Iron Deficiency Anaemia

EPIDEMIOLOGY

Iron deficiency is the most common nutritional deficiency worldwide and the leading cause of anaemia globally. It is disproportionately prevalent in refugee and migrant populations due to the intersecting effects of poor nutrition during displacement, food insecurity, chronic helminth infection (which causes occult gastrointestinal blood loss), and inadequate dietary iron in refugee camp settings.

Women of reproductive age and children under 5 are at greatest risk. In Canada, iron deficiency anaemia (IDA) has been identified as one of the 20 priority conditions for clinical prevention in immigrants and refugees by the CCIRH Delphi consensus. Concurrent conditions that increase risk include: GI parasite infections (particularly hookworm and whipworm), malnutrition, and recent pregnancy.

CLINICAL PRESENTATION

Mild to moderate IDA is commonly asymptomatic or presents with non-specific symptoms that may be attributed to other causes:

•        Fatigue and reduced exercise tolerance

•        Pallor (conjunctival, palmar)

•        Exertional dyspnoea and palpitations

•        Headache and reduced concentration

•        Pica (craving non-food substances: ice, clay, starch) — classic but often not volunteered

Examination findings in moderate to severe IDA: conjunctival pallor, angular stomatitis, glossitis, koilonychia (spoon-shaped nails). In children: irritability, reduced activity, developmental delay, poor school performance.

CONTEXT-SPECIFIC INVESTIGATION

Initial CBC will show: low haemoglobin, low MCV (microcytic anaemia), low MCH. Note that microcytic anaemia in a refugee patient has a broader differential than in the general population:

–       Iron deficiency anaemia (most common)

–       Thalassaemia trait (alpha or beta) — very common in sub-Saharan African, Mediterranean, Middle Eastern, and Southeast Asian populations; ferritin is NORMAL

–       Anaemia of chronic inflammation — ferritin may be normal or elevated; iron stores are reduced but ferritin is an acute phase reactant

Confirmatory investigations:

•        Serum ferritin: most sensitive marker of iron stores. Low (<12 μg/L definitively confirms iron deficiency; <30 μg/L in the presence of anaemia is highly suggestive). Note: ferritin is an acute phase reactant — may be falsely elevated in inflammatory states.

•        Serum iron and TIBC (total iron-binding capacity): low iron + high TIBC = iron deficiency pattern

•        Haemoglobin electrophoresis: if thalassaemia trait suspected (microcytosis + normal ferritin)

•        Consider stool O&P (ova and parasites): if eosinophilia present or patient at high risk for helminth infection

MANAGEMENT AND TREATMENT

Oral iron replacement:

•        Ferrous sulphate 300 mg TID (elemental iron 60 mg per dose), taken on an empty stomach for maximum absorption. Vitamin C co-administration increases absorption.

•        Alternative: ferrous gluconate 600 mg TID (better tolerated GI profile); ferrous fumarate

•        Duration: continue oral iron for 3 months after haemoglobin has normalized, to replenish iron stores. Confirm with repeat ferritin.

Address underlying cause:

•        Treat helminth infections if identified (mebendazole or albendazole depending on species)

•        Dietary counselling: increase dietary iron (red meat, legumes, dark leafy greens, fortified cereals); reduce concurrent calcium, tea, and coffee which reduce iron absorption

•        GI source investigation if no other cause identified (especially in adult males or post-menopausal women)

IV iron: consider if severe anaemia, malabsorption, intolerance to oral iron, or need for rapid repletion (e.g., near-term pregnancy).

⚑  G6PD deficiency: check G6PD levels in males before initiating iron therapy if G6PD deficiency is suspected. Iron supplementation in G6PD deficiency is generally safe unless the patient is iron-replete, in which case it should be avoided due to the theoretical risk of oxidative stress.

CONTEXTUAL CONSIDERATIONS

Concurrent helminth infection: GI parasites — particularly hookworm — are a major and treatable cause of IDA in refugees from sub-Saharan Africa and Asia. Treating the parasite without replacing iron will not fully resolve the anaemia, and vice versa. Empirical treatment for helminths with mebendazole is reasonable in patients from high-prevalence regions with unexplained IDA and eosinophilia.

Dietary transition: patients transitioning from traditional iron-rich diets (e.g., legume and grain-based diets in East African communities) to processed Canadian food may develop IDA. Culturally sensitive dietary counselling that incorporates traditional foods alongside Canadian options is more effective than generic dietary advice.

Children and development: IDA in children under 2 years has lasting effects on neurodevelopment even after iron repletion. Early identification and treatment is critical. Confirm adequate dietary iron sources are available in the household.