Andre Tan Surgical Notes

March 24, 2018 | Author: Aqsa Ghazanfar | Category: Esophagus, Major Trauma, Medical Specialties, Diseases And Disorders, Injury


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CONTENTSSurgery Notes For the M.B.B.S. By Andre Tan I TRAUMA (MULTI-SPECIALTY APPROACH) Page 2 II APPROACH TO ABDOMINAL PAIN 10 III APPROACH TO ABDOMINAL MASSES 11 IV OESOPHAGEAL DISEASES 12 V UPPER BLEEDING GIT AND ITS CAUSES 21 VI COLORECTAL DISEASES 19 VII LIVER DISEASES 39 VIII PANCREATIC DISEASES 45 IX BILIARY TRACT DISEASES 51 X BREAST DISEASES 60 XI HEAD AND NECK MASSES 69 XII SALIVARY GLAND SWELLINGS 74 XIII THYROID DISEASES 78 XIV PERIPHERAL ARTERIAL DISEASE 85 XV ABDOMINAL AORTIC ANEURYSM 93 XVI PERIPHERAL VENOUS DISEASE 95 XVII UROLOGICAL DISEASES 99 XVIII SURGICAL INSTRUMENTS 110 TRAUMA (MULTI-SPECIALTY APPROACH) ADVANCED TRAUMA LIFE SUPPORT ALGORITHM MAIN PRINCIPLES: - Treat greatest threat to life first - Definitive diagnosis is less important - Time is important – the “golden hour” after trauma is when 30% of trauma deaths occur, and are preventable by ATLS APPROACH 1. Primary survey and Resuscitation with adjuncts 2. Re-evaluation of the patient 3. Secondary survey with adjuncts 4. Post-resuscitation monitoring and re-evaluation 5. Optimise for transfer and definitive care PRIMARY SURVEY – ABCDE 1. AIRWAY Assessment of airway patency - Is patient alert, can patient speak? Gurgling, stridor Maxillofacial injuries Laryngeal injuries Caution: C-spine injury Establishing patent airway - Chin-lift or modified jaw thrust (protect C-spine) Remove any foreign objects in the mouth where possible Oro/nasopharyngeal airway Definitive airway – endotracheal tube, cricothyroidotomy, tracheostomy 2. BREATHING Assessment of breathing - 2 Look, listen, feel: chest rise, breath sounds – rhythm and equality bilaterally Rate of respiration Effort of respiration Colour of patient Percuss chest Look for chest deformities e.g. flail chest Management of breathing - Supplemental oxygen Ventilate as required if patient requires assistance with breathing Needle thoracotomy for tension pneumothorax, followed by chest tube Occlusive dressing for open pneumothorax 3. CIRCULATION Assessment of organ perfusion - Level of consciousness Skin colour and temperature, capillary refill Pulse rate and character – all major pulses Blood pressure Classes of haemorrhagic shock Bld loss Amt (ml) Percentage Ht rate BP Cap refill Resp rate Ur output (ml/h) Mental state Fluid replacement I II III IV <750 <15 <100 Normal Normal 14-20 >30 Sl anxious 750-1500 15-30 >100 Normal Prolonged 20-30 20-30 Mild anxiety Crystalloid Crystalloid 1500-2000 30-40 >120 Decreased Prolonged 30-40 5-15 Anxiousconfused Crystalloid + blood >2000 >40 >140 Decreased Prolonged >35 Oliguric-anuric Confusedlethargic Blood Management - Sources of bleeding  apply direct pressure or pressure on proximal pressure point - Be suspicious about occult bleeding e.g. intraperitoneal, retroperitoneal (pelvic fracture), soft tissue (long bone fracture) - Venous access – large bore, proximal veins - Restore circulatory volume with rapid crystalloid infusion – Ringer’s lactate - Blood transfusion if not responsive to fluids or response is transient - Reassess frequently 3 SECONDARY SURVEY 4. DISABILITY - Glasgow coma scale Eye Spontaneous opening Opens to voice Opens to pain No response When to do secondary survey 4 3 2 1 Verbal Oriented speech Confused Inappropriate Incomprehensible No verbal response 5 4 3 2 1 Motor Obeys Purposeful Withdraws Flexion response Extension response No response 6 5 4 3 2 1 GCS: 14-15 (minor); 8-13 (moderate); 3-7 (severe) - AVPU score: Alert, Verbal stimuli (responds to), Pain stimuli, Unresponsive - Pupillary reactivity - Primary survey and resuscitation completed - ABCDEs reassessed - Vital functions returning to normal i.e. no need for active resuscitation at the moment 1. AMPLE HISTORY - Allergy - Medications - Past history - Last meal - Events leading to injury, Environment in which trauma occurred 2. COMPLETE HEAD-TO-TOE EXAMINATION - Call for neurosurgical consult as indicated Head - 5. EXPOSURE - Remove all clothes - Check everywhere for injuries (log-roll to look at the back) - Prevent hypothermia Complete neurological examination GCS or AVPU assessment Comprehensive examination of eyes and ears for base of skull fractures Caution: unconscious patient; periorbital oedema; occluded auditory canal Maxillofacial - 6. ADJUNCTS TO PRIMARY SURVEY Monitoring - Vital signs – BP, pulse rate, saturation (pulse oximeter) - ECG monitoring - Arterial blood gas Cervical spine Diagnostic tools - - Screening X-ray films (trauma series): CXR, AP pelvis, lateral C-spine - Focused abdominal sonography in trauma (FAST) - Diagnostic peritoneal lavage Urinary catheter - Functions: decompress bladder, measurement of urinary output - Caution in urethral injury: blood at urethral meatus, ecchymosis/haematoma, high-riding prostate Bony crepitus/deformity Palpable deformity Comprehensive oral/dental examination Caution: potential airway obstruction in maxillofacial injury; cribriform plate fracture with CSF rhinorrhoea  do not insert nasogastric tube perineal Gastric catheter (orogastric or nasogastric) - Function: decompress stomach, look at aspirate (bloody? bilious?) - Caution in base of skull fracture: CSF otorrhoea/rhinorrhoea, periorbital ecchymosis, mid-face instability (grab the incisors and rock), haemotympanum  insert orogastric tube instead of nasogastric Palpate for tenderness, any step deformity Complete neurological examination C-spine imaging Caution: Injury above clavicles; altered consciousness (cannot assess accurately); other severe, painful injury (distracts from cervical spine pain) Neck (soft tissues) - Blunt versus penetrating injuries Airway obstruction, hoarseness Crepitus (subcutaneous emphysema), haematoma, stridor, bruit Caution: delayed symptoms and signs of airway obstruction that progressively develop; occult injuries percuss. retroperitoneum.Intravenous analgesia as appropriate 4 ABDOMINAL TRAUMA TYPES OF INTRA-ABDOMINAL INJURY IN BLUNT TRAUMA .Vascular injury with bleeding INDICATIONS FOR IMMEDIATE LAPAROTOMY . but should not delay transfer 4. increase in chest tube drainage Abdomen - Inspect.Any penetrating injury to the abdomen with haemodynamic instability or peritoneal irritation . right upper quadrant.Vaginal examination: blood. FREQUENT RE-EVALUATION .Obvious signs of peritoneal irritation . left upper quadrant. PAIN MANAGEMENT . lacerations . liver – bleeding (may be quite massive) . DPL.Evisceration. high-riding prostate.g.Have a high index of suspicion for injuries to avoid missing them . percuss. auscultate Abrasions and ecchymosis – “seat-belt sign” Lower rib fractures  liver and spleen injury Re-evaluate frequently Special studies: FAST.If patient is unstable: FAST and/or DPL FOCUSED ABDOMINAL SONOGRAPHY IN TRAUMA (FAST) . excessive pelvic manipulation Perineum . soft-tissue or ligamentous injuries.Disadvantages  Does not image solid parenchymal damage. no radiation risk . CT scan Caution: hollow viscus and retroperitoneal injuries. rectal wall integrity. blood . subcutaneous air  Less sensitive. deformity Pain Perfusion Peripheral neurovascular status X-rays as appropriate Caution: potential blood loss is high in certain injuries (e.Obvious or strongly suspected intra-abdominal injury with shock or difficulty in stabilising haemodynamics .X-ray evidence of pneumoperitoneum or diaphragmatic rupture INVESTIGATIONS .Urethral blood .If patient is stable: FAST and/or CT scan . gunshot wounds traversing abdominal cavity .Chest - Inspect.As required according to suspicion. palpate. femoral shaft fracture). stab wounds with implement in-situ.Hollow viscus injury with rupture . pelvic fracture. examine patient’s back 3. ADJUNCTS AND SPECIAL DIAGNOSTIC TESTS .DRE: Sphincter tone. more operator-dependent than DPL and cannot distinguish blood from ascites  Intermediate results require follow-up attempts or alternative diagnostic tests . diaphragmatic defects or bowel injury  Compromised in uncooperative.Persistent fresh blood aspirated from nasogastric tube (oropharyngeal injuries excluded as source of bleeding) . lacerations Musculoskeletal – extremities - Contusion.Rectal exam reveals fresh blood . pelvic fracture (may feel fragments of bone). obesity.Ultrasonographic evaluation of four windows: Pericardial.Contusions.Advantages     Portable Can be done quickly in <5min Can be used for serial examination Does not require contrast. auscultate Re-evaluate frequently Look at CXR Caution: missed injury.Frequent re-evaluation and continuous monitoring  rapidly recognise when patient is deteriorating 5. missed fractures. pelvis . palpate. substantial bowel gas.Solid organ injury: spleen. haematomas. agitated patient. Definitive airway – ETT.Management  Aggressive fluid resuscitation – helps maintain cardiac output and buys time  Pericardiocentesis: ECG lead-guided or 2D-echo guided AIRWAY OBSTRUCTION . CARDIAC TAMPONADE .5 CT SCAN . suction blood/secretions .When 2 or more ribs are fractured at 2 points forming a flail segment that moves paradoxically with breathing .Advantages  Can promptly reveal or exclude the presence of intraperitoneal haemorrhage  Valuable in discovery of potentially lethal bowel perforation . diaphragmatic injuries. then instillation of saline and re-aspiration . WBC >500. muffled heart sounds are least reliable  Pulseless electrical activity  Kussmaul’s signs (increased neck distension during inspiration. age > 65. electrical alternans (uncommon)  Pericardial fluid demonstrated on FAST or 2D-echo .definitive .Positive DPL  Frank blood (>5ml) or obvious bowel contents aspirated  Lavage fluid seen to exit from chest drain or urinary catheter  RBC >100.Consider mechanical ventilation in high risk patients: shock.Indications:  Any unstable patient with suspicion of abdominal trauma or where clinical exam is difficult or equivocal  Unexplained hypotension in multiple trauma  Patient requiring immediate surgery for extra-abdominal injuries . fracture of >8 ribs. severe head injury.Disadvantages  Expensive  Time required to transport patient  Use of contrast DIAGNOSTIC PERITONEAL LAVAGE (DPL) . airway obstruction. haemothorax. early hollow viscus injury.Involves making a cut in the infraumbilical region and inserting a catheter into the peritoneal cavity. injuries to retroperitoneal structures CARDIOTHORACIC TRAUMA There are 5 clinical scenarios in chest trauma where bedside procedures are lifesaving: cardiac tamponade.Management: ensure adequate oxygenation and ventilation.Remove any foreign body manually.Only suitable for stable patient as quite long time involved in imaging with only patient in the room  can collapse . infection). and pneumothorax. >3 associated injuries . contributed to by pain with restricted chest wall movement . distended neck veins) – only seen in 50% of cases as hypovolaemia may prevent neck vein distension. judicious fluid therapy (avoid fluid overload). previous pulmonary disease. intraperitoneal injury  False negative rate of 2% when there is failure to recover lavage fluid.Disadvantages  Morbidity involved – wound complications (haematoma.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 .Diagnostic clues  Enlarged cardiac shadow in CXR (globular heart – very rarely seen)  Small ECG voltages.Chin lift or jaw thrust . aspirate. adequate intravenous analgesia . pulsus paradoxus) . Gram stain positive for bacteria in effluent .000 per mm3. tracheostomy FLAIL CHEST . cricothyroidotomy.Clinical features  Chest trauma and hypotension  Beck’s triad (hypotension. flail chest.High index of suspicion required .Contraindications      Absolute indication for laparotomy already exists Previous abdominal surgery or infections Gravid uterus Morbid obesity Coagulopathy .Results in hypoxaemia mainly due to underlying pulmonary contusion. muffled heart sounds. taping it down on 3 sides to produce a fluttervalve effect.Immediate needle thoracotomy in second intercostal space in mid-clavicular line . Contusion . hypotension. increased ICP etc) since neuronal death is irreversible. will require evacuation 4. producing a “sucking chest wound” . a line just anterior to the mid-axillary line laterally. PATHOLOGIES: (a) Hypoxic (cellular)  Decreased blood supply (oxygenation)  loss of function of Na-K pump as ATP decreases  increased intracellular sodium  cellular swelling (b) Interstitial  Breakdown of blood-brain barrier  proteins enter interstitial space  oedema 1.Tension pneumothorax is a clinical diagnosis (CXR will only delay treatment. Diffuse axonal injury .(Physiological dysfunction is the first step towards cell death. underlying brain is minimally damaged. Intracranial haemorrhage (a) Extradural haemorrhage  Lens-shaped haematoma outside the dura (between skull and dura)  Pathology: expanding space-occupying lesion  20% of patients with EDH are alert and well. call urgent cardiothoracic consult (b) Subdural haemorrhage  Crescent shaped haematoma under the dura (between the dura and the arachnoid)  More severe than EDH (usually due to nature of injury that causes SDH to occur – associated with higher impact.Open pneumothorax occurs in a large chest wall defect with equilibration between intrathoracic and atmospheric pressure.Physiological dysfunction without anatomical or radiological abnormality .Be wary of sudden cessation of chest tube drainage as tube can get blocked by clot .Removal of any reversible cause of raised ICP will improve cerebral perfusion .Insert chest tube (not through the wound) . Monroe-Kellie doctrine . severe respiratory distress . and may cause death) – signs of pneumothorax.Usually recovers in 2-3 hours 2. but is reversible if no further insult occurs) .If blood >1500mls  massive haemothorax.Small haematoma <1cm PATHOPHYSIOLOGY 1. neck vein distension. blood) are relatively incompressible . Concussion . location  If large haematoma. will see punctate haemorrhages at the grey-white border 5.HAEMOTHORAX .Cover defect with a sterile dressing.Chest tube insertion in the triangle of safety (bound by the lateral border of the pectoralis major medially. thus drainage gives good results 6 .Followed by chest tube insertion (c) Traumatic subarachnoid haemorrhage  Usually only small amount of blood  conservative treatment sufficient (d) Intraparenchymal haemorrhage  Any shape. size. letting air out of the pleural cavity but not back in . and the upper border of the fifth rib inferiorly) . thus brain has other injuries)  Pathology: underlying brain damage in addition to expanding SOL  Removal of blood does not solve underlying brain damage  poorer results PNEUMOTHORAX (OPEN/TENSION) .Compensatory mechanisms: (a) Hyperventilation  vasoconstriction of cerebral vessels due to increased partial pressure of carbon dioxide  decrease in blood volume (b) CSF pushed into spinal canal (but limited volume available) .Thus increase in intracranial volume  raised ICP Cerebral perfusion pressure = Mean arterial pressure – Intracranial pressure 3.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 .Global injury of axons . hypoxaemia. CSF.Intracranial cavity is of fixed volume and its contents (brain.If severe. Cerebral oedema (2 types) NEUROSURGICAL TRAUMA AIM in management of head injuries is the prevention of secondary brain injury (from hypotension.Maximal effects at corpus callosum and brainstem . Constrictor fibres to the pupil run in the oculomotor nerve. the uncus herniates over the edge of the tentorium. exclude metabolic causes (e.Always explore to ensure underlying dura is intact.Screen for other life-threatening injuries (likely to be multi-trauma patient) .All will be CT-scanned at ED  NES will operate if any indication to do so . which exits the brainstem at the upper midbrain – nerve fibres lie just under the tentorium . Moderate head injury . hypoglyc). Assessment . GCS. moderate injury: 813. Severe head injury . Minor head injury .Thus a fixed dilated pupil occurs on the side of the compression due to unoppressed sympathetic supply (dilates the pupil) 3. Cushing’s reflex .In ward: as per mild head injury 4.There is through-and-through skin laceration over the fracture .In raised ICP. an increase in mean arterial pressure helps to maintain cerebral perfusion pressure when ICP is raised . do not give if patient is unstable) .In ward: NBM. compressing the fibres of the oculomotor nerve just below .Most common . and repair if dura is torn (since meningitis can occur with a torn dura) .Indications for admission:  Persistent headache and/or vomiting  CSF leak  Neurological deficit  Skull fracture  History of loss of consciousness  Amnesia .A triad of: (a) Raised ICP (b) Hypertension (c) Bradycardia .Baroreceptors detect abnormally raised blood pressure and try to decrease it  heart rate falls MANAGEMENT 3. ward in ICU  Prevents patient from struggling which will raise ICP 1.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.Uncus of the temporal lobe sits on the tentorium .Operate if reversible cause found (a) Craniectomy (i.Glasgow coma scale (see above) – Minor head injury: 14-15. monitor GCS .Achieve haemodynamic stability (a) Check for long bone fractures (b) FAST for bleeding into abdominal cavity (c) ABG to detect acidosis (d) Keep monitoring patient and re-investigate where appropriate . no sedation.From Monroe-Kellie doctrine. IV drip (no dextrose saline!). Depressed skull fracture .If patient deteriorates  CT scan.7 2. severe injury: 3-7 5. (c) increases BP .Total sedation after operation.3 important parameters: ABCs.Must scan to look for reversible causes of raised ICP but stabilise patient first . pupil size . bone flap not replaced) or craniotomy (bone flap replaced after blood evacuated) [Burrhole usually not big enough to drain an acute bleed] (b) Evacuate clot (c) Insert endoventricular drain (EVD) if there is hydrocephalus .e.Medical methods to lower ICP (a) Intubate and hyperventilate (b) IV mannitol (must catheterise patient also.g. Fixed dilated pupil . do septic workup (exclude sepsis) . Compound depressed fracture 2.Can leave alone unless depression is greater than the thickness of the skull bone 6. fracture stabilisation (internal or external fixation depending on Gustilo classification) .But occult blood loss can occur in large volumes especially in certain types of injuries – pelvic fracture (up to 3L). early signs of shock . malleable splint .Perfusion: colour.Soft tissue assessment .Extremity trauma tends not to be life-threatening .Appropriate X-rays (at least 2 planes) .Abnormal joint mobility – ligamentous injury around the joint.Temporary immobilisation – backslab. femoral shaft fracture (up to 2L) .Analgesia .Betadine dressing .Need to have high level of suspicion and treat with urgency .Deformity . avulsions or flaps Type IIIA  Extensive soft tissue damage. if in the knee. especially in open fractures).  Massive contamination common Type IIIC  Arterial injury requiring repair SOFT TISSUE INJURIES Types - 8 Open: laceration. skin temperature. irrigation (within 4-8 hours.Skin colour/temperature . with thrombosis and occlusion)? .Any joint instability (dislocation of a joint can result in intimal tear in the major vessel running across it.Neurovascular examination.Viability of the limb 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? 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 patient) .Post-reduction tibial pulse in knee dislocation – if still absent.Recognise fracture and/or dislocation . pulses. abrasion Crushing Degloving: open or closed Closed .Complete neurovascular examination of the limb involved before reduction .Circulation chart OPEN FRACTURES Definition: there is communication between the fracture or fracture haematoma and the external environment Gustilo-Andersen classification Physical examination .Neurological assessment . examine for compartment syndrome . do an urgent angiogram! Type I  <1cm AND clean Type II  >1cm AND no extensive soft tissue damage.Any limb deformity (can result in kinking of vessels)? .In OT: generous debridement.MUSCULOSKELETAL TRAUMA GENERAL POINTS . highly likely that the popliteal artery is injured as well .Correction of deformity .Prepare to resuscitate patient ASSESSMENT OF THE EXTREMITY .Wounds – open or closed injury.Leave wound OPEN MANAGEMENT OF FRACTURES .Look out for any tachycardia. abrasion over a fracture is considered open fracture . capillary refill . avulsions or flaps but adequate soft tissue coverage of bone OR  High-energy trauma cause irregardless of size of wound Type IIIB  Extensive soft tissue loss with periosteal stripping and exposure of bone. PT/PTT. GXM. CXR Arrange for emergency operation Angiogram if needed Surgery involves: (a) Generous debridement of the wound with irrigation to decrease bacterial load (b) Treat any soft-tissue injuries (c) Stabilise fracture – usually using external fixator . prognosis similar to closed fracture  Treat with ORIF within 6 hours . ECG.Grade IIIA  Skin graft usually possible .Grade II  Moderate velocity. more trauma .Grade IIIC  Neurovascular injuries present in addition to musculoskeletal injuries Management of open fractures - Recognise an open fracture Stabilise patient first Pain relief and analgesia Cover the wound with moist gauze Temporary immobilisation and splinting IV broad spectrum antibiotics Appropriate X-rays Nil by mouth Pre-op investigations: FBC. U/E/Cr.Grade IIIB  Skin graft alone often not adequate  Local and free flaps will be necessary  Secondary bone procedures .9 .Grade I  Low velocity injury. NOF. autoimm etc)  Hepatomegaly  Abscess Thoracic  MI  Pericarditis  Aortic aneurysm Others  Subphrenic abscess  Pancreatitis  PUD  Appendicitis Gastrointestinal  Oesophagitis  GERD  PUD  Gastric outlet obstructn  CA stomach Rt Loin Periumbilical Biliary (see RUQ) Gastrointestinal  Appendicitis (early)  I/O  Mesenteric ischaemia  Colitis  IBD Urological Infection  Pyelonephritis  Abscess Others  PKD  Renal cyst  Angiomyolipoma  Infarction Obstruction  Hydronephrosis  Nephrolithiasis  Ureteral obstruction CA  RCC  TCC renal pelvis  Bladder ca (ureteral obstructn) 10 Thoracic  Pneumonia  Pleural effusion  MI Others  Subphrenic abscess  Splenomegaly  Pancreatitis Gastrointestinal  PUD  Diverticulitis  Mesenteric ischaemia Lt Loin Others  Aortic Aneurysm  Pancreatitis 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 LHC Others  Pancreatitis Hypogastric O&G  Ovarian cyst  Ovarian torsion  Ectopic pregnancy  PID Orthopaedics (See LIF) Gastrointestinal  Colorectal CA Urological  ARU  Bladder calculi  Cystitis / UTI LIF O&G  Ectopic pregnancy  Abortion  PID  Uterine rupture  Fibroid complications  Adenomyosis  Endometriosis 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  # .ABDOMINAL PAIN RHC Thoracic  Pneumonia  Pleural effusion Biliary  Cholangitis  Cholecystitis  Gallstone disease Epigastric Hepatic  Hepatitis (viral. 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) . IMS Endocarditis  Autoimm – SLE. CLL)  H’lytic anaemia (thal. PAN  Myeloprolftve dz – PRV. essential thrombocytopaenia  Infiltratn – sarcoid. amoebic abscss  Biliary obstruction  Cirrhosis Epigastrium Gallbladder  Pancreatic/periampullary ca  Acute cholecystitis  Hydrops  Empyema  Mirizzi syndrome Ascending colon  Cancer  Diverticular mass/abscess  Faeces Orthopaedics  Chondroma/sarcoma of ilium  Bony metastasis Transverse colon  Cancer  Diverticular mass/abscess  Faeces Aorta  Aortic aneurysm Retroperitoneal lNpathy  Lymphoma  Teratoma  Other malignancies Massive  Infxns  CML  Myelofibrosis Moderate  Above causes  Portal hypt  Lymphoprolftve dz (lymphoma. VHL Liver (see RHC) LHC Spleen Mesenteric cyst Retroperitoneal lNpathy  Lymphoma  Teratoma  Other malignancies Hypogastrium O&G  Ovarian cyst/tumour  Fibroids Bladder  Acute retention of urine  Chronic retention of urine Others  Transplanted kidney  Iliac artery aneurysm  Psoas abscess  Iliac lymphadenitis  Malignant change in undesc testis Anal/rectal mass  Cancer Descending colon  Cancer  Diverticular mass/abscess  Faeces LIF Uterus  Gravid uterus  Fibroids  Tumour Ovary  Cyst  Tumour Gastrointestinal  Diverticular mass/abscess  Ca colon/sigmoid  Crohn’s dz (terminal ileitis)  Faeces Orthopaedics  Chondroma/sarcoma of ilium  Bony metastasis O&G  Ovarian cyst/tumour  Fibroids Others  Transplanted kidney  Iliac artery aneurysm  Psoas abscess  Iliac lymphadenitis  Malignant change in undesc testis .11 ABDOMINAL MASS RHC Liver Massive  Cancer: HCC Metastases Myeloprolftve dz  Alcoholic liver dz  Rt ht failure/tricuspid regurg Moderate  Above causes  Lymphoprolftve dz  Haemochromatosis  Amyloidosis Mild  Above causes  Infxns: Viral – Hep. IMS Bacterial – abscess Parasitic – hydatid cyst. RA. HS)  Storage dz (Gaucher’s) Stomach Descending colon  Cancer  Diverticular mass/abscess  Faeces Left kidney(see Rt lumbar) Left adrenal gland Mild  Above causes  Infxns: Viral hep. amyloid Right kidney(see Rt lumbar) Umbilical Left Lumbar Right adrenal gland Liver (see RHC) Pancreas (see Epigastrium) Spleen (see LHC) Liver (see RHC) Stomach(see Epigastrium) Aorta  Aortic Aneurysm Left kidney (see right lumbar) Ascending colon mass  Cancer  Diverticular mass/abscess  Faeces Small intestine  Obstruction RIF Gastrointestinal  Appendiceal mass/abscess  TB gut  Ca caecum  Distended caecum (due to distal obstruction)  Crohn’s dz (terminal ileitis) Pancreas  Pseudocyst  Tumour Stomach  Cancer  Distension (GOO) Right adrenal gland Right Lumbar Right Kidney  Hydro/pyonephrosis  Cancer – RCC  Polycystic dz  Single cyst  Amyloidosis  Tuberous sclerosis. MS Peripheral neuropathy Myasthaenia gravis Myopathies e.Lower sphincter is not an anatomical sphincter.OESOPHAGEAL DISEASES ANATOMY . striated and smooth muscle in the middle third.Upper oesophageal sphincter is formed by cricopharyngeus muscle . adventitia (no peritoneal lining except for a short segment of intra-abdominal oesophagus) Muscularis propria is composed of striated muscle in the upper one-third.Blood supply (roughly divided into thirds): Inferior thyroid artery to upper third. thus preventing reflux (iii) Angle of His where the oesophagus joins the stomach – acts as a valve (iv) Intra-abdominal pressure being higher than intra-thoracic pressure . at the same time. oesophageal branches of the aorta to the middle third. myotonic dystrophy Obstructive lesions Tumours Inflammatory masses e. left gastric vein (lower) --. muscularis propria.Further elevation of tongue pushes food bolus into oropharynx . abscess Oesophageal webs Pharyngeal pouch (Zenker’s divert) Anterior mediastinal mass Achalasia Spastic motor disorders Diffuse oesophageal spasm Hypertensive lower oesophageal sphincter Nutcracker oesophagus Scleroderma Obstructive lesions Intrinsic structural lesions Tumours Strictures: Peptic (reflux oesophagitis) Radiation Chemical (caustic ingestion) Medication Lower oesophageal rings (Schatzki’s ring) Oesophageal webs (Plummer-Vinson) Foreign bodies Extrinsic structural lesions PHYSIOLOGY OF SWALLOWING . sneezing etc when intra-abdominal pressure increases. lymphadenopathy Others Oesophagitis: Reflux Infectious (candida. and smooth muscle in the lower third .Pharyngeal muscles contract to propel food bolus past the relaxed cricopharyngeus into the oesophagus . oesophageal branches of left gastric artery to lower third .Dysphagia can be divided into oropharyngeal and oesophageal dysphagia . submucosa.Once in the oesophagus.Starts at the cricoid cartilage (C6 vertebra) from the oropharynx and continues into the stomach at the level of T10 . involuntary contractions of the muscularis propria form peristaltic waves to propel food bolus into stomach APPROACH TO DYSPHAGIA CAUSES OF DYSPHAGIA . the epiglottis falls back. the pharyngeal muscles contract to bring the posterior surface of the larynx upwards to make the laryngeal inlet smaller  closed off by the epiglottis 12 Vascular compression (enlarged aorta or left atrium) Mediastinal masses – retrosternal thyroid.Venous return also divided into thirds: Brachiocephalic veins (upper).g.a portosystemic anastomosis exists at the lower oesophagus thus leading to formation of varices in portal hypertension .Process of mastication forms a food bolus on the dorsum of the tongue .Oesophagus is a muscular tube that is 25cm (10 inches) long . but physiological: (i) Increased tone of the muscularis propria at the lower oesophageal sphincter (ii) Fibres of the right diaphragmatic crus loop around the cardio-oesophageal junction and ontract during coughing.As the base of the tongue is elevated posterior.g.The tongue then contracts upwards and backwards pushing the food bolus against the hard palate .g. ALS.Structure: mucosa. herpes) Radiation-induced Medication-induced Chemical-induced (alcohol) . azygos veins (middle).In each anatomic region the dysphagia can be caused by neuromuscular dysfunction (impaired physiology of swallowing) or mechanical obstruction to the lumen Oropharyngeal Oesophageal Neuromuscular diseases Neuromuscular diseases Stroke Parkinson’s disease Brain stem tumours Degenerative conditions e.3 narrow points along the course of the oesophagus (i) Cricopharyngeus muscle (15cm from incisor teeth) (ii) Carina where the left bronchus crosses the oesophagus (27cm from incisors) (iii) Where the oesophagus passes through the diaphragm (40cm from incisors) .Soft palate elevates (contraction of palatoglossus) to close off nasopharynx . may be toxic. Differentiating mechanical obstruction from neuromuscular dysfunction (i) Mechanical .Patient’s localisation of the symptom often does not correspond to actual site of pathology .Signifies some form of oesophagitis: infectious (candida.Intermittent symptoms are suggestive of webs. sclerodactyly.May have regurgitation of undigested food .May have history of stroke. History of predisposing conditions .Tube feeding through NG tube. cough and haemoptysis (tracheo-oesophageal fistula) Haematemesis (invasion into aorta) Neck lump (lymph node) PHYSICAL EXAMINATION 1.g.Smoking.Patient complains of more trouble swallowing fluids than solids .Recent onset dysphagia that is progressively worsening.Total parenteral nutrition . skin turgor. Complications of disease . Parkinson’s 5. General condition .Can be due to either neuromuscular dysfunction or mechanical obstruction 3.Intermittent symptoms suggestive of diffuse oesophageal spasm.Symptoms of anaemia (bleeding from tumour. Disease - Presence of cervical lymph nodes (esp Virchow’s node) Scars/marks over the chest and abdomen suggesting previous surgery. Treatment .Conjunctival pallor: bleeding from tumour.Reflux symptoms e. or as part of Plummer-Vinson syndrome) .Oesophageal spasm .Scleral icterus: metastases to liver .Vitals: the patient may be hypovolaemic from vomiting/decreased intake . Is there odynophagia (pain associated with difficulty swallowing)? .13 HISTORY: 1. nutcracker oesophagus . post-radiation. slowly progressive . nasal regurgitation . retrosternal burning pain (heartburn). coughing.Symptoms of systemic disease e. Tumour spread - Hoarseness (recurrent laryngeal nerve) Fever.Loss of weight occurs in cancer and achalasia. or associated with P-V syndrome . postural aggravation on lying down . oesophagitis ulcerations. gastrostomy/jejunostomy – if aspirates seen.Presenting complaint is that of food “getting stuck” in the throat or chest . Raynaud’s).Medication history . sour fluid reflux into mouth (acid brash).Pain occurs late in achalasia and oesophageal cancer (not painful from the start) 2. lung crepitations. reflux oesophagitis . stroke (focal neurological deficits). but of much later onset in achalasia compared to cancer . herpes). Differentiating oropharyngeal from oesophageal dypshagia (i) Oropharyngeal . what is the colour? . calcinosis.Signs of pneumonia: patient febrile.May be associated with choking. etc) 2. chronic alcohol intake .Caustic chemical ingestion in the past . decreased air entry usually over right lower lobe 4. radiation Palpable mass in abdomen (not likely) Hepatomegaly Ascites PR examination for malaena 3. scleroderma (telangiectasia.Scleroderma .Presenting complaint is usually of difficulty in initiating swallowing .g.Radiation to the chest .Cause of oropharyngeal dysphagia is usually neuromuscular rather than mechanical. neuromuscular disease 4.Nutrition: presence of cachexia . excessive salivation (water brash). shortness of breath 6.Patient complains of more difficulty swallowing solids than fluids .Dehydration (mucous membranes. rings (ii) Neuromuscular . cough. chemical-induced (usually alcohol).Dysphagia more long-standing. with loss of weight  high suspicion of oesophageal cancer .Voice may sound nasal (bulbar palsy) . Systemic review . stroke is the most common cause (ii) Oesophageal .Symptoms of aspiration pneumonia – fever. Liver function tests – low albumin with nutritional deprivation 2.Advantage of barium swallow is that it is less invasive than OGD.Diffuse oesophageal spasm gives a corkscrew appearance 2. Barium swallow .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 1.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 . . Videofluroscopic examination of swallowing (VFES) or flexible-endoscopic examination of swallowing (FEES) . poor intake. diverticula in the oesophagus where OGD may cause perforation.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 2. barium swallow is dangerous. especially when suspecting webs. CXR . Oesophagogastroduodenoscopy (OGD) . however if patient is at high risk of aspiration.Advantage is direct visualisation of the lesion and ability to take tissue biopsy (especially useful in malignancy).Visualisation of pharyngeal pouch or oesophageal diverticulum .Used to assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various consistencies of food during swallowing INVESTIGATIONS Supportive Diagnostic 1. electrolytes. Blood investigations: .Treat any aspiration pneumonia – NBM. Investigate for underlying cause and treat it 4. Manometry . may also be therapeutic (stopping bleeding from a tumour.If patient complains of reflux symptoms and no signs are seen on OGD (see later section on Gastro-oesophageal reflux disease) Achalasia Benign stricture Carcinoma . raised creat and urea in dehydration (creat will be raised more than urea if patient has prerenal failure from dehydration) . 24-hour pH probe monitoring . IV antibiotics 3. etc) 14 .Full blood count – Low Hb (anaemia from chronic blood loss) High TW (aspiration pneumonia) . Stabilise patient . stenting the lumen.Keep NBM if patient cannot tolerate even fluids . creatinine – electrolyte disturbances from vomiting.Resuscitate if patient is haemodynamically unstable .Consolidation (aspiration pneumonia) 3.IV fluids (correct fluid deficits and also any electrolyte derangements) .Urea.MANAGEMENT 1. Third most common gastrointestinal tract cancer in Singapore . 1.g. Oesophagogastroduodenoscopy . 4-7=1b. Regurgitation 4.Caustic injury (ca occurs at site of scar/stricture. and is about 1% per year) . Endoscopic ultrasound .Smoking (100x increased risk for SCC.Pain develops late and is usually due to extra-oesophageal involvement 2. lung.Increasing incidence with age RISK FACTORS .Achalasia (2-8% incidence of SCC) .SCC can arise anywhere in the oesophagus while adenocarcinoma occurs in lower third and gastro-oesophageal junction (related to reflux and Barrett’s oesophagus) .Obesity (related to reflux. and most patients already have advanced disease when they are diagnosed – 75% have lymph node involvement at time of diagnosis. risk is 3040x higher than in individual without Barrett’s. preserved foods (nitrosamines). Aspiration pneumonia 7.70% squamous cell carcinoma. 10x for adenocarcinoma) .92% accuracy in showing mucosal irregularity and annular constrictions but not able to diagnose malignancy with confidence 2. vitamin E. beta-carotene) . lymphatic spread . 30% adenocarcinoma .Male predominance .Plummer-Vinson (or Paterson-Brown-Kelly) syndrome – Post-cricoid oesophageal web and iron deficiency anaemia.Allows biopsy of the lesion  confirmatory histological diagnosis Staging 1. increased risk of cancer due to metaplasia-dysplasia-carcinoma sequence. “indigestion”. bone Tis T1a T1b N T2 T3 T4 N1 M M1a M1b High-grade dysplasia/carcinoma in-situ Tumour invading lamina propria or muscularis mucosa Tumour invading submucosa but does not breach submucosa Tumour invades the muscularis propria Tumour invades adventitia Invasion of surrounding structures Regional node involvement (1-3 nodes involved =1a. (10% develop cancer in upper third of oesophagus) PATHOLOGY . retrosternal discomfort. Barium swallow .Barrett’s oesophagus (intestinal metaplasia of oesophageal mucosa due to reflux. mostly middle third of oesophagus) . 60% in the middle third. betel nuts.If endoscope can pass around the lesion.Alcohol (2x increased risk) . increases adenocarcinoma incidence) .Tumour spread: direct extension into surrounding structures. Weight loss 3. and also to identify enlarged regional lymph nodes . Dysphagia .15 CANCER OF THE OESOPHAGUS STAGING T EPIDEMIOLOGY . Vocal cord paralysis (left more than right) 6.Tylosis (autosomal dominant disorder with keratosis of palms and soles .Overall: 10% of cancers occur in the upper third. Anaemia (with or without malaena/frank haematemesis – bleeding is usually occult) 5. Tracheo-oesophageal or broncho-oesophageal fistula INVESTIGATIONS Diagnosis 1. with earliest symptoms being non-specific e. the EUS is good for T staging. vitamin and mineral deficiencies (selenium.Three growth patterns:  Fungating (60%)  Ulcerative (25%)  Infiltrative (15%) .Common sites of metastases: liver.Present in 80% of patients – most common presentation . >7=1c) Nonregional lymph node involvement Other distant metastases Stage 0 I IIA IIB III IVA IVB T N M is 1 2/3 1/2 3 4 any any 0 0 0 1 1 any any any 0 0 0 0 0 0 1a 1b PRESENTATION Usually of insidious onset.Diet: Hot beverages. 30% in the lower third . vascular invasion. Bone scan for bony metastases 6.Reflux can result in the long term due to loss of the LES .Surgical treatment is usually performed with curative intention.SCCs are radiosensitive .Three modalities available – surgery. life expectancy. Urea. N.Usually given in combination with chemotherapy . Chest X-ray . Bronchoscopy . chemotherapy. electrolytes. chest.Intraoperatively.Presence of any lung metastases .Oesophagectomy (i) Ivor-Lewis Two-stage procedure involving gastric mobilisation (first stage. gastric mobilisation. radiotherapy – used singly or in combination .Curative in early lesions (in-situ. pain and bleeding . done through upper midline abdominal incision).Pleural and/or pericardial effusion .Can be used for T.Endoluminal surgery – for early lesions. thus patients have to be carefully selected in order to maximise survival benefit from surgery  Complications of surgery dependent on extent of surgery and incisions used .Aspiration pneumonia .Modalities: External beam radiation or brachytherapy . through right thoracotomy incision) (ii) Trans-hiatal Done via two incisions – one in the abdomen and one in the neck Blunt oesophagectomy. nutritional state. co-morbidities. CT scan or MRI of the thorax with extension to include liver and adrenals . and also left neck incision for gastrooesophageal anastomosis in the neck  Performed with two-field lymphadenectomy (upper abdominal and mediastinal)  No difference in survival between trans-hiatal and I-L modalities. and gastro-oesophageal anastomosis in the neck Less morbidity than Ivor-Lewis as the chest is not opened. RLN can occur .Palliative debulking for obstructive symptoms Radiotherapy . and M staging 4. the stage of the cancer when the operation is performed is a greater factor influencing survival  Radical en-bloc dissections not shown to improve survival  Oesophagectomies have high mortality (5%) and morbidity (25%) rates.Anastomotic leak and resultant mediastinitis (for chest anastomosis) most feared . stricture .Aims of treatment: Curative or palliative (50% of patients have unresectable cancer on presentation) .2.Widened superior mediastinum in an upper oesophagus tumour .Choice of treatment depends on several patient factors: age. but controversial (iii) Tri-incisional Three incisions – abdominal. pneumonia .Primary treatment for poor-risk patients. Liver function tests – low albumin with nutritional deprivation TREATMENT Principles . 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) 3.Anastomotic stricturing can also occur . poor intake. injury to lung. oesophagectomy and gastro-oesophageal anastomosis in the chest (second stage. Laryngoscope to assess for vocal cord paralysis Supportive 1.Tracheal deviation or extrinsic compression of tracheobronchial system .Exclude bronchial involvement especially in tumours involving upper two-thirds of oesophagus 5.Raised hemidiaphragm with phrenic nerve involvement 3.Respiratory complications higher in thoracotomies – atelectasis.Obstructive symptoms may worsen temporarily after radiotherapy due to oedema . Full blood count – Low Hb (anaemia from chronic blood loss) High TW (aspiration pneumonia) 2. T1a) and part of multimodal therapy in more advanced stages .Resection should not be done in patients with distant metastases or contraindications to surgery 16 .Complications: tracheo-oesophageal fistula. palliation for unresectable lesions with obstructive symptoms. but can also achieve good long-term palliation of symptoms . thoracic duct. and prognosis of cancer Surgery . no attempt to remove any LNs (usually no LN involvement) . consider PEG placement for long-term feeding if able to get scope around tumour .Lower oesophageal sphincter is a physiological sphincter with various mechanisms that help to prevent reflux (see above. particularly a heavy meal.80% mortality at 1 year. etc. scleroderma .Current regimen: 5-Fluorouracil and cisplatin . but most techniques are not long-lasting and dysphagia will return with tumour growth PROGNOSIS . sedatives.Some physiological reflux occurs that is rapidly cleared by peristaltic movements in the oesophagus . anticholinergics.Chronically increased intra-abdominal pressure – pregnancy. .e.g.Relief of obstruction via various techniques as listed above help to enable oral feeding.Eating habits – lying down after a heavy meal .Motility disorder of oesophagus e. stricture.e. sinusitis).g.Chronic inflammation results in complications of GORD: oesophagitis. tight garments.These symptoms occur usually after food. calcium channel blockers.Chemotherapy given preoperatively and postoperatively improves survival EPIDEMIOLOGY Incidence in Singapore not known Increasing prevalence. consider open gastrostomy . hiatal hernia.Long-standing disease can lead to dysphagia due to stricture formation. overall 5-year survival <10% PATHOPHYSIOLOGY . Barrett’s oesophagus CAUSES/RISK FACTORS . constipation. and postoperative adjuvant chemoradiotherapy for responsive tumours Palliative treatment - Surgical debulking Bypass surgery rarely done nowadays Endoscopic laser fulguration to relieve obstruction Photodynamic therapy is a new treatment option Stenting to maintain lumen patency Feeding in oesophageal obstruction .Total parenteral nutrition is another option but has more complications.Addition of chemotherapy to external beam radiation for unresectable cancers shown to have improved survival compared to EBRT alone . Coffee and smoking also cause LES relaxation. large meal  Motor failure of oesophagus with loss of peristalsis . and are aggravated by lying flat (posturally related) .17 Chemotherapy GASTRO-OESOPHAGEAL REFLUX DISEASE (GORD) .Drugs that cause smooth muscle relaxation e.Feeding via oropharyngeal route is preferred unless the passage is obstructed or it is unsafe for the patient to feed via that route (i. dysphagia can also result from an underlying oesophageal motility disorder. chronic cough.Acid incites inflammation in the lower oesophagus – extent of inflammation increases with increasing duration of contact with acid . odynophagia suggests oesophagitis with ulceration . more costly .Hiatal hernia (loss of normal LES mechanisms) .If unable to pass tube or scope around tumour. regurgitation .GORD results from various pathophysiological factors (loss of the normal protective mechanisms. erosions around nasal area. or the mechanisms are overwhelmed) singly or in combination:  Loss of LES function – decreased tone. beta agonists.Heartburn: retrosternal pyrosis . etc .g.Malfunction of LES .If still able to pass NG tube around tumour  feed via NG (but also consider complications with long-term NG placement e. iatrogenic injury  Delayed gastric emptying  Increased intra-abdominal pressure – obesity. Anatomy of the oesophagus) .Acid brash: reflux of sour gastric juices into back of mouth i.Any cause of decreased gastric emptying PRESENTATION . obesity. more common in males than females Overall curative treatment Preoperative neoadjuvant chemoradiotherapy (increases rates of complete resection). risk of aspiration) . oesophagectomy. The probe is placed 5cm above the manometrically-determined upper limit of the LES (for the wired probe). and exclude malignant cause of dysphagia 2. also. with or without exudates Grade II: Erosive and exudative lesions. and also pick up oesophageal ulceration and stricturing resulting from reflux . Manometry . Avoid drugs that relax LES e. Stricture 3. Elevate head of bed 5. but not between the tops of adjacent mucosal folds Grade C: at least one mucosal break that is continuous between the tops of adjacent mucosal folds. Los Angeles classification Grade A: one or more mucosal breaks. History is important as most patients with reflux are seen in the primary setting with no facilities for detailed investigation . 3.Confirmatory test for reflux is the ambulatory 24hr oesophageal pH probe especially if oesophagitis is not seen on OGD . alternative is the Bravo capsule (a wireless capsule that is temporarily attached to the oesophageal wall) .Antimony probe most commonly used. water brash (hypersalivation in response to reflux) COMPLICATIONS 1.Diagnosis based on the percentage of time in 24hrs the pH reading is below 4 4. etc. Barium swallow and follow-through . each <5cm in length Grade B: at least one mucosal break >5cm long. Dysmotility 8. Shortening of oesophagus 5.May see a hiatal hernia which is associated with reflux (though not all patients with hiatus hernia will have reflux) 3.Reflux can also lead to pulmonary symptoms: chronic cough. Ulceration 6. but which is not circumferential Grade D: mucosal break that involves at least three-quarters of the luminal circumference .Relevance of classification schemes: subjective and dependent on assessment by the endoscopist. chocolate. Savary-Miller classification Grade I: One or more supravestibular non-confluent reddish spots. Smoking and alcohol intake cessation . arm).Other symptoms: globus (feeling of a lump at the throat).g.Can sometimes see reflux of barium contrast into oesophagus 5. Malignancy (adenocarcinoma arising from Barrett’s oesophagus) DIAGNOSIS 1. Haemorrhage (occult more common than frank) 4. eat small meals 2. just mentioning a grade may not have any meaning if the actual abnormalities are not described TREATMENT Lifestyle 1.Can visualise and grade oesophagitis if present. Oesophagogastroduodenoscopy . stenosis. chest pain (can mimic anginal pain with radiation to neck. Diet and eating habits  Avoid coffee. and take biopsy specimens for confirmation (see below) . anticholinergics. may be confluent but not circumferential Grade III: Circumferential erosions covered by haemorrhagic and pseudomembranous exudate Grade IV: Presence of chronic complications such as deep ulcers. or 6cm above the endoscopically-determined squamocolumnar junction (for the wireless capsule) . fatty foods. Barrett’s oesophagus (see below) 7.Can detect motility disorders that cause reflux. or scarring with Barrett’s metaplasia 2. nausea..Cannot actually diagnose reflux . Weight reduction if obese 4.No value in reflux except for detecting motility disorder GRADING OF OESOPHAGITIS 1.Exclude cardiac cause of chest pain.Not of much value in diagnosing reflux 18 . due to the multitude of classification schemes available. chest infections (aspiration) . jaw. or anything that worsens symptoms  Do not eat 2 hours prior to sleeping  Walk after eating  Avoid excessive eating. Pain and spasm 2. Oesophageal pH probe . Schatzki’s ring (constrictive ring at the squamocolumnar junction composed of mucosa and submucosa) 9. muscle relaxants. may result in mediastinitis if not promptly detected and repaired intraoperatively  Excessively tight wrap resulting in dysphagia  Excessively loose or short wrap – reflux recurs (failure of treatment)  “Slipped-Nissen” occurs when the wrap slides down.Indications:  Failure of medical therapy (or incomplete resolution of symptoms)  Oesophagitis with frank ulceration or stricture  Complications of reflux oesophagitis – respiratory complications. the GE junction retracts into the chest.e.g.Outcome of surgery  80-90% Excellent to good (no symptoms. and the stomach is partitioned. anterior 180 deg. 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. anterior 90 degrees. Acid suppression therapy: proton pump inhibitors or H2-receptor antagonists 2. as well as higher risk of dysplasia and subsequent adenocarcinoma development than short segment Barrett’s . and posterior 270 deg fundoplications are various options available .Surgery versus conservative treatment  Surgery has higher rates of cure and better long-term results  No need to adhere to strict lifestyle and diet change as well as long-term medication  Disadvantage of surgery is the associated morbidity and mortality . .Management of stricture  Rule out malignant cause of stricture by taking biopsy  Dilatation (variety of means available – balloon.Intestinal metaplasia of the oesophageal epithelial lining (stratified squamous epithelium converted to mucus-secreting columnar epithelium with goblet cells) . 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 . while in long segment Barrett’s the distance between the two junctions is >3cm.Fundoplication is the mainstay of surgical therapy  Can be done via open surgery or laparoscopic surgery (most laparoscopic now)  Nissen fundoplication is the most commonly done – a 360 degree (total) wrap of the fundus around the gastro-oesophageal junction  Partial fundoplications can also be done in patients where oesophageal motility is poor or the oesophagus is foreshortened. they do not align) and biopsy of the junction shows intestinal metaplasia. Barrett’s oesophagus  Severe symptoms or progressive disease  Compliance problems . Prokinetics to increase LES pressure e. metoclopramide Surgical .19 Medication 1.Diagnosed on endoscopy and histology:  The squamocolumnar junction (or Z line) is visible on endoscopy as gastric and intestinal type epithelium is pink and granular in appearance.Long segment Barrett’s is associated with more severe reflux.Risk of development of adenocarcinoma is about 10-15% in 10 years .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) . etc)  Treatment of underlying reflux  If resistant to dilatation  resection and reconstruction .Complications of surgery  Perforation of the oesophagus – most feared complication.Short segment Barrett’s is defined as the squamocolumnar junction being <3cm above the gastro-oesophageal junction. domperidone. the patient is diagnosed to have Barrett’s oesophagus . dilators. usually due to a foreshortened oesophagus unrecognised in the first operation  “Gas bloat syndrome” – patient experiences difficulty burping gas that is swallowed BARRETT’S OESOPHAGUS Features .Associated with long-term reflux – an adaptation mechanism where intestinal epithelium withstands exposure to acidic reflux better than oesophageal epithelium .patient does not want to be on medication for life (despite good results) . Endoscopic surveillance .Abnormal peristalsis secondary to absence or destruction of Auerbach’s (myenteric) plexus and failure of the LES to relax. with incomplete LES relaxation on swallowing. but is associated with high morbidity and mortality (worth it?) . there is a 3% chance of developing reflux  addition of fundoplication helps prevent this .Surgical treatment  Laparoscopic Heller cardiomyotomy (much like Ramstedt pyloromyotomy for pyloric stenosis) – good results with 85% symptom-free after 5 years. repeat OGD once every 3 years . argon plasma coagulation  will not remove all dysplastic cells thus potential for malignancy still remains .Mainly palliative in nature .Non surgical treatment:  Injection of botulinum toxin (problem is that it is not long lasting and only used in patients not fit for surgery)  Pneumatic balloon dilatation (about 65% of patients improve. regurgitation. Treatment of underlying reflux . retrosternal chest pain.Patients present with dysphagia. photodynamic therapy.Manometric studies (required for diagnosis) show abnormally high pressures at the LES.Lifestyle changes.Main purpose of surveillance is to pick up dysplasia .Not shown to decrease risk of cancer  still requires surveillance 2.Management 1.g. acid suppression. Treatment of high-grade dysplasia . otherwise to undergo intensive surveillance (q3mths for at least one year) to detect cancer development 3.Endoscopic therapies to ablate the dysplastic tissue e. and recurrent pulmonary infections . weight loss. and lack of progressive peristalsis (often aperistaltic) .Barium swallow demonstrates “bird’s beak” narrowing of distal oesophagus with proximal dilatation . it should be treated (see below).Not certain regarding benefit for surveillance if patient has Barrett’s but no dysplasia  if 2 scopes in a year reveal no dysplasia.Aetiology unknown .Possibility of endoscopic mucosal resection as a treatment modality (research still undergoing) 20 ACHALASIA FEATURES . laser therapy.1-10% of patients develop SCC after 15-25 years of disease TREATMENT .If patient has high grade dysplasia.Oesophagectomy is the only definitive treatment to remove all dysplasia. affects body and distal oesophagus . 40% response rate at 5 years) . surgery etc . TCM Varices .Altered blood. aortoenteric fistula HISTORY (if patient is stable) 1.Binge-drinking with subsequent severe retching and vomiting leading to haemetemesis Malignancy . lethargy. Complications .Any history of chronic liver disease Mallory-Weiss tear .21 UPPER BLEEDING GIT AND ITS CAUSES APPROACH TO BLEEDING UPPER GIT CAUSES 1. AV malformation .Other comorbidities: liver disease. gastritis/erosions. Rare causes: AV malformation (Dieulafoy lesion). antiplatelets. or variceal blood that has entered the stomach Malaena . palpitations. Gastric malignancy 6.Very brisk upper GI bleed can present as frank PR bleeding as blood passes down so fast it doesn’t get altered 2. Mallory-Weiss tear. chest pain . Mallory-Weiss tear 5.Blood pressure.Recent constitutional symptoms e. non-particulate (almost liquid in consistency) (b) Stale malaena – black-grey.Compare current vitals with vitals in ambulance. Abdomen . mixed with normal stool. malaena indicates bleeding from the upper GIT i. Gastritis. Vitals! . IHD  high risk PHYSICAL EXAMINATION 1. . General inspection .Pallor . gastric erosions 4. ED – is there a worsening trend? 2.Stigmata of chronic liver disease 3.If patient is having haematemesis. above the ligament of Treitz . but iron stool will sedimentate and turn the water green Frank PR bleeding .Any drugs that may predispose – NSAIDs. heart rate stable? Any postural hypotension? (Tachycardia is an early sign of shock) . malaena will “dissolve” completely with no sedimentation and turn the water black.Any history of dyspepsia. Nature of bleeding Haematemesis . Amount of blood . steroids. particulate.Elderly patient (>60)  high risk . decreased effort tolerance. malaise .Early satiety . Gastro-oesophageal varices 3.May even be having AMI if it’s an old patient with history of IHD 5. Comorbidities .Malaena or frank blood . tarry. ask how much blood  Cup? Bowl? 3. occasionally particulate (c) Iron stool – greenish hue on rubbing between gloved fingers. anticoagulants. gastric ulcer (any OGD done in the past showing these problems? On any “gastric” medications?) .Any tenderness (not very helpful) 4. Peptic ulcer disease (bleeding peptic ulcer) 2.Can be fresh red blood as in variceal bleeding.Patient’s conscious level – confused? .Different types of malaena: (a) Fresh malaena – jet black with sheen.Cold clammy peripheries  impending shock .Symptoms of anaemia: postural giddiness.e. renal disease. dull.Coffee grounds vomitus is altered blood (due to gastric acid) and can come from gastric ulcer. LOW. shortness of breath. Aetiological clues Gastric ulcer/gastritis/erosions .If gloved finger is stirred in a cup of water. LOA.g.Dyspepsia 4. Digital rectal examination . and blood investigations 4.Protect airway before inserting tube.Previous history of variceal bleed . breathing. Resuscitate . oesophageal balloon is not inflated nowadays .e.NG tube if patient is having haematemesis – prevents aspiration. Prophylaxis 3. postural hypotension . IJV) Send bloods – GXM. Acute bleeding 2. LFT. confirm diagnosis  Therapeutic interventions – injection of ulcer.Airway. FBC.FFP if patient is on anticoagulants or PT/PTT prolonged (+ vitamin K) 2. ligation/sclerotherapy for varices 22 - 2 large-bore IV cannula in proximal veins (cubital.Monitor for:  Increase in heart rate  Decrease in BP  Decrease in urine output  Increasing confusion and lethargy VARICEAL BLEEDING PATHOPHYSIOLOGY A result of portal hypertension (i.IV omeprazole 80mg bolus (increases stomach pH and stabilises clot formation) .IMMEDIATE MANAGEMENT 1.Packed cells if Hb is less than 10. U/E/Cr Infuse fluids Under-resuscitate in variceal bleed (cf ulcer bleed) to keep Hb around 9. supplemental oxygen. IV antibiotics. Close monitoring .Inflate gastric balloon and pull upwards against cardioesophageal junction (balloon will press on perforator veins entering oesophagus from stomach.1 pint N/S over half to one hour if patient is in shock. portal venous pressure >20 cmH2O or >12 mmHg – normal should be 7-14 cmH2O or 5-10 mmHg) WHEN TO SUSPECT VARICEAL SOURCE IN UBGIT . U/E/Cr. as enthusiastic transfusion can increase portal pressure and cause more bleeding 4. GXM 4 pints .Role of endoscopy  Identify source of bleeding. or anticipating surgery . EJV.ECG to detect any acute myocardial ischaemia/infarction . .Indications:  Shock (resuscitated)  Ongoing BGIT  Suspected variceal bleed . 2 large-bore IV cannula in antecubital fossa . to keep Hb above 10g/dL . ACUTE BLEEDING – MANAGEMENT 1.If suspecting varices – IV somatostatin/octreotide. Emergency oesophagogastroduodenoscopy .Catheterisation – monitor input/output balance especially in elderly patient or when large amount of fluid resuscitation required. look for early signs of shock – tachycardia.Jaundice or stigmata of chronic liver disease MANAGEMENT OF VARICES can be divided into three categories: 1. Resuscitation . . PT/PTT.If patient is hypotensive and bleeding is still continuing – may require use of Sengstaken-Blakemore tube. Adjuncts . vitamin K 3. circulation . Chronic management I. and thus decrease oesophageal variceal bleeding).Chronic alcohol intake .Look at hydration status 2. followed by more fluids if necessary (be wary in patients with renal failure. Vascular access.Protect airway. Assess mental state .Take blood for investigations: FBC.If patient has altered mental state (encephalopathy)  need to protect airway (may require intubation) 3. Management of severe bleeding . fluids/blood resuscitation.May consider platelets if patient is on antiplatelet medication (qualitative defect in platelets) .If patient appears well. heart failure) . allows gastric lavage prior to OGD (DO NOT insert if suspecting varices) . Needs to be done emergently (on that night of admission) as soon as patient is stabilised since bleeding can be torrential and life-threatening .Best option is combination of band ligation and non-selective beta-blockers e. propranolol unless propranolol is contraindicated II.Preferably started before endoscopy (procedures increase bacteraemia) If bleeding is not remediable by endoscopic intervention: . 7. Hepatic vein thrombosis . Secondary prophylaxis . end-to-side  Mesocaval shunts (joining superior mesenteric vein to IVC)  Proximal splenorenal shunt (splenectomy with end-to-side anastomosis of portal side of splenic vein to left renal vein)  Distal splenorenal shunt (Warren-Zeppa shunt – splenic vein divided and splenic side anastomosed end-to-side to left renal vein) .Studies have shown that cover with broad spectrum antibiotics (with Gram neg cover) decreases infectious complications.g.Shunt surgery  Portocaval shunts (joining portal vein to IVC) – side-to-side. aids haemostasis . possibly mortality.Purpose: confirm diagnosis and institute management . proximal gastric devascularisation. PRIMARY PROPHYLAXIS OF VARICEAL BLEEDING Use of non-selective beta-blocker e. ?benefit of gastric decompression using NG tube (c) risks of procedure – OGD-related risks 10.Also acts indirectly to inhibit secretion of gut hormones that increase portal blood flow 6.Sugiura procedure (last resort): splenectomy. Antibiotics .Radiologically guided insertion of transjugular intrahepatic porto-systemic shunt (TIPSS) .Gastric varices are usually too large to be banded. oesophageal transection 8.Banding is the best modality for stopping oesophageal variceal bleeding (sclerotherapy is associated with higher morbidity e.Not given in ulcer bleed. propranolol can be used to prevent development of varices in patients without varices. IV somatostatin/octreotide .Anticipate complications: (a) encephalopathy – fleet and lactulose. sclerotherapy used instead 9.Continue somatostatin up to the point where haemostasis is achieved or 5 days (exact ideal duration not well studied) . Acid suppression . and can decrease the size of and prevent bleeding from varices in patients who already have them. mode of action is as a splanchnic vasoconstrictor which decreases portal blood flow and hence portal pressures  decreased variceal bleeding . the use of propranolol is of questionable benefit – repeat OGD to monitor varices. etc. In patients with small varices with no risk of bleeding.Continue antibiotics and omeprazole . mucosal ulceration) . treat hypokalaemia from vomiting (b) aspiration – protect airway.Agents available: omeprazole.Insert Sengstaken-Blakemore tube (only temporary) and repeat endoscopy 10-12 hours later . and also risk of recurrent bleed .Increasing intragastric pH increases clot stability. pyloroplasty. Observation .NSAIDs.23 5. Management of possible precipitants . Predictors of variceal haemorrhage: 1 Site: varices at the gastro-oesophageal junction have the thinnest coat of supporting tissue and are at highest risk of rupture and bleeding 2 Size: F1: Small straight varices F2: Enlarged tortuous varices that occupy less than one-third of the lumen F3: Large coil-shaped varices that occupy more than one-third of the lumen 3 Child’s score – patients with higher Child’s score have higher risk 4 Red signs: Red wale marks (longitudinal red streaks) Cherry red spots (flat discrete spots) Haematocystic spots (raised discrete spots – resemble “blood blisters”) Diffuse erythema 5 Previous variceal haemorrhage: 70% of patients will have further variceal bleeds after an index bleed 30% rebleed within 6 weeks (risk highest in first 48 hours after first bleed). pantoprazole. 30% rebleed after 6 weeks 11.Not given in ulcer bleed .g.g. selective vagotomy. esomeprazole. oesophageal devascularisation. Endoscopy . pylori .Overall mortality is 7-10%. Perforation .000 per year .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) .Protective mechanisms: mucus secretion.Board-like rigidity. and 50% of gastric ulcers NSAIDs .If patient bleeds again  failed ablation  consider surgery (as above – shunts. as well as maintaining mucosal blood flow PRESENTATION PEPTIC ULCER DISEASE 1. prostaglandin secretion by mucosa to maintain blood flow 24 (a) Ulcer-like dyspepsia: pain in the upper abdomen is the predominant symptom (b) Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen. pylori . but increase the risk of bleeding in an existent ulcer PATHOGENESIS .Aggressive forces: gastric activity and pepsin activity . Symptoms of dyspepsia EPIDEMIOLOGY .About 10-20% of infected patients develop an ulcer . guarding will be present on examination (signs of peritonism) . epithelial regenerative capacity. pylori by age 21 .30% of patients on NSAIDs will get an ulcer. bicarbonate secretion into mucus. early satiety.Incidence about 100 per 100. of which one-fifth will have a clinically significant ulcer i. pylori . associated with upper abdominal fullness.Cigarette smoking . Bleed . symptomatic.Erect CXR will show air under diaphragm ENDOSCOPY (OGD) .60% of population are positive for H. CHRONIC MANAGEMENT . Incidentally detected on OGD 2.An imbalance between mucosal protective mechanisms against acid. bleeding Other factors . belching. and also enhances gastric acid secretion and decreases bicarbonate production .As above. robust mucosal blood flow to remove protons.68% of patients are over 60 years of age .Roles of endoscopy: (a) Diagnosis     Confirmation of ulcer disease Location of ulcer Biopsy to rule out malignancy (usually 6 bites) Biopsy of antral tissue for CLO (Campylobacter-like organism) test for H.Accounts for 90-95% of duodenal ulcers. presenting with haematemesis (coffee-grounds vomitus) or malaena 4. unchanged for last 2 decades – mostly due to ulcer bleeding especially in elderly with significant comorbidities MAIN AETIOLOGICAL FACTORS H. while it is relieved by food in a duodenal ulcer 3. bloating.Accounts for most of the rest of ulcer disease not caused by H.Pain is usually worse with food in a gastric ulcer. pylori causes a local inflammatory reaction and secretes enzymes that break down the gastric mucosal barrier.NSAIDs impair mucosal prostaglandin production (through non-selective COX inhibition)  prostaglandins are important for mucosal bicarbonate and mucin production and inhibiting gastric acid secretion.H. or Sugiura) .e. and aggressive forces that damage the gastric mucosa .Steroids and anticoagulants do not increase the risk of ulcer formation. nausea (c) Unspecified dyspepsia .III.Patient presents with sudden generalised abdominal pain that is aggravated by even the slightest movements .Alcohol .The most important and valuable investigation . can treat similar to duodenal ulcer . urea breath test or stool serology testing  Treatment failure occurs in up to 20% . Persistent bleeding (e. PPI. erosion of a posterior duodenal ulcer into gastroduodenal artery) 2. Gastrectomy 3. pylori) GASTRIC ULCER Indications for surgery 1. pylori eradication  First line triple therapy: omeprazole 20mg BD. ooze (venous) 2a Non-bleeding ulcer with visible vessel 2b Non-bleeding ulcer with adherent clot 2c Ulcer with haematin-covered base (flat spot) 3 Ulcer with clean base Bleeding risk 90% 20% 40% 20% 10% 5% (c) Endotherapy (in UBGIT)     Injection with adrenaline (1:10.Vagotomy can be truncal. 4. Failure of medical management (ulcer does not heal) Surgery: 1. biopsy ulcer again (exclude malignancy for gastric ulcer) and also do antral biopsy for CLO test (to confirm eradication of H.000) or absolute alcohol Thermal coagulation (heater probe) Haemostatic clipping (endoclip) Argon plasma coagulation CONSERVATIVE MANAGEMENT 1. IV antibiotics. Antrectomy with truncal vagotomy 4. omeprazole 20mg BD for 7 days Re-scope in 6 weeks to document ulcer healing If ulcer still present. Oversewing the bleeding vessel 2. or highly selective . Gastric outlet obstruction (patient presents with vomiting of undigested food not long after meal. Vagotomy with gastric drainage procedures . parietal cells also become less responsive to histamine and gastrin. Gastrectomy 5. metronidazole 400mg BD.25 (b) Prognostication of bleeding risk (in UBGIT)  Forrest classification (or endoscopic stigmata of recent haemorrhage – ESRH) SURGICAL MANAGEMENT DUODENAL ULCER Forrest grade 1a Spurting (arterial) 1b Non-spurting. selective. characteristic electrolyte abn of hypokalaemic hypochloraemic metabolic alkalosis with paradoxical aciduria) 4. Failure to heal after 3 months of conservative therapy Dysplasia or carcinoma Recurrence Perforation. succussion splash. air-fluid levels on AXR. ulcers will not heal with ongoing NSAID therapy Indications for surgery: 1. surgery (patch repair) 2.Drainage procedures usually done with vagotomy as gastric emptying is decreased with denervation  gastrojejunostomy or pyloroplasty 3. H. If prepyloric ulcer. 2. persistent bleeding Surgery 1. Omental patch repair is sufficient for small perforated ulcer Perforated ulcer: IV fluids.treat with quadruple therapy: colloidal bismuth subcitrate 120mg QDS. amoxicillin 1g BD.Rationale for vagotomy is to eliminate direct cholinergic stimulation to gastric secretion. 3. Perforation 3. substitute amoxicillin with metronidazole 400mg BD  Document eradication by endoscopy with CLO test. and vagal stimulus for gastrin release is abolished .g. 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. tetracycline 500mg QDS. Oversewing the bleeding vessel 2. clarithromycin 500mg BD for 7 days  In penicillin-allergic patients. Types: SCC.000 per year . in older men.Female to male ratio 2:1 .Early gastric cancer  Confined to mucosa and submucosa  Good survival and prognosis regardless of size. rubber Low socioeconomic status 2. pancreatic and intestinal secretions at the anastomotic zone 2.Lauren classification: (a) Intestinal type (most common overall) – occurs in high risk population. H.3-6X increased risk of gastric cancer EPIDEMIOLOGY . lymph node status. up to 10% risk of malignant change .Usually occurs >15 years after surgery . growing intraluminally Ulcerated. more aggressive. histological grade Non-adenocarcinoma . pylori infection .37% in cardia . leiomyosarcoma. sixth most common in females in Singapore . in younger and female patients. heavy metals. smoked foods. 2-10% risk of gastric cancer 4. proximal third and cardiooesophageal junction. neuroendocrine tumour.Incidence increases steeply after 50 years old RISK FACTORS 1. Chronic atrophic gastritis . associated with erbB2 and erbB3 receptor stimulation (b) Diffuse type – occurs in low risk population. linitis plastica) MORPHOLOGY Borrmann’s classification: - Type I (3%): Type II (18%): Type III (16%): Type IV (63%): Nonulcerated. polypoid. Peptic ulcer disease .30% in pyloric channel or antrum . may be ulcerated. distal third of the stomach. present later.Make up less than 10% of stomach tumours . primary gastric nonHodgkin’s lymphoma (MALT.12% in entire stomach .Make up 90-95% of stomach tumours . Genetic - Blood type A HNPCC – Lynch syndrome II P53 mutation Germline mutation of e-cadherin Family history of gastric cancer PRECURSOR CONDITIONS 1. GIST. Partial gastrectomy for benign disease with Bilroth II reconstruction . infiltrating. associated with K-sam oncogene .<1% risk of malignant change 26 HISTOLOGY Adenocarcinomas . polycyclic hydrocarbons Smoking Alcohol Occupational exposure: asbestos.GASTRIC CARCINOMA 5. worse prognosis. may diffuse entire stomach (linitis plastica) LOCATION .Fourth most common cancer in males.Hypertrophic gastritis (Menetrier’s disease) – inflammatory disease of gastric epithelium.Due to chronic exposure of gastric mucosa to biliary. margin not sharply circumscribed Diffuse.Pernicious anaemia – autoantibodies to parietal cells with achlorhydria.20% in body .Also increased risk of adenocarcinoma elsewhere in the stomach 3. circumscribed with sharp margins Ulcerated. Gastric polyps .Highest risk in inflammatory polyps: 75-90% .Incidence 10-18 per 100.10-20% risk in adenomatous polyps especially in large polyps (>2cm) or those with villous histology . Environmental - Diet: preserved foods (nitrosamines). higher chance of leak  Oesophagojejunostomy (after total gastrectomy) Complications of gastrectomy: Early 1. bone.Direct extension to neighbouring organs . Anastomotic leak . 2.Nausea/vomiting 40% . low chloride.Palpable mass 30% .Haematogenous spread – liver. parietal peritoneum.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 one-fifth of patients whose disease was thought to be resectable)  change in stage of disease 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: .Weight loss 50% .Anaemia 40% .27 SPREAD . body) as well as diffuse-type tumours and cardio-oesophageal junction tumours .Peritoneal seeding to omentum. but involves 2 anastomoses. alkalosis LFTs – albumin as a marker of nutritional status (alb<35 is poor). neurological deficits.Gastric outlet obstruction  vomiting (dehydration. Infection 3. lung. 4.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. brain . etc)  New onset dyspepsia at age>35 years old should cause concern COMPLICATIONS . liver mets CXR – lung mets Endoscopic ultrasound – gold standard for T staging and good for N staging 6. better functional outcome (some residual reservoir function preserved)  Total gastrectomy is the resection of choice for proximal tumours (fundus.Haematemesis/malaena 25% . cardia.Wide resection of the tumour to negative margins (at least 6cm margins) . 3.Perforation . or cul-de-sac (Blumer’s shelf) PRESENTATION Very non-specific symptoms and signs: .Malnutrition INVESTIGATIONS Diagnosis by OGD – best for visualisation and biopsy (usually an ulcer with heaped- up edges) Supportive/staging investigations 1. low potassium.Early satiety 17% . FBC – low Hb U/E/Cr – if vomiting.Lymphatic spread (a) Regional nodes (b) Supraclavicular nodes (Virchow’s node) (c) Umbilical (Sister Joseph’s node) . aspiration) . hypokalaemic metabolic alkalosis. CT scan – good for T and N staging 7.Bleeding . 5. Bleeding 2.Abdominal pain 60% .Metastatic symptoms late (bony tenderness. ovaries (Krukenberg’s tumour).Reconstruction  Bilroth I (end-to-end gastroduodenostomy) – rarely done as it is difficult to mobilise duodenum up to anastomose with residual stomach  Bilroth II/Polya (gastrojejunostomy) – no protection against biliary reflux into stomach  Roux-en-Y – to prevent biliary reflux. nausea. gastrojejunostomy for obstruction . methotrexate. doxorubicin.Occurs in Bilroth II/Polya reconstruction .Need to supplement with B12 injections and iron supplements CHEMOTHERAPY/RADIOTHERAPY Adjuvant therapy 5-fluorouracil with chemotherapy 5-fluorouracil with epirubicin for advanced disease Neoadjuvant therapy . Early satiety 2. followed by intraperitoneal 5-FU  improved resection rates.Late dumping syndrome: reactive hyperinsulinaemia with hypoglycaemia. obstruction .For resectable disease: preoperative 5-FU. palpitations. median survival 28 PALLIATIVE THERAPY .For palliation of symptoms such as pain. Dumping syndromes .Surgical options: subtotal gastrectomy (6-15% mortality).Embolisation for bleeding .Iron deficiency – mixed picture (a) Loss of intrinsic factor  B12 deficiency (b) Decreased conversion of iron from Fe3+ to Fe2+ by gastric acid  decreased iron absorption in terminal ileum . Nutritional deficiency . locally advanced disease with a significant increase in resectability (61%  79%) . Intestinal hurry .External beam radiotherapy for pain.5-FU and cisplatin can be used to downstage unresectable. cisplatin.Not enough antrum removed leads to increased acidity in residual stomach.Endoscopic laser ablation for obstruction .Can be decreased by doing Roux-en-Y surgery (but may still occur) 7. Biliary/intestinal reflux into stomach .Stage II 70% .Late 1.Inadequate reservoir function leads to poor digestion  may have phytobezoar formation 4. treat by eating small frequent meals with low carbo and high protein/fat . Afferent limb syndrome . anastomotic narrowing. bleeding.Stage I 90% 5-year survival . resulting in flushing.Stage III 40% .Early dumping syndrome: due to increased osmotic load in bowel occurring half to one hour after meal. treat by eating more carbohydrates 5. low-level ongoing bleeding (not for heavy bleeding as it takes weeks to cause fibrosis) PROGNOSIS .Mechanical obstruction of the afferent jejunal loop due to kinking. total gastrectomy (20-40%). Retained antrum syndrome . or adhesions  postprandial epigastric pain with non-bilious vomiting .Stage IV 0% . with formation of marginal ulcers on the jejunal side of the anastomosis 3. dizziness.Leads to symptoms of dyspepsia 6. response rates. 25% in transverse colon . APC pathway (adenoma-carcinoma sequence) . and without clearly identifiable morphologic correlates i.Like the APC pathway.Tumours that arise from this pathway have a better prognosis than tumours that arise from the APC pathway SITE: .Due to mutations in one of the five DNA repair genes (MSH2. Defects in DNA mismatch repair . MSH6. Intraluminal 4.90% of tumours are sporadic . MLH1. PMS1. but due to a different mechanism.Characterised by chromosomal instability . Nodular SPREAD 1.Almost all tumours are adenocarcinomas . Intramural – along bowel wall 2.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 . Direct extension into surrounding tissues e. ovary 3. no adenomas . Polypoid – more common in the right colon as there is more space to grow 2.Accounts for 80% of sporadic colorectal carcinomas . betacatenin accumulates and activates various genes in the nucleus (such as MYC and cyclin D1) which promote cell proliferation  K-RAS (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering mitotic signals and prevent apoptosis  Loss of tumour suppressor gene at 18q21  Loss of p53 late in carcinogenesis .29 COLORECTAL DISEASES COLORECTAL CARCINOMA EPIDEMIOLOGY Commonest cancer in Singapore men. small bowel.1% arise in association with long-standing ulcerative colitis (>10 years) PATHOGENESIS There are 2 pathways for cancer development in the colorectal mucosa: 1. Ulcerated 4.Stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes:  Loss of the APC suppressor gene on 5q21 (congenitally absent in patients with familial adenomatous polyposis – APC) is the earliest event in adenoma formation  APC is required to break down beta-catenin.8% arise in association with hereditary non-polyposis colon carcinoma (HNPCC) and 1% in association with familial adenomatous polyposis (APC) .25% in caecum and ascending colon . number 2 cancer in Singapore women Peak incidence at 60-70 years of age PATHOLOGY . Scirrhous – annular “apple-core” lesions. there is accumulation of mutations. Transcoelomic . more dysplastic adenoma  carcinoma in-situ  invasive cancer 2. more common in the left colon 3. Lymphatic 5.e. Haematogenous – to liver.Most are left-sided though there is an increasing incidence of right-sided tumours MORPHOLOGY 1. with the loss of APC. PMS2) of which MSH2 and MLH1 are the most commonly involved in sporadic colorectal carcinomas .g.The molecular evolution of colon cancer through this pathway occurs through a series of morphologically identifiable stages: localised epithelial proliferation  small adenoma  large.Involved in 10-15% of sporadic cases . lungs 6.25% in distal sigmoid and rectum .25% in descending colon and proximal sigmoid . preserved foods (nitrosamines). while metachronous adenomas occur at a rate of 25-40% . and risk is further increased if there are 2 first-degree relatives with CRC. palpitations. malaise Note: Site of CA . decreased effort tolerance. LOW. amoeba.Metastatic symptoms – bone pain .Diet: high in red meat.Bloody diarrhoea – ddx:  IBD  Infective e. should be screened starting at age 45. and polyps with tubulovillous or villous histology. Environmental factors . brown . Adenomatous polyps . particularly if multiple (3-6X increased risk) . other polyposis syndromes such as Peutz-Jegher’s. difficile) .Haematochezia – ddx:  Diverticulitis  Angiodysplasia (AVM. accounting for 8% of cancers 4.Ascending: anaemia.Lower down: I/O.Family history of one first-degree relative with CRC increases risk of CRC 1. or if the relative had CRC before the age of 55 . tenesmus 30 .Increased risk if there is a personal history of large (>1cm )adenomatous polyps. or two first or second degree relatives from the same side of the family with CRC at any age.Small (<1cm) tubular polyps do not have increased risk 6. Family history or personal history of colorectal carcinoma .Associated secretions  Blood o Mixed in stool? o Separate from stool?  Mucus . shortness of breath. Age >50 years A) 5 things to ask about bowel habits – FACCE .Metachronous colorectal cancers occur at a rate of 3-5% in the first five years after resection of a primary CRC.Frequency .Constitutional symptoms – LOA.7X.>3x/day=diarrhoea. normal. Cronkhite-Canada have a small increased malignant potential (b) HNPCC – more common than FAP. postural giddiness.Family history of colonic adenoma appears to have the same significance as family history of colonic carcinoma  Anyone with one first degree relative diagnosed with CRC younger than 45 years old. vitamins. watery . TB. Genetic predisposition (a) Polyposis syndromes – FAP and its variants. after 15-20 years if the patient has disease limited to the left colon 5.RISK FACTORS HISTORY 1.Consistency – pellet.Effort – tenesmus Stool Changes . minerals .Iron deficiency anaemia – fatigue. chest pain . no obstructive symptoms usually .Abdominal mass . soft. clay. bleed. common in old)  Massive upper GI  Hemorrhoids - Progressively worsening constipation requiring chronic laxatives Spurious diarrhoea Mucoid stools Progressive intestinal obstruction symptoms Tenesmus (rectal ca) Other Symptoms . hookworm  Antibiotic Associated Colitis (C. Gardner’s and Turcot’s syndromes are associated with near 100% risk of cancer formation.Increased risk after 10 years of disease if the patient has pancolitis. or 10 years earlier than the youngest cancer in the family .Colour – black.g.NSAIDs may be protective against CRC 3. low in fibre. <2x/week=constipation 2. Ulcerative colitis . cervix. or transrectal ultrasound for rectal tumour .Enables therapeutic procedures e. ovarian cancer FAP history INVESTIGATIONS Aims .Haemorrhage (usually occult)  anaemia .Classically can see an apple core lesion with barium enema C) Other risk factors . breast.Local T staging .Obesity .Staging of regional and no-regional lymph note involvement .Can also assess local lymph node status (c) CXR + CT scan of the chest (d) MRI of the tumour . hepatomegaly .Fistula – colovesical fistula causing faecuria.Metastases to the liver (b) Endoscopic ultrasound. peritonitis PHYSICAL EXAM 1. FAP and HNPCC considered very high-risk (b) Double-contrast barium enema (barium + air) .Cachexia .FAP is excluded (a) Colonoscopy – first-line investigation . bladder and kidney II.Can take biopsies of the lesion . cholangitis and cancers of the stomach. non-tender.g.Perforation . bronchitis. 2.Low fibre diet . 2.3 or more family members from the same side with CRC.1 of the CC must occur prior to age 50 .Stage the cancer .Superior to CT for delineating fat planes in T staging especially in rectal cancer (e) Bone scan if appropriate .Not adequate for diagnostic purposes.At least 2 of which must be first-degree relatives .2 successive generations . it is likely tumour has been totally removed .Follow-up after surgery with CEA levels to detect tumour recurrence . Complications.Jaundice.Cervical lymphadenopathy – Virchow’s node synchronous cancer in 3-5% .Obstruction (left sided lesion) .Investigate for complications of cancer I. 1] . lung.A tumour marker for colorectal carcinoma – >90% of tumours produce CEA .2 or more 1st/2nd deg same side relative with CC at any age . irregular. polypectomy.Causes of false positive raised CEA: smoking. may miss small lesions . stenting of obstructed colon (c) Carcinoembryonic antigen level (CEA) .1 or more 1st deg relative with CC at age <40 .Red meat .Personal or family history of breast.Bone tenderness . Mass on DRE – hard. pancreas.Lungs . .Ulcerative colitis D) Complications . STAGING (a) CT scan of the abdomen and pelvis .Brain . contact bleeding 3. DIAGNOSIS Amsterdam Criteria for Hereditary Non-Polyposis Colorectal Ca (HNPCC) – [3. Metastases .Anaemia .  Family history alone considered high-risk.Measured pre-operatively as a baseline level – if the CEA is raised pre-op and falls to within normal range post-op.Can visualise lesion and have an idea of which part of the colon it is in .Enables detection of synchronous lesions – synchronous polyps in 30%. pneumaturia. polypoid. pregnancy.Very good for T staging to determine depth of involvement by tumour . Abdominal mass 2.31 B) High-risk factors Positive Family history . recurrent UTI .Infection – abscesses.Diagnose colorectal cancer . e. together with iron studies (b) Urea. ALP (d) If patient presented with symptoms of intestinal obstruction – erect and supine AXR can help in diagnosis and location of obstruction (e) Erect CXR in perforated tumour to detect air under diaphragm DUKE’S STAGING Stg Description 5yr surv A Tumor confined to bowel wall with no extension into extrarectal/ extracolic tissue. no LN mets 75% B Invades past muscularis propria into extrarectal/ extracolic tissue. III. creatinine may be elevated due to pre-renal failure (c) Liver function tests for derangements caused by metastasis (though these changes will only occur late) – raised bilirubin. COMPLICATIONS (a) FBC for low Hb.Prophylactic antibiotics  ampi/ genta/ metronidazole at induction of anesthesia Principles of surgery for colonic carcinomas . tumour removed with proximal end of colon brought out as a colostomy) as compared to creating a primary anastomosis  On-table bowel decompression is equivalent to 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 . 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 . may have third space losses (intraluminal) with fluid and electrolyte abnormatlities.Site of surgery for colonic carcinoma .Bowel prep  Modification of diet – 3 days low residue diet. 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% Distant mets/ extensive local mets such that surgically incurable poor D TREATMENT SURGERY Pre-operative measures . NBM day before operation)  Bowel clearance with polyethylene glycol .En-bloc resection of tumour with adequate margins  For colonic tumours.Obstructed left sided carcinoma  No difference shown for doing a staged procedure (i. electrolytes and creatinine in patient with obstruction – may be vomiting. a margin of 5 cm proximally and distally is adequate 32  While segmental resection (excision of only the segment of colon containing the tumour) is sufficient for primary tumour removal. Division of left colic and inferior mesenteric arteries .Division of ileocolic and right colic arteries.Excision of sigmoid colon .e. usually taken to be at the level of the dentate line (which is 5cm above the anal verge) i.Descending colon Left hemicolectomy . adherent tumours (T4).Ascending colon Right hemicolectomy .Division of inferior mesenteric artery and/or sigmoid branches Transverse colectomy Left segmental colectomy Principles of surgery for rectal carcinomas . done when there is difficulty creating the colonic J-pouch .Neoadjuvant chemoradiotherapy  Neoadjuvant therapy with radiotherapy in combination with 5-fluorouracil can downstage tumour significantly  ability to preserve sphincter. mesorectal excision of 5 cm distal to the distal margin of the tumour is adequate (see Mesorectal excision below) .Sphincter-sparing versus loss of sphincter  The anal sphincter can be spared if the distal margin is >2cm above the level of the sphincter complex.Division of supplying vessels – left branch of middle colic artery. and the right branch of the middle colic artery .Sigmoid colon Sigmoid colectomy .Extended resections  For locally advanced.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) – for upper rectal tumours.Transverse colon near splenic flexure Extended right hemicolectomy .Stoma creation  A defunctioning loop ileostomy (or loop colostomy) is usually created during an anterior resection as the manipulation of the colon deep within the pelvic cavity causes increased risk of an anastomotic leak  A defunctioning stoma does not protect against anastomotic leak.Division of ileocolic and right colic arteries.Hepatic flexure . then an abdominoperineal resection is performed where the entire anus and sphincter complex is dissected. the apex of the J being anastomosed to the anus) is associated with improved post-operative function  Coloplasty is another alternative that is equivalent to colonic J-pouch (the distal colon is cut longitudinally but sewn transversely.Excision of transverse colon . distal margin of the tumour must be >7cm from the anal verge  Sphincter-sparing surgery involves a low anterior resection  If the tumour is so low that it cannot be resected without removing the sphincter complex.Mid-transverse colon . with the creation of an end colostomy .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) .Excision of descending colon . and the two limbs opened and stitched together to form a pouch.Reconstruction  Formation of a straight coloanal anastomosis in anterior resections is associated with poor function due to the lack of reservoir function  Creation of a colonic J-pouch using the proximal end of colon (the end of the colon is folded back on itself to form a J. and proximal transverse colon . but mitigates against disastrous complications should a leak occur .Division of middle colic artery . ascending colon.Caecum . ability to resect previously unresectable tumour. widening the diameter at that segment to form a small pouch).33 Tumour site Surgery Structures involved . multivisceral resection of organs involved (pelvic exenteration) is associated with improved local control and overall survival compared with standard resection. though high morbidity of 2550% is associated  Consider neoadjuvant chemoradiotherapy prior to surgery to downstage disease .Excision of distal transverse colon and proximal descending colon . and the middle colic artery at its origin .Excision of caecum. left colic artery .Excision of caecum and ascending colon . etc .Transverse colon near the hepatic flexure . Resection of asymptomatic primary is controversial. or pericolic fat. perforation.Yearly colonoscopy .Rectal cancer: post-operative adjuvant therapy in combination with radiotherapy in stage II or III disease (5-FU based regimen used) Palliative therapy . muscularis propria a) Local excision + adjuvant Chemo/RT OR b) radical resection T3 Penetration through muscularis propria into subserosa (if present).Surgical treatment according to stage Stage of disease Treatment T1 Involvement of submucosa.Colon cancer: 5-FU + folinic acid (leucovorin) for 6 months.Follow-up visits 3-monthly for the first 2 years. capecitabine or UFT (uracil combined with tegafur) plus folinic acid FOLLOW UP .Isolated liver metastases (synchronous or metachronous) may be resected with survival benefit.CXR and liver ultrasound to detect metastases (recommended frequency not known) .Alternatives for first-line therapy: Raltitrexed when 5-FU is not tolerated. but in the rare setting that there is an isolated lung secondary. but may confer survival benefit in a select group of patients where metastatic tumour burden is restricted to one side and liver involvement is not extensive 34 Adjuvant therapy .Surgery for metastases . ureters Early (<30 days) Wound infection Bleeding Abscess Anastomosis breakdown/leak Early stoma complications Late (>30 days) Diarrhoea Impotence (damage of pelvic nerves) Adhesions (I/O) Anastomotic stricture Late stoma complications Surgery for palliation . 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 . but not penetration through. and subsequently yearly. measure CEA at each visit . then 6-monthly for the next three years.Loco-regional recurrence.Resection of primary for palliation of symptoms such as bleeding.Role as neoadjuvant therapy in rectal cancer to downstage tumour . or 5-FU + levamisole for 12 months in Duke’s C cancer (node positive). can confer survival benefit RADIOTHERAPY .g. if detected early with adequate resection. obstruction or pain . neoadjuvant chemotherapy can be given to downstage the metastases if they are initially resectable . but no penetration through muscularis propria Local excision (AR or APR) T2 Invasion into.Post-operative adjuvant therapy in stage II or III rectal cancer CHEMOTHERAPY Operative complications Immediate (<24h) Damage to other organs e.5-FU in combination with folinic acid is first-line therapy . not recommended in Duke’s B or less .Lung metastases usually indicate systemic dissemination of disease. resection can provide survival benefit Surgery for recurrence . treated with chemo.Sited away from old surgical scars (hernia risk) .g. the bowel that forms the stoma must not be overstretched – tension causes decreased vascularity of the stoma and may cause stoma necrosis Types of stomas Permanent (end colostomy) . enema . not under a large fold of abdominal fat .Surveillance  Yearly colonoscopy for at-risk family members from 12y onwards  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 . Familial adenomatous polyposis (FAP) - 1 in 10. as ileal contents are corrosive.Extraintestinal manifestations  Epidermoid cysts  Lipoma  Osteoma of skull. discuss best site for stoma placement Stoma siting . to prevent contact with skin) . . double check by passing a proctoscope into the stoma to look at colour of mucosa)  refashion stoma .Intra-operatively. but care must also be taken not to site it too near a midline surgical incision due to fears of wound contamination and infection .g.Defunctioning – to protect a distal bowel anastomosis  Previously contaminated bowel  Technical considerations e.Other sites for polyps: stomach. while ileal stoma protrudes 3cm (a ‘spout’.35 STOMA PRINCIPLES Stoma Complications Nursing intervention Early . after low anterior resection. fecal impaction  explore with finger.e.When no distal bowel remaining  Low rectal/ anal tumor requiring abdomino-perineal resection  Panproctocolectomy without ileal pouch anal anastomosis e. duodenum . colostomies in the epigastric/hypochondriac [transverse colostomy] or left side) .Obstruction e. autosomal dominant inheritance Germline mutation of APC gene on 5q21 >100 adenomatous polyps all over colon. RT or hormonal   Rx. acute Crohn’s Note: Colonic stoma is usually flushed with skin.To rest an inflamed distal portion e. mandible  Dental abnormalities  Congenital hypertrophy of retinal pigment epithelium (CHRPE)  Desmoid tumours (intraabdominal tumours.g.Decompression – relief of large bowel obstruction causing proximal dilatation .Stoma nurse to counsel. polyps take 5-6 yrs to turn malignant 50% patients will have polyps by 16yrs. Not treated by surgery) Follicular or papillary thyroid cancer Periampullary CA – requires 5 yearly OGD for surveillance of CA.Necrosis of terminal bowel (stoma appears dusky.Should be sited away from skin creases or bony prominences such that stoma wafer can be attached flush with the skin (otherwise there are gaps between skin and wafer  leakage of fluid) .Sited where the bag will be easily accessible and visible to the patient i.Diagnosis  Colonoscopy showing >100 polyps  Genetic testing .000.g. where risk of anastomotic leakage is high  Usually loop ileostomies or colostomies with 2 openings (ileostomies usually on the right side.Leakage between skin and appliance causing skin erosion  resite Late - Prolapse of bowel  refashion Parastomal hernia  refashion Stenosis  refashion Retraction  refashion Psychological problems ASSOCIATED CONDITIONS I. 90% will have colorectal CA by 45yrs .Siting of a stoma over the rectus sheath decreases the risk of prolapse. FAP  Usually sited on the left side with a single opening Temporary . Diverticulitis – inflammation of diverticula EPIDEMIOLOGY .Diverticulosis coli – presence of acquired pseudodiverticula .Diverticular disease – symptomatic diverticulosis coli .Usually at point of entry of terminal arterial branches where serosa is weakest . ovarian. d.Increases with age . constipation 2. themselves and stitching or stapling them together to form a reservoir pouch which is them anastomosed to the anus) at ~ 20 YO Subtotal colectomy is an option if the rectum is relatively spared of polyps PATHOGENESIS 1. b. NBM.Associated with weakening of collagen structure with age PRESENTATIONS 1.10-30% of diverticulosis coli are symptomatic .Surveillance – 1-3yrly colonoscopy starting at 20 years old Ulcerative colitis . colovaginal STAGING .Passage of mucus PR 3.Diagnosis is based on the Amsterdam criteria – see above . pressure) 36 . and renal pelvis/ureter cancers .ABx.Resultant tumour is often poorly differentiated . most commonly endometrial cancer. diameter. IV fluids . colo-uterine.Recurrent LIF pain .Screening – yearly colonoscopy starting after 10 years of UC DIVERTICULAR DISEASE PATHOLOGY – acquired herniation of colonic mucosa through muscular wall. Chronic diverticulitis .Consider 1 stage surgery after acute episode – resection of affected bowel segment with primary anastomosis . colo-enteric. hepatobiliary.Lynch syndrome type II is differentiated from Lynch syndrome I as it is associated with increased risk of cancer elsewhere.Irregular bowel habit .Hinchey classification of acute diverticulitis – need for surgery is reflected by degree of infective complications Stage 1 Pericolonic / Mesenteric abscess Stage 2 Pelvic / retroperitoneal abscess Purulent peritonitis Faecal peritonitis Stage 3 Stage 4 . operation or drainage of pericolic abscess. c. small bowel. Degenerative changes in colonic wall Hereditary Non-Polyposis Colorectal CA (HNPCC) . Increased intraluminal pressure .Divided into Lynch syndrome I or Lynch syndrome II based on clinical features . Acute diverticulitis - LLQ pain Tender palpable mass Low grade fever N/V Constipation / diarrhoea  WBC 2. with a covering of colonic serosa TERMS .Associated with lack of dietary fibre.Percutaneous drainage . May present with urinary symptoms.Elective 1 stage surgery . inc.Risk factors – dietary fibre & genetics .2 stage operation – Hartmann’s procedure (partial colectomy + diverting end colostomy & rectal stump formation) + secondary re-anastomosis 3 months later .Tumours usually proximal to splenic flexure (~70% proximal to splenic flexure) .Site – majority are in the sigmoid colon (dec. Complicated diverticulitis a. with villous histology . and also gastric.Tumours tend to arise from polyps which are commonly flat. Others – colo-cutaneous. Perforation Paracolic abscess / inflammatory mass – 2o to localized perforation Bowel obstruction – 2o to structure or adherence to a diverticular mass LGIT haemorrhage – ulcerated vessel @ neck of diverticulum Fistula formation (commonest: colovesical fistula) – 2o to pericolic abscess discharging. e. Vomiting .Usually temporary.Surgery if does not resolve .Bed rest . abscess.Resuscitate . histology after bowel resection .LIF pain – colicky.Barium enema – ‘saw-tooth’ appearance. progressing to constant.Surgical  Peritoneal toilet  Resection of affected segment  End sigmoid colostomy (Hartmann’s procedure) Pericolic abscess - .Nausea . ↑Hb (dehydration) .Pyrexia .Other causes of peritonitis – perforated PUD. ALWAYS exclude CA colon e.Ba enema &/or Colonoscopy – confirm dx & exclude CA colon Chronic Diverticulitis . due to attachment of enteric loop against area of acute diverticulitis .Severe / recurrent attacks of diverticulitis . oral for small bowels.Irregular bowel habits – constipation & bouts of diarrhoea . relieved by defecation . mesenteric fat infiltration.CT – differentiate between inflammatory phlegmon & pericolic abscess Persistent inflammatory mass .Tachycardia .NBM. extraluminal gas & contrast.CT scan w triple contrast is gold std for diagnosis  Contrast: IV for vascular lesions. tenderness & palpable mass .CXR – free gas under diaphragm . appendicitis etc Mgmt as for acute abdomen .LIF pain.Rigid sigmoidoscopy – oedematous mucosa & rigidity of rectosigmoid junction .Palpable LIF mass . pericolic fat inflammation. enema for large bowels  Features – diverticula. air-fluid level w/in an abscess Barium enema ± CT or U/S: thickened bowel wall.Abdominal guarding & rigidity . Ca colon) . concentric bowel thickening.FBC – ↑ TW. strictures .Recurrent LIF pain .Possible CA colon . pelvic abscess - Conservative .Laparoscopy – if diagnosis is in doubt .CT/US guided percutaneous aspiration .Fever .Passage of mucus PR .LIF tenderness .e.Surgery – evacuation of pus ± resection of affected segment .Pyrexia . free fluid & gas .Increase pulse rate - FBC – leucocytosis ↑ ESR AXR – ileus.Ischaemic colitis . diverticula.Broad-spectrum antibiotics – augmentin or metronidazole or ciprofloxacin .U/E/Cr – dehydration & ARF .CA colon – may coexist.Flexible sigmoidoscopy – diverticular orifices .Radiation colitis .FBC – ↑ TW .37 Presentation Clinical features Investigations Differentials Management Acute Diverticulitis .Acute onset abdominal pain – severe & continuous .Colonoscopy – exclude differentials (i.Antispasmodics Acute salpingitis Acute appendicitis GE Irritable bowel syndrome After acute phase has settled . IV fluid .Segmental resection of affected colon + anastomosis . Hard to differentiate – therefore.Colonic endometriosis Conservative – see above Generalised peritonitis / perforation .g.Malaise Small bowel I/O May follow acute diverticulitis LIF tenderness & guarding LIF mass – may be detected on DRE Swinging fever Surgical Indications: . invesigations + colonoscopy & angiography to locate site of bleed .PHx of recurrent acute diverticulitis or irregular bowel habit .Surgery – Resection of affected colon + anastomosis + closure of bladder fistula opening Sepsis Perforation Diverticulitis not responding to conservative management Emergency bleed a. faecal debris.Massive bleed usually right-sided .Water soluble contrast enema .70% of patients will not have recurrence after first attack . 4. constipation & abdo distension .Other causes of fistula – CA colon. pneumaturia. 3. haematuria.Advise high fibre diet & to drink lots of fluid 38 UFEME – pus. renal transplant) – may not show S/S of acute attack or complications Advice to patients: . Hence. post-irradiation necrosis .Usually in the elderly who have higher density of sigmoid diverticula . Obstruction – need to rule out cancer at the same time Stricture Fistula Recurrent attacks – occurs in 30% of patients after 1st episode. 2.AXR – dilated bowels proximal to stenosis .Surgery – Resection ± primary anastomosis Hemorrhage . .Invx as for LGIT bleed – resus. Previous bleed 5. CA bladder. freq. 2. Crohn’s disease. Indications for elective operation 1. 4. 3.NBM. Haemodynamically unstable b. a/w higher mortality & complication rates Young patientss <40YO – high recurrence rates Immunocompromised patients (e.± on-table enteroscopy if required .g. intestinal organisms Cystoscopy – cystitis Sigmoidoscopy – usually normal KUB – air in bladder Barium enema – diseased diverticular bowel segment Anorectal bleed Angiodysplasia Ischaemic colitis UGIT bleed Colorectal CA IBD Other colitis Coagulopathy .± tagged RBC scan (not as sensitive compared to angiogram) - .CA colon . Need > 4 units of PCT c. angiogram is the preferred invx as it is of diagnostic AND therapeutic value Vesicocolic fistula .PHx of chronic diverticulitis & UTI . 5. Drip & suck .Presentation Clinical features Investigations Differentials Management Large bowel I/O .Surgery – resection or radiologic embolisation of site of bleeding – done while doing angiography.Resuscitate & correct coagulopathy . faecaluria - Indications for emergency operation 1.Colicky abdominal pain.Hx of dysuria. urogenital tract. pancreas.The transverse plane is at the level of the main branches of the portal vein.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) .Segments II to VIII are named clockwise.The sagittal planes are formed by the three main hepatic veins (right. with a small proportion of intrahepatic cholangiocarcinoma (6%) . breast.The segments are divided by one transverse plane and three sagittal planes as shown in the picture .The liver is divided into two lobes.Primary cancers of the liver are mainly hepatocellular carcinomas (85%).The anatomical division of the liver lobes is demarcated by the falciform ligament .Segment I is the caudate lobe .Drainage is via the three hepatic veins into the inferior vena cava CAUSES FOR A LIVER NODULE ON IMAGING Benign Cyst Haemangioma - Single Multiple – familial (polycystic) or non-familial Small Big Adenoma Fibronodular hyperplasia Malignant Secondary Primary Colorectal. where IVa is the superior subsegment and IVb is the inferior subsegment .000 per year in males. lung Hepatocellular carcinoma (or hepatoblastoma in children) Cholangiocarcinoma (only 10% intrahepatic) – presents like HCC except no background of cirrhosis HEPATOCELLULAR CARCINOMA . overall fourth most common cancer .Incidence in Singapore is 18 per 100. stomach.Peak age of onset: 30-40 years old . and divides the liver into an upper half and a lower half . starting from the upper right corner (i. the upper left segment of liver) – see picture .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) .000 in females . and biliary drainage.More common in men.Third most cancer among males. right and left . middle and left) EPIDEMIOLOGY .6 per 100.The liver can be further divided into 8 functional segments (Couinaud segments) that each have their own vascular inflow. independent of the other segments .Segment IV can be further divided into IVa and IVb.e. while facing the patient. with a ratio of 3:1 . outflow. and 4.39 SURGICAL LIVER PROBLEMS ANATOMY OF THE LIVER . which leads to increased rates of genetic mutation in the cells and accumulation of these mutations leading to carcinoma formation . watery diarrhoea. hypercalcaemia. biochemical and radiological tests WHO criteria for HCC: (a) Risk factors for HCC e. Dynamic MRI scan of the liver . compression of a major duct 3. Local symptoms .Adjunct investigation done when CT findings are equivocal . Tumour rupture .Obstructive jaundice due to invasion of intrahepatic biliary tree.Upper abdominal pain .Pyrexia (central tumour necrosis) .Metastasises to lymph nodes.Incidentally found on imaging of the abdomen 2. hep B/C carrier (b) Characteristic CT findings (of a hypervascular lesion) (c) Raised AFP (>400) 1.In a patient with hepatitis B/C and raised AFP. etc. Asymptomatic . can be used to exclude benign conditions .During screening (ultrasound) for chronic hepatitis B carrier . more common in females. good prognosis .Investigations for liver cirrhosis .Pathogenesis involves a chronic inflammatory process or ongoing hepatocellular damage with high cellular regeneration. no association with hep B or cirrhosis. Metastases . Liver decompensation (on top of underlying cirrhosis) - Worsening liver function Ascites Variceal bleeding Encephalopathy 4. erythrocytosis (tumour produces erythropoietin).Hepatitis C infection . Other manifestations PATHOLOGY . bones.Triphasic CT involves scanning the liver at three different times after intravenous contrast: (a) Arterial phase – aorta lights up as contrast fills arteries. resulting in portal hypertension) .Abdominal pain (peritonitis) . lungs and adrenals INVESTIGATIONS PRESENTATION 1. Alpha-foetoprotein (AFP) .Elevated in 80% of hepatocellular carcinoma 2. IVC and portal vein are dark (b) Portal venous phase – contrast enters portal system so portal vein is as bright as the aorta (c) Delayed phase – contrast drains out.Cirrhosis (of which cirrhosis resulting from hep B. hep C and haemochromatosis are associated with the highest risk) .Two histological subtypes:  Nonfibrolamellar – associated with hep B and cirrhosis  Fibrolamellar – associated with younger patients. DIAGNOSIS Biopsy is usually not performed due to risk of tumour seeding (1-2% risk) along the needle track – diagnosis is based on clinical.CT can also look for nodal involvement. a liver lesion that is not a haemangioma on imaging should be considered HCC until proven otherwise .AETIOLOGY AND RISK FACTORS .g.Bone pain . and metastases to the adrenals 3.Hepatomegaly found on examination .Dyspnoea 40 . so none of the vessels in the liver are lighted up .Paraneoplastic syndromes – hypoglycaemia (high metabolic demands of tumour).Images liver in greater detail.Hepatitis B infection (high HBV DNA load.Aflatoxin ingestion 6.Budd-Chiari syndrome (occlusion of portal vein. 70% resectable. Triphasic CT scan is the gold standard investigation . HBeAg positivity increase the risk) .Characteristic feature of HCC is enhancement in the arterial phase (as HCCs have a rich arterial supply derived from the hepatic arterial system) with rapid contrast washout in the portal venous phase (hypodense) .Shock 5. If patient has cirrhosis. thus a new tumour can still develop in the remnant liver .Use of indocyanin green (ICG) – the percentage of ICG remaining in the liver after 15 minutes indicates the level of liver function. If indicated. bleeding and infection . high HBV DNA levels) – can be aggressively treated with anti-viral drugs 2 months before transplant and anti-HBV immunoglobulin longterm after transplant PALLIATIVE THERAPY Loco-regional ablation (a) Radiofrequency ablation – best results for locoregional strategies (b) Percutaneous ethanol injection (c) Cryotherapy . because tumour is non-functional .Dependent on tumour size and how much of the liver it takes up. Degree of portal hypertension .CEA. Adrenals – CT abdomen 3.Lipiodol will be retained in HCC even after many days as the HCC does not contain Kupffer cells to ingest lipiodol . there is a risk for reinfection of the donor liver (high risk factors are HBeAg positivity.Hepatic angiogram may reveal abnormal blood vessels within the HCC .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. Stage of disease .Milan criteria for transplantation (>75% 5-year survival if followed) (a) Single tumour 5cm or smaller.CT scan of the liver weeks after lipiodol ingestion will pick up the areas of tumour (where the pre-lipiodol CT may not have demonstrated the tumour clearly) 5.2 surgical possibilities: (a) Resection of tumour (partial hepatectomy) (b) Liver transplantation Factors affecting resectability: 1. CA 19-9. while a small tumour means that more functional tissue is removed with the same resection margins 5.Multicentric disease affecting both lobes is a contraindication to hepatectomy 2. endoscopy STAGING (looking for metastases) 1. Lung – chest X-ray. If >15% remains after 15 minutes.Has to be located in a suitable location for resection Hepatectomy .The only curative treatment for HCC is surgical removal of the tumour . Location of tumour . Residual liver function post-operatively . CT thorax 2.Metastatic disease is not suitable for resection .Problems with availability of donor organ – the disease might have progressed past being suitable for transplant by the time donor organ is available  Possibility of “bridging therapy” such as radiofrequency ablation to shrink disease and prevent progression until donor liver is available .Good immediate and short-term results. or 3 or less tumours none larger than 3cm (b) No evidence of gross vascular invasion (c) No regional nodal or distant metastasis .A large tumour taking up most of the liver segments being resected translates to smaller amount of functional liver tissue being resected. General fitness for operation 3. only Child’s A and good Child’s B . the patient cannot tolerate major liver resection (>3 segments removed) 4. but not long term (<30% 5-year survival) due to occurrence of new primaries in the cirrhotic liver Transplantation .Only about 10-20% of patients with HCC will have disease amenable to surgery . Bone – bone scan if clinically indicated TREATMENT SURGERY . investigations to look for GI primary .In hepatitis B carriers.Problem in patients with cirrhosis is that there is already a “field-change” effect in the liver.41 4. Hepatic angiogram with lipiodol and post-lipiodol CT scan .Resection of the liver results in worsened portal hypertension since the effective portal venous capillary bed has decreased  increased resistance to flow 6.Requires a fine balance between adequate resection margins and preservation of sufficient functional liver to prevent liver failure . assess the Child’s status  Child’s C and most of Child’s B will not be fit for operation. Liver function pre-operatively . sibling has hep B. irregular nodular hepatomeg . but should be increased in patients at increased risk – HbeAg positivity.Combination of six-monthly to yearly ultrasound with AFP levels .Jaundice early. gastric.Prevalence 0. oesophageal mets .Possible role for prophylactic surgery in large.Hepatomegaly may not be present . inferior lesions since there is higher risk for rupture .Promising results with colorectal and neuroendocrine metastases if isolated resectable metastatic disease – 5-yr survival >50% .Hard. but it is not associated with radiation exposure .Jaundice is a late sign .Both obstructive and transaminitis picture . thrombocytopaenia 6.Poor results for stomach.Ultrasound alone is not very sensitive or specific as it is operator dependent and may miss certain areas of the liver where imaging is difficult.Hard mass . breast.Radiological Characteristic features on triphasic CT – slow enhancement of the rims on arterial and portal venous phase. high HBV DNA levels . lateral.Symptoms of obstructive jaundice  Yellow sclera  Tea-coloured urine  Pale stools P/E .Obstructive picture in early stages Invx 42 ROLE OF SURGERY . pancreatic. Usually small and asymptomatic. breast mets .Vascular malformation that enlarges by ectasia. mother had hep B/HCC. etc LIVER METASTASES .Pain from rupture . congenital in origin PRESENTATION 1. lung PRESENTATION DEPENDS ON SITE OF METASTASIS Mets to liver parenchyma Mets to porta hepatis LN Hx .g. brightest in the delayed phase .AFP is also not a perfect screening test as 20% of HCC will not have raised AFP .Palliation for symptoms in neuroendocrine metastases LIVER HAEMANGIOMA EPIDEMIOLOGY . Pain from liver capsule stretch 4.Primaries: Colorectal. Kassabach-Merritt syndrome for large haemangiomas – consumptive coagulopathy. found incidentally 2.Incidentally found on follow up (for cancer) .Frequency of screening is controversial. progressive .Increasing contrast uptake on portal venous and delayed phases Intra-arterial therapy (a) Transarterial chemoembolisation (b) Transarterial embolisation (c) Radioactive isotopes – Yttrium-90 Systemic therapy – limited results SCREENING FOR CHRONIC HEPATITIS CARRIERS . Mass effects compressing on surrounding organs 3. Rupture (<1%) 5.Only for symptomatic or complicated lesions . urogenital.Female to male ratio 3:1 PATHOGENESIS .TRIPHASIC CT .Thus the combination of ultrasound and AFP can increase the sensitivity and specificity of screening . Heart failure from large arteriovenous shunt DIAGNOSIS .Important to also screen family for chronic hepatitis B carrier status especially if there is a family history! – e.4-20% .Heaviness .Hypodense on arterial phase (as metastases are usually hypovascular compared to hypervascular HCC) .DO NOT BIOPSY TREATMENT .Still more common than primary liver tumour for malignancy occurring in the liver .Increasing role in urogenital. Ethanol sclerotherapy (painful) .Causative organisms: Klebsiella pneumoniae.Bleeding .Prevalence 1-3% .g.Fistulation into duodenum .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) . stains. cultures .Torsion . and one-third have hepatomegaly . may be multiloculated. CA 19-9.More common than amoebic abscess locally PATHOGENESIS . diverticulitis.Cholestasis due to compression of CBD . pancreatitis.Routes of infection: (a) Ascending infection from biliary system (ascending cholangitis) (b) Intra-abdominal source through portal vein – acute appendicitis.Presentation: Spiking fever with chills. traumatic . Antibiotics  Empirical antibiotics – Ampicillin/Gentamicin/Metronidazole  Change to definitive antibiotics when blood c/s results return  Total duration of 6 weeks – first 2 weeks intravenous.Portal hypertension .Investigations:         FBC.Mass effect . cysts and parasites Ultrasound CT scan to exclude liver tumour (KIV endoscopy to rule out GI malignancy) If any aspiration done. Enterococcus. coli. air-fluid levels.Treatment 1.Imaging: Irregular lesion with central area of necrosis. pelvic abscess (c) Contiguous spread – from gallbladder empyema (d) Haematogenous spread in sepsis e. infective endocarditis (e) External inoculation – iatrogenic.Carcinoma (rare) TREATMENT (IF SYMPTOMATIC) . Rim-enhancing appearance on triphasic CT scan. aspirates for histology. next 4 weeks oral .Excision/resection .No solid component and not septated (mixed cysts with septations are suggestive of malignancy) .Compression of inferior vena cava . inflammatory bowel disease.50% of cysts are single .Fenestration (open or laparoscopic) . 50% of patients have jaundice.[Cysts that communicate with the biliary system are called choledochal cysts] PRESENTATION – WITH COMPLICATIONS . CEA (may resemble tumour on imaging) Stool ova. Staph aureus .43 SIMPLE LIVER CYSTS HEPATIC ABSCESS EPIDEMIOLOGY .9:1 female predominance for symptomatic cysts 2 types depending on aetiology: pyogenic or amoebic PYOGENIC ABSCESS .Aspiration . Enterobacter. E. . rigors.Rupture . U/E/Cr Blood cultures Melioidosis serology Tumour markers: AFP. then spreads to the liver through the portal vein) . forming ulcers in the colon. performed under radiologic guidance . Drainage Drainage if >3cm – open drainage or percutaneous aspiration Percutaneous aspiration Open drainage .Causative organism: Entamoeba histolytica (infects the gut. jaundice Hepatomegaly often present Complications: rupture into pleural/peritoneal spaces .2.Contraindications:  Ascites (pus can leak into peritoneal cavity)  Uncorrected coagulopathy  Proximity to vital structures - Invasive procedure.Minimally invasive.Transmission is faecal-oral .May require multiple attempts if unable to completely drain pus .Treatment:  Metronidazole  Aspiration if amoebic serology inconclusive.Can be done under LA . pregnancy (metronidazole contraindicated). suspicion of secondary infection.Presentation     Usually single abscess No sepsis. severe symptoms from distension or fever. or pt not getting better)  Ascites  Ruptured abscess AMOEBIC ABSCESS . impending rupture 44 .Longer stay for patient as drainage tube stays in patient for a longer time . done under GA Shorter hospital stay Single procedure Not dependent on location Indications  Concomitant pathology requiring surgery  Multiple abscesses or multiloculated abscess  Immunocompromised patient  Failed percutaneous drainage (tube blocked. Interstitial oedema . azathioprine.Pancreatic or peripancreatic necrosis .Uneventful recovery 2.45 PANCREATIC DISEASES ACUTE PANCREATITIS DEFINITION An acute inflammatory process of the pancreas with variable involvement of regional tissues or remote organ systems EPIDEMIOLOGY Incidence is difficult to measure accurately as many patients with mild pancreatitis may not be diagnosed. Scorpion toxin 9. worse on movement  Nausea and vomiting  Anorexia . Hypercalcaemia. Patients with acute pancreatitis make up 7-10% of those presenting with abdominal pain. suggest severe haemorrhagic pancreatitis associated with profound fluid loss (third-spacing) . Gallstones 3. pancreas divisum Gallstones and alcohol are the most common causes (>90% of acute pancreatitis) PATHOPHYSIOLOGY . alleviated by sitting up. hypertriglyceridaemia. Mumps and other infections (VZV also) 7. severe blunt trauma. usually occurs after a heavy meal. CAUSES (I GET SMASHED) 1. Severe acute pancreatitis (any 1 of the following) . Mild acute pancreatitis .Signs (also non-specific)  Epigastric tenderness (less than one third have signs of peritonism)  Tachycardia. Ethanol 4.The activated lytic enzymes destroy the pancreatic acinar cells resulting in release of potent cytokines that attract neutrophils and macrophages. NSAIDs.Symptoms (generally non-specific):  Abdominal pain (most consistent.The cytokine cascade amplifies the local inflammatory response and also results in a systemic inflammatory response (resulting in systemic complications of acute pancreatitis such as ARDS and multiorgan dysfunction) . diuretics) 12.Gallstones are thought to cause acute pancreatitis due to obstruction of the pancreatic duct causing interstitial oedema which impairs blood flow to the pancreatic cells  ischaemic cellular injury  predisposition to enzyme activation . in >90% of patients) – constant epigastric pain. Idiopathic 2. maximal intensity within several hours of onset. PAN 8. Trauma 5. Drugs (SAND: Sulphonamides. Steroids 6. ERCP 11. classically radiating to the back (in 50%).Associated with organ failure .The mechanisms in which alcohol cause pancreatitis are not known. low grade fever  Abdominal distension with diminished or absent bowel sounds (paralytic ileus)  Ecchymoses: flank (Grey-Turner’s sign) or umbilical (Cullen’s) – formed by blood-stained peritoneal fluid tracking to the flank or umbilicus. Rare causes: Cystic fibrosis.Minimal organ dysfunction . hypothermia 10. Autoimmune – SLE.The final common pathway of pancreatitis involves inappropriate activation of proenzymes stored within zymogen granules in the pancreatic cell – trypsin is implicated in this mechanism as it activates most of the proenzymes secreted by the pancreas when they are secreted into the duodenum .May be associated with local complications PRESENTATION . and may sensitise the pancreas to injury by other agents ATLANTA CLASSIFICATION (FOR SEVERITY) 1. cancer of the head of the pancreas. which themselves secrete pro-inflammatory cytokines . though it is believed alcohol itself results in injury to pancreatic cells through generation of free radicals during its metabolism. FBC (TW for Ranson. cholangitis Peptic ulcer disease Kidney stone Ectopic pregnancy Intestinal obstruction. Ultrasound . base excess for Ranson) 6. Fasting lipids (hyperlipidaemia – aetiology) 2. CT scan DIAGNOSTIC GI sources . elevated hemidiaphragm.MANAGEMENT STRATEGY 3. Urinary diastase . as urinary diastase will be elevated for a longer time after onset of symptoms Diagnosis 4. usually more than 1000 or 3 times normal .Not the first investigation of choice unless considering pathologies other than pancreatitis.Pancreas may be diffusely enlarged and hypoechoeic – often difficult to visualise due to overlying bowel gas 6.Serum amylase is raised within 12 hours of onset of acute pancreatitis. Serum amylase . ECG (rule out AMI as a cause of epigstric pain) . obstructive picture in gallstone pancreatitis) 4.Value of CT is at a later point in the disease time course to look for complications such as fluid collections.Similar function to serum lipase. Serum lipase . IV contrast needs to be given to detect necrosis PROGNOSTIC / SUPPORTIVE / LOOKING FOR AETIOLOGY 1.Preferred over CT scan .Good for visualising biliary tree and picking up gallstones .Other causes of elevated serum amylase: Non-GI sources 5. X-rays of the chest. pulmonary infiltrates. perforation Salivary gland injury or inflammation Macroamylasaemia Impaired clearance due to chronic renal failure .Erect CXR may show pleural effusion. U/E/Cr (urea and glucose for Ranson and Glasgow) 3. since CT may worsen pancreatitis . used when serum amylase is equivocally raised or normal.Returns to normal level 48 to 72 hours after onset – not useful in late diagnosis . Lactate dehydrogenase (for Ranson and Glasgow) 5. Glasgow.Abdominal X-ray 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) – these occur in more severe disease and are due to functional spasm of the bowel around the pancreas resulting from inflammation - Ischaemic bowel (can cause elevated amylase in the thousands) Cholecystitis.High sensitivity and moderate specificity (specificity increased when cut-off taken at 3 times normal upper limit) . in severe cases. ABG (PaO2 for Ranson and Glasgow. haematocrit for Ranson) 2.Rises within 8 hours of onset of symptoms and returns to normal after 7-10 days .Thus more useful in late diagnosis of acute pancreatitis 46 8. there will be signs of ARDS – complete whiteout . albumin for Glasgow. Ca/Mg/PO4 with albumin (hypercalcaemia – aetiology) 7. abdomen Severity stratification Assess for aetiology Supportive treatment Monitor for complications Treat aetiology (reverse / control) Manage complications Prevent future recurrence INVESTIGATIONS 1. LFTs (AST for Ranson and Glasgow. 2mmol/L >600U/L >120U/L Fall in Hct >10% Rise in urea >0.As a single prognostic marker . C-reactive peptide Present at admission Within 48 hours of admission 1. Danger signs in the first few hours - Encephalopathy Hypoxaemia Tachycardia >130/min Hypotension <90mmHg Haematocrit >50 Oliguria <50mls/hr Azotemia Presence of Gray Turner’s/Cullen’s sign >3 criteria  severe IV. but it is difficult to tell aetiology in acute setting  Cumbersome to wait for 48 hours. 7. and will recover without much treatment unless comorbidities cause deterioration .Ranson’s criteria prognosticates mortality according to score .Shortfalls of Ranson’s:  Was originally validated in patients in whom the aetiology was mostly alcohol. 5. 4. 8.Death is bimodally distributed: (a) Early  Within first week of disease  Occurs due to severe organ failure.Preferred over Ranson’s scoring in certain centres II. and difficult to assess for negative fluid balance . thus questionable to apply it in pancreatitis secondary to other conditions. 2. such as gallstones  A revised Ranson’s score was created for gallstone pancreatitis.Not very useful as CT is not usually done in the first week in local context.9% 15% 50% 90% .20-25% have more severe outcome – one-third of these patients will ultimately die . Glasgow/Imrie score 1. 2. 2. 3.Overall mortality rate <10% . Balthazar’s CT severity index .If CRP is >210mg/dL at 48 hours. 1. 3.Grades severity of disease according to CT findings .75% of patients have a mild course of disease. 6. and disease is still evolving (CT findings lag behind) in the early stages COURSE OF DISEASE .9mmol/L Calcium <2mmol/L PaO2 <60mmHg Base excess >4mmol/L Neg fluid balance >6L .No relevance beyond three days of onset as other confounding factors come into the picture . >55 yrs >16x109/dL >11.47 SEVERITY STRATIFICATION III. 3. I. 4. Ranson’s criteria Age White cell count Fasting bld gluc LDH AST Age White cell count Glucose LDH AST Urea Calcium PaO2 Albumin 0.Mortality: <3 3-4 5-6 >6 >55yrs >15x109/dL >10mmol/L >600U/L >100/L >16mmol/L <2mmol/L <60mmHg <32g/L . 9. the pancreatitis is more likely to be severe . 6.Any patient with a score of 3 and above is considered to have severe pancreatitis . 4.Combination of Glasgow score and CRP improves overall prognostic value V. 5. 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 . 5. g. with metronidazole (b) Fluoroquinolone e.In general ward for patients with mild pancreatitis .Fast patients for at least 48 hours until more stable . significant gastroparesis. pain) .Do not give NSAIDs as they can worsen pancreatitis.Acid suppression does not change course of disease.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%) .Either prophylactic or therapeutic .Pancreatic necrosis  Areas of no contrast uptake on CT with intravenous contrast .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. imipenem rarely used due to inability to escalate therapy in situation of resistance) . cystoduodenostomy or cystojejunostomy .Use opioid analgesics other than morphine (morphine causes increased tone of sphincter of Oddi) 7. Analgesia . or open jejunostomy creation early in patients with severe pancreatitis.Patients with severe pancreatitis will require HD/ICU monitoring 2. and cause renal failure (since there is already decreased renal perfusion in acute pancreatitis) . pancreatic infection . or intestinal obstruction (ileus) .Necrosectomy for infected necrosis  Some kind of lavage and drainage procedure is done after necrosectomy to decrease infective load . but protects against stress ulcer formation . 70-80% resolve spontaneously .g. Monitoring .May include gastric decompression if there is persistent vomiting.Therapeutic in cholangitis. ciprofloxacin. ceftriaxone.Abscess  Infection of fluid collection (not necrosis) .g. vomiting.ERCP should be done within first 48-72 hours for maximum benefit MONITORING FOR COMPLICATIONS AND TREATING Local complications: . Antibiotics . then consider TPN 3.Indications:  Severe pancreatitis  Evidence of ductal stones  Cholangitis  No response to treatment within 48 hours . Nil by mouth (bowel rest) and intravenous fluid replacement .g.Not shown to have any benefit in patients with mild pancreatitis unless patient is having cholangitis secondary to a biliary obstruction that also caused the pancreatitis .May start feeding early with fluids in mild pancreatitis unless symptoms do not permit (e. percutaneous (radiologically guided) or endoscopic  Endoscopic – internal drainage via a cystogastrostomy.Prolonged NBM results in poorer recovery due to nutritional debilitation – think about NJ feeding.SUPPORTIVE TREATMENT 1. haemorrhage. if not tolerable.Acute fluid collections  Due to increased vascular permeability.Infected necrosis 4. Support for organ failure 48 Surgery for local complications .No benefit in mild biliary pancreatitis . with metronidazole (c) Carbapenem on its own (e.Pseudocyst  Persistent fluid collection walled off by fibrosis and not an epithelium-lined surface (can only be called a pseudocyst after 4 weeks) .Use for 14-28 days 6.CT-guided aspiration of pancreatic necrosis  Can help differentiate between sterile and infected necrosis  Consider surgery if patient doing poorly . Endoscopic retrograde cholangiopancreatography (ERCP) . Treatment of fluid and electrolyte abnormalities such as hypocalcaemia 5.3 main regimens to choose from: (a) Third-generation cephalosporin e. laparoscopic. rupture) is high  Surgery can be open. 20% in the body. 25-65% will develop the 2nd episode within 30 days of the initial one Cholecystectomy can be done in the same admission for pts with mild pancreatitis In patients with severe pancreatitis. anorexia.Metastatic symptoms: ascites.Bleeding upper GIT (haematemesis and/or malaena) . p16 gene) . weight loss.Obstructive jaundice (painless obstructive jaundice with palpable GB) + cholangitis .Chronic pancreatitis . there is reluctance to do the surgery early.Familial cancer syndromes e.Genetic factors (mutations in K-ras gene.Duodenal obstruction . overall 5-year survival <3% ASSOCIATIONS .Exocrine insufficiency with duct obstruction  steatorrhoea.Eighth cause of cancer death in Singapore .Can be used as a marker for tumour recurrence during post-op follow-up 2.Anatomic distribution: 75% in the head.000 per year in each gender .Not a screening test for pancreatic cancer as it can be false positive .Very poor prognosis – median survival for unresectable disease is 6 months (80% of patients have unresectable disease at presentation). CT scan .Treat any life-threatening complications such as cholangitis. 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) .7:1 male to female ratio . pancreatitis. CNS symptoms. bleeding INVESTIGATIONS DIAGNOSTIC 1.g. bile and pancreatic duct dilatation in head of pancreas tumours (double duct sign) .Malaise.Coeliac and mesenteric plexus invasion – dull constant pain in the epigastrium radiating to the back . ascites 3. picked up on imaging for some other purpose Pancreatic head or periampullary Pancreatic body/tail .Lower socioeconomic class .Paraneoplastic syndromes – migratory thrombophlebitis in 6% PANCREATIC CANCER EPIDEMIOLOGY . nausea Late presentation . 5% in the tail .Most common histology is ductal adenocarcinoma (90% of tumours) . malabsorption .49 MANAGEMENT OF AETIOLOGY & PREVENTION OF RECURRENCE Cholecystectomy for biliary pancreatitis - 18-21% of patients with biliary pancreatitis will have another episode Among these. weight loss.1. MRI pancreas with MRCP – MRI pancreas is not superior to CT scan.Any evidence of extra-pancreatic spread: Involvement of regional lymph nodes. CA 19-9 .Diabetes mellitus . bone pain. anorexia.Can act as a prognostic marker: high CA 19-9 levels usually associated with unresectable disease with poorer prognosis .Distinct category of tumours collectively called periampullary tumour:  Malignant cells arise from one of a few cells: (a) Duodenal epithelium (best outcome out of all three) (b) Biliary ductular epithelium (c) Ampullary ductular epithelium  The periampullary tumours have better tumour biology than pancreatic adenoca  Prognosis is also better as they present earlier with obstructive jaundice IMMEDIATE MANAGEMENT .Industrial carcinogens – benzidine. Peutz-Jeghers PATHOLOGY .Cigarette smoking (most clearly established – 2-5X increased risk) .Malaise. nausea . liver metastases.Incidence about 3-5 per 100.Better sensitivity (85-90%) and equal specificity (90-95%) in diagnosing pancreatic cancer . as the patient may develop complications that require surgical intervention – better to do all surgery in the same operation instead of opening the patient twice PRESENTATION May be asymptomatic. betanaphthylamine .Features: Mass lesion within pancreas. dyspnoea . N stage. peritoneum)  Patent superior mesenteric vein and portal vein  Definable tissue plane between tumour and superior mesenteric artery as well as coeliac axis . common bile duct.FNA with EUS guidance is preferred to transcutaneous biopsy as there is less risk of tumour seeding . close up and abort surgery TREATMENT SURGERY Curative resection .Can be used to stage tumour and nodal involvement . Bones – bone scan when suspicion is high 5.Not shown to provide good outcomes . Staging laparoscopy – for peritoneal metastases.Only about 15-20% of patients will have resectable disease at presentation – usually in periampullary or head of pancreas tumours.Complications of Whipple’s operation  Mortality rate is 2-7%. otherwise. Lungs – CXR + CT thorax 4.Stenting of obstructed duodenum 2. pseudocyst formation may occur due to anastomotic leaks Late (a) Long-term exocrine insufficiency resulting in malabsorption and steatorrhoea (b) Gastric stasis with pylorus-preserving Whipple’s (c) Diarrhoea resulting from autonomic nerve injury during lymph node dissection (d) Endocrine insufficiency  DM Palliative surgery Surgical bypass of obstruction . 4560cm proximal to the gastrojejunostomy 50 Intraoperative/early complications  Injury to other organs – liver. Endoscopic ultrasound + FNA biopsy .Triple bypass involving anastomosis between (a) Stomach and jejunum (gastrojejunostomy) (b) Biliary system and jejunum (choledocho-/hepatico-/cholecysto-jejunostomy) (c) Jejunum and jejunum. Palliative chemotherapy/radiotherapy/chemoradiotherapy .However. N stage 3. ERCP with stenting to relieve obstruction (in cholangitis) 5.Improves chances of survival . Coeliac plexus block for pain 3. Endoscopic stenting . liver.4. recurrence rates after surgery are high – 5 year survival only 10 to 30% . proximal 15cm of jejunum. and distal part of the stomach  Common hepatic duct and pancreas are then anastomosed to the jejunum. metastasis to the liver 2. with a morbidity rate of up to 20-30% (mostly mild complications)  (a) (b) (c) (d) (e) (f) (g) STAGING 1. Endoscopic ultrasound – T. duodenum. kidney.Stenting of obstructed biliary duct . continue with surgery. bone.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.Resectable disease:  No metastases (lung. to prevent reflux of food into biliary tree – essentially a Roux-en-Y loop (jejunojejunostomy) NON-SURGICAL PALLIATIVE MEASURES 1. bowel Bleeding Infection  sepsis Pancreatitis Pancreatic anastomotic leak (5-20%) Biliary anastomotic breakdown Fistulation. just before definitive operation for a resectable tumour (since CT/MRI may miss small peritoneal deposits)  if no peritoneal disease found. CT/MRI of the abdomen – T. tumours of the body and tail present too late to be resectable . gallbladder. hepatic.Gallstones .Liver decompensation: encephalopathy . Complications . Abdomen . needlestick injuries.Generalised distension? (ascites could be due to malnutrition.g. sexual contact  Alcohol intake  Drug history: any TCM intake recently. Vitals: Is patient haemodynamically stable? Any fever? HISTORY 2. DRE: Pale stools? 6. operation) . drug abuse/needle sharing. myalgia. leg swelling? 1. Respiratory examination . D.Metastatic symptoms: bone pain. etc. or primary liver pathology) .Any scars of abdominal surgery? . malaise . family history of hepatitis (esp mother.Pain is a late symptom of pancreatic cancer and tends to be constant and relentless compared to biliary colic which subsides after a few hours 3.Strictures from other causes (gallstones. the cause is unlikely to be stones) . General inspection: Jaundice.Metastases to the porta hepatis 2. dyspnoea.Choledochal cyst Malignant .Previous history of gallstone disease or biliary colic symptoms . Bony tenderness 8.A young patient with painful jaundice  usually benign cause . painless progressive jaundice) .Constitutional symptoms: loss of appetite. malaise. stones. E.Splenomegaly? (Portal hypertension – think prehepatic. Confirm obstructive jaundice 3. loss of weight. chills.  Risk factors for viral hepatitis: travel history. arthralgia.Fat malabsorption: steatorrhoea.Recurrent spikes of similar jaundice that resolve on their own with time suggest benign obstruction e. K) – especially coagulopathy (very unlikely in acute setting) . posthepatic) 5.Parasitic infections (recurrent pyogenic cholangitis) Mural Benign . etc . Peripheries: Stigmata of chronic liver disease? Scratch marks? Conjunctival pallor? . blood transfusions.Previous history of surgery to the biliary tract or ERCP .Hepatomegaly? (Could be due to metastatic disease. chronic pancreatitis) . jaundice is of new onset and progressively worsening. ingestion of seafood. Aetiology – benign or malignant . neck lump.Primary sclerosing cholangitis . pale stools .Pruritus as a result of bile salt retention PHYSICAL EXAMINATION 1. peritoneal malignancy.Head of pancreas cancer .Establish obstructive jaundice – tea-coloured urine. siblings).Malignancy is suggested if the patient is old.Symptoms of cholangitis: fever.e.Confirm jaundice – patient’s sclera are yellow .Cholangiocarcinoma (distal) Extramural Benign . rigors with RHC pain and jaundice . fat-soluble vitamin deficiency (A.51 DISEASES OF THE BILIARY SYSTEM APPROACH TO OBSTRUCTIVE JAUNDICE CAUSES Intraluminal Benign .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. nausea/vomiting. or obstruction of portal vein by cancer) .Periampullary cancer . any new medications taken  History of chronic liver disease 4.Enlarged gallbladder? (Recall Courvoisier’s law – if the gallbladder is palpable in a person with painless obstructive jaundice. strictures .Mirizzi syndrome Malignant .Post-instrumentation strictures (ERCP. Pallor? Any abdominal distension. Cervical and supraclavicular lymph nodes 7. and there is no associated pain (i. g. hepatic duct. Decreased emptying of the gallbladder  Gallbladder malignancy is an important cause to exclude  Truncal vagotomy  Spinal cord injury Pigment stones - More common in younger patients Pigment stones are soft stones and crumble easily Can be divided into black pigment stones and brown pigment stones Black pigment stones are composed of mostly calcium salts and bilirubin – predisposing factors include increased secretion of bilirubin into bile (e. decreased bilirubin solubilisers. female. chronic liver disease.Brown stones are composed of calcium salts. and 10% form stones CLINICAL COURSE Asymptomatic .Consistent 2:1 female to male ratio . liver dysfunction 5. and more cholesterol than black pigment stones. and bilirubin .INVESTIGATIONS (guided by clinical suspicion after Hx and P/E) STONE COMPOSITION AND PATHOPHYSIOLOGY Bloods Cholesterol stones 1. ALP and GGT should be raised more than AST and ALT in an obstructive picture 4. flatulent NORMAL PHYSIOLOGY OF BILE .Typical picture (the F’s): Fat. more direct bilirubin than indirect in obstructive jaundice. Increased cholesterol secretion in bile  Obesity  Hyperlipidaemia  Increased oestrogens: female. 18% at 15-20 yrs . and gallbladder stasis . U/E/Cr 3.Ultrasound versus CT  Both useful in demonstrating dilated biliary system and site of obstruction as well as the cause of obstruction  Ultrasound is sufficient if malignancy is unlikely. TPN). cholesterol. 15% at 10 yrs. but CT is preferred if there is a suspicion of malignancy as it can define the tumour better and also have a staging function at the same time to determine involvement of nodes and other organs MANAGEMENT The patient is managed as for the causative aetiology (see relevant sections) GALLSTONE DISEASE DEFINITION Gallstone is a generic term for any kind of stone (cholesterol.Exact incidence in Singapore not known . protein. anaemia 2. they form in the biliary ducts due to infection with bacterial degradation of biliary lipids. cystic duct.Risk of symptom occurrence is 1 to 2% per year. bilirubin. pigment) in any part of the biliary system (gallbladder. but not all sludge becomes stones 20% of biliary sludge will disappear. common bile duct. CEA (cholangioca and pancreatic ca) - Imaging . phospholipids. PT/PTT – any prolonged PTT from vitamin K malabsorption.Normal bile contains bile salts (primary and secondary). chronic haemolysis. of which the greatest risk is within the first 5 years of diagnosis – 10% at 5 yrs.80-95% of patients will have asymptomatic gallstones . a milieu that predisposes to stone formation Can be visualised on the ultrasound scan as layering in the biliary tree Sludge is a pre-stone condition. etc) EPIDEMIOLOGY . LFT – bilirubin raised. FBC – any infection. pregnancy. the degradation products of which then precipitate Biliary sludge - Microlithiasis suspended in bile. fertile.Bile salts and phospholipids are amphiphatic and help to solubilise cholesterol 52 More common in older patients (peak at 40-50 years) Cholesterol stones are hard and faceted Cholesterol stones results from disruption in the solubility equilibrium of bile Risk factors for cholesterol stones formation: 1. 60% recur. forty. exogenous administration 2.In the West: overall 10-15%. Tumour markers – CA 19-9. 20% in women and 10% in men . sickle cell anaemia. Ultrasound of the hepatobiliary system Symptomatic sequlae 1.53 .Lasts for minutes to hours. so the resolution is not as good as MRI . or tip of right shoulder . abdominal distension .Radiation to the inferior angle of the right scapula. and 3-5% severe. haemorrhage 2-3%  Perforation into bile duct.5-1%  Overall risk of complications is 10-15% . 7-10% will have moderate symptoms. and select patients carefully . or in patients with high risk of malignancy (gallbladder polyp.Of those who develop symptoms. bloating. Cholangitis and septic sequelae (see below) 7. if not homogeneous  sludge 3. fried oily foods. Biliary colic . Magnetic resonance cholangiopancreatography (MRCP) . with posterior acoustic shadowing .Pickup rate for gallstones is less than 10% since most stones are radiolucent .The largest value of ERCP lies in its therapeutic potential  Stone removal (using balloon catheter. Fistulation and passage into gut resulting in gallstone ileus – subacute IO 1. Acute pancreatitis (see above) 8. Acute cholecystitis (see below) 3. the rest will have minor symptoms . Endoscopic retrograde cholangiopancreatography (ERCP) .Usually not done to diagnose stones (as mentioned above) .Waxing-waning in character but rarely have any pain-free intervals between waves of pain (unlike ureteric colic where pain will resolve completely between waves) . Empyema of the gallbladder (see below) 4.Often triggered by meals – binge-eating. need to assess the benefits and risks.Biliary colic is a “herald” symptom that indicates risk of further sequelae 2.Thus the majority of patients do not require removal of the stones or the gallbladder  expectant management INVESTIGATIONS FOR GALLSTONE DISEASE .Usually done in symptomatic patient where it is uncertain what is the cause of symptoms  looking for other possible causes as well 4. porcelain gallbladder)  prophylactic surgery (b) Immunocompromised patient where presentation of gallstone disease is not like the normal patient (c) Patients with chronic haemolytic disease (e.Role of surgery in the asymptomatic patient: (a) Predisposing cause for gallbladder stasis that should be surgically treated e. dehydration . or Dormia basket)  Sphincterotomy (in order to relieve obstruction or facilitate removal of stone)  Stenting . and also minimally invasive  preferred to ERCP if patient does not require any therapeutic intervention that ERCP provides 5.Typically epigastric or right hypochondriac pain . CT scan .Associated with nausea and vomiting (patient gets better after vomiting). Plain abdominal X-ray .Even more sensitive than CT scan for stones since CT may miss small stones due to the spacing of the cuts taken . thalassaemia) – as high as 50-60% will develop symptomatic disease in their lifetime 2.g.Before doing ERCP.Bile should appear as black patch in gallbladder. Choledocholithiasis with obstructive jaundice (see below) 6. gallbladder mass suspicious of malignancy.Investigation of choice for gallstones .Comparable to ERCP. Mirizzi syndrome with obstructive jaundice (see below) 9.g. duodenum 0.Features of stone on ultrasound: strong echogeneic rim around the stone. Mucocoele of the gallbladder or hydrops (see below) 5.High level of complications  Pancreatitis in 2-3%  Cholangitis 1-2%. often resolves spontaneously .MRCP is not the same as MRI liver/pancreas – only selected cuts taken in order to reconstruct the biliary tree. Presence of gallstones in biliary system . worst case scenario is empyema .No longer used commonly.Constant.Septic workup . cholecystitis – up to 1 in 3 to 1 in 4  Injury to bowel  Injury to biliary structures e.Non. except in biliary atresia 5 criteria for a normal cholangiopancreatogram (a) Normal intrahepatic ducts (b) No filling defects (c) Smooth common bile duct (d) No stricture/narrowing of the common bile duct (e) Good and free flow of contrast into duodenum TREATMENT Asymptomatic .Pericholecystic fluid (oedema of gallbladder wall) .Analgesia .(Fat stranding around gallbladder not seen on ultrasound but on CT) MANAGEMENT . severe RHC pain (less commonly epigastric) .g.Gallbladder becomes distended and inflamed PRESENTATION . sepsis  Haemorrhage 54  Infection .Gallbladder may be palpable – omentum wrapping around GB. less pain. conversion rate is higher if there is ongoing infection e.LFTs usually normal.RHC tenderness with guarding found on clinical examination.Gallstone gets stuck in the cystic duct causing obstruction of biliary flow . etc Symptomatic .Mostly for therapeutic rather than diagnostic purposes .Risks of laparoscopic cholecystectomy  Conversion to open operation up to 5% (due to abnormal anatomy. main indications: 1) high obstruction not well visualised in ERCP.PTC involves a tube being inserted into the liver under radiologic guidance into one of the biliary ducts (must be dilated duct) .g. no jaundice ULTRASOUND FEATURES OF ACUTE CHOLECYSTITIS .Associated with fever. vomiting . acute cholecystitis.Complications: bleeding. HIDA scan .Expectant management and close follow-up .Counsel patient about symptoms – biliary colic.No surgery required unless patient has indications for surgery (see above) . Percutaneous transhepatic cholangiography (PTC) /biliary drainage (PTBD) . good results only for cholesterol stones   All not shown to work for long-term ACUTE CHOLECYSTITIS PATHOPHYSIOLOGY . Murphy’s sign positive . CBD  Spilled bile  peritonitis.6.Radiates to the inferior angle of the scapula . less complications post-operatively .Rarely done now.Can be open or laparoscopic – laparoscopic is preferred as it is associated with shorter hospital stay. leakage of bile when tube is removed 7. obstructive jaundice.surgical means of stone treatment  Chemodissolution  Liver diet  Shockwave lithotripsy – more morbidiy cf renal lithotripsy as less fluid around to dampen waves.Resuscitate the patient . iatrogenic injury).Contracted gallbladder (from chronic gallstone disease) .Bowel rest and intravenous fluids . difficult or complicated dissection. 2) therapeutic purpose of drainage for an obstructed system that cannot be drained from below .Cholecystectomy is the only way to treat gallbladder stones that are symptomatic .Sonographic Murphy’s positive .Empirical intravenous antibiotics – IV ceftriaxone and metronidazole . nausea. then colon.Chance of recurrence during the time . mostly in elderly patients in whom gallstone ileus is more common .Dependent on several factors:  Severity of illness  Response to resuscitation and antibiotic therapy  Logistical considerations (availability of OT. in very sick patients who are not doing well/not responding to treatment) ii.55 .Small bowel enterotomy proximal to the point of obstruction is usually required to remove the stone . Delayed/interval (after 6-8 weeks) 4.Higher conversion rate to open chole . surgeon etc) 3.Most commonly occurs in duodenum. Cholecystenteric fistula Early Delayed Advantages .Symptomatic fistulas should be treated with cholecystectomy and fistula closure 5.Better laparoscopic success Disadvantages . Gangrene and perforation . requiring urgent surgery .Small stones (<2-3cm) usually pass spontaneously without problems .Increased risks of post-op infection Disadvantages . Early (within few days of onset) iii.Treatment involves emergent cholecystectomy .Can be done under LA.Usually asymptomatic . poor nutrition. labile blood pressure. Emergency (immediate.Fibrosis  difficulty mobilising gallbladder .Cystic duct obstruction leads to a tense gallbladder filled with mucus . Gallstone ileus .Definitive treatment – laparoscopic cholecystectomy Timing of cholecystectomy .Need for another admission .Mortality is 10-15%. aerobilia is seen in 40% of cases .In moribund patients who are not fit for surgery .Ongoing inflammation  higher risk of bleeding .Accounts for 1-2% of IO overall .May lead to gallbladder wall necrosis if pressure exceeds capillary bld pressure 2.Possibilities available: i.Lower risks . requiring emergency laparotomy . sepsis COMPLICATIONS OF ACUTE CHOLECYSTITIS .Gallbladder is filled with pus due to bacterial infection of the stagnant bile (cystic duct being obstructed by a stone) .On AXR.Easier to operate as the gallbladder is oedematous Advantages . Empyema . after repeated attacks of cholecystitis .Immediate cholecystectomy not warranted as <4% of patients will have further symptoms  Early surgery has been found to be more beneficial than delayed surgery Cholecystostomy ACALCULOUS CHOLECYSTITIS .Everything done in one admission .Most common site of obstruction is terminal ileum .Poor nutrition leads to biliary stasis.Localised perforation  abscess that is confined by the omentum .Stones causing cholecystenteric fistula pass into the enteric lumen causing intermittent bouts of small bowel obstruction .Free perforation  generalised peritonitis and sepsis.Drains the gallbladder and alleviates the inflammation  better outcomes . or more commonly under radiologic guidance (percutaneous) .Patient is usually toxic. and stomach. while dehydration and hypotension leads to formation of viscous bile and gallbladder ischaemia  bile may get infected  cholecystitis 1.Higher risk of injuring some other structure due to difficulty in visualisation . Hydrops .Occurs in very ill patients with prolonged stay in ICU – prolonged fasting. coli.Definitive treatment dependent on:  Medical condition of patient  Success of biliary decompression .Investigate for cause of obstruction – ultrasound or CT (depending on what facilities are available.Gallstone in CBD . imipenem if the patient is in shock 3.e. jaundice (only 50-70% of patients have the classic triad) . ultrasound is preferred if suspecting stones) . EUS .Most common cause is choledocholithiasis (60%).FBC (check TW for any rise suggestive of infection) . E. up to 11-12mm in size MANAGEMENT .Usually results from obstruction to the biliary system with infection of stagnant bile . Enterococcus MANAGEMENT 1.If unsure of presence of stone  less invasive investigation such as MRCP.Dilated CBD (normally <8-9mm)  >10mm is abnormal  In older patients.Previous Bilroth II (unsuitable anatomy for ERCP) CHOLEDOCHOLITHIASIS CHOLANGITIS PRESENTATION .If infection sets in  cholangitis (see below) PRESENTATION . try again (+ stent in between to drain bile) Operative removal – Open CBD exploration – Lap CBD exploration ..Amylase (CBD stone may cause pancreatitis) . biliary) .A surgical emergency! BLOODS .Common causative organisms are gram negative bacteria and anaerobes – Klebsiella. Biliary decompression and definitive treatment .LFTs (raised bilirubin – direct. also consider benign strictures and malignancy (pancreatic.Biliary decompression and definitive treatment can be combined or separate .g. Resuscitation - Anticipate rapid deterioration Obtain good intravenous access and fluid resuscitate as appropriate Take bloods for investigations – cultures especially Close monitoring of vitals in HD/ICU Catheterise and watch urine output CVP line insertion if patient has shock unresponsive to fluid resuscitation 2.Gallstones in gallbladder . pale stools .If no facilities to do ERCP: open or laparoscopic cholecystectomy with CBD exploration When to do operative removal of stones (i.Reynold’s pentad: Charcot’s triad plus mental obtundation and shock .Biliary colic . Enterobacter. not suitable for ERCP) - Stone >25mm Intrahepatic stone Large number of stones Impacted stone Dual pathology Tortuous duct 56 PATHOLOGY .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.Decompression commonly performed using ERCP  Decompression is the primary objective – stenting or external drainage (nasobiliary drain)  If cause of obstruction can be treated in the same setting (e. stones to be removed) then treat the cause also  Success rate 90% . or patients on long-term opiates. the CBD may be larger. post-cholecystectomy.Obstructive jaundice – tea-coloured urine. ALP raised more than transaminases) ULTRASOUND .Classically Charcot’s triad: RHC pain.IV ceftriaxone and metronidazole. Antibiotics . fever. Grade II: Fistulation into common bile duct with the fistula <1/3 diameter of the CHD .Bile duct adenoma . the CBD is more than 2cm in diameter. and no free leak of contrast into peritoneum  If all normal  release anchoring stitch and exert gentle traction on the tube.Related to chronic cholestasis:  Primary sclerosing cholangitis / Ulcerative colitis  Hepatolithiasis  Parasitic infection – Clonorchis sinensis. if not. the tube should slip out easily. quite unlikely that it will function normally even after removal of the obstruction) MIRIZZI’S SYNDROME PATHOLOGY .Grade I: No fistula. Type II: tumour reaching confluence iii. thus not as sensitive. one should anticipate swelling and oedema of the biliary system resulting in postoperative obstruction and buildup of bile  higher risk of biliary leakage (a) Stent – removed later by endoscopy (b) T-tube  A T-shaped tube with its horizontal limb placed in the CBD and the vertical limb leading out to drain bile  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. Type IV: multicentric or involving confluence and both hepatic ducts ASSOCIATIONS .57  Logistical considerations . extrinsic compression on CHD .Cholangiogram or choledochoscopy is performed    Cholangiogram involves injection of dye – can image higher ducts Choledochoscopy involves using a scope to visualise the large biliary ducts – cannot image higher ducts. 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 CHOLANGIOCARCINOMA SITE .Gallstone in the Hartmann’s pouch compressing the common hepatic resulting in obstructive jaundice . Opisthorchis viverrini  Caroli’s disease (multifocal segmental dilatation of large intrahepatic bile ducts) . Type IIIA/B: involving common hepatic duct and either right or left hepatic duct iv. Type I: below confluence of hepatic ducts ii. only when there is obstruction to flow will bile be diverted out through the vertical limb  Allows for post-op cholangiogram to check for remaining stones (at POD 910) before removal – free flow of contrast into duodenum.Compression effect is not just physical (the stone) but also contributed by the surrounding inflammation .One of the caveats to Courvoisier’s law GRADING .Grade IV: Fistula >2/3 diameter of CHD .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.Choledochal cyst .Distal 25% .Perihilar 65% (Altemeier-Klatskin tumour) Bismuth classification i. but can be used to remove stones visualised in the duct Choice of imaging depends on site of obstruction and the cause . no residual stones.Grade III: Fistula 1/3 to 2/3 diameter of CHD .Consider biliary bypass if there are multiple stones.Intrahepatic/peripheral 10% .Removal of stones     Manual removal with stone-grasping forceps Flushing out stones Dredging stones out using balloon catheter or Dormia basket Lithotripsy .Choices for definitive treatment: (a) Open cholecystectomy with CBD exploration (b) Laparoscopic cholecystectomy (c) Laparoscopic cholecystectomy with CBD exploration CBD EXPLORATION . or there are strictures (since the CBD has been chronically dilated. endoscopic procedures.Intrahepatic pigment stones . jaundice.Pruritus .Perihilar 10-30% (worse prognosis due to early lymphatic spread) PALLIATION . . Clonorchis sinensis)  epithelial damage  predispose to seeding of coliforms into biliary system  stone formation  recurrent cholangitis HISTORY: .Intrahepatic biliary obstruction.. specificity 86%) .FBC . Dx based on history.Acholic stools . AST .LFT with ALP>ALT.CA 19-9 >100μl/ml (good sensitivity of 89%.Intrahepatic: 35-45% .If after opening up and finding that tumour is not resectable.Distal 35-45% . 2) drainage of obstructed system if ERCP cannot drain) CURATIVE TREATMENT . is characterized by: . malaise  Weight loss  Hepatomegaly DIAGNOSIS .Contrast CT .Thorotrast exposure PRESENTATION .Recurrent bacterial cholangitis . DIFFERENTIALS Primary Sclerosing Cholangitis INVESTIGATIONS For diagnosis For Complications Bloods . or percutaneous biliary drainage procedures.Painless jaundice (painful if there is cholangitis) .Endoscopic/percutaneous transhepatic biliary stenting . or recurrent pyogenic cholangitis (RPC). can perform surgical bypass 58 RECURRENT PYOGENIC CHOLANGITIS BACKGROUND Cholangiohepatitis.A history of recurrent attacks of cholangitis – typical hx:  1-2 episodes of fevers. and RUQ abdominal pain per year  Hx of prev biliary surgery.Surgery is the only chance of long-term cure .PTC (2 functions: 1) roadmapping for surgery. PATHOPHYSIOLOGY Helminthic infxn (eg Ascaris lumbricoides.Complications of pyogenic cholangitis  cirrhosis with portal hypertension  cholangiocarcinoma PHYSICAL EXAMINATION No specific physical findings are evident in RPC.Only 25% of tumours are resectable .Prothrombin time: N/ (if prolonged cholestasis causes fat malabsorption and vitamin K deficiency)  Impt to exclude – correct with parenteral Vit K before invasive procedures .Bilateral drainage for hilar cholangiocarcinoma .Advanced signs and symptoms:  Abdominal pain  Fatigue.Contraindications to surgery  Bilateral or multifocal intrahepatic disease  Invasion of portal vein trunk or hepatic artery  Bilateral involvement of hepatic arterial or portal venous branches  Unilateral hepatic vascular invasion with contralateral ductal spread  Distant metastases PROGNOSIS FOR RESECTABLE DISEASE (5-year survival) . Usual surgical approach includes:  Initial biliary decompression – ERCP sphincterotomy / stent placement  Definitive biliary drainage procedure – e.59 .g. .Ova and parasites: RPC freq a/w Clonorchis infxn – look for it and treat when present. .Death occurs in approximately 15-20% of patients over 5-6 years.Treat current infection .CT scan  centrally dilated bile ducts with peripheral tapering  bile duct stones  pyogenic liver abscesses. TREATMENT PRINCIPLES: . .Management of other complications e.U/S HBS  segmental biliary dilatation  hepatolithiasis  liver abscesses  helps determine choice of supplemental axial imaging techniques.ERCP or PTC – imaging modality of choice for delineating the biliary tree.Biliary drainage . Roux-en-Y choledochojejunostomy PROGNOSIS . Radiology . dehydration etc Surgical .Blood C/S: bacteremia – results help guide antibiotic choice.g. . posterior. dimpling. and provide structural support to the breast (involvement of these ligaments by malignancy causes dimpling of the overlying skin) Level II: posterior to pectoralis minor Level III: medial to pectoralis minor. extending up to apex of axilla 2. from the second to the sixth rib . 10% present with pain) HISTORY 1.DISEASES OF THE BREAST ANATOMY . medial. 3. 1. Drain secondarily into supraclavicular and jugular nodes 3. swelling? Any general asymmetry of the breasts noticed? Any increase in size from first noticed to now? Any changes in the nipple e. Internal mammary nodes  Account for about 20% of drainage from the ipsilateral breast – upper and lower inner quadrants  About 4 nodes per side. with one node in each of the first three interspaces and one in the fifth or sixth interspace 3.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. History of lump . Interpectoral (Rotter’s nodes) – between pec major and pec minor muscles PRESENTATION OF BREAST DISEASE 1. Pain with no lump (cyclical vs non-cyclical) 3. what is the colour and consistency? Any other lumps elsewhere – other breast? Axilla? Neck? . 6. self-examination. Anatomic division into levels I.The base of each breast extends from the lateral border of the sternum to the midaxillary line. 3. Nipple changes or discharge APPROACH TO BREAST LUMP DIFFERENTIALS Painless lump Painful lump 1. Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes 1. 7. 4. 40-50 nodes in total.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 . lateral.The axillary tail pierces the deep fascia and enters the axilla . etc)? Duration since first noticed Painful or painless? Overlying skin changes noted: erythema. Carcinoma Cyst Fibroadenoma Area of fibroadenosis (nodularity) Area of fibroadenosis Cyst Abscess (usually in lactating women) Galactocoele (lactating women) Periductal mastitis Fat necrosis Carcinoma (rare. 5. 2. 4. retraction Nipple discharge? If present.Lymphatic drainage: 1. 2.Each mammary gland consists of 15-20 lobules that are drained by lactiferous ducts that open separately on the nipple . apical 2. in 5 groups: Anterior. II and III by the pectoralis minor muscle: Level I: lateral to pectoralis minor 60 - Site of the lump? Single or multiple? When was it first noticed? Why was it noticed (pain.g. warmth. Breast lump (painful vs painless) 2. for how long after birth Is patient currently postmenopausal? If so. any obvious skin changes (peau d’orange.Use one hand to retract and stabilise the breast and palpate with the other . then ask patient to relax and try to move the lump again . if patient cannot do it. or hard)  Fluctuance  Margins (regular and smooth. consistency (firm.Characterise the lump:  Site (which quadrant)  Tender or non-tender  Warmth of overlying skin  Size  Shape  Surface (smooth or nodular/irregular)  Consistency (soft.Bone pain (metastasis) PHYSICAL EXAMINATION Preliminaries - Introduce yourself to the patient.If any lymph nodes are found to be enlarged. check with the patient whether this is the same lump she detected on her own . how old was she when she became menopausal? (>55 years old) Use of hormonal replacement therapy and/or oral contraceptive pills Family history of breast cancer or ovarian cancer (BRCA gene) especially if cancer occurs in first degree relative below the age of 40. how many children (nulliparity) Age at which first child was born (>30 years old) Whether patient breastfed her children.Start off with patient’s hands relaxed at her sides – look for any asymmetry in the breast contours.Look for nipple changes (7 D’s):  Discolouration  Depression (retraction)  Destruction  Discharge  Deviation  (Duplication – unlikely)  Displacement Palpation .Patient should be lying down at 45 degrees to the horizontal with her hand tucked behind her head – this splays the breast out so it can be palpated properly . or procedure e. posterior. puckering) .Start with the normal side first! . Oestrogen exposure history and other risk factors for cancer - Age of menarche (early menarche <12 years old  increased risk) Whether married.Ask for any pain before starting to palpate .Palpate the normal side first . Systemic review .Palpate gently.Then ask patient to raise her arms (to accentuate any tethering to the skin which shows up as dimpling) . punch biopsy . covering the major groups of nodes: anterior. and apical . ask for permission to examine the breast Always have a chaperone to accompany you if you are male Expose patient adequately from the waist up with exposure of axillae Good lighting Position the patient at 45 degrees or sitting position if a bed is not available Inspection . quadrant by quadrant from centre outwards .Fever (infective cause) . mobility .Loss of appetite. and if so.Palpate in a systematic manner e. erythema. especially before age of 30 3. loss of weight .61 2. note the number of lymph nodes. then try to move the lump in 2 perpendicular directions. usually fibroadenoma or fibroadenosis) . then ask the chaperone to help Axillary lymph nodes .Rest the patient’s right forearm on your right forearm and use your left hand to palpate the right axilla (vice versa for the left side) .g. tenderness. matted).Ask the patient to push her hands against her hips to contract the pectoralis major muscles – this may reveal a previously unnoticeable lump . medial.Don’t be happy just finding one lump. and systematically. still examine carefully for other lumps (multiple lumps are unlikely to be malignant. or in bilateral breasts Previous breast cancer that has been treated Previous biopsy of the breast showing atypical ductal hyperplasia or LCIS Exposure to ionising radiation Alcohol intake. lateral.Be thorough and examine the entire breast including the axillary tail . ask patient if she can show you the discharge by expressing it herself (NEVER squeeze the nipple yourself!). and if married. or irregular and ill-defined)  Fixation to the skin – try to pick up the skin above the lump  Fixation to underlying muscle – ask patient to press her hands against her hips to contract the pectoralis major muscle.g. hard. their site. firm.When the lump is located. size.Look for any scars of previous operation. slowly.If the patient complains of nipple discharge and none is visible. 95% of spiculated masses on mammography are due to malignancy 62 .Evaluates consistency (solid vs cystic).Calcifications <0.2% risk) Category 4: Suspicious. radial scar (a benign lesion). non-standardised techniques. bosselated Irregular Soft to hard Mixed.Evaluation of mass in mammographically-difficult areas e. poor resolution.05% risk still present) Category 2: Benign Category 3: Probably benign. but provides good soft tissue definition . biopsy should be considered (25-74% risk) Category 5: Highly suggestive of malignancy (75-99% risk) Category 6: Known malignancy 2. Ultrasound . done on request to help magnify areas of abnormality or help visualise breast better .5mm in size (if >0.Causes: Invasive cancer. fat necrosis. short-term follow-up suggested (<0. 0. fibrocystic disease. heterogeneous appearance.Features of malignancy:  Markedly hypoechoeic + thick echogenic halo  Irregular edges  Hypoechoeic shadowing  Taller than it is wide (fir-tree appearance)  High central vascularity 3. (ii) Imaging. margins .Pitalls: Operator dependent. lactating patients . MRI of the breast . and (iii) Histology. abscess. invasive cancer.Stellate lesion is a localised distortion of the breast parenchyma without perceptible mass lesion – high chance of it being malignant . Mammography . papilloma . underlying density .Usually used as the first investigation in young patients (<35 years old) or pregnant.Can be used to guide interventional procedures such as biopsy.To complete the examination - Examine the cervical lymph nodes especially the supraclavicular nodes Examine the lungs for any pleural effusion Percuss the spine for bony tenderness Examine the abdomen looking for hepatomegaly . drainage of abscess.Benign microcals are punctate.5mm  macrocalcifications) .Look at the axilla on the MLO view for any enlarged lymph nodes FINDINGS FOR THE COMMON BREAST LUMPS Type of lump Cyst Nodularity Age Pain Surface Consistency Mobility 30-55 20-55 Occ Occ Smooth Indistinct Not fixed Not fixed Fibroadenoma Cancer 15-25 35+ No No Smooth. and may have a “tea-cup” appearance (c) Spiculated mass or stellate lesion .BI-RADS (Breast Imaging Reporting and Data System) classification Category 0: Need additional imaging evaluation Category 1: Negative (nothing to comment on. localisation of a lump preoperatively. “partially blind” to microcalcifications .Most sensitive of the proven breast imaging modalities . axilla . aspiration of cyst .Usually performed in older women (>40 years old) as the breast tissue in younger women is denser.Sole feature of 33% of cancers detected on mammography . more difficult to pick up abnormalities on mammogram . fluctuant Rubbery Stony hard Very mobile May be tethered or fixed INVESTIGATIONS “The evaluation of a breast lump is via the TRIPLE ASSESSMENT – (i) Clinical examination.Abnormal features: (a) Neo-density or asymmetric density (b) Microcalcifications .Indications:  Positive axillary lymph node but mammogram and ultrasound negative  Suspicion of multifocal or bilateral malignancy (esp ILC which has a high incidence of multifocality/bilaterality)  Assessment of response to neoadjuvant chemotherapy  When planning for breast conservation surgery  Screening in high-risk patient? .g.Normally. closely grouped or arranged in a linear pattern (ductal distribution).Causes: DCIS.Evaluation of a palpable mass with a negative mammogram . 2 views are done: craniocaudal (CC) and mediolateral oblique (MLO) . etc (d) Architectural disortion .Rarely used due to high cost.Additional specialised views: magnification and coned compression. chest wall.Localisation of lesion seen in only one mammographic projection .Features of malignancy: pleomorphic microcals.” Imaging 1. 63 Histology . will result in a larger wound.If triple assessment suggests benign disease (i.If malignancy found.Can be guided by clinical palpation (if there is a palpable mass) or radiologic guidance if the mass is small or there is no palpable mass  more accurate but still not 100%  Ultrasound guidance  Stereotactic guidance (stereotactic mammotome) MANAGEMENT .Antibiotics for mastitis/abscess + incision and drainage for abscess . Is the discharge worrisome? - Unilateral or bilateral (unilateral more worrisome) Discharge from multiple ducts or single duct (single duct more worrisome) Nature of discharge (bloody more worrisome) Age of the patient (more worrisome in older patient >60) 4. may require excisional biopsy APPROACH TO NIPPLE DISCHARGE CAUSES Colour of discharge Cause Red or pink (blood + serum) Ductal papilloma Ductal carcinoma Ductal papilloma Duct ectasia (= periductal mastitis) Cyst Ductal carcinoma Duct ectasia Mastitis/abscess Galactorrhoea/lactation Clear yellow (serous) Green. eczema. less painful. follow patient up with physical examination for a year (q3-6mths) to make sure the lump is stable or regresses . brown. requires local anaesthetic. requires skilled cytopathologist  Core biopsy is more invasive. all three aspects suggest benign nature of lump). Is the discharge true? . smaller wound. Ductography MANAGEMENT .If all three aspects of triple assessment suggest malignancy  further staging and treatment . Histology of lesion if found on imaging 4.e. but can obtain tissue specimen.Spontaneous discharge or discharge only on pressing (spontaneous is sig) . Is the discharge significant? . etc 2. improper angling may result in puncture of the lung or heart).g. more painful. white fluid (milk) HISTORY: 1. Mammography/ultrasound of both breasts to detect any underlying malignancy 3. foul-smelling Thin.Relation to breastfeeding (significant if >1yr after stopping breastfeeding) 3.Conservative management for most other pathologies unless discharge persists and is troubling patient  microdochectomy of offending duct .Exclude other conditions that can cause discharge but not from the nipple e.If one or two out of three aspects suggest malignancy  further workup. Is it troubling the patient? PHYSICAL EXAMINATION (as described above) INVESTIGATION 1. but only cells are obtained with no histology  cannot differentiate between in-situ cancer and invasive cancer.Options available: (a) Fine needle aspiration cytology (b) Core biopsy (Trucut) (c) Incisional biopsy (d) Excisional biopsy . can stain for ER/PR status  better diagnostic value . Paget’s. does not require any local anaesthetic. Discharge for cytology to detect malignant cells 2. black (cell debris) Purulent.Mostly a choice between FNAC and core biopsy  FNAC is less invasive.Microdochectomy for intraductal papilloma . manage malignancy . risk of complications higher (because biopsy needle is a spring-loaded firing mechanism.Intermittent or persistent (persistent is sig) . Good prognosis if treated .Presents as erythematous.Histologically not specialised . especially if first degree relative. young onset <40 years old. nulliparity.In patients presenting late.35% multicentric. Hormonal replacement therapy 8. papillary . pain alone. bone pain (metastases from breast cancer spread to lung. bland round nuclei . tubular. bone. swollen breast w/o palpable mass . peau d’orange.Most common cancer in females in Singapore .Better prognosis than IDC Inflammatory carcinoma .70-80% of invasive breast cancer . late menopause >55y/o) 10.Epithelial tumours arise from cells lining the ducts or lobules. but a marker for increased risk of invasive disease in both breasts (7-10x increased risk) . High oestrogen exposure (early menarche <12y/o. liver.Bimodal age distribution. Ionising radiation to breast PATHOLOGY .Progress to ca within 10 yrs.Not premalignant. incidentally detected . incidence is half that of the West .Usually does not form palpable mass and not detected by mammo. cause distortion of lobules. Oral contraceptive usage 7. colloid (mucinous).Malignant cells arise from terminal duct lobular unit (like DCIS) but do not distort lobular architecture . rapidly fatal PRESENTATION . primary sarcomas) and are very uncommon .g.Very poor prognosis. tethering (means mass is still mobile but overlying skin will be indented when moving the lump).60-80% multicentric and bilateral . and can be further divided into invasive and non-invasive based on invasion of the basement membrane Ductal 64 Non-invasive Invasive DCIS IDC . discharge. will be IDC usually. Alcohol consumption 6.Malignant cells arise from terminal duct lobular unit.Similar prognosis to IDC Specialised types . Previous breast cancer 5. bilateral cancer in relative affected) 3.WHO classification divides breast cancers into epithelial and non-epithelial tumours.Gender ratio is about 100-150:1 RISK FACTORS 1. considered pre-malignant . Age (increases with increasing age with two peaks as mentioned) 2.Non-palpable. enlarged. lymph nodes.Poorer prognosis than a carcinoma of specialised type . a cell-adhesion molecule) . there may be overlying skin changes e. onethird overexpress C-erbB2 Others LCIS ILC .10-20% multicentric and/or bilat . fixation (means the mass is not mobile).BREAST CANCER Lobular EPIDEMIOLOGY . malignant phyllodes tumour.g. angiosarcoma.No histo features of inflammation . even fungation .000 in 2002. occurs >15 years after diagnosis .g. Li-Fraumeni syndrome involving p53 mutation) 4. Previous biopsy showing atypical ductal hyperplasia or lobular carcinoma in-situ 9.Age-standardised incidence 55 per 100. nipple retraction .5-10% of invasive cancers .Non-epithelial tumours arise from supporting stroma (e. . brain) .Increasing number of patients with abnormalities detected on mammographic screening but with no palpable lump DIAGNOSIS – BY TRIPLE ASSESSMENT (see above) . one peak at 45-55 years and another in older women (>75) . but do not invade BM .Includes all cancers that cannot be subclassified into a specialised type  “no special type” .May have symptoms of metastatic spread e. Genetic predisposition (BRCA1 on 17q.Medullary.Most patients present with self-detected lump in the breast (more than one-third of patients).Cells invade individually into stroma (due to loss of E-cadherin. Family history (breast or ovarian cancer.Cells morphologically similar to cells of LCIS: monomorphic.If ca develops.Diffuse invasion of breast parenchyma by ca cells blocking numerous dermal lymphatic spaces  swelling . late childbearing with first child at >30y/o. detected on mammo as microcals . occult invasive ca in 10-20% . other presentations include painful lumpiness. ~30% risk.Two-thirds express ER/PR. nipple-areolar complex. lymphoedema .0 cm N3: N3a – Ipsilat infraclav nodes N3b – Ipsilat int mammary nodes N3c – Ipsilat supraclav nodes (b) Systemic control: Chemotherapy Hormonal therapy Targeted therapy T3: >5cm T4: T4a – Chest wall involvmt T4b – Skin involvmt T4c – Both 4a and 4b T4d – Inflammatory ca Stage 0 Tis Options can be divided into aims of control: Surgery Radiotherapy T2: 2 to 5 cm Stage I Stage II T1N0 T2N0. N3 T4.Investigations: (i) Chest X-ray (for lung metastases) (ii) CT chest (iii) CT abdomen (iv) Bone scan M stage M1: distant mets (70% in 10 years) (40-50%) (20-30%) (<2%) THERAPEUTIC OPTIONS T stage Tis: Carcinoma in-situ.g.e. T3N2 Any T. shoulder stiffness.Removal of tumour with clear margins. T1N2.Not required for DCIS (because theoretically cancer cells are confined to the breast) . 4% in 5 years) . 6.0 to 2. progress of disease) C-erbB2/Her-2 positivity indicates more aggressive tumour  worse ER/PR positivity is good – more of a “predictive factor” because it predicts response to treatment with tamoxifen. any N M1 Aaaaa – Stage Xb (e. 3. IIb. and overlying skin . while achieving good cosmetic result . T1N1. 5. no skin or chest wall involvement (i.Criteria:  Tumour <5cm in size. Axillary clearance . 2.1 to 0. IIIb) PROGNOSIS Prognostic factors: Stage of disease – tumour size.Performed for all invasive carcinoma (WEAC or SMAC) .Complications: numbness/pain along inner aspect of arm. T2 or less)  Only one tumour.5 to 1.5 cm T1b – 0. Paget’s with no tumour N stage N1: Mobile ipsilat axillary nodes N2: Fixed/matted ipsilat axillary nodes (a) Locoregional control: T1: <2cm T1a – 0.Removal of breast tissue. 90% 60% 30% 10% 1. Simple mastectomy . T2N1 Surgery Stage III Stage IV T3 N1 T0N2.0 cm T1c – 1.65 STAGING Survival Stage I: Stage II: Stage III: Stage IV: . 4.Lower rates of local recurrence 3. lymph node involvement [Major prognostic factor] Histological grade of tumour Lymphovascular invasion Age (younger patient  higher chance of recurrence. not multiple (unless in the same quadrant)  No metastatic disease  Appropriate tumour size-to-breast ratio (to achieve good cosmetic result)  Patient must agree to post-operative radiotherapy .Overall survival at 25 years for WEAC comparable to SMAC . T3N0 T0N1.Slightly higher local recurrence rates for WEAC (1% per year. T2N2. p53 mutation 1. Wide excision (breast-conserving surgery) .Higher risk in younger patients as cancer tends to be more aggressive 2. also means tumour is less undifferentiated 7. infected tumour) . Neoadjuvant .Safe. Need to clean even minor wounds with antiseptic solution + prophylactic ABx vs staphstrep .Of these tumours. endometrial cancer (0.e.Common regimens: AC (anthracycline. FAC (5-FU.Preferred for postmenopausal women as response to hormonal therapy is better than to chemotherapy . decompression of spinal cord compression. increase survival Hormonal therapy . being the first lymph node draining the breast. Palliative Chemotherapy 1.Sentinel lymph node biopsy is a new modality of treatment  Principle: the sentinel lymph node.Lymphoedema – RT is contraindicated with AC as it worsens oedema . doxorubicin. 66 Radiotherapy 1. if positive.Premenopausal patients tend to have better response to chemotherapy than hormonal therapy (and vice versa for postmenopausal patients) . CMF (cyclophos.Surgery at other sites: Fixation of pathological fractures.Shoulder stiffness – require physiotherapy .1% per year).Need to place a clip into the tumour before starting neoadjuvant therapy to guide surgery in case the tumour “disappears” 2. fungating. look for the SLN by colour.Anthracyclines and taxanes are the mainstay . no more tumour cells . Palliative . Adjuvant .Options: (i) Prosthesis (ii) Muscle flap from rectus abdominis or latissimus dorsi Complications of surgery Early Haemorrhage (POD1) Wound Infection (POD3) Seroma formation (accumulation of serum) in 50% Flap ischemia Late Cosmetic deformity Complications of Axillary Clearance: . 1 cycle per day from Monday to Friday over five to six weeks 2.No delay in subsequent treatment and no increase in rates of relapse . methotrexate. Adjuvant . cyclophosphamide). due to lymphoedema. deep vein thrombosis .Intercostobrachial nerve transection – numbness over inner aspect of arm.20% of tumours achieve complete clinical response (cCR) i. epirubicin) and the taxanes (e. 25% reduction in mortality .Regimen consists of 25 to 30 cycles in total. methylene blue) or radioactive isotope (Tc99 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  During the op.Palliative mastectomy for symptoms (bleeding.Given in all locally advanced cancers after resection. then the rest of the axillary nodes should be negative as well  Use of blue dye (isosulphan blue.Mostly used as adjuvant therapy but can also be used as palliative treatment Classes (a) Selective oestrogen receptor modulators (SERMs) .. perform axillary clearance  False negative rate 8% (quite good)  No difference in axillary recurrence between full axillary clearance versus only sentinel node biopsy  SLN biopsy is now standard of care in many hospitals in SG 4.Helps to reduce load of disease to alleviate symptoms. and in some early breast cancers depending on stage (see below) .Tamoxifen  50% reduction in recurrence. is representative of the rest of the axilla. paclitaxel.Usually done after breast-conserving surgery . surgical excision of brain metastases 5. docetaxel) . or using a Geiger-Muller counter to detect the node with highest radioactivity  Send node for frozen section  If negative.For hormone receptor-positive disease . can be done during breast surgery or at a later time . 5-FU) 3. a further 20% will achieve complete pathological response (cPR) i. Breast reconstruction . etc). Palliative surgery .Main active agents are the anthracyclines (e.Side effects: menopausal symptoms (hot flushes.g. do not clear axilla.Cellulitis – even in minor trauma.g.Given in locally advanced cancer to shrink the tumour before surgical resection .Used in adjuvant setting . anthracycline. if the SLN is negative for tumour cells. tumour is no longer palpable . cyclophosphamide).e. osteoporosis Targeted therapy . N=0 Look at histological grade (minor prognostic factor).6-monthly for the next 3 years (i.Inhibit peripheral conversion of testosterone and androstenedione to oestradiol .At each visit – ask about symptoms and do clinical examination . used in advanced cancers) TREATMENT BY TUMOUR STAGE Tumour can be divided into in-situ cancer. the skin defect will be very large  inoperable) . asymptomatic 40-49 YO 50-64 YO >65 YO Increased risk Start screening 5 yrs before onset of breast dz in youngest family member HRT therapy 40-49 YO 50-65 YO Annual mammogram Biannual mammogram (by invitation) Optional 2 yrly mammogram    Monthly BSE 6 mthly CBE & U/S breast Annual mammography Annual mammogram Biannual mammogram up to 5 yrs after cessation of HRT . infusion reactions. or advanced breast cancer.Distant metastases . third to fifth years) .Main agent is Herceptin (trastuzumab) which targets Her-2-neu a.Systemic therapy:  Neoadjuvant therapy to downstage inoperable tumour (in addition. targets vascular endothelial growth factor [VEGF] receptor. Locally advanced breast cancer .Used in C-erbB2 positive tumours. N stage >1  Adjuvant therapy usually involves chemotherapy if tolerable and/or hormonal therapy if ER/PR positive  In general: In premenopausal pt  chemotherapy + hormonal In postmenopausal pt  hormonal + chemotherapy Intermediate 11mm < T < 20mm. pulmonary toxicity.3-monthly for first 2 years .k. Lapatinib (targets Her-1 and Her2.a.67 (b) Aromatase inhibitors . N=0    Normal risk. Early breast cancer .Yearly for another 5 years (to tenth year) . exemestase . DCIS .Wide excision without axillary clearance . tamoxifen reduces overall breast cancer risk by 50% (in contralateral breast as well) – strictly not adjuvant therapy 3. febrile neutropaenia .Lanastrazole. it helps by predicting the tumour response to chemotherapy before resection)  Adjuvant therapy after resection – chemotherapy or hormonal (as above) 4.Some patients given hormonal therapy to reduce recurrence at surgical site. used in advanced cancer). locally advanced breast cancer. early breast cancer.Locoregional therapy: SMAC.Surgical resection dependent on size of tumour and resectability (if tumour is too large. 1.Only suitable for post-menopausal patients as use of these agents will cause overactivity of the HPA axis in premenopausal women . C-erbB2 receptor (a type of epidermal growth factor receptor [EGFR] that is overexpressed in 18-20% of cancers) .T2 or less (<5cm).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 T >20mm.e.Other agents include Avastin (or bevacizumab.Minimal locoregional therapy except for palliative purposes . or WEAC with postop radiotherapy .Systemic therapy is the mainstay of treatment – chemotherapy or hormonal therapy FOLLOW-UP .Usually no adjuvant therapy . N1 or less (no nodes or non-fixed nodes) . N2 or N3 (fixed lymph node involvement or supraclavicular node involvement) .Side effects of Herceptin: cardiomyopathy. Advanced breast cancer .T3 or T4 (tumour >5cm or skin/chest wall involvement).Side effects: musculoskeletal pain. if high grade  chemo No chemo T <10mm. early or late stage .Repeat mammo of same breast 1yr postop. letrozole. then 2-yrly bilateral mammo subsequently BREAST SCREENING 2. Prognosis of the underlying cancer is not altered by the presence of Paget’s disease of the nipple . breaking the normal epidermal barrier thus allowing fluid to be extruded onto the nipple .Punch biopsy of the nipple may be required .PAGET’S DISEASE OF THE NIPPLE .If no palpable mass or mammographic abnormality is detected.Often associated with intraductal carcinoma (DCIS) or invasive carcinoma just beneath the nipple .Examination and investigations should be targeted towards detecting an underlying tumour – may find a palpable mass and/or mammographic abnormalities . may develop into erosions and ulcerations .Treatment should be planned according to the underlying cancer if found .Malignant cells invade across the epithelial-epidermal junction and enter the epidermis of the nipple. wide excision is an adequate treatment 68 .Presents as erythema and eczematous change of the nipple (not the areola) with crusting exudates. 5. . hyoid pathology e. 2. 3. and the anterior border of the sternocleidomastoid posteriorly . Pathology: A cystic expansion of the remnant thyroglossal tract (the embryological origin of the thyroid gland which descends from the foramen caecum on the tongue). enlarged lymph nodes are the most common cause of a lump in the neck. 5. Submental lymph node Thyroglossal cyst Thyroid nodule in the isthmus Sublingual dermoid cyst Plunging ranula (retention cyst of the sublingual) Rarely. 2. 8. 4.The neck is composed of two triangles on each side – anterior and posterior triangles . IV) Thyroid nodule Submandibular gland mass (see later section on Salivary gland swellings) Branchial cyst + fistula Chemodectoma (carotid body tumour) Carotid aneurysm Pharyngeal pouch Laryngocoele (rare. 2. 6. does it move with tongue protrusion – thyroglossal cyst moves with protrusion but a thyroid nodule does not - - Masses in the neck region can be subdivided according to the triangle they occur in as there are pathologies peculiar to each triangle Locations: (i) Midline (ii) Anterior triangle (iii) Posterior triangle In general. Occurs mostly in children and adolescents but up to onethird occur in patients older than 20 years. compressible structure seen in glass-blowers) Posterior triangle 1.If it moves with swallowing. regardless of location (see section on Lymph node enlargement) Thyroglossal cyst Epidemiology: Equal in males and females.Does it move with swallowing – divides the thyroglossal cyst and thyroid nodule from the other causes . 7.g. 3. Lymph node – along anterior border of sternocleidomastoid (levels II. the anterior border of the trapezius posteriorly. and the clavicle inferiorly 1. 4. bursa Anterior triangle 1.The posterior triangle is bounded by the posterior border of the sternocleidomastoid anteriorly. 4. Lymph node – level V and supraclavicular lymph node groups Cystic hygroma Cervical rib Brachial plexus neuroma/schwannoma CAUSES OF MIDLINE MASS Approach: . an air-filled. 6.The anterior triangle is bounded by the lower border of the mandible superiorly. 3. III. the midline anteriorly.69 APPROACH TO NECK MASSES MASSES BY LOCATION Midline NECK MASSES ANATOMY . Management: . usually on fingers. .If complete resection not possible. passing between the external and internal carotid arteries. sebaceous glands and sweat glands. it is usually a papillary carcinoma (~90%).Features: Smooth. inject Bonney’s blue dye into tract prior to surgery to allow accurate surgical excision. Features: . 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 CAUSES OF ANTERIOR TRIANGLE MASS Pathology: Can be congenital or acquired. present since birth). with evidence of adnexal structures such as hair follicles. cystic lump. It is lined by squamous epithelium.If fistula present. Treatment: . XR. Branchial cyst and/or fistula Histology: Cyst lined by epidermis. . CT) are important especially for cysts on the skull as they can communicate with cerebrospinal fluid.Complete resection if possible. history of trauma to area (may have associated scar). .g. Management . (i) Congenital – developmental inclusion of epidermis along lines of fusion of skin dermatomes (seen in younger patients.Smooth firm swelling that is ovoid in shape.May be fluctuant.Surgical excision of the cyst where possible. rounded. 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. fixation to surrounding structures. . The cyst may also contain thyroid and lymphoid tissue. with its long axis running downwards and forwards. If fistula/sinus present. usually in young adults in their 20s.Imaging investigations (e. . may be fluctuant. 70 Epidemiology: Affects both sexes equally. . often in continuity with the associated sublingual gland (but often difficult due to close association with the lingual nerve and submandibular duct).Treatment of infection with antibiotics.Fine needle aspiration of the cyst will yield opalescent fluid with cholesterol crystals under microscopy. chronic discharging sinus. Pathology: A branchial cyst is thought to develop because of failure of fusion of the embryonic second and third branchial arches.Look for fistula in this area – a branchial fistula will run between tonsillar fossa and the anterior neck.Occurs anterior to the upper or middle third of the sternocleidomastoid muscle. usually not transilluminable (due to desquamated epithelial cell contents).May be complicated by recurrent infections – purulent discharge. Ranulas can be congenital or acquired after oral trauma. no previous history of mass. If malignancy occurs (carcinoma of the thyroglossal duct). . Features: Small non-tender mobile subcutaneous lump. U/S. Usually asymptomatic but may become infected with sinus formation and seropurulent discharge (occurs with incision or rupture of cyst) Histology: Cyst with columnar or squamous epithelial lining which may be ciliated.Complete surgical excision of the cyst. Treatment: Sistrunk procedure – resection of the cyst and mid-portion of the hyoid bone in continuity and resection of a core of tissue from the hyoid upwards towards the foramen caecum. Plunging ranula Pathology: A pseudocyst associated with the sublingual glands and submandibular ducts. perform fistulogram to delineate course. . marsupialisation and suturing of the pseudocyst wall to the oral mucosa may be effective. 75% are in the midline while 25% are slightly to the left or right.Complications: cyst recurrence. . . . Seen in older patients. skin-coloured or bluish. hoarseness. regurgitation of undigested food with coughing and dysphagia in the neck. the risk of malignancy is 10%. Treatment: .May obstruct delivery . They are usually benign.Radiotherapy is an effective alternative for patients who are unfit for surgery or whose tumours are too large. look for signs of Horner’s syndrome.DO NOT PERFORM FNA .Cystic hygroma seen on prenatal ultrasound in the first trimester suggests chromosomal abnormality (50% of foetuses. .Compressive problems after delivery – respiratory. Features: .Complications: chest infection (due to aspiration).Squelching sound on deep palpation .Occurs in older patients . . It consists of thin-walled. but locally invasive. .Solid. single or multiple interconnecting or separate cysts which insinuate themselves widely into the tissues at the root of the neck. dangerous) o Diverticulopexy (done in high risk patients. swallowing .Surgical approaches (several available) o Diverticulectomy + cricothyroidotomy (diverticulectomy associated with risk of mediastinitis.A large cyst may extend deeply into the retropharyngeal space Complications: . CT reveals homogenous mass with intense enhancement following IV contrast administration.Patient complains of halitosis. listen for bruit. 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. and undetected synchronous tumours. Features: . Differentials and investigation: . as the diverticulum is still present.50-65% present at birth. fluctuant.CT and/or MRI can be used to delineate tumour anatomy in relation to surrounding structures. due to transmitted pulsation from carotids. but occasionally may present later in childhood or adulthood .A cystic swelling low down in the anterior triangle. May also show vessel compromise by tumour invasion.Due to close association with carotid arteries. involves suspending the lumen of the pouch in the caudal direction so that food and secretions cannot enter the pouch.Minimally invasive treatment: endoscopic cricothyroid myotomy . diverticular neoplasm (<1%) Diagnosis by barium swallow Treatment . thus malignant nature can only be diagnosed by presence of metastasis). . probably formed during coalescence of primitive lymph elements. usually congenital heart anomalies) . weight loss .Angiography is the gold standard investigation – shows a hypervascular mass displacing the bifurcation.If suspecting aneurysm. and facilitates resection). Pharyngeal pouch (also called Zenker’s diverticulum) Pathology: A herniation of the pharyngeal mucosa (pulsion diverticulum) through its muscular coat at the weakest point – Killian’s dehiscence – between the cricopharyngeus muscle and the lower inferior constrictor muscles. with metastasis to local lymph nodes (no histopathological features for malignancy.May be bilateral.Mass is pulsatile but not expansile. . any enlarged ipsilateral lymph nodes are also removed due to the small possibility of malignancy . usually trisomy 21) or other structural abnormalities (33% of foetuses with no chromosomal abnormality. . the risk for malignancy still remains) CAUSES OF POSTERIOR TRIANGLE MASS Cystic hygroma Pathology: A cystic hygroma is a congenital cystic lymphatic malformation found in the posterior triangle of the neck. Features .Classically “brilliantly transilluminable” .71 Chemodectoma Pathology: A chemodectoma is a tumour of the paraganglion cells (paraganglionoma) of the carotid body located at the bifurcation of the common carotid artery (into the internal and external carotids). and compressible (usually into another part of the cyst). located in the posterior triangle at the root of the neck .Main differential is carotid artery aneurysm. examine the rest of the peripheral vascular system.Surgical excision with pre-operative embolisation (reduces bleeding and complications.Lobulated cystic swelling that is soft. lump can be moved side to side but not up and down.Leave it alone if small and asymptomatic . aneurysm can occur at any level but carotid body tumour occurs at the level of the hyoid bone. usually on the left . CXR. 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 . cervical plexus.DO NOT PERFORM FNA – excruciatingly painful 72 Levels There are six levels of lymph nodes in the neck.Slow growing tumour arising from peripheral neural structures of the neck e.g. cyanosis o Neurological: complaints of radicular symptoms (pain.Radiological investigations e.Symptoms/signs: o Arterial: pallor. occasionally with reproduction of radicular symptoms in the limb .g. brachial plexus.Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful) . paraesthesia). etc.A hard mass in the posterior triangle at the root of the neck . gangrene or necrosis of the tips of the fingers o Venous: oedema.Adson’s test can be done – ask patient to extend neck and rotate it towards side of symptoms  radial pulse will be diminished.Usually benign .Diagnosis by CXR Neuroma/Schwannoma Features: . is mobile in plane perpendicular to axis of nerve but not parallel .Usually more symptoms than signs as it causes thoracic outlet syndrome . . vagus nerve. CT to delineate extent of cyst .Management: .May be Tinnel’s positive – tap on the mass for any paraesthesia occurring in distribution of the nerve .Fusiform. wasting of the small muscles of the hand .Surgical excision – partial (to alleviate symptoms) or complete CERVICAL LYMPHADENOPATHY ANATOMY: Cervical rib Features: . phrenic nerve. oral/tongue ulcer. ultrasound. sulphur granules seen in actinomycosis) Palpate from behind. adenocarcinoma – look for breast.Fine needle aspiration provides most definitive results (though there is still the possibility of false positive and false negative results) . Other primary sites (4B’s) Bowel (stomach. .Tenderness to palpation . one side at a time – start at submental.Examination of the thyroid gland . Staphylococcus.Complete examination of the face and scalp for any primary site of infection or neoplasia . discharging sinus (multiple lymph node enlargement with discharging sinuses can be TB or actinomycosis. arthralgia. lastly occipital.g. B symptoms of lymphoma).lymphoma Inflammatory SLE Kikuchi’s (necrotising lymphadenitis occurring in young females.Malignant – work up for primary if present (e.g. tooth decay. malaise. ENT. larynx.Nasopharynx  II – V (usually upper neck – level II and high level V) CAUSES: Can be divided into three main groups: infective. rate of growth.Fixation to overlying skin or underlying structures To complete the examination: . along anterior border of sternocleidomastoid. oropharynx. o Night sweats.Full respiratory and abdominal examination especially if supraclavicular lymph node found . low-grade fever (TB. myalgia (viral prodrome). throat examination especially looking at the post-nasal space for nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged cervical lymph nodes) . lung malignancy. erythema. and neoplastic Infective Viral Epstein-Barr virus. extent. GI tract malignancy) and treat as appropriate . tonsillitis . etc. hypopharynx. HIV Bacteria Streptococcus. matted nodes are more suspicious for malignancy .Consistency – hard. then submandibular. colon). skin.g. TB (contact? Diagnosed? treated or untreated?) . malignancy) . inflammatory.According to FNAC results .Infective/Inflammatory – treat underlying condition . presenting as painful cervical lymphadenopathy) Sarcoidosis HISTORY .Social history: travel and contact history. postauricular. breast. loss of weight (chronic infection. Klebsiella (from intraoral pathology e.g.g.Breast examination in female patient INVESTIGATIONS: . balls (testicular) Primary . spleen .The lump itself – onset.Local symptoms – intra-oral diseases e. Use pulps of the fingers in a gentle rolling movement.Past medical history – cancer. lumps elsewhere .Examination of lymphoreticular system – other lymph node groups. squamous cell carcinoma – look for oral cavity. nose. associated symptoms. CT – to assess nature of lump. liver.Constitutional symptoms o Fever.Location .Oral cavity and oropharynx  levels I – III .Radiological investigation e.Formal ear. bronchus (lung).73 Drainage: .Thyroid and larynx  levels II – VI . o Loss of appetite. cytomegalovirus (infectious mononucleosis). and can be used to visualise primary tumour if present MANAGEMENT: . dental abscess. posterior triangle. tonsillitis) Tuberculosis Parasitic Toxoplasma Fungi Actinomycosis Neoplastic Head and neck primary Metastatic Nasopharyngeal carcinoma Oral cavity. other enlarged nodes that are not clinically palpable. any pain. supraclavicular. sexual history for HIV PHYSICAL EXAMINATION Inspection . preauricular. thyroid. duration.Any overlying skin changes e. Submandibular duct (of Wharton) arises from the superficial part of the gland.Each gland has 15 or so ducts.Sandwiched between the posterior border of the ramus of the mandible and the mastoid process . sensory supply of the capsule from the great auricular nerve. (ii) Somatic sensory supply of the gland from auriculotemporal nerve.Nerve supply is similar to the submandibular gland .SALIVARY GLAND SWELLINGS .Histology: mixed serous and mucous acini.Nerve supply: parasympathetic secretomotor supply from lingual nerve carrying postganglionic fibres from the submandibular ganglion (preganglionic fibres in superior salivary nucleus) .Histology: predominantly serous acini. and the hypoglossal nerve and submandibular duct below it – surgery may injure these nerves . drains into the mouth opposite to the upper second molar tooth 74 .Consists of a large superficial part and a small deep part that are continuous with one another around the free posterior border of the mylohyoid . half of which drain into the submandibular duct. many ducts (other glands have few ducts) ANATOMY: Submandibular gland Parotid gland .The deep part of the gland is closely associated with the lingual nerve (with the attached submandibular ganglion) above it.Parotid duct (of Stensen) runs 5cm across the masseter (surface marking: along the line joining the intertragic notch to the midpoint of the philtrum).Histology: almost solely mucous acini. runs forwards deep to mylohyoid and drains into the oral cavity at the sublingual papilla just adjacent to the frenulum . . the superficial temporal and maxillary arteries) .Surrounded by tough fibrous capsule – the parotid sheath (thus mumps is painful as the gland swells within a tight envelope) . few ducts Sublingual gland . the rest draining directly into the oral cavity .A small almond-shaped gland sitting just under the mucosa of the floor of the oral cavity . few ducts .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.Nerve supply: (i) Parasympathetic secretomotor supply from auriculotemporal nerve carrying postganglionic fibres from the otic ganglion (preganglionic fibres from inferior salivary nucleus). Symptoms of infection e. o Look for red inflamed duct opening.g.g. tenderness. o For the parotid duct. if considering mumps.Look for fistula/sinus . progress. can palpate the duct along the masseter for stone.Examination of the duct openings: o Using a torch and a tongue depressor. SLE . duration. ask patient to clench the teeth to contract the masseter.g. drooping corner of the mouth. then try to move the gland .If pain is present.Palpate for cervical lymphadenopathy Other tests .History of connective tissue disease e. drooling .Palpate the gland openings for stones. surface. consistency. Warthin’s Malignant tumours Lymphoma and leukaemia* Sialolithasis Mumps* Acute sialadenitis Chronic recurrent sialadenitis HIV Sjogren’s syndrome* Sarcoidosis* Alcoholic liver disease Diabetes mellitus Pancreatitis Acromegaly Malnutrition Lymph node Facial neuroma Temporal artery aneurysm Skin and soft tissue swellings e. pain . and look for discharge inside the mouth while palpating. and under the tongue for the opening of the submandibular duct. fever.Palpate the obviously enlarged gland.Look at the patient’s face for asymmetry (facial nerve palsy) Suspicious features of malignancy: - Hyperaemic hot skin over lump Pain Fixation to underlying structures or skin Hard consistency Irregular surface or ill-defined border Facial nerve involvement Parenchymal swelling Stones Infection/ Inflammation Autoimmune Infiltration Systemic disease* Palpate from behind . is it precipitated by food ingestion? (suggestive of sialolithiasis) . and lifts the earlobe if large. Neoplasia Nonparenchymal swelling Benign e. associated symptoms e.Bimanual palpation of the submandibular gland . .Fixation to overlying skin . ask about testicular pain and swelling (orchitis). abdominal pain (pancreatitis) . submandibular mass is located just under the mandible .Facial nerve examination PHYSICAL EXAMINATION CAUSES OF SWELLING OF THE PAROTID Inspect . lipoma * are conditions in which parotid swelling is bilateral . examine opposite the second upper molar tooth for the opening of the parotid duct. and always remember to also palpate the contralateral gland for any swelling .About the lump: onset.Check for warmth of overlying skin.Look for scars – parotidectomy scar runs anteriorly to the ear. rheumatoid arthritis. or any visible stone. malaise.g.Ask patient about any pain before starting to palpate . below the earlobe and around posteriorly before looping forward again under the jaw .g. sebaceous cyst.Any noticed asymmetry of the face – incomplete closure of the eye on one side.g.Put yourself at the level of the patient’s face and look from front for any asymmetry with an obvious mass on one side – parotid mass is located between the angle of the jaw and the ear. xerophthalmia .Fixation to underlying structures – for parotid. pleomorphic adenoma.75 HISTORY . margins . discharge (purulent). cannot eat a piece of biscuit or bread without water).Does the patient have symptoms of xerostomia (e. but histology shows multiple sites of capsular penetration by tumour cells.Surgical removal o Transoral removal of stones for submandibular duct stones (50% can be removed thus).Other options: Lithotripsy.Usually occurs in males more than females.3% occur in sublingual glands.Can result in sialadenitis.Most common benign tumour . milking the duct. and even abscess formation  worsening of symptoms of pain and redness. occurs in younger patients less than 50 years old Histology: Very heterogeneous appearance. partial gland resection can be performed .80% of salivary stones occur in the submandibular gland (due to its higher mucus and calcium content with a long duct. while 50% of parotid stones occur in the gland itself. systemic symptoms such as fever. and between the ages of 30 and 60.Stones of the salivary gland that may be impacted within the gland itself or in the duct.General measures: o Good hydration. and CT is better. and interspersed islands of myoepithelial cells. containing epithelial cells surrounded by loose stroma with islands of chondromyxoid (mesenchymal components).Sialogram (rarely done today as it is invasive and technically demanding.80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the floor of the mouth. . . sialoendoscopy SALIVARY GLAND TUMOURS Epidemiology: . of which 80% are benign (80% of the benign tumours are pleomorphic adenomas) . of which 50% are benign (all benign tumours are pleomorphic adenomas) . of which 60% are benign (95% pleomorphic adenoma) . Presentation .0.85% occur in the parotid gland . application of moist hot towel o Analgesia – NSAIDs such as ibuprofen o Antibiotics if patient has sialadenitis – usually antibiotics to cover Staph and Strept e.Most submandibular gland stones occur in the duct. resolves about an hour after the meal.Plain X-rays can pick up radio-opaque stones .Stone may be palpable along the duct or at the opening of the duct .15% occur in minor salivary glands. 7% sublingual.Complete obstruction Acute pain and swelling of the gland involved at meal times. wire basket removal. and 60% of parotid stones are radio-opaque. rapid onset within minutes of starting to eat. purulent discharge from duct opening .Partial obstruction Occasional symptomatic episodes interspersed by asymptomatic periods of days to weeks.80% occur in the parotid. .g. .Noncontrast CT scan – can pick up almost all stones when fine cuts are requested . soft diet. chronically enlarged mass in the submandibular region . chills.SIALOLITHIASIS Epidemiology . . Augmentin o Refer specialist treatment if symptoms persist for several days.Equal sex ratio.10% occur in the submandibular. good oral hygiene o Massage of the gland. and slow flow of the saliva against gravity). . or sialadenitis persists despite antibiotic therapy 76 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: . Contraindicated in acute sialadenitis and contrast allergy.) Management . 10% occur in the parotid. The tumour appears to be encapsulated. of which all are malignant Pathology Epithelial Adenomas (benign) Pleomorphic adenoma Warthin’s tumour Investigations . less for parotid duct stones o If stones cannot be removed via transoral surgery or is intraglandular. Radical neck dissection if neck nodes positive . damage to the hypoglossal and/or lingual nerves can occur intraoperatively) 2.Only occurs in the parotid gland (10% of parotid tumours) . soft to firm cystic fluctuant swelling in parotid tail . 4.Postoperative radiotherapy COMPLICATIONS OF PAROTIDECTOMY Immediate (within 24 hrs) 1.Occurs in older patients (>50 years) .Slow-growing.Irregular and lobulated surface. FNAC.Postoperative radiotherapy Submandibular: . Features: .Does not invade or metastasise .Usually occurs in pre-existing pleomorphic adenoma. while adenoid cystic ca is the most common in the submandibular.Related to cigarette smoking Histology: Also called papillary cystadenoma lymphomatosum or just adenolymphoma. sublingual and minor salivary glands Malignant pleomorphic adenoma . Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to the submandibular gland. texture of cartilage (slightly harder than Warthin’s) . due to reinnervation of divided sympathetic nerves to the facial skin by fibres of the secretomotor branch of the auriculotemporal nerve . Reactionary haemorrhage Early (1 to 30 days) 1. if tumour is deep or large. cosmetic problems 2. since there is no malignant potential . painless swelling occurring in the lower pole of the parotid . 3.Superficial parotidectomy if causing trouble to patient Mucoepidermoid ca is the most common malignant tumour in the parotid. can occur in any salivary gland.Radical excision of gland with lymphatic clearance of submandibular triangle .Chance of malignant transformation if left for 10-15 years (1-6% risk) .If not completely excised. sparing lingual and hypoglossal nerves Warthin’s tumour Epidemiology: . 6.Invariably benign with no risk of malignant change Diagnosis by clinical.Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be grafted with great auricular nerve) .More common in males than females (4:1) . + MRI Treatment – surgical excision . Wound dimple.Worst prognosis of any salivary gland tumour . Wound infection Skin flap necrosis Temporary facial weakness (neuropraxia of facial nerve) Salivary fistula Division of great auricular nerve  loss of sensation over pinna Trismus (inability to open mouth due to spasm of masseter) Late (more than 30 days) Malignant tumours Most common malignancies are mucoepidermoid (34%) and adenoid cystic carcinomas (22%) – equal sex ratio.77 Features: .Can be left alone if absolutely certain that the entire mass is composed of only Warthin’s tumour cells.30-70% recurrence and metastasis rate Treatment of salivary gland cancers Parotid: . can recur (recurrence rate of 2%) Diagnosis by clinical. 5. 2. total parotidectomy with preservation of the facial nerve . Frey’s syndrome – increased sweating and redness of facial skin when eating.Submandibular: Total gland excision together with adjacent connective tissue. surrounded by a stroma of well-developed lymphoid tissue with germinal centres. Consists of cleftlike or cystic spaces lined by two-tiered epithelium. containing mucin. FNA + MRI Treatment . rarely de novo . in older patients (usually >60 yrs) 1. Hyperaesthesia of local skin 3.Parotid: Superficial parotidectomy for superficial tumour.Radical neck dissection if neck nodes positive .Slowly enlarging. loss of outer third of eyebrows Muscle fatigue Constipation Bradycardia Menorrhagia Slow thought. insomnia Fine tremor 78 - Medications given e. INSPECT FROM THE FRONT 1. compression (of airway. dementia Carpal tunnel syndrome symptoms A. RA. do not swallow until I tell you to. pernicious anaemia (associations with Graves and Hashimoto’s) History of cancer elsewhere – metastatic disease to thyroid. any complications? Follow-up – what investigations done? PHYSICAL EXAMINATION About the LUMP - - History of autoimmune disease e. Problem with configuration/anatomy (i) (ii) (iii) - Solitary thyroid nodule (most common in exam) Multinodular goitre Diffuse enlargement 2. rarely nerve) . please stick your tongue out and back in again. oesophagus. duration Size (Diffuse or one side predominant? Any sudden increase in size? – malignant growth. Any skin changes over the mass? 4. without moving your jaw. atrial fibrillation Oligomenorrhoea.g. THYROID GLAND GREET PATIENT. papillary cancer is associated with familial polyposis syndromes  ask about GI polyps/ca History of thyroid disease – long-standing MNG can progress to lymphoma Occupational history – any exposure to radiation (papillary cancer risk) Family history of thyroid cancer – ~20% of medullary cancers are familial (MEN2. type I DM. Now. propylthiouracil. subacute thyroiditis) Any pain – bleeding into cyst can result in sudden increase in size and pain. AD inheritance).g. propranolol – for how long.Look for any complications e. ddx includes haemorrhage into necrotic nodule or cyst. easily irritable.Exclude cancer! . Any scars (thyroidectomy scar may be difficult to spot as it is often hidden in a skin crease)? Sinuses? 3. amenorrhoea Nervousness.” 5.Address issues of thyroid function .Cosmesis – is patient bothered by lump? - - Hypothyroid Decreased appetite. hoarseness of voice (benign pathologies almost never compress the recurrent laryngeal nerve) Cosmetic effects - About THYROID FUNCTION Hyperthyroid Weight loss despite increased appetite Heat intolerance Increased sweating Proximal myopathy (Graves’) Diarrhoea. 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. 6. Check for plethora of face. lymphoma. rarely pain can occur in anaplastic carcinoma and thyroiditis Compressive symptoms: difficulty swallowing. 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.” NB. . carbimazole. lethargy Cold intolerance Dry skin. weight gain. ~5% of papillary cancers About previous TREATMENT for any thyroid disease AIMS OF ASSESSMENT IN THYROID NODULE/ENLARGEMENT: . speech and action. Any swelling? Where is it? 2.g. distended neck veins – may be due to compressive nature of mass (but rarely seen). SLE. difficulty breathing. a thyroglossal cyst will move on both swallowing and protrusion of the tongue. side effects Radioactive iodine treatment – what was the result? Is the patient receiving replacement? Surgery – what kind of surgery. depression. A thyroid swelling moves only on swallowing.THE THYROID GLAND About RISK FACTORS APPROACH TO THYROID PROBLEMS – 2 MAIN TYPES 1. emotional lability. efficacy. Problem with function (usually hyperfunctioning) (i) (ii) (iii) (iv) Graves’ disease Toxic adenoma Toxic multinodular goitre Hashimoto’s disease - HISTORY-TAKING Onset (gradual or sudden). frequent bowel movement Tachycardia. Check if mass moves on protruding the tongue – “Please open your jaw slightly. History and physical examination – as above Differential diagnoses: 1. unblinking (hyperthyroid).Lid lag (eyelid lags behind eye when patient follows your finger downwards) . Feel palms – warm sweaty palms 2. Fine postural tremor – accentuate by placing a sheet of paper on the hands 5. Complexion – dry. lethargic. but need to exclude!) Follicular adenoma Cyst (simple. 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. Important to visualise nerve and avoid damaging it!  B. or haemorrhagic) Dominant nodule of a multinodular goitre . Ask for pain before palpating! 1. ask about diplopia!) . Eyes . onycholysis (both seen in Graves’) 3.Chemosis (oedema and erythema of conjunctiva) . palms down) 1. Palms up – palmar erythema Embryonic origin: FACE 1. 4. PERCUSS – any retrosternal extension? AUSCULTATE – bruit in Graves’ OFFER to do Pemberton’s sign to check for thoracic inlet obstruction. Check swallowing while palpating to confirm mass moves on swallowing. ‘peaches-and-cream’ complexion. Level VI lymph nodes – first nodes that a thyroid malignancy spreads to. 4. Recurrently laryngeal nerve – supplies all the other intrinsic muscles of the larynx (except for cricothyroid) and runs close to the branches of the inferior thyroid. the opposite hand stabilises the gland. Nails – thyroid acropachy. 2.Exophthalmos (sclera between lower limbus and lower eyelid) . mobility (fixed to skin? Fixed to underlying structures?). hard. Palpate lymph nodes PALPATE TRACHEA from in front for tracheal deviation. 2. colloid. 3rd and 4th tracheal rings. apathetic (hypothyroid) 2. Expression – staring. cystic. consistency (soft. Strap muscles of the neck lie superficial to the thyroid gland. NEUROMUSCULAR 1.Proptosis (look from above patient’s head – eye visible over supraorbital ridge) the tracheo-oesophageal groove and are not palpable. they lie in PART II: APPROACH TO THE SOLITARY THYROID NODULE Prevalence: About 4-8% of population in US have palpable thyroid nodules. Legs for pretibial non-pitting oedema (Graves’ or hypothyroid) Thyroglossal tract from foramen caecum of the tongue (in the midline. Parathyroid glands: 2 superior and 2 inferior glands that lie behind the lateral lobes. Cancer (only 10-20% of nodules is malignant. Check tongue protrusion. Reflexes – slow to relax in hypothyroidism 3. ask patient about compressive symptoms. runs close to superior thyroid artery.  External laryngeal nerve – supplies the cricothyroid muscle which controls pitch of voice. multinodular?). check thyroid status. 3.Lid retraction (can see sclera between upper limbus of iris and upper eyelid) . The nerve runs behind the pretracheal fascia and so will not be damaged if the fascia is not breached during operation.79 PALPATE FROM BEHIND – one side at a time. PROBLEMS WITH GLAND CONFIGURATION PART I: RELEVANT ANATOMY Structure: 2 lateral lobes joined by an isthmus that lies in front of the 2nd. loss of outer third of eyebrows (hypothyroid) 3. Proximal myopathy (Graves’) 2. 3. size (discrete nodule or multinodular enlargement or diffuse enlargement?). tenderness. Feel pulse – tachycardia. atrial fibrillation (AF more in toxic MNG than Graves’) 4. a branch of the first part of the subclavian artery). Characteristics of lump: site (anterior triangle).Ophthalmoplegia (restriction of eye movements. THYROID STATUS HANDS (get patient to stretch arms out in front of him. Nerves and vessels:   Superior thyroid artery (from external carotid) Inferior thyroid artery (from thyrocervical trunk. prevalence in Singapore not known. detect any abnormal function . Hard. release suction before pulling out needle. Rapidly enlarging nodule 6.Procedure: inject local anaesthetic in area. dominant nodule of MNG) (ii) Malignant (papillary. Age <15yrs or >60yrs (majority of nodules occurs in 3rd to 6th decades – likely benign) 3.No real diagnostic value 4. Other symptoms of invasion e.Best to have experienced cytologist on hand to view slides and re-do FNAC if the sample is inadequate 2. not causing any symptoms  can follow-up and monitor any increase in size A lump >4cm has a greater risk for malignancy . Hurthle cell change in follicular lesion) (iv) Inadequate  repeat FNAC . RADIO-ISOTOPE SCAN . BASELINE TUMOUR MARKERS (IF SUSPECTED OR CONFIRMED MALIGNANCY) . cystic. FAP) 5.Not routine in thyroid nodular study . Hoarseness (i. History of head and neck radiation or thyroiditis 4. then fix . anaplastic. but cold nodule: 10-20% malignant . mets) (iii) Suspicious (follicular.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 . haemoptysis.Easy to perform.Can be both therapeutic and diagnostic for cyst – chocolate-brown fluid aspirated.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. small. round nodule with benign FNAC results. Gardner’s syndrome. medullary.90-95% sensitivity and specificity . single nodule and/or nodules fixed to surrounding structures 7.The most important investigation modality! .Clinical features suspicious of malignancy: 1. dysphagia Investigations: 1. expel contents onto slide. THYROID FUNCTION TEST .In the rare occasion that there is pre-existing vocal cord palsy on one side  take extra care not to injure opposite recurrent laryngeal nerve as that can cause bilateral vocal cord palsy Management of benign nodule: - Soft. feel lump after aspiration to check for resolution .For medullary thyroid cancer: calcitonin. Family history of thyroid cancer (or MEN2. insert 20-22G needle and apply suction while fanning needle in region of nodule. stridor.e. Cervical lymphadenopathy 9.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.MRI has same functions as CT but higher cost 7.Uses: (i) Evaluating invasion of surrounding structures (ii) Retrosternal extension (iii) Lymph node involvement .4 possible results: (i) Benign (thyroiditis. Male gender (thyroid nodules less common in male but more likely to be malignant) 2.But not very useful diagnostically 5. ENT EXAMINATION OF VOCAL CORDS .Ultrasound still does not provide as good diagnostic value as FNAC 3. carcinoembryonic antigen (CEA) 6.For differentiated thyroid cancer: thyroglobulin . establish baseline.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 . CT SCAN OR MRI . or complex 80 . non-functional. ULTRASOUND OF THYROID . FINE NEEDLE ASPIRATION CYTOLOGY . recurrent laryngeal nerve invasion) 8.g. Tracheostomy Chemotherapy and/or radiotherapy depending on type of lymphoma Adjuvant therapy .Unilat LN involved in 60-80%. and neck dissection if neck nodes are positive .Aggressive growth.Radioactive iodine at ablative levels to ablate remnant thyroid and any cancer tissue (only for total thyroidectomy) .Follicular structures similar to normal thyroid . KIV TT Surgical resection .External radiotherapy (only shown to have good results in pts with locally advanced follicular ca) Follow-up .High calcitonin – screen for residual or metastatic disease.Serum calcitonin and CEA six mths after surgery (if normal.Total thyroidectomy for the majority . etc.Characteristic Orphan Annie nuclei.Thyroxine replacement (not for TSH suppression but to maintain euthyroid state) . size>4cm (more details on risk stratification below) Treatment TSH suppression – give L-thyroxine to suppress TSH levels to <0. liver. spread via local.Longstanding goitre . with RT or chemo as appropriate Median survival <6mths Dependent on histo.Multiple metastases probably present at presentation . lymphatic.Small blue round cells that are highly anaplastic – may resemble lymphoma . extrathyroid invasion. treat surgically. haematological routes . 24hr urinary catecholamines .Hurthle cell variant – worse prognosis .Papillary architecture with psammoma bodies .Check TSH levels .Iodine deficiency may be associated . complete penetrance. Slow-growing tumour Spread by lymphatics 30-50% multicentric LN involvement in 80% of disease at diagnosis (level VI first) . contralat LN in 40% .Significant family history in the familial type – MEN2 (AD. 20-30 years for familial 60-70 years >50 years F:M ratio 3:1 3:1 1:1 3:2 2:1 Risk factors .95% produce calcitonin.Tall cell variant (nuclear features of papillary ca within follicular lesion) behaves like papillary ca.Haematologic spread to bone. considered cured – 5% 5yr recurrence) .Poor prognostic factors (AMES): Age>40.Very good prognosis .Chemotherapy to shrink tumour . followed by ablation 5yr survival 95% in low-risk pts. worse prognosis .Diagnosis of cancer made on evidence of capsular or vascular invasion by tumour cells (vs follicular adenoma) . Gardner’s.History of previous differentiated thyroid ca (30% of anaplastic ca) .Thyroglobulin as a tumour marker of recurrence .81 PART III: THYROID CANCERS Differentiated thyroid carcinoma Papillary carcinoma Follicular carcinoma Medullary carcinoma Anaplastic carcinoma Lymphoma Proportion 75% 10% 7% 3% 5% Age 25-40 years 40-50 years >50 years for sporadic type. 50% in high-risk pts Slightly worse for follicular ca No good adjuvant therapy 60-70% . better prognosis .Arise from parafollicular C cells (which produce calcitonin) . associated with parathyroid adenoma and phaeochromocytoma – see notes below) . etc) .Positive family history in 5% .History of lymphoma or MALT elsewhere .LN clearance: tracheo-oesophageal nodes cleared.Hashimoto’s thyroiditis (60X increased risk) Pathological features .Sporadic cases usually solitary.Distinctive deposits of acellular amyloid material – altered calcitonin collections .For suspicious lesion – hemithyroidectomy with histology.Radioactive iodine scan to detect recurrence.Surgical debulking .Familial cases all multicentric.60-80% aggressive and 30% more indolent Surgical resection . presence of metastases.005U/L Follow-up . brain . stage.Follicular adenoma is NOT a risk factor .FNAC may suggest lymphoma but definitive diagnosis requires trucut or excision biopsy . 88% in intermediate-risk pts. treatment.Sampling of cervical and mediastinal nodes and modified dissection where positive Palliative therapy for compressive effects .Radiation exposure .Always exclude MEN2 – serum calcium.Solitary .Hemithyroidectomy for selected low-risk patients (see below) .Almost always nonHodgkin’s of B-cell type Clinical features - .Multicentric C-cell hyperplasia may be seen in familial cases . nuclear pseudoinclusions .Aggressive resection – total thyroidectomy with level VI node clearance . lung. has worse prognosis . 80% produce CEA .LN involvement in 10% (rare) .Usually presents as rapidly enlarging goitre with compressive symptoms .Polyposis syndromes (FAP.Aggressive growth .Large bulky mass involving neck structures – locally advanced . Age. hypoglossal nerve.Differentiated thyroid cancer Disadvantages of TT: . and high risk patients 50% TOTAL THYROIDECTOMY VERSUS HEMITHYROIDECTOMY Advantages of TT: .Ability to use serum thyroglobulin as a cancer marker for recurrence 82 Lymph node clearance . irradiation  resus.Papillary and follicular cancers are considered differentiated thyroid cancer (as opposed to anaplastic – undifferentiated – thyroid cancer) . phrenic nerve .Risk factors can be divided into patient factors and disease factors . from the infrahyoid muscles medially to the anterior border of the trapezius laterally .Classic radical neck dissection (Crile’s) – internal jugular vein.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 .Patient factors: Age – >45 years old is high risk. or high risk patient with low risk disease (iii) High risk – high risk patient and high risk disease .Ability to use adjuvant radioiodine to ablate any residual cancer tissue after surgery .Patients can be divided into three groups: (i) Low risk – low risk patient and low risk disease (i. salivary fistula (v) Carotid blowout – risk factors: infection.Various score systems have been formulated to stratify risk: AMES – Age. thus the presence of the thyroid gland will decrease the ability of RAI to pick up recurrent cancer) and as treatment for recurrence . from the mandible superiorly to the clavicle inferiorly. and accessory nerve are resected. no high risk features) (ii) Intermediate risk – low risk patient with high risk disease. RISK STRATIFICATION: . Size) – rarely used as histological grading is not commonly performed MACIS – Metastasis. Invasion.The removal. Extent. Grade (Histological). risk stratification helps to guide the extent of surgical resection in differentiated thyroid cancer according to the patient’s disease. weakest point is the junction of the trifurcate incision . while high risk patients undergo total thyroidectomy with post-op ablative RAI treatment.e. sternocleidomastoid muscle.Complications of radical neck dissection: (i) Injury to nerves – vagus (vocal cord paralysis).Modified radical neck (i) Type I: one of the three structures not removed.Risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism . 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.Very low incidence of cancer recurrence in residual thyroid – microfoci probably not clinically significant . and if the upper GI tract was opened during the surgery) – infection can result (iv) Wound infection – risk factors: previous irradiation. 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 . Size . brachial plexus.Ability to use radioiodine to detect recurrent disease (normal thyroid picks up iodine better than cancer cells. Size AGES – Age. of the entire ipsilateral lymphatic structures of the neck. but usually is similar to that in high risk patients . Completeness of resection. en-bloc. cervical sympathetic chain (Horner’s). Gender – male is high risk . Metastases. Structures not resected: carotid arteries.5 year survival is also prognosticated by the risk: low risk patients have a survival of 95-98%.Risk helps to guide treatment – low risk patients can undergo hemithyroidectomy without ablative radioiodine therapy post-op. intermediate risk patients 88%. Extent.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 .Prognosis is excellent . vagus nerve. treatment in intermediate risk patients is tailored to the disease.Limited thyroidectomy may spare patient from having to be on lifelong thyroid hormone replacement Thus. if upper aerodigestive tract is opened during surgery with salivary contamination. apply constant pressure all the way to the OT! (vi) Poor healing – usually in irradiated skin.Tracheo-oesophageal groove (level VI) node clearance usually done .Evidence for microfoci of disease and multicentricity of cancer – removal of the entire thyroid decreases risk of recurrence . of which less than 10% are malignant) Parathyroid hyperplasia and hyperparathyroidism (30%) 2. thus the patient will require life-long thyroid replacement and follow-up  problems with compliance.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?).Multiple endocrine organs involved.Two distinct groups of disorders: 1. SCFE.Autosomal dominant inheritance . Indications for surgery: FEATURES: . delayed puberty 1. Total thyroidectomy – entire gland removed completely.Gene involved is RET protooncogene at 10q11.83 Multiple endocrine neoplasia PART IV: SURGERY IN BENIGN THYROID DISEASE A group of inherited diseases resulting in proliferative lesions (hyperplasia. Subtotal thyroidectomy . 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 . cost. some have growth hormone-secreting tumours MEN 2 . MEN 2b (William syndrome) Thyroid and adrenal involvement like MEN 2a. Hemithyroidectomy – removal of one lobe of the gland.Multifocal tumours in each organ involved . but no hyperparathyroidism Neurocutaneous manifestations: ganglioneuromas on oral mucosa.g.2 where activating mutations occur . but weigh this against the benefits of not requiring any medication (for which there is a good chance) .Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides . 5.Tumour usually preceded by asymptomatic stage of endocrine hyperplasia .Harley-Dunhill subtotal thyroidectomy – leave a thumb-sized amount only on one side with removal of the rest of the gland Total versus subtotal thyroidectomy (for hyperfunctioning thyroid disease) . usually done in MNG 3. either synchronously or metachronously .Result of total thyroidectomy is always hypothyroidism. usually for suspicious thyroid nodules 2. but not RAI) Types of surgery available: 1.Tumours occur at younger age than sporadic cancers . inconvenience . Child-bearing (not a very strong indication since medical therapy can still be given. 3. 2.Autosomal dominant inheritance . carcinomas) of multiple endocrine organs.More aggressive and higher chance of recurrence compared to sporadic type of tumours in the same organs MEN 1 . gastrinoma.failed medical therapy or unsuitable for medical tx Cancer Compression on neighbouring structures Cosmesis Compliance/cost problems – with long-term medical therapy (but patient may still require long-term therapy after op if he/she becomes hypothyroid or is still hyperthyroid) 6.Three P’s: Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands Pancreas (>40%) – aggressive metastatic tumours (e. lips eyelids Other features: Marfanoid habitus. insulinoma). MEN 2a (Sipple syndrome) Medullary carcinoma of the thyroid (almost all) Phaeochromocytoma (50%. including the isthmus and the pyramidal lobe. Cannot be treated medically . adenomas. 4. Complications of thyroid surgery: (Mostly H’s, one I and one T) IMMEDIATE (<24HRS) 1. Haemorrhage with haematoma formation - Haematoma forms in the paratracheal region, mostly below the strap muscles  can result in compression of airway if not released (patient can die!) - Cut the subcuticular stitches and also the stitches holding the strap muscles opposed to let the blood drain out 2. Hoarseness or airway compromise from recurrent laryngeal nerve injury - Risk of nerve injury is <1% - Unilateral nerve injury for hemithyroidectomy, bilateral nerve injury for total or subtotal thyroidectomy - If bilateral nerve palsy resulting in compromised airway, will require tracheostomy 3. Hyperthyroidism - Resection of gland can release large amounts of stored thyroid hormone into bloodstream - May result in thyroid storm (see Management of thyroid storm) 4. Tracheomalacia - Floppiness of trachea resulting from chronic compression e.g. by large goitre - Requires intubation to secure airway INTERMEDIATE (1 DAY TO 1 MTH) 1. Infection 2. Hypoparathyroidism leading to hypocalcaemia - Risk of permanent hypoparathyroidism is 1-4% (only in total or subtotal thyroidectomies); 10-20% of patients may have temporary hypocalcaemia - Important to check the serum calcium levels post-operatively – POD 1,3,5 - Ask patient for any symptoms and look for signs of hypocalcaemia – paraesthesia around the mouth, difficulty breathing, carpopedal spasm, Chvostek’s sign (spasm of the facial muscles on tapping the facial nerve), Trousseau’s sign (carpopedal spasm on inflating blood pressure cuff over arm) - Dangerous as it can cause laryngeal spasm and airway compromise - Check serum calcium together with albumin to get corrected calcium! Measured serum calcium + 0.02 (40 – Albumin) - Replacement: 5mmol/6h if symptoms mild, 10ml of 10% calcium gluconate over 30 minutes if severe - Hypocalcaemia may also occur due to “hungry bone syndrome” after thyroidectomy in long-standing thyrotoxicosis 84 LATE (MORE THAN 30 DAYS) 1. Hypothyroidism 2. Hyperthyroidism (failed treatment) 3. Permanent hypoparathyroidism 4. Hypertrophic scarring or keloid formation – ask patient if he/she has keloids 85 PERIPHERAL ARTERIAL DISEASE ANATOMY OF THE LOWER LIMB ARTERIES - The anterior tibial crosses into the anterior compartment of the leg and supplies the muscles there, and then continues as the dorsalis pedis in the foot (surface landmark: one third of the way down a line joining the midpoint of the two malleoli to the cleft between the first and second toes) - The posterior tibial supplies the posterior compartment of the leg and passes posterior to the medial malleolus (surface landmark: one third of the way down a line joining the medial malleolus to the heel) before dividing into medial and lateral plantar arteries to supply the sole of the foot - Refer to diagram – important to know the arrangement of the anterior tibial, posterior tibial and peroneal vessels at the trifurcation as you may be asked to read an angiogram of these vessels. - From lateral to medial: Anterior tibial, Peroneal, Posterior tibial FORMS OF PERIPHERAL ARTERIAL DISEASE Peripheral arterial disease Acute Chronic Critical - External iliac artery continues as the femoral artery after crossing the inguinal ligament (surface landmark: the mid-inguinal point i.e. midway between the pubic symphysis and the anterior superior iliac spine) - The femoral artery then divides into the superficial femoral and the profunda femoris (or deep femoral) arteries about 4cm below the inguinal ligament - The profunda femoris supplies the compartments of the thigh via two main branches, the medial and lateral circumflex femoral arteries - The superficial femoral runs distally and passes through the adductor hiatus to reach the popliteal fossa, where it changes its name to become the popliteal artery - The popliteal artery divides into the anterior tibial artery and the posterior tibial (also called tibioperoneal trunk by some), and the posterior tibial will give off the peroneal artery Asymptomatic Non-critical. Claudicants. ACUTE LIMB ISCHAEMIA Acute limb ischemia is defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within two weeks of the acute event (if >2 weeks, it is considered chronic ischaemia). The decrease in perfusion is usually due to sudden occlusion of a feeding arterial vessel, and this may be in a setting of already narrowed vessel lumen (acute on chronic ischaemia) or in a normal lumen. CAUSES: 1. Arterial embolism - Most common cause of acute limb ischaemia (60-80% of the time) - The most likely source of embolus is the heart (80%), of which 70% is due to atrial fibrillation, 20% to AMI with left ventricular mural thrombus, and a small proportion to prosthetic heart valves - Non-cardiac emboli arise from other arteries where there are atherosclerotic plaques or an aneurysm (the embolic material may be thrombus or part of a plaque, but atheroemboli are less likely to cause complete arterial occlusion) - Most common sites where emboli lodge:  Bifurcation of the femoral artery (most common site)  Trifurcation of the popliteal artery (next most common site in the lower limb)  Aortic bifurcation  External and internal iliacs  Arm (about 20% of emboli) - Emboli usually cause lower limb ischaemia mostly - After emboli obstructs the vessel, thrombus can propagate distally (due to stasis of blood) and proximally (due to turbulence of incoming blood hitting embolus) by derangements in the Virchow’s triad 2. Acute thrombosis - Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel) - Less common cause of acute limb ischaemia - When thrombotic occlusion of a vessel does occur, the resulting ischaemia is usually less severe than in an embolic occlusion, because collaterals have had time to form around the chronically stenosed vessel - Other less common causes of acute thrombosis include the arteritides (usually affecting medium-sized arteries), ergotism, and hypercoagulable states (notably antiphospholipid syndrome). 3. Arterial trauma - Increasing incidence of acute arterial occlusion due to endovascular diagnostic or interventional procedures - Trauma can cause development of an arteriovenous fistula that shunts blood away from the limb - Fracture or dislocations can stretch an artery and cause an intimal tear while the media and adventitia layers are intact (because they contain elastin and can stretch)  a thrombus forms at the site of the tear where underlying thrombogenic collagen is exposed - Compartment syndrome can result from trauma as well 86 4. Dissecting aortic aneurysm - As the blood dissects between the intima and media of the aorta, it can cause occlusion of the aortic branches at their origins PATHOPHYSIOLOGY In order of sensitivity to ischaemia, the tissues affected are nerves (most sensitive), muscle, skin, and bone (least sensitive); thus early signs of ischaemia involve pain and numbness, and muscle paralysis as well as skin changes occur later. The lower limb can survive about 6 to 8 hours in an ischaemic state before injury becomes irreversible. PRESENTATION The classic 6 P’s of acute limb ischaemia: Pain, Paraesthesia, Pallor, Pulselessness, Paralysis, Perishingly cold Pain - Develops acutely - Starts off in a distal part of the extremity and then progresses proximally, increasing in severity with time - Further progress leads to decrease in pain as the nerves die off from ischaemia - Important to ask for any previous claudication pain (10% of claudicants can develop acute ischaemia due to thrombosis of the stenosed vessel) Paraesthesia - Starts off with paraesthesia (develops relatively early in the course of ischaemia) and develops to complete loss of sensation Pallor - Assess skin colour, temperature, and capillary refill - The limb may still be slightly pink though pale, but in severe ischaemia it can be marble-white (especially in embolus where there are no collaterals) - Other colours:  Mottling/Marbling (patches of blue on white): deoxygenation of stagnated blood; surrounding areas of pallor are due to vasoconstriction  Duskiness: due to deoxygenation of stagnated blood; if there is fixed staining (i.e. does not blanch on pressure) then the limb is non-viable  Black: gangrene - The disclouration usually affects a large part of the distal limb e.g. the toes, foot; rarely does it only affect one toe (more in chronic ischaemia) - The site of arterial occlusion is usually one joint above the line of demarcation between normal and ischaemic tissue but still possible . do cardiac enzymes . embolectomy is done for embolic occlusion. no emergency to operate.Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites in the muscle CLASSIFICATION OF SEVERITY (SVS/ISCVS) Three categories: viable.Important to start anticoagulation with heparin if the suspicion of acute limb ischaemia is high . assess with a handheld Doppler the arterial and venous flow in the limb – there can still be flow without a palpable pulse .Thrombolysis . while dead muscle will be dull and will not twitch . free spontaneous flow from proximal and distal ends of the artery when unclamped) . Embolectomy . but in patients with threatened limb there is no time for angiogram  may do on-table angiography [Angiography is useful in confirming an occlusion.Can assess viability of muscle by making a cut – viable muscle will be shiny and twitches in response to flicking.Give IV heparin bolus 3000-5000 units .If unable to feel. sharp cut-off. quite unlikely that the limb is ischaemic.Flush with heparinised saline .Stenting Embolectomy Endarterectomy Bypass grafting Fasciotomy Primary amputation In general.Total paralysis occurs late and usually indicates that the limb is non-viable .Pre-operative investigations .Check for forward-bleeding and back-bleeding of the vessel (i.If able to feel one good pulse (PT or DP).Also feel the pulses on the other limbs – gives a clue as to whether the cause is embolic or thrombotic (see below) Paralysis .Ideal PTT is 2 to 2.Angiogram can be done in patients with viable limb.5 times normal INVESTIGATIONS . PT/PTT.87 Pulselessness .Involves clamping of the involved artery and making an arterotomy . and hyperkalaemia with cardiac arrhythmia can occur after reperfusion .A Fogarty balloon catheter is inserted into the artery until distal to the clot.CXR and ECG if patient is older than 40 yrs old .Can be done under LA but still require anaesthetist to monitor patient as he may be quite sick (e. recent AMI Negative Contralat pulses present White limb (no blood) Minimal atherosclerosis.If suspecting an AMI with mural thrombus. AMI).e. Patient may require revascularisation to allow lower amputation or help the amputation to heal Pain Capillary refill Motor deficit Sensory deficit Arterial Doppler Venous Doppler Treatment Viable Mild Intact None None Audible Audible Urgent work-up Threatened Severe Delayed Partial Partial Inaudible Audible Emergency surgery Non-viable Variable Absent (fixed stain) Complete Complete Inaudible Inaudible Amputation DIFFERENTIATING BETWEEN EMBOLIC AND THROMBOTIC CAUSE Identifiable source Claudication hx Physical findings Angiography Embolic Present – AF. welldeveloped collaterals EARLY ANTICOAGULATION . U/E/Cr. the cause – thrombotic or embolic – and also pinpointing the level of occlusion and the anatomy] DEFINITIVE TREATMENT OPTIONS Surgical Endovascular - . irregular cut-off.FBC.Check foot – warm foot with good pulse indicates reperfusion .Follow with IV heparin infusion at 1000 units/hour . 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. then the balloon is inflated to trawl the clot out of the artery .Angioplasty . GXM .g. while thrombolysis is done for thrombotic occlusion. few collaterals Thrombotic Less common Positive Contralat pulses diminished Dusky limb (collaterals still supplying limb) Diffuse atherosclerosis. FEATURES: 1.Need to convert to full warfarin anticoagulation.Closure of arterotomy with meticulous haemostasis as patient is on heparin . and/or gangrene) in patients who present more than two weeks after the acute event (the converse of the definition of acute limb ischaemia).After complete lysis of the clot.Takes much longer than embolectomy . foot but may involve more proximal areas if disease is severe) occurring at rest .After 6 hours. 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 . lateral malleolus (as opposed to venous ulcers that occur over the medial malleolus) 88 . and the thrombolytic agent is infused .Patient will be in high-dependency with thrombolytic infusion for 6 hours (~10004000 units per minute) . increasing pressure in the compartments of the leg.Pain is aggravated or precipitated by lifting the limb. uptitrating dose until INR 2-2. only 35% successful CHRONIC LIMB ISCHAEMIA Chronic limb ischaemia can be divided into critical and non-critical limb ischaemia.Not easily controllable with analgesia – requires opioids to control pain II.Angiogram done before thrombolysis to locate occlusion ..Important to monitor ECG for any arrhythmias! .Embolectomy has a 20% mortality.Usually arise from minor traumatic wounds with poor healing .So severe as to disturb sleep at night . Gangrene or ulcers over the toes or feet AND 3. Multiple collaterals form to bypass the obstructed vessels as a compensatory mechanism CRITICAL LIMB ISCHAEMIA Critical limb ischaemia is defined as decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain.Most often occur on the tips of the toes. can do angioplasty . Objective indication of poor vascular supply to the lower limbs (a) Ankle brachial pressure index <0.Post-op: patient monitored in high-dependency.Severe pain in the distal portion of the lower limb (usually toes. over the metatarsal heads (ball of the foot).Thrombolysis may be preferred for embolism in a diseased artery. if some clot remains. ischemic ulcers. look out for reperfusion injury  The reperfused muscles become oedematous.Thrombolysis has a 10% mortality. codeine) lasting >2 weeks AND/OR 2. relieved by dependency of the limb – many patients sleep with the leg hanging over the side of the bed to relieve the pain . 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). almost full success rate .Thrombolysis catheter inserted into the clot.Discharge patient to anticoagulation clinic for follow-up with warfarin advice Thrombolysis . since it may be difficult to trawl out the clot in a diffusely stenosed vessel – the clot may get caught on a proximal stenosed segment Results: . Rest pain requiring regular opioid analgesia (e.Often painful . and non-critical ischaemia further subdivided into that which causes symptoms (usually claudication) and that which is asymptomatic. bunion area. adjust catheter into the clot and infuse for 6 more hours . redo angiogram to check for residual clot.g. Rest pain .5 before stopping heparin (patient at risk of further embolic events) .5 (b) Toe pressure <30 mmHg I. Ischaemic ulcers . Occurs in patients with atherosclerotic disease. 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. 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? .g. Any ulcer or gangrene in the lower limb? .Thigh claudication results in common femoral artery or aortoiliac disease . Usually described as the patient as a cramping. septic arthritis III. swollen. impotence in LeRiche’s When did pain first start Progress since first noticed until currently (worsening pain.How has symptoms affected lifestyle e. extension of the spine further narrows the spinal canal while flexion widens it) . Often has a clear demarcation between viable and necrotic tissue. getting worse) . vasospasm NEUROGENIC CLAUDICATION . Often occurs in diabetics with decreased sensation and unrecognised trauma. anaesthetic tissue associated with or progressing to necrosis .If ulcer. Any rest pain - Site.The characteristic of neurogenic claudication is “park bench to park bench” where the patient has to sit down and flex the spine to relieve the pain (pain results from compression of the cord and spinal nerves in spinal stenosis. .Important to determine the “claudication distance” – within a short period of time the distance is usually fairly constant.Usually deep.Either dry or wet: DRY – hard.89 . diffuse) . impaired mobility 2. punctate (unlike venous ulcers that tend to be superficial. and is composed of a classical tetrad of buttock claudication.Occurs when arterial blood supply falls below that which is necessary to meet minimal metabolic requirements . Safe and can be allowed to autoamputate after demarcation with precautions against infection. aching pain in the muscle group on exertion such as walking. severity Aggravating factors – raising the limb Relieving factors – putting limb in a dependent position Able to relieve with normal analgesics? Or require opioid analgesia? How long has rest pain lasted for requiring opioid analgesia (if more than 2 weeks. An emergency requiring surgical debridement or amputation. pain on less exertion.May become infected resulting in cellulitis. dry texture.Progress (stable. and occasionally presence of aortoiliac bruits. . impotence in men. Takayasu’s arteritis. dry. frequently blistered. WET – moist. absent femoral pulses (and distal pulses). nature. even abscess formation. or increasing in size.Most commonly atherosclerotic disease .“Claudication distance” of neurogenic claudication is more variable . but can shorten as the disease progresses CAUSES OF VASCULAR CLAUDICATION .Pulses will be absent/diminished in vascular but not in neurogenic claudication TAKING A HISTORY OF CHRONIC LIMB ISCHAEMIA 1. and spread to involve the underlying bone and joints  osteomyelitis. moist.Current claudication distance . considered a feature of critical limb ischaemia) 3.Ask about onset of ulcer/gangrene .Other less common causes: ergot toxicity. and alleviated on stopping (patient does not have to sit down for pain to go away) – “shop window to shop window”. development of rest pain) . or the popliteal artery  calf pain .g.LeRiche’s syndrome arises from occlusion of the aortoiliacs.Foot claudication results from involvement of the tibial and peroneal arteries.Vascular intermittent claudication needs to be differentiated from neurogenic claudication which can also present as pain in the lower limb on exertion . Buerger’s disease (thromboangiitis obliterans). Claudication - Which part of the lower limb does the pain occur in Nature of the pain Radiation Severity Aggravating factors – exertion Relieving factors – rest (just standing is sufficient) Associated symptoms e.Usually affects the superficial femoral near to the adductor hiatus.Cyanotic. increasing areas of lower limb affected. Gangrene . but rarely do patients with claudication due to atherosclerosis get foot pain alone (more common in Buerger’s) . Patient is supine with the bed flat.Dry. suspect a popliteal aneurysm] .Any systemic signs of infection – fever. Drug history .. usually between the toes.Ergots 6. Warmth of the skin . shape Edges (punched out – arterial.Site of the ulcer  Venous ulcers form at the medial malleolus  Arterial ulcers are more distal. Presence of any diabetic dermopathy 4. chills.If gangrene. with the patient exposed optimally (from the thighs to the feet. blood? Surrounding skin  Erythema (cellulitis) – there may be an underlying abscess (confirm on palpation)  Blistering. then palpate deeply in the popliteal fossa with the fingers of one hand pressing the fingers of the other [If the pulse is very well felt. 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. Palpating the ulcer if present . blue/dusky (cyanosed).Popliteal pulse: Ask patient to bend the knee ~60-90 degrees.Social support and home condition (need to climb stairs?) PHYSICAL EXAMINATION Examine the patient’s lower limbs in a warm room. Social history .Nail changes .Use the dorsum of the fingers of both hands to simultaneously run up the patient’s feet to the shins and thighs bilaterally .Wasting 3.Posterior tibial pulse: one-third of the way down a line joining the medial malleolus to the heel . Risk factors (“Arteropath”) - Diabetes mellitus – take a full diabetic history including other complications Hyperlipidaemia Heart disease Stroke Smoking Family history 5. check for blanchability (fixed staining = dead toe) 3. malaise 4.Wet (infected) or dry (not infected) . may see deformities – Charcot’s joint) Feel 1.If one limb feels cool. 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.See if any discharge from the ulcer when palpating 4. limb? . shiny skin . Look 1.Compare the temperature on both sides (note if one side is cooler) .Press hard on a toe for a few seconds. then release . purplish colour (possibility of necrotising fasciitis) 5. Presence of gangrene . including the heels (ask patient to flex at the knee so you can look at the heel) and between the toes . mottled 2.Aspirin intake . (If the patient has diabetes. rigors.Any allergies to contrast (for angiography) .Normal capillary refill should be 2 seconds or less . Pulses . wearing underwear).White (pallor). Colour of the lower limb . Capillary refill .Look carefully at the entire lower limb.Dorsalis pedis pulse: one third of the way down a line joining the midpoint of the two malleoli to the cleft between the first and second toes . Trophic changes .Feel the distal pulses and work your way proximally . foot. and at pressure points such as the lateral malleolus.Bogginess of surrounding tissue (may have abscess formation) .If a toe is blue. Presence of ulcer .Extent of gangrene (level of demarcation) 6.Any surrounding tenderness (infection) .Premorbid function and current function .Loss of hair . 90 - -  Neuropathic ulcers form at areas such as the ball of the foot and the heel Size. feel for the level where the skin becomes warm 2. pink (normal). often associated with claudication  ABPI <0. Buerger’s test . good alternative to angiogram . renal disease.g. suggests non-compressible calcified vessel)  ABPI between 0.Can define anatomy of occlusions and also look for relatively good arteries distally for “landing zone” of bypass graft 3. creatinine .Duplex (means two modalities) = 2D ultrasound (like the normal kind) plus Doppler ultrasound (measures flow and waveforms) .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 . Duplex ultrasound . this indicates severe ischaemia .How the ankle-brachial pressure index is done  Brachial pressure is measured with a blood pressure cuff around the arm and a Doppler probe at the brachial artery – cuff is inflated until the arterial signal is obliterated.Do one side at a time .Look at the leg for reactive hyperaemia (the leg turns purple-red) Complete the exam - Examine the rest of the pulses Offer to auscultate over the femoral and popliteal arteries for bruits Examine the abdomen for any abdominal aortic aneurysm Measure the ankle-brachial pressure index (ABPI) INVESTIGATIONS 1.5: Critical ischaemia . 1+ is diminished (but may be normal for popliteal). biphasic and monophasic waves are abnormal .5 to 0. dissection/damage to artery with worsening ischaemia . Angiogram (arteriogram) .Angiogram with digital subtraction – the images of the underlying bone are removed so as to better visualise the arteries (if the bones are visible.2  claudication 2. then slowly deflated until the signal just starts being detected. at which the pressure is recorded  Ankle pressures are measured in a similar manner. metformin  Investigations: FBC (platelets impt).Preparing for angiogram:  Take informed consent from patient  Ask about contrast allergy. if the Buerger’s angle is less than 20 degrees.There may be venous guttering of the lower limb at this angle as well .Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior superior iliac spine (mid-inguinal point). stenting . asthma.Non-invasive test.Holding the heel of the foot.Stop when the toes become pale (white) . 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 . slowly lift the entire lower limb.Accuracy of the index  ABPI below 0.Grading of pulses: 2+ is normal. Ankle-brachial pressure index .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. looking at the colour of the toes . angioplasty.If the patient is lying near the side of the bed.Exercise treadmill testing  Measure ABPI before and after patient exercises on a treadmill  If the ABPI falls by >0. 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 .91 .3. negative if not felt  label on a stick-figure diagram Move 1. if >1. just below the inguinal ligament .Usually only done if planning intervention e.9 (can be more than 1.0 as ankle pressures tend to be higher than brachial.Normal arterial flow waveform should be triphasic. with the patient’s lower limb straightened.Interpreting the values  Normal ABPI is greater than 0.9 – occlusion. without digital subtraction) . PT/PTT. then it is a normal angiogram.Invasive and associated with risks of bleeding from arterial puncture. Dead  Necrotic tissue 2. stroke.Level of amputation depends on vascularity of the limb and the indication (e. Damn nuisance  Non-functional limb. walk again  Keep a walk diary recording daily claudication distance in paces  Will stimulate collateral formation  symptoms get better . the guidewire is threaded into the subintimal space to create a dissection around the occluded segment.As far as possible try to preserve function of the lower limb .g. otherwise the wound will not heal .ASSESSMENT OF SEVERITY The three L’s of peripheral arterial disease: Life – does disease threaten life (e. to return to ED if such symptoms arise . other complications of atherosclerosis e. constant need to dress wound .g. sepsis. or to enable lower amputation .g. need to amputate above level of infection) .Teach patient about symptoms of critical ischaemia. AMI.Exercise training  Exercise at least half to one hour every day  Walk until pain comes. Dangerous  Gangrene.?Use of Vasteral (methoxyphylline) .Antiplatelets e. aspirin .Smoking cessation . if infected. rest 2-3 minutes.) or will intervention cause risks (ii) Limb – will patient lose the limb (iii) Lifestyle – is the lifestyle of the patient severely handicapped. and this space is then angioplastied to create a channel parallel to the actual lumen for blood to flow through 2. difficult to perform bypass TREATMENT OF CRITICAL LIMB ISCHAEMIA Need to revascularise – see interventions above AMPUTATION Indications (3 D’s) 1.e.Monitor regularly with measurement of ABPI  Intervention (endovascular or surgical) . Angioplasty  Stenting usually not done for lower limbs except in aortoiliacs (since stent needs to be placed in a vessel which is relatively fixed and won’t be kinked/bent by movement)  Angioplasty only effective for focal stenotic lesions and better for large vessels  Problem with angioplasty is that it is not long-lasting – restenosis can occur  New method: subintimal angioplasty – if lumen is so occluded that guide wire cannot pass through. bad smell. does it require intervention (i) Fontaine system Stage I: Asymptomatic Stage IIa: Mild claudication Stage IIb: Moderate to severe claudication Stage III: Ischaemic rest pain Stage IV: Ulceration or gangrene TREATMENT OF CLAUDICATION Conservative . 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. ascending sepsis 3. pain.At least 6 months of conservative treatment first . Bypass grafting  Consider bypass when lesions cannot be treated by angioplasty i.May require revascularisation interventions before amputation to ensure good healing.g. discuss with patient about whether he can accept the level of symptoms.If parameters improve but then plateau. and the risks of intervention  weigh risks against benefits .Usually do angioplasty rather than bypass as it is less invasive.Assessment of cardiovascular risk factors and treatment to optimise control – cardiologist .Monitor claudication distance and ABPI – intervene if deteriorating despite conservative management .Do not simply amputate without ensuring good vascular supply to the surgical site.Podiatrist to teach foot care . though may not be as effective in treating the symptoms 92 1. True aneurysms are bound by all layers of the blood vessel wall.g. Synthetic graft (Dacron – polytetrafluoroethylene) is placed within the aorta and the vessel wall closed up over the graft i. Do not intubate as neuromuscular blocking agents will reduce tamponade effect. Stabilise patient – resuscitation with fluid and blood products 2.93 ABDOMINAL AORTIC ANEURYSM EPIDEMIOLOGY More common in men than in women (4:1 ratio) Predominantly in older patients (>60 years old) Other risk factors: smoking.Check the other arteries – femoral. the fingers are pushed upwards and outwards .Size: 3 to 15 cm (normal aorta is 2cm in diameter) . trauma. mesenteric. hypertension. may extend to involve common iliac arteries.Most commonly asymptomatic.Mass is expansile – when fingers of both hands are placed at the edges on either side of the mass. iliac. Most common complication postoperatively is renal insufficiency – can be reduced by giving frusemide or mannitol pre-operatively before anaesthesia induction .Ensure vitals stable . After clamping the aorta. infection (mycotic) . infection. Bring to operating theatre for open repair – surgeon’s main task is to quickly isolate the aorta and clamp it proximally (can be clamped for about 30 minutes without significant visceral ischaemia) 5. found incidentally during imaging . the graft forms the lumen of the aorta 7.Location: usually infrarenal (95% of cases). and listen for bruits .Often contains mural thrombus due to turbulence and stasis RISK OF RUPTURE . Call for vascular surgeon 3.Very high mortality – nearly 100% if frank rupture (will not get to ED in time) . while a false aneurysm is a breach in the blood vessel wall leading to an extravascular haematoma that freely communicates with the intravascular space . or ruptured? Ruptured AAA . renal. worsening haemorrhage 4.Pulsations and mass in epigastric region felt on deep palpation . ureter . the surrounding haematoma and mural thrombus within the AAA are cleared out 6.g.Local compression on neighbouring structures e.Visible pulsation over abdomen . rarely beyond .e.75% of aneurysms 7cm or larger will rupture in 5 years PRESENTATION . may feel a pulsatile mass in the abdomen 1.Thromboembolism distally – gangrene of feet (trash feet) .Shape: Usually fusiform – long dilated segment (versus saccular which is spherical) . symptomatic but not yet ruptured.Mortality rate of repair operation in this setting is about 50% .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 .Other causes: cystic medial degeneration (in Marfan). popliteal – for any aneurysm.Small aneurysms <5cm have a 2-3% chance of rupture per year. etc INVESTIGATIONS Mostly imaging to delineate aneurysm  CT Scan MANAGEMENT Dependent upon clinical context – is patient asymptomatic.Auscultate for bruit over the mass . strong family history (Marfan.An aneurysm is a localised abnormal dilatation of a blood vessel wall or the heart . becomes rapidly hypotensive and goes into shock . Ehler-Danlos) PATHOLOGY .Most feared presentation is that of rupture – patient complains of intense abdominal pain radiating to the back. the AAA is incised. while aneurysm larger than 5.Obstruction of branches from aorta e.5 cm will have a 10% risk of rupture per year .Look at the lower limbs for any gangrene. vertebral PHYSICAL EXAMINATION .High suspicion in unstable hypotensive patient complaining of severe sharp pain radiating to the back.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 . Aortoenteric fisula – frank PR bleeding.Indications for surgery: (a) Aneurysm > 5.Operation is the same except that it is done under elective setting .An alternative to open repair which is less invasive. but serious morbidity rate is similar to open repair: 10% .Involves deployment of a non-porous stent within the aneurysm to form the lumen of the aorta – requires adequate “neck” proximally and good landing site distally . Renal insufficiency 4.Non-ruptured AAA . ruptured/leaking aneurysm . serious morbidity ~10% Endovascular stenting . Colon ischaemia – occurs in 2-6% 5.5 cm in largest diameter (b) Increase in diameter of more than 1cm per year (c) Symptomatic aneurysm – back pain. distal embolism. Infection of graft 7. Trash foot – embolism of thrombus from the aneurysm 6.Not as good results as open surgery. Stroke (due to hypotension or embolism) 3. need to do an angiogram every 6 months to check position of the stent (ensure that stent has not migrated) COMPLICATIONS OF SURGERY Intraoperative/early 1. Spinal cord ischaemia (quite uncommon) Late 1. tenderness on palpation. Late infection of prosthetic graft material 3.Mortality ~1%. torrential 2.Patient’s fitness for surgery needs to be properly assessed because it is a major operation – need to optimise cardiovascular function .Time available for investigation of size of AAA and related anatomy . Sexual dysfunction 94 . can be done under GA . 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.Mortality is <5% in the elective setting. The deep venous system is composed of veins corresponding to the arterial supply e.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 .Physiology of venous drainage:     .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 .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 .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 . femoral vein . popliteal vein. so blood only flows towards the heart During calf muscle relaxation.95 PERIPHERAL VENOUS DISEASE ANATOMY OF THE VENOUS SYSTEM OF THE LOWER LIMB .g. squeezing the blood into the popliteal vein and back to the heart The deep veins have many valves to prevent backflow. the intramuscular veins open and suck blood in from the superficial system through the communicating veins.The superficial venous system is composed of two major veins.5 cm below and lateral to the pubic tubercle Hunterian perforator: mid-thigh Dodd’s perforator: distal thigh Boyd’s perforator: knee Calf perforators: at 5. 10. the great saphenous vein and the small saphenous vein Main mechanism is the calf muscle pump Contraction of the calf muscles compresses large venous sinuses in the muscles. thus draining the superficial veins . anterior and posterior tibial veins.Locations of the communicating veins:      Saphenofemoral junction (great saphenous drains into femoral vein): located 2. aching discomfort. Failure of the “venous pump” – dependent on adequate muscle contraction (stroke. they are more superficial and not bound down to the deep fascia) (d) Corona phlebectactica (a network of small dilated venules beneath the lateral and/or medial malleolus with severe venous hypertension) 4. which can result from: 1. pregnancy. hyperpigmented skin that is fixed to subcutaneous tissue. nocturnal leg cramps. which result from proximal venous obstruction. tumour compression in the pelvis. weeping. scaling. . They can be divided into primary varicose veins. varicose veins 3. if inguinal lymph nodes are enlarged These manifestations can be asymptomatic or associated with symptoms of leg fullness. unlike the saphenous veins. becomes painful and malodorous. edge becomes thickened or raised. Dysfunction of venous valves e. CEAP CLASSIFICATION OF CHRONIC VENOUS INSUFFICIENCY 2.g. flat ulcer with sloping edges. with erosions and crusting (d) Lipodermatosclerosis – a fibrosing panniculitis of the subcutaneous tissue that results in a firm area of tender. Venous ulcer formation . heaviness.Typical location is over the medial malleolus .In long-standing ulcer SCC can develop (Marjolin’s ulcer) – If ulcer enlarges. muscular weakness can cause failure) as well as competent venous valves MANIFESTATIONS OF CHRONIC VENOUS INSUFFICIENCY: 1.g. where the cause is unknown (may be related to posture and components and structure of the vein wall). or bursting pain upon standing. tortuous veins. Skin changes (a) Hyperpigmentation of the skin over medial lower third of the leg (gaiter area) – due to extravasation with haemosiderin deposits (b) Atrophie blanche – hypopigmented scars of healed venous ulcers (avascular and fibrotic skin) (c) Venous stasis eczema – pruritic.  Results from severe venous hypertension  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 96 VARICOSE VEINS Varicose veins are dilated.Shallow. deep vein thrombosis 2.Surrounding skin will show signs of CVI . formed by main tributaries of the saphenous veins because these do not have a strong coat of smooth muscle in their walls. usually quite moist-looking . present in all but the earliest stages Unilateral oedema worsened by dependency (worse at the end of the day) and better with recumbency 3. Obstruction to venous flow e. Venous dilatations (a) Telangiectasias (spider veins or venous stars – intradermal veins) (b) Reticular veins (slightly larger intermediate veins) (c) Varicosities (visible. base may be sloughy or granulating. dilated tortuous superficial veins.CHRONIC VENOUS INSUFFICIENCY Chronic venous insufficiency develops when there is venous hypertension. indurated. Oedema – pitting: The hallmark of CVI. destruction of the valves by thrombosis or an increase in flow and pressure caused by an arteriovenous fistula. and secondary varicose veins. Parity .Tie a tourniquet around the calf or thigh and ask patient repeatedly stand on tiptoe and then relax . there are other sites of incompetence (the SFJ may or may not be incompetent) PERTHES’ TEST .Weight .5 cm below and lateral to the pubic tubercle) with the patient lying down .Look for filling up of the varicosities above and below the tourniquet . Presence of signs of chronic venous insufficiency (as above) .Ask the patient to stand up . Palpate along the course of the saphenous veins and their tributaries to feel any varicosities present (may be more palpable than visible especially in fat legs) 3. then the incompetent perforator is below the level of the tourniquet . First percuss the distal veins to feel the wave of blood flowing orthogradely  normal. Do the cough test to feel for reflux at the saphenofemoral junction (2. Look at the inguinal region for any saphena varix Palpate 1.Lie the patient down and empty the varicosities . 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 . leading to dilation and separation of valve cusps so they become incompetent . Then percuss the proximal veins – if the distal hand can feel the wave of blood flowing retrogradely then there is valvular incompetence (not a very valuable test) Special tests TOURNIQUET TEST .Get the patient to stand while holding the SFJ occluded . Feel any dilated varicosities 2. the SFJ is the site of incompetence.97 PATHOPHYSIOLOGY . if they fill up.This may be aggravated by obstruction to venous return (as above) RISK FACTORS .Skin changes . Percussion (tap test) – place two hands some distance apart.Repeat the test. chronic cough.Posture – crossing legs all the time . Look at course of great saphenous vein and short saphenous vein for varicosities 3.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 .The SFJ is occluded (landmark is 2. etc .Pelvic tumour or other lesion compressing on the deep veins HISTORY Usually varicose veins do not cause symptoms and problems unless they are related to chronic venous insufficiency EXAMINATION: Examine patient standing with adequate exposure of the lower limbs Inspection (look all around the limb!) 1.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.If varicosities do not fill up.Auscultate over the varicosities for any bruit (indicate arteriovenous malformation) .Increased abdominal pressure – constipation. 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 .If the patient’s varicosities remain enlarged then he or she has obstructed deep venous drainage or incompetent valves in the communicating veins Completing the examination .If the veins below the tourniquet are dilated when the patient stands up.Examine the abdomen for any mass that may be causing the varicosities . placing the tourniquet at different sites: (i) Mid thigh (just below the Hunterian perforator (ii) Below the knee (iii) Mid-calf .5 cm below and lateral to the pubic tubercle) 5.Tie a tourniquet just below the SFJ .Occupation – requiring long periods of standing .Inherent weakness in the vein wall.Oedema .Age .If the veins dilate above but not below the tourniquet.Venous ulcers from pressure necrosis from insude 2. Palpate the inguinal region for a saphena varix (compressible lump that refills when released) 4. Exclude presence of deep vein thrombosis – stripping is contraindicated MANAGEMENT Conservative 1. Graduated compression stockings 3. neuromuscular disease INVESTIGATIONS Venous duplex ultrasound .g. deep vein reflux (post-DVT) 3. compression stockings should be fitted and continued for life Surgical .Decrease amount of time spent standing .FBC for raised total white count . Endovenous laser therapy (burns vein from within) 98 INVESTIGATIONS 1.Split skin graft can be considered with excision of dead skin and graft attached to healthy granulation tissue . Incompetent valves – varicose veins.When the calf is relaxed there should not be any sound – a second whoosh indicates reflux of blood i.First. Once healed. Most commonly done: High tie with great saphenous vein stripping.X-ray of the area to exclude underlying gas. change job or ask for change to position that involves less standing and walking 2. Exclude infection of the ulcer and other complications . Lifestyle changes . Complications – signs of chronic venous insufficiency. there is valvular incompetence CAUSE – ANY CAUSE OF CHRONIC VENOUS INSUFFICIENCY 1. Warn patient to avoid trauma to affected area 5.Doppler probe is placed in the popliteal fossa between the two heads of the gastrocnemius – over small saphenous vein . discomfort 3. Cosmesis – large unsightly varicosities 2. Symptoms – pain. and stab avulsion of varicosities 2.If ulcer fails to heal . Obstruction to venous flow – thrombosis 2. exclude malignancy or other causes of ulcer (biopsy) .Indications:  Recurrent varicose veins  History of superficial thromobophlebitis  History of DVT  Venous eczema  Haemosiderin staining  Lipodermatosclerosis  Venous ulceration . Encourage rest and elevate leg 6.Use of a handheld Doppler probe to detect incompetence VENOUS ULCERS . Analgesia 3. bone involvement 2. Daflon Surgical Indications: 1.Venous surgery for the underlying pathology . Antibiotics if infected 4.If due to job. venous ulceration Available modalities: 1. Muscle pump failure – stroke. Venous duplex to map out venous system 3. Biopsy if cannot exclude malignant transformation (Marjolin’s ulcer) MANAGEMENT: Conservative 1.Squeeze the calf to empty the veins – should hear a whoosh as blood flows through the small saphenous vein .g. Check for peripheral arterial disease by doing ABPI 4. Ultrasound-guided foam sclerotherapy 3. 4 layer compression stockings (change once per week) (a) Non-adherent wound dressing over ulcer (e. Menolin) followed by wool bandage (b) Crepe bandage (c) Blue-line bandage (Elset) (d) Adhesive bandage (Coban) 2.e. Medications e.Can delineate deep and superficial venous systems and locate sites of incompetence .Swabs of the ulcer for Gram stain and cultures . nocturia. skin infxns. myalgia. bleeding diathesis.Storage problem – frequency. BPH) Vascular  AV malformations  Renal artery disease – thromboembolism. Screen for pre-renal causes LOW / bone pain / sickness Rash. Other urological symptoms .End – bladder neck or prostate . bladder outflow obstruction (men e.Bleeding diathesis . renal dzes (eg Alport syndrome – ask for deafness).Malignancy – RCC. Prostate . oliguria. malignant hypertension  Renal vein thrombosis 4. hesitancy. bladder (TCC). medications causing discoloration of urine (eg rifampicin. hypt. sickle cell disease.Pyelonephritis . arthritis. urethra  Nephrolithiasis 5. Frequency + dysuria + haematuria . arthralgia. TB etc  Cancers of ureter. sickle cell dz PKD. malignancy.g. malaria Renal disease. dissecting aneurysms. Painful vs painless haematuria Painful . phenytoin) CAUSES Drugs PreRenal Renal Analgesics (NSAIDs) Anticoagulants Cytotoxic/immunosuppressive agents (eg cyclophosphamide) OCP Penicillin Quinine Warfarin 2.Voiding problem – strangury. schistosomiasis . dribbling. URTI Ongoing URTI or GE Iatrogenic Travel history PMHx Family history Malignancies. prostate. malaria 6. incomplete emptying etc .99 UROLOGICAL DISEASES HISTORY Post-renal Causes APPROACH TO HAEMATURIA DEFINITION: . HPT. incontinence .Beginning – urethra distal to UG diaphragm .Ureteric stone / clot .Hydronephrosis . BPH.DDx: nephrolithiasis (colicky).Tumour .ITP / HSP . urethral discharge Vasculitis  HSP  PAN  Wegener granulomatosis Pre-renal & Renal Causes Glomerular Tubulointerstitial dz Postrenal        1.Infections – malaria.DDx: haemoglobinuria. vasculitis Post-strep / post-infective GN IgA nephropathy Drug causes.Others – polyuria. urgency. fever. TCC.Drugs .>3 RBC / hpf. strictures) Painless .Renal cysts . urolithiasis . Which part of urine stream is blood stained? . UTI (women & children). urethra – eg schistosomiasis. TB. radiotherapy Schistosomiasis.g.Throughout – upper urinary tract or upper bladder      Post-strep GN Post-infectious GN IgA nephropathy Lupus nephritis Other GNs      Polycystic kidney disease Nephrolithiasis Malignancy – RCC. bladder.UTI . systemic illnesses Autoimmune causes. prostate.Exercise Systemic  Bleeding diathesis  Sickle cell disease Metabolic  Hypercalciuria  Hyperuricosuriia 3. . metastatic Pyelonephritis Renal cysts  Infxns of ureter. diabetic nephropathy.GN . myoglobinuria. oedema Sore throat. Associated fever – pyelonephritis.Bladder outflow obstruction (e. pseudohaematuria (menstruating women). may have specks of calcification .Renal size .Renal dz. rash. Scrotum – varicocoele on the left (may have RCC of the left kidney with extension of tumour into renal vein.LOW. Plain KUB .Increased residual volume in bladder after micturition due to BPH 11. blocking the testicular vein where it drains into the left renal vein) 5. Intravenous urogram (IVU) – see below for more details . 5. . bladder – any filling defects. Urine dipstick . etc) 5.Stones (filling defect.Detection of bladder tumour (IVU may not pick up small tumours <1cm) . filling defects.Casts  nephritis .Other necessary history 1. any filling defects (iv) Release film (abdominal binder which was placed to slow the flow of contrast into the bladder is released) – shows ureters.Contraindicated in: (a) Contrast allergy (b) Renal impairment (Cr >200) (c) Patients on metformin (can cause lactic acidosis. organisms  infection 3. patients need to stop metformin 2 days before and after study) (d) Patients with asthma (given steroids for 3 days before study) . drugs (rifampicin).RBCs – isomorphic or dysmorphic? Dysmorphic RBCs suggest a tubular source. metabolic (alkaptonuria. Urine culture and sensitivity 6.Elevated TW – infection 7.Any renal impairment and electrolyte abn (renal or pre-renal dz more likely) 100 8. Digital rectal examination – prostate enlargement (BPH versus cancer) INVESTIGATIONS 1. Infection . can detect dilated calyces/pelvis (hydronephrosis). Check patient’s vitals.Renal stones 10.systemic dz (DM HPT Bleeding sickle cell) 6.Stones. joint pain.Various phases: (i) Control film – plain KUB (ii) Nephrogram phase (taken 1 minute after contrast given) – contrast fills kidney parenchyma so the kidneys become more visible. bone pain. proximal dilatation. Conjunctival pallor 3. oedema Malignancy . travel and contact history Sorethroat .Distortion of renal outline and pelvic calyces by RCC. Family history – PKD.Biopsy can be taken at the same time KUB FILM .How low is the Hb? . electrolytes and creatinine . renal dz. UFEME . beetroot. decreased distal passage of contrast) + hydroureter and/or hydronephrosis . Abdomen – renal mass. abnormal appearance of the bladder (fir-tree appearance in neurogenic bladder) (v) Post-micturition – any residual urine in bladder after voiding . size of kidney 9. Urine cytology for malignant cells 4. 4. Drug history / Hx of radiation 7.Confirm presence of red blood cells . 3.stable? 2. Sickle cell. Urine phase contrast .Fever. bladder. inferiorly needs to show the pubic symphysis INTRAVENOUS UROGRAM .Presence of any hydronephrosis . neuro deficits. Urea. palpable bladder/bladder mass 4. while isomorphic RBCs suggest post-renal source (ureter.Fever. liver function PMHx .Elevated WBC (pyuria is >5 WBC per hpf).Filling defect in bladder due to TCC .Margins: Superiorly needs to be above the upper pole of the right kidney (T12).Causes of false-positive for blood: haemoglobinuria. SOB.Post-strep/infective GN. Full blood count .Intravenous contrast used to delineate anatomy of the kidneys and urinary system . Ultrasound of the kidneys . Cystoscopy . can measure size (iii) Pyelogram phase (3-5 minutes) – contrast fills calyces and pelvis. HPT PHYSICAL EXAMINATION 1. IgA nephropathy Autoimmune . porphyria) 2. 2. any hydroureter. and chromophobe renal cell carcinoma (5%) . MRI of abdomen and heart .Arise from the renal tubular epithelium .Peak incidence 60-70 years PATHOLOGY .In these resectable lesions. but not beyond Gerota’s fascia T4 Tumour invades beyond Gerota’s fascia .When tumour has grown large enough. hypercalcaemia. biopsy of the metastatic site may be easier STAGING 1. lymphoma RISK FACTORS . etc)  clear cell carcinomas  Hereditary papillary RCC (HPRCC) due to mutation of the MET proto-oncogene on chromosome 7q31  multifocal bilateral papillary carcinomas . liver dysfunction. limited to the kidney T3 Tumour extends into major veins or invades adrenal gland or perinephric tissues.2:1 male predominance .Three cell types: clear cell carcinoma (70-80%). Wilms’ tumour.Other renal tumours: TCC of renal pelvis. IVC Lymph node enlargement Liver metastases 2. extension of tumour into left renal vein can cause a left varicocoele as the left testicular vein becomes occluded .For lung metastases 3. liver.Smoking .Paraneoplastic syndromes are uncommon – Cushing’s. adjacent organ invasion Extension into renal vein. malaise . Pathological diagnosis .Symptoms of metastases – lungs. CT scan of the chest . palpable renal mass (indicates late stage disease) . pulmonary embolism . bilateral multicentric retinal angiomas.3% of adult malignancy . brain. LOA.For left renal tumour.Only done if patient complains of bone pain and/or alkaline phosphatase is raised 4.Most common primary renal tumour (80-85% of all tumours of the kidney) .Presumptive diagnosis is made on imaging – a renal parenchymal mass with thickened irregular walls and enhancement after contrast injection suggests malignancy 2. ascites.Most frequent occurring solid lesion within kidney .Needle biopsy usually not done for resectable lesions due to fears of tumour seeding . Imaging – CT and/or ultrasound . LOW. dull flank pain and palpable mass may result  Classical triad of RCC: flank pain. limited to the kidney T1a: tumour <4cm T1b: tumour >4cm but <7cm T2 Tumour >7cm. Bone scan .Polycythaemia occurs in 1-5% (due to increased erythropoietin) . bones.Exposure to cadmium . lymph nodes . painless haematuria.Family history  von-Hippel Lindau syndrome due to mutation of the VHL gene on chromosome 3p25 (associated with CNS haemangioblastomas (usually cerebellar). and provides the tissue diagnosis post-operatively .In tumours with metastatic disease on presentation.Superior to CT for evaluation of IVC and right atrium involvement T1 Tumour <7cm. a partial or total nephrectomy is often performed. papillary renal cell carcinoma (1015%). hypertension DIAGNOSTIC 1.101 RENAL CELL CARCINOMA INVESTIGATIONS EPIDEMIOLOGY . CT scan of the abdomen - Perinephric invasion.Extension into IVC can cause lower limb oedema.May have fever a/w night sweats.Painless gross haematuria is the most common presenting symptom – >50% of cases .Acquired polycystic kidney disease (secondary to chronic dialysis) PRESENTATION .Initially asymptomatic (may be detected incidentally) . phaeochromocytomas. Schistosomiasis . cryotherapy of lesions PATHOLOGY . urgency) suggestive of carcinoma in-situ.Occupational (hairdressers – exposure to hair dyes) . LOA.4:1 male predominance Surgery . aniline-containing dyes.High dose interleukin-2 – associated with good results in patients whose tumours respond to treatment. feeling of incomplete voiding. intermittent voiding.Industrial chemicals – naphthylamine.Sorafenib – an inhibitor of tyrosine kinase  blocks intracellular domain of the vascular endothelial growth factor (VEGF) receptor .Most small tumours grow slowly and do not become symptomatic or metastasise – reasonable to manage conservatively with periodic re-evaluation . bone pain due to metastasis . suprapubic pain due to local invasion.Other types of bladder tumours: adenocarcinoma (1%.Increasing incidence with age (80% diagnosed in patient >60 years old) .Constitutional symptoms – LOW. intermittent.Thought to arise due to exposure to carcinogenic substances in the urine  field change effect. adrenal gland Adjuvant chemotherapy Surveillance after resection to detect relapse early Patients who cannot undergo resection .Alternatives: radiofrequency ablation. arises from remnant of the urachus in the dome of the bladder). while obstructive symptoms (decreased stream.g.In T3 disease.Done in T1b disease – entire kidney removed 3. strangury) indicate a tumour at the bladder neck or prostatic urethra .g.Analgesic abuse (phenacetin) . fatigue DIAGNOSIS 1. However.TCC is the most common tumour of the bladder (>90%) . occurring throughout the stream . etc . thus urothelial tumours often occur multifocally .Haematuria is the most common presenting symptom (90%) – typically gross.Ninth most common cancer in Singaporean males .Chronic cystitis . Urine cytology for malignant cells 2. associated with high toxicity and often not tolerable .Chemotherapy (cyclophosphamide) ADVANCED TUMOURS Immunotherapy . as treatment can induce long-term remissions without relapse.Radiation (pelvic) .LUTS – irritative symptoms (frequency.Pain – in locally advanced or metastatic tumour  flank pain due to urinary obstruction. painless.Bevacizumab – monoclonal antibody against VEGF Prognosis Stage I (T1N0): Stage II (T2N0): Stage III (T3N0/N1): Metastatic disease: 102 >90% 5 year survival 75-90% 60-70% <10% PRESENTATION . Total nephrectomy . Radical nephrectomy .Retroperitoneal versus transperitoneal approach 1. Partial nephrectomy . due to chronic irritation e. long term indwelling catheter or untreated bladder stone) RISK FACTORS .Cytoreductive nephrectomy performed prior to starting immunotherapy can improve survival Molecular targeted therapy . Cystoscopy with cell brushings and biopsy 3.Done in T2 disease – entire kidney together with Gerota’s fascia .Cigarette smoking .Laparoscopic versus open methods . IVU or CT urogram to detect synchronous lesions (3% chance of proximal tumour) .Done in T1a disease – spares part of the kidney that is not involved  nephronsaving 2. dysuria.TREATMENT BLADDER TRANSITIONAL CELL CARCINOMA RESECTABLE TUMOURS EPIDEMIOLOGY . SCC (<5%. aim for radical nephrectomy and removal of structures affected e. 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.Urinary tract infections can also cause stone formation – struvite stones form in Proteus vulgaris infections as this organism splits urea into ammonium. not continent) o o Ileal conduit (a segment of ileum with ureters attached.Most important cause of stone formation is increased urine concentration of the stone’s constituents. such that they exceed their solubility  precipitate as stones . multiple recurrences. hyperuricuria .Bacteria can also form nidi for the formation of any kind of stone PRESENTATION DEPENDS ON SITE Renal stones . tumour size >3cm.Vague flank pain may occur Ureteric stones - Even small stones can cause severe symptoms as the ureter is narrow Classically ureteric colic pain – severe. intermittent loin-to-groin pain Haematuria – gross or microscopic Irritative symptoms – frequency. generating alkaline urine .Intravesical therapy indicated in patients with high risk of tumour recurrence or tumour progression (high grade.Follow-up:  3-monthly cystoscopy for 1 year  6-monthly cystoscopy for next 4 years  Yearly cystoscopy thereafter  IVU every 2 years Urine cytology with every cystoscopy MUSCLE-INVASIVE .Most often asymptomatic unless the stone gets lodged in the pelviureteric junction causing hydronephrosis and subsequent infection  pyonephrosis . abdominal wall Generally can be divided into 2 main groups: (a) Superficial tumour (70-80% of patients) – Ta. Transurethral resection of bladder tumour (TURBT) with histopathology Ta Tis T1 T2a T2b T3a T3b T4a T4b Superficial. not continent) Neobladder construction using ileum (only if urethra not removed. prostatic urethral involvement)  BCG – 1 instillation per week for 6 weeks  Mitomycin C – single instillation within 24hrs of TURBT. as a stoma. continent. hypercalciuria with or without hypercalcaemia. urgency Can cause upper urinary tract infection  fever. multiple primary sites. but easily stenosed due to small calibre. or weekly/monthly treatments for up to 2 years .Magnesium ammonium phosphate (struvite) stones – 15% .Primary treatment is TURBT of the tumour .g. does not involve lamina propria Carcinoma in-situ: “flat tumour” Superficial.E.Calcium oxalate or calcium phosphate stones – 75% .Radical cystectomy  Radical cystoprostatectomy with pelvic lymphadenectomy in male  Anterior exenteration with pelvic lymphadenectomy in female  Ways of diverting urine output o Cutaneous ureterostomy (use ureters to create stoma. etc . Tis.Uric acid and cystine stones – 10% PATHOLOGY . primary or coexisting carcinoma in-situ. urgency Haematuria If infection is present – dysuria. but most commonly in the kidney . uterus Invasion of lateral pelvic walls. pain Bladder stones - May be asymptomatic Can cause irritative urinary symptoms – frequency. vagina.103 o STAGING 1.Radiotherapy (not as good as surgery) UROLITHIASIS STONE COMPOSITION . better quality of life) Stoma with pouch construction under abdominal wall (not continent) . CT abdo/pelvis for T. T1 (b) Muscle-invasive tumour (20-30%) – >T2 MANAGEMENT DEPENDENT ON STAGE SUPERFICIAL TUMOUR . fever.Can occur at any level in the urinary tract. N and M staging 2. Urine tests – dipstick.Can show dilated urinary system secondary to stone obstruction – hydroureter and/or hydronephrosis 4.If pyelonephritis present due to stone obstruction. only if failed other management strategies. KUB . altered anatomy. untreated UTI. looking for ureteric stones . rebound. distal obstruction that cannot be bypassed with a stent 3. any renal stones .If underlying disease present that causes increased urinary concentration of stone components e.PHYSICAL EXAMINATION .Contraindicated in pregnancy. Cystolitholapaxy for bladder stone 5. refined sugars Increase citrus fruit intake SURGICAL INTERVENTION INVESTIGATIONS Indications: 1.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) .Otherwise unremarkable examination - High fluid intake Low salt intake Restriction of red meat. Intravenous urogram . and/or cause symptoms . it is not worth salvaging the kidney TREATMENT CONSERVATIVE Stones smaller than 5mm can be treated conservatively as 60% will be passed out.g. hypercalcaemia  treat disease if possible 104 Constant pain Does not pass after one month Too large to pass spontaneously Obstructs urine flow Causes urinary tract infection Damages renal tissue or causes significant bleeding Increase in size Types of treatment available: 1. or if system is obstructed to begin with. and medially into bladder.In ureteric colic. can also be done by pneumatic drill. only treat if they do not pass out after 4 to 6 weeks.Look for bladder stones 3.Done for renal stones that are too large for ESWL to disintegrate .g. patients unfit for GA 2. Ultrasound of kidney or bladder .Haematuria . when ESWL used for treatment of a large stone. untreated bleeding diathesis.Pyuria. UFEME.If the patient has pyelonephritis. micro-organisms (UTI) 2.Can also help to visualise a stone . etc . but calcium phosphate and cystine do not .Used for renal stones and upper ureter stones – not so good for lower system due to difficulty in access . symptoms are often out of proportion to signs – no guarding. across sacroiliac joint.Look at kidney size.May be able to see radio-opaque stone (90% of renal stones are radio-opaque) .Contraindicated in uncorrected bleeding diathesis. dairy produce.Trace path of ureter along tips of transverse processes.If one kidney has less than 15% of total renal function. may want to stent to ensure good drainage after surgery . Ureteroscopy with lithotripsy (usually laser lithotripsy.For stones along the ureter 4. performing open surgery for another reason anyway. non-functioning kidney Adjuncts: . urine culture/sensitivity - . Percutaneous nephrolithotomy (PCNL) .Used for stones below 10mm in size . electrohydraulic means) . it is valuable to measure the renal function using the MAG-3 renogram .Calcium oxalate. uric acid and struvite stones fragment easily. MAG-3 renogram .Features of stone: echogeneic rim. renal punch may be positive . Extracorporeal shock wave lithotripsy (ESWL) .Treatment of any urinary tract infection . posterior acoustic shadowing 5. Open surgery (pyelolithotomy or ureterolithotomy) – rarely done.Double-J stent (or DJ stent) – inserted to stent the urinary system when worried that stone fragments after ESWL may cause obstruction e. Digital rectal examination  Any saddle anaesthesia  Anal tone  Prostate enlargement – firm and smooth? Or hard. frequency. malaise (any tumour in general) CAUSES Complications: Mechanical Extraluminal Intramural Intraluminal Nonmechanical Cord disease/ injury Neuropathy Drugs Others Prostate enlargement (benign/malignant) Faecal impaction Pelvic tumour Pregnancy UV prolapse Tumour of the bladder neck (TCC) Urethritis (UTI) Urethral stricture from STD.Symptoms of urinary tract infection: dysuria. pedal oedema. history of spinal disease e.Lower limb weakness/paralysis. LOA. bladder stone .g. back trauma.General condition – sallow appearance. rectal mucosa not mobile?  Stool impaction .Neurological examination  LMN paralysis of the lower limbs?  Any sensory level present? . alcohol Prolonged immobility Post-anaesthesia Pain .Constipation .Stone disease (if in the bladder.Renal failure (more likely in chronic retention) – vomiting. haematuria .Immobility History suggestive of aetiology: APPROACH TO ACUTE RETENTION OF URINE . bowel incontinence.g. usually asymptomatic) . nocturia.Suprapubic distension with pain (unlike chronic retention of urine which is painless) Precipitating factors: .Abdomen  Palpable bladder – tender  Other pelvic masses – fibroid. urgency. cough mixture.Previous urethral instrumentation or STD  stricture .Previous history of ureteric colic pain or stones . prev instrumentation Stones Blood clot (clot retention in haematuria) Foreign body Cord compression Multiple sclerosis Tabes dorsalis Diabetic autonomic neuropathy Anticholinergics (cough medicine). drowsiness PHYSICAL EXAMINATION . gravid uterus.Gross painless haematuria recently  TCC. PID. etc (uraemia) . antihistamines.Previous history of obstructive symptoms e.Infection – symptoms of UTI .Constitutional symptoms: LOW. spinal stenosis  neurogenic bladder .Inability to pass urine . irregular. lethargy. terminal dribbling etc  BPH . poor stream. ovarian cyst  Faecal loading  Bilateral enlarged kidneys (hydronephrosis) .Drugs e. anti-depressants. scratch marks. hesitancy. craggy. antihistamines .g.105 Summary of treatment modalities Location Renal Size < 5mm 5-10mm 10-20mm > 20mm Treatment Conservative management unless symptomatic/persistent ESWL Either ESWL or PCNL PCNL Upper ureter < 5mm 5-10mm > 10mm Conservative management unless symptomatic/persistent ESWL URS with lithotripsy Middle ureter/ Distal ureter < 5mm > 5mm Conservative management unless symptomatic/persistent URS with lithotripsy Bladder < 30mm > 30mm Cystolitholapaxy Open cystolithotomy (also if there are multiple stones) HISTORY Symptoms of ARU: . Full blood count for raised TW (infection) 2.Try urethral catheterisation first (impt: urethral catheterisation contraindicated if patient has signs suggestive of urethral injury – blood at urethral meatus.Major stimulus for hyperplasia appears to be dihydrotestosterone (produced from testosterone by the enzyme 5-alpha reductase) . Treat reversible causes . tumour. perform suprapubic catheterisation  Requires distended bladder which pushes the surrounding bowel loops away so that risk of bowel injury is lower  Local anaesthetic injected 2 fingerbreadths above pubic symphysis  Small incision made in the skin and fascia.Commonly occurs in the central zone of the prostate . PSA – keeping in mind causes of raised PSA (cancer. Urine dipstick.Age-related increases in oestrogen levels may also contribute to BPH by increasing the expression of dihydrotestosterone receptors on prostatic parenchymal cells PRESENTATION . hypokalaemia. hypovolaemia) Requires close monitoring of urine output and fluid/electrolyte status with appropriate replacement and resuscitation (b) Haemorrhage ex-vacuo  Bladder mucosal disruption with sudden emptying of greatly distended bladder  Usually self-limiting 3. intravesical protrusion of prostate TREATMENT 1. easier to pass through)  For stricture (when you feel the catheter is stuck quite proximally along the penile urethra. and 2) urethral stricture  For enlarged prostate. Urea.Take off catheter and watch patient’s output. UFEME and culture/sensitivity for infection 4. Ultrasound of the bladder for stones. and also do bladder scan post-micturition to check residual volume . resulting in transient impairment of concentrating function Can result in hypotension and electrolyte abnormalities (hyponatraemia. and trocar inserted  When a gush of urine is seen.If urethral catheterisation fails. lactulose. can perform uroflow to investigate severity of outlet obstruction. senna etc .If patient cannot pass urine and bladder volume >400ml  re-catheterise BENIGN PROSTATIC HYPERPLASIA (BPH) INVESTIGATIONS (FOR CAUSES) 1.Relieve constipation with fleet enema. try a smaller gauge catheter  Do not push too hard – may cause false passage creation if the obstruction is due to a stricture  .Results from proliferation of both the epithelial and stromal components of the prostate with resultant enlargement of the gland . there are two possibilities: 1) enlarged prostate. as well as perform bladder scan to measure bladder volume . it is more likely to be a stricture). try again with a thicker catheter (stiffer.Frequency rises with age after the age of 30.When patient passes urine. reaching 90% in men older than 80 PATHOLOGY .Main result of BPH is obstruction of the prostatic urethra resulting in lower urinary tract symptoms (LUTS) which can be divided into irritative and obstructive symptoms – obstructive symptoms predominate . BPH [usually <40]. KUB for stones. faecal loading 6.Treat any urinary tract infection if present 2. the suprapubic catheter is inserted and secured  Due to tubular damage from obstruction of drainage of the pelvicalyceal system. instrumentation >11days) 5.Stop drugs that may have precipitated ARU . Trial-off catheter . electrolytes and creatinine for raised creatinine (renal impairment secondary to obstructive nephropathy) 3. Anticipate complications (a) Post-obstructive diuresis  Urine output >200ml/hr for 2 hours or more 106 EPIDEMIOLOGY . high-riding prostate – more relevant in the trauma setting)  If urethral catheterization cannot pass into bladder. prostatitis.IMMEDIATE MANAGEMENT – CATHETERISATION  .Very common problem in men . Obstruction leads to hypertrophy of the detrusor muscle and trabeculation of the bladder mucosa as the bladder tries to empty against increased resistance PHYSICAL EXAMINATION . 5-alpha reductase inhibitors .In the chronic setting.Bladder calculi . medical management.Divided into watchful waiting. no complications and normal invx . Doxazosin. Terazosin.Most common side-effect is sexual dysfunction III. hypertension. Perforation of the urethra or bladder dome Late 1.Risk increases with prolonged operation and increased pressure of irrigation.Symptoms: Nausea.Creatinine level (renal impairment due to chronic obstruction) .Suitable for patients with minimal symptoms. and surgical management .May progress to the point of acute urinary retention  admitted to hospital .Patient usually given spinal anaesthesia during TURP so the surgeon can assess the patient’s mental status during the operation 3. bladder stone .Treats the disease (not just the symptoms) by inhibiting the conversion of testosterone to dihydrotestosterone by 5-alpha reductase  reduced prostate size .Ultrasound of kidney and bladder – hydronephrosis. vomiting.Digital rectal examination: smooth enlarged prostate.Irrigation fluid is hypotonic. thus water enters open vasculature during surgery .Result in decreased outflow resistance and decreased bladder instability . prevent long-term complications.Palpable tender bladder in ARU (non-tender in chronic retention) .Refractory urinary retention . post-void residual volume >100ml. TUR syndrome .Prazosin. Watchful waiting . rubbery. improve patient’s quality of life I.Objectives of treatment: Rapid and sustained relief of symptoms.Finasteride. and in prostates >40g .Renal impairment secondary to outflow obstruction . confusion.Side effects include postural hypotension.Obstructive uropathy .Urinary investigations for infection (stasis predisposes to UTI) .Co-existence of prostate cancer MANAGEMENT .Gross haematuria .Acute/chronic urinary retention .Recurrent gross haematuria Complications of surgery (TURP) Early 1.Monitor patient’s symptoms and clinical course annually II. may have overflow incontinence . thus op is kept to shorter than one hour. Surgery – Transurethral resection of prostate (TURP) Indications: . the patient may have chronic urinary retention with high postvoid residual volume in the bladder  asymptomatic.Proven to decrease need for surgery and acute retention rates . prostate and urethra . dizziness 2. Alfuzosin .Recurrent urinary tract infection .Only effective after 6 months. and irrigation pressures <60mmHg . visual disturbances . Alpha blockers .107 Obstructive Hesitancy Straining to pass urine Weak stream Prolonged micturition Terminal dribbling Feeling of incomplete voiding Double voiding (pis-en-deux) Irritative Frequency Urgency Nocturia Dysuria Urge incontinence .Recurrent UTI . Medical treatment 1. Bleeding 2.Bladder stones .Uroflow to confirm obstruction to urinary outflow (normal peak flow rate should be more than 15ml/sec) PROBLEMS .Hyponatraemia due to constant irrigation during TURP (glycine used for irrigation – cannot use N/S.KUB for bladder stone .Treatment of symptoms of BPH by acting on the alpha-1 adrenergic receptors that are abundant in the bladder neck. Dutasteride . as ionic solutions make diathermy non-functional) . Retrograde ejaculation . non-tender INVESTIGATIONS . 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.Oestrogen therapy (diethylstilbestrol) METASTATIC DISEASE 1. PSA level . Chemotherapy  Docetaxel + Prednisone (gold standard)  Mitoxantrone + Prednisone .Genetic – racial variations in onset and prevalence.PROSTATIC CANCER EPIDEMIOLOGY . Secondary hormonal manipulation  Glucocorticoids – prednisone. family history .Percuss spine for any bone pain DIAGNOSIS 1.Peak incidence between 65 and 75 years of age PATHOLOGY .Adenocarcinoma .4-10ng/ml: biopsy advised. bladder outlet obstruction . aminoglutethimide 2.Anti-androgen  Non-steroidal e.Metastatic symptoms – bone pain PHYSICAL EXAMINATION . TRUS biopsy for staging purpose 3.Environmental – industrial chemical exposure.Digital rectal examination: Asymmetric area of induration. Androgen ablation HORMONAL REFRACTORY PROSTATIC CANCER .Histology of prostate carcinoma is graded by the Gleason score looking at glandular architecture at low magnification 108 1.Arise in the outer parts of the prostate 70-80% of the time and are thus palpable on digital rectal examination RISK FACTORS . non-regional) 4.2 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 . Radiotherapy .Can cause local symptoms such as obstruction of the prostatic urethra (uncommon as most cancers arise in peripheral zones) – LUTS.Castration  Surgical  Medical – LHRH agonist . dexamethasone. laparoscopic or robot-assisted . diet containing high animal fat STAGING 1. Clinical examination (palpable tumour  T2) 2.5th common cancer in Singapore .Brachytherapy LOCALLY ADVANCED DISEASE PRESENTATION .g.<4ng/ml: majority will have negative biopsies.Open – retropubic or perineal approaches 2.>10ng/ml: biopsy recommended as >50% of patients will have prostate cancer .75ng/ml per year 2. CT scan of the abdomen and pelvis to assess extent of tumour invasion and nodal status (regional. Transrectal ultrasound (TRUS) with biopsy .Combined androgen blockade . Flutamide  Steroidal – cyproterone acetate .Prostate Cancer is the 6th commonest cancer among men in Singapore. Radiotherapy with androgen ablation .Hormonal – growth of tumour can be inhibited by orchidectomy or administration of oestrogens . may be incidentally picked up on digital rectal examination or due to elevated prostate-specific antigen (PSA) level . Radical prostatectomy .Open. . hydrocortisone  Progesterone – megestrol acetate  Adrenal suppressives – ketoconazole. though only 20% will have prostate cancer .Often asymptomatic.External beam radiotherapy (EBRT) . or frank hard irregular nodule . Bone scan for metastasis TREATMENT LOCALISED DISEASE 1.Management: 1. Can you identify the testis and the epididymis? 3.109 APPROACH TO SCROTAL SWELLINGS ANSWER 4 QUESTIONS: 1. Is the swelling transilluminable? 4. Is the swelling tender? Cannot get above swelling Can get above swelling Cough impulse Reducible Testis palpable Opaque Hernia No cough impulse Not reducible Testis not palpable Transilluminable Infantile hydrocoele Testis not definable from epididymis Opaque Non tender Chronic haematocoele Gumma Tumour Tender Torsion Epididymo-orchitis Acute haematocoele 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 . Can you get above the swelling? 2. Drain potential collections .Corrugated drain.g. rely on gravity .May allow the early detection of anastomotic leaks or haemorrhage .Passive drains have no suction. T-tube .Drain fluid collects in gauze pad or stoma bag . biliary t-tube) Open drains .Function by the differential pressure between body cavities and the exterior . Incisional hernia.active drainage systems have a clear graduated scale by which you can see the FUNCTIONS OF DRAINS Drains are inserted to: . Yeates drain.Prevent Infection. Where a drain has been put in to drain an infected site e.If the tubing isn't sutured in place.Drainage of fluid removes further fluid collections .create a separate incision site for drain! TYPES OF DRAINS . blood or other fluids (e. Infection 2.g. Passive drains rely on gravity. remove it when the fever settles or when there is evidence of complete drainage. Bleeding 3.Red rubber drains induce an intense tissue reaction allowing a tract to form .In some situations this may be useful (e.by mechanical pressure or suction 4. Drain failure. refix as required .maintain meticulous skin care and aseptic technique around the insertion site .Consist of tubes draining into a bag or bottle .Drains are often made from inert silastic material . abscess. an air leak will cause the collection chamber to rapidly fill with air and the system won't drain properly. Drains put in to cover perioperative bleeding and haematoma formation.Never hold a drainage collection device higher than the tube insertion site to prevent the drainage from flowing backward into the patient .occurs when drain inserted through incision wound site. The following are general guidelines: 1. so be careful. Penrose drain .Prevent slippage by securing drain carefully to skin.The risk of infection is reduced Active drains . If a portion of the tube is pulled outside his skin.Note amount of drainage daily REMOVAL OF DRAINS A drain is removed as soon as it is no longer required.SURGICAL INSTRUMENTS . lymph) .They include chest and abdominal drains . Redivac Drain.Jackson-Pratt Drain.Prevent blockage of the drain.g.Active drains require suction.Evacuate collections of pus.Tubing of the low-pressure active drainage system is placed through a separate drainage system won't provide adequate drainage Rationale: . Passive drains .Used when small to moderate amounts of drainage are expected or when a passive DRAINS .They induce minimal tissue reaction .Leave a tract for potential collections to drain following removal COMPLICATIONS: 1. .Easier to drain infected collections Closed drains .blocked/slipped/kinked 5.Have expandable chambers to create low-pressure suction 110 type and amount of drainage and determine when to empty the drainage chamber puncture wound or the tube may exit the edge of the surgical wound .Used when a moderate to large amount of drainage is expected CARE AND PREVENTION OF COMPLICATIONS OF TUBES: . .Drains classified as:  Open or closed  Active or passive . 2.do not allow bottles to fill up . can come out after 24— 48 hours. Tissue damage. it could become dislodged when you change dressings or reposition the patient. attached to an empty 10 ml syringe. Advance guide wire. External jugular vein CANNULATION OF THE INTERNAL JUGULAR VEIN The internal jugular vein (IJV) is accessible. 3. Avoid internal jugular vein if carotid aneurysm present on the same side. Measurement of central venous pressure 5. Cleanse the skin and drape the area. Remove syringe. 7. Direct the needle caudally. When vein is entered. aiming towards the ipsilateral nipple. 2. 3. Sterile gloves and a gown should be worn to avoid catheter-related sepsis. Hence. On the left side. Use a dilator to enlarge the hole in the vein. Perform check chest X-ray to confirm position and exclude pneumothorax. Maintain a firm grip on the guide wire at all times. Air embolism . Cardiac catheterization 6. Transvenous cardiac pacing. dome of the pleura. Septicaemia 6. Thread tip of catheter into the vein through the guidewire. Apply dressing according to hospital protocol. 3. The catheter tip should lie in the superior vena cava above the pericardial reflection. Bleeding diatheses 5. 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. 9. 2. Hypercoagulable states ROUTES FOR CENTRAL VENOUS CANNULATION INCLUDE: 1. CONTRAINDICATIONS: 1. Hold catheter and REMOVE GUIDEWIRE.ensure head-down position. Now. flush of blood appears in the syringe.111 CENTRAL VENOUS PRESSURE LINE INSERTION INDICATIONS 1. observe rhythm on cardiac monitor during insertion. 6. Check lumen placement by aspirating through all the pigtails and flushing with saline next. The vein is initially posterior to. Anatomy of the IJV The vein originates at the jugular foramen and runs down the neck. Introduce the large calibre needle. Infusion of irritant drugs 4. parallel to the sagittal plane. Arrhythmias – This happens if cathether “irritates” the heart. 10. 15. so cannulation of this vein is associated with a lower complication rate than with other approaches. 13. Remove the dilator. 4. Avoid passing guidewire too far. Pneumothorax/haemothorax 2. Internal jugular vein 2. Medial: Carotid arteries. J-shaped end first. holding needle firmly in place. Vascular access 2. Turn the head away from the venepuncture site. to terminate behind the sternoclavicular joint. Total parenteral nutrition 3. 4. It lies alongside the carotid artery and vagus nerve within the carotid sheath. into the vessel through the needle. Procedure 1. Palpate the carotid artery and ensure that the needle enters the skin lateral to the artery. cannulate the vein via the Seldinger technique as described below. Avoid infraclavicular approach to subclavian vein if patient has apical emphysema or bullae. the IJV lies anterior to the thoracic duct. Hold guide wire in place and remove needle. Posterior: C1. Do not insert into an infected area. . Femoral vein 4. While needle is advanced. where it joins the subclavian vein. 14. The vein lies most superficially in the upper part of the neck. 5. then lateral and then anterolateral to the carotid artery during its descent in the neck. 12. cranial nerves IX-XII Technique of IJV cannulation Place the patient in a supine position. Subclavian vein 3. Grasp the catheter near the skin and advance it into the vein with a slight twisting motion. maintain gentle aspiration. Pulmonary artery catheterization 7. Complications 1. Relations of the IJV Anterior: Internal carotid artery and vagus nerve. Use local anaesthetic to numb the venepuncture site. Occlude needle to prevent air embolism or bleeding. 16. 11. Suture the catheter to the skin to keep it in place. it is the vessel of choice for central venous cannulation. Advance catheter into final indwelling position. sympathetic chain. 8. at least 15 degrees head-down to distend the neck veins and to reduce the risk of air embolism. if feeding. The catheter tip should lie in the superior vena cava above the pericardial reflection. a) bleeding from the upper gastrointestinal tract.palpate artery and ensure needle is lateral to it. follow the Seldinger approach. 2. 5. Patient has a cervical spine injury 2. Adopt full asepsis. slightly cephalad. The subclavian vein (SVC) may be preferred for central venous access if 1. Base of skull fracture 2. sit patient upright for optimal neck/stomach alignment with the head forward. Gather equipment. Severe facial injury The cuffed endotracheal and tracheostomy tubes should be deflated prior to nasogastric tube insertion. Explain the procedure to the patient and show equipment. Oesophageal tear 3. 5. Place the patient in a supine position. Don non-sterile gloves. 3. 8FG) because it is more comfortable in the long term. The external jugular vein joins the SCV at the midpoint of the clavicle. transduce needle before dilating and passing central line into vessel. Chylothorax. Deflate the endotracheal tube or tracheostomy cuff 6. Line is for long-term use e.4. This site may be more comfortable for the patient. a smaller tube may be used (eg. particularly in patients at risk of hepatic encephalopathy therapeutic and prophylactic decompression after major abdominal surgery prevention of further soilage after gastric perforation prevention of anastomotic rupture after gastric surgery prevention of obstruction of the operative field by air in the stomach Nutrition a) patients with dysphagia b) comatose or weak patients 4. 6. haematemesis b) pentagastrin studies (rarely done now) 2. 8. feeding. Complications As listed for internal jugular venous cannulation.Avoid cannulating the vein on the left side as the thoracic duct lies there. and posteriorly behind the clavicle toward the suprasternal notch. head-down. Introduce a needle attached to a 10 ml syringe. or remove syringe from needle and ensure blood is venous. PRE-PROCEDURE 1. . Surface mark the subclavian vein 1 cm below the junction of the middle and medial thirds of the clavicle. 5.g. use as large a tube as possible to reduce the risk of blocking during use or the formation of a false passage during introduction. 4. When a free flow of blood appears. Lavage a) poisoning b) gastrointestinal bleeding CONTRAINDICATIONS 1. 4. If possible. Turn the head to the contralateral side (if C-spine injury excluded). Carotid artery puncture/cannulation . The SCV passes over the first rib anterior to the subclavian artery. dialysis. 2. prop the patient up at 45 degrees. Determine the size of the nasogastric tube required (usually 14 – 16FG). Otherwise. The risk of pneumothorax is far greater with this technique. 112 Decompresssion a) b) c) d) e) f) g) CANNULATION OF THE SUBCLAVIAN VEIN The SCV is the continuation of the axillary vein and originates at the lateral border of the first rib. Damage to the subclavian artery may occur. direct pressure cannot be applied to prevent bleeding. Ensure that a chest X-ray is ordered. to join with the internal jugular vein at the medial end of the clavicle. Slowly advance the needle while gently withdrawing the plunger. 3. as detailed previously. 7. 6. If aspirating. or use ultrasound-guided placement. intestinal obstruction pyloric stenosis haematemesis. Direct the needle medially. Perform check chest X-ray to confirm position and exclude pneumothorax. Diagnostic 3. to identify the position of the line and to exclude pneumothorax. Anatomy of the SCV Technique 1. Catheter-related sepsis NASOGASTRIC TUBE INDICATIONS 1. coiling and reentry into the oesophagus (rare). if the tube coils in the mouth. 10. 2. especially sodium. Mark the Mark measured length with a marker or note the distance. 5. chloride and hydrogen ions. If for suction. Examine nostrils for deformity/obstructions (eg. rotate the tube slowly with downward advancement towards the closer ear. gastroesophageal reflux due to functional incompetence of the lower oesophageal sphincter. dislodgement perforation of the pharynx and oesophagus. bend his head to elicit a swallowing reflex. Document the reason for the tube insertion. the nature and amount of drainage. oesophagus or the external nares. Loss of fluids and electrolytes. PROBLEMS AND COMPLICATIONS 1. Lubricate tube with water. auscultating the epigastrium while injecting air through the tube. type & size of tube. Secure the tube with adhesive tape. 5. 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. Advance the tube until mark is reached (approximately 40cm). 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. Do not force the tube down against resistance as this may form a false passage. the type of suction and pressure setting if for suction. Instruct the patient to swallow (you may offer ice chips/water if not contraindicated) and advance the tube as the patient swallows. traumatic haemorrhage of varices. remove the syringe from the free end of the tube. 4. or if the patient begins to cough or turns pretty colours. Dry mouth and parotitis due to fluid loss and mouth breathing. There should not be resistance. 3. erosions of the oesophagus leading to strictures. or obtaining an x-ray to verify placement before instilling any feedings/medications or if you have concerns about the placement of the tube. Technical a) b) c) d) e) insertion into the trachea. and the effectiveness of the intervention. 6. Withdraw the tube immediately if changes occur in the patient's respiratory status. resulting in choking. the nature and amount of aspirate. Resistance may be felt as tip reaches the nasopharynx. the McGill’s forceps may be used to guide the tube down. The nose may be lubricated with lignocaine gel.113 PROCEDURE 1. If patient is uncooperative. connect to suction. 11. passing the tube along the floor of the nose. 13. Select the largest nostril for inserting the tube. Introduce the tube through the nostril. 4. If resistance is met. set machine on type of suction and pressure as prescribed. 9. trauma to the nose and the pharynx. potassium. choanal stenosis) to determine best side for insertion. Re-inflate the endotracheal tube or tracheostomy cuff if necessary. Stop. Continue to advance the tube down the oesophagus. which is the most uncomfortable part of the procedure. Gastrointestinal a) b) c) d) e) gastric erosions pressure necrosis of the pharynx. 12. 2. 7. 8. In the operation theatre. . Lung complications a) decreased ventilation b) aspiration pneumonia 3. when the patient is under general anaesthesia. Swallowing of small sips of water may enhance passage of tube into esophagus. TRACHEOSTOMY INDICATIONS FOR TRACHEOSTOMY 1. Maintenance of airway patency. 2. Protection of the airway from aspiration. 3. Application of positive pressure to the airway. 4. Facilitation of secretion clearance. 5. Delivery of high oxygen concentrations. RELATIVE CONTRAINDICATIONS 1. Evidence of infection in the soft tissues of the neck at the prospective surgical site. 2. Medically uncorrectable bleeding diatheses. 3. Gross distortion of the neck anatomy due to hematoma, tumour, thyromegaly, high innominate artery or scarring from previous neck surgery. 4. Documented or clinically suspected tracheomalacia. 5. Need for positive end-expiratory pressure (PEEP) of more than 15 cm of water. 6. Patient obesity with short neck that obscures neck landmarks. 7. Patient age younger than 15 years. TYPES OF TRACHEOTOMY 1. Temporary: Portex (cuffed). 2. Permanent: Consist of inner and outer tubes made of stainless steel. Tracheostomy is more useful in the elective setting compared to endotracheal intubation because: 1. Better tolerated. 2. Avoids risk of laryngeal stenosis 3. Avoids risk of endotracheal obstruction. PROCEDURE 1. Position the patient. Place rolled towel under the patient’s neck to hyperextend the neck for better exposure. 2. Clean and drape. Clean the skin of the neck from the chin to the suprasternal notch and laterally to the base of the neck and clavicles. Drape field. 3. Identify anatomical landmarks (thyroid cartilage, cricoid cartilage). 4. Administer local anaethesia. 5. Incise skin. In the emergency setting, make a vertical incision 3cm from cricoid cartilage downwards. In the elective setting, make a tranverse incision 4cm wide, 3cm above the suprasternal notch. 6. Dissect through the subcutaneous layers and platysma. 7. Identify the communicating branch of the anterior jugular vein, clamp and ligate the artery (ignore this in an emergency). 114 8. Visualise the thyroid isthmus and retract isthmus. 9. Retract cricoid cartilage upwards wth cricoid hook. 10. Incise the trachea between the 2nd and 3rd tracheal rings, making an inverted U-flap incision. 11. Insert tracheal dilator through the tracheostoma and remove the cricoid hooks. 12. Suction of blood and secretions in the lumen. 13. Insert the tracheostomy tube. 14. Remove the obturator and insert the inner cannula. 15. Dress wound and secure to the neck using sutures and adhesive tape. COMPLICATIONS During Procedure 1. Bleeding if damage to the innominate or inferior thyroid artery. 2. Damage to surrounding structures, eg esophagus, recurrent laryngeal nerve, brachiocephalic vein. 3. Pneumothorax. 4. Pneumomediastinum. Immediate post-op 1. 2. 3. 4. 5. Surgical emphysema. Obstruction, eg clot, mucus. Bleeding. Dislodgment. Subcutaneous emphysema. Late post-op 1. 2. 3. 4. 5. 6. 7. Infection . Obstruction, eg dislodgment of tube, crust formation from secretions. Tracheo-esophageal fistula. Tracheal stenosis. Wound breakdown. Scarring. Tracheomalacia. POST-OP CARE 1. Position patient in a propped up position. 2. Prevent obstruction by suction, saline irrigation, mucolytic agents (mucomyst, guaifenesin) and humidified air. 3. Change Portex tube every 3rd day and remove the inner tube for cleaning everyday. 4. Unlock the metal tube every night so that the patient can cough it out if it becomes obstructed. 115 SENGSTAKEN-BLAKEMORE TUBE (OR MINNESOTA TUBE) URINARY CATHETERISATION INDICATIONS Oesophageal varices INDICATIONS FOR SHORT-TERM CATHETERISATION 1. Relief of acute retention of urine, e.g. benign prostatic hypertrophy, bladder outflow obstruction. 2. Bladder washout, e.g. blood clots causing acute retention of urine. 3. Cystourethrogram. 4. Administration of intra-vesical drugs. 5. As an adjunctive measure pre/post-operatively a) Pre-operatively: (i) to drain the bladder so as to improve access to the pelvis in urologic or pelvic surgery. (ii) to allow accurate measurement of urine output in major surgery. b) Post-operatively: (i) to relieve acute urinary retention because post –op pain results in failure of the sphincter to relax. 6. Urinary output monitoring, e.g. in patient with hypovolaemic shock or the critically ill. CONTRAINDICATIONS 1. Base of skull fracture 2. Oesophageal tear 3. Severe facial injury PROCEDURE 1. Measure the length of the tube. Test balloons. Test patency of the tube. 2. Sit the patient upright or at 45 degrees. 3. Apply local anaesthesia (lignocaine nasal spray). 4. Lubricate and insert the tube through the nose, asking the patient to swallow or drink water to aid in smoother passage of the tube through the pharynx and oesophagus. 5. Inflate the gastric balloon slowly with 100-150ml saline. 6. Check that the tube is in the stomach by: (i) aspirating fluid and testing it with litmus, (ii) auscultating the epigastrium while injecting air, or (iii) doing an X-ray. 7. Traction. 8. Inflate the oesophageal balloon to 35 – 45mmHg: use the Y-connector piece with one arm to the BP set and the other to the syringe to pump in air. 9. Aspirate fluid from the oesophagus through the Ryle’s tube, or if using the Minnesota tube, use the additional lumen provided (with the additional lumen for aspirating fluid in the oesophagus, the Minnesota tube decreases the likelihood of aspiration pneumonia occurring). 10. Check the oesophageal balloon pressure hourly and release 5mins hourly. 11. Release oeophageal balloon after 24hrs. 12. Release gastric balloon after 48hrs. 13. The tube should not be used for more than 72hrs. COMPLICATIONS 1. Aspiration pneumonia 2. Respiratory obstruction 3. Oesophageal ulceration and rupture 4. Rebleeding 5. Gastric varices not controlled INDICATIONS FOR LONG-TERM INDWELLING CATHETERIZATION 1. Refractory bladder outlet obstruction. 2. Chronic retention of urine, eg. neurogenic bladder. 3. Incontinence, e.g. in palliative care of terminally ill or patient’s preference. CONTRAINDICATIONS 1. Presence of urethral injury, as manifested by: a) blood from the meatus, b) scrotal haematoma, c) pelvic fracture, or d) high-riding prostate, elicited from a genital and digital rectal examination. (alternative: suprapubic drainage) 2. Urinary tract infection, as an indwelling catheter causes difficulty in treatment. PROCEDURE 1. Gather equipment. 2. Explain procedure to the patient. Maximize patient’s privacy. Have a chaperone if performing the procedure on a member of the opposite sex. 3. Assist patient into supine position with legs spread and feet together. 4. Open the catheterization kit and catheter. 5. 6. 7. 8. Prepare sterile field. Don the sterile gloves from the kit. Test the balloon at the tip of the catheter. Generously coat the distal portion (2 - 5cm) of the catheter with lubricant. Using the non-dominant hand to come in contact with the patient and the dominant hand to use items from the kit (recall that once your hand comes in contact with the patient, it is no longer sterile and cannot be used to obtain items from the kit), cleanse the peri-urethral mucosa with antiseptic-drenched swabs held by forceps. Cleanse anterior to posterior, inner to outer, one swipe per swab, discard swab away from sterile field. a) Male: Hold the penis and retract the foreskin. Swab the penis and surrounding area, making sure to cleanse beneath the foreskin. b) Female: Retract the labia majora. Swab the perineum. 9. Apply sterile drape. 10. Installation of local anaesthesia. a) Male: (i) Smear lignocaine gel around the meatus and apply the gel gently into urethra. (ii) Massage gel carefully down the urethra to sphincter, squeezing the meatus shut (iii) Wait for for 5 minutes (alternatively, with less anaesthetic effect, smear gel over the catheter tip). b) Female: (i) Apply lignocaine gel to urethra or catheter tip. 11. In the male, lift the penis to a position perpendicular to patient's body and apply light upward traction (with non-dominant hand); in the female, expose the external urethral orifice. 12. Gently insert tip of catheter into the meatus using forceps until 1 to 2 inches beyond where urine is noted to drain into kidney dish. If no urine appears although the catheter seems to be in the right place, flush with sterile saline as the lumen may be blocked with gel. If this is still unsuccessful, withdraw and reinsert. 13. Inflate balloon, using correct amount of sterile saline (usually 20 – 30mls but check actual balloon size). This process should be painless. If patient feels pain, deflate balloon immediately and reposition catheter. 14. Gently pull catheter until inflation balloon is snug against bladder neck. 15. Connect catheter to drainage system. 16. Secure catheter to abdomen or thigh, without tension on tubing. 17. Place drainage bag below level of bladder. 18. Evaluate catheter function and amount, color, odour and quality of urine. 116 19. Remove gloves. Dispose equipment appropriately. Wash hands. 20. Document size of catheter inserted, amount of water in balloon, patient's response to procedure and assessment of urine. COMPLICATIONS 1. Infection, which may lead to stone formation. 2. Stricture formation due either to faulty technique or an irritant material used in the catheter. 3. Creation of a false passage due to wrong technique of insertion. 4. Occasionally, irritation of the bladder may cause severe bladder spasms. CHEST TUBE Chest tubes are inserted to drain blood, fluid, or air and allow full expansion of the lungs. The tube is placed between the ribs and into the space pleural space. The area where the tube will be inserted is anesthetized locally. The patient may also be sedated. The chest tube is inserted through an incision between the ribs into the chest and is connected to a bottle or canister that contains sterile water (underwater seal). Suction is attached to the system to encourage drainage. A suture and adhesive tape is used to keep the tube in place. The chest tube usually remains in place until the X-rays show that all the blood, fluid, or air has drained from the chest and the lung has fully re-expanded. When the chest tube is no longer needed, it can be easily removed, usually without the need for medications to sedate or numb the patient. Antibiotics may be used to prevent or treat infection. INDICATIONS 1. Pneumothorax. 2. Hemothorax. 3. Drainage of pleural effusion. 4. Chylothorax 5. Drainage of empyema/lung abcesses 6. Prophylactic placement of chest tubes in a patient with suspected chest trauma before transport to specialized trauma center CONTRAINDICATIONS 1. Infection over insertion site 2. Uncontrolled bleeding diathesis/coagulopathy 5. Locate the triangle of safety. Laceration or puncture of the intrathoracic and/or abdominal organs. 3. Scalpel blade & handle 4. 6. and prevent normal fluids from collecting in the lungs. 6. 10. Look for fogging of the chest tube with expiration or listen to air movement. COMPLICATIONS 1. etc. Frequent deep breathing and coughing is necessary to help re-expand the lung. and need for additional oxygen. Inform the patient of the possibility of major complications and their treatment 3. assist with drainage. 25. Suture the tube in place. While the chest tube is in place. 3. Determine the site of insertion. 2. 5. 8. Locally anaesthetized the skin and rib periosteum. 11. Anaphylactic or allergic reaction to surgical preparation or anaesthesia. 2. depending on clinical setting) 12. 5th or 6th intercostal space. just over the top of the rib. Recovery from the chest tube insertion and removal is usually complete. 9. Suction apparatus (Pleuravac)/underwater seal apparatus 11. Subcutaneous emphysema. Do a chest X ray 12. clots. Introduction of pleural infection. 1% lignocaine with epinephrine. Explain the major steps of the procedure. Incorrect intrathoracic or extrathoracic tube position. Connect the end of the chest tube to an underwater seal apparatus. imaginary vertical line between the anterior and mid axillary lines. artery or vein. 10. Apply a dressing and tape the tube to the chest. bronchoscopy required. Damage to the intercostals nerve. The patient will stay in the hospital until the chest tube is removed. 7. Sterile drapes & gloves 3. bounded by the lateral border of the pectoris major. Make a 2-3cm transverse incision at the predetermined site and bluntly dissect through the subcutaneous tissues. all of which can be prevented by using the finger technique before inserting the chest tube. Silk suture 6. Lungs fail to expand due to plugged bronchus. . Surgically prepare and drape the chest at the predetermined site of the tube insertion. Persistent pneumothorax 7. 8. 10 cc syringe. Obtain informed consent 2. Petrolatum-impregnated gauze 8. breathing difficulties. with only a small scar. Chest tube (size 32 to 40 Fr. the nursing staff will carefully check for possible air leaks. 4. Tape 10. clogging or dislodging from the chest wall or disconnection from the underwater seal apparatus.117 MATERIALS 1. Clamp 5. Clamp the proximal end of the chest tube and advance the tube into the pleural space to the desired length. Sterile gauze 9. Iodine & alcohol swabs for skin prep 2. 4. 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. usually at tube site.& 22-g needles PRE-PROCEDURE PATIENT EDUCATION 1. Obtain arterial blood gas values and/or institute pulse oximetry monitoring as necessary. and necessity for repeated chest radiographs PROCEDURE 1. Needle holder 7. 9. Recurrence of pneumothorax upon removal of the chest tube. Chest tube kinking.
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