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Question

What are the symptoms and signs of a PE?

Answer 1

Highly variable, may include: ``` Symptoms: SOB Pleuritic chest pain (shoulder pain if diaphragm is irritated by lower lobe PE) Cough +/- haemoptysis (if infarction) Shock (if severe) – dizziness, syncope ``` ``` Signs: Tachypnoeic Tachycardic Elevated JVP Parasternal heave Loud pulmonic component of 2nd heart sound (P2) Crackles (pleural effusion) Shock – hypotensive (SBP <90), altered LOC, pale/mottled skin, central cyanosis ```

Answer 2

Approach is based on assessment of pre-test probability via Modified Well’s Score: Modified Well’s Criteria Clinical signs/symptoms of DVT (+3) PE is #1 diagnosis OR equally likely (+3) Heart rate >100 (+1.5) Immobilization at least 3 days OR surgery in past 4 weeks (+1.5) Previous, objectively diagnosed PE or DVT (+1.5) Haemoptysis (+1) Malignancy with treatment within 6 months or palliative (+1) Low risk (<2) Consider D-dimer Negative – PE excluded Positive – consider CTPA (CT pulmonary angiography) PERC (PE rule-out criteria) All negative – PE excluded as <2% chance ``` PERC (+1 per criteria) Age >50 HR >100 SaO2 on RA <95% Unilateral leg swelling Haemoptysis Surgery or trauma <4wks Prior PE/DVT Hormone use ``` Moderate risk (2-6) High sensitivity D-dimer Negative – PE excluded Positive – CTPA ``` High risk (>6) CTPA (D-dimer not recommended) ``` If patient hemodynamically unstable despite resuscitation: Consider bedside lower extremity compression U/S to diagnose DVT to allow initiation of therapy Refer to PERT (PE response team) who will consider risk/benefit of initating therapy Findings: CTPA Embolism appear dark against contrast in pulmonary vessels RV enlargement V/Q scan 2nd line choice if eGF <30 i.e. renal failure or allergy to contrast Inhale helium and inject contrast to compare V and Q ``` Other Ix: Pathology FBC, ESR, CRP, Troponin Elevated BNP ABG Respiratory alkalosis (hyperventilation) If massive with severe shock can be metabolic acidosis CXR Usually normal, may exclude ddx Non-specific atelectasis and effusion ECG Sinus Tachycardia (most common finding) S1Q3T3 pattern (non-specific ST segment and T wave changes) T wave inversions in anterior and inferior leads RBBB Right axis deviation ```

Answer 3

Supportive: A – Intubation if in CV collapse/arrest B – High Flow O2 C – IV fluids, vasopressors (adrenaline/dobutamine), analgesia Specific: Severe/life-threatening: Thrombolysis Indicated if sustained hemodynamically instable patients Absolute CI is bleeding, recent stroke Alteplase 10mg IV bolus followed by 90mg IV infusion over 2h If bleeds – FFP and anti-fibrinolytics Embolectomy Catheter insertion via femoral/brachial) to reach clot Anticoagulation Initial: Enoxaparin (LMWH) 1.5mg/kg SC OD OR 1mg/kg BD Ongoing: (3-6m or more) Rivaroxaban (NOAC) – start immediately after diagnosis OR Warfarin – continuing LMWH for 5 days until in therapeutic range (INR 2-3) Venous filter Placed in inferior vena cava for 3-6months in patient with absolute CI to anticoagulation

Answer 4

Definition: Obstruction of the pulmonary artery or one of its branches by material that originated elsewhere in the body. ``` Origin: 80% Thrombus from lower limb Proximal DVT embolises to PE in 50% Distal DVT embolises to PE in 5% Other: tumour tissue, fat, air, septic (endocarditis of tricuspid or pulmonary valves), ``` Classification: Massive: acute PE with obstructive shock or SBP <90mmHg Sub-massive: acute PE without systemic hypotension but with either RV dysfunction or myocardial necrosis Low risk: none of the above features Pathogenesis As per DVT, Virchow’s triad of hypercoagulable state + stasis of blood + endothelial injury Thus, similar RF Pathophysiology: PE are typically multiple, with lower lobes being involved in majority of cases Effects are proportional to the rapidity and degree of obstruction Physiological responses: Due to obstruction, there is Increased pulmonary vascular resistance (PVR) which impedes RV outflow. This causes RV dilation as it attempts to maintain adequate pulmonary flow. As it fails to compensate hypotension ensues. Obstruction results in increased alveolar dead space, i.e. ventilation with no perfusion. This results in the V/Q mismatch that triggers pulmonary vasoconstriction to optimise gas exchange. This results in hypoxaemia, stimulating respiratory drive resulting in hypocapnia and respiratory alkalosis. In 10% of cases, small thrombi lodge distally in segmental vessels resulting in pulmonary infarction, that presents as pleuritic chest pain and haemoptysis.

Answer 5

Relevant factors on: Modified Well’s Criteria Immobilization at least 3 days OR surgery in past 4 weeks (+1.5) Previous, objectively diagnosed PE or DVT (+1.5) Malignancy with treatment within 6 months or palliative (+1) ``` PERC (+1 per criteria) Age >50 Surgery or trauma <4wks Prior PE/DVT Hormone use ```

Answer 6

Absolute CI: Hypovolaemia (as it may precipitate hypovolaemic shock) Raised ICP (early morning vomiting and headache, papilledema, altered LOC, dilated unresponsive pupil) Infection at site Allergy to anaesthetic Coagulopathy - INR >1.4 - Platelet count <100 - LMWH within the last 12hrs (prophylactic dose) or 24hrs (therapeutic dose) - Clopidogrel (within the last 7 days) Patient refusal ``` Relative CI: INR 1.2-1.4 Sepsis Abnormal anatomy of spine Severe aortic or mitral stenosis ```

Answer 7

**Catheter Related** 1. Epidural abscess -- Back pain, infection, possible neurological deficit, if so, then MRI. Mx: Incision + drainage + fluclox 2. Infection -- sore, exudate, redness, swelling, fevers. Mx: Fluclox 3. Epidural haematoma -- back pain, tenderness, possible motor block, of so, then MRI. Can lead to compression + ischaemia of spinal cord, leading to paralysis. Prevention: Know coag status of pts, check site prior to administraion of anticoagulants. Management: Notify anaesthetists, CT/MRI + surgical evacuation. 4. Inadequate block/no block -- can feel ice cold or pain sensation. Mx: Retry 5. Dural puncture -- postural occipito-frontal headache, neck stiffness, photophobia, tinnitus, hearing disturbance. Mx: Supine position, hydration, analgesia 6. Total spinal -- ascending motor loss with LOC **Drug Effects** 1. Local anaesthesia toxicity Initial: Light headedness, drowsiness, tinnitus, circumoral tingling, metallic taste. Undetected: convulsions, hypoventilation, arrhythmias, hypotension, tachycardia, arrest Prevention: Aspirate catheter to check for blood, give block slowly. Mx: Stop infusion, MET call, IV fluids, O2, airways and ventilation support, bag + mask PRN, anticonvulsants. 2. High block (Unintentional anaesthetic into CSF) -- Respiratory depression, weakness, bradycardia, hypotension, arm neuropathy. Mx: Stop infusion, MET call, IV fluids, O2, airways and ventilation support, bag + mask PRN, anticonvulsants, adrenaline. 3. Sympathetic block: Hypotension, bradycardia, vasodilation. Prevention: position in L lateral, administer slowly. Mx: Stop infusion, IV fluid bolus, elevate legs, adrenaline. 4. Opioid effects: sedation, respiratory depression, vasodilation. 5. Sub-arachnoid opioid: N/V, severe itch, drowsiness -> coma, bradypnoea -> apnoea. Mx: Stop infusion, MET call, IV naloxone, IV fluids, O2, airways and ventilation support, ICU. 6. Urinary retention anaphylaxis: Confusion, pain, full bladder. Mx: Catheterisation

Answer 8

Consider causes of hypotension: • Hypovolaemia- haemorrhage, insufficient fluid replacement/maintenance • Cardiogenic: MI, arrhythmia • Obstructive: saddle PE, tension pneumothorax, cardiac tamponade • Distributive- sepsis, side effect of epidural, anaphylaxis ABCDE assessment; • Trial of fluid challenge 500mL N Saline • Anaesthetics consult- consider turning down the epidural or stopping Once stable: • Review patients fluid balance and medications • Treat any underlying cause as well as fluid balance • Elevate legs • Administer oxygen • If refractory- get ICU involved to administer vasopressors Jessica Redmond 29 NB: A transient drop in blood pressure is to be expected as the sympathetic blockage produces vasodilation. This is usually compensated for by an increase in cardiac output. If the sympathetic blockage should reach T4 level, where the sympathetic chain to the heart leaves the spinal column the compensatory mechanism is blocked preventing increase in heart rate. This can result in profound hypotension, bradycardia, thready pulse or anxiety. A common problem as Epidurals tend to unmask the patients volume status.

Answer 9

``` Normal Saline: 0.9% NaCl 1L H2O Na 154 mmol Cl 154 mmol ``` Daily requirements: 2.5L of H2O (30ml/kg/day) Na 1-2mmol/kg K 0.5-1mmol/kg Daily requirements for 70kg man: 2.1L (approx.2.5L) of H2O 70-140mmol/kg/day Na 70mmol K

Answer 10

The average daily intake of sodium is 1-2mmol/kg/day. The average daily intake of potassium is 0.5- 1mmol/kg/day.

Answer 11

The average daily intake of potassium is 0.5-1mmol/kg/day. Potassium is prescribed as additive to other fluids. It can be given with 5% dextrose and 0.9% saline 30 mmol KCl additive to IL N Saline or 10mmol in 100 mL

Answer 12

The adult water volume requirement is 25-30mL/kg/day | That is a maintenance of of 1500-2500mL/day

Answer 13

Note: maintenance glucose = 50-100mg/day 1% =10mg/mL

Answer 14

``` Hartmann’s: 1L H20 Na 131mmol/L K 5mmol/L Cl 111mmol/L Ca2+ 2mmol/L Lactate (HCO3-) 29mmol/L (as lactate gets first pass metabolised into bicarbonate) ```

Answer 15

``` 4% and 1/5th NS: 1L H20 Dextrose 40g Na 30mmol/L Cl 30mmol/L ``` 5% dextrose: 1L H20 Dextrose 50g

Answer 16

Immunological complications: • Febrile non-haemolytic transfusion reaction • Acute Haemolytic transfusion reaction • Urticarial reactions • Anaphylactic transfusion reactions • Transfusion related Acute Lung Injury • Post transfusion purpura • Transfusion associated graft vs host disease • Delayed haemolytic transfusion reaction Febrile Non-haemolytic transfusion reaction Caused by release of cytokines by WBCs in a product that has not been leukoreduced. Presentation: within 1-6 hours Characterised by fever, usually with chills in the absence of systemic symptoms. Diagnosis of exclusion Mx is symptomatic e.g. paracetamol for fever, cease transfusion, antihistamines Prevention: leucodepletion of blood products Acute Haemolytic Reactions Life threatening reaction within first 24 hours caused by intravascular haemolysis of transfused RBCs when major ABO incompatibility. Can lead to acute renal failure, DIC and haemodynamic collapse. Presentation: fever, chills, flank pain, oozing from IV sites, chest pain, pink serum or urine. Classic triad = fever, flank pain and red urine. Treatment: Immediate communication to transfusion service Aggressive hydration and diuresis- Normal saline Urticarial Transfusion Reaction Urticaria but no other allergic findings. Antigen-antibody reaction- antigens in plasma interact with recipient's pre-existing IgE antibodies. Mast cells and basophils then release histamine Presentation = wheal and itch. No wheezing, angioedema, hypotension Mx: Can continue remainder of blood product if no wheezing, angioedema, hypotension after antihistamine. ``` Anaphylactic Transfusion Reaction Various mechanisms: • Recipients with IgA deficiency and IgG anti-IgA antibodies • Anhaptoglobinaemia • Passive transfer of food allergen ``` Presentation = rapid onset. Angioedema, wheezing, hypotension. May occur in IgA deficient individuals. Management: cease transfusion, adrenaline repeat every 5 minutes as necessary IM, antihistamines, vasopressors, airway management. TRALI Life threatening occurs when recipient neutrophils are activated by the transfused products in short time or have underlying cardiovascular disease. Neutrophils release inflammatory mediators and damage pulmonary capillaries. Presentation: fever, chills, respiratory distress, hypotension. Mx: supportive, may include intubation and mechanical ventilation. Post-transfusion Purpura Occurs after transfusion of any platelet containing produce. Caused by platelet-specific alloatbodies. Presentation--> 5-10 days post infusion -bleeding -thrombocytoapenia Mx: high dose IVIg for several days Transfusion Associated Graft vs Host Disease Donor lymphocytes recognise recipient cells as foreign, initiating GvHD- (usually, donor lymphocytes destroyed by recipients immune system) Risk factors: -immunocompromised pts -specific type of partial HLA matching between donor and recipient Presentation- 4- 30 days post op • Fever • Erythematous, maculopapular rash --> TENS • n/v • Abdo pain often RUQ • Produse diarrhoea • Cough • Ix: pancytopaenia- hypocellular marow, deranged LFT, electrolyte abnormalities Dx is supported by skin biopsy and HLA phenoytping Mx- no effective treatment- almost always universally fatal Prevent by irradiating products to inactivate T cells Delayed Haemolytic Transfusion Reaction Haemolytic tractions that occur more than 24 hours after completing the transfusion. Often, they occur days to weeks later. They are typically gradual and less severe and often clinically silent. Autoantibodies to minor antigens e.g. Rh, Kell ,Duffy, Kidd. Presentation: 2-30 days post transfusion. -falling Hct, anaemia Fever- mild Unconjugated bilirubin increase Mx: No treatment required in the absence of rapid haemolysis Future avoidance of implicated antigen (must report to patient)

Answer 17

``` Non-immunological complications: • Infection/Sepsis • Transfusion related circulatory overload (TACO) • Primary hypotensive reactions • Iron overload ``` Infection/Sepsis Caused by transfusion of a product that contains a microorganism. Presentation: fever, chills, hypotension Broad spectrum antibiotics and haemodynamic support. TACO Pulmonary oedema due to volume excess or circulatory overload. Diuresis, supplementary oxygen. Presentation: respiratory distress, rales, SOB, orthopnoea, PND, hypertension, Abnormal CXR, hypoxaemia. Prevention: non rapid infusion rates Drop in blood pressure without other causes of hypotension. Exclude TRALI, sepsis, anaphylaxis. Most often reported in platelet transfusions. Iron Overload In chronically transfused patients- e.g. sickle cell, thalassemia, myelodysplastic syndrome.

Answer 18

Definition: Occurs due to insufficient blood flow through one or more coronary arteries usually due to atherosclerotic disease. ``` Classification: Stable angina Retrosternal chest discomfort Exacerbated by exercise Relieved by rest or GTN May be silent in diabetics, elderly and females Acute Coronary Syndrome Unstable angina STEMI NSTEMI ``` Indications: Patient with chronic stable angina in which: Failure of medical therapy Maximum does not improve symptoms Maximum intolerable Significant risk factors on non-invasive testing: Smoking Obesity Dyslipidaemia Co-morbid DM, HTN ST changes on stress ECG Patient categories with better survival post-surgical intervention i.e. Stenosis of Left Main Triple vessel disease (RCA, LAD and circumflex) Two vessel disease (proximal LAD and another) Method: Percutaneous coronary intervention (PCI) Indications: 1-2 vessel disease Suitable anatomically Low risk CVD CI: Anatomically unsuitable (long, near bifurcations) Procedure: Insertion via femoral artery Coronary guidewire inserted into stenotic area and balloon catheter is pushed above. Inflation results in plaque compression and stretches stenosis to allow stent placement Requires dual antiplatelet therapy + heparin post-op Cx: Thromboembolism – MI, stroke Access site – haematoma, pseudoaneurysm, perforation Contrast induced AKI Restenosis (1/3 in 6 months) Stent thrombosis Advantages: Minimally invasive (better for comorbidities i.e. pulmonary disease) Cheaper Faster recovery time Less adverse events Superior for acute STEMI Disadvantages: High re-stenosis rates Not suitable for 3 vessel disease or LMCA Not suitable for non-compliant patients i.e. anti-platelets Potentially incomplete revascularisation Coronary Artery Bypass Graft Indications: Failure of medical therapy Three vessel disease or two vessel involving proximal LAD Failed PCI or restenosis with angina High risk CVD CI: Unfit for surgery Procedure: Internal vein used to bypass stenotic artery Most commonly long saphenous vein, radial artery, mammary artery Must continue strict lifestyle modification/therapy Cx: Thromboembolic events – MI, stroke Haemorrhage Pericarditis Graft failure Advantages: More complete revascularisation More effective for multi-vessels Better long-term results – lower risk of recurrent angina Mortality benefit in diabetic patients Disadvantages: More peri-operative complications – death, stroke, GA, surgical risks Longer recovery and hospital stay

Answer 19

``` Indications: Extent Stages: 1-2 considered operable 3A limited patients operable 3-4 inoperable ``` Patient preference Fitness Co-morbidities that CI surgical Mx – cardiac disease, CCF, end-stage renal disease Recovery and rehabilitation Psychosocial impact Predicted post-operative FEV1 >80% Requires adequate respiratory reserve to tolerate pneumonectomy and maintain quality of life CI: CI in patients with disease extending past the diaphragm: Intra-abdominal Contralateral hemithorax Invading structures of the mediastinum – aorta, IVC, heart, oesophagus Ribs Malignant disease Surgical options: Wide resection + mediastinal lymph node sampling Segmentectomy Lobectomy Sleeve resection Involves removing infected lobe and primary bronchus and then the remaining lobes are re-joined to the remainder of the primary bronchus. ``` Lung cancer: Non-small cell cancer (NSCLC) 85% Adenocarcinoma 40% Squamous cell carcinoma 25% Large cell (undifferentiated) 10% Small cell lung cancer (SCLC) 10% ```

Answer 20

Function: Temporarily replaces the function of the heart and lungs during surgery to maintain systemic circulation and oxygenation. Method: Removes blood from the intravascular space, commonly RA or SVC + IVC. This is filtered through a membrane oxygenator which both oxygenates blood and removes CO2. It is then passed through a heat exchanger and then a filter to remove air bubbles. The blood then returns to the body via the ascending aorta, which is pumped under pressure. ``` Method: Pre-operative Anticoagulation – high dose Heparin CPB circuit primed with crystalloid, heparin +/- mannitol Systolic BP is lowered Prior to cannulation SBP 80-100 During bypass MAP 50-70 Cardioplegic solution administered (K+/Mg2+, procain) – decrease myocardial oxygen demand ``` During Lungs are deflated by turning off ventilator BP maintained with vasodepressors and dilators Induce slight hypothermia (28-34) – prevent ischemia Post-operative Air excluded from cardiac chambers and aortic clamp removed May require cardioversion or pacing if arrhythmia or heart block Machine gradually switched off Cannulas removed and anticoagulation reversed with protamine sulphate

Answer 21

Mechanical ``` Advantages: Durability Sterile – decreased risk of infection Availability Simple procedure ``` ``` Disadvantages: Thrombogenic – increased VTE risk Lifelong Warfarin Bleeding risk Sometimes audible when open/close Endocarditis ``` Tissue Advantages: Reduced VTE risk Reduced anticoagulation need – decreased bleeding risk ``` Disadvantages: 10-15-year lifespan May need replaced – mortality risk Higher rates of infection Difficult procedure ``` Therefore, mechanical valves are normally used in younger patients and tissue valves in older patients.

Answer 22

There are 3 urgent considerations for surgery: 1. Cardiac Tamponade a. Dx: FAST scan b. Initial MX ED = pericardiocentesis and catheter c. Definitive Mx – thoracotomy – release tamponade, control haemorrhage i. Indications: pts with pulseless ECG activity 2. Significant haemorrhage a. >1-1.5L initial loss or >200mL/hour ongoing for 2-4hrs b. Suggests major vascular wall injury unlikely to stop without surgical 3. Massive air leak a. One present during all respiration – suggests major bronchial injury 4. Flail chest Other Considerations for Surgery Direct injury Ruptured blood vessel – endovascular stent or open repair Aorta – if unstable BP emergency surgical repair Trachea/bronchus – tube thoracotomy then open repair Diaphragm – laparoscopic repair Oesophagus – open repair Pulmonary laceration – open repair Haemothorax PC: reduced chest expansion/breath sounds, dull to percussion Mx: Emergency thoracotomy Pneumothorax PC: persistent air leak from chest tube Mx: thoracotomy Overview of Chest Wall Injury - Many penetrating chest wall injuries do not require surgery and can be managed conservatively with: - Serial CXRs - Simple chest tube thoracotomy (15-30% of chest wall traumas will require surgery) Approach to Penetrating Chest Injuries - Primary survey and resuscitation - Detect and immediately treat life-threatening conditions such as: - Tension pneumothorax - Massive haemothorax - Open pneumothorax - Cardiac tamponade - Flail chest Rapid diagnostic testing: - CXR - FAST Scan - ABGs

Answer 23

Assessment: Primary survey (ABCDE) Basic manoeuvre: patient sits upright, bends at hips, and applies digital pressure on cartilage for >10mins. History PC: duration, severity, localisation (nose/throat), causative factor (trauma, coagulopathy, medications, environmental, iatrogenic) PMHx: previous bleed and method of control Evidence of anaemia Examination GI: nasal symmetry, deviation, tenderness, associated injuries Identify source of bleeding: Nasal speculum +/- suctioning To reduce pain o/e consider 5% lignocaine with 0.5% phenylephrine nasal spray Posterior bleeding: Suggested by failure to identify anterior, bleeding from both nares, visualisation of blood in posterior pharynx Refer to ENT for rigid endoscopy Mx: Pain management Cauterisation Apply silver nitrate stick 10-15s (reacts with mucosal lining to produce chemical burn) Never cauterize both sides of septum to avoid perforation Nasal packing Anterior - Rapid Rhino --Nasal tampon with inflatable balloon coated in a compound that acts as a platelet aggregator, may remain in place for 3-4days --Ribbon gauze soaked in paraffin paste or Kaltostat Posterior (if bleeding continues despite anterior packing) - Foley catheter Inserted along floor of nasal cavity into the posterior pharynx then inflated to sit in nasopharyngeal space. Re-insert anterior packing. As increased risk of hypovolaemic shock – insert IV cannula, send bloods (FBC, coagulation studies, cross-match), commence IV fluids Surgical options (refer to ENT) Arterial ligation (SPA – most common, external carotid, internal maxillary) Embolization (useful if failed SPA ligation or unfit for general anaesthesia) For reference: Definition: bleeding from the nasal cavity and/or nasopharynx (common due to rich vascular supply) Classification: Anterior (90%) Located in anteroinferior nasal septum Formed by anastomoses of four arteries “GASS” – greater palatine, anterior ethmoidal, sphenopalatine, septal branches of superior labial Posterior Located in inferior lateral nasal wall, posterior to inferior turbinate Formed by anastomoses of two arteries – Sphenopalatine and pharyngeal Greater risk of airway compromise, aspiration and uncontrollable haemorrhage A vs P Division occurs at piriform aperture (pear-shaped bony inlet of the nose formed by the nasal and maxillary bones)

Answer 24

``` History: • Duration of voice complaints and whether the symptoms are constant or intermmittent • Characteristics of onset o Sudden or gradually progressive o Pattern- worse on voice use, worse in morning • Potential triggering factors o Vocal abuse o Concurrent URTI o Change in medications o Exposure to known allergens or toxins • Exacerbating and ameliorating factors o Improvement with voice rest o Fatigue with use • Other head and neck symptoms o Dysphagia o Otalgia o Odynophagia (pain on swallowing) o Bleeding o Throat pain o Post nasal drip • History of smoking and alcohol use • Red Flags- (when not a/w acute RTI) o SOB o Stridor o Cough o Haemoptysis o Throat pain o Dysphagia o Odynophagia o Weight loss • Use of meds affecting voice o Steroids - inhaled • History of reflux or sinonodal disease • History of past surgery involving neck, base of skull or chest o Thyroid o Carotid o Cervical spine • History of trauma and endotracheal intubation • Occupation, hobbies, habits impacting voice use • Medical comorbidities that can affect voice – rheumatoid, tremor, hypothyroidism ``` Following Hx I would also like: • Physical examination • Referral for ENT for laryngoscopy +- FNA and imaging • Any patient with hoarseness >3 weeks needs CXR • Indications for referral o SCALD o S- smoker, stridor o C- constant/persistent hoarseness, coughing up blood o A- acute onset (not related to URTI or EtoH) o L- Loss (of weight) o D- Dyspnoea or dysphagia • Early referral and detection essential o 70-90% 5 year survival, worse prognosis in stages 3-4 Ddx Causes of hoarseness may be considered in the following categories: • Acute laryngitis, which is self-limited and related to acute respiratory illness or acute voice misuse o Moraxella catarrhalis, haemophilus influenzae, pneumococcus isolated from larynx o Acute vocal strain – such as screaming or protracted coughing= can result in submucosal microtrauma of the vocal fold • Chronic laryngitis, which is related to irritants, reflux, chronic infection (such as fungal), or habitual vocal misuse- beyond 3 weeks o Irritants o Laryngopharyngeal reflux o Muscle tension dysphonia • Benign vocal fold lesions o Polyps and nodules • Malignancy • Neurologic dysfunction o Unilateral or bilateral paralysis o Parkinsons o MND o MG o Tremor • Non-organic ("functional") issues Laryngeal anatomy: Function: Phonation (production of a primary vocal tone at the level of the vocal folds) Respiration Swallowing (laryngeal elevation, posterior deflection of the epiglottis, inhibition of respiration, closure of the vocal folds to prevent aspiration of ingested material) Gross: Extends from the epiglottis to the inferior aspect of the cricoid cartilage Divided into supraglottis, glottis (location of true vocal cords), subglottis Supply: Above vocal cords: superior laryngeal artery (branch of superior thyroid) Below vocal cords: inferior laryngeal artery (branch of inferior thyroid) Innervation: Motor: recurrent laryngeal (branch of vagus), except for the cricothyroid muscle supplied by external laryngeal Sensory: Above vocal cords: internal laryngeal nerve (branch of superior laryngeal) Below: recurrent laryngeal

Answer 25

Dx: Peritonsillar abscess DDx: Epiglottitis: rapidly progressive, younger children Retropharyngeal abscess: neck pain and tenderness, minimal peritonsillar findings Parapharyngeal abscess: bulging posterior to tonsillar pillar, rather than superior Tonsillopharyngitis: bilateral swelling, no trismus, no palpable fluctuance Peritonsillar cellulitis: U/S, response to Abx Clinical diagnosis confirmed by collection of pus on drainage. If diagnostic uncertainty U/S or trial of Abx may help. Q2. Pathogenesis Infective Preceding tonsillitis or pharyngitis that progresses from cellulitis to phlegmon to abscess Most common pathogens include S.Aureus, B-haemolytic strepoccoci, S.Pyogenes, H.influenza Non-infective Due to obstruction of the Weber glands (salivary glands in soft palate), associated with smokers For reference: Peritonsillar abscess Definition: Peritonsillar abscess (quinsy) is a collection of pus located between the capsule of the palatine tonsil and the pharyngeal muscles in the superior pole. Epidemiology: Most common deep neck infection 20-40s, M>F, smokers Hx: Unilateral sore throat +/- ipsilateral ear pain Fever Muffled “hot potato” voice Dysphagia with pooling/drooling of saliva, odynophagia Trismus (inability to open mouth due to inflammation and spasm of the internal pterygoid muscle) Distinguishes PTA from severe pharyngitis or tonsillitis O/E: Swollen, erythematous, fluctuant tonsil (note: bilateral PTA is rare) Deviation of the uvula to the opposite side Cervical lymphadenopathy Ix: CT – fluid collection with large and inflamed tonsil Cx: Retropharyngeal effusion or abscess Septic thrombophlebitis of internal jugular vein Extension into surroundings 🡪 airway obstruction

Answer 26

Dx: Peritonsilar abscess (quinsy) Mx: Resuscitation (ABCDE): Airway - ?ET intubation Breathing – pulse oximeter, O2 as required Circulation – IV access, bloods (FBC, UEC, culture), IV fluids Immediate: Analgesia Empirical IV Abx – benzylpenicillin or clindamycin + metronidazole Definitive: Needle aspiration OR incision and drainage WITH MCS (outpatient or in OT) Emergency tonsillectomy Significant airway obstruction, recurrent episodes, failure of drainage On discharge: Follow-up within 7 days Return if worsening or recurrence of symptoms Oral Abx 10-14days

Answer 27

The most important differential diagnosis is epiglottitis. Epiglottitis describes inflammation of the epiglottis and adjacent supraglottic structures. Without treatment, epiglottitis can progress to life-threatening airway obstruction. It is often caused by Haemophilus influenza type B (which is part of the immunisation program thus often only seen in unvaccinated children). Maintenance of the airway is the first priority for patients with epiglottitis. In patients with signs of total or near-total airway obstruction, airway control should occur prior to diagnostic evaluation. • Defer attempts at visualizing the epiglottis (tongue blade or any other instrument) or invasive procedures (eg, IV placement, phlebotomy, or any other painful or frightening intervention) until after airway assessment and management • Prepare to manage the airway and immediately involve airway specialists (anesthesiologist or critical care physician and otolaryngologist) whenever available Patient not able to maintain the airway: Attempt bag-valve mask ventilation • Unable to oxygenate (pulse oximetry lower than high 80s or falling): Attempt endotracheal intubation by rapid sequence intubation first but be prepared to establish a surgical airway (eg, needle cricothyrotomy or surgical cricothyrotomy)* • Able to oxygenate (pulse oximetry high 80s and steady or improving): Endotracheal intubation by the most capable provider, preferably in the operating with an otolaryngologist present Patient able to maintain the airway: • Provide supplemental humidified oxygen and maintain the child in a position of comfort with the parent present (eg, sitting on the parent's lap on the stretcher) • Keep the patient in a setting where the airway can be rapidly managed if necessary with capable personnel and specialized airway equipment constantly available • Soft-tissue radiograph of the lateral neck (portable if possible) may be helpful but necessary personnel and equipment to manage an acute airway event must remain with the patient at all times during the imaging process. • Do not image patients with severe respiratory distress in whom it will delay definitive airway management Radiographic findings of epiglottitis: Enlarged epiglottis ("thumb" sign), loss of vallecular air space, thickened aryepiglottic folds, and/or distended hypopharynx Attempts at direct visualization are only appropriate in patients with no stridor or stridor without significant distress, no increase in symptoms with agitation, and no cyanosis In children <6 years of age with confirmed epiglottitis or older children who are toxic-appearing or have >50 percent obstruction of the lumen by direct visualization, perform endotracheal intubation in the operating room with an otolaryngologist present Under GA: examine throat + swabs, intubate, take blood cultures ICU Start IV Abx – ceftriaxone or cefotaxime.

Answer 28

Post-operative cervical haematoma (usually in paratracheal area) – rare but life-threatening complication. Management: Call senior + transfer to OT Resuscitation (ABCDE): Airway If non-critical may perform in OT, if critical perform at bedside Establish airway: Relieve pressure on airway by removal of sutures and evacuation of haematoma. Keep pressure without occluding trachea or carotids. Attempt intubation If all else fails, then cricothyroidotomy Breathing – immediate high flow O2 Circulation - establish IV access, control haemorrhage OT Re-opening and inspecting for location of bleed Place drain to remove fluid collecting in bed of haematoma Transfer to ICU for observation For reference: Post thyroidectomy haematoma Description: Haematoma is a collection of blood within the tissue Due to major vessel ligature, re-opening of cauterized veins, bleeding from traumatized sternocleidomastoid muscle. Causes life-threatening airway obstruction from direct tracheal compression and lymphatic/venous congestion Presentation: Commonly 12-24hrs post-op Progressive neck swelling Signs of airway obstruction Respiratory distress (dyspnoea, stridor, anxiety, tachycardia) Hypoxia (tachycardia, sweating, irritability, confusion) Bleeding along suture line or significantly into drain Transient vocal cord paralysis

Answer 29

Dx: Secondary (>24hrs) post-op haemorrhage Occurs when fibrin clot (eschar) separates between day 5-10 exposing vessels to local trauma. There is significant vascular supply to the tonsil (primarily from tonsillar branch of the facial artery) which predisposes it to haemorrhage. Mx: Admit Resuscitation (ABCDE): Airway – position patient forward, encourage spitting blood into bowel, suction as required Breathing – O2, OBS Circulation – IV access, bloods (FBC, coagulation studies, G&S), IV fluids Immediate: Urgent ENT review IV analgesia NBM 24hrs monitoring Definitive: Examine oropharynx for source of bleeding – visualise greyish white eschar Apply pressure to tonsillar fossa with gauze soaked in lignocaine and adrenaline If non-resolving 🡪 OT: Electrocautery or silver nitrate Topical haemostasis (topical thrombin, fibrin sealant) Suture ligation Surgical embolization

Answer 30

Dx: Squamous cell carcinoma (SCC) of the larynx O/E: General observation Hoarseness or vocal change Respiratory distress, noisy breathing Cachexia, weight loss Head and neck Ear: otalgia Oral cavity and oropharynx: masses or leucoplakia Laryngeal inlet: lesions of vocal cords, tumours Neck: cervical lymph nodes or masses (size, location, shape, mobility, firmness, tenderness) Respiratory Signs of distress: stridor, diminished breath sounds, obstruction Refer to ENT for Ix Urgent laryngoscopy Visualise lesions and document vocal cord mobility Imaging (assess local infiltration, LN involvement, presence of Mets or secondary tumours) CT contrast neck and chest Whole body PET/CT scan FNA of neck mass or cervical LN (under U/S guidance) Rigid direct laryngoscopy with biopsy (FNA or excisional) under GA For reference: Laryngeal cancer Background: Laryngeal cancer approx. 20% of all cases of head and neck cancer 90-95% are SCC Glottic (59%) > Supraglottic (40%) > subglottic (1%) Metastatic patterns: Larger (especially if located in supraglottis) spread lymphatically to the neck Lungs most common site for metastases Prognosis: If localised 5-year survival 77% ``` Risk factors: M>F >40y/o 40 pack year, EtOH Chronic viral infection – HPV, HIV ``` Pathophysiology: Chronic tobacco exposure irritates the epithelial surfaces causing pre-malignant changes of hyperplasia and dysplasia, pre-disposing the area to malignancy. If alcohol is consumed as well, it more than doubles the risk compared to exposure to one factor alone. Presentation: Hoarseness >3wks (early in glottic, late in supraglottic and subglottic) Dysphagia, odynophagia Otalgia (referred ear pain via CN X – suggests advanced disease) Cervical lymphadenopathy (poor prognosis – may be only sing of supraglottic lesion) Stridor, dyspnoea Haemoptysis, chronic cough Unexplained weight loss, fatigue, night sweats ``` DDx: Chronic Laryngitis Polyps on the vocal cords Reinke’s oedema Contact granuloma HPV papilloma’s Benign tumours (rare) ```

Answer 31

``` Pathology: Thyroid function tests (TFTs) Decreased TSH Increased free T4, free T3 Thyroid autoantibodies (positive) Thyroid peroxidase (TPO) antibody TSH-receptor antibody Other: FBC (normochromic normocytic anaemia, mild leukopenia) LFTs (elevated ALT and AST) Hypercalcemia ``` Imaging: Radionuclide thyroid scan (Technetium-99m) Normal or elevated uptake Homogenous: graves Heterogenous: toxic multinodular goitre Decreased uptake: thyroiditis, exogenous thyroid hormone Thyroid U/S +/- FNA Indicated if suspicious nodules (i.e. macrocalcification, irregular border, increased vascularity) ECG (document any arrhythmias or other changes) For reference: Hyperthyroidism Causes: Autoimmune (Grave’s disease) – most common Thyroid-stimulating antibodies (IgG) bind to TSH receptors causing excess thyroid hormone secretion. Over time the thyroid hypertrophies and becomes diffusely enlarged. TSH-secreting pituitary adenoma Toxic multinodular goitre Thyroiditis Exogenous intake of thyroid hormones Clinical features: Increased MR: weight loss, heat intolerance, sweating CNS overactivity: tremor, nervousness, irritability, lethargy Beta-adrenergic sympathetic overactivity: palpitations, tachycardia, arrhythmias Eye signs: soft tissue oedema, exophthalmos, diplopia, ophthalmopathy Thyroid storm (thyrotoxic crisis): Precipitated by non-thyroid surgery, major trauma, infection, imaging with iodinated contrast Features: insomnia, anorexia, vomiting, diarrhoea, sweating, fever, tachycardia

Answer 32

Traumatic perforation of tympanic membrane O/E: Anatomic inspection: External ear: Haematoma, bruising, trauma, discharge Otoscopy: TM perforation (central or marginal – unsafe as allow skin invasion into middle ear) Blood crust Physiological assessment: Hearing Positive Rinne’s test (conductive: bone conduction > air) Weber’s test (conductive: loudest on ipsilateral side to affected ear) Facial nerve (CN VII) palsy Symmetry, facial movements, taste Advice: Most perforations heal spontaneously within 8wks Keep dry and clean to avoid infection (i.e. use plug when showering) If signs of infection (pain/discharge) 🡪 Abx Follow-up in 4-6wks If not improved, refer to ENT for surgical management (tympanoplasty) For reference: Rupture tympanic membrane Causes: Blunt force trauma to external ear canal (car accident, blow to side of head, explosion) Penetrating trauma (cotton buds, iatrogenic during irrigation or FB removal) Barotrauma (air travel, scuba diving) Red flags: Significant polytrauma Battle’s sign (mastoid ecchymosis indicating skull base fracture) Facial nerve palsy Presentation: Sudden severe pain (otalgia) Serosanguinous drainage (fresh blood leakage) Conductive hearing loss (sound does not reach the inner hear) Tinnitus (ringing or buzzing in ears) Fullness in the ears (aural fullness) Disequilibrium/imbalance

Answer 33

Cholesteatoma (abnormal growth of epithelium in the middle ear that results in bone erosion and infections) Actions: Initial workup: Otoscopy: (confirm diagnosis) Attic (posterosuperior portion of TM) retraction containing keratin Migration of keratin through perforated TM White crust within or behind intact TM Audiometry (assess hearing loss) CT temporal bone (assess for extent and complications) Ear swab of discharge ``` Mx: Immediate: Analgesia (paracetamol/NSAID) Topical Abx +/- wick Definitive: Refer to ENT Mastoidectomy Canal wall up (closed) – heals better, but risk that disease will recur Canal wall down (open) – decreases risk of recurrence, will need to wear earplug when swimming and have wax cleaned Tympanoplasty ``` For reference: Cholesteatoma Causes: Eustachian tube dysfunction (from allergies, sinusitis, chronic middle ear infections) Perforated TM due to infection of injury Congenital remnant of skin trapped in middle ear Implantation of keratinocytes following otologic surgery or traumatic blast injury Presentation: Hearing loss or tinnitus Chronic offensive discharge Otalgia, vertigo, facial nerve palsy

Answer 34

**VIVA I** Dx: Acute Otitis media The condition that this could develop into that causes swelling behind the ear and the ear to stick out/forwards is Mastoiditis -- a bacterial infection of the mastoid cells surrounding the inner and middle ear, causing swelling behind the ear and the ear to stick out or forwards. There will be oedema, erythema and tenderness over the mastoid process. This is also managed with analgesia and antibiotics. **VIVA II** Dx: Acute Otitis media Management: 1. Acute pain relief with analgesia (usually paracetamol +/- ibuprofen) 2. Antibiotics (usually penicillin/amoxycillin. Refer to local guidelines). 3. As the patient will likely have an ongoing viral respiratory infection, the patient should also be encouraged to drink plenty of fluids and rest. 3. ENT referral for surgical mx **VIVA III** Dx: Acute Otitis media ``` Dangerous Complications: Intratemporal complications that can result include: 1. Hearing loss 2. Balance and motor problems 3. Tympanic membrane perforation 4. Cholesteatoma 5. Mastoiditis 6. Seventh cranial nerve palsy ``` Other complications include: 1. Meningitis 2. Epidural abscess 3. Subdural abscess 4. Brain abscess 5. Lateral sinus thrombosis 6. Cavernous sinus thrombosis 7. Carotid artery thrombosis For reference: Acute otitis media ``` Clinical features: Ear: 1. Otalgia (ear pain) 2. Postauricular tenderness 3. Decreased hearing ``` - Physical examination will reveal a bulging, opacified tympanic membrane with decreased mobility. - The membrane may be white, yellow, pink or red. - Diagnosis is generally made with conventional otoscopy Resp: 1. Usually ongoing viral respiratory infection Neuro: 1. Facial nerve palsy Systemic: 1. Irritability/Lethargy 2. Fever GI: 1. Anorexia 2. Nausea/Vomiting Protruding auricle/external auditory canal oedema Ix (not routine): CT -> bony destruction of mastoid air cells ``` Pathophysiology: Preceding event (e.g. URTI) -> inflammatory response. Inflammatory oedema obstructs the isthmus in the eustachian tube -> accumulation of secretions in middle ear space -> viral/bacterial growth. ``` Pathogens: Viral (most common): RSV, Rhinovirus, enterovirus Bacterial: S.pneumoniae (50%), H.influenzae (45%), Moraxella, GAS

Answer 35

While I am still on the call, I would ask the nurse to check for any surrounding dangers, rechek the patient's observations, and ensure their immediate stability. I would urgently review this patient as there is a concern this patient may be hypovolaemic due to post-operative blood loss. ``` Whilst on my way to the patient's bedside, I will be considering differentials categorised by system: Cardiovascular System -Hypovolaemia - MI - Arrhythmia - Fluid imbalance or acid/base imbalance - Exacerbation of valvular pathology ``` Neurologic System - Vasovagal or micturition syncope - CVA - Delerium - Seizure - Also consider psychiatric aetiology Respiratory System - PE Musculoskeletal System - Muscle weakness - Functional issue e.g. slippery surface/severe pain Endocrine - Hypoglycaemia Once at the patient's bedside, or rather toiletside, I would begin by ensuring their: 1. Airway is patent and assess for signs of bleeding 2. Breathing and Circulation are adequate Look for chest rise, whilst listening and feeling for breath sounds with my ear and assess fluid status by checking pulse, cap refill and checking urine output. 3. Checking for disability. GCS (pupils, limb strength, motor/sensory assessment, focal deficit assessment) 4. Checking exposure Examine for injuries sustained during fall (head/neck, fracture, bruises/lacerations) ``` Secondary survey: Hx - Mechanism of fall - Precipitants/preceding symptoms (straining, constipation, standing, dizziness, palpitations, SOB) - LOC, time to recovery - Witnesses? - Subsequent pain/concerns ``` O/E - Cardiorespiratory - Neurological + cranial nerve - Surgical site? bleeding Review: - OBS - Operation report - Progress notes - Fluid balance - Medications (particularly anti-hypertensives) - Consider ENT review Ongoing monitoring: - OBS hourly for 4hrs - Observe for headache, nausea, vomiting or changes in behaviour - Observe for occult bleeding: flank pain, increased intra-abdominal pressure, swelling, bruising - Review falls risk (now high) and risk prevention strategies For reference: Sinus surgery Indications for frontal sinus surgery: Chronic rhinosinusitis e.g. ethmoidectomy Cerebrospinal fluid leak Benign and malignant tumours of the frontal sinuses Complications: Open/external: osteomyelitis, ocular muscle injury, haemorrhage, CSF leak, meningitis Endoscopic: Epistaxis, bruising, dental pain, brain abscess, haemorrhage, CSF leak, meningitis Post-op advice: Avoid straining or blowing nose for 10days Do not recommence aspirin or NSAID until 2wks post-op Avoid steroid nasal spray for 2wks Nasal saline sprays every 2-3hrs Sinus irrigation twice daily Normal to have intermittent blood discharge first 3-5days after surgery

Answer 36

The most likely diagnosis is Acute Otitis Media • May present with otalgia, irritability, decreased hearing, anorexia, vomiting, or fever, usually in the presence of an ongoing viral respiratory infection. o Risk factors: male, young age, exposure to respiratory viruses (day care attendance, older siblings), positive family history, aboriginal • Physical examination will reveal a bulging, opacified tympanic membrane with decreased mobility. The membrane may be white, yellow, pink, or red. • Diagnosis is generally made with conventional otoscopy. Additional tests might include pneumatic otoscopy or tympanometry to confirm the presence of an effusion. • Treatment includes pain control with analgesics and might include antibiotics. • Complications include perforation of the tympanic membrane and, rarely, mastoiditis, seventh cranial nerve palsy, or sigmoid sinus thrombosis. The condition that could develop causing swelling behind the ear and the ear to stick out/forwards is acute mastoiditis. • There is oedema, erythema, and tenderness over the mastoid process. • Because the mastoid air cells are connected to the distal end of the middle ear through a small canal or antrum, most episodes of AOM are associated with some inflammation of the mastoid • Also managed with analgesia and abx

Answer 37

The most likely diagnosis is Acute Otitis Media Management: • Oral analgesia o Pain control is central to the management o Paracetamol/ibuprofen • Antibiotic therapy with penicillin (amoxicillin)

Answer 38

``` The most likely diagnosis is Acute Otitis Media Complications that can result include: • Intratemporal complications o Hearing loss o Balance and motor problems o TM perforation o Choleastoma o Mastoiditis ``` ``` • Intracranial complications o Meningitis o Epidural abscess o Brain abscess o Lateral sinus thrombosis o Cavernous sinus thrombosis o Subdural empyema o Carotid artery thrombosis ```

Answer 39

Urgently go to review the patient, concerned that patient may be hypovolemic due to post-op bloodloss ABCDE Response – patient conscious or unconscious, alert or obtunded Airway – patent? Breathing – RR, SaO2 Circulation: HR, BP, mucous membranes, 2x large bore IV cannulas with resuscitation fluids if needed, review fluid balance chart Disability - GCS Review obs chart, medications (anticoagulants?), operation report, patient notes Hx of fall • Mechanism of fall? Injuries? • LOC? • Post-ictal period? • Dizziess • anticoagulation • Events leading up to fall – dizzy? Lightheaded? Palpitations? • Amount of bloodloss • Past hx of bleeding disorders, seizures, IHD • Review: chart, operative report, perioperative progress notes, adequacy of fluid replacement, omission of important meds? Examination: • Repeat obs • Examine site of bleeding • Surgical site examination • Neurological exam – focal defecits? Global defecits? • Cardiovascular exam – including check for orthostatic hypotension DDx – Hypovolaemia, aortic stenosis, seizures, arrhythmias, vasovagal/micturition syncope, MI, CVA, PE Ix: B – FBC, UEC, Coags, Group and hold O – X – X-ray for fractures E – ECG for arrhythmias, MI S – CT head looking for site of bleeding/ ?CVA if suspected/ head trauma Mx: Attempt to bring about haemostasis – upright position, packing if needed Provide fluid resuscitation and treat any injuries as required Contact ENT surgeon who performed operation for advice- urgent ENT review Complications of functional endoscopic sinus surgery: • CSF leaks, orbital injury, intracranial haemorrhage, meningitis Important causes of post-operative collapse or rapid deterioration: Cardiovascular MI, sudden arrhythmia, fluid overload, PE, stroke, haemorrhage Respiratory Failed reversal of anaesthesia, drug induced respiratory depression Surgical/infective Hypovolaemic shock- blood loss, decompensation, systemic sepsis, SSI Metabolic Electrolyte disturbance, BGL abnormality, adrenal insufficiency --> hypotension drugs Drug reaction e.g. anaphylaxis

Answer 40

DDx - VITAMIN CDEF ``` Neoplasm (most likely): Parotid tumours Causes: Benign (70%) - Pleomorphic adenoma Malignant – Mucoepidermoid carcinoma, SCC, acinus cell carcinoma Hx: painless, firm, slow-growing mass Red flags: Red flags on Hx: Facial n. weakness, rapidly increasing size, ulceration of mucosa/skin Others: Lipoma (tumour of being adipose tissue) Non-Hodgkin Lymphoma Odontogenic Muscles of mastication ``` ``` Infective/inflammatory: Parotid infection Bacterial (S.aureus, streptococci) Hx: sudden onset pain, swelling, purulence from duct, salivary stones Viral (Mumps, HIV, coxsackievirus) Hx: usually bilateral swelling, tenderness Odontogenic infection and abscess Hx: acute onset pain, swelling, trismus Lymphadenitis ``` Obstructive: Sialolithiasis (salivary stone) Hx: chronic/recurrent pain and swelling, occurs with meals, recurrent infections O/E: swelling, milking gland produces saliva, intraoral palpable stone Autoimmune: Sjogren’s syndrome Hx: xerostomia, keratoconjunctivitis sicca, abnormal taste, intermittent swelling Idiopathic: Sialadenosis (non-specific bilateral enlargement of the salivary glands)

Answer 41

Approach: “Triple Test” Positive if any component is indeterminant, suspicious or malignant Sensitivity (true positive) 99.6% Specificity 62% i.e. false positive 38% Hx and O/E Imaging (mammography and/or ultrasound +/- MRI) Non-excisional biopsy (FNA +/- core biopsy) ``` Hx: HxPC Site (1/2+, localised or generalised) Onset/duration (rapid – cyst, slow – carcinoma) Growth or change (fluctuate with menstrual cycle – fibroadenoma, fibroadenosis) Previous lump Associated symptoms Pain/tenders (non-malignant) Nipple retraction or inversion Nipple discharge Skin changes (redness, swelling or puckering of the skin) Systemic features: Fever, weight loss, anorexia ``` PMHx/SHx Previous breast problems (any previous Ix or results) Obstetric history (RF for malignancy – late age at first pregnancy, low parity) Menstrual history (RF for malignancy – early menarche, late menopause) Obesity Medications: the pill, HRT FHx Family history of breast/ovarian cancer – age of onset, bilaterality O/E: General inspection - patient sitting upright on side of bed Asymmetry Scars (small – lumpectomy, large diagonal – mastectomy) Masses – size, location Skin changes – erythema, puckering, peau d’orange (inflammatory breast cancer) Nipple changes (retraction, discharge (green, blood-stained), scale) Closer inspection - hands on hips (tenses pectoralis major), hand on head and lean forward Palpation – hand behind head of breast you’re examining, including axillary tail and nipple Location (quadrant of breast or clock face) Size and shape Consistency (smooth and round -benign, firm/hard – probable malignancy) Edges (well-defined/irregular) Mobility (mobile – benign, fixed – probably malignancy) Fluctuance (fluid-filled – cyst) Temperature Overlying skin changes (erythema, ulceration, punctum) General lymph node examination (axillary lymphadenopathy – probably malignancy)

Answer 42

``` Non-modifiable: Increasing age (peak incidence 70-80s) Female Family or personal hx BRAC-1 or BRAC-2 mutation (5-10%) Menses <12y/o Late menopause >55y/o Previous breast biopsies showing non-malignant abnormalities ``` ``` Modifiable: Obesity (fat tissue produces oestrogen) Alcohol (limits liver’s ability to control the levels of oestrogen and can damage DNA cells) Smoking First pregnancy >30y/o OCP/HRT Radiation exposure ``` Protective factors: Regular physical activity First pregnancy <20y/o Breast feeding >12mths

Answer 43

Adjuvant therapy is given following primary surgical management to reduce the risk of local recurrence or prevent metastatic spread. Radiotherapy Indications: Post breast-conserving therapy (lumpectomy) Post mastectomy if high recurrence risk or nodal involvement Delivered daily (except weekends) for 3-6wks via external beam to chest wall +/- local nodes SE: Fatigue, skin reactions (sunburn), lymphedema, loss of appetite, predisposed to other cancers Chemotherapy Indications: Lymph node involvement (regardless of size or menopausal status) Premenopausal with invasive cancers (generally more aggressive) HR -ve and HER2 +ve Contraindications: Less effective if node negative or post-menopausal Non-invasive cancer Combination: Anthracycline (doxorubicin) + Taxane (paclitaxel) SE: nausea, vomiting, alopecia, neutropenia, fatigue, mouth ulcers, infertility Hormone therapy Indications: ER +ve Types: Ovarian ablation (premenopausal) GnRH agonists (supress ovarian function) or oophorectomy Tamoxifen (premenopausal and low-risk postmenopausal) Selective oestrogen receptor modulator that blocks peripheral action of oestrogen by binding to the receptor SE: menopausal symptoms (vaginal dryness, hot flushes), clotting risk, endometrial cancer Aromatase inhibitors (high-risk postmenopausal) Prevents oestrogen synthesis in peripheral adipose tissues by blocking conversion of androgens to oestrogen by aromatase enzyme. SE: osteoporosis, fractures, worsening menopausal symptoms Delivered as daily oral medication for 5+ years post other treatments Biological therapy Indications: HER2 +ve Trastuzumab (Herceptin) Monoclonal antibody that targets HER2 receptors to downregulate action and initiate immune mediated destruction. SE: flu-like, fever, anorexia, muscle/joint pain, diarrhoea Delivered post-surgery and chemotherapy (must have or won’t be covered by PBS) at 3wk intervals for 1yr

Answer 44

1. Breast conservation surgery Background Removal of tumour with margin of surrounding breast tissue + radiotherapy Lumpectomy (1cm margins), wide local excisions (2-3cm margins), quadrantectomy ``` Indications Patient’s choice Single lesion, Stage I/II, <4cm Nil skin, nipple/areola involvement No node involvement CI: pregnancy, BRCA, SLE, lupus ``` ``` Advantages Comparable survival Better cosmetic and psychological result Less invasive Shorter recovery ``` ``` Disadvantages Follow-up radiotherapy Higher rate of recurrence Anxiety/fear of recurrence May require additions surgeries (poor margin or recurrence) ``` ``` 2. Mastectomy Background Simple/total: breast + level I nodes Modified: breast + lvl I-III nodes + pec minor Radical: modified + pec major ``` ``` Indications Not a candidate for BCS Multicentric disease Positive margins after resection Radiation CI (pregnancy, recurrence of cancer) ``` ``` Advantages Comparable survival Better cosmetic result if smaller breast Reconstruction potential Lower risk of recurrence No follow-up radiation if low risk ``` ``` Disadvantages Comparable survival Better cosmetic result if smaller breast Reconstruction potential Lower risk of recurrence No follow-up radiation if low risk ```

Answer 45

Malignancy: 10% Non-invasive/pre-cancerous: Ductal carcinoma in situ (DCIS) 80% Lobular carcinoma in situ (LCIS) 12% ``` Invasive: Infiltrating ductal carcinoma (IDC) 75% Infiltrating lobular carcinoma (ILC) 10% Other: Medullary (5%), mucinous (colloid), inflammatory, tubular, Paget’s disease, papillary Metastases from another primary site ``` Benign: Cyst (blockage of duct resulting in fluid-filled mass) Hx: premenopausal/perimenopausal O/E: compressible, ballotable solitary mass Fibroadenoma Hx: asymptomatic, incidental finding, <40y/o O/E: smooth, rubbery, mobile mass Fibrocystic change or fibroadenosis Hx: breast pain, increase with menstrual cycles O/E: not well-defined mass, nodular breast tissue Fat necrosis Hx: obese, large breast, blunt trauma, injection of substance, breast surgery, radiation therapy O/E: skin ecchymosis, hard irregular lump Breast abscess Hx: lactating, mastitis, fever, malaise, painful mass O/E: fluctuant, tender, palpable mass Galactocele (milk retention cyst) Hx: breastfeeding Phylloides tumour Hx: 40-60, rapid enlargement breast O/E: well-delineated, large breast mass ``` Intraductal papilloma (local epithelial proliferation in mammary ducts) Hx: blood stained discharge Duct ectasis Hx: menopause, green nipple discharge ```

Answer 46

Indications: >30 Mammography <30 U/S or MRI if high risk (family hx, BRCA in first degree relatives, hx chest radiation) Reasoning: Denser breast tissue in younger women limits the sensitivity of mammography. In patient <35 false-negative rate for mammography is >50% MRI not affected by age or density of breast tissue More sensitive, but not very specific which can result in unnecessary biopsies

Answer 47

Dx: Lactational breast abscess Mx: Needle aspiration (+/- U/S guidance) or surgical incision/drainage. Empirical abx (flucloxacillin) – modify based on culture of swab. Pain relief – simple analgesia, ice pack. Continue breast feeding/expressing milk – important for resolution of infection and relief of breast fullness. ? referral to lactation nurse consultant. For reference: Lactational breast abscess Definition: collection of infected fluid within the breast Background: 20% breastfeeding women develop lactational mastitis, with 3% developing an abscess Peak within first 6wks post-partum Causative organism: S.aureus Risk factors: hx mastitis, primiparity, maternal age >30, GA >41wks Pathophysiology: Milk stasis or milk overproduction coupled with bacterial invasion of the breast tissue through a traumatised nipple results in mastitis. As the breast tissue becomes inflamed it further blocks milk ducts and allows for progression of the infection. Left untreated, it can cause tissue destruction resulting in an abscess. Presentation Hx: worsening mastitis unresponsive to abx Breast pain, fever, flu-like (malaise, lethargy, myalgia, sweating, headache, nausea/vomiting) O/E: Inflammation, fluctuant tender mass

Answer 48

Dx: Fibroadenoma (most common lesion between 15-35y/o) Reassure patient that most breast lumps benign, but must complete “Triple Test” Triple testing is a combination of clinical examination, imaging and nonsurgical biopsy. History: HxPC Site, onset, duration Growth or change (fluctuate with menstrual cycle – fibroadenoma, fibroadenosis) Previous lump Associated symptoms (discharge, pain, tenderness, skin changes) Systemic features (fever, weight loss, anorexia) PMHx/SHx Previous breast problems (any previous Ix or results) Gynaecological, menstrural and obstetric hx Medications – OCP Hx cancer FHx Family history of breast/ovarian cancer – age of onset, bilaterality, BRAC genes O/E: Inspection: Asymmetry, scars, masses, skin changes, nipple changes/discharge Palpation: Location, size, shape, consistency, mobility, temperature, tenderness/painless, skin changes Lymph nodes Ix: U/S (well-defined, solid mass – fibroadenoma) FNA or CNB (especially if red flags or suspicious imaging)

Answer 49

Dx: Lactational mastitis +/- abscess O/E: Describe breast + quadrant Nipple cracking (+/- retraction/inversion) Localised area of inflammation (erythema, swelling) Purulent discharge Abscess punctum Lactational localised to peripheral wedge-shaped areas of the breast (non-lactational central)

Answer 50

Staphylococcus Aureus

Answer 51

Needle aspiration (+/- U/S guidance) or surgical incision/drainage Empirical abx (flucloxacillin) – modify based on culture of swab Pain relief – simple analgesia, ice pack Continue breast feeding/expressing milk – important for resolution of infection and relief of breast fullness ? referral to lactation nurse consultant

Answer 52

Dx: Lactational mastitis +/- abscess ``` Mx mastitis: Flucloxacillin 500mg 6hrly for 5days Effective milk removal Pain relief – analgesia, warm/cold compress Increased fluid intake ``` Mx abscess: Needle aspiration (+/- U/S guidance) or surgical incision/drainage Empirical abx (flucloxacillin) – modify based on culture of swab Pain relief – simple analgesia, ice pack Continue breast feeding/expressing milk – important for resolution of infection and relief of breast fullness ? referral to lactation nurse consultant DDx: Breast engorgement (occurs day 3-5 post-partum, requires frequent breast emptying) Inflammatory breast cancer

Answer 53

For this patient I would recommend radiotherapy, hormone therapy and chemotherapy. I would not recommend biological therapy as she is HER2-ve and this would not be effective. Radiotherapy Indicated after breast conserving surgery Aims to achieve local disease control by eradicating any residual disease and preventing its recurrence. Hormone therapy (e.g. tamoxifen or aromatase inhibitors) Indicated in hormone receptor positive cancers Aims to reduce the level of circulating oestrogen and block hormonal stimulation of remanet cancer cells. Chemotherapy Indicated in HER2-ve grade 3 cancers >10mm Aims to eradicate microscopic cancer cells that could recur as metastases Most common regimen is Anthracycline + Taxane Both local and systemic adjuvant therapies aim to improve survival by preventing disease recurrence. However, they can be distinguished by their mechanism of action. Local therapy acts directly on the breast to prevent recurrence of the primary tumour, systemic therapy acts through the whole body targeting metastatic spread or occult disease.

Answer 54

For: Staging and prognostic purposes Determining appropriate adjuvant therapy Reduce risk of further spread Improves quality of life if bulky adenopathy in neck Stage T3 or T4 (>2.0mm) If macro metastases >2.0mm Against: No overall survival benefit (in comparison to observation alone) May not prevent recurrence elsewhere Approx. 80% of patients with positive sentinel node have no additional disease i.e. unnecessary surgery Surgical risks – lymphedema, wound infections, nerve damage Stage T1 or T2 (<2.0mm) If micro metastases Older patient, unstable patient, high peri-operative risk, life-shortening comorbidity Definition: removal of all lymph nodes and possible tumour containing tissue from the armpit region. Levels: Lateral to pec minor Up to medial border pec minor Beyond medial border pec minor

Answer 55

Dx: Nodular basal cell carcinoma ``` History: HxPC: Site, onset, duration Growth or change Association symptoms (pain, bleeding – after trauma) Risk factors: Previous skin malignancies Sun exposure (occupational/recreational) Exposure to radiation ``` O/E Inspection: ABCDE approach: (more for pigmented lesions) Asymmetry, irregular borders, colour, diameter >6mm, evolution Characteristic features: Pearly/waxy, central depression, central ulceration, raised border, telangiectasias Closer inspection via dermatoscope Full skin check Mx: Surgical: Excision biopsy (gold-standard) with >4mm margins – cure rate approx. 90% Curettage and cautery – approx. 90% Non-surgical: Radiation therapy – cure rate approx. 90% Cryotherapy – approx. 85-90% Photodynamic therapy – approx. 80% Topical immunotherapy (e.g. imiquimod) – approx. 80% For reference: Nodular BCC Definition: Locally invasive skin cancer Risk factors: Sun exposure Fair skin Previous skin cancer ``` Clinical features: Slow growing plaque/nodule Shiny/pearly nodule with smooth surface Variable size mm-cms Spontaneous bleeding or ulceration Rarely - rapid growing, invasive and/or metastatic to local lymph nodes ```

Answer 56

Clinical features (alone not sufficient to differentiate): ``` Benign Multiple lesions “Rubbery” Mobile Well circumscribed border Bilateral, milky discharge Fluctuating ``` ``` Malignant Single lesion Hard Immobile Irregular borders Unilateral, bloody, clear or coloured discharge Skin changes Hx of cancer or systemic symptoms ``` Mammographic features: ``` Benign Round/oval shape Well circumscribed border Low density Large, coarse (‘popcorn-like’) or smooth, round calcifications ``` ``` Malignant Stellar shape Irregular (spiculated) border High density Clustered or linear branching micro-calcifications ```

Answer 57

Gold-standard Ix is the triple test, as no test alone has greater sensitivity or specificity. In terms of a single most reassuring investigation, it would be a core biopsy for cytology and histopathology. Although, this usually requires imaging first. Reassuring findings: Histology of tissue specimen being void of malignant change (e.g. differentiated or irregular cells, abnormal proliferation)

Answer 58

Relative risk reduction: relative/proportional risk reduction of an event happening in 2 groups with different interventions Current risk of death in 5yrs is 80%, and chemotherapy offers a 25% reduction relative to that risk i.e. new risk of death is 0.25*0.8 = 0.6 = 60% So, if the new risk of death is 60% with chemotherapy, the new chance of 5yr survival with chemotherapy is 40%

Answer 59

For this patient I would recommend radiotherapy, hormone therapy and chemotherapy. I would not recommend biological therapy as she is HER2-ve and this would not be effective. Radiotherapy (via external beam) Indicated after breast conserving surgery Aims to achieve local disease control by eradicating any residual disease and preventing its recurrence. Hormone therapy (e.g. tamoxifen or aromatase inhibitors) Indicated in hormone receptor positive cancers Aims to reduce the level of circulating oestrogen and block hormonal stimulation of remanet cancer cells. Chemotherapy Indicated in HER2-ve grade 3 cancers >10mm Aims to eradicate microscopic cancer cells that could recur as metastases Most common regimen is Anthracycline + Taxane Both local and systemic adjuvant therapies aim to improve survival by preventing disease recurrence. However, they can be distinguished by their mechanism of action. Local therapy acts directly on the breast to prevent recurrence of the primary tumour, systemic therapy acts through the whole body targeting metastatic spread or occult disease.

Answer 60

Conservative: General measures: Avoid straining Mx constipation – Fibre, stool softeners e.g. Movicol, fluids Sx analgesia Warm anal bathing – stimulates somatoanal reflex Topical ointment (1st line) GTN – smooth muscle (sphincter) relaxation and vasodilation CCB (diltiazem) – blocks smooth muscle contraction Botulinum toxin injection (2nd line) Sphincter relaxation (paralysis) for 8-12wks Surgical: Lateral internal sphincterotomy Indicated post 6-8wks of conservative therapy Method: Divide 1cm of the lower portion of the internal sphincter Risks: incontinence of flatus or stools, infection

Answer 61

Definition: Longitudinal tear in the mucosa and skin of the anal canal distal to the dentate line. Approx. 90% occur in the posterior midline, whereas secondary causes more associated with lateral tears. ``` Aetiology: Acute Primary: Passage of hard stools Explosive diarrhoea Vaginal delivery Foreign body penetration Secondary: IBD Malignancy Infection (syphilis, HIV) Chronic Approx. 40% develop into chronic form due to: Repeated tearing “Fear of defecation” which aggravates constipation and straining Impaired healing If extends into internal anal sphincter (involuntary smooth muscle) it can lead to spasm and reduced blood flow with ischemia. Exposure to faeces also slows healing ``` ``` Presentation: Pain post defecation Tearing, ripping, burning character Minutes to hours Hx constipation Irritation or itchiness around skin Haematochezia Fissure or small skin tag (sentinel pile) at 6 or 12 O’clock position PR exam extremely painful ```

Answer 62

``` DDx: Colorectal Ca Benign polyps Haemorrhoids, fissures IBD Diverticular disease Infectious (gastroenteritis) ``` ``` Hx: PC Bleeding Onset, duration, previous bleeds, mucous, colour Bright red – anorectal Dark red, clots – rectosigmoid Dark red mixed in stool – ascending/transverse Melena – Upper GI Associated Sx Pain, weight loss, fever, night sweats, changes in bowel habits PMHx Any of the DDx Abdominal surgery Hx Coagulopathies (incl. medications) RF for Colorectal Ca Polyposis syndromes (FAP, HNPCC, juvenile polyposis) FHx PMHx polyps or CRCa Chronic UC or Crohn’s Diet poor in fruit and vegetables Smoking/alcohol Long term NSAIDs ``` O/E Vitals Abdo (conjunctival pallor, palmar pallor) PR (haemorrhoids, anal fissure, abscess, distal carcinoma or polyp) All patients >45 with new onset rectal bleeding must be investigated due to high risk of CR Ca Ix: Pathology FBC, UECs, coagulation studies, LFTs (metastatic disease) Bedside rigid sigmoidoscopy Visualised up to splenic flexure (75% of CR Ca) Note that most PR bleeding with CR Ca will be distal to descending colon Colonoscopy +/- biopsy Other: ? Upper GI endoscopy If CR CA suspected - CT colonography, abdominal CT

Answer 63

DDx: Microcytic Decreased intake (lack of red meat ingestion) Blood loss (CR Ca, haemorrhoids, IBD, menorrhagia, PUD) Decreased absorption (surgery, Crohn’s disease) Increased demand (puberty, pregnancy) Normocytic Increased reticulocytes i.e. Hyperproliferative Haemorrhage Haemolytic (thalassemia, sickle cell, autoimmune, infection, drugs) Decreased reticulocytes i.e. hypoproliferative Aplastic, leukaemia ``` Macrocytic Megaloblastic (hyper segmented neutrophils) B12 deficiency Folate deficiency Non-megalobalastic Alcohol Liver disease ``` ``` Hx: PC Source of bleeding? (GIT, bladder, menstural) Previous Hx Diet (iron, folate, B12) PMhx IBD, coeliac, GORD, malignancy Coagulopathy Surgical Hx (gastrectomy, bariatric) Medications NSAIDs, steroids Antiplatelet, anticoagulant Smoking, alcohol, drugs ``` O/E: Vitals Abdo (conjunctival pallor, SOB, mass, hepatomegaly etc.) PR ``` Ix: Pathology FBC RBC <130 in M OR <120 W Microcytic 🡪 iron studies Normocytic 🡪 reticulocytes Macrocytic 🡪 blood film + serum B12/folate Blood film/peripheral smear Cell morphology e.g. sickle cell Iron, B12, Folate UECs, LFTs Other: If occult blood – FOBT, colonoscopy If haemoptysis/melena – upper GI endoscopy If cause unclear – bone marrow biopsy (hypo proliferative normocytic anaemia) ```

Answer 64

``` DDx: IBS, IBD (especially UC) CR Ca Haemorrhoid, fissure, villous adenoma Bacterial infection Obstruction, colostomy ``` ``` Hx: PC Bowel habits – duration, frequency, Bristol stool chart Associated Sx – bleeding, abdo pain, n/v/a, weight loss, fever Sick contacts, recent travel Previous Hx PMHx Any DDx RF CR Ca Polyposis syndromes (FAP, HNPCC, juvenile polyposis) FHx PMHx polyps or CRCa Chronic UC or Crohn’s Diet poor in fruit and vegetables Smoking/alcohol Long term NSAIDs Previous Ix Medications Abx – Clostridium Difficile ``` O/E: Vitals Abdo + PR ``` Ix: Pathology FBC UECs Electrolyte disturbances from diarrhoea) – hypokalaemia, hyponatremia CRP, ESR Nutritional deficiencies (B12, vitamin D) Stool culture + MCS FOBT Consider: Rigid/flexible sigmoidoscopy Colonoscopy +/- biopsy Upper GI endoscopy +/- biopsy Barium studies (IBD) Contrast CT (localise extent, assess mural and extra mural involvement) ```

Answer 65

``` Epidemiology: CR Ca 2nd commonest tumour, most common GI malignancy Approx. 1/12 Australians M>F, Peak: 55-75y/o ``` ``` RF: Modifiable Diet (high red meat, low fibre (fruit/vegetables)) Obesity Physical inactivity Smoking Heavy ETOH Long term NSAIDs Non-modifiable Age >50 FHx 1# PMHx polyps or CRCa IBD Hereditary polyposis syndromes (FAP, HNPCC – lynch syndrome), juvenile polyposis) ```

Answer 66

``` Screening: Low Risk Asymptomatic, Nil FHx Method: FOBT Two stool samples on consecutive days to assess for blood 50-74y/o every 2 years 70% sensitivity (i.e. 30% false negatives) Moderate Risk 1# relative OR 2x2# relative Method: FOBT – 2yearly Colonoscopy – 5yearly or 10yrs before FHx diagnosis High Risk 3x1# relative, extensive premature adenomas Method: Refer to bowel cancer specialist ? Flexible sigmoidoscopy or colonoscopy 1-2yearly >25y/o or 5yrs before affected family member Genetic screening Symptomatic Colonoscopy not FOBT ```

Answer 67

``` Neoadjuvant: Definition: Treatment given prior to definitive surgery to shrink tumour making it more easily resectable Initiations: T3/T4 T1/T2 with nodal involvement Distal rectal tumour where APER is required Tumour that invades mesorectal fascia Benefits: Higher sphincter preservation Improved resectability Tumour regression Therapy: Conventional fractioned radiotherapy +/- chemotherapy (fluropyrimidine) Long course approx. 7-10wks All pts who receive neoadjuvant also require 4m of adjuvant chemotherapy ``` Definitive: Surgical resection +/- lymphadenectomy ``` Site of cancer Type of resection Anastomosis Caecal, ascending or proximal transverse colon Right hemicolectomy Ileo-colic Distal transverse, descending colon Left hemicolectomy Colo-colon Sigmoid colon High anterior resection Colo-rectal Upper rectum Anterior resection (TME) Colo-rectal Low rectum Anterior resection (Low TME) Colo-rectal (+/- Defunctioning stoma) Anal verge Abdomino-perineal excision of rectum None ``` ``` Palliative For unresectable metastases or tumours Method: Chemotherapy Obstructing tumours may be endoluminally stented with self-expanding metal stents or transanally ablated if rectal ```

Answer 68

Metastatic: Background Approx. 15-20% have metastasis at time of diagnosis Location Lymphatic spread Lower rectum – internal iliac Middle/upper rectum – pararectal, inferior mesenteric Descending/sigmoid colon – inferior mesenteric Transverse/ascending colon – superior mesenteric Haematogenous spread 70% Liver (via portal venous system) 35% Lungs (via venous spread) 21% Peritoneum Other: Bone, ovaries, kidneys, brain Distal extension Outer bowel wall direct contact – liver, greater curvature of stomach, duodenum, small bowel, pancreas, spleen, bladder Rectal cancer – bladder, prostate, vaginal wall, sacrum Staging Ix: Assessment of metastases (liver, lung or para-aortic) Thoracoabdominopelvic CT CT PEP scan to evaluate equivocal lesions Assessment of local extent Colonic – CT adequate Rectal – Pelvic MRI and TRUS Assessment of synchronous tumours Colonoscopy or barium enema to confirm no secondary tumour Tumour marker CEA not useful for diagnosis or staging but can indicate relapse if high at time of diagnosis and falls to normal after resection

Answer 69

``` Pathological staging: Dukes (approx. %5yr survival) A – confined to bowel wall only (90%) B – through bowel wall (70%) C – any with +ve lymph nodes (50%) D – any with metastases (<10%) TNM T1-4 – stages of invasion of bowel wall N0/1/2. No/up to 4/more than 4 lymph nodes involved M0/1, Metastases not present/present ``` ``` Confirming Metastases Imaging CT FDG-PET Biopsy FNA Laparoscopic needle biopsy ``` Regional Mx: Surgical resection (Approx. 50% 5YS) Eligibility discussed by MDT Patient factors – fitness for surgery, preference Cancer factors No extrahepatic metastasis No portal vein, hepatic artery or bile duct involvement Adequate hepatic function post resection (2/8 segments) Radiofrequency ablation (14-55% 5YS) Insertion of image guided probe percutaneously into tumour which emits high energy electrical currents effectively burning cancer If not eligible for surgery Selective internal radiation therapy (SIRT) Injection of tiny radioactive beads providing specific radiation to liver Trans-arterial chemoembolization Chemotherapy injected directly into liver vessels Based on principle that hepatic cancers preferentially receive blood supply from hepatic artery whilst normal parenchyma are supplied predominantly by the portal vein ``` Systemic Mx: Chemotherapy Neoadjuvant Transitions 10-15% of unresectable to resectable Adjuvant Post-surgery for 6m Palliative 10% 5YS, prolongs survival 5-20months Decrease symptoms of jaundice, pain, nausea, fatigue ```

Answer 70

Background: Process by which mutational activation of oncogenes and inactivation of tumour suppressor genes result in cancer. In CR Ca, this is the process in which benign polyps undergo dysplastic change to become malignant adenocarcinomas. Process takes approx. 5-10years ``` Pathophysiology: Pathway of mutation Chromosomal instability (85%) Microstallite instability (15%) Genes: Oncogenes: KRAS Tumour suppressor genes: APC and p53 Progression Normal mucosal cells of intestine continuously lost into lumen due to apoptosis and exfoliation, and continually replaced by proliferation at the crypt base. Subsequent to mutations it progresses from normal to low-grade dysplasia to high-grade dysplasia to carcinoma ``` CR Ca: Predominant type adenocarcinoma May occur as a polypod, ulcerating, stenosing, or infiltrative tumour mass Majority (75%) lie on left side of colon and rectum

Answer 71

Definition: Chronic immune-mediated inflammatory disorder that can affect any part of the GIT. Most commonly small/large bowel, particularly terminal ileum and right colon. Epidemiology: >incidence the further from the equator Peak 15-30y/o and 55-80y/o Idiopathic RF: Smoking Sx: RIF Abdo pain + diarrhoea (+/-blood/mucus) + weight loss Constitutional: malaise, fever, n/v/a Extra intestinal: conjunctivitis, iritis, gallstone formation O/E: Abdo Inspection: wasting, anaemia, red fat tongue, oral ulcers Palpation: tenderness, RIF mass (when omentum wraps around inflamed terminal ileum) PR: nodules, perianal fissures Ix: Diagnosis: Colonoscopy (most sensitive) + Biopsy Consider: Pathology FBC, ESR, CRP, Iron/B12 Decreased Hb and albumin (protein-losing enteropathy) Stool MCS + culture – exclude infection (e.g. C.Difficile) Antibody tests to distinguish from UC Imaging Abdo CT Assess strictures, disease location, wall thickening, complications Small bowel contrast study (barium enema or from duodenum via NG tube) Narrowing of lumen, fibrosis, nodularity, cobblestones, ulceration Gross Appearance: Scope Pink (preserved mucosa) between Yellow/white (ulcers) – “Skip lesions” Fissures extending from epithelium into muscle wall – “Cobblestone appearance”, abscess, fistula, strictures Transmural inflammation – thickened bowel wall Fat wrapping (fingers of mesenteric fat wrap around the bowel due to chronic inflammation) Histological Non-caseating granuloma (approx. 50% of biopsies) Lymphoid aggregates Transmural inflammation Submucosal oedema Fibrosis ``` Cx: Fissures Fibrosis – Strictures, bowel obstruction Fistulas Adhesions Perforation – Peritonitis ``` Fistula’s: Approx. 35% affected Commonly involve small bowel Mx: Regression with aggressive medical mx Resection of affected bowel segment + closure of other viscera Note: high risk of leak due to impaired healing process in CD ``` Perianal disease: Approx. 20% Involves fissures, abscesses and fistulas Presentation: Devastatingly painful Bleeding Mx: Fissures: Sitz baths, stool softeners, analgesics Abscess: incision and drainage under GA Fistula: Surgical Setons (rubber band threat through fistula to keep it open and allow drainage preventing infection) Fistulotomy Bowel resection Abx cover ``` Medical Mx: Anti-inflammatory agents 5-ASA (Sulfasalazine and Mesalazine) – first-line acute and long-term Corticosteroids (prednisolone, budesonide) – acute exacerbations Immunomodulators Azathioprine, 6-mercaptopurine Infliximab (anti-TNFalpha antibodies) Dietary modification Elemental diet to reduce inflammatory factors Liquid/low fibre diets if at risk of obstruction Supplemental calories, iron and vitamins ``` Surgical Mx: Approx. 50% end up with surgery Indications: Acute complications – fistula, obstruction, abscess, fulminant colitis, toxic megacolon Failure of medical therapy Cancer Growth retardation ```

Answer 72

A diverticulum is an outpouching of a hollow or fluid filled structure. Diverticular disease is defined as clinically significant and symptomatic diverticulosis due to diverticular bleeding, diverticulitis, segmental colitis associated with diverticula, or symptomatic uncomplicated diverticular disease. Diverticular disease is extremely common, affecting more than 50% of people over age of 70. Common sites affected: Potential defects can occur between longitudinal muscle bands (teniae coli) where mucosal vessels penetrate the wall from the outside • Sigmoid colon most commonly affected • Right sided diverticular- rare but often ddx for appendicitis • Isolate caecal diverticula - common in Western countries- susceptible to perforation The pathophysiology is likely related to functional hypersegmentation - lack of dietary fibre --> high intraluminal pressure -->mucosa herniate through muscle layers at weak points of intestinal wall. Aetiology: dietary fibre deficiency, obesity, red meat consumption, NAIDS, coffee and alcohol, steroids, decreased physical activity, altered colonic wall structure

Answer 73

Diverticulitis is the inflammation of a diverticulum. It be acute or chronic, uncomplicated or complicated. Jessica Redmond 81 Usually presents with continuous LIF pain, altered bowel habits, nausea and vomiting, flatulence and bloating, and is systemically unwell with fever, tachycardia leucocytosis in symptomatic acute diverticulitis. It can also present with sign of perforation (peritonism, distended tympanic abdomen, reduced/absent bowel sounds), and signs of fistula (PV discharge, UTI) CT is imaging of choice. Management involves bowel rest, antibiotics (amoxicillin, met, gent, tazocin) and surgical intervention for complications in particular such as perforation, fistula, abscess. Uncomplicated -bowel rest -abx (cipro + met) -high fibre diet -colonoscopy 6 weeks post to exclude colon cancer Complicated Empirical Abx - taz or ceftriaxone and met Mx complications - surgical - colonic resection etc.

Answer 74

The major complications of diverticulitis are: • Diverticular abscess o Pericolic abscess often presents with persistent pain and tenderness, swinging pyrexia, incomplete obstruction, or even sepsis o Dx made on CT o Abx if <4cm, or >4cm drained percutaneously under radiological guidance • Fistula o Can occure when inflammed diverticlum lies close to another hollow viscus o Vesicolic fistula = pneumaturia and severe UTI o Colo-ileal fistula = diarrhoea o Colovaginal - PV discharge o Surgical intervention • Bowel obstruction o May occur due to relative luminal narrowing from pericolonic inflammation or compression from abscess • Free perforation o Often from abscess • Segmental colitis • Acute PR haemorrhage although not common in diverticulitis as much as diverticulosis

Answer 75

Haemorrhoids are normal vascular structures in the anal canal, arising from a channel of arteriovenous connective tissues that drains into the superior and inferior haemorrhoidal veins. They can enlarge and thus become symptomatic. The cardinal features of haemorrhoidal disease include bleeding, anal pruritus, prolapse, and pain due to thrombosis. Constipation and pregnancy are the most common triggers for their development . Straining raises intra- abdominal pressure which obstructs venous return, causing venous plexuses to engorge, they are dragged distally by hard stool. Haemorrhoids are classified as either internal or external, or mixed. External haemorrhoids are distal to the dentate line in the anal canal and are covered by skin. Internal haemorrhoids are proximal to the dentate line, and are classified into 4 grades based on extent of prolapse. Classification of haemorrhoids: Grade I: never prolapse- protrusion limited within anal canal Grade II: prolapse during defecation and then return spontaneously Grade III: piles remain outside anal margin unless replaced digitally. Grade IV: irreducible and may strangulate Jessica Redmond 82 Symptoms and signs of haemorrhoids: • Attacks can last days-weeks, intermittent symptoms • May bleed from stool trauma during defecation • May prolapse and thrombose- acute severe pain • Atrophy- by thrombosis and fibrosis --> skin tags at anal margin • Strangulated haemorrhoids

Answer 76

Treatment is generally conservative, medical or surgical. Conservative: (all) • High fibre diet to reduce constipation • Squatting or feet up to reduce straining • Avoid straining and excessive time on toilet • Moist gentle wiping • Adequate fluid intake Medical: Creams, suppositories and topical preparations • Grade 1- hydrocortisone cream short term for pruritus and pain • Anaesthetics - benzocaine rectal ointment • Stool softeners to decrease straining • antispasmodics Surgical • Sclerotherapy - grade 2+ o Indication: First degree haemorrhoids that don’t regress with dietary, and secondary o Outpatient o Injection of sclerosing agent with proctoscope o Injected into submucosal tissue (NOT the haemorrhoid itself) fibrotic action rapidly obliterating the haemorrhoidal vessels. o Usually repeated on 2-3 occasional 4-6 weeks apart o not for people with nut allergy • Banding - grade 2+ o Cone around base of haemorrhoid to constrict the vessels o Uses anoscope o Ischaemic necrosis occurs distal o l to bands and they fall off • Haemorrhoidectomy (grade 4+, external) o Indications 3rd degree haemorrhoids o Mass excised with overlying skin and mucosa. Secondary intention healing o Stapled - sometimes for large

Answer 77

• Colectomy indications: o Patients with persistent symptoms o Chronic disabling symptoms of intractable diarrhoea, urgency, recurring anaemia, failure to maintain weight and nutrition o Children with failure to thrive o Patients with increased cancer risk o Patients with longstanding colitis o Patients with dysplastic or adenomatous polyps Most patients undergo a restorative proctocolectomy with ileal pouch anal anastomosis

Answer 78

* Intra-abdominal, retroperitoneal, abdominal wall abscess * Symptomatic fibrotic stricture causing intestinal obstruction * Enteric fistula * SB or CRC from longstanding Crohn's * Intractable disease

Answer 79

For emergency or urgent indications, a total abdominal colectomy with end ileostomy is typically performed. • Colectomy indications: o Toxic megacolon o Perforation o Major haemorrhage o Urgent rx for fulminant cases failing to respond to intensive medical management. The rectum is not resected but left as a defunctionalised Hartmann’s pouch with or without a mucus fistula. In patients who develop significant rectal bleeding after total abdominal colectomy, completion proctectomy with an ultralow Hartmann’s pouch or transanal suturing of the bleeding rectal ulcers can be performed to achieve haemostasis. After the patient is stabilized, a completion proctectomy with reconstruction can be performed at a later time.

Answer 80

The most likely diagnosis is a perianal abscess. Perianal abscess - originates from an infected anal crypt gland • Perianal abscesses transverse distally in the intersphincteric groove into the perianal skin where they present as a tender fluctuant mass • If undrained, a perianal abscess can expand into adjacent tissues (e.g. ischiorectal space, supralevator space) and progress to sepsis Epidemiology: mean age 40 years (but any age from 20-60), M:F = 2:1 Pathogenesis: A perianal abscess usually originates from an infected anal crypt gland– the glands penetrate the internal sphincter and end in the intersphincteric plane. An abscess develops when an anal crypt gland becomes obstructed permitting bacterial growth and abscess formation An anal fistula is a connection between two epithelial lined structures, and connects the anal abscess to the skin of the buttocks Clinical features: • Severe pain in anal/rectal area • Pain may be constant or associated with walking/sitting • Constitutional symptoms such as fever, malaise • Purulent discharge if abscess has started to drain spontaneously • Erythema, lump • May be no findings of inspection- abscess felt upon DRE Approximately half of anal abscesses will result in the development of a fistula from the inciting anal gland to the skin DDx: • Supralevator abscess, ischiorectal abscess, intersphincteric abscess • Anorectal fistula- epithelialsed track between the abscess and perirectal skin or an adjacent organ e.g. bladder ``` Jessica Redmond 84 • Internal haemorrhoid • Pilonidal abscess Ix: B –FBC, abscess culture if starting antibiotics, blood cultures if septic O –PR exam X – E S –CT if suspicious of nonpalpable abscess Mx: • Incision and drainage • Antibiotics -especially in valvular heart disease, immunosuppression, cellulits, diabetes ```

Answer 81

Perianal abscess • Most result from infection of the anal glands with colonic bacteria (cryptoglandular infections) o The anal canal has 6-14 glands that lie in the plane between the internal and external anal sphincters o Ducts from these glands pass through the internal sphincter and drain in to the anal crypts at the dentate line o This glands may become infected when the crypt is occluded by impacted faeces, oedema (from anal trauma e.g. passage of hard stool) or as a result of inflammation e.g. Crohns Aetiological factors/ risk factors: • Male (M:F = 2:1) • Crohn's disease (1/3 of patients) • Hard stools • Age 20-60 (mean 40)

Answer 82

Ulcerative Colitis is an inflammatory disorder of the mucosa and submucosa of the large bowel. It is characterised by recurrent acute exacerbations and intervening periods of quiescence or chronic low grade activity. Epidemiology • Typically a young adult with a history of several weeks of frequent loose stools, later streaked with blood and mucous. • Attack often starts with attack of gastroenteritis or traveller's diarrhoea that fails to settle Aetiology • Unclear Jessica Redmond 85 Pathophysiology • the disease always involves the rectum and extends proximally • Can processed to backwash colitis in pancolitis patients • Colonic mucosa becomes acutely inflamed --> neutrophil accumulation --> crypt abscesses • Sloughing of mucosa --> small superficial ulcers • Dysplastic changes occur over time --> prolonged or repeated episodes of inflammation can cause progression to adenocarcinoma o 5% after 10 years of colitis o Aggressive o On average occurs 20 years earlier than general population • Lead pipe colon - fibrosis from longstanding colitis causing smoothing of haustrations an shortening of colon Clinical Features • Acute attacks: o Loose blood stained stools streaked with mucous o Diarrhoea severity corresponds to extent of inflammation • May pass 20+ stools/day • Preceded by abdominal cramps o Fulminant colitis • Severe dehydration and electrolyte imbalances and blood loss • Subgroup of patients with severe ulcerative colitis who have more than 10 stools per day, continuous bleeding, abdominal pain, and distension, and acute, severe toxic symptoms including fever and anorexia. o Weight loss o Extra-colonic features tend to flare up in parallel with colitis, except liver-related ones. o Tenesmus • O/E o PR exam, proctoscopy and sigmoidoscopy Extra-colonic features: • Anaemia o Normochromic normocytic- typically chronic and non specific • Arthropathy o Sacroillitis/ankylosing spondylitis, enteropathic arthropathy • ~20% cases • Anterior uveitis o ~10% cases • Primary sclerosing cholangitis o Progressive fibrosis of intrahepatic biliary system --> cirrhosis, progressive liver failure, jaundice, death o Other liver presentations: chronic active hepatitis, bile duct carcinoma • Erythema nodosum or pyoderma gangrenosum (purulent skin ulcers) Complications: • Toxic megacolon o Colon dilates massively and patchy necrosis eventually occurs. The patient is systemically ill with high fever, marked tachycardia and dehydration. o Perforation and fatal peritonitis required emergency colectomy o Causes: • Inflammatory: UC, Crohn's • Infectious: bacterial (C diff, salmonella, shigella, campylobacter), parasitic, viral, pseudomembranous colitis The diagnosis of toxic megacolon should be considered in all patients presenting with abdominal distension and acute or chronic diarrhoea. The diagnosis is clinical, based upon the finding of an enlarged dilated colon on abdominal imaging accompanied by severe systemic toxicity. o Medical therapy is the first line of treatment for patients with IBD and toxic megacolon and includes fluid resuscitation and correction of laboratory abnormalities, administration of broad- spectrum antibiotics, intravenous corticosteroids, complete bowel rest, bowel decompression with a nasogastric or long intestinal tube, and a surgical consultation. o The operative procedure of choice is a subtotal colectomy with end-ileostomy and is reserved for patients who do not improve on medical management. Investigations • B: FBC, UEC, LFT, CRP, ESR o Raised inflammatory markers, anaemia, hypoalbuminemia • O: stool samples: MCS, OCP, C Diff • X: barium enema usually not in acute disease, AXR monitoring dilatation as a sign of toxic megacolon - likely do a CT tbh • E • S: proctoscopy, sigmoidoscopy, biopsy, colonoscopy in non acute setting Ddx • Crohn's disease • Radiation colitis • Infectious colitis • Diverticulitis • Ischaemic colitis • Vasculitis • IBS Management Management depends on the severity of an individual attack, amount of colon involved, extent of chronic symptoms and risks of long term complications. Medical • 5-ASA o Mild attacks of proctitis/procto-sigmoiditis treated with local 5-ASA suppositories or enemas o Mild attack of pan colitis with orals o Avoid aspirin and NSAIDs as exacerbate despite being related • Corticosteroids o Suppositories or enemas used for local rx of rectal inflammation o Short course high dose oral for severe exacerbations, IV if seriously ill • No evidence for bowel rest and TPN • Immunosupressives o Ciclosporin and azathioprine • settles on steroids but flares as weaned off steroids • Maintenance therapy recommended in all patients with left sided colitis, pancolitis, extensive colitis. • Supportive: o Avoid anti-diarrhoeals e.g. loperamide - precipitate toxic dilatation o High calorie and protein diet to counteract losses Surgical • Only needed in ~20% patients • Colectomy indications: o Urgent rx for fulminant cases failing to respond to intensive medical management o Acute cases which progress to toxic megacolon, perforation or major haemorrhage o Chronic disabling symptoms of intractable diarrhoea, urgency, recurring anaemia, failure to maintain weight and nutrition o Children with failure to thrive o Patients with longstanding colitis who develop dysplasia or malignancy • Total colectomy is curative • Three main options: o Subtotal colectomy with ileostomy • Safest in emergency situation in sick patient on high dose corticosteroids • Patient left with inflamed rectal stump • Can change to other option when patient is well o Proctocolectomy with permanent ileostomy • Includes removal of rectum • Generally recommended for elderly patients with sphincter preserving procedures are inadvisable o Restorative proctocolectom- ileoanal pouch • Sphincter preserving operation avoiding permanent ileostomy • Pouch from terminal ileum anastomosed into upper anal canal Health maintenance: • Immunisations o Live vaccines contraindicated in immunosuppressed people • Screening for cancer o CRC, skin, cervical - skin because therapies • Screening for anxiety and depression • Prevention and monitoring of bone loss o Increased risk, especially if on glucocorticoids • Lab monitoring of complications of IBD o Anaemia, b12 and folic acid deficiency • Medication side effect monitoring

Answer 83

If Polyp: Classified as: • Non-neoplastic o Hamartomatous – glandular epithelium supported by smooth muscle cells that is contiguous with the musularis mucosa – associated with Peutx-Jeghers syndrome o Serrated (neoplastic or non-neoplastic) o Submucosal (neoplastic or non-neoplastic) • Neoplastic – adenoma or carcinoma Management • Polypectomy during colonoscopy Surveillance • If only 1-2 adenomas ≤10mm on baseline colonoscopy = lower risk – follow-up colonoscopy in 5 years • If advanced adenomas (≥10mm, villous histology or high-grade dysplasia) or multiple adenomas (between 3-10) at baseline colonoscopy = higher risk – follow-up colonoscopy in 3 years • 3-6 month and 12 months if sessile and laterally spreading

Answer 84

?Likely Crohn's: ``` Abnormality • Cobblestoning • Linear ulcers • Granulomas • Stricture ``` ``` Likely histology: • Transmural inflammation- lymphoid aggregates • Granulomas - nonnectrotising • Cobblestoning • Linear ulcers/fissures • Skip lesions • Submucosal fibrosis ``` ``` Possible diagnoses: • Crohn's disease • Ulcerative Colitis with backwash ileitis if pancolitis • NSAID enteropathy • Vasculitis • Eosinophilic gastroenteritis • Sarcoidosis ```

Answer 85

CRC Initial treatment If the metastases are potentially resectable for cure, then an aggressive surgical approach is warranted for both the primary and metastatic sites with the aim of curing the patient. If there are five or more simultaneous, potentially resectable hepatic metastases (unless all are located in one lobe), bilobar involvement, or if disease is borderline resectable due to location, initial chemotherapy followed by reassessment and delayed resection is probably a better strategy than upfront surgery. There are two main options for this bowel lesion. Acute resection or stenting to decompress the bowel ``` Jessica Redmond 90 followed by resection if deemed appropriate for the patient at a later stage. I believe the best option is stenting. Stenting is largely palliative Major risks of approach: Risks of neoadjuvant chemo: -failure to work -toxicity -risk of becoming unfit for surgery - ``` ``` Risks of liver resection: • haemorrhage • Intra-abdominal sepsis • Liver failure • Bile leak • Liver steatosis • Mortality Risks of stenting: - perforation - failure to decompress - tumour ingrowth and re-obstruction - stent migration - bleeding - risks of anaesthetic -------- This patient's bowel obstruction needs to be managed. This 85 yo man may not be able to survive surgery, and metastases means most likely need palliative intervention. To manage the bowel obstruction: There are two main options for this bowel lesion. Acute resection or stenting to decompress the bowel followed by resection if deemed appropriate for the patient at a later stage. I believe the best option is stenting. Risks of stenting: - perforation - failure to decompress - tumour ingrowth and re-obstruction - stent migration - bleeding - risks of anaesthetic ``` --------- With integration of surgery and chemotherapy, long-term survival can be achieved in as many as 50 percent of cases. For patients with borderline resectable metastatic disease, downstaging with neoadjuvant chemotherapy may permit later successful resection. Even patients who are not candidates for a curative resection can benefit from surgical palliation for symptoms of obstruction and bleeding from the primary tumor. 4 rules for considering liver metastases resectable: 1) primary cancer is resectable, Jessica Redmond 91 2) no extra-hepatic metastases, 3) at least 2 of 8 liver segments will remain preserving adequate hepatic function, 4) no involvement of major structures (portal vein, hepatic artery) There is the possibility of neoadjuvant chemotherapy to allow for stage resection of liver metastases, however, it is likely that if there is not enough preserved hepatic function from resection, than this would not be possible, and definitely not curative. On the other hand, if there are five or more simultaneous potentially resectable hepatic metastases (unless all are located in one lobe), bilobar involvement, or if disease is borderline resectable due to location, initial chemotherapy followed by reassessment and delayed resection is probably a better strategy. As such, the focus would be on palliative control as opposed to curative control. Although this decision likely needs to be made post-neoadjuvant chemotherapy If 2 stage metastases resection: There are two main options for this bowel lesion. Acute resection or stenting to decompress the bowel followed by resection if deemed appropriate for the patient at a later stage. I believe the best option is stenting. Can do palliation

Answer 86

``` ?volvulus Initial treatment of large bowel obstruction • Flexible sigmoidoscopy to detorse twisted segment • Rectal tube Prevent recurrence: • Endoscopic detorsion If acutely unwell: • O2 • IV fluids • Blood transfusions if anaemic • NG decompression • Pre-operative Abx • If perf- laporatomy ``` Volvulus? – Mx: Endoscopic decompression of sigmoid volvulus followed by elective resection for sigmoid volvulus because of high rate or recurrence (up to 50%) with endoscopic decompression alone • Urgent intervention needed due to risk of perf • Rectal tube in situ for 24 hours with repeat AXR • Endoscopic detorsion • ?resection of sigmoid to prevent recurrence • the literature indicates that sigmoid resection, done either as a Hartmann's procedure when a gangrenous colon is discovered at laparotomy or as a one-stage resection with primary anastomosis in the setting of a viable colon, has the lowest rate of recurrence Colorectal tumour? – Mx: Stenting • May be ‘bridge to surgery’ i.e. provide time to correct fluid and electrolyte balance prior to operation or be palliative

Answer 87

Parastomal Hernia Most frequent complication - 50% pts Type of incisional hernia. Stoma creation introduces an abdominal wall defect, the trephine, for which no healing is expected. A parastomal hernia forms as the trephine is continually stretched by the forces tangential to its circumference. Mx: Asymptomatic: conservative management Prosthetic mesh repair for acute obstruction or elective repair Mucocutaneous separation Separation of stoma from peristomal skin. Leakage and skin irritation. Mx: Surgery Stomal Necrosis Early post operative period- venous congestion or arterial insufficiency from tight fascial opening. Mx: Surgery Dermatitis Exposure to damaging effluent can produce severe skin breakdown in the area exposed to the drainage; this type of skin damage is characterized by severely denuded skin along the inferior aspect of the stoma and is most common among ileostomy patients and patients with problematic stomas. Mx: Steroids Stomal retraction Stomal retraction is defined as a stoma that is 0.5 cm or more below the skin surface within six weeks of construction, typically as a result of tension on the stoma. Mx: Use of a convex pouching system and the use of a belt or binder. If these measures fail to provide a secure pouch seal, surgical revision may be needed. Stomal Prolapse Prolapse is the telescoping of the intestine out from the stoma and can occur with any type of stoma. Large abdominal trephine, increased intraabdominal pressure, and a redundant loop of bowel proximal to the stoma. Mx: Mannaged conservatively with cool compress and/or application of an osmotic agent (eg, table sugar or honey) to reduce edema, followed by manual reduction of the prolapse and application of a binder with a prolapse over-belt to keep the bowel recued into the abdomen, or by pouching modifications to accommodate the prolapsed bowel when reduction cannot be established or maintained.

Answer 88

?polyp - polypectomy Histology- adenoma, adenocarcinoma ?adenoma – by definition histology is dysplasia • Most colorectal cancers are caused by adenomas but only 5% of adenomas progress to cancer • Development of adenoma to cancer usually takes 7-10 years • Advanced adenoma is any adenoma with high-grade dysplasia, size >10mm, an adenoma with a villous component • Adenomas can be classified as tubular, villous or tubulovillous • Mx: Polypectomy via snare excision

Answer 89

Anal cancer The lesions is likely a squamous cell carcinoma Staging consists of biopsy of the primary tumour, CT chest abdomen and pelvis and PET scans. Chemoradiotherapy is the first line treatment, with radiation therapy administered to the sites of the primary disease and lymphatic spread, usually with prophylactic irradiation of clinically negative groins. Local excision is an option for patients with T1 tumours less than 1 cm in size with followup prophylactic chemoradiotherapy. Surgery also has a place in recurrent or persistent disease after chemoradiotherapy. Although prognosis is poor abdominoperineal resection offers the potential for long term survival. NB- tumours above the dentate line, similar to rectal cancers, drain to the mesorectal and internal iliac nodes whereas tumours below the dentate line may also spread to the superficial inguinal and external iliac nodes. Note: May also be a fistula. Initial management is surgery, and the mainstay of treatment is a fistulotomy.

Answer 90

Prolapsed internal haemorrhoid. Management: Medical Grade 1 hydrocortisone cream short term for pruritis and pain Anaesthetics- benzocaine rectal ointment Stool softeners to decrease straining Antispasmodics Surgical: Sclerotherapy- injection into the submucosal tissue of sclerosing agent with proctoscope to obliterate the haemorrhoidal vessels Banding- Cone around the base of the haemorrhoids to constrict the vessels Haemorrhoidectomy- Indications include 3rd degree haemorrhoids. The mass is excised with the overlying skin and mucosa, followed by secondary intention healing or staples for larger haemorrhoids. NB- external haemorrhoids are painful whereas internal haemorrhoids are not painful

Answer 91

Q1: What is the common presentation of this problem? Constant and severe perianal pain and local tenderness Q2: What is the first line of management? Surgical incision and drainage Q3: What bacteria are usually cultured? Staphylococcus or E.coli Q4: What is the usual cause of this? Usually begin as acute purulent infections of the anal glands in intersphincteric spaces and obstruct the ducts. Obstruction- constipation, trauma or inflammation (Crohn’s disease or UC)

Answer 92

1. What are the complications of this procedure? Bleeding- 2-11% Perforation Failure to completely resect polyp 2. What is the likely Pathology here? Adenoma 3. What would normally occur if there is found to be a tiny focus of completely excised, well differentiated invasive cancer in the specimen that is far from the resection line? Frequent surveillance. If advanced adenomas (>1cm or high grade dysplasia) or multiple adenomas (between 3 and 10) at baseline colonoscopy = high risk = colonoscopy in 3 years. 12 month if sessile and laterally spreading

Answer 93

``` Q1. What does this show? ?haemorrhoids Anal rectal carcinoma Fissure polyp Anal cancers ``` Q2. How do these present clinically? Haematochezia (45% of patients), anal pain, sensation of an anal mass, pruritis, anal discharge, on DRE they may have a localised firm or hard ulcer/ growth with an irregular surface and edge, possibly surrounded by woody induration. Q3. How are they treated? The lesion is confirmed by biopsy 1. Chemoradiotherapy 2. Abdominoperineal resection

Answer 94

Q1. What are the lesions you can see in the perianal area? Anogenital warts/ perianal warts/ condylomata acuminata Other causes: - Faecal soilage - Herpes - Mucous leakage - Diarrhoea - Haemorrhoids - Skin disorders - contact dermatitis from soaps, shower gel, cream, talc etc - Fungal infections (candida) - Genital warts: - > Chlamydia trachomatis, syphillis, gonorrhoea Q2. What is the responsible agent that causes this condition? HPV. Types 6 and 11 are normally the causative agents of anal warts. Transmitted sexually. Q3. What treatments are available? All patients should be offered treatment although although warts may resolve. Topical agents- podophyllin (anti-mitotic) Trichloracetic acid (caustic causing chemical coagulation of protein) Immunomodulators such as imiquimod Cryotherapy Surgical excision under local or general anaesthetic (only practical option when large numbers are present). Care must be taken to prevent the complication of anal stenosis.

Answer 95

The assessment of a neck lump requires a thorough history, examination and further investigations: History Characteristics of the mass- duration, growth pattern, absence or presence of pain. Masses that are present for years with little changes are more likely to be benign neoplasms (e.g benign salivary gland tumours, schwannomas or paragangliomas) Rapidly expanding masses raise concern for infectious processes or rapidly growing lymphomas. Masses that fluctuate over time and increase with viral illness are often congenital cysts. Symptoms- pain, voice change, hoarseness, dysphagia and otalgia. Pain is often associated with rapid growth but can also be related to direct neural invasion in the setting of certain malignancies. Voice change, hoarseness, dysphagia and otalgia may indicate cervical lymph node metastasis from an underlying aerodigestive malignancy. Presence of fever, night sweats, or weight loss- suspicious of lymphoma. Tobacco, alcohol and drug use HIV status Occupational exposures Recent travel history Examination: Mass location Pre auricular and angle of jaw- likely related to the parotid gland. Posterior triangle- high index of suspicion for malignancy Supraclavicular masses- metastasis from below the neck, especially the lungs and GIT Characteristics of the mass- size, shape, consistency, tenderness, mobility and colour Discrete, firm, mobile or rubbery but not rock hard masses are usually lymph nodes Rock hard masses that are fixed are likely malignancy Soft ballotable masses are usually congenital cysts A firm lateral neck mass that moves side to side but not up and down indicates involvement with the carotid sheath such as a carotid body tumour or schwannoma. Pulsatile mass or bruit suggests a vascular lesion An immobile midline neck mass that elevates with swallowing indicates a thyroid source ``` Cranial nerve exam Abdominal exam GIT exam Investigations FBC, ESR/CRP, EBV serology when adenopathy is diffuse, HIV serology in at risk patients Ultrasound CT MRI? PET? FNA or core biopsy in suspicious lesions Consider excision biopsy ``` NB- A neck mass in an adult over the age of 40 should be considered neoplastic and potentially malignant until proven otherwise.

Answer 96

There are 5 main types of thyroid cancer: 1. Papillary thyroid cancer- Papillary thyroid cancer is the most common type of thyroid cancer. It develops from follicular cells and usually grows slowly. Papillary thyroid cancers can often spread to the lymph nodes. They are usually curable. 2. Follicular thyroid cancer- develop from follicular cells and usually grow slowly. They rarely spread to the lymph nodes. They are usually curable. 3. Hurthle cell cancers- Arise from the Hurthle cells, a specific type of follicular cell, and are more likely to spread to the lymph nodes than other follicular thyroid cancers. 4. Medullary thyroid cancer- develop in the C cells. Medullary thyroid cancers can be controlled if diagnosed before lymphatic spread occurs. Medullary thyroid cancers are genetic in 25% of cases. 5. Anaplastic thyroid cancers- This type is rare, accounting for about 1% of thyroid cancer. It is fast growing, poorly differentiated thyroid cancer. As anaplastic thyroid cancers are so fast growing they have a poor prognosis.

Answer 97

Thionamides (carbimazole and propylthiouracil) are used in patients with thyrotoxicosis and a goitre due to Grave’s disease. Patients with multinodular goitre will also respond to thionamide medication, but definitive treatment with surgery is generally preferred. Radioactive iodine is another option and reduces goitre size by about 50% in the majority of patients over 6-12 months. It can be used in patients with toxic adenoma. However radioactive iodine carries a significant risk of causing hypothyroidism over time and so patients require annual TSH follow up. Surgery is appropriate for patients who have troubling compressive symptoms or who fail to respond to medical management. Surgical treatment is with a thyroidectomy, which involves partial or total removal of the thyroid gland.

Answer 98

Supernumerary nipple?- commonly arise along the two vertical milk lines that originate in the axilla, descend through the region where nipples are typically situated and terminate at the groin. NB may also be a melanocytic naevi Q2. What is it's significance Supernumerary nipples are typically asymptomatic however may enlarge during puberty, swell and become premenstrually tender and undergo lactation. Supernumerary nipples can also undergo similar disease to normal breast tissue including fibroadenoma, adenoma, cyst, abscess, mastitis and breast cancer. Q3. What treatment is needed? Usually no treatment is required. Surgical removal can be considered for cosmetic purposes or if there is discomfort from lactation or tenderness.

Answer 99

- Femoral hernia that has become incarcerated and strangulated and causing a small bowel obstruction. - Inguinal hernia - Lymphadenopathy - Spigelian hernia (a hernia through the spigelian fascia, which is the aponeurotic layer between the rectus abdominus muscle medially and the semilunar line laterally) Q2. What is the most likely diagnosis here? Incarcerated femoral hernia causing a mechanical bowel obstruction. Q3. What is the most appropriate treatment strategy? Resuscitation and urgent surgery to resect and infarcted bowel and mesh repair the abnormality that lead to the hernia.

Answer 100

Q1. What is the most likely diagnosis? Lipoma- benign neoplasm of adipose tissue Differential diagnosis- epidermoid/ sebaceous cyst (has a punctum), liposarcoma, abscess, malignancy. Q2. What tests other than physical examination are likely to be helpful? Ultrasound- diagnostic MRI- a lipoma will appear as homogenous and superficial. MRI is normally done to rule out differentials such as liposarcoma. Biopsy- shows histopathological features of a lipoma. Q3. What are the common complications of operative removal of this? Operative removal of lipoma is needed if there is pain, for cosmetic reasons or if there is concerns over diagnosis. Complications of surgery include scarring, seroma (pocket of clear serous fluid), haematoma, wound infection, nerve injury

Answer 101

Q1. What does this show? Likely shows a hernia Q2. What does the surgical registrar do the minute he sees this scan? The surgical registrar should attempt to reduce the hernia Q3. What does he find? What is the treatment? It is most likely irreducible. Therefore treatment should be as per SBO and hernia repair. ``` Initial: Primary survey and fluid resuscitation Correct electrolyte imbalances NG tube decompression of GI tract Pain management Preoperative antibiotics FBC, UEC, group and hold, coags ``` Definitive: Surgical repair

Answer 102

The massive transfusion protocol is a protocol used in critically bleeding patients anticipated to require a massive transfusion in order to maintain adequate tissue perfusion and oxygenation, A massive transfusion is defined as a replacement of the entire blood volume in 24 hours or 50% of the blood volume in 4 hours. The massive transfusion protocol should be activated for patients with any of the following: - Actual or anticipated transfusion of 4 units of red blood cells in less than 4 hours + haemodynamically unstable + anticipated ongoing bleeding. - Severe thoracic, abdominal, pelvic or multiple long bone trauma. - Major obstetric, gastrointestinal or surgical bleeding

Answer 103

``` Q1 Adhesions Hernia Crohns disease Malignancy- adenocarcinoma Volvulus Benign mass- adenoma, lipoma Intra-abdominal abscess ``` Q2 Primary survey and appropriate resuscitation AXR and erect CXR Surgical consult- urgent if potentially strangulated bowel or very dilated as there is a risk of perforation and peritonitis. Correct electrolyte abnormalities and losses from vomiting. Decompression with an NG tube since the patient is vomiting. Pain management

Answer 104

Q1) Gallbladder + cholecystectomy Q2) Symptoms of cholecystitis Clinically it presents as prolonged (>4 hours) severe RUQ pain that may radiate to the right shoulder or back with fever, abdominal guarding, tachycardia, nausea and vomiting, anorexia and a positive Murphy’s sign. Q3) Management is with analgesia, IV fluids, NBM, broad spectrum antibiotics (not required in simple biliary colic) and a laprascopic cholecystectomy in the same admission.

Answer 105

Causes of abdominal pain are best categorised based on location, by dividing the abdomen into 9 anatomical location. Pain in each location has common causes. Can also mention Surgical sieve: VINDICATE or VITAMIN CDEF

Answer 106

The appendix is a blind-ending tube arising from the caecum at the meeting point of three taeniae coli, just distal to the ileocaecal junction. The appendix base thus lies in the right iliac fossa close to Mcburney’s point (two thirds of the way along a line from the umbilicus to the ASIS). Apart from the true retrocaecal appendix (appendix lies retroperitoneally posterior to the caecum) the organ probably floats in a broad arc about its base. In about 30% of cases it lies over the pelvic brim. It is Retrocaecal and pelvic.

Answer 107

Although several studies have shown that uncomplicated appendicitis can be treated with antibiotics alone there is not enough evidence to currently recommend that approach. Therefore antibiotic therapy should only be started once the surgeon has decided to operate. Ideally the antibiotics should be given 1-2 hours before the surgery commences however in practice they are usually given in the operating theatre. For uncomplicated appendicitis (appendicitis without localised ischaemia, perforation and the development of appendiceal abscess or generalised peritonitis) antibiotics may be discontinued post operatively. For complicated cases antibiotic treatment should be continued for at least 5 days post op. Antibiotic choice is usually with triple therapy (ampicillin + gentamicin + metronidazole)

Answer 108

Ectopic pregnancy- presents with missed menstrual period, right lower quadrant pain or pelvic pain, generally with some degree of vaginal bleeding or spotting. Cervical motion tenderness may be present on pelvic exam. Investigations include beta HCG hormone levels, which will be raised in the urine and blood and ultrasound which will reveal a mass in the fallopian tubes. Ovarian torsion- Presents with right lower quadrant pain and may present with a mass in the right lower quadrant. Investigation is with ultrasound, which will show an ovarian cyst and decreased blood flow/ ischaemia. Pelvic inflammatory disease- Occurs when bacteria from the vagina spread to the cervix or uterus. Presents with bilateral lower quadrant tenderness, usually within 5 days of the last menstrual cycle with purulent discharge from the cervical os. Investigation is with an endocervical swab which may show chlamydia trachomatis. Ruptured Graafian follicle- occurs mid menstrual cycle (12-16 days post menstruation) and causes a brief period of lower abdominal pain not usually associated with nausea, vomiting or fever. The tenderness is usually diffuse. - Pyelonephritis/ cystitis- UTI - Right sided ureteric stones - Pancreatitis - Cholecystitis - Crohn’s disease - Mesenteric adenitis - Gastroenteritis - Meckel’s diverticulum

Answer 109

ABCDE: History: Socrates of pain Nausea and vomiting (75% of patients with acute appendicitis) Anorexia (almost always associated with appendicitis) Migration of pain from periumbilical to RIF Changes in bowel habits (uncommon with acute appendicitis) Recent cold/ flu like symptoms (mesenteric adenitis) Sexual activity (STI and ectopic pregnancy) Menstrual history Ongoing GIT issues such as IBD Active or past malignancy Past appendectomy ``` Examination: Vital signs Abdominal exam including signs of peritonism, McBurney’s sign (tenderness and rebound tenderness at McBurney’s point [1/3 of the way from the ASIS to the umbilicus on the right side]), Rovsing sign (pain in RLQ after compressing LLQ), psoas sign (pain on flexion of the right leg) Reduced bowel sounds Pelvic examination ``` ``` Investigations: FBC, UEC, bHCG, CRP Urine MCS and dipstick Erect CXR if considering bowel perforation ? abdo/pelvis USS ``` This information can then be used to assess the Alvarado score for appendicitis. ``` Initial management for an appendicitis; NBM IV fluids Analgesia Monitor vital signs Antibiotics according to local protocols if the decision to operate is made Call surgical registrar ```

Answer 110

Imaging is not essential for the diagnosis of appendicitis, the diagnosis is made clinically. Imaging is indicated when the diagnosis of appendicitis is unclear and the patient isn't too unwell such that delaying surgery may lead to perforation. An abdominal and pelvic ultrasound scan is performed mostly in female patients when the history is unclear and clinical findings are equivocal. In obese patients the use is limited due to body habitus. CT abdomen and pelvis may have some place in imaging in acute appendicitis. However CT should not be used in younger populations due to the radiation exposure or in female patients who may be pregnant. It is more classically used in older patients who present with a possible appendicitis as the incidence is lower in this population and common differentials, such as cancer, are potentially more life threatening.

Answer 111

Acute appendicitis classically begins with poorly localised, colicky central abdominal visceral pain, lasting a few hours. This results from smooth muscle spasm and stretching as a reaction to appendiceal obstruction. The pain is poorly localised due to the relatively small number of nociceptors. The pain also travels along non-myelinated C-fibres, which are slow conducting and cause a dull, poorly localised pain. As inflammation advances over the ensuing 12-24 hours it progresses through the appendiceal wall to involve the parietal peritoneum, which is innervated somatically by a larger number of nociceptors containing a-delta fibres. Consequently the pain typically becomes localised to the right iliac fossa. NB- Non myelinated C fibres run with autonomic nerves and terminate in the superficial dorsal horn, transmitting signals to the brain through the dorsal column to the limbic area. A-delta fibres run in somatic nerves, terminate in the deeper dorsal horn and transmit signals up the faster spinothalamic spinal tract, which terminates in the thalamus and cortex.

Answer 112

The indications for laprascopic approach to appendicectomy are: Patients who are clearly unwell and in need of a diagnosis if unclear. Women of menstruating age to allow for visualisation of other organs. Children. Obese patients to reduce the risk of wound infection from a large incision. ``` Advantages Diagnostic as well as therapeutic Quicker return to work post op Less post op pain Fewer adhesions Better cosmetically Fewer wound infections Technical ease in obese patients Ability to visualise other organs- particularly pelvic organs ``` ``` Disadvantages: Higher rate of intra-abdominal abscess Longer operative time Higher operative costs Technically more demanding on the surgeon ```

Answer 113

Acute appendicitis classically begins with poorly localised, colicky central abdominal visceral pain, generally lasting less than 72 hours. Anorexia, nausea and vomiting (1-3 episodes of vomiting) and pyrexia (fever of less than 38˚C) often occur at this stage. As inflammation advances it progresses through the appendiceal wall to involve the parietal peritoneum. The pain typically becomes localised to the right iliac fossa. Signs of local peritonitis can be elicited such as tenderness, guarding and rebound tenderness. Specifically, McBurney’s sign (pain and guarding on palpation of McBurney’s point), Rovsing sign (pain elicited in the right lower quadrant in response to palpation of the left lower quadrant), Obturator sign (internal rotation of flexed right thigh causes pain in RLQ) and Psoas sign may be present. This classic picture is seen in less than half of all cases, largely because localising symptoms and signs vary with anatomical relations of the inflamed appendix and the vigour of the bodies defences. NB: If the inflamed appendix lies in the pelvis near the rectum it may cause local irritation and diarrhoea. If it lies near the bladder or ureter inflammation may cause urinary frequency, dysuria and pyuria (the presence of pus in the urine). An inflamed retrocaecal appendix produces none of the usual localising symptoms or signs but may irritate the psoas major muscle causing involuntary hip flexion and pain on extension. A high retrocaecal appendix may cause pain and tenderness below the right costal margin. An inflamed appendix near the fallopian tubes causes pelvic pain suggestive of an acute gynaecological disorder. If left untreated the inflamed appendix may become gangrenous (tissue death due to loss of blood supply) after 12-24 hours and perforate, causing peritonitis unless sealed off by the omentum. The whole abdomen becomes rigid and tender and there is marked systemic toxicity.

Answer 114

A sentinel lymph node is defined as the first lymph node to which cancer cells are most likely to spread from a primary tumour. In breast cancer the lymphatic drainage is generally to the axillae (can be internal mammary and supraclavicular nodal groups). Lymphatic spread nearly always follows a predictable pattern with a sentinel node the first to be affected, so the standard diagnostic procedure is a sentinel lymph node biopsy. The operation is performed after a diagnosis of breast cancer is made. The node is identified using a radioactive isotope bound to albumin, injected next to the tumour 12 hours before surgery and a blue dye injected into the periareolar area at the start of the surgery. Radioactivity is detected at surgery and the visibly blue nodes are excised and examined. If the nodes are positive an axillary lymph node clearance can be completed and is the standard approach for ned []? positive patients. NB inflammatory breast cancer is a contraindication to sentinel lymph node biopsy

Answer 115

A hernia is a protrusion, bulge or projection of an organ through the body wall that normally contains it, such as the abdominal wall. They are typically classified by aetiology and location. Hernias can be reducible (contents of the sac returns spontaneously or with manual pressure), irreducible (contents can not be returned with manual pressure) or strangulated (blood supply to the contents of the hernia is compromised causing significant pain). Some examples of hernias include inguinal (direct and indirect), femoral, epigastric and umbilical.

Answer 116

In terms of the anatomical difference between inguinal and femoral hernias it is important to note that inguinal hernias can be direct or indirect. Inguinal and femoral hernias are both considered to be groin hernias. The inguinal hernias occur in the inguinal canal superior to the inguinal ligament whereas femoral hernias occur in the femoral canal, inferior to the inguinal ligament. * Indirect inguinal- These are the most common type of hernia in males and females (5x more common than direct) and are 7x more common in males (due to persistence of the processes vaginalis in the testicular descent). They are usually congenital abnormalities where abdominal contents, such as mesenteric fat, small bowel loops or mobile colon segments, protrude through the internal inguinal ring, follow anterior to the spermatic chord in males, and exit through the external inguinal ring into the scrotum in males and into the labia majorus in females. * Direct inguinal- Occur through Hesselbach’s triangle (protruding through transversals fascia on the posterior wall of the inguinal canal) which is formed by: - Inguinal ligament inferiorly - Inferior epigastric vessels laterally - Rectus abdominus medially * Direct hernias occur as a result of weakness in the floor of the inguinal canal, often due to connective tissue abnormalities or acquired causes of increased intra abdominal pressure (COPD, bladder outflow obstruction, chronic constipation. They are more common in men over 50 and often occur bilaterally * Femoral hernias develop in the empty space of the femoral canal in the medial aspect of the femoral triangle, entering through the femoral ring, inferior to the inguinal ligament. They are more common in women due to wider bony pelvis’ and are more likely to strangulate as the borders are tough and not easily extendible. They will also cause compression of the femoral vein. The femoral canal (the opening of which is the femoral ring where the femoral hernias protrude through) has four borders: - Medial border- lacunar ligament - Lateral border- femoral vein - Anterior border- inguinal ligament - Posterior border- pectineal ligament, superior ramus of the pubic bone and the pectineus muscle

Answer 117

The key is the position of the hernia in relation to the inguinal ligament. Inguinal hernias are above the inguinal ligament whereas femoral hernias are below the inguinal ligament. Initially in the exam the patient is standing and the groin/labia majora is checked for the hernia. The patient is then asked to cough or valsalva with the hand over the bulge. An inguinal hernia is above the inguinal ligament, is likely reducible, is better felt on cough, often descends laterally and above the pubic tubercle and is more likely indirect if it is in the scrotum or labia majora. When placing a finger over the pubic tubercle hernias felt against the side of the finer are likely direct and hernias felt against the tip of the finger are likely indirect. A femoral hernia is below the inguinal ligament and medial to the femoral artery, is rarely reducible and is likely strangulated.

Answer 118

It is important to decide whether a hernia is inguinal or femoral because the approach to management is different for each. Watchful waiting may be an option for asymptomatic or minimally symptomatic inguinal hernias, but this is not recommended in femoral hernias as they are more likely to strangulate. The surgical options for hernia repair include either an open repair or laprascopic repair with stitching of the protrusion point and placing of a mesh. In a femoral hernia the approach may be from above (doesn't interfere with inguinal structures) or below (the usual approach as compromised bowel can be resected) the inguinal ligament.

Answer 119

An incarcerated/ irreducible hernia is entrapped. The hernia is trapped in the hernial sac and hence can not be reduced back into the abdominal wall In a strangulated hernia the blood supply to the contents of the hernia have ceased due to compression of the hernial orifice. Initially, lymphatic and venous channels are obstructed thus there is oedema and venous congestion, and if arterial pressure and tissue pressure are equal arterial flow ceases and tissue necrosis ensues due to ischaemia. When bowel is involved the patient could present with peritonitis, and will be in severe pain. NB- Femoral hernias are more likely to strangulate as the surrounding structures are not as extensible as in an inguinal hernia.

Answer 120

The most likely diagnosis is a mechanical bowel obstruction secondary to a strangulated groin hernia, likely femoral due to the age, gender and strangulation. This is a surgical emergency and the patient requires immediate work up for theatre: ABCDE IV access and consider fluid resuscitation if the patient is hypotensive Catheterisation FBC, UEC, group and hold, coags, lactate NBM Perioperative antibiotics Analgesia Contact general surg consultant/ registrar for consultation and definitive treatment Surgical repair of the hernia by either a laprascopic or open approach.

Answer 121

Lower GI bleeding refers to blood loss of recent onset originating from a site distal to the suspensory ligament of Treitz (connects to both the third an fourth parts of the duodenum, as well as the duodenojejunal flexure). The causes of lower GI bleeding may be grouped into several categories including: - Anatomical- diverticulosis - Vascular- angiodysplasia (small vascular malformation of the gut), haemorrhoids, ischaemia - Inflammatory- Inflammatory bowel disease, radiation colitis, other colitis (infectious, antibiotic associated, ischaemic, colitis of unclear etiology) - Neoplastic- polyp or cancer - Other- Anal fissures, rectal ulcers, postpolypectomy (removal of polyps)

Answer 122

Signs and symptoms include: Haematochezia (passage of maroon or bright red blood or blood clots per rectum). In general anatomic and vascular causes of bleeding present with painless, large volume blood loss Rarely melena in a right sided lower GI bleed. Abdominal pain- may be caused by IBD, ischaemia and colitis Rectal pain- anal fissures Constipation/ diarrhoea- colitis and IBD Weight loss- IBD, cancer Anaemia- more common with occult blood loss and may lead to dyspnea, palpitations, fatigue, conjunctival pallor Signs of haemodynamic instability in severe bleeds- tachypnoea, tachycardia, hypotension

Answer 123

Initially ABCDE should be performed with particular interest in circulation. Haemodynamic status should be initially assessed with intravascular volume resuscitation started as needed. Upper GI bleed should be excluded with upper endoscopy Colonoscopy should be the initial investigation and should be performed within 24 hours of patient presentation after adequate bowel preparation. Endoscopic haemostasis therapy should be provided to all patients with high risk stigmata of bleeding including active bleeding, non bleeding visible vessels or adherent clot. Endoscopic haemostasis therapy involves mechanical, thermal, injection of adrenaline or a combination and is most often guided by the aetiology of bleeding. Radiologic interventions (tagged red blood cell scintigraphy [technetium], CT angiogram and angiography) should be considered in high risk patients with ongoing bleeding who do not respond adequately to fluid resuscitation and who are unlikely to tolerate bowel preparation for colonoscopy. In a patient who is acutely unstable surgical intervention with a laparotomy may be required and can also be used when other means of controlling an established source of bleeding have failed. For an unidentified source of bleeding a subtotal colectomy (removal of the entire colon) and ileostomy may be necessary Specific management may be necessary depending on the cause of the LGI bleed. Acute colitis can be managed with antibiotics if there is an infectious source or hydrocortisone if the source is IBD. 90% of diverticulosis bleeding will resolve spontaneously, however 10% will require a blood transfusion.

Answer 124

A Meckel’s diverticulum is a true diverticulum, meaning it contains all layers of the small bowel wall (mucosa, submucosa, muscular layer and serosa), found in the small bowel and particularly the middle to distal ileum. It is the most common congenital abnormality of the GI tract, resulting from the incomplete obliteration of the vitelline duct during the fifth week of foetal development. Patients are often asymptomatic and majority of symptomatic patients present before the age of 2. Signs and symptoms include GI bleeding, obstruction and Meckel’s diverticulitis (clinically indistinguishable from appendicitis). The rule of twos is the classic description of the essential features: Occurs in about 2% of the population Male to female ratio of 1:2 Is about two feet (60cm) above the ileocaecal valve Is about two inches long 2 types of heterotopic mucosa- gastric and pancreatic Approximately 2% of the population develop a complication over their lifetime (typically before the age of 2)

Answer 125

Meckel’s diverticulum are often clinically silent, however they can present as abdominal pain, symptoms of GI bleeding and bowel obstruction GI bleeding: - Most common presentation in children - GI bleeding is caused by ulceration of the small bowel due to acid secretion by ectopic gastric mucosa within the diverticulum. - This usually occurs distal to the diverticulum such as in the perianal region. Obstruction - Intussusception (a process in which a segment of intestine invaginate into the adjoining intestinal lumen) - Volvulus (the small bowel twists around its mesentery) - Torsion of the diverticulum - Littre hernia (protrusion of a Meckels diverticulum through the abdominal wall) - Meckel’s diverticulitis Acute abdominal pain: - Diverticular inflammation - Bowel obstruction - Perforation of the bowel leading to peritonitis - Entrapment of enterolith (a mixed concretion formed in the GIT) causing obstruction, bacterial growth and inflammation (similar process to acute appendicitis)

Answer 126

``` Extramural: Adhesions Hernia Volvulus Intrabdominal abscess Endometriosis Prostatic hypertrophy Tumours Congenital bands ``` ``` Intramural: Congenital malformations Neoplasms Strictures Intramural haematoma Post op ileus ``` Atherosclerosis Vasoconstriction Vasospasm ``` Intraluminal: Intussusception Gallstones Faeces Foreign body Parasites Kidney stones ``` Thrombosis Emboli

Answer 127

The main causes of an upper GI bleed are: Peptic ulcer- epigastric or right upper quadrant pain Severe or erosive gastritis/ duodenitis Severe or erosive oesophagitis Oesophageal varices- jaundice, fatigue, anorexia and abdominal distension Angiodysplasia Mallory-Weiss tears- emesis, retching or coughing Tumours (benign or malignant) In 10-15% of patients no cause can be identified General signs and symptoms include: Haematemesis- either fresh blood or “coffee ground” (a sign the blood has been in the stomach) blood Melena In severe cases signs of hemorrhagic shock/ haemodynamic instability- tachypnoea, tachycardia, hypotension, diaphoresis Signs of anaemia

Answer 128

Low risk patients should be admitted to the ward, made NBM, observed for continued bleeding or signs of haemodynamic instability and may receive an elective endoscopy with definitive management if necessary High risk patients: Initially resuscitation with a large calibre IV access and fluid resuscitation if the patient is tachycardic or hypotensive. Call blood bank and give a blood transfusion if there is a large volume haematemesis or if there are still signs of haemodynamic instability after fluid resuscitation. ``` Bloods: FBC, UEC, LFT, coagulation and cross match Alert HDU/ICU Alert appropriate surgical team Vitals monitoring NG tube Cease all NSAIDs and give IV PPI. ``` Gastroscopy (within 12 hours of first bleed) to determine the site of the bleeding and for management. If no obvious lesion is identified further imaging such as angiography/ small bowel capsular imaging/ enteroscopy (endoscopy of the small bowel). If a major bleed is identified on gastroscopy, therapeutic endoscopic interventions such as endoclipping, heater probe and injection therapy are available. Surgery (laparotomy) if endoscopic treatment fails or for patients who suffer 2 or more re- bleeds.

Answer 129

ABCDE Assess for haemodynamic instability/ shock by checking vital signs Give high flow oxygen Call surgical registrar/ consultant Call ICU Venous access 2x large bore cannulas and fluid boluses x2 Blood transfusion if patient still shocked after fluid boluses Catheter to monitor urine output Considering call for rapid response if the patient is still unstable NBM Bloods- FBC, UEC, coags, LFTs, Group and hold Correct electrolyte and clotting abnormalities History; How much bleeding and over what time period Associated symptoms such as haematemesis, melena, dysphagia, pain Use of NSAIDs (peptic ulcers) Alcohol history including drinking just prior to bleeding and vomiting Cirrhosis or liver disease (oesophageal varices) Smoking ``` Examination: Vitals Cardio exam Gastrointestinal exam Looking for signs of liver disease ``` ``` Differentials: Peptic ulcer disease- (duodenal or gastric) Reflux oesophagitis Gastritis/ duodenitis Oesophageal varices Mallory-Weiss tears Vascular malformations Aortoenteric fistulas (post aortic surgery) Neoplasm ```

Answer 130

``` Heliobacter pylori infection NSAID use Smoking Increasing age Personal history of peptic ulcer disease Family history of peptic ulcer disease Patient in intensive care ```

Answer 131

``` Bloods: FBC- leukocytosis (infection) CRP- inflammation or infection UECs- kidney function and SIRS LFTs ECG- MI may present as epigastric pain Serum gastrin levels- Zollinger-Ellison syndrome (gastric screwing tumours or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid, resulting in recurrent peptic ulcers) ``` Erect chest x-ray: 75% of PPU have free air under the diaphragm. Abdominal X-ray - Rigler’s sign- appearance of gas on both sides of the bowel/ double wall - Football sign- a large volume of free gas resulting in a round black area - Gas outlining soft tissue structures such as the liver edge or falciform ligament Serum lipase/amylase- checking for the differential of acute pancreatitis CT scan: Diagnostic accuracy of 98% Free air anteriorly just below the anterior abdominal wall Visible falciform ligament when air is present on both sides Exclude acute pancreatitis

Answer 132

Physical signs are generally those suggestive of peritonitis due to the gastric contents spilling out into the abdomen: - Involuntary guarding - Rebound tenderness - Board like rigidity - Epigastric tenderness Mild fever, pallor, tachycardia and hypotension Absent bowel sounds

Answer 133

``` Sudden onset of severe epigastric pain that becomes generalised and is worse on movement. It may also radiate to the back and shoulders Abdominal distension Brownish bloodstained vomiting Nausea Constipation Fever ```

Answer 134

Conservative therapy has been shown to be effective in 40-80% of perforated peptic ulcer disease: Nasogastric tube Intravenous fluids Gastric acid suppression with a PPI Antibiotics- triple antibiotic therapy, usually with ampicillin (gram positive), gentamicin (gram negative) and metronidazole (anaerobes) Repeated clinical assessment In patients who become clinically unstable or who are shown to have a leakage with gastrograffin, dye study surgery is indicated: Laparotomy is the most common form of surgery and will involve an abdominal cavity washout with saline solution and closure of the perforation by suturing a vascularised flap of omentum over the defect. Post surgery patients will have to undergo H.pylori eradication with triple therapy for 7 days: PPI Amoxicillin Clarithromycin ``` Prompt resuscitation Analgesia Nasogastric tube Urinary catheter Omeprazole and triple therapy Surgery ```

Answer 135

Resuscitation ABCDE Known relevant history and examination findings NBM Catheterisation Contact the relevant people including the surgical team, anaesthetic team, operating theatre, blood bank Medical management- analgesia, IV fluids, IV PPI, antiemetics, pre op antibiotics Consent patient and give the booking slip to the NUM

Answer 136

This patient likely has a pseudo-obstruction of the colon (Ogilvie’s syndrome). Differentials include opiate induced pseudo-obstruction, paralytic ileus, toxic megacolon and bowel obstruction. As the resident I would: Start with a primary survey and adequate resuscitation replacing losses from vomiting and from lack of food NBM NG tube since the patient is vomiting Decrease meds that decrease colonic motility and give analgesia with paracetamol/ ibuprofen and minimal opioids if necessary History- op report, SOCRATES of pain Exam- Abdominal and PR exam- bowel sounds can help distinguish between a functional and mechanical obstruction (bowel sounds are present in 90% of cases of Ogilvie’s syndrome) Bloods- FBC, UEC, LFTs Serial abdominal radiographs and consider abdominal CT Neostigmine if there is greater than 12cm of dilatation of colonic distension and conservative management has failed for 48 hours. Neostigmine is a anti cholinesterase inhibitor to increases parasympathetic nervous system activity. However it can cause the side effects of bradycardia, hypotension, asystole, seizures and bronchoconstriction. Colonic decompression if neostigmine fails or is contraindicated

Answer 137

The common skin cancers are: Basal cell carcinomas Squamous cell carcinomas Melanomas

Answer 138

ABCDE of melanoma suspicion Asymmetry- irregularity in shape Border irregularity Colour change- an increase in pigmentation, red halos around the lesion, multiple colour and even uneven distribution of colours are all important prognostic factors. Diameter- > 6mm in diameter is often concerning Evolution- increase in size, bleeding, ulceration or crusting, spreading of pigmentation, satellite lesion (smaller lesions near the edges of a principal lesion) or pain and itching are poor prognostic signs.

Answer 139

Investigations: Diagnostic biopsy- Excision biopsy is always preferred as it always gives you more information about invasion but shave and punch are done as they are more convenient. For an excision biopsy of a melanoma there should be 1mm margins. Sentinel node biopsy- indicated for a melanoma with depth greater than 1mm Imaging CT chest abdomen pelvis for staging and looking for metastatic spread. Note that there is a 98% chance of the CT not showing anything and a 2% chance of the CT showing metastasis, which have a very poor prognosis anyways. Management: Surgery- wide local excision of primary lesions with margins - BCC and SCC- 1-2mm margin - Carcinoma in situ (no spread past the basement membrane)- 5mm margins wide excision - Invasive (below the epidermis) melanoma- wide excision with 1cm margin Resection of metastases Lymph node clearance if sentinel node biopsy is positive Adjuvant treatment- radiotherapy and chemotherapy (relatively ineffective) or immunotherapy

Answer 140

A volvulus is a closed loop obstruction of the large bowel, often of the sigmoid or the caecum. It occurs when a large loop of bowel distended with gas and faeces, twists in on its mesentery, leading to a closed loop obstruction. Presentation is more common in the elderly and there is an association with chronic neurological conditions such as Parkinson’s disease and MS and with antipsychotic medications. This can rapidly lead to strangulation, infarction and then perforation and generalised peritonitis. Classic clinical features include: - Constipation - Nausea and vomiting - Abdominal distension and pain - Tympanic abdomen - Peritonitis if perforated - Shock, tachycardia and severe pain if there is ischaemia Abdominal radiographs will show a large, dilated loop of the colon, often with a few gas-fluid levels and commonly a collapsed rectum. Specific signs include coffee bean sign. CT may also be performed. Rectal tube insertion is successful in treating 90% of cases. The mortality rate is 20-25%, with the most common complication being bowel ischaemia.

Answer 141

The goal of treatment of sigmoid volvulus is to reduce the sigmoid volvulus and to prevent recurrent episodes A flexible sigmoidoscopy should be performed first line to detours the volvulus, thereby restoring blood supply. An additional advantage is that it allows for an assessment of the viability of the colon. Visualisation of a dilated proximal segment filled with gas and stool or a sudden expulsion of air and stool indicates successful reduction of the volvulus. Decompression should then be confirmed with AXR. A rectal tube should also be left in place with the proximal end beyond the area of torsion as it lessens colonic distension and reduces the chance of recurrence. The surgical approach for sigmoid volvulus includes sigmoidectomy and primary anastomosis. It is indicated in recurrent episodes of the sigmoid volvulus. Hartmann’s procedure (proctosigmoidectomy with closure of the anorectal stump and end colostomy) may also be used.

Answer 142

The most likely diagnosis is an indirect inguinal hernia. The differential diagnosis include: - Direct inguinal hernia- bulging of abdominal contents through the posterior wall (transversalis fascia) of the inguinal canal. - Femoral hernia- Abdominal contents migrate through the abdominal canal. Rarely has a cough impulse, rarely reducible and more likely to strangulate - Inguinal lymphadenopathy- The inguinal nodes drain the lower limb, abdominal wall below the umbilicus, anal canal, scrotal skin and penis - Saphena varix- dilatation of the long saphenous vein superficial to the deep facia before entering the femoral vein - Femoral artery aneurysm- Dilatation of the common femoral artery. This is classically found in males >65yoa and is classically expansile and pulsatile - Psoas abscess- Classically seen in TB - Hydrocele - Spermatocele - Varicocele

Answer 143

Inguinal hernia: - Omentum - Small intestine - Peritoneum (if small) - Extra-peritoneal fat (if small) - Large intestine (less common) - Appendix (less common) Femoral hernia: - Small bowel - Omentum

Answer 144

Laprascopic surgery- mesh repairs are required in laprascopic procedures and normally involve approaching the hernia from the posterior aspect. Open surgery- a tension free mesh placed anterior to the hernial defect is used to plug and patch the hernia. A non-mesh open repair is also possible where a patch of external oblique aponeurosis may be used to patch the defect. ``` Indications for laprascopic approach: Bilateral hernias Recurrent hernias Femoral hernia Prevention of post repair neuralgia Patients with physically active jobs or lifestyles as laprascopic repair reduces pain and has a quicker return to normal activity ``` ``` Indications for open approach: Prior pelvic surgery Infection Complicated hernia (i.e strangulated) Large scrotal hernia (greater than 3cm) ``` The indications for repair are; for a symptomatic hernia, a femoral hernia, or a strangulated or incarcerated hernia The contraindications for surgery are elective repair in pregnancy in asymptomatic hernias and in active infection.

Answer 145

``` Common: Seroma Haematoma Bruising Superficial wound infection ``` ``` Serious complications: Urinary retention Bladder injury Persistent groin pain Testicular complications such as pain, ischaemic orchitis, testicular atrophy, transection or obstruction of the vas deferens Deep wound and mesh infections Recurrent hernias Mesh migration and erosion into bladder, spermatic chord or gastrointestinal structures ```

Answer 146

The neck can be divided into the anterior and posterior triangles: Posterior triangle- bordered by the trapezium muscle, sternocleidomastoid muscle and the clavicle. It can be further divided int the occipital triangle (superior to the posterior belly of the omohyoid muscle, and then subclavian triangle, inferior to the posterior border of the omohyoid muscle. Anterior triangle- made up of the submental triangle, carotid triangle, submandibular triangle and the muscular triangle. ``` Differential diagnosis of neck lumps: Inflammatory Reactive viral lymphadenopathy Bacterial lymphadenopathy Parasitic lymphadenopathy ``` Neoplastic Metastatic head and neck cancer - Posterior triangle- nasopharyngeal cancer - Upper jugular- oral cavity, oropharynx or laryngeal cancer - Virchow’s node- tracheobronchial, oesophagus, stomach carcinoma Thyroid masses - Diffuse goitre- Grave’s disease and Hashimoto’s disease - Toxic multinodular goitre - Thyroid cancer Salivary gland neoplasms - 80% of neoplasms arise from the parotid gland with 80% of those tumours being benign (mostly pleomorphic adenomas) - 50% of submandibular neoplasms are malignant Paragangliomas- tumours in the peripheral nervous system. Occur in the superior part of the neck (just inferior to the ear) near the carotid artery. Schwannomas- tumour of the Schwann cells that line the peripheral nerves Lymphoma- common in children with Hodgkin’s lymphoma Lipoma and benign skin cysts Congenital - Brachial cleft cyst- epithelial cyst, arising on the lateral part of the neck from a failure of obliteration of the second branchial cleft in embryonic development - Thyroglossal duct cyst- an embryonic remnant that forms due to failure of closure of the thyroglossal duct extending from the foramen cecum in the tongue to the thyroid - Vascular anomalies - laryngocele- congenital anomalous air sac communicating with the larynx - Teratoma- tumour containing fully developed tissue such as bone, hair or muscle - Dermoid cyst- saclike growth containing structures such as hair, fluid, bone or sebaceous glands) NB: A neck mass in an adult should be considered neoplastic, and potentially malignant, until proven otherwise. This likelihood is further increased if there is a smoking or alcohol history.

Answer 147

History: - Duration- masses present for years without change are likely benign neoplasms (benign salivary gland tumours, schwannomas or paragangliomas) - Growth pattern- rapid expanding masses are likely due to an infectious process or rapidly growing lymphoma - Absence or presence of pain - Voice changes, hoarseness, otalgia, dysphagia may indicate cervical node metastasis. - Other features- fever, night sweats, weight loss - Risk factors- smoking, alcohol, illicit drug use, occupational history and exposures, recent travel Examination: - Location - Characteristics of mass- size, shape, consistency, tenderness, mobility and colour • Neck masses that are due to reactive lymph nodes are usually discrete, mobile, firm, rubbery, but not rock hard • Rock hard masses increase the chance of malignancy • Soft, ballotable, mobile masses are usually congenital cysts - Cranial nerve exam - Abdo exam looking for masses and organomegaly - Examination of the oropharynx and oral cavity

Answer 148

I. Q1. What can you see and what is the diagnosis? Most likely umbilical hernia An umbilical hernia is a defect of the anterior abdominal wall fascia that occurs when the umbilical ring fails to close. The defect allows protrusion of a peritoneal sac that is covered by skin and may contain intrabdominal content, such as omentum and bowel. Ddx epigastric hernia II. Q2. What is the likely contents? Mainly omentum and and pre peritoneal fat and also small bowel and colon III. Q3. What is the risk of serious complications with this hernia as it stands. Incarceration and strangulation and bowel obstruction and perforation IV. Q4. What would be the correct approach if this were to become acutely painful and incarcerated? ABCDE with adequate resuscitation and open surgical repair with mesh

Answer 149

172. This is the laparoscopic view of the lower abdomen. I. Q1. What is visible here? II. Q2. How can the bowel be injured at Laparoscopy and what are the consequences? 1/3 of bowel injury occurs during abdominal access. Other mechanisms include dissection, electrocoagulation (diathermy), tissue grasping, placing of pneumoperitoneum needles. Bowel injury is the 3rd leading cause of death, following anaesthesia and major vascular injury, after a laprascopic procedure. Apart from mortality, other consequences include peritonitis, bowel necrosis and perforation.

Answer 150

Biliary colic is when a colic (sudden pain) occurs due to a gallstone temporarily blocking the cystic duct. The pain is severe, located in the RUQ, commonly occur post-prandially, may radiate to the back or right shoulder blade and it typically rises to a plateau over a few minutes then continues unrelentingly. Note that the pain does not have the strikingly intermittent brief peaks of other forms of colic (e.g ureteric). These patients may be in agony until the pain resolves spontaneously after several hours or after opiate analgesia. Vomiting is often associated with the attack and the patient feels exhausted and sore for the next few days or so. There is commonly a history of similar episodes. There are few positive findings on examination; the patient is afebrile, but there may be some local tenderness due to gallbladder distension. If the attack lasts more than 24 hours acute cholecystitis is the more likely diagnosis. Other differentials to consider include perforated peptic ulcer.

Answer 151

Cholangitis is an infection of the biliary tree, most commonly caused by biliary obstruction, bile stasis and dilatation of the distal common bile duct. This allows for bacteria in the duodenum to enter the common bile duct. The most common infecting organisms are gram negative organisms such as E.coli, Klebsiella and enterobacter and gram positive organisms such as enterococcus. Causes of the obstruction are biliary calculi, benign stenosis, malignancy and stent placement.

Answer 152

In its less severe form cholangitis will present with Charcot’s triad of intermittent right upper quadrant pain, swinging pyrexia and jaundice. In the more severe, life threatening form known as toxic cholangitis patients will present with Reynolds’s pentad of Charcot’s triad + hypotension and confusion/ altered mental status. Investigations include FBC (for WCC) inflammatory markers (CRP), LFTs (raised bilirubin) The bile duct should be drained urgently, preferably by endoscopic sphincterotomy.

Answer 153

Acute cholecystitis is acute gallbladder inflammation and is one of the major complications of cholelithiasis/ gallstones. It develops in up to 10% of patients with symptomatic gallstones. In most cases (90%) it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall. In 10% of cases bile inspissation (thickening), due to dehydration, or bile stasis, due to trauma or severe systemic illness, can block the cystic duct, causing an acalculous cholecystitis (cholecystitis without evidence of cystic duct obstruction). Clinically it presents as prolonged (>4 hours) severe RUQ pain that may radiate to the right shoulder or back with fever, abdominal guarding, tachycardia, nausea and vomiting, anorexia and a positive Murphy’s sign. It is often associated with episodes of fatty foods approximately 1hr before onset. Suspected with fever, Murphy’s sign or leucocytosis. Diagnosed by abdominal ultrasound Management is with analgesia, IV fluids, NBM, broad spectrum antibiotics (not required in simple biliary colic) and a laprascopic cholecystectomy in the same admission. NB: gallstones typically contain 20-80% cholesterol and calcium carbonate, phosphate, bilirubin and other bile pigments

Answer 154

Choledocholithiasis is the presence of gallstones in the common bile duct. They are mostly asymptomatic, but can present with RUQ pain, nausea and vomiting. Stones may pass conservatively but often do not if they are larger than the size of the common bile duct. In this case there are two main techniques to remove them: ERCP- Sphincterotomy of sphincter of Oddi to allow the passage of the stones. Papillary balloon dilatation has also been tried to preserve the sphincter however this technique has less supporting evidence. The ERCP should be followed by cholecystectomy. Surgical- Largely only occurs if the stones are found intraoperatively during a laprascopic cholecystectomy. If found intraoperatively an intraoperative CBD exploration can be done or an intra-operative ERCP.

Answer 155

ERCP related complications can be divided into two main groups: General complications common to all endoscopic procedures: - Medication reactions and anaphylaxis - Oxygen desaturation - Cardiopulmonary accidents - Haemorrhage or perforation caused by passage of the endoscope Selective complications specific to pancreatobiliary instrumentation: - Pancreatitis- caused by physical irritation of the pancreatic duct. Amylase should be tested 24 hours post-ERCP and levels greater than 3x normal are suggestive of acute pancreatitis. This occurs in approximately 3% of patients undergoing ERCP. - Infection- cholangitis leading to subsequent septicaemia. The most common causative organisms are E.coli, Klebsiella, haemolytic streptococci, Pseudomonas, Enterococcus and Staphylococcus. - Perforation of the pancreatic duct, bile duct or duodenum- reported in less than 1% of patients. - Haemorrhage- postsphincterotomy bleeding has been reported in up to 2% of patients

Answer 156

Biliary colic is usually caused by the gallbladder contracting in response to a fatty meal, pressing a stone against the gallbladder outlet or cystic duct. This then results in increased intra-gallbladder pressure and pain. The pain is felt in the RUQ, however, unlike acute cholecystitis the pain is visceral in origin, without gallbladder wall inflammation, so peritoneal signs are absent. In addition patients with biliary colic are afebrile with normal laboratory studies. As the gallbladder relaxes the stones often fall back from the cystic duct and as a result the pain reaches a crescendo over a number of hours and then resolves spontaneously, generally in less than 6 hours. Cholecystitis has symptoms similar to biliary colic but will also present with fever, tachycardia, leucocytosis, Murphy’s sign and rebound tenderness and guarding of the RUQ.

Answer 157

Jaundice is a yellow colour of the skin, mucous membranes or eyes. The yellow comes from bilirubin, a byproduct of red blood cell haemolysis. Obstructive jaundice is a specific type of jaundice where symptoms develop due to a narrowed or blocked bile duct or pancreatic duct, preventing the normal drainage of bile into the intestines. Painless obstructive jaundice may be caused by: - Pancreatic carcinoma near the head of the pancreas - Pancreatic cysts - Ampulla of vater carcinoma - Biliary stricture (often secondary to chronic to alcoholism) - Cholangiocarcinoma (cancer of the bile duct) - Autoimmune causes such as primary sclerosing cholangitis - Drugs

Answer 158

``` Pancreatic cancer rarely causes symptoms. Symptoms often only present once the cancer is large enough to affect nearby organs or once it has metastasised. Signs and symptoms include: - Intractable upper abdominal pain which is described as: • Severe and continuous • Deep and gnawing • Often nocturnal and poorly relieved by analgesia • Partially relieved by sitting forward • Radiating to the back (60% of cases) - Weight loss- 80% of cases - obstructive jaundice- 50% of cases - Nausea and vomiting - Diarrhoea - Anorexia - Dark urine - RUQ mass or epigastric mass - Hepatomegaly - Cachexia - Gastric outlet obstruction - Steatorrhoea (the excretion of abnormal quantities of fat with the faeces) ``` Note that courvosier's sign is that a palpable gall bladder in the setting of jaundice is unlikely to be due to gallstones.

Answer 159

Pancreatic tumours present with jaundice due to compression of the common bile duct causing a cholestatic pattern. Haematological consequences: LFT derangement in an obstructive pattern- high alkaline phosphatase and high GGT as both of these substages are produced by the biliary epithelium (alkaline phosphatase also produced by the bones) Elevated conjugated bilirubin Liver failure causes haematological consequences including decreased clotting factors especially vitamin K clotting factors as the pancreas helps absorb vitamin K, decreased albumin, decreased platelets, protein C and S

Answer 160

Gallstones can cause pancreatic duct obstruction at the point of the ampulla of Vater. This causes reflux of pancreatic enzymes into the pancreas which can lead to inflammation and self digestion of the pancreas which will care interstitial oedematous pancreatitis. Findings on liver function tests, particularly ALT levels greater than 150 units per litre, have a positive predictive value of 95% in diagnosing gallstone pancreatitis.

Answer 161

Idiopathic (10-20%) Gallstones (50%) and genetic (cystic fibrosis) Ethanol (30%) Trauma Steroids Mumps/ malignancy Autoimmune Scorpion stings/ spider bites Hyperlipidaemia/ hypercalcemia/ hyperparathyroidism ERCP Drugs (tetracyclines, furosemide, azathioprine, thiazides) Note: - Clinical findings consistent with acute pancreatitis- acute onset of persistent, severe epigastric pain (pain may also be in the RUQ or more rarely confined to the left side), radiating to the back (in 50% of cases) and partially relieved by sitting up or bending forward, with associated nausea and vomiting (90% of cases), and occasionally dyspnoea - Laboratory findings- serum amylase or lipase (more commonly used in practice) greater than three times the upper limit of normal - Imaging (CT, MRI or ultrasound) criteria suggestive of acute pancreatitis

Answer 162

There are various prognostic scores that have been developed to assess disease severity in acute pancreatitis. The Glasgow system is a simple prognostic system that uses age and 7 laboratory values collected during the first 48 hours following admission for pancreatitis. It is applicable to both biliary and alcoholic pancreatitis. A point is assigned for each breakpoint that is met at any time during the first 48 hours of admission. A score of greater than 3 is suggestive of severe pancreatitis. ``` PaO2 < 60 Age > 55 Neutrophils > 15 Calcium < 2 Renal function high serum urea Enzymes- AST or ALT > 200 and LDH > 600 Albumin < 32 Sugar > 10 ```

Answer 163

Fluid resuscitation with 2 large bore IV cannulas (with isotonic crystalloid solution such as Hartmann’s solution)!!!! (very important) Oxygen supplementation NBM/NG tube- oral intake can be restarted in mild pancreatitis once pain and nausea and vomiting have resolved. Antiemetics- for example with ondansetron Analgesia Patients with biliary pancreatitis should have an ERCP within 24 hours of presentation.

Answer 164

Pancreatic necrosis Bile duct or pancreatic duct obstruction Pseudocyst (fluid filled cavity not lined by epithelium) formation in the pancreas. Diabetes mellitus Chronic pancreatitis Pseudoaneurysm- pancreatic enzymes in the blood causing breakdown of blood vessels. The most commonly affected vessels are the splenic and gastroduodenal arteries. Enteric fistula formation Lung complications- pleural effusion and pulmonary oedema

Answer 165

``` It is an ERCP. It shows the common bile duct, biliary tree and gallbladder Complications include: - Pancreatitis - Bleeding - Sepsis - Perforation ``` ERCP is indicated for therapeutic intervention, whereas MRCP should be used for diagnosis ERCP with sphincterotomy and stone removal are valuable therapeutic interventions in choledocholithiasis with jaundice, dilated common bile duct, acute pancreatitis, cholangitis. In patients with pancreatic or biliary cancer ERCP can also be used for palliation with plastic or mental stenting of the bile duct to relieve obstruction.

Answer 166

ARDS- pancreatic enzymes cause leakage of pulmonary capillaries Shock Peripancreatic fluid collection forming into a pseudocyst Infection- necrotising pancreas or pancreatic abscess Multiple organ failure AKI Abdominal compartment syndrome- increased intraabdominal pressure reducing blood flow to abdominal organs and leading to multi-organ failure Respiratory compromise Haemorrhage- adjacent inflamed stomach/duodenum, ruptured pseudocyst, peptic ulcer, pseudoaneurysm.

Answer 167

Q1: What does this show? A bile leak Q2: What might this patient present with? Fever, chills, nausea, vomiting, RUQ pain, distension, General discomfort, jaundice Q3: What are the features of Cholangitis? Charcot’s triad- Fever, jaundice and RUQ pain. It may also present with altered mental status and hypotension in more severe cases.

Answer 168

Q1: What does the patches of white on the fat represent? Fat necrosis/ saponification Q2: What is the mechanism of this? Enzyme damage to the membranes of the adipocytes near the affected pancreatic tissue. Acute pancreatitis —> activation of lipase —> hydrolysis of peripancreatic fat —> release of free fatty acids —> FFA precipitate with circulating calcium (saponification) Q3: Leads to hypocalcaemia due to the sequestration of Calcium.

Answer 169

Q1: Gallbladder Q2: This means that the gallbladder is abnormally large. This is Courvoisier’s sign (in the presence of an enlarged gallbladder which is non-tender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones). The enlarged gallbladder is likely to be from neoplasm of the head of the pancreas or cholangiocarcinoma until proven otherwise. Q3: Pressure in the gallbladder increases from obstruction of the biliary tree which causes a build up of bile and inflammation of the gallbladder. Q4: Courvoisier’s sign

Answer 170

Cystic lesion, CT and ultrasound Hepatic cysts can be broken into simple and complex cysts - Simple- congenital cysts, biliary hamartomas, Caroli disease and polycystic liver disease - Complex cysts- mucinous cystic neoplasms, hydatid cysts, haemorrhagic cysts, endometrial cysts and cystic hepatocellular carcinoma Complications of large hepatic cysts include: Haemorrhage, rupture, infection, biliary obstruction, secondary cholangitis if cysts rupture into the biliary tree, anaphylaxis if a hydatid cyst ruptures, malignant transformation of benign cysts and compression of the venous system in the liver.

Answer 171

Q1 Stent in the biliary tree Q2 ERCP with stenting Metal or plastic: The placement of a plastic stent is inexpensive and effective and the stent can easily be removed or exchanged. Plastic stents however eventually develop occlusion by sludge and/or bacterial biofilm and maintaining biliary drainage with plastic stents usually requires repeated ERCP. Metal stents extend the duration of stent patency. However, metal stents have significantly higher costs and may not be removable Q3 Enteral stenting and surgical bypass to solve a gastric outlet obstruction which obstructs gastric emptying at the pyloric sphincter. The procedure involves passing a guide wire through the obstruction and deploying a stent to keep the obstruction open. The stents are self expanding metal stents and can be covered or uncovered depending on whether they are coated. The advantage of covered stents is that they prevent tumour ingrowth.

Answer 172

Q1 Intra-operative cholangiogram Q2 A cholangiogram shows the gallbladder, cystic duct, the left and right hepatic ducts, the common bile duct and the ampulla of vater. Stones of the common bile duct

Answer 173

Q1 Sphincterectomy ``` Q2 Short term: - Bleeding - Infection - Pain - Pancreatitis - Perforation of duodenal wall - Abscess or fistula formation ``` Long term: - Stone recurrence - papillary stenosis - Cholangitis

Answer 174

Q1 This is the main cause for primary biliary stent failure and the occlusion reduces the quality of life of these patients and increases the risk of complications as there is a new blockage. Q2 Jaundice, RUQ pain and nausea Elevated liver enzymes in a cholestatic pattern (raised GGT and ALP) Q3 Mechanical Cleaning With a Baloon Plastic stent insertion Percutaneous transhepatic biliary drainage if endoscopic attempts fail NB- biliary stenting is recommended in patients with a potentially resectable malignant biliary obstruction, in those who require palliative care drainage of the common bile duct or hilar strictures, in treatment of strictures related to chronic pancreatitis, liver transplantation or cholecystectomy and in leaks and failed biliary stone extraction.

Answer 175

Q1 Symptomatic common bile duct stones Treatment of papillary stenosis Facilitation of endotherapy such as stenting, stricture dilatation, tissue sampling ``` Q2 Short term - Haemorrhage - Acue pancreatitis - Perforation of duodenal wall Long term: - Papillary stenosis - Ascending cholangitis - Stone recurrence ``` Q3 Lap cholecystectomy to prevent stone recurrence Rectal NSAIDs to prevent acute pancreatitis (rarely used) Coags preoperatively and cease anticoagulation therapy Prophylactic antibiotics to prevent ascending cholangitis

Answer 176

In ulcerative colitis there is mucosal inflammation with continuous involvement of the affected part of the colon, there is always rectal involvement, there may be backwash ileitis, there is widespread irregular ulceration and there is no granuloma formation and minimal fibrosis of the bowel wall. In Crohns disease there is transmural inflammation of the bowel with skip lesions and fissured ulcerations causing cobblestoning. Any part of the GIT may be affected with the most common areas being the ileum (affected in 80% of cases and exclusively affected in 50% of cases) and proximal colon. There is also non- caseating granuloma formation and marked fibrosis of the bowel wall.

Answer 177

This indicates that the patients oxygen saturation is significantly low despite nasal prong oxygen. Additionally there increased respiratory rate indicates further increase in oxygen requirements. This patient is hypoxemic, which could lead to inadequate perfusion. This is likely due to type 1 respiratory failure (if the CO2 is low or normal) which can be caused by acute asthma, pulmonary oedema, ARDS, pneumonia, pneumothorax, fibrosing alveolitis or PE.

Answer 178

``` This is likely due to type 1 respiratory failure (if the CO2 is low or normal) which can be caused by: Pneumonia PE Atelectasis Pleural effusion Acute upper airway obstruction Pulmonary oedema ARDS Pneumothorax Fibrosing alveolitis Acute asthma ```

Answer 179

Criteria for bariatric surgery BMI over 35 and at least one major comorbidity such as type II diabetes, hypertension or sleep apnoea BMI over 40 There are 3 main types: 1. Gastric Banding: Adjustable silicon band placed just below the gastrooesophageal junction applying gentle pressure that suppresses hunger. Level of restriction can be adjusted by varying the amount of fluid in the band. Expected Weight Loss: (17-20%) Advantages: - Effective with good long term weight maintenance. - Degree of restriction adjustable. - Reversible. - Lowest morbidity and mortality rate Disadvantages: - Highest long term re-operation rate - Gastric pouch dilatation - Erosion of the band into the stomach - Weight regain - Leaks to the adjustable gastric band 2. Sleeve Gastrectomy Greater portion of the fundus and body of the stomach is removed. Gastric volume is reduced by 80%. Expected Weight Loss: 20-30% Advantages: - Very effective with good mid-term weight maintenance Disadvantages: - Staple line leak - GORD - Dilatation of the gastric remnant - Weight regain - Limited long term data - Moderate nutritional deficiencies due to malabsorption 3. Roux-en Y gastric bypass - Small stomach pouch created, thereby reducing gastric volume. - The pouch is joined to the jejunum, hence, diverting nutrients from the lower stomach, duodenum and proximal jejunum. Advantages: - Largest amount of weight loss with good long term weight maintenance - Highest rates of diabetes remission (for patients with pre-existing type II diabetes mellitus) Disadvantages: - Staple line leak - Dumping - Stomach ulcer - Intestinal obstruction - Gallstones - Nutritional deficiencies due to malabsorption - Altered alcohol metabolism - Right regain

Answer 180

Overall the aim is to accurately characterise: Extent of the primary tumour Regional lymph node involvement Presence of distant metastasis This TNM staging of the disease is important for deciding if the tumour is resectable, if neoadjuvant therapy is required or if palliation is indicated Note that there are often metastases to the lungs. Investigations: 1. Endoscopic Ultrasound Scan (USS) Evaluation of choice for the primary tumour and its relationship to the oesophageal wall layers, having an 80-90% accuracy for T and N staging 2. CT Chest/abdomen Evaluate local lymph node and distant metastatic disease and also helps to evaluate the primary tumour, although there is limited value in this 3. PET Scan Detects distant metastatic disease 4. Diagnostic Laparoscopy Controversial however it does detect intraperitoneal metastases that are heard to diagnose non-invasively 5. Pre-op bronchoscopy with biopsy and brush cytology Indicated for patients with locally advanced tumours that are non-metastatic and above the level of the carina

Answer 181

Oesophagectomy is the only curative treatment for oesophageal cancer, but it has a high associated morbidity and mortality. Factors to consider are: His age (65) Pulmonary function and smoking status- spirometry and blood gases Comorbid illnesses- especially lung disease or cirrhosis (LFTs) Cardiac fitness- ECG, echo, stress test Nutritional status Previous surgeries and the response to anaesthetic Consider a trimodal approach with chemoradiotherapy and cancer Whether or not the patient consents Alcohol and weight His kidney function- UECs, coagulations

Answer 182

The main concern in this lady is oesophageal carcinoma (age > 50, progressive dysphagia and weight loss). History: Problems initiating swallowing or is food getting stuck at a certain point (oropharyngeal dysphagia is difficulty initiating swallowing, oesophageal is food getting stuck) Coughing, choking or nasal regurgitation (oropharyngeal cancer) Do you have problems swallowing solids, liquid or both (liquids and not solids suggests a motility disorder) Have the symptoms progressed or remained the same? and if they have progressed then over what time period? Associated symptoms- appetite changes, nausea, vomiting, heartburn, vomiting blood, pain on swallowing Other medical conditions Previous surgery on the larynx Radiation therapy in the past? Medications? ``` Examination: Wasting Hepatomegaly- tumour unresectable Virchow’s node (supraclavicular node) lymphadenopathy- tumour unresectable Hoarseness ``` Investigations: Gastroscopy and biopsy Staging- oesophageal ultrasound, CT and PET scan Management: Neoadjuvant chemoradiotherapy prior to surgery if there is a chance of cure Oesophagectomy after chemoradiotherapy for definitive treatment. Type of oesophagectomy is dependent on whether the cancer is below or above the level of the carina. Palliative care- laser treatment, stent insertion or argon tissue coagulation for oesophageal patency squamous cell carcinomas- high likelihood of responding to chemoradiotherapy- more proximal Adenocarcinomas- oesophagectomy ``` Differentials: Food impaction- most common cause of acute onset dysphagia Oesophageal strictures Oesophagitis Radiation therapy Achalasia Spastic motility dosorders Scleroderma Sjogren’s syndrome Functional motility disorder ```

Answer 183

There are three main categories of management for GORD; conservative, medical and surgical ``` Conservative: Weight loss Moderate exercise If GORD is nocturnal elevation of the bed head and avoidance of food 2-3 hours before bed Smaller meals Smoking and alcohol cessation Avoid anticholinergics ``` Medical: PPI single dose once daily for 4-8 weeks and then reduction of dosage to the lowest possible dosage that adequately controls symptoms. If standard therapy is not adequate to control symptoms high dose PPI therapy may be used, which involves taking double the dosage of standard therapy, preferably over 2 doses 12 hours apart. ``` Surgical: Laprascopic Nissen fundoplication Constructs a 360˚ cuff of gastric tissue around the lower oesophageal sphincter. Stomach contraction will therefore contract the lower oesophageal sphincter preventing reflux of gastric contents. Indications for surgery include: - GORD with refractory symptoms despite maximal medical management - Intolerance of treatment - Symptomatic complications unresponsive to medical therapy such as hoarseness, laryngitis, wheezing, nocturnal asthma, aspiration pneumonia or dental erosion - Benign stricture - Noncompliance with medical therapy - High volume reflux Complications include: - Post op IBS for approximately 2 weeks - Inadequate control of GORD - Dysphagia - Increased flatus - Delayed gastric emptying - Dumping syndrome- when food, especially sugar, moves into the small intestine too quickly - Gas bloat syndrome - Achalasia - Vagus nerve injury - Mortality in less than 1% of patients ```

Answer 184

Duodenal ulcer Complications: perforation for anterior ulcers, erosion into gastroduodenal artery in posterior ulcers causing bleeding Common causes- H.Pylori, NSAIDs, smoking Management: Mucosal patch for perforation (laprascopic intervention) Cytoprotective agents- misoprostol Eradication therapy for H.pylori- triple therapy (PPI + clarithromycin + amoxicillin)

Answer 185

Achalasia results from progressive degeneration of ganglion cells in the myenteric plexus in the oesophageal wall, leading to failure of relaxation of the lower oesophageal sphincter, accompanied by a loss of peristalsis in the distal oesophagus. It commonly affects people aged 30-50 and is associated with stress, drastic weight loss, slowly progressive (months to years) dysphagia of both solids and liquids and regurgitation (recognisable food). Investigations include barium swallow which may show: - Bird beak appearance - Oesophageal dilatation - Tram track sign- central longitudinal lucency bounded by barium on both sides - Incomplete lower oesophageal sphincter relaxation that is not coordinated with oesophageal contraction - Failure of normal peristalsis to to clear the oesophagus of barium and then manometry to confirm the high pressure and the non relaxing lower oesophageal sphincter. An endoscopy may also be performed to ensure the symptoms are not caused by a neoplasm. Management is with GTN, calcium channel blockers, botox, or endoscopic balloon dilatation. Surgical management is with oesophagomyotomy (cut outer longitudinal layer of oesophagus from above the sphincter to the cardia of the stomach) or oesophagectomy (removal of oesophagus).

Answer 186

Normal laprascopic insufflation pressure is less than 15mmHg. This is to allow for adequate surgical exposure without causing pneumoperitoneum and vasoconstriction leading to reduced organ perfusion. The normal intrabdominal pressure is 0-5mmHg and increases above 10mmHg are clinically significant, with > 15mmHg causing abdominal compartment syndrome.

Answer 187

Q1 The lower oesophageal sphincter is higher than usual, and some of the stomach has been pulled up into the oesophagus. There may be some oesophagitis or Barrett’s oesophagus. Q2 Barrett’s oesophagus = severe reflux Q3 Most sliding hernias can be managed conservatively, with surgery reserved for intractable cases: Reducing reflux- weight reduction, alcohol reduction, smoking cessation, avoiding trigger foods, not exercising after eating, not eating 3 hours before bed. Reducing acid production- PPI therapy for 4 weeks. If this works the dose should be gradually reduced until the patient is on the lowest maintenance dose possible. If single dosing is insufficient double dosing by adding a second dose 12 hours apart is another option. Q4 Surgery: Laprascopic reduction of hiatus hernia 360˚ fundoplication

Answer 188

Q1. The most likely cause of this is duodenal ulcer from H.pylori Q2. The two main complications are bleeding and perforation. If the ulcer is posterior it will more likely cause haemorrhage as the gastro-duodenal artery will be effected. If the ulcer is anterior it is more likely to perforate. Q3. The treatment is triple therapy- PPI + amoxicillin + clarithromycin

Answer 189

Q1 Progression of dysphagia Is it associated with liquids and solids- association with liquids is more likely to be achalasia Is it associated with coughing or nasal regurgitation (more likely oropharyngeal cancer) Known neuromuscular diseases such as myasthenia gravis? Family history of oesophageal cancer Previous radiotherapy or surgery on the anterior neck Red flag symptoms- weight loss, night sweats, painful swallowing, otalgia, haematemesis etc Q2 The most important differential to exclude is oesophageal cancer Q3 Investigations depend on the history and may include: Endoscopic ultrasound with biopsy, barium swallow (achalasia), oesophageal manometry, PET scan

Answer 190

Q1 Adenocarcinomas are by far the most common type of gastric tumour (90-95%) Lymphoma- cancers of the gut associated lymphoid tissue (GALT) Gastrointestinal stromal tumours Neuroendocrine tumours Squamous cell cancer Leiomyosarcoma- sarcoma developed from smooth muscle cells Q2 Staging of the tumour: - CT scan of chest and abdomen- determine tumour invasion, lymph node involvement and hepatic and more distant metastasis. - Endoscopic ultrasonography via a flexible endoscope for determining the depth of penetration and therefore the T stage of the cancer as well as local spread int lymph nodes, the liver and the pancreas - PET scan- for metastatic disease Q3 Preoperative chemotherapy Total gastrectomy with a Roux-en-Y reconstruction or a proximal subtotal gastrectomy Post operative radiotherapy for a proximal subtotal gastrectomy

Answer 191

Q1 Reflux oesophagitis?- damage to the cells that line the lower portion of the oesophagus (squamous epithelium) Q2 GORD or hiatus hernia Q3 PPI and conservative management

Answer 192

Q1 This is likely an ectopic kidney and the kidney is likely located in the pelvis, however ectopic kidneys may be located in the abdomen, lumbar region or pelvis. Q2 Ectopic kidneys are generally not harmful, however can lead to: - increased risk of calculus formation with consequent hydronephrosis. - Recurrent UTI as normal drainage can be affected - Abdominal pain - Palpable abdominal masses - Hydronephrosis from obstruction - Trauma - Vesico-ureteric reflux Q3 If the kidney is located in the pelvis there could be complications during pregnancy with the expanding uterus and thus obstruction of the outflow of the kidney.

Answer 193

Varicose veins are dilated superficial veins, usually in the legs, measuring greater than 3mm. It is caused by valvular insufficiency resulting in venous hypertension, reflux and dilatation of veins. There is a strong genetic component to varicose veins. Q1 [] Q2 Venous duplex ultrasound, documenting: Patency and competency of the deep system Patency and competency of the superficial system, including the incompetent segments, site of junctions and perforators Location and relationship of the sapheno-popliteal junction Diameter of the affected veins Q3 Pain Oedema Skin pigmentation- commonly seen in Gaiter area of the leg and associated with increased melanin production and deposition of haemosiderin. Champagne bottle appearance of the leg Eczema Atrophie blanche- white scarring Venous ulceration- usually located on the medial aspect of the leg between the ankle and calf (Gaiter area) Superficial thrombophlebitis- blood clotting of the vein that causes swelling and pain Haemorrhage Q4 While surgery, with great saphenous vein stripping, remains the gold standard most veins can be treated with a range of other endovenous therapy options including: - Sclerotherapy- using injected liquid or foam to cause venospasm and sclerosis of veins - Endogenous laser therapy- now covered by medicare - Radio frequency ablation- now covered by medicare - Mechanical therapy- using steam or rotating catheter

Answer 194

The most likely diagnosis is an epidural/ extradural haematoma which is a collection of blood that forms between the inner surface of the skull and the dura mater. They are usually associated with a history of head trauma and the source of bleeding is usually arterial, most often a torn middle meningeal artery. The classical clinical presentation is of a patient involved in a head strike who may or may not lose consciousness transiently. Following the injury they regain a normal level of functioning but usually have an ongoing but severe headache. Over the next few hours the gradually lose consciousness. Investigations to order include a: CT scan- extradural haematomas are almost always seen on CT and are typically biconvex (lentiform) in shape, hyperdense and most frequently beneath the temporal bone. There may also be secondary features of mass effect including midline shift, subfalcine herniation and uncle herniation. MRI- may be ordered if a CT is not conclusive Other useful investigations include: Fundoscopy- papilledema indicative of raised ICP IV access and bloods- FBC, UEC, ABG, BSL, LFT, coagulation study ECG Urinalysis

Answer 195

The most likely diagnosis is an extradural/ epidural haemorrhage. An extradural haematoma occurs when blood accumulates in the space between the skull and dura mater. It is almost always associated with a skull fracture, typically in the temporal bone, and rupture of the middle meningeal artery. The expansion of the haematoma strips the dura mater from the cranium causing the headache. Further haematoma expansion causes a raised intracranial pressure which decreases cerebral perfusion and (as cerebral perfusion pressure is increased above blood pressure) leading to a decline in consciousness and eventually death.

Answer 196

The most likely diagnosis is a subarachnoid haemorrhage. The major cause of this (in 80% of cases) is a rupture of an intracranial saccular aneurysm, most commonly occurring in the communicating arteries. Factors contributing to the formation of a saccular aneurysm are: Smoking Alcohol abuse Hypertension Connective tissue disorders (Marfans, Ehlers Danos) Sickle cell disease Congenital arteriovenous malformations Anticoagulants Sympathomimetic drugs (cocaine, caffeine, amphetamines) Family history Diabetes mellitus

Answer 197

The most likely diagnosis is a subarachnoid haemorrhage. During initial assessment this patient should receive clinical monitoring: Regular monitoring of their vital signs Airway evaluation GCS Full neurological examination Early referral to ICU

Answer 198

The most likely diagnosis is a subarachnoid haemorrhage. The main investigation used to diagnose SAH is CT brain. History: - Presence of risk factors- smoking, alcohol, hypertension, pregnancy, anticoagulation, known aneurysm - Thunderclap headache - Nausea and vomiting - Photophobia - Loss of consciousness Examination: - Neck stiffness - Altered mental status - CN abnormalities in cranial nerves 3 and 6 Investigations: - Bloods- FBC, UEC, troponin, coagulation studies - ECG- non specific ECG patterns including bradycardia are common with SAH - Lumbar puncture- elevated opening pressure, elevated RBC count and xanthochromia due to lysed RBCs - CT- blood in the subarachnoid space, most commonly around the circle of Willis - MRI- more sensitive to SAH - Digital subtraction catheter- gold standard for the diagnosis of an aneurysm post diagnosis

Answer 199

The likely diagnosis is a subarachnoid haemorrhage. Primary survey Correct electrolyte and coagulation (FFP) imbalances Manage hypertension- nimodipine (dihydropyridine CCB that quickly reduces blood pressure) Discontinuation of antithrombotics Prophylactic anti-emetics and stool softeners Analgesia Normothermia Specific: Surgery and coil embolisation (most common management) Prevent delayed cerebral ischaemia- nimodipine to prevent vasospasm Seizure prophylaxis Manage raised ICP- osmotic therapy and diuresis (mannitol)

Answer 200

The most likely diagnosis is a chronic subdural haematoma. Differentials include delirium, alcohol withdrawal, stroke, epidural haematoma, seizure, substance abuse Investigations: CT brain is most important. A chronic subdural haematoma will appear as an isodense or hypodense crescent shaped lesion. ``` Vitals Full neurological exam and MMSE Bloods- FBC, UEC, BGL, LFTs, coagulation studies MRI Angiography ```

Answer 201

Subdural haemorrhages are believed to be due to stretching and tearing of bridging cortical veins as they cross the subdural space to drain into adjacent dural sinus. These veins rupture due to shearing forces when there is a sudden change in the velocity of the head. 10-30% of chronic subdural haematomas show evidence of repeated haemorrhage. Rebleeding usually occurs from the rupture of stretched cortical veins as they cross the enlarged fluid filled subdural space. Subdural haematomas are interspersed between the dura and arachnoid mater, typically crescent shaped and are usually more extensive than extradural haematomas as they are limited only by the dural reflections. Initially the haematoma is encapsulated by a thick collagen and fibroblast membrane. When the haematoma becomes large enough and blood is drawn into the surrounding area by osmosis symptoms will begin to occur. At this point the haematoma can be evacuated via burr holes and the subdural space irrigated with warm saline or a hemicraniectomy and duraplasty can be performed. In the interim mannitol (an osmotic diuretic) can be used. For patients with chronic SDH and the potential for recovery, surgical haematoma evacuation is recommended if there is evidence of moderate to severe cognition impairment or progressive deterioration. Surgical intervention is also recommended if the clot thickness is >10mm or midline shift > 5mm. Conservative management with monitoring and serial CT scans can be used if the patient does not meet these criteria. In the patient alcohol + age = cortical atrophy stretching the cortical veins Fall = shearing forces Craniotomy and evacuation of haematoma as visible on CT and therefore likely greater than 1cm

Answer 202

Primary injury occurs at the time of the initial traumatic event, and may be local or diffuse. Focal injuries include haematomas, contusions and lacerations resulting from blunt or penetrating trauma. Diffuse injuries typically result from acceleration/ deceleration forces and affect the whole brain resulting in axonal shearing or concussion. Secondary injury is potentially preventable and reversible and occurs after the time of the injury. Mechanisms of injury include oedema (raised intracranial pressure), ischaemia/hypoxia, hypotension, and metabolic disturbance. Once the primary brain injury has been recognised the main objective of the management of acute traumatic brain injury is the prevention of secondary brain injury.

Answer 203

Primary survey Determine consciousness level on AVPU GCS- eye opening response (4), best verbal response (5), best motor response (6) 3-8 = severe head injury = 1 in 7 probability of haematoma 9-12 = moderate head injury = 1 in 50 probability of head injury 13-14 = mild head injury = 1 in 3500 probability of haematoma Systemic analgesia should be avoided until the full neurological assessment is performed Secondary survey Full assessment of head and neck Signs of basal skull fracture (panda eyes, Battles sign [bruising over the mastoid process], CSF otorrhoea or rhinorrhea) Repeated monitoring of vitals and GCS/AVPU Pupil size and reactivity Limb movements and responses ``` Indications for CT in head injury: GCS < 13 at any point Suspected open or depressed skull fracture Any sign of basal skull fracture Post-Traumatic seizure Focal neurological deficit More than one episode of vomiting Amnesia for greater than 30 minutes Age > 65 years, coagulopathy, dangerous mechanism of injury provided there is amnesia or loss of consciousness experienced. ```

Answer 204

The history sounds like colitis, which can be caused by: Inflammation- UC or Crohn’s disease Infective- C.difficile, campylobacter Ischaemic- likely inferior mesenteric artery if distal bowel The main sign of colitis is thumb printing of the bowel There may also be toxic megacolon

Answer 205

Given the history of previous laparotomy there is a high suspicion of adhesion small bowel obstruction, also the classical presentation is cramping abdominal pain, abdominal distension with nausea and vomiting. Look for: Dilated loops of bowel proximal to the obstruction with gas fluid levels and free gas in the peritoneum. The dilated loops will be predominantly centralised in a small bowel obstruction. Transition point of obstruction Decompressed small bowel distal to the obstruction Signs of herniation NB- other causes of small bowel obstruction include neoplasm, herniation and gallstone ileus Mucosal folds will be spread all the way across the diameter of the small bowel loops whereas the mucosal folds (haustra) are only spread across part of the diameter of the bowel loops.

Answer 206

Excellent spatial resolution (very good for assessment of bony structures) Good contrast resolution (the ability to distinguish between differences in intensity in an image)- 10x better than plain X-ray Fast and therefore less susceptible to motion artefact Widely available Can be used to image bones, organs, tissues and tumours Multiple planes can be seen without repositioning the patient Reproducible findings Gold standard for many pathologies- e.g intracranial haemorrhage

Answer 207

Radiation dose (100x higher than plain x-ray) and therefore shouldn't be used for children or in pregnancy Use of contrast has potential adverse effects including constipation and renal dysfunction Not portable to patient bedside Cost is more expensive than x-ray and ultrasound

Answer 208

Extradural/ epidural = biconvex/ lentiform shape Subdural = crescent shaped Unilateral 85% of the time

Answer 209

Crohn’s disease? []

Answer 210

``` Things to look for include: Hip dislocation Hip fracture Patella fracture/ dislocation Femoral fracture Tibial plateau fracture ```

Answer 211

``` Most common is splenic injury in blunt trauma. Findings on CT include lacerations, sub scapular or parenchymal haematomas, active haemorrhage and vascular injuries. Haemoperitoneum Lacerations Haematomas Contusions Pneumoperitoneum Devascularisation of organs or parts of organs Sub scapular haematomas ```

Answer 212

Rib fractures Pneumothorax/ haemothorax Pulmonary contusions Haematoma, aortic dissection

Answer 213

Excellent contrast resolution (gold standard for differentiating different types of tissue) Very good spatial resolution (not quite as good as CT) No ionising radiation Non-contrast vascular imaging Lots of detail available without use of a contrast Large field of view Image acquired in multiple plains without the patient having to move

Answer 214

``` Long scan times Large chance of motion artefact Suboptimal bony detail Contraindicated in patients with metal in situ Large cost Not mobile Not widely available, especially in rural settings Claustrophobia ```

Answer 215

``` No Ionising radiation Mobile Dynamic imaging, viewing structures and flow of blood in real time Relatively cheap Fantastic in pregnancy Readily available Easily transportable Minimal contraindications No need for contrast ```

Answer 216

``` Unable to visualise gas filled or bony structures well Limited field of view Heavily operator dependent Very difficult in obese patients Low penetration Requires pressure- discomfort if in pain Lots of artefacts ```

Answer 217

A chest drain allows the removal of blood from the pleural space. Removing blood allows the lung to expand against the chest wall and helps to arrest continuing haemorrhage from intercostal vessels. The goals of chest drain in acute haemothorax are drainage of fresh blood, measurement of the rate of bleeding, improvement of ventilation, decreasing risk of clotted haemothorax and evacuation of any coexisting pneumothorax. The aim of treatment of a haemothorax is fluid resuscitation as needed, usually tube thoracotomy and sometimes a thoracotomy. Patients with sign of hypovolaemia (e.g tachycardia and hypotension) are given IV crystalloid and sometimes blood transfusions. If blood volume is sufficient to be visible on chest x-ray (usually requiring 500ml) or if pneumothorax is present a large calibre chest tube is inserted in the 5th or 6th intercostal space mid-axillary line. Blood collected via tube thoracosotmy can be autotransfused. Urgent thoracotomy is indicated when there is more than 1500ml of blood loss or bleeding rate is greater than 200ml/hour for more than 2 hours and causes haemodynamic compromise.

Answer 218

Rib fractures are often simple fractures that heal while managed conservatively with analgesia and physiotherapy. However they may also result in other significant injuries that can become life threatening. Immediate: Cardiac damage- bleeding into the pericardial cavity causing severe haemodynamic shock and may be the cause of a cardiac arrest Tension pneumothorax Haemothorax Pulmonary contusion Aortic rupture Splenic laceration Hepatic injury Flail chest- which can lead to respiratory compromise failure. On inspiration the detached segment gets sucked in leading to paradoxical movement and the inhaled air shunts back and forth between the lungs Late: Pneumonia- this is the most common complication as the pain prevents the patient from breathing deeply and coughing Empyema- result from residual haematoma

Answer 219

Mechanical prophylaxis: Treatment of avoidable risk factors Active mobilisation Thromboembolic deterrent stockings (TEDs)- graded compression stockings increase venous return by continuous direct compression of the infrapopliteal veins. This should be accompanied by elevation of the legs. Intermittent pneumatic compression devices- cuffs around the legs that fill with air squeezing veins and increasing venous blood flow. Drugs that act on the clotting cascade: Heparin LMWH- e.g enoxaparin (activates antithrombin III) NB: Risk factors for VTE in trauma patient include spinal cord injury, head trauma, lower extremity fracture, pelvic fracture, need for surgical intervention, increasing age, femoral vein line insertion, surgical repair of venous injuries, prolonged immobilisation, prolonged hospital stay, high injury severity score. Prophylaxis should be used until patients regain full mobility.

Answer 220

WHY: The ABCDE mnemonic for the primary survey of patients allows for the ability to identify and treat life threatening conditions according to priority, with a clear, simple, organised and easily remembered approach to managing a severely injured patient. This also allows for consistency between doctors and centres and allows for life threatening injuries to be addressed during the ‘golden hour’ (the period of time following traumatic injury in which there is the highest likelihood that prompt medical and surgical treatment will prevent death). WHAT DOES IT STAND FOR: Airway protection, including stabilisation of the cervical spine Breathing (maintain adequate oxygenation) Circulation (control haemorrhage and maintain adequate organ perfusion) Disability (perform basic neurologic evaluation) Exposure (undress patient and search everywhere for possible injury while preventing hypothermia) Airway Head tilt + chin lift or jaw thrust + look inside oropharynx for foreign bodies Endotracheal intubation (if GCS < 8 or other indication) + CXR to check intubation Crichothyroidotomy (if intubation not possible) Breathing Assess ventilation with inspection, palpation, percussion/ auscultation Oxygen saturation, RR CXR Manage specific injuries such as open chest wound, flail segment, pneumothorax, haemothorax, cardiac tamponade, diaphragmatic rupture Circulation Assess pallor, HR, BP, temp, cap refill, ECG and urine output Control haemorrhage Insert two large bore IV cannulas into large veins Urgent cross matching and standard biochemical and haematological analysis If shocked rapid infusion of 2L warmed crystalloid solution in both cannulas If failure to respond consider transfusion of packed red cells + FFP FAST scan and reduction of fractures Disability Basic neuro assessment: AVPU (alert, respond to verbal stimuli, responds to painful stimuli, unresponsive) + pupil size, reactivity, inequality BSLs Estimate GCS Exposure: Rapid top to toe assessment for external injury and for signs of injury while ensuring the patient does not become hypothermic and patient dignity. Imaging that has not already been performed (FAST, CXR, CT etc)

Answer 221

There are two main indications for a laparotomy in trauma; peritonitis and haemorrhage The main priorities are: 1. To control haemorrhage- immediate blunt pressure control of haemorrhage sites 2. Control contamination- rapid closure of hollow viscus injuries. 3. Provide temporary abdominal closure to prevent abdominal compartment syndrome 4. Facilitate subsequent procedures once the patient has been resuscitated. The strategy aims to bring the lethal triad of acute coagulopathy (hypothermia, coagulopathy, acidosis) under control so that the patient will be able to tolerate further surgery once he or she improves. ``` This is achieved by: Short time in OT Limited focused surgery to control haemorrhage and decontaminate Packing Partially resect organs Staple off and remove injured bowel Fibrin sealants Leave abdomen open ```

Answer 222

Pneumothorax is air in the pleural space causing partial or complete lung collapse. Pneumothorax can occur spontaneously or result from trauma or medical procedures. Management of a pneumothorax includes: - Observation and follow up x-ray for small asymptomatic, primary spontaneous (no underlying lung pathology) pneumothraces - Catheter aspiration for large or symptomatic primary spontaneous pneumothraces- small bore catheter into 2nd intercostal space midclavicular line and attached to 3-way stopcock and syringe, followed by air withdrawing from the pleural space until the lung re-expands or until 4L of air is removed. - Tube thoracostomy for secondary (underlying pulmonary disease) and traumatic pneumothraces

Answer 223

Tension pneumothorax is accumulation of air in the pleural space under pressure, compressing the lungs and decreasing venous return to the heart. Tension pneumothorax develops when a lung or chest wall injury is such that is allows air into the pleural space but not out of it. As a result air accumulates and compresses the lung, eventually shifting the mediastinum, compressing the contralateral lung and increasing intrathoracic pressure enough to decrease venous return to the heart, causing shock. Causes include mechanical ventilation and simple pneumothorax with lung injury that fails to seal following penetrating or blunt chest trauma or failed central venous cannulation.

Answer 224

Symptoms of pneumothorax include dyspnoea and pleuritic chest pain. Dyspnoea may be sudden or gradual in onset depending on the rate of development and size of the pneumothorax. Pain may also be referred to the shoulder or abdomen. Physical findings typically consist of absent tactile fremitus, hyperresonance to percussion, and decreased breath sound on the affected side.

Answer 225

Symptoms and signs initially are those of simple pneumothorax. As intrathoracic pressure increases, patients develop hypotension, tracheal deviation and neck vein distension. The effected hemithorax (half of the thorax) is hyper resonant to percussion and often feels somewhat distended, tense and poorly compressible to palpation.

Answer 226

Tension pneumothorax is a medical emergency and should be diagnosed clinically; time should not be wasted confirming the diagnosis with a chest x-ray. It should be treated immediately by inserting a 14 or 16 gauge needle with a catheter through the chest wall in the 2nd intercostal space at the midclavicular line, just above the third rib to avoid the neuromuscular bundle just below the second rib. The sound of high pressure air escaping confirms the diagnosis. The catheter can be left open to air or attached to a Heimlich valve (one way valve that prevents air going back into the chest). Emergency decompression must be followed immediately by tube thoracostomy (insertion of a chest tube into the pleural space), after which the catheter is removed.

Answer 227

Shock is inadequate perfusion of vital organs due to circulatory failure, especially the heart and the brain. If untreated shock rapidly proceeds to irreversible organ damage and death of the patient. The most common cause of shock in trauma patients is hypovolaemic shock, usually as a result of haemorrhage. A reduction in circulating volume results in a reduction in stroke volume and cardiac output. Initially the body compensates by increasing sympathetic activity, raising the systemic vascular resistance and therefore the blood pressure. As volume loss increases blood pressure falls leading to the signs and symptoms of hypotension, hyperventilation, rapid weak pulse, cold, clammy cyanotic hands and oliguria. Other types of shock include: Cardiogenic- occurs when heart function is impaired Septic/ distributive- systemic inflammation causes cardiac depression and microvascular changes Anaphylactic- acute hypersensitivity to an allergen

Answer 228

Permissive hypotension and haemostatic resuscitation are terms relating to hypovolaemia and are components of damage control resuscitation. Permissive hypotension is a strategy to suggest that limited volume replacement the maintains minimally adequate organ perfusion may improve outcomes. Permissive hypotension targets early fluid resuscitation only to a systolic BP of 70 mmHG. Controlled hypotension may be beneficial in patients with haemorrhagic shock due to torso injuries, from gun shots or stab wounds, or patients with ruptured AAA. However it may be detrimental to patients with brain injury as hypotension reduces cerebral perfusion and increases mortality. The rationale behind permissive hypotension is that aggressive fluid resuscitation might lead to dilution of clotting factors, production of hypothermia, oedema leading to compartment syndrome and acute lung injury and disrupt thrombus formation and enhance bleeding. Haemostatic resuscitation aids to avoid or ameliorate acute coagulopathy of trauma and the complications of aggressive crystalloid fluid resuscitation while maintaining circulating volume. It involves the use of blood products in ratios resembling that of whole blood, often 1:1 FFP to packed red blood cells. This is also to prevent the lethal triad of hypothermia, metabolic acidosis and acute coagulopathy of trauma.

Answer 229

Neurogenic shock is classically characterised by hypotension, bradycardia and peripheral vasodilation. Neurogenic shock is due to loss of sympathetic vascular tone and happens only a significant portion of the sympathetic nervous system has been damaged- as occurs with lesions at the T6 level or higher. This affects vasomotor tone and cardiac function due to failure of descending sympathetic pathways of the upper thoracic cord. Spinal shock is not a true form of shock. It refers to flaccid areflexia with possible priapism (prolonged erection of the penis) that may occur after spinal cord injury, and may last hours to weeks. It resolves as soft tissue swelling improves.

Answer 230

Pelvis- pelvic X-ray Long bones- exposure/ inspection or X-ray Abdomen- FAST scan or diagnostic peritoneal lavage or CT (more accurately diagnosis solid organ injuries but is not as specific for blunt bowel and mesenteric injuries) Chest- CXR External- exposure/ inspection

Answer 231

Primary survey Organise trauma team, call surgeon, notify blood bank. Perfusion indices including ABGs, lactate, Hb and HCT Definitive management: Apply direct pressure to the open haemorrhaging wound If bleeding persists consider sutures, cautery, interventional radiology or damage control surgery

Answer 232

The aim of treatment of a haemothorax is fluid resuscitation as needed, usually tube thoracotomy and sometimes a thoracotomy. Patients with sign of hypovolaemia (e.g tachycardia and hypotension) are given IV crystalloid and sometimes blood transfusions. If blood volume is sufficient to be visible on chest x-ray (usually requiring 500ml) or if pneumothorax is present a large calibre chest tube is inserted in the 5th or 6th intercostal space mid-axillary line. Blood collected via tube thoracosotmy can be autotransfused. Urgent thoracotomy is indicated when there is more than 1500ml of blood loss or bleeding rate is greater than 200ml/hour for more than 2 hours and causes haemodynamic compromise.

Answer 233

Primary survey Organise trauma team, notify blood bank, call surgeon Interventional radiology and demobilisation Damage control laparotomy

Answer 234

Primary survey Organise trauma team, notify blood bank, call surgeon Non-surgical management is only indicated in patients with minimal neurological symptoms or haemorrhage volume <10ml. ``` Surgical options are generally for decompression of the brain to release pooled blood and relieve pressure. This may be done through: Burr hole procedure Craniectomy incision (partial removal of the skull to allow the brain swelling to expand) Craniotomy (opening of the skull cavity) after which the skull fragment is immediately put back into place. ``` Other treatments include: Anti-anxiety medications to control blood pressure Anti-epileptic drugs for seizure control Analgesia for pain Stool softeners to prevent straining during constipation Fluids and nutrients as necessary

Answer 235

Primary survey and secondary survey Organise trauma team, notify blood bank, call surgeon The leg should be realigned and splinted with skin traction and a Thomas splint. This will help to control pain and haemorrhage. An x-ray should only be attained after splinting has occurred. If the fracture is an open fracture the wound should be photographed, cleaned, dressed with a butadiene dressing, IV antibiotics should be commenced and tetanus given if necessary and the fracture should be reduced. NB: the average blood loss from a femoral fracture is 1-2.5L.

Answer 236

Primary survey Organise trauma team, notify blood bank, call surgeon Definitive management: Reducing the pelvic volume by use of a pelvic binder or binding a bedsheets tightly around the pelvis and internally rotating the hips (emergency procedure) or by application of an external pelvic fixator in theatre as a more definitive solution Emergency laparotomy, during which pelvic stabilisation and/or pelvic packing is performed pending definitive management of the injury. Once the parent is haemodynamically stable the patient may have an abdominopelvic CT with IV contrast and surgical fixation as required.

Answer 237

The combination of packed red blood cells, fresh frozen plasma (FFP), platelets and cryoprecipitates is given in order to achieve haemostasis and correct coagulopathy caused by massive haemorrhage. It has been shown that FFP to packed RBC ratios of 1:1 drastically improve survival rate. Cryoprecipitate provides an additional option for factor replacement for a lower volume of fluid, notably replacing factor VIII (and therefore Von Willebrand’s factor) and fibrinogen. Blood products also provide additional advantages over isotonic crystalloid solutions in trauma patients as large volumes of crystalloid solution can lead to dilution coagulopathy and exacerbate bleeding as well as decrease organ function due to volume overload and oedema. Furthermore, crystalloid solutions have no O2 carrying capacity and do little to correct the anaerobic metabolism associated with shock. Cryoprecipitates- contains factor VIII of the intrinsic pathway (so it decreases your aPTT), Von Willebrand’s factor (as it is bound to factor VIII in circulation) and fibrinogen. Fresh frozen plasma- contains all of the clotting factors, fibrinogen, plasma proteins electrolytes, physiological anticoagulants (protein C, protein S, antithrombin etc) and added anticoagulants. NB to reverse warfarin prothrombinex is the preferred agent as it contains factors II, IX and X and a small amount of factor VII. When prothrombinex is not readily available FFP may also be used.

Answer 238

History: - Timing of haematuria- blood from the kidneys, ureters and bladder will completely mix in the urine whereas urethral bleeding may occur independently of micturition - Acute trauma - Currently in menses (false positive for haematuria) Associated symptoms- colic pain, retention, symptoms of UTI (dysuria, frequency, urgency, pneumaturia) - Difficulty initiating urine stream, slow stream, hesitancy or post void dribbling - Systemic symptoms- fever, weight loss - PMHx- bleeding diathesis, sickle cell, stones, cancer, structural kidney diseases, pelvic surgery/ radiation, catheterisation, endometriosis - Medications- anticoagulants - Past surgical history- renal or urological procedures - Smoking history Examination: Loin inspection and palpation/ ballot kidneys DRE for prostate assessment Blood pressure Investigations: Urine dipstick MSU and MCS Urine cytology Bloods- FBC, ESR/CRP, serum albumin, UEC, PSA, CMP, uric acid and PTH levels (stone disease), coags Imaging- renal ultrasound, cystoscopy, X-ray KUB (stones), CT KUB (renal/prostate/ stones/ bladder mass) Differential diagnosis: Urinary tract infection- most common cause Renal stones Malignancy (typically painless haematuria) Renal cell carcinoma Transitional cell carcinoma Post interventional (e.g post TURP or post cystoscopy) Glomerulonephritis Vasculitis Obstruction such as BPH Trauma of kidney- polycystic kidney disease especially susceptible Emboli or renal vein thrombosis

Answer 239

The important diagnosis to exclude is a urinary malignancy, likely a transitional cell/ urothelial carcinoma. Investigations include: FBC- may show mild anaemia Urinalysis- haematuria and pyuria (pus in the urine) Renal and bladder ultrasound or CT urogram to image the urinary tract Urine cytology- identifies malignant cells that have been exfoliated from the urothelium or squamous cells into the urine. The specificity is greater than 90% while the sensitivity for high grade disease and carcinoma in situ is 80-90% however there is low sensitivity for detecting low grade neoplasms (20-50%). Cystoscopy- Low grade tumours are papillary and readily visible, while high grade tumours may be flat and more difficult to see. Carcinoma in situ is often not visible. To evaluate metastatic disease I would also like to do LFTs- increased alkaline phosphatase indicates bony metastasis Bone scan- if alkaline phosphatase is raised NB: Overall 80-90% of cancers of the bladder are urothelial carcinomas (previously termed transitional cell carcinomas). Squamous cell carcinomas are the next most common form of bladder cancer and adenocarcinomas are the rarest form. The most common presenting symptoms include: - Presence of risk factors- risk factors include tobacco exposure, male gender, age > 55, exposure to chemical carcinogens, pelvic radiation, systemic chemotherapy and family history of bladder cancer. - Haematuria- present in over 80% of cases. Gross, painless haematuria which is present throughout the entire urinary stream is the most common. - Dysuria- typical of carcinoma but also seen in high grade urothelial carcinoma - Urinary frequency Urine cytology Cystoscopy

Answer 240

The patient has acute urinary retention which is a urologic emergency and should be promptly managed. History: - Signs and symptoms- inability to pass urine, abdominal pain, haematuria, fever, dysuria, neurologic symptoms, low back pain - Previous history of retention or lower urinary tract symptoms - History of prostate disease - Pelvic or prostate surgery, pelvic trauma or radiation - Recent medication changes ``` Examination: - General inspection - Vitals - Percuss bladder - Rectal examination- masses, faecal impaction, perineal signs, prostate - Neurologic exam- strength, sensation, reflexes, muscle tone Investigations: - FBC, UEC - Urinalysis - Bladder ultrasound, cystoscopy ``` Management: - Analgesia- relaxation and may aid spontaneous micturition - Cease any causative medication - Catheterise if retention persists - Alpha blockers in the case of BPH and consider TURP Differential diagnosis of acute urinary retention: - BPH - Carcinoma - Post urologic surgery - Bladder or urethral stone impaction - Pressure on bladder (pregnancy or faecal impaction) - Infection- acute prostatic - Trauma - Pharmacological- anticholinergics, anaesthetics, alpha agonists - Loss of neurological control- spinal injury, epidural/spinal anaesthesia

Answer 241

The diagnosis is benign prostatic hyperplasia which is causing a bladder outlet obstruction and chronic urinary retention leading to overflow incontinence. He is complaining of bedwetting because BPH leads to compression of the urethra leading to a bladder outflow obstruction. This leads to chronic urinary retention, bladder distension, an atonic bladder (loss of muscle tone) and overflow incontinence. This primarily affects him at night because the combination of the full bladder and nocturnal relaxation of the pelvic floor, tends to occur. NB: The symptoms of bladder obstruction include: - Incomplete bladder emptying after urination - Frequency (less than 2 hours) - Intermittent flow (stopping and starting during urination) - Urgency (difficult to postpone urination) - Week stream - Straining to begin urination - Nocturia - Hesitancy - Post micturition dribbling - Symptoms precipitated by excessive fluid intake

Answer 242

The diagnosis is most likely benign hypertrophic hyperplasia Management options include: Drug treatment: - 5 alpha reductase inhibitors (finasteride)- block the conversion of testosterone to dihydrotestosterone, preventing hyperplasia - Alpha adrenergic receptor blocker (tamsulosin)- present in the bladder neck and prostate- relax smooth muscle of prostatic urethra to decrease outlet resistance Surgical therapy: - Transurethral resection of prostate (TURP)- This is the standard surgical therapy and involves removing the bulk of the prostate and leaving a compressed venous plexus to prevent bleeding. It has a 5-10% risk of erectile impotence. - Retropubic prostatectomy- rarely performed - Laser vaporisation Long term catheterisation- only recommended for patients with significant perioperative morbidity. Management is determined by the IPSS score, with alpha adrenergic blockers given in mild disease and 5 alpha reductase inhibitors given in more severe disease.

Answer 243

The diagnosis is most likely benign prostatic hyperplasia. It is hard to clinically differentiate between benign prostatic hyperplasia and prostate cancer however concern for prostate cancer from examination of the prostate would be due to: Smooth enlargement Nodular asymmetrical surface Large, hard irregular gland with evidence of extension beyond the capsule or into the seminal vesicles. General features to note are tenderness, nodules, asymmetry and induration (hardened mass) Other features on history that would make cancer more likely include; fatigue, weight loss, night sweats, bone pain, age > 50, FHx, ethnicity, high dietary fibre

Answer 244

- Low risk test - Easily reproducible and not operator dependent - Early PSA tests can detect cancer before symptoms occur - Most prostate cancers detected in patients with a > 15 year life expectancy are significant tumours that are likely to cause significant morbidity and mortality. Therefore testing is likely to be more beneficial in men between the ages of 50 and 70, especially if there is a family history of prostate cancer

Answer 245

- PSA is not specific- PSA is also raised in other conditions such as benign prostatic hyperplasia and prostatitis. - Only 40% of patients with PSA between 4 and 10 will have cancer - 20% of patients with PSA less than 4 will have cancer - Most prostate cancers are slow growing and are not a threat to life. These cancers may be treated unnecessarily leading to the risk of side effects such as impotence, urinary incontinence and proctitis. - There is no good clinical trial evidence that PSA screening saves lives - Prostate biopsies can cause rectal bleeding, dysuria, haematuria, haematospermia and infection and sepsis

Answer 246

A renal cell carcinoma is a malignant tumour of the renal parenchyma originating in the renal tubules. The classic presentation is with the triad of haematuria, a renal mass and flank pain; although all three features only occur in about 15% of cases, one is present in 40% of patients. Uncommon presentations include iron deficiency anaemia, polycythaemia due to erythropoietin production, hypertension due to renin production, hypercalcemia due to parathormone-like protein production, pyrexia of unknown origin, elevated ESR or as secondary lesions. NB- renal cell carcinoma is a renal cell malignancy arising from the real parenchyma/ cortex and accounts for about 85% of renal cancers.

Answer 247

The important diagnosis to exclude = carcinoma in situ of bladder History: - How long? Has it happened before? Recent trauma? - Painful or painless? (painless suggests malignancy) - Timing of blood in urine stream • Initial haematuria = urethral cause • Terminal haematuria = bladder stones • Throughout urine stream = bleeding of bladder or upper tract (kidney/ ureteral) - Lower urinary tract symptoms (e.g. dysuria, frequency, urgency, urethral discharge) • Presence suggests infectious or inflammatory process - Risk factors – smoking, pelvic radiation, occupational exposure to benzenes and amines (dry cleaners) - Symptoms of glomerular cause (e.g. oedema, weight gain, oliguria, dark urine) - Family history (inc. kidney stones, cancer, prostatic enlargement, sickle cell anaemia, collagen vascular disease, renal disease) - Menstruation - Trauma - Sexual activity - Medications (aspirin, NSAIDs, warfarin, NOACs, cytotoxic agents, rifampicin) - Recent sore throat - ? glomerulonephritis - Other respiratory tract infection - ?IgA nephropathy - Systemic illness - Travel abroad - ?malaria, ?schistosomiasis Investigations: - Urinalysis for haematuria (and exclude infection) - Urine cytology – positive in 90% of carcinoma in situ - US renal and bladder – for bladder tumour or upper tract obstruction - Cystoscopy enables pathological diagnosis • Typically, via a flexible cystoscopy under local anaesthetic • Rigid cystoscopy will then be required for more definitive assessment • Biopsy of any tumours identified and potential resection via transurethral resection of bladder tumour (TURBT) - CT urogram with contrast in excretory phase - FBC – will show reduced haemoglobin levels - Urinary markers of bladder cancer

Answer 248

The likely diagnosis is a ureteric stone that is acting as a nidus for infection leading to urosepsis. The patient is clearly septic and likely as a consequence of the obstruction has developed pyenephrosis (collection of pus in the renal pelvis[ broaden top part of the ureter]) of the kidney. This has likely occurred as a result of the failed passage of calculus fragments from lithotripsy, leading to steinstrasse (acute stone fragment impaction). Considering this, she needs initial resuscitation, followed by relief of the obstruction as this is a urological emergency. Resuscitation: Primary survey O2 with non rebreather 2x large bore IV cannulas- fluid resuscitation Bloods- FBC, UEC, lactate, cultures, serum calcium, phosphate and uric acid, CRP (with WCC raises suspicion for infection) Analgesia Antiemetics Indwelling catheter and monitor hourly urine output IV antibiotics- gentamicin and ampicillin Urological consult for decompression with a retrograde ureteric stent insertion. Investigations: Urine dipstick, midstream urine MCS, 24 hour urine for calcium, phosphate, oxalate, urate, cystine and xanthine KUB x-ray (90% of ureteric stones are radio-opaque as they contain calcium Renal ultrasound CT abdo/pelvis- gold standard for locating stones and evidence of complications Management: 1. Conservative management for stones less than 1cm with no complications- hydration, pain control, anti-emetics) 2. Stones between 1cm and 2cm are in general treated with extracorporeal shock wave lithotripsy. 3. Percutaneous nephrostolithotomy is a minimally invasive form of treatment that is usually reserved for renal and proximal ureteric stones and more distal stones > 2cm or that don't respond to lithotripsy.

Answer 249

The most likely diagnosis is a testicular cancer. Signs and symptoms include a testicular mass, swelling of the testis, heaviness in the scrotum and discomfort or pain. Cryptochordism, family history and infertility are risk factors for testicular cancer. Germ cell tumours account for the majority of testicular cancers. Germ cells give rise to two main kinds of cancer, seminomas and nonseminomatous tumours. • Seminomas- Are the most common germ cell type of testis cancer. They occur most often in men between the ages of 20 and 45 years old. They are usually treated surgically sometimes with adjuvant radiotherapy and may also be treated with chemotherapy in the case of metastasis. • Nonseminomatous germ cell tumours- may be more aggressive and are treated somewhat differently from seminomas. These tumours also occur in men in their 20s and 30s. The histologic types are: - Embryonal carcinoma - Yolk sac carcinoma - Choriocarcinoma - Teratoma • Carcinoma in situ- a non-invasive form of germ cell cancer that hasn't spread beyond the tubes in the testes. Sometimes the best option for treatment is watchful waiting. • Stromal cell tumour- Cancers that develop in the stromal cells, the supportive tissue of the testes that produce testosterone. However the tumours are usually benign. They account for fewer than 1 in 20 adult testicular tumours but up to 1 in 5 testicular tumours in boys. There are two types, Leydig cell tumours and sertoli cell tumours. They are usually cured by surgery. • A tumour in the testicles can also be secondary from lymphoma, leukaemia, prostate, lung, skin and kidneys. • Scrotal doppler ultrasound - First line investigation - Can confirm a solid intratesticular mass, as opposed to a fluid filled cyst, that is indicative of testicular cancer. • Tumour markers: - Beta HCG- secreted by synctiorophoblastic cells - Alpha fetoprotein (AFP)- produced by yolk sac elements - LDH- elevated in more than half of metastatic seminomas. - Seminomas- occasionally raised beta HCG but never raised AFP - Nonseminomatous- often raise AFP and/or beta HCG ``` • Urine: - MSU and MCS • Blood tests: - Raised inflammatory markers (WCC, CRP) - Low haemoglobin and albumin - Tumour markers as above • Surgical orchidectomy and histology of the mass to confirm diagnosis ```

Answer 250

The likely diagnosis is testicular cancer. Inspection: Rash, ulcers, erythema (cellulitis/ fungal infections) Enlargement of the testis and is it bilateral or unilateral Examination of the testes: - Use both thumbs and index fingers to gently palpate the whole testicle - Determine the size/ shape of the mass - Is the mass regular or irregular - Consistency- hard (solid), soft (cystic), bag of worms (varicocele) - Are you able to get above the mass: - No = inguinal hernia - Yes = hydrocele - Is the mass fixed to the testicle or separate: - Separate and hard = epididymitis/ orchitis - Separate and soft = epididymal cyst / spermatocele - Is there a cough impulse- suggests hernia/ varicocele - Does the mass transilluminate- transillumination suggests the mass is filled with fluid (e.g hydrocele) Epididymal cysts- separate from the body of the testicle. Found posterior to the testicle. Does transilluminate. Smooth surface with a fluctuant consistency. Hydrocele- Soft non tender swelling usually below and anterior to the testicle. It is confined to the scrotum and you can get above it on examination. It does transilluminate. The testes may be difficult to palpate if the hydrocele is large. Varicocele- Classically described as a bag of worms. Cough impulse present. Hard to get above. Varicoceles do not transilluminate. Inguinal hernia- Hard to get above, does not transilluminate, found superior to the testes. ``` Differential Diagnosis: Epididymal cysts • Epididymal cysts are the most common cause of scrotal swellings seen in primary care. - Features - Separate from the body of the testicle - Found posterior to the testicle • Associated conditions - Polycystic kidney disease - Cystic fibrosis - Von Hippel-Lindau syndrome • Diagnosis may be confirmed by ultrasound. • Management is usually supportive but surgical removal or sclerotherapy may be attempted for larger or symptomatic cysts. ``` Hydrocele • A hydrocele describes the accumulation of fluid within the tunica vaginalis. They can be divided into communicating and non-communicating: - Communicating: caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum. Communicating hydroceles are common in newborn males (clinically apparent in 5-10%) and usually resolve within the first few months of life - Non-communicating: caused by excessive fluid production within the tunica vaginalis • Hydroceles may develop secondary to: - Epididymo-orchitis - testicular torsion - testicular tumours • Features - Soft, non-tender swelling of the hemi-scrotum. Usually anterior to and below the testicle - The swelling is confined to the scrotum, you can get 'above' the mass on examination - Transilluminates with a pen torch - The testis may be difficult to palpate if the hydrocele is large • Diagnosis may be clinical but ultrasound is required if there is any doubt about the diagnosis or if the underlying testis cannot be palpated. • Management - Infantile hydroceles are generally repaired if they do not resolve spontaneously by the age of 1-2 years - In adults a conservative approach may be taken depending on the severity of the presentation. Further investigation (e.g. ultrasound) is usually warranted however to exclude any underlying cause such as a tumour Varicocele • A varicocele is an abnormal enlargement of the testicular veins. They are usually asymptomatic but may be important as they are associated with infertility. • Varicoceles are much more common on the left side (> 80%). • Features: - classically described as a 'bag of worms' - Subfertility • Diagnosis - ultrasound with Doppler studies • Management - Usually conservative - Occasionally surgery is required if the patient is troubled by pain. There is ongoing debate regarding the effectiveness of surgery to treat infertility

Answer 251

Medical indications: All patients with chronic kidney disease at stage 4 or 5 (GFR < 15 and GFR between 15 and 30 respectively) with progressive disease likely to require renal replacement therapy within the next 6 months Anticipated low perioperative mortality 80% likelihood of surviving for at least 5 years after transplantation Psychosocial indications: Ability to understand risks and benefits and cooperate with medical regimen Adequate psychosocial support Able to afford follow up care, post transplant medications etc No absolute contraindications to transplantation such as: Untreated malignancy Active infection Untreated HIV or AIDS Any condition where life expectancy is under 2 years

Answer 252

``` HLA typing: - HLA antigen type - HLA antibody screening - Lymphocyte cross matching- if recipient cells attack and kill donor cells this is indicative of rejection and transplantation should not go ahead ABO blood group compatibility ``` HLA = chromosome 6 ABO []

Answer 253

Q1 Likely to be polycystic kidney disease Q2 Hypertension Chronic renal failure Recurrent UTIs Renal stones Preeclampsia during pregnancy Liver cysts (most common extra-renal manifestation) Berry aneurysm- leading to subarachnoid haemorrhage Heart valve abnormalities (mitral valve prolapse) Diverticulosis in patients who have had a renal transplant Q3 Often asymptomatic Patients often present in adulthood as the cysts slowly expand, compressing the parenchyma disrupting local control of blood pressure and impairing renal function May present with chronic renal failure, hypertension, haematuria, loin pain or recurrent urinary tract infections The other main possibility is a horseshoe kidney. Complications include pleviureteric junction (PVJ) obstruction, renal stones, infection, tumours and trauma. Patients will often present with hydronephrosis, obstructive symptoms or urinary retention. NB- echogenic spaces within the kidneys on ultrasound is a characteristic finding of polycystic kidney disease

Answer 254

Abdominal aortic aneurysm (AAA) is a permanent pathological dilation of the aorta with a diameter > 1.5 times the expected AP diameter of that segment, given the patients sex and body size. The most commonly adopted threshold is a diameter of 3cm or more. More than 90% of aneurysms originate below the renal arteries. The usual indications for considering repair of an abdominal aortic aneurysm are: Ruptured or leaking aneurysm Symptomatic aneurysm (usually abdominal, back and groin pain) Aneurysm that is larger than 5.5 cm in males or 5cm in females Rapidly expanding AAA (>0.5cm/year) AAA associated with peripheral arterial aneurysm or peripheral artery disease Saccular aneurysm (aneurysm that only bulges on one side of the artery wall)

Answer 255

A patient with a ruptured AAA classically presents with a triad of acute abdominal pain (severe epigastric + or - back pain), abdominal distension and haemodynamic instability (hypotension, diaphoresis, tachycardia, tachypnoea) and possible cardiovascular collapse. Other possible symptoms include flank or groin pain or an expansile, pulsatile abdominal mass. Risk factors include; increasing age, male, smoker, FHx, atherosclerosis, hypertension, hypercholesterolaemia, other vascular aneurysms.

Answer 256

The diagnosis is most likely to be a ruptured abdominal aortic aneurysm. Urgent or emergent AAA repair is generally indicated for patients with ruptured AAA and diagnosis is therefore made from clinical picture in order to save time. No investigations are warranted except for those that facilitate the emergency surgery. These include UECs for renal function, coagulation screen, cross match, and ECG. If there is uncertainty in the diagnosis a FAST scan may be performed as long as this does not delay the time to theatre. Initial management is to notify ED and surgical staff and the insertion of two large bore IV cannulas for fluid resuscitation while maintaining a permissive hypotension due to risk of worsening AAA with aggressive fluid resuscitation. The patient should receive oxygen and analgesia (morphine). Theatre should also be booked, consent for surgery attained, catheterisation and calling of the blood bank. Two methods of aneurysm repair are currently available: Open AAA repair- open aneurysm repair involves replacement of the diseased aortic segment with a tube or bifurcated prosthetic graft through a midline abdominal or retroperitoneal incision Endovascular aneurysm repair- guide wire inserted in femoral artery or iliac artery up to the abdominal aorta followed by a sheathed stent graft, which is positioned with fluoroscopy. The stents are then deployed and the guide wires and removed.

Answer 257

The size of the AAA (>5.5cm) indicates the need for surgery due to his 10-22% risk per year of AAA rupture. Two methods of aneurysm repair are currently available: Open AAA repair- open aneurysm repair involves replacement of the diseased aortic segment with a tube or bifurcated prosthetic graft through a midline abdominal or retroperitoneal incision Endovascular aneurysm repair- guide wire inserted in femoral artery or iliac artery up to the abdominal aorta followed by a sheathed stent graft, which is positioned with fluoroscopy. The stents are then deployed and the guide wires are removed. This surgery requires fulfilment of anatomic criteria including a sealing zone above and below and adequate access vessels (commonly femoral and iliac) to accomodate stent graft. If the patient declines surgery or is not fit for surgery watchful waiting and cardiovascular risk reduction (smoking cessation, BP control, lipid control and weight loss) is also an option. NB EVAR has a lower mortality rate (0.5-2%) compared to open AAA repair

Answer 258

Complications associated with endovascular abdominal aortic repair are most commonly related to some technical aspect of the endograft placement and include: Access site complications such as infection, haematoma, thrombosis of accessed vessels, pseudoaneurysm, dissection, distal embolism and AV fistula Endograft complications include device migration, separation of components and endloeak, which is a term that describes the presence of persistent flow of blood into the aneurysm sac after endograft placement. This causes a continued risk of expansion and rupture. There can also be endograft infection with staphylococcus epidermidis or staphylococcus aureus and this can cause enterovascular fistula formation between the aorta and duodenum Systemic complications such as cardiopulmonary, IV contrast nephropathy and allergy and ischaemia Other complications such as abdominal compartment syndrome, post-implantation syndrome and conversion to open repair Endoleak type I- incompetent seal at the proximal or distal Endoleak type II- sac filling via a branch vessel III- mechanical failure of the graft IV- intentional leaking V- continuos expansion of the aneurysm sac with evidence of a leak

Answer 259

Carotid endarterectomy (CEA) is a surgical procedure used to treat carotid artery stenosis in which an incision is made in the anterior side of the neck, a filter and balloon catheter is used to removed the atherosclerotic plaque from the artery and the artery is closed with stitching or a graft. CEA is recommended for: - Symptomatic individuals with moderate (50%-70%) stenosis - Symptomatic individuals with high grade (70%-99%) stenosis. - Asymptomatic individuals with stenosis greater than 60% stenosis Symptomatic is defined as causing focal neurological symptoms, sudden in onset and referable to the carotid artery distribution (ipsilateral to the significant carotid atherosclerotic pathology) with symptoms in the last 6 months. Symptoms include transient visual obscuration from retinal ischaemia, contralateral weakness or numbness of an arm, leg or face, visual field defect, dysarthria and aphasia. The only absolute contraindication to CEA is asymptomatic individuals with complete carotid occlusion as the chance of stroke would be higher with CEA than without. Other relative contraindications include history of neck irradiation, concurrent tracheostomy, prior radical neck dissection, contralateral vocal chord paralysis, atypical surgically inaccessible lesion, unacceptably high medical risk. [] double check [] vascular runoff

Answer 260

The diagnosis is likely a TIA. Differentials include stroke, hypoglycaemia, seizure, complex migraine, subdural haematoma and brachial plexus injury. Initial investigations include FBC, UEC, cholesterol studies, lipids, glucose and PT, INR and APTT and a CT brain. A 12 lead ECG and carotid imaging with a carotid doppler ultrasound should also be performed. As an outpatient Holter monitor testing should also be performed to check for AF and an echocardiogram with bubble study may be performed in patients with a high clinical suspicion of a cardiac shunt, valvular disease or intraventricular thrombus.

Answer 261

The likely diagnosis is a TIA. Differentials include stroke, hypoglycaemia, seizure, complex migraine, subdural haematoma, brachial plexus injury ``` Risk factors for TIA include: Increasing age Alcohol abuse Smoking Diabetes mellitus Hypertension Congestive heart failure Carotid stenosis Valvular disease- especially aortic disease Atrial fibrillation ``` ``` Patent foramen ovale Hyperlipidaemia Inactivity Obesity Hypercoagulability ```

Answer 262

``` The arterial blood gas shows metabolic acidosis (as shown by low pH and base deficit), with lactic acidosis (elevated lactate), with partial respiratory compensation (low PaCO2). The most likely diagnosis is intestinal ischaemia, given the clinical history it is most likely to be secondary to emboli from atrial fibrillation. The reasonable differential diagnoses include: - Infectious colitis - Ulcerative colitis or Crohn’s disease - Diverticular disease - Peptic ulcer disease - Acute pancreatitis - SBO or LBO - Gastroenteritis - Bowel perforation - Acute myocardial infarction ```

Answer 263

The ABG shows metabolic acidosis with lactic acidosis (elevated lactate) with partial respiratory compensation (low PaCO2). The most likely diagnosis is intestinal ischaemia. Given the clinical history it is most likely to be secondary to emboli from atrial fibrillation. Management: Primary survey and resuscitation and supportive measures: supplemental oxygen Fluids Gastrointestinal decompression- NBM and NG tube Haemodynamic monitoring and support Correction of electrolyte abnormalities Pain control- parenteral opioids Anticoagulation- parenteral heparin Broad spectrum antibiotics- acute mesenteric or colonic coverage (triple therapy) Abdominal exploration, especially if peritoneal signs are present NB- Intestinal ischaemia develops as a consequence of severe hypoperfusion leading to transmural necrosis of the bowel wall, which can progress to sepsis, peritonitis, free intrabdominal air or extensive gangrene. Surgery should not be delayed patients suspected of having intestinal infarction or perforation based upon clinical findings, regardless of aetiology. For patients with non-occlusive mesenteric ischaemia, surgical exploration should be limited to patients with peritoneal signs.

Answer 264

Primary survey assessing vitals and haemodynamic stability Assess levels of pain and provide appropriate analgesia History: SOCRATES of pain and assess for the presence of rest pain Past medical history- ulcers, gangrene, MI, carotid artery disease, AF, smoking history, diabetes, hypertension Examination: Cardiovascular examination Neuromuscular examination- pain, paraesthesia, pulses, pallor, perishingly cold, paralysis Investigations: Bloods- FBC, UEC, LFTs, group and hold, coags, lipids, BGL ECG- AF or AMI Ankle brachial index Call vascular surgeon as soon as possible, potentially start heparin, possible CT angiography

Answer 265

The likely diagnosis is an acute ischaemic limb, most likely due to an emboli and this case likely secondary to atrial fibrillation or could be from thrombosis due to atherosclerotic occlusion. This is a surgical emergency and I would therefore call a vascular surgeon, call the operating theatre and call the anaesthetist. I would insert a cannula and correct any dehydration with fluids as hypotension is an exacerbating factor for an acute ischaemic limb. I would also give IV heparin and consider a CT angiography depending on the surgeons advice. I would also keep the patient NBM and give appropriate analgesia. I would take bloods including an FBC, UEC, CK, coagulation profile, lactate (which may be helpful in assessing and tracking the degree of tissue hypoperfusion) and group and save. I would also perform an ECG to check cardiovascular function and determine if AF is present at the moment, making an embolic cause of ischaemia more likely. Causes of ischaemic limb: Embolisation- AF, valvular vegetation, tumours such as an atrial myxoma (benign primary heart tumour most commonly found in the atrium), atherosclerotic, aneurysm Thrombosis- atherosclerosis or occlusion of a bypass graft Trauma- Blunt, penetrating or intravenous drug use Rarer- hypoperfusion, vasculitis, drugs, aortic dissection, venous gangrene Presentation of ischaemic limb: Pain, pallor, pulselessness, perishingly cold, paraesthesia and paralysis. Paraesthesia and paralysis indicate a threatened limb that requires emergency surgical review, regardless of the cause.

Answer 266

``` Determination of whether a leg is salvageable depends on the viability of the tissue. This is determined based on clinical findings and investigations including: Pain Capillary refill time Motor deficit Sensory deficit Arterial doppler findings Venous doppler findings ``` If tissue is not viable it needs amputation. However, tissue commonly presents as threatened and revascularisation with heparin infusion is continued post-operatively in continued revascularisation attempts. The ischaemic area is initially white but later becomes mottled/ livedo reticularis. If this blanches on pressure the limb is still viable. If the mottling does not blanch then the limb is not viable.

Answer 267

The clinical appearance in this patient suggests peripheral vascular disease with critical limb ischaemia (rest pain relieved with dependency), an abscess at the base of the right toe with possible cellulitis surrounding the abscess and poorly controlled diabetes. Investigations include: FBC, UEC, blood cultures, coags, LFT, HBA1c Foot x-ray looking for osteomyelitis ECG ABI (the ratio of the blood pressure at the ankle to the blood pressure in the arm, with lower blood pressures at the ankle suggesting peripheral artery disease), duplex doppler ultrasound, ?CT angiogram Treatment needed is three pronged: For the abscess this patient needs incision and drainage, wound debridement and antibiotics, likely iV tazocin in diabetic foot infection patients but depends on the swab results Diabetes control with lifestyle modification, inpatient endocrine consult and management of insulin dosing Control of ischaemic limb with vascular surgeon for possible intervention such as angioplasty or bypass (if arterial thrombosis is present).

Answer 268

Management considerations for peripheral vascular disease: Is the limb viable or not? Is revascularisation possible or is there a need for amputation Chronic presentation: Disease activity- claudication (does it limit lifestyle) and is there critical limb ischaemia Age and expected lifespan Patient compliance to medical therapy and lifestyle modifications Comorbidities such as diabetes Treatment Mild-moderate claudication- stop smoking, exercise, statin, aspirin, weight loss, BP control. consider balloon angioplasty Disabling claudication- balloon angioplasty or reconstructive arterial surgery Critical ischaemia- IV drug therapies such as prostacyclin (vasodilation), balloon angioplasty, reconstructive arterial surgery, amputation, appropriate analgesia

Answer 269

While determining the level of amputation several factors are taken into account including: Physical factors- tissue necrosis or infection, transcutaneous oxygen level and circulation of the extremity Co-existing diseases- diabetes, peripheral vascular disease and other systemic infections Experience and skills of the surgeon Nutritional status of the patient Some of the important principles include: The amputation is made through a level of healthy tissue to ensure all of the necrosis is removed Fitting of a prosthetic limb. Therefore common levels of amputation include transferral (just above the knee), transtibial (just below the knee), Syme’s malleolar amputation and mid tarsal amputation.

Answer 270

``` Above knee femoral amputation Below knee tibial amputation Knee disarticulation/ through knee Syme’s malleolar amputation Mid tarsal amputation ```

Answer 271

The most likely diagnosis is acute upper limb ischaemia (possibly secondary to AF) Investigations include a cardiovascular examination, difference in blood pressure between the two arms or an ankle brachial index (ABI), bloods (FBC, UEC, coags, thrombophilia screen, CRP), ECG, duplex ultrasound of upper limb and CT angiogram.

Answer 272

The most likely diagnosis is acute upper limb ischaemia. Causes of ischaemic limb: Embolisation- AF, valvular vegetation, tumours such as an atrial myxoma (benign primary heart tumour most commonly found in the atrium), atherosclerotic, aneurysm Thrombosis- atherosclerosis or occlusion of a bypass graft Trauma- Blunt, penetrating or intravenous drug use Rarer- hypoperfusion, vasculitis, drugs, aortic dissection, venous gangrene Diagnosis includes: History: Palpitations, family Hx of AF, known AF or valvular disease Diabetes, hypertension, smoking, alcohol, sedentary lifestyle History of trauma Intravenous drug use Examinations Cardiovascular examination Investigations ECG Echocardiogram Doppler ultrasound

Answer 273

The most likely diagnosis is acute upper limb ischaemia possibly secondary to atrial fibrillation. Treatment options angioplasty, stenting, carotid-subclavian bypass or embolectomy. Treatment should also include secondary prevention measures such as: Control of hypertension Control of AF with anticoagulation therapy (warfarin or apixaban) Lipid modification Smoking cessation Antithrombotic therapy (anticoagulants or anti platelets)

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