Andre Surgery notes (ed 3, 2013) w Washington+ChinYee

SURGERY Jeremy Chee Faith Leong (Information from Washington added on to ChinYeeedited-Andre’s) 2013 spellchecked version

Pre-operative Care Peri-Operative Principles General Anesthesia Local and General Anesthesia Blood Products Post-Operative Care Fluid Management Surgical Nutrition Post-Op Pyrexia Post-Op Pulmonary Problems Cardiovascular Problems Wound dehiscence Other Post-Op Complications Surgical Techniques Wound Healing Suturing and Skin Closure Surgical Drains Surgical Dressings Abdomen Abdominal Trauma Abdominal Incisions Abdominal Masses Approach to Abdominal Masses Approach to Abdominal Pain Acute Appendicitis Perforated Ulcer Mesenteric Ischemia Approach to Intestinal Obstruction Small Bowel Obstruction Large Bowel Obstruction Approach to Bleeding GIT Upper BGIT Lower BGIT Variceal Bleed Groin Hernia Groin Lumps Abdominal Stomas Upper GI The Esophagus Approach to Dysphagia GERD Barrett’s Esophagus

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Achalasia Esophageal Cancer Peptic Ulcer Disease Gastric Carcinoma Hepatobiliary and Pancreas Approach to Jaundice Approach to Cirrhosis Approach to Ascites Gallstones Acute Cholecystitis Choledocholithiasis Mirizzi’s Syndrome Cholangitis Recurrent Pyogenic Cholangitis Cholangiocarcinoma Acute Pancreatitis Chronic Pancreatitis Pancreatic Carcinoma Liver Hemangioma Simple Liver Cyst Hepatocellular Carcinoma Liver Metastases Pyogenic Liver Abscess Amoebic Liver Abscess Colorectal Inflammatory Bowel Disease Benign Colonic Polyps which may not be so benign Familial Adenomatous Polyposis, Hereditary Non-polyposis Colorectal Cancer Colorectal Carcinoma Diverticular Disease Hemorrhoids Anal Fistulae Anal Fissures Breast Breast Assessment Approach to Breast Lump Approach to Nipple Discharge Breast Pain Breast Cancer Gynaecomastia Paget’s Disease of the Nipple

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Lumps and Bumps Approach to Lumps and Bumps Lipoma Sebaceous Cyst Ganglion Basal Cell Carcinoma Squamous Cell Carcinoma Malignant Melanoma Neurofibroma Dermoid Cyst Seborrhoeic Keratosis Hemangioma Kaposi’s Sarcoma Fibrosarcoma Neck Lumps Anatomy of the Neck Cervical Lymphadenopathy Salivary Glands Salivary Gland Swellings Approach to Salivary Gland Swellings Sialolithiasis Salivary Gland Tumours Thyroid Thyrotoxicosis Thyroglossal Cysts Thyroid Gland Multiple Endocrine Neoplasia Surgery in Thyroid Disease Vascular Anatomy of Lower Limb Arteries Arterial Assessment Acute Limb Ischemia Chronic Limb Ischemia Treatment of Chronic Limb Ischaemia Diabetic Foot Abdominal Aortic Aneurysm Varicose Veins Venous Ulceration Venous Thrombosis

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! PERIOPERATIVE PRINCIPLES ASA Grading • Medical co-morbidity increases risk a/w anaesthesia & surgery • ASA accurately predicts morbidity and mortality • 50% of patients presenting for elective surgery are ASA grade 1 • Operative mortality for these patients is less than 1 in 10,000. Grade Definition I Normal healthy individual II Mild systemic disease that does not limit activity Severe systemic disease that limits activity but is III not incapacitating Incapacitating systemic disease which is IV constantly life-threatening Moribund, not expected to survive 24 hours with V or without surgery

Mortality (%) 0.05 0.4 4.5 25 50

Respiratory function • Lung function tests predict the type and severity of lung disease • Can predict risk of complications and postoperative mortality • Tests fall in to three categories o Lung volumes (spirometry) o Airway caliber (peak flow rate) o Gas transfer (ABG) • Arterial blood gases may be invaluable Cardiac function • Chest x-ray (presence of cardiorespiratory symptoms or signs) • ECG (ischemia or previous infarct) • Echocardiography (cardio anatomy and function) • Exercise test Renal function • Glomerular filtration rate is the gold standard test of renal function • Can be calculated by measuring creatinine clearance rate • Requires 24-hour urine collection • Use of serum creatinine may be inaccurate in patients with: o Obesity, Oedema, Pregnancy, Ascites

PRE-OPERATIVE CARE

Pre-operative Investigations The request for pre-operative investigations should be based on: • Factors apparent from the clinical assessment • The likelihood of asymptomatic abnormalities • The severity of the surgery contemplated • 5% of patients have abnormalities on investigations not predicted • 0.1% of these investigations ever change the patients management • 70% of pre-operative investigations eliminated without adverse effect Investigations: • CXR • ECG • FBC • PT/PTT • U/E/Cr • Random blood glucose • Urinalysis • Blood gases (ABG) • Lung function tests

Recommendations are based on: • Age • ASA Grade of patient • Grade of surgery

Preoperative anaemia • Tissue oxygenation is dependent on o Arterial oxygen content o Capillary blood flow o Position on the oxygen dissociation curve • Haemoglobin concentration affects all of these factors o Anaemia reduces arterial oxygen content o Reduced plasma viscosity increases capillary blood flow o Increases 2,3 DPG and shifts dissociation curve to the right • Both anaemia and polycythaemia increase postoperative mortality • Perioperative haemoglobin concentration of approximately 10 g/dl is ideal

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! Anaesthetic Risk

Operative Risk

Conditions rendering patients at increased anaesthetic risk • Difficult airway • Obesity o HDU bed post op o Increased M&M • Cardiac disease o Revised cardiac risk index  High-risk surgery  Ischaemic heart disease  At least 6 months after AMI  risk of post op AMI  History of congestive heart failure  History of cerebrovascular disease  Insulin therapy for diabetes mellitus  Renal impairment o Hypertension  Assess degree of HTN and end organ damage • Respiratory disease o Bronchospasm o URTI o Atelectasis o Smoking o Bronchopneumonia o Hypoxaemia o Respiratory failure o Pulmonary embolism • Gastrointestinal disease o GERD o Liver function • Renal failure • Diabetes o Wound healing and infections • Haematological disorders • Allergic reactions

As above, and:

PRE-OPERATIVE CARE

Obstructive Jaundice • Coagulation disorders o Reduces the absorption of fat soluble vitamins o Reduces production of factors II, VII, IX, X o Disorders can be reversed with Fresh Frozen Plasma or Vitamin K • Reduced wound healing • Increased risk of infection • Hepato-renal syndrome o Acute renal failure in patient with jaundice o Probably due to systemic endotoxaemia o Requires adequate hydration and diuretics o Value of mannitol unproven • Altered drug metabolism o Half-life of many analgesics is prolonged (e.g. morphine). Chronic renal failure • Chronic renal failure affects multiple organ systems • Effects that need to be considered by both surgeons and anaesthetists include o Electrolyte disturbances o Impaired acid-base balance o Anaemia o Coagulopathy o Impaired autonomic regulation o Protection of veins, shunts and fistulae

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! Pre-Op Assessment • • •

Reduce morbidity and mortality associated with surgery Prevent unnecessary cancellations Reduce hospital stay

Aim of preoperative planning • Obtain informed consent for the procedure • Assess pre-existing medical conditions • Plan pre and postoperative management of these conditions Issues that should be discussed • Time of admission and starving instructions • Management of usual medication • Any specific pre-operative preparation that may be required • Transport to theatre • Any specific anaesthetic issues • Anticipated duration of surgery • Likely recovery period • Need for drains, catheters • Likely discharge date • Need for dressing change or specific postoperative care • Follow up requirements • Likely date of return to work or full activity Important medical diseases that increase morbidity and mortality • Ischaemic heart disease • Diabetes mellitus • Congestive cardiac failure • Endocrine dysfunction • Hypertension • Chronic renal failure • Cardiac arrhythmias • Nephrotic syndrome • Chronic respiratory disease • Obstructive jaundice Advantages of pre-admission clinic • Allows pre-operative optimisation of patients • Reduces duration of hospital stay • Reduces risk of unnecessary cancellations • Guidelines minimise unnecessary preoperative investigations

PRE-OPERATIVE CARE

Informed consent • • •

Patients autonomy must be respected at all times This could adversely affect outcome or result in their death Patients must be given sufficient information to make these decisions

Types of consent • Express consent - oral or written o Needed for most investigations or treatments with risks attached o e.g. consent for operation • Implied consent o Non-written consent when patient co-operates with a particular action o e.g. physical examination Information required for valid consent • When obtaining consent patients should be informed of: o Details of diagnosis and prognosis with and without treatment o Uncertainties about the diagnosis o Options available for treatment o The purpose of a proposed investigation or treatment o The likely benefits and probability of success o Any possible side effects o A reminder that the patient can change his or her mind at any stage o A reminder that the patient has the right to a second opinion • The person who obtains consent must be: o Suitably trained and qualified o Have sufficient knowledge of the proposed treatment and its risks Children • At age of 16 years a child can be presumed to have the capacity to decide on treatment • Below the age of 16 years the child may have the capacity to decide depending on their ability to understand what the treatment involves • If a competent child refuses treatment a person with parental responsibility may authorise treatment which is in the child's best interests

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! Premedication and Induction Principles of premedication • Anxiolysis • Analgesia • Amnesia • Antiemetic • Antacid • Anti-autonomic • Adjuncts Induction • Induction agents are usually administered intravenously • Distributed to organs with a high blood flow (e.g. brain) • Have rapid onset and without maintenance would have rapid recovery Perioperative Monitoring Airway management • General anaesthesia removes muscle tone • Methods of maintaining airway include o Manual methods (e.g. Jaw thrust) o Endotracheal tube Complications of endotracheal intubation • Failure to intubate & loss of airway control • • Unrecognised oesophageal intubation • • Accidental intubation of a main bronchus • • Trauma to the larynx, trachea or teeth

Pulmonary aspiration Disconnection or blockage of the tube Tracheal stenosis

Hypothermia • Hypothermia develops rapidly during general anaesthesia • Heat loss can be reduced by use of: o Warming blanket o Warm intravenous fluids o Warm fluid to irrigate body cavities o Forced air warming

Monitoring during anaesthesia • Accurate monitoring of vital signs • Facilities for cardiopulmonary resuscitation • Monitoring of the following is considered essential for all patients: o Temperature o Oxygen content of o Heart rate inspiratory gas mix o Blood pressure o End-tidal carbon dioxide o ECG o Pulse oximetry • Alarms should indicate o Oxygen supply failure o Ventilator disconnection • The following may be considered for major surgery o Invasive blood pressure monitoring o Central venous pressure o Urine output Recovery from anaesthesia • Causes of failure to breath after general anaesthesia include: o Obstruction of airway o Central sedation due to opiates or anaesthetic agent o Hypoxia o Hypercarbia o Hypocarbia due to overventilation o Persistent neuromuscular blockade o Pneumothorax o Circulatory failure leading to respiratory arrest Postoperative nausea and vomiting Mechanisms of postoperative nausea and vomiting • Chemoreceptor trigger zone • Vestibular apparatus • Vagal sensory neural endings

Prevent Injury • Ensure patient is appropriately fastened to table • Movement of patient should be coordinated Preserve Circulation

PRE-OPERATIVE CARE

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! GENERAL ANAESTHESIA Ideal inhalational anaesthetic agent Preparation • Easily administered • Boiling point above ambient temperature • Low latent heat of vaporization • Chemically stable • Compatible with soda-lime, metals and plastics • Non-flammable • Cheap • Pharmacodynamic • High potency - allows high FiO2 • High therapeutic index • Analgesic

Pharmacokinetic • Low solubility • Rapid onset, rapid offset, adjustable depth • Minimal metabolism • Predictable in all age groups Adverse actions • Minimal toxicity • Minimal unwanted effects nausea, vomiting, cardiac arrhythmias • No toxicity with chronic lowlevel exposure of staff

Adverse effects of inhalational anaesthetic agents Cardiovascular Central nervous system • Decreased myocardial contractility • Increased cerebral blood flow • Reduced cardiac output • Reduced cerebral • Hypotension metabolic rate • Arrhythmias • Increased risk of epilepsy • Increased myocardial sensitivity to • Increased ICP catecholamines Respiratory • Depress ventilation • Laryngospasm and airway obstruction • Decreased ventilatory response to hypoxia and hypercapnia • Bronchodilatation

PRE-OPERATIVE CARE

Others • Decreased renal blood flow • Stimulate nausea and vomiting • Precipitate hepatitis

Maintenance of anaesthesia • Balanced anaesthesia has three aspects to it o Hypnosis = suppression of consciousness o Analgesia = suppression of physiological responses to stimuli o Relaxation = suppression of muscle tone and relaxation • MAC = Minimum alveolar concentration (required to keep 50% of population unresponsive) Specific anaesthetic agents Halothane • Potent anaesthetic but poor analgesic agent (MAC = 0.75) • Can be used for gaseous induction in children Isoflurane • Potent anaesthetic but poor analgesic agent (MAC = 1.05) • Less cardiotoxic but causes greater respiratory depression Nitrous oxide • Weak anaesthetic agent (MAC = 103) • Cannot be used as an anaesthetic agent alone without causing hypoxia • Used in anaesthesia mainly for its analgesic properties Muscle relaxants Depolarizing agents (suxamethonium) • Used during induction of anaesthesia • Side effects: o Histamine release producing a 'scoline rash' o Bradycardia o Somatic pain resulting from fasciculation o Hyperkalaemia o Persistent neuromuscular blockade = 'scoline apnoea' o Malignant hyperpyrexia o Increased intra-ocular pressure o Increased gastric pressure Non-depolarizing agents (vecuronium) • Act over 2-3 minutes and effects last for 30 minutes to one hour • Competitive antagonism of acetylcholine receptor • Used for muscle relaxation

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! LOCAL AND REGIONAL ANESTHESIA Local anaesthesia • Reduces membrane permeability to sodium • Act on small unmyelinated C fibres before large A fibres • Reduce pain and temperature sensation before touch and power Lignocaine • Lignocaine is a weak base (pKa=7.8) • Has a duration of action of about one hour o With addition of adrenaline duration of action increased to 2 hrs • Main toxicity is on central nervous and cardiovascular systems • Plain lignocaine should be used for local anaesthesia in digits and appendages (adrenaline containing solutions can cause tissue ischaemia)

Postoperative epidural infusions • Attenuates postoperative stress response • Improves postoperative pain control • Reduces incidence of postoperative pulmonary complications • Allows more rapid return of gastrointestinal function • Reduces duration of hospital stay Opioid alone • Allows opioid analgesia without sedation • No motor or sympathetic blockade • Itch is common • Serious respiratory depression can occurs after stopping infusion Combination of LA and opioid • Synergy between sites of action • Reduced doses of both drugs • Optimal analgesia possible

PRE-OPERATIVE CARE

Local anaesthetic alone • Potential for complete anaesthesia • No sedative effects or respiratory depression • Sympathetic and motor blockade are common • Cardiovascular side effects can occur

Spinal and epidural anaesthesia • Spinal anaesthesia - local anaesthetic or opiate into CSF below termination of cord at L1 • Epidural anaesthesia - local anaesthetic or opiate into fatty epidural space • Both can produce good anaesthesia for up to 2 hours • The quality of the block is often better with a spinal • Epidural anaesthesia is technically more demanding Contraindications • Pre-existing neurological disease • Coagulopathy Complications Timing Characteristic Hypotension Immediate LA toxicity High Blockade Urinary retention Headache Local infection Early Meningism Epidural haematoma Backache

Spinal Common Rare Occasional Common 1-5% Almost never Uncommon Almost never Common

Epidural Less common Occasional Occasional Less common Never unless dural puncture Uncommon Very rare Very rare Common

Hypotension • Sympathetic outflow form spinal cord occurs between T1 and L2 • Blocked to varying degrees in both spinal and epidural anaesthesia • In hypovolaemic patients there is a greater risk of hypotension • Hypotension during spinal and epidural anaesthesia usually requires fluid resuscitation Post spinal headache • Seen following in 1 - 5% of spinal anaesthetics, usually due to CSF leak • In most patients is settles after about 3 days • Headache is characteristically occipital, worse on standing and relieved by lying down • Initial treatment is with bed rest, simple analgesia and fluids • If persists consider 'blood-patch' (patient’s own blood injected into epidural space)

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! BLOOD PRODUCTS Cross Matching Blood grouping • Patients red cells grouped for ABO and Rhesus antigens • Serum tested to confirm patients ABO group Antibody screening • Detects atypical red cell antibodies in recipients serum Crossmatching • Tests donor red cells against patients serum Blood products • Whole blood • Packed red cells • Granulocyte concentrates • Platelet concentrates • Human plasma - fresh frozen plasma / freeze-dried plasma • Plasma protein fraction • Human albumin 25% • Cryoprecipitate • Clotting factors - Factor VIII / IX • Immunoglobulins Complications of blood transfusion Early • Haemolytic reactions (immediate or delayed) • Bacterial infections from contamination • Allergic reactions to white cells or platelets • Pyogenic reactions Late • Infection - cytomegalovirus / hepatitis • Immune sensitization • Iron overload

PRE-OPERATIVE CARE

• • • • • •

Circulatory overload Air embolism Thrombophlebitis Citrate toxicity Hyperkalaemia Clotting abnormalities

Acute haemolytic or bacterial transfusion reactions • Due to acute haemolysis or bacterial contamination • May occur after infusion of small volume of incompatible or infected blood • Associated with high morbidity and mortality • In unconscious patient bleeding due to DIC may be only sign • Most ABO mismatched transfusions are due to human error o Usually occurs soon after start of transfusion o Patient feels unwell and agitated o Symptoms include back pain and pain at infusion site o Associated with shortness of breath, rigors o Examination will show hypotension, oliguria and bleeding from venepuncture sites o Urinalysis will show haemoglobinuria Management • Discontinue transfusion immediately and remove giving set • Check unit of blood against patients identity • Give intravenous crystalloid • Consider transfer to the intensive care unit • Take blood for FBC, plasma haemoglobin, clotting, blood cultures and repeat grouping • Give broad spectrum antibiotics • Monitor urine output and ECG Anaphylaxis • Usually occurs soon after start of transfusion • May be seen in IgA deficient patients reacting to transfused IgA • Presents with circulatory collapse and bronchospasm Management • Discontinue transfusion and remove giving set • Maintain airway and give oxygen • Administer adrenaline, chlorpheniramine, salbutamol • If the patient is IgA deficient any further transfusion must be carefully planned

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! FLUID MANAGEMENT Daily requirements For the ‘average’ 70 Kg man • Total body water 60% of body weight • 40% is in the intracellular and 20% in the extracellular compartments • The plasma volume is 7% • The extravascular volume is 13% + • Total body Na is 4200 mmol (50% in ECF) + • Total body K is 3500 mmol (only about 50-60 mmol in ECF) • Normal osmolality of ECF is 280 –295 mosmol/kg Fluid replacement Fluid replacement = fluid deficit + maintenance fluid + ongoing losses *70ml of blood per kg

Composition of crystalloids Hartmann’s N/S Dextrose Sodium (mmol/l) 131 150 30 Chloride (mmol/l) 111 150 30 Potassium 5 Nil Nil (mmol/l) Lactate (mmol/l) 29 Nil Nil Calcium (mmol/l) 2 Nil Nil • 3L of Dextrose saline is not equivalent to 2L 5% Dextrose and 1L Normal saline • 3L Dextrose Saline = 3L water and 90 mmol sodium • 2L 5% Dextrose saline + 1L Normal saline = 3L water and 154 mmol sodium •

Fluid deficit • Fluid deficit in dehydration (ml/l) = body weight x % dehydration Maintenance requirements • Daily maintenance fluid requirements (Holliday-Segar formula) o 0-10 kg is 100 ml/kg/day o 10-20 kg is 1000 ml + 50 ml/kg for each kg > 10 o >20 kg is 1500 ml + 25 ml/kg for each kg > 20 Replacement of losses • Pre-operative or pre-admission o Ongoing losses o Nasogastric aspirate o Vomit, diarrhoea o Stoma, drains, fistula etc. • Most ‘surgical ‘ ongoing losses are rich in sodium and should be replaced with 0.9% saline Insensible losses • Faeces approximately 100 ml/ day • Lungs approximately 400 ml/ day • Skin approximately 600 ml/ day

POST-OPERATIVE CARE

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0.45% saline/5% dextrose for replacement and maintenance needs o Maintenance + replacement fluid over 24hr st o ½ given in 1 8hr, ½ over the next 16 hrs in acute GE o Replacement slower in meningitis and DKA 0.22% saline/5% dextrose used for maintenance in patients with renal, liver, cardiac failure Isotonic 0.9% saline used for resuscitation o Fluid bolus 20ml/kg over 20 min for severe dehydration

Electrolyte requirements • Na: 2-3 mmol/kg/day • K: 1-2 mmol/kg/day • Ca: 3-5 mmol/kg/day • Glucose: 3 g/kg/day Assessment of adequacy of resuscitation • Clinical history and observations – Pulse, blood pressure, skin turgor • Urine output – oliguria < 0.5 ml/kg/hr • CVP or pulmonary capillary wedge pressure • Response of urine output or CVP to fluid challenge • A fluid challenge should be regarded as a 200-250 ml bolus of colloid • This should be administered as quickly as possible • A response in the CVP or urine output should be seen within minutes • The size and duration of the CVP response rather the actual values recorded is more important

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! SURGICAL NUTRITION Malnutrition causes:

Delayed wound healing, Reduced ventilatory capacity, Reduced immunity and increased risk of infection

Nutritional assessment • Clinical assessment o Weight loss, BMI o 10% = mild malnutrition o 30% = severe malnutrition • Anthropometric assessment o Triceps skin fold thickness o Mid arm circumference o Hand grip strength

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Blood indices o Reduced serum albumin, prealbumin or transferrin o Lymphocyte count ‘End-of-bedogram’

Methods of nutritional support • Use gastrointestinal tract if available • Prolonged post-operative starvation is probably not required • Early enteral nutrition reduced post-operative morbidity Enteral feeding • Prevents intestinal mucosal atrophy, • Supports gut associated immunological shield • Cheaper than TPN and has fewer complications • Polymeric liquid diet o Short peptides, medium chain triglycerides and polysaccharides o Vitamins and trace elements • Elemental diet o L-amino acids, simple sugars o Expensive and unpalatable; High osmolarity cause diarrhoea • Enteral feed can be taken orally or by NGT Nasoenteral tube - usually fine bore • Long term feeding can be by: o Surgical gastrostomy, jejunostomy o Percutaneous endoscopic gastrostomy (PEG) o Needle catheter jejunostomy • Rate of infusion – often started at low rate and increased • Strength of initial feed – often diluted and strength gradually increased

Parenteral nutrition • Intestinal failure = ‘A reduction in functioning gut mass below the minimal necessary for adequate digestion and absorption of nutrients’ • Useful concept for assessing need for TPN • Can be given by either a peripheral or central line Indications for total parenteral nutrition • Absolute indications o Enterocutaneous fistulae • Relative indications o Moderate or severe malnutrition o Acute pancreatitis o Abdominal sepsis o Prolonged ileus o Major trauma and burns o Severe inflammatory bowel disease Monitoring of parenteral nutrition • Feeding lines should only be used for that purpose • Drugs and blood products should be given via separate peripheral line • 5% patients on TPN develop metabolic derangement • Nutrition should be monitored: o Clinically – Weight o Biochemically twice weekly o FBC, U+Es, LFTs, 2+ 2+ 22+ o Mg , Ca , PO4 , Zn o Nitrogen balance • Blood cultures on any sign of sepsis Metabolic complications of parenteral nutrition • Hyponatremia • Hypokalaemia • Hyperchloremia • Trace element and folate deficiency • Deranged LFTs • Linoleic acid deficiency

Complications of enteral feeding • Malposition and blockage of tube • Gastroesophageal reflux • Feed intolerance POST-OPERATIVE CARE

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! POST-OP PYREXIA Category Wind

POD 1-2

Water Walking Wound Wonder Drugs

3-5 4-6 5-7 7+

POST-OP PULMONARY PROBLEMS Description the lungs, i.e. pneumonia, aspiration, and pulmonary embolism urinary tract infection, related to indwelling catheter deep vein thrombosis or pulmonary embolism Surgical site infection drug fever, infections related to intravenous lines or reaction to blood products

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• Assessment of patient • Adequate assessment requires a full clinical examination • Respiratory complications often associated with breathlessness, cough and chest pain • Wound infections may show erythema, purulent discharge or dehiscence • Abdominal pain, distension and ileus may suggest a collection • Calf pain and tenderness may suggest a DVT • Appropriate clinical signs may be present Investigation • Useful investigations may include: o Chest x-ray o ECG o Arterial blood gases o Ventilation / perfusion scan o Abdominal ultrasound or CT scan

Lack of alveolar ventilation o Hypoventilation (airway obstruction, opiates) o Bronchospasm o Pneumothorax o Arteriovenous shunting (collapse, atelectasis) Lack of alveolar perfusion o Ventilation-perfusion mismatch (pulmonary embolism) o Impaired cardiac output Decreased alveolar diffusion o Pneumonia o Pulmonary oedema

Atelectasis • Significant atelectasis is more often seen o In those with pre-existing lung disease o With upper rather than lower abdominal incisions o Obese patients o Cigarette smokers • The basic mechanisms leading to atelectasis are: o Increased volume of bronchial secretions o Increased viscosity of secretions o Reduced tidal volume and ability to cough Treatment • Intensive chest physiotherapy • Nebulised bronchodilators • Antibiotics for associated infection Pneumonia Aspiration pneumonitis • Aspiration of gastric contents results in a chemical pneumonitis • Most commonly seen in apical segments of right lower lobe • If unrecognised or inadequately treated it can result in a secondary bacterial infection • Secondary infection is usually with gram-negative and anaerobic organisms Treatment • Tilt table head down and suck out pharynx • Consider intubation and endotracheal suction • Prophylactic antibiotics should be given • No evidence that steroids reduce inflammatory response

POST-OPERATIVE CARE

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! CARDIOVASCULAR PROBLEMS • • • • • • •

Hypotension Hypovolaemia Ventricular failure Cardiogenic shock Arrhythmias Conduction defects Hypertension

Causes of perioperative arrhythmias • Physiological disturbances o Acidosis o Hypercapnia o Hypoxaemia o Electrolyte imbalance o Vagal manoeuvres o Hypovolaemia • Pathological disturbances o Myocardial ischaemia or infarction o Pulmonary embolus o Phaeochromocytoma • Pharmacological causes o General anaesthesia o Local anaesthetic toxicity o Positive and negative inotropes

WOUND DEHISCENCE • • •

• • •

Affects about 2% of mid-line laparotomy wounds Serious complication with a mortality of up to 30% Due to failure of wound closure technique o Broken sutures or slipped knots o Inadequate muscle bites Usually occurs between 7 and 10 days post operatively Often heralded by serosanguinous discharge from wound Should be assumed that the defect involves the whole of the wound

Management • Opiate analgesia • Sterile dressing to wound • Fluid resuscitation • Early return to theatre • Resuture under general anaesthesia • Exact technique is variable • Interrupted or mass closure with non-absorbable sutures often used • The use of 'deep tension' sutures is controversial • Believed by some to strangulate muscle and weaken the closure • Also painful and associated with increased risk of infection

Causes of postoperative hypertension • Pain • Pre-existing hypertension • Hypoxaemia • Hypercapnia • Positive inotropic drugs • Hyper-reninemia

POST-OPERATIVE CARE

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! OTHER POST OP COMPLICATIONS Causes of postoperative hepatic dysfunction • Increased bilirubin load o Blood transfusion o Haemolysis o Haemolytic disorders o Abnormalities of bilirubin metabolism • Hepatocellular damage o Pre-existing hepatic disease o Viral hepatitis o Sepsis o Hypotension o Hypoxaemia o Drug-induce hepatitis o Congestive cardiac failure o General anaesthetic induced hepatic necrosis • Extra-hepatic biliary obstruction o Gallstones o Ascending cholangitis o Pancreatitis o Common bile duct injury Causes of postoperative renal failure • Prerenal (hypoperfusion) o Shock (hypovolaemia, cardiogenic, septic) o Renal artery disease • Renal (direct injury) o Acute tubular necrosis (following prerenal, drugs, myoglobin) o Glomerulonephritis o Interstitial nephritis • Postrenal (obstruction) o Bladder outflow obstruction o Single ureter (calculus, tumour) o Both ureters (bladder malignancy)

POST-OPERATIVE CARE

Urinary tract infections • 10% of patients admitted to hospital have a urinary catheter inserted • Risk of catheter-related infection depends on: o Age and sex of patient o Duration of catheterisation o Indication for catheterisation • Bacterial colonisation of catheters is common • If catheter required for more than 2 weeks 90% patients will develop bacteriuria • Commonest organisms are Enterobacter and enterococci • Does not require treatment unless patient is systemically unwell • Infection can be prevented by: o Maintaining closed drainage system o High infection control standards o Preventing backflow from catheter bag Postoperative confusion • Occurs in 10% of postoperative patients • Associated with increased morbidity and morality • Leads to increased duration of hospitalisation • Clinical features include o Reduced level of consciousness o Impaired thinking o Impaired memory o Abnormalities in perception o Disturbed emotion o Psychomotor disturbance Causes • Hypoxia - respiratory disease, cardiac failure, arrhythmia • Trauma - head injury • Infection - intracranial, extracranial • Neoplasia - primary and secondary cerebral tumours • Vitamin deficiency - Thiamine (Wernicke's encephalopathy), B12 deficiency • Endocrine - hypothyroidism, hyperthyroidism, Addison's disease • Degenerative • Vascular - CVA, TIAs • Drugs • Metabolic derangement

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! WOUND HEALING Skin anatomy • Skin has natural tension lines o Incisions placed along these lines -- heal with narrower and stronger scar  More favourable cosmetic result Pathophysiology of wound healing (3 phases) • Acute inflammatory phase st o 1 2-5 days o Bleeding stops (hemostasis) - platelet clot + scab formation o Inflammation - opens blood ss and cleanses wound • Proliferative phase (cell proliferation + deposition of extracellular matrix) o 5 days to 3 weeks o Granulation -- angiogenesis + fibroblasts synthesizing ECM  Pink and granular! (due to rich network of capillary vessels) o Contraction of wound - due to myofibroblasts o Epithelialization • Maturation phase (remodelling of ECM) o Occurs from 3weeks to 2 years! o Increase in tensile strength o Formation of avascular scar o Scar tissue only 80% as strong as normal tissue st  Strength increases rapidly over 1 7 days  Full maturation of scar takes up to 12months  Time required to regain strength depends on tissue type and thickness  Bowel - 1month  Skin - 6 months  Abdominal incisions through muscle layers take 3-4 months b4 they no longer require suture support  Close with either loop nylon that persists in the wound  or a strong, slowly absorbing suture material such as PDS  Superficial skin wounds require little support  Close with quickly absorbable suture material or stapler

SURGICAL TECHNIQUES

Classification of wound healing • Primary intention (oppose skin) o Uncontaminated wounds with minimal tissue loss o Wound edges can be easily approximated (sutures/staples/adhesive strips) w/o excessive tension o Heals by rapid epithelialization with minimal granulation tissue • Secondary intention o Wounds with substantial tissue loss o Edges cannot be apposed w/o excessive tension o Leave open and allow to heal from bottom up by granulation tissue, epithelialization and contraction o Takes much longer, more intense inflammatory response o Scar quality and cosmesis poor result (Butt abscess saucerization/ulcers) • Delayed primary intention o A period of healing by secondary intention - control infection/ reduce tissue edema; Close by primary intention! Rate of healing • Site o Scalp and face heal v quickly o Bone and intestine can regenerate with no/minimal loss of fx o Cardiac - little regenerative potential o Nerve - partial fx may be regained through slow neuronal growth • Age - rate of healing declines with age Causes of delayed wound healing • Local factors o Wound infection/dirty o Dead tissue wound o Surgical technique o Hematoma o Ischemia (Acute; Damage to o Excessive mobility e.g. vascular ss; Sutures too tight) Situated over a joint o Previous irradiation o Foreign body • General factors o Age - elderly o Chronic diseases  Cardiorespiratory disease; Diabetes Mellitus; Vascular disease (Atherosclerosis, Venous disease)  Anaemia, Renal/liver failure, Obesity, Malnutrition  Immunosuppressive disease e.g. AIDS o Drugs - Steroids, Immunosuppressive drugs 13!

! Ideal conditions for wound healing • Absence of things o No infx or foreign body • Surgical factors o Accurate apposition of tissue in layers (eliminating dead space) o No excess tension • Vascular factors o Good blood supply, good hemostasis, prevent hematoma Wound dehiscence • Failure of wound healing • Partial or total disruption of any or all layers of operative wound • Evisceration (burst abdomen) = extrusion of abdominal viscera o Usually preceded by blood-stained fluid • Mgt o Resuscitation, reassurance, analgesia o Protection of organs with moist sterile towels o Re-operation and closure • Incisional hernias - @ sites of partial dehiscence Classification of wounds • Depth o Superficial - only epidermis and dermis  No granulation tissue, no scar  E.g. Superficial burn/ graze o Deep  Involves layers deep to the dermis  Healing process: migration of fibroblasts, granulation tissue formation, scar formation  If deep wound not closed with good approximation - can cause contractures (problem) Related to the rate of surgical site infections • Principles of wound closure • Optimize wound healing & cosmesis • Incise along natural tension lines • Avoid hematoma and obliterate potential spaces -- use of surgical drain • Eliminate all dead tissue & infx • Avoid excess wound tension, ensure good blood ss • Handle tissues gently • Use appropriate suture material • Choose appropriate closure technique SURGICAL TECHNIQUES

Classification of surgical wounds Class Definition Class I Operative wound clean Clean Non-traumatic, with no inflammation encountered No break in technique Respiratory, gastrointestinal and genitor-urinary tracts not entered

Class II Clean contaminated

Class III contaminated

Class IV Dirty infected

Operative wound cleancontaminated Non-traumatic wound with minor break in technique Gastrointestinal, respiratory or genitor-urinary tracts entered without significant spillage Wound contaminated Fresh traumatic wound from clean source Major break in technique Gross spillage from the gastrointestinal tract Entrance into the genitourinary or biliary tracts Incision encountering acute non-purulent inflammation. Operative wound dirty Traumatic wound from dirty source or delayed treatment Fecal contamination Foreign body Retained devitalized tissue Operative wound w/ acute bacterial inflammation or perforated viscus Operative wound where clean tissue is transected to gain access to a collection of pus

Examples Vascular, Neurological, Endocrine, Eye, Orthopedic procedures (unless: trauma III, old wound IV, amputation II), Skin ( mastectomy, lumpectomy, lesions, lipoma, cosmetic, I&D IV, old wounds III, inflamed III, infected IV) Exploratory Lap (no bowel involvement II) (herniorrhaphy) Thoracic procedures GI procedures (including: laparoscopy, colonoscopy, gastroscopy, cholycystectomy) GU procedures Ear surgery Nose/Oropharynx Inflammation Gross spillage Fresh accidental wound

Infected I&D abscess Wound debridement

14!

! Scar formation • Factors influencing scar formation o Individual genetic make up o Race o Anatomical site o Wound tension o Age o Placement of incision o Surgical technique • To minimise the degree of postoperative scarring: o Incisions should run along Langer's lines o The finest suture possible should be used o Tension should be avoided o Sutures should be removed as soon as possible o Traumatic wounds should be clean and edges excised o Exposure to sunlight should be avoided in the early postoperative period Management 1. If large defect -- takes very long to heal, conservative mgt not recommended as scar will be large, ugly and granulation tissue may overgrow 2. Reconstruct o Secondary closure -- allow for healthy granulation tissue to form, excise the edges to rebleed wound, appose the skin and re-stitch with a strong stitch o Skin graft (partial thickness for large wounds) o Rotation flap o Muscle flap with blood ss o Free flap with microvascular reconstruction -- re-perfuse

SURGICAL TECHNIQUES

Problematic scars Contractures • Result if scars shorten • Particularly seen in badly aligned scars not corresponding to Langer's lines • Can reduce joint mobility • May require a z-plasty or skin graft Depressed scars • Result if skin becomes attached to deep tissue • Can be treated by release of normal skin from margins of scar • Scar is then de-epithelialized and skin edges closed over the top Keloid and hypertrophic scars • All scars become red and thickened during the normal healing process • After several months maturation results in flattening of the wound • In some scars collagen formation is excessive • Results in elevated and red scar • If confined to wound = hypertrophic scar • If extends beyond wound into normal tissue = keloid scar • Seen particularly in patients of Afro-Caribbean origin • Particularly affects scars on the presternal and deltoid areas • Treatment is often difficult • Treatment options include: o Intra-lesional steroid injections (e.g. triamcinolone) o Compression dressings with elasticated compression garments o Silastic gel therapy o Excision and radiotherapy o Laser therapy

15!

! SUTURING AND SKIN CLOSURE • • • •

Staples, skin clips • Sutures - interrupted or continuous Subcuticular sutures • Self-adhesive steristrips Glue Adequate apposition of tissues under the skin may eliminate the requirement for skin closure

Choosing sutures To hold a wound together in good apposition until such time as the natural healing process is sufficiently well established to make the support from the suture material unnecessary and redundant. • Properties of suture material • Size of suture • Absorption rate • Type of needle • Handling characteristics and knotting properties Properties of materials • Suture materials vary in their physical characteristics o Monofilament sutures (e.g. polypropylene) are smooth  The slide well in tissues but if handles inappropriately they can fracture o Multifilament sutures (e.g. polyglactin) are braided  They have a greater surface area  They are easier to handle and knot well • Absorbancy - depends on duration of support required o Non-absorbable e.g. Prolene (polypropylene) o Absorbable e.g. Vicryl (polyglactin) • Synthetic vs biological (biological - have unpredictable length of time persistence in tissues + strength and have ) Absorbable Non-Absorbable o Polyglycolic Acid (Dexon) o Polyamide (Nylon) o Polyglactin (Vicryl) o Polyester (Dacron) o Polydioxone (PDS) o Polypropylene (Prolene) o Polyglyconate (Maxon) o Silk, Linen, Stainless Steel o Catgut • Ideal suture material = o Have good handling characteristics o Not induce a significant tissue reaction o Allow secure knots o Have adequate tensile strength o Not cut through tissue o Be sterile, non-electrolytic, non-allergenic, cheap SURGICAL TECHNIQUES

Classification of needles • Shape o Straight o Curved o Circular o J-shaped • Type (point of needle) o Conventional cutting needle o Reverse cutting needle o Round-body taper-point needle o Taper cutting needle o Blunt point needle • Thickness o Should be appropriate to weight of suture o Choice of a larger or smaller curved needle may aid suture placement  Large for large bites of tissue e.g. Abdominal closure  Small for accurate placement e.g. Vascular anastomosis Common errors of suture use • Too many throws. Increases foreign body size. Causes stitch abscesses • Intra-cuticular rather than subcuticular sutures causing hypertrophic scars • Holding monofilament sutures with instruments reduces tensile strength by over 50% • Holding butt of needle causes needle and suture breakage Timing of suture removal • Vary according to site o Areas that are very mobile - may req longer to heal o Face 4-5 days o Scalp 6-7 days o Hands and limbs 10days o Abdominal wounds 10-20days

16!

! SURGICAL DRAINS • •

SURGICAL DRESSINGS

Drains are often made from inert silastic material They induce minimal tissue reaction

Purpose of surgical drains • Minimise dead space in a wound e.g. Axillary clearance, mastectomy, thyroidectomy • When there is risk of leakage e.g. Pancreatic surgery, bowel anastomosis • To drain actual fluid collections e.g. Subphrenic abscess • To divert fluid away from blockage or potential blockage o Biliary T-tube, suprapubic urinary catheter, ventricular CSF drain • To decompress and allow air to escape e.g. Chest drain Classifying surgical drains • Open (into dressing) vs closed (into container) o Closed = reduce risk of infx • Suction vs non-suction (passive gravity drainage) o Suction = better drainage but may damage adjacent organs/structures e.g. Bowel - precipitate leak Open drains Closed drains • Include corrugated rubber or • Consist of tubes draining into a plastic sheets bag or bottle • Drain fluid collects in gauze • They include chest and pad or stoma bag abdominal drains • Increase the risk of infection • The risk of infection is reduced Active drains • Active drains are maintained under suction • They can be under low or high pressure

Dressings - provide optimal healing environment for wounds • Moist • Infection free, with minimal slough • Free of chemicals and foreign bodies e.g. Dressing fibres • At optimum temperature • Reduce wound disruption - minimum change in dressings • Correct pH (4.8 - 6) Requirements of dressings • Provide protection from infx and trauma • Allow debridement - chemical and mechanical • Be absorbent and remove excess exudates while keeping wound moist • Maintain temp & gaseous exchange • Comfortable and cosmetically acceptable • Stimulate healing • Inexpensive and easy to change

Passive drains • Passive drains have no suction • Function by the differential pressure between body cavities and the exterior

Complications of drains • Infx via drain track • Injury to adjacent structures by drain e.g. Bowel • Anastomosis leakage • Retraction of drain into the wound • Bleeding by erosion into blood vessel • Pain e.g. Chest drain irritating diaphragm • Herniation @ drain site

SURGICAL TECHNIQUES

17!

! ABDOMINAL TRAUMA Assessment of abdominal trauma • Can be difficult due to altered sensorium (head injury, alcohol), altered sensation (spinal cord injury), injury to adjacent structures (pelvis, chest) • Differentiate between penetrating and blunt trauma Indications for immediate laparotomy • Unexplained shock (third spacing) with strongly suspected intraabdominal injury • Rigid silent abdomen (i/o + perf viscus) • Evisceration, gunshot wounds, stab wounds with implement in-situ • Obvious signs of peritoneal irritation • Radiological evidence of o Intraperitoneal gas o Ruptured diaphragm • Positive result on peritoneal lavage FAST (Focused Assessment for the Sonographic assessment of Trauma) • U/S for intraperitoneal fluid • Probe placed on pericardial, RUQ, LUQ, suprapubic region o Detects fluid in subphrenic, subhepatic spaces or Pouch of Douglas in hypotensive patient o Confirms need for emergency laparotomy Advantages Disadvantages Portable Does not image solid parenchyma, retroperitoneum, Can be done in <5min diaphragmatic defect or bowel injury Can be used for serial Compromised in uncooperative, obese patient w exam substantial bowel gas No contrast/radiation Operator dependent Cannot differentiate blood from ascites Not conclusive; may need alternatives CT Scan Advantages Precisely locate intra-abdominal lesions pre-op Evaluate retroperitoneum Non-invasive Possibility of conservative tx

ABDOMINAL TRAUMA

Disadvantages Expensive Time consuming Use of contrast

Peritoneal Lavage Indication Contraindication Equivocal clinical examination Absolute indication for laparotomy Difficulty in assessing patient already exists Persistent hypotension despite Previous abdominal surgery or infx adequate fluid resuscitation Gravid uterus; Morbid obesity Multiple injuries Coagulopathy Advantages Disadvantages Reveal or exclude presence of Morbidity – wound complications, intraperitoneal hemorrhage intraperitoneal injury, viscus injury Discover bowel perforation False negative rate 2% • Method o Ensure that catheter and NGT are in place o Under LA make vertical sub-umbilical incision dividing linea alba o Aspirate any free blood or enteric contents from peritoneal cavity o If no blood aspirated infuse 1L of normal saline and allow 3 min to equilibrate o Place drainage bag on floor and allow to drain o Send 20 ml to laboratory for measurement of RBC, WCC and microbiological examination • Positive result 3 o Red cell count > 100 000 / mm 3 o White cell count > 500 / mm o Presence of bile, bacteria or faecal material o Frank blood >5ml Damage Control Surgery • Ensure hypothermia, coagulopathy and severe acidosis is not exacerbated o Injury severity score >25 o Core temperature < 34ºC o Arterial gas pH <7.1 • Principles o Control hemorrhage o Remove dead tissue o Control contamination o Lavage abdominal cavity o Close abdomen without tension (can use Bogota bag) o Send to SICU for rewarming, ventilation, restoration of perfusion, correction of deranged biochemistry commence nutrition o ‘Second look laparotomy’ allows definitive treatment

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! ABDOMINAL INCISIONS Abdominal incisions • They must allow adequate access to the abdomen • They should be capable of being extended if required • Ideally muscle fibres should be split rather than cut • Nerves should not be divided • The rectus muscle has a segmental nerve supply • It can be cut transversely without weakening a denervated segment • Above the umbilicus tendinous intersections prevent retraction of the muscle

Midline incision • Midline incisions are the commonest approach to the abdomen • The following structures are divided: o Skin o Linea alba o Transversalis fascia o Extraperitoneal fat o Peritoneum • The incision can be extended by cutting through or around the umbilicus • Above the umbilicus the Falciform ligament should be avoided • The bladder can be accessed via an extraperitoneal approach through the space of Retzius • The wound can be closed using a mass closure technique • The most popular sutures are either non-absorbable or absorbable monofilaments • At least 1 cm bits should be taken 1 cm apart • Requires the use of one or more sutures four times the wound length Paramedian incision • A paramedian incision is made parallel to and approximately 3 cm from the midline • The incision transverse: o Skin o Anterior rectus sheath o Rectus - retracted laterally o Posterior rectus sheath - above the arcuate line o Transversalis fascia o Extraperitoneal fat o Peritoneum • The potential advantages of this incision are: o The rectus muscle is not divided o The incisions in the anterior and posterior rectus sheath are separated by muscle • The incision is closed in layers  Takes longer to make and close • Had a lower incidence of incisional hernia (when sutures were not so good)

ABDOMINAL INCISIONS

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! ABDOMINAL MASSES

Physical signs of abdominal masses Signs of hepatomegaly • Mass descending below right costal margin and costal angle • Moves with respiration and cannot get above it th • Dullness to percussion up to the level of the 8 rib in the mid-axillary line Signs of splenomegaly th • Mass descending below the left 10 rib and enlarging in a line towards the umbilicus • Often has a palpable notch on the medial border • Moves with respiration and cannot get above it • Dullness to percussion • Can be brought forward by lifting the lower ribs • Cannot be felt bimanually or balloted Signs of a renal mass • Mass lies in paracolic gutter • Moves with respiration but usually only lower border is palpable • Can be felt bimanually or balloted; not dull to percussion

.

Signs of an enlarged gallbladder th • Mass arising from below the tip of the right 9 rib • Smooth and hemi-ovoid in shape • Moves with respiration • Dull to percussion • Cannot feel space between mass and liver Signs of an enlarged urinary bladder • Hemi-ovoid smooth mass arising from the pelvis • Can extend above umbilicus • Non-mobile and dull to percussion • Does not bulge into the pelvis • Cannot be felt on rectal examination Signs of an ovarian cyst • Smooth mass arising from the pelvis • Mobile from side-to-side but not up and down • Dull to percussion • Palpable fluid thrill • Lower extremity can be felt on pelvic examination

APPROACH TO ABDOMINAL MASSES

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! APPROACH TO HEPATOMEGALY • •

•

•

Physical examination o Normal Impalpable in adults; 2FB below right costal margin in infants o Features  Enlarged mass extending downwards below right costal margin  Gross hepatomegaly - may fill subcostal angle and extend below left costal margin  Moves with respiration  Dull to percussion - may extend above normal upper level of 5th right intercostal space Specific features to aid diagnosis o Edge  Smooth - fatty liver/micronodular cirrhosis/congestive cardiac failure  Knobbly - metastatic/macronodular cirrhosis o Consistency - hard if mets o Tenderness (occurs with distention of capsule)  Hepatitis  HCC  CCF/AV malformation o Pulsatility only in TR Always feel for associated splenomegaly and lymphadenopathy o Causes of hepatosplenomegaly  Cirrhosis (portal HTN)  Polycythaemia  Leukaemia  Amyloidosis o Causes of hepatosplenomegaly + lymphadenopathy  Lymphoma


Causes of hepatomegaly Smooth generalized enlargement • Congestion due to cardiac failure • Micronodular cirrhosis • Reticuloses • Hepatic vein obstruction (BuddChiari syndrome) • Infective hepatitis • Cholangitis • Portal pyaemia • Amyloidosis

Knobbly generalized enlargement • Secondary carcinoma • Macronodular cirrhosis • Polycystic disease

Congenital • Riedel’s lobe (right lobe) • Polycystic liver disease

Cirrhosis (often shrunken) • Chronic viral hepatitis • Alcoholic • Rare: biliary, cardiac, hemochromatosis, Wilson’s

Inflammatory • Infective hepatitis • Viral - Hepatitis viruses, EBV, CMV, HIV • Bacterial - pyogenic abscess, TB • Parasite - amoebiasis, malaria • Portal pyaemia and liver abscess • Leptospirosis (Weil’s disease) or actinomycosis Vascular • Right heart failure • Tricuspid regurgitation • Budd-Chiari syndrome

Localised swelling • Riedel's lobe • Hydatid cyst • Liver abscess • Hepatocellular carcinoma

Metabolic • Fatty liver • Amyloid/Gaucher’s disease Neoplastic • Primary -- HCC • Secondary mets Hemopoietic disease & reticuloses • Lymphoma – Hodgkin’s disease & NHL • Leukaemia • Polycythaemia

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! Causes of a palpable gall bladder • Obstruction of the cystic duct o Stone in Hartmann's pouch o Cholangiocarcinoma • Obstruction of the common bile duct o Carcinoma of the head of the pancreas/periampullary carcinoma Courvoisier's law • 'If in the presence of jaundice the gallbladder is palpable, the obstruction of the bile duct causing the jaundice is unlikely to be due to a stone.' • Stones causes a thickened non-distensible gall bladder; leading to fibrosis (longstanding process) Causes of splenomegaly Infection • Bacterial - typhoid, typhus, TB • Viral - glandular fever • Protozoal - malaria, kala-azar

Congestion • Portal hypertension • Hepatic vein obstruction • Congestive heart failure

Cellular proliferation • Myeloid and lymphatic leukaemia • Pernicious anaemia • Polycythaemia rubra vera • Spherocytosis • Thrombocytopenia purpura • Myelosclerosis

Others • • • • •


Causes of a renal mass • Hydronephrosis • Pyonephrosis • Perinephric abscess • Hypernephroma • Nephroblastoma • Solitary cyst • Polycystic disease Causes of a right iliac fossa mass • Appendicitis • Tuberculosis • Carcinoma of the caecum • Crohn's disease • Iliac lymphadenopathy • Psoas abscess

Amyloidosis Gaucher's disease Felty's syndrome Angioma Lymphosarcoma

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! APPROACH TO ABDOMINAL PAIN History Pain • • • •

•

A/w • •

• •

•

Frequency Site and radiation Onset Character: o Colicky – obstruction of the bowel or ureters o Sharp – peritonitis Aggravating and relieving factors: o Relationship to meals, movement, defecation o Patient lies perfectly still – peritonitis o Patient leans forward – pancreatitis Fever GIT symptoms o Bloating/distension o Nausea/vomiting  Amount, colour, contents, presence of blood, relationship to eating/pain  GI infections, small b/o, increased ICP o Reflux  Acid brash, water brash, heartburn, hematemesis  Gastritis, PUD o Bowel habits  Constipation/diarrhea – ask about frequency, stool, what kind of change  Bowel obstruction, biliary tract problems o PR bleed  Melena/Hematochezia – ask about colour of blood, relationship to stool  Cancer, diverticulosis LOW/LOA – malignancy or depression o If appetite increased: malabsorption of hypermetabolic state Liver o Jaundice, pruritus, sclera, variceal bleeding, pale stools, tea coloured urine, hepatic encephalopathy Urinary syndromes – possible post-op pain related o FUNDSHIP (frequency, urgency, nocturia, dribbling, poor stream, hesitancy, incontinence, pis-en-deux) + ARU o Hematuria

APPROACH TO ABDOMINAL PAIN

Tenderness localized to: RHC Epigastric region Cholangitis RHC pain, fever, jaundice + shock, altered mental Acute cholecystitis Biliary colic, nausea, vomiting, pain (Murphy+) Hepatitis Jaundice Liver abscess Pyelonephritis Fever, pain radiating to back, nausea, tenderness I/O or perf colon

Peptic ulcer Dull, burning pain after/unrelated to meals, relieved with antacids, episodic. Radiation to back = perforation Pancreatic pain Steady epigastric pain, may be partially relived by sitting up and leaning forwards. Radiation of pain to back, vomiting common.

LHC Splenic pain Infarct/aneurysm (due to AF or emboli) Atypical AMI Perf colon Pyelonephritis

Biliary colic (cystic duct) Sharp, severe, constant pain that lasts for hours. Hx of episodes. Colonic pain Relieved by passing motion Gastric cancer Early satiety

Right flank

Left flank Umbilical region

Renal colic Severe, colicky pain, constant pain in the renal angle, radiation to the groin. Right iliac fossa Appendicitis Perf Cecum

Bowel obstruction Colicky pain. Frequent (2-3 mins) – small bowel, less frequent (10-15 mins) – large bowel. Associated with vomiting, constipation, abdominal distension. Pancreatitis Appendicitis

Crohn’s Terminal ileitis

Renal colic Severe, colicky pain, constant pain in the renal angle, radiation to the groin. Left iliac fossa Diverticulitis (sigmoid) PID, salpingitis

AAA Rupture Radiates to back, shock, hypotension

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! PMHx • Biliary/Liver disease o Gallstones, biliary colic, jaundice, hepatitis, chronic liver disease • Pancreatic disease o Assess risk factors (I GET SMASHED) o Possible pancreatic pseudocyst formation from pancreatitis • Hematological disease o Sickle cell anemia associated with biliary diseases due to pigment gallstones • Autoimmune diseases - pancreatitis • Surgical/medical history o Adhesion I/O o Biliary strictures • Comorbidities o HTN, Hypercholesterolemia, DM, strokes, cancers Medications • Drug allergies • NSAIDS/Steroids – ulcers • Nitrates – reflux inducing • Antivirals, diuretics – pancreatitis • TCM – acute liver failure Social history • Travel / eating • Food allergies • Smoking/alcohol Family history • Cancer • GERD problems • Liver problems • Hereditary diseases

APPROACH TO ABDOMINAL PAIN

Investigations • Lab o FBC, UECr, INR/PTT o LFT / Amylases / Lipases • Imaging o Ultrasound o CTAP o Endoscope o CXR Functional Disorders Upper abdominal discomfort after meals, often associated with a sensation of fullness, belching, nausea, early satiety or inability to finish a meal are typical features of functional disease. Irritable bowel syndrome due to spasm of the intestine and gives rise to upper or lower generalized abdominal pain. There is usually associated constipation and/or diarrhoea, and defecation may relieve the pain. Structural disorders Peptic ulcer disease usually gives rise to upper abdominal pains worse on hunger, relieved by food and sometimes waking the patient up at night. Stomach cancer can give rise to similar pains but usually of shorter duration and associated with loss of appetite and weight. Gallbladder give rise to very severe upper abdominal pain lasting up to several hours, sometimes going to the back or right shoulder. There may also be darkening of the skin and eyes (jaundice) or of the urine. Renal colic is due to a stone passing down from the kidneys. It results in excruciating pain lasting up to hours, usually in one loin but often going into the lower abdomen and groin on the same side. The urine may turn dark due to the presence of blood. The acute abdomen The pain of acute appendicitis is often generalized initially but becomes concentrated in the right lower abdomen. This pain is constant and becomes increasingly severe. It may get worse on touching the abdomen, on movement or even on breathing or coughing. There may be vomiting and fever. The pain from perforated ulcer is similar in character but occurs in the upper abdomen. In intestinal obstruction, there is generalized abdominal pain which comes in waves (colic). The abdomen becomes distended and vomiting occurs. Stools and flatus are not passed.

24

! ACUTE APPENDICITIS •

Acute abdominal pain is defined as previously undiagnosed pain of <72 hours duration

Causes of right iliac fossa mass • Appendix mass • Crohn's disease • Caecal carcinoma • Mucocele of the gallbladder • Psoas abscess • Pelvic kidney • Ovarian cyst

Causes of right iliac fossa pain • Appendicitis • Mesenteric adenitis • Urinary tract infection • Non-specific abdominal pain • Pelvic inflammatory disease • Renal colic • Ectopic pregnancy • Constipation

Etiology • Obstruction of appendiceal lumen o Fecaliths: Calcium salts and fecal debris collect around nidus of faecal material within appendix o Lymphoid hyperplasia: a/w inflammatory and infective disease  Crohn’s/UC  GE, URTI o Less common: TB, parasites, tumor • Increased intraluminal pressure o Due to continued mucosal secretion and bacterial overgrowth o Wall thins, lymphatic and venous obstruction occurs • Necrosis and perforation develops when arterial flow is compromised • The risk of perforation is: o Less than 10 years old = 50% o 10-50 years old = 10% o Over 50 years old = 30% Clinical features of appendicitis • Central abdominal pain moving to localized tenderness in right iliac fossa o Right iliac fossa peritonism o Percussion tenderness is a kinder sign of peritonism than rebound o Rovsing's sign = pain in RIF on palpation of the LIF • Nausea, vomiting, anorexia (should precede pain in order to exclude i/o) • Associated with o Low-grade pyrexia o LOA o +/- diarrhea or constipation o +/- irritative voiding symptoms & hematuria (due to inflamed appendix near bladder/ureter) APPROACH TO THE ACUTE ABDOMEN

Physical examination • RIF (McBurney’s point - 2/3 from umbilicus to ASIS) tenderness • Rebound tenderness, rigidity & guarding • May have palpable RIF mass (periappendiceal abscess or phlegmon) • May have LIF tenderness (situs inversus or lengthy appendix) • Cough sign: RIF pain on coughing (localized peritonitis) • Rovsing sign: RIF pain with palpation of LIF (peritoneal irritation) • Obturator sign: RIF pain with internal rotation of flexed right hip (pelvic) • Psoas sign: RIF pain with passive extension & active flexion of right hip • Infants/children may present with inflamed hemiscrotum o Due to migration of pus through patent processus vaginalis o Often mistaken for acute testicular torsion Differential diagnoses Gastrointestinal disease • Gastroenteritis o Characterized by nausea and vomiting before onset of pain o A/w malaise, high fever, diarrhea and poorly localized pain o WBC count usually normal • Mesenteric lymphadenitis o No rebound tenderness or muscular rigidity usually o Self-limiting inflammation of mesenteric LNs in RIF o A/w viral infections • Meckel’s diverticulitis o Clinically indistinguishable, but usually in infants o PUD, diverticulitis, cholecystitis Urologic diseases • Pyelonephritis o High fevers, rigors, costovertebral pain, tenderness o Diagnose by urinalysis + culture • Ureteric colic o Classical loin to groin pain, little localized tenderness, hematuria o XR-KUB often shows stones O&G • Pelvic inflammatory disease o S/S may be indistinguishable o Pain usually bilateral, may have vaginal discharge o Do transvaginal US to visualize ovaries & tubo-ovarian abscesses • Ectopic pregnancy (do urine pregnancy test) • Ovarian cysts (do transvaginal/transabd US) • Ovarian torsion (sudden, acute intense pain with simultaneous frequent and persistent vomiting) 25

! Investigations • Appendicitis is essentially a clinical diagnosis • Predictors of appendicitis in patients with abdominal pain o Raised inflammatory markers o Clinical signs of peritoneal irritation o Migration of abdominal pain Bloods • FBC: Total white cell count (inflammation) • UECr • CRP (trends inflammatory process) • Blood c/s • Pre-op prep o PT/PTT o GXM Urine • UFEME - may have pyuria (TRO UTI) and haematuria (TRO urolithiasis) • Pregnancy test (TRO ectopic pregnancy) Imaging • Erect CXR • CTAP o Distended, thick-walled appendix with inflammatory streaking of surrounding fat, pericecal phlegmon or abscess o Right lower quadrant free air indicates perforation • Ultrasound o Useful in women of child-bearing age to exclude O&G causes; may be helpful in the assessment of an appendix mass or abscess

Management • NBM, IV fluids/analgesia/anti-emetics e.g. Maxolon, correct electrolyte imbalances • Opiate analgesia does not mask the signs of peritonism • Active observation o In cases of diagnostic doubt o Active observation reduces negative appendicectomy rate without increased risk of perforation • Conservative treatment for appendiceal mass/abscess o When omentum wraps around inflamed appendix and contained the inflammatory process  Inflammation localized to RIF, patient pyrexial with palpable mass o Symptomatic Rx + Abx + monitor patient and size of mass → Do surgery only when mass has reduced in size and patient is stable (less inflammation = easier surgery) o Give IV o Fluids, analgesia and antibiotics o Appendicular abscess suspected → Incision & drainage • Definitive treatment: appendectomy o IV roc/Flagyl o Diagnostic laparoscopy should be considered particularly in young women o Open appendicectomy is usually performed via a Lanz incision and muscle splitting approach

Alvarado scoring system A score below 5 is strongly against a diagnosis of appendicitis, while a score of 7 or more is strongly predictive 1. Migratory right iliac fossa pain 1 point 2. Anorexia 1 point 3. Nausea and vomiting 1 point 4. Right iliac fossa tenderness 2 points 5. Rebound tenderness 1 point 6. Fever 1 point 7. Leukocytosis 2 points 8. Shift to left (segmented neutrophils) 1 point

APPROACH TO THE ACUTE ABDOMEN

26

! PERFORATED ULCER Clinical features • Most occur in patients with pre-existing dyspepsia • 10% have no previous symptoms • Classic presentation is with: o Sudden onset epigastric pain o Rapid generalization of pain o Examination shows peritonitis with absent bowel sounds • 10% have an associated episode of melaena • 10% have no demonstrable gas on an erect chest x-ray • Water soluble contrast enema may confirm perforation Management • Most patients require surgery after appropriate resuscitation • Conservative management may be considered if significant co-morbidity • More likely to fail if perforation is of a gastric ulcer Preoperative preparation • Fluid resuscitation with CVP or Swan Ganz monitoring • Analgesia • Antibiotics • Nasogastric intubation Operation • Oversew of ulcer • Oversew perforation with omental patch o Use 2/0 synthetic absorbable. o Take 1 cm bites either side of ulcer • Thorough wash out and irrigation of peritoneal cavity with 0.9% saline • All gastric ulcers require biopsy to exclude malignancy • Definitive ulcer surgery probably not required • 50% patients develop no ulcer recurrence • Postoperatively patients should receive H. pylori eradication therapy Outcome • Operative mortality depends on four major risk factors o Long period from perforation to admission o Increasing age o Coexisting medical disease o Hypovolaemia on admission APPROACH TO THE ACUTE ABDOMEN

MESENTERIC ISCHEMIA • •

•

Occurs as result of either SMA or SMV occlusion nd Affects bowel from 2 part of duodenum to transverse colon o 50% embolic arterial occlusion o 25% atheromatous arterial occlusion o 10% venous occlusion o Whatever the underlining aetiology reduced capillary flow causes intestinal necrosis Overall mortality is approximately 90%

Clinical features • Severe central abdominal pain out of proportion to clinical signs • Vomiting and rectal bleeding may also occur • No single clinical feature provided conclusive evidence of the diagnosis o As a result the diagnosis is difficult and often delayed o Early diagnosis requires a high index of suspicion • May also be evidence of an embolic source (e.g., recent MI, arrhythmia) o May also be other features of atherosclerotic disease  History of intestinal angina leading to “food fear” – chronic mesenteric ischemia o 75% have ischaemic heart disease Investigations • No single investigation provides pathognomic evidence • Raised WBC • ABG may show a metabolic acidosis • Serum amylase is raised in 50% of patients • Abdominal x-ray may be normal early in the disease process o Late features include dilated small bowel and 'thumb printing' due to mucosal oedema • Mesenteric angiography may confirm the diagnosis Management • Papaverine infusion into the SMA may be beneficial • Laparotomy allows: o Confirmation of diagnosis and assessment of extent of ischaemia o Opportunity to revascularize SMA o Resect necrotic small intestine • Revascularization may be achieved by embolectomy, graft/bypass or endarterectomy • Resection and primary anastomosis may be possible 27

! APPROACH TO INTESTINAL OBSTRUCTION Causes Intraluminal Mechanical

Functional

Foreign body Bezoar Mural Strictures 2º to: Divert, Crohn’s, RT Extraluminal Volvulus LN compression SMA syndrome Paralytic ileus (post-op, inflammatory, ischemic, metabolic, hypothyroid/opiate induced) Hirschsprung’s disease (absent ganglia in Auerbach’s plexus) Ogilvie syndrome (in severely ill patients)

Types Small Bowel I/O Adhesions Herniae

Ileocecal tumor Intussusception

Impacted stool Gallstone ileus Tumors Intussusception Adhesions Hernia

Large Bowel I/O Cancer Post-divert strictures

Sigmoid volvulus

History • 4 cardinal symptoms o Pain (Usually colicky - 4-5 days duration)  Complete obstruction: constant sharp pain  Volvulus: acute onset severe pain o Vomiting  Ask if projectile; Color - bilious/feculent o Abdominal distention o Constipation (vs normal frequency)  Ask if obstipated - no flatus even! (severe) • Other pertinent history o Previous surgeries o Underlying or previous GIT disorders  Previous Ca, IBD o Symptoms of GI bleed - melena/frank PR bleed o Symptoms of GI infection o Recent change in bowel habits - frequency, tenesmus, stool calibre o Suspicion of malignancy - LOW/LOA o Family history of cancer o Risk factors for ischaemic bowel - atherosclerosis, heart disease, previous CVA ABDOMINAL EMERGENCIES

Physical Exam • Vitals • General inspection o Hemodynamic stability - HR, BP o Cachexia o Febrile? o Confusion/AMS o Toxic-looking/sepsis o Abdo distention • Abdomen o Distention o Scars - previous surgery o Visible peristalsis -- severe obstruction o Signs of peritonitis - guarding, rebound tenderness vs SNT abdo o Masses, herniae o Bowel sounds  Initially hyperactive (peristalsis trying to pass obstruction), later sluggish or absent  Tinkling BS = SBIO o Succussion splash + epigastric tenderness = gastric outlet obstruction • DRE - look for stools felt, masses Acute management • Resuscitate if necessary o Monitor vitals - IDC to monitor urine O/P • NBM (bowel rest) + IV drip (correct dehydration) • NG tube on constant suction • Correct electrolyte imbalances, replace K+ • Start broad-spectrum Abx (as IO affects normal translocation of bacterial flora) • Rule out any surgical emergencies (history/PE/inx) o Obstructed hernia o Volvulus (sigmoidal, caecal, gastric) o Closed loop obstruction o Ischemic bowel with necrosis (impending perf) o Perforation/peritonitis -- do erect CXR to look for free gas

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! Investigations Bloods • FBC o TW for infx o Hb for anemia • UECr rd o Dehydration 2/2 vomiting or intra-luminal 3 space loss (damaged enterocytes unable to reabsorb) • ABG o Acidosis from bowel ischaemia o Alkalosis due to vomiting (esp for GOO/pyloric stenosis) • Pre-op o PT/PTT; GXM - 4 pints of blood o ECG & cardiac enzymes Imaging • Erect CXR - look for free gas under diaphragm, any aspiration pneumonia • AXR o Rigler’s sign (obvious bowel wall due to extraluminal air) o Erect to look for air-fluid levels (>6 is significant) o Supine  Look for bowel dilation on radiograph (>3cm sig for small bowel, >5 for large bowel)  Jejunum & proximal ileum - centrally located, stack of coins appearance  Distal ileum - lead pipe appearance  Colon - incomplete bands/haustrations o Sigmoid volvulus - coffee bean + parrot’s beak sign o Closed loop obstruction - distal lesion with very distended caecum (thinnest wall, most prone to distention up to 12cm); ileum not dilated o Bowel ischaemia +/- necrosis -- gas in bowel wall (pneumatosis intestinalis) due to gas gangrene o Rectal gas absent may mean complete obstruction (may require KUB to see) • Barium enema o Gastrografin preferred if risk of perf (avoid barium peritonitis) • Colonoscopy contraindicated (risk of perf) • CT colonography

ABDOMINAL EMERGENCIES

Definitive management is cause-dependent • Obstructed hernia -- herniorrhaphy • Sigmoid volvulus o Ryle’s tube decompression o Flexible sigmoidoscopic decompression with sigmoid colectomy and formation of double-barrel colostomy with secondary reanastomosis • Closed loop obstruction (if due to distal tumor) o Resect bowel + primary anastomosis with proximal defunctioning (loop) colostomy o Hartmann’s procedure (sigmoid resection with end colostomy + rectal stump w 2ndary anastomosis) if bowel too inflamed/edematous to anastomose (high risk of leak) • Ischaemic bowel (at watershed areas e.g. splenic flexure, rectosigmoidal jx) o Ischaemia alone can cause paralytic ileus o Supportive mgt - NBM, drip & suck, abx while waiting for collaterals to re-supply bowel and for peristalsis to begin o Surgical intervention indicated if bowel is non-viable i.e. Necrosis/gangrene nd  Requires 2 laparotomy after initial resection 2-3/7 later to ensure bowel margins are clear (no gangrenous gut left) o Perforation (usually at thin-walled caecum)  Usually occurs due to ischaemic of distended bowel (>12cm)  Emergency laparotomy: resect lesion and perforated bowel with generous peritoneal lavage  Type of resection - hemi-colectomy vs total colectomy dependent on site of lesion  Continue abx after surgery (dirty surgery) o Intussusception  Children - usually due to hypertrophic Peyer’s patches • Rx = administer barium enema and watch intussusception reduce on fluoroscopy  Elderly - usually due to polyp or Ca (barium enema unlikely to work/high recurrence) • Rx - surgical is first-line o Post-op paralytic ileus (>3 days post-op)  Drip and suck, wait for peristalsis to restart  Oral Gastrografin: hyperosmotic - causes intraluminal osmosis, can re-establish peristalsis  Other prokinetic agents - erythromycin, metoclopramide (Maxolon), cisapride

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! SMALL BOWEL OBSTRUCTION Mechanical obstruction Aetiology • Small bowel obstruction accounts for 5% of acute surgical admissions • Adhesions (60%), Strangulated hernia (20%), Malignancy (5%), Volvulus (5%) Pathophysiology • Proximal dilatation occurs above obstructing lesion • Results in the accumulation of gas and fluid and reduced reabsorption • Dilation of the gut wall produced mucosal oedema • This impairs venous and then arterial blood flow o Intestinal ischaemia eventually results in infarction and perforation of that segment of bowel o Ischaemia also results in bacterial and endotoxin translocation o The overall effect is progressive dehydration, electrolyte imbalance and systemic toxicity Clinical feature • Colicky central abdominal pain • Vomiting - early in high obstruction • Abdominal distension - extent depends on level of obstruction • Absolute constipation - late feature of small bowel obstruction • Dehydration associated with tachycardia, hypotension and oliguria • Features of peritonism indicate strangulation or perforation Investigation • Supine abdominal X-ray shows dilated small bowel • Valvulae conniventes (plicae circulares) – stack of coins • Erect abdominal film rarely provided additional information Management • Resuscitation prior to surgery o May require more than 5 litres of intravenous crystalloid o Adequacy of resuscitation should be judged by urine output or central venous pressure o Surgery in under resuscitated patient is associated with increased mortality o Exact procedure will depend on underlying cause


Indications for surgery • If features of peritonism or systemic toxicity present, need to consider early operation o Absolute o Relative  Generalized peritonitis  Palpable mass lesion  Localised peritonitis  'Virgin' abdomen  Visceral perforation  Failure to improve  Irreducible hernia • If obstruction presumed to be due to adhesions and there are no features of peritonism o Conservative management for up to 48 hours is often safe o Requires regular clinical review  Incomplete obstruction  Previous surgery (intestinal obstruction)  Advanced malignancy Paralytic ileus • Functional obstruction most commonly seen after abdominal surgery • Also associated with trauma, intestinal ischaemia, sepsis • Absorption of fluid, electrolytes and nutrients is impaired • Significant amounts of fluid may be lost from the extracellular cmpt Clinical features • Usually history of recent operation or trauma • Abdominal distension is often apparent; usually no pain • If no nasogastric tube in-situ vomiting may occur • Flatus will not be passed until resolution of the ileus • Auscultation will reveal absence of bowel sounds Investigation • Plain abdominal x-ray may show dilated loops of small bowel • Gas may be present in the colon • Water soluble contrast study to distinguish mechanical or functional Management • Bowel should be handled as little as possible • Fluid and electrolyte derangements should be corrected • Sources of sepsis should be eradicated • Nasogastric tube • No drugs are available to reverse the condition • Usually resolves spontaneously after 4 or 5 days

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! LARGE BOWEL OBSTRUCTION • • • • • •

15% colorectal cancers present with obstruction Most patients are over 70 years old Risk of obstruction greatest with left sided lesions Usually present at a more advanced stage 25% have distant metastases at presentation Perforation can occur at site of tumour or in a dilated caecum

Clinical presentation • Caecal tumours present with small bowel obstruction o Colicky central abdo pain o Early vomiting o Late absolute constipation o Variable extent of distension

•

Left sided tumours present with large bowel obstruction o Change in bowel habit o Absolute constipation o Abdominal distension o Late vomiting

Investigation • Plain supine abdominal x-ray will show dilated large bowel (Haustrations) • Small bowel may be dilated depending on competence of ileocaecal valve • If doubt over diagnosis or site of obstruction consider a water soluble contrast enema • Colonoscopy; CT Colonography Management • All patients require • At operation o Adequate resuscitation o Full laparotomy should be o Prophylactic antibiotics performed o Consenting and marking o Liver should be palpated for for potential stoma metastases formation o Colon should be inspected for synchronous tumours • Appropriate operations include: o Right sided lesions – right hemicolectomy o Transverse colonic lesion – extended right hemicolectomy o Left sided lesions – various options Three-staged procedure • Defunctioning colostomy • Resection and anastomosis • Closure of colostomy


Two-staged procedure • Hartmann’s procedure • Closure of colostomy

One-stage procedure • Resection, on-table lavage and primary anastomosis • Three stage procedure will involve 3 operations! • Associated with prolonged total hospital stay • Transverse loop colostomy can be difficult to manage • With two-staged procedure only 60% of stomas are ever reversed • With one-stage procedure stoma is avoided • Anastomotic leak rate of less than 4% have been reported • Irrespective of option total perioperative mortality is about 10% Sigmoid Volvulus • Volvulus = rotation of the gut on its own mesenteric axis o Produces partial or complete intestinal obstruction o Blood supply compromised resulting in intestinal ischaemia o Venous congestion leading to infarction can occur o Arterial supply rarely compromised o Long narrow based mesentery predisposes to volvulus Clinical features • Large bowel obstruction – pain, constipation and vomiting • Disproportionate abdominal distension • 50% patients have had a previous episode • Severe pain and tenderness suggests ischaemia • Plain abdominal x-ray may show a large ‘bean’ shaped loop of large bowel arising from pelvis • If diagnostic doubt consider a water soluble contrast enema • Will demonstrate site of obstruction Management • Resuscitation with intravenous fluids is essential • Conservative management can be attempted if no clinical features of ischaemia o Sigmoidoscopy can be both diagnostic and therapeutic o Flatus tube can be inserted and left for 2-3 days o 80% of patients will settle with conservative management o If decompression occurs no emergency treatment required • 50% further episode of volvulus within 2 years • If decompression fails or features of peritonitis o Sigmoid colectomy and primary anastomosis o Hartmann’s procedure o Paul Mikulicz Colostomy

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! APPROACH TO BLEEDING GIT History Nature of bleed

Amount Etiology clues

Complx

Comorb

Upper Lower Hematemesis Hematochezia - fresh red (variceal, AV malform) - mixed with or coating stool - coffee grounds (ulcer, gastritis) - torrential/drops, any clots Melaena - bright/dark red - above ligament of Treitz - mucous - fresh (jet black with sheen, - relation to defecation tarry, liquid consistency) vs stale (black grey, dull, mixed w normal stool, particulate) vs iron (greenish hue) st 1 Episode? Measurement – cup/bowl? Frequency? Ulcer/gastritis/erosions TRO UBGIT - Hx dyspepsia, ulcer (past - Melaena, hematemesis, coffee OGD) grounds vomitus - Drugs (NSAIDs, steroids, - Hx of PUD, gastritis, varices, Ca antiplatelets, anticoags) stomach Varices Bleeding divert/angiodysplasia - Hx of CLD - Torrential, stops spontaneously Mallory-Weiss tear - Altered clots - Binge drinking w severe CRC retching’ - constitutional symptoms Malignancy - change in bowel habits, tenesmus - LOW, LOA, malaise - occult bleed from anemia - Early satiety - fam Hx - Dyspepsia Colitis - Infective: fever/chills/rigors/n/v/ pain/travel/food etc - Inflammatory: UC/Crohn’s Hemorrhoids - blood coating stools, pain - Hx of constipation, hard stools, chronic straining, low fibre Coagulopathy Anemia - Postural giddiness, SOB, lethargy, ↓ effort tolerance, palpitations, CP Dehydration & shock - Thirst, confusion, pallor, ↓ urine output Elderly, CLD, renal disease, IHD


Associated symptoms • Fever • GIT symptoms o Abdominal bloating/distension o Nausea/vomiting  Amount, colour, contents, presence of blood, relationship to eating/pain  GI infections, small b/o o Reflux  Acid brash, water brash, heartburn, hematemesis  Gastritis, PUD o Bowel habits  Constipation/diarrhea – ask about frequency, stool, what kind of change  Bowel obstruction o PR bleed  Melena/Hematochezia – ask about colour of blood, relationship to stool  CRC, diverticulosis • LOW/LOA – malignancy or depression o If appetite increased: malabsorption of hypermetabolic state • Liver o Jaundice, pruritus, sclera, variceal bleeding, pale stools, tea coloured urine, hepatic encephalopathy o CLD • Urinary syndromes – possible post-op pain related o FUNDSHIP (frequency, urgency, nocturia, dribbling, poor stream, hesitancy, incontinence, pis-a-deux) + ARU o Hematuria Fam + Personal Hx • IBD, IBS, CRC • Cancer • GERD problems • Liver problems • Hereditary diseases • Comorbidities – DM

Social Hx • Alcohol excess – diarrhea and pancreatitis • Smoking – Crohn’s, CRC • HIV risk factors – immunocompromised host • Contact history – similar symptoms

Drug Hx • Medications as above • Drug allergies

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! Physical Examination • Vitals o BP & postural BP, HR o Conscious level/confusion - GCS • General inspection o Pallor, cold, clammy peripheries o Cachetic? Jaundice? o Stigmata of CLD • Abdomen o Any tenderness, mass o Hepatosplenomegaly, ascites -- CLD o DRE - melaena (fresh vs stale) or frank blood Investigations • Vitals – assess state of shock, conscious level • FBC, UECr, INR/PTT • LFT • GXM


Management • Resuscitation o Airway (intubate nasal prongs), Breathing (oxygen), Circulation (ECG) o 2 large-bore IV cannula in antecubital fossa o Take blood for investigations - FBC, UECr, LFT, PT/PTT, GXM (4 pints)  IV fluids/crystalloids - 1 pint N/S over 1/2 - 1hr if patient is in shock  May follow with more if req  Beware fluid overload in patients with renal/heart failure  Correct any coagulopathy - if patient is on  Antiplatelets e.g. aspirin - consider platelet replacement  Anti-coagulants e.g. warfarin / PT/PTT prolonged consider FFP +/- Vit K • Adjunct o NG tube if hematemesis (therapeutic and diagnostic) – contraindicated if variceal bleed suspected o Catheterization – i/o monitoring o IV omeprazole (80mg bolus) o IV somatostatin/octreotide, IV abx, Vit K for Varices • Monitor o HR, BP, Urine output, mental status • Emergency OGD/Colonoscopy o Indications:  Persistent shock after resuscitation  Ongoing BGIT  Suspected variceal bleed o Role:  Diagnostic: Identify source of bleeding  Therapeutic: Injection of ulcer, ligation/sclerotherapy, cauterization • Laparotomy and on-table lavage + angiogram in crazy LBGIT

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! UPPER BGIT Causes • Peptic ulcer (50%) • Gastric erosions • Oesophageal or gastric varices

LOWER BGIT • • • •

Mallory-Weiss tear Angiodysplasia Dieulafoy malformation Gastric neoplasia

Management • Aggressive fluid resuscitation is important o Circulating blood volume restored with crystalloid o Cross-matched blood should be given when available • All patients require closed monitoring in an HDU or ITU environment with central and arterial pressure monitoring • Proton-pump inhibitors Bleeding peptic ulcer • 80% bleeding stops spontaneously • 25% require intervention for recurrent bleeding within 48 hours • Duodenal ulcer bleeding usually from gastroduodenal artery o Close gastroduodenotomy as a pyloroplasty o Consider truncal vagotomy and pyloroplasty o All patients should be given H. pylori eradication therapy post op o If a pyloroplasty will be difficult because of large ulcer consider Poly-a gastrectomy • Gastric ulcer consider local resection or partial gastrectomy All patients require early endoscopy (± intervention) to determine: • Site of bleeding • Features of recent bleed o Ooze from ulcer base • Continued o Clot covering ulcer base bleeding o Black spot in ulcer base o Visible vessel Endoscopic therapy • Laser photocoagulation using the Nd-YAG laser • Bipolar diathermy; Heat probes • Adrenaline or sclerosant injection Indications for surgery • Continued bleeding that fails to respond to endoscopic measures • Recurrent bleeding / gastric ulcer bleed • Patients > 60 years • Cardiovascular disease with predictive poor response to hypotension ABDOMINAL EMERGENCIES

• •

Accounts for 20% cases of acute gastrointestinal haemorrhage Most cases settle spontaneously without the need for emergency surgery

Causes • Diverticular disease • Angiodysplasia • Inflammatory bowel disease

• • •

Ischaemic colitis Infective colitis Colorectal carcinoma

Angiodysplasia • Acquired malformation of intestinal blood vessels o 80% lesions occur in the right side of the colon o Often associated with cardiac valvular disease • Dilated vessels or 'cherry red' areas may be seen at colonoscopy • Bleeding may be visible during capillary phase of angiogram Investigation • Most patients are stable and can be investigated once bleeding stops • In the actively bleeding patient consider: o Colonoscopy Rate of bleeding for detection o Sigmoidoscopy Investigation Rate of bleed o OGD TRO varices Radiolabel red cell scan 0.1 ml/min o Emergency exploratory Mesenteric angiography 1.0 ml/min laparotomy Non-selective aortic angiography 6.0 ml/min o Selective mesenteric Colonoscopy Any angiography Intraoperative endoscopy Any (can be on table) o Radionuclide scanning  Uses technetium-99m labeled red blood cells Management • Acute bleeding tends to be self-limiting • Consider selective mesenteric embolization if life threatening haemorrhage • If bleeding persists perform endoscopy to exclude upper GI cause • Proceed to laparotomy, consider on-table lavage and panendoscopy o If right-sided angiodysplasia perform a right hemicolectomy o If bleeding diverticular disease perform a sigmoid colectomy o If source of colonic bleeding unclear perform a subtotal colectomy and end-ileostomy

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! VARICEAL BLEED •

Suspect variceal UBGIT in patients with history of variceal bleed, chronic alcohol intake, jaundice or stigmata of CLD

Primary prevention • Bleeding from varices more likely if poor hepatic function or large varices • Primary prevention of bleeding is possible with β blockers like propanolol o Prevents varices formation o Reduces risk of bleed by 40-50% • Band ligation may also be considered • Predictors of hemorrhage: o Site: varices at gastroesophageal jx have thinnest coat of tissue - highest risk of rupture & bleed o Size (fraction of lumen occupied and shape of varices) o Child’s score o ESRH; Previous bleed

Secondary prevention • 70% patients will have a rebleed; 30% in first 6wks • Ablation regimen o Endoscopy with initial ligation/sclerotherapy o Subsequent endoscopic monitoring and repeated ligation/sclerotherapy as required to completely ablate varices • If patient bleeds again and ablation fails → TIPSS; Surgical shunt *The mortality of a variceal bleed is approximately 50%

Active bleeding • Resuscitation should be as for other causes of upper GI haemorrhage o Airway - endotracheal intubation to protect airway, prevent aspiration, facilitate OGD o Breathing - supplemental oxygen o Circulation - 2 large-bore IV cannula in proximal veins  Infuse crystalloids while awaiting bloods - N/S • Assess: Vitals, hydration status, Mental state • Investigations: Blood tests - GXM 4 pints, FBC, UECr, LFT, PT/PTT • IV regimen o IV somatostatin/octreotide  Acts as splanchnic vasoconstrictor → decreases portal flow & portal pressures (not given in ulcer bleed)  Also inhibits secretion of gut hormones that ↑ portal flow o IV omeprazole - acid suppression  ↑ in intragastric pH → ↑ clot stability, aids hemostasis  Decrease formation of stress ulcers o IV antibiotics (Roc/flag)  Infection a strong prognostic indicator in acute variceal bleed  Abx reduces risk of rebleed & mortality • Lactulose may be used to decrease GI transit & ↓ ammonia absorption ABDOMINAL EMERGENCIES

Endoscopy should be performed to confirm site of haemorrhage o To confirm diagnosis and institute management o Needs to be done emergently, as soon as patient is stabilized o Note: half of pts with known esophageal varices have upper GI bleed from an alternative source - need to do thorough endoscopy o Emergency endoscopic therapy includes:  Endoscopic banding of varices (best)  Intravariceal or paravariceal sclerotherapy (higher morbidity)  Only for large gastric varices • Temporary tamponade with Sengstaken-Blackmore tube for 12 hrs (repeat endoscopy after) o Should be considered as a salvage procedure if first endoscopy fails; always protect airway first o Inflate gastric balloon and pull upwards against CE jx - balloon will compress perforator veins entering esophagus from stomach, decreasing esophageal variceal bleed o Tamponade is 90% successful at stopping haemorrhage o Unfortunately 50% patients rebleed within 24 hours of removal of tamponade o A Sengstaken-Blackmore tube has three channels  Inflation of gastric balloon, inflation of oesophageal balloon, aspiration the stomach • If endoscopic methods fail need to consider: o Transection or devascularization o Porto-caval or mesenterico-caval shunting  Emergency shunting associated with 20% operative mortality and 50% encephalopathy  Transjugular intrahepatic porto-systemic shunting (TIPSS)  Radiologically-guided  Stent between branches of hepatic and portal venous circulation  In patient with good Child’s score (A is best; it’s for CLD/cirrhosis) only to avoid ppt encephalopathy  Reduces risk of rebleeding but increases risk of encephalopathy  Mortality of the procedure ~1%  Surgery – portacaval/mesocaval/splenorenal shunt  Sugiura procedure

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! GROIN HERNIA A hernia is a protrusion of an organ through the wall that normally contains it • The two main aetiological factors for acquired hernias are o Increased intra-abdominal pressure (e.g. straining or lifting) o Abdominal weakness (e.g. advancing age or malnutrition) • A hernia consists of: o A sac, its coverings, its contents • Hernias can be: o Reducible o Irreducible  Narrow neck or adherent contents to sac wall o Obstructed or incarcerated  Obstructed but viable intestine o Strangulated  Venous drainage from sac contents compromised Clinical features • The hernia often increases in size on coughing or straining • It reduces in size or disappears when relaxed or supine • Examination may show it to have a cough impulse and to be reducible o Irreducible but non-obstructed hernias may cause little pain o If the hernia causes obstruction colicky abdominal pain, distension and vomiting may occur • The hernia will be tense tender and irreducible o If strangulation occurs the lump will become red and tender • Diagnosis is usually based on clinical features •

Mortality of strangulated hernia repair • The peak incidence of hernia strangulation is approximately 80 years • In those with acute onset of a hernia the greatest risk is in the first 3 months • Risk of strangulation depends on type of hernia o Femoral is approximately 40% o Direct inguinal is approximately 3% • Operative mortality remains at approximately 10% o Is ten times greater than that following an elective repair • Risk of death is dependent on: o Age and presence of necrotic bowel requiring resection

ABDOMINAL HERNIA

Femoral hernias • Account for 7% of all abdominal wall hernia • Female : male ratio is 4:1 • Commonest in middle aged and elderly women • Much less common than inguinal hernias but are as common as inguinal hernias in older women Anatomy of the femoral canal • Anterior border is the inguinal ligament • Posterior border is the pectineal ligament • Medial border is the lacunar ligament • Lateral border is the femoral vein

Management of femoral hernia • All uncomplicated femoral hernias should be repaired as an urgent elective procedure • Three classical approaches to the femoral canal have been described o Low (Lockwood) o Transinguinal (Lotheissen) o High (McEvedy) • Irrespective of approach used the following will be achieved o Dissection of the sac o Reduction / inspection of the contents o Ligation of the sac o Approximation of the inguinal and pectineal ligaments 36

! Inguinal hernias • Male : female ratio is 12:1 • Elective : emergency operation 12:1 • Peak incidence is in the 6th decade • 65% inguinal hernias are indirect • In females inguinal hernias are as common as femoral hernias Anatomy • Inguinal canal lies between the superficial and deep inguinal rings o Deep ring lies deep to the mid-inguinal point  In men it contains vas deferens & testicular artery & veins  In women it contains the round ligament o Anterior border is the external oblique aponeurosis o Posterior border is the transversalis fascia o Inferior border is the inguinal ligament o Superior border is the conjoint tendon - the lower fibres of internal oblique and transversus abdominis • Indirect hernias arise lateral to the inferior epigastric vessels o Bulges directly ant though a weakened fascia: Hesselbach’s triangle, post to the inguinal canal o Hesselbach’s ∆: inf. Epigastric art., rectus abd, inguinal ligament • Direct hernias arise medial to the inferior epigastric vessels Classification of inguinal hernias (Nyhus) Type 1 Indirect hernia with normal internal ring Type 2 Indirect hernia with dilated internal ring. Posterior wall intact Type 3 Posterior wall defect A: Direct inguinal hernia C: Femoral hernia B: Indirect inguinal hernia, internal ring dilated Type 4 Recurrent hernia Indirect Hernia Neck lies lateral to inferior epigastric artery, out of Hesselbach’s triangle

Direct Hernia Neck lies medial to inferior epigastric artery, within Hesselbach’s triangle

Reduces upwards, laterally & backwards Reduces upwards & straight backwards Controlled after reduction by pressure over the deep ring May descend down the scrotum

Controlled after reduction by pressure over the superficial ring Does not descend down the scrotum

Narrow; strangulation at superficial ring

Rarely causes strangulation

Does not readily reduce on lying down More common in young adults & infants

Readily reduces on lying down More common in old men

ABDOMINAL HERNIA

Techniques of inguinal hernia repair • Herniotomy involves removal of the sac and closure of the neck • Herniorrhaphy involves a form of reconstruction to o Restore the disturbed anatomy o Increase the strength of the abdominal wall o Construct a barrier to recurrence • Shouldice or Liechtenstein now regarded as 'gold standard' • Laparoscopic hernia repair should be reserved for bilateral or recurrent hernia Complications of hernia repairs • Urinary retention • Scrotal haematoma • Damage to the ileoinguinal nerve • Ischaemic orchitis • Recurrent hernia Recurrent inguinal hernia • Recurrence rate varies with herniorrhaphy technique and duration of follow up • Factor involved in recurrence include: o Inadequate preoperative selection o Type of hernia o Type of operation o Postoperative wound infection • Recurrent hernias should be repaired using a mesh technique • Can be performed as either an open or a laparoscopic procedure • Patients should be consented for a possible orchidectomy Differentials of inguinal and femoral hernias Inguinal hernia Femoral hernia Femoral hernia Inguinal hernia Vaginal hydrocele Lymphadenopathy Hydrocele of the cord Saphena varix Undescended testis Ectopic testis Lipoma of the cord Psoas abscess Psoas bursa Lipoma

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! Umbilical hernias • Two types of umbilical hernia occur in adults • True umbilical hernias are rare o Occur with abdominal distension (e.g. ascites) • Para-umbilical hernias are more common o Occurs through the superior aspect of the umbilical scar • Female : male ratio is 5:1 • Usually contain omentum • Neck is often tight and the hernias are often irreducible Differential diagnosis • Cyst of the vitello-intestinal duct • Urachal cyst • Metastatic tumour deposit (Sister Joseph's nodule) Management • Management of true and para-umbilical hernias is similar • Surgery is usually performed through a infra-umbilical incision • Occasionally the umbilicus needs to be excised • Contents of the hernia are reduced • Defect in linea alba can be repaired with: o An overlapping Mayo repair o A mesh repair Epigastric hernia • Arises through a congenital weakness if the linea alba • Hernia usually consists of extra-peritoneal fat from near to falciform ligament • Male : female ratio is 3:1 • Strangulation is rare • Can be repaired with either sutures or a mesh Spigelian hernia • Occurs at the lateral edge of the rectus sheath • Interparietal hernia in the line of the linea semilunaris • Usually occurs at the level of the arcuate line Obturator hernia • Occurs in the obturator canal • Usually asymptomatic until strangulation occurs • May complain of pain on the medial aspect of the thigh • Vaginal examination may allow identification of a lump in the region of the obturator foramen ABDOMINAL HERNIA

Incisional hernia • Occurs through the scar from a previous operation • 1% of all transparietal abdominal incisions result in a hernia • Account for 10% of all abdominal wall hernias • Partial dehiscence of all deep fascial layers occurs • Skin remains intact • Most develop within a year of surgery • Symptoms are often minimal with cosmetic appearance the main concern • Most are wide necked but strangulation can occur Aetiological factors • Preoperative o Increasing age o Malnutrition o Sepsis o Uraemia o Jaundice o Obesity o Diabetes o Steroids

•

•

Operative o Type of incision o Technique and materials used o Type of operations o Use of abdominal drains Postoperative o Wound infection o Abdominal distension o Chest infection or cough

Management • CT or ultrasound may clarify muscular defect and hernial sac content • The elderly or infirm may be helped by an abdominal wall support • If surgery is required the following should be considered o Fascial closure or mayo-type repair using sutures o A 'keel repair' using sutures o A mesh repair using polypropylene or PTFE o Mesh can be placed as a sublay, onlay or inlay • The results with mesh are superior to suture repairs o Composite meshes may offer reduced risk of complications o A sublay mesh repair may have the lowest recurrence rate Special types of hernia • Richter's hernia o Partial enterocele o presents with strangulation and obstruction • Maydl's hernia o W loop strangulation o Strangulated bowel within abdominal cavity • Littre's hernia o Strangulated Meckel's diverticulum o Can cause small bowel fistula 38

! GROIN LUMPS Hydrocele

Epididymal Cyst

Points from examination: • Very swollen scrotum; uniformly enlarged • Cannot define testis well; no separable from testis • Maybe firm, tense or lax • Maybe transilluminable if acute (less in chronic hydrocele) • Can get above the mass; the superficial ring is distinct

Points from examination: • Small mass separate from testis; can get above it • Firm; maybe loculated; transilluminable if large cyst • Often multiple in the head of epididymis • May occur as a complication of vasectomy (spermatoceles)

Definition of hydrocele: • Excess accumulation of fluid in processus vaginalis (fold of peritoneum as testis descends; usually patent for fluid to accumulate) o

Types of 1 hydrocele: • Vaginal hydrocele: o Only in tunica vaginalis & does not extend into the cord • Hydrocele of the cord o Mass around the cord; attached distally to the testis o Difficult to distinguish from irreducible inguinoscrotal hernia o May extend up and beyond • Congenital hydrocele: patent processus vaginalis filled with peritoneal fluid • Infantile hydrocele: hydrocele of cord and congenital hydrocele o

Types of 2 hydrocele • From testicular tumours • From torsion • From trauma • From orchitis (any inflm) Treatment options: • Conservative: o Watch & wait or Aspiration [tend to reaccumulate] o o Must exclude a 2 cause • Surgical: o Lord’s plication of the sac o Jaboulay’s operation to evert the sac

OTHER GROIN LUMPS

Treatment: • Conservative [mainstay] • Surgical: if painful, very large or frequent recurrences. Complicated by operative damage and fibrosis of epididymis  subfertility Varicocele Points from examination: • Best noticed on palpating the standing patient • Mass is separate from testis; can get above it • Feels like a bag of worms; +ve cough impulse • Not transilluminable Definition: • Dilated, tortuous pampiniform plexus • 98% on Left side: left vein is more vertical, connects to left renal vein, longer than right one, often lacks a terminal valve Causes: • Idiopathic in younger males around puberty • In older men with retroperitoneal disease: RCC Treatment options: • Conservative: risk of infertility • Surgical: o Transfemoral radiological embolization with coil or sclerosant o Excise the surrounding veins via high retroperitoneum, inguinal or laparoscopic approach

39

! Testicular Torsion (Surgical emergency) Testicular Tumor Points from examination: • Inseparable from the testis; can get above i • Hard, nodular, irregular, non-tender • Not transilluminable (but maybe a/w hydrocele) DDx: • •

Chronic infection with scarring Long standing hydrocele with calcification,

Classification: • Mostly seminomas or teratomas o Seminomas: 30-40YO, normal tumour markers, Rx with RT to paraaortic nodes and CT according to staging o Teratomas: 20-30YO, AFP/ BHCG raised in 90%, Rx with CT • Others: embryonal carcinoma, choriocarcinoma, yolk sac tumour, Leydig cell tumours (10% malignant ; a/w gynaecomastia), Sertoli cell tumour (a/w gynaecomastia), Lymphoma (look for lymphoma elsewhere; poor prognosis) Treatment: • Staging, excision of whole testis with combination chemotherapy

OTHER GROIN LUMPS

Clinical features: • Children/ teenagers • acute abdomen (T10 innervation) & acute scrotum a/w vomiting • swollen and tender scrotum, testis is high in scrotum; pain worsen by lifting testis up • Previous attacks of self-limiting pain; ppt by trauma, cycling, straining, coitus DDx: • • •

Epididymitis Torsion of testicular appendage (pea coloured lump through scrotum) Strangulated inguinoscrotal hernia

Cause: • Maldescended testis hanging like a bell clapper within tunica vaginalis Treatment: • Emergency exploration if Doppler US –ve for flow or clinical suspicion o Untwisting (lateral) of affected testis and orchidopexy of both testis to scrotum o Warm up with warm pad to see reperfusion or check with doppler after untwisting [4h before ischaemia] • If dead, excise and replace with prosthesis

40

! ABDOMINAL STOMAS • •

A stoma is a surgically created communication between a hollow viscus and the skin Functionally they can be end, loop or continent stoma

Indications • Input: feeding (PEG) • Output: decompression/lavage, defunctioning/diversion, draining Stoma siting • Over the rectus sheath (decrease risk of prolapse) • Away from: o Surgical incision – risk of wound contamination and infection o Skin creases or bony prominence – allow flushing with skin to prevent leakage o Old hernia scars – risk of hernia • Easy accessibility • Ensure compatible with the clothing worn by the patient • Ideally should be marked preoperatively by stoma nurse Colostomy RUQ or LIF Flushed with skin Firm brown fecal output Larger diameter of stoma

Ileostomy RIF 3cm ‘sprout’ as ileal contents corrosive Watery greenish ilieal output Small diameter

Types of stomas Permanent (end colostomy) • When no distal bowel remaining • Low rectal/ anal tumor requiring abdomino-perineal resection • Panproctocolectomy without ileal pouch anal anastomosis e.g. FAP • Usually sited on the left side with a single opening Temporary • Decompression – relief of large bowel obstruction causing proximal dilatation • Defunctioning – to protect a distal bowel anastomosis o Previously contaminated bowel o Technical considerations e.g. after low anterior resection, where risk of anastomotic leakage is high o Usually loop ileostomies or colostomies with 2 openings (ileostomies usually on the right side, colostomies in the epigastric/hypochondriac [transverse colostomy] or left side) • To rest an inflamed distal portion e.g. acute Crohn’s Complications Functional disorders • Excess action (stoma diarrhea) o Distal colostomy should produce solid faeces o Ileostomy will produce 500-700 ml/day of liquid effluent o If excess output consider  Inflammatory bowel disease  Para-intestinal sepsis  Subacute obstruction o Correct electrolyte and water imbalance • Reduced action • Consider simple constipation or obstruction Structural complications • Necrosis – especially if tension over stoma intra-op • Detachment • Prolapse – refashion stoma • Parastomal herniation – refashion stoma • Stenosis – refashion stoma • Recession • Ulceration • Fistula formation • Skin excoriation due to corrosive ilieal output

GASTROINTESTINAL STOMA

41

! THE ESOPHAGUS Anatomy • 25cm long muscular tube o Starts @ cricoid cartilage (C6) linking oropharynx - upper esophageal sphincter is formed by cricopharyngeus muscle  To stomach @ T10 o LES is not an anatomical sphincter but a physiological one  Increased tone of muscularis propria  Fibres of right diaphragmatic crus looping around cardioesophageal jx that contract during coughing/sneezing/any increase in intra-abdo pressure to prevent reflux  Angle of His where esophagus joins stomach -- acts as valve  Intra-abdo pressure is higher than intra-thoracic pressure • 3 narrow points o Cricopharyngeus muscle (15cm from incisors) o Carina where left bronchus crosses esophagus (27cm from incisors) o Esophagus passes through diaphragm (40cm from incisors) • Structure: mucosa, submucosa, muscularis propria, adventitia (no serosa except for short segment of intra-abdominal esophagus) o Muscularis propria is striated muscle in upper 1/3, striated and smooth in lower 1/3, smooth in lower 1/3 • Blood supply o Upper 1/3: inferior thyroid artery ; brachiocephalic veins o Middle 1/3: esophageal branches of aorta ; azygos veins o Lower 1/3: esophageal branches of left gastric a. ; left gastric v. Physiology of swallowing Oral Mastication forms bolus on dorsum of tongue Tongue contracts upwards and backwards - bolus pushed against hard palate Soft palate elevates to close nasopharynx Further elevation of tongue pushes food into oropharynx Pharyngeal Epiglottis falls back + pharyngeal muscles contract to bring larynx upwards -- makes laryngeal inlet smaller such that it is closed off by epiglottis Pharyngeal muscles contract to propel food bolus pass the relaxed cricopharyngeus into esophagus Esophageal Involuntary contractions of muscularis propria -- peristaltic waves to propel food bolus! UPPER GASTROINTESTINAL SURGERY

42

Mechanical

Neuromuscular

! APPROACH TO DYSPHAGIA Oropharyngeal Coordination - Stroke - Parkinson’s disease - Brainstem tumors Nerve & muscle dysfx - Degenerative conditions e.g. ALS, MS - Peripheral neuropathy - Myasthenia gravis - Myopathies e.g. Myotonic dystrophy Tumors Inflammatory masses e.g. Abscess Esophageal webs Pharyngeal pouch Anterior mediastinal mass

Esophageal Achalasia Spastic motor disorders e.g. Diffuse esophageal spasm, hypertensive LES Scleroderma

Intrinsic structural lesions - Tumors - Strictures – secondary to inflammation/ radiation/chemicals/medication - Lower esophageal rings/esophageal webs - Foreign bodies Extrinsic structural lesions - Vascular compression (aorta/LA) - Mediastinal mass - thyroid/enlarge LN

•

•

Others e.g. Esophagitis due to reflux, infection, RT, medication or chemicals History • Is there odynophagia (pain a/w difficulty swallowing) o Signifies some form of esophagitis: infectious (candida/herpes) or post-RT or chemical-induced (usually alcohol) or reflux o Esophageal spasm o Scleroderma o Pain occurs late in achalasia and ca esophagus • Diffx oropharyngeal from esophageal dysphagia o Oropharyngeal  Complains of difficulty initiating swallowing  May be a/w choking, coughing, nasal regurgitation  Voice may be nasal (bulbar palsy)  Cause is usually neuromuscular rather than mechanical (most commonly stroke) UPPER GASTROINTESTINAL SURGERY

Esophageal  Pt c/o food getting stuck in throat or chest  Note: pt’s localization of symptom usually does not correspond to actual site of pathology  Can be due to neuromuscular dysfx or mechanical obs Diffx mechanical from neuromuscular dysfx o Mechanical  More difficulty swallowing solids than fluids  May have regurg of undigested food  Recent onset of dysphagia that is progressively worsening + LOW = high suspicion for esophageal ca  Intermittent symptoms suggest webs/rings o Neuromuscular  More trouble swallowing fluids than solids  Dysphagia is long-standing and slowly progressive  Intermittent symptoms suggest diffuse esophageal spasm, nutcracker esophagus  May have hx of stroke or neuromuscular dz History of predisposing conditions o Reflux symptoms i.e. Retrosternal burning pain (heartburn), sour acid reflux into mouth (acid brash), excessive salivation (water brash), aggravated by lying down o Caustic chemical ingestion e.g. Suicidal swallowing sulfuric acid o Smoking, chronic alcohol ingestion o Radiation to chest o Medical hx o S/S of systemic disease e.g. Stroke, scleroderma, Parkinson’s Systemic review o LOW - occurs in ca and achalasia (but onset much later in achalasia) o Complications  S/S of anaemia - bleeding from tumor?  S/S of aspiration pneumonia - fever, cough, SOB Tumor spread o Hoarseness of voice (RLN) o Fever, cough, hemoptysis (tracheo-esophageal fistula) o Hematemesis (invasion into aorta) o Neck lump (LN mets) o

•

•

43

! Physical examination • General condition o Vitals (HR/BP) - pt may be hypovolemic due to vomiting/decreased fluid intake o Cachetic? - nutritional status o Conjunctival pallor - bleeding from tumor, esophagitis ulcerations o Scleral icterus/jaundice? Mets to liver o Dehydration - mucus membranes • Disease o Cervical LNs (esp Virchow’s nodes) o Scars/RT marks on abdo/chest o Any masses in abdo o Hepatomegaly? Ascites? o PR exam for melaena (UBGIT 2/2 esophageal ca) • Complications of disease o Signs of pneumonia - febrile, toxic, lung creps, decreased air entry (usually over right lower lobe) • Treatment o Enteral  NGT feeding  Gastrostomy/jejunostomy o Parenteral - TPN Initial management • Stabilize o Resus if hemodynamically unstable o IV fluids + correct any electrolyte imbalances o Feed with fluids if patient can tolerate (i.e. Only solid foods are the problem), otherwise - tube feeding or TPN (may have to correct state of malnutrition) o Keep NBM if even fluids are not tolerated o Treat any aspiration pneumonia - NBM, NGT, IV abx • Investigate for underlying cause - treat

UPPER GASTROINTESTINAL SURGERY

Investigations • Diagnostic o Barium swallow  Adv: Less invasive than OGD, esp when suspecting webs or divert where OGD may cause perforation • But if pt has high risk of aspiration - barium swallow is dangerous  Visualize obstructive lesion • Shouldering of a stricture o Benign: smoother contour o Malignant: abrupt right-angled contour • Bird’s beak sign of achalasia • Visualize any pouch/diverticulum • Diffuse esophageal spasm - corkscrew appearance o OGD  Adv: direct visualization of lesion, able to take biopsy in suspected malignancy  Adv: can be therapeutic i.e. Stop any bleed, stent lumen o Manometry -- gold standard for diagnosing achalasia  Criteria: 1) absence of peristalsis 2) very high LES pressure 3) absence of relaxation @ LES on swallowing food o Videofluoroscopic examination of swallowing (VFES) or flexible endoscopic examination of swallowing (FEES)  Can assess oropharyngeal dysphagia (neuromuscular causes) by looking for penetration and aspiration of various consistencies of food during swallowing • Supportive o Bloods  FBC - Low Hb (anaemia 2/2 chronic tumor bleed); high TW in aspiration pneumonia  UECr - electrolyte disturbances 2/2 vomiting, poor intake, raised creat/urea in dehydration (creat will be raised more than urea in dehydration/prerenal failure) o Imaging  CXR - consolidations in aspiration pneumonia • 24hr probe monitoring: if pt c/o reflux S/S but no signs on OGD o diagnostic test for reflux

44

! GASTRO-ESOPHAGEAL REFLUX DISEASE • • • • •

Affects approximately 40% of the adult population Due to acid or bile reflux Delayed oesophageal clearance also important Gastric hypersecretion rarely implicated Poor correlation between symptoms and endoscopic evidence of oesophagitis o 20% patients with oesophagitis are symptom free o Most gain symptomatic relief with conservative treatment o 30% of patients with symptoms have no endoscopic evidence of mucosal injury

Causes of GERD • Loss of LES function • Delayed gastric emptying • Increased intra-abd pressure • Motor failure of esophagus • Drugs causing smooth muscle relaxation

Natural barriers to gastro-oesophageal reflux Lower oesophageal sphincter • Basal tone • Adaptive pressure changes • Transient lower oesophageal sphincter relaxation External mechanical factors • Flap valve mechanism o Cardio-oesophageal angle o Diaphragmatic pinchcock o Mucosal rosette • Distal oesophageal compression o Phreno-oesophageal ligament o Transmitted abdominal pressure

Conservative treatment Lifestyle modification Drug treatment • Stop smoking • H2 antagonists o Symptomatic relief in 60% at 6 wks • Avoid alcohol o Endoscopic evidence of healing in 40% • Lose weight • Proton pump inhibitors • Raise head of o 80% healing at 8 weeks in H2 bed antagonist resistant disease o More than 20% relapse o Life-long therapy often required Management of strictures • TRO malignancy • Treat using balloon dilatation • Treat underlying reflux UPPER GASTROINTESTINAL SURGERY

Presentation • Heartburn • Acid brash (reflux) • Symptoms occurring after food, and aggravated by lying flat • Long-standing stricture causing disease, odynophagia • Pulmonary symptoms due to aspiration • Chest pain mimicking anginal pain Diagnosis • History – TRO cardiac and malignant cause • OGD - provides histological confirmation and grading o Look for peptic stricture, esophagitis, Barrett’s, hiatal hernia o Savary-Miller grading of oesophagitis 1. Isolated (or sometimes multiple) erythematous or erythematoexudative erosion(s), covering a single mucosal fold 2. Multiple erosions covering several mucosal folds, partly confluent but never circumferential 3. Circular extension of erosive and exudative lesions 4. (a) Ulcer (b) Fibrosis (leading to stenosis and brachyesophagus) 5. Presence of cylindric cell epithelialization acquired in the form of a disc, strip or sleeve • Barium swallow and follow through for motility disorders • 24-hour pH monitoring - probe placed 5 cm above lower oesophageal sphincter (LOS) – Diagnostic • Oesophageal manometry (motility disorder) Surgical options • Indications: o Failure of medical therapy; Recurrent symptomatic relapse o Esophagitis with frank ulceration or stricture o Complications of reflux esophagitis (Barrett’s, aspiration) • Fundoplication o Mobilization of gastric fundus, tension free wrap around 50 Fr oesophageal bougie, wrap suture line of less than 3 cm o Partial fundoplication is associated with less dysphagia and fewer gas related symptoms (anterior 90º/180º, posterior 270º) • Complications: o Perforation of the esophagus o 3% develop dysphagia o 11% develop gastric bloat (difficulty burping) o Failure of treatment 45

! BARRETT’S ESOPHAGUS Features • Intestinal metaplasia of the oesophageal epithelial lining (stratified squamous epithelium converted to mucus-secreting columnar epithelium with goblet cells) • Associated with long-term reflux – an adaptation mechanism where intestinal epithelium withstands exposure to acidic reflux better than oesophageal epithelium • Diagnosed on endoscopy and histology: o The squamocolumnar junction (or Z line) is visible on endoscopy as gastric and intestinal type epithelium is pink and granular in appearance, but stratified squamous epithelium is smooth and pale o If the squamocolumnar junction is above the gastro-oesophageal junction (where gastric folds begin) (i.e. they do not align) and biopsy of the junction shows intestinal metaplasia, the patient is diagnosed to have Barrett’s oesophagus • Short segment Barrett’s is defined as the squamocolumnar junction being <3cm above the gastro-oesophageal junction, while in long segment Barrett’s the distance between the two junctions is >3cm. • Classic Long segment Barrett’s is associated with more severe reflux, as well as higher risk of dysplasia and subsequent adenocarcinoma development than short segment Barrett’s • Risk of development of adenocarcinoma is about 10-15% in 10 years Management Treatment of underlying reflux • Lifestyle changes, acid suppression, surgery etc Endoscopic surveillance • If patient has high grade dysplasia, it should be treated (see below), otherwise to undergo intensive surveillance (q3mths for at least one year) to detect cancer development Treatment of high-grade dysplasia • Endoscopic therapies to ablate the dysplastic tissue e.g. photodynamic therapy, laser therapy, argon plasma coagulation  will not remove all dysplastic cells thus potential for malignancy still remains • Oesophagectomy is the only definitive treatment to remove all dysplasia, but is associated with high morbidity and mortality • Possibility of endoscopic mucosal resection as a treatment modality UPPER GASTROINTESTINAL SURGERY

ACHALASIA •

•

Due to reduced number of ganglion cells in myenteric plexus o Abnormal peristalsis o Failure of LES to relax o Affects body and distal esophagus Aetiology is unknown but a neurotropic virus may be important

Clinical features • Commonest in patients between 40 - 70 years • Male : female ratio is approximately equal • Presents with dysphagia, weight loss, regurgitation, retrosternal chest pain • 10% of patients develop squamous carcinoma after 15-25 yrs Investigations • CXR - widening of mediastinum, air / fluid level and absence of gastric fundus gas bubble • Barium Swallow – proximal dilatation & residue, small tertiary contractions and distal Bird’s Beak narrowing • Manometry - absent primary peristaltic wave & non-propulsive tertiary contractions; high pressure at LES • Endoscopy TRO 'pseudoachalasia' due to submucosal carcinoma o Tight lower oesophageal sphincter which relaxes with gentle pressure Differential diagnosis • Diffuse oesophageal spasm • Infiltrating carcinoma • Hypertrophic LES

• •

Scleroderma Chagas' disease

Treatment options Conservative • Injection of botulinum toxin • Rider Moeller Pneumatic Balloon – inflated to 300 mmHg for 3 minutes o 40% dysphagia free at 5 years Surgical: Laparoscopic Heller Cardiomyotomy • Splitting of muscular wall at LES • 85% will have an improvement in symptoms at 5 yrs • 10% develop oesophageal reflux; 3% will develop oesophageal stricture • Some combine cardiomyotomy with an antireflux operation

46

! ESOPHAGEAL CANCER •

• • • •

rd

3 most common GIT cancer, especially in males o 70% are squamous cell carcinomas in the upper or middle 1/3 o 30% are adenocarcinomas in lower 1/3 Overall 5 year survival is very poor and is at best 20% Less than 50% patients are suitable for potentially curative treatment Of those undergoing 'curative' treatment less than 40% survive 1 year Overall prognosis - 80% mortality at 1yr, 5yr-survival <10%

Risk factors • Squamous cell carcinoma o Alcohol 2x / tobacco 10x o Achalasia (2-8%) o Diet high in nitrosamines o Coeliac Disease o Aflatoxins o Genetic – Tylosis (keratosis) o Trace element deficiency o High incidence in Transkei, molybdenum Areas of Northern China and o Vitamin deficiencies - A & C the Caspian littoral region o Plummer-Vinson (webs) o Fe-deficiency anemia • Adenocarcinoma o 15% associated with Barrett's Oesophagus o Reflux; Smoking 10x Pathology • Site

•

•

•

o 10% in upper 1/3 o 60% in middle 1/3 o 30% in lower 1/3 3 growth patterns o Fungating (60%) o Ulcerative (25%) o Infiltrative (15%) Tumor spread o Direct extension into adj strs o Vascular invasion o Lymphatic spread Common sites of mets: liver, lungs, bone


Clinical features • Progressive dysphagia, insidious onset o Retrosternal discomfort/indigestion • Dysphagia – first solid then liquid • Pain develops late • Anaemia +/- melaena or hematemesis (occult bleed usually) • Vocal cord paralysis - left more than right • Aspiration pneumonia • Respiratory symptoms due to overspill or occasionally a tracheaoesophageal fistula • Weight loss Assessment Diagnosis confirmed by: • Endoscopy plus biopsy / cytology • Barium swallow

Resectability and fitness for surgery assessed by: • Chest x-ray • Lung function tests(FEV1 > 1L) • Liver ultrasound • Endoscopic ultrasound • Bronchoscopy • Laparoscopy • Thoracic CT

Staging T: Tis does not breach basement membrane T1 does not invade muscularis, T2 does T3 invades adventitia, T4 invades surrounding strs N: according to number of regional nodes involved M: nonregional LN involvement vs distant mets

Feeding in esophageal obstruction • Feeding via oropharyngeal route is preferred unless passage is obstructed or it is unsafe (high risk of aspiration) • If able to pass NG tube around tumor -- feed via NG o Also consider problems with long-term NG placement o Consider PEG placement for long-term feeding  PEG = percutaneous endoscopic gastrostomy (scope in stomach - can poke tube percutaneously) • If unable to pass tube/scope around tumor - consider open gastrostomy • Total parenteral nutrition (TPN) an option but more complications and higher cost • Relief of obstruction (above) can enable oral feeding but dysphagia will return as tumor grows 47

! Investigations • Diagnosis o Barium swallow - high accuracy in showing mucosal irregularity and annular constrictions but no histo diagnosis o OGD - allows biopsy with histo confirmation • Staging o Endoscopic Ultrasound  If endoscope can pass around lesion - EUS is good for T staging and can identify enlarged LNs o CXR  Presence of lung mets, pleural/pericardial effusion  Aspiration pneumonia  Tracheal deviation or extrinsic compression of tracheobronchial system  Widened superior mediastinum in upper tumor  Raised hemidiaphragm if phrenic nerve involved o CT or MRI of thorax with extension to liver and adrenals -- TNM o Bronchoscopy - exclude bronchial involvement o Laryngoscope to assess for vocal cord paralysis o Bone scan - bony mets • Supportive o FBC - Low Hb (anaemia), high TW (aspiration pneumonia) o UECr - electrolyte disturbances from vomiting/poor intake/dehydration (crea>>urea) o LFTs - low albumin in malnutrition states Management • 3 modalities available: surgery, chemo, RT (use singly or in combination) • Aims: curative vs palliative (half of cancers unresectable on ppt) o Surgical Rx usually is performed with curative intention, but can also achieve good long-term palliation of symptoms • Choice of treatment depends on patient factors like age, co-morb, nutritional state, life expectancy and cancer prognosis • Curative treatment: o Pre-op neoadjuvant chemoRT, esophagectomy, post-op adjuvant chemoRT (for responsive tumors) Radiotherapy • Improved survival compared to surgery for SCC (radiosensitive) • Usually given together with chemo o External beam radiotherapy or Brachytherapy • Complications: fistula, strictures UPPER GASTROINTESTINAL SURGERY

Chemotherapy • 5-FU and cisplatin, given as neoadjuvant and adjuvant Surgery • Only 40% tumours are resectable (but curative in early lesions o Operative mortality now less than 10% o Should not be done in patients with mets or contraindications • Operative approaches o Endoluminal surgery for early lesions o Esophagectomy  Need 10 cm proximal clearance  Total gastrectomy via thoracoabdominal (Adeno CA)  Subtotal two-stage oesophagectomy (Ivor-Lewis)  Subtotal three-stage oesophagectomy (McKeown)  Transhiatal oesophagectomy  Complications:  Intraop injury to lungs, thoracic duct, RLN  Early: respi (atelectasis, pneumonia), mediastinitis from anastomotic leak  Late: reflux, strictures Palliative treatment Aim to relieve obstruction and dysphagia with minimal morbidity • Surgical debulking • Oesophageal stenting o Endoscopic or radiological placement most commonly practiced o Atkinson tube is the most commonly placed endoscopically o Requires dilatation with risk of oesophageal perforation o Complications of stents and tubes:  Oesophageal perforation  Tube displacement or migration  Tube blockage due to ingrowth or overgrowth • Endoscopic laser fulguration o Produces good palliation in over 60% of cases o May need to be repeated every 4 to 6 weeks o Associated with oesophageal perforation in about 5% cases • Radiation: for unresectable, bleeding, painful lesions o External beam radiotherapy o Brachytherapy • Diathermy; Alcohol injection; Photodynamic therapy

48

! PEPTIC ULCER DISEASE • •

Incidence about 100 per 100,000 per year 68% of patients are over 60 years of age

An imbalance between mucosal protective mechanisms against acid, and aggressive forces that damage the gastric mucosa • Aggressive forces: gastric activity and pepsin activity • Protective mechanisms: mucus secretion, bicarbonate secretion, robust mucosal blood flow to remove protons, epithelial regenerative capacity, prostaglandin secretion by mucosa to maintain blood flow Etiology H. pylori (Gram-negative spiral flagellated bacterium, produces urease) • Causes a local inflammatory reaction and secretes enzymes that break down the gastric mucosal barrier, and also enhances gastric acid secretion and decreases bicarbonate production • 90% patients with duodenal ulcer, 70% patients with gastric ulcer • 60% patients with gastric cancer NSAIDs • Impair mucosal prostaglandin production (through non-selective COX inhibition)  prostaglandins are important for mucosal bicarbonate and mucin production and inhibiting gastric acid secretion, as well as maintaining mucosal blood flow • Accounts for most of the rest of ulcer disease not caused by H. pylori • 30% of patients on NSAIDs will get an ulcer, of which one-fifth will have a clinically significant ulcer i.e. symptomatic, bleeding Other factors • Vices: Cigarette smoking, Alcohol • Steroids and anticoagulants do not increase the risk of ulcer formation, but increase the risk of bleeding in an existent ulcer


Presentation • Incidentally detected on OGD • Symptoms of dyspepsia o Ulcer-like dyspepsia: pain in the upper abdomen o Dysmotility-like dyspepsia: non-painful discomfort in the upper abdomen, associated with upper abdominal fullness, early satiety, bloating, belching, nausea o Unspecified dyspepsia: Pain is usually worse with food in a gastric ulcer, while it is relieved by food in a duodenal ulcer • Bleed (presenting with haematemesis (coffee-grounds vomitus) or melaena) • Perforation o Sudden generalized abdominal pain aggravated movement o Board-like rigidity, guarding (signs of peritonism) o Erect CXR will show air under diaphragm Investigation • Endoscopy (OGD) o Diagnostic  Confirm ulcer disease & localize ulcer  Biopsy - TRO malignancy  Biopsy antral tissue - for CLO (campylobacter-like organism to test for H. pylori) o Prognostic  Forrest classification (or endoscopic stigmata of recent  hemorrhage ESRH) – bleeding risk  Ia: spurting (arterial) -- 90%  Ib: non-spurting ooze (venous) -- 20%  IIa: non-bleeding w visible vessel -- 40%  IIb: non-bleeding ulcer w adherent clot -- 20%  IIc: ulcer w hematin-covered base -- 10%  III: ulcer w clean base -- 5% o Therapeutic  Injection with adrenaline -- to create edema and tamponade effect  Thermal coagulation with heater probe  Hemostatic clipping (endoclip)  Argon plasma coagulation • Microscopy – silver or Giemsa staining of antral biopsies • Culture – difficult and requires special culture techniques • CLO rapid urease test – colour changes due to change in pH 13 14 • C or C breath test – Ingested radioactive urea is broken down to CO2 • Serology – detected immunologically using an ELISA 49

! Conservative Management Gastro-protection: Proton Pump inhibitors • 20mg omeprazole OM • Promotes ulcer healing even with ongoing NSAID use • 90 - 100% healing at 2 months • Low recurrence on long term maintenance H2 Antagonists • Give 40mg BD famotidine if allergic to omeprazole • 65% healing at 1 mth, 85% healing at 2 • If stop treatment - 90% recurrence at 2yr • If maintenance therapy - 20% recurrence at 5 years H. Pylori eradication • Two weeks amoxicillin, clarithromycin and omeprazole o If allergic to penicillin, substitute amox with metronidazole o Document eradication with endoscopy + CLO, urea breath test or stool serology (after 6 wks) o 80% cured with dual or triple therapy o Treatment failure occurs in up to 20% - go for quadruple therapy (add bismuth) • The number of complications however remain unchanged o May be increasing due to increased NSAID use in elderly o Bleeding and perforation still have mortality of >10% Surgical Management Gastric ulcer Indication for surgery: • Failure to heal after 3 months conservative therapy • Dysplasia/ carcinoma • Recurrence • Persistent bleed/perf Surgery (if prepyloric ulcer - can treat like duodenal ulcer): • Oversew bleeding vessel • Gastrectomy


Duodenal Ulcer Indications: • Persistent bleeding (e.g. Erosion of posterior D1 ulcer into gastroduodenal artery) • Perforation - contained or free • Gastric outlet obstruction - patient presents with vomiting of undigested food not long after meal + succussion splash positive + air-fluid levels on AXR + hypokalemic hypochloraemic metabolic alkalosis with paradoxical aciduria • Failure of medical management (ulcer does not heal) Surgical options for duodenal ulceration: • Oversew bleeding vessel with omental patch repair • Reduce acid production by the stomach via Truncal vagotomy o Cephalic phase reduced by vagotomy o Antral phase reduced by antrectomy • May require gastric drainage procedure to overcome effects of vagotomy on gastric drainage Surgical Procedures Open surgical procedures • Truncal vagotomy with: o Pyloroplasty o Gastrojejunostomy o Antrectomy • Highly selective vagotomy • Anterior seromyotomy and posterior truncal vagotomy Post gastrectomy complications Percentage Diarrhoea 16 Dumping 14 Bilious vomiting 10 Iron deficiency anaemia 12 B12 deficiency 14 Folate deficiency 32 Recurrent ulceration 2

Laparoscopic peptic ulcer operations • Thoracoscopic truncal vagotomy and pyloric stretch • Highly selective vagotomy • Posterior truncal vagotomy with: o Selective anterior vagotomy o Anterior seromyotomy Post vagotomy complications Percentage Diarrhoea 2 Dumping 2 Bilious vomiting <2

50

! GASTRIC CARCINOMA Epidemiology th th • Gastric carcinoma 5 in men, 8 in women in Singapore • Incidents increases after 50yo Risk factors • Environmental o Diet low in Vitamin C; preserved food, nitrosamines, polycyclic hydrocarbons o Alcohol, Smoking o Occupational exposure: asbestos, heavy metal, rubber • Genetic - Blood group A, , e-cadherin mutation, family history, HNPCC Precursor states • Post gastrectomy (Bilroth II) o Chronic exposure of gastric mucosa to biliary, pancreatic & intestinal secretions @ anastomotic zone, >15yrs after surgery • Gastric polyps o Inflammatory polyps - highest risk (75-90%) o Adenomatous polyps - 10-20% risk, increased if large (>2cm) &/or villous histology • Chronic gastritis • Hypertrophic gastritis - inflammatory disease of gastric epithelium - up to 10% risk of malignant change • Pernicious anemia - autoAbs to parietal cells with achlorhydria - 2-10% risk of gastric ca • PUD -- <1% risk of malignant change • H. Pylori infection -- 3-6x increased risk

Clinical presentation • Asymptomatic o Most present late and are not amenable to radical surgery o Upper GI endoscopy should be considered in all with dyspeptic symptoms over 40 years • Symptomatic -- very non-specific o Abdo pain o Dysphagia - a/w proximal cancers  New onset dysphagia in >35yo should be cause for concern o Nausea, vomiting, anorexia (and LOW) o Palpable mass o Early satiety • Complications (bleed, block, burst, burrow) o Bleed  Anaemia - SOB, CP, decreased ET, palpitations, fatigue, postural giddiness  UBGIT - coffee grounds vomitus / melena o Block  Gastric outlet obstruction - projectile vomiting shortly after meal  Vomiting, aspiration pneumonia, dehydration, hypokalemic hypochloremic metabolic alkalosis with aciduria  Malnutrition o Burst  Perforation - peritonism o Burrow  Fistulas  Metastasis - LOA/LOW/malaise

Morphology – Borrmann’s classification • Type I (3%): non-ulcerated, polypoid, growing intraluminally • Type II (18%): Ulcerated, circumscribed with sharp margins • Type III (16%): Ulcerated, margins not sharply circumscribed • Type IV (63%): Diffuse, infiltrating, may be ulcerated, may infiltrate extensively (entire stomach) - linitis plastica Location • 30% pylorus/antrum • 20% body • 37% cardia • 12% entire stomach UPPER GASTROINTESTINAL SURGERY

51

! Histology Adenocarcinoma (90-95%) Lauren classification • Intestinal type *more common overall o Occurs in high risk population (i.e. Older, male) o Distal 1/3 of stomach; arise from mucosa o H. pylori --> chronic gastritis --> intestinal metaplasia --> dysplasia --> carcinoma o a/w ERB2, ERB3 receptor stimulation • Diffuse type o Occurs in low risk population - younger, female o Proximal 1/3, cardio-esophageal jx; arise from submucosa o More aggressive, invasive growth pattern - rapid submucosal spread o Present later, worse prognosis  Transmural and lymphatic spread w early mets o Associated with K-sam oncogene • If detected early (early gastric ca) o Confined to mucosa and submucosa o Good prognosis and survival regardless of size, LNs status, histological grade Leiomyosarcoma (2-3%) • Arises from the smooth muscle of the stomach wall • Lymphatic spread is rare • 75% present with an upper gastrointestinal bleed • 60% have palpable abdominal mass • Diagnosis can be confirmed by endoscopy and CT scanning • Partial gastrectomy; 5-year survival is approximately 50% Gastric lymphoma (1%) • Stomach - commonest extranodal primary site for non-Hodgkin's lymphoma • Clinically presents similar to gastric carcinoma • 70% of tumours are resectable; 5-year survival is approximately 25% • Both adjuvant radiotherapy and chemotherapy may be useful Sister Mary Joseph Nodule • Presents as firm, red, non-tender nodule a/w advanced malignancy • Results from spread of tumour within the falciform ligament • 90% of tumours are adenocarcinomas • Commonest primaries are stomach and ovary


Spread • Direct extension - to neighbouring organs • Lymphatic spread o Regional nodes i.e. Perigastric nodes o Virchow’s node, Umbilical nodes - Sister Mary Joseph node • Hematogenous spread o Liver (look for hepatomegaly with ascites & jaundice on PE) o Lung (SOB?) o Bone (pain over the axial skeleton/spine) o Brain (changes in behavior) • Peritoneal seeding o Omentum - omentum caking o Parietal peritoneum o Ovaries – Krukenberg’s tumor o Cul-de-sac (Blumer’s shelf) Investigations Requires a combination of preoperative investigations & intra-op assessment Diagnostic Staging • OGD confirms diagnosis, • Endoscopic ultrasound may allow site & extent of tumour assessment of intramural tumour penetration (gold standard) • Visualize and biopsy • CXR • Usually ulcer with heaped up edges • CT will assess nodal spread and extent of metastatic disease • Laparoscopy will identify peritoneal seedlings occult on CT (1/5) Supportive • FBC - low HbUECr - if vomiting -- electrolyte disturbances (low K, low Cl, acid-base balance) • LFTs - as a marker of nutritional status (<35 is poor); liver metastases • β-hCG (beta-human chorionic gonadotropin), CA-125, and CEA (carcinoembryonic antigen) TNM staging Tis Carcinoma in situ (does not breach BM) N0 No LNs involved T1 Tumor limited to mucosa & submucosa N1 1-6 regional LNs T2 Tumor invades muscularis mucosa N2 7-15 regional LNs T3 Tumor penetrates serosa N3 >15 regional LNs involved T4 Tumor invades adjacent structures • Prognosis if generally very poor • Overall 5 year survival is approximately 5% • Survival is 70%, 32%, 10% and 3% for Stages 1,2,3 and 4 respectively 52

! Management Principles • A tumour is considered resectable if confined to stomach or N1 or N2 nodes (less than 6 nodes) involved (Stage I and II) o Nodes less than 3 cm from tumour = N1 nodes o Nodes greater than 3 cm from tumour = N2 nodes • If tumour and N1 nodes resected = D1 gastrectomy • If tumour and N2 nodes resected = D2 gastrectomy • Even in patients with incurable disease surgery may palliate symptoms • Chemoradiotherapy may reduce relapse and improve survival Chemotherapy/Radiotherapy Adjuvant therapy • 5-flurouracil with chemotherapy • 5-flurouracil with epirubicin for advanced dz Neoadjuvant therapy • 5-FU and cisplatin can be used to downstage unresectable locally advanced disease -- significant increase in resectability • For resectable disease: pre-op 5-FU, cisplatin, doxorubicin, methotrexate followed by intraperitoneal 5-FU --> improved resection rates, response rates, median survival


Curative Surgery - Wide resection of the tumor to negative margins (at least 6cm) - En-bloc excision of regional LNs & any structures involved by local invasion - Choice btwn subtotal (1/3 of stomach left) and total gastrectomy • Proximal tumors o Total or proximal subtotal possible o Total gastrectomy with Roux-en-Y esophagojejunostomy preferred  avoid post-op morbidity of reflux esophagitis and impaired gastric emptying (a/w prox subtotal gastrect) o Tumors of GE jx  may require esophagogastrectomy with cervical or thoracic anastomosis • Midbody tumors o Generally req total gastrect to achieve adequate margins • Distal tumors o Distal subtotal gastrect - superior post-op nutritional status and quality of life (maintains gastric remnant - residual reservoir fx) and hence preferred if adequate margins can be obtained • Diffuse-type tumors - total gastrectomy - Reconstruction • Billroth I: end to end gastroduodenostomy o Rarely done as it is difficult to mobilize duodenum up to anastomose with residual stomach • Billroth II: gastrojejunostomy o No protection against biliary reflux into stomach • Roux-en-Y o Prevents biliary reflux o Involves 2 anastomoses -- higher chance of leak

53

! Complications of gastrectomy Early • Bleeding, Infx, Anastomotic leak Late • Nutritional disturbances (30%) o Prolonged iron, folate, vitamin B12, calcium, vitamin D deficiencies o Can result in anemia, neuropathy, dementia and osteomalacia (respectively) o Supplementation required - B12 injx, Fe supplementation • Early satiety -- further nutritional status deterioration • Retained antrum syndrome o Prox subtotal gastrect - too much antrum left behind -- increased acidity in residual stomach -- formation of marginal ulcers on jejunal end of anastomosis • Dumping syndrome o Due to loss of reservoir fx & pylorus - rapid emptying of highosmolar carbo load into small intestine o Most common after Billroth II reconstruction o Early (within 30mins)  Nausea, epigastric distress, explosive diarrhea, vasomotor symptoms (dizziness, palpitations, flushing, diaphoresis)  Relieved by recumbence or saline infusion o Late (1-4hrs)  Symptoms are primarily vasomotor  Hormonal response to high simple carbo loads results in  hyperinsulinaemia and reactive hypoglycaemia  Hypoglycaemic s/s relieved by carbohydrate ingestion o Tx: smaller volume meals, increased frequency, avoid simple carbohydrates, liquids should be taken 30mins after solids • Alkaline reflux gastritis o Most commonly a/w Billroth II o Triad of constant epigastric pain, nausea, bilious emesis  Vomiting does not relieve pain, not a/w meals o Endoscopy: inflamed, beefy red, friable proximal mucosa +/- bile reflux o No mechanical obstruction (diffx from loop syndromes) o Rx  Non-surgical: frequent meals, antacids, cholestyramine  Surgical: Roux-en-Y gastrojejunostomy (preferred)


•

•

• •

Roux stasis syndrome (up to 30% of patients after Roux-en-Y) o Chronic abdo pain, nausea, vomiting aggravated by eating o Functional obstruction - due to disruption of peristalsis in duodenum & altered motility in gastric remnant Loop syndromes - mechanical obstruction of either afferent or efferent limbs of Billroth II o Afferent loop (duodenal) syndrome  Caused by bowel kink/volvulus/internal herniation  Severe abdo pain, non-bilious emesis (no bile in NG aspirate)  Elevated bilirubin/amylase  Acute complication: duodenal stump blowout progressive dilation,  peritonitis/abscess/fistula  Chronic complication (with partial obstruction) - blind loop syndrome • Steatorrhea, B12, folate, iron deficiency (due to lack of B12 and fat absorption) (B12 bound to R factor digested by proteases, B12 released to bind to IF to be absorbed) o Efferent loop syndrome  Abdominal pain and bilious emesis o Rx: remove adhesions, revise anastomosis, bowel resection, conversion to Roux-en-Y Intestinal hurry o Inadequate reservoir fx -- poor digestion -- phytobezoar formation Post-vagotomy diarrhea o Watery and episodic o Rx: anti-diarrheals, reduce excessive fluid intake, reduce lactose intake

Palliative • Objective: Prevent obstruction, bleeding, perforation, relieve pain • Obstruction: endoscopic laser ablation, surgical resection (subtotal/total), bypass • Bleed: angioembolization • Pain: external beam radiotherapy (also for low-level ongoing bleed) Prognosis -- stage-dependent Stage I: 90% 5yr survival Stage II: 70% Stage III: 40% Stage IV: 0% 54

Hepatic

Pre-hepatic

• •

Normal serum bilirubin <17umol/L (1mg/dL) Serum bilirubin >35umol/L (2mg/dL) o clinically detectable jaundice/icterus (yellowing of skin & sclera)

Pathogenesis - Increased production of unconj bilirubin by reticuloendothelial sys - Excessive destruction of RBCs (hemolysis) exceeds ability of liver to conjugate - unconj bili accumulates in blood - No increase in conj bili in blood --> none will be found in pee - Increased amt of urobilinogen in gut – reabsorbed & overflow into systemic circulation - excreted by kidneys - Hepatocellular damage -hepatic ability to conjugate bilirubin drops - less excreted into canaliculi - Both unconj and conj bilirubin accumulate in blood

Causes Hereditary - G6PD deficiency - Thalassemia - Hereditary spherocytosis - Sickle cell anaemia

Symptoms and signs - Normal urine/stools - May have anaemic symptoms - Unconj hyperbilirubinaemia - Raised LDH, decreased haptoglobin - Peripheral blood film if Acquired malaria suspected - Malaria - Direct Coomb’s test for - Incompatible blood autoimm transfusions - Stool ova/cyst/ parasites for - Mechanical heart malaria valves - Hemolytic uraemic syndrome (in acute renal failure) - Autoimmune SLE - Infectious - viral - Mixed signs: urine may be hepatitis, dark with normal stool EBV/CMV, TB - LFT - raised AST/ ALT - Cirrhosis / CLD disproportionate to ALP/GGT alcoholic, viral, - In cirrhosis – decreased metabolic or albumin, raised INR infiltrative - AFP to exclude malignancy - Hepatotoxic drugs - Do viral hepatitis serology e.g. Paracetamol (HBV - anti-HBc, HBsAg, O/D, TCM HCV - anti-HCV, HCV RNA, - Autoimmune e.g. HAV - Anti-HAV) SLE - Autoimmune (ANA, anti- Hereditary inability dsDNA) to conjugate or - Metabolic screen excrete ceruloplasmin or 24hr Cu urine O/P - Do abd U/S: look for surface nodularity, increased echogenicity in cirrhosis, signs of portal HTN (splenomeg & ascites)

HEPATOBILIARY AND PANCREATIC SURGERY

Obstructive

! APPROACH TO JAUNDICE

- Obstruction of intrahep or extrahep bile ducts, preventing excretion of conjugated bilirubin - No pigment -- pale stools + conj bili builds up in blood and excreted in pee – dark tea-colored pee - Hepatic and post-hep forms co-exist e.g. CBD stones can also cause biliary cirrhosis, tumor deposits or cirrhosis can destroy liver tissue and compress intrahepatic ducts

Intraluminal - gallstones/ parasites e.g. Ascaris lumbricoides

- Tea-colored pee, pale stools, intense pruritus - Conj hyperbilirubinaemia - Increased ALP/GGT disproportionate to AST/ALT

Mural - Biliary strictures post-ERCP or gallstones of chronic pancreatitis - PBC - intrahepatic bile ducts - PSC - intra&extra hepatic ducts - Cholangitis/ choledochal cyst/ distal cholangio CA

Do abdo U/S - If ducts dilated (>8mm) – do ERCP/MRCP/PTC - If not dilated – further serological testing e.g. For AMA, p-ANCA (PSC), ANA, anti-SMA

Extraluminal - Ca head of pancreas - Other periampullary ca - Mirizzi’s syndrome

•

• •

•

RBCs reach end of life in circulation after ~120 days -- destroyed in reticuloendothelial system -- porphyrin ring of Hb disrupted; iron is recycled for further Hb synthesis -- bilirubin-globin reaches liver (lipidsoluble; water-insoluble) Liver: Bilirubin conjugated with glucuronic acid in hepatocytes -- excreted in bile as water-soluble bilirubin glucuronide Bowel: Bilirubin reduced by bacteria to colourless urobilinogen -- majority excreted in faces where it is broken down to urobilin and stercobilin -colors stool brown o Small amt reabsorbed from intestine - portal venous sys - liver -re-excreted as bile into gut o Some reach systemic circulation and excreted in pee Urine exposed to air - urobilinogen ox to urobilin (darker)

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! History • Onset o Acute (days)  Gall stone disease, Acute hepatitis  Acute Budd-Chiari syndrome, hemolysis o Subacute (weeks to months)  Pancreatic and hepatobiliary malignancy  Intrahepatic cholestasis  RHF o Recurrent episodes – gallstone disease o Resolution? – if yes, benign obstruction; painless progressive = Ca • Associated symptoms o Fever (Chills and rigors)  Sign of inflammation/infection  Cholangitis, viral hepatitis, cholecystitis, Mirizzi’s syndrome o RUQ pain  Cholangitis, acute hepatitis, Budd Chiari, Mirizzi’s  Lack of pain + gradual onset + obstructive suggests pancreatic/bile duct/periampullary malignancy/ drug/autoimmune o Confusion – sepsis (cholangitis) or hepatic encephalopathy o Easy bruising  Ask about gum bleeding, nosebleeds, easy bruising – coagulopathy can be caused by liver failure.  Jaundice can also be due to hemolysis – DIC, malaria o Back pain  Viral hepatitis and severe hemolysis o Dark urine/pale stools  Excessive conjugated bile appearing in urine  May not distinguish obstruction from hemolysis o Pruritus  Cholestatic picture  Bile duct obstruction, drug induced o Weight loss (Malignancy, chronic liver disease) Travel History • Hep A/B • Liver flukes Medications and vaccines • Current and previous medications • Hep A and B vaccinations

Gynae • Liver disease in pregnancy Family history • Liver disease, hepatitis, blood disorders • Hemochromatosis, Wilson’s disease, Gilbert’s syndrome • Hemolytic anemias – sickle cell, G6PD deficiency


Associated risk factors • Viral hepatitis o Needle and blood exposure, tattoos, sexual history (number of partners, barrier protection), vaccination history o Travel/eating/shellfish history o Immunosuppressive therapy • Alcoholic hepatitis • Acute liver failure o Paracetamol/herbal remedies causing acute liver failure • Cholestatic jaundice o Cholelithiasis – history of gallstones, post-prandial RUQ pain  Hemolytic anemia, gastric bypass surgery (risk factors) o Hepatic/biliary surgery (Risk of biliary strictures o Previous pancreatitis Formation of pancreatic pseudocyst – compression o Sickle cell anemia  Ischaemic cholangiopathy – sickling in end arteries o Ulcerative colitis (a/w primary sclerosing cholangitis) Complications • Ascending cholangitis o Charcot's triad is classical clinical picture  Intermittent pain, jaundice and fever o Cholangitis can lead to hepatic abscesses o Need parenteral antibiotics and biliary decompression o Operative mortality in elderly of up to 20% • Clotting disorders o Vitamin K required for gamma-carboxylation of Factors II, VII, IX, XI o Vitamin K is fat soluble. No absorbed. o Needs to be given parenterally o Urgent correction will need Fresh Frozen Plasma o Also endotoxin activation of complement system • Hepato-renal syndrome o Renal failure post intervention o Due to gram negative endotoxinaemia from gut o Preoperative lactulose may improve outcome o Improves altered systemic and renal haemodynamics • Drug Metabolism o Half-life of some drugs prolonged. (e.g. morphine) • Impaired wound healing • Fat malabsorption – steatorrhea, vitamin deficiency – coagulopathy • Liver decompensation – encephalopathy, hepatic fetor, ascites • Gallstone pancreatitis – abdominal pain radiating to back with n&v 56

! Investigation of Jaundice Blood results • FBC – infection/anemia • Prolonged PTT • UECr • Hepatitis serology • Amylase, Lipase • Blood cultures if febrile • Cancer markers: CA19-9, CEA • LFT o Bilirubin (↑ in direct), rarely >100umol/L in pre-hep causes, can be much higher in obstruction  >1000 - late malignant dz  Direct > indirect; normal 3:7 o ALP/GGT > 2 x AST/ALT (obstructive) o 5 x ALP/GGT < AST/ALT (hepatic) o AST/ALT raised in acute viral hep  AST:ALT = 2:1 → alcoholic hepatitis o Albumin may be reduced Urinalysis findings Conjugated bilirubin Urobilinogen

Haemolysis normal increased

Hepatocellular normal normal

Obstruction increased nil

Ultrasound • Normal CBD <8 mm diameter; abnormal if >10mm • CBD diameter increase with age and after previous biliary surgery • For obstructive jaundice ultrasound has a sensitivity 70 - 95% and specificity 80 - 100% o GB stones or sludge; thickened GB wall, pericholecystic fluid, duct dilation, liver consistency o Demonstrates dilated biliary system and site of obstruction  Unable to detect distal CBD stone well; CT preferred if malignancy + staging o Demonstrates fattiness/cirrhosis of liver CT AP (Tri-phasic) • Stages and assesses operability of tumours • Demonstrates intra-hepatic lesions e.g. Tumor/abscess/cyst which can then be biopsied under radiological guidance • Assess intrahepatic ducts • Delineate pancreatic mass - ca vs chronic pancreatitis hard to diffx o CT is preferred if malignancy is suspected (ca head of pancreas/periampullary tumor - can stage TNM) HEPATOBILIARY AND PANCREATIC SURGERY

HIDA Radionuclide scanning 99 • technetium iminodiacetic acid (HIDA); taken up by hepatocytes and actively excreted into bile; allows imaging of biliary tree o Failure to fill gallbladder = acute cholecystitis o Delay of flow into duodenum = biliary obstruction • Now mainly used for biliary atresia Endoscopic retrograde cholangiogram (ERCP) • Per oral endoscope cannulate ampulla of Vater in D2 o Diagnostic:  Localization/nature of obstruction  Visualize any tumor  Biopsy or brush cytology o Therapeutic:  Stone extraction or stenting for decompression • Complications o Pancreatitis o Duodenal perf o Ascending cholangitis Percutaneous transhepatic cholangiography • Cannulates a dilated bile duct • May be req if ERCP is impossible • Can introduce stent - decompress bile duct & resolve jaundice • Lower risk of bleed but higher infx risk MRCP (magnetic resonance cholangiopancreatography) • Non-invasive, high-res imaging of biliary tree • But no therapeutic purpose Summary • Exclude pre-hepatic cause: haptoglobin level, reticulocyte level, Coombs’ test • Liver synthetic fx: PT & albumin • Hepatocellular damage: AST/ALT, GGT • Bile duct obstruction: ALP/GGT, US of HBS, MRCP, ERCP, PTC; CT for pancreatic lesion • Intrahepatic mass: U/S or CT with needle biopsy

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! APPROACH TO CIRRHOSIS • •

Definition: consequence of chronic hepatic injury with healing by regeneration and fibrosis. Fibrosis leads to further cell damage and destruction of hepatic architecture, progressing to liver failure and portal HTN

Etiology • Parenchymal o Alcoholic o Viral (Hep B, Hep C) • Metabolic o Fe overload - hemochromatosis o Cu overload - Wilson’s disease • Biliary o Primary biliary cirrhosis (autoimmune) o Secondary to prolonged biliary obstruction • Hepatic venous outflow obstruction o Budd-Chiari Syndrome (hepatic vein occlusion) o Severe chronic CCF (cardiac cirrhosis) • Others o Chronic active hepatitis in autoimmune disease o Schistosomiasis e.g. In Egypt o Nutritional - protein-deficient diet o Idiopathic (cryptogenic) o Parental nutrition related (possible due to fat content) o Non-alcoholic steatohepatitis (NASH) Consequence • Hepatocellular failure • Portal HTN • Ascites • Malignant change Clinical features • Gynaecomastia • Testicular atrophy • Amenorrhea • Spider naevi • Finger clubbing • Palmar erythema (hyperestrinism - failure of liver to inactivate estrogen)


APPROACH TO ASCITES Causes of ascites Transudate (<30g/L protein) • Cardiac: CCF, RHF, TR, constrictive pericarditis • Abdo: CLD (low albumin) • Renal: ESRF, nephrotic syndrome (loss of albumin) • GIT: protein losing enteropathy

Exudate (>30g/L protein) • Cirrhosis • Malignancy • Infective cause - TB • Chylous ascites

Pathogenesis in cirrhosis • Raised portal pressure -- transudation of fluid into peritoneal cavity alone does not cause ascites (not seen in pre-hepatic obstruction of the portal venous sys) • Liver damage -- low albumin -- low plasma osmotic pressure -- deficient reabsorption of ascetic fluid o A/w increased aldosterone levels and Na retention • Increased lymphatic pressure in a cirrhotic liver -- lymph transudation from liver surface o Also present in post-hepatic block e.g. Hepatic veins/IVC Physical Examination • Abdominal distention • Peripheral stigmata of CLD and portal HTN o Clubbing, jaundice/scleral icterus, spider naevi etc. • Signs of fluid overload - LL/sacral edema, bibasal crepitations • Other signs of malignancy - cachexia • Flank dullness -- shifting dullness -- fluid thrill Investigations • Peritoneal tap (see below) o SAAG (serum albumin-ascites gradient) = serum albumin conc ascitic albumin conc  Normal = 1.1 -- ascites 2/2 portal HTN (i.e. Due to increased hydrostatic pressure)  If (absolute) albumin level is high - CCF/Budd-Chiari syndrome; if albumin is low - cirrhosis • CT AP (triphasic) - look for liver pathologies e.g. HCC that can develop on background of cirrhosis

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! Rx of ascites • Conservative o Low salt, high protein diet + fluid restriction o Diuresis - spironolactone +/- thiazide or loop diuretic o Drip - IV albumin •

•

Peritoneal tap/paracentesis o Role  Diagnostic: send fluid for FEME, protein, microbiology, cytology  Therapeutic: relieve discomfort and diaphragm splinting due to distention o Indications  Failed medical treatment  Symptomatic o Procedure  Aseptic technique, LA, U/S guidance  May insert pigtail catheter via Seldinger technique  Open drain into stoma bag o Complications: patient loses protein  Replace 10g albumin/L of ascitic fluid removed Surgical o Shunt surgery  Anastomosis of portal vein/SMV to IVC • Peritoneovenous shunting • Portacaval shunting  Trans-jugular intrahepatic portosystemic shunt (TIPSS) • Under radiologic control • Involves the creation of an intrahepatic portosystemic shunt o Hepatic vein is cannulated via the internal jugular vein o Intrahepatic portal vein punctured percutaneously o Guide wire passed from portal to hepatic vein o Stent is then passed along guide wire • But porto-systemic shunts predispose to encephalopathy - pt has to be maintained on low-protein diet forever and must be Child’s A o Liver Transplantation  For intractable ascites secondary to hepatic cirrhosis


GALLSTONES • Gallstones are found in 10% men and 20% women • Prevalence increases with advancing age o 10-20% become symptomatic • Female, Fatty, Fertile, Forty, Flatulent Pathophysiology • 10% of gallstones are radio-opaque • Cholesterol stones result from a change in solubility of bile constituents • Bile acids act as a detergent keeping cholesterol in solution • Bile acids, lecithin and cholesterol result in the formation of micelles o Biliary infection, stasis and changes in gallbladder function can precipitate stone formation o Bile is infected in 30% of patients with gallstones o Gram-negative organisms are the most common isolated • Three types of stones are recognized o Cholesterol stones (15%)  40-50 y/o  Risk factors for increased cholesterol secretion: obesity, hyperlipidaemia, increased estrogens  Risk factors for decreased GB emptying: GB malignancy must be excluded o Pigment stones (5%)  black (found in GB) or brown (found in ducts)  Risk: increased secretion of bilirubin into bile e.g. Chronic hemolysis, CLD, TPN, gallbladder stasis, infection with bacterial degradation of biliary lipids (insoluble pdts) o Biliary sludge = microlithiasis suspended in bile  Predispose to stone formation, pre-stone condition  On US - layering in biliary tree o Mixed stones (80%)  Variant of cholesterol stones  Bile is often supersaturated with cholesterol  This favours the formation of cholesterol microcrystals

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! Clinical Course • Asymptomatic (80-95% of gallstones) o Risk of symptom occurrence is 1-2% per year, greatest risk within 1st 5yrs of diagnosis o Majority of patients do not require removal of stones or GB -expectant management o Role of surgery in the asymptomatic patient  Predisposing cause for GB stasis e.g. GB mass with suspicion of malignancy (polyp, porcelain GB) -prophylactic surgery  Immunocompromised - abnormal presentation, difficult to detect  Patients with chronic hemolytic disease (e.g. Sickle cell anaemia) - ~50% chance of symptomatic disease in their lifetime • Symptomatic o Biliary colic  Typically epigastric or RHC pain (may radiate to inferior angle of right scapula or tip of right shoulder)  Waxing-waning in character but rarely pain-free intervals between waves of pain (unlike ureteric colic)  Often triggered by meals - oily  Lasts for few mins-hrs; resolves spontaneously  Associated with N/V (relieved by vomiting), bloating, abdominal distention – flatulent dyspepsia  Biliary colic is ‘herald’ symptom for risk of further sequelae o Acute cholecystitis o Mucocoele (hydrops) of GB or empyema o Mirizzi’s syndrome o Choledocholithiasis with obstructive jaundice o Cholangitis +/- sepsis o Acute pancreatitis o Fistula formation and passage into gut -- gall stone ileus (subacute IO)


Investigations Laboratory • FBC, UECr, Amylase, Lipase , PT/PTT, Hepatitis serology, blood cultures if febrile, Cancer markers: CA19-9, CEA, LFT, Albumin • Urinalysis for conjugated bilirubin and urobilinogen Imaging • Plain AXR (but only 10% of stones are radio-opaque) • US HBS - investigation of choice for gallstones o More sensitive than CT scan for stones (5mm cuts) o Features of stone: strong echogenic rim with posterior acoustic shadowing o Bile in GB should be a black homogenous patch, otherwise -sludge • CT scan o Not usually done for stones in particular, done when diagnosis is uncertain and looking for other causes • Magnetic Resonance Cholangiopancreatography (MRCP) o Cuts taken to construct biliary tree, w/o contrast o Resolution comparable to ERCP, plus it’s minimally invasive preferred unless pt requires therapeutic interventions • Endoscopic Retrograde Cholangiopancreatography o Diagnostic + therapeutic  Stone removal (balloon catheter or Dormia basket)  90% success, 8% morbidity  Sphincterotomy (to relieve obstruction + stone removal)  Stenting o High level of complications  Pancreatitis 2-3%, cholangitis 1-2%  Hemorrhage 2-3%, perforation into bile duct/duodenum 0.5-1% o Therefore, risk and benefits must be assessed and patients must be selected carefully • Percutaneous transhepatic cholangiography (PTC)/biliary drainage (PTBD) o Tube into liver under radiologic guidance into a dilated biliary duct o Rarely done now unless  High obstruction which cannot be seen well on ERCP  Therapeutic purpose: drainage of obstructed system that ERCP failed to drain from below • HIDA scan - only used in biliary atresia 60

! •

5 criteria for normal cholangiopancreatogram (ERCP/MRCP/IOC) o No filling defects o Normal intrahepatic ducts o Smooth CBD w normal diameter (no stricture/narrowing or dilation) o Tapering of distal CBD (rat-tailing) o Good and free flow of contrast into duodenum

Perioperative management of obstructive jaundice • Preoperative biliary decompression improves postoperative morbidity • Broad spectrum antibiotic prophylaxis • Parenteral vitamin K +/- fresh frozen plasma • IV line & catheter o Pre-operative fluid expansion o Need careful post-operative fluid balance to correct depleted ECF compartment Management Asymptomatic • No surg required unless pt has indication (e.g. GB polyp, hemolytic anaemia, immunocompromised) • Counsel symptoms - biliary colic, acute cholecystitis, obstructive jaundice Symptomatic • Initially: ERCP – Therapeutic, but if failed, consider: o Open cholecystectomy + exploration of CBD o Laparoscopic exploration of CBD o Mechanical lithotripsy (80% successful after failure of ERCP) o Extra-corporeal shockwave lithotripsy o Chemical dissolution with cholesterol solvents  Administered via T Tube or nasobiliary catheter  25% complete response and 30% partial response o If retained stones after CBD exploration need to consider:  Early ERCP or Exploration via T tube tract at 6 weeks • Cholecystectomy only definitive Rx for symptomatic GB stones (Open or lap - lap has shorter hospital stay, less pain & post-op complications) o Risk of lap  Conversion to open ~5% (due to abnormal anatomy, difficult/complicated dissection/iatrogenic injury)  Conversion rate higher if there is ongoing infection e.g. Cholecystitis/pancreatitis o Risks of both  Injury to surroundings - bowel and biliary strs e.g. CBD  Spilled bile - peritonitis & sepsis  Infection and bleeding HEPATOBILIARY AND PANCREATIC SURGERY

ACUTE CHOLECYSTITIS • • • •

90% cases result from obstruction to the cystic duct by a stone Increased pressure within the gallbladder results in inflammation Secondary bacterial infections occurs in 20% Most common organisms are E. coli, Klebsiella and strep. faecalis

Presentation • Constant pain (usually greater than 12 hours duration) in RUQ o Radiating to inferior angle of scapula • Fever, tachycardia • Murphy's sign - guarding in right upper quadrant on deep inspiration o Possible palpable GB (omentum or empyema) Complications of acute cholecystitis • Hydrops o Tense GB filled with mucus (sec to cystic duct obstruction) o If pressure exceeds capillary blood pressure - GB wall necrosis • Empyema o GB filled with pus due to bacterial infx of stagnant bile o Patient usually toxic, surgery required • Gangrene & perforation o Localized perforation -- abscess confined by the omentum o Free perforation -- generalized peritonitis, sepsis, requires emergency laparotomy • Fistula formation - cholecystenteric o Most commonly to duodenum, 2nd colon, 3rd stomach o Occurs after repeated attacks of acute cholecystitis o Usually asymptomatic o On AXR, may see aerobilia (40%) i.e. Accumulation of air o Rx if symptomatic: cholecystectomy and fistula closure • Gallstone ileus o Due to cholecystenteric fistula passing into enteric lumen o Causes intermittent bouts of SBIO (1-2% of all IOs)  Most common site of obstruction is terminal ileum  Small stones usually pass w/o symptoms o Mortality is 10-15%, mainly in elderly patients o Rx  Small bowel enterotomy proximal to the point of obstruction is usually required to remove stone  Immediate cholecystectomy not warranted, <4% of patients will have further symptoms 61

! Investigation • Ultrasound is the initial investigation of choice o Presence of gallstones / sludge o Distended thick-walled gallbladder o Pericholecystic fluid o Murphy's sign demonstrated with ultrasound probe • CT – as above, with the addition of fat stranding • ** LFTs usually normal and no jaundice • Will show failure of isotope uptake by gallbladder Management Conservative (80% patients improve with conservative treatment) • Resuscitate – ABC • Septic workup (blood c/s) • NBM, IV fluids, opiate analgesia • Empirical IV roc/flagyl • 80% patients improve with conservative treatment • If fit, should be considered for a laparoscopic cholecystectomy Surgery • Pre-operative ERCP is indicated if: o Recent jaundice o Abnormal liver function tests o Significantly dilated common bile duct o Ultrasonic suspicion of bile duct stones • Evidence now suggests that early surgery (less than 72 hours) is safe o Less fibrosis, easier to operate on edematous DB o No need for readmission; decreased length of hospitalization o Slightly higher rate of conversion to open chole or injury of adjacent structures o But depends on severity of illness, response to resus and IV abx, and logistical factors • Std practice: Delayed/interval cholecystectomy (6-8wks) if presentation delayed >3 days after symptoms, if gallbladder if palpable or if WBC >18 • If patient unfit for surgery, percutaneous cholecystotomy may be beneficial o In moribund patients not fit for surgery who have failure of systemic therapy i.e. IV Abx o Usually done under LA, percutaneous with radiological guidance o Drains GB and alleviates inflammation --> better outcomes o Particularly useful in acalculous cholecystitis  Ill patients with prolonged stay + fasting + TPN  biliary stasis + dehydration  bile infection  Maintenance before emergency cholecystectomy HEPATOBILIARY AND PANCREATIC SURGERY

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! CHOLEDOCHOLITHIASIS Presents with: Obstructive jaundice + Biliary colic Investigations Bloods • FBC -- TW must be trended for any sign of inflammation • Amylase -- CBD stone may cause pancreatitis • LFTs -- raised bilirubin (direct/conjugated), ALP raised > AST/ALTs Imaging • US HBS o Stones in GB o Gallstone in CBD (but only visible in 50% due to obscuring gas in duodenum) o Dilated CBD (normally 5mm or less)  >10mm is abnormal • EUS/MRCP/ERCP or PTC -- can confirm intraductal stones Management • If not sure about stone -- less invasive investigation e.g. EUS/MRCP • If likelihood of CBD stone is high -- ERCP with stone removal • If ERCP successful -- plan for lap chole • If ERCP failed -o Patient well, can tolerate another ERCP -- try again (+/- stent in between to drain bile) o If not -- (Intra-operative cholangiogram) operative removal  Open CBD exploration  Lap CBD exploration • If no facility to do ERCP - open or lap cholecystectomy with IOC and CBD exploration

MIRIZZI’S SYNDROME Pathology • Gallstone in Hartmann’s pouch (infundibulum of GB) compressing the common hepatic duct resulting in obstructive jaundice o Compression effect is physical (stone) and also contributed by the surrounding inflammation • One of the caveats to Courvoisier’s law (in the presence of jaundice, a non-tender enlarged GB is unlikely to be due to stones) o Because stones causing obstruction occurs in chronic cholecystitis - gallbladder wall is thickened -- no distention possible Grading • Grade I - no fistula, only extrinsic compression of CHD • Grade II - fistula formation with common bile duct, with the fistula <1/3 diameter of the CHD • Grade III - fistula 1/3 to 2/3 diameter of CHD • Grade IV - fistula >2/3 diameter of CHD Management • Grade I & II - attempt lap chole • Grade II - IV - open cholecystectomy with CBD exploration

Indications for surgical stone removal (i.e. Not suitable for ERCP) • Stone problems o Stone >25mm o Intrahepatic stone o Large number of stones o Impacted stone • Duct problems o Duct pathology o Tortuous duct o Previous bilroth II surgery (anatomy no can do ERCP)


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! CHOLANGITIS Presentation • Classically: Charcot’s triad (Fever, RUQ pain, jaundice) • Reynolds’ pentad: Charcot’s triad + altered mental status and hemodynamic instability (esp in elderly) • Surgical emergency! Pathology • Obstruction to biliary system -- stagnant bile gets infected • Causes: o Choledocholithiasis (60%) o Benign strictures o Malignancy - pancreatic (extramural) or biliary e.g. Cholangiocarcinoma (intramural) • Common organisms - Gram negative bacteria + anaerobes o Klebsiella, E.coli, Enterobacter, Enterococcus Management • Resuscitation o ABC - obtain good IV access and fluid resuscitate as appropriate o Bloods + C/S o Close monitoring  Vitals in ICU/HD  Urine output - put in-dwelling catheter (IDC)  If patient has shock that does not respond to fluid challenge -- CVP line insertion • Antibiotics - IV rocephin, flagyl; add imipenem if patient in shock • Biliary decompression & definitive Rx o Investigate for cause of obstruction - U/S or CT scan  U/S HBS preferred if suspecting stones o Decompression commonly performed using ERCP  Primary objective = Decompression - stenting or nasobiliary drain can be used  If cause of obstruction i.e. Stone is found - can be treated/removed  Success rate 90% o Definitive Rx dependent on  Medical condition of patient  Success of biliary decompression  Logistical considerations o Choices for definitive Rx  Lap or open cholecystectomy +/- intra-operative cholangiogram (IOC done in cholangitis) HEPATOBILIARY AND PANCREATIC SURGERY

CBD Exploration • Based on site and cause of obstruction o Cholangiogram - inject dye to image higher ducts o Choledochoscopy - scope to see large biliary ducts, cannot image higher ducts, not as sensitive (but can remove stone) • Removal of stone o Manual = forceps to grasp stone o Flushing out of stones o Dredging stones with ballon catheter or Dormia basket o Lithotripsy • Consider use of biliary stent or T tube after stone removal (If significant instrumentation of biliary sys during operation would result in swelling & edema of biliary system -- post-op obstruction and build-up of bile -higher risk of biliary leakage) o Stent -- removed later by endoscopy o T-tube (usually after CBD exploration) o Horizontal limb in CBD, vertical limb leading out o Functions as pressure release valve - most of bile flows through into distal CBD, only diverted out if there is obstruction to flow o Allows for post-op cholangiogram to check for remaining stones (POD9-10) before removal  Normal: Free flow of contrast into duodenum, no residual stones, no free leak of contrast into duodenum  If normal - release anchoring stitch and pull gently  If stones are present, leave tube in for 4-6 wks to form a fibrous tract -- allows for instrumentation of tract with scope to remove stones • Consider biliary bypass if o Multiple stones, CBD >2cm diameter, or strictures present (as chronically dilated CBD unlikely to function normally after removal of obstruction)

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! RECURRENT PYOGENIC CHOLANGITIS AKA cholangiohepatitis Pathophysiology Helminth infx (e.g. Ascaris/clonorchis) -- epithelial damage -- predispose to seeding of coliforms into biliary system -- stone formation -- recurrent cholangitis • Recurrent bacterial cholangitis • Intrahepatic pigment stones • Intrahepatic biliary obstruction

Management • Treat current infx • Biliary drainage - stent • Definitive (surgical) biliary drainage - e.g. Roux-en-Y choledochojejunostomy above the level of strictured CBD Prognosis = death in approximately 20% of patients over 5-6yrs

History • Recurrent attacks of cholangitis o 1-2 episodes of fever, jaundice, RUQ abdo pain/yr o Hx of previous biliary surg/endoscopic procedures/perc drainage • Complications of recurrent pyogenic cholangitis o Cirrhosis with portal HTN (secondary biliary cirrhosis) o Cholangio CA • DDx: primary sclerosing cholangitis Investigations -- for diagnosis & complications • Bloods o FBC o LFT with ALP>ALT/AST o PT: may be normal or increased (prolonged cholestasis causes fat malabsorption & Vit K deficiency)  Important TRO increased PT / correct with parenteral Vitamin K before any invasive procedures e.g. PTC o Blood C/S: can guide choice of Abx • Stool ova parasites: freq a/w clonorchis infx -- treat if present • Imaging • US HBS o Segmental biliary dilation o Hepatolithiasis o Liver abscess • ERCP/PTC - to delineate biliary tree • CT scan


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! CHOLANGIOCARCINOMA Arises from bile duct epithelium, occurs anywhere along biliary tree Tumors usually locally invasive (spread microscopically along bile ducts) Metastasize to involve liver & peritoneum Site • • •

Intrahepatic - 25% Extrahepatic upper duct a.k.a. Hilar/Klatskin tumor Extrahepatic lower duct

Bismuth Classification • Type I: below confluence of L & R hepatic ducts • Type II: tumor involves confluence of L & R hepatic duct • Type IIIA/B: involving common hepatic duct & either L or R hepatic duct • Type IV: multicentric or involving confluence and both hepatic ducts Associations and Risk Factors • Age • Related to chronic cholestasis o Primary sclerosing cholangitis (inflammation, destruction, scarring of bile ducts)/ulcerative colitis o Hepatolithiasis o Parasitic infection - Opisthorchis and Clonorchis species o Caroli’s disease (multifocal segmental dilation of large intrahepatic bile duct) • Bile duct adenoma • Choledochal cyst • Thorotrast exposure Presentation • Painless jaundice (only painful if there is cholangitis) • Acholic stools (pale)/tea-colored pee • Advanced s/s: Abdominal pain, LOW, Fatigue/malaise, Hepatomegaly Investigations Bloods • LFTs to confirm increased bilirubin • CA 19-9 > 100ul/ml (good sensitivity of 89%, specificity 86%) o Usually used for pancreatic ca • CA 125


Imaging (from simplest least invasive to more advanced less invasive) • Diagnostic: o *CT AP - to delineate mass and define its relation to liver o *MRCP - look at tumor, r/s to key vessels & intrahepatic mets o U/S - look at bile duct masses, dilation, assess extent of tumor involvement within the liver and portal vein o EUS with FNA - lower bile duct strictures and masses • Diagnostic and therapeutic o *ERCP  Diagnostic - biopsy for histological analysis! • Distal tumors vs small pancreatic carcinomas • But if obstruction is complete - may not be able to delineate upper limit of tumor  Therapeutic - decompression of the biliary tree • If cholangitis is present or if bilirubin very high o PTC - when MRCP/ERCP fails/cannot delineate the upper limit  Diagnostic - FNA cytology  Therapeutic: decompression (may be palliative) Curative Treatment • Surgery only chance for long-term cure • Tumour is resected and biliary reconstruction is performed • 1 in 4 tumors resectable o Extent of tumor, vascular invasion, hepatic lobar atrophy, metastatic lobar atrophy, metastatic disease • Contraindications to surgery: o Distant mets o Can’t resect both lobes of liver  Bilateral or multifocal intrahepatic disease  Unilateral hepatic vascular invasion w contralateral ductal spread o Vessels involvement  Invasion of portal vein trunk or hepatic artery (proximal vessel that supplies both lobes)  Bilateral involvement of hepatic artery or portal vein branches • Prognosis for resectable disease (5yr survival) • Intrahepatic ~40% ; Distal ~40% • Perihilar 10-30% -- early lymphatic spread (LNs at portal hepatis) Palliation • ERCP or PTC biliary stenting • Bilateral drainage for hilar cholangiocarcinoma • Surgical bypass can be performed 66

! ACUTE PANCREATITIS Aetiology • Gallstones and alcohol account for 80% cases of acute pancreatitis • Gallstones less than 5mm diameter are more likely to cause pancreatitis than larger ones • Less than 5% patients with gallstones develop pancreatitis • Aetiological factors can be summarized as follows: o Idiopathic - 20% o Obstruction  Choledocholithiasis – 40%  Ampullary or pancreatic tumours o Pancreatic structural anomalies o Toxins  Alcohol – 40%  Drugs – Steroids, NSAIDs, diuretics, sulphonamides o Trauma (Accidental or Iatrogenic) o Metabolic abnormalities  Hyperlipidemia – 7% o Infection (Mumps) o Vascular anomalies Epidemiology • 80% have mild disease • 40% of those with severe disease develop infected pancreatic necrosis • The mortality associated with infected necrosis is about 40% • 50% of deaths occur within first week due to multi-organ failure Pathophysiology • Final common p/w - inappropriate activation of proenzymes stored within zymogen granules in pancreatic cell o Trypsin is implicated as it activates most of the proenzymes secreted by the pancreas • Activated lytic enzymes destroy pancreatic acinar cells -- release potent cytokines  attract neutrophils & macrophages  pro-inflamm cytokines • Cytokine cascade amplifies local inflammatory response + results in systemic inflammatory response: T<36 or >38, HR > 100, RR >20, TW>15) • May progress to sepsis and septic shock and multi-organ dysfunction • Gallstones obstruct pancreatic duct -- interstitial edema -- impairs blood flow to acinar cells -- ischaemic cellular injury -- predispose to enzyme activation • Alcohol generates free radicals during metabolism - direct injury o May sensitize pancreas to injury by other agents HEPATOBILIARY AND PANCREATIC SURGERY

Clinical features • Sudden onset constant epigastric pain radiating to the back o Tenderness may be localised to epigastrium or generalized o Palpable pseudocyst or phlegmon o Abd distension due to ileus • Alleviated by sitting up and leaning forward • N/V, anorexia, fever, dehydration • Elicit etiology! • Differential diagnosis includes o PUD (ask PMHx of dyspepsia) o Perf viscus o Acute cholecystitis / hepatitis – assess jaundice/hepatitis o Mesenteric ischaemia o AMI (ask CP, diaphoresis, palpitations) • Ecchymoses of retroperitoneal haemorrhage are rare and appear late o Cullen's sign, Grey Turner's sign Causes of hyperamylasaemia • Perforated peptic ulcer • Cholecystitis • Generalized peritonitis

• • • •

Intestinal obstruction Mesenteric infarction Ruptured AAA Ruptured ectopic pregnancy

Diagnosis • Serum amylase (normal = 100) o >3x upper limit of normal (sensitivity 60%, specificity 95%) or >1000iu/l o Raised between 12-72 hrs – not useful in late diagnosis o 20% cases of pancreatitis have normal serum amylase (particularly alcoholic aetiology) • Serum lipase more sensitive and may remain elevated longer o >3x upper limit of normal has higher sensitivity and good specificity o Rises within 8 hrs of onset, returns to normal after 7-10 days • Urine diastase (similar to lipase) • Features suggestive of a gallstone aetiology include: o Female sex o Bilirubin > 25 umol/L o Age more than 50 years o AST > 100 IU/L o Amylases > 4000 IU/L o ALP > 300 IU/L

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! Severity stratification and etiology Imaging • Erect CXR - look for free gas, pleural effusion, pulmonary infiltrates, ARDS complete whiteout • AXR o Sentinel loop sign or colon cut off sign -- due to ileus (functional spasm due to nearby inflammation) o Calcification in chronic pancreatitis • US HBS - Can visualize biliary tree and pick up gallstones, can visualize diffusely enlarged and hypoechoic pancreas o Alternatively - MRCP/EUS/ERCP if stone is likely • CT AP - if looking for complications of pancreatitis (1 wk or more later), if other findings unequivocal A Normal B Focal or diffuse glandular enlargement Small intra-pancreatic fluid collection C Any of the above Peripancreatic inflammatory changes Less than 25% gland necrosis D Any of the above Single extrapancreatic fluid collection 25-50% gland necrosis E Any of the above Extensive extrapancreatic fluid collection Pancreatic abscess More than 50% gland necrosis Laboratory • FBC - TW, hematocrit • UECr - Urea, any electrolyte imbalances or dehydration • LFTs - AST, albumin, to look for obstructive picture in gallstone pancreatitis • LDH • ABG - PaO2, base excess • Ca/Mg/PO4 with albumin - hypercalcemia etiology • Fasting lipids - hyperlipidaemia etiology • ECG & cardiac enzymes - to exclude AMI Danger signs in 1st few hours • Encephalopathy • Hypoxaemia • Tachycardia >130/min, hypoBP <90mmHg, hematocrit >50 • Presence of ecchymoses signs • Oliguria <50mls/hr, azotemia HEPATOBILIARY AND PANCREATIC SURGERY

Prognostic factors (identify severe pancreatitis) Ranson's criteria (>=3 is severe) • On admission • Within 48 hours o Age > 55 yrs o Haematocrit fall >10% o WCC > 16,000 o Urea rise >0.9 mmol/l o LDH > 600 U/l o Calcium < 2 mmol o AST > 120 U/l o pO2 < 60 mmHg o Glucose > 10 mmol/l o Base deficit > 4 o Fluid sequestration > 6L APACHE II score • Multivariate scoring system (assesses ICU patient condition) • Measure objective parameter - vital signs and biochemical analysis • Account for premorbid state and age • Can be used throughout course of illness C-Reactive Peptide • At 48hrs, if >210mmHg - more likely to be severe • More than 3/7 - useless as other confounding factors enter Complications of acute pancreatitis Local • Necrosis +/- infection • Pancreatic fluid collections • Colonic necrosis • Gastrointestinal haemorrhage • Splenic rupture

Systemic • Hypovolaemia and shock • Coagulopathy • Respiratory failure • Renal Failure • Hyperglycaemia • Hypocalcaemia

Course of disease • 75% mild course, will recover unless comorbidities cause deterioration • 20-25% severe outcome, 1/3 of these eventually die (mortality overall <10%) o Death is bimodal  Early (within 1/52) - due to SIRS and severe organ failure  Late - usually due to infection & resultant sepsis -- MOF Timing of intervention in pancreatitis • All patients should undergo ultrasound within 24 hours of admission • If confirms gallstones and severe pancreatitis consider ERCP in 48 hrs • If not stable after 1 wk → Contrast enhanced CT to assess pancreatic necrosis • If suspicion of infection - CT guided aspiration • Consider pancreatic necrosectomy if o Clinical deterioration o Bacteriological proof of infection • Antibiotics do not prevent infected necrosis in acute necrotizing pancreatitis • Operative mortality >40% 68

! Supportive treatment of pancreatitis • Monitor (after resuscitating) o If severe -- HD/ICU monitoring o Fluid resuscitate with crystalloids o Monitor vitals (SpO2, BP, HR, Temp), urine O/P and CVP • NBM (bowel rest) and IV fluids o NGT decompression if required (severe vomiting, ileus or gastroparesis) o Acid suppression (IV omeprazole) to protect against stress ulcer formation o NBM for at least 2/7 until more stable - restart clear fluids if tolerated (mild disease) o Correct any dehydration and electrolyte abnormalities (hypocalcemia, hypoglycaemia) • Analgesia o No NSAIDs - can worsen pancreatitis & cause renal failure o Use opioids - tramadol/pethidine (just not morphine) • Abx (?) o Current practice not to give for pancreatitis o Two situations to give - cholangitis or infection of necrosis or abscess (CTAP + TW)  Imipenem for infected (or fluoroquinolones); IV Roc/flag for cholangitis • Support for organ failure o Hypoxaemia -- ventilate with PEEP (positive end-expiratory pressure) o Acute renal failure -- Dialysis & CVP monitoring o Hypotensive -- fluid resuscitate + inotropes • ERCP may be of benefit within the first 48 hours in patients with predicted severe disease Monitor for complications & manage Treat etiology • Avoid alcohol • Stop any offending meds • Control hyperlipidaemia • Biliary pancreatitis - cholecystectomy • If mild, can do cholecystectomy in same admission • 1 in 5 patients with biliary pancreatitis will have recurrence, 1/4 - 1/2 of these will occur in the next month


Local • •

• • • •

Acute fluid collections (35%) Pseudocyst (15%) = persistent fluid collection walled off by fibrosis -- no epithelial-lined surface >6cm for >6wks o Presents as GOO, infx, peritonitis, h’ge (due to erosion of vessels), persistently raised amylase (after resolution of pancreatitis) o Usually resolve spontaneously (half). Even if they don’t, don’t poke them  intervention at 6 weeks o U/S, CT, ERCP o Check for duct anatomy and fistula Abscess = fluid collection of pseudocyst Pancreatic necrosis - CT shows areas of no IV contrast uptake Infected necrosis - CT shows gas bubbles, positive culture on FNA (CT or US guided) Chronic pancreatitis (with endocrine or exocrine insufficiency)

Systemic complications • Peritoneal sepsis • Pancreatic ascites -- massive fluid accumulation of fluid in peritoneum • Intra-abdominal h’ge -- erosion of vessels, usually splenic • Multi-organ failure - ARDS, ARF, hypovolemic shock, DIVC Intervention for local complications • ERCP o Indications: severe pancreatitis/pt not improving, evidence of ductal stones, concomitant cholangitis • CT-guided aspiration of pancreatic necrosis o Differentiate between sterile and infected necrosis - to consider surgery if patient deteriorating • Role of surgery o Infected necrotic pancreas - mortality 100% w/o op -- do necrosectomy/resection of pancreas o Sterile necrotic pancreas (necrosectomy)  Delay surgery till as late as possible for demarcation of necrotic areas (repeated surgeries if required)  Surgery can be open, lap, endoscopic or percutaneous o Diagnostic uncertainty o Complications e.g. Intra-abdominal h’ge Nutritional support • Pancreatitis is associated with a catabolic state • Evidence that early enteral nutrition is safe (Nasojejunal feeding limits pancreatic secretion, preferred over oral or nasogastric feeding) 69

! CHRONIC PANCREATITIS •

Chronic inflammatory disease of the pancreas o Results in irreversible destruction of both the endocrine & exocrine pancreatic tissue o Pancreas may appear macroscopically normal

Aetiological factors • Alcohol • Tobacco • Pancreatic duct strictures • Pancreatic trauma • Hereditary pancreatitis • Tropical pancreatitis Epidemiology • Male to female ratio is approximately 4:1 • Mean age of onset is approximately 40 years Clinical progression • Early stages of the disease → episodes of acute pancreatitis • Late stage of disease is characterized by pancreatic fibrosis & calcification • Pancreatic duct dilatation and stricture formation occurs o Cysts form within the pancreatic tissue • Chronic pancreatitis increases the risk of pancreatic carcinoma Clinical features • Local chronic pain is the principal symptom in most patients o Usually epigastric, sub-costal and radiating to the back o Pain may be continuous or episodic o Often interferes with life and may lead to opiate abuse • Nausea and vomiting • Weight lost may occur + Decreased appetite • Loss of exocrine function produces malabsorption and steatorrhoea • Loss of endocrine function results in diabetes • Complications: o Pancreatic pseudocyst o Fistulae o Ascites o Pancreatic cancer


Investigation • Serum amylase is often normal • Plain abdominal x-ray may show pancreatic calcification • CT or MRI is the most useful investigation for imaging the pancreas • May confirm pancreatic enlargement, fibrosis and calcification • ERCP has a high sensitivity for detecting chronic pancreatitis • MR pancreatogram will outline the state of the pancreatic duct • Pancreatic function test rarely provide useful information o Direct tests - e.g. secretin-pancreozymin test, Lundh test o Indirect tests - e.g. serum trypsin, faecal fat analysis • On imaging criteria it can be difficult to differentiate chronic pancreatitis from carcinoma Treatment • Treat underlying cause (e.g. alcohol, ductal stricture) • Low fat diet and alcohol abstention is essential o Surgery is associated with significant morbidity and mortality  Does not arrest loss of endocrine and exocrine function; used for:  Persistent local complications e.g. Pseudocyst/fistulae/local obstruction of CBD/duodenum 2/2 fibrosis  Pain relief - pancreatectomy, celiac plexus block, thoracic splanchnicectomy  If performed is aimed at:  Removing any mass lesion  Relieving pancreatic duct obstruction  Mass lesion can be removed by pancreaticoduodenectomy or a Beger procedure  Duct obstruction can be relieved by  Puestow procedure - side-to-side pancreaticojejunostomy  Pancreaticojejunostomy  Frey procedure  Disease confined to pancreatic tail may require distal pancreatectomy  Surgery relieves symptoms in 75% of patients • Symptomatic o Analgesia (avoid opiates to prevent addiction o Pancreatic enzyme supplements may  Reduce steatorrhoea  Reduce frequency of painful crises o Control blood sugar with insulin 70

! PANCREATIC CARCINOMA • • • •

More than 80% of cases occur between 60 and 80 years of age Male : female ratio is 2 : 1 Median survival for unresectable disease is 6 months (80% of patients) Overall 5-year survival <5%

Clinical features • Asymptomatic (incidental screening finding) vs symptomatic • Most are gradual - dull, mid-epig pain, malaise/fatigue, nausea, LOW, LOA • 30% present with painless progressive obstructive jaundice Head of pancreas or periampullary Pancreatic body/tail (late) - Obstructive jaundice (painless with - Celiac and mesenteric plexus invasion – palpable GB, +/- cholangitis) dull constant pain in epigastrium icterus, pruritus, stool/pee radiating to back changes (note: Courvoisier sign in - Malaise, LOW, LOA, nausea periampullary tumors) - Exocrine insufficiency if duct obstructed - Duodenal obstruction steatorrhea/malabsorption - Bleeding upper GIT - Metastatic symptoms: ascites, bone hematemesis/melaena pain, SOB, dyspnea - Constitutional - Paraneoplastic syndromes – migratory LOW/LOA/malaise, nausea thrombophlebitis in 6% Pathology • Most commonly ductal adenocarcinoma (75% head, 20% body, 5% tail) • Neuro-endocrine tumours of the pancreas (PNET) o Often produce hormones causing defined clinical syndromes o Non-functioning tumours have increased risk of malignancy Insulinoma Gastrinoma • Commonest PNET • Presents with Zollinger-Ellison syndrome • Presents with: o Impaired consciousness • Causes intractable peptic ulcer o Personality change disease at unusual or multiple o Sweating and fainting sites, resistant to normal therapy attacks in 30% • 20% patients develop diarrhoea • Fits occur in 30% of patients & weight loss • Associated with • Diagnosis confirmed by hypoglycaemia, symptoms increased serum gastrin on relieved by food secretin stimulation • Diagnosis confirmed by • Also need to confirm gastric increased insulin and CRP hypersecretion • 10% tumours are malignant • 60% tumours are malignant HEPATOBILIARY AND PANCREATIC SURGERY

Associations • Well-known: Cigarette smoking, alcoholism & industrial carcinogens • Disease states: Chronic pancreatitis • Genetic factors (K-ras, p16), familial cancer syndromes (FAP, Von Hippel Lindau, hereditary breast ca, Gardner’s syndrome) Investigations Differentiate with peri-ampullary tumor • Duodenum (best outcome), bile duct or ampullary duct • Better tumor biology; present earlier with obstructive jaundice (better prognosis) Computerized tomography (most useful) • Spiral CT has improved on resolution of conventional CT • Has sensitivity of greater than 95% for detection of pancreatic tumours • Contrast-enhanced triple-phase imaging is modality of choice • Features: o Hypoattenuating indistinct mass that distorts normal architecture of pancreas, bile & pancreatic duct dilation in head of pancreas tumors (double duct sign) o Look for evidence of extra-pancreatic spread - TNM staging: regional LNs, liver mets, ascites o Determine resectability of tumor: no distant mets, preserved fat plane btwn mass and SMV/portal vein, no tumor encasement of celiac, hepatic or superior mesenteric artery Ultrasound • Abdominal ultrasound has sensitivity of about 80% for the detection of pancreatic cancer; Detects level of biliary obstruction, excludes gallstones and may identify pancreatic mass • Doppler ultrasound allows assessment of vascular invasion Staging • CT AP - T, N staging + liver mets • EUS - T, N • CXR + CT thorax - lung mets • Bone scan - if there is suspicious signs and symptoms • Laparoscopy o Laparoscopy will identify liver or peritoneal metastases in 25% of patients deemed resectable after conventional imaging o Laparoscopic ultrasound has improved predictability of resection

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! Curative Management Resectional surgery • Resection is the only hope of cure (15% tumours are resectable) o Tumour size (<4 cm) o Presence of ascites, nodal, peritoneal or liver metastases o Patent veins (superior mesenteric and portal which run behind & emerge from top) o Definable fat plane between tumour and SMA and celiac axis • Pre-operative biliary drainage of unproven benefit • Has not been shown to reduce post-operative morbidity or mortality • High recurrence rate Whipple's operation • Octreotide given for one week to reduce pancreatic secretion • Preceded by staging laparoscopy to confirm absence of peritoneal mets • Remove head of pancreas, CBD, GB, duodenum, prox 15cm jejunum, distal stomach • Head of pancreas and duodenum excised followed by: o End to side pancreaticojejunostomy o End to side hepaticojejunostomy o Duodenojejunostomy • Mortality - 2-7%; morbidity up to 30% (mostly mild) • Postoperative chemotherapy may improve survival • Complications Intra-op/early Late • Injury to liver, kidney, bowel • Long-term exocrine insufficiency - steatorrhea, • Bleeding, infection/sepsis malabsorp (Vit ADEK) – 30% • Pancreatitis • Endocrine insufficiency – DM • Anastomotic leak (5-20%) – (10%) o may cause fistula formation or • Gastric stasis in PPPD pseudocyst • Diarrhea resulting from • Intra-abdominal abscess autonomic nerve injury during • Biliary anastomotic breakdown LN dissection • GIT/Op-site hemorrhage Pylorus-preserving proximal pancreaticoduodenectomy • Preserves gastric antrum and pylorus • Compared with Whipple's procedure o Reduced morbidity, no change in mortality o Fewer post gastrectomy symptoms o Less entero-gastric reflux o Improved post-operative nutrition • May be associated with gastric stasis & increased risk of local recurrence HEPATOBILIARY AND PANCREATIC SURGERY

Palliative Management • 85% of patients are not suitable for curative resection • Palliation of symptoms can be achieved either surgically or endoscopically • Surgical palliation has initially higher complication rate • Produces better long-term symptom control. • Palliative treatment should achieve: o Relief of jaundice by either endoscopic stenting or surgery o Prevention of duodenal obstruction by gastrojejunostomy o Relief of pain by coeliac plexus block • External biliary drainage now rarely required • Palliative chemotherapy (e.g. gemcitabine) controversial Endoscopic stenting • Achievable in over 95% of patients • Complications include bleeding, perforation, pancreatitis • Mortality less than 3% • 20% develop duodenal obstruction • Patency of plastic stents often only 3 to 4 months • Can be improved with the use of self-expanding wall stents Palliative surgery • Biliary drainage can be achieved by choledocho- or cholecystojejunostomy • 10% will develop duodenal obstruction • Triple bypass o Choledocho/hepatico-/cholecysto-jejunostomy o Gastrojejunostomy o Jejuno-jejunostomy (prevents food reflux into biliary tree) • Removes risk of duodenal obstruction and often avoid recurrent jaundice Analgesia • Pain occurs in over 80% with advanced malignancy • Can be palliated with: o Slow release morphine o Coeliac nerve block o Thoracoscopic section of splanchnic nerves

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! LIVER HEMANGIOMA Epidemiology • Prevalence of up to 20% • Female: male - 3:1 Pathogenesis • Congenital vascular malformation • Enlarges by ectasia (dilation) Presentation • Incidental finding, Usually small & asymptomatic o Most less than 5cm o If large (>5cm) - may have nonspecific abdo symptoms e.g. Upper abdo fullness or vague abdo pain • Mass effects o Compression on surrounding organs • Pain - due to stretching of liver capsule • Rupture (<1%) • Kasabach-Merritt syndrome (for large hemangiomas) o Consumptive coagulopathy + thrombocytopaenia • Heart failure o Secondary to large AV shunt • Note: Malignant transformation does not occur Diagnosis - radiological • US HBS o Well-defined, lobulated, homogenous, hyperechoic mass (may have hypoechoic regions - hemorrhage, fibrosis, calcifications) o Compressibility of lesion is pathognomonic • Triphasic CT o Slow enhancement of rims during arterial & portal-venous phase o Enhancement progresses towards the centre of the lesion o Brightest in delayed phase o Note: biopsy contraindicated -- may precipitate severe hemorrhage

SIMPLE LIVER CYST Epidemiology • Prevalence 1-3% • 9:1 female predominance for symptomatic cysts • Half of cysts are solitary Pathogenesis • Congenital malformation when an aberrant bile duct loses communication with the rest of biliary tree & becomes progressively dilated (fluid within cysts is not bilious) • No solid component, no septa o Mixed cysts with septations are suggestive of malignancy • Note: cysts that communicate with biliary system = choledochal cysts Presentations (with complications) • Torsion • Bleeding & rupture • Mass effect o IVC compression o Cholestasis due to CBD compression o Portal HTN • Fistula formation with duodenum • Malignant change -- rare Treatment if symptomatic • Aspirate • Ethanol sclerotherapy (painful) • Fenestration (open or lap) i.e. Unroofing of cyst • Excision/resection

Treatment - only if symptomatic or complicated • Follow-up/observation • Surgical • Indicated when symptomatic, complications or unable to exclude malignancy • Possible role for prophylactic surgery in large, lateral, inferior lesions  Higher risk for rupture! HEPATOBILIARY AND PANCREATIC SURGERY

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! HEPATOCELLULAR CARCINOMA th

Singapore: 4 most common cancer in men; Male : female ratio = 4:1 Peak presentation is 40 years; usually with background of cirrhosis Aetiology Types: Fibrolamellar (non-cirrhotic, non hepatitic) vs non-fibrolamellar (cirrhotic) • Cirrhosis • Alcohol • Viral hepatitis - particularly • NAFLD Hepatitis B and C • Anabolic steroids • Metabolic triad: • Primary liver diseases - e.g. alpha-1 anti-trypsin deficiency, primary biliary cirrhosis Wilson’s disease, • Mycotoxins - e.g. aflatoxin hemochromatosis produced by Aspergillus flavus Clinical presentation Asymptomatic • Suspect in any patient with cirrhosis with evidence of clinical deterioration • Detected during screening for chronic hep B carriers Symptomatic • Local o o o o

• •

•

•

RUQ dull, persistent pain (secondary to capsular stretch) RUQ mass - hepatomegaly Low grade pyrexia (tumor necrosis) Jaundice is a late feature  Compression/invasion of intrahepatic ducts  Lymphadenopathy at porta hepatitis  Pre-existing cirrhosis Constitutional: Malaise, LOW, LOA Tumor rupture: o Haemobilia or haemoperitoneum are often the immediate cause of death  pallor with shock o Severe abdo pain + peritonism o U/S, DPL, then treat with Transarterial Embolization Liver decompensation o Background of existing HCC + CLD/cirrhosis especially n o Liver f - jaundice/pruritus, coagulopathy, edema, encephalopathy o Portal HTN - ascites, LL edema, hematemesis, melena (varices) o Hepatorenal syndrome in late stages Metastases • Paraneoplastic syndromes o Bone pain o High metabolic demands – hypoglycaemia o Dyspnea o Tumor produces EPO – erythrocytosis


Investigations As most tumours cause symptoms late, screening of high risk patients advocated. Laboratory • FBC (low Hb from BGIT, raised TW from spontaneous bact peritonitis) rd • UECR (dehydration, 3 spacing, diuretics for ascites, contrast nephropathy) • LFT (albumin, bilirubin, ALP, transaminases) • Hepatitis Markers • Alpha-fetoprotein - produced by the yolk sac & liver o Normal <5; WHO criteria >400 o Progressive increases in serum levels in 70-90% of HCC o Slightly increased and often fluctuating serum levels also seen in hepatitis, cirrhosis, pregnancy, teratoma o In HCC serum levels correlate with tumour size  Rate of increase in serum levels correlate with tumor growth  Tumour resection results in a fall in serum concentrations  Serial assessment useful in measuring response to tx Imaging • CT Triphasic - Conventional or lipoidal enhance o Arterial phase  Contrast in aorta/ any bleed & HCC  IVC and portal vein are dark o Portal venous phase (most CT scans taken @ this phase)  Portal vein as bright as aorta  Visualize metastasis o Delayed phase  Contrast drains out - none of the vessels in liver are lit up  Visualize hemangioma (also rim enhancement in others) o Characteristic features of HCC  Enhancement in arterial phase (due to hepatic arterial ss)  Rapid contrast washout in portal venous phase - hypodense • Dynamic MRI scan - greater detail • Hepatic angiogram (reveals abnormal blood vessels) • Lipiodol and post-lipoidal CT with hepatic angiogram o CT scan a week later WHO Criteria for HCC: o Lipiodol will be retained in HCC (a) Risk factors for HCC even after many days - tumor e.g. HBV/HCV carrier has no Kupffer cells (b) Characteristic CT Staging triphasic findings: • Lung: CXR, CT thorax Hypervascular lesion • CT AP: liver, adrenals, peritoneum, LNs (c) Raised AFP (>400) • Bone: Bone scan if indicated

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! Screening for chronic hepatitis carriers • 6 monthly - yearly U/S with AFP levels o Frequency of screening controversial, but should be increased in high risk pts (i.e. HBeAg positive, high HBV DNA levels) • Important to detect smaller and resectable HCCs -- increases survival from 26 to 88 weeks (~6 months to 2yrs) • Remember to screen family for Hep B carrier status! Especially if famhx is positive o U/S  Operator dependent  May miss certain areas of liver where imaging is difficult  Not a/w with radiation exposure o AFP  Not perfect as 1 in 5 (20%) of HCC will not have raised AFP o Combining both increase sensitivity and specificity! Surgery for hepatocellular carcinoma • Only about 20% patients are suitable for surgery Surgical resection • Surgical resection involves either hemi-hepatectomy or segmental resection • Presence of ‘field change’ effect in the cirrhotic liver -- new tumor can develop in remnant liver o Fine balance between adequate resection margins and preservation of sufficient functional liver to prevent liver failure o Good immediate and short-term results, but long term <30% 5yr survival due to occurrence of new primaries in cirrhotic liver • Most tumours are unresectable to: o Stage of disease  Metastatic or multicentric not suitable o Fitness for op o Liver function  Advanced cirrhosis  ICG test pre-op must <15% remains after 15mins for >3 segments removed (major resection)  CT liver scan program to calculate residual function o Involvement of major vessels o Crazy portal HTN (increased resistance to flow) • The presence of cirrhosis increases the operative mortality (to >20%) o Consider only Child’s A and good Child’s B • After resection, 5 year survival is typically 30-60% • The 5-year recurrence rate is over 80% HEPATOBILIARY AND PANCREATIC SURGERY

Child-Pugh Classification of CLD Measure Albumin, g/l Coagulation PT INR Bilirubin, µmol/l Distension Ascites Encephalopathy Points 5-6 7-9 10-15

Class A B C

1 point >35 <1.7 <34 None None

2 points 28-35 1.71-2.20 34-50 Mild Grade I-II

3 points <28 > 2.20 >50 Moderate to Severe Grade III-IV (or refractory)

One year survival Two year survival 100% 85% 81% 57% 45% 35%

1) Prognosis 2) Strength of medical treatment 3) Necessity of liver transplant

Liver transplantation • Useful for unresectable disease confined to the liver • Operative mortality is often 10-20% • After transplantation, 5-year survival is less than 20% • Milan criteria for transplantation (>75% 5yr survival if followed!) o Single tumor 5cm or smaller OR 3 or less tumors, > 3cm o No evidence of gross vascular invasion o No regional nodal or distant metastasis • Problems with availability of donor organ - disease may no longer by suitable for transplant when organ is available o Possibility of ‘bridging therapy’ such as radiofrequency ablation to shrink disease and prevent progression until organ is available • In HBV carriers - risk of reinfection of donor liver (esp if HBeAg positive, high HBV DNA levels) o Can be aggressively treated with anti-viral drugs 2 months before o Anti-HBV Ig long-term after transplant Palliative therapy • Loco-regional o Radiofrequency ablation (RFA) - best among the 3 o Percutaneous ethanol injx o Cryotherapy • Intra-arterial o Transarterial chemoembolization TACE o Transarterial embolization TAE o Selective intrahepatic radiation - Yttrium-90 • Systemic o Sorafenib improves median survival by 3 months (limited results + expensive) 75

! LIVER METASTASES • • • •

PYOGENIC LIVER ABSCESS

50% patients with colorectal cancer develop liver metastases 20% have metastases at time of initial surgery 25% develop metastases within 5 years of a 'curative' resection Median survival with metastases is about one year

Presentation Mets to liver parenchyma History - Incidentally found on f/u for cancer - Hard mass/heaviness - Pain on rupture O/E - Hard, irregular nodular hepatomegaly - Jaundice is late sign Invx Both obstructive and transaminitis

Mets to porta hepatis LNs S/S of obstructive jaundice - Scleral icterus - Tea-colored urine, pale stools - Progressive early jaundice - Hepatomegaly may be absent Obstructive in early stages

Detection of metastases • Ultrasound will detect lesion more than 0.5 cm in diameter • CT allows assessment of resectability • Intra-operative ultrasound superior to extra-corporeal scanning • Elevated tumour marker - CEA, CA 19.9, CA 242 Investigation: Triphasic CT • Hypodense on arterial phase – Mets are usually hypovascular (c.f. HCC) • Spread by portal vein – ↑ contrast uptake on portal venous & delayed phases Liver resection for metastatic disease • Resectional surgery is only chance of cure for patients with liver mets • Only 10% of patients w metastases suitable for 'curative' hepatic resection • Aim is to resect tumour with more than 1 cm margin by segmentectomy, lobectomy or hepatectomy • 5 year survival 35% and 10 year survival 20% Relative indications • Single lobe involvement • Less than three lesions without evidence of satellite lesions • No invasion of inferior vena cava • More than 20% of liver spared Palliation of liver metastases • Cryotherapy • Hepatic artery infusion therapy • Laser photo-coagulation

Relative contra-indications • Hilar & coeliac nodal involvement • Distant metastases • Poor cardiovascular reserve • Pre-operative portal vein embolization - atrophy of segments to be excised • Neoadjuvant chemotherapy


• • • • •

Usually seen in elderly patients (more common in SG than amoebic) Can be multiple or solitary Arise as a result of biliary sepsis Mortality is high as diagnosis is often delayed Commonest organisms involved - E. coli, Klebsiella, Proteus and Bacteroides species, strep milleri, enterococcus/bacter

Aetiology • Portal pyelophlebitis - appendicitis, diverticulitis or pelvic infections • Biliary disease - cholecystitis, ascending cholangitis or pancreatitis • Trauma - blunt or penetrating or iatrogenic • Direct extension - empyema of the gall bladder, subphrenic or perinephric abscess • Septicaemia • Infected liver cysts or tumours Clinical features • Patients are generally systemically unwell • Severe abdominal pain usually localised to right hypochondrium • Swinging pyrexia, rigors and weight loss • 25% present with jaundice • Examination shows an hypochondrial or epigastric mass • 30% have a pleural effusion Investigation • Serology shows a raised TW, increased ESR and deranged LFTs • Hepatitis markers TRO hepatitis • Blood c/s, melioidosis, stool ova/cysts/parasites • Tumor markers • Aspirates for cytology, staining, c/s • Chest x-ray often shows a raised right hemidiaphragm & pleural effusion • Ultrasound will localised the abscess and will guide drainage • CT triphasic – TRO tumor; irregular+necrotic, multi-loculated, rim-enhancing Management • Early: resus, vitals monitoring with i/o charting • Antibiotics  1st 2/52 IV; next 4/52 PO • Percutaneous drainage under ultrasound guidance if >3cm • If biliary obstruction will need to consider decompression • Open surgery if failure of resolution with percutaneous drainage or intraperitoneal rupture (esp w gallstones/multiple abscess/ascites) 76

! AMOEBIC LIVER ABSCESS • • • •

•

Prognosis in uncomplicated cases is good (<1%)

Due to infection with the protozoan parasite Entamoeba histolytica o Transmitted by the faecal-oral route 10% of affected patients develop liver abscesses Liver abscesses can be solitary or multiple o 80% of abscess develop in right lobe of the liver Can present several years after intestinal infection

Clinical features • Presents with malaise, persistent pyrexia and weight loss • Right hypochondrial pain is often mild o Tender hepatomegaly • Less than 20% of patients present with diarrhoea • NO jaundice or sepsis • Complications can arise as a result of abscess rupture or extension of infection – peritonitis • Complications occur in 5% patients and include: o Amoebic empyema o Hepato-bronchial fistula o Lung abscess o Pericarditis o Peritonitis Investigations • Serology shows raised WCC and ESR o Latex agglutination assay positive in more than 90% o Sigmoidoscopy, stool microscopy and rectal biopsy may identify the organism • Chest x-ray may show a raised right hemidiaphragm, atelectasis or abscess • U/S HBS o Aspiration produces a typical 'anchovy sauce' appearing pus o Pus is odourless and sterile on routine culture • CT Tri-phasic Management • Metronidazole is the antibiotic of choice o If ineffective chloroquine and dehydroemetine may be considered • Ultrasound guided aspiration may be useful o In pregnancy, or suspicion of secondary infection o Symptomatic – distension or fever o Esp in impending rupture HEPATOBILIARY AND PANCREATIC SURGERY

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! INFLAMMATORY BOWEL DISEASE Causes of colonic inflammation • Infection - bacteria, viruses, parasites • Ulcerative colitis • Crohn's' disease Ulcerative colitis • Peak age of onset 20 - 35 yrs • Characteristic feature acute mucosal inflammation with crypt abscesses

• • • •

Radiation enteritis Ischaemic colitis Microscopic colitis Drug-induced colitis

Crohn’s disease • Incidence is increasing possibly due to increased recognition • Characteristic feature - patchy transmural inflammation with noncaseating granuloma

Epidemiology • Bimodal distribution o Young: 2nd and 3rd decades of life o Middle: 5th and 6th decades of life • Equal gender predominance • Genetic association • Higher prevalence among Ashkenazi Jews and in cooler climates e.g. Scandinavia, UK, Germany Pathophysiology • Both Crohn's disease and ulcerative colitis have some pathophysiological features in common • Both result from inappropriate activation of the mucosal immune system • This process is driven by the normal luminal flora • May result from defective barrier function of the intestinal epithelium • Genetic factors contribute to susceptibility as demonstrated by: o Variable prevalence in different populations o Increased incidence in first degree relatives o Increased concordance in monozygotic twins o Concordance in site and type of disease in affected families • Possible environmental factors include: o Smoking o Use of NSAIDs o Luminal flora

Pathological features Crohn's disease Skip lesions - penetrating Can affect entire GIT (mouth, terminal ileum) Rectum normal in 50% Terminal ileum involved in 30% Discretely ulcerated mucosa Serositis common Fibrous shortening Strictures common Enterocutaneous or intestinal fistulae in 10% Anal lesions in 75% (fistulae, fissures) Possible malignant change Macroscopic: bowel is thick-walled & nodular (cobblestone appearance) with creeping fat, mesenteric thickening and deep linear ulcers Microscopic: transmural involvement, noncaseating granulomas (pathognomonic, but only present in 2/3)

History GIT symptoms Non-specific symptoms • Abdo pain • LOW/LOA/fatigue • D/N/V • Fever • Bloating, distention • Anemia • Bloody stools with mucus and pus • Malnutrition • Crohn’s fistula • Extra-intestinal manifestations • Colovesical fistula or colo-ovarian fistula: e.g. Skin fecaluria, pneumaturia, feces per vagina/PID O/E: usually normal (may have extra-intestinal manifestations) DDx •

• • COLORECTAL SURGERY

Ulcerative colitis Lesions continuous - superficial Begins in rectum, expends prox Rectum always involved Terminal ileum involved in 10% Granulated ulcerated mucosa Normal serosa Muscular shortening of colon Fibrous strictures rare Fistulae rare Anal lesions in <20% Malignant change well recognized Macroscopic: granular appearance of mucosa, loss of vascular markings, pseudopolyps interspersed with areas of shallow ulceration Microscopic: only mucosal and submucosal involvement; crypt abscesses

Gastroenteritis (Exclude by doing stool microscopy and culture) o Bacterial: E coli/ campylobacter/ salmonella/ shigella o Parasitic: Entamoeba histolytica o Viral: rotavirus Other infective causes: diverticulitis, TB colon Ischaemic colitis; Bleeding diverticulosis; Ca colon 78

! Clinical features of inflammatory bowel disease Ulcerative colitis • 30% disease confined to rectum • 15% develop more extensive disease over 10 years • 20% total colonic involvement from onset • Patients generally fall into following categories: o Severe acute colitis o Intermittent relapsing colitis o Chronic persistent colitis o Asymptomatic disease • Assessment of disease severity o Mild = < 4 stools per day. Systemically well o Moderate = > 4 stools per day. Systemically well o Severe = > 6 stools per day. Systemically unwell o Systemic features: tachycardia, fever, anemia, hypoalbuminaemia • Endoscopic grading of ulcerative colitis 0 = normal 1 = loss of vascular pattern or granularity 2 = Granular mucosa with contact bleeding 3 = Spontaneous bleeding 4 = Ulceration Crohn’s disease • Clinical features depend on site of disease • 50% have ileocaecal disease, 25% present with colitis • Systemic features are more common than in ulcerative colitis Extraintestinal manifestations Associated with disease activity • Skin o Erythema nodosum o Pyoderma gangrenosum • Joints o Asymmetrical nondeforming arthropathy • Eyes o Anterior uveitis o Episcleritis o Conjunctivitis • Hepatobiliary conditions o Acute fatty liver • Thromboembolic disease COLORECTAL SURGERY

Unrelated to disease activity • Joints o Sacroiliitis o Ankylosing spondylitis • Hepatobiliary conditions o Primary sclerosing cholangitis o Cholangiocarcinoma o Chronic active hepatitis o Gallstones • Amyloid • Nephrolithiasis

Medical management of inflammatory bowel disease • Treatment depends on o Type, site, severity of disease • Different drugs may be used for active disease and those in remission 5-Aminosalicylic acid • Used in mild / moderate ulcerative colitis and Crohn's disease • 5-ASA block production of prostaglandins and leukotrienes • Mesalazine is conjugated to prevent absorption in small intestine • Topical preparation may be used in those with left-sided colonic disease • Maintenance therapy of proven benefit in those with ulcerative colitis • Of unproven benefit in those with Crohn's disease Corticosteroids • Often used in those in whom 5-ASA therapy is inadequate o Also used in those presenting with acute severe disease • Can be given orally, topically or parenterally • Use should be limited to acute exacerbations of disease o Of no proven value as maintenance therapy in either ulcerative colitis or Crohn's disease o Use must be balanced against side effects Immunosuppressive and immunomodulatory agents • Often used in those in whom steroids cannot be tapered or discontinued • Agents used include: o Azathioprine - effective in both UC & Crohn's disease o Methotrexate - effective in Crohn's disease o Cyclosporin o Infliximab - anti-TNF-alpha therapy

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! Surgery for Crohn’s Disease

Surgery for Ulcerative Colitis

Indications for surgery - Crohn’s disease Absolute • Perforation with generalized peritonitis • Massive haemorrhage • Carcinoma • Fulminant or unresponsive acute severe colitis

Indications for surgery • 20% of patients with ulcerative colitis require surgery at some time • 30% of those with total colitis require colectomy within 5 years

Elective • Chronic obstructive symptoms • Chronic ill health or debilitating diarrhoea • Intra-abdominal abscess or fistula • Complications of perianal disease • Surgery should be as conservative as possible • No evidence that increased resection margins reduce risk of recurrence • If possible improve preoperative nutritional state Surgical Options • Limited resections • 30% undergoing ileocaecal resection require further surgery • Strictureplasty often successful • Bypass procedures rarely required

Emergency • Toxic megacolon • Perforation • Haemorrhage • Severe colitis failing to respond to medical treatment

Elective • Chronic symptoms despite medical therapy • Carcinoma or high grade dysplasia

Surgical options Emergency Elective • Total colectomy • Panproctocolectomy & Brooke ileostomy with ileostomy • Panproctocolectomy & Kock continent ileostomy and mucus • Total colectomy and ileorectal anastomosis fistula o Maintains continence but proctitis persists • Restorative proctocolectomy with ileal pouch o Need adequate anal musculature o Need for mucosectomy unclear o May need defunctioning ileostomy Pouch design Functional results of ileoanal pouch • Mean stool frequency six per day • Perfect continence o During day (90%) o At night (60%) • Gross incontinence (5%) Morbidity • 50% develop significant complications • Small bowel obstruction (20%) • Pouchitis (15%) • Genitourinary dysfunction (6%) • Pelvic sepsis (5%) • Fistula (5%) • Pouch failure (6%) • Anal stenosis (5%) • Larger capacity pouches reduce stool frequency

COLORECTAL SURGERY

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! BENIGN COLONIC POLYPS WHICH MAY NOT BE SO BENIGN •

A polyp is a pedunculated lesion o Not all polyps are tumours o Not all polypoid tumours are benign o Not all benign tumours are polypoid

Classification of large bowel polyps Epithelial Mesodermal • Adenomas - tubular, • Lipoma villous, tubulovillous • Leiomyoma • Metaplastic polyps • Haemangioma

Hamartoma • Juvenile polyps • Peutz-Jeghers syndrome

Juvenile polyps • Commonest form of polyp in children • Can occur throughout large bowel but are most common in the rectum • Usually present before 12 years o Prolapsing lump or rectal bleeding • Not pre-malignant, treated by local endoscopic resection Peutz-Jeghers syndrome • Rare familial disorder • Polyps found throughout gut but most common in the small intestine o Presents in childhood with bleeding, anaemia or intussusception • Circumoral pigmentation and intestinal polyps • Polyps can become malignant Metaplastic polyps • Small plaques approximately 2 mm in diameter • Not pre-malignant Adenomas • Benign epithelial neoplasm (pre-malignant) o Risk of malignancy increases with size o Malignancy more common in villous rather than tubular lesions • Most adenomas are asymptomatic o p/w bleeding, mucous discharge or prolapse o Villous adenomas may produce hypokalaemia but this is rare • Diagnosis is often by sigmoidoscopy or colonoscopy o Full colonoscopy essential to exclude other lesions • Treatment is by transanal excision or colonoscopic snaring o Patients require regular colonoscopic surveillance COLORECTAL SURGERY

FAMILIAL ADENOMATOUS POLYPOSIS (FAP) • • • •

<1% of colorectal cancers Definition: >100 adenomatous polyps all over colon & APC mutation o Attenuated FAP – <100 polyps, usually about 30 Autosomal Dominant mutation of APC gene on 5q21 p/w symptomatically but non-specifically with: loose stools, diarrhea, lower abdominal pain, weight loss, passage of blood and mucus

Clinical Manifestations • Gastrointestinal: >100 Colonic polyps in 50% of 16yo, 90% of 45yo o Also presents in stomach, duodenum and periampullary • Extra-gastrointestinal manifestations: o *Eye: Congenital hypertrophy of retinal pigmented epithelium o Bone: Osteomas o Skin: Epidermoid cysts, Lipomas o Thyroid: Papillary Thyroid Cancer o Desmoid cancers (treated with chemoRT), Adrenal cortex tumor Surveillance • Genetic testing (confirm plus chop become cancer) • At-risk members: yearly colonoscopy from 12yo + 5-yearly OGD o 80% detected by screening BUT 20% asymptomatic Treatment • Prophylactic proctocolectomy w ileal pouch anal anastomosis (formation of reservoir pouch) at ~20yo • Subtotal colectomy if rectum no polyps (NB surveillance of rectal stump)

HEREDITARY NON-POLYPOSIS COLORECTAL CANCER (HNPCC) 80% becomes cancer, accounts for 8% of colorectal cancers Genetics: microsatellite instability due to mutated mismatch repair gene Left sided in Asians, Right sided in Westerners Polyps tend to be flat, villous; often poorly differentiated Lynch I – familial colonic cancer Lynch II – associated with other GIT or urogenital cancers o Endometrial cancer, and also gastric, ovarian, small bowel, hepatobiliary, and renal pelvis/ureter cancers Diagnosis • The Amsterdam clinical criteria identifies candidates for genetic testing, and genetic testing can make a diagnosis of Lynch syndrome. o 3 or more family members are diagnosed with colorectal cancer o 2 are first degree relatives & 2 successive generations affected o 1 or more of the colon cancers is diagnosed under age of 50 o 0 – FAP (familial adenomatous polyposis) is excluded • • • • • •

Surveillance – 1-3yrly colonoscopy starting at 20 years old 81

! COLORECTAL CARCINOMA • • • •

Colorectal cancer is most common cancer in Singapore 40% are rectal and 60% are colonic tumours 3% patients present with more than one tumour (=synchronous tumours) A previous colonic neoplasm increases the risk of a second tumour (=metachronous tumour)

Pathology • Almost all tumours are adenocarcinomas • 90% of tumours are sporadic • 8% a/w HNPCC and 1% a/w FAP • 1% arise in association with long-standing ulcerative colitis (>10 years) Risk factors • Sporadic colorectal cancer (85%) o Older age o Obesity o Male sex o Smoking o Cholecystectomy o Hx of colorectal polyps/cancer o Ureterocolic anastomosis o Familial colorectal cancer (20%) o Diet rich in meat and fat • Colorectal cancer in inflammatory bowel disease (1-2%) o Ulcerative colitis • Adenomatous polyps (villous, >2cm, multiple) • Hereditary colorectal cancer (5-10%) o FAP and its variants (Gardner’s and Turcot’s syndromes) o Hereditary non-polyposis colorectal cancer (HNPCC) o Hamartomatous polyposis syndromes (Peutz-Jeghers) Site • 20% in cecum and ascending colon • 5% in transverse colon • 15% in descending colon and proximal sigmoid • 60% in distal sigmoid and rectum Morphology • Polypoid (more common in right colon) • Scirrhous (annular apple core in left colon) • Ulcerated • Nodular

COLORECTAL SURGERY

Pathogenesis APC pathway (adenoma-carcinoma sequence) • Accounts for 80% of sporadic colorectal carcinomas • Adenomas: 70% tubular, 10% villous, 20% tubulovillous o Most cancers believed to arise within pre-existing adenomas o Risk of cancer greatest in villous adenoma • Characterized by chromosomal instability • Stepwise accumulation of mutations in a series of oncogenes and tumour suppressor genes (APC – DCC – K-RAS – p53) 1. Loss of the APC suppressor gene on 5q21 (congenitally absent in patients with familial adenomatous polyposis – APC)  APC is required to break down beta-catenin; with the loss of APC, beta-catenin accumulates and activates various genes in the nucleus (such as MYC and cyclin D1) which promote cell proliferation 2. K-RAS (12p12) mutation follows the loss of APC – an activating mutation that causes the RAS to keep delivering mitotic signals and prevent apoptosis 3. Loss of tumour suppressor gene at 18q21 4. Loss of p53 late in carcinogenesis • The molecular evolution of colon cancer through this pathway occurs through a series of morphologically identifiable stages: localised epithelial proliferation  small adenoma  large dysplastic adenoma  carcinoma in-situ  invasive cancer Defects in DNA mismatch repair • Involved in 10-15% of sporadic cases • Accumulation of mutations, but due to a different mechanism, and without clearly identifiable morphologic correlates i.e. no adenomas • Due to mutations in one of the five DNA repair genes (MSH2, MSH6, MLH1, PMS1, PMS2) of which MSH2 and MLH1 are the most commonly involved in sporadic colorectal carcinomas o Loss of DNA mismatch repair results in microsatellite instability which affects coding or promoter regions of genes involved in cell growth such as the BAX gene and the type II TGF-β receptor • Tumours that arise from this pathway have a better prognosis than tumours that arise from the APC pathway

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! Clinical presentation History Right sided Occult presentation • Iron deficiency anaemia due occult GI Blood loss • Weight loss • Right iliac fossa mass

Left Sided Mass effect • Abdominal pain • Alteration in bowel habit • Rectal bleeding + mucus • Tenesmus

Complications in 40% of patients Bleed • Iron deficiency anaemia - SOB, CP, decreased ET, palpitations, fatigue, postural giddiness • LBGIT (blood and possible mucus) Block • Change in bowel habits (<3x/week = constipation) • Progressive constipation, possible spurious diarrhea • Mucoid stools • Change in consistency of stools • Tenesmus Burst • Perforation – peritonism – super super super super super pain Burrow • Colovesical fistulae (fecaluria, pneumaturia, recurrent UTI) • Metastasis – Constitutional symptoms – LOA/LOW/malaise Examination • Abdominal Mass • DRE (rectal mass) o Hard, non-tender, polypoid, irregular, contact bleeding o Distance from anal verge >7cm (internal anal sphincter) Screening • Screen asymptomatic population for pre-disease state (based on observational studies) o Prevalent and lethal disease o Precursor can be detected early (long asymptomatic period) o Early detection makes a difference (can institute treatment) o Safe, effective, feasible test available • FOBT (detection) o Test for heme component broken down by upper GIT • Colonoscopy (prevention) o Allows for polypectomy o Recommended after 40yo (official is 50), once every 10 years

COLORECTAL SURGERY

Investigation Diagnostic • Colonoscopy (98% accuracy) o Diagnostic:  Visualize (size and location) and biopsy lesion  Enables detection of synchronous lesions (polyps 30%, cancers 5%) o Therapeutic: e.g. polypectomy, stenting of obstructed colon o Ensure good bowel prep (PEG for renal impaired, Oral fleet) o Risks: Perforation, Bleeding, Failure to complete • CT colonography (95% accuracy) – second line o Spiral CT (IV contrast, air, contrast enema) – 6mm polyps • Double-contrast barium enema (barium + air) o Not adequate for diagnostic purposes, may miss small lesions  Classically can see an apple core lesion o In patients presenting with large bowel obstruction single contrast enema (after rigid sigmoidoscopy) is the investigation of choice o Barium prep: bisacodyl oral or magnesium salt o Risks: inssipation of barium stones Staging • CT scan of the abdomen and pelvis o Local T staging & invasion into bladder, ureter, uterus o Staging of regional and no-regional lymph node involvement o Metastases to the liver, peritoneal seeding, omental kinking o Ascites, hydroureter/hydronephrosis, intestinal obstruction • CXR + CT scan of the chest • Bone scan if appropriate • Endoscopic ultrasound, or transrectal ultrasound for rectal tumour o T staging to determine depth of involvement by tumour o Can also assess local lymph node status Monitoring • FBC for low Hb, together with iron studies rd • UECr: fluid and electrolyte abnormalities from vomiting or 3 space losses (intraluminal); assess risk of contrast nephropathy • LFT: derangements caused by metastasis (though these changes will only occur late) – raised bilirubin, ALP • PTT/GXM: for surgery • CEA (used only for trending) o >90% of tumours produce CEA o Compare pre-op, immediate post-op, and follow up for recurrence o Causes of false positive raised CEA: smoking, pregnancy, bronchitis, cholangitis and cancers of the stomach, lung, breast, pancreas, cervix, bladder and kidney 83

! Surgical pre-operative measures • Bowel prep o 3 days low residue diet, NBM day before op o Bowel clearance with PEG • Prophylactic antibiotics o Cefuroxime and Metronidazole 30min before induction of anaesthesia • Heparin – anti-coagulant

•

Principles of Surgery for the Colon • 5 cm proximal and 5 cm distal clearance for colonic lesions • Radial margin should be histopathologically free of tumour if possible • Lymph node resection should be performed to the origin of the feeding vessel • En Bloc resection of adherent tumours should be performed • Preferentially segmental colectomy with intraoperative decompression • Depending on site of lesion surgical options are: o Caecum, ascending colon, hepatic flexure – Right hemicolectomy o Transverse colon – Extended right hemicolectomy o Splenic flexure, descending colon – Left hemicolectomy o Sigmoid colon – High anterior resection • Principles of Surgery for Rectum • Because it is so common: o Upper rectum: where the tenia coli coalesce into a single longitudinal muscle layer. o Rectum measures ~12 to 15 cm in length and contains three valves o Middle rectal valve be located 9 to 10.5 cm from the anal verge  At anterior peritoneal reflection: the anterior cul-de-sac  Lesions at or beneath the middle rectal valve are considered to lie in the extraperitoneal portion of rectum o Anorectal junction  Anatomically at dentate line – 3 cm from anal verge  Surgically 2cm above dentate line, at proximal edge of anal sphincter – 5cm from anal verge • Clearance margins o 5 cm proximal and 2 cm distal clearance for higher rectal lesions o 1 cm distal clearance for super low rectal lesions is adequate o Radial margins are very important o Local recurrence reduced by performing total mesorectal excision (TME) COLORECTAL SURGERY

• •

Surgical options o Sphincter-sparing (with temporary defunction ileostomy)  Low Anterior Resection (Upper Rectum)  If distal margin >2cm above sphincter complex, which is 2 cm above dentate line, which is 3 cm from anal verge (total 7cm from anal verge)  Ultra Low Anterior Resection (Lower Rectum)  If distal margin 1cm above sphincter complex o Sphincter-sacrificing  Abdomino-perineal resection  For lower rectal cancers or invasion into external sphincter complex  Anus and sphincter complex dissected with creation of end colostomy o Even for the lowest of rectal cancers, using a combination of neoadjuvant chemo/radiation, total mesorectal excision, and intersphincteric proctectomy and colonic J-pouch to anal anastomosis, sphincter preservation can be achieved for most patients. o Unless the rectal tumor involves the external sphincter muscle, there is no oncologic need to remove it, and following resection of the tumor, gastrointestinal tract continuity can be restored. Reconstruction o Formation of colonic J pouch to improve function o Coloplasty – creation of a pouch Extended resections for locally advanced, adherent tumors o Consider neoadjuvant therapy to downstage Stoma creation o Defunctioning loop ileostomy/colostomy due to increased risk of an anastomotic leak & also poorer blood supply to anastomosis o A defunctioning stoma does not protect against anastomotic leak, but mitigates against disastrous complications of faecal peritonitis should a leak occur o Closed in 2-6/12 after check with Gastrografin reveals no leak

Operative complications Intra-op

Early (<30d)

Late (>30d)

Damage to other organs e.g. ureters

Wound infection; Bleeding; Abscess Anastomosis breakdown/leak → faecal peritonitis Early stoma complications

Diarrhoea Impotence (pelvic nerves) Adhesions (I/O) Anastomotic stricture Late stoma complications 84

! Adjuvant Chemoradiotherapy Principles • Adjuvant therapy for T2 and above • Neoadjuvant for T3 and above • Chemoradiotherapy o Good evidence for ≥T3 tumours, CRM<2mm: benefits > risk o Only for rectal cancers because of the radio risk

Staging Duke’s (more important) Stg A

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

5yr surv 75%

B

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

55%

Chemotherapy • 5FU and folinic acid is effective as adjuvant therapy • Given for both colon and rectal cancers

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)

Radiotherapy • Colon cancers, and tumors of the upper rectum, do not have tendency for local failure and therefore, except in specific situations, are not treated with radiation – also radiation may harm intra-abdominal organs • Tumors at or below the level of the middle rectal valve are considered to be extraperitoneal, and depending on their stage, may be treated with, in addition to surgery, radiation and chemotherapy to help in reducing local recurrence rates and maximizing the odds of achieving a sphinctersparing operation. • Risk factors for local recurrence include: o Local extent of tumour o Nodal involvement o Circumferential margin status o Risk of local recurrence can be reduced by radiotherapy • Can be given either preoperatively or postoperatively • Preoperative radiotherapy given as short course immediately prior to surgery o Reduces local recurrence o Increases time to recurrence o Improves 5-year survival

D

C1:40% C2:20%

Distant mets/ extensive local mets such that surgically Poor incurable

TNM made easy T 1 Invades Submucosa 2 Invades Muscularis propria 3 Penetrates muscularis into surrounding 4 Penetrates to visceral peritoneum N 1 Mets in 1-3 2 Mets in 4 or more M 0 No 1 Yes (a = only 1 organ or site, b = good luck to you)

Follow-up • Follow-up visits 3-monthly for the first 2 years, then 6-monthly for the next three years, and subsequently yearly, measure CEA at each visit • Yearly colonoscopy • CXR and liver ultrasound to detect metastases

COLORECTAL SURGERY

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! DIVERTICULAR DISEASE Pseudodiverticulum - acquired herniation of colonic mucosa & submucosa through the colonic wall, with covering of colonic serosa • Diverticulosis coli – presence of acquired pseudodiverticula • Diverticular disease – symptomatic diverticulosis coli • Diverticulitis – inflammation of diverticula Features • Increases with age • Risk factors – dietary fibre & genetics • Majority are asymptomatic; 10-30% are symptomatic • Classically at the mesenteric border but usually circumferential o Majority are in the sigmoid colon, right sided genetic o Asians: 40% right, 60% left, Caucasians: 20% right, 80% left Pathogenesis • Increased intraluminal pressure a/w lack of dietary fibre • Degenerative changes in colonic wall a/w weakening of collagen w age o Usually at point of entry of terminal arterial branches where serosa is weakest Staging (for acute diverticulitis) Severity staging by CT scanning may allow not only the selection of patients most likely to respond to conservative treatment, but may also predict the risk of failure of medical therapy and of secondary complications after initial conservative treatment. Hinchey Classification for acute diverticulitis Stage 1

Pericolonic / Mesenteric abscess (small)

Stage 2

Pelvic / retroperitoneal abscess (large) Purulent peritonitis (fm perf diverticulitis)

Stage 3 Stage 4

- Conservative: ABx, NBM, IV fluids - Surgery: 1 stage surgery after acute episode – resection of affected bowel segment with primary anastomosis

- Percutaneous drainage - Elective 1 stage surgery - 2 stage operation – Hartmann’s procedure (partial colectomy + diverting end colostomy & rectal stump formation) Faecal peritonitis 2º re-anastomosis 3 months later (fm ruptured diverticula)

COLORECTAL SURGERY

Presentation Acute diverticulitis • Typical presentation: 50yo male with fever, localized abdominal tenderness and GI symptoms, commonly diarrhea Symptoms Signs Pain: usually at LLQ (sigmoid), colicky Vitals: usually low grade → constant; relieved by defecation fever + tachycardia GI symptoms: N/V/C/D Abdo exam: tenderness Urinary symptoms e.g. Urgency +/- palpable mass • Differentials o GI: appendicitis, colitis (including GE & IBD), mesenteric adenitis/ ischaemia, ca colon, IBS o Uro: UTI, renal colic, renal tumor, renal cyst, hydronephrosis o Obgyn: PID, ectopic pregnancy, torsion of cyst/ovary, endometriosis • Investigations o Bloods: FBC  TWC raised + raised ESR o Imaging  Erect CXR: look for free air under the TRO perf  AXR: look for air-fluid levels in an abscess, I/O  CT scan (CTAP, triple contrast) • Contrast enema NOT recommended due to the risk of barium peritonitis • Visualize diverticula elsewhere (but not the one that is inflamed) • Confirm colitis (suggests divert) - mesenteric fat infiltration, concentric bowel thickening • Spot abscess, free gas, segmental colonic thickening • Cannot differentiate Hinchey III and IV because shit and pus look the same on CT  Sigmoidoscopy not recommended due to risk of perf  Laparoscopy if diagnosis in doubt • Management o Conservative  NBM, IV fluids, IV rocephin, flagyl  Antispasmodics/analgesia/antipyretics  Fibre supplements + stool softeners when oral feeds are restarted  Colonoscope after acute inflammation has subsided ~6wks • Confirm diagnosis, TRO colon cancer • Not to be done immediately due to risk of colonic perforation o Surgical -- see Hinchey classification 86

! Chronic diverticulitis • Presentation o Recurrent LIF pain o Irregular bowel habits with passage of mucus (due to edema) o Due to healing by strictures and adhesions -- I/O may result • Management o Colonoscopy should be done to rule out ca colon o Conservative mgt as above o Surgery considered if severe/recurrent Diverticular abscess • Presentation (may follow acute diverticulitis) o Localized tenderness & guarding o Palpable mass that may be detected on DRE o Swinging fever • Investigations: identified on CT scan (air-fluid levels) o Can diffx inflammatory phlegmon and abscess • Management: Percutaneous CT/US guided abscess drainage Generalized peritonitis secondary to perforation • Presentation o Acute onset continuous abdominal pain; guarding, rigidity o Vomiting; Febrile + tachycardic • Investigations o FBC – raised TWC, raised Hb o UECr – dehydration o CXR – free gas o CTAP TRO other causes e.g. PUD, appendicitis, ischaemic bowel • Management: Resuscitate (ABC) then surgery (refer Hinchey’s) Obstruction • Small bowel I/O o Usually temporary, due to adhesions of enteric loop to acute diverticulitis inflammation o Conservative - drip and suck, surgery considered if does not resolve • Large bowel I/O o Occurs with recurrent acute diverticulitis o Presents as colicky abdominal pain, constipation & distention o Investigation: CT - dilated bowels proximal to stenosis o Differential: Ca colon o Management: NBM, drip & suck; resection + primary anastomosis

COLORECTAL SURGERY

Hemorrhage • 80% self-limiting, but 40% will have recurrent bleed • Presentation o Usually elderly with high density of sigmoid diverticula o Massive bleed - torrential; altered blood with clots (not melena) o Colicky pain as blood is irritative & causes spasm o Syncope – from seeing blood, haha • Invx as per LBGIT and mgt o Assess vitals, resus if required o Always always PR and proctoscope to rule out piles o Rule out UBGIT - history + NGT o Correct any coagulopathies - drug-induced or congenital or acquired disease o CT mesenteric angiography  Diagnose, localize bleed and intervene – angioembolization  But low success rate -- bleed usually stops spontaneously - no active bleed for blush to form o Colonoscopy - may be able to find active bleed but intervention may be difficult o Exploratory laparotomy  Wash out rectum - exclude rectal bleed  Colonoscope small bowel (small incision at ileocecal jx) make sure there’s no blood  Colonoscope large bowel + wash out - resect bleeding segment Fistula • Vesicocolic (most common) o PMHx of chronic diverticulitis + UTI o Hx of dysuria, frequency, hematuria, pneumaturia, fecaluria o Investigations  Urine tests: • Dipstick/UFEME • Urine c/s  Imaging • Cystoscopy - cystitis • KUB – air in bladder o Differentials - other causes of fistula  Ca colon, ca bladder  Crohn’s  Post-irradiation necrosis (e.g. Ca prostate) o Management: resection of diseased colon + closure of fistula • Colovaginal – not pleasant • Coloenteric – enteritis and malnutrition 87

! HEMORRHOIDS Presentation • Affect 50% of population over the age of 50 years • Painless bright red rectal bleeding (coating, dripping) • Prolapsing perianal lump • Acute pain due to thrombosis • Faecal soiling or pruritus ani Anatomy • Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses • Internal hemorrhoids are not supplied by somatic sensory nerves and therefore cannot cause pain - internal hemorrhoids can produce perianal pain by prolapsing and causing spasm of the sphincter complex around the hemorrhoids • Internal hemorrhoids can also cause acute pain when incarcerated and strangulated Pathogenesis • 80% of patients have high resting anal pressure o Dilatation of venous plexus o Distension of AV anastomoses o Displacement of anal cushions

Treatment • All should have high residue diet • Lifestyle modifications – less straining • Local preparations rarely produced long-term clinical benefit Outpatient • Conservatively treat with Daflon • Surgical options for first and second degree haemorrhoids include: o Injection with 5% phenol in arachis or almond oil o Rubber band ligation Inpatient • Treatment options include: o Dilatation and banding; Haemorrhoidectomy • Haemorrhoidectomy is usually performed as an open procedure (3º) • Secondary infection and postoperative pain may be reduced with oral metronidazole • Anal stenosis may develop if adequate skin bridges are not maintained • Other haemorrhoidectomy techniques include closed or stapled procedures o Reduced operating time o Less postoperative pain o Shorten hospital stay, More rapid return to normal activity

Classification • Haemorrhoids are often classified as internal or external • Internal haemorrhoids arise above the dentate line • Banov grading of internal hemorrhoids Description Rx I Hemorrhoids do not prolapse Lifestyle modifications; meds (Daflon) – improves venous tone II Hemorrhoids prolapse on BO Rubber band ligation but reduce spontaneously Injection sclerotherapy (phenol emollient oil) III Hemorrhoids prolapse on BO Staple hemorrhoidectomy but manually reduced IV Hemorrhoids are prolapsed, Excision ( due to high recurrence) cannot be reduced

ANAL AND PERIANAL CONDITIONS

88

! ANAL FISTULAE Anal fistulae are abnormal communications, hollow tracts lined with granulation tissue connecting the primary opening inside the anal canal to a secondary opening in the perineal skin. They are usually associated with anorectal abscesses (obstruction of ducts  infection). Conditions associated with multiple anal fistulas: 1. Crohn’s disease 2. TB 3. Actinomycosis 4. Hydra-adenitis suppurativa Goodsall’s Law • Posterior ½: (All fistula tracts with external openings within 3 cm of the anal verge and posterior to a line drawn through the ischial spines) o Curvilinear o Internal opening in posterior midline (at level of dentate line) • Anterior ½: o Straight tracts • Tracts closer to anal verge = simpler, shorter • Tracts further away = transphincteric, long, high tracts

ANAL FISSURES A painful linear tear or crack in the distal anal canal, which, in the short term, usually involves only the epithelium and, in the long term, involves the full thickness of the anal mucosa. • •

Most will heal because of good blood supply (within 1 day / 2 days) If they don’t heal: usually due to spasm of internal sphincter muscle

Features of a chronic anal fissure: 1. Boat shaped 2. Punched out 3. Exposing internal sphincter 4. Sentinel skin tag 5. Hypertrophic anal papilla Management • Internal anal sphincterotomy o Definitive for chronic anal fissure o But do not cut through muscle – irreversible • Medical sphincterotomy (reversible) o GTN paste, botulinum toxoid injections

Investigations • Endoanal U/S (H2O2 aided for hyperechoic effect) – to view course of fistula tract • MRI – able to visualise entire pelvis, beyond the sphincter complex • CT/fistulography (in emergency situation) – for complex fistulas / unusual anatomy Management • Fistulotomy (for simple, short tracts) – cut & lay open tract • Fistulectomy – core along tract & remove tract entirely • Seton – for complex, long, high tracts

ANAL AND PERIANAL CONDITIONS

89

! BREAST ASSESSMENT Modified sweat gland that lies in the subcutaneous tissue of the anterior chest wall between superficial and deep layers of the superficial fascia • The base of each breast extends from the lateral border of the sternum to the mid-axillary line, from the second to the sixth rib • The axillary tail pierces the deep fascia and enters the axilla Lymphatic drainage • Axillary nodes – 75% of ipsilateral breast drains to the axillary nodes o 40-50 nodes: Anterior, posterior, medial, lateral, apical o Drains into supraclavicular and jugular nodes o Levels:  Level I: lateral to pectoralis minor  Level II: posterior to pectoralis minor  Level III: medial to pectoralis minor, up to apex of axilla • Internal mammary nodes--20% of drainage from the ipsilateral breast o Drains upper and lower inner quadrants o About 4 nodes per side, with one node in each of the first three interspaces and one in the fifth or sixth interspace • Interpectoral (Rotter’s nodes) – between pec major and pec minor Symptoms requiring specialist referral • Lumps (any new lump, even one in pre-existing nodularity) • Asymmetrical nodularity persisting after menstruation • Breast abscess • Persistently refilling or recurrent cysts • Axillary lymphadenopathy • Breast pain o Pain associated with a lump o Persistent unilateral pain in a postmenopausal woman • Nipple discharge o All women aged over 50 years, or women <50 with: o Women aged below 50 years with:  Bilateral discharge sufficient to stain clothes  Blood-stained nipple discharge  Persistent discharge from a single duct • Family history

BREAST SURGERY

Symptoms that may indicate breast cancer • Breast lump • • Breast pain • • Change in breast size or shape • • Arm lymphedema • • Dimpling of the breast skin •

Involution or inversion of nipple Axillary lymphadenopathy Nipple discharge or bleeding Ulceration of the breast skin Bone or abd pain / jaundice

Triple assessment Clinical Exam • Features of lump that are highly suspicious for breast cancer o Surface: irregular or nodular o Edge: poorly defined o Consistency: firm (rather than hard, usually) o Tenderness: non-tender o Fluctuation: usually not o Fixation: to skin or underlying chest wall • Nipple involvement - either in the lump or concurrent nipple changes o Lymphadenopathy Pathological • FNAC o Less invasive, less painful, smaller wound (23G needles), does not require LA o But only cells are obtained with no histology  cannot differentiate between in-situ cancer and invasive cancer, requires skilled cytopathologist o If FNAC shows malignant cells, do frozen section intraop before proceeding with surgery (recommended). • Core biopsy (gold standard) o Core biopsy is more invasive, requires local anaesthetic, will result in a larger wound (14G needle), more painful, risk of complications higher (because biopsy needle is a spring-loaded firing mechanism, improper angling may result in puncture of the lung or heart), more ex as requires tissue processing. o But can obtain tissue specimen, can stain for ER/PR status →better diagnostic value – especially for metastatic disease because first line treatment is chemoRT o Usually done intra-op o Can be guided by radiology - US or stereotactic guidance 90

! Breast imaging (esp for symptomatic patients) Mammography ***most sensitive! • Screening in asymptomatic women >40yo or symptomatic women >35yo o Breast tissue in younger women is denser - more difficult to pick up abnormalities • 2 views: craniocaudal (CC) & mediolateral oblique (MLO) o Look at axilla on MLO for any enlarged LNs • Features of malignancy o Pleomorphic microcalcifications  Heterogenous appearance  Segmental, closely grouped or arranged in a linear pattern (ductal distribution) o Underlying density o Spiculated mass or stellate lesion with poor outline or comet sign - 95% due to malignancy o Architectural distortion, tent sign, nipple changes • Abnormalities: o Spiculated masses  Soft tissue mass with spicules extending into surrounding tissue, 95% due to invasive cancer  DDx: DCIS, fibromatosis or fat necrosis o Stellate lesions  Localised distortion of the breast parenchyma with no perceptible mass lesion  DDx: radial scar, invasive Ca, DCIS, surgical scar o Circumscribed masses  Analyzed according to density, outline and size  DDx: Fibroadenoma, cyst, medullary carcinoma, abscess o Microcalcification  Debris within the duct wall or lumen  Sole feature of 33% of screen-detected cancers  Malignant usually linear or branching  Benign is usually rounded and punctate  DDx: invasive cancer, DCIS, fibroadenoma, fat necrosis BI-RADS Assessment • 0: Incomplete • 1: Negative • 2: Benign finding(s) • 3: Probably benign (short term follow up recommended) • 4: Suspicious abnormality 25-74% • 5: Highly suggestive of malignancy 75-99% BREAST SURGERY

•

6: Known biopsy – proven malignancy

Breast ultrasound • First investigation in pts <40yo, pregnant or lactating • Other uses: o Guide procedures e.g. Biopsy, drainage of abscess, cyst aspiration o Evaluate consistency - cystic vs solid - & margins o Localisation of lesion seen in only one mammographic projection o Evaluation of a palpable mass when mammogram is negative o Evaluation in mammographically-difficult areas e.g. Chest wall/axilla • Downsides o Operator-dependent, non-standardized techniques, poor resolution o Cannot see microcalcifications • Features of malignancy o Markedly hypoechoic, may have thick echogenic halo o Irregular edges due to destruction of surrounding strs o Hypoechoic shadowing - posterior acoustic shadow o Taller than its width (fir-tree appearance), invasion of fascia o High central vascularity • Abnormalities: o Cysts  Smooth walls; Sharp anterior and posterior borders  Black hypoechoic centres without internal echoes o Solid lesions (have internal echoes) Malignant Benign Heterogenic, hypoechoic Isoechoic or hypoechoic patterns Irregular edges Smooth well defined borders Cast hypoechoic shadows Cast no hypoechoic shadows Screening Normal risk, asymptomatic Increased risk

HRT therapy

40-49 YO  Annual mammogram 50-64 YO  Biannual mammogram (by invitation) >65 YO  Optional 2 yrly mammogram Start screening 5 yrs  Monthly BSE before onset of breast dz in  6 mthly CBE & U/S breast youngest family member  Annual mammography 40-49 YO Annual mammogram 50-65 YO Biannual mammogram up to 5 yrs after cessation of HRT

91

! APPROACH TO BREAST LUMP History • Lump-related o Site & number o Painful vs painless o Onset: when + why was it first noticed o Progression: change in size o Overlying skin changes: Erythema, Dimpling, Swelling, Asymmetry o Single lump ddx: fibroadenomas, cysts, fat necrosis, cancer • Any nipple changes (retraction) or discharge (blood, colour?) • Any other lumps anywhere else - other breast/axilla/neck • Estrogen exposure o Menarche/menopause/perimenopausal o Use of HRT/OCP o Number of children (+ before 30), breast-feeding (>6mths) • Other risk factors o Previous breast disease  Treated cancer  Previous atypical ductal hyperplasia / LCIS o Family history of breast cancer or ovarian or CRC (possible Lynch II)  Both paternal and maternal side (BRCA)  If yes - age of diagnosis, bilateral? o Exposure to ionizing radiation esp RT for previous breast dx o Daily alcohol intake (especially before age of 30) • Systemic review o LOA/LOW, fever, bone pain, shortness of breath Malignant - Ductal Ca (~70%) - Lobular Ca (~20%) - Others e.g. Mucinous, tubular (~10%)

Benign - Congenital abnormalities - supernumerary nipples - Hypoplasia

Painless Older age group: Breast cancer Younger age group: - Fibroadenoma - Cyst - Area of fibroadenosis BREAST SURGERY

Aberrations of normal development and involution (ANDI) - Fibroadenomas - Breast cysts - Sclerotic/fibrotic lesions

Painful - Area of fibroadenosis - Cyst - Abscess (usually in the lactating)

Non-ANDI - Infective - Lipomas - Fat necrosis

- Fat necrosis (post-trauma) - Periductal mastitis - Carcinoma (rare)

Physical Examination • Lump o Size, tenderness, site: quadrant o Surface: smooth/irregular/nodular o Edge: poorly/well-defined, temperature o Consistency: hard/soft/firm, fluctuation o Fixation: skin or underlying chest wall (in 2 directions) • General appearance o any asymmetry in the breast contours, o any obvious skin changes o peau d’orange –infiltration of malignant cells into lymphatics causing edema (not compression), erythema, puckering o any scars of previous operation or procedure e.g. punch biopsy • Look for nipple changes (7 D’s):  Discolouration  Depression  Displacement  Discharge  Deviation  Destruction  Duplication • Manoeuvres: o Ask patient to raise her arms (to see the axilla and underside of breasts, and accentuate any tethering to skin → dimpling) o Ask the patient to contract the pectoralis major (push her hands against her hips) → may reveal a previously unnoticeable lump if tethered to both skin and muscle o Press arms down & lean forward → the rest of the breast will flop fwd. but not the CA that is attached to underlying muscle Pain Surface Some- Smooth times Indistinct NO!! Smooth/ bosselated Irregular

Consistency Soft to hard

Mobility Not fixed

Mixed/fluctuant Not fixed Rubbery Very mobile Stony hard

Triple Assessment • Clinical: history and PE • Radiological: Ultrasound (if <35yo) or mammography • Pathological

Age 30-55; especially perimenopausal Wide: 20-55 Young:15-25

May be 35+ tethered/fixed

Diagnosis Cyst Nodularity Fibroadenoma Cancer

Management • If all 3 assessments suggest a benign lump -F/U with physical exam for 1 year to ensure lump is stable or regresses • If all 3 concordant for malignancy -- stage & treat • If mixed -- further workup e.g. Excisional biopsy

92

! APPROACH TO NIPPLE DISCHARGE Causes Colour of discharge Red or pink (blood + serum) Clear yellow (serous)

Green, brown, black (cell debris) Purulent, foul-smelling Thin, white fluid (milk)

Cause Ductal papilloma (benign) Ductal carcinoma Ductal papilloma Duct ectasia (= periductal mastitis) Cyst Ductal carcinoma Duct ectasia Mastitis/abscess Galactorrhoea/lactation

History • Is the discharge true? o Exclude other conditions may mimic e.g. eczema, Paget’s, etc. • Is the discharge significant? o Spontaneous or only on pressing (spontaneous is sig) o Intermittent or persistent (persistent is sig) o Relation to breastfeeding (significant if >1yr after stopping) • Is the discharge worrisome? o Unilateral or bilateral (unilateral more worrisome) o Discharge from multiple ducts or single duct (single duct more worrisome) o Nature of discharge (bloody more worrisome) o Age of the patient (more worrisome in older patient >60) • Is it troubling the patient? Investigation • Discharge for cytology to detect malignant cells • Mammography/ US of both breasts to detect any underlying malignancy • Histology of biopsied lesion if found on imaging • Ductography, ductoscope & biopsy Management • If malignancy found, manage malignancy • Excision for intraductal papilloma (microdocholectomy, total ductal excision, hookwire localised excision) – scarring may affect other ducts • Antibiotics for mastitis/abscess + incision and drainage for abscess • Conservative management for most other pathologies unless discharge persists and is troubling patient  microdochectomy of offending duct BREAST SURGERY

BREAST PAIN Cyclical mastalgia • Usually bilateral, affects upper outer quadrant • Mostly minor and accepted by many women as 'part of normal life' • Average age of onset is 24 years • No consistent hormonal abnormality • Prolactin levels may be increased • Essential fatty acid profiles may be abnormal Treatment • 80% require no treatment other than reassurance • Treatment should be considered if: o Symptoms for more than 6 months o For >7 days per cycle • Evening primrose oil (EPO) o Require treatment for at least 4 months o 50% response rate o 1% complications - nausea • Danazol o 80% response rate o 25% complications - acne, weight gain, hirsutism o Requires mechanical contraception • Bromocriptine o 50% response rate o 20% complications - postural hypotension • Tamoxifen effective but not licensed for use in mastalgia Non-cyclical mastalgia • Affects older women • Average age = 45 yrs • Usually unilateral, often localised • True non-cyclical mastalgia o Usually has a musculoskeletal cause o Rarely cancer Treatment • Support bra & NSAID

93

Breast cancer affects 1:12 women It is the commonest cause of cancer death in women, 6% of female deaths

Risk Factors • Age (increases with increasing age with two peaks as mentioned) • Genetic: o Family history: maternal & paternal (breast or ovarian cancer, especially if in first degree relative, young onset <40 YO, bilateral cancer in relative affected) o Known BRCA1 (on 17q; maternal side) or BRCA2 (both sides), o Li-Fraumeni syndrome involving p53 mutation) or HNPCC • High oestrogen exposure: o early menarche <12YO, nulliparity, late childbearing at >30YO, late menopause >55YO o Oral contraceptive usage (pure oestrogen type) o HRT (>5yrs, small increase in risk; reduced when stopped) • Previous breast disease: o Previous breast cancer (10X) o Previous biopsy with atypical ductal hyperplasia or LCIS (7-10X) • Ionizing radiation to breast (previous RT) • Alcohol consumption (daily)

WHO Classification Non-invasive

Ductal

• •

Epithelial Lobular

! BREAST CANCER

Spread • Local: skin & subcut tissues, underlying ribs and muscle (chest wall) • Lymphatics: axillary, internal mammary LNs, supraclavicular LNs • Haematogenous: lungs, liver, brain, bone, adrenals, ovaries

BREAST SURGERY

IDC - 70-80% of invasive breast Ca - Includes all cancers that cannot be subclassified into a specialised type  “no special type” - Poorer prognosis than a carcinoma of specialised type - 2/3 express ER/PR, - 1/3 overexpress C-erbB2 ILC - 5-10% of invasive cancers - 10-20% multicentric and/or bilat - Cells morphologically similar to cells of LCIS: monomorphic, bland round nuclei - Cells invade individually into stroma (due to loss of Ecadherin, a cell-adhesion molecule) - Similar prognosis to IDC

Others

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

Nonepithelial

Presentation • Asymptomatic: detected on mammographic screening • Local: o Self-detected lump in the breast (>1/3 of patients) o Nipple change: distortion, destruction, retraction, deviation, discharge, eczema o Overlying skin changes e.g. peau d’orange, tethering (means mass is still mobile but overlying skin will be indented when moving the lump), fixation (means the mass is not mobile), even fungating ulcer o Other lumps in axilla • Pain is uncommon. • Constitutional: LOW, LOA • Metastatic: bone pain/ #, SOB (metastases to lung, liver, LNs, bone, brain, adrenals)

DCIS = malignant - From terminal duct lobular unit, - Cause distortion of lobules, - Do not invade BM - Non-palpable, detected microcalcifications - 35% multicentric, occult invasive in 10-20% - Progress to CA within 10 yrs ~30% risk; considered malignant - Good prognosis if treated - Tx similar to IDC LCIS = RF - From terminal duct lobular unit (like DCIS) - Do not distort lobular architecture - Usually presents with a lump, seldom detected by mammogram (microcalcifications) - 60-80% multicentric and bilateral - Not premalignant, but a marker for increased risk of invasive disease in both breasts (7-10x increased risk) - If ca develops, will be IDC usually, occurs >15 years after diagnosis - Usually proceed with excision biopsy.

Invasive

Inflammatory carcinoma - Presents as erythematous. enlarged, swollen breast w/o palpable mass - Histologically not specialised - Diffuse invasion of breast parenchyma by ca cells blocking numerous dermal lymphatic spaces  swelling - No histo features of inflammation - Very poor prognosis, rapidly fatal Primary nonepithelial malignancies of the breast arising from supporting stroma comprise an important minority of breast neoplasms, including primary breast sarcomas, therapy-related breast sarcomas, the phyllodes tumors, primary breast lymphomas and angiosarcomas

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! Diagnosis and assessment • Most symptomatic cancers present as a painless lump • Breast pain is an uncommon presentation of breast cancer • Diagnosis is by Triple Assessment o Clinical Evaluation – Lump and regional nodes o Imaging (ultrasound <35 years old or mammogram >35 years) o Cytology or Histology • Imaging is reported as BI-RADS • Can help divide it into: o DCIS or early Breast Cancer (max with small mobile axillary LNs) o Locally advanced BC (matted LNs, skin and rib involvement) o Continue to stage to look for metastasis in advanced BC Prognostic factors • To select appropriate therapy according to prognosis • To allow comparison of treatment between similar groups of patient at risk of recurrence or death • To improve the understanding of the disease Patient factors • Age: Younger women have poorer prognosis of equivalent stage • Comorbidities • Social Support Tumor factors • Tumour size: Diameter of tumour correlates directly with survival • Histological type (some associated with improved prognosis) o Tubular, Cribriform, Mucinous, Papillary, Micro-invasive • Histological grade (for scoring of grades [1,2,3] ) o Tubule formation, Nuclear pleomorphism, Mitotic frequency • Lymph node status o Single best prognostic factor o Correlation between number & level of nodes involved & survival • Lymphatic / vascular invasion o 25% operable breast cancers have lympho-vascular invasion o Double risk of local relapse; ↑ risk of short term systemic relapse o Presence confers a poorer prognosis • Metastases: Distant metastases worsen survival

BREAST SURGERY

Predictive factors (predict response to a Tx): • C-erbB2/Her-2 positivity indicates more aggressive tumour • ER or PR positivity is good – predicts 90% response to treatment with tamoxifen; also means tumour is less undifferentiated • p53 mutation NOT for prog purpose. Staging Investigations: • CXR (for lung metastases; look for isolated hyperdensity) • CT thorax , abdomen (for liver and adrenal metastasis) • Bone scan • LFT (raised ALP) + Hepatitis screen (may flare up with chemoTx) • CT or MRI brain – if patient symptomatic T stage Tis: Carcinoma in-situ, Paget’s with no tumour T1a: 0.1-0.5cm T1b: 0.5-1.0cm T1c: 1.0-2.0cm T2: 2 to 5 cm T3: >5cm T4a: Chest wall T4b: Inv skin T4c: 4a+4b T4d: Inflammatory

N stage M stage N1: Mobile ipsilat axillary nodes M1: distant mets N2: Fixed/matted ipsilat axillary N3: N3a – Ipsilat infraclav nodes N3b – Ipsilat int mammary nodes N3c – Ipsilat supraclav nodes

Stage 0 Stage I Stage II

Stage III

Stage IV

Tis

T1N0

T2N0, T3N0 *skin, rib inv., matted LNs M1 T0N1, T1N1, T2N1 T3 N1 T0N2, T1N2, T2N2, T3N2 Any T, N3 T4, any N

5yr life

90%

60%

DCIS

Early Breast Cancer

80%

10%

Locally advanced BC

Advanced BC

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!

Palliative Surgery • Indications o Bleeding, fungating, infected tumor – toilet mastectomy o Fixation of pathological fractures o Decompression of spinal cord compression o Surgical excision of brain metastases BREAST SURGERY

Early

Surgical options for the breast • Wide Excision + radiotherapy (breast conserving surgery, std of care) o Removal of tumour with clear margins, while achieving good cosmetic result o Contraindications: [Nodal status does not influence decision for WE or SM] 1. Multifocal (tumour originates from 1 tumour and breaks off) +/- Multicentric (synchronous tumours) 2. No metastatic disease 3. Appropriate tumour size-to-breast ratio (to achieve good cosmetic result) - not about T staging anymore 4. Patient must agree to post-operative radiotherapy (daily RT in hosp) 5. CI to RT a. PREGNANT (the only absolute CI) b. No CT disorder –underlying inflammation may get worse c. Previous RT to the chest o Central lumpectomy: Must remove nipple-areolar complex o Overall survival at 25 years for WEAC comparable to SMAC, with Slightly higher local recurrence rates (for WEAC: 1% per year, 4% in 5 years) o Higher risk in younger patients as cancer tends to be more aggressive • Simple Mastectomy o Removal of breast tissue, nipple-areolar complex, & overlying skin o Indications  Contraindication to wide excision  Patient prefers to remove entire breast o If done for DCIS, don’t need to give adjuvant therapy o Reconstructed with rectus abdominis or latissimus dorsi  S/E: abnormal sensation of breast, no breastfeeding

Complications of surgery

Late

Aims of breast cancer surgery • To achieve cure if excised before metastatic spread has occurred • To prevent unpleasant sequelae of local recurrence

Haemorrhage (POD1) Wound Infection (POD3) Seroma formation (accumulation of serum) in 50% Flap ischemia Cosmetic deformity Complications of Axillary Clearance: - Lymphoedema – RT to axilla is contraindicated with AC as it worsens oedema - Cellulitis – even in minor trauma, due to lymphoedema. Need to clean even minor wounds with antiseptic solution + prophylactic ABx - Shoulder stiffness – require physiotherapy - Intercostobrachial nerve transection – numbness over inner aspect of arm

Sentinel node biopsy • SLN is representative of the rest of the axilla; if the SLN is negative for tumour cells, then the rest of the axillary nodes should be negative • Done in any breast surgery • Aims to accurately stage the axilla without the morbidity of axillary clearance • Can be located following the injection of radioisotope, blue dye, or a combo • Can be injected in peritumoural, subdermal or subareolar site • Positive node sent for frozen section o If -ve do not clear axilla; if +ve, perform axillary clearance Axillary Clearance • 30-40% of patients with early breast cancer have nodal involvement • The aims of axillary surgery is to: o To eradicate local disease o To determine prognosis to guide adjuvant therapy (nodal stage) • Surgical evaluation important and should be considered for all patients with invasive cancer o Routinely done in clinically palpable LN or ≥T3 (5cm) o Previous surgery which may disrupt lymphatic flow • Levels of axillary clearance are assessed relative to pectoralis minor o Level 1 - below pectoralis minor o Level 2 - up to upper border of pectoralis minor (routine) st o Level 3 - to the outer border of the 1 rib Benefits of axillary clearance • Axillary clearance both stages and treats the axilla • Surgical clearance possibly gains better local control • Avoids complications of axillary radiotherapy 96

! Chemotherapy (polyCT with 3 drugs; 4-6cycles, eliminate micrometastasis) Neoadjuvant • Shrink tumors – for conservation surgery as well as to downstage locally advanced cancers before mastectomy • 70% tumours show a clinical response; in 20–30% it is complete o 80% of these patients still have histological evidence of tumour o Surgery required even in those with complete clinical response • Complications: as for CT drug, e.g. mouth ulcers, N/V, hair loss, immunosuppression (main disadvantage pre-op) Adjuvant • Start 3 weeks after surgery o For T1c and above o Surgical margins <1mm or invasive o T1b with lymphovascular invasion o +ve nodal status • Premenopausal patients tend to have better response to chemotherapy than hormonal therapy (vice versa for postmenopausal patients) • Main active agents: anthracyclines (e.g. doxorubicin, epirubicin) and the taxanes (e.g. paclitaxel, docetaxel) • Common regimens: CMF (cyclophos, methotrexate, 5-FU) Palliative • Anthracyclines & taxanes are the mainstay • Helps to reduce load of disease to alleviate symptoms, increase survival Radiotherapy Adjuvant • To decrease local recurrence rate • Indications: o Usually done 6 weeks after Wide Excision o High risk of local recurrence: ≥ T3 (5cm) OR ≥ 4 LN +ve o 1-3 LN in any young pre-menopausal woman • Targeted at breast with or without internal mammary, infra/supraclavicular LN (Axillary LN are tackled during Surgery) • Contraindications: o Pregnancy, previous RT, patient choice o No chemo, no WE • Regimen consists of 25 to 30 cycles in total, 1 cycle per day from Mon Fri over 5-6/52 until max dose (no repeat RT for recurrences) • Complications: radiation injury (e.g. pneumonitis, skin changes), risk of cancers 1 in 2000 in 20yrs Palliative: Brain mets; Bone mets to painful areas / impending fractures BREAST SURGERY

Hormonal Therapy Used largely in post-menopausal patients – basically principle is to give therapy which tumor responds best to • Adjuvant therapy to eradicate micrometasis o Can also be used as palliation or preventive treatment in high risk patient o Reduces risk in contralateral breast • For ER/PR +ve → will have 90% response • Preferred for postmenopausal women • May render patient postmenopausal for better response to HT via medical ablation with LHRH-a or surgical oophorectomy Selective oestrogen receptor modulators (SERMs): Tamoxifen • 50% reduction in recurrence, 25% reduction in mortality • Taken daily for 5 years • Contraindications: o PMHx of CVA/DVT ; Immobile patients • Side effects: o Menopausal symptoms (hot flushes, etc.) o Endometrial cancer (0.1% per year) o Deep vein thrombosis Aromatase inhibitors: Anastrozole, letrozole, exemestane • Inhibit peripheral conversion of testosterone and androstenedione to oestradiol (still present in post-menopausal women) • Only suitable for post-menopausal patients as use of these agents will cause overactivity of the HPA axis in premenopausal women • Side effects: o Musculoskeletal pain; Osteoporosis Targeted Therapy Herceptin (trastuzumab) • targets Her-2-neu a.k.a. C-erbB2 receptor (an epidermal growth factor receptor [EGFR] that is overexpressed in 18-20% of cancers) • Used in C-erbB2 positive tumours, early or late stage • Her-2-neu indicates worse prognosis  Herceptin improves prog to normal • Side effects of Herceptin: o cardiomyopathy & CCF ; pulmonary toxicity o infusion reactions ; febrile neutropaenia Avastin: Targets vascular endothelial growth factor [VEGF] receptor, used in advanced cancer Lapatinib: Targets Her-1 and Her-2, used in advanced cancers 97

! Treatment by tumour stage DCIS • WE (+radiotherapy) vs SM • Core biopsy and SLN biopsy • ± hormonal therapy (if WE) to reduce recurrence at surgical site; tamoxifen reduces overall breast cancer risk by 50% in both breast

Biochemical measurements • ER positivity predicts for response to endocrine manipulation • C-erb-B2 o Likely to be resistant to CMF chemotherapy & hormonal therapy o Respond to anthracycline and taxols • Proteases: Urokinase and cathepsin D found in breast cancer

Early breast cancer (stage 1 & 2) • T2 or less (<5cm), N1 or less (no nodes or non-fixed nodes) • SMAC, or WEAC with postop RT • Adjuvant therapy to destroy systemic micrometastases o CT if tolerable and/or HT if ER/PR +ve Chemo Intermediate No chemo T >20mm, N >1 11mm < T < 20mm, N=0 T <10mm, N=0 High grade = chemo o Premenopausal pt → chemotherapy + hormonal o Postmenopausal pt → hormonal + chemotherapy

Recurrent breast cancer • Most local recurrences are symptomatic, a/w development of metastases • Restaging is therefore essential • Commonest sites for ductal carcinoma are liver, bone and lung o Lobular carcinoma less predictable often spreading to bowel, retroperitoneum etc • Recurrence whilst on adjuvant tamoxifen consider: o Further surgery for  Isolated 'spot' recurrence after mastectomy  Local recurrence in the conserved breast o Radiotherapy if not previously given o Change of hormonal agent to anastrozole or megestrol acetate

Locally advanced breast cancer (stage 3) • T3 or T4, N2 or N3 • Surgical resection dependent on size of tumour and resectability • Systemic therapy: o Neoadjuvant chemo  Downstage inoperable tumour (and predicts tumor response)  eliminate micrometastasis o Adjuvant therapy after resection  CT & HT (depends on the histology)  Usually not done if patient has completed the course of chemo during neoadjuvant phase Advanced breast cancer (stage 4) – aim for disease control • Distant metastases: treat symptoms and prevent potential problems • Minimal locoregional therapy except for palliative purposes o May reduce mets! • Systemic therapy – CT, HT, TT • Mets specific: o Bone: RT to painful areas, Fixation/RT to impending fractures, Decompression if cord compression • Treat hypercalcemia from mets o Brain: RT o Pleural: drain effusion o Liver (usually liver failure > obstructive jaundice) BREAST SURGERY

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! GYNAECOMASTIA • • • •

Due to enlargement of both ductal and stromal tissue 'True' gynaecomastia = enlarged breast glandular tissue 'Pseudo' gynaecomastia = excess adipose tissue Benign and often reversible, presents as unilateral non-tender enlargement

Aetiology Idiopathic Physiological (estrogen excess) Pathological

Neonatal Puberty (may be painful) Senile Primary Testicular Failure • Endocrine Tumors o Anorchia o Testicular o Klinefelter's Syndrome o Adrenal o Bilateral Cryptorchidism o Pituitary o Acquired Testicular Failure • Non-Endocrine Tumours o Mumps o Bronchial carcinoma o Irradiation o Lymphoma • Secondary Testicular Failure o Hypernephroma o Generalized hypopituitarism • Hepatic Disease o Isolated gonadotrophin o Cirrhosis deficiency o Hemochromatosis • Drugs o Oestrogens and oestrogen agonists - digoxin, spironolactone o Hyperprolactinaemia - methyldopa, phenothiazines o Gonadotrophins o Testosterone target cell inhibitors - cimetidine, cyproterone acetate • • • •

PAGET’S DISEASE OF THE NIPPLE Presentation • Eczematoid change of the nipple +/- surrounding areola • Burning, pruritus, hypersensitivity, with crusting exudate • May have palpable mass (60%) Work-up • Mammography to identify other areas of involvement • Pathologic diagnosis - core biopsy of nipple and underlying tissue • Almost always accompanied by an underlying malignancy - invasive ductal ca or DCIS Prognosis • Related to tumor stage Treatment • Surgery + RT

Classification (Simon's) • Grade 1 - Minor breast enlargement without skin redundancy • Grade 2a - Moderate breast enlargement without skin redundancy • Grade 2b - Moderate breast enlargement with skin redundancy • Grade 3 - Gross breast enlargement with breast ptosis Management • Reassurance that it is a benign and self-limiting condition • Investigate: o Thyroid function tests, testosterone/LH LFT, alpha-FP, beta-HCG Medical: Danazol may reduce breast size in 80% of patients Surgery: Excision can be considered if gynaecomastia is painful or cosmetically embarrassing (small = periareolar incision) BREAST SURGERY

99

! APPROACH TO LUMPS AND BUMPS Inspection • Number: solitary / multiple • Site: take reference from bony points • Shape / Symmetry: o Hemispherical, Round, Exophytic

• • •

Size Scars Colour & skin changes? o Sinuses, discharge o Ulceration o Erythema / cellulitis

Palpation (Ask patient: Is area painful?) • Overlying skin temperature • Consistency o Hard > Firm > Tense > Soft • Tenderness • Mobility • Surface: o Fully mobile in all directions? o Smooth/Irregular/ o Fixed and immobile? Rough o Mobile only in certain directions? • Margins clearly defined? • Relations to surrounding tissues (over lump in 2 perpendicular planes) o Attached to skin? muscle / tendon / bone? o If appears to be attached to muscle:  Ask patient to tense muscle; Reassess mobility in the 2 planes • Intramuscular or below the muscle, it will disappear. • Above the muscle it will be more prominent. • Fixed to muscle, it will become less mobile. • Fluctuant? (for small / medium lumps) o Paget’s sign: Rest 2 fingers on opposite sides of lump, press down on middle of lump +ve: Feel fingers moving apart •

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

LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Request – “I would like to complete my examination by…” • Examine the draining LNs • If sebaceous cyst / lipoma  “Looking for other lumps elsewhere” • Ganglion  “Looking for other lumps elsewhere” + “Asking for hand dominance” + “Taking an occupational history” Characteristics of lumps: • S: site, size, shape, scars, skin changes, surface • E: edge, expansibility/ pulsatility • C: colour, consistency, compressibility • T: tenderness, temperature, transilluminability • O: others [fluctuance, fluid thrill] • R: reducibility, relationship to each other Ulcers: • Base: granulation tissue, slough, fascia, muscle, bone • Edge: sloping (healing), punched out, undermined, rolled (BCC), everted (SCC) • Discharge: serous, sanguinous, haemoserous, purulent “Mr. X is a young Chinese gentleman…” “On inspection, there is a (single) (hemispherical) lump on the (dorsum of the forearm)” “It measures (x by x cm)” “There are (?scars, sinuses, ulceration, or discharge seen, nor overlying or surrounding skin changes)” “Is the lump tender?” “On palpation, the overlying skin is (not) found to be warm. It is (non-tender)” “The surface is (smooth), with clearly-defined margins” “The consistency is firm, and it is (non-fluctuant)” “The lump is (not) attached to the overlying skin, and it is non-pulsatile.” “It (appears to be attached to underlying muscle, as it is mobile horizontally but not longitudinally)”

100

! Symptoms and signs

Diagnostic significance

1. Lump in or on the skin

Character of the ulcer margin

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

Behaviour of the ulcer

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

Size, shape and surface features Revealed by inspection-is the lesion smooth-surfaced, irregular, exophytic (i.e. projecting out of the surface)? Depth within the skin Superficial and deep attachments. Which tissue is the swelling derived from?

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

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

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

Character of the margin Discreteness, tethering to surrounding tissues, threedimensional shape

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

Red or purple

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

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

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

Deeply pigmented

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

Pulsatility

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

Emptying and refilling

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

Transilluminability Temperature 2. Pain, tenderness and discomfort

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

Lesions filled with clear fluid such as cysts 'light up' when transilluminated Excessive warmth implies acute inflammation, e.g. pilonidal abscess These symptoms often indicate acute inflammation. Pain also develops if a non-inflammatory lesion becomes inflamed or infected (e.g. inflamed epidermal cyst). Malignant lesions are usually painless Malignant lesions and keratoacanthomas tend to ulcerate as a result of central necrosis. Surface breakdown also occurs in arterial or venous insufficiency (e.g. ischaemic leg ulcers), chronic infection (e.g. TB or tropical ulcers) or trauma, particularly in an insensate foot


5. Rapidly Keratoacanthoma, warts and pyogenic granuloma may all develop developing lesion rapidly and eventually regress spontaneously. When fully developed, these conditions may be difficult to distinguish from malignancy. Spontaneous regression marks the lesion as benign 6. Multiple, In certain rare syndromes, multiple similar lesions develop over a recurrent and period. Examples include neurofibromatosis and recurrent lipomata in spreading lesions Dercum's disease. Prolonged or intense sun exposure predisposes a large area of skin to malignant change. Viral warts may appear in crops. Malignant melanoma may spread diffusely (superficial spreading melanoma) or produce satellite lesions via dermal lymphatics 7. Site of the lesion

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

8. Age when lesion noticed

Congenital vascular abnormalities such as strawberry naevus or portwine stain may be present at birth. Benign pigmented naevi (moles) may be detectable at birth, but only begin to enlarge and darken after the age of 2

101

! LIPOMA Inspection o Can be single, often multiple o Usually at neck, trunk o Hemispherical – may appear lobulated o Scars  Implies recurrent lipoma Palpation o Smooth or lobulated on firm pressure – bulging between strands of fibrous tissue) o Soft / firm (depending on nature of fat) o Well defined edges (may not be regular; series of curves corresponding to each lobule o Pseudo-fluctuance if large – lipomas are not liquid; but fat may be liquid o Mobile in all directions (if subcutaneous) o Positive slip sign; No transillumination / thrill o Usually in the subcutaneous tissue. [check attachment skin & muscle] Background Information  Definition: Benign tumour consisting of mature fat cells (distended with fat from over-activity) o Malignant change does not occur o Liposarcomas arise de novo; occur in older age (deeper tissues – retroperitoneal, deep tissues of thigh, subscapular)  Liposarcoma classification 1. Well-differentiated 2. Myxoid, round cell (poorly differentiated myxoid) 3. Pleomorphic liposarcoma  Clinical features o Can occur at all ages (not common in children) o Slow-growing, never regress o May be multiple: lipomatosis (multiple continuous lipomata)  Occur in buttocks / neck  Can cause distortion of subcutaneous tissues.  Treatment o Non-surgical – watch & wait o Surgical – If patient wants it removed (Pain / peripheral neuropathy – Dercum’s disease, Cosmesis)  Can be removed under LA  Nuchal lipomas (back of the neck): extremely fibrous septae: difficult to excise  If close to joint: LA may not be possible (may communicate with joint) LUMPS, LUMPS, LUMPS, LUMPS, LUMPS



Variants of lipomas / syndromes associated with lipomas o Adiposis dolorosa (Dercum’s disease)  Multiple painful lipomas in limbs, sometimes trunk  Associated with peripheral neuropathy  Angiolipomas: prominent vascular component o Hibernomas: brown fat cells o Cowden’s disease – associated with:  Thyroid cancers  Lipomas  Palmoplantar keratoses  Multiple facial papules  Oral papillomatoses o Bannayan-Zonana syndrome – rare AD dz: lipomas with macrocephaly and haemangiomas, intestinal polyps

“Mr. X is a young Chinese gentleman…” “On inspection, there is a hemispherical lump over the right scapula” “It measures 10 by 8 cm” “There are no scars, punctum, ulceration, or discharge seen, nor any overlying or surrounding skin changes” “On palpation, the overlying skin is not warm, it is non-tender” “The surface is lobulated, and its margins are not well-defined” “The consistency is soft, and it is fluctuant” “The lump is not attached to the overlying skin” “It is mobile in all directions with a positive slip sign” “It is not transilluminable” “I would like to complete my examination by looking for other similar lumps” “My provisional diagnosis is a lipoma” “My differential diagnosis is: large sebaceous cyst”

102

! SEBACEOUS CYST Inspection • Usually solitary (can be multiple), Hemispherical • Site: face, trunk, back, neck, scalp, shoulders (none on palms / soles) • Variable size ; few mm to 4-5 cm • May have bluish discolouration, May exhibit plastic deformation on palpation • Punctum in apex: in 50% Palpation • Normal Temperature, non-tender (unless inflamed) • Smooth surface • Well-defined margins (lies in subcutaneous fat) • Tense consistency, may stretch overlying skin ( plastic deformation) • Non fluctuant, not transilluminable • Attached to skin, not attached to deeper structures, mobile in all directions Background Information • 2 histological types (Arise from infundibular parts of hair follicles) o Epidermal cyst: from infundibular portions of hair follicles o Trichilemmal cyst: from hair follicle epithelium (most common on scalp), frequently multiple (AD inheritance) • Definition: Distension of sebaceous glands w sebum from blockage of opening • Clinical features o Occur in all age groups, rarely present before adolescence o Slow growing,– may appear suddenly at adolescence o May become infected: acutely painful, sudden increase in size o May spontaneously discharge contents through punctum, regress  Point of fixation & discharge along a hair follicle  Point gets pulled inwards on enlargement of the mass – creates punctum  Sebaceous horn may form from hardening of slow discharge from wide punctum • Treatment: excision / curettage along with base + histological assessment Complications 1. Infection (±discharge) 2. Ulceration 3. Calcification (trichilemmal cyst) (may lead to cyst hardening) 4. Sebaceous horn formation, [hardening of a slow discharge of sebum from a large, central punctum.] 5. Malignant change LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Treatment • Non-surgical: leave alone (if small, asymptomatic). • Surgical o Complete excision of cyst and contents under LA. o Prevention of recurrence: by removal of elliptical portion of skin containing punctum along the Langer’s lines. o If at the angle of jaw, be careful of the facial nerve during operation. Damage to zygomatic branch can cause eye ulceration. • •

•

If lump is increasing in size, what to exclude? o Malignancies: BCC, Malignant melanoma. Cock’s peculiar tumour (complication) o Proliferating trichilemmal cysts that can grow to large size, ulcerate  may become infected, open, granulating & edematous  Boggy, painful, discharging swelling  solitary, 90% occur in scalp o often mistaken for SCC scalp; Angry, malignant-looking (malignant transformation rare)  Heaping up of granulation tissue from the lining of the cyst  burst through skin, giving everted appearance  regional lymphadenopathy may be present Gardner’s syndrome (If multiple lumps found) o Genetic disorder associated with:  Multiple osteomata of skull & epidermal cysts  Adenomatous polyposis of large bowel & CRCs  Desmoid tumours  Thyroid cancers

“Mr. X is a young Chinese gentleman…” “On inspection, there is a single hemispherical lump in the middle of the forehead just above the eyebrows” “It measures 1 by 1 cm in diameter” “There is a visible punctum over the lump” “There are no scars, sinuses, ulceration, or discharge seen, nor any overlying or surrounding skin changes” “On palpation, the overlying skin is not warm. It is non-tender.” “The surface is smooth, with clearly-defined margins” “The consistency is firm, and it is non-fluctuant” “The lump is attached to the overlying skin” “It is mobile in all directions” “Slip sign is negative” “I would like to complete my examination by…” “Looking for other lumps elsewhere” “My provisional diagnosis is a sebaceous cyst” My differentials are: Lipoma / Dermoid cyst

103

! GANGLION Inspection • Single; may have overlying scar [recurrent mass] • Hemispherical, flattened, • Near joint capsules, tendon sheaths (90% on wrist, hand – ventral / dorsal) • Variable (0.5 – 6 cm) Palpation • Normal temperature, non-tender • Smooth surface with Well-defined margins • May be multilocular • Soft & fluctuant if large > firm consistency if small • Weakly transilluminant. (gelatinous material) • Mobility: o Should assess mobility in 2 perpendicular planes, then with underlying muscles tensed (less mobile when tensed) o Not attached to overlying skin (mobile over it) o Attached to fibrous structures of origin [to joint capsule, tendon sheath, intramuscular septum, fixed when tensed] • Reducibility: may slip between deep structures when pressed (appears falsely reduce into joint) Request • Other similar lumps; ask dominant hand, occupation Background Information • Definition: Cystic myxomatous degeneration related to synovial lined cavity [joint capsule or tendon sheath] • Origin controversial: pockets of synovium communicating with joint, tendon sheath / degeneration of mucoid fibrous tissue • Site: o Can occur anywhere in body o Common in areas of fibrous tissue (e.g. around joints, esp. Dorsal > Volar wrist @ scapholunate joint)  Most common soft-tissue mass in the hand • Types: o Simple o Compound – chronic inflammation distends tendon sheath above and below the flexor retinaculum. o Occult o Interosseous LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

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

Differentials • Bursae (soft) • Cystic protrusion of synovial cavity in OA (joint will be abnormal) • Benign giant cell tumours of flexor sheath (Pigmented Villonodular Synovitis) • Lipoma • Sebaceous cyst

Treatment Non-surgical • Watch & wait, usually may disappear after a few months. • Aspiration + 3/52 of immobilisation (successful in 30-50%). High chance of recurrence 6-12/12 later. Surgical • Complete excision to include neck of ganglion at site of origin. Along Langer’s lines. • Complications o Wound complications: Scar, haematoma, infection o Recurrence <10% o Damage to adjacent neurovascular structures. o Stiffness & Contractures

“Mr. X is a young Chinese gentleman, who is alert and comfortable…” “On inspection, there is a single hemispherical lump on the dorsum of the left wrist” “It measures 3 by 2 cm” “There are no scars, ulcerations, or discharge seen, nor any overlying or surrounding skin changes” “On palpation, the overlying skin is not warm. It is non-tender” “The surface is smooth, with clearly-defined margins” “The consistency is soft, and it is fluctuant” “The lump is not attached to the overlying skin” “It appears to be attached to underlying muscle, as it is mobile horizontally but not longitudinally” “It is transilluminant” “I would like to complete my examination by…” “Looking for other similar lumps” “Asking Mr. X for his hand dominance” “Taking an occupational history” “My provisional diagnosis is a ganglion” My differential is a 1. Bursa 2. Cystic protrusions of synovial cavity of arthritic joints 3. Benign giant cell tumours of flexor sheath”

104

! BASAL CELL CARCINOMA Most common skin malignancy in Singapore Inspection • Single (often multiple) • Commonly found on the face, (above line drawn from angle of mouth to earlobe) • Hair-bearing, sun-exposed skin (especially around the eye) • Lesions raised above the skin: o Nodular/ nodulo-ulcerated type (most common):  Pearly, rolled edges [smooth, glistening, slightly transparent]  May be pigmented, with telangiectasia over the lump  May have central ulceration; erode facial structures if advanced o Cystic: large cystic nodule • Lesions not raised: o Pigmented: contains melanin; confused with malignant melanoma o Sclerosing: flat or depressed with ill-defined edges; maybe ulcerated o Bush-fire / Cicatricial: multiple superficial erythematous lesions with pale atrophic areas o Superficial: erythematous scaly patches • Base: o May be covered with coat of dried serum & epithelial cells o If deep: may expose deeper tissues (bone, muscle, etc.), covered with poor-quality granulation tissue o On face: may erode deep into facial structures Palpation (Important to palpate for mobility: fixation and deep local invasion) • Normal temperature, may be painful / itchy • Firm / solid consistency • should be mobile over underlying structures, confined to skin o If fixed, immobile  deeper invasion • Regional LAD (metastases are extremely rare, to rule out SCC) + Ask about pre-disposing factors

Xeroderma pigmentosum (familial, associated with failure of DNA transcription)  Gorlin’s syndrome (rare autosomal dominant cancer) o Acquired  Sunlight (especially UV light; UV-B range)  Carcinogens (smoking, arsenic)  Previous RT  Malignant transformation in previous skin lesions (e.g. naevus sebaceous) Clinical features o In elderly people (incidence increases with age) o Rare in dark-skinned races o Males > females o Grow very slowly; months / years typically o May spread radially – leaving central scar o Persistent nodule / ulcer with central scab (repeatedly falls off, reforms) o May have itch / pain o If neglected: deep infected ulcer 

Macroscopic appearances • Above the skin: o Nodular o Nodulo-ulcerative / Deeply eroding ulcer (“rodent ulcer”) o Cystic • Not raised above the skin: o Pigmented o Geographical / cicatricial / “bush-fire” (advancing edge, healing centre) o Sclerosing (flat / depressed tumour, illdefined edge) o Superficial (erythematous scaly patches)

Microscopic features • Most commonly islands and nests of basaloid cells in dermis • High mitotic rates, peripheral palisading • (islands arranged radially with long axes in // alignment)

Background Information • Locally invasive carcinoma of basal layer of the epidermis • Does not metastasize, but can infiltrate adjacent tissues • Common in sun-exposed skin • Pre-disposing factors: o Congenital (rare) LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

105

! Origin of various appearances: o Tumour always starts as a nodule o When central epithelium dies, ulcer develops (nodulo-ulcerative)  Edge rolled – raised up and rounded (but not everted) (may be only clue to diagnosis) o If centre of tumour does not necrose / ulcerate: nodule enlarges → cystic appearance  Not really cystic: solid and non-fluctuant o If pigmented brown by excess melanin: pigmented BCC o Geographical appearance:  When nodule first ulcerates, rolled edge is circular  Shape becomes irregular as malignant cells spread  As ulcer heals: irregular, raised edge around flat white scar – “bush-fire” BCC

“Mr. X is an elderly Chinese gentleman…” “On inspection, there is a single hemispherical lump just above alar of the nose” “It measures 2 by 2 cm” “The edges of the lump are well defined, with a pearly, rolled appearance” “There is a small area of pigmentation on the periphery of the lump, and fine telangiectasia are seen over the lump” “There are no visible scars, ulceration, or discharge seen, nor any other overlying or surrounding skin changes” “On palpation, the overlying skin is not warm. It is non-tender.”

Differentials • SqCC o Especially if ulcerated o But if rolled edge: more likely BCC • Keratoacanthoma (adenoma sebaceum, molluscum pseudocarcinomatosum) o But scar will be deep (see below) • If pigmented: malignant melanoma (rare in Singapore) Treatment • Raised above skin: excision with 0.5 cm margin (maximum) • Not raised above skin: wider margin of excision, especially if at inner acanthus of eye, nasolabial fold, nasal floor, ear o Frozen section may be needed to ensure adequate excision • Alternative: o RT • Eyes, ears, nasolabial fold lesions: Mohs chemosurgery o Staged chemosurgery, histological assessment of margins & electrodessication


“The surface is smooth” “The consistency is firm” “The lump arises from the skin” “It is freely mobile over the underlying tissues” “My provisional diagnosis is basal cell carcinoma” “My differentials include SqCC, keratoacanthoma” “I would like to complete my examination by…” Examining for cervical lymphadenopathy (although very rare in BCC)

106

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

Background Information • Carcinoma of the cells of the epidermis forming superficial keratinous squamous layer • Local invasion into epidermis, dermis, adjacent tissues, & lymphatic spread to LNs • Microscopy: o Tongues of tumours cells spreading in all directions o “Epithelial pearls” – nest of squamous epithelium, cells are arranged in concentric circles surrounding a central focus of acellular keratin • Clinical features o Incidence increases with age (usually elderly male) o Predisposition:  Congenital: • Xeroderma pigmentosum (AD, failure of DNA transcription)  Acquired n • Env : sunlight, Irradiation, Chemicals • Pre-existing lesions: Solar keratosis, Bowen’s disease • Chronic ulcers: old burns, chronic venous ulcers • Immunosuppression (post-transplant, HIV) o Usually has been growing for 1 – 2 months before being noticed  Begins as small nodules on skin  As enlargement occurs, centre necroses, sloughs  Nodule turns into ulcer  Ulcer initially circular with prominent everted edges  Subsequently enlarges & changes to any shape • Bleeding (more common with SCC than BCC) • Discharge • Pain (invasion of deep structures) • Lymphadenopathy Complications • Infection • Bleeding (massive / fatal if erosion into large vessel) Treatment (depending on site of lesion) • Wide-excision with 1 cm margin • Radiotherapy (if unresectable, nodal spread) • + Block dissection of regional lymph nodes (if involved) • Eyes, ears, nasolabial fold lesions: Mohs chemosurgery o Staged chemosurgery, histological assessment of margins & electrodessication


107

! Lesions Associated with SqCC

“Mr. X is an elderly Chinese gentleman…”

Marjolin’s ulcer

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

“On inspection, there is a single irregular ulcer on the dorsum of the right st nd hand, proximal to the 1 & 2 MCP joints”

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

“The base of the ulcer is shallow and contains red granulation tissue.”

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

“My provisional diagnosis is squamous cell carcinoma”

•

• Bowen’s disease (SqCC in situ)

• •

•

• •

• Solar (actinic) keratosis (SqCC in situ)

•

• • •

•


“It measures 1.5 by 1.5 cm. The edge of the ulcer is well-defined, red and heaped up.”

“There are no scars, or discharge seen, nor any surrounding skin changes.” “On palpation, the surrounding skin is not warm. It is non-tender” “The edges are firm” “The lump arises from the skin” “It is fixed and immobile”

“My differentials are…” o Benign: Keratoacanthoma, infected seborrhoeic wart, solar acanthosis, pyogenic granuloma o Malignant: BCC, malignant melanoma, solar keratosis “I would like to complete my examination by…” “Examining the local lymph nodes for lymphadenopathy” “Taking a history looking for sites of metastases” “Examining the abdomen and lungs for signs of metastases”

108

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

Background information 4 commonest types of malignant melanoma • Superficial spreading melanoma (70%) • Nodular melanoma (15 - 30%) • Lentigo maligna melanoma • Acral lentigous melanoma Microscopic features • Consists of loose nests of melanocytes in basal cell layer: • Invade epidermis (leading to destruction, ulceration) & deeper into dermis, subcutaneous fat Clinical Features • Very rare before puberty (usually > 20 years old) • Equally in both sexes (but distribution different – see below) • > 25% arise de novo o Change in surface, size, colour, Halo, satellite nodules o Ulceration, bleeding o Itch, No pain o Lymphadenopathy • Symptoms of distant metastases: LOW, SOB, jaundice o Lymphatogenous spread to: regional LN o Haematogenous spread to: Lungs [pleural effusion], Liver [hepatomegaly], Brain [focal neurological signs] & Skin and subcutaneous tissues Predisposing Factors • Congenital / non-modifiable o Light skinned race o Xeroderma pigmentosum o Dysplastic naevus syndrome (B-K mole, FAMM syndrome) – 100% risk if 2 family members affected o Large congenital naevi st o FHx in 1 degree relatives (1.5X risk) • Acquired / modifiable o Sunlight exposure o Pre-existing skin lesions  Lentigo  > 20 benign pigmented naevi (3 x risk) o Previous melanoma (3.5 x risk)

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! Features of pigmented skin lesion suspicious of malignancy • Asymmetry • Bleeding & ulceration (late) • Change in: colour, size, shape, surface, number (early) o Surface:  Loss of normal surface markings (e.g. skin creases) around lesion  Skin may become rough / scaly  Itchy with pale-pink halo (inflammation) o Size:  Growth of newly-formed / long-standing mole  Increase in edge, width, thickness o Colour:  Becoming darker  Halo of brown discolouration in skin around the lesion  Patchy colour change (black, to blue-purple  ↑ vascularity)  Occasionally colourless: no melanin production o Number:  Satellite nodules of tumour around the lesion  Enlarged inguinal, axillary lymph nodes • Diameter >6mm • Elevation (flat plaque → nodule) Request • Examine draining lymph nodes • Take a history for: o Cardinal symptoms of malignant change in a mole  Rapid increase in size  Itching  Bleeding  Change in colour / shape / thickness o Predisposing factors

Staging by depth of invasion Clark’s levels of invasion Level Extent of Tumour I II III IV V

Epidermis only Invades papillary dermis Fills papillary dermis Invades reticular dermis Subcutaneous tissue invasion

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

Breslow’s thickness (different in absolute depth of invasion, LN involvement) Breslow Thickness 10-Year Survival < 0.76 mm 92% < 3 mm 50% < 4 mm 30% LN Involvement < 40% (8 yr) •

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

Differentials • Benign o Moles (pigmented naevus – ↑ melanocytes, ↑ melanin) o Freckles (normal number of melanocytes, ↑ melanin from each) o Lentigo (↑ melanocytes, normal amount of melanin from each) o Pigmented seborrhoeic keratoses o Dermatofibroma o Thrombosed haemangioma • Malignant o Pigmented BCC LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

110

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

%

Superficial Spreading

Nodular

Lentigo Maligna

Acral Lentiginous

70%

15-30%

–

Rare

Trunk

Face; Dorsum of hand / forearm

Hairless skin (palms, soles, subungual area)

Site

♂: Back ♀: Legs

Colour

Red, white, blue Most often (varying black pigmentation)

Edge

Irregular

Shape

Palpable, but Thick, polypoid, Flat thin raised

Surface -

Remarks -

“Mr. X is a middle aged Chinese gentleman…” “On inspection, there is a single flat-looking lesion over the right foot” “It measures 2 by 4 cm” “It is variegated in appearance, and exhibits red, white, and black discolouration” “The margins are clearly-defined and irregular” “There are no scars, nor any surrounding pigmentation, erythema, or ulceration, bleeding, or discharge” “On palpation, the overlying lesion is palpable. It is not warm. It is non-tender” “The surface is smooth, and its consistency is firm” “The lump is attached to the skin, and moves with it over deeper structures” “My provisional diagnosis is malignant melanoma” “My differential diagnoses are: BCC, pigmented naevus” “I would like to complete my examination by…”

Brown / black

Regular outline Irregular

Brown / black Irregular

“Take a history for: cardinal symptoms of malignant change, and any predisposing factors”

Flat

Smooth

-

-

• Frequently ulcerated, bleeding

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

• Rare type • Often misdiagnosed as haematoma, paronychia


“Examining for regional lymphadenopathy”

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! NEUROFIBROMA Inspection • Often multiple • Anywhere in skin, subcutaneous tissues, e.g. forearm • Spherical / Pedunculated / Fusiform (long axes lie along length of limb) • Rarely more than few cm • Comment on any café-au-lait spots

Palpation • normal temp., Non-tender • Smooth, Well-defined • Soft/ fleshy, rubbery consistency • Non-fluctuant • If in subcutaneous tissue: mobile within it • Move most freely perpendicular to course of nerve

Request • Look for other similar lesions & other manifestations of NF-1: café-au-lait spots, axillary freckling, Lisch nodules, optic glioma o • Measure the BP (HPT 2 to phaeochromocytoma, CoA, RAS) • Examination of cranial nerve VII & VIII (acoustic neuroma) Background Information Sporadic Neurofibroma • Benign tumour containing mixture of elements from peripheral nerves: o Neural (ectodermal); Fibrous (mesodermal) • Often multiple • History o Any age (but usually adult) o Symptoms: usually cause no discomfort, rarely disfiguring o If related to nerve trunk, may be tender  Patient may get tingling sensations in distribution of nerve • Histology o Schwann cells: appear as bundles of elongated wavy spindle cells o Collagen fibrils, myxoid material o Often not encapsulated (unlike neurilemmomas) • Complications of Neurofibroma o Pressure effects: spinal cord, nerve root compression o Deafness: involvement of VIII o Neurofibrosarcoma (only in NF-1): 5-13 % o Intra-abdominal effects: obstruction, chronic GI bleeding o Skeletal changes: kyphoscoliosis, cystic changes, pseudoarthrosis • Treatment (single neurofibroma) o Non-surgical: leave alone if asymptomatic, patient agreeable o Surgical: indicated only if malignancy suspected  Local re-growth common (cannot be surgically detached from underlying nerve) LUMPS, LUMPS, LUMPS, LUMPS, LUMPS

Neurofibromatosis I (Von Recklinghausen’s disease) • AD, neurocutaneous syndrome; chr 17 • Characterised by pigmentary changes, • tumours, and skeletal, vascular dysplasias o Fibroma ≥2 NF or ≥1 plexiform NF o Iris hamartomas (Lisch Nodules) o Bone: dysplasia, pseudoarthrosis o Relatives o Optic glioma o Macules >6; >15mm post-pubertal o Axillary freckling

Neurofibromata of all sizes (few mm to large subcutaneous nodules), related differently to skin o Within skin o Tethered to skin o Pedunculated

Plexiform Neurofibroma (elephantiasis neurofibromatosis) • Very rare • Excessive overgrowth of neural tissue in subcutaneous layers, giving tissue swollen oedematous appearance o Often mistaken for lymphoedema, but lymphatic drainage is normal • Can result in severe deformity: diffuse enlargement of peripheral nerve with skin involvement “Mr. X is a young Chinese gentleman…” “On inspection, there are two spherical, pedunculated masses on the back” “One measures 2 cm, and the other 0.5 cm in diameter” “They are pink in colour, with well-defined margins” “There are no scars, sinuses, ulceration, or discharge seen, nor any surrounding skin changes” “On palpation, they are not warm and non-tender” “Their surfaces are smooth, and are firm, and rubbery” “They are attached to the skin, and are mobile over the deeper tissue layers” “My provisional diagnosis is neurofibromata” “I would like to complete my examination by…” • "Looking for other similar lesions” • “Looking for manifestations of neurofibromatosis” • “Examining the cranial nerves”

112

! DERMOID CYST Inspection • Usually single • Ovoid / spherical • Site: o Congenital, 1-2 cm usually  Along lines of fusion of ophthalmic & maxillary facial processes  Inner & outer ends of upper eyebrow o Acquired, 0.5-1 cm usually  Beneath skin likely to be injured e.g. fingers  Scars often present Palpation • Not warm, maybe tender if infected • Smooth surface, Well-defined margins • Consistency o Congenital: Soft (not tense / hard) o Acquired: Hard & tense (sometimes stony hard) • Fluctuant (if large) • Mobile over deeper tissues o Deep to skin, in subcutaneous tissue i. Congenital: Not attached to skin or underlying structures ii. Acquired: may be tethered to scar Background Information • A dermoid cyst is a cyst deep to the skin, lined by skin • 2 different methods of formation: o Congenital: Accident during antenatal development o Acquired: Implantation of skin into subcutaneous tissue by injury Treatment • Congenital o Surgical treatment; complete excision o Full extent should first be established with X-ray / CT  Midline cysts may communicate with CSF; must exclude bony defect • Acquired o Complete excision of cyst


Clinical features • Congenital (suspect if in child, young adult) o Formed intra-utero, when skin dermatomes fuse o Occur at any point in mid-line, common in neck / face / nose  Particularly along lines of fusion of ophthalmic & maxillary facial processes  Also: inner & outer ends of upper eyebrow o May be seen at birth o Distends a few years later, becomes obvious; few symptoms other than cosmetic problems o Rarely infected • Acquired – Implantation dermoid (suspect if in adult – Browse pg 60) o Develop when piece of skin survives after being forcibly implanted into subcutaneous tissue  Often by injury: cut, stab, etc. o Symptoms  Small, tense lump  Painful and tender (in areas subjected to repeated trauma)  Local effects (e.g. problems with grip / touch if on finger)  Also rarely infected o Differentials  Sebaceous cyst (look for old injury, presence of scar near cyst: more likely dermoid) “Ms. X is a young Chinese girl…” “On inspection, there is a single ovoid lump just above the lateral edge of the left eyebrow” “It measures 3 by 2 cm” “There are no scars, ulceration, or discharge seen, nor any overlying or surrounding skin changes)” “On palpation, the overlying skin is not warm. It is non-tender.” “The surface is smooth, with clearly-defined margins” “The consistency is firm, and it is fluctuant” “The lump is not attached to the overlying skin or underlying tissues.” “It is fully mobile in all directions.” “My provisional diagnosis is a congenital dermoid cyst” “My differentials are: sebaceous cyst, lipoma”

113

! SEBORRHOEIC KERATOSIS

HAEMANGIOMA

(Senile wart / seborrhoeic wart / verruca senilis / basal cell papilloma) Inspection • Often multiple • Any part of skin; most found on back & face • Round / oval • Light brown → black • “stuck on appearance”; appears warty • Varying size; Few mm to 2-3 cm • Distinct margins Request to look for similar lesions elsewhere

Palpation • No warmth, no tenderness • Rough surface (sometimes papilliferous) • More firm than surrounding skin • Attached to skin • Special tests o May be picked off gently – reveals patch of pale-pink skin, 1-2 surface capillaries (bleed slightly) o (DON’T DO THIS IN EXAM)

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

Background Information • Vascular malformations o Types  Capillary: ⅔ of cases, include the cutaneous haemangiomata, telangiectasias  Predominantly venous: venous angioma • Deeper levels of subcutaneous tissue, may extend into muscle / joint • May have distended veins over the surface of the mass • Empty with pressure, may have bruit  Predominantly lymphatic: lymphangioma circumscriptum o Features  Develop as abnormal proliferation of embryonic vascular network  Hamartomas  May ulcerate, induce hyperkeratosis in overlying stratum corneum • Many forms of cutaneous haemangiomata: (see table) o Strawberry naevus (cavernous haemangioma) o Port-wine stain (naevus flammeus) o Spider naevus o Campbell de Morgan spot Also • Telangiectasias o Dilatation of normal capillaries o Can be secondary to irradiation o Can be part of hereditary haemorrhagic telangiectasia (Osler-RenduWeber syndrome)  Autosomal dominant disease  Overt and occult haemorrhage can present as haematuria, haematemesis, melaena, epistaxis, iron-deficiency anaemia • Vin rosé patch o Congenital intradermal vascular abnormality o Mild dilatation of vessels in sub-papillary dermal plexus o Can occur anywhere, gives skin pale-pink colour o Associated with other vascular abnormalities (e.g. haemangiomata, AV fistulae, lymphoedema) o Usually not disfiguring 114

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


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

115

! ANATOMY OF THE NECK • •

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•

The neck is composed of two triangles on each side – anterior and posterior triangles The anterior triangle is bounded by the lower border of the mandible superiorly, the midline anteriorly, and the anterior border of the sternocleidomastoid posteriorly The posterior triangle is bounded by the posterior border of the sternocleidomastoid anteriorly, the anterior border of the trapezius posteriorly, and the clavicle inferiorly In general, enlarged lymph nodes are the most common cause of a lump in the neck, regardless of location

Masses by location Midline 1. Submental lymph node 2. Thyroglossal cyst 3. Thyroid nodule in the isthmus 4. Sublingual dermoid cyst 5. Plunging ranula (retention cyst of the sublingual) 6. Rarely, hyoid pathology e.g. bursa Anterior Triangle 1. Lymph node – along anterior border of sternocleidomastoid (levels II, III, IV) 2. Thyroid nodule 3. Submandibular gland mass (see later section on Salivary gland swellings) 4. Branchial cyst + fistula 5. Chemodectoma (carotid body tumour) 6. Carotid aneurysm 7. Pharyngeal pouch 8. Laryngocoele (rare; an air-filled, compressible structure seen in glassblowers)

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

Posterior Triangle 1. Lymph node (mainly) – level V and supraclavicular lymph node groups 2. Cystic hygroma 3. Cervical rib 4. Brachial plexus neuroma/schwannoma

NECK LUMPS

116

! Dermoid Cyst

Branchial Cyst/Fistula

Pathology: Can be congenital or acquired. • Congenital – developmental inclusion of epidermis along lines of fusion of skin dermatomes (seen in younger patients, present since birth). Locations include: o medial and lateral ends of the eyebrows (internal and external angular dermoid cysts) o midline of the nose (nasal dermoid cysts) o midline of the neck and trunk • Acquired – due to forced inclusion of skin into subcutaneous tissue following an injury, usually on fingers. Seen in older patients, no previous history of mass, history of trauma to area (may have associated scar).

Epidemiology: Affects both sexes equally, usually in young adults in their 20s.

Histology: Cyst lined by epidermis, with evidence of adnexal structures such as hair follicles, sebaceous glands and sweat glands. Features: Small non-tender mobile subcutaneous lump, may be fluctuant, skin-coloured or bluish. Management - Imaging investigations (e.g. XR, U/S, CT) are important especially for cysts on the skull as they can communicate with cerebrospinal fluid. - Complete surgical excision of the cyst. Plunging Ranula Pathology: A pseudocyst associated with the sublingual glands and submandibular ducts. Ranulas (frog mouth) can be congenital or acquired after oral trauma.

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

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

117

! Chemodectoma

Pharyngeal Pouch

Pathology: A chemodectoma is a tumour of the paraganglion cells (paraganglionoma) of the carotid body located at the bifurcation of the common carotid artery (into the internal and external carotids). They are usually benign, but locally invasive; the risk of malignancy is 10%, with metastasis to local lymph nodes (no histopathological features for malignancy, thus malignant nature can only be diagnosed by presence of metastasis).

Pathology: A herniation of the pharyngeal mucosa (pulsion diverticulum) through its muscular coat at the weakest point – Killian’s dehiscence – between the cricopharyngeus muscle and the lower inferior constrictor muscles.

Features: - Solid, firm mass at the level of the hyoid bone (where the bifurcation is) – be gentle during palpation as pressure on the carotid body can cause vasovagal syncope. - Mass is pulsatile but not expansile, due to transmitted pulsation from carotids. - Due to close association with carotid arteries, lump can be moved side to side but not up and down. - May be bilateral. Differentials: - Main differential is carotid artery aneurysm - Aneurysm can occur at any level but carotid body tumour occurs at the level of the hyoid bone. - If suspecting aneurysm, (a) listen for bruit, look for (b) signs of Horner’s syndrome, (c) examine the rest of the peripheral vascular system. Investigation: - DO NOT PERFORM FNA - Angiography (gold standard) – shows a hypervascular mass displacing the bifurcation. May also show vessel compromise by tumour invasion, and undetected synchronous tumours. - CT and/or MRI can be used to delineate tumour anatomy in relation to surrounding structures; CT reveals homogenous mass with intense enhancement following IV contrast administration.

Features - Occurs in older patients - A cystic swelling low down in the anterior triangle, usually on the left - Squelching sound on deep palpation - Patient complains of o halitosis, o regurgitation of undigested food with coughing o dysphagia in the neck, o hoarseness, o weight loss - Complications: aspiration pneumonia; diverticular neoplasm (<1%) Diagnosis by barium swallow Treatment - Leave it alone if small and asymptomatic - Minimally invasive treatment: endoscopic cricothyroid myotomy - Surgical approaches (several available) o Diverticulectomy + cricothyroidotomy (diverticulectomy associated with risk of mediastinitis, dangerous) o Diverticulopexy (done in high risk patients, involves suspending the lumen of the pouch in the caudal direction so that food and secretions cannot enter the pouch; as the diverticulum is still present, the risk for malignancy still remains)

Treatment: - Surgical excision with pre-operative embolization (reduces bleeding and complications, and facilitates resection); any enlarged ipsilateral lymph nodes are also removed due to the small possibility of malignancy - Radiotherapy is an effective alternative for patients who are unfit for surgery or whose tumours are too large.

NECK LUMPS

118

! Cystic Hygroma

Cervical Rib

Pathology: A cystic hygroma is a congenital cystic lymphatic malformation found in the posterior triangle of the neck, probably formed during coalescence of primitive lymph elements. It consists of thin-walled, single or multiple interconnecting or separate cysts which insinuate themselves widely into the tissues at the root of the neck.

Features: - Usually more symptoms than signs as it causes thoracic outlet syndrome (diagram below) - A hard mass in the posterior triangle at the root of the neck - Symptoms/signs: o Arterial: pallor, gangrene or necrosis of the tips of the fingers o Venous: oedema, cyanosis o Neurological: complaints of radicular symptoms (pain, paraesthesia), wasting of the small muscles of the hand - Adson’s test can be done – ask patient to extend neck and rotate it towards side of symptoms  radial pulse will be diminished, occasionally with reproduction of radicular symptoms in the limb

Features: - 50-65% present at birth, but occasionally may present later in childhood or adulthood - cystic swelling that is soft, fluctuant, and compressible (usually into another part of the cyst), located in the posterior triangle at the root of the neck - Classically “brilliantly transilluminable” - A large cyst may extend deeply into the retropharyngeal space Complications: - Cystic hygroma seen on prenatal ultrasound in the first trimester suggests chromosomal abnormality (50% of foetuses, usually trisomy 21) or other structural abnormalities (33% of foetuses with no chromosomal abnormality, usually congenital heart anomalies) - May obstruct delivery - Compressive problems after delivery – respiratory, swallowing Management: - Radiological investigations e.g. CXR, CT to delineate extent of cyst - Non-surgical treatment – aspiration and injection of sclerosant (usually unsuccessful) - Surgical excision – partial (to alleviate symptoms) or complete

NECK LUMPS

Diagnosis by CXR Neuroma/Schwannoma Features: - Slow growing tumour arising from peripheral neural structures of the neck e.g. brachial plexus, cervical plexus, vagus nerve, phrenic nerve, etc. - Fusiform, is mobile in plane perpendicular to axis of nerve but not parallel - Usually benign - May be Tinel’s positive – tap on the mass for any paraesthesia occurring in distribution of the nerve - DO NOT PERFORM FNA – excruciatingly painful

119

! CERVICAL LYMPHADENOPATHY

Causes: • Cancer (3): SCC, NPC, Adenocarcinoma • Lymphoma • TB Infective

Neoplastic

Inflammatory

There are six levels of lymph nodes in the neck, and different structures drain to different groups of nodes: Ia – submental Ib – submandibular II – long internal jugular vein from skull base to bifurcation of carotids (includes jugulodigastric nodes) III – along internal jugular vein from carotid bifurcation to omohyoid IV – along internal jugular vein from omohyoid to clavicle Va – Posterior triangle Vb – Supraclavicular VI – Tracheo-oesophageal groove (not palpable) VII – Superior mediastinum Drainage: • Oral cavity and oropharynx  levels I – III • Thyroid and larynx  levels II – VI • Nasopharynx  II – V (usually upper neck – level II and high level V) NECK LUMPS

Viral (esp 1-2cm firm LN. No need Abx unless obvious infx) Epstein-Barr virus, cytomegalovirus (infectious mononucleosis); HIV Streptococcus, Staphylococcus, Klebsiella (from intraoral pathology e.g. dental abscess, tonsillitis) Tuberculosis Toxoplasma; Actinomycosis Mets Head and neck primary Nasopharyngeal carcinoma Oral cavity, oropharynx, larynx, hypopharynx, thyroid, etc. Other primary sites (4B’s) Bowel (stomach, colon), breast, bronchus (lung), balls (testicular). Also UL. Primary – lymphoma SLE Kikuchi’s (necrotising lymphadenitis occurring in young females, presenting as painful cervical lymphadenopathy) Sarcoidosis

History • Age • RF for CA: smoking, alcohol. Betel nut • The lump itself o onset, duration, associated symptoms, lumps elsewhere o Pain: inflammatory > CA o Growth pattern / rate of growth: • last few days = infx / inflammatory / haemorrhage into cyst • last few months = CA • Constitutional symptoms o Fever, malaise, arthralgia, myalgia (viral prodrome); o Night sweats, low-grade fever (TB, B symptoms of lymphoma); o Loss of appetite, loss of weight (chronic infection, malignancy) • Local symptoms – intra-oral diseases e.g. tooth decay, oral/tongue ulcer, tonsillitis. Use of dentures. • Past medical history – cancer, TB (contact? Diagnosed? treated or untreated?) • Social history: travel and contact history, sexual history for HIV, oral sex 120

! Physical examination • Inspection o Site, size, shape, surface: erythema, discharging sinus (multiple lymph node enlargement with discharging sinuses can be TB or actinomycosis; sulphur granules seen in actinomycosis) • “Is there any pain? I am going to feel the lump, if any pain, let me know” o Palpate from behind, one side at a time – start at submental, then submandibular, preauricular, postauricular, along anterior border of sternocleidomastoid, supraclavicular, posterior triangle, lastly occipital. Use pulps of the fingers in a gentle rolling movement. o Tenderness to palpation • Consistency – hard, matted nodes are more suspicious for malignancy o Fixation to overlying skin or underlying structures Potential drainage sites: • Upper LN (5) : MOUTH!!, face, scalp, thyroid, salivary glands • Lateral LN: thyroid • Lower LN: UL, Breast, Lungs, Abdomen (if Virchow’s), Oesophagus • Susp lymphoma (3): axilla, parotid, inguinal + liver/spleen To complete the examination: • Formal ear, nose, throat examination especially looking at the post-nasal space for nasopharyngeal carcinoma (NPC being the most common cancer causing enlarged cervical lymph nodes) • Full respiratory and abdominal examination especially if supraclavicular lymph node found • Examination of the thyroid gland • Examination of lymphoreticular system – other lymph node groups, liver, spleen • Breast examination in female patient

NECK LUMPS

Investigations • Fine needle aspiration o Able to definitively diagnose CA and TB. (still the possibility of false positive and false negative results) o Only lymphoma requires excision Bx to diagnose (to be done after FNAC) o Do not do excision Bx first as it can compromise resection later if LN mets is from H&N CA, because LN mets counted as locally advanced dz (still resectable). •

Radio: CT, ultrasound (esp thyroid), MRI (mainly CA as pre-op w/u) o to assess nature of lump, extent, other enlarged nodes that are not clinically palpable, and can be used to visualise primary tumour if present

•

Panendoscopy: to look for synchronous tumors as smoking/alc affect squamous cells o Nose – airway: nasolaryngoscopy, bronchoscopy o Mouth – CE junction: OGD

Management • According to FNAC results • Malignant – work up for primary if present (e.g. squamous cell carcinoma – look for oral cavity, skin, ENT, lung malignancy; adenocarcinoma – look for breast, GI tract malignancy) and treat as appropriate • Infective/Inflammatory – treat underlying condition

121

! SALIVARY GLAND SWELLINGS

Anatomy of the Submandibular Gland

Anatomy of the Parotid Gland

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

SALIVARY GLANDS

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

Anatomy of the Sublingual Gland • • • •

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

122

! APPROACH TO SALIVARY GLAND SWELLINGS History • About the lump: onset, duration, progress, associated symptoms o If pain is present, is it precipitated by food ingestion? (suggestive of sialolithiasis) o Intermittent swelling a/w food (inflammatory) • Symptoms of infection e.g. fever, malaise; if considering mumps, ask about testicular pain and swelling (orchitis), abdominal pain (pancreatitis) • Any noticed asymmetry of the face – incomplete closure of the eye on one side, drooping corner of the mouth, drooling • Does the patient have symptoms of Sjogren: xerostomia (e.g. cannot eat a piece of biscuit or bread without water), xerophthalmia • History of connective tissue disease e.g. rheumatoid arthritis, SLE Physical examination Inspect • Put yourself at the level of the patient’s face and look from front for any asymmetry with an obvious mass on one side o Parotid mass is located between the angle of the jaw and the ear o submandibular mass is located just under the mandible • Look for scars – parotidectomy scar runs anteriorly to the ear, below the earlobe and around posteriorly before looping forward again under the jaw • Look for fistula/sinus • Look at the patient’s face for asymmetry (facial nerve palsy)

Other tests • Examination of the duct openings: o Using a torch and a tongue depressor, examine opposite the second upper molar tooth (opening of the parotid duct), and under the tongue (opening of the submandibular duct) o Look for (1) red inflamed opening, (2) discharge-purulent, (3) visible stone. o For the parotid duct, can palpate the duct along the masseter for stone, and look for discharge inside the mouth while palpating • Tonsillar fossa: enlargement of deep lobe of the parotid (in retropharyngeal space) pushes tonsils and arches aside  see asymmetry of the arches • Palpate the gland openings for stones. • Bimanual palpation of the submandibular gland • Facial nerve examination Suspicious features of malignancy: 1. Facial nerve involvement 2. LN involvement 3. Skin involvement: eg Hyperaemic hot skin over lump 1+2+3 = CA until proven otherwise Causes of swelling of the parotid Parenchymal swelling

“Is there any pain? I am going to feel the lump, if any pain, let me know” Palpate from behind • Palpate the obviously enlarged gland: • Check for warmth, tenderness, consistency, surface, margins • Fixation to underlying structures – for parotid, ask pt to clench the teeth to contract the masseter, then try to move the gland • Fixation to overlying skin • Palpate the contralateral gland for any swelling • Palpate for cervical lymphadenopathy Investigations • FNAC: malign vs benign • CT: confirm salivary gland (vs LN) o esp parotid – multiple swelling likely LN (DDx Warthin)

SALIVARY GLANDS

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

Nonparenchymal swelling

Neoplasia

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

Stones Infection/ Inflammation Autoimmune Infiltration Systemic disease: bilateral Lymph node Facial neuroma Temporal artery aneurysm Skin and soft tissue swellings e.g. sebaceous cyst, lipoma

123

! SIALOLITHIASIS Epidemiology • Stones of the salivary gland that may be impacted within the gland itself or in the duct. • Usually occurs in males more than females, and between the ages of 30 and 60. • 80% occur in the submandibular gland (due to its higher mucus and calcium content with a long duct, and slow flow of the saliva against gravity); 10% occur in the parotid, 7% sublingual. • Most submandibular gland stones occur in the duct, while 50% of parotid stones occur in the gland itself. • 80-95% of submandibular stones are radio-opaque and can be seen on an X-ray of the floor of the mouth, and 60% of parotid stones are radioopaque. Presentation • Complete obstruction o Acute pain & swelling of the gland involved at meal times, rapid onset within minutes of starting to eat, resolves about an hour after the meal. • Partial obstruction o Occasional symptomatic episodes interspersed by asymptomatic periods of days-weeks, chronically enlarged mass in submandibular region • Cx: sialadenitis, and even abscess formation  worsening of symptoms of pain and redness; systemic symptoms such as fever, chills; purulent discharge from duct opening • Stone may be palpable along the duct or at the opening of the duct

Management • General measures: o Good hydration, good oral hygiene, soft diet, avoid sour food (increase salivation) o Massage of the gland, milking the duct, application of moist hot towel o Lifestyle changes: activities that exacerbate the pain eg. Blowing instruments o Analgesia – NSAIDs such as ibuprofen • If sialadenitis present: o Antibiotics– usually to cover Staph and Strept e.g. Augmentin o Refer specialist treatment if symptoms persist for several days, or sialadenitis persists despite antibiotic therapy • Surgical removal o Transoral removal of stones for submandibular duct stones (50% can be removed thus), less for parotid duct stones o If stones cannot be removed via transoral surgery or is intraglandular, partial gland resection can be performed • Other options: Lithotripsy, wire basket removal, sialoendoscopy

Investigations • CT scan (Noncontrast) – can pick up almost all stones when fine cuts are requested • Plain X-rays can pick up radio-opaque stones • Sialogram (rarely done as it is invasive and technically demanding; CT is better. Contraindicated in acute sialadenitis and contrast allergy.)

SALIVARY GLANDS

124

! SALIVARY GLAND TUMOURS

PLEOMORPHIC ADENOMA

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

Epithelial Carcinomas (malignant) Adenoid cystic ca Pleomorphic adeno CA Mucoepidermoid ca Acinic cell ca Adeno CA Squamous cell ca Undifferentiated

Non-epithelial Haemangioma Lymphangioma Neurofibroma Neurilemmoma Lipoma Sarcoma Malignant lymphoma

Epidemiology: • Most common benign tumour • 85% occur in the parotid gland • Equal sex ratio, occurs in younger patients (<50 years old) Histology: Very heterogeneous appearance, containing epithelial cells surrounded by loose stroma with islands of chondromyxoid (mesenchymal components), and interspersed islands of myoepithelial cells. The tumour appears to be encapsulated, but histology shows multiple sites of capsular penetration by tumour cells. Features: • Slow-growing, painless swelling occurring in the lower pole of the parotid • Irregular and lobulated surface, texture of cartilage (slightly harder than Warthin’s) • Does not invade or metastasise • Cx o Malignant transformation (carcinoma ex pleomorphic) if left for 10-15 years (1-6% risk) o If not completely excised, can recur due to frequent capsular penetration (recurrence rate of 2%) Diagnosis by clinical, FNAC, + MRI Treatment – surgical excision (sufficient margin) - Parotid: Superficial parotidectomy for superficial tumour; if tumour is deep or large, total parotidectomy with preservation of the facial nerve (or any way possible as long as margins are sufficient) - Submandibular: Total gland excision together with adjacent connective tissue, sparing lingual and hypoglossal nerves

SALIVARY GLANDS

125

! WARTHIN’S TUMOUR AKA PAPILLARY CYSTADENOMA LYMPHOMATOSUM

TREATMENT OF SALIVARY GLAND CANCERS

Epidemiology: • Only occurs in the parotid gland (10% of parotid tumours) • More common in males than females (4:1) • Occurs in older patients (>50 years) • Related to cigarette smoking

Parotid: • Total parotidectomy with sacrifice of facial nerve if tumour has infiltrated it (may be grafted with great auricular nerve) • Radical neck dissection if neck nodes positive • Postoperative radiotherapy If localised in superficial lobe • Superficial parotidectomy only (if sufficient margin) • + RT (in higher grade tumor / adenoid cystic – may have spread to nerves)

Histology: • Consists of cleft like or cystic spaces lined by two-tiered epithelium, containing mucin, surrounded by a stroma of well-developed lymphoid tissue with germinal centres. Features: • Slowly enlarging, soft to firm cystic fluctuant swelling in parotid tail (inferior) • Invariably benign with no risk of malignant change • 10% bilateral (check contralateral side) Diagnosis by clinical, FNA + MRI Treatment • Can be left alone if absolutely certain that the entire mass is composed of only Warthin’s tumour cells, since there is no malignant potential • Superficial parotidectomy if causing trouble to patient MALIGNANT TUMOURS • Tumor grade • Nerve involvement Most common malignancies • Mucoepidermoid (34%) - most common malignant tumour in the parotid. Younger patients. • Adenoid cystic carcinomas (22%) – most common in the submandibular, sublingual and minor salivary glands. Equal sex ratio, can occur in any salivary gland, in older patients (usually >60 yrs). Tends to spread along nerves. • Malignant pleomorphic adenoma o Usually occurs in pre-existing pleomorphic adenoma, rarely de novo o Worst prognosis of any salivary gland tumour o 30-70% recurrence and metastasis rate SALIVARY GLANDS

Submandibular: • Radical excision of gland with lymphatic clearance of submandibular triangle • Radical neck dissection if neck nodes positive • Postoperative radiotherapy Complications of parotidectomy Immediate (within 24 hrs) • Intraoperative facial nerve transection – lower motor neurone palsy (in surgery to the submandibular gland, damage to the hypoglossal and/or lingual nerves can occur intraoperatively) • Reactionary haemorrhage: early post-op bleeding due to displacement of a clot in a BV / slippage of a ligature Early (1 to 30 days) • 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) • Wound dimple, cosmetic problems • Hyperaesthesia of local skin • Frey’s syndrome (gustatory sweating syndrome / auriculotemporal syndrome) o Increased sweating and redness of facial skin when eating o Auriculotemporal nerve: symp branches (sweat glands of the scalp), parasympathetic branches (parotid gland secretion) o due to reinnervation of divided sympathetic nerves to the facial skin sweat glands by fibres of the secretomotor branch of the auriculotemporal nerve 126

! THYROTOXICOSIS Aetiology and diagnosis • Affects 2% women and 0.2% of men o Graves, Toxic nodular goitre, Toxic solitary nodule, Thyroiditis • Serum free T4 is normally increased o Serum total T4 can be variable due to changes in serum levels of thyroid binding globulin o Occasionally free T3 is increased in T3-toxicosis • Diagnosis of thyrotoxicosis can be confirmed by the measurement of TSH level o A normal TSH excludes the diagnosis (except in rare case of TSH secreting pituitary tumours) Clinical features of thyrotoxicosis • Palpitation, • Myopathy tachycardia, • Tiredness and cardiac lethargy arrhythmias, • Weight loss Heat cardiac failure intolerance • Sweating, tremor • Diarrhoea and • Hyperkinetic vomiting movements • Irritability • Nervousness • Emotional disturbance

• • • • • • •

Behavioral abnormalities Ophthalmic signs Irregular menstruation and amenorrhoea Pretibial myxoedema Thyroid acropachy Vitiligo Alopecia

Graves' disease • Usually occurs in women between 20 and 40 years • Immunological disorder due to release production of thyroid stimulating IgG antibodies • Bind to TSH receptor stimulating thyroid hormone production • Produces a diffuse goitre • Clinically patients have features of thyrotoxicosis often with eye signs: o Exophthalmos and proptosis - usually bilateral o Diplopia due to weakness of external ocular muscles o Chemosis and corneal ulceration Pretibial myxoedema • Occurs in 1-2% patients with Graves' disease • Painless thickening of the skin in nodules or plaques • Usually occurs on shins or dorsum of foot • Strongly associated with ophthalmopathy

THYROID SURGERY

Thyroid acropachy • Occurs in less than 1% patients with thyrotoxicosis • Closely resembles finger clubbing • Almost all patients also have ophthalmopathy or pretibial myxoedema Treatment of thyrotoxicosis • Rapid symptomatic relief can be achieved with beta-blockers Thyroid function can be reduced by o Anti-thyroid drugs o Radioactive iodine o Surgery Anti-thyroid drugs • Inhibit synthesis of thyroxine by reducing incorporation of iodine into tyrosine residues • Most commonly used drugs are carbimazole and propylthiouracil • Used short-term (3-4 months) prior to definitive treatment (radioiodine or surgery) • Used long-term (12-24 months) induce remission in Grave's disease • 40% of patients with Grave's disease respond to carbimazole • Side effects of carbimazole include agranulocytosis, aplastic anaemia, hepatitis o Patients need to be warned to seek medical attention if they develop sore throat etc. • Advantage - no surgery or the use of radioactive materials • Disadvantages o Treatment is prolonged o Failure rate after 2 years treatment is approximately 50% o Impossible to predict which patients will remain in remission o Some goitres enlarge during treatment Radioactive iodine 131 • I is commonest isotope used • 400 MBq renders 50% patients hypothyroid but about 20% remain hyperthyroid • Contraindicated in children, pregnancy and breast feeding • Pregnancy should be avoided for 4 months after treatment • Advantage - no surgery or prolonged drug therapy • Disadvantages o Isotope facilities must be available o 80% hypothyroid at 10 years o Indefinite follow up required 127

! Surgery • Indications for surgery in Grave's disease are: o Relapse after adequate course of anti-thyroid drugs o Large goitre o High T4 levels at diagnosis (>75 pmol/l) • Subtotal thyroidectomy is treatment of choice. • Preserves about 4g (10%) of thyroid tissue • Patients must be euthyroid prior to operation • Advantages - goitre is removed and cure rate is high • Disadvantages o 5% develop recurrent thyrotoxicosis o 20% develop postoperative hypothyroidism o 0.5% develop parathyroid insufficiency Thyroid storm • Uncommon life-threatening exacerbation of thyrotoxicosis • Has a mortality of 50% Precipitating factors • Thyroid surgery • Radioiodine • Withdrawal of antithyroid drugs • Iodinated contrast agents • Acute illness (e.g. stoke, infection, trauma) Clinical features • Severe thyrotoxicosis • Fever • Delirium • Seizure or coma • Jaundice

THYROID SURGERY

Treatment • Propylthiouracil 600mg loading dose • Lugol's iodine at least one hour later • Beta-blocker • Supportive measures • Treatment of precipitating cause

THYROGLOSSAL CYSTS Epidemiology • Thyroglossal cysts are usually found in subhyoid portion of tract • 75% present as midline swellings • Remainder can be found as far lateral as lateral tip of hyoid bone • The cyst elevates on protrusion of the tongue • Male : female ratio is approximately equal • 40% present < 10 years of age • 65% present < 35 years of age • Often present as an infected cyst due lymphoid tissue in the cyst wall Pathology • Cystic expansion of the remnant thyroglossal tract (embryological origin of the thyroid which descends from the foramen caecum on the tongue). Features • Smooth, rounded, cystic lump. • 75% are in the midline while 25% are slightly to the left or right. • Usually asymptomatic but may become infected. Complications • Infected with sinus formation and seropurulent discharge (occurs with incision or rupture of cyst) • Malignant change (carcinoma of the thyroglossal duct) Histology • Cyst with columnar or squamous epithelial lining which may be ciliated. • The cyst may also contain thyroid and lymphoid tissue. If malignancy occurs, it is usually a papillary carcinoma (~90%). Treatment • Sistrunk procedure – resection of the (a) cyst and (b) mid-portion of the hyoid bone in continuity and resection of a (c) core of tissue from the hyoid upwards towards the foramen caecum (remove the entire tract to prevent recurrence!) • If infected aspirate cyst rather than incise o Prevents formation of thyroglossal fistula

128

! THYROID GLAND Anatomy Structure nd th • 2 lateral lobes joined by an isthmus overlying the 2 -4 tracheal rings • Strap muscles are superficial to the thyroid gland - sternothyroid, sternohyoid; platysma also Nerves and vessel • Superior thyroid artery from external carotid st • Inferior thyroid artery from thyrocervical trunk (1 part of subclavian A) • External laryngeal nerve - ss the cricothyroid muscle o Controls pitch of voice o Runs close to superior thyroid A • Recurrent laryngeal nerve - ss all the other intrinsic muscles of the larynx o Runs close to branches of inferior thyroid o Very important to localize/visualize nerve and not damage it Embryology • Thyroglossal tract from foramen caecum of tongue (midline, jx of anterior 2/3 and posterior 1/3) o Descends close to hyoid bone, expansion at caudal end of the tract forms the thyroid gland • Parathyroid glands - 2 superior, 2 inferior, behind the lateral lobes Presentation Goitre (not all anterior masses are goitres) • Solitary nodule • MNG - 1 vs 2 lobes • Diffuse - physiological or Graves’ Thyroid function change • Hypo/Eu/Hyperthyroid • Graves, Hashimoto’s, Toxic adenoma/MNG Malignant changes • Mets to LNs • Bony pain - atypically for follicular ca o Proceed to exclude other CAs that have bone mets

THYROID SURGERY

Aims of assessment: • Exclude cancer • Address issues of thyroid fx • Look for complications mass effect • Cosmesis - is patient bothered by lump?

History • Rate of growth can diffx benign and malignant disease o Anaplastic ca is fast growing • Onset; duration; progression o Overnight appearance is unlikely to be malignant - more likely to be bleeding into a cyst o A/w pain - unlikely to be malignant (hemorrhage into cyst) o A/w URTI - unlikely to be malignant • Thyroid functional status – Hyperthyroid vs hypothyroid vs euthyroid Hyperthyroid Metabolic: LOW, increased appetite Heat intolerance Increased sweating Proximal myopathy (Graves’) Bowel changes - diarrhea, frequent BO CVS - tachycardia, atrial fibrillation Oligomenorrhea/amenorrhea Behavioural changes - easily irritable, emotional liability, insomnia Fine tremor Loss of outer third of eyebrows

•

•

•

Hypothyroid Decreased appetite weight gain Cold intolerance Dry skin Muscle fatigue Constipation Bradycardia Menorrhagia Slow though, speech & actions, depression, dementia, lethargy Carpal tunnel syndrome symptoms

Mass effects o Swallowing difficulty due to weight of gland as trachea rises o Airway  Dyspnea on lying down  Stridor due to airway narrowing, especially on coughing o Recent onset hoarseness of voice (appearing after the goitre)  Due to RLN invasion (benign growths do not invade) Previous thyroid disease or investigations o If yes - on what meds, any ADRs o Any radioactive iodine o Ask for FNAC (poked) or US (jelly) Etiology o Family history  Dyshormonogenesis  Papillary ca  20% medullary carcinomas a/w MEN 2 Syndrome or FAP o Autoimmune disease o Radiation exposure  Due to RT or nuclear fallouts  33% will be malignant - affects threshold for total thyroidectomy  Increased incidence of thyroid malignancy - usually papillary  Most occult (<1.5 cm diameter) and multifocal  Usually good prognosis 129

! Physical Examination Objectives: 1. Confirm abnormality in the thyroid gland 2. Determine if there is a diffuse enlargement (smooth vs nodular - MNG) or solitary nodule 3. Examine structures around the thyroid 4. Assess thyroid status of patient IPPE

- Ask for how to address them -- hoarseness - Shake their hands -- warm/sweaty - Exposure: neck & clavicles Inspect - Lump: Size, shape, site (midline/anterior triangle) - Skin and color changes, scars - Swallow and stick out tongue tests - Any distended neck veins/raised JVP Palpate *Always ask for tenderness first Thyroid Front: Back: - Lump: inferior border - Thyroid ask patient to protrude tongue/ - Trachea: deviation swallow again with your hands on gland from midline - features of lump: size, tenderness, consistency, mobility Thyroid status - diffuse enlargement -- smooth or nodular Hands: - Cervical LNs • Fine tremor • Acropachy (pseudoclubbing) and onycholysis • Palmar erythema and sweating • Pulse - tachycardia or Afib in hyper, bradycardia in hypo Eyes: • Hypo - loss of hair on outer-third of eyebrows • Lid retraction/exophthalmos/chemosis/proptosis • Assess for lid lag & ophthalmoplegia (H - diplopia @ up & out) Neuromuscular: Prox. myopathy, reflexes, pretibial non-pitting edema Percuss/ - Percuss sternum only if you can’t see the inferior border auscultate - Auscultate if there are signs of thyrotoxicosis/large pulsatile goitre Wish list Limb exam - proximal myopathy, reflexes, pretibial myxoedema Cardiovascular exam - for signs of heart failure Assess the patient’s biochemical thyroid status ?Pemberton’s sign Present Function - clinically euthyroid, hyperthyroid or hypothyroid Any evidence of thyroid eye disease or pretibial myxedema (Graves) Any goitre (nodular or diffuse), any retrosternal extension THYROID SURGERY

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

Clinical features suspicious of malignancy: 1. Male gender (thyroid nodules less common in male but more likely to be malignant) 2. Age <15yrs or >60yrs (majority of nodules occurs rd th in 3 to 6 decades – likely benign) 3. History of head and neck radiation or thyroiditis 4. Family history of thyroid cancer (or MEN2, Gardner’s syndrome, FAP) 5. Rapidly enlarging nodule 6. Hard, single nodule and/or nodules fixed to surrounding structures 7. Hoarseness (i.e. recurrent laryngeal n. invasion) 8. Cervical lymphadenopathy 9. Other symptoms of invasion e.g. haemoptysis, stridor, dysphagia

Investigation Biochemical assessment • Thyroid functional status - Free T4 and TSH • Thyroid Antibodies - anti-thyroglobulin and anti-microsomal • If suspicion of MEN2 Syndrome will need 24 hr urinary catecholamine estimations to exclude phaeochromocytoma prior to surgery • CEA and Calcitonin for Medullary Thyroid CA (+ve fam Hx) CXR; CT Thorax • Chest radiography and thoracic inlet views if obstructive symptoms Isotope scanning 131 123 99 • I , I or Tch scanning provides functional assessment of thyroid • Nodules classified as cold, warm or hot o Unable to differentiate benign and malignant nodules o Most solitary thyroid nodules are cold o Most cancers arise in cold nodules o Risk of cancer in a cold nodule is 10-15% o Risk of tumour in a hot nodule is negligible • Scintigraphy of minimal use in evaluation of solitary thyroid nodules • Useful in recurrent thyroid swellings and retrosternal goitres Ultrasound • Solitary vs dominant nodule; solid vs cystic lesions (consistency) o Most sonographically solid lesions are benign o Cancer can occur in the wall of a cystic lesion • Features that might suggest malignancy are: o Hypoechogenicity, Microcalcification, Irregular margins o Increased nodular flow (vascularity) on Doppler o Regional lymphadenopathy • Measurement of nodule, detection of subclinical nodule

130

! ENT examination of vocal cords Fine needle aspiration cytology • Should be first line investigation of the solitary thyroid nodule • Accuracy improved if performed under ultrasound guidance • With experienced cytologist diagnostic accuracy can be >95% • Possible cytopathological diagnoses are: o Benign (thyroiditis, dominant nodule of MNG) o Malignant (papillary, medullary, anaplastic, mets) o Suspicious (follicular, Hurthle cell change in follicular lesion) o Inadequate  repeat FNAC • Can distinguish benign & malignant tumours except follicular neoplasms • Diagnosis of follicular carcinoma depends on capsular visualization • If follicular neoplasm on FNA lesion will require surgical excision • False negative rate less than 5% in most institutions • Definitive FNA cytology allows: o Non-operative treatment with benign disease o Appropriate surgical treatment of thyroid cancers at initial op o Surgery can be avoided in anaplastic tumours and lymphomas o Reduces total number of thyroid lobectomies o Increases yield of thyroid cancers Indications for surgery after FNA cytology • All proven malignant nodules • All cytologically diagnosed follicular neoplasms • All lesions exhibiting an atypical but non-diagnostic cellular pattern on cytology • Cystic nodules which recur after aspiration • When on clinical grounds the index of suspicion of malignancy is high even if the cytology report suggests it is benign

Benign thyroid tumours • Most are follicular adenomas • Papillary adenomas are rare • All papillary tumours should be considered malignant Follicular adenoma • Of all follicular lesions - 80% benign and 20% malignant • They are smooth and discrete lesions with glandular or acinar pattern • They are encapsulated usually 2-4 cm in diameter • Adenomas cannot be differentiated from carcinoma on FNA cytology • Requires histological assessment of capsular invasion • Various histological types are described: o Embryonal - rudimentary acini. No Colloid o Foetal o Simple o Colloid - Well formed acini. Much colloid o Macrofollicular, Microfollicular Toxic adenoma • Account for 5% of cases of thyrotoxicosis • Female : Male ratio is 9:1 • Presentation - 54% with a nodule and 37% with thyrotoxicosis • 95% of toxic adenomas are benign • Thyrotoxicosis not usually associated with eye signs • Hot nodule on scintigraphy • Treatment is by thyroid lobectomy • Require post-operative thyroxine until suppressed gland returns to normal Malignant thyroid tumours • Differentiated thyroid cancer accounts for 80% of thyroid neoplasms • Female : Male ratio is 4:1 • Usually presents as solitary thyroid nodule in young / middle age adult • Nodule more likely to be malignant in man or child • Papillary and follicular tumours are biologically very different Comparison of papillary and follicular tumours Papillary tumours Follicular tumours Multifocal Solitary Unencapsulated Encapsulated Lymphatic spread Haematogenous spread Metastasize to regional nodes Metastasize to lung, bone and brain

THYROID SURGERY

131

! Differentiated thyroid carcinoma Proportion Age

Medullary carcinoma

Anaplastic carcinoma

Lymphoma

10%

7%

3%

5%

40-50 years

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

60-70 years

>50 years

Papillary carcinoma

Follicular carcinoma

75% 25-40 years

F:M ratio

3:1

3:1

1:1

3:2

2:1

Risk factors

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

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

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

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

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

Patho features

- Characteristic Orphan Annie nuclei, - Follicular structures similar nuclear pseudoinclusions to normal thyroid - Papillary architecture with - Diagnosis of cancer made psammoma bodies on evidence of capsular or - Tall cell variant (nuclear features of vascular invasion (vs papillary ca in follicular lesion) behaves follicular adenoma) like papillary ca, worse prognosis - Hurthle cell variant – poor

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

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

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

Clinical features

-

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

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

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

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

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

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

Chemotherapy and/or radiotherapy depending on type of lymphoma

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

No good adjuvant therapy

Median survival <6mths

Dependent on histo, stage, treatment, etc.

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

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

- Very good prognosis - Poor prognostic factors (AMES): Age>40, presence of metastases, extra-thyroid invasion, size>4cm Treatment

TSH suppression – give L-thyroxine, suppress TSH to <0.005U/L Follow-up - Check TSH levels - Thyroglobulin as a tumour marker of recurrence - Radioactive iodine scan to detect recurrence, followed by ablation 5yr survival

95% in low-risk pts, 88% in intermediate-risk pts, 50% in high-risk pts Slightly worse for follicular ca

THYROID SURGERY

Follow-up - Thyroxine replacement (not for TSH suppression but to maintain euthyroid state) - Serum calcitonin and CEA six mths after surgery (if normal, considered cured – 5% 5yr recurrence) - High calcitonin – screen for residual or metastatic disease, treat surgically, with RT or chemo as appropriate 60-70%

132

! Risk stratification • Patient factors: Age – >45 years old is high risk; Gender – male high risk • Tumour factors: o Size – nodule >4cm has higher risk o Histology – tall cell variant of papillary ca and Hurthle cell variant of follicular ca are considered unfavourable o Extrathyroidal extension into surrounding structures – worse o Lymph node or distant metastases – worse Scoring systems • AMES – Age, Metastases, Extent, Size • AGES – Age, Grade (Histological), Extent, Size) – rarely used as histological grading is not commonly performed • MACIS – Metastasis, Age, Completeness of resection, Invasion, Size Patients can be divided into three groups: • Low risk – low risk patient and low risk disease (i.e. no high risk features) • Intermediate risk – low risk patient with high risk disease, or high risk patient with low risk disease • High risk – high risk patient and high risk disease •

•

Risk helps to guide treatment – low risk patients can undergo hemithyroidectomy without ablative radioiodine therapy post-op, while high risk patients undergo total thyroidectomy with post-op ablative RAI treatment; treatment in intermediate risk patients is tailored to the disease, but usually is similar to that in high risk patients 5 year survival is also prognosticated by the risk: low risk patients have a survival of 95-98%, intermediate risk patients 88%, and high risk patients 50%

Management Surgery • Therapeutic o Hemi vs total • Diagnostic o For lymphoma - incisional biopsy needed to type the lymphoma (incidentally, Rx for lymphoma is RT only) o For follicular/Hürthle cell lesions  To diffx benign and malignant, capsular invasion has to be seen  Lobectomy is done

THYROID SURGERY

Total thyroidectomy vs thyroid lobectomy for differentiated tumours Arguments for total thyroidectomy (Treatment, monitoring, recurrence, low mortality) • Multifocal disease occurs in opposite lobe in 50% cases • Total thyroidectomy reduces risk of local recurrence • Ablation with radioiodine is facilitated • Serum thyroglobulin can be used as a tumour marker for progression or recurrence • In experienced hands, morbidity of total thyroidectomy is low Arguments for thyroid lobectomy • Many patients do not require radioiodine • Progression to undifferentiated carcinoma is rare • Significance of micro-foci in contralateral lobe is uncertain • No evidence that more extensive procedure is associated with better prognosis • Higher incidence of hypoparathyroidism after total thyroidectomy Complications of thyroidectomy • Haemorrhage • Wound Complications o Sepsis o Hypertrophic scarring • Respiratory Obstruction o Laryngeal mucosal oedema/hematoma o Clot deep to strap muscles o Bilateral incomplete recurrent laryngeal nerve palsies o Tracheomalacia • Nerve Damage o Recurrent laryngeal nerve palsy o Incomplete - cord moves to midline o Complete - cord in cadaveric position o Preoperative cord inspection is essential o 3% population have asymptomatic recurrent laryngeal nerve palsy • Hypocalcaemia • Thyroid Crisis o Fulminating • Pneumothorax hyperthyroidism • Air Embolism o Hyperpyrexia • Recurrent hyperthyroidism o Arrhythmia • Hypothyroidism o Cardiac Failure 133

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

THYROID SURGERY

MULTIPLE ENDOCRINE NEOPLASIA A group of inherited diseases resulting in proliferative lesions (hyperplasia, adenomas, carcinomas) of multiple endocrine organs. Features: • Tumours occur at younger age than sporadic cancers • Multiple endocrine organs involved, either synchronously or metachronously • Multifocal tumours in each organ involved • Tumour usually preceded by asymptomatic stage of endocrine hyperplasia • More aggressive and higher chance of recurrence compared to sporadic type of tumours in the same organs MEN 1 • Autosomal dominant inheritance • Gene involved is the tumour suppressor gene MEN1 located on chromosome 11q13 where mutations cause loss of function of the gene • Three P’s: o Parathyroid (95%) – hyperparathyroidism from hyperplasia of parathyroid glands o Pancreas (>40%) – aggressive metastatic tumours (e.g. gastrinoma, insulinoma), leading cause of death in MEN 1 patients o Pituitary (>30%) – most commonly prolactin-secreting macroadenoma; some have growth hormone-secreting tumours MEN 2 • Autosomal dominant inheritance • Gene involved is RET protooncogene at 10q11.2 where activating mutations occur Two distinct groups of disorders: • MEN 2a (Sipple syndrome) o Medullary carcinoma of the thyroid (almost all) o Phaeochromocytoma (50%, of which less than 10% malignant) o Parathyroid hyperplasia and hyperparathyroidism (30%) • MEN 2b (William syndrome) o Thyroid and adrenal involvement like MEN 2a, but no hyperparathyroidism o Neurocutaneous manifestations: ganglioneuromas on oral mucosa, lips eyelids • Other features: Marfanoid habitus, SCFE, delayed puberty 134

! SURGERY IN THYROID DISEASE Indications for surgery: • Cannot be treated medically - failed or unsuitable • 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) • Child-bearing (not a very strong indication since medical therapy can still be given, but not RAI) Types of surgery available: • Hemithyroidectomy – removal of one lobe of the gland, including the isthmus and the pyramidal lobe; usually for suspicious thyroid nodules • Total thyroidectomy – entire gland removed completely; usually done in MNG • Subtotal thyroidectomy o Conventional subtotal thyroidectomy – leave a thumb-sized amount (about 4-6g) of remaining thyroid tissue on both sides o Harley-Dunhill subtotal thyroidectomy – leave a thumb-sized amount on one side with removal of the rest of the gland Total versus subtotal thyroidectomy (for hyperfunctioning thyroid disease) • Result of total thyroidectomy is always hypothyroidism, thus the patient will require life-long thyroid replacement and follow-up  problems with compliance, cost, inconvenience • Results of subtotal thyroidectomy (at 5 years): o 60-70% euthyroid (do not require medication but still have to be followed up closely) o 16-20% hypothyroid (usually becomes evident within 1 year of surgery) o 8-10% hyperthyroid (percentage increases proportionately with time  failure of surgical therapy)  Difficulty in managing post-operatively and in the long term as patients need close monitoring (better off to just replace everyone after TT?), but weigh this against the benefits of not requiring any medication (for which there is a good chance)

THYROID SURGERY

Complications of thyroid surgery: (Mostly H’s, one I and one T) Immediate (<24hrs) • Haemorrhage with haematoma formation o Haematoma forms in the paratracheal region, mostly below the strap muscles → compression of airway if not released (DIE) o Cut the subcuticular stitches and also the stitches holding the strap muscles opposed to let the blood drain out • Hoarseness or airway compromise from recurrent laryngeal nerve injury o Risk of nerve injury is <1% o Unilateral nerve injury for hemithyroidectomy, bilateral nerve injury for total or subtotal thyroidectomy o Bilateral nerve palsy = compromised airway = tracheostomy  • Hyperthyroidism o Resection of gland can release large amounts of stored thyroid hormone into bloodstream o May result in thyroid storm (see Management of thyroid storm) • Tracheomalacia o Floppiness of trachea resulting from chronic compression o Requires intubation to secure airway Intermediate (1 day to 1 mth) • Infection • Hypoparathyroidism leading to hypocalcaemia o Risk of permanent hypoparathyroidism is 1-4% (only in total or subtotal thyroidectomies)  10-20% of patients may have temporary  Ca2+  Important to check the serum calcium levels – POD 1,3,5 o 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 BP cuff over arm) o Dangerous as it can cause laryngeal spasm & airway compromise o Check serum calcium together with albumin to get corrected calcium! → Measured serum calcium + 0.02 (40 – Albumin) o Replacement: 5mmol/6h if symptoms mild, 10ml of 10% calcium gluconate over 30 minutes if severe o Hypocalcaemia may also occur due to “hungry bone syndrome” after thyroidectomy in long-standing thyrotoxicosis Late (more than 30 days) • Hypothyroidism • Hyperthyroidism (failed treatment) • Permanent hypoparathyroidism • Hypertrophic scarring or keloid formation – ask patient have prev keloids 135

! ANATOMY OF LOWER LIMB ARTERIES •

•

•

External iliac artery continues as the femoral artery after crossing the inguinal ligament (surface landmark: the mid-inguinal point i.e. midway between the pubic symphysis and the anterior superior iliac spine) The femoral artery then divides into the superficial femoral and the profunda femoris (or deep femoral) arteries about 4cm below the inguinal ligament o The profunda femoris supplies compartments of the thigh via 2 main branches, the medial & lateral circumflex femoral arteries o 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 o 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) o 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

VASCULAR SURGERY

136

! ARTERIAL ASSESSMENT Clinical Assessment Claudication • Calf or thigh pain precipitated by exercise o Usually occurs after predictable distance o Described as 'cramp' or 'tightness' o Relieved by rest • Progression of symptoms is important - worsening or improvement o Impact on social function should be identified • Need to differentiate form spinal stenosis (shop window vs park bench o Also causes exercise induced leg pain o Usually associated with neurological symptoms and relieved by spinal flexion • Peripheral pulses can be present in patients with intermittent claudication Critical limb ischaemia • Characterized by rest pain • Occurs when foot is elevated (e.g. in bed) • Improved with foot dependency • May be associated with ulceration or gangrene • Foot pulses are invariably absent Non-invasive testing of arterial patency Arterial investigations are used to: • Confirm the clinical impression of arterial disease • Assess disease severity • Preoperative planning of surgical or radiological interventions Duplex ultrasound • Combined pulsed doppler and real time B mode ultrasound • Allows imaging of vessels and any stenotic lesion • Flow and pressure wave form can be also be assessed • Doppler wave forms from normal and diseases arteries In normal individuals a 'triphasic' wave is obtained • Rapid antegrade flow during systole • Transient reverse flow in early diastole • Slow antegrade flow in late diastole

VASCULAR SURGERY

Hand-held Doppler • Reflection of an ultrasound wave off a stationary object does not change its frequency • Reflection off a moving object results in a change of frequency • The change in frequency is proportional to velocity or blood flow • Hand held 8 MHz doppler probe is used to assess arterial system • Measurements can be made at rest and after exercise • Ankle-brachial pressure index (ratio of best foot systolic to brachial systolic pressure) o Normal >1.0 o Claudication 0.4 -0.7 o Critical Ischaemia 0.1-0.4 • In normal individuals pressures do not fall flowing exercise o In claudicants the ABPI falls and recovery is delayed o In diabetic lower limb pressures are falsely elevated due to calcification in the vessel wall Toe pressures • Provides accurate assessment of distal circulation • Not influenced by calcification in pedal vessels • Medical calcification particularly seen in diabetics • Normal toe pressures are 90-100 mmHg • Toe pressure less than 30 mmHg suggests critical limb ischaemia Invasive vascular assessment Angiography • Usually performed using digital subtraction techniques • Catheter inserted using Seldinger technique • Femoral artery is commonest site of venous access • Generally safe procedure performed under local anaesthetic Potential complications include: • Contrast-related • Technique-related o Anaphylactic reaction o Haematoma o Toxic reactions o Arterial spasm o Deterioration in renal o Sub-intimal dissection function o False aneurysm o Arteriovenous fistula o Embolization o Infection CT angiography • Required intravenous contrast and ionizing radiation • Spiral CT and reconstruction can provide detailed images • Particularly useful for the assessment of aneurysmal disease 137

! ACUTE LIMB ISCHEMIA •

•

Defined as a sudden decrease in limb perfusion that causes a potential threat to limb viability (manifested by ischemic rest pain, ischemic ulcers, and/or gangrene) in patients who present within 2/52 of the acute event (if >2/52, it is considered chronic ischaemia).Effects of sudden arterial occlusion depends on state of collateral supply Collateral supply in leg usually inadequate unless pre-existing occlusive disease

Aetiology of acute limb ischaemia • Embolism (60-80%) o Arising from:  Left atrium in patients in atrial fibrillation  Mural thrombus after myocardial infarct  Prosthetic and diseases heart valves  Aneurysm or atheromatous stenosis  Tumour, foreign body, paradoxical o Lodging commonly at  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 • Acute Thrombosis o Thrombosis of a previously stenotic but patent artery (atherosclerotic vessel) o Resulting ischaemia is usually less severe than in an embolic occlusion, because collaterals have had time to form • Other • Trauma • Dissecting aneurysm • Raynaud's Syndrome Clinical features of limb ischaemia • Fixed staining is a late sign • Objective sensory loss requires urgent treatment • Need to differentiate embolism from thrombosis • Important clinical features include o Rapidity of onset of symptoms o Features of pre-existing chronic arterial disease o Potential source of embolus o State of pedal pulses in contralateral leg VASCULAR SURGERY

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 • Progression: Light touch Vibration  Proprioception  (late) Deep pain  Pressure sense Pallor; Perishingly cold • Assess skin colour, temperature (Perishingly cold), 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: Pale  Cyanosis  Mottling  Fixed cyanosis and mottling • 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 • The discolouration 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 Pulselessness • If able to feel one good pulse (PT or DP), quite unlikely that the limb is ischaemic • If unable to feel, assess with a handheld Doppler the arterial and venous flow in the limb – there can still be flow without a palpable pulse • Also feel the pulses on the other limbs – gives a clue as to whether the cause is embolic or thrombotic (see below) Paralysis • Initial: heavy limb, Late irreversible ischemia: muscle turgidity • Total paralysis occurs late and usually indicates that the limb is non-viable • Intrinsic foot muscles > Leg muscles (toe mvmts produced by leg muscles  detect late) • Can assess viability of muscle by making a cut – viable muscle will be shiny & twitches in response to flicking, while dead muscle will be dull & will not twitch • Dangerous to save dead muscle as reperfusion can cause circulation of toxic metabolites in the muscle 138

! Severity of ischemia

Management of acute ischaemia

Three categories: viable, threatened and non-viable • Viable: No immediate threat of tissue loss • Threatened: Salvageable if revascularized promptly • Non-viable: Limb cannot be salvaged and has to be amputated, no emergency to operate. Patient may require revascularisation to allow lower amputation or help the amputation to heal

Initial • • • •

Severity depends on: • capability of existing collaterals to carry blood around occlusion • location of obs relative to no. of axial arteries (pop=1, fem=2, tib=3) • extent of obs: larger  lose more collaterals • duration Pain Capillary refill Motor deficit Sensory deficit Arterial Doppler Venous Doppler Treatment

Viable Mild Intact None None Audible Audible Urgent work-up

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

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

Investigations Pre-operative investigations • FBC, U/E/Cr, PT/PTT, GXM • CXR and ECG if patient is older than 40 yrs old • If suspecting an AMI with mural thrombus, do cardiac enzymes • Biochemical abnormalities (muscle necrosis): K, CK, lactic acidosis Angiogram • Can be done in pts with viable limb; in pts with threatened limb there is no time for angiogram  may do on-table angiography • High clinical probability of embolism does not need angiography Useful in 1. confirming an occlusion, 2. cause – thrombotic or embolic 3. pinpointing the level of occlusion and the anatomy VASCULAR SURGERY

Doppler to analyze viability and level of obstruction Heparinize (5000mg bolus then 1000mg/hr) & analgesia Improve perfusion (foot dependency, avoid heel pressure, max O2 sat) Treat associated cardiac disease (CHF, AF)

Identifiable source Claudication hx Physical findings Angiography

Embolic Present – AF, recent AMI Negative Contralat pulses present White limb (no blood) Minimal atherosclerosis, sharp cut-off, few collaterals

Thrombotic Less common Positive Contralat pulses diminished Dusky limb (collaterals) Diffuse atherosclerosis, irregular cut-off, collaterals

Emergency embolectomy • Under LA, but monitor for AMI, AF, arrhythmia & hyperK after reperfusion • Transverse arteriotomy performed over common femoral artery • Fogarty balloon catheter is inserted into artery until distal to the clot, then balloon is inflated to trawl clot out of the artery • If embolectomy fails - angiogram + consider bypass graft/thrombolysis • Convert to full warfarin (INR 2.5) before stopping heparin • Complications: reperfusion injury (edema, compartment syndrome – calf pain and inability to dorsiflex ankle – do a 3 compartment fasciotomy) • Embolectomy has a 20% mortality, almost full success rate Intra-arterial thrombolysis • Arteriogram and catheter (multiple side hole) advanced into thrombus o Urokinase 5000u/hr + heparin 250u/hr for 6 hours o Alternative thrombolytic agents include streptokinase or tissue plasminogen activator (tPA) • Repeat arteriogram at 6 -12 hours • Advance catheter and continue thrombolysis for 48 hours or until clot lysis • Indicated for embolism in diseased artery – easier than trawling • Contraindications o Absolute: CVA (2m), active bleeding (10d), intracranial trauma (3m) o Relative: CPR (10d), major trauma (10d), uncontrolled HTN • Angioplasty of chronic arterial stenosis may be necessary • Complications: o Mortality of 1-2%; Bleeding (CVA, retroperitoneal) • Thrombolysis has a 10% mortality, only 35% successful 139

! CHRONIC LIMB ISCHEMIA Most common cause is atherosclerosis with gradually developing diffuse stenosis of the peripheral arteries resulting in diminished blood supply to the lower limb (imbalance between supply and demand). Multiple collaterals form to bypass the obstructed vessels as a compensatory mechanism. Intermittent claudication Epidemiology of claudication • 5% of males older than 50 years have intermittent claudication • 5% of claudicants progress to critical ischaemia each year • 75% of patients remain stable and show clinical improvement • Peripheral vascular disease is an independent risk factor for cardiovascular disease • At 5 years of follow-up o 10% claudicants and 50% of those with critical ischaemia have had an amputation. o 20% claudicants and 50% have died usually from ischaemic heart disease • Calf claudication: Usually affects the superficial femoral near to the adductor hiatus, or the popliteal artery • Foot claudication: tibial & peroneal arterial disease, but rarely do patients with claudication due to atherosclerosis get foot pain alone (more common in Buerger’s) • Thigh claudication: common femoral artery or aortoiliac disease • Leriche’s syndrome  occlusion of the aortoiliacs, and composed of a classical tetrad of buttock claudication, impotence in men, absent femoral pulses (and distal pulses), and occasionally presence of aortoiliac bruits. Assessment of claudication • History to assess disability associated with symptoms (claudication distance) o Neurogenic claudication usually must flex spine, variable distance, pulse present, parasthesia present • Exclude rest pain or tissue loss • Doppler studies to measure pressures and assess wave forms

VASCULAR SURGERY

Critical limb ischaemia • Rest pain requiring regular opioid analgesia (e.g. codeine) lasting >2 weeks • +/- Tissue loss (Gangrene or ulcers over the toes or feet) • Objective indication of poor vascular supply to the lower limbs (a) Ankle brachial pressure index <0.5 (b) Toe pressure index < 0.3 (c) Toe pressure <30 mmHg, Ankle pressure <55mmHg Rest pain • Severe pain in the distal portion of the lower limb (usually toes, foot but may involve more proximal areas if disease is severe) occurring at rest (calf pain without toe pain is not) • Pain is aggravated or precipitated by lifting the limb, relieved by dependency of the limb – many patients sleep with the leg hanging over the side of the bed to relieve the pain • So severe as to disturb sleep at night –  blood supply as pt is not in dependent position and decrease BP during sleep • Not easily controllable with analgesia – requires opioids to control pain Ischaemic ulcers (most are neuroarteriopathic ulcers) • Usually arise from minor traumatic wounds with poor healing • Often painful • Most often occur on the tips of the toes, bunion area, over the metatarsal heads (ball of the foot), lateral malleolus (as opposed to venous ulcers that occur over the medial malleolus) • Usually deep, dry, punctate (unlike venous ulcers that tend to be superficial, moist, diffuse) • May become infected  cellulitis / abscess, and spread to involve the underlying bone and joints  osteomyelitis, septic arthritis Gangrene • Cyanotic, anaesthetic tissue associated with or progressing to necrosis • Occurs when arterial blood supply falls below that which is necessary to meet minimal metabolic requirements • Dry – hard, dry texture. Often has a clear demarcation between viable and necrotic tissue. Occurs in patients with atherosclerotic disease. Safe and can be allowed to autoamputate after demarcation with precautions against infection. • Wet = infected dry gangrene. Moist, swollen, frequently blistered. Often occurs in diabetics with decreased sensation and unrecognised trauma, requiring an emergency surgical debridement or amputation. 140

! History Claudication = muscular pain, reproducible, increased on walking/dec w rest • Which part of the lower limb does the pain occur in – depends on level of obstruction • Nature of the pain, Radiation, Severity • Aggravating factors – exertion • Relieving factors – rest (just standing is sufficient) • Associated symptoms e.g. impotence in Leriche’s • Duration: When did pain first start (>2/52?) • Progress since first noticed until currently (worsening pain, ing areas of lower limb affected, pain on less exertion, rest pain) • Current claudication distance • How has symptoms affected lifestyle e.g. impaired mobility Any rest pain • Site, nature, severity • Aggravating factors – raising the limb • Relieving factors – putting limb in a dependent position • Able to relieve with normal analgesics? Or require opioid analgesia? • How long has rest pain lasted for requiring opioid analgesia (if > 2 wks, considered a feature of critical limb ischaemia)

Drug history • Aspirin and statin intake – commonly prescribed for vasculopathy • Any allergies to contrast (for angiography) • Ergots Social history • Premorbid function and current function • Social support and home condition (need to climb stairs?) Physical examination Look • •

• •

Any ulcer or gangrene in the lower limb? • Ask about onset of ulcer/gangrene • Progress (stable, or increasing in size, getting worse) • If ulcer, any preceding trauma? Ill-fitting shoes? Altered sensation in the foot? Does patient take care to protect foot? Pain? Redness/swelling/warmth in surrounding skin? Purulent/foul-smelling discharge from the ulcer? • If gangrene, is it wet or dry? Redness/swelling/warmth in surrounding skin? Any feeling in the toe involved? Any sensory changes in the other normal toes, foot, limb? • Any systemic signs of infection – fever, chills, rigors, malaise Risk factors (“Arteriopathy”) • Diabetes mellitus – take a full diabetic history including other complications • Hyperlipidaemia / Heart disease (IHD) / Stroke (CVA) • Smoking (very strong RF; 3-6X risk of claudication, higher than the risk for IHD) • Family history VASCULAR SURGERY

•

•

Colour of the lower limb o White (pallor); pink (normal); blue/dusky (cyanosed); mottled Trophic changes o Loss of hair o Dry, shiny skin o Nail changes o Wasting Presence of any diabetic dermopathy Presence of ulcer o Look carefully at the entire lower limb, including the heels (ask pt to flex at the knee) & between the toes o Site of the ulcer o Venous ulcers form at the medial malleolus o Arterial ulcers are more distal, usually between the toes, and at pressure points such as the lateral malleolus; o Neuropathic ulcers form at areas such as the ball of the foot & heel o Size, shape, Edges (punched out – arterial; sloping – venous), Base o Depth of the ulcer (can see underlying tendon? Down to bone?) o Appearance of the base – Necrotic? Granulating (beefy-red)? Sloughy? o Any discharge – pus, blood? o Surrounding skin o Erythema (cellulitis) – there may be an underlying abscess (confirm on palpation) o Blistering, purplish colour (possibility of necrotising fasciitis) Presence of gangrene o Wet (infected) or dry (not infected) o Extent of gangrene (level of demarcation) (If the patient has diabetes, may see deformities – Charcot’s joint) 141

! Feel •

•

•

•

Move Warmth of the skin o Use the dorsum of the fingers of both hands to simultaneously run up the patient’s feet to the shins and thighs bilaterally o Compare the temperature on both sides (note if one side is cooler) o If one limb feels cool, feel for the level where the skin becomes warm Capillary refill o Press hard on a toe for a few seconds, then release o Normal capillary refill should be 2 seconds or less o If a toe is blue, check for blanchability (fixed staining = dead toe) Palpating the ulcer if present o Any surrounding tenderness (infection) o Bogginess of surrounding tissue (may have abscess formation) o See if any discharge from the ulcer when palpating Pulses – compare both legs. Check regularity of pulses. Grading of pulses: 2+ normal; 1+ diminished (but may be normal for popliteal); negative if not felt o Feel the distal pulses and work your way proximally o Posterior tibial pulse: one-third of the way down a line joining the medial malleolus to the heel o Dorsalis pedis pulse: just lateral to the ext hallucis longus tendon/ one third of the way down a line joining the midpoint of the two malleoli to the cleft between the first and second toes o Popliteal pulse: Ask patient to bend the knee ~60-90 degrees, then palpate deeply in the popliteal fossa with the fingers of one hand pressing the fingers of the other. Thumbs on the tibial tuberosity. [If the pulse is very well felt, suspect a popliteal aneurysm] o Femoral pulse: Midpoint of the line joining the pubic symphysis to the anterior superior iliac spine (mid-inguinal point), just below the inguinal ligament o Abdominal aorta

VASCULAR SURGERY

Buerger’s test • Lift both legs together to compare • Holding the heel of the foot, with the pt’s LL straightened, slowly lift the entire LL, looking at the colour of the toes • Stop when the toes become pale (white) • Estimate the angle the lower limb makes with the horizontal – this is the Buerger’s angle • Normal lower limb can be raised to 90 degrees without turning white; if the Buerger’s angle is less than 30-40 degrees, this indicates critical ischaemia • There may be venous guttering of the lower limb at this angle as well • Hold for 1 min (to induce ischemic environment) • If the patient is lying near the side of the bed, tell the patient that you’re going to put his leg over the edge of the bed before gently abducting the hip and then letting the leg drop over the edge of the bed • Look at the leg for reactive hyperaemia (the leg turns purple-red) – due to ischemic env causing increased acidity and triggering autonomic response Complete the exam • Examine the rest of the pulses • Offer to auscultate over the femoral and popliteal arteries for bruits • Examine the abdomen for any abdominal aortic aneurysm • Measure the ankle-brachial pressure index (ABPI)

142

! Investigations Ankle-brachial pressure index •

•

•

•

How the ankle-brachial pressure index is done o Lie patient supine (so that ankle pulse will not increase sec to dependency) o Brachial pressure is measured with a blood pressure cuff around the arm and a Doppler probe at the brachial artery – cuff is inflated until the arterial signal is obliterated, then slowly deflated until the signal just starts being detected, at which the pressure is recorded o Ankle pressures are measured in a similar manner, with the cuff around the calf and the Doppler at the dorsalis pedis and posterior tibial arteries – one reading for each artery o The ankle pressure to be used for each leg is the higher of the two taken o This ankle pressure is then divided by the brachial pressure (the higher of the two brachial pressures for both upper limbs) to get the ankle-brachial pressure index Interpreting the values o Normal ABPI is > 0.9 (can be more than 1.0 as ankle pressures tend to be higher than brachial; o ABPI between 0.5 - 0.9 – occlusion, often associated with claudication o ABPI <0.5: Critical ischaemia Rest pain o if >1.25, suggests non-compressible calcified vessel esp seen in DM patients  do Toe pressure index instead (every value minus 0.2) Accuracy of the index o ABPI below 0.9 has 95% sensitivity and 100% specificity for detecting angiogram-positive peripheral arterial disease and is associated with >50% stenosis in one or more major vessels Exercise treadmill testing o Measure ABPI before and after patient exercises on a treadmill o If the ABPI falls by >0.2  claudication

VASCULAR SURGERY

Arterial Duplex ultrasound • Non-invasive test, good alternative to angiogram • Duplex (means 2 modalities) = 2D ultrasound plus Doppler ultrasound (measures flow and waveforms) • Normal arterial flow waveform should be triphasic (rapid antegrade flow reaching a peak during systole, transient reversal of flow during early diastole, and slow antegrade flow during late diastole.); biphasic & monophasic waves are abnormal • Distal to stenosis: rate of rise is delayed, the amplitude decreased, and the transient flow reversal in early diastole is lost • A twofold increase in peak systolic velocity compared with the velocity in an adjacent segment of the artery usually signifies a stenosis of 50% or more • Can define anatomy of occlusions and also look for relatively good arteries distally for “landing zone” of bypass graft Angiogram (arteriogram) • Invasive and associated with risks of  bleeding from arterial puncture,  dissection  damage to artery with worsening ischaemia • Usually only done if planning intervention e.g. angioplasty, stenting • Preparing for angiogram: o Take informed consent from patient o Ask about contrast allergy, asthma, renal disease, metformin o Investigations: FBC (platelets impt), PT/PTT, UECr • Angiogram with digital subtraction – the images of the underlying bone are removed so as to better visualise the arteries (if the bones are visible, then it is a normal angiogram, without digital subtraction) Basic laboratory investigation • FBC, UECr, PT/PTT, septic workup: bld c/s, wound c/s 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

143

! TREATMENT OF CHRONIC LIMB ISCHEMIA Conservative (for claudicants) Mainstay for all cases of claudicants, esp. foot and calf claudicants • RF control o Assessment and treatment to optimise control of CVS risk factors– cardiologist o Antiplatelets [e.g. aspirin] and statins (target lipid levels are much lower) o Smoking cessation • Exercise training to stimulate collateral formation  symptoms get better o Exercise at least half to one hour every day o Walk until pain comes, rest 2-3 minutes, walk again o Keep a walk diary recording daily claudication distance in paces o Supervised exercise 3X/wk helps. Advice to exercise alone does not. • Patient education: o Teach patient to go to ED if symptoms of critical ischaemia arises o Podiatrist to teach foot care • Medications o Praxilene and Cilostazol shown to increase claud dist - Ex. o Use of Vasteral (methoxyphylline) is controversial • Monitor regularly with measurement of ABPI Indications for intervention in peripheral vascular disease • Disabling claudication or Critical limb ischaemia • Arteriography is essentially a preoperative investigation • Three options are: o Stenting o Percutaneous angioplasty o Bypass surgery Intervention (endovascular or surgical) • At least 6 months of conservative treatment first; mainly for aortoiliac disease • Monitor claudication distance & ABPI – usually intervene if claudication distance <50m (poor QOL, almost critical limb ischemia) • Confirm disease outline with CT angiogram or angiogram • If parameters improve but then plateau, discuss with patient about whether he can accept the level of symptoms, and the risks of intervention • Usually do angioplasty rather than bypass as it is less invasive, though may not be as effective in treating the symptom VASCULAR SURGERY

Percutaneous transluminal angioplasty • Angioplasty of the aorto-iliac segment has a 90% 5 year patency • Angioplasty of the infra-inguinal vessels has a 70% 5 year patency • Angioplasty only effective for focal stenotic lesions and better for large vessels. Problem with angioplasty is that it is not long-lasting – restenosis can occur • New method: subintimal angioplasty – if lumen is so occluded that guide wire cannot pass through, the guidewire is threaded into the subintimal space to create a dissection around the occluded segment, and this space is then angioplastied to create a channel parallel to the actual lumen for blood to flow through • Complications occur in less than 2% of patients o Acute thrombosis; Distal embolization o Wound haematoma; Arterial wall rupture Bypass surgery Only used when lesions cannot be treated by angioplasty Types of bypass graft include: • Biological grafts o Autograft: Long saphenous vein or Internal mammary artery o Allografts: Dacron coated umbilical vein • Synthetic grafts o Dacron - woven or knitted +/- albumin coated o Woven grafts - smaller pores. No preclotting required o Velour - Polyfluorotetraethylene (PTFE) Choice of graft material • Determined by long term patency rates • Autologous vein is best graft material but not always available • Interposition of vein between PTFE graft and artery at distal anastomosis can improve long term patency Reasons for graft failure • Less than 30 days - technical failure • 30 days to 1 years - neointimal hyperplasia at distal anastomosis • More than 1 years - progression of distal disease Amputation • Indications: Dead (necrotic), dangerous (gangrene, infection), damn nuisance (non-functional, bad smell, pain) • Level of amputation depends on vascularity of the limb; indications (where the infection is etc) • Try to preserve function – must revascularize to ensure good healing 144

! DIABETIC FOOT • • • •

Foot problems are common in type-1 and type-2 diabetics 20-40% of diabetics have peripheral neuropathy Many also have features of peripheral vascular disease o 15% of diabetics develop foot ulceration Diabetes is the leading cause of non-traumatic lower limb amputation

Pathophysiology • The diabetic foot results from a combination of neuropathy and ischaemia • Neuropathy has sensory, motor and autonomic components o Sensory loss results in loss of protective sensation and unnoticed foot injuries o Loss of motor control to the small muscles of the feet results in a claw foot deformity • Autonomic neuropathy leads to vasomotor denervation and arteriovenous shunting o This compromises the ability to direct blood flow to the capillary beds • Ischaemia can affect both the large and small vessels o Large vessels disease results in atheroma of the femoral, popliteal and tibial vessels o Small vessel disease affects the microcirculation • Other contributing factors include: o Poor vision o Cerebrovascular disease o Limited joint mobility o Peripheral oedema • In patients with foot ulceration healing is impaired o Impaired fibroblast function o Deficiency in growth factors o Abnormalities of the extracellular matrix

VASCULAR SURGERY

Management • Prevention of complications is preferable to the need for active management • Patients should be monitored and self-care encouraged • They should be educated about o Washing o Care of cores and calluses o Toenail cutting o Suitable footwear • In those with ulceration assessment should be made of: o Infection o Vascular insufficiency Management of infection • Wound swabs often show both gram-negative, gram-positive and anaerobic bacteria • Osteomyelitis if usually due to Staph. aureus • Plain radiography or MRI may demonstrate the extent of the infection • The threshold for antibiotic use should be low • The antibiotics used should be based on culture sensitivities • Surgery may be required if progression despite antibiotic treatment Management of vascular insufficiency • All patients with diabetic ulceration should undergo non-invasive vascular assessment • The ABPI should be calculated o This may be falsely elevated due to arterial calcification o Normal values may still be recorded in diabetics with significant major vascular disease • Revascularization should be considered if arterial insufficiency is present • Diabetics have a predisposition for disease in medium-sized vessels especially at the popliteal trifurcation o The distal pedal vessels are often spared • Femoro-distal bypass grafting may be required

145

! ABDOMINAL AORTIC ANEURYSM • • • •

AAA = localised abnormal dilatation of a blood vessel wall or the heart; diameter >3cm More prevalent in elderly men, Male : female ratio is 4:1 Risk factors – hypertension, peripheral vascular disease, family history Accounts for 2% male deaths above the age of 55 years o Mortality of emergency operation is greater than 50% o Mortality of elective surgery is less than 5%

Natural history • AAA diameter expands exponentially at approximately 10% / year • Risk of rupture increases as aneurysm expands (5 yr risk) o 5.0 – 5.9 cm = 25% o 6.0 – 6.9 cm = 35% o More than 7 cm = 75% • Overall only 15% aneurysms ever rupture; 85% die from unrelated cause • 95% infrarenal, but may extend to common iliac arteries • Usually fusiform in shape (vs saccular), containing mural thrombus Screening • AAA are suitable for screening as elective operation of asymptomatic aneurysms can reduce mortality associated with rupture • Probably males over 65 years especially hypertensives • Single US at 65 years reduces death from ruptured AAA by 70% in screened population Clinical features (75% are asymptomatic) Possible symptoms: Rupture presents with • Epigastric pain • Sudden onset abdominal pain • Back pain • Hypovolaemic • Malaise and shock weight loss (with inflammatory • Pulsatile aneurysms) epigastric mass

Rare presentations: • Trash feet • Aorto-caval fistula • Primary aortointestinal fistula

Indication for operation • Rupture • Symptomatic aneurysm • Rapid expansion 10% a year • Asymptomatic > 5.5 cm – exact lower limit controversial

VASCULAR SURGERY

Pre-operative investigation • Need to determine o Extent of aneurysm o Fitness for operation (Pre-op) • Ultrasound, conventional CTAP and more recently spiral CT o Determines – aneurysm size, relation to renal arteries, involvement of iliac vessels • Most significant post op morbidity and mortality related to cardiac disease o If pre-operative symptoms of cardiac disease need cardiological opinion • May need thallium scan or cardiac catheterization • Cardiac revascularization required in up to 10% patients Endovascular aneurysm repair • Morbidity of conventional open aneurysm surgery related to: o Exposure of infra-renal aorta o Cross clamping of aorta • Endovascular repair may be associated with: o Reduced physiological stress o Reduced morbidity & mortality Technique Complications • Three main types of graft • Graft migration o Aorto-aortic • Endovascular leak o Bifurcated aorto-iliac • Graft kinking o Aorto-uniiliac graft with femoro• Graft occlusion femoral crossover and contralateral iliac occlusion Popliteal artery aneurysms • Defined as a popliteal artery diameter greater than 2 cm • Account for 80% of all peripheral aneurysms o 50% are bilateral o 50% are associated with an abdominal aortic aneurysm o 50% are asymptomatic • Symptomatic aneurysms present with features of: o Compression of adjacent structures (veins or nerves) o Rupture o Limb ischaemia due to emboli or acute thrombosis • Treatment is by proximal and distal ligation • Revascularization of the leg with a femoropopliteal bypass • With a symptomatic popliteal aneurysm 20% patients will undergo an amputation 146

! Management Ruptured AAA • Very high mortality – nearly 100% if frank rupture (will not get to ED in time) • Most of the patients who reach the ED (about 50% reach ED alive) have a leaking AAA with a tamponade effect by the retroperitoneal structures • High suspicion in unstable hypotensive patient complaining of severe sharp pain radiating to the back; may feel a pulsatile mass in the abdomen •

• •

•

Stabilise patient – resuscitation with fluid and blood products o Do not intubate as neuromuscular blocking agents will reduce tamponade effect, worsening haemorrhage Call for vascular surgeon Bring to OT for open repair – quickly isolate the aorta and clamp it proximally o can be clamped for about 30 minutes without significant visceral ischaemia o AAA is incised, the surrounding haematoma and mural thrombus within the AAA are cleared out o Synthetic graft (Dacron – polytetrafluoroethylene) is placed within the aorta and the vessel wall closed up over the graft i.e. the graft forms the lumen of the aorta  Mortality rate of repair operation in this setting is about 50% Most common complication postoperatively is renal insufficiency – can be reduced by giving frusemide or mannitol pre-operatively before anaesthesia induction

Non-ruptured AAA • Time available for investigation of size of AAA and related anatomy • Indications for surgery: o Aneurysm > 5.5 cm in largest diameter [risk of surgery outweighs that of AAA] o Increase in diameter of more than 1cm per year o Symptomatic aneurysm – back pain, tenderness on palpation, distal embolism, ruptured/leaking aneurysm • Patient’s fitness for surgery needs to be properly assessed because it is a major operation – need to optimise CVS function • Operation is the same except that it is done under elective setting • Mortality is <5% in the elective setting, serious morbidity ~10% VASCULAR SURGERY

Endovascular stenting • An alternative to open repair which is less invasive, can be done under GA • Mortality ~1%, but serious morbidity rate is similar to open repair: 10% • Involves deployment of a non-porous stent within the aneurysm to form the lumen of the aorta – requires adequate “neck” proximally and good landing site distally • Not as good results as open surgery; need to do an angiogram every 6 months to check position of stent (ensure not migrated) Complications of surgery Intraoperative/early • Acute myocardial infarction – most patients already have atherosclerotic disease of coronary vessels and are at risk of AMI (responsible for 5060% of mortality) • Stroke (due to hypotension or embolism) • Renal insufficiency • Colon ischaemia – occurs in 2-6% • Trash foot – embolism of thrombus from the aneurysm • Infection of graft • Spinal cord ischaemia (quite uncommon) • Haemorrhage Late • • •

Aortoenteric fistula – frank PR bleeding, torrential Late infection of prosthetic graft material Sexual dysfunction

Post-operative investigations: • FBC: Hb and plt (blood loss and consumptive coagulopathy) • UECr: renal insufficiency or contrast nephropathy • KUB: check position of stent

147

! VARICOSE VEINS •

Varicose veins affect o 20-25% of adult females o 10-15% of adult males

Assessment of varicose veins • History o Poor correlation exists between symptoms and signs o Cough, tap and thrill tests are inaccurate o Important to identify those with history of DVT or lower limb fracture o If history of DVT need preoperative investigation with duplex scanning • Examination o Identify distribution of varicose veins - long saphenous (LSV) vs short saphenous (SSV) o Confirm with tourniquet testing & hand held-doppler probe (5 MHz) o Recurrent varicose veins need duplex ultrasound Indications for duplex scanning • Suspected short saphenous incompetence • Recurrent varicose veins • Complicated varicose veins (e.g. ulceration, lipodermatosclerosis) • History of deep venous thrombosis Indications for varicose vein surgery • Most surgery is cosmetic or for minor symptoms • Absolute indications for surgery : o Lipodermatosclerosis leading to venous ulceration o Recurrent superficial thrombophlebitis o Bleeding from ruptured varix

VASCULAR SURGERY

Surgical Options LSV surgery • Saphenofemoral junction (SFJ) found 2 cm below and lateral to pubic tubercle • Flush ligation of the LSV: Individually divide and ligate tributaries of LSV o Superficial circumflex iliac vein o Superficial inferior epigastric vein o Superficial and deep external pudendal vein • Check that femoral vein clear of direct branches for 1 cm above and below SFJ • Stripping of LSV reduces risk of recurrence o Only strip to upper calf. o Stripping to ankle is associated with increased risk of saphenous neuralgia (association with saphenous nerve) • Post-operative care: o Elevate foot of bed for 12 hours o Class 2 varix stocking should be worn for at least 2 weeks SSV surgery • Saphenopopliteal junction (SPJ) has very variable position • Preoperative localisation with duplex ultrasound • Identify and preserve the sural nerve • Stripping associated with risk of sural nerve damage • Subfascial ligation inadequate Perforator surgery • Significance of perforator disease is unclear • Perforator disease may be improved by superficial vein surgery • Perforator surgery (e.g. Cockett's and Todd's procedure) associated with high morbidity • Subfascial endoscopic perforator surgery (SEPS) recently described • Not indicated for uncomplicated primary varicose veins • May have a role in addition to saphenous surgery in those with venous ulceration

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! Endovascular laser treatment • Laser energy deliver via narrow laser fibre to obliterate the vein • Causes heat injury to vessel wall • Usually performed under local anaesthesia • Clinical and symptomatic improvement seen in 95% patients • Patient satisfaction high and early return to work is possible • Complications include paraesthesia and skin burns • Recanalization seen in less than 10% patients Radiofrequency ablation • Uses high frequency alternating current delivered via a bipolar catheter • Placed intraluminally under duplex guidance • Local heating results in venous spasm and a collagen seal • Performed under general anaesthesia • Long saphenous vein accessed at the knee using Seldinger technique • 90% vein occlusion achieved in first week after treatment • Associated with less pain than open surgery o Improved quality of life and earlier return to work • Complications include paraesthesia and skin burns • Recurrence rates are similar to open surgery

Recurrent varicose veins • 15 - 25 % of varicose vein surgery is for recurrence • Outcome of recurrent varicose veins surgery is less successful • Can be avoided with adequate primary surgery Reasons for recurrence • Inaccurate clinical assessment o Confusion as to whether varicosities are in LSV or SSV distribution o Can be avoided with use of hand held doppler • Inadequate primary surgery o 10% cases SFJ not correctly identified o 20% cases tributaries mistaken for LSV  Failure to strip LSV • Injudicious use of sclerotherapy o 70% of those with SF incompetence treated with sclerotherapy alone will develop recurrence • Neovascularization o With recurrent varicose vein need to image with duplex or varicography

Sclerotherapy • Only suitable for below knee varicose veins • Need to exclude SFJ or SPJ incompetence • Main use is for persistent or recurrent varicose veins after adequate saphenous surgery • Sclerosants o 5% Ethanolamine oleate o 0.5% Sodium tetradecyl sulphate • Recently foam ( mixture of air / sclerosant) has been shown to be more effective • Different to sclerosants used for haemorrhoids • Needle placed in vein when full with patient standing • Empty vein prior to injection • Apply immediate compression and maintain for 4-6 weeks • Do not exceed maximum volume • Injection about 5 sites possible Complications of sclerotherapy • Extravasation causing pigmentation or ulceration • Deep venous thrombosis VASCULAR SURGERY

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! VENOUS ULCERATION • • •

•

Leg ulceration is common Most are due to venous hypertension o 40% of venous ulcers are due to superficial venous disease Rare causes include: o Rheumatoid arthritis o Malignancy o Syphilis Surgical correction of superficial venous disease often results in healing

Assessment • Clinical assessment should o Identify previous DVT o Assess arterial disease o Identify varicose veins and underlying valvular incompetencies • Assessment requires o Clinical examination o Hand held doppler assessment o Possible duplex scanning Venous hypertension • Affects 1-2% of population • Due to chronic venous insufficiency and distal vein hypertension • Usually due to post thrombotic syndrome • Can be due to primary valvular incompetence

Causes of chronic venous insufficiency Gravitational reflux • Venous insufficiency classified as primary or secondary • Primary insufficiency has no obvious cause of valvular dysfunction • Insufficiency results in early refilling of venous pool after muscle contraction o Causes progressive and sustained increase in calf vein pressure = Ambulatory venous hypertension o Results in capillary dilatation and leakage of plasma proteins Compartmental pressures • Incompetent perforating veins exposes superficial veins to high pressures during muscle contraction = hydraulic ram effect o Produces localised venous hypertension and filtration oedema o Continues until tissue pressures rise to restore equilibrium Leucocyte trapping • Accumulation of leucocytes occurs in dependent limbs of those with venous hypertension • Trapping of WC associated with activation o Hypoxic endothelial cells stimulate adherence of WC o Activate WC release O2 radicals, collagenases and elastases which injure surrounding tissue Evaluation of venous insufficiency • History of chronic venous insufficiency • Exclude other causes of leg ulceration Signs of venous hypertension • Perimalleolar oedema • Pigmentation • Lipodermatosclerosis

• •

Eczema Ulceration

Doppler ultrasonography • Used to assess presence of venous reflux • LSV, SSV and perforators should be assessed • Patency of femoral and popliteal veins should be checked • Flow augmented by compression of calf, deep inspiration or Valsalva manoeuvre Duplex ultrasonography • Allow anatomical and functional assessment • Flow rate and anatomy can be measured VASCULAR SURGERY

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! Treatment of venous ulceration Compression • Elastic compression stockings o Provide graduated compression o Produce local alteration of microvascular haemodynamics o Minimal effect on deep vein dynamics o Do not cure hypertension - Protect skin from the effects o Occlusive arterial disease is a relative contraindication • Gel paste gauze boots • CircAid • External pneumatic compression • Drug treatment • Systemic agents - minimally effective o Zinc o Fibrinolytic agents o Pentoxifylline • Topical agents - not recommended o Antibiotics o Free radical scavengers o Hydrocolloid dressings

Marjolin's ulcer • Marjolin's ulceration is a squamous cell carcinoma arising at sites of chronic inflammation • Recognized underlying causes include: o Chronic venous ulceration o Burns o Osteomyelitis sinuses • Usually a long-period between injury and malignant transformation o This period may be 10-25 years • 40% occur on lower limb • Malignant change is usually painless • Nodal involvement is uncommon • Diagnosis is confirmed by biopsy of the edge of the ulcer • Management involves adequate excision and skin-grafting or amputation

Surgery • Aims of venous ulcer surgery are: o Cure venous hypertension o Heal the ulcer • Combination of superficial venous surgery and compression may be beneficial • Surgical options include: o Skin grafting o Free flap grafting o Superficial vein stripping o Perforating vein interruption o Valve plasty o Thrombolysis, dilation, stenting

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! VENOUS THROMBOSIS • • •

Venous thrombosis is significant cause of morbidity and mortality Pulmonary embolus accounts for 10 - 25 % of hospital deaths At least 20% patients with a DVT develop a post-thrombotic limb o 80% of calf DVTs lyse spontaneously without treatment o 20% of calf DVTs propagate to the thigh and increased risk of PE

Pathophysiology • Thrombus formation and propagation depends on Virchow's triad o Venous stasis (immobility) o Hypercoagulable state (drugs or malignancy) o Endothelial damage (external compression) Risk of venous thrombosis during surgery • Low risk o Minor surgery (<30 min) + no risk factors other than age o Major surgery (> 30 min) , age <40 yrs + no other risk factors • Moderate risk o Major general, urological, gynaecological, cardiothoracic, vascular or neurological surgery + age >40 yrs o Major medical illness or malignancy, trauma or burn o Minor surgery, trauma or illness with prev DVT, PE or thrombophilia • High risk o Fracture or major orthopaedic surgery of pelvis, hip or lower limb o Major pelvic or abdominal surgery for cancer o Major surgery, trauma or illness with prev DVT, PE or thrombophilia o Major lower limb amputation Risk factors for venous thrombosis Patient Factors - Age - Puerperium - Obesity - High-dose oestrogen therapy - Varicose veins - Previous DVT or PE - Immobility - Thrombophilia: - Pregnancy - Antithrombin III deficiency

VASCULAR SURGERY

- Protein C deficiency - Protein S deficiency - Antiphospholipid antibody - Lupus anticoagulant

Potential for DVT can be investigated by thrombophilia screen • FBC and blood film • >Clotting studies - APPT / PT / TT • Reptilase test • Protein C & S and Antithrombin III assay • Lupus anticoagulant Prevention of thromboembolism Prevention of stasis • Early mobilization • Graduate compression stockings (reduce incidence of DVT by 50%) o The stocking profile should be  18 mmHg at the ankle  14 mmHg at the mid-calf  8 mmHg at the upper thigh • Intermittent pneumatic compression (e.g. Flowtron boots) Pharmacologically reduce hypercoagulable state Heparin • Unfractionated heparin (MW = 15 kDa) 5000u 3x daily • Low Molecular Weight Heparin (MW = 5 kDa) Enoxaparin 20 or 40 mg daily • Potentiate Antithrombin III by inactivating activated clotting factors o Unfractionated heparin anti-Xa activity = anti IIa activity o Low Molecular Weight Heparin = anti-Xa activity 4x > anti IIa • Does not have significant effect on APPT • Reduce DVTs by 70% and PEs by 50% • Side effects of unfractionated Heparin o Osteoporosis o Idiosyncratic thrombocytopenia New drugs • New drugs useful in DVT prophylaxis include o Thrombin inhibitors (e.g. hirudin) o Specific factor Xa inhibitors (e.g. fondaparinux)  Factor Xa inhibitors may be more effective than LMWH Current recommendations for DVT prophylaxis • Assess for clinical risk factors and overall risk of thromboembolism • Should receive prophylaxis according to degree of risk o Prophylaxis should continue until discharge • Low risk patients should be mobilized early • Moderate risk patients should receive specific prophylaxis 152

! Clinical features of DVT • Many are asymptomatic • Clinical features depends on site of venous occlusion • Classical clinical features of a calf DVT are: o Calf pain and tenderness o Pyrexia o Persistent tachycardia • Homan's sign = pain on passive dorsiflexion of the ankle • Occlusion of the ilio-femoral vein can result in venous gangrene (phlegmasia cerulea dolens) Investigation of suspected DVT D-dimers • A fibrin degradation product that can be assayed in plasma • Levels raised in the presence of recent thrombus • A negative result almost excludes the presence of venous thrombosis • Decision to proceed to venography or ultrasound often based on D-dimer result Venography • Gold standard, Will identify both calf vein and proximal thrombus • Painful and time consuming investigation. o 2-3% of patients develop contrast reaction Ultrasound • Technique has three components - all operator dependent. o Venous compressibility o Detection of Doppler flow o Visualization of clot • Able to exclude femoro-popliteal or major calf DVT in symptomatic patients

Treatment of venous thrombosis • Prevention of pulmonary embolus • Restore venous and valvular function to prevent the post thrombotic limb Anticoagulation • Initially with unfractionated or low molecular weight heparin • Followed by oral anticoagulation Surgical thrombectomy • Considered in massive ilio-femoral thrombosis associated with phlegmasia cerulea dolens o Good early results with 62% complete and 38% partial clearance of ilio-femoral segment o Unfortunately re-occlusion common o Thrombolysis of unproven benefit Pulmonary embolism Investigations of possible pulmonary embolus • Arterial blood gases - hypoxia, hypocarbia but may be normal • ECG - Signs of right heart strain - classically S1Q3T3 • CXR - Show oligaemia + central pulmonary markings and excludes other dx • Ventilation / Perfusion scanning - May confirm or refute diagnosis • Pulmonary angiography and echocardiography • Spiral CT might replace pulmonary angiography • Lower limb investigations for DVT as above Management of pulmonary embolus • If high degree of suspicion but stable: o Anti-coagulate with heparin or LMWH o Oxygen, analgesia, colloid to increase CVP o Warfarinise for at least 3 months • If haemodynamically unstable: o Consider pulmonary thrombolysis via pulmonary artery catheter o If thrombolysis contraindicated consider pulmonary embolectomy Inferior vena caval filters • Inserted percutaneously usually via femoral vein • Indicated if: o Recurrent pulmonary emboli despite adequate anti-coagulation o Extensive proximal venous thrombosis and anticoagulation is contraindicated

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Andre Surgery notes (ed 3, 2013) w Washington+ChinYee

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