Iron Deficiency — Written Clinical Reasoning

Model answer — Part A: severe iron-deficiency anaemia in an older man

Frame the problem. This is confirmed absolute iron-deficiency anaemia — ferritin 12 µg/L with TSAT 7% admits no argument — with a reactive thrombocytosis typical of chronic blood loss. In a 68-year-old man, the working diagnosis is occult GI blood loss, and GI malignancy must be excluded; the ibuprofen is a contributor to prove innocent, not a cause to assume [1] [3].

Assessment. Establish severity and stability: symptoms of anaemia (exertional dyspnoea, angina, syncope), haemodynamic observations, and any red flags — weight loss, anorexia, change in bowel habit, dysphagia, family history of GI cancer. Medication review for NSAIDs, anticoagulants and antiplatelets; dietary history; examination for abdominal masses, lymphadenopathy and PR findings [1].

Investigations. Complete the phenotype first: B12/folate, renal and liver function, CRP, reticulocytes and film. Then the cause hunt: coeliac serology (tTG-IgA with total IgA) and bidirectional endoscopy — gastroscopy with duodenal biopsies plus colonoscopy — because in this demographic a causative GI lesion is found in the majority and roughly one in ten harbours a cancer; a negative FOBT would change nothing and should not be performed as a gatekeeper [1] [2] [4].

Management. Transfusion is NOT indicated in a stable, compensating patient — iron deficiency is treated with iron. Start oral ferrous sulfate (65 mg elemental iron per tablet) once daily or alternate days on an empty stomach if tolerated, counsel on side effects, and stop the ibuprofen. Set expectations: reticulocyte response within about a week, haemoglobin rise of about 20 g/L per 2–3 weeks, and continue about 3 months after normalisation to replete stores. Switch to IV iron if oral iron fails or is not tolerated. Close the loop: recheck Hb and ferritin at 4 weeks, and ensure the endoscopy happens regardless of how the numbers respond [3] [8].

Model answer — Part B: functional iron deficiency in CKD

Interpretation. Ferritin 380 µg/L with TSAT 16% in an inflamed CKD patient is functional iron deficiency: stores exist on paper, but hepcidin-mediated sequestration plus darbepoetin-driven erythropoiesis means iron cannot reach the marrow at the required rate — the falling haemoglobin on a stable ESA dose is the clinical signature. Ferritin here must not be read against general-population cut-offs [7] [3].

Thresholds. KDIGO deliberately permits an iron trial in CKD at much higher numbers than elsewhere — TSAT at or below 30% with ferritin at or below 500 µg/L — precisely because of this physiology. She qualifies comfortably [6] [5].

Management. Give intravenous iron rather than escalating the ESA: in non-dialysis CKD, FIND-CKD showed IV ferric carboxymaltose achieves haemoglobin targets faster and more reliably than oral iron without added adverse events, and PIVOTAL in dialysis patients showed proactive IV iron is cardiovascular-safe while reducing ESA requirements and transfusions. Recheck iron studies and Hb after repletion before touching the darbepoetin dose, and address contributors — inflammation, hyperparathyroidism, adequacy of nutrition [6] [5].

Avoid the traps. Do not transfuse a stable CKD patient (allosensitisation matters for future transplantation); do not interpret ferritin 380 as "stores adequate"; and do not escalate the ESA into unopposed iron-restricted erythropoiesis — replete iron first [5] [7].