Haematology: Anatomy Physiology and Pharmacology

• Anatomy: Bone Marrow and Blood Cell Production | The Spleen | Lymph Nodes, Thymus and Lymphoid Tissue
• Physiology: Red Cells and Haemoglobin | Sickle Cell and Thalassaemia | What the Marrow Needs — Anaemia by MCV | Iron Metabolism | Red Cell Breakdown and Haemolysis | White Cells | Platelets | Coagulation and Fibrinolysis | Bleeding and Clotting Disorders | Clotting Tests | Blood Groups and Transfusion | The Blood Film | Normal Values
• Pharmacology: Iron, B12 and Folate | Heparins and Fondaparinux | Warfarin | Direct Oral Anticoagulants | Antiplatelet Drugs | Thrombolytics, Tranexamic Acid and Reversal Agents | Blood Components and Products | Growth Factors and Immune Treatments | Sickle Cell, Chelation and Venesection | Chemotherapy Basics | Targeted Drugs in Blood Cancers | Drugs That Cause Blood Problems
• Revision: Drug Reference Table | Spot the Answer | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🩸 Haematology anatomy, physiology and pharmacology — blood carries oxygen (red cells), fights infection (white cells) and stops bleeding (platelets and clotting factors). Most blood problems are too few cells, too many cells, abnormal cells, or a clotting system that bleeds or clots too easily. The commonest haematology drugs in everyday practice are iron, anticoagulants, antiplatelets and blood products — all high-risk if used wrongly.
Your four questions for every drug: How does it work? What is it used for? What are the important side effects and safety issues? What does it interact with, and how is it monitored?

Bone Marrow and Blood Cell Production

• Where blood is made:
  • Fetus — yolk sac (first weeks), then liver and spleen (mid-pregnancy), then bone marrow (from about 5 months).
  • Children — marrow in almost all bones.
  • Adults — mainly the axial skeleton: pelvis, sternum, vertebrae, ribs, skull and the ends of the femur and humerus. Marrow samples (aspirate and trephine) are taken from the posterior iliac crest.
  • Extramedullary haematopoiesis — liver and spleen start making blood again when the marrow fails or is overworked (myelofibrosis, thalassaemia) → hepatosplenomegaly.
• Stem cells — a small number of haematopoietic stem cells make all blood cells; they can renew themselves (the basis of stem cell transplantation):
  • Myeloid line — red cells, platelets (from megakaryocytes), neutrophils, eosinophils, basophils, monocytes.
  • Lymphoid line — B cells, T cells and natural killer cells.
• Growth factors control production — erythropoietin (kidney — red cells), thrombopoietin (liver — platelets), G-CSF (neutrophils), interleukins. Several are given as drugs.
• Scale — the marrow makes about 200 billion red cells a day; it can increase output several-fold (e.g. after bleeding or in haemolysis — rising reticulocytes).
• Marrow failure (aplastic anaemia, leukaemia, infiltration by cancer or fibrosis, chemotherapy, drugs, B12 or folate deficiency) → pancytopenia — anaemia, infections and bleeding.
• Leucoerythroblastic film (immature red and white cells in the blood) — suggests marrow infiltration (metastatic cancer, myelofibrosis, TB) or severe stress.

The Spleen

• Position — left upper quadrant under the 9th–11th ribs; not normally palpable. An enlarged spleen grows towards the right iliac fossa, has a notch, moves with breathing, you can't get above it, and it is dull to percussion (unlike a kidney).
• Functions:
  • Red pulp — filters old and damaged red cells; removes inclusions from red cells (after splenectomy — Howell–Jolly bodies, target cells and raised platelets).
  • White pulp — immune responses, especially against encapsulated bacteria (pneumococcus, meningococcus, Haemophilus influenzae type b).
  • Stores about a third of platelets — so a big spleen lowers the platelet count (hypersplenism).
• Causes of splenomegaly:
  • Massive — CML, myelofibrosis, malaria, visceral leishmaniasis (and Gaucher disease).
  • Moderate — lymphoma, leukaemias, portal hypertension, haemolytic anaemias, thalassaemia.
  • Mild — infections (EBV, endocarditis, hepatitis), sarcoidosis, autoimmune disease.
• Hyposplenism (reduced function) — splenectomy, sickle cell disease (repeated infarction — autosplenectomy), coeliac disease, alcohol-related liver disease, after radiotherapy.
• Preventing infection after splenectomy or in hyposplenism (UKHSA Green Book):
  • Vaccines — pneumococcal, Hib/MenC, MenACWY, MenB, yearly influenza (and COVID-19) — ideally 2 weeks before planned splenectomy or 2 weeks after.
  • Antibiotic prophylaxis (phenoxymethylpenicillin, or a macrolide if allergic) — at least for the first years and lifelong in high-risk patients; a stand-by course for fever.
  • Alert card; warn about severe malaria when travelling and infection from dog bites (Capnocytophaga).
  • Overwhelming post-splenectomy infection — fever in an asplenic patient is an emergency — IV antibiotics immediately.
• Splenic rupture — trauma, or with minor trauma in infectious mononucleosis (avoid contact sport for several weeks) — referred pain to the left shoulder tip (Kehr's sign).

Lymph Nodes, Thymus and Lymphoid Tissue

• Lymph nodes — filters along lymphatic vessels:
  • Cortex — B cells in follicles (germinal centres — where antibodies are refined).
  • Paracortex — T cells.
  • Medulla — plasma cells and macrophages.
• Lymphadenopathy — infection (tender, recent), inflammation (sarcoid, autoimmune), cancer spread (hard, fixed), lymphoma (rubbery, painless, often large; Hodgkin's nodes may hurt after alcohol). Red flags — node over 2 cm, persisting over 6 weeks, supraclavicular, with weight loss, night sweats or fever (NICE NG12).
• Important nodes — left supraclavicular (Virchow's) node — gastric and other abdominal cancers (Troisier's sign); axillary — breast cancer, arm infections; inguinal — legs, perineum, anus below the dentate line.
• Thymus — where T cells mature and learn to ignore the body's own tissues; large in children, shrinks with age. Thymoma is linked to myasthenia gravis, pure red cell aplasia and low antibodies.
• MALT (mucosa-associated lymphoid tissue) — in the gut (Peyer's patches), airways and elsewhere; gastric MALT lymphoma is driven by H. pylori and can regress after eradication.
• Lymphocytes recirculate between blood, nodes and tissues — the reason lymphomas often involve several sites.
• Plasma cells — mature B cells that make antibodies; a malignant clone causes myeloma (paraprotein, bone lesions, high calcium, kidney injury, anaemia — "CRAB").

Red Cells and Haemoglobin

• Structure — a biconcave disc about 7–8 micrometres across, with no nucleus or mitochondria; flexible enough to squeeze through capillaries and the spleen. Lifespan about 120 days.
• Membrane — supported by proteins such as spectrin and ankyrin; defects cause hereditary spherocytosis (round, fragile cells removed by the spleen — anaemia, jaundice, gallstones, splenomegaly; crises with parvovirus B19).
• Energy — red cells rely on glycolysis (pyruvate kinase deficiency → haemolysis) and the pentose phosphate pathway, which makes NADPH to protect against oxidation (G6PD deficiency → haemolysis with oxidant drugs, infection, fava beans). 2,3-DPG is made here (shifts the oxygen curve right).
• Haemoglobin — four globin chains, each with a haem group containing iron, which binds oxygen:
  • HbA (α2β2) — about 97% of adult haemoglobin.
  • HbA2 (α2δ2) — under about 3.5% (raised in beta-thalassaemia trait).
  • HbF (α2γ2, fetal) — under 1% in adults; binds oxygen more tightly. The switch from gamma to beta chains happens in the first 6 months of life — so beta-chain disorders (sickle cell, beta-thalassaemia) show up after about 3–6 months.
  • Alpha-globin genes — 4 copies (chromosome 16); beta-globin genes — 2 copies (chromosome 11).
• Reticulocytes — young red cells (still with some RNA) that circulate for about 1–2 days; the reticulocyte count shows whether the marrow is responding:
  • High — bleeding, haemolysis, recovery after treatment (e.g. iron or B12).
  • Low — marrow not responding (deficiency, marrow failure, CKD, parvovirus aplastic crisis).
• Red cell indices — MCV (size — the key to classifying anaemia), MCH (haemoglobin per cell), RDW (variation in size — high in iron deficiency and mixed deficiencies).
• Polycythaemia — high haemoglobin and haematocrit: primary (polycythaemia vera — JAK2 mutation, low EPO) or secondary (high EPO — hypoxia, COPD, sleep apnoea, smoking, high altitude, kidney tumours, testosterone); relative (dehydration, diuretics).

Sickle Cell and Thalassaemia

• Sickle cell disease (HbSS, also HbSC and HbS/beta-thalassaemia):
  • A single change in the beta-globin gene (glutamic acid → valine at position 6) makes HbS, which polymerises when deoxygenated → stiff sickle-shaped cells → blockage of small vessels (pain, organ damage) and haemolysis.
  • Triggers — infection, dehydration, cold, low oxygen, acidosis, exertion, stress, alcohol.
  • Complications — painful crises, acute chest syndrome, stroke (children — transcranial Doppler screening), splenic sequestration (children), aplastic crisis (parvovirus), infections (hyposplenism), priapism, avascular necrosis, kidney disease, leg ulcers, retinopathy, gallstones, pulmonary hypertension.
  • Sickle cell trait (HbAS) — usually no symptoms; protects against severe malaria; risk at extreme exertion, dehydration or altitude; haematuria; important in genetic counselling.
  • Screened for at birth (heel-prick test) and in pregnancy in England.
• Thalassaemias — reduced production of globin chains (the other chain builds up and damages cells):
  • Alpha-thalassaemia — depends on how many of the 4 genes are lost: 1 (silent), 2 (trait — microcytosis with normal or slightly low Hb), 3 (HbH disease — moderate anaemia, splenomegaly), 4 (Hb Barts — hydrops fetalis, usually fatal before birth).
  • Beta-thalassaemia trait — microcytosis with a normal or high red cell count and raised HbA2; mild or no anaemia; iron studies normal — don't give iron unnecessarily.
  • Beta-thalassaemia major — severe anaemia from about 6 months; regular transfusions → iron overload (heart, liver, endocrine glands) needing chelation; marrow expansion (skull bossing, facial changes), splenomegaly; stem cell transplant or gene therapy can cure.
• Iron deficiency vs thalassaemia trait — both microcytic; thalassaemia trait has a higher red cell count for the degree of anaemia, normal ferritin and (beta) raised HbA2. Check ferritin before haemoglobin electrophoresis (iron deficiency can lower HbA2).

What the Marrow Needs — Anaemia by MCV

• Making red cells needs — erythropoietin (kidney), iron (haemoglobin), vitamin B12 and folate (DNA synthesis — deficiency causes large, immature "megaloblastic" cells), plus vitamin B6, copper, thyroid hormone and androgens.

• Anaemia of chronic disease — inflammation raises hepcidin, which locks iron away in macrophages and blocks gut absorption → low serum iron with normal or high ferritin and low transferrin; often mild and normocytic.
• B12 deficiency also damages nerves — peripheral neuropathy, subacute combined degeneration of the cord, memory problems, optic neuropathy — may occur without anaemia; folate deficiency doesn't cause these (but matters for neural tube defects in pregnancy).
• Pernicious anaemia — autoimmune loss of intrinsic factor (intrinsic factor antibodies; parietal cell antibodies less specific); linked to other autoimmune diseases and gastric cancer risk.

Iron Metabolism

• Body iron — about 3–4 g, mostly (about two-thirds) in haemoglobin; the rest stored as ferritin and haemosiderin in the liver and macrophages.
• Daily balance — only about 1–2 mg a day is absorbed, matching losses from skin and gut cells; menstruation, pregnancy and growth increase needs. The body has no way to excrete extra iron — so transfusions and haemochromatosis cause iron overload.
• Absorption — in the duodenum, as ferrous (Fe2+) iron; helped by acid and vitamin C; reduced by tea, calcium, PPIs and coeliac disease. Iron leaves gut cells via ferroportin and travels on transferrin.
• Hepcidin — the master regulator (made by the liver); it blocks ferroportin:
  • High in inflammation → anaemia of chronic disease; also high for about a day after an oral iron dose (the reason alternate-day or once-daily dosing absorbs better).
  • Low in iron deficiency and hereditary haemochromatosis (HFE C282Y — too much absorption → liver, heart, pancreas, joint and skin damage).
• Iron tests:
  • Ferritin — the best single test; low ferritin confirms iron deficiency (under about 15–30 micrograms/L). Ferritin is an acute phase protein — it rises with inflammation, infection, liver disease and cancer, so a "normal" ferritin doesn't exclude deficiency if inflamed (deficiency still possible up to about 100).
  • Transferrin saturation — low (under about 20%) in iron deficiency and chronic disease; high in haemochromatosis (over about 45–50%).
  • TIBC (transferrin) — high in iron deficiency, low in chronic disease.
• Iron deficiency anaemia is a sign, not a diagnosis — in men and postmenopausal women, investigate for GI blood loss (gastroscopy and colonoscopy, coeliac serology, urine dipstick for blood) — BSG guidance; in younger women, consider menstrual loss, diet and coeliac disease first.

Red Cell Breakdown and Haemolysis

• Normal breakdown — old red cells are removed by macrophages in the spleen → iron is recycled; haem becomes unconjugated bilirubin (see the Gastroenterology Anatomy, Physiology and Pharmacology chapter).
• Signs of haemolysis — anaemia with raised reticulocytes, raised unconjugated bilirubin (jaundice without dark urine), raised LDH, low haptoglobin (it mops up free haemoglobin), abnormal film.
• Two places it happens:
  • Extravascular (in the spleen and liver) — hereditary spherocytosis, warm autoimmune haemolysis, sickle cell disease — splenomegaly, gallstones.
  • Intravascular (inside blood vessels) — ABO-incompatible transfusion, G6PD deficiency, microangiopathic haemolysis (TTP, HUS, DIC), mechanical heart valves, malaria, PNH — haemoglobinuria (dark red-brown urine), very low haptoglobin, AKI.
• Direct antiglobulin (Coombs) test (DAT) — detects antibody or complement on red cells:
  • Positive — autoimmune haemolysis (warm — IgG: idiopathic, CLL, lymphoma, lupus, drugs; cold — IgM complement: Mycoplasma, EBV, lymphoma — worse in the cold, Raynaud's, agglutination), alloimmune (transfusion reactions, haemolytic disease of the newborn), drug-induced (penicillins, cephalosporins, methyldopa).
  • Negative — hereditary (spherocytosis, G6PD, pyruvate kinase, haemoglobinopathies), microangiopathic, mechanical, infection, PNH.
• G6PD deficiency — X-linked (mostly males of African, Mediterranean, Middle Eastern and Asian descent); haemolysis after oxidant stress:
  • Drugs — primaquine and tafenoquine (test before use), dapsone, nitrofurantoin, sulfonamides (co-trimoxazole), quinolones, rasburicase, methylene blue, high-dose aspirin.
  • Also fava beans and infections; film shows bite cells and Heinz bodies.
  • The enzyme test can be falsely normal straight after a crisis (young cells have more enzyme) — repeat later.
• Thrombotic microangiopathy — haemolysis with fragmented red cells (schistocytes), low platelets and organ damage:
  • TTP — low ADAMTS13 (the enzyme that cuts von Willebrand factor) → fever, confusion or stroke, kidney injury, purpura; an emergency — urgent plasma exchange, steroids, rituximab, caplacizumab; avoid platelet transfusion (feeds clotting).
  • HUS — after E. coli O157 diarrhoea (children) — AKI; atypical HUS (complement) — eculizumab.
  • Also DIC, HELLP syndrome and pre-eclampsia, malignant hypertension, drugs (quinine, calcineurin inhibitors, gemcitabine).
• Paroxysmal nocturnal haemoglobinuria (PNH) — red cells lack complement protection → intravascular haemolysis (dark morning urine), thrombosis in unusual sites, marrow failure; complement inhibitors.

White Cells

• Neutropenia severity — under 1.5 × 10⁹/L mild; under 1.0 moderate; under 0.5 severe (high risk of life-threatening infection).
• Neutropenic sepsis — temperature over 38°C or signs of sepsis with neutrophils 0.5 × 10⁹/L or less (usually after chemotherapy) — IV broad-spectrum antibiotics within 1 hour (e.g. piperacillin–tazobactam) without waiting for the count if chemotherapy is recent (NICE).
• Benign ethnic neutropenia (Duffy-null phenotype) — lower neutrophil counts (often 1.0–1.5) in many people of African and Middle Eastern ancestry, without extra infection risk — important when starting drugs like clozapine.
• Blasts on a blood film — suggest acute leukaemia — same-day haematology review.
• Very high white count (over 100 × 10⁹/L) — risk of leucostasis (stroke, breathlessness) — urgent haematology input.

Platelets

• Production — fragments of megakaryocytes in the marrow (driven by thrombopoietin from the liver); lifespan about 7–10 days; about a third are held in the spleen.
• Forming a platelet plug:
  • Adhesion — von Willebrand factor links exposed collagen to the platelet receptor GPIb.
  • Activation — platelets change shape and release ADP (acts on P2Y12 receptors — blocked by clopidogrel, prasugrel, ticagrelor) and thromboxane A2 (made by COX-1 — blocked by aspirin).
  • Aggregation — GPIIb/IIIa receptors bind fibrinogen and link platelets together (blocked by tirofiban and eptifibatide).
  • Activated platelets also provide the surface where clotting factors work.
• Low platelets (thrombocytopenia) — causes:
  • Less production — marrow failure or infiltration, chemotherapy, B12 or folate deficiency, alcohol, viral infection, drugs.
  • More destruction — ITP (immune), HIT, TTP and HUS, DIC, drugs (quinine, heparin, valproate), sepsis, pregnancy (gestational thrombocytopenia, HELLP).
  • Pooling — big spleen (portal hypertension).
  • Dilution — massive transfusion.
  • False low (pseudothrombocytopenia) — platelets clumping in the EDTA tube — check the film or repeat in a citrate tube.
• Bleeding risk — usually little bleeding above 50 × 10⁹/L; spontaneous bruising and mucosal bleeding more likely under about 20–30; serious spontaneous bleeding risk under 10. For procedures — usually over about 50 for most surgery and lumbar puncture (40–50 depending on guidance), over 80 for epidurals and spinal anaesthesia, over 100 for neurosurgery and eye surgery.
• Platelet-type bleeding — petechiae, purpura, bruising, gum and nose bleeding, heavy periods, oozing after procedures (versus clotting factor problems — deep muscle and joint bleeding).
• High platelets (thrombocytosis):
  • Reactive (most) — infection, inflammation, iron deficiency, bleeding, after splenectomy, cancer.
  • Primary — essential thrombocythaemia and other myeloproliferative neoplasms (JAK2, CALR or MPL mutations) — clotting and bleeding risk.

Coagulation and Fibrinolysis

• Stopping bleeding — blood vessel narrowing → platelet plug (primary haemostasis) → fibrin clot (secondary haemostasis) → clot breakdown later (fibrinolysis).
• The clotting cascade (classic model, used to interpret lab tests):
  • Extrinsic pathway — tissue factor (exposed by injury) + factor VII — the real starting point in the body; measured by the PT/INR.
  • Intrinsic pathway — factors XII, XI, IX and VIII — amplifies the process; measured by the APTT.
  • Common pathway — factors X and V → thrombin (factor II) → converts fibrinogen into fibrin; factor XIII cross-links fibrin to strengthen the clot.
  • Thrombin is the key enzyme — it also activates platelets and factors V, VIII and XI (positive feedback) — and is a drug target (dabigatran).
• Vitamin K-dependent factors — II, VII, IX and X (and the natural anticoagulants protein C and protein S) need vitamin K to work — blocked by warfarin.
  • Factor VII has the shortest half-life (about 6 hours) — so the INR rises first when warfarin starts or vitamin K is lacking.
  • Protein C also falls quickly → a brief pro-clotting state when warfarin starts (the reason for heparin cover in VTE and the rare warfarin skin necrosis).
• Natural anticoagulants (keep clotting in check):
  • Antithrombin — switches off thrombin and factor Xa (heparin boosts it about 1,000-fold); lost in nephrotic syndrome.
  • Protein C and protein S — switch off factors Va and VIIIa; factor V Leiden resists this.
  • Tissue factor pathway inhibitor.
• Fibrinolysis — tissue plasminogen activator (tPA) turns plasminogen into plasmin, which breaks down fibrin → D-dimer (fibrin breakdown products).
  • Thrombolytic drugs (alteplase, tenecteplase) are forms of tPA.
  • Tranexamic acid blocks plasminogen activation — helps stop bleeding.
• Virchow's triad — clots form with slow blood flow (immobility, long travel, heart failure), vessel wall damage (surgery, trauma) and increased clotting tendency (cancer, pregnancy, oestrogen, thrombophilia, dehydration, inflammation).

Bleeding and Clotting Disorders

• Inherited bleeding disorders:
  • Von Willebrand disease — the commonest inherited bleeding disorder; mucosal bleeding (nosebleeds, heavy periods, bleeding after dental work); vWF also carries factor VIII (so APTT may be long); desmopressin or vWF concentrate; tranexamic acid.
  • Haemophilia A (factor VIII) and B (factor IX) — X-linked (mainly males; female carriers may bleed); bleeding into joints (haemarthrosis) and muscles; long APTT, normal PT; factor concentrates, emicizumab (haemophilia A), gene therapy; avoid IM injections and NSAIDs.
• Acquired bleeding problems — anticoagulants and antiplatelets, liver disease (fewer clotting factors and platelets — but also fewer natural anticoagulants, so clots still occur), vitamin K deficiency (malnutrition, cholestasis, antibiotics, newborns), uraemia (platelet dysfunction — desmopressin, dialysis), massive transfusion (dilution), acquired haemophilia (older people — sudden large bruises, long APTT that doesn't correct on mixing).
• Disseminated intravascular coagulation (DIC) — widespread clotting uses up platelets and factors → bleeding and clotting together:
  • Causes — sepsis, trauma, obstetric emergencies (abruption, amniotic fluid embolism), cancer (especially acute promyelocytic leukaemia), severe pancreatitis, snake bites.
  • Tests — low platelets, long PT and APTT, low fibrinogen, high D-dimer, schistocytes.
  • Treat the cause; blood products if bleeding (platelets, FFP, cryoprecipitate).
• Inherited thrombophilia — factor V Leiden (commonest — about 1 in 20 people of European descent), prothrombin gene mutation, protein C, protein S and antithrombin deficiency (rarer, higher risk). Testing rarely changes management (NICE — not routinely after a first provoked VTE).
• Antiphospholipid syndrome — antibodies (lupus anticoagulant, anticardiolipin, anti-beta-2-glycoprotein I) cause venous and arterial clots and pregnancy loss; lupus anticoagulant prolongs the APTT in the lab but causes clotting in the body; treat with warfarin — DOACs are not recommended, especially in triple-positive patients (MHRA); aspirin and LMWH in pregnancy.
• Acquired clotting risk — cancer (and its treatment), pregnancy and the puerperium, oestrogen (combined pill, oral HRT), surgery, immobility, obesity, inflammatory disease, nephrotic syndrome, myeloproliferative neoplasms, PNH, heparin-induced thrombocytopenia.

Clotting Tests

• Mixing study — mix patient plasma with normal plasma: if the long APTT corrects, a factor is missing; if it doesn't, there is an inhibitor (lupus anticoagulant, acquired haemophilia, heparin).
• INR — the PT standardised for warfarin monitoring; not reliable for liver disease or DOACs.
• Anti-Xa level — monitors LMWH (pregnancy, kidney disease, extremes of weight) and can measure factor Xa-inhibiting DOACs.
• D-dimer — sensitive but not specific — useful to rule out VTE when clinical probability is low (Wells score); raised in infection, cancer, pregnancy, surgery, older age (age-adjusted cut-offs are used in some places).
• Fibrinogen — low in DIC, massive bleeding (including postpartum haemorrhage), liver failure; give cryoprecipitate or fibrinogen concentrate if bleeding with low fibrinogen.
• Viscoelastic tests (TEG, ROTEM) — bedside whole-blood clotting tests used to guide transfusion in major bleeding.

Blood Groups and Transfusion

• ABO system — people have naturally occurring antibodies (mainly IgM) against the A or B antigens they lack:
  • Giving the wrong ABO group causes immediate intravascular haemolysis (fever, loin pain, hypotension, haemoglobinuria, DIC, AKI) — usually from a patient identification error — a "never event".
  • Group O negative red cells — the emergency "universal donor" for red cells (O positive is often used for men and older women in emergencies).
  • Group AB plasma — the universal plasma donor (AB has no anti-A or anti-B).
• Rhesus D — RhD-negative people make anti-D only after exposure (transfusion or pregnancy). Anti-D (IgG) crosses the placenta → haemolytic disease of the fetus and newborn in later pregnancies.
  • Anti-D prophylaxis for RhD-negative pregnant women — routine antenatal anti-D (around 28 weeks, unless the baby is known RhD-negative from fetal DNA testing) and after sensitising events (bleeding, trauma, procedures, delivery of an RhD-positive baby).
• Other antibodies (Kell, Kidd, Duffy and others) — from previous transfusion or pregnancy; cause delayed haemolytic reactions and HDFN; patients with sickle cell disease receive extended phenotype-matched blood.
• Pre-transfusion testing — group and screen (ABO, RhD and antibody screen) then crossmatch or electronic issue; two samples from separate occasions may be needed for patients without a history (to prevent wrong blood in tube).
• When to transfuse red cells (NICE NG24) — restrictive thresholds in stable patients: Hb under 70 g/L (target 70–90), or under 80 g/L in acute coronary syndrome (target 80–100); one unit at a time then reassess (one unit raises Hb by about 10 g/L in an average adult). Don't transfuse for iron, B12 or folate deficiency unless severe or symptomatic — treat the cause.
• Bedside safety — positive patient identification at every step, check the blood component against the wristband and prescription, observations before, 15 minutes after starting and at the end; complete each red cell unit within 4 hours of leaving storage.

The Blood Film