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]

Short Case Discussion

Scenario: "Classify and investigate this anaemia"

Provided data: A 45-year-old woman with fatigue. Hb 88 g/L, MCV 104 fL, reticulocyte count 1.5 per cent. Blood film: oval macrocytes and hypersegmented neutrophils. B12 92 pmol/L (low), folate normal. LDH 580 U/L (raised). [1]

Candidate presentation (model): [1]

"I classify this anaemia as macrocytic — the MCV is 104 femtolitres. The reticulocyte count is low at 1.5 per cent, which tells me the marrow is underproducing, not haemolysing or recovering. The blood film shows oval macrocytes and hypersegmented neutrophils with six or more lobes — these are the morphological hallmarks of megaloblastic haematopoiesis, which means impaired DNA synthesis from B12 or folate deficiency. The B12 is low at 92 and the folate is normal, so this is B12 deficiency. The mildly raised LDH is from ineffective erythropoiesis — the megaloblastic marrow produces cells that are destroyed in the marrow before they are released, releasing LDH." [1]

"My next steps are: first, to ask about the cause — is this pernicious anaemia, dietary, post-surgical, or malabsorption from terminal ileum disease or metformin? I would check anti-intrinsic factor antibodies to look for pernicious anaemia. Second, to examine for neurological features of B12 deficiency — loss of vibration and proprioception in the legs, extensor plantars, cognitive change — because their presence makes the treatment more intensive and more urgent. Third, to treat with intramuscular hydroxocobalamin, not oral, because the IM route is reliable regardless of the cause of deficiency." [1]

Examiner: "What is the critical safety point in treating this patient?" [1]

"Do not give folate without B12. If I were to give folic acid alone, it would correct the blood picture — the megaloblastic anaemia would improve — but it would not address the B12 deficiency in the nervous system, and the patient could develop or worsen subacute combined degeneration of the spinal cord while her blood counts looked better. The rule is: always check B12 before starting folate, and if there is any doubt, treat both together. In this patient, the B12 is low and the folate is normal, so I would treat with IM hydroxocobalamin and I would not give folate at all [2]."

Examiner: "Name three causes of a macrocytic anaemia other than B12 or folate deficiency." [1]

"First, alcohol — it alters red cell membrane lipids and produces round macrocytes (not oval, and without hypersegmentation); the clue is a raised GGT and a drinking history. Second, liver disease — which also produces round macrocytes from membrane lipid changes and is often accompanied by target cells and features of chronic liver disease. Third, myelodysplastic syndrome — which produces dysplastic, often macrocytic red cells in an older patient, frequently with cytopenias in other lineages; the film shows dysplastic features and the marrow is hypercellular with dysplasia. Other causes include hypothyroidism (usually a mild macrocytosis), reticulocytosis (large young cells from haemolysis or recovery — but the reticulocyte count would be high, not low), and drug-induced macrocytosis from hydroxycarbamide, zidovudine, or chemotherapy." [1]

Examiner: "How does the direct antiglobulin test classify haemolytic anaemia?" [1]

"The DAT, or Coombs test, detects antibody or complement bound to the surface of the patient's red cells, and it separates immune from non-immune haemolysis. A positive DAT with IgG is warm autoimmune haemolytic anaemia — the antibody binds at body temperature and the coated cells are removed by splenic macrophages; it responds to corticosteroids. A positive DAT with C3d complement alone is cold agglutinin disease — an IgM antibody binds in the cooler peripheral circulation and fixes complement, and the cells are removed by the liver; it does not respond to steroids and is treated with rituximab. A negative DAT points to a non-immune cause: hereditary spherocytosis, G6PD deficiency, a microangiopathic process like TTP or DIC, or a haemoglobinopathy [3]."

Examiner: "What is the single most common error candidates make in the anaemia viva?" [1]

"Treating the number and not the cause. Iron deficiency is not a diagnosis — it is a sign of blood loss, and in a man or a postmenopausal woman that blood loss is from the gut until proven otherwise. The candidate who starts oral iron and rechecks the haemoglobin in three months has improved the blood count but may have missed a colon cancer. The disciplined approach is: confirm the deficiency with iron studies, find the cause with endoscopy and colonoscopy, and treat both — the deficiency and the source." [1]