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

Anaemia is defined as a haemoglobin (Hb) level below 13 g/dL in adult men and below 12 g/dL in adult women (WHO criteria), resulting in reduced oxygen-carrying capacity of the blood and causing tissue hypoxia. It is not a single disease but a sign of one or more underlying conditions affecting red blood cell production, survival, or loss. The most common type worldwide is iron-deficiency anaemia (IDA) — responsible for approximately 50% of all anaemia cases and the single most common nutritional deficiency globally, affecting predominantly women of reproductive age, children under 5, and pregnant women in low-income countries. Other major types include: anaemia of chronic disease/inflammation (associated with rheumatoid arthritis, IBD, malignancy, chronic kidney disease); vitamin B12 deficiency anaemia (most commonly pernicious anaemia — autoimmune gastric atrophy); folate deficiency anaemia; haemolytic anaemias (autoimmune, hereditary spherocytosis, G6PD deficiency, sickle cell haemolytic crises); sickle cell disease; thalassaemia major (severe transfusion-dependent); and aplastic anaemia (bone marrow failure). Anaemia affects 1.6 billion people globally — 24.8% of the world population — and is a major contributor to maternal and child mortality, cognitive development impairment, and reduced productivity in low-income settings.

Anaemia results from three main pathophysiological mechanisms, often in combination. Blood loss — the most common cause: menorrhagia (heavy menstrual bleeding — the leading cause of IDA in premenopausal women globally), gastrointestinal bleeding (peptic ulcer, colorectal cancer, oesophageal varices, angiodysplasia, NSAIDs), postpartum haemorrhage, and surgical or traumatic haemorrhage. Decreased red blood cell production: nutritional deficiencies (iron — impairs haemoglobin synthesis; vitamin B12 — needed for DNA synthesis in erythropoiesis; folate — required for erythrocyte maturation); bone marrow failure or infiltration (aplastic anaemia, myelodysplastic syndrome, leukaemia, lymphoma, myeloma metastases); anaemia of chronic disease (elevated inflammatory cytokines — IL-6, IL-1 — increase hepcidin, reducing iron bioavailability); chronic kidney disease (reduced erythropoietin production); and myelosuppressive chemotherapy or radiation. Increased red blood cell destruction (haemolysis): autoimmune haemolytic anaemia (warm or cold-antibody mediated); hereditary red cell membrane disorders (spherocytosis, elliptocytosis); enzyme defects (G6PD deficiency, pyruvate kinase deficiency); haemoglobinopathies (sickle cell disease — vaso-occlusive crises with haemolysis; thalassaemia major); microangiopathic haemolytic anaemia (TTP, HUS, DIC, HELLP syndrome); and falciparum malaria. Risk factors: female sex, pregnancy, infancy and childhood, inadequate dietary iron or B12, malabsorption (coeliac disease, Crohn's, post-gastrectomy), and chronic alcohol use (bone marrow suppression, folate deficiency).

Symptoms depend on the severity of anaemia, its rate of onset, and the underlying cause. Mild anaemia (Hb 10-12 g/dL) may be asymptomatic or cause only subtle fatigue — particularly in young, otherwise healthy individuals who compensate through cardiovascular adaptation. As anaemia worsens, symptoms develop from tissue hypoxia and compensatory cardiorespiratory responses: fatigue and generalised weakness (most common — caused by reduced oxygen delivery to muscles); pallor of the skin, conjunctivae, nail beds, and mucous membranes; dyspnoea on exertion and reduced exercise tolerance; palpitations and tachycardia (the heart works harder to maintain oxygen delivery); dizziness, lightheadedness, or syncope (especially postural); headaches; difficulty concentrating and cognitive slowing; and cold extremities. Severe acute anaemia (Hb below 7-8 g/dL) causes angina (chest pain from myocardial hypoxia — particularly in those with coronary artery disease), haemodynamic instability, and high-output cardiac failure. Iron deficiency anaemia specifically causes additional symptoms from iron-dependent enzymatic dysfunction: pica (craving and consumption of non-food items such as ice/pagophagia, clay, chalk, or soil — present in 50-70% of IDA patients); brittle, spoon-shaped nails (koilonychia); angular stomatitis and glossitis (smooth, painful tongue); dysphagia (Plummer-Vinson syndrome — associated with post-cricoid web); and restless legs syndrome. B12 deficiency causes neurological symptoms — subacute combined degeneration of the spinal cord (peripheral neuropathy, sensory ataxia, cognitive decline) — that may precede or occur without anaemia.

A full blood count (FBC/CBC) is the first step and characterises anaemia by MCV (mean corpuscular volume) and red cell morphology. Microcytic anaemia (MCV below 80 fL): iron deficiency (most common — confirmed by low serum ferritin, below 30 mcg/L; low transferrin saturation, below 20%), thalassaemia trait (ferritin normal or elevated; haemoglobin electrophoresis diagnostic), or anaemia of chronic disease (ferritin normal or high). Normocytic anaemia (MCV 80-100 fL): anaemia of chronic disease (most common normocytic cause — normal or high ferritin, low transferrin saturation, high hepcidin; elevated ESR/CRP), acute blood loss, renal anaemia (low erythropoietin), early iron or B12 deficiency, or mixed deficiency. Macrocytic anaemia (MCV above 100 fL): vitamin B12 deficiency (serum B12 below 150-200 pg/mL; serum methylmalonic acid and homocysteine elevated — more sensitive markers), folate deficiency (serum folate, RBC folate), hypothyroidism (TFTs), alcohol toxicity, myelodysplastic syndrome, or drugs (methotrexate, hydroxyurea). Peripheral blood film examination: hypochromic microcytes (IDA), macroovalocytes and hypersegmented neutrophils (megaloblastic; B12/folate), sickle cells, target cells, spherocytes (hereditary spherocytosis or haemolytic), or blast cells (haematological malignancy). Further testing guided by findings: reticulocyte count (low — production failure; high — haemolysis or blood loss); direct Coombs/antiglobulin test (AIHA); LDH and haptoglobin (haemolysis); haemoglobin electrophoresis or HPLC (haemoglobinopathies); bone marrow aspirate and trephine (unexplained, suspected marrow failure or malignancy); anti-intrinsic factor and anti-parietal cell antibodies (pernicious anaemia); and renal function with eGFR.

Treatment must address both the anaemia and its underlying cause. Iron-deficiency anaemia: oral ferrous sulphate 200 mg two to three times daily (providing approximately 120-200 mg elemental iron per day) for 3-6 months to replenish stores — taken on an empty stomach 30 minutes before food, with vitamin C, to maximise absorption; reticulocyte response should be confirmed at 2-4 weeks and Hb rechecked at 4-8 weeks. IV iron (ferric carboxymaltose, iron sucrose, low molecular weight iron dextran) is used when oral iron fails, is not tolerated, or absorption is impaired (post-bariatric surgery, coeliac disease, IBD); single large doses of ferric carboxymaltose 500-1000 mg can be given over 15 minutes. Vitamin B12 deficiency (pernicious anaemia): intramuscular hydroxocobalamin 1 mg every other day for 2 weeks, then monthly lifelong (lifelong because pernicious anaemia is a permanent autoimmune condition); oral high-dose B12 (1000-2000 mcg daily) is effective in dietary deficiency without malabsorption. Folate deficiency: folic acid 5 mg once daily for 4 months (give only after excluding B12 deficiency — supplementing folate alone without treating co-existing B12 deficiency risks precipitating irreversible neurological damage from B12 deficiency). Anaemia of chronic disease: best treated by effectively managing the underlying inflammatory condition; erythropoiesis-stimulating agents (ESAs — darbepoetin alfa, epoetin) for renal anaemia or chemotherapy-induced anaemia; IV iron if ferritin is below 100 mcg/L. Haemolytic anaemia: prednisolone 1 mg/kg/day for autoimmune warm haemolytic anaemia; rituximab for refractory cases; splenectomy for refractory warm AIHA or hereditary spherocytosis. Aplastic anaemia: haematopoietic stem cell transplant (HSCT) is curative in eligible patients; anti-thymocyte globulin (ATG) plus cyclosporin for those unsuitable for transplant; eltrombopag (thrombopoietin receptor agonist) improves responses. Blood transfusion: packed red cells for symptomatic anaemia when Hb below 7 g/dL (below 8 g/dL if cardiovascular disease) or haemodynamic compromise.

Chronic untreated anaemia causes persistent fatigue, reduced physical work capacity, impaired cognitive function, and significantly reduced quality of life. In children, iron deficiency anaemia (even subclinical) causes irreversible neurodevelopmental damage — reduced cognitive performance, poor academic achievement, impaired attention, and behavioural difficulties that may not fully recover even after iron repletion. Severe anaemia (Hb below 70 g/L) precipitates high-output cardiac failure — the heart increases cardiac output to compensate for reduced oxygen delivery, leading to left ventricular hypertrophy, cardiomegaly, and decompensated heart failure. In patients with underlying coronary artery disease, even moderate anaemia (Hb below 10 g/dL) can precipitate angina and myocardial infarction. Untreated B12 deficiency left uncorrected causes permanent subacute combined degeneration of the spinal cord — progressive demyelination causing sensory ataxia, peripheral neuropathy, and cognitive decline that may be irreversible. In pregnancy, untreated anaemia significantly increases risk of preterm birth, low birth weight, impaired foetal brain development, increased vulnerability to postpartum haemorrhage (already depleted iron stores), and maternal mortality — particularly in resource-limited settings where maternal anaemia-related deaths remain common. Aplastic anaemia without treatment is rapidly fatal from bleeding and infections.

Prevent iron-deficiency anaemia — the most common type globally — through dietary optimisation: haem iron from red meat, poultry, and fish is absorbed at 15-35%; non-haem iron from dark leafy greens (spinach, kale), legumes, tofu, fortified cereals absorbs at 2-20% but is enhanced 2-3-fold by concurrent vitamin C (orange juice, tomatoes, kiwi). Avoid tannins (tea, coffee) and calcium with iron-rich meals as they inhibit absorption. For heavy menstrual bleeding (the most common cause of iron deficiency in premenopausal women): investigate and treat the underlying cause — tranexamic acid 1g TDS, levonorgestrel intrauterine system (Mirena), or COC to reduce menstrual blood loss; if refractory, gynaecological assessment is essential. Pregnant women must take folic acid 400 mcg daily from preconception through the first 12 weeks (5 mg for high-risk groups — previous neural tube defect, epilepsy, diabetes) and iron supplementation if deficient. Vegans and strict vegetarians require vitamin B12 supplementation (1000 mcg cyanocobalamin sublingual daily or monthly IM injections) or consumption of fortified foods (plant milks, cereals, yeast extract). Population strategies for low-income settings: WHO-recommended flour and rice fortification programmes; supplementation campaigns targeting infants, pregnant women, and adolescent girls. Annual FBC monitoring in all patients on proton pump inhibitors (which reduce iron and B12 absorption), those with coeliac disease, and in elderly individuals with reduced dietary intake.

See a GP for persistent fatigue, pallor, breathlessness on exertion, palpitations, or dizziness that may indicate anaemia — a simple full blood count confirms the diagnosis. Seek urgent evaluation for: anaemia in adult men or postmenopausal women (requires investigation for gastrointestinal blood loss and malignancy — do not assume dietary cause without investigations); any new anaemia accompanied by unexplained weight loss, night sweats, or lymphadenopathy (possible haematological malignancy); anaemia with abnormal white blood cell count or platelet abnormalities on the FBC (warrants urgent haematology referral to exclude bone marrow disorders); and haemoglobin below 7-8 g/dL with chest pain or haemodynamic instability (may require emergency transfusion). Children with developmental concerns alongside pallor, poor appetite, or excessive cow's milk consumption should be assessed promptly for iron deficiency anaemia, which causes irreversible cognitive impacts if untreated.