Synopsis
Confirm iron deficiency, identify bleeding, malabsorption or increased demand, start effective replacement and prove both haematological response and completion of the source investigation.
- Confirm iron deficiency with ferritin and the inflammatory context rather than diagnosing it from microcytosis alone; early or mixed deficiency may remain normocytic.
- Low ferritin is highly supportive of depleted stores, but inflammation can raise ferritin. Transferrin saturation, CRP, reticulocyte haemoglobin where available and response help when the result is equivocal.
- Find the cause at the same time as starting replacement. Menstrual loss, gastrointestinal symptoms, diet, blood donation, pregnancy, medicines, bariatric surgery and coeliac risk require explicit review.
Key red flags
Chest pain, syncope, heart failure, shock or severe breathlessness with rapid anaemia indicates threatened oxygen delivery or continuing bleeding, not a routine oral-iron problem.
Investigation priorities
Define severity, morphology, mixed deficiency and marrow response.
Management branches
Anaemia is microcytic, hypochromic, otherwise unexplained or accompanied by symptoms suggesting depleted iron.
- Obtain FBC, reticulocytes, film, ferritin, transferrin saturation and CRP, assess symptoms and haemodynamics, and compare previous haemoglobin and MCV.
- The preferred diagnosis uses depleted stores plus the clinical phenotype; an alternative inflammation-adjusted assessment uses saturation, specialist thresholds and treatment response when ferritin is misleading.
Key medicines
Ferrous sulfateA common adult BSG regimen is one 200 mg tablet by mouth once daily; if not tolerated, use one tablet every other day or another oral preparation.
Ferric carboxymaltose (intravenous example)Calculate the Ferinject requirement from weight and haemoglobin; an infusion must not exceed 20 mg iron/kg or 1,000 mg, and the cumulative weekly maximum is 1,000 mg.