After reading this note you will be able to recognise the clinical picture of iron‑deficiency anaemia, list the common Kenyan aetiologies, interpret the key laboratory results, grade severity and outline the immediate and definitive management plan – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
Iron‑deficiency anaemia (IDA) is a microcytic, hypochromic anaemia caused by a total body iron deficit that is insufficient to sustain normal haemoglobin synthesis.
Anatomy and physiology you need
| Structure / Function | Relevance to IDA |
|---|---|
| Erythropoietic marrow | Site of red‑cell production; requires iron for haemoglobin assembly. |
| Duodenal mucosa (proximal) | Main site of dietary iron absorption (ferrous Fe²⁺). |
| Transferrin | Plasma iron‑binding protein; low saturation signals deficiency. |
| Ferritin | Intracellular iron store; serum level reflects total body iron. |
| Hepcidin | Hormone that down‑regulates ferroportin; raised in inflammation, blocks iron release. |
| Reticulo‑endothelial system | Recycles iron from senescent erythrocytes; impaired recycling contributes to deficiency. |
| Kidney (EPO production) | Stimulated by hypoxia; may be blunted in chronic disease, worsening anaemia. |
Causes and risk factors
| Category | Kenyan‑relevant examples |
|---|---|
| Inadequate intake | Low‑iron diets (maize‑based, limited meat), vegetarianism, poverty. |
| Increased loss | Menstrual bleeding, gastrointestinal bleeding (ulcers, hemorrhoids, parasites), postpartum haemorrhage. |
| Increased demand | Pregnancy, rapid infant growth, chronic infections (TB, HIV). |
| Malabsorption | Celiac disease, tropical sprue, chronic diarrhoea, post‑gastrectomy. |
| Chronic inflammation | HIV infection, active TB, malaria, rheumatic fever, sickle‑cell disease (functional iron sequestration). |
| Other tropical contributors | Hookworm infestation, schistosomiasis, repeated malaria episodes causing haemolysis and iron loss. |
Pathophysiology
- Reduced dietary iron intake → ↓ luminal Fe²⁺ → ↓ absorption.
- Blood loss (chronic GI, menstrual, hookworm) → ↑ iron loss > intake.
- Infection/inflammation (HIV, TB, malaria) → ↑ hepcidin → ferroportin internalisation → ↓ iron release from macrophages & enterocytes.
- Increased physiological demand (pregnancy, growth) → iron utilisation outpaces supply.
- Net effect: ↓ serum ferritin & transferrin saturation → ↓ iron delivered to marrow → impaired haemoglobin synthesis → microcytic, hypochromic red cells → anaemia.
Arrows format:
Inadequate intake / loss / sequestration → ↓ plasma iron → ↓ transferrin saturation → ↓ marrow iron → ↓ haemoglobin → microcytic hypochromic anaemia.
Clinical features
| Aspect | Key questions / findings | Why it occurs |
|---|---|---|
| General symptoms | Fatigue, easy tiredness, reduced exercise tolerance, breathlessness on exertion, dizziness, palpitations. | Reduced oxygen‑carrying capacity → tissue hypoxia → compensatory increase in cardiac output and perception of low energy. |
| Gastro‑intestinal | Change in appetite, pica (craving for ice, dirt, clay), dysphagia, early satiety, abdominal pain, melena or occult blood loss. | Iron deficiency stimulates craving for non‑nutritive substances; chronic blood loss (ulcers, parasites, hemorrhoids) depletes iron stores. |
| Genitourinary | Menstrual history (heavy, prolonged bleeding, intermenstrual spotting), post‑partum bleeding, urinary symptoms suggestive of schistosomiasis. | Menstrual or genital blood loss is a common source of iron loss in women of reproductive age. |
| Infectious / inflammatory | History of recent or recurrent malaria episodes, TB treatment, HIV status, chronic cough, night sweats, weight loss, rheumatic fever, sickle‑cell crises. | Chronic infection or inflammation can cause iron sequestration and increased loss (e.g., hemolysis in sickle cell, hematuria in schistosomiasis). |
| Dietary | Frequency of meat, leafy greens, legumes; vegetarian/vegan diet; use of tea/coffee with meals; socioeconomic constraints. | Low dietary heme iron intake or inhibitors of iron absorption (phytates, polyphenols) limit iron availability. |
| Medication / supplements | Use of antacids, PPIs, iron chelators, chronic NSAIDs, anti‑malarial prophylaxis. | Reduced gastric acidity or drug‑induced GI bleeding impair iron absorption or increase loss. |
| Family / past medical | Family history of haemoglobinopathies, previous anaemia, surgeries (gastric bypass). | Genetic conditions or prior surgeries can affect iron metabolism or loss. |
Examination findings
| Finding | Interpretation |
|---|---|
| Pallor – conjunctiva, palmar creases, nail beds | Visible reduction in perfused hemoglobin; early sign of moderate anaemia. |
| Tachycardia (resting) | Compensatory increase in cardiac output to maintain tissue oxygen delivery. |
| Systolic flow murmur (soft, ejection) | Turbulent flow due to increased blood velocity in a low‑viscosity circuit. |
| Glossitis (smooth, beefy red tongue) | Rapid turnover of mucosal epithelium with iron‑dependent enzymes impaired. |
| Angular cheilitis / atrophic mucosa | Iron is required for epithelial integrity; deficiency leads to fissuring. |
| Koilonychia (spoon‑shaped nails) | Chronic iron shortage affects keratin synthesis. |
| Splenomegaly (if co‑existing hemolysis e.g., sickle cell) | May indicate overlapping haemolytic process rather than pure iron deficiency. |
| Peripheral edema (rare) | Severe anaemia can precipitate high‑output cardiac failure. |
Differential diagnosis
| Condition | Points to it | How to separate from iron‑deficiency anaemia |
|---|---|---|
| Thalassaemia trait | Family history, microcytosis, mild anaemia, often asymptomatic. | Normal or elevated ferritin, HbA2 ↑, iron studies normal; RBC indices show target cells. |
| Anemia of chronic disease | Chronic infection (TB, HIV), inflammatory markers ↑, low serum iron with normal/high ferritin. | Ferritin high/normal, transferrin saturation low, CRP/ESR ↑; iron studies differ from true deficiency. |
| Sideroblastic anaemia | Exposure to drugs (isoniazid), alcohol, congenital forms, ringed sideroblasts on marrow. | Serum iron ↑, ferritin ↑, transferrin saturation ↑; bone marrow shows sideroblasts. |
| Hemolytic anaemia (sickle cell, G6PD) | Jaundice, dark urine, splenomegaly, episodic pain crises. | Elevated LDH, indirect bilirubin, reticulocytosis; peripheral smear shows sickled cells or bite cells. |
| Lead poisoning | Occupational exposure, abdominal pain, neurocognitive changes. | Basophilic stippling on smear, blood lead level ↑, iron studies usually normal. |
| Vitamin B12/folate deficiency | Neurological signs, macrocytosis, dietary deficiency. | MCV ↑, hypersegmented neutrophils, normal iron studies, low B12/folate levels. |
| Chronic kidney disease | Reduced eGFR, uremic symptoms. | Low erythropoietin, normocytic anaemia, iron studies may be normal or low depending on concurrent deficiency. |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Full blood count (FBC) | Morphology, severity, indices. | Low Hb, low MCV, low MCH → microcytic anaemia; reticulocyte count low in deficiency. |
| Serum ferritin | Iron stores. | < 15 µg/L → depleted stores; > 100 µg/L suggests alternative cause. |
| Serum iron | Circulating iron. | Low in deficiency; normal/high in sideroblastic. |
| Total iron‑binding capacity (TIBC) | Binding capacity of transferrin. | Elevated in deficiency; low/normal in anemia of chronic disease. |
| Transferrin saturation | Ratio of serum iron to TIBC. | < 15 % typical of deficiency. |
| Peripheral blood smear | Red cell morphology. | Microcytosis, hypochromia; absence of target cells (thalasemia) or basophilic stippling (lead). |
| Stool occult blood | GI blood loss. | Positive → source of chronic loss; negative directs search elsewhere. |
| C‑reactive protein / ESR | Inflammation. | Elevated suggests anemia of chronic disease or active infection. |
| HIV test, TB screening (GeneXpert, chest X‑ray) | Co‑morbid infections. | Positive results guide concurrent treatment. |
| Pregnancy test (women of reproductive age) | Pregnancy‑related demand. | Positive → increased iron requirement. |
Diagnosis and severity
- Confirm iron deficiency – combination of microcytic hypochromic anaemia on FBC and at least two iron studies consistent with depletion (low ferritin, low serum iron, high TIBC, low transferrin saturation). In the Kenyan setting, a ferritin < 30 µg/L is often used as the cut‑off when inflammation is present.
- Assess severity (based on haemoglobin concentration):
- Mild – Hb 10–11 g/dL (women) or 10–12 g/dL (men). Usually asymptomatic or mild fatigue.
- Moderate – Hb 7–9.9 g/dL. Marked fatigue, tachycardia, exertional dyspnoea.
- Severe – Hb < 7 g/dL. Resting tachycardia, orthostatic hypotension, high‑output cardiac failure, possible chest pain.
- Stage the aetiology – identify and document the source of loss or malabsorption (e.g., heavy menstrual bleeding, helminthic infection, chronic malaria, TB, HIV, dietary insufficiency). This determines definitive therapy beyond iron replacement.
- Document comorbidities – HIV status, renal function, pregnancy, sickle‑cell disease, which influence choice of iron formulation and need for adjunctive therapy (e.g., erythropoietin in CKD).
The clinical approach therefore proceeds from confirming the iron‑deficiency pattern, quantifying the haemoglobin deficit, and pinpointing the underlying cause to guide both immediate replenishment and long‑term prevention.
Management
| Phase | What to do | Rationale / safety notes |
|---|---|---|
| Immediate stabilisation | • Assess airway, breathing, circulation; give supplemental O₂ if SpO₂ < 94 % | Anaemia can precipitate tissue hypoxia, especially in severe cases or co‑existing cardiopulmonary disease. |
| • Obtain rapid bedside haemoglobin (point‑of‑care) and full blood count | Guides urgency of transfusion. | |
| • Transfuse packed red cells only if haemoglobin < 7 g/dL (or < 8 g/dL with cardiac disease, active bleeding, or pregnancy) | Avoids volume overload; monitor for transfusion reactions. | |
| • Correct any active bleeding (e.g., GI bleed, menorrhagia) before iron replacement | Ongoing loss will negate replacement. | |
| Definitive treatment | Oral iron (ferrous salts) – first line for uncomplicated IDA | Improves stores in 2–3 weeks; give on empty stomach if tolerated, otherwise with food to reduce GI upset. |
| Parenteral iron (IV iron sucrose, ferric carboxymaltose) – for intolerance to oral iron, malabsorption, severe anaemia needing rapid repletion, or when oral therapy is contraindicated (e.g., active infection, inflammatory bowel disease flare) | Faster repletion; monitor for hypotension, rash, or rare anaphylaxis during infusion. | |
| Treat underlying cause – anti‑TB therapy, antiretroviral therapy optimisation, malaria treatment, deworming, surgical correction of chronic blood loss, etc. | Without addressing source, anaemia recurs. | |
| Nutritional optimisation – ensure adequate folate, vitamin B12, protein, and calories; counsel on iron‑rich foods (red meat, beans, dark leafy greens) and enhancers (vit C) and inhibitors (tea, coffee, calcium) | Improves absorption and overall haematopoiesis. | |
| Monitoring | • Repeat full blood count at 2–4 weeks; reticulocyte count rises within 7‑10 days if therapy effective | Detects non‑response early. |
| • Serum ferritin and transferrin saturation after 8‑12 weeks of therapy to confirm repletion | Ferritin normalises before haemoglobin. | |
| • Watch for side‑effects: GI irritation (oral), infusion reactions (IV), iron overload (rare, in repeated IV courses) | Stop or switch therapy if severe. | |
| Follow‑up | • Continue oral iron for at least 3 months after haemoglobin normalises to replenish stores | Prevent relapse. |
| • Re‑evaluate for occult bleeding if anaemia recurs despite adherence | Ensures hidden source is not missed. |
Contra‑indications / safety
- Oral iron: known hypersensitivity to ferrous salts, active haemochromatosis.
- IV iron: previous severe hypersensitivity to any IV iron product, active severe infection (iron may fuel pathogens), uncontrolled asthma (risk of bronchospasm).
- Blood transfusion: patient refusal, religious objection, or severe allo‑immunisation risk without compatible units.
Complications and prognosis
- Cardiac strain – chronic severe IDA can cause high‑output heart failure, especially in pregnant women and the elderly.
- Pregnancy adverse outcomes – pre‑term delivery, low birth weight, and perinatal mortality increase with maternal IDA.
- Neurocognitive effects – impaired concentration, fatigue, and reduced exercise tolerance; children may have delayed psychomotor development.
- Infection susceptibility – iron deficiency impairs neutrophil function; however, excess iron (especially IV) can promote bacterial growth, so balance is key.
- Refractory anaemia – if underlying cause (e.g., chronic malaria, TB, gastrointestinal malignancy) is missed, anaemia persists despite replacement.
With timely diagnosis, appropriate iron repletion and treatment of the precipitating condition, most patients recover fully. Relapse rates are low when iron stores are re‑established and the source of loss is eliminated.
High‑yield exam points
- Look‑alike conditions: Thalassaemia trait (microcytosis with normal ferritin), anemia of chronic disease (low iron, low TIBC, normal/high ferritin), sideroblastic anaemia (ringed sideroblasts, high iron).
- Common wrong first step: Starting iron therapy without confirming iron deficiency (e.g., in anemia of chronic disease).
- Examiner bedside question: “What would you look for on abdominal examination and why in a patient with iron‑deficiency anaemia?” – Expected answer: palpate for splenomegaly (rule out hemolysis), examine for signs of chronic blood loss (e.g., hemorrhoids, uterine enlargement).
- Key investigation interpretation: Low serum ferritin is the most specific test; a normal ferritin does not exclude IDA in inflammation.
- Management nuance: In a pregnant woman with Hb 7 g/dL, give oral iron and consider a single unit of packed cells if symptomatic, but avoid routine transfusion.
Clinical case
Case: A 28‑year‑old Kenyan woman, gravida 2 para 1, presents with a 3‑month history of progressive fatigue, exertional dyspnoea, and heavy menstrual bleeding (≈ 8 pads/day). Physical exam shows conjunctival pallor, tachycardia 110 bpm, and a mildly enlarged, non‑tender uterus. Labs: Hb 7.8 g/dL, MCV 68 fL, serum ferritin 8 µg/L, transferrin saturation 10 %.
Questions
- What is the most appropriate immediate management?
Answer: Give a single unit of packed red cells because she is symptomatic with Hb < 8 g/dL and is pregnant; start oral iron concurrently.
- Which investigation should be performed next to identify the source of blood loss?
Answer: Pelvic ultrasound to assess for uterine fibroids or polyps causing menorrhagia; also consider endometrial sampling if indicated.
- What counselling point is essential regarding oral iron therapy?
Answer: Advise taking the tablets on an empty stomach with vitamin C‑rich juice to enhance absorption and to avoid tea/coffee within an hour to reduce inhibition.
Practice questions
Question 1
A 65‑year‑old man with known chronic kidney disease presents with fatigue and Hb 6.5 g/dL. His ferritin is 30 µg/L and transferrin saturation 12 %. What is the next best step?
A. Start oral ferrous sulfate
B. Give a unit of packed red cells
C. Initiate intravenous iron therapy
D. Begin erythropoiesis‑stimulating agent only
Answer: C. Initiate intravenous iron therapy – CKD patients often have poor oral iron absorption and need IV iron to replenish stores efficiently.
Question 2
A 10‑year‑old boy from a malaria‑endemic area has microcytic anaemia, low ferritin, and a recent positive malaria smear. Which statement is true?
A. Treat malaria first, then start iron after 2 weeks
B. Give iron immediately; malaria does not affect iron absorption
C. Withhold iron until malaria is cleared to avoid fueling parasites
D. Use high‑dose oral iron to overcome malaria‑induced loss
Answer: C. Withhold iron until malaria is cleared to avoid fueling parasites – iron can exacerbate malaria infection; treat the infection first.
Question 3
A pregnant woman at 20 weeks gestation has Hb 9.2 g/dL, MCV 72 fL, ferritin 15 µg/L. Which is the safest iron preparation?
A. Ferrous gluconate tablets
B. Intravenous iron sucrose
C. Iron dextran infusion
D. No iron until delivery
Answer: A. Ferrous gluconate tablets – oral iron is first‑line in pregnancy; IV iron is reserved for intolerance or severe deficiency.
Question 4
A 45‑year‑old woman with heavy menstrual bleeding has a normal ferritin but low serum iron. Which diagnosis is most likely?
A. Iron‑deficiency anaemia
B. Anemia of chronic disease
C. Thalassaemia trait
D. Sideroblastic anaemia
Answer: B. Anemia of chronic disease – normal/high ferritin with low serum iron suggests iron sequestration rather than true deficiency.
Question 5
During follow‑up, a patient on oral iron reports persistent diarrhoea and no rise in haemoglobin after 4 weeks. What is the best next action?
A. Increase the oral iron dose
B. Switch to a different oral iron formulation
C. Start intravenous iron therapy
D. Add folic acid supplement
Answer: C. Start intravenous iron therapy – intolerance and lack of response indicate need for parenteral iron.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.