/3 of patients) .5 to 1. retraction. T2N1 Stage III *skin. bone.locally advanced BC (matted LNs.Staging Investigations: (i) CXR (for lung metastases.0 cm M1: distant mets N2: Fixed/matted ipsilat axillary nodes N3: N3a – Ipsilat infraclav nodes N3b – Ipsilat int mammary nodes N3c – Ipsilat supraclav nodes T2: 2 to 5 cm T3: >5cm T4: T4a – Chest wall involvmt T4b – Skin involvmt T4c – Both 4a and 4b T4d – Inflammatory ca Stage 0 Stage I Stage II Tis T1N0 T2N0. 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 .Triple assessment can help divide it into: .Local: skin & subcut tissues.Lymphatics: axillary. liver. brain. Tumor factors . but if recurs have poor prognosis Surgery 1. Appropriate tumour size-to-breast ratio (to achieve good cosmetic result) .to predict RECURRENCE rate to decide on the SYSTEMIC TREATMENT 1.Criteria: [Nodal status does not influence decision for WE or SM] 1.Removal of tumour with clear margins. Predictive factors (predict response to a Tx): . Patient factors . TT 2.ER or PR positivity is good – predicts 90% response to treatment with tamoxifen. discuss breast reconstruction 2.Lymphovascular invasion 3. Wide excision (breast-conserving surgery. ± CT. Previously conserved breast 5. HT.Social support 2. lymph node involvement [Major prognostic factor] .Psychological counselling. Only 1 tumour.not about T staging anymore 4.Stage of disease – tumour size. No metastatic disease 3. also means tumour is less undifferentiated p53 mutation NOT for prog purpose. 4% in 5 years) .Age (younger patient higher chance of recurrence.+/. Eradicate micrometastasis a. Mark out the site .C-erbB2/Her-2 positivity indicates more aggressive tumour worse . Patient must agree to post-operative radiotherapy (daily RT in hosp) 6. ± RT Reduces recurrence by 1/3.Grade of tumour . No previous RT to the chest . No CTD –underlying inflammation may get worse c. consent taking.Higher risk in younger patients as cancer tends to be more aggressive 191 . with Slightly higher local recurrence rates (for WEAC: 1% per year. standard of care) . Prevent local recurrence a. not multicentric/ multiple DCIS/ LCIS (multifocal) unless same quadrant 2. TT b. not PREGNANT (the only absolute CI) b. HT.PROGNOSIS Prognostic factors: . CT. RT b. progress of disease) .Comorbidities . while achieving good cosmetic result .Anaesthesia workup and necessary imaging. No CI to RT a. Preparing for operation: . Recurrence score: to identify people who will recur using gene typing THERAPEUTIC OPTIONS Options can be divided into aims of control (with either curative of palliative intent): (a) Locoregional control: Surgery (WEAC vs SMAC) Radiotherapy Systemic control: (size >10mm.ability to tolerate chemo .Results: overall survival at 25 years for WEAC comparable to SMAC. <70YO) Chemotherapy Hormonal therapy Targeted therapy (b) Aim of adjuvant therapy: 1. Axillary clearance . decompression of spinal cord compression. look for the SLN by colour. fungating. radical or extended radical mastectomy) are not performed anymore. false –ve rate of FS ~ 33% if so.does not confer survival benefit . if +ve. unable to breastfeed Options: (i) Prosthesis – 6 wks post-op (ii) Muscle flap from rectus abdominis or latissimus dorsi Complications of surgery Early Late Haemorrhage (POD1) Wound Infection (POD3) Seroma formation (accumulation of serum) in 50% Flap ischemia Cosmetic deformity Complications of Axillary Clearance: .Purpose of removal: NODAL STAGING (for prognostication) .2. 192 .Ind 1. surgical excision of brain metastases 5.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). Send node for frozen section (FS) If -ve do not clear axilla. Simple mastectomy (if any CI to Wide excision) . due to lymphoedema. can be done during breast surgery or at a later time No delay in subsequent treatment and no increase in rates of relapse Cx: abnormal sensation of breast.Sentinel lymph node (SLN) biopsy (SLN) is a new standard of care Only in Early CA (</= 5cm) Principle: the sentinel lymph node. Need to remove nipple (WE cannot give good cosmesis) . similar long term prognosis as WE (Italian trial) . methylene blue) or radioactive isotope (Tc-99 sulphur colloid or colloidal albumin) injected in the area of the breast just before surgery concentrates in the first lymph node (sentinel node) that drains the breast after 5mins During the op.Lymphoedema – RT to axilla is contraindicated with AC as it worsens oedema . dont need to give adjuvant therapy Other forms of mastectomy (modified raical. CI to wide excision 2. being the first lymph node draining the breast.Palliative mastectomy for symptoms (bleeding.Routinely be done in (1) Clinically palpable LN / detected on US (2) BrCA >/= T2 (5cm) .Complications: see below . and overlying skin .If done for DCIS. perform axillary clearance False –ve rate of SLN Bx <5%.Surgery at other sites: Fixation of pathological fractures. then the rest of the axillary nodes should be negative as well o Solitary internal mammary LAD is rare Use of blue dye (isosulphan blue. Breast reconstruction - Safe. Need to clean even minor wounds with antiseptic solution + prophylactic ABx vs staphstrep . is representative of the rest of the axilla. infected tumour) . .Intercostobrachial nerve transection – numbness over inner aspect of arm.Cellulitis – even in minor trauma. if the SLN is negative for tumour cells.Removal of breast tissue. or using a Geiger-Muller counter to detect the node with highest radioactivity.Shoulder stiffness – require physiotherapy . Patient prefers to remove entire breast 3.'toilet mastectomy' . Palliative surgery . re-explore if histology +ve and do AC No difference in axillary recurrence between AC vs SLN biopsy 4. nipple-areolar complex. 3.Lower rates of local recurrence. etc). Palliative .k. musculoskeletal pain. letrozole.Place clip into tumour before neoadjuvant therapy to guide surgery in case tumour “disappears”.Avastin (or bevacizumab. febrile neutropaenia . paclitaxel. pneumonitis.Side effects: 1.Lapatinib (targets Her-1 and Her-2.Anthracyclines and taxanes are the mainstay .Radiotherapy 1.(b) High risk of local recurrence: >/= 5cm OR >/= 4 LN +ve . given in stage III / LABC (LN+ve) & in some early breast cancers depending on stage (see below) .Main purpose: eliminate micrometastasis! 1.1% per year). early or late stage .Regimen consists of 25 to 30 cycles in total. deep vein thrombosis (b) Aromatase inhibitors: Lanastrazole.; operate according to preop staging .20% achieve complete clinical response (cCR) i. pulmonary toxicity. 5-FU) 3. 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 . previous RT.g. hair loss.CI: PHx of CVA/DVT.Main active agents: anthracyclines (e.g. risk of cancers 1 in 2000 in 20yrs 2. menopausal symptoms (hot flushes. targets vascular endothelial growth factor [VEGF] receptor. e.Only suitable for post-menopausal patients as use of these agents will cause overactivity of the HPA axis in premenopausal women .50% reduction in recurrence.Premenopausal patients tend to have better response to chemotherapy than hormonal therapy (vice versa for postmenopausal patients) .Side effects: 1. FAC (5-FU. each over 1/12) . 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 .Bone mets to painful areas / impending fractures Chemotherapy (polyCT with 3 drugs is better. methotrexate. 3. 25% reduction in mortality .Inhibit peripheral conversion of testosterone and androstenedione to oestradiol (still present in post-menopausal women) . exemestase . infra/supraclavicular LN (Axillary LN are tackled during Surgery) . N/V.e. anthracycline.Common regimens: AC (anthracycline. infusion reactions. CMF (cyclophos. . used in advanced cancers) 193 . mouth ulcers. endometrial cancer (0. immunosuppression (main disadvantage pre-op) 2. Adjuvant .Herceptin (trastuzumab) .Fri over 5-6/52 until max dose (no repeat RT for recurrences) .taken daily for 5 years . cyclophosphamide). 4. 2. cyclophosphamide).a. Adjuvant: to decrease local recurrence rate . C-erbB2 receptor (an epidermal growth factor receptor [EGFR] that is overexpressed in 18-20% of cancers) . tumour is no longer palpable further 20% will achieve complete pathological response (cPR) i.e. 2. patient choice .Her-2-neu indicates worse prognosis Herceptin improves prog to normal . skin changes). doxorubicin.Also reduces risk in contralateral breast Selective oestrogen receptor modulators (SERMs): Tamoxifen . 4-6cycles.Brain mets .Helps to reduce load of disease to alleviate symptoms. 1 cycle per day from Mon .g.g. osteoporosis! Targeted therapy . no more tumour cells = good prognosis .Cx: as for CT drug. docetaxel) . immobile patients . used in advanced cancer).(a) Usually done 6/52 after WE .Side effects of Herceptin: 1. 3.Targeted at Breast with or without internal mammary.Cx: radiation injury (e. Palliative .CI: pregnancy.Start 3/52 after surgery. cardiomyopathy & CCF 2.Used in C-erbB2 positive tumours. epirubicin) and the taxanes (e.targets Her-2-neu a. N stage >1 11mm < T < 20mm. Fixation/RT to impending fractures. N2 or N3 (fixed lymph node involvement or supraclavicular node involvement) . Advanced BC palliative intention curative intention 1.Systemic therapy: Neoadjuvant chemo to (1) downstage inoperable tumour (in addition. or WEAC with postop RT .T3 or T4 (tumour >5cm or skin/chest wall involvement). Liver (usually liver failure > obstructive jaundice) FOLLOW-UP . the skin defect will be very large inoperable) . then 2-yrly bilateral mammo for life (previous BC is a strong Risk factor for future Breast cancer) . locally advanced BC 2.MMG: same breast 1yr postop.Systemic therapy is the mainstay of treatment – CT. HT or TT (to prevent worsening of mets) .± 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.Adjuvant therapy Purpose of adjuvant therapy is to destroy systemic micrometastases Likelihood of patient having micromets is deduced from T and N stage (major prognostic factors): Chemo Intermediate No chemo T >20mm. Decompression if cord compression Treat hypercalcemia from mets 2. Bone: RT to painful areas. if high grade chemo Adjuvant therapy: CT if tolerable and/or HT if ER/PR +ve In general: In premenopausal pt chemotherapy + hormonal In postmenopausal pt hormonal + chemotherapy 3. ie does patient still require adj tx) Usually not done if patient has completed the course of chemo during neoadjuvant.e.Minimal locoregional therapy except for palliative purposes (new study shows that removing primary in metastatic BrCA confers survival benefit) . in-situ cancer.Surgical resection dependent on size of tumour and resectability (if tumour is too large. N1 or less (no nodes or non-fixed nodes) .Same Tx as invasive carcinoma: WE vs SM .6-monthly for the next 3 years (i. N=0 T <10mm.3-monthly for first 2 years . early BC.T2 or less (<5cm). Locally advanced breast cancer (stage 3) . N=0 Look at histological grade (minor prognostic factor). 4. 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. Early breast cancer (stage 1 &2) .Distant metastases: treat symptoms and prevent potential problems .CEA and CA15-3 are used in some centres for trending 194 .symptoms + P/E . third to fifth years) . Pleural: drain effusion 4.Locoregional therapy: SMAC. DCIS .TREATMENT BY TUMOUR STAGE Tumour can be divided into 1.Mets specific: 1. Advanced breast cancer (stage 4) . Brain: RT 3.aim for dz control .Yearly for another 5 years (to tenth year) .Sentinel LN biopsy if DCIS not very certain (ie diagnosed on Core biopsy) . Treatment . PAGET’S DISEASE OF THE NIPPLE .Surgical excision 195 . breaking the normal epidermal barrier thus allowing fluid to be extruded onto the nipple .LFT.Causes: .Prognosis of the underlying cancer is not altered by the presence of Paget’s disease of the nipple . 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. may develop into erosions and ulcerations . α-FP.Drugs: Recreational drugs Cimetidine (H2 blockers) Digosin Spironolactone Antimicrobials (Isoniazid.Endocrine disorders: Thyroid disorders Acromegaly Hypogonadism (testicular atrophy.If no palpable mass or mammographic abnormality is detected.TFT.Investigation: . GYNAECOMASTIA .BREAST SCREENING Normal risk.Conservative management .Malignancy: testicular tumours. Klinefelters’ syndrome) . ß-HCG .Punch biopsy of the nipple may be required .Often associated with intraductal carcinoma (DCIS) or invasive carcinoma just beneath the nipple .Chronic liver disease: cirrhosis . ketoconazole) .Treatment should be planned according to the underlying cancer if found .Presents as erythema and eczematous change of the nipple (not the areola) with crusting exudates.Physiological: puberty (maybe painful) . testosterone/ LH .Examination and investigations should be targeted towards detecting an underlying tumour – may find a palpable mass and/or mammographic abnormalities . lymphomas . wide excision is an adequate treatment 7.Malignant cells invade across the epithelial-epidermal junction and enter the epidermis of the nipple. In general. Pharyngeal pouch 8.The posterior triangle is bounded by the posterior border of the sternocleidomastoid anteriorly.13. Sublingual dermoid cyst 5. ANATOMY OF THE NECK . Cervical rib 4. Submental lymph node 2. III. NECK MASSES 1. Submandibular gland mass (see later section on Salivary gland swellings) 4. Plunging ranula (retention cyst of the sublingual) 6. Branchial cyst + fistula 5. Carotid aneurysm 7. Lymph node – along anterior border of sternocleidomastoid (levels II. and the anterior border of the sternocleidomastoid posteriorly .If it moves with swallowing. 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 .Does it move with swallowing – divides the thyroglossal cyst and thyroid nodule from the other causes . Rarely. Thyroglossal cyst 3. compressible structure seen in glass-blowers) Posterior triangle 1. IV) 2.g. enlarged lymph nodes are the most common cause of a lump in the neck. Brachial plexus neuroma/schwannoma 196 . the anterior border of the trapezius posteriorly. the midline anteriorly. bursa Approach: . Laryngocoele (rare.Locations: (i) Midline (ii) Anterior triangle (iii) Posterior triangle . does it move with tongue protrusion – thyroglossal cyst moves with protrusion but a thyroid nodule does not Anterior triangle 1. Thyroid nodule 3.The neck is composed of two triangles on each side – anterior and posterior triangles . Lymph node (mainly) – level V and supraclavicular lymph node groups 2. an air-filled. hyoid pathology e. Cystic hygroma 3. regardless of location MASSES BY LOCATION Midline (5) 1.The anterior triangle is bounded by the lower border of the mandible superiorly. Thyroid nodule in the isthmus 4. Chemodectoma (carotid body tumour) 6. Treatment: . If malignancy occurs. history of trauma to area (may have associated scar). CT) are important especially for cysts on the skull as they can communicate with cerebrospinal fluid.2. Management . . THYROGLOSSAL CYST Epidemiology: Equal in males and females. Complications: 1. XR. Pathology: Cystic expansion of the remnant thyroglossal tract (embryological origin of the thyroid which descends from the foramen caecum on the tongue). Ranulas (frog mouth) can be congenital or acquired after oral trauma. with evidence of adnexal structures such as hair follicles.If complete resection not possible. 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. DERMOID CYST Pathology: Can be congenital or acquired. 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. 4.Imaging investigations (e. . usually on fingers. Histology: Cyst lined by epidermis. Infected with sinus formation and seropurulent discharge (occurs with incision or rupture of cyst) 2. The cyst may also contain thyroid and lymphoid tissue. it is usually a papillary carcinoma (~90%). Typically appears as a blue-grey dome-like swelling beneath the tongue. Occurs mostly in children and adolescents but up to one-third occur in patients older than 20 years. no previous history of mass. Incomplete removal leads to recurrence. 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. often in continuity with assoc sublingual gland (but often difficult due to close association with the lingual nerve and submandibular duct). PLUNGING RANULA Pathology: A pseudocyst associated with the sublingual glands and submandibular ducts. 197 .Complete resection if possible. rounded. Features: Smooth.g.Complete surgical excision of the cyst. 75% are in the midline while 25% are slightly to the left or right. U/S. 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. Usually asymptomatic but may become infected. (i) Congenital – developmental inclusion of epidermis along lines of fusion of skin dermatomes (seen in younger patients. skin-coloured or bluish. cystic lump. Malignant change (carcinoma of the thyroglossal duct) Histology: Cyst with columnar or squamous epithelial lining which may be ciliated. may be fluctuant. Features: Small non-tender mobile subcutaneous lump. sebaceous glands and sweat glands. present since birth). Seen in older patients. Treatment of infection with antibiotics. Management: . . fixation to surrounding structures. Pathology: A branchial cyst is thought to develop because of failure of fusion of the embryonic second and third branchial arches.Fine needle aspiration of the cyst will yield opalescent fluid with cholesterol crystals under microscopy. . usually in young adults in their 20s. .Surgical excision of the cyst where possible. .Smooth firm swelling that is ovoid in shape.May be complicated by recurrent infections – purulent discharge.5.May be fluctuant. 198 .Look for fistula in this area – a branchial fistula will run between tonsillar fossa and the anterior neck. .If fistula present. perform fistulogram to delineate course. usually not transilluminable (due to desquamated epithelial cell contents). It is lined by squamous epithelium. BRANCHIAL CYST/FISTULA Epidemiology: Affects both sexes equally. . passing between the external and internal carotid arteries. . with its long axis running downwards and forwards. Features: .Occurs anterior to the upper or middle third of the sternocleidomastoid muscle.Complications: cyst recurrence. chronic discharging sinus. (perc drainage rarely permanently successful) If fistula/sinus present. inject Bonney’s blue dye into tract prior to surgery to allow accurate surgical excision. . as the diverticulum is still present. o hoarseness. They are usually benign. .Surgical approaches (several available) o Diverticulectomy + cricothyroidotomy (diverticulectomy associated with risk of mediastinitis.Leave it alone if small and asymptomatic . thus malignant nature can only be diagnosed by presence of metastasis). o weight loss . and facilitates resection).Aneurysm can occur at any level but carotid body tumour occurs at the level of the hyoid bone.Patient complains of o halitosis. usually on the left .Main differential is carotid artery aneurysm . the risk of malignancy is 10%. o regurgitation of undigested food with coughing o dysphagia in the neck.Squelching sound on deep palpation . look for (b) signs of Horner’s syndrome.Minimally invasive treatment: endoscopic cricothyroid myotomy .DO NOT PERFORM FNA . 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. Differentials: . 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). Treatment: . involves suspending the lumen of the pouch in the caudal direction so that food and secretions cannot enter the pouch. (c) examine the rest of the peripheral vascular system. due to transmitted pulsation from carotids. with metastasis to local lymph nodes (no histopathological features for malignancy. the risk for malignancy still remains) 199 . CT reveals homogenous mass with intense enhancement following IV contrast administration.Due to close association with carotid arteries. Features . any enlarged ipsilateral lymph nodes are also removed due to the small possibility of malignancy .Occurs in older patients . but locally invasive. (a) listen for bruit.A cystic swelling low down in the anterior triangle.Angiography (gold standard) – shows a hypervascular mass displacing the bifurcation. and undetected synchronous tumours. .Radiotherapy is an effective alternative for patients who are unfit for surgery or whose tumours are too large. Features: .Solid.May be bilateral. 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. diverticular neoplasm (<1%) Diagnosis by barium swallow Treatment . May also show vessel compromise by tumour invasion.Surgical excision with pre-operative embolisation (reduces bleeding and complications.Mass is pulsatile but not expansile. 7.If suspecting aneurysm. lump can be moved side to side but not up and down.Complications: aspiration pneumonia. .CT and/or MRI can be used to delineate tumour anatomy in relation to surrounding structures. dangerous) o Diverticulopexy (done in high risk patients.6. . Investigation: . . fluctuant.Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful) .Surgical excision – partial (to alleviate symptoms) or complete 9. phrenic nerve. single or multiple interconnecting or separate cysts which insinuate themselves widely into the tissues at the root of the neck.Radiological investigations e.g. etc.Fusiform. located in the posterior triangle at the root of the neck . is mobile in plane perpendicular to axis of nerve but not parallel . paraesthesia). usually congenital heart anomalies) .May be Tinnel’s positive – tap on the mass for any paraesthesia occurring in distribution of the nerve . cervical plexus.Classically “brilliantly transilluminable” . brachial plexus.DO NOT PERFORM FNA – excruciatingly painful 200 .May obstruct delivery . CERVICAL RIB Features: . Features: .A large cyst may extend deeply into the retropharyngeal space Complications: .Cystic hygroma seen on prenatal ultrasound in the first trimester suggests chromosomal abnormality (50% of foetuses.Diagnosis by CXR 10.A hard mass in the posterior triangle at the root of the neck . and compressible (usually into another part of the cyst).Usually benign . . swallowing Management: . usually trisomy 21) or other structural abnormalities (33% of foetuses with no chromosomal abnormality.50-65% present at birth. wasting of the small muscles of the hand . NEUROMA/SCHWANNOMA Features: .Compressive problems after delivery – respiratory. gangrene or necrosis of the tips of the fingers o Venous: oedema. CT to delineate extent of cyst .Usually more symptoms than signs as it causes thoracic outlet syndrome (diagram below) . probably formed during coalescence of primitive lymph elements. but occasionally may present later in childhood or adulthood . CYSTIC HYGROMA Pathology: A cystic hygroma is a congenital cystic lymphatic malformation found in the posterior triangle of the neck.Adson’s test can be done – ask patient to extend neck and rotate it towards side of symptoms radial pulse will be diminished.Slow growing tumour arising from peripheral neural structures of the neck e. CXR. vagus nerve. cyanosis o Neurological: complaints of radicular symptoms (pain.g.Symptoms/signs: o Arterial: pallor. occasionally with reproduction of radicular symptoms in the limb .8.cystic swelling that is soft. It consists of thin-walled. cytomegalovirus (infectious mononucleosis). and different structures drain to different groups of nodes: Level Ia – submental Ib – submandibular II – long internal jugular vein from skull base to bifurcation of carotids (includes jugulodigastric nodes) III – along internal jugular vein from carotid bifurcation to omohyoid IV – along internal jugular vein from omohyoid to clavicle Va – Posterior triangle Vb – Supraclavicular VI – Tracheo-oesophageal groove (not palpable) VII – Superior mediastinum Drainage: . Other primary sites (4B’s) Bowel (stomach. Primary . breast. Staphylococcus. No need Abx unless obvious infx) Epstein-Barr virus.11. TB Infective Neoplastic Inflammatory Viral (esp 1-2cm firm LN. etc.lymphoma SLE Kikuchi’s (necrotising lymphadenitis occurring in young females. hypopharynx. bronchus (lung). Lymphoma 3. presenting as painful cervical lymphadenopathy) Sarcoidosis 201 . Cancer (3): SCC. oropharynx. NPC. balls (testicular). Klebsiella (from intraoral pathology e. tonsillitis) Tuberculosis Parasitic Toxoplasma Fungi Actinomycosis Metastatic Head and neck primary Nasopharyngeal carcinoma Oral cavity. thyroid.Thyroid and larynx levels II – VI . Adenocarcinoma 2. HIV Bacteria Streptococcus. Also UL.Oral cavity and oropharynx levels I – III . dental abscess. colon). larynx. CERVICAL LYMPHADENOPATHY There are six levels of lymph nodes in the neck.g.Nasopharynx II – V (usually upper neck – level II and high level V) CAUSES: 1. ultrasound (esp thyroid). Abdomen (if Virchows).HISTORY . ENT.According to FNAC results . supraclavicular. tooth decay. lung malignancy. tonsillitis.Panendoscopy: to look for synchronous tumors as smoking/alc affect squamous cells o Nose – airway: nasolaryngoscopy. along anterior border of sternocleidomastoid. surface: erythema. sulphur granules seen in actinomycosis) “Is there any pain? I am going to feel the lump. other enlarged nodes that are not clinically palpable. inguinal + liver/spleen To complete the examination: .parotid.Consistency – hard. Oesophagus .Age . Breast. arthralgia. posterior triangle.Examination of lymphoreticular system – other lymph node groups. . spleen . liver. loss of weight (chronic infection. shape.Susp lymphoma (3): axilla.Radio: CT.g. skin.Infective/Inflammatory – treat underlying condition 202 . let me know” Palpate from behind. lumps elsewhere o Pain: inflammatory > CA o Growth pattern / rate of growth: last few days = infx / inflammatory / haemorrhage into cyst last few months = CA . and can be used to visualise primary tumour if present . associated symptoms. sexual history for HIV. malaise.Social history: travel and contact history.Upper LN (5) : MOUTH!!.Formal ear.Past medical history – cancer. duration.Full respiratory and abdominal examination especially if supraclavicular lymph node found . .Examination of the thyroid gland .Size. extent. nose. preauricular.g. if any pain. Betel nut . .RF for CA: smoking. B symptoms of lymphoma).Breast examination in female patient INVESTIGATIONS . postauricular. alcohol.Malignant – work up for primary if present (e. discharging sinus (multiple lymph node enlargement with discharging sinuses can be TB or actinomycosis.Constitutional symptoms o Fever. Use pulps of the fingers in a gentle rolling movement. scalp. adenocarcinoma – look for breast.Local symptoms – intra-oral diseases e.Fine needle aspiration o Able to definitively diagnose CA and TB. oral/tongue ulcer. GI tract malignancy) and treat as appropriate . lastly occipital.Fixation to overlying skin or underlying structures Potential drainage sites: . Use of dentures. bronscopy o Mouth – CE junction: OGD MANAGEMENT . o Night sweats.Lateral LN: thyroid . MRI (mainly CA as pre-op w/u) to assess nature of lump. low-grade fever (TB. because LN mets counted as locally advanced dz (still resectable). matted nodes are more suspicious for malignancy . one side at a time – start at submental. myalgia (viral prodrome).The lump itself o onset. o Loss of appetite. salivary glands . throat examination especially looking at the post-nasal space for nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged cervical lymph nodes) .Lower LN: UL. then submandibular. face. thyroid. malignancy) .SITE . (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.Tenderness to palpation . squamous cell carcinoma – look for oral cavity. ORAL SEX PHYSICAL EXAMINATION Inspection . Lungs. TB (contact? Diagnosed? treated or untreated?) . Sandwiched between the posterior border of the ramus of the mandible and the mastoid process . ANATOMY OF THE SUBMANDIBULAR GLAND . half of which drain into the submandibular duct.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. many ducts (other glands have few ducts) 2.Parotid duct (of Stensen) runs 5cm across the masseter (surface marking: along the line joining the intertragic notch to the midpoint of the philtrum). few ducts 203 .Submandibular duct (of Wharton) arises from the superficial part of the gland. (ii) Somatic sensory supply of the gland from auriculotemporal nerve. .Histology: mixed serous and mucous acini. drains into the mouth opposite to the upper second molar tooth . 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.Nerve supply: (i) Parasympathetic secretomotor supply from auriculotemporal nerve carrying postganglionic fibres from the otic ganglion (preganglionic fibres from inferior salivary nucleus).Surrounded by tough fibrous capsule – the parotid sheath (thus mumps is painful as the gland swells within a tight envelope) .14. SALIVARY GLAND SWELLINGS ANATOMY OF THE PAROTID 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 superficial temporal and maxillary arteries) .The deep part of the gland is closely associated with the lingual nerve (with the attached submandibular ganglion) above it.Nerve supply: parasympathetic secretomotor supply from lingual nerve carrying postganglionic fibres from the submandibular ganglion (preganglionic fibres in superior salivary nucleus) . 1. few ducts 3. and the hypoglossal nerve and submandibular duct below it – surgery may injure these nerves . runs forwards deep to mylohyoid and drains into the oral cavity at the sublingual papilla just adjacent to the frenulum . the rest draining directly into the oral cavity Nerve supply is similar to the submandibular gland Histology: almost solely mucous acini. sensory supply of the capsule from the great auricular nerve.Histology: predominantly serous acini. LN involvement 3. Facial nerve involvement 2.Fixation to underlying structures – for parotid. surface. drooling . ask pt to clench the teeth to contract the masseter. associated symptoms e. can palpate the duct along the masseter for stone. fever. For the parotid duct.Palpate the contralateral gland for any swelling . Examination of the duct openings: Using a torch and a tongue depressor. is it precipitated by food ingestion? (suggestive of sialolithiasis) o Intermittent swelling a/w food (inflammatory) . xerophthalmia .History of connective tissue disease e. tenderness.g. Bimanual palpation of the submandibular gland 5.Symptoms of infection e.Fixation to overlying skin .4.g. ask about testicular pain and swelling (orchitis). and lifts the earlobe if large. drooping corner of the mouth. Palpate the gland openings for stones. malaise. (3) visible stone. margins .Any noticed asymmetry of the face – incomplete closure of the eye on one side.Look for scars – parotidectomy scar runs anteriorly to the ear.g. and under the tongue (opening of the submandibular duct) Look for (1) red inflamed opening.g. let me know” Palpate from behind .Look for fistula/sinus . SLE PHYSICAL EXAMINATION Inspect . (2) discharge-purulent. consistency.Palpate for cervical lymphadenopathy Other tests 1. below the earlobe and around posteriorly before looping forward again under the jaw .About the lump: onset. then try to move the gland . rheumatoid arthritis. o submandibular mass is located just under the mandible . cannot eat a piece of biscuit or bread without water).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. duration.Palpate the obviously enlarged gland: .Check for warmth of overlying skin. if considering mumps. 4.Look at the patient’s face for asymmetry (facial nerve palsy) “Is there any pain? I am going to feel the lump. and look for discharge inside the mouth while palpating 2. Facial nerve examination Suspicious features of malignancy: 1. examine opposite the second upper molar tooth (opening of the parotid duct). if any pain. Tonsillar fossa: enlargement of deep lobe of the parotid (in retropharyngeal space) pushes tonsils and archs aside see asymmetry of the arches 3. abdominal pain (pancreatitis) . progress.Does the patient have symptoms of Sjogren: xerostomia (e. APPROACH TO SALIVARY GLAND SWELLINGS HISTORY . Skin involvement: eg Hyperaemic hot skin over lump 1+2+3 = CA until proven otherwise - Pain Fixation to underlying structures or skin Hard consistency Irregular surface or ill-defined border 204 . pain o If pain is present. 80% occur in the submandibular gland (due to its higher mucus and calcium content with a long duct. sebaceous cyst.Cx: sialadenitis.Most submandibular gland stones occur in the duct. purulent discharge from duct opening .g. and even abscess formation worsening of symptoms of pain and redness.Partial obstruction Occasional symptomatic episodes interspersed by asymptomatic periods of days-weeks. and slow flow of the saliva against gravity). Presentation .Other options: Lithotripsy.If sialadenitis present: o Antibiotics– usually to cover Staph and Strept e.FNAC: malign vs benign .80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the floor of the mouth.CT: confirm salivary gland (vs LN) o esp parotid – multiple swelling likely LN (DDx Warthin) 5. application of moist hot towel o Lifestyle changes: activities that exacerbate the pain eg.Sialogram (rarely done as it is invasive and technically demanding. systemic symptoms such as fever. . rapid onset within minutes of starting to eat. avoid sour food (increase salivation) o Massage of the gland.Stones of the salivary gland that may be impacted within the gland itself or in the duct.CT scan (Noncontrast) – can pick up almost all stones when fine cuts are requested . and between the ages of 30 and 60.g. . Augmentin o Refer specialist treatment if symptoms persist for several days. 10% occur in the parotid. Blowing instruments o Analgesia – NSAIDs such as ibuprofen .Stone may be palpable along the duct or at the opening of the duct Investigations .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. and 60% of parotid stones are radio-opaque.) Management .General measures: o Good hydration. while 50% of parotid stones occur in the gland itself. partial gland resection can be performed .pleomorphic adenoma . less for parotid duct stones o If stones cannot be removed via transoral surgery or is intraglandular.Complete obstruction Acute pain & swelling of the gland involved at meal times. SIALOLITHIASIS Epidemiology . sialoendoscopy 205 . chronically enlarged mass in submandibular region . . chills. good oral hygiene. Contraindicated in acute sialadenitis and contrast allergy. CT is better.Plain X-rays can pick up radio-opaque stones . wire basket removal.Usually occurs in males more than females. milking the duct.CAUSES OF SWELLING OF THE PAROTID Parenchymal swelling Neoplasia Stones Infection/ Inflammation Autoimmune Infiltration Systemic disease: bilateral Nonparenchymal swelling Benign . resolves about an hour after the meal. or sialadenitis persists despite antibiotic therapy . lipoma INVESTIGATIONS . . .Surgical removal o Transoral removal of stones for submandibular duct stones (50% can be removed thus). soft diet. 7% sublingual. 3% occur in sublingual glands. total parotidectomy with preservation of the facial nerve (or any way possible as long as margins are sufficient) .Irregular and lobulated surface.Superficial parotidectomy if causing trouble to patient 206 . sparing lingual and hypoglossal nerves WARTHIN’S TUMOUR AKA PAPILLARY CYSTADENOMA LYMPHOMATOSUM / ADENOLYMPHOMA Epidemiology: .Slowly enlarging. of which 80% are benign (80% of the benign tumours are pleomorphic adenomas) . containing mucin. FNAC.Most common benign tumour .85% occur in the parotid gland .Parotid: Superficial parotidectomy for superficial tumour.10% occur in the submandibular. since there is no malignant potential .Cx o Malignant transformation (carcinoma ex pleomorphic) if left for 10-15 years (1-6% risk) o If not completely excised. containing epithelial cells surrounded by loose stroma with islands of chondromyxoid (mesenchymal components). + MRI Treatment – surgical excision (sufficient margin) .10% bilateral (check contralateral side) Diagnosis by clinical. soft to firm cystic fluctuant swelling in parotid tail (inferior) .More common in males than females (4:1) . of which 50% are benign (all benign tumours are pleomorphic adenomas) . but histology shows multiple sites of capsular penetration by tumour cells. texture of cartilage (slightly harder than Warthin’s) .Occurs in older patients (>50 years) .6. if tumour is deep or large.Does not invade or metastasise .Equal sex ratio.Slow-growing.Submandibular: Total gland excision together with adjacent connective tissue.0. and interspersed islands of myoepithelial cells. SALIVARY GLAND TUMOURS Epidemiology: (80% rule for parotid) .Related to cigarette smoking Histology: Consists of cleftlike or cystic spaces lined by two-tiered epithelium. FNA + MRI Treatment . of which 60% are benign (95% pleomorphic adenoma) . occurs in younger patients (<50 years old) Histology: Very heterogeneous appearance.80% occur in the parotid. can recur due to frequent capsular penetration (recurrence rate of 2%) Diagnosis by clinical.15% occur in minor salivary glands. The tumour appears to be encapsulated. 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: .Only occurs in the parotid gland (10% of parotid tumours) . surrounded by a stroma of well-developed lymphoid tissue with germinal centres.Can be left alone if absolutely certain that the entire mass is composed of only Warthin’s tumour cells. painless swelling occurring in the lower pole of the parotid . Features: .Invariably benign with no risk of malignant change . Features: . Superficial parotidectomy only (if sufficient margin) .Radical neck dissection if neck nodes positive . Skin flap necrosis 3. sublingual and minor salivary glands. Division of great auricular nerve loss of sensation over pinna 6. damage to the hypoglossal and/or lingual nerves can occur intraoperatively) 2. Tends to spread along nerves.MALIGNANT TUMOURS Tumor grade Nerve involvement Most common malignancies 1. Increased sweating and redness of facial skin when eating b. Hyperaesthesia of local skin 3. due to reinnervation of divided sympathetic nerves to the facial skin sweat glands by fibres of the secretomotor branch of the auriculotemporal nerve 207 .most common malignant tumour in the parotid. rarely de novo o Worst prognosis of any salivary gland tumour o 30-70% recurrence and metastasis rate TREATMENT OF SALIVARY GLAND CANCERS Parotid: . Wound infection 2. cosmetic problems 2. Wound dimple. 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. Frey’s syndrome (gustatory sweating syndrome / auriculotemporal syndrome) a. 3. Adenoid cystic carcinomas (22%) – most common in the submandibular. Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to the submandibular gland.Radical neck dissection if neck nodes positive . Equal sex ratio. in older patients (usually >60 yrs). can occur in any salivary gland. Trismus (inability to open mouth due to spasm of masseter) Late (more than 30 days) 1.Postoperative radiotherapy If localised in superficial lobe . parasympathetic branches (parotid gland secretion) c.Postoperative radiotherapy COMPLICATIONS OF PAROTIDECTOMY Immediate (within 24 hrs) 1. Salivary fistula 5. 2. Auriculotemp nerve: symp branches (sweat glands of the scalp).Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be grafted with great auricular nerve) . Mucoepidermoid (34%) . Younger patients.+ RT (in higher grade tumor / adenoid cystic – cos may have spread to nerves) Submandibular: .Radical excision of gland with lymphatic clearance of submandibular triangle . Temporary facial weakness (neuropraxia of facial nerve) 4. Malignant pleomorphic adenoma o Usually occurs in pre-existing pleomorphic adenoma. 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.15. THYROID DISEASES 1. External laryngeal nerve – supplies the cricothyroid muscle which controls pitch of voice. Parathyroid glands: 2 superior and 2 inferior glands that lie behind the lateral lobes. they lie in the tracheo-oesophageal groove and are not palpable. runs close to superior thyroid artery. The nerve runs behind the pretracheal fascia and so will not be damaged if the fascia is not breached during operation. a branch of the first part of the subclavian artery). Important to visualise nerve and avoid damaging it! Embryonic origin: Thyroglossal tract from foramen caecum of the tongue (in the midline. Nerves and vessels: Superior thyroid artery (from external carotid) Inferior thyroid artery (from thyrocervical trunk. 3rd and 4th tracheal rings. Level VI lymph nodes – first nodes that a thyroid malignancy spreads to. Strap muscles of the neck lie superficial to the thyroid gland. ANATOMY OF THE THYROID GLAND Structure: 2 lateral lobes joined by an isthmus that lies in front of the 2nd. 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. 208 . duration . amenorrhoea Nervousness. compression (of airway. type I DM. rarely nerve) . lethargy Cold intolerance Dry skin.Cosmesis – is patient bothered by lump? HISTORY-TAKING About the LUMP . hoarseness of voice (benign pathologies almost never compress the recurrent laryngeal nerve) . lymphoma. weight gain.g. frequent bowel movement Tachycardia.Address issues of thyroid function . AD inheritance). rarely pain can occur in anaplastic carcinoma and thyroiditis .g. carbimazole. any complications? . atrial fibrillation Oligomenorrhoea.2. easily irritable.Surgery – what kind of surgery.Cosmetic effects About THYROID FUNCTION Hyperthyroid Weight loss despite increased appetite Heat intolerance Increased sweating Proximal myopathy (Graves’) Diarrhoea. SLE.Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2. difficulty breathing. side effects .History of cancer elsewhere – metastatic disease to thyroid. speech and action. propranolol – for how long. pernicious anaemia (associations with Graves and Hashimoto’s) .Onset (gradual or sudden).History of autoimmune disease e.Look for any complications e.Radioactive iodine treatment – what was the result? Is the patient receiving replacement? . ~5% of papillary cancers About previous TREATMENT for any thyroid disease . APPROACH TO THYROID PROBLEMS 1. depression. Problem with configuration/anatomy (i) Solitary thyroid nodule (most common in exam) (ii) Multinodular goitre (iii) Diffuse enlargement 2.History of thyroid disease – long-standing MNG can progress to lymphoma .Any pain – bleeding into cyst can result in sudden increase in size and pain. papillary cancer is associated with familial polyposis syndromes ask about GI polyps/ca . loss of outer third of eyebrows Muscle fatigue Constipation Bradycardia Menorrhagia Slow thought. ddx includes haemorrhage into necrotic nodule or cyst. subacute thyroiditis) . insomnia Fine tremor Hypothyroid Decreased appetite. dementia Carpal tunnel syndrome symptoms About RISK FACTORS . efficacy. oesophagus.Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth.Follow-up – what investigations done? 209 . 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! .Medications given e. RA. emotional lability. propylthiouracil.Compressive symptoms: difficulty swallowing.g.Occupational history – any exposure to radiation (papillary cancer risk) . THYROID GLAND GREET PATIENT. check thyroid status. INSPECT FROM THE FRONT 1. onycholysis (both seen in Graves’) 3.Lid retraction (can see sclera between upper limbus of iris and upper eyelid) . please stick your tongue out and back in again. mobility (fixed to skin? Fixed to underlying structures?). Check for plethora of face. hard. Ask for pain before palpating! 1. 3. ask patient to swallow) 2. Palpate lymph nodes PALPATE TRACHEA from in front for tracheal deviation. 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. Any skin changes over the mass? 4. Complexion – dry. loss of outer third of eyebrows (hypothyroid) 3. ‘peaches-and-cream’ complexion. Palms up – palmar erythema FACE 1. Check swallowing while palpating to confirm mass moves on swallowing. atrial fibrillation (AF more in toxic MNG than Graves’) 4. A thyroid lump moves only on swallowing.” NB. Now. distended neck veins – may be due to compressive nature of mass (but rarely seen). the opposite hand stabilises the gland. Eyes . 2. Expression – staring. size (discrete nodule or multinodular enlargement or diffuse enlargement?). cystic. PERCUSS – any retrosternal extension? AUSCULTATE – bruit in Graves’ OFFER to do Pemberton’s sign to check for thoracic inlet obstruction. Nails – thyroid acropachy. do not swallow until I tell you to. THYROID STATUS HANDS (get patient to stretch arms out in front of him. palms down) 1. tenderness. Fine postural tremor – accentuate by placing a sheet of paper on the hands 5. consistency (soft. multinodular?). PALPATE FROM BEHIND – one side at a time. apathetic (hypothyroid) 2. Reflexes – slow to relax in hypothyroidism 3. Feel pulse – tachycardia. Characteristics of lump: site (anterior triangle). 6.PHYSICAL EXAMINATION A. a thyroglossal cyst will move on both swallowing & protrusion of the tongue. ask patient about compressive symptoms. Legs for pretibial non-pitting oedema (Graves’ or hypothyroid) 210 .Lid lag (eyelid lags behind eye when patient follows your finger downwards) . 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. B.Chemosis (oedema and erythema of conjunctiva) . Any swelling? Where is it? (if unable to see.Proptosis (look from above patient’s head – eye visible over supraorbital ridge) NEUROMUSCULAR 1. without moving your jaw. 4. Check if mass moves on protruding the tongue – “Please open your jaw slightly. ask about diplopia!) . Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a skin crease)? Sinuses? 3. Check tongue protrusion. Feel palms – warm sweaty palms 2.Ophthalmoplegia (restriction of eye movements.Exophthalmos (sclera between lower limbus and lower eyelid) . Proximal myopathy (Graves’) 2. lethargic. unblinking (hyperthyroid).” 5. Other symptoms of invasion e. BASELINE TUMOUR MARKERS (IF SUSPECTED OR CONFIRMED MALIGNANCY) . RADIO-ISOTOPE SCAN . establish baseline.Easy to perform. not causing any symptoms . FINE NEEDLE ASPIRATION CYTOLOGY .Ultrasound still does not provide as good diagnostic value as FNAC 3.Can be both therapeutic and diagnostic for cyst – chocolate-brown fluid aspirated. Hoarseness (i. dysphagia INVESTIGATIONS 1. round nodule with benign FNAC results.The most important investigation modality! .But not very useful diagnostically 5. APPROACH TO THE SOLITARY THYROID NODULE Prevalence: About 4-8% of population in US have palpable thyroid nodules.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. colloid. but cold nodule: 10-20% malignant . prevalence in Singapore not known.Not routine in thyroid nodular study . medullary.Procedure: inject local anaesthetic in area. detect any abnormal function . feel lump after aspiration to check for resolution . Rapidly enlarging nodule 6. Male gender (thyroid nodules less common in male but more likely to be malignant) 2. Hard. insert 20-22G needle and apply suction while fanning needle in region of nodule.A lump >4cm has a greater risk for malignancy 211 can follow-up and monitor for in size . ENT EXAMINATION OF VOCAL CORDS . Gardner’s syndrome. ULTRASOUND OF THYROID . History of head and neck radiation or thyroiditis 4. stridor. Hurthle cell change in follicular lesion) (iv) Inadequate repeat FNAC . recurrent laryngeal nerve invasion) 8. mets) (iii) Suspicious (follicular. dominant nodule of MNG) (ii) Malignant (papillary. Family history of thyroid cancer (or MEN2.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 . Cyst (simple. Dominant nodule of a multinodular goitre Clinical features suspicious of malignancy: 1.For medullary thyroid cancer: calcitonin.No real diagnostic value 4. Follicular adenoma 3.g. non-functional.90-95% sensitivity and specificity .e. but need to exclude!) 2. CT SCAN OR MRI . haemoptysis.Best to have experienced cytologist on hand to view slides and re-do FNAC if the sample is inadequate 2.Soft. small. single nodule and/or nodules fixed to surrounding structures 7.MRI has same functions as CT but higher cost 7.Uses: (i) Evaluating invasion of surrounding structures (ii) Retrosternal extension (iii) Lymph node involvement . or haemorrhagic) 4.4 possible results: (i) Benign (thyroiditis. Cancer (only 10-20% of nodules is malignant. release suction before pulling out needle. or complex . Cervical lymphadenopathy 9. then fix .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 .For differentiated thyroid cancer: thyroglobulin . cystic. FAP) 5. expel contents onto slide. anaplastic. Differential diagnoses: 1. carcinoembryonic antigen (CEA) 6.3. Age <15yrs or >60yrs (majority of nodules occurs in 3rd to 6th decades – likely benign) 3.Care to be taken with CT as contrast contains iodine and will affect post-op radioactive iodine body scan once given .Hot nodule: only 1% malignant.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 . THYROID FUNCTION TEST . presence of metastases. etc) .Sampling of cervical and mediastinal nodes and modified dissection where positive No good adjuvant therapy Follow-up .Surgical debulking .005U/L Follow-up .Poor prognostic factors (AMES): Age>40.LN involvement in 80% of disease at diagnosis (level VI first) . 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 . 88% in intermediate-risk pts.Polyposis syndromes (FAP.Radioactive iodine at ablative levels to ablate remnant thyroid and any cancer tissue (only for total thyroidectomy) . 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.60-80% aggressive and 30% more indolent Palliative therapy for compressive effects .Significant family history in the familial type – MEN2 (AD.Thyroglobulin as a tumour marker of recurrence .Follicular structures similar to normal thyroid . better prognosis .Papillary architecture with psammoma bodies . 24hr urinary catecholamines .Radioactive iodine scan to detect recurrence.Radiation exposure .Tall cell variant (nuclear features of papillary ca within follicular lesion) behaves like papillary ca. lung. with RT or chemo as appropriate 60-70% 212 .Aggressive resection – total thyroidectomy with level VI node clearance . associated with parathyroid adenoma and phaeochromocytoma – see notes below) .Aggressive growth. and neck dissection if neck nodes are positive . worse prognosis . brain . complete penetrance.LN involvement in 10% (rare) .History of lymphoma or MALT elsewhere .Unilat LN involved in 60-80%.Chemotherapy to shrink tumour .Characteristic Orphan Annie nuclei. stage.Tracheostomy Chemotherapy and/or radiotherapy depending on type of lymphoma Median survival <6mths Dependent on histo. treat surgically.Usually presents as rapidly enlarging goitre with compressive symptoms . considered cured – 5% 5yr recurrence) . lymphatic.Sporadic cases usually solitary. spread via local.LN clearance: tracheo-oesophageal nodes cleared. extra-thyroid invasion.Always exclude MEN2 – serum calcium.Slow-growing tumour .Very good prognosis .Spread by lymphatics . treatment.Total thyroidectomy for the majority . Gardner’s. etc.Distinctive deposits of acellular amyloid material – altered calcitonin collections . nuclear pseudoinclusions .Aggressive growth . liver. . size>4cm (more details on risk stratification below) Treatment Surgical resection . followed by ablation 5yr survival 95% in low-risk pts.Positive family history in 5% . has worse prognosis . 50% in high-risk pts Slightly worse for follicular ca Surgical resection .Small blue round cells that are highly anaplastic – may resemble lymphoma .Hurthle cell variant – worse prognosis .Almost always nonHodgkin’s of B-cell type Clinical features .95% produce calcitonin.History of previous differentiated thyroid ca (30% of anaplastic ca) .30-50% multicentric .Solitary .Multiple metastases probably present at presentation .Check TSH levels . contralat LN in 40% .FNAC may suggest lymphoma but definitive diagnosis requires trucut or excision biopsy .Follicular adenoma is NOT a risk factor . 80% produce CEA . haematological routes .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 <0.High calcitonin – screen for residual or metastatic disease.Iodine deficiency may be associated .Longstanding goitre .For suspicious lesion – hemithyroidectomy with histology.Hashimoto’s thyroiditis (60X increased risk) Pathological features . KIV TT Adjuvant therapy .Familial cases all multicentric.Arise from parafollicular C cells (which produce calcitonin) .Large bulky mass involving neck structures – locally advanced .Haematologic spread to bone.Hemithyroidectomy for selected low-risk patients (see below) .Diagnosis of cancer made on evidence of capsular or vascular invasion by tumour cells (vs follicular adenoma) .4.Thyroxine replacement (not for TSH suppression but to maintain euthyroid state) .Serum calcitonin and CEA six mths after surgery (if normal.Multicentric C-cell hyperplasia may be seen in familial cases . and accessory nerve are resected. 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 .Patients can be divided into three groups: (i) Low risk – low risk patient and low risk disease (i. but usually is similar to that in high risk patients . from the mandible superiorly to the clavicle inferiorly. Size) – rarely used as histological grading is not commonly performed MACIS – Metastasis.5 year survival is also prognosticated by the risk: low risk patients have a survival of 95-98%. if upper aerodigestive tract is opened during surgery with salivary contamination. en-bloc. and if the upper GI tract was opened during the surgery) – infection can result (iv) Wound infection – risk factors: previous irradiation. apply constant pressure all the way to the OT! (vi) Poor healing – usually in irradiated skin. and high risk patients 50% - TOTAL THYROIDECTOMY VERSUS HEMITHYROIDECTOMY Advantages of TT: .e. 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. treatment in intermediate risk patients is tailored to the disease. irradiation resus. Size . Grade (Histological). while high risk patients undergo total thyroidectomy with post-op ablative RAI treatment. Size AGES – Age. 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: .Ability to use radioiodine to detect recurrent disease (normal thyroid picks up iodine better than cancer cells.Modified radical neck (i) Type I: one of the three structures not removed. weakest point is the junction of the trifurcate incision - 213 . of the entire ipsilateral lymphatic structures of the neck. Age. from the infrahyoid muscles medially to the anterior border of the trapezius laterally .Complications of radical neck dissection: (i) Injury to nerves – vagus (vocal cord paralysis). no high risk features) (ii) Intermediate risk – low risk patient with high risk disease.RISK STRATIFICATION: .Risk factors can be divided into patient factors and disease factors - Patient factors: Age – >45 years old is high risk. intermediate risk patients 88%. hypoglossal nerve. Metastases. cervical sympathetic chain (Horner’s).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. Completeness of resection. Extent. sternocleido-mastoid muscle. 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.Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism . Structures not resected: carotid arteries. salivary fistula (v) Carotid blowout – risk factors: infection. brachial plexus.Evidence for microfoci of disease and multicentricity of cancer – removal of the entire thyroid decreases risk of recurrence . 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. 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. Extent.Ability to use adjuvant radioiodine to ablate any residual cancer tissue after surgery . Invasion.Classic radical neck dissection (Crile’s) – internal jugular vein. phrenic nerve .Very low incidence of cancer recurrence in residual thyroid – microfoci probably not clinically significant . vagus nerve. delayed puberty 214 . lips eyelids Other features: Marfanoid habitus.Tumours occur at younger age than sporadic cancers .Autosomal dominant inheritance .g.Tumour usually preceded by asymptomatic stage of endocrine hyperplasia . of which less than 10% are malignant) Parathyroid hyperplasia and hyperparathyroidism (30%) 2. adenomas. insulinoma).Multiple endocrine organs involved. FEATURES: .More aggressive and higher chance of recurrence compared to sporadic type of tumours in the same organs MEN 1 . some have growth hormone-secreting tumours MEN 2 . leading cause of death in MEN 1 patients Pituitary (>30%) – most commonly prolactin-secreting macroadenoma.Gene involved is the tumour suppressor gene MEN1 located on chromosome 11q13 where mutations cause loss of function of the gene . gastrinoma.Multifocal tumours in each organ involved .Two distinct groups of disorders: 1.Autosomal dominant inheritance .2 where activating mutations occur .Gene involved is RET protooncogene at 10q11. MEN 2a (Sipple syndrome) Medullary carcinoma of the thyroid (almost all) Phaeochromocytoma (50%. SCFE. but no hyperparathyroidism Neurocutaneous manifestations: ganglioneuromas on oral mucosa. MEN 2b (William syndrome) Thyroid and adrenal involvement like MEN 2a.Multiple endocrine neoplasia A group of inherited diseases resulting in proliferative lesions (hyperplasia. either synchronously or metachronously .Three P’s: Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands Pancreas (>40%) – aggressive metastatic tumours (e. carcinomas) of multiple endocrine organs. including the isthmus and the pyramidal lobe. 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. Hypothyroidism 2. but not RAI) Types of surgery available: 1. Infection 2. cost. Permanent hypoparathyroidism 4. Cosmesis 5. 10ml of 10% calcium gluconate over 30 minutes if severe Hypocalcaemia may also occur due to “hungry bone syndrome” after thyroidectomy in long-standing thyrotoxicosis LATE (MORE THAN 30 DAYS) 1. by large goitre . bilateral nerve injury for total or subtotal thyroidectomy . Hypoparathyroidism leading to hypocalcaemia .Unilateral nerve injury for hemithyroidectomy.Check serum calcium together with albumin to get corrected calcium! Measured serum calcium + 0. Chvostek’s sign (spasm of the facial muscles on tapping the facial nerve). Hypertrophic scarring or keloid formation – ask patient if he/she has keloids 215 .3. one I and one T) IMMEDIATE (<24HRS) 1. mostly below the strap muscles compression of airway if not released (patient can die!) . Subtotal thyroidectomy . Haemorrhage with haematoma formation . Cannot be treated medically .failed medical therapy or unsuitable for medical tx 2. will require tracheostomy 3. Hoarseness or airway compromise from recurrent laryngeal nerve injury . usually done in MNG 3.Dangerous as it can cause laryngeal spasm and airway compromise . carpopedal spasm. Hyperthyroidism .02 (40 – Albumin) - Replacement: 5mmol/6h if symptoms mild. SURGERY IN BENIGN THYROID DISEASE Indications for surgery: 1.If bilateral nerve palsy resulting in compromised airway. Hyperthyroidism (failed treatment) 3. Child-bearing (not a very strong indication since medical therapy can still be given.Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides . usually for suspicious thyroid nodules 2. Total thyroidectomy – entire gland removed completely.Haematoma forms in the paratracheal region. thus the patient will require life-long thyroid replacement and follow-up problems with compliance.5 . Compression on neighbouring structures 4.Risk of permanent hypoparathyroidism is 1-4% (only in total or subtotal thyroidectomies).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) . difficulty breathing. Trousseau’s sign (carpopedal spasm on inflating BP cuff over arm) .Requires intubation to secure airway INTERMEDIATE (1 DAY TO 1 MTH) 1.Important to check the serum calcium levels post-operatively – POD 1.Ask patient for any symptoms and look for signs of hypocalcaemia – paraesthesia around the mouth.Resection of gland can release large amounts of stored thyroid hormone into bloodstream . Cancer 3.Result of total thyroidectomy is always hypothyroidism.5. inconvenience .Risk of nerve injury is <1% . Tracheomalacia . 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.May result in thyroid storm (see Management of thyroid storm) 4.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?). 10-20% of patients may have temporary Ca2+ .g.Floppiness of trachea resulting from chronic compression e.Cut the subcuticular stitches and also the stitches holding the strap muscles opposed to let the blood drain out 2. Hemithyroidectomy – removal of one lobe of the gland. and mortality. where it changes its name to become the popliteal artery .Refer to diagram – important to know the arrangement of the anterior tibial.The posterior tibial supplies the posterior compartment of the leg and passes posterior to the medial malleolus (surface landmark: one third of the way down a line joining the medial malleolus to the heel) before dividing into medial and lateral plantar arteries to supply the sole of the foot .From lateral to medial: Anterior tibial. .16.The femoral artery then divides into the superficial femoral and the profunda femoris (or deep femoral) arteries about 4cm below the inguinal ligament . ANATOMY OF THE LOWER LIMB ARTERIES . and the posterior tibial will give off the peroneal artery . the medial & lateral circumflex femoral arteries .External iliac artery continues as the femoral artery after crossing the inguinal ligament (surface landmark: the mid-inguinal point i.e. 216 .The superficial femoral runs distally and passes through the adductor hiatus to reach the popliteal fossa. Peroneal.The profunda femoris supplies compartments of the thigh via 2 main branches.The anterior tibial crosses into the anterior compartment of the leg and supplies the muscles there. Posterior tibial PAD is a very powerful predictor of CVD/CAD. midway between the pubic symphysis and the anterior superior iliac spine) .The popliteal artery divides into the anterior tibial artery and the posterior tibial (also called tibioperoneal trunk by some). and then continues as the dorsalis pedis in the foot (surface landmark: one third of the way down a line joining the midpoint of the two malleoli to the cleft between the first and second toes) . PERIPHERAL ARTERIAL DISEASES 1. posterior tibial and peroneal vessels at the trifurcation as you may be asked to read an angiogram of these vessels. Emboli usually cause lower limb ischaemia mostly .2. and hypercoagulable states (notably antiphospholipid syndrome). skin.As blood dissects between the intima and media of the aorta. Dissecting aortic aneurysm . ACUTE LIMB ISCHAEMIA Acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain. but atheroemboli are less likely to cause complete arterial occlusion) . and bone (least sensitive).Most common sites where emboli lodge: Bifurcation of the femoral artery (most common site) Trifurcation of the popliteal artery (next most common site in the lower limb) Aortic bifurcation External and internal iliacs Arm (about 20% of emboli) .After emboli obstructs the vessel. 3. because collaterals have had time to form around the chronically stenosed vessel . 20% to AMI with left ventricular mural thrombus. and this may be in a setting of already narrowed vessel lumen (acute on chronic ischaemia) or in a normal lumen. muscle. ischemic ulcers. The decrease in perfusion is usually due to sudden occlusion of a feeding arterial vessel.Other less common causes of acute thrombosis include the arteritides (usually affecting medium-sized arteries). the tissues affected are nerves (most sensitive).Fracture or dislocations can stretch an artery and cause an intimal tear while the media and adventitia layers are intact (because they contain elastin and can stretch) a thrombus forms at the site of the tear where underlying thrombogenic collagen is exposed . it is considered chronic ischaemia).Less common cause of acute limb ischaemia . Arterial trauma . Arterial embolism . of which 70% is due to atrial fibrillation. 217 . The lower limb can survive about 6 to 8 hours in an ischaemic state before injury becomes irreversible. ergotism. it can cause occlusion of the aortic branches at their origins PATHOPHYSIOLOGY In order of sensitivity to ischaemia. and muscle paralysis as well as skin changes occur later.Most common cause of acute limb ischaemia (60-80% of the time) . thus early signs of ischaemia involve pain and numbness.The most likely source of embolus is the heart (80%). the resulting ischaemia is usually less severe than in an embolic occlusion. Acute thrombosis .Compartment syndrome can result from trauma as well 4. thrombus can propagate distally (due to stasis of blood) and proximally (due to turbulence of incoming blood hitting embolus) by derangements in the Virchow’s triad 2.Non-cardiac emboli arise from other arteries where there are atherosclerotic plaques or an aneurysm (the embolic material may be thrombus or part of a plaque. and a small proportion to prosthetic heart valves .When thrombotic occlusion of a vessel does occur. CAUSES 1.Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel) .Increasing incidence of acute arterial occlusion due to endovascular diagnostic or interventional procedures . and/or gangrene) in patients who present within 2/52 of the acute event (if >2/52.Trauma can cause development of an arteriovenous fistula that shunts blood away from the limb . foot. the toes.Assess skin colour. Pallor.e. while dead muscle will be dull and will not twitch . surrounding areas of pallor are due to vasoconstriction Duskiness: due to deoxygenation of stagnated blood. but still possible .If able to feel one good pulse (PT or DP). does not blanch on pressure) then the limb is non-viable Black: gangrene . if there is fixed staining (i. rarely does it only affect one toe (more in chronic ischaemia) .The disclouration usually affects a large part of the distal limb e.Also feel the pulses on the other limbs – gives a clue as to whether the cause is embolic or thrombotic (see below) Paralysis Initial: heavy limb.Non-cardiac: AAA? Bruit? 218 . prosthetic click .The site of arterial occlusion is usually one joint above the line of demarcation between normal and ischaemic tissue Pulselessness . Pulselessness.Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites in the muscle - P/E Search for sources of embolisation: .If unable to feel. temperature (Perishingly cold). increasing in severity with time Further progress leads to decrease in pain as the nerves die off from ischaemia Important to ask for any previous claudication pain (10% of claudicants can develop acute ischaemia due to thrombosis of the stenosed vessel) Paraesthesia . Late irreversible ischemia: muscle turgidity Total paralysis occurs late and usually indicates that the limb is non-viable Intrinsic foot muscles > Leg muscles (toe mvmts produced by leg muscles detect late) Can assess viability of muscle by making a cut – viable muscle will be shiny and twitches in response to flicking.Other colours: Pale Cyanosis Mottling Fixed cyanosis and mottling Mottling/Marbling (patches of blue on white): deoxygenation of stagnated blood. Perishingly cold Pain - Develops acutely Starts off in a distal part of the extremity and then progresses proximally. but in severe ischaemia it can be marble-white (especially in embolus where there are no collaterals) .Cardiac: AF. Paraesthesia.The limb may still be slightly pink though pale.Progression: Light touch Vibration Proprioception (late) Deep pain Pressure sense Pallor .g. Paralysis.PRESENTATION The classic 6 P’s of acute limb ischaemia: Pain. and capillary refill . quite unlikely that the limb is ischaemic. assess with a handheld Doppler the arterial and venous flow in the limb – there can still be flow without a palpable pulse .Starts off with paraesthesia (develops relatively early in the course of ischaemia) and develops to complete loss of sensation . murmur (MDM). DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE (IMPT AS THE MANAGEMENT IS DIFFERENT) Embolic Thrombotic Identifiable source Present – AF. Patient may require revascularisation to allow lower amputation or help the amputation to heal Severity depends on: . Diffuse atherosclerosis. sharp cut-off. 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.extent of obs: larger lose more collaterals . no emergency to operate.capability of existing collaterals to carry blood around occlusion . few collaterals irregular cut-off. fem=2. of axial arteries (pop=1. well-developed collaterals CLASSIFICATION OF SEVERITY (SVS/ISCVS) Three categories: viable. tib=3) .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 219 Non-viable Variable (anaesthesia) Absent (fixed stain) Complete Complete Inaudible Inaudible Amputation . 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.location of obs relative to no. Follow with IV heparin infusion at 1000 units/hour . CK.Endarterectomy .5 before stopping heparin (pt at risk of further embolic events) discharge patient to anticoagulation clinic for follow-up with warfarin advice 220 .Give IV heparin bolus 3000-5000 units . while thrombolysis is done for thrombotic occlusion. lactic acidosis .Important to start anticoagulation with heparin if the suspicion of acute limb ischaemia is high.Embolectomy . MEASURES TO IMPROVE EXISTING PERFUSION . DOPPLER U/S: viable vs threatened vs non-viable + level of obstruction 2. extremes of temp . Embolectomy . pinpointing the level of occlusion and the anatomy DEFINITIVE TREATMENT OPTIONS Surgical . 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.Fasciotomy .Involves clamping of the involved artery and making an arterotomy . free spontaneous flow from proximal and distal ends of the artery when unclamped) . then balloon is inflated to trawl clot out of the artery .Flush with heparinised saline . 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 . TREAT OTHER ASSOCIATED CONDITIONS (CHF.5 times normal 3.ACUTE MANAGEMENT 1.Ideal PTT is 2 to 2.e. AMI).Primary amputation Endovascular .Avoid pressure to heel. 2. uptitrating dose until INR 2-2.A Fogarty balloon catheter is inserted into artery until distal to the clot.Max tissue oxygenation (O2 supp) .Bypass grafting . to avoid clot propogation . AF) INVESTIGATIONS - Pre-operative investigations FBC. cause – thrombotic or embolic 3.Can be done under LA but still require anaesthetist to monitor patient as he may be quite sick (e.Angioplasty .Post-op: patient monitored in high-dependency.Keep foot dependent . confirming an occlusion.Check foot – warm foot with good pulse indicates reperfusion .Important to monitor ECG for any arrhythmias! .Stenting In general. do cardiac enzymes Biochemical abnormalities (muscle necrosis): K.ANGIOGRAM Can be done in pts with viable limb.Closure of arterotomy with meticulous haemostasis as patient is on heparin . EARLY ANTICOAGULATION . ANALGESIA 4. ing pressure in the compartments of the leg.Need to convert to full warfarin anticoagulation.Thrombolysis .Correct hypotension 5. and hyperkalaemia with cardiac arrhythmia can occur after reperfusion . embolectomy is done for embolic occlusion. U/E/Cr. PT/PTT. look out for reperfusion injury The reperfused muscles become oedematous (due to ROS tt injure cells).Check for forward-bleeding and back-bleeding of the vessel (i.g. GXM CXR and ECG if patient is older than 40 yrs old If suspecting an AMI with mural thrombus. 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 221 3. CHRONIC LIMB ISCHAEMIA Chronic limb ischaemia can be divided into critical and non-critical limb ischaemia, and non-critical ischaemia further subdivided into that which causes symptoms (usually claudication) and that which is asymptomatic. Most common cause is atherosclerosis with gradually developing diffuse stenosis of the peripheral arteries resulting in diminished blood supply to the lower limb (imbalance between supply and demand). Multiple collaterals form to bypass the obstructed vessels as a compensatory mechanism. Progression: CRITICAL LIMB ISCHAEMIA Critical limb ischaemia is defined as decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present more than two weeks after the acute event (the converse of the definition of acute limb ischaemia). FEATURES: 1. Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks +/- Tissue loss (Gangrene or ulcers over the toes or feet) 2. Objective indication of poor vascular supply to the lower limbs (a) Ankle brachial pressure index <0.5 (b) Toe pressure index < 0.3 (c) Toe pressure <30 mmHg, Ankle pressure <55mmHg I. Rest pain - Severe pain in the distal portion of the lower limb (usually toes, foot but may involve more proximal areas if disease is severe) occurring at rest (calf pain without toe pain is not) - Pain is aggravated or precipitated by lifting the limb, relieved by dependency of the limb – many patients sleep with the leg hanging over the side of the bed to relieve the pain - So severe as to disturb sleep at night – blood supply as pt is not in dependent position and decrease BP during sleep - Not easily controllable with analgesia – requires opioids to control pain II. Ischaemic ulcers (most are neuroarteropathic ulcers) - Usually arise from minor traumatic wounds with poor healing - Often painful - Most often occur on the tips of the toes, bunion area, over the metatarsal heads (ball of the foot), lateral malleolus (as opposed to venous ulcers that occur over the medial malleolus) - Usually deep, dry, punctate (unlike venous ulcers that tend to be superficial, moist, diffuse) - May become infected cellulitis / abscess, and spread to involve the underlying bone and joints osteomyelitis, septic arthritis III. Gangrene - Cyanotic, anaesthetic tissue associated with or progressing to necrosis - Occurs when arterial blood supply falls below that which is necessary to meet minimal metabolic requirements - Either dry or wet: DRY – hard, dry texture. Often has a clear demarcation between viable and necrotic tissue. Occurs in patients with atherosclerotic disease. Safe and can be allowed to autoamputate after demarcation with precautions against infection. WET – = infected dry gangrene. Moist, swollen, frequently blistered. Often occurs in diabetics with decreased sensation and unrecognised trauma, requiring an emergency surgical debridement or amputation. 222 NON-CRITICAL LIMB ISCHAEMIA WITH CLAUDICATION Intermittent claudication is defined as a reproducible discomfort of a defined group of muscles that is induced by exercise and relieved with rest. Usually described as the patient as a cramping, aching pain in the muscle group on exertion such as walking, and alleviated on stopping (patient does not have to sit down for pain to go away) – “shop window to shop window”. - Calf claudication Usually affects the superficial femoral near to the adductor hiatus, or the popliteal artery - Foot claudication tibial & peroneal arterial disease, but rarely do patients with claudication due to atherosclerosis get foot pain alone (more common in Buerger’s) - Thigh claudication common femoral artery or aortoiliac disease - LeRiche’s syndrome arises from occlusion of the aortoiliacs, and is composed of a classical tetrad of buttock claudication, impotence in men, absent femoral pulses (and distal pulses), and occasionally presence of aortoiliac bruits. - Determine “claudication distance” – within a short period of time it is usu fairly constant, but can shorten as the disease progresses - Need to differentiate the various causes: vascular vs neurogenic vs musculoskeletal CAUSES OF VASCULAR CLAUDICATION - Mainly an atherosclerotic disease; pain is due to acidosis & buildup of metabolites - Other less common causes: ergot toxicity, Takayasu’s arteritis, Buerger’s disease (thromboangiitis obliterans), vasospasm DDX NEUROGENIC CLAUDICATION!!! Vascular intermittent claudication needs to be differentiated from neurogenic claudication (can also present as pain in the lower limb on exertion) The characteristic of neurogenic claudication is “park bench to park bench” 1. patient has to sit down and flex the spine to relieve the pain (pain results from compression of the cord and spinal nerves in spinal stenosis; extension of the spine further narrows the spinal canal while flexion widens it) 2. “Claudication distance” of neurogenic claudication is more variable 3. Pulses will be absent/diminished in vascular but not in neurogenic claudication 4. Parasthesia is common in neurogenic claudication TAKING A HISTORY OF CHRONIC LIMB ISCHAEMIA 1. Claudication = muscular pain, reproducible, incr on walking/dec w rest - Which part of the lower limb does the pain occur in – depends on level of obstruction - Nature of the pain - Radiation - Severity - Aggravating factors – exertion - Relieving factors – rest (just standing is sufficient) - Associated symptoms e.g. impotence in LeRiche’s - Duration: When did pain first start (>2/52?) - Progress since first noticed until currently (worsening pain, ing areas of lower limb affected, pain on less exertion, rest pain) - Current claudication distance - How has symptoms affected lifestyle e.g. impaired mobility 2. Any rest pain - Site, nature, severity - Aggravating factors – raising the limb - Relieving factors – putting limb in a dependent position - Able to relieve with normal analgesics? Or require opioid analgesia? - How long has rest pain lasted for requiring opioid analgesia (if > 2 wks, considered a feature of critical limb ischaemia) 3. Any ulcer or gangrene in the lower limb? - Ask about onset of ulcer/gangrene - Progress (stable, or increasing in size, getting worse) - If ulcer, any preceding trauma? Ill-fitting shoes? Altered sensation in the foot? Does patient take care to protect foot? Pain? Redness/swelling/warmth in surrounding skin? Purulent/foul-smelling discharge from the ulcer? - If gangrene, is it wet or dry? Redness/swelling/warmth in surrounding skin? Any feeling in the toe involved? Any sensory changes in the other normal toes, foot, limb? - Any systemic signs of infection – fever, chills, rigors, malaise 4. Risk factors (“Arteropath”) - Diabetes mellitus – take a full diabetic history including other complications - Hyperlipidaemia / Heart disease (IHD) / Stroke (CVA) - Smoking (very strong RF; 3-6X risk of claudication, higher than the risk for IHD) - Family history 5. Drug history - Aspirin and statin intake – commonly prescribed for vasculopath - Any allergies to contrast (for angiography) - Ergots 6. Social history - Premorbid function and current function - Social support and home condition (need to climb stairs?) 223 PHYSICAL EXAMINATION Examine the patient’s lower limbs in a warm room, exposed optimally (from the thighs to the feet, wearing underwear). Patient is supine with the bed flat. Look 1. Colour of the lower limb - White (pallor); pink (normal); blue/dusky (cyanosed); mottled 2. Trophic changes - Loss of hair - Dry, shiny skin - Nail changes - Wasting 3. Presence of any diabetic dermopathy 4. Presence of ulcer - Look carefully at the entire lower limb, including the heels (ask pt to flex at the knee) & between the toes - Site of the ulcer Venous ulcers form at the medial malleolus Arterial ulcers are more distal, usually between the toes, and at pressure points such as the lateral malleolus; Neuropathic ulcers form at areas such as the ball of the foot and the heel - Size, shape - Edges (punched out – arterial; sloping – venous) - Base Depth of the ulcer (can see underlying tendon? Down to bone?) Appearance of the base – Necrotic? Granulating (beefy-red)? Sloughy? Any discharge – pus, blood? - Surrounding skin Erythema (cellulitis) – there may be an underlying abscess (confirm on palpation) Blistering, purplish colour (possibility of necrotising fasciitis) 5. Presence of gangrene - Wet (infected) or dry (not infected) - Extent of gangrene (level of demarcation) 6. (If the patient has diabetes, may see deformities – Charcot’s joint) Feel 1. Warmth of the skin - Use the dorsum of the fingers of both hands to simultaneously run up the patient’s feet to the shins and thighs bilaterally - Compare the temperature on both sides (note if one side is cooler) - If one limb feels cool, feel for the level where the skin becomes warm 2. Capillary refill - Press hard on a toe for a few seconds, then release - Normal capillary refill should be 2 seconds or less - If a toe is blue, check for blanchability (fixed staining = dead toe) 3. Palpating the ulcer if present - Any surrounding tenderness (infection) - Bogginess of surrounding tissue (may have abscess formation) - See if any discharge from the ulcer when palpating 4. Pulses – compare both legs. Check regularity of pulses. - Feel the distal pulses and work your way proximally - Posterior tibial pulse: one-third of the way down a line joining the medial malleolus to the heel - Dorsalis pedis pulse: just lateral to the ext hallucis longus tendon/ one third of the way down a line joining the midpoint of the two malleoli to the cleft between the first and second toes - Popliteal pulse: Ask patient to bend the knee ~60-90 degrees, then palpate deeply in the popliteal fossa with the fingers of one hand pressing the fingers of the other. Thumbs on the tibial tuberosity. [If the pulse is very well felt, suspect a popliteal aneurysm] - Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior superior iliac spine (mid-inguinal point), just below the inguinal ligament - Abdominal aorta Grading of pulses: 2+ normal; 1+ diminished (but may be normal for popliteal); negative if not felt 224 Move 1. Buerger’s test - Lift both legs together to compare - Holding the heel of the foot, with the pt’s LL straightened, slowly lift the entire LL, looking at the colour of the toes - Stop when the toes become pale (white) - Estimate the angle the lower limb makes with the horizontal – this is the Buerger’s angle Normal lower limb can be raised to 90 degrees without turning white;; if the Buerger’s angle is less than 30-40 degrees, this indicates critical ischaemia - There may be venous guttering of the lower limb at this angle as well - Hold for 1 min (to induce ischemic environment) - If the patient is lying near the side of the bed, tell the patient that you’re going to put his leg over the edge of the bed before gently abducting the hip and then letting the leg drop over the edge of the bed - Look at the leg for reactive hyperaemia (the leg turns purple-red) – due to ischemic env causing increased acidity and triggering autonomic response Complete the exam - Examine the rest of the pulses Offer to auscultate over the femoral and popliteal arteries for bruits Examine the abdomen for any abdominal aortic aneurysm Measure the ankle-brachial pressure index (ABPI) INVESTIGATIONS 1. Ankle-brachial pressure index - How the ankle-brachial pressure index is done Lie patient supine (so that ankle pulse will not increase sec to dependency) Brachial pressure is measured with a blood pressure cuff around the arm and a Doppler probe at the brachial artery – cuff is inflated until the arterial signal is obliterated, then slowly deflated until the signal just starts being detected, at which the pressure is recorded Ankle pressures are measured in a similar manner, with the cuff around the calf and the Doppler at the dorsalis pedis and posterior tibial arteries – one reading for each artery The ankle pressure to be used for each leg is the higher of the two taken This ankle pressure is then divided by the brachial pressure (the higher of the two brachial pressures for both upper limbs) to get the ankle-brachial pressure index - Interpreting the values Normal ABPI is > 0.9 (can be more than 1.0 as ankle pressures tend to be higher than brachial; ABPI between 0.5 - 0.9 – occlusion, often associated with claudication ABPI <0.5: Critical ischaemia Rest pain if >1.25, suggests non-compressible calcified vessel esp seen in DM patients do Toe pressure index instead (every value minus 0.2) - Accuracy of the index ABPI below 0.9 has 95% sensitivity and 100% specificity for detecting angiogram-positive peripheral arterial disease and is associated with >50% stenosis in one or more major vessels - Exercise treadmill testing Measure ABPI before and after patient exercises on a treadmill If the ABPI falls by >0.2 claudication 2. Arterial Duplex ultrasound - Non-invasive test, good alternative to angiogram - Duplex (means 2 modalities) = 2D ultrasound plus Doppler ultrasound (measures flow and waveforms) - Normal arterial flow waveform should be triphasic (rapid antegrade flow reaching a peak during systole, transient reversal of flow during early diastole, and slow antegrade flow during late diastole.); biphasic & monophasic waves are abnormal - Distal to stenosis: rate of rise is delayed, the amplitude decreased, and the transient flow reversal in early diastole is lost - A twofold increase in peak systolic velocity compared with the velocity in an adjacent segment of the artery usually signifies a stenosis of 50% or more - Can define anatomy of occlusions and also look for relatively good arteries distally for “landing zone” of bypass graft 225 renal disease. angioplasty. then it is a normal angiogram. mainly for aortoiliac disease Monitor claudication distance & ABPI – usually intervene if claudication distance <50m (poor QOL. walk again Keep a walk diary recording daily claudication distance in paces Supervised exercise 3X/wk helps.Monitor regularly with measurement of ABPI Intervention (endovascular or surgical) At least 6 months of conservative treatment first. stenting .Exercise training to stimulate collateral formation symptoms get better Exercise at least half to one hour every day Walk until pain comes.Usually only done if planning intervention e. other cxs of atherosclerosis e.g. almost critical limb ischemia) Confirm disease outline with CT angiogram or angiogram If parameters improve but then plateau. Use of Vasteral (methoxyphylline) is controversial . aspirin] and statins (target lipid levels are much lower) Smoking cessation – not shown to be useful .) or will intervention cause risks (ii) Limb – will patient lose the limb (iii) Lifestyle – is the lifestyle of the patient severely handicapped.Ex. Angiogram (arteriogram) . bleeding from arterial puncture.Patient educaton: Teach patient to go to ED if symptoms of critical ischaemia arises Podiatrist to teach foot care . PT/PTT.g. 2. septic workup: bld c/s. AMI.Preparing for angiogram: Take informed consent from patient Ask about contrast allergy.Invasive and associated with risks of 1. metformin Investigations: FBC (platelets impt).FBC. stroke. . without digital subtraction) 4. Advice to exercise alone does not. Basic laboratory investigation . and the risks of intervention weigh risks against benefits . esp. UECr . PT/PTT. sepsis.g. wound c/s ASSESSMENT OF SEVERITY The three L’s of peripheral arterial disease: (i) Life – does disease threaten life (e.Angiogram with digital subtraction – the images of the underlying bone are removed so as to better visualise the arteries (if the bones are visible. damage to artery with worsening ischaemia . asthma. discuss with patient about whether he can accept the level of symptoms. though may not be as effective in treating the symptoms - 226 . 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.Usually do angioplasty rather than bypass as it is less invasive. foot and calf claudicants .RF control Assessment and treatment to optimise control of CVS risk factors– cardiologist Antiplatelets [e.g.Medications Craxilen and Cilasterzol shown to increase claud dist . dissection 3. rest 2-3 minutes. UECr.3. Dangerous: Gangrene.1. lesion extends for long distance through the vessel and/or no lumen for guide wire to pass through (complete occlusion) Needs a good “landing zone” for graft distally – if vessel is diffusely diseased. Angioplasty only effective for focal stenotic lesions and better for large vessels. New method: subintimal angioplasty – if lumen is so occluded that guide wire cannot pass through. and this space is then angioplastied to create a channel parallel to the actual lumen for blood to flow through 2. Problem with angioplasty is that it is not long-lasting – restenosis can occur 3. constant need to dress wound .Need to revascularise – either angioplasty or bypass grafting (C) AMPUTATION Indications (3 D’s) 1. ascending sepsis 3.Level of amputation depends on vascularity of the limb (palpable pop pulse: BKA) indication (e. otherwise the wound will not heal 227 . Damn nuisance: Non-functional limb. Angioplasty 1.e. need to amputate above level of infection) - As far as possible try to preserve function of the lower limb May require revascularisation interventions before amputation to ensure good healing. difficult to perform bypass (B) TREATMENT OF CRITICAL LIMB ISCHAEMIA . if infected. or to enable lower amputation Do not simply amputate without ensuring good va scular supply to the surgical site. bad smell. pain. Stenting usually not done for lower limbs except in aortoiliacs (since stent needs to be placed in a vessel which is relatively fixed and won’t be kinked/bent by movement) – not true: can even stent foot arteries! 2. Bypass grafting Consider bypass when lesions cannot be treated by angioplasty i.g. Dead: Necrotic tissue 2. the guidewire is threaded into the subintimal space to create a dissection around the occluded segment. while a false aneurysm is a breach in the blood vessel wall leading to an extravascular haematoma that freely communicates with the intravascular space .Obstruction of branches from aorta e. pancreatitis. or ruptured? 228 . vertebral .g. PT/PTT. mesenteric. iliac. may extend to involve common iliac arteries. smoking. 5% are juxtarenal. HPT. and listen for bruits . trauma.Small aneurysms <5cm have a 2-3% chance of rupture per year.True aneurysms are bound by all layers of the blood vessel wall. perforated viscus. ECG & CXR MANAGEMENT Dependent upon clinical context: asymptomatic. UECr. Ehler-Danlos) PATHOLOGY . previous CVA.Check the other arteries – femoral. while aneurysm larger than 5.Local compression on neighbouring structures e.Size: 3 to 15 cm (normal aorta is 2cm in diameter) .Auscultate for bruit over the mass .Also ask for vascular risk factors (DM. pyonephrosis INVESTIGATIONS Imaging: CT AbdoPelvis Other investigations: FBC. AMI . BGIT. hyperlipidemia. hypertension.Pale: ruptured AAA.Often contains mural thrombus due to turbulence and stasis RISK OF RUPTURE . symptomatic.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 .5 cm will have a 10% risk of rupture per year 75% of aneurysms 7cm or larger will rupture in 5 years PRESENTATION .Shape: Usually fusiform – long dilated segment (versus saccular which is spherical) . ureter .Not pale: sepsis. mesenteric bleed . thoracic or both . becomes rapidly hypotensive and goes into shock (Most feared presentation) . AAA risk factors (smoking. etc - DIFFERENTIAL DIAGNOSIS OF UPPER ABDOMINAL PAIN WITH SHOCK .Rupture: intense abdominal pain radiating to the back. infection (mycotic) .Trash feet: distal Thromboembolism gangrene of feet . ruptured spleen in trauma.Asymptomatic (Most commonly. GXM for 4 units.Look at the lower limbs for any gangrene. renal. lung or kidney diseases) PHYSICAL EXAMINATION Ensure vitals stable Visible pulsation over abdomen Pulsations and mass in epigastric region felt on deep palpation Mass is expansile – when fingers of both hands are placed at the edges on either side of the mass. HPT.Location: 95% of cases are infrarenal.17.g. ABDOMINAL AORTIC ANEURYSM EPIDEMIOLOGY More common in men than in women (4:1 ratio) Predominantly in older patients (>60 years old) Other risk factors: smoking. rarely beyond. found incidentally during imaging) . popliteal – for any aneurysm.Other causes: cystic medial degeneration (in Marfan). the fingers are pushed upwards and outwards . strong family history (Marfan. infection. Marfan’s/ Ehler-Danlos) & GA risk factors (any heart.An aneurysm is a localised abnormal dilatation of a blood vessel wall or the heart . IHD). ruptured hepatoma. Most of the patients who reach the ED (about 50% reach ED alive) have a leaking AAA with a tamponade effect by the retroperitoneal structures . Most common complication postoperatively is renal insufficiency – can be reduced by giving frusemide or mannitol preoperatively before anaesthesia induction Non-ruptured AAA .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.Not as good results as open surgery. distal embolism. Aortoenteric fisula – frank PR bleeding.e.Time available for investigation of size of AAA and related anatomy . serious morbidity ~10% Endovascular stenting . Trash foot – embolism of thrombus from the aneurysm 6. can be done under GA .Mortality ~1%. Haemorrhage Late 1. but serious morbidity rate is similar to open repair: 10% . Stroke (due to hypotension or embolism) 3.Very high mortality – nearly 100% if frank rupture (will not get to ED in time) .Involves deployment of a non-porous stent within the aneurysm to form the lumen of the aorta – requires adequate “neck” proximally and good landing site distally . Infection of graft 7. Stabilise patient – resuscitation with fluid and blood products Do not intubate as neuromuscular blocking agents will reduce tamponade effect.Ruptured AAA . tenderness on palpation. Colon ischaemia – occurs in 2-6% 5. Late infection of prosthetic graft material 3. Sexual dysfunction Post operative investigations: FBC: Hb and plt (blood loss and consumptive coagulopathy) UECr: renal insufficiency or contrast nephropathy KUB: check position of stent 229 .Operation is the same except that it is done under elective setting . Call for vascular surgeon 3. need to do an angiogram every 6 months to check position of stent (ensure not migrated) COMPLICATIONS OF SURGERY Intraoperative/early 1. may feel a pulsatile mass in the abdomen 1. the surrounding haematoma and mural thrombus within the AAA are cleared out Synthetic graft (Dacron – polytetrafluoroethylene) is placed within the aorta and the vessel wall closed up over the graft i.Patient’s fitness for surgery needs to be properly assessed because it is a major operation – need to optimise CVS function . worsening haemorrhage 2.Indications for surgery: (a) Aneurysm > 5. Bring to OT for open repair – quickly isolate the aorta and clamp it proximally can be clamped for about 30 minutes without significant visceral ischaemia AAA is incised. the graft forms the lumen of the aorta o Mortality rate of repair operation in this setting is about 50% 4. Renal insufficiency 4.High suspicion in unstable hypotensive patient complaining of severe sharp pain radiating to the back.Mortality is <5% in the elective setting. ruptured/leaking aneurysm . Acute myocardial infarction – most patients already have atherosclerotic disease of coronary vessels and are at risk of AMI (responsible for 50-60% of mortality) 2. torrential 2. Spinal cord ischaemia (quite uncommon) 8.An alternative to open repair which is less invasive. Course of the great saphenous vein: Arises from the medial end of the dorsal venous arch of the foot Passes anterior to the medial malleolus Runs up the leg posteriorly to pass behind the medial surface of the knee Then runs anteriorly and laterally up the thigh Pierces the cribriform fascia at the saphenofemoral junction to drain into the femoral vein 230 . the great saphenous vein and the small saphenous vein . popliteal vein. PERIPHERAL VENOUS DISEASES 1.18.The superficial venous system is composed of two major veins.g. femoral vein .The deep venous system is composed of veins corresponding to the arterial supply e.The venous drainage of the lower limb is divided into a deep venous system and a superficial venous system separated by the deep fascia of the lower limb . anterior and posterior tibial veins. ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB . The superficial system and the deep system communicate through communicating veins that contain valves which allow only one-way flow of blood from the superficial vein into the deep vein (Foot perforators allow bi-directional flow directed by muscle movements) .Locations of the communicating veins: a. Boyd’s perforator: knee e. 10. squeezing the blood into the popliteal vein and back to the heart (The deep veins have many valves to prevent backflow. Dodd’s perforator: distal thigh d.5 cm below and lateral to the pubic tubercle [HDB] b.Physiology of venous drainage: Main mechanism is the calf muscle pump: Contraction of the calf muscles compresses large venous sinuses in the muscles.Course of the small saphenous vein: Arises from the lateral end of the dorsal venous arch of the foot Passes posterior to the lateral malleolus Runs up the midline of the calf Pierces the deep fascia over the popliteal fossa to drain into the popliteal vein . and 15 cm above the medial malleolus . the intramuscular veins open and suck blood in from the superficial system through the communicating veins. Hunterian perforator: mid-thigh c. so blood only flows towards the heart) During calf muscle relaxation. Saphenofemoral junction (great saphenous drains into femoral vein): located 2.. Calf perforators: at 5. thus draining the superficial veins 231 . telangiectasias are classified as type I veins. enlarges. Oedema – pitting: The hallmark of CVI. scaling. nocturnal leg cramps. reticular veins are considered type III veins. varicose veins 3. Obstruction to venous flow e. inguinal lymph nodes are enlarged SYMPTOMS 1. 4. 2. Venous ulcer formation - Typical location is over the medial malleolus Shallow. base may be sloughy or granulating. itch (40%) 7. asymptomatic 2.2. edge becomes thickened or raised. dilated tortuous superficial veins. CHRONIC VENOUS INSUFFICIENCY Chronic venous insufficiency develops when there is venous hypertension. unlike the saphenous veins. with erosions and crusting Lipodermatosclerosis (fats and skin hardening) – a fibrosing panniculitis of the subcutaneous tissue that results in a firm area of tender. heaviness. (b) Reticular veins (slightly larger intermediate veins) also known as blue veins and intradermal varices. shooting 5. hyperpigmented skin that is fixed to subcutaneous tissue. Skin changes[5] (a) (b) (c) (d) Hyperpigmentation over medial lower third of the leg (gaiter area) – extravasation with haemosiderin deposits Atrophie blanche – hypopigmented scars of healed venous ulcers (avascular and fibrotic skin) Venous stasis eczema – pruritic. Results from severe venous hypertension hemosiderin deposits at fats inflammation chronic inflammation Starts in the gaiter area and extends circumferentially to surround the leg If severe can result in an “inverted champagne bottle” appearance of the leg with brawny oedema above and below the area of lipodermatosclerosis (e) Cellulitis 4. non-specific pain: aching discomfort. (c) Varicosities (visible. Failure of the “venous pump” – dependent on adequate muscle contraction (stroke. formed by main tributaries of the saphenous veins because these do not have a strong coat of smooth muscle in their walls. Venous dilatations[4] (a) Telangiectasias (spider veins or venous stars – intradermal veins) 15 % of men and 25 % of women in the general population. which can result from: 1.g. bursting pain upon standing. they are more superficial and not bound down to the deep fascia) Trunk varicosities – along main trunk of LSV/SSV. dull. flat ulcer with sloping edges. (d) Corona phlebectactica (a network of small dilated venules beneath the lateral and/or medial malleolus with severe venous hypertension) 2. deep vein thrombosis 2. muscular weakness can cause failure) as well as competent venous valves MANIFESTATIONS OF CHRONIC VENOUS INSUFFICIENCY: [4] 1. becomes painful 3.In the classification of veins. 4. pregnancy. weeping. leg fullness / swelling 3. In the classification of veins. usually quite moist-looking Surrounding skin will show signs of CVI In long-standing ulcer SCC can develop (Marjolin’s ulcer) – If ulcer 1. 5. 232 . tumour compression in the pelvis. Dysfunction of venous valves e. present in all but the earliest stages Unilateral oedema worsened by dependency (worse at the end of the day) and better with recumbency 3. malodorous. 6.g. Spider veins are amenable to laser therapy and sclerotherapy. 2.Family history: 1 parent (50% risk. hyperpigmentation. family history 233 . 50% 1 parent. swelling.cancer 2. ulceration +/. bleeding. pelvic masses – compress on deep veins PATHOPHYSIOLOGY . both parents (up to 80% risk) HISTORY Asymptomatic Symptomatic: local (non specific pain. commonly mistaken as cellulitis) 3. chemical rather than infective. obstetrics history.Inherent weakness in the vein wall.Parity . chronic cough. 4. VARICOSE VEINS Varicose veins are dilated. proximal venous obstruction.Posture – crossing legs all the time . 4. Primary varicose veins: cause is unknown (may be related to posture and components and structure of the vein wall) GENETIC! (20% risk in gen pop. 6.CEAP CLASSIFICATION OF CHRONIC VENOUS INSUFFICIENCY 3.Weight . 80% both parents) Secondary varicose veins: 1.Increased abdominal pressure – constipation. heavy legs) Complications : 1. 5. thrombophlebitis (= thrombosis inflammation. increase in flow and pressure caused by an arteriovenous fistula. itching.Occupation – requiring long periods of standing . infection (due to dependent oedema) Risk factors: Ask for Past history of DVT & thrombophlebitis.in already predisposed people . destruction of the valves by thrombosis (DVT most common secondary cause). tortuous veins of the superficial venous system (secondary to incompetent leg valves resulting in reflux). leading to dilation and separation of valve cusps so they become incompetent . 3.This may be aggravated by obstruction to venous return (as above) RISK FACTORS (NOT CAUSES!) . etc . eczema.Age . Palpate the inguinal region for a saphena varix (compressible lump that refills when released) 4.If varicosities do not fill up. the SFJ is the site of incompetence.Repeat the test. Percussion (tap test) – test for valvular incompetence (not a very valuable test) – Ensure good distance between both hands first.Oedema .Get the patient to stand while holding the SFJ occluded . placing the tourniquet at different sites: (i) Mid thigh (just below the Hunterian perforator) (ii) Below the knee (iii) Mid-calf . there are other sites of incompetence (the SFJ may or may not be incompetent) PERTHES’ TEST (Test of deep venous obstruction) .If veins below the tourniquet are dilated when pt stands up.Venous ulcers from pressure necrosis from insude 2. feel thrill on top) 6. Look at the inguinal region for any saphena varix Palpate 1.EXAMINATION Examine patient STANDING with adequate exposure of the lower limbs Inspection (look all around the limb!) 1.5 cm below and lateral to the pubic tubercle) 5. warn patient that ankle/calf pain may not go away after surgery as the pain may not be directly from the veins) 2.8) 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.The SFJ is occluded (landmark is 2. 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 . to cover valves in between.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 234 .5 cm below and lateral to the pubic tubercle) with the patient lying down . Feel any dilated varicosities: Direct tenderness that can account for patient’s pain symptoms (if patient’s varicosities are not tender.Skin changes. Feel the peripheral pulses!!! of Lower limb to exclude any ischaemia as the management will involve compression of limbs (ABI >0. 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 . Do the cough test to feel for reflux at the saphenofemoral junction (2.Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe and then relax . stasis eczema.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 . v tight) . then the incompetent perforator is below level of the tourniquet . Look at course of great saphenous vein and short saphenous vein for varicosities 3. Palpate along the course of the saphenous veins and their tributaries to feel any varicosities and for tenderness (may be more palpable especially in fat legs) 3. if they fill up. Positive if the distal hand can feel the wave of blood flowing retrogradely after tapping the proximal varicosities (normal: tap bottom. lipodermatosclerosis (feels like leather.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. Presence of signs of chronic venous insufficiency (as above) . Skin manifestations of CVI: Venous eczema. Therefore. 3. 4. like painkillers) Surgical – the only definitive treatment Indications: 1. can opt for selective stripping.If due to job. Complications – signs of chronic venous insufficiency. and stab avulsion of varicosities 2. Daflon (only symptomatic.5s indicates reflux of blood i. discomfort 3.Examine the abdomen for any mass that may be causing the varicosities Use of a handheld Doppler probe to detect incompetence 1. 235 . 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. change job or ask for change to position to stand & walking less 2. 2. Available modalities: 1. Complications of CVI: History of superficial thromobophlebitis 3. (b) perforator. (slow healing ulcers that are not infected can still operate as it may improve the ulcer) 2. Lifestyle changes . Cosmesis – large unsightly varicosities 2. Symptoms – pain. Medications e. 4. DVT: can rescan after medical treatment.Exclude presence of deep vein thrombosis – stripping is contraindicated MANAGEMENT Conservative 1. INVESTIGATIONS Venous duplex ultrasound . Ultrasound-guided foam sclerotherapy 3. venous ulceration Contraindications: 1. Recurrent varicose veins 2. Endovenous laser therapy (burns vein from within) 20% recurrence: due to large number of perforators left over even after stripping. 3. Everyone with varicosities to exclude subclinical DVT .g. Lipodermatosclerosis.Can delineate deep and superficial venous systems and locate sites of incompetence . usually grade II ensure good pulses 3.e.Decrease amount of time spent standing . Haemosiderin staining. Venous ulceration .Auscultate over the varicosities for any bruit (indicate arteriovenous malformation) .Ask for (a) SFJ and SPJ reflux.Completing the examination . If DVT resolves. Thrombotic tendencies: patient may dev DVT in the future. Infected ulcers. Graduated compression stockings. High tie with great saphenous vein stripping. deep venous incompetency (c) DVT screen . you may be getting signals from the deep perforators instead. 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.Indications: 1. 2. Biopsy if cannot exclude malignant transformation (Marjolin’s ulcer) MANAGEMENT Conservative 1. Lifestyle (a) Warn patient to avoid trauma to affected area (b) Encourage rest and elevate leg Surgical If ulcer fails to heal: . Muscle pump failure – stroke.Swabs of the ulcer for Gram stain and cultures . neuromuscular disease INVESTIGATIONS 1. Exclude infection of the ulcer and other complications . exclude malignancy or other causes of ulcer (biopsy) . 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.Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue . 4 layer compression stockings (change 2X/week if ulcer.g. Check for peripheral arterial disease by doing ABPI 4. Antibiotics if infected 5. 1X/wk if no ulcer) (a) Non-adherent wound dressing over ulcer (e. Venous duplex to map out venous system 3. 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. deep vein reflux (post-DVT) 3.Venous surgery for the underlying pathology 236 . Obstruction to venous flow – thrombosis 2.First.4. Incompetent valves – varicose veins. compression stockings should be fitted and continued for life 3. Stockings: Once healed (cannot use with ulcer/wound). VENOUS ULCERS CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY 1.FBC for raised total white count . bone involvement 2. Symptomatic: Analgesia 4.X-ray of the area to exclude underlying gas. 237 . prostate. bladder (TCC).Bladder outflow obstruction (e.End – bladder neck or prostate .DDx: haemoglobinuria.Beginning – urethra distal to UG diaphragm . meds causing discoloration (eg rifampicin.Clots .UTI .Hydronephrosis . 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. UROLOGICAL DISEASES 1.Infections – malaria. Severity .Drugs .Renal cysts .S/S of anemia 238 . RCC.Bleeding diathesis . schistosomiasis .Malignancy – TCC. . pseudohaematuria (menstruation).>3 RBC / hpf.g.Tumour .Exercise (jogger’s hematuria) 3. APPROACH TO HAEMATURIA DEFINITION: .19.GN . strictures) Painless . Which part of urine stream is blood stained? .ITP / HSP .Throughout – upper urinary tract or upper bladder 2. bladder. urethra – eg schistosomiasis. BPH. urethra Nephrolithiasis HISTORY Post-renal Causes 1.Pyelonephritis . metastatic Pyelonephritis Renal cysts Infxns of ureter. myoglobinuria. Prostate . Painful vs painless haematuria Painful .Ureteric stone / clot . prostate. 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. TB etc Cancers of ureter. dissecting aneurysms. oliguria. arthralgia. UTI (women & children).DDx: nephrolithiasis (colicky). vasculitis Post-strep / post-infective GN IgA nephropathy Drug causes. etc) 5.Carcinoma in situ (imaging cannot see) 4. travel and contact history 2. urethral discharge Pre-renal & Renal Causes 6. Sickle cell. Urine cytology for malignant cells . Check patient’s vitals. Drug history / Hx of radiation 7.Elevated WBC (pyuria is >5 WBC per hpf). rash.Post-strep/infective GN. oedema Sore throat. sickle cell disease.RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source. Family history – PKD. Abdomen – renal/bladder mass. Other urological symptoms . bleeding diathesis.Causes of false-positive for blood: haemoglobinuria. incomplete emptying etc . Frequency + dysuria + haematuria . radiotherapy Schistosomiasis. metabolic (alkaptonuria. Associated fever – pyelonephritis. while isomorphic RBCs suggest postrenal source (ureter.Voiding problem – strangury. malaria 7. liver function 5. IgA nephropathy 3. Digital rectal examination – prostate enlargement (BPH versus cancer) INVESTIGATIONS URINE 1. Malignancy . malignancy. URTI Ongoing URTI or GE Iatrogenic Travel history PMHx Family history Malignancies. Infection . systemic illnesses Autoimmune causes. Urine culture and sensitivity 239 . EC <5) . oedema 4.g. Urine dipstick . organisms . Autoimmune . incontinence . HPT. skin infxns. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension of tumour into renal vein. bladder outflow obstruction (men e.Casts nephritis infection 3. neuro deficits. renal dzes (eg Alport syndrome – ask for deafness). dribbling.Fever. joint pain.useful for: . blocking the testicular vein where it drains into the left renal vein) 5.Storage problem – frequency.Others – polyuria. Screen for pre-renal causes LOW / bone pain / sickness Rash.Fever. renal dz. drugs (rifampicin). HTN. sickle cell dz PKD. myalgia. External genitalia – blood from urethra 6. bladder. Sorethroat . urgency. TB. hesitancy. HPT PHYSICAL EXAMINATION 1. BPH – vascular prostate may bleed) 5.stable? 2. urolithiasis Other necessary history 1. UFEME (normal (all below 5): RBC 3-5. beetroot.LOW. systemic dz (DM HPT Bleeding sickle cell) 6. palpable bladder (clot causing retention) 4. porphyria) 2. Conjunctival pallor 3. bone pain. PMHx . diabetic nephropathy.Renal dz. arthritis. WBC 2-5. nocturia. malaria Renal disease.4. Urine phase contrast .High grade urothelial carcinoma (LG hardly shed cells) . fever. SOB.Confirm presence of red blood cells . Intravenous contrast used to delineate anatomy of the kidneys and urinary system . Stones (filling defect.How low is the Hb? . Intravenous urogram (IVU) .Margins: Superiorly needs to be above upper pole of the right kidney (T12). Filling defect in bladder due to TCC 6. inferiorly needs to show pubic symphysis . any hydroureter. any filling defects (v) Release film (abdominal binder which was placed to slow the flow of contrast into the bladder is released) – shows ureters. GXM!!! IMAGING (HEMATURIA – IMAGE ENTIRE URINARY SYSTEM) Upper tract: imaging. 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. may have specks of calcification 2. electrolytes and creatinine . outline (iv) Pyelogram phase (3-5 min) – contrast fills calyces & pelvis. Contrast UPTAKE: present or not (no contrast in obstruction / non-functioning).Presence of any hydronephrosis.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. lower tract: cystoscopy 10. abnormal appearance of the bladder (fir-tree appearance in neurogenic bladder) (vii) Post-micturition – any residual urine in bladder after voiding . proximal dilatation. Ultrasound of the kidneys .BLOOD 6. hydroureters . CT urogram / IVP .Renal size .Disadv: Radiation ++ (3 CT scans) 14.any filling defects. Cystoscopy .Any renal impairment and electrolyte abn (renal or pre-renal dz more likely) 8. Distortion of renal OUTLINE and pelvic calyces by RCC.Look for 1. size of kidney 11. Urea.Elevated TW – infection 7.Contraindicated in: (a) Contrast allergy (b) Renal impairment (Cr >200) (c) Patients on metformin (can cause lactic acidosis. Full blood count . equal and symmetrical uptake 3. filling defects (vi) Cystogram .Renal stones 12.Anycoagulopathy 9. Increased residual volume in bladder after micturition due to BPH .Detection of bladder tumour (IVU may not pick up small tumours <1cm) . PT/PTT .Non-contrast phase (stones) Nephrogram (tumors) Delayed phase . decreased distal passage of contrast) + hydroureter and/or hydronephrosis 5. Plain KUB .Stones.Adv: Ability to see renal parenchyma tumors (IVU only sees outline) .Biopsy can be taken at the same time 240 . can detect dilated calyces/pelvis (hydronephrosis). Configuration of the kidneys eg. Horseshoe kidneys 4. brain. (d) pulmonary embolism 5. Metastasis .2.Arise from the renal tubular epithelium . phaeochromocytomas.Exposure to cadmium (industrial) . etc) Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene on chromosome 7q31 multifocal bilateral papillary carcinomas . (c) liver dysfunction. painless haematuria. For left renal tumour.Peak incidence 60-70 years PATHOLOGY .2:1 male predominance .Acquired polycystic kidney disease (secondary to chronic dialysis) PRESENTATION . Complications 1. LOA. Extension into IVC can cause (a) lower limb oedema. angiomas (associated with CNS haemangioblastomas (usually cerebellar).When tumour has grown large enough. RENAL CELL CARCINOMA EPIDEMIOLOGY . 3.Symptoms of metastases – lungs. chromophobe renal cell carcinoma (5%) Other renal tumours: TCC of renal pelvis.Initially asymptomatic (may be detected incidentally) 1. (b) ascites.Most frequent occurring solid lesion within kidney . May have fever a/w night sweats. Local S/S .Three cell types: 1. malaise 2. hypertension 3. lymph nodes 241 . bilateral multicentric retinal angiomas.Most common primary renal tumour (80-85% of all tumours of the kidney) . liver. LOW. bones. dull flank pain and palpable mass may result Classical triad of RCC: flank pain. 2. papillary renal cell carcinoma (10-15%). clear cell carcinoma (70-80%). extension of tumour into left renal vein can cause a left varicocoele as the left testicular vein becomes occluded 4. Paraneoplastic syndromes are uncommon – Cushing’s. Polycythaemia occurs in 1-5% (due to increased erythropoietin) 3.Family history von-Hippel Lindau syndrome clear cell carcinomas Due to mutation of the VHL gene on chromosome 3p25 resulting in abnormal growth of BV ie.Smoking . palpable renal mass (indicates late stage disease) 2.Painless gross haematuria is the most common – >50% of cases . lymphoma RISK FACTORS . Wilms’ tumour. hypercalcaemia.3% of adult malignancy . Extension into renal vein.Liver metastases 2. Pathological diagnosis .Lymph node enlargement . limited to the kidney T1a: tumour <4cm T1b: tumour >4cm but <7cm T2 Tumour >7cm. adjacent organ invasion .In tumours with metastatic disease on presentation.size and shape of nucleus . limited to the kidney T3 Tumour extends into major veins or invades adrenal gland or perinephric tissues.Only done if patient complains of bone pain and/or alkaline phosphatase is raised MRI of abdomen and heart .For lung metastases Also.Presumptive diagnosis is made on imaging – a renal parenchymal mass with (a) thickened irregular walls and (b) enhancement after contrast injection suggests malignancy 2.In these resectable lesions.chromatin clumping I (best) IV (worst) Prognosis Stage I (T1N0): Stage II (T2N0): Stage III (T3N0/N1): Metastatic disease: >90% 5 year survival >75% >60% <10% 242 .no and size of nucleoli .Perinephric invasion. Imaging – CT and/or ultrasound . and provides the tissue diagnosis postoperatively . CT scan of the abdomen .Superior to CT for evaluation of IVC and right atrium involvement T1 Tumour <7cm. but not beyond Gerota’s fascia T4 Tumour invades beyond Gerota’s fascia Fuhrman grading prognosis (not tx) . IVC . biopsy of the metastatic site may be easier STAGING 1.INVESTIGATIONS DIAGNOSTIC 1. a partial or total nephrectomy is often performed. CT scan of the chest . Bone scan .Needle biopsy usually not done for resectable lesions due to fears of tumour seeding . High dose interleukin-2 – associated with good results in patients whose tumours respond to treatment.TREATMENT A. RESECTABLE TUMOURS Surgery + Adj chemo + Surveillance after resection to detect relapse early . However. as treatment can induce long-term remissions without relapse.Cytoreductive nephrectomy performed prior to starting immunotherapy can improve survival Molecular targeted therapy: Sorafenib.Alternatives: radiofrequency ablation.Most small tumours grow slowly and do not become symptomatic or metastasise – reasonable to manage conservatively with periodic re-evaluation . cryotherapy of lesions B.In T3 disease. Partial nephrectomy (T1a) . Radical nephrectomy (T2 and beyond) .entire kidney removed 3. Bevacizumab 1.entire kidney together with Gerota’s fascia .spares part of the kidney that is not involved nephron-saving 2. aim for radical nephrectomy and removal of structures affected e.Retroperitoneal versus transperitoneal approach 1.Laparoscopic versus open methods . associated with high toxicity and often not tolerable . ADVANCED TUMOURS Immunotherapy . Sorafenib – an inhibitor of tyrosine kinase blocks intracellular domain of the vascular endothelial growth factor (VEGF) receptor 2. Bevacizumab – monoclonal antibody against VEGF 243 . Total nephrectomy (T1b) . adrenal gland Patients who cannot undergo resection .g. 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. LOA.Pain – in locally advanced or metastatic tumour (a) flank pain due to urinary obstruction. painless. uterus Invasion of lateral pelvic walls.Increasing incidence with age (80% diagnosed in patient >60 years old) . etc .obstructive symptoms: indicate a tumour at the bladder neck or prostatic urethra . does not involve lamina propria Carcinoma in-situ: “flat tumour” Superficial.LUTS – irritative symptoms suggestive of carcinoma in-situ.g.Adenocarcinoma (1%.Ninth most common cancer in Singaporean males . . intermittent. due to chronic irritation e. Tis. . Urine cytology for malignant cells (not very sensitive but very specific) Cystoscopy with cell brushings and biopsy IVU or CT urogram to detect SYNCHRONOUS LESIONS (3% chance of proximal tumour) STAGING 1. T1 (b) Muscle-invasive tumour (20-30%) – >T2 Grading is also important T1 15% becomes invasive T1G3 75-80% invasive 244 thus used for staging . long term indwelling catheter or untreated bladder stone) RISK FACTORS . (c) bone pain due to metastasis . 2. thus urothelial tumours often occur multifocally Screen ENTIRE urothelium every f/u Papillary in nature (more differentiated) .Occupational (hairdressers – exposure to hair dyes) .Chronic cystitis (SCC) Schistosomiasis Radiation (pelvic) Chemotherapy (cyclophosphamide) .Haematuria most common (90%) – typically gross. 2. arises from remnant of the urachus in the dome of the bladder). involves lamina propria (up to muscularis propria) Superficial involvement of muscularis propria – up to inner half of muscle Deep involvement of muscularis propria – up to outer half of muscle Microscopic extension outside bladder (from TURBT specimen) Macroscopic extension outside bladder Invasion of prostate. CT abdo/pelvis for T.3.4:1 male predominance PATHOLOGY . aniline-containing dyes.Industrial chemicals – naphthylamine.Analgesic abuse (phenacetin) PRESENTATION . N and M staging Transurethral resection of bladder tumour (TURBT) with histopathology – can reach the muscular layer Ta Tis T1 T2a T2b T3a T3b T4a T4b Superficial. vagina. fatigue DIAGNOSIS 1.Cigarette smoking (Urothelial CA!) – ask secondary smoking . (b) suprapubic pain due to local invasion. abdominal wall Generally can be divided into 2 main groups: (a) Superficial tumour (70-80% of patients) – Ta. 3. BLADDER TRANSITIONAL CELL CARCINOMA EPIDEMIOLOGY . occurring throughout the stream .SCC (<5%.Constitutional symptoms – LOW. Intravesical therapy BCG – 1 instillation per week for 6 weeks Mitomycin C – single instillation within 24hrs of TURBT. 6. not continent) o Neobladder construction using ileum (only if urethra not removed.MANAGEMENT DEPENDENT ON STAGE SUPERFICIAL TUMOUR .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 . multiple primary sites. or weekly/monthly treatments for up to 2 years Indicated in patients with high risk of tumour recurrence or tumour progression: 1. as a stoma.Radiotherapy (not as good as surgery) METASTATIC Chemotherapy 245 . 5. multiple recurrences. tumour size >3cm. but easily stenosed due to small calibre. continent. 3. 4. prostatic urethral involvement . better quality of life) o Cutaneous ureterostomy (use ureters to create stoma. primary or coexisting carcinoma in-situ.Primary treatment is TURBT of the tumour . not continent) o Stoma with pouch construction under abdominal wall (not continent) .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. high grade. 2. May be asymptomatic (a) Can cause irritative urinary symptoms – frequency. such that they exceed their solubility precipitate as stones E.4.Most often asymptomatic unless the stone gets lodged in the pelviureteric junction causing hydronephrosis and subsequent infection pyonephrosis . symptoms are often out of proportion to signs – no guarding.Otherwise unremarkable examination 246 . hypercalciuria with or without hypercalcaemia.Even small stones can cause severe symptoms as the ureter is narrow (a) Classically ureteric colic pain – severe.In ureteric colic.Calcium oxalate or calcium phosphate stones – 75% .DECOMPRESSION using PCN or URS with stenting (no need to remove stone in same setting) Loin pain DDx: MSK (diff to differentiate) Bladder stones . hyperuricuria .Can occur at any level in the urinary tract.Vague flank pain may occur.g. UROLITHIASIS STONE COMPOSITION .Broad spec Abx eg. Ceftriaxone . but most commonly in the kidney PATHOLOGY .Uric acid and cystine stones – 10% .Urinary tract infections– struvite stones form in Proteus vulgaris infections ( splits urea into ammonium). pain. etc PHYSICAL EXAMINATION . can be very ill (sepsis) Management: .Most important cause of stone formation is increased urine concentration of the stone’s constituents. Bleeding? Ureteric stones . etc . intermittent loin-to-groin pain (b) Haematuria – gross or microscopic (c) Irritative symptoms – frequency. urgency (b) Haematuria (c) If infection is present – dysuria. renal punch may be positive (DDx spinal pain by pressing on the spine) .If the patient has pyelonephritis. fever. rebound.Magnesium ammonium phosphate (struvite = MAP) stones – 15% . generating alkaline urine Bacteria can also form nidi for the formation of any kind of stone PRESENTATION DEPENDS ON SITE Renal stones . urgency (d) Can cause upper urinary tract infection Pyonephrosis! (infected purulent urine in an obstructed collecting system) fever with C&R. Unlikely to resolve with conservative Tx: Does not pass after one month Too large to pass spontaneously 247 treat . UFEME. 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.Features of stone: echogeneic rim.Cx: Obstructs urine flow Causes urinary tract infection Damages renal tissue or causes significant bleeding Increase in size .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) .May be able to see radio-opaque stone (90% of renal stones are radio-opaque) . micro-organisms (UTI) Intravenous urogram .If one kidney has less than 15% of total renal function. looking for ureteric stones . dairy produce. False positive: Phlebolith (perfectly round.U: Trace path of ureter along tips of transverse processes. any renal stones .Can also help to visualise a stone . posterior acoustic shadowing Complications 4. urine culture/sensitivity . Found in pelvis near ureters).INVESTIGATIONS Diagnosis 1.S/S: Constant pain . it is not worth salvaging the kidney TREATMENT CONSERVATIVE Stones smaller than 5mm can be treated conservatively as 60% will be passed out. it is valuable to measure the renal function using the MAG-3 renogram . sometimes with lucent centre.If pyelonephritis present due to stone obstruction. KUB . 2. Urine tests – dipstick. 6. in front of bifurcation of common iliac arteries and medially into bladder at ischial tuberosity. stools . across sacroiliac joint. 5. 3.B: Look for bladder stones Intravenous urogram . only treat if they (a) do not pass out after 4 to 6 weeks.Haematuria .Can show dilated urinary system secondary to stone obstruction – hydroureter and/or hydronephrosis Ultrasound of kidney or bladder . hypercalcaemia disease if possible (c) Diet: High fluid intake Low salt intake Restriction of red meat. refined sugars Increase citrus fruit intake SURGICAL INTERVENTION Indications: .g.as above MAG-3 renogram .Pyuria.False neg: too small.K: Look at kidney size. non-functioning kidney Adjuncts: Double-J stent (or DJ stent) – inserted to stent the urinary system when . when ESWL used for treatment of a large stone. (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) .g.Used for stones below 2cm in size .CI : uncorrected bleeding diathesis.Done for renal stones that are too large for ESWL to disintegrate . Percutaneous nephrolithotomy (PCNL) . uric acid and struvite stones fragment easily.worried that stone fragments after ESWL may cause obstruction e. can also be done by pneumatic drill. (c) untreated bleeding diathesis. electrohydraulic means) .Used for renal stones and upper ureter stones – not so good for lower system due to difficulty in access . (b) untreated UTI. performing open surgery for another reason anyway. or if system is obstructed to begin with. Ureterorenoscopy with lithotripsy (URS + LL) (usually laser lithotripsy. Extracorporeal shock wave lithotripsy (ESWL) .For stones along the ureter .CI: (a) pregnancy.Calcium oxalate. may want to stent to ensure good drainage after surgery .Cx: (a) Bleeding (capsular hematoma) (b) Sepsis (if stone is infected) (c) Injuries to surr tissues 3. Cystolitholapaxy (stone crushing) for bladder stone Open surgery (pyelolithotomy or ureterolithotomy) – rarely done. but calcium phosphate and cystine do not . only if failed other management strategies.Types of treatment available: [from top to bottom] 1. patients unfit for GA 2.Retrograde pyelogram to see the stone? 4. altered anatomy.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/ 248 . Overactive bladder Tx).Suprapubic pain (unlike chronic retention of urine which is painless) – severe! . 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.Renal failure (more likely in chronic retention) – vomiting. antihistamines (d) Immobility 3. PID.Sudden inability to pass urine . drowsiness 249 . FAECES. Precipitating factors: (if present.Previous history of ureteric colic pain or stones . bladder stone.5. ANTICHOL. antihistamines.Constitutional symptoms: LOW. spinal stenosis neurogenic bladder .Inguinotesticular pain. STRICTURE. ovarian cyst.Infection – symptoms of UTI . Complications: [3] . history of spinal disease e.Lower limb weakness/paralysis.g. UTI. blood clot . LOA.Suprapubic distension 2. nocturia. alcohol Prolonged immobility Post-anaesthesia Pain HISTORY 1. bowel incontinence.Stone disease (if in the bladder. Confirm Dx (Symptoms of ARU) [3] . frequency. retroverted gravid uterus UV prolapsed Tumour of the bladder neck (TCC) Urethritis (UTI) Urethral stricture from STD. haematuria (b) Constipation (c) Drugs e.Previous urethral instrumentation or STD stricture . cough mixture. back trauma. cauda equina Multiple sclerosis Tabes dorsalis (Tertiary syphilis) Diabetic autonomic neuropathy Anticholinergics (cough medicine. dribbling Prostatitis . usually asymptomatic) . malaise (any tumour in general) 4.g. History suggestive of aetiology: . prev instrumentation Phimosis Urethral trauma/rupture Stones Blood clot (clot retention in haematuria) Foreign body Cord compression. fibroid Pregnancy. lethargy. APPROACH TO ACUTE RETENTION OF URINE CAUSES: BPH.Gross painless haematuria recently TCC.Previous history of obstructive symptoms BPH . higher the chances of retaining bladder abilities after Tx with TURP) [4] (a) UTI: dysuria. anti-depressants.Recent trauma to urethra . urethral burning. urgency. (b) high-riding prostate – more relevant in the trauma setting) If cannot pass into bladder: a) enlarged prostate use thicker catheter (stiffer. ovarian cyst Faecal loading Bilateral enlarged kidneys (hydronephrosis) desire to micturate (large bladder up to umb suggests b/g of . cancer BPH [usually <40] prostatitis instrumentation /catheterization >11days ARU 250 . pedal oedema.External genitalia: narrow maetus. (3) prostate volume. the suprapubic catheter is inserted and secured INVESTIGATIONS 1. pressure chronic retention) Other pelvic masses – fibroid. 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. FBC: raised TW (infection) – not usually done Imaging 1) KUB for stones. free/total PSA. hydroureters (obstructive complication) PSA .>/= 2 readings 2/52 apart . ureters: hydronephrosis. Urine dipstick.1st choice: URETHRAL CATHETERISATION (14F) (CI!!: S/S of urethral injury – (a) blood at urethral meatus. ii. gravid uterus.Abdomen Palpable bladder – tense. (4) intravesical protrusion of prostate 3) U/S kidney. (2) tumour. craggy. and trocar inserted When a gush of urine is seen. tender.PHYSICAL EXAMINATION .to be done 4-6/52 later (as ARU can cause raised PSA) . iv.PSA velocity (rate of rise).Causes of raised PSA i. UECr: raised creatinine (renal impairment secondary to obstructive nephropathy) c. tight foreskin . scratch marks. 2. etc (uraemia) . v. Bloods/Urine a. hematuria) b.General condition Vitals (fever) sallow appearance. iii. rounded. dull. rectal mucosa not mobile? Tender? (prostatitis) Stool impaction . PSA density (= PSA/prostate volume) . faecal loading 2) U/S bladder: (1) stones. irregular. UFEME and culture/sensitivity (UTI.Neurological examination LMN paralysis of the lower limbs? Any sensory level present? IMMEDIATE MANAGEMENT – PROMPT BLADDER DECOMPRESSION .Digital rectal examination Any saddle anaesthesia (buttock and perineum – ind cauda equina) Anal tone Prostate enlargement (>2FB) – firm and smooth? Or hard. 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. hypokalaemia. 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. rarely clinically significant drain urine in 500-750ml aliquots. resulting in transient impairment of concentrating function. Usually seen in CRU. TURP (if sec to BPH): refer to indications 1 and 2 are done while waiting for medical therapy to work.Relieve constipation with fleet enema. lactulose.Stop drugs that may have precipitated ARU . Long term catheterization 2.Treat any urinary tract infection if present 2. Urinary obstruction + Fever Admit! (Uro emergency) 251 .Take off catheter and watch patient’s output. decrease UTI 3. and also do 2) bladder scan post-micturition to check residual volume Failed Trial of void: after how long can try TOC? 1. senna etc . Clean intermittent catheterization: a. Can result in hypotension and electrolyte abnormalities (hyponatraemia. representing appropriate attempt to get rid of excess fluid in the body during period of obstruction. with 15-20min intervals between each (c) Hypotension secondary to vasovagal response or relief of pelvic venous congestion 3. Adv: improved rate of spontaneous voiding (pt can PU in btw).When patient passes urine. can perform 1) uroflow to investigate severity of outlet obstruction.TREATMENT 1. as well as perform bladder scan to measure bladder volume . Treat reversible causes .If patient cannot pass urine and bladder volume >400ml re-catheterise . Trial-off catheter . pyelonephrosis: loin pain.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. stones .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) .Rule out other DDx (refer ARU): Stricture/ bladder neck contractures: previous instrumentation or STDs causing urethritis/ post.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 . TCAs Chronic constipation Ca bladder neck/ Ca Prostate: LOW.Frequency rises with age after the age of 30.6. BENIGN PROSTATIC HYPERPLASIA EPIDEMIOLOGY .Fever (UTI . fever Renal impairment: polyuria/ anuria.6 COMPLICATIONS of an obstructive uropathy: a) Acute urinary retention (previous admissions and IDC) b) UTI: irritative symptoms. haematuria c) Stones: irritative symptoms.Other aspects of history: Social history (effect on lifestyle) 252 . haematuria d) Hydronephrosis.Very common problem in men . anti-cholingerics. Irritative [FUNI] Frequency Urgency Nocturia Urge incontinence Dysuria Irritative S/S significant for Cx of urine retention: UTI. bone pain.Results from proliferation of both the epithelial and stromal components of the prostate with resultant enlargement of the gland . reaching 90% in men older than 80 PATHOLOGY . LOA. BB.pyelonephritis from ascending infection) .Haematuria (UTI or rupture of enlarged veins) .TURP Drug causes: codeine (cough mixture). haematuria Neurogenic bladder . e) Overflow incontinence 2o to Chronic urinary retention with high post-void residual volume in the bladder f) Hernia sec to chronic straining . 253 . strictures/ bladder neck obstruction or cancer.DRE impacted stools prostate (benign): 1.Cystoscopy to rule out stones.PSA (done 4-6/52 later to avoid false +ves): normal <4 Imaging .US kidney – hydronephrosis . median sulcus. Pyelonephritis) .KUB for bladder stone .± urodynamic studies. urine c/s: for UTI and screen for cancer . peak flow rate may be normal or high.Pedal/ sacral oedema (CRF) .Hernia repair scar? (hernia) Palpation . non-tender. Volume voided (>100ml to be valid): too low (falsely low peak flow rate).Sallow? Anaemia? (of CRF/ underlying malignancy) Cachexia (CA) . raised WBC .Bony tenderness (tumor) Confirm diagnosis and R/O DDx: . rubbery. increase RU) 3. especially if outlet resistance is reduced .Abdominoperineal masses (fecal loading. masses to compress) . stones) .UECr: dehydration. prolonged flow. raised creatinine renal impairment due to chronic obstruction . B) BOO with abdo straining: intermittent flow. smooth enlarged 2. Residual urine 0 in young males. TRUS with biopsy TRO prostate cancer if PSA >10 254 .Renal punch? (Pyelonephritis) . 4.Already on IDC? (ARU) Diapers? (incontinence) Hematuria? (UTI. saw tooth appearance 2.US bladder – post-void residual volume >100ml. mobile mucosa INVESTIGATIONS Blood . .Check for hernias . normal bell shaped curve.Vitals: BP for HPT? (CRF) Fever? (UTI) Urine output? (CRF) . too high (falsely long duration.Uroflowmetry to confirm obstruction to urinary outflow (IMPT!!) 1. cytology. 5.FBC: anaemia. 3. Normal peak flow rate (Qmax) > 15ml/sec 4.Any ballotable kidneys? (Hydronephrosis.Palpable tender bladder in (ARU) non-tender (CRU) .PHYSICAL EXAMINATION Inspection . bladder stone. measure intravesical prostatic protrusion (IPP) .UFEME. can accept up to 50ml in elderly A) BOO with normal detrusor muscle: max flow rate 10ml/sec. Monitor patient’s symptoms and clinical course annually II. Bladder calculi. Watchful waiting . prostate and urethra – relaxing the area) . good flow (Qmax) 255 . no complications and normal invx . Bleeding. 5-alpha reductase inhibitors (Finasteride.Objectives of treatment: Rapid and sustained relief of symptoms. - III. Void: detrusor pressure should be sufficient. lethargy. and irrigation pressures <60mmHg Patient usually given spinal anaesthesia during TURP so the surgeon can assess the patient’s mental status during the operation Now uncommon as new technology allows isotonic irrigation Failure of procedure: S/S recur Caution: Must rule out Neurogenic bladder / Detrusor hypotonia before TURP!! Do Urodynamic studies 1. 3. Insert narrow catheter with pressure gauge at the end into a. 4. Alpha blockers (Prazosin. Bladder: intravesical pressure b. Ex: $3/pill. prostate size make small Indications: 1.SEs: include postural hypotension. and in prostates >40g Most common side-effect is Sexual dysfunction. thus water enters open vasculature during surgery Risk with prolonged operation & pressure of irrigation. Medical treatment 1. Always check if pt is planning to have children! TUR syndrome (<1%) = hyponatremia Symptoms: Nausea. Rectum: intraabdominal pressure Detrusor pressure = a – b 2. hypertension.Treatment of symptoms (blocking the α-1 adrenergic receptors in the bladder neck. visual disturbance. Alfuzosin) . Hair growth. Combi therapy better than monotherapy. improve patient’s quality of life I. Warn patient about Gynaecomastia (1%) and stop med when they notice it developing. 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. infection. thus op is kept to < 1 hour. vomiting. Obstructive uropathy 3. and surgical management . Fill up bladder: look for detrusor contractions 3. dizziness. Significant Complications (4): Refractory urinary retention.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 .Suitable for patients with minimal symptoms.Divided into watchful waiting. Failed medical treatment 2.Result in decreased outflow resistance and decreased bladder instability . etc. Recurrent gross haematuria Aim: to widen bladder neck Complications of TURP: bold = must mention during consent taking 1. cryoablation. stricture / bladder neck stenosis Perforation of the urethra or bladder dome can form fistula Retrograde ejaculation (100%) impotence: (incompetent bladder neck). seizure Hyponatraemia due to constant irrigation during TURP (glycine used for irrigation – cannot use N/S. 5. Terazosin. 6. 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!). risk of GA/ spinal analgesia Local injury causing incontinence (1%).dynamic . as ionic solutions make diathermy non-functional) Irrigation fluid is hypotonic. Adv: 50% chance of Retrograde ejaculation Laser prostectomy is promising (pending long term results) Other techniques do not show good results: stenting. prevent long-term complications. medical management. giddiness. confusion. Cough when erect: stress incontinence 4. Doxazosin. Recurrent UTI. lightheadedness 2. 2. DIAGNOSIS 1. 4.Local symptoms: obstructive LUTS. and yet there is a significant proportion of men with prostate cancer with PSA <4ng/ml biopsy if the rate of rise of PSA is >0.gold standard .>10ng/ml: biopsy recommended as >50% of patients will have prostate cancer .4-10ng/ml: biopsy advised.Histology of prostate carcinoma is graded by the Gleason score looking at glandular architecture at low magnification PSA level .Adenocarcinoma .7.Genetic – racial variations in onset and prevalence.DRE: Asymmetric area of induration. . though only 20% will have prostate cancer . or frank hard irregular nodule . Transrectal ultrasound (TRUS) with biopsy. 2. bladder outlet obstruction. 2.Asymptomatic (mostly): incidentally picked up on DRE or due to elevated prostate-specific antigen (PSA) level (>100 is highly suggestive) .Arise in the outer parts of the prostate 70-80% of the time and are thus palpable on digital rectal examination RISK FACTORS .5th common cancer in Singapore .Percuss spine for any bone pain Staging (TNM staging) T1: non-palpable lesions o 1a: diagnosed on TURP (Gleason score <7.75ng/ml per year STAGING 1.Prostate Cancer is the 6th commonest cancer among men in Singapore.Environmental – industrial chemical exposure. diet containing high animal fat PRESENTATION . 3. haematospermia. >5% involvement) o 1c: diagnosed with PSA screening and TRUS biopsy T2: confined to prostate o 2a: confined to 1 lobe o 2b: both lobes of prostate involved T3: extra-prostatic spread (beyond prostatic capsule) T4: prostate stuck down to pelvic structures Gleason score for prostate Ca is based on its microscopic appearance.Hormonal – growth of tumour can be inhibited by orchidectomy or administration of oestrogens . non-regional) Bone scan for metastasis 256 .Metastatic symptoms – lower back pain (from Batson’s venous plexus) PHYSICAL EXAMINATION . (uncommon as most cancers arise in peripheral zones) haematuria. Clinical examination (palpable tumour T2) TRUS biopsy for staging purpose CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal status (regional. PROSTATIC CANCER EPIDEMIOLOGY . family history .Peak incidence between 65 and 75 years of age PATHOLOGY .<4ng/ml: majority will have negative biopsies. Higher scores means more aggressive lesion and worse prognosis. new onset erectile dysfunction . <5% involvement) o 1b: diagnosed on TURP (Gleason score >7. Combined androgen blockade (A + B) D. Castration (decrease Testosterone by 90-95%) a. aminoglutethimide 2.External beam radiotherapy (EBRT) or Brachytherapy LOCALLY ADVANCED DISEASE (T3/4) 1. 257 . dexamethasone. Surgical orchidectomy b. Radical prostatectomy . Chemotherapy (relieves pain from bone mets + slow dz progression) Docetaxel + Prednisone (gold standard) Mitoxantrone + Prednisone Watchful waiting is possible in elderly (>75yo). laparoscopic or robot-assisted . After: pituitary stops signaling testicles castration level testosterone B. S/E: CVS HORMONAL REFRACTORY PROSTATIC CANCER . binds Testosterone-R at hypothalamus decrease LHRH b. 7-10 days: hormone flare (raised testosterone) ii.Open. Medical – LHRH agonist (luteinizing hormone releasing hormone) i. Flutamide b. Secondary hormonal manipulation Glucocorticoids – prednisone. Non-steroidal e. Anti-androgen a. NO N/M) AND <75YEARS OLD 1. Steroidal – cyproterone acetate C. Oestrogen therapy (diethylstilbestrol) a. Radiotherapy .Open – retropubic or perineal approaches 2.2 consecutive PSA rises no less than 2 wks apart and/or documented dz progression based on clinical/radiological findings in pts with castrate levels of testosterone . Androgen ablation A.Management: 1.TREATMENT LOCALISED DISEASE (T1/2.g. Radiotherapy with androgen ablation METASTATIC DISEASE 1. hydrocortisone Progesterone – megestrol acetate Adrenal suppressives – ketoconazole.