Anaemia

Anaemia means that your blood has less haemoglobin than expected, reducing oxygen carrying capacity. It is not one disease. Reduced production, increased destruction and blood loss are the main mechanisms, so safe treatment depends on identifying the cause.

What anaemia means Anaemia means that the haemoglobin concentration in your blood is below the appropriate reference range. Haemoglobin is the oxygen binding protein inside red blood cells. When there is less haemoglobin available, the blood carries less oxygen from the lungs to tissues. Anaemia is a physiological state rather than one disease. It can result from reduced red cell production, increased red cell destruction or blood loss. The cause determines the urgency, investigations and treatment. Iron tablets are appropriate for confirmed iron deficiency but can be ineffective or harmful when another process is responsible. Haemoglobin and oxygen transport Each haemoglobin molecule contains iron bearing haem groups that bind oxygen in the lungs. Red blood cells carry haemoglobin through the circulation. Oxygen separates from haemoglobin within tissues according to local demand, temperature, acidity and other factors. The total oxygen content of blood depends heavily on how much haemoglobin is present. A person with anaemia can therefore have normal lungs and a normal oxygen saturation while still carrying less oxygen overall. This distinction explains why a normal pulse oximeter reading does not exclude clinically important anaemia. Red blood cells and the bone marrow Red blood cells are produced mainly within bone marrow. Developing cells require iron, vitamin B12, folate, amino acids and functioning marrow stem cells. The kidneys produce erythropoietin, a hormone that signals the marrow to increase red cell production when oxygen delivery falls. A mature red blood cell normally circulates for about 120 days before being removed, mainly by the spleen and liver. Anaemia develops when production cannot match ordinary turnover, when cells are destroyed early or when blood leaves the circulation. Oxygen delivery depends on more than haemoglobin Haemoglobin is central to oxygen delivery, but it is not the only factor. The heart must pump effectively, the lungs must load oxygen, blood vessels must distribute flow and tissues must extract oxygen appropriately. Someone with heart or lung disease may become symptomatic at a higher haemoglobin than a healthy person. A fit person with slowly developing anaemia may initially tolerate a lower level. Clinical decisions therefore use symptoms, speed of change, cause and cardiovascular reserve rather than one haemoglobin number alone. Anaemia is not a diagnosis of cause A full blood count can show that anaemia is present. It cannot establish the cause by itself. The same haemoglobin level can arise from iron deficiency, bleeding, kidney disease, inflammation, haemolysis, marrow failure or an inherited haemoglobin disorder. The red cell indices, reticulocyte count, blood film and targeted biochemical tests narrow the possibilities. A safe assessment asks why the haemoglobin is low rather than treating the number automatically. How anaemia is defined Clinically, anaemia is defined as haemoglobin below the lower limit expected for the relevant population and laboratory. Reference ranges vary with age, sex, pregnancy, altitude and laboratory method. Children require age specific interpretation. Haemoglobin concentration is easier to measure than total red cell mass and is used in routine practice. A result just outside the range may still be important when it is new, progressive or associated with abnormal white cells, platelets, bleeding or systemic symptoms. Plasma volume can alter haemoglobin concentration Haemoglobin is reported as a concentration within blood, so changes in plasma volume can influence the result. Pregnancy normally expands plasma volume more than red cell mass, producing physiological dilution. Intravenous fluids can also lower the measured concentration without immediate loss of red cells. Severe dehydration can make haemoglobin appear higher and temporarily conceal anaemia. Clinicians interpret the result with fluid status, pregnancy and previous measurements rather than assuming that concentration always equals total red cell mass. Why the speed of onset matters Symptoms depend on how quickly anaemia develops as well as how low the haemoglobin becomes. During slow decline, the heart, circulation and tissues adapt partly. You may notice gradually reduced stamina before severe symptoms appear. Acute blood loss gives the body little time to adapt. Dizziness, collapse, chest pain or shock can occur even before the measured haemoglobin has fallen fully. A rapid change is therefore often more urgent than a stable chronic result at a similar concentration. Fatigue and reduced exercise capacity Fatigue is common because muscles and other tissues receive less oxygen during activity. You may feel unusually exhausted, weak or unable to complete tasks that were previously straightforward. Fatigue is non specific. Poor sleep, depression, infection, thyroid disease, medicines and many chronic disorders can produce the same symptom. Anaemia becomes more likely when fatigue occurs with breathlessness, pallor, palpitations or an abnormal blood count. Breathlessness Anaemia can cause breathlessness, particularly during physical activity, because the circulation must deliver more blood to supply the same amount of oxygen. You may notice difficulty climbing stairs, walking quickly or exercising. Breathlessness at rest, sudden deterioration, chest pain or low oxygen saturation should not be attributed automatically to anaemia. Heart failure, pulmonary embolism, infection and other emergencies may coexist. The symptom provides a clue to severity but does not identify the cause. Palpitations and cardiovascular strain The heart may beat faster or more forcefully to compensate for reduced oxygen carrying capacity. This can cause palpitations, a rapid pulse and sometimes a flow murmur caused by increased blood movement across normal heart valves. Severe or prolonged anaemia can worsen angina, heart failure or arrhythmia in susceptible people. Chest pain, fainting, marked breathlessness or a sustained abnormal rhythm requires urgent assessment rather than waiting for routine iron treatment. Headache, dizziness and concentration Anaemia can cause headache, light headedness, reduced concentration and a feeling of faintness. Symptoms may worsen when standing or exercising because circulatory demand increases. These features also occur with dehydration, low blood pressure, migraine, anxiety and neurological disease. Sudden severe headache, one sided weakness, speech difficulty or persistent loss of consciousness is not explained safely by uncomplicated anaemia and requires emergency assessment. The three main mechanisms A practical framework divides anaemia into three broad mechanisms. First, the marrow may produce too few red cells because required materials, hormonal signals or healthy stem cells are lacking. Second, red cells may be destroyed before the end of their expected lifespan. This is called haemolysis. Third, red cells and iron may be lost through acute or chronic bleeding. More than one mechanism can operate at the same time. Reduced production Reduced production usually produces a reticulocyte response that is lower than expected for the degree of anaemia. Common causes include iron deficiency, vitamin B12 or folate deficiency, inflammation and chronic kidney disease. Bone marrow disorders, cancer treatment, alcohol, endocrine disease and selected medicines can also reduce production. The mean cell volume helps organise these possibilities, but normal cell size does not exclude nutritional deficiency or marrow disease. Iron and haemoglobin production Iron is required to build the haem groups that bind oxygen. Most iron used each day comes from recycling old red cells rather than new dietary absorption. The body has no controlled pathway for removing large amounts of excess iron. Iron is stored mainly within ferritin and transported in blood by transferrin. Deficiency develops when losses or requirements exceed intake and absorption. Iron stores usually fall before haemoglobin becomes low. Iron deficiency is the commonest global cause Iron deficiency is considered the commonest cause of anaemia worldwide. Its importance varies by population. Diet, pregnancy, menstrual bleeding, gastrointestinal disease, parasitic infection and access to healthcare all influence risk. Anaemia in any individual should not be assumed to be iron deficiency solely because this cause is common. Confirmation with iron studies prevents unnecessary supplementation and helps identify a potentially serious source of loss. Low iron intake Low dietary intake can contribute when meals contain little available iron or total food intake is restricted. Plant foods provide non haem iron, while meat and fish contain more readily absorbed haem iron. A balanced vegetarian or vegan diet can still provide enough iron with appropriate planning. Diet alone is less often the sole explanation for new severe iron deficiency anaemia in an adult. Food insecurity, eating disorders and restrictive diets should be approached sensitively and without blame. Impaired iron absorption Iron is absorbed mainly in the duodenum and upper small bowel. Coeliac disease, inflammatory bowel disease, autoimmune gastritis, gastrectomy and some bariatric operations can reduce absorption. Proton pump inhibitors may reduce absorption in some circumstances, although they are rarely the only explanation for substantial anaemia. A previous gastrointestinal operation does not remove the need to consider bleeding or another new cause. Increased iron requirements Pregnancy increases iron requirements because maternal red cell mass expands and the fetus and placenta need iron. Infancy, adolescence and recovery from major blood loss also increase demand. People receiving erythropoiesis stimulating treatment can develop functional or absolute iron deficiency because marrow production accelerates. Increased requirement may contribute, but clinicians still assess diet, absorption and bleeding when anaemia is significant. Chronic blood loss causes iron deficiency Because blood contains iron, repeated small losses can gradually exhaust iron stores. Heavy menstrual bleeding is a common cause before menopause. Gastrointestinal bleeding is important in adults of any sex and becomes particularly concerning in men and after menopause. Other sources include frequent blood donation, nosebleeds, urinary bleeding and repeated medical blood sampling. Replacing iron treats the deficiency but does not stop continued loss. Heavy menstrual bleeding Heavy or prolonged periods can cause iron deficiency over months or years. The history includes duration, flooding, clots, changing protection at night, bleeding through clothing and the effect on daily life. Fibroids, adenomyosis, bleeding disorders and hormonal changes are possible causes. Menstrual loss may explain the deficiency, but severe, recurrent or disproportionate anaemia still requires assessment for additional dietary, gastrointestinal or bleeding causes. Occult gastrointestinal bleeding Occult bleeding means blood loss that is not obvious to you. Stomach ulcers, inflammation, vascular lesions, bowel polyps and gastrointestinal cancers can bleed slowly without visible red blood or black stools. NSAIDs and anticoagulants can contribute but should not be accepted automatically as the complete explanation. New confirmed iron deficiency anaemia in an adult requires cause assessment even when bowel symptoms are absent. Why adult iron deficiency must be investigated Iron deficiency can be the first sign of gastrointestinal cancer or another treatable disease. The risk is particularly important in adult men, postmenopausal women, older adults and people with weight loss, bowel change, abdominal symptoms or recurrent deficiency. British gastroenterology guidance recommends urgent gastrointestinal investigation for new unexplained iron deficiency anaemia in at risk adults. Treatment and investigation usually proceed together. A rise in haemoglobin after iron confirms replacement response but does not prove that the source was harmless. FIT and suspected colorectal cancer pathways NICE recommends quantitative faecal immunochemical testing, called FIT, to guide colorectal cancer referral in adults with iron deficiency anaemia. A FIT result at or above 10 micrograms of haemoglobin per gram of faeces leads to a suspected cancer pathway referral. A lower result reduces but does not eliminate cancer risk. Persistent symptoms, an abdominal or rectal mass, ongoing unexplained anaemia or strong clinical concern still require safety netting and possible referral. FIT assesses lower gastrointestinal bleeding risk. It does not evaluate upper gastrointestinal causes. Coeliac and renal tract assessment in iron deficiency Coeliac disease is found in a meaningful minority of adults investigated for iron deficiency anaemia. Serological screening is commonly included, with interpretation adjusted when IgA deficiency or a gluten free diet could affect results. Urinalysis can identify blood loss from the urinary tract. The investigation plan may include upper endoscopy, colon assessment, gynaecological review or small bowel testing according to age, sex, symptoms, treatment response and previous results. Vitamin B12 and folate Vitamin B12 and folate are required for normal DNA synthesis during red cell development. Deficiency slows nuclear maturation while cell growth continues, producing large abnormal precursor cells. This is called megaloblastic change. The resulting anaemia is often macrocytic, but the mean cell volume can be normal when iron deficiency, inflammation or another process coexists. Vitamin B12 deficiency can damage the nervous system even without anaemia or macrocytosis. Megaloblastic anaemia Megaloblastic anaemia describes ineffective blood cell production caused most often by vitamin B12 or folate deficiency. The marrow may be active but many abnormal precursors die before entering the circulation. White cells and platelets can also fall in severe deficiency. The blood film can show oval macrocytes and neutrophils with too many nuclear segments. Megaloblastic morphology is a mechanism clue rather than proof of one vitamin deficiency. Causes of vitamin B12 deficiency Vitamin B12 is obtained mainly from animal derived foods and fortified products. Autoimmune gastritis reduces intrinsic factor and is an important cause of impaired absorption. Total gastrectomy and terminal ileal resection create permanent absorption problems. Coeliac disease, Crohn's disease, bariatric surgery, metformin, acid suppressing medicines and recreational nitrous oxide can contribute. Testing and treatment take account of supplements because over the counter B12 can raise blood levels without fully correcting deficiency. Neurological vitamin B12 deficiency Vitamin B12 deficiency can cause pins and needles, numbness, impaired vibration sense, unsteady walking, weakness, visual symptoms, cognitive change and bladder disturbance. Subacute combined degeneration affects long spinal cord pathways and can progress to permanent disability. NICE advises not delaying vitamin B12 replacement when megaloblastic anaemia and neurological symptoms are suspected. Treatment begins after diagnostic blood samples when possible, but urgent replacement takes priority over waiting for results. Folate deficiency Folate deficiency can result from low intake, alcohol excess, malabsorption, pregnancy, increased red cell turnover and medicines that affect folate metabolism. It causes megaloblastic anaemia but does not usually produce the characteristic neurological syndrome of vitamin B12 deficiency. Folic acid can improve the blood count while untreated B12 related nerve damage continues. Clinicians therefore assess B12 before or alongside folate treatment, especially when neurological symptoms are present. Anaemia of chronic disease and inflammation Inflammation changes how the body handles iron and red cell production. The liver increases hepcidin, which reduces intestinal iron absorption and traps recycled iron within storage cells. The marrow receives less usable iron even when total stores are adequate. Inflammatory cytokines also reduce erythropoietin response and shorten red cell survival. The anaemia is often normocytic but can become microcytic. Ferritin may be normal or raised because it increases during inflammation. Chronic kidney disease Healthy kidneys produce erythropoietin, which stimulates marrow red cell production. As chronic kidney disease advances, erythropoietin signalling becomes insufficient. Inflammation, functional iron deficiency, blood loss and shortened red cell survival add to the problem. Anaemia should not be attributed to kidney disease until other important causes, including bleeding and nutritional deficiency, have been considered. Treatment can include iron and specialist erythropoiesis stimulating therapy, with careful haemoglobin and blood pressure monitoring. Bone marrow failure Bone marrow failure reduces production of red cells and often other blood cell types. Causes include aplastic anaemia, myelodysplastic syndromes, leukaemia, marrow infiltration, chemotherapy, radiotherapy and severe infection. Anaemia accompanied by low white cells or platelets is more concerning than an isolated mild haemoglobin reduction. Fever, recurrent infection, unexplained bruising or bleeding can indicate a broader marrow problem requiring urgent haematology assessment. Aplastic anaemia Aplastic anaemia is a rare, potentially life threatening disorder in which the marrow becomes markedly hypocellular and fails to produce enough blood cells. The full blood count commonly shows pancytopenia, meaning anaemia, neutropenia and thrombocytopenia together. Most acquired cases involve immune destruction of marrow stem cells, although medicines, toxins, viruses and inherited disorders can contribute. Diagnosis requires marrow examination and exclusion of other causes. Treatment can involve stem cell transplantation or immunosuppressive therapy with intensive infection and transfusion support. Myelodysplastic syndromes and marrow infiltration Myelodysplastic syndromes are clonal marrow disorders causing ineffective and abnormal blood cell production. They become more common with age and can produce macrocytic anaemia, low platelets, low neutrophils or abnormal cells on the film. Leukaemia, lymphoma, myeloma and metastatic cancer can replace or disrupt normal marrow. Persistent unexplained anaemia with abnormal white cells, platelets or film findings requires haematology assessment rather than repeated nutritional treatment alone. Increased red cell destruction Haemolytic anaemia develops when red cells are destroyed faster than the marrow can replace them. The marrow usually responds by releasing more reticulocytes, provided iron, folate and marrow function are adequate. Haemolysis may be inherited or acquired and can occur mainly within blood vessels or within the spleen and liver. Rapid haemolysis can cause severe anaemia, jaundice, dark urine, gallstones and kidney injury. Laboratory clues to haemolysis Common clues include a raised reticulocyte count, raised unconjugated bilirubin and raised lactate dehydrogenase. Haptoglobin binds free haemoglobin and often becomes low during intravascular haemolysis. It can also change with inflammation or liver disease. The blood film may show spherocytes, fragments, sickle cells or other diagnostic clues. No single marker proves haemolysis in every setting. Results are interpreted together with the clinical pattern. Intravascular and extravascular haemolysis Intravascular haemolysis occurs within the bloodstream and can release free haemoglobin into plasma and urine. Extravascular haemolysis occurs mainly when the spleen or liver removes abnormal or antibody coated red cells. Many disorders use both pathways rather than fitting one category perfectly. Dark urine can result from haemoglobin, red cells, myoglobin or bilirubin, so urine appearance alone cannot identify the mechanism. Sickle cell disease Sickle cell disease is a group of inherited haemoglobin disorders involving haemoglobin S. When deoxygenated, haemoglobin S can polymerise and make red cells rigid. Cells haemolyse early and can obstruct small blood vessels. Chronic haemolytic anaemia occurs alongside painful vaso occlusive episodes and risks involving the lungs, brain, spleen, kidneys and other organs. Treatment can include vaccination, infection prevention, hydroxycarbamide, transfusion and specialist disease modifying or curative therapies. Thalassaemia Thalassaemias are inherited disorders in which production of alpha or beta globin chains is reduced. The red cells are usually markedly microcytic. A carrier can have small cells and mild anaemia without iron deficiency. More severe disease causes ineffective production, haemolysis, marrow expansion and transfusion dependence. Iron should not be prescribed solely because the MCV is low. Ferritin and other iron tests help avoid harmful unnecessary iron in a haemoglobinopathy. Other inherited haemolytic anaemias Glucose 6 phosphate dehydrogenase deficiency can cause episodic haemolysis after selected medicines, foods or infections. Hereditary spherocytosis alters the red cell membrane and promotes splenic destruction. Pyruvate kinase deficiency and other enzyme or membrane disorders are less common. Family history, age at onset, jaundice, gallstones and characteristic blood film findings guide specialist testing. Autoimmune haemolytic anaemia In autoimmune haemolytic anaemia, antibodies target the person's own red cells. Warm antibody disease commonly causes splenic destruction, while cold antibody disease is triggered more strongly at lower temperatures and uses complement pathways. The condition can be primary or associated with autoimmune disease, infection, lymphoma or medicines. The direct antiglobulin test helps identify antibody or complement attached to red cells. Treatment depends on the type and severity and may include glucocorticoids, rituximab or other specialist therapy. Mechanical and microangiopathic haemolysis Artificial heart valves, severe burns and mechanical circulatory devices can physically damage red cells. Microangiopathic haemolytic anaemia occurs when red cells fragment within abnormal small blood vessels. The film shows schistocytes. Thrombotic thrombocytopenic purpura, haemolytic uraemic syndrome, malignant hypertension and disseminated intravascular coagulation are important causes. Anaemia with low platelets, fragments, neurological symptoms or kidney injury can represent a haematological emergency. Acute blood loss Acute blood loss can follow trauma, surgery, gastrointestinal haemorrhage, ruptured ectopic pregnancy or major obstetric bleeding. The immediate danger is loss of circulating volume and tissue perfusion as well as loss of oxygen carrying cells. Possible features include visible bleeding, vomiting blood, black stool, abdominal pain, dizziness, collapse, rapid pulse and low blood pressure. Emergency treatment controls the bleeding and restores circulation. Transfusion decisions are made within the major haemorrhage pathway rather than by a routine threshold alone. Haemoglobin may initially appear normal after acute bleeding Whole blood contains both red cells and plasma. During the first phase of rapid haemorrhage, both components are lost together, so the measured haemoglobin concentration may initially remain near baseline. The concentration falls after fluid moves into the circulation or intravenous fluid is given. A normal early haemoglobin therefore does not exclude dangerous acute blood loss. Clinical signs and the bleeding history take priority. Chronic blood loss Slow blood loss usually produces iron deficiency because the body cannot recycle iron that has left the circulation. Sources include heavy periods, gastrointestinal lesions, regular blood donation, urinary bleeding and repeated nosebleeds. In many regions, hookworm, schistosomiasis and malaria contribute through blood loss, haemolysis or inflammation. The source may be silent. Replacing iron without investigating ongoing loss can delay diagnosis and lead to repeated deficiency. The full blood count The full blood count reports haemoglobin, haematocrit, red cell number and red cell indices. It also reports white blood cells and platelets, which can reveal infection, marrow failure, leukaemia or a broader cytopenia. The haemoglobin confirms the anaemia pattern but does not identify the cause. Comparing current and previous results shows whether the change is acute, progressive, stable or recurrent. MCV is the first morphological branch point Mean cell volume, shortened to MCV, describes the average size of circulating red cells. A low MCV is called microcytosis. A normal MCV is normocytosis, and a high MCV is macrocytosis. This is a useful first branch point, but it is not a diagnosis. Mixed deficiencies can produce a normal average size. Reticulocytes are larger than mature cells and can raise MCV during recovery or haemolysis. Microcytic anaemia Iron deficiency is the commonest cause of microcytic anaemia. Thalassaemia trait, anaemia of inflammation, sideroblastic disorders and lead toxicity are other possibilities. A relatively high red cell count with marked microcytosis can suggest thalassaemia trait, while a high red cell distribution width often supports evolving iron deficiency. These are clues only. Iron studies and haemoglobin analysis establish the next steps. Normocytic anaemia Normocytic anaemia includes acute blood loss, haemolysis, chronic inflammation, kidney disease and marrow failure. Early iron deficiency or combined iron and vitamin deficiency can also appear normocytic. The reticulocyte count is particularly useful in this group. A high response suggests loss or destruction, while a low response suggests underproduction. Kidney function, inflammation, blood film and the other blood cell lines then narrow the differential. Macrocytic anaemia Vitamin B12 and folate deficiency are important causes of macrocytosis. Alcohol, liver disease, hypothyroidism, reticulocytosis and medicines such as hydroxycarbamide, methotrexate and some antiretrovirals can also increase MCV. Myelodysplastic syndromes become important when macrocytosis is persistent, unexplained or accompanied by other cytopenias. Macrocytosis without anaemia still deserves interpretation in context but does not always indicate disease. The reticulocyte count Reticulocytes are young red cells recently released from marrow. A raised count suggests that marrow is responding to blood loss, haemolysis or treatment. A low or inappropriately normal count suggests impaired production. The raw percentage can be misleading in severe anaemia because the total number of red cells is reduced. Laboratories may provide an absolute count or corrected production index. A reticulocyte response can take several days after treatment begins. The blood film A blood film allows direct examination of red cell size, shape, colour and inclusions. Target cells can occur in thalassaemia and liver disease. Spherocytes suggest immune or membrane related haemolysis. Schistocytes suggest mechanical fragmentation. Oval macrocytes and hypersegmented neutrophils support megaloblastic change. Blasts, marked cell abnormalities or several abnormal blood cell lines require urgent laboratory and haematology review. Ferritin Ferritin is the single most useful routine marker of stored iron. A low ferritin strongly supports absolute iron deficiency. Ferritin is also an acute phase protein and can rise with inflammation, infection, liver disease and malignancy. A result within or above the reference range may therefore conceal deficient available iron. When inflammation is possible, transferrin saturation, inflammatory markers and the overall pattern improve interpretation. Serum iron, transferrin and transferrin saturation Serum iron varies during the day and after food and should not be interpreted alone. Transferrin carries iron through blood. Total iron binding capacity estimates available binding capacity. In uncomplicated iron deficiency, transferrin often rises while serum iron and transferrin saturation fall. In inflammation, transferrin can be low or normal while ferritin is normal or raised and saturation remains low. A low transferrin saturation means little circulating iron is available, but it does not by itself distinguish absolute from functional deficiency. Functional iron deficiency Functional iron deficiency means that iron stores exist but iron is not released or delivered efficiently to the marrow. It occurs commonly with inflammation, chronic kidney disease and erythropoiesis stimulating therapy. Ferritin may appear adequate while transferrin saturation is low. Treatment depends on the clinical setting. Giving oral iron alone may be ineffective when hepcidin remains high or absorption is poor. Response to iron treatment A clear haemoglobin rise after iron replacement supports iron deficiency when initial studies were equivocal. British gastroenterology guidance notes that a rise of at least 10 grams per litre within about two weeks is highly suggestive in an anaemic person. Failure to respond prompts review of adherence, dose, absorption, continued bleeding, inflammation and the original diagnosis. A response confirms that iron was limiting production. It does not identify why iron became deficient. Vitamin B12 testing Total vitamin B12 or active B12 is used as an initial test in most adults. Borderline results may require methylmalonic acid testing, clinical judgement or treatment when symptoms create high risk. Blood should be taken before replacement when this can be done safely. Supplements can make concentrations look reassuring without fully correcting tissue deficiency. A negative intrinsic factor antibody does not completely exclude autoimmune gastritis. Folate testing and combined deficiency Serum folate reflects recent intake and can fall quickly. Local laboratories guide interpretation. B12 and folate deficiency can coexist with iron deficiency, chronic disease or alcohol related illness. Treating folate alone can improve megaloblastic anaemia while B12 related neurological injury continues. When both are deficient, vitamin B12 is started before or with folate according to clinical guidance. Tests for haemolysis The haemolysis assessment commonly includes reticulocytes, bilirubin, lactate dehydrogenase and haptoglobin. A direct antiglobulin test assesses immune coating of red cells when autoimmune haemolysis is possible. Urinalysis can detect haemoglobin, while kidney function identifies complications. Haemoglobin electrophoresis or high performance liquid chromatography investigates haemoglobin variants, and enzyme or membrane tests are selected from the history and film. Bone marrow examination Bone marrow aspiration and biopsy are not needed for most straightforward nutritional anaemias. They become important when aplastic anaemia, myelodysplasia, leukaemia, marrow infiltration or unexplained cytopenias are suspected. The aspiration examines individual cells, while the biopsy shows marrow architecture and cellularity. The decision considers bleeding risk, likely diagnostic benefit and whether less invasive testing has already explained the pattern. Treatment follows the cause Anaemia treatment varies entirely by mechanism and underlying disease. Iron replaces iron deficiency. Vitamin B12 or folate corrects the relevant deficiency. Bleeding requires source control. Inflammation, kidney disease, haemoglobinopathy, haemolysis and marrow failure each need different management. Transfusion can restore red cell oxygen carrying capacity rapidly but does not correct the cause and is not the routine treatment for every low haemoglobin. Oral iron treatment Oral ferrous sulphate, fumarate or gluconate is commonly used for iron deficiency anaemia. British guidance recommends one tablet daily initially. A tablet on alternate days, a different preparation or intravenous iron can be considered when treatment is not tolerated. Haemoglobin response is checked during the first weeks. Treatment usually continues for about three months after haemoglobin normalises to restore iron stores. The investigation of the cause continues while iron is being replaced. Taking oral iron safely Iron is absorbed best away from food, but nausea or abdominal discomfort may make taking it with food more practical. Constipation, diarrhoea, nausea and dark stools are common adverse effects. Dark stools from iron do not remove the need to assess true melaena when symptoms suggest bleeding. Tea, coffee, calcium and some medicines reduce absorption when taken close to the dose. Iron is toxic in overdose and must be stored securely away from children. Intravenous iron Intravenous iron replaces iron directly into the circulation. It is considered when oral iron is ineffective, not tolerated, poorly absorbed or when correction is particularly urgent. Different preparations allow different doses and infusion times. Hypersensitivity reactions are uncommon but require monitoring and access to emergency treatment. Intravenous iron can replenish stores but still does not explain or stop ongoing blood loss. Vitamin B12 replacement Vitamin B12 replacement can be oral or intramuscular depending on cause, severity, neurological features and absorption. Autoimmune gastritis, total gastrectomy and complete terminal ileal resection usually require lifelong intramuscular replacement. High dose oral treatment can be effective in selected dietary, medicine related or uncertain cases. Neurological recovery may take months and can be incomplete when treatment is delayed. Folate replacement Folic acid treats confirmed folate deficiency after vitamin B12 deficiency has been considered. The underlying cause may require dietary support, alcohol treatment, coeliac assessment or medicine review. Requirement is increased during pregnancy, and recommended preventive supplementation differs from treatment of established deficiency. Treatment response is monitored through symptoms and blood count rather than indefinite supplementation without reassessment. Treating anaemia of inflammation and kidney disease The primary treatment for anaemia of inflammation is control of the underlying infection, inflammatory disease or malignancy when possible. Iron may still be required when absolute deficiency coexists. In chronic kidney disease, specialist treatment can include oral or intravenous iron and an erythropoiesis stimulating agent. These medicines are monitored carefully because excessive haemoglobin targets can increase cardiovascular and thrombotic risk. Treating haemoglobinopathies Sickle cell disease and clinically significant thalassaemia require specialist lifelong care. Hydroxycarbamide reduces complications in many people with sickle cell disease. Transfusion is used for selected acute events and prevention strategies. Thalassaemia treatment can include regular transfusion, iron chelation, splenectomy in selected cases and curative stem cell or gene based treatment. Carrier states usually do not need anaemia treatment, but genetic counselling can be important. Treating haemolysis and marrow failure Autoimmune haemolytic anaemia may require glucocorticoids, rituximab, transfusion and treatment of an associated disorder. Aplastic anaemia can require urgent infection management, blood and platelet support, immunosuppressive therapy or stem cell transplantation. Microangiopathic haemolysis is treated as an emergency directed at the underlying syndrome. These disorders should not be managed by iron supplementation unless iron deficiency is separately confirmed. When red cell transfusion is considered Red cell transfusion increases haemoglobin and oxygen carrying capacity immediately. It is considered for major bleeding, severe symptoms, cardiovascular compromise or selected very low haemoglobin states. The decision uses the clinical situation rather than a number alone. Chronic stable anaemia allows more time for cause specific treatment than rapidly developing anaemia with chest pain or shock. Where possible, alternatives such as iron or vitamin replacement reduce avoidable exposure to donor blood. Restrictive transfusion thresholds For most stable people who need transfusion and do not have major haemorrhage, acute coronary syndrome or a regular transfusion programme, NICE recommends a restrictive approach. A threshold around 70 grams per litre and a post transfusion target of 70 to 90 grams per litre are considered. For acute coronary syndrome, a threshold around 80 grams per litre and target of 80 to 100 are considered. Adults without active bleeding commonly receive one unit followed by clinical and haemoglobin reassessment. Transfusion risks Transfusion can cause fever, allergy, haemolytic reactions, fluid overload and rarely serious lung injury. Incorrect blood given to the wrong person is a preventable life threatening event, so identity checks are essential. Transmitted infection risk is very low in the UK but not zero. Repeated transfusion can cause antibodies and iron overload. Benefits and risks are discussed whenever circumstances allow, with monitoring before, during and after the transfusion. Recovery and prognosis Prognosis depends on the cause and how quickly it is recognised. Nutritional deficiency and controlled blood loss often improve fully with appropriate treatment. Inherited haemoglobin disorders, chronic inflammation, kidney disease and marrow disorders may require long term care. Neurological damage from prolonged B12 deficiency, organ injury from severe haemolysis and complications of delayed cancer diagnosis may not reverse completely. Follow up Follow up confirms that haemoglobin, cell size and relevant nutrient stores are improving. It also checks whether the cause has been treated, whether bleeding continues and whether another blood cell line becomes abnormal. Recurrent iron deficiency after initial correction requires renewed assessment rather than repeated indefinite prescriptions alone. Return earlier for worsening breathlessness, chest pain, fainting, bleeding, fever, jaundice, neurological symptoms or failure to improve. The main safety message Anaemia is reduced oxygen carrying capacity, not a final diagnosis. The full blood count identifies a pattern. MCV, reticulocytes, blood film and targeted tests help separate reduced production, destruction and loss. Confirmed iron deficiency in an adult requires investigation of its cause, with urgent gastrointestinal pathways when clinically indicated. Acute bleeding, severe cardiopulmonary symptoms, rapidly progressive haemolysis, pancytopenia and neurological B12 deficiency require prompt escalation rather than routine supplementation alone.

Anaemia is reduced oxygen carrying capacity caused by low haemoglobin, not a diagnosis of cause. MCV, reticulocytes, blood film and targeted tests separate reduced production, destruction and blood loss so that treatment addresses both the deficiency and the underlying disease.