Micronutrient deficiencies — structured clinical encounter

Task

You have twelve minutes to read this case and prepare, then a structured discussion with the examiner covering the recognition, the workup, the management, the differential and the public-health rationale. [1]

Domain 1 — Recognition and initial assessment

The examiner asks you to summarise the key findings and give the most likely diagnosis. [1]

A strong answer names iron-deficiency anaemia and ties it to the microcytic anaemia on the film, the fallen growth centile, the excessive cow's milk intake that displaces iron-rich solids and causes microscopic gut blood loss, and the pica, the eating of soil, which is a classic behavioural clue. The pallor, tiredness and irritability are the symptoms, and the cardiovascular examination should seek a flow murmur or tachycardia that marks severe anaemia. [1]

Domain 2 — Confirmatory investigations

The examiner asks how you confirm the diagnosis and why a C-reactive protein is needed. [3]

The confirmatory iron studies are a low serum ferritin, a low transferrin saturation, a raised transferrin and a low reticulocyte count. The C-reactive protein is required because ferritin is an acute-phase reactant that rises with inflammation, so a normal or borderline ferritin in an inflamed child can hide iron deficiency, and the soluble transferrin receptor, which is not affected by inflammation, can help when the ferritin is equivocal. A haemoglobin electrophoresis excludes thalassaemia trait when the ferritin is normal. [3]

Domain 3 — Management and counselling

The examiner asks for the treatment, the expected timeline and the dietary advice. [2]

The treatment is oral elemental iron at around three milligrams per kilogram per day, given once daily or in divided doses and away from milk and antacids. The reticulocyte count should rise within one to two weeks, the haemoglobin should normalise within two to three months, and the iron should be continued for about three months after the haemoglobin normalises to replete the stores. The dietary advice limits cow's milk to around five hundred millilitres a day, introduces iron-rich solids such as meat, legumes and iron-fortified cereals, and pairs iron with vitamin C to aid absorption. Intravenous iron is reserved for the severe, non-responsive or malabsorbing child. [2]

Domain 4 — Differential diagnosis

The examiner asks for the differential of microcytic anaemia and how you separate iron deficiency from thalassaemia trait. [1]

The differential is iron deficiency, thalassaemia trait, anaemia of chronic disease, lead poisoning and sideroblastic anaemia. The serum ferritin separates iron deficiency, which is low, from thalassaemia trait, which is normal or raised, alongside a normal or near-normal haemoglobin, a family history and a haemoglobin electrophoresis. [1]

Domain 5 — Public health and prevention

The examiner closes by asking why universal iron screening at around twelve months is recommended. [1]

Universal screening is recommended because iron deficiency harms the developing brain, through dopamine metabolism and myelination, before the anaemia appears, so waiting for pallor is waiting too long. The neurodevelopmental argument, not the anaemia alone, is the case for screening every infant, and prevention rests on iron-fortified complementary foods, limiting cow's milk in the toddler, and iron supplementation of the preterm and low-birth-weight infant from one month of age. [1]