Anaemia: diagnostic approach — formative SAQs

SAQ 1 (10)

A 20-month-old has a haemoglobin of 78 g/L with a mean corpuscular volume of 66 femtolitres, microcytic hypochromic indices, and a normal white cell and platelet count. The child drinks about 800 millilitres of cow's milk a day. [1]

1. State a one-sentence problem representation and justify the MCV and reticulocyte classification grid you used. (3) [1] [3]
2. Outline the directed second-line tests and how you would interpret ferritin as an acute-phase reactant. (4) [1] [6]
3. Detail cause-directed management including the oral iron dose, expected response, and how to avoid missing the microcytic mimics. (3) [1] [4] [6]

Model answer

Problem representation. Twenty-month-old with dietary risk, microcytic hypochromic anaemia, low or normal reticulocytes, and no red flags for marrow disease, consistent with iron deficiency. The grid sorts by mean corpuscular volume into micro, normo or macro, and by reticulocyte count into high (loss or destruction) versus low (production failure); this child sits in microcytic and low reticulocyte, the iron-deficiency cell. [1] [3]

Directed tests. Iron studies: ferritin, serum iron, transferrin or total iron-binding capacity, and transferrin saturation. Low ferritin with high binding capacity confirms deficiency, but ferritin is an acute-phase reactant, so a normal or high value in inflammation does not exclude iron deficiency and the soluble transferrin receptor or full iron panel helps. Add a haemoglobinopathy screen if microcytosis is disproportionate, the red cell count is high, or ancestry suggests trait. [1] [6]

Management. Reduce cow's milk to about 500 millilitres daily, improve iron-rich solids, start oral elemental iron at 3 to 6 milligrams per kilogram per day, and plan a response check. Expect a reticulocyte rise within seven to ten days then a haemoglobin climb; failure to rise means wrong diagnosis, ongoing loss, non-adherence or malabsorption, not more iron. Avoid empiric iron when thalassaemia trait, anaemia of inflammation or lead is plausible. [1] [4] [6]

SAQ 2 (10)

A 14-year-old vegetarian girl has a haemoglobin of 74 g/L with a mean corpuscular volume of 108 femtolitres and hypersegmented neutrophils on the film. On the same shift, a six-year-old presents with fever, bruising, bone pain, and a haemoglobin of 69 g/L with low reticulocytes and thrombocytopenia. [2] [5]

1. What is the mechanism and what directed tests confirm the macrocytic anaemia? (3) [5]
2. What immediate actions protect the febrile, bruised child with cytopenias? (3) [2]
3. State the transfusion and sampling principles for stable versus unstable anaemia. (4) [2]

Model answer

Macrocytic pathway. A high mean corpuscular volume with hypersegmented neutrophils and oval macrocytes points to megaloblastic anaemia from vitamin B12 or folate deficiency. Confirm with serum B12 and red-cell or serum folate, review for malabsorption or pernicious anaemia, and replace the missing vitamin under specialist guidance; a marked reticulocytosis from haemolysis can also raise the volume, so read the reticulocyte count. [5]

Threat pathway. This is a suspected marrow pathology or malignancy. Same-day full blood count with film, assess stability, treat neutropenic fever as a time-critical infection risk with empirical broad-spectrum antibiotics, and involve haematology early for marrow examination with cytogenetics. Do not trial iron at home. [2]

Transfusion and sampling. If stable, draw diagnostic samples including film, reticulocytes, group and screen and special tests before transfusion so they remain interpretable. If unstable, resuscitate and transfuse per local paediatric protocol for physiological compromise; do not delay rescue blood for a perfect pre-transfusion panel. Transfuse for physiology, not a number alone, and beware over-rapid volume expansion in chronic compensated anaemia. [2]