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The book is organized into 16 chapters, each offering trainees and trainers complete examinations as in the real structured oral examination, covering around 70 relevant topics. Each chapter includes clinical anaesthesia and basic science broadly organized into the six areas covered by the exam: long-cases, short-cases, applied anatomy, physiology, pharmacology and clinical measurement. The book also includes a hot topics chapter addressing recent advances beloved of examiners.
Chapter Clinical anaesthesia Long case: A young boy with Guillain–Barré syndrome 163 Short cases 168 Questions 168 Answers 169 Short case 1: Pre-eclampsia 169 Short case 2: A patient in recovery following TURP 172 Short case 3: Autonomic neuropathy 173 Clinical science Questions 176 Answers 177 Anatomy: Femoral triangle 177 Physiology: Intraocular pressure 179 Pharmacology: Local anaesthetic 181 Physics and clinical measurements: Tourniquets 183 161 This page intentionally left blank Clinical anaesthesia Long case: A young boy with Guillain–Barré syndrome A 13-year-old boy is admitted with complaints of days’ history of malaise, lethargy, intermittent headache, and weak legs He also complains of features suggestive of bulbar weakness His parents are Jehovah’s Witnesses On examination, he was apyrexial Clinical examination Temperature: 36.4°C; weight: 49 kg; height 160 cm Pulse: 110/min, irregular; BP: 150/75 mmHg; respiratory rate: 26/min; SaO2; 92% with L/min O2 Chest: bilateral air entry present, harsh vesicular breath sounds, crepitations over right lower lung base Cardiovascular system: normal heart sound with no murmurs Central nervous system: blurred vision, dysphasia, and dysarthria Power of 3/5 in all limbs areflexia in all limbs Laboratory investigations Hb MCV WBC Platelets 13.0 g/dL 89 fL 5.1 × 109/L 350 × 109/L Na K Urea Creatinine 142 mEq/L 3.7 mEq/L 6.6 mmol/L 107 μmol/L 110 Glucose PaO2: 10 PaCO2: 6.5 pH: 7.22 HCO3−: 31 kPa kPa Protein >400 mg/L, no elevation in cell counts 6.4 mmol/L Lactate: 0.9 mmol/L CRP CSF BE: QUESTIONS 10 11 12 13 14 15 Summarize the case Do you want to know any other details from history and examination? Comment on the chest X-ray and ECG What are the differential diagnoses? Why is it not botulism? Why is it not polio? Can this be aseptic meningitis? What is your probable diagnosis? What are the clinical features of Guillain–Barré syndrome (GBS)? What are the indications for admitting a GBS patient to ICU? What are the treatment options available? Which is better—plasmapheresis or immunoglobulins? Why? Which treatment options are you going to use in this patient and why? Can this boy decide for himself about treatment? What are the supportive treatments you can provide? 163 Structured Oral Examination Practice for the Final FRCA Figure 8.1 Chest X-ray aVR V1 V4 aVL V2 V5 aVF V3 V6 Figure 8.2 ECG 164 Chapter ANSWERS Summarize the case A 13-year-old boy presents with a history of lethargy, intermittent headache, weak legs and bulbar weakness On examination all his limbs are weak 3/5 and areflexic He is apyrexial, hypertensive, tachycardic, and blood gases show a compensated respiratory acidosis CSF shows evidence of increased protein Blood count and CSF show no evidence of infection Do you want to know any other details from history and examination? History Any preceding illness—gastrointestinal infection/respiratory infection? Recent vaccines, travel, trauma, toxic ingestion z Any sensory symptoms, visual disturbance, problems with balance/ataxia? z Does he have pain? z Any difficulty voiding urine/excessive sweating? z Degree of difficulty with coughing, swallowing, speaking z Previous history of similar events Past medical history, medications, allergies, family history z z Examination Sensory abnormalities Cranial nerve examination—facial weakness, bulbar palsy, ophthalmoplegia, reactivity of pupils z Ataxia z Ability to cough, clear secretions, vital capacity z z Comment on the chest X-ray and ECG Chest X-ray: posterio-anterior chest X-ray Normal cardiomediastinal contour Lungs and pleural spaces clear Normal bones ECG: sinus rhythm, HR: 75 bpm, normal P waves, normal PR interval (duration of 0.12–0.2 sec), QRS complex (duration of 0.06–0.1 sec), normal axis (between 0–90°) My Impression is of a normal ECG What are the differential diagnoses? The differential diagnosis can be subdivided into: Spinal cord lesions: trauma, transverse myelitis, epidural abscess, tumours, vascular malformations, cord infarctions, cord compression, lumbosacral disc syndromes, poliomyelitis, enteroviral infections of the anterior horn cells, Hopkins syndrome z Peripheral neuropathies: toxic neuropathy (glue sniffing, heavy metals, organophosphate pesticides, vincristine), HIV, diphtheria, Lyme disease, inborn errors of metabolism (porphyria, Leigh disease, Tangier disease), critical illness polyneuropathy z Neuromuscular junction disorders: tick paralysis, myasthenia gravis, botulism, hypercalcaemia, Lambert–Eaton syndrome z Myopathies: periodic paralysis, hypokalaemia, dermatomyositis, critical illness myopathy, benign acute childhood myositis z Why is it not botulism? Botulism is an acute bilateral symmetrical descending paralysis, it affects neck and arms before legs unlike this patient who complains of leg weakness z Tendon reflexes are normally present except in severe cases of botulism z History of nausea, vomiting, or abdominal pain is common with botulism (not wound botulism) z 165 Structured Oral Examination Practice for the Final FRCA Why is it not polio? This is not poliomyelitis because: Poliomyelitis is a disease caused by one of three small RNA enteroviruses transmitted by the respiratory of faecal–oral routes z Polio gives a picture of meningeal symptoms and asymmetrical paralysis following an acute febrile illness Although the patient has a headache there is no other evidence of meningeal symptoms such as confusion, decreases consciousness level, irritability z He also has a symmetrical paralysis which affects his arms and legs unlike polio which is mostly lower limbs and cranial nerves only z CSF examination in polio also differs, showing an increased number of lymphocytes and only minimal increase in protein z Can this be aseptic meningitis? No, as patients with aseptic meningitis often have flu-like symptoms and headache; they not have focal neurological signs and are not critically unwell This is not the case for this patient who has bulbar and limb weakness What is your probable diagnosis? My probable diagnosis is Guillain–Barré syndrome What are the clinical features of Guillain–Barré syndrome (GBS)? The clinical features of GBS are: Progressive motor weakness, usually ascending from the legs (proximal more than distal) Areflexia z Facial palsy and bulbar weakness z Ophthalmoplegia z Sensory symptoms z Severe pain, often affecting the girdle area z Weakness of the respiratory musculature leading to respiratory failure z Autonomic dysfunction—under/over activity of sympathetic and parasympathetic systems leading to arrhythmias, wide fluctuations in BP and pulse, urinary retention, ileus, and excessive sweating z z 10 What are the indications for admitting a GBS patient to ICU? The management of patients with GBS can be challenging because of its unpredictable course These patients can rapidly deteriorate leading to respiratory failure It is suggested that any patient without sound evidence of stable neuromuscular status on initial evaluation or presentation will require admission to ICU One in three patients with GBS will need prolonged ICU monitoring and possible intubation 25–30% need mechanical ventilation A vital capacity 110 mmHg diastolic on two occasions at least hours apart z Proteinuria >5 g in 24 hours or 40 years z Booking BMI >35 z Chronic hypertension (booking BP >140 systolic) z Multiple pregnancy z Hydropic fetus z Associated medical conditions: diabetes mellitus, renal disease and anti-phospholipid syndrome z z What is the pathogenesis of eclampsia? This is a disease of heterogeneous cause of both maternal and placental origin 169 Structured Oral Examination Practice for the Final FRCA Exact aetiology is not known but there are association to immunological, genetic, endothelial, platelet, and coagulation factors z There is endothelial damage or altered sensitivity which leads to decreased production of vasodilatory substances, increased sensitivity to vasoconstrictors, and increased glomerular permeability These changes leads to: Increased systemic vascular resistance Increased sodium and water retention In severe conditions there is platelet aggregation, haemolysis, and hepatic dysfunction (HELLP syndrome) z What are the pathophysiological changes to various systems? Pre-eclamptic toxaemia (PET) is a multisystem disorder of unknown origin but widespread endothelial dysfunction Cardiovascular system: Generalized vasoconstriction leading to increased SVR and diastolic hypertension Increased capillary permeability—peripheral oedema, intravascular depletion, and decreased colloid oncotic pressure Poor correlation between CVP and pulmonary capillary wedge pressure measurements and are prone for pulmonary and cerebral oedema Hypercoagulability, platelet activation, and activation of fibrinolytic systems are seen z Respiratory system: Upper airway oedema—face, tongue, neck, and larynx may lead to difficult laryngoscopy and intubation Fluid management requires special care as the patient is prone to pulmonary oedema, especially postpartum stage z Renal system: There is decreased GFR and increased permeability leading to proteinuria and hypoalbuminaemia Decreased uric acid excretion leads to increased plasma levels and acts as a marker for severity of the disease There is tubular dysfunction leading to acute renal failure z Hepatic changes: Serum transaminase levels frequently increase, in extreme cases HELLP syndrome Epigastric or subcostal pain is a serious sign—indicating hepatic oedema, subcapsular haematoma, or impending hepatic rupture z CNS changes: Neurological signs/symptoms like headache, visual disturbances, vomiting, confusion, hyperreflexia indicate altered cerebral perfusion Cerebral ischaemia due to oedema and vasoconstriction may lead to seizures— eclampsia Cerebral haemorrhage due to severe hypertension is also seen and can be fatal z Haematological changes: Altered coagulation, thrombocytopenia, and rarely DIC is seen Microvascular haemolysis and anaemia is seen in HELLP z Feto-placental unit: many of the changes seen are due to decreased placental perfusion Intrauterine growth restriction (IUGR) is a serious risk and so is placental abruption z 170 Structured Oral Examination Practice for the Final FRCA Opioids Classically not used as older opioids had slower onset and longer duration But newer opioids like alfentanil (20–30 mcg/kg) and remifentanil (1 mcg/kg) are quicker onset and quicker offset The addition of opioids may reduce the dose of induction agents and make the entire process haemodynamically stable The disadvantage on the other hand is in the possibility of respiratory depression in a difficult intubation situation and that opioids can cause chest wall rigidity and vocal cord closure Non-depolarizing relaxants When suxamethonium is contraindicated, non-depolarizing relaxants are used The primary disadvantage of this situation is the much slower onset time and the resulting risk for aspiration On the other hand, with the use of rocuronium (0.6–1.5 mg/kg) it has become much faster onset with intubating conditions similar to that of suxamethonium Further, with availability of sugammadex it is now possible to use in patients with a difficult airway Manual ventilation Classically IPPV is not performed with RSII for fear of gastric insufflation, regurgitation, and aspiration The view has been that people with normal airways who are pre-oxygenated adequately not need PPV due to the short duration of apnoea But many clinicians use IPPV with RSII If the peak airway pressures are kept