Anaemia — Systematic Workup Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Kaur is a 68-year-old man who presents with three months of progressive fatigue, exertional dyspnoea, a six-kilogram unintentional weight loss, and darker-than-usual stools. He takes amlodipine for hypertension and has been taking ibuprofen 400 milligrams daily for six months for osteoarthritis. His full blood count shows a haemoglobin of 76 grams per litre with an MCV of 71 femtolitres. His iron studies confirm iron deficiency, with a ferritin of 6 micrograms per litre, a transferrin of 4.1 grams per litre, and a transferrin saturation of 7 per cent. His reticulocyte count is low at 1 per cent. Digital rectal examination reveals dark stool positive for occult blood." ^[1]

"His main problems are:

1. Severe iron deficiency anaemia from chronic gastrointestinal blood loss, symptomatic with exertional dyspnoea
2. Possible gastrointestinal malignancy — the weight loss and occult blood in a man of this age mandate urgent endoscopic investigation
3. NSAID-related gastrointestinal injury — the daily ibuprofen is a likely contributor to mucosal bleeding
4. Chronic comorbidity — hypertension — which is relevant to transfusion decisions." ^[1]

"My immediate priorities are to stop the ibuprofen, start oral iron replacement, and arrange urgent coeliac serology, oesophagogastroduodenoscopy and colonoscopy to find and treat the source of bleeding. I would not transfuse him at present — he is chronically anaemic, haemodynamically stable, and his haemoglobin of 76 is above the restrictive threshold of 70." ^[1]

Examiner probing questions and model answers

Q1: "Take me through how you classified this anaemia and confirmed the cause." ^[1]

"I started with the mean cell volume. The MCV is 71 femtolitres — that is microcytic, which puts the differential at iron deficiency, thalassaemia trait, anaemia of chronic disease, sideroblastic anaemia, or lead poisoning. The iron studies sorted it: the ferritin is 6, the transferrin is high at 4.1, and the transferrin saturation is 7 per cent. That is the classic iron deficiency pattern — the body upregulates transferrin in an attempt to capture more iron, and the saturation falls because there is no iron to load onto it. The reticulocyte count is low at 1 per cent, confirming the marrow is not responding because it has no iron to make haemoglobin. I then looked for the source of the iron loss, and the occult blood in the stool plus the weight loss point to a gastrointestinal cause." ^[1]

Q2: "Why are you so insistent on endoscopy? Could this not be the ibuprofen?" ^[1]

"The ibuprofen is almost certainly contributing — daily NSAID use is a major cause of gastroduodenal erosion and ulceration, and I would stop it immediately. But the weight loss is the discriminator. NSAID-related gastritis causes bleeding and anaemia but does not cause six kilograms of weight loss in three months. That symptom raises colorectal or gastric malignancy, and in a man of this age the British Society of Gastroenterology guideline is explicit: iron deficiency anaemia in men and postmenopausal women is investigated with coeliac serology, an OGD, and a colonoscopy, no exceptions, because the cost of missing a cancer is too high. The OGD may show an NSAID ulcer — and if so, I will treat it with a proton pump inhibitor and stop the NSAID. But the colonoscopy may show a cancer, and that is what I must not miss ^[1]."

Q3: "His haemoglobin is 76. Would you transfuse him?" ^[1]

"No, not at this time. The TRICC trial and the AABB guideline support a restrictive transfusion strategy — a threshold of 70 grams per litre in a stable inpatient. He is chronically anaemic, not acutely, so his circulation has adapted; he is haemodynamically stable; and he has no ischaemic features. Transfusing him to a higher haemoglobin would expose him to the risks of transfusion — transfusion-associated circulatory overload, transfusion-related acute lung injury, infection, and transfusion reactions — without evidence of benefit. If he were to develop chest pain, ischaemic ECG changes, or heart failure, the threshold rises to 80 grams per litre, and I would transfuse a single unit at a time with diuretic cover. But on current information, treating the iron deficiency is the correct approach ^[4]."

Q4: "What would change your transfusion decision?" ^[1]

"Three things. First, if his haemoglobin fell below 70 and he was symptomatic, I would transfuse. Second, if he developed ischaemia — chest pain, troponin rise, or new ECG changes — I would transfuse to keep the haemoglobin above 80, because the heart is the organ that suffers first from acute anaemia. Third, if he presented in acute haemodynamic collapse from a GI bleed — tachycardia, hypotension, postural drop — I would resuscitate with blood in parallel with urgent endoscopy, because that is a different scenario entirely: acute blood loss, not chronic iron deficiency." ^[1]

Q5: "How would you manage his iron replacement?" ^[1]

"Oral ferrous sulfate 200 milligrams three times daily for a minimum of three months — long enough to correct the haemoglobin and replete the stores. I would counsel him that the dark stools are from the iron and not a sign of worsening bleeding, that constipation is common and can be managed, and that a reticulocyte response should appear within seven to ten days with a haemoglobin rise of about 20 grams per litre over three weeks. If he cannot tolerate oral iron, or if the haemoglobin does not rise as expected, I would switch to intravenous iron — ferric carboxymaltose allows a large single-dose infusion. I would not give intravenous iron first-line because oral iron is effective, cheaper, and avoids the small but real risk of infusion reaction." ^[1]