Approach to the Patient

Seminars 1–16 · 18,015 words · Download this chapter as PDF

How Part II Differs

In Part I you were told the diagnosis in the title and the case taught you how to confirm and manage it. That is not how patients arrive. A patient arrives with a symptom, and the diagnosis is the thing you are trying to produce.

These cases therefore run in a different order. The differential comes first, before any history is taken, because the differential is what the history is for. A student who takes a history before generating a differential is collecting facts without knowing which ones matter.

Seminar 1 · Approach to the Patient with Jaundice

1. Think First — Three Compartments, Three Questions

Answer three questions in order, and the diagnosis narrows at each step:

• Is the bilirubin conjugated or unconjugated? This separates haemolysis and Gilbert syndrome from everything else, and it costs one extra box on the request form.

• Is the enzyme pattern hepatitic or cholestatic? Aminotransferases out of proportion means the hepatocytes; alkaline phosphatase and gamma-glutamyl transferase out of proportion means the biliary tree.

• Are the bile ducts dilated? This is what the ultrasound is for, and it is the pivotal investigation in the whole assessment.

2. What Could Kill in the Next Hour

• Acute liver failure — jaundice with encephalopathy and a rising INR. See Case 35.

• Paracetamol toxicity — check a level in every jaundiced patient regardless of the history.

• Severe haemolysis, and sepsis with jaundice as a manifestation rather than a cause.

3. The History That Discriminates

4. The Examination That Discriminates

• The presence or absence of chronic liver disease stigmata — spider naevi, palmar erythema, gynaecomastia, ascites. Their absence, as here, argues against cirrhosis and for an acute obstructive process in a previously normal liver.

• Mental state and asterixis, which convert this from a diagnostic problem into an emergency.

• Liver edge — smooth and tender in hepatitis, hard and irregular in malignancy or cirrhosis; splenomegaly (portal hypertension or haemolysis); left supraclavicular node; abdominal masses; ascites.

• Pallor in haemolysis; Kayser–Fleischer rings in any patient under 40; scratch marks; xanthelasma in chronic cholestasis.

5. Investigations, in Tiers

• Bedside: urinalysis — bilirubin in the urine means it is conjugated; capillary glucose.

• First line: split bilirubin, full liver enzyme profile, INR and albumin as the measures of function, complete blood count with reticulocytes and blood film, haptoglobin and lactate dehydrogenase, direct antiglobulin test if unconjugated, amylase, renal function, paracetamol level, viral hepatitis serology, autoimmune screen with immunoglobulins, and — under 40 — caeruloplasmin and iron studies.

• Magnetic resonance cholangiopancreatography is diagnostic; endoscopic retrograde cholangiopancreatography is therapeutic. Do not use the latter as a purely diagnostic test — it carries a real risk of post-procedure pancreatitis and should be reserved for when you intend to intervene.

• CA 19-9 rises in biliary obstruction of any cause, including benign, so interpret it only after the obstruction is relieved and never as a screening test.

6. Management While You Are Still Deciding

• Vitamin K for a prolonged prothrombin time — in obstructive jaundice the deficiency is of absorption, and it corrects.

• Cholangitis: broad-spectrum antibiotics and urgent biliary drainage. Do not wait for the fever to settle before referring for drainage.

• Maintain hydration and monitor renal function. Jaundiced patients are prone to acute kidney injury, particularly around contrast and procedures.

• Treat the itch — it is genuinely disabling and is often ignored. Cholestyramine, with other agents where that fails.

• Nutrition, including fat-soluble vitamins; stop hepatotoxic drugs; and refer to the multidisciplinary team where malignancy is suspected, for staging and for biliary stenting, which relieves symptoms whether or not resection is possible.

7. Teaching Points and Viva Questions

• Split the bilirubin, read the enzyme pattern, then ask the ultrasound whether the ducts are dilated.

• Painless jaundice with weight loss is malignancy until proved otherwise.

• A palpable non-tender gallbladder points away from stones.

• Fever plus pain plus jaundice means the biliary tree needs draining, not just antibiotics.

• The INR and albumin tell you how the liver is working. The bilirubin does not.

• Endoscopic retrograde cholangiopancreatography is a treatment, not an investigation.

Questions you should be able to answer:

• His urine contains bilirubin. What does that exclude?

• Explain the reasoning behind Courvoisier’s sign.

• The ultrasound shows no duct dilatation. How does your plan change?

• A different patient has jaundice, fever and rigors with a blood pressure of 84/50. What are your first three actions?

• A 24-year-old has an isolated unconjugated bilirubin of 45 with normal enzymes after a period of fasting. What is the diagnosis?

Seminar 2 · Approach to the Patient with Generalised Anasarca

1. Think First — Four Mechanisms

Oedema forms when the Starling forces are disturbed. There are only four ways to do that, and every cause sits in one of them.

Add two that fit awkwardly: hypothyroid myxoedema, which is non-pitting, and pregnancy.

2. What Could Kill in the Next Hour

• Pulmonary oedema with hypoxia; cardiac tamponade; massive pulmonary embolism — for which the nephrotic patient is at high risk; severe hyponatraemia; sepsis; and anasarca with acute kidney injury and hyperkalaemia.

3. The History That Discriminates

• Where did it start and when is it worst? Face on waking versus ankles by evening. This one question separates the renal from the cardiac patient more efficiently than any test.

• Frothy urine, haematuria, reduced urine output — renal. Orthopnoea, paroxysmal nocturnal dyspnoea, chest pain, palpitations — cardiac.

• Jaundice, alcohol, known liver disease, abdominal swelling preceding leg swelling — hepatic.

• Diarrhoea, weight loss, malabsorption — protein-losing enteropathy or malnutrition.

• Drugs — calcium channel blockers are a very common and entirely reversible cause of ankle oedema, and anti-inflammatory drugs cause fluid retention and worsen every other cause.

• Underlying disease that causes nephrotic syndrome: diabetes, hepatitis B and C, human immunodeficiency virus, systemic lupus erythematosus, amyloidosis, myeloma, malignancy, and recent infection.

4. The Examination That Discriminates

• Jugular venous pressure, weight, blood pressure, and the urine dipstick — which you perform yourself rather than waiting for.

• Distribution of oedema: periorbital, sacral in a bedbound patient, scrotal, and whether it pits.

• Ascites and shifting dullness; pleural effusions; third heart sound and murmurs; pulsatile hepatomegaly; Kussmaul sign for constrictive pericarditis.

• Stigmata of chronic liver disease; thyroid examination; lymphadenopathy; and xanthelasma, which accompanies the hyperlipidaemia of nephrotic syndrome.

5. Investigations, in Tiers

• Bedside: urine dipstick, and a urine protein-to-creatinine or albumin-to-creatinine ratio. This single test immediately separates the renal cause from all the others, and it is available within minutes.

• First line: serum albumin and total protein, liver and renal function, lipids, complete blood count, C-reactive protein, thyroid function, glucose, natriuretic peptide, chest radiograph, electrocardiogram.

• Targeted — if nephrotic: hepatitis B and C, human immunodeficiency virus, antinuclear antibody, anti-double-stranded DNA and complement, antineutrophil cytoplasmic antibodies, serum immunoglobulins with protein electrophoresis and serum free light chains to exclude myeloma and amyloidosis, and renal biopsy — which in an adult determines the treatment and is not optional.

• Targeted — otherwise: echocardiography, abdominal ultrasound, and faecal alpha-1 antitrypsin clearance for protein-losing enteropathy.

6. Management While You Are Still Deciding

• Salt restriction and fluid restriction, with daily weights as the measure of response.

• Loop diuretic — and expect to need more than usual. Gut wall oedema impairs absorption of oral diuretics, so intravenous administration or a higher dose is frequently required, sometimes combined with a thiazide for sequential blockade.

• An angiotensin-converting enzyme inhibitor or receptor blocker to reduce proteinuria, with monitoring of potassium and creatinine.

• Statin for the hyperlipidaemia; thromboprophylaxis, and formal anticoagulation where the albumin is very low or there is another risk factor.

• Vaccination, including pneumococcal; treat infection promptly and with a low threshold.

• Then treat the cause, which in an adult means acting on the biopsy — immunosuppression for the primary glomerular diseases, and treatment of the underlying disorder in secondary causes.

7. Teaching Points and Viva Questions

• Look at the neck before the ankles. The jugular venous pressure divides the differential in two.

• Puffy eyes in the morning is a renal history; swollen ankles in the evening is a cardiac one.

• Dipstick the urine yourself, in the first five minutes.

• Nephrotic patients clot, and they get infected. Anticipate both.

• Oral diuretics are poorly absorbed through an oedematous gut.

• In an adult, the biopsy determines the treatment.

Questions you should be able to answer:

• His jugular venous pressure is normal. Which half of your differential does that remove?

• Why is he at risk of thrombosis, and what would you do about it?

• He is not responding to 40 mg of oral furosemide. Give two reasons and your next step.

• What must be excluded before you attribute this to a primary glomerular disease?

• A different patient has ankle oedema, a normal albumin and a normal jugular venous pressure, and takes amlodipine. What is your first move?

Seminar 3 · Approach to the Patient with Acute Chest Pain

1. Think First — The Six That Kill, Then Everything Else

Then the rest: pericarditis, myocarditis, pneumonia and pleurisy, gastro-oesophageal reflux and oesophageal spasm, musculoskeletal and costochondral pain, herpes zoster before the rash appears, biliary and pancreatic pain referred to the chest, and anxiety — which is a diagnosis of exclusion, not a first impression.

2. What Could Kill in the Next Hour

• Electrocardiogram within 10 minutes, repeated if the first is unremarkable and the pain continues.

• Oxygen only if hypoxic; intravenous access; continuous monitoring beside a defibrillator; analgesia.

3. The History That Discriminates

• How quickly did it reach its worst? Instantaneous and maximal at onset suggests dissection or pneumothorax. Crescendo over minutes suggests ischaemia.

• Character and radiation. Heaviness to the arm or jaw suggests ischaemia; tearing to the back suggests dissection; sharp and pleuritic suggests pleura, pericardium or embolism.

• What changes it? Worse on inspiration — pleuritic. Relieved by sitting forward — pericarditis. Reproduced by movement or palpation — musculoskeletal, though this does not exclude a serious cause. Related to food or lying flat — oesophageal.

• What came with it? Sweating, nausea and vomiting favour ischaemia. Syncope raises dissection, embolism and arrhythmia. Vomiting immediately before the pain began raises oesophageal rupture.

• Risk factors for each of the six, taken deliberately — including recent surgery, immobility and long-haul travel for embolism, as in this patient, and cocaine use in a younger one.

4. The Examination That Discriminates

• Both arms, all pulses, respiratory rate and oxygen saturation, perfusion and conscious level.

• Jugular venous pressure — raised in tamponade, right ventricular infarction and massive embolism.

• Heart sounds: a new early diastolic murmur suggests dissection into the aortic root; a rub suggests pericarditis; muffled sounds suggest tamponade. Test for pulsus paradoxus.

• Chest: tracheal position, asymmetry of expansion, percussion note, breath sounds, and surgical emphysema.

• Calves; abdomen; chest wall palpation; and the skin over the dermatomes for early zoster.

5. Investigations, in Tiers

• Bedside: electrocardiogram within 10 minutes and repeated; oxygen saturation; glucose.

• First line: high-sensitivity troponin using the local pathway with a repeat sample; complete blood count, renal function, coagulation; chest radiograph.

• Targeted: D-dimer only where pulmonary embolism is being considered and the pre-test probability is low or intermediate — a positive result in a high-probability patient adds nothing and a negative one cannot be relied on. Then computed tomographic pulmonary angiography, or computed tomographic aortogram, or echocardiography, as the differential dictates.

6. Management While You Are Still Deciding

• Monitored area, oxygen to target, analgesia, and treatment of the specific diagnosis once identified — thrombolysis or thrombectomy for infarction, anticoagulation for embolism, urgent surgical referral for dissection or rupture, needle decompression for tension pneumothorax.

• Where the diagnosis remains uncertain, the disposition decision is the clinical act. Use a validated pathway, and if discharging, provide explicit safety-netting and arranged follow-up rather than an instruction to return if worse.

• Remember that a patient may have two diagnoses at once — an embolism and demand ischaemia, or pneumonia and an arrhythmia. Do not stop looking once the first explanation is found.

7. Teaching Points and Viva Questions

• Electrocardiogram in ten minutes, and repeat it if the pain persists.

• Both arms before the aspirin.

• Hypoxia with a clear chest is pulmonary embolism until proved otherwise.

• Tension pneumothorax is treated before it is imaged.

• Troponin is a marker of injury, not of a diagnosis.

• Reproducible chest wall tenderness lowers the probability of a dangerous cause but never excludes it.

Questions you should be able to answer:

• Give the six immediately life-threatening causes and one discriminating feature of each.

• Why is her troponin raised, and what does the T wave inversion represent?

• When is a D-dimer useful, and when is it worse than useless?

• What features in a history would make you withhold aspirin?

• A patient collapses with chest pain, a blood pressure of 70/40, a raised jugular venous pressure and a clear chest. Give three diagnoses.

Seminar 4 · Approach to the Patient with Acute Dyspnoea

1. Think First — Follow the Oxygen

Four questions sort most patients within a minute of walking to the bedside:

• Is there stridor, or wheeze, or neither? Stridor is upper airway and is an emergency; wheeze is lower airway; neither points elsewhere.

• Is the chest clear despite hypoxia? Then think pulmonary embolism, anaemia, acidosis, or shunt.

• Is the jugular venous pressure raised? Cardiac, embolic or tamponade.

• Is it unilateral? Pneumothorax, effusion or consolidation.

2. What Could Kill in the Next Hour

• Sit the patient up. Give oxygen to an explicit target — 94–98%, or 88–92% where there is a risk of carbon dioxide retention, written on the chart. Monitoring, intravenous access, and senior help early.

• Look immediately for the causes that are reversible within minutes: tension pneumothorax, anaphylaxis, upper airway obstruction, and opioid toxicity.

3. The History That Discriminates

• Speed of onset is the most informative single item. Seconds to minutes — pneumothorax, embolism, aspiration, anaphylaxis, arrhythmia. Hours — asthma, pulmonary oedema, pneumonia. Days to weeks — effusion, anaemia, interstitial disease, malignancy.

• Orthopnoea and paroxysmal nocturnal dyspnoea favour a cardiac cause; fever and purulent sputum an infective one; pleuritic pain and unilateral leg swelling an embolic one; wheeze with a known diagnosis an airways one.

• Weight gain, ankle swelling, and any recent change to diuretic dose or adherence — a very common and entirely correctable precipitant.

• Exposure history, occupational history, drugs, and the patient’s baseline exercise tolerance, without which "breathless" cannot be quantified.

4. The Examination That Discriminates

• Respiratory rate counted, saturation on air with the device and flow recorded, ability to complete a sentence, accessory muscle use, cyanosis, conscious level.

• Jugular venous pressure; tracheal position; percussion and auscultation comparing sides; heart sounds, third sound and murmurs; peripheral oedema and calves; peak flow; temperature; capillary glucose.

5. Investigations, in Tiers

• Bedside: arterial or venous blood gas — which tells you the type of respiratory failure, whether there is acidosis, the lactate, and the bicarbonate as a marker of chronicity; electrocardiogram; glucose; peak flow.

• First line: chest radiograph, complete blood count, renal function, C-reactive protein, natriuretic peptide, troponin.

• Targeted: computed tomographic pulmonary angiography where embolism is suspected; echocardiography; sputum and blood cultures; carboxyhaemoglobin.

• Bedside ultrasound is increasingly the fastest discriminator available — B-lines of pulmonary oedema, pleural effusion, absent lung sliding in pneumothorax, gross cardiac function and inferior vena cava filling, all in a few minutes at the trolley.

6. Management While You Are Still Deciding

• Controlled oxygen to a written target, with a repeat gas after 30–60 minutes.

• Treat the most likely and the most dangerous simultaneously, then subtract treatments as the picture clarifies rather than adding indefinitely.

• Continuous positive airway pressure for cardiogenic pulmonary oedema, or non-invasive ventilation for hypercapnic acidosis, with early critical care involvement.

• Reassess after every intervention. Improvement or its absence is itself diagnostic information.

7. Teaching Points and Viva Questions

• Write the target saturation range on the chart. "Give oxygen" is not a prescription.

• Speed of onset narrows the differential faster than any investigation.

• Hypoxia with a clear chest, and the jugular venous pressure, are the two highest-yield observations.

• Elderly patients are allowed more than one diagnosis, and usually have them.

• Hyperventilation is what you conclude at the end, never what you assume at the start.

Questions you should be able to answer:

• What oxygen target would you set for this man, and why?

• Name the three processes contributing to his breathlessness and the treatment for each.

• His gas shows pH 7.28, carbon dioxide 8.4 kPa, bicarbonate 31. Interpret it.

• A 24-year-old is acutely breathless with a clear chest and normal saturations. What must you exclude before diagnosing hyperventilation?

• Which four bedside ultrasound findings would you look for, and what would each tell you?

Seminar 5 · Approach to the Patient with Headache

1. Think First — Primary and Secondary

• Primary headache disorders: migraine with and without aura, tension-type headache, and the trigeminal autonomic cephalalgias including cluster headache.

• Secondary headache is where the danger lies:

2. What Could Kill in the Next Hour

• Bacterial meningitis — antibiotics immediately, before imaging and before lumbar puncture (Case 44).

• Subarachnoid haemorrhage with rebleeding or hydrocephalus.

• Giant cell arteritis with visual symptoms — start high-dose corticosteroids on suspicion, before the biopsy, because the visual loss is sudden, painless and irreversible.

• Raised intracranial pressure with impending herniation; carbon monoxide poisoning; hypertensive emergency with encephalopathy.

3. The History That Discriminates

• Time to maximum intensity, as above. Then duration, frequency and whether the pattern has changed.

• Positional variation: worse lying flat and on waking suggests raised pressure; worse on standing and relieved by lying suggests low cerebrospinal fluid pressure, as after a dural puncture.

• Triggers: exertion, coughing, straining and sexual activity all raise the concern for haemorrhage on a first occurrence.

• Associated features: fever, rash, visual disturbance, diplopia, weakness, seizure, jaw pain on chewing, lacrimation and nasal congestion with a strictly unilateral orbital pain (cluster), and aura.

• Analgesic use — how many days per month, which identifies medication overuse headache, a very common and entirely reversible cause of daily headache.

• Pregnancy or recent delivery; anticoagulation; immunosuppression; malignancy; recent trauma or neck manipulation; and whether anyone else at home has a headache.

4. The Examination That Discriminates

• Temperature and blood pressure, conscious level, and a full neurological examination.

• Fundoscopy for papilloedema — omitted far more often than it is performed, and the finding changes the plan entirely.

• Neck stiffness; the skin for a non-blanching rash; temporal artery tenderness, thickening and absent pulsation in anyone over 50; the eye itself for redness and a mid-dilated pupil; visual acuity, fields and colour vision; and pupillary responses including Horner syndrome.

5. Investigations, in Tiers

• Giant cell arteritis: erythrocyte sedimentation rate and C-reactive protein urgently, then temporal artery ultrasound or biopsy within days — the biopsy remains informative for a week or two after starting steroids, so treatment is never delayed for it. Same-day ophthalmology assessment if there are visual symptoms.

• Meningitis: blood cultures, polymerase chain reaction, and lumbar puncture — with antibiotics given first.

• Cerebral venous sinus thrombosis: computed tomographic or magnetic resonance venography — plain imaging is frequently normal.

• Dissection: angiography with fat-suppressed sequences. Glaucoma: intraocular pressure and immediate ophthalmology referral. Carbon monoxide: carboxyhaemoglobin on a blood gas.

• Magnetic resonance imaging for a suspected mass lesion or where the picture is progressive.

6. Management While You Are Still Deciding

• Analgesia and antiemetics while investigation proceeds — treating the pain does not obscure the diagnosis.

• Avoid opioids in primary headache disorders, which promote medication overuse headache and rarely work well.

• Treat the specific cause: neurosurgical referral and nimodipine for subarachnoid haemorrhage; antibiotics for meningitis; corticosteroids for arteritis; anticoagulation for venous thrombosis.

• For primary headache: acute treatment with a triptan or an anti-inflammatory drug, consideration of prophylaxis where attacks are frequent, a headache diary, attention to sleep, hydration and caffeine, and explicit review of analgesic frequency.

7. Teaching Points and Viva Questions

• Ask how long it took to peak, not how severe it is.

• Computed tomography sensitivity falls after six hours; xanthochromia needs twelve.

• Start steroids in suspected giant cell arteritis before the biopsy, not after.

• Do fundoscopy. Papilloedema changes everything that follows.

• Take the temperature and the blood pressure in every headache.

• Ask how many days a month she takes painkillers, and whether anyone else at home has a headache.

Questions you should be able to answer:

• Her computed tomogram at 7 hours is normal. What do you do, and when?

• What is xanthochromia and why must you wait 12 hours?

• A 72-year-old has a new headache and pain in her jaw when chewing. What do you do, in what order?

• Give five red flags from the SNOOP list and the diagnosis each suggests.

• A patient has daily headache and takes codeine most days. What is the likely diagnosis and the treatment?

Seminar 6 · Approach to the Patient with Arthritis

1. Think First — By Number of Joints and Tempo

Then refine by symmetry, joint size, axial involvement, and whether the distal interphalangeal joints are affected — as set out in the rheumatology system opener.

2. What Could Destroy or Kill

• Septic arthritis — including of a prosthetic joint, which has a different microbiology and needs orthopaedic involvement immediately.

• Disseminated gonococcal infection — migratory arthralgia, tenosynovitis and pustular skin lesions in a sexually active patient.

• Necrotising fasciitis — pain out of proportion, rapid spread, systemic toxicity. Not a joint problem, but it presents as one.

• Giant cell arteritis in an older patient with a polymyalgic presentation — because untreated it blinds.

3. The History That Discriminates

• Speed of onset and number of joints, and whether previous episodes followed the same pattern.

• Risk factors for sepsis: diabetes, immunosuppression, chronic kidney disease, a prosthetic joint, intravenous drug use, a skin breach or ulcer, and recent joint injection or aspiration.

• Risk factors for gout: diuretics, alcohol, chronic kidney disease, obesity, previous podagra, family history, and a diet high in purines.

• Preceding infection — gastrointestinal or genitourinary, one to four weeks earlier, for reactive arthritis. Sexual history for gonococcal disease.

• Unpasteurised milk and animal contact — brucellosis causes sacroiliitis and large joint arthritis and is a realistic cause here. Recent travel for chikungunya and dengue.

• Psoriasis, inflammatory bowel disease, red eye, urethral discharge, oral and genital ulcers, rash, and every drug.

4. The Examination That Discriminates

• Fever — but its absence does not exclude sepsis, particularly in the elderly and the immunosuppressed.

• Restriction of movement in every direction with severe pain indicates the joint itself. Bursitis and cellulitis over a joint preserve most passive movement — this distinction is made at the bedside in thirty seconds and prevents an unnecessary aspiration or, worse, a missed one.

• Examine all the other joints, the entheses, and the spine; look for psoriasis in the scalp, natal cleft, umbilicus and nails; look for tophi, pustules, erythema nodosum and conjunctivitis.

5. Investigations, in Tiers

• Blood cultures before antibiotics; complete blood count, C-reactive protein and erythrocyte sedimentation rate, renal and liver function, glucose, and serum urate — interpreted with the caution above.

• Radiograph as a baseline, and to look for chondrocalcinosis, erosions or avascular necrosis. Ultrasound to confirm an effusion and guide aspiration; magnetic resonance imaging where osteomyelitis or spondylodiscitis is suspected.

• Targeted: rheumatoid factor and anti-cyclic citrullinated peptide antibody, antinuclear antibody, brucella serology, parvovirus and hepatitis serology, and nucleic acid amplification testing for gonorrhoea and chlamydia from the appropriate sites.

6. Management While You Are Still Deciding

• Aspirate, culture, then start empirical antibiotics covering staphylococci according to local resistance patterns, adjusted once cultures return. Do not wait for the culture result to start treatment, and do not start treatment before taking the sample.

• Refer to orthopaedics for washout or arthroscopic lavage, with repeated aspiration where surgery is delayed. Splint briefly for comfort, then mobilise early to preserve function.

• If it proves to be crystal disease: an anti-inflammatory drug, colchicine, or corticosteroid — oral or intra-articular — chosen according to renal function and comorbidity. In this patient, with chronic kidney disease, anti-inflammatory drugs are a poor choice.

• Do not start urate-lowering therapy during an acute attack — but do not stop it if the patient is already taking it. Begin allopurinol or febuxostat several weeks later, with colchicine or anti-inflammatory cover for the first months, and treat to a target urate level.

• Review the thiazide, which is contributing, and address alcohol, weight and renal function.

7. Teaching Points and Viva Questions

• Aspirate every hot joint. It is the investigation, and it takes minutes.

• Crystals in the fluid do not exclude infection in the same joint.

• A normal urate during an attack tells you nothing.

• Bursitis and cellulitis preserve passive movement; septic arthritis does not.

• Ask about milk, animals, sexual history and recent joint injections.

• Never start urate-lowering therapy in an acute attack, and never stop it either.

Questions you should be able to answer:

• The aspirate shows 30,000 white cells and urate crystals. Have you excluded sepsis?

• Why is his urate normal, and when should you measure it?

• He has chronic kidney disease. How does that change your choice of anti-inflammatory treatment?

• Distinguish septic arthritis from prepatellar bursitis at the bedside.

• A 26-year-old has migratory arthralgia, tenosynovitis and pustules. What is the diagnosis and what do you send?

Seminar 7 · Approach to the Patient with Chronic Cough

1. Think First

Chronic cough means more than eight weeks. Under three weeks is acute, and three to eight weeks subacute — most often post-infectious and self-limiting.

2. The History That Discriminates

• Check the drug chart before you take the history. An angiotensin-converting enzyme inhibitor explains a large number of chronic coughs, and the temporal link is often missed because the cough may begin months after the drug was started.

• Dry or productive, and how much. Large daily volumes of purulent sputum means bronchiectasis until proved otherwise.

• Timing and triggers: worse at night suggests asthma, reflux or heart failure; worse on lying flat suggests reflux; provoked by cold air, exercise or laughing suggests airway hyper-responsiveness; provoked by eating or talking suggests reflux or aspiration.

• Nasal symptoms and throat clearing for upper airway cough syndrome; heartburn and regurgitation for reflux — although reflux-related cough frequently occurs with no heartburn at all.

• Exposures: smoking including waterpipe, occupational dusts, biomass fuel and incense smoke, birds and moulds, and tuberculosis contact.

3. The Examination That Discriminates

• Expect it to be normal, and record that it is. A normal examination in chronic cough is the usual finding, not a failure to examine properly.

• Examine the nose and post-nasal space, the throat, and the ears — impacted wax against the drum stimulates the auricular branch of the vagus and causes cough.

• Cervical lymph nodes, clubbing, the chest, the heart, and — importantly — watch the patient use her inhaler if she has one.

4. Investigations, in Tiers

• First line for everyone: chest radiograph, spirometry with reversibility testing, and a complete blood count looking for eosinophilia.

• Where tuberculosis is possible — which is often, here: three sputum specimens for smear, nucleic acid amplification testing and culture.

• Targeted: fractional exhaled nitric oxide or bronchial provocation testing for cough-variant asthma; computed tomography of the chest for suspected bronchiectasis, malignancy or interstitial disease; ear, nose and throat assessment with nasendoscopy; oesophageal pH and impedance monitoring where reflux is suspected and empirical treatment has failed; bronchoscopy for a suspected foreign body or endobronchial lesion; echocardiography.

5. Management While You Are Still Deciding

• Then treat the likely causes one at a time, each for long enough to be a fair trial. Treating three things simultaneously means that when the cough settles you will not know why, and when it does not you will not know what to change.

• Upper airway cough syndrome: intranasal corticosteroid, with an antihistamine where there is an allergic component. Asthma or eosinophilic bronchitis: a trial of inhaled corticosteroid. Reflux: a proton pump inhibitor with dietary and postural measures, recognising that the evidence for acid suppression in cough is modest.

• Smoking cessation where relevant, which alone resolves a substantial proportion of coughs within weeks.

• Refractory chronic cough: speech and language therapy with cough suppression techniques, and neuromodulator therapy such as gabapentin or low-dose morphine, under specialist supervision.

• Acknowledge the impact. Chronic cough causes urinary incontinence, sleep loss, social embarrassment, exhaustion and occasionally rib fractures. Patients are frequently told it is nothing.

6. Teaching Points and Viva Questions

• Eight weeks defines chronic cough. Read the drug chart before the history.

• Angiotensin-converting enzyme inhibitor cough can start months after the drug and takes weeks to settle after stopping.

• A normal examination and a normal film are expected — but red flags and regional tuberculosis risk override the empirical pathway.

• Reflux cough often occurs without heartburn.

• Treat one cause at a time, for long enough to know whether it worked.

Questions you should be able to answer:

• Name the three commonest causes in a non-smoker with a normal film.

• She stopped the ramipril a week ago and is no better. What do you tell her?

• Which findings in this history would make you send sputum before starting any trial?

• Why should you not start a nasal steroid, an inhaler and a proton pump inhibitor together?

• A 63-year-old smoker has coughed for three months and has lost 5 kg. What is your first investigation?

Seminar 8 · Hypertensive Urgencies and Emergencies

1. Think First — Where Is the End-Organ Damage?

2. How Fast, and With What — the Targets Differ by Situation

Sublingual short-acting nifedipine has been abandoned because it produces an uncontrolled and unpredictable fall in pressure. It should not be used.

3. The History That Discriminates

• Ask what medication was stopped, and when. Non-adherence, or an abrupt withdrawal — particularly of clonidine or a beta blocker — is among the commonest precipitants, and it is entirely correctable.

• Symptoms of each organ system: headache, visual change, confusion, seizure, chest pain, breathlessness, oliguria, frothy or bloody urine.

• Drugs: anti-inflammatory drugs, decongestants, corticosteroids, the combined oral contraceptive, ciclosporin, erythropoietin, liquorice — and cocaine and amphetamines, which change the treatment.

• Features of a secondary cause, as in Case 14 — because severe hypertension in a young patient, or hypertension that suddenly becomes uncontrolled, is far more likely to be secondary.

• Pregnancy or recent delivery in any woman of childbearing age.

4. The Examination That Discriminates

• Blood pressure measured properly, in both arms, and repeated — with the correct cuff size, after rest. Severe readings are frequently artefactual.

• Fundoscopy in every patient. This is the examination that most often converts an urgency into an emergency, and it is the one most often skipped.

• Full neurological examination; heart and lungs; radio-femoral delay and peripheral pulses; abdominal and renal bruits; volume status.

5. Investigations, in Tiers

• Bedside: urinalysis — blood and protein indicate renal involvement and are available in a minute; electrocardiogram.

• First line: urea, electrolytes and creatinine, complete blood count with a blood film for fragments, lactate dehydrogenase, troponin, natriuretic peptide, glucose, chest radiograph, pregnancy test.

• Targeted: computed tomography of the head where there are neurological features; computed tomographic aortogram where dissection is suspected; echocardiography; renal imaging.

• Once stabilised, screen for a secondary cause — aldosterone-to-renin ratio, plasma metanephrines, renal artery imaging, and a sleep study.

6. Management While You Are Still Deciding

• Monitored bed with continuous blood pressure monitoring, ideally intra-arterial, and an intravenous agent titrated to a defined target that is written down.

• Identify and remove the precipitant, and restart oral therapy early so that the infusion can be weaned.

• Expect the creatinine to rise transiently as the pressure falls — this is haemodynamic and is not a reason to stop treating, provided the fall is controlled.

• In a hypertensive urgency: do not treat in the emergency department with repeated intravenous boluses. Restart or adjust oral therapy, arrange review within days, and address why the medication stopped.

7. Teaching Points and Viva Questions

• The organs define the emergency, not the number.

• Do fundoscopy. Papilloedema changes the diagnosis and the disposition.

• Twenty to twenty-five per cent in the first hour — except in dissection, and except in acute ischaemic stroke where you do not lower it at all.

• Beta blocker before vasodilator in dissection; alpha before beta in cocaine and phaeochromocytoma.

• Always ask which tablets were stopped and why.

Questions you should be able to answer:

• Is this an urgency or an emergency, and what exactly makes it so?

• What is your target pressure at one hour, and why not lower?

• Why do the fragments on his blood film matter?

• A patient with the same pressure has tearing interscapular pain. How does your plan change, and in what order do you give the drugs?

• A 22-year-old with a pressure of 230/130 has taken cocaine. What must you avoid?

Seminar 9 · Approach to the Patient with Pyrexia of Unknown Origin

1. Think First — Four Categories

Pyrexia of unknown origin is conventionally fever above 38.3 °C on several occasions for more than three weeks, remaining undiagnosed after appropriate initial investigation. The causes fall into four groups, and the proportions differ substantially by region.

2. The Method — Which Matters More Than the List

3. What Could Kill

• Infective endocarditis; disseminated tuberculosis; an occult abscess progressing to sepsis; aggressive lymphoma; giant cell arteritis with impending visual loss; and adrenal crisis.

4. Investigations, in Tiers

• First tier: complete blood count with a blood film, erythrocyte sedimentation rate and C-reactive protein, renal and liver function, lactate dehydrogenase, three sets of blood cultures taken off antibiotics, urinalysis and culture, chest radiograph, human immunodeficiency virus and hepatitis serology, antinuclear antibody and rheumatoid factor, protein electrophoresis, thyroid function, creatine kinase, and ferritin.

• Regionally targeted: brucella serology with prolonged blood cultures — and tell the laboratory; tuberculin or interferon-gamma release assay with sputum and tissue for tuberculosis; *Coxiella* and *Bartonella* serology; malaria films; leishmania serology.

• Imaging: echocardiography, proceeding to transoesophageal study where endocarditis is possible; computed tomography of chest, abdomen and pelvis; magnetic resonance imaging of the spine for spondylodiscitis; dental panoramic radiograph; and fluorodeoxyglucose positron emission tomography where available, which has a high diagnostic yield in this setting.

• Tissue, when imaging is unrevealing: lymph node biopsy; bone marrow aspirate and trephine sent for culture as well as histology, which has a good yield for tuberculosis, lymphoma and leishmaniasis; liver biopsy; and temporal artery biopsy or ultrasound in anyone over 50 with a raised erythrocyte sedimentation rate.

5. Management While You Are Still Deciding

6. Teaching Points and Viva Questions

• Re-examine the patient every day. That is where the diagnosis usually comes from.

• Stop the drugs. Drug fever is common and free to exclude.

• Three sets of blood cultures, off antibiotics.

• In this region, tuberculosis and brucellosis head the list — and both need the laboratory to be told.

• Check the ferritin.

• Empirical treatment feels active and usually destroys the diagnosis.

Questions you should be able to answer:

• Define pyrexia of unknown origin and give the four diagnostic categories.

• Which two diagnoses does this man’s occupation and diet put at the top of your list?

• He has had two courses of antibiotics. How does that affect your investigation?

• A colleague wants to start empirical antituberculous therapy. Argue both sides.

• Which single investigation would you request if a positron emission tomogram were unavailable and the computed tomogram was normal?

Seminar 10 · Approach to the Patient in Coma

1. Think First — Two Mechanisms

Consciousness requires both cerebral hemispheres and the reticular activating system in the brainstem. Coma therefore means either diffuse bilateral hemispheric dysfunction or a brainstem lesion — and the examination tells you which.

Infection sits across both: meningitis, encephalitis and cerebral malaria can produce either picture, and they are treated before imaging.

2. The History — From Everybody Except the Patient

• The circumstances in which she was found, and when she was last known to be well — which determines the treatment window if this proves to be a stroke.

• Access to drugs: what is in the house, and what is missing. Ask the ambulance crew about empty packets, bottles and syringes, and about the state of the room.

• Preceding headache, fever, confusion, focal symptoms, seizures, vomiting or trauma — including a fall days earlier, which raises subdural haematoma.

• Comorbidity: diabetes, liver disease, kidney disease, epilepsy, psychiatric illness, malignancy, and alcohol use.

• Whether anyone else in the household is unwell or has a headache — carbon monoxide poisoning affects the whole house, and is repeatedly missed.

3. The Coma Examination

• Record the Glasgow Coma Scale as its three components, not as a total. "GCS 7" hides whether the patient is deteriorating in eye opening or in motor response, and the motor score is the most prognostically important.

• Respiratory pattern and temperature, both of which are diagnostic clues and both of which are frequently omitted.

• Eye movements: spontaneous movement, gaze deviation (towards the lesion in a hemispheric stroke, away from it in a seizure focus), corneal reflexes, and oculocephalic testing — only once the cervical spine has been cleared.

• Fundoscopy for papilloedema and for the subhyaloid haemorrhage of subarachnoid bleeding.

• Motor response to a standardised stimulus, tone, reflexes, plantars, asymmetry, and abnormal posturing.

• Neck stiffness — with caution if trauma is possible. Skin for rash, needle marks, jaundice, cyanosis, bruising, and signs of head injury including periorbital and mastoid bruising and cerebrospinal fluid leak. Smell the breath. Look for a medical alert bracelet.

4. Investigations, in Tiers

• Bedside: glucose, arterial blood gas including carboxyhaemoglobin and lactate, electrocardiogram, temperature.

• First line: urea and electrolytes, calcium, magnesium, liver function, ammonia, complete blood count, C-reactive protein, coagulation, creatine kinase, thyroid function, cortisol, blood and urine cultures, paracetamol and salicylate levels, toxicology screen, and serum osmolality with an osmolar gap where a toxic alcohol is possible.

• Computed tomography of the head in all but the most obvious metabolic cases; lumbar puncture after imaging where infection is suspected — with antibiotics given first.

5. Management While You Are Still Deciding

• Secure the airway — intubate for a score of 8 or less, an absent gag, or a rising carbon dioxide. Maintain oxygenation and normocapnia.

• Treat the reversible causes empirically in sequence: glucose, thiamine, naloxone; then antibiotics and aciclovir if infection is possible, before imaging.

• Nurse head-up at 30 degrees; maintain normothermia, normoglycaemia and normal sodium; treat seizures; treat raised intracranial pressure and involve neurosurgery urgently for a mass lesion or herniation.

• Eye care, pressure area care, nutrition, thromboprophylaxis, and a urinary catheter.

• Talk to the family early and honestly, and establish what the patient would have wanted before decisions become urgent.

6. Teaching Points and Viva Questions

• Airway, glucose, thiamine, naloxone — in that order, in the first two minutes.

• Record the coma score in its three components.

• Symmetrical signs with reactive pupils point to a metabolic cause; asymmetry points to a structural one.

• A unilateral fixed dilated pupil is a neurosurgical emergency.

• Ask whether anyone else at home is unwell.

• If nothing explains it, ask for an electroencephalogram.

Questions you should be able to answer:

• What is the likely cause here, and what would you give first — and in what order?

• Why does she need thiamine considered before glucose?

• Her pupils are equal and reactive. What does that make more likely?

• The glucose is corrected but she does not wake. What are your next three steps?

• A patient has a right pupil of 6 mm that does not react. What has happened and whom do you call?

Seminar 11 · Approach to the Patient with Venous Thromboembolism

1. Think First

Deep vein thrombosis and pulmonary embolism are one disease presenting in two places. This patient has both, and finding one is sufficient reason to treat.

• Differential for the leg: cellulitis, ruptured Baker cyst, calf muscle tear or haematoma, superficial thrombophlebitis, chronic venous insufficiency, lymphoedema, compartment syndrome.

• Differential for the chest: as in Seminar 3.

Generate the risk factors from Virchow’s triad rather than memorising a list:

2. What Could Kill in the Next Hour

3. Score Before You Test

4. Investigations

• Suspected deep vein thrombosis: proximal leg vein compression ultrasound. If negative but the probability is high, repeat it after about a week, or proceed to further imaging.

• Suspected pulmonary embolism: computed tomographic pulmonary angiography.

• Supporting tests, none of which diagnose: electrocardiogram — sinus tachycardia is the commonest finding, and the classical S1Q3T3 pattern is uncommon; chest radiograph, whose main role is to exclude alternatives; blood gas; and troponin and natriuretic peptide, which are used for risk stratification and not for diagnosis.

• Echocardiography for right ventricular strain in the haemodynamically unstable patient.

5. Management

• Start anticoagulation on clinical suspicion while awaiting imaging where the probability is high and the bleeding risk is acceptable. Do not wait several hours for a scan with the patient untreated.

• Duration: three months where the event was provoked by a major transient risk factor that has now resolved; at least three to six months if unprovoked, with a considered decision about extended therapy weighing recurrence risk against bleeding risk; indefinite therapy in active cancer, antiphospholipid syndrome, and recurrent unprovoked events.

• Low-risk pulmonary embolism can be managed as an outpatient using a validated severity score, which is safe and avoids admission.

• Stop the combined oral contraceptive and counsel on alternative contraception — a progestogen-only method or a non-hormonal method — and on future pregnancy, which will require thromboprophylaxis.

• Graduated compression for post-thrombotic symptoms; explain the risk of recurrence and the symptoms that should bring her back; and follow up persisting breathlessness at three to six months for chronic thromboembolic pulmonary hypertension, which is treatable and easily missed.

6. Teaching Points and Viva Questions

• Score the probability before you choose the test.

• D-dimer excludes; it never confirms — and it is useless in a high-probability patient.

• Ventilation–perfusion scanning in pregnancy and in young women; leg ultrasound first in pregnancy.

• Anticoagulate on suspicion when the probability is high.

• The exceptions to direct oral anticoagulants are antiphospholipid syndrome, pregnancy and severe renal impairment.

• No thrombophilia screen, and no whole-body cancer hunt.

Questions you should be able to answer:

• Would you send a D-dimer on this patient? Justify your answer.

• Which imaging would you choose for her, and why not computed tomography?

• She is 8 weeks pregnant. How does everything change?

• When is a thrombophilia screen actually useful?

• Six months later she remains breathless on exertion. What must you exclude?

Seminar 12 · Approach to the Patient in Shock

1. Think First — Four Mechanisms

The jugular venous pressure and the temperature of the hands divide the four mechanisms in about ten seconds, and they are available before any test.

2. What Could Kill in the Next Minutes

3. The History and Examination That Discriminate

• From whoever is available: onset and course; bleeding of any kind; fever; chest pain; breathlessness; vomiting and diarrhoea; drugs — antihypertensives, beta blockers, insulin, anticoagulants, and recently stopped corticosteroids; allergies and exposures; recent surgery or procedure; immobility; and the possibility of pregnancy.

• Examination: full vital signs including the respiratory rate, capillary refill, peripheral temperature, conscious level; jugular venous pressure; heart sounds, murmurs and pulsus paradoxus; chest; abdomen for peritonism, a pulsatile mass or distension; rectal examination; calves; the whole skin for a non-blanching rash, urticaria or cellulitis; every line and wound; and a pregnancy test in any woman of childbearing age.

4. Investigations, in Tiers

• Bedside: lactate, blood gas, glucose, electrocardiogram, pregnancy test — and bedside ultrasound, which in a few minutes gives cardiac function, inferior vena cava filling, free intraperitoneal fluid, pneumothorax and the aorta.

• First line: complete blood count, coagulation, cross-match, urea and electrolytes, liver function, amylase, C-reactive protein, blood cultures, troponin, urinalysis, chest radiograph.

• Targeted: echocardiography, computed tomography of the aorta, chest or abdomen, random cortisol, and toxicology.

5. Management While You Are Still Deciding

• Vasopressors once fluid responsiveness is exhausted — noradrenaline first line. A central line is preferable, but peripheral administration while one is being placed is better than delay.

• Sepsis: antibiotics within one hour, and source control — remembering that no antibiotic treats an undrained collection (Cases 32 and 48).

• Anaphylaxis: intramuscular adrenaline, repeated as needed, plus fluid, and observation for a biphasic reaction.

• Correct calcium, potassium and severe acidosis; give hydrocortisone if adrenal crisis is conceivable, including in any patient on long-term steroids (Case 26); and actively rewarm the hypothermic.

• Document the escalation plan and ceiling of care early, while the patient or family can still participate.

6. Teaching Points and Viva Questions

• Shock is a perfusion diagnosis. A normal blood pressure does not exclude it.

• The jugular venous pressure and the hands divide the four mechanisms.

• Treat the reversible causes before the diagnosis is complete.

• Fluid in boluses with reassessment after each — never a bag prescribed and forgotten.

• Blood, not crystalloid, in haemorrhage; caution with fluid in cardiogenic shock.

• Follow the lactate.

Questions you should be able to answer:

• Which mechanism is this, and which two bedside findings told you?

• A shocked patient has a raised jugular venous pressure and a clear chest. Give three diagnoses.

• Why is a lactate of 5.8 more useful to you than the blood pressure?

• A trauma patient is hypotensive from abdominal bleeding. How does your fluid strategy differ?

• He does not respond to two litres. What do you do next, and where?

Seminar 13 · Approach to the Patient with Chronic Diarrhoea

1. Think First — Define It, Then Classify by Mechanism

• Chronic means more than four weeks. First distinguish it from faecal incontinence and from overflow diarrhoea with underlying constipation — patients call all three "diarrhoea", and the management of each is entirely different.

• Regionally: giardiasis, amoebiasis, intestinal tuberculosis, schistosomiasis, tropical sprue and brucellosis. Chronic diarrhoea with weight loss here requires stool parasitology and active consideration of tuberculosis (Case 39).

2. The History That Discriminates

• Frequency, consistency, volume, blood, mucus, urgency, tenesmus, incontinence, and nocturnal symptoms.

• Steatorrhoea — pale, bulky, offensive stool that floats and is difficult to flush.

• Does it stop when she does not eat? This single question separates osmotic from secretory diarrhoea.

• The drug chart, which is a common and entirely reversible cause: metformin, magnesium-containing antacids, proton pump inhibitors, antibiotics, laxatives — including covert use — non-steroidal anti-inflammatory drugs, colchicine, selective serotonin reuptake inhibitors, orlistat and chemotherapy.

• Previous surgery: cholecystectomy or ileal resection causes bile acid diarrhoea; gastrectomy and bariatric surgery cause malabsorption. Also radiotherapy.

• Extraintestinal clues: an itchy vesicular rash on the elbows and knees (dermatitis herpetiformis — Case 76), arthritis, mouth and eye lesions, thyroid symptoms, flushing, diabetes.

• Travel, water source, unpasteurised dairy, contacts, and human immunodeficiency virus risk. Family history of coeliac disease, inflammatory bowel disease and colorectal cancer.

3. Examination

• Weight and nutritional state; pallor; angular stomatitis and glossitis; clubbing; mouth ulcers; thyroid; abdominal masses and tenderness; perianal inspection and rectal examination; skin, joints and lymph nodes.

4. Investigations, in Tiers

• First line: complete blood count, ferritin, B12, folate, urea and electrolytes, liver function, albumin, calcium, C-reactive protein, thyroid function, faecal calprotectin, stool culture with ova and parasites on three samples and *Clostridioides difficile* toxin, and a human immunodeficiency virus test.

• Second line, by suspicion: faecal elastase for pancreatic insufficiency; bile acid testing or a therapeutic trial of a sequestrant; breath testing for bacterial overgrowth and lactose intolerance; gut hormones and urinary 5-hydroxyindoleacetic acid; duodenal biopsy for coeliac disease and giardia; colonoscopy with ileal intubation; computed tomography or magnetic resonance enterography; and a faecal laxative screen where surreptitious use is suspected.

5. Management While You Are Still Deciding

• Rehydrate, correct electrolytes, and replace deficiencies — iron, B12, folate, calcium, vitamin D, magnesium and zinc.

• Stop the culprit drug, which may be the entire treatment.

• Avoid antidiarrhoeal agents until infection and inflammatory colitis have been excluded (Case 39).

• Then treat the cause: a gluten-free diet with dietetic support, coeliac follow-up, pneumococcal vaccination and bone density assessment in coeliac disease; pancreatic enzyme replacement; antimicrobials for giardiasis or overgrowth; a sequestrant for bile acid diarrhoea; budesonide for microscopic colitis; and the therapy of Case 39 for inflammatory bowel disease.

• In coeliac disease, explain the timescale: symptoms improve over weeks, the serology falls over many months, and adherence must be lifelong — with first-degree relatives offered testing.

6. Teaching Points and Viva Questions

• Four weeks defines chronic. Distinguish diarrhoea from incontinence and from overflow.

• Nocturnal diarrhoea, weight loss, blood and anaemia are red flags, not features of irritable bowel syndrome.

• Read the drug chart before ordering anything.

• Send total IgA with the coeliac serology, and biopsy before starting the diet.

• Biopsy a normal-looking colon — microscopic colitis is invisible to the eye.

• Think of bile acid diarrhoea after a cholecystectomy, and try a sequestrant.

Questions you should be able to answer:

• Which three red flags does she have, and what do they exclude?

• Her tissue transglutaminase is negative. What must you check before accepting that?

• A 62-year-old has watery nocturnal diarrhoea and a normal colonoscopy. What was not done?

• A patient develops urgent watery diarrhoea after a cholecystectomy. What is the diagnosis and how would you test it?

• Why should the biopsy come before the gluten-free diet?

Seminar 14 · Approach to the Patient with Ascites

1. Think First — the Albumin Gradient Divides It in Two

Serum-ascites albumin gradient = serum albumin minus ascitic albumin, on samples taken at the same time.

2. What Must Not Be Missed

• Spontaneous bacterial peritonitis — ascitic neutrophils of 250/mm³ or more, with or without fever, pain or a positive culture. Every patient admitted with ascites is tapped (Case 37).

• Tense ascites causing respiratory compromise; hepatorenal syndrome; a surgical abdomen — perforation or ischaemia — presenting as distension; and malignancy or tuberculosis mistaken for cirrhosis.

3. The History and Examination That Discriminate

• Speed of onset; abdominal pain and fever; alcohol quantified and hepatitis risk; cardiac symptoms — orthopnoea, oedema, known heart disease; weight loss and night sweats, pointing to malignancy or tuberculosis; gynaecological history — pelvic pain, irregular bleeding, and family history of ovarian or breast cancer; frothy urine; diarrhoea; previous abdominal surgery or peritoneal dialysis; tuberculosis contact and unpasteurised milk.

• First confirm it is ascites: shifting dullness requires about 1.5 litres, and a fluid thrill more. Distinguish it from obesity, a large ovarian cyst, a distended bladder, pregnancy and gross organomegaly — ultrasound settles it in a minute.

• Then: the presence or absence of chronic liver disease stigmata · the jugular venous pressure · a pelvic and rectal examination, and in women a vaginal examination · the umbilicus for a Sister Mary Joseph nodule · the left supraclavicular fossa · the breasts · peripheral oedema · and the mental state for encephalopathy.

4. Investigations, in Tiers

• Diagnostic paracentesis, under ultrasound. Send: cell count and differential; culture in blood culture bottles inoculated at the bedside; albumin and total protein with a paired serum albumin; glucose; lactate dehydrogenase; cytology — and where indicated adenosine deaminase and mycobacterial culture, amylase, and triglycerides.

• Interpretation: the gradient as above; neutrophils ≥250 means peritonitis; a lymphocyte-predominant, high-protein fluid with a high adenosine deaminase suggests tuberculous peritonitis — where the culture yield is low, so laparoscopic peritoneal biopsy is often needed and empirical treatment is sometimes justified; and a negative cytology does not exclude malignancy, since sensitivity is moderate at best.

• Blood: liver function, INR, albumin, renal function, complete blood count, C-reactive protein, natriuretic peptide, alpha-fetoprotein, and CA-125 — which is raised in cirrhotic ascites as well, so interpret it with the imaging rather than alone.

• Imaging: ultrasound with Doppler for liver texture, portal and hepatic vein patency, nodules and the pelvis; echocardiography where a cardiac cause is possible; computed tomography of chest, abdomen and pelvis; and laparoscopy where the cause remains unexplained.

5. Management While You Are Still Deciding

• Cirrhotic ascites: sodium restriction, spironolactone with furosemide, daily weights, and large-volume paracentesis with albumin replacement — Case 37.

• Malignant ascites: treat the cancer; repeated therapeutic paracentesis or an indwelling drain for symptom control; diuretics help only where the mechanism is massive hepatic metastasis.

• Tuberculous peritonitis: standard antituberculous therapy.

• Cardiac ascites: treat the heart failure — here diuretics are the treatment (Case 12).

• Nutrition and symptom control; and where malignancy is confirmed, early palliative care involvement and an honest conversation.

6. Teaching Points and Viva Questions

• Tap every ascites, and tap it on admission.

• The albumin gradient divides the differential in two; the ascitic protein then separates cirrhosis from heart failure.

• Neutrophils of 250 or more is spontaneous bacterial peritonitis.

• A negative cytology does not exclude malignancy.

• Lymphocytic, high-protein fluid with a raised adenosine deaminase is tuberculosis.

• Examine the pelvis and the umbilicus, and do not diurese an undiagnosed ascites.

Questions you should be able to answer:

• What does her albumin gradient of 6 tell you, and what does it exclude?

• A patient has a gradient of 14 with an ascitic protein of 45 and a raised jugular venous pressure. What is the diagnosis?

• The cytology is negative but you still suspect malignancy. What next?

• What would make you suspect tuberculous peritonitis, and how would you prove it?

• Why is starting spironolactone before the tap a mistake?

Seminar 15 · Approach to the Patient with Dementia

1. Think First — Three Questions in Order

• Delirium is frequently superimposed on dementia. So a sudden change in someone with established dementia is delirium, and it needs a cause found — infection, pain, constipation, urinary retention, drugs, metabolic disturbance — not an increase in the antipsychotic.

• Depression can present as pseudodementia, with prominent "don’t know" answers, and it is reversible with treatment.

Question three: which dementia?

2. The History — Which Must Come From an Informant

• Always take a collateral history. The patient’s own account is unreliable by the nature of the condition, and a consultation conducted with the patient alone will underestimate the problem.

• Which domain failed first — memory, language, behaviour or visuospatial function — because that is what distinguishes the subtypes.

• Function, in specifics rather than generalities: finances, medication, cooking, driving, appliances, getting lost, washing and dressing. This is what determines risk and the support required, and it is more useful than any score.

• Behavioural and psychological symptoms; hallucinations and fluctuation; dream enactment; falls; continence; mood and sleep; alcohol; the complete drug history; vascular risk factors; family history.

• Safety, asked explicitly: driving, gas and fire, wandering, and financial vulnerability and exploitation. This patient has already left the gas on twice and become lost while driving.

3. Examination

• A validated cognitive assessment, noting which domains are impaired; test attention specifically, to exclude delirium; assess mood.

• Hearing and vision.

• Full neurological examination — focal signs, gait, parkinsonism; postural blood pressure; cardiovascular examination.

• Evidence of self-neglect or of neglect by others: weight loss, dehydration, poor dentition, unexplained bruising, pressure damage.

4. Investigations, in Tiers

• First line: complete blood count, urea and electrolytes, calcium, glucose or glycated haemoglobin, liver function, thyroid function, B12 and folate, C-reactive protein — and human immunodeficiency virus and syphilis serology where there is risk or the picture is atypical.

• Structural imaging — computed tomography, or preferably magnetic resonance imaging — to exclude a subdural haematoma, tumour or hydrocephalus, to assess vascular burden, and to look at the pattern of atrophy. It is not performed to "confirm dementia".

• Specialist: neuropsychometry; electroencephalography where prion disease or non-convulsive status is suspected; dopamine transporter imaging in suspected Lewy body disease; cerebrospinal fluid or amyloid biomarkers in young-onset or atypical cases; genetic testing in familial disease.

• Refer urgently rather than routinely if: the onset is before 65, progression is rapid, behaviour or language change dominates, or there are focal neurological signs.

5. Management While You Are Still Deciding

• Treat what is treatable first. A medication review — stopping anticholinergic and sedative drugs — is among the highest-yield interventions in the whole assessment. Correct deficiencies, treat depression and sleep apnoea, fit hearing aids and correct vision, and manage vascular risk.

• Cholinesterase inhibitors — donepezil, rivastigmine or galantamine — in Alzheimer, Lewy body and Parkinson disease dementia; memantine in moderate to severe Alzheimer disease or where inhibitors are not tolerated. The benefit is modest and symptomatic: say so, or the family will expect reversal.

6. Teaching Points and Viva Questions

• Dementia, delirium or depression — decide that first, and test attention to do it.

• A sudden change in someone with dementia is delirium, and needs a cause.

• Always take an informant history, and ask about function in specifics.

• Review the drugs — it is the highest-yield intervention.

• Fit the hearing aid.

• Find the cause of agitation before prescribing an antipsychotic, and never use one lightly in Lewy body disease.

• Do the legal planning while capacity remains.

Questions you should be able to answer:

• How would you distinguish this from delirium at the bedside?

• Name six reversible contributors you would exclude, and the test for each.

• Why does his hearing matter to his cognition?

• His daughter reports he has become aggressive at bath time. What do you do before prescribing anything?

• What must be arranged while he still has capacity?

Seminar 16 · Approach to the Patient with Acute Poisoning

1. Think First — Four Questions

• What, how much, when, and with what else? — and the history in poisoning is frequently wrong, whether through confusion, shame or intent. Assume the worst plausible scenario and treat it.

• Is there a specific antidote or elimination strategy, and is there a time window?

• Does the toxidrome fit the story? If it does not, believe the patient’s physiology rather than their account.

• Why did this happen, and what is the risk of it happening again? The psychosocial assessment is part of the medical management, not an addendum to it.

2. What Could Kill in the Next Hour

• Airway and breathing — the commonest cause of death in poisoning is airway obstruction and aspiration, not the drug itself.

• Hypoglycaemia; arrhythmia — check the electrocardiogram for a wide QRS from sodium channel blockade, which is treated with sodium bicarbonate, and for a prolonged QT interval; seizures; hyperthermia, which requires active cooling.

• And the patient who looks well. Paracetamol produces no symptoms for 24 hours and then destroys the liver. The level, not the appearance, decides the treatment.

• Use the poisons information service or database in every significant case. It is a core clinical resource, not a last resort, and it should be consulted early.

3. Decontamination and Elimination

• Activated charcoal within about one hour of ingestion, in a patient who can protect their airway. It is of limited value later, and useless for iron, lithium, alcohols and corrosives.

• Gastric lavage and ipecac are obsolete. Do not use them.

• Whole bowel irrigation for modified-release or enteric-coated preparations in selected cases.

• Urinary alkalinisation for salicylate; haemodialysis for lithium, salicylate, toxic alcohols, metformin-associated lactic acidosis, valproate and theophylline; intravenous lipid emulsion in refractory local anaesthetic and some lipophilic drug toxicity.

4. Management While You Are Still Deciding

• Airway, breathing and circulation; oxygen; glucose; monitoring; intravenous access; electrocardiogram with attention to the QRS width and the QT interval; temperature; and a pregnancy test.

• Supportive care is the mainstay for most poisons: most patients survive because of good airway and circulatory management, not because of an antidote.

• Correct electrolytes and acid–base disturbance; treat seizures with benzodiazepines; cool the hyperthermic patient actively; and observe for the delayed effects of modified-release preparations.

5. Teaching Points and Viva Questions

• Treat the patient, not the poison — supportive care saves more lives than antidotes.

• The history is often wrong. Let the toxidrome and the tests guide you.

• Use the poisons information service early.

• Charcoal only within the hour and with a protected airway; lavage is obsolete.

• Paracetamol is silent then lethal — treat on the level, or blind if staggered, late or unwell.

• The INR and the pH, not the aminotransferase, tell you how sick the liver is.

• Check the QRS width on the electrocardiogram.

• No self-poisoning is discharged without a mental health assessment.

Questions you should be able to answer:

• She cannot say how much she took or when. How does that change your management?

• Give three situations in which you would start N-acetylcysteine without a level.

• Her aminotransferase is normal at eight hours. Is that reassuring?

• A patient arrives drowsy with a QRS of 140 ms. What is the likely poison and the treatment?

• She is medically fit at 24 hours and wants to go home. What must happen first?