Anaemia — Causes, Types, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Anaemia is defined as a reduction in the number of circulating red blood cells (RBCs) or haemoglobin (Hb) concentration below the normal threshold for age and sex — WHO defines anaemia as Hb below 130 g/L in adult men, below 120 g/L in non-pregnant adult women, and below 110 g/L in pregnant women. It is the world's most common blood disorder, affecting 1.62 billion people — 24.8% of the global population. Anaemia is not a diagnosis in itself but a sign of an underlying cause requiring investigation. The physiological consequence is reduced oxygen delivery to tissues, causing the characteristic symptoms of fatigue, breathlessness, and pallor. Iron deficiency anaemia (IDA) accounts for approximately 50% of all anaemia globally, predominantly affecting children, women of reproductive age, and people in low- and middle-income countries. Other major types include anaemia of chronic disease (ACD), vitamin B12 and folate deficiency, haemolytic anaemias, haemoglobinopathies (sickle cell disease, thalassaemia), aplastic anaemia, and renal anaemia.

Anaemia is classified by mechanism: decreased production, increased destruction, or blood loss. Decreased RBC production: iron deficiency (inadequate dietary intake, chronic blood loss — most common cause worldwide); vitamin B12 deficiency (pernicious anaemia — autoimmune gastric atrophy, strict vegan diet, gastric surgery, metformin use); folate deficiency (poor diet, alcohol, pregnancy, methotrexate); anaemia of chronic disease (ACD) — chronic inflammation suppresses erythropoiesis via hepcidin; renal failure (reduced erythropoietin production); bone marrow failure (aplastic anaemia, haematological malignancy, myelodysplastic syndrome, chemotherapy); thalassaemia (reduced globin chain production). Increased RBC destruction (haemolysis): hereditary spherocytosis, sickle cell disease, glucose-6-phosphate dehydrogenase (G6PD) deficiency, autoimmune haemolytic anaemia (AIHA), thrombotic thrombocytopenic purpura (TTP), haemolytic uraemic syndrome. Blood loss: acute (trauma, GI haemorrhage) or chronic (peptic ulcer, colorectal cancer, menorrhagia — commonest cause of IDA in women of reproductive age).

Symptoms depend on the severity of anaemia and speed of onset. Chronic gradual anaemia allows physiological compensation and may be surprisingly asymptomatic even at Hb 70-80 g/L. Symptoms: fatigue and exhaustion (most common), breathlessness on exertion (reduced O2 delivery), palpitations (compensatory tachycardia), pallor (conjunctival, palmar, mucous membrane — check conjunctival pallor for clinical assessment), headache, dizziness, poor concentration, and cold extremities. Severe anaemia (Hb below 70 g/L or rapid onset): angina, cardiac failure, and haemodynamic instability. Type-specific features: IDA — koilonychia (spoon-shaped nails), glossitis, angular cheilitis, pica (craving non-food items — ice, dirt), and dysphagia (Plummer-Vinson syndrome); B12 deficiency — glossitis, peripheral neuropathy (subacute combined degeneration of the spinal cord — dorsal column and corticospinal tract demyelination), neuropsychiatric symptoms; Haemolytic anaemia — jaundice, splenomegaly, dark urine; Aplastic anaemia — pancytopaenia with bleeding and infections.

Full blood count (FBC): haemoglobin, MCV (mean corpuscular volume), MCH, MCHC, reticulocyte count, and white cell and platelet counts. MCV classifies anaemia: microcytic (MCV below 80 fl) — IDA, thalassaemia, ACD; normocytic (MCV 80-100 fl) — ACD, haemolysis, renal anaemia, bone marrow failure; macrocytic (MCV above 100 fl) — B12/folate deficiency, alcohol, hypothyroidism, haematological malignancy. Reticulocyte count: elevated in haemolysis and haemorrhage; low in bone marrow failure. Iron studies: serum ferritin (most sensitive marker of iron stores — below 30 ng/mL confirms IDA; above 100 ng/mL unlikely IDA); serum iron, TIBC, transferrin saturation. Vitamin B12 and folate levels. Peripheral blood film: morphology of RBCs (hypochromic microcytes in IDA; macroovalocytes with hypersegmented neutrophils in B12 deficiency; sickle cells; spherocytes; schistocytes in haemolysis). LFTs, renal function, TSH, LDH, haptoglobin (low in haemolysis), Coombs' test (positive in AIHA). Bone marrow aspirate and biopsy for unexplained cytopaenias or suspected haematological malignancy.

Treatment is directed at the underlying cause. Iron deficiency anaemia: oral ferrous sulfate 200 mg (65 mg elemental iron) three times daily — taken with vitamin C (orange juice) to enhance absorption; avoid with calcium, tea, antacids; causes GI side effects (constipation, nausea) — if intolerant, ferrous gluconate or ferrous fumarate. IV iron (ferric carboxymaltose — Ferinject; low molecular weight iron dextran) for patients unable to tolerate oral iron, malabsorption (coeliac, IBD, post-bariatric surgery), severe IDA, or chronic kidney disease. Treat underlying cause (menorrhagia, peptic ulcer, colorectal cancer). B12 deficiency: hydroxocobalamin 1 mg IM every 2-3 days for 2 weeks, then 3-monthly (pernicious anaemia) or oral cyanocobalamin 1 mg daily for dietary deficiency or malabsorption without pernicious anaemia. Folate deficiency: folic acid 5 mg daily for 4 months (always exclude B12 deficiency first — folate supplementation in B12 deficiency risks precipitating subacute combined degeneration). Anaemia of chronic disease: treat underlying condition; EPO therapy for renal anaemia. Blood transfusion: indicated for symptomatic severe anaemia (typically Hb below 70 g/L) or cardiac/haemodynamic compromise.

Untreated or poorly managed anaemia causes serious systemic complications. Severe anaemia (Hb below 70 g/L) leads to high-output cardiac failure — the heart increases output to compensate for reduced oxygen delivery, causing left ventricular hypertrophy, cardiomegaly, and decompensated heart failure, which is potentially fatal. In children, iron deficiency anaemia (even subclinical) causes irreversible neurodevelopmental impairment — reduced cognitive function, poor academic performance, and behavioural difficulties. Vitamin B12 deficiency left untreated causes permanent subacute combined degeneration of the spinal cord — progressive demyelination of dorsal columns and corticospinal tracts producing sensory ataxia, peripheral neuropathy, and cognitive decline. In pregnancy, severe anaemia significantly increases risk of preterm birth, low birth weight, maternal mortality from postpartum haemorrhage, and impaired foetal brain development. Aplastic anaemia is rapidly fatal without immunosuppression or bone marrow transplantation. Untreated haemolytic crises in sickle cell disease precipitate acute chest syndrome, stroke, and multi-organ damage.

Iron deficiency prevention: dietary iron optimisation — haem iron (red meat, poultry, fish — 15-35% absorbed) is better absorbed than non-haem iron (legumes, fortified cereals, dark leafy vegetables — 2-20% absorbed); enhance absorption with vitamin C; avoid tea and coffee with meals. Folic acid 400 mcg daily for all women planning pregnancy (5 mg/day for high-risk) reduces neural tube defect risk. Deworming programmes (albendazole, mebendazole) reduce IDA in endemic regions. Routine anaemia screening in pregnancy — all pregnant women. Annual B12 monitoring in strict vegans, elderly, and long-term metformin users. In children with heavy cow's milk consumption, limit to 500 mL/day (displaces iron-rich foods). National food fortification programmes (iron and folate in flour) are highly effective public health interventions.

Seek emergency medical care immediately for: severe breathlessness at rest, chest pain, or rapid heart rate with known or suspected anaemia; collapse or haemodynamic shock from acute blood loss (vomiting blood, rectal bleeding, black stools). Seek urgent medical attention (within days) for: pallor with extreme fatigue that limits daily activities; any unexplained haematuria, rectal bleeding, or persistent menorrhagia; features of haemolysis — jaundice and dark urine. Routine GP review is needed for: persistent unexplained fatigue and pallor (Hb may be monitored at home with some devices but always confirm with laboratory FBC); known anaemia that has not responded to 4-6 weeks of treatment; recurrence after completing iron therapy without investigation of cause.