Hematological Medicines: Pharmacology, Dosage, Safety and Nursing Care
Hematological medicines prevent or treat disorders of blood formation, haemostasis, coagulation and thrombosis. They include haematinics, growth factors, medicines for haemoglobin disorders, anticoagulants, antiplatelets, thrombolytics, haemostatics and blood products. Incorrect selection, dosing or monitoring can cause catastrophic bleeding, thrombosis, marrow suppression, haemolysis or death.
Dosage note: Doses below are common educational adult examples, not a substitute for a prescription. Always confirm the exact indication, age, current weight, pregnancy status, renal and liver function, laboratory results, product strength and the latest Uganda Clinical Guidelines or facility protocol. Paediatric doses are usually weight-based and should never be extrapolated from adult doses.
Learning Objectives
- Relate normal haemopoiesis and haemostasis to drug action.
- Classify hematological medicines and explain pharmacodynamics and pharmacokinetics.
- State common indications, dosage principles, contraindications, interactions, side effects, serious adverse effects and monitoring.
- Administer iron, anticoagulants, haemostatics and blood components safely.
- Recognise major bleeding, thrombosis, heparin-induced thrombocytopenia and transfusion reactions.
- Develop patient-centred nursing care plans and discharge education.
Foundations of Blood Pharmacology
Haematopoietic stem cells in bone marrow produce erythrocytes, leucocytes and platelets. Erythropoietin from the kidney stimulates red-cell formation. Iron forms haem; folate and vitamin B12 support DNA synthesis. Platelets create the primary plug, coagulation factors stabilise it with fibrin, and plasmin later removes fibrin.
| Target | Normal function | Drug effect | Clinical implication |
|---|---|---|---|
| Red-cell production | Requires iron, folate, B12, erythropoietin and functioning marrow. | Haematinics replace deficiencies; erythropoiesis-stimulating agents promote production. | Anaemia must be classified; haemoglobin alone does not identify the cause. |
| Platelets | Adhere, activate and aggregate at vascular injury. | Aspirin and P2Y12 inhibitors reduce aggregation. | Useful mainly for arterial thrombosis but increase mucosal and intracranial bleeding. |
| Coagulation cascade | Produces thrombin and cross-linked fibrin. | Heparins, warfarin and direct oral anticoagulants inhibit selected steps. | Prevent clot propagation; they do not instantly dissolve an existing thrombus. |
| Fibrinolysis | Plasmin breaks down fibrin. | Thrombolytics accelerate breakdown; tranexamic acid inhibits it. | Drug selection depends on whether a clot must be lysed or preserved. |
Baseline Assessment Before Any Hematological Medicine
- Confirm the indication: anaemia, thrombosis, prophylaxis, acute coronary syndrome, stroke, bleeding disorder or replacement of a defined component.
- Assess bleeding: haematemesis, melaena, haematuria, epistaxis, heavy menses, bruising, recent surgery, trauma, falls, ulcer disease and neurological symptoms.
- Assess thrombosis: unilateral limb pain/swelling, sudden dyspnoea, chest pain, haemoptysis, focal deficit or catheter failure.
- Review tests: full blood count, reticulocytes, ferritin/iron studies when indicated, renal/liver function, PT/INR, aPTT, fibrinogen or anti-Xa according to the medicine.
- Reconcile medicines: NSAIDs, antiplatelets, anticoagulants, antimicrobials, anticonvulsants, antiretrovirals, alcohol and herbal products.
- Check procedures: surgery, lumbar puncture, neuraxial anaesthesia or invasive procedures require coordinated interruption and restart plans.
Haematinics and Blood-Cell Stimulating Medicines
Comprehensive Haematinic Drug Table
| Medicine | Pharmacodynamics and pharmacokinetics | Indications and common dosage guidance | Contraindications and precautions | Interactions | Side effects and serious adverse effects | Monitoring and nursing responsibilities |
|---|---|---|---|---|---|---|
| Oral ferrous salts Ferrous sulfate, fumarate, gluconate | PD: supply elemental iron for haemoglobin, myoglobin and enzymes. PK: absorption occurs mainly in duodenum/proximal jejunum and increases when stores are depleted. Food, phytates, calcium and antacids reduce absorption. Iron is stored as ferritin/haemosiderin; the body has no regulated excretory pathway. | Confirmed iron-deficiency anaemia and policy-based prevention. Adult treatment commonly provides about 100–200 mg elemental iron daily, though once-daily or alternate-day regimens may improve tolerance and absorption. Pregnancy regimens must follow current national/WHO guidance. Continue after haemoglobin normalises as prescribed to replenish stores. | Iron overload, haemochromatosis, anaemia not caused by iron deficiency. Use caution with active peptic disease, inflammatory bowel disease and repeated transfusions. Do not give blindly in unexplained anaemia. | Antacids, calcium, tea/coffee and some foods reduce absorption. Iron reduces absorption of tetracyclines, quinolones, levothyroxine and bisphosphonates; separate administration according to pharmacy guidance. Vitamin C may increase absorption. | Common: nausea, epigastric pain, constipation/diarrhoea and dark stool. Liquid stains teeth. Serious: overdose causes corrosive GI injury, shock, metabolic acidosis, hepatic failure and death. | Confirm elemental iron content, not tablet mass. Teach expected stool change and adherence. Give on an empty stomach if tolerated; use food if needed for adherence. Use a straw for liquid. Store locked away from children. Recheck Hb response and investigate non-response. |
| Intravenous iron Iron sucrose, ferric carboxymaltose and locally available products | PD: iron-carbohydrate complex is taken up by macrophages and releases iron to transferrin for erythropoiesis. PK: bypasses intestinal absorption; product stability, maximum dose and half-life differ markedly. | Confirmed deficiency when oral therapy is ineffective, not tolerated, poorly absorbed or too slow; selected CKD and ongoing loss. Dose is calculated from iron deficit and product limits. Iron sucrose is often given in smaller repeated doses; ferric carboxymaltose may permit larger single doses. Never interchange protocols. | Known hypersensitivity to product, anaemia without iron deficiency, iron overload. Defer during active systemic infection when clinically appropriate. Caution in asthma/atopy and liver disease. | Do not start oral iron simultaneously unless directed; it adds little during immediate IV replacement and may increase GI effects. Avoid mixing with unapproved drugs/solutions. | Common: metallic taste, headache, nausea, flushing, infusion-site pain. Serious: hypersensitivity/anaphylaxis, hypotension, bronchospasm; extravasation causes persistent skin staining. Some formulations cause hypophosphataemia. | Verify calculated total need, exact preparation, dilution and rate. Ensure patent IV access and resuscitation readiness. Observe during and after. Stop for chest/back pain, wheeze, facial swelling, hypotension or collapse. Never use another product’s instructions. |
| Folic acid | PD: converted to tetrahydrofolate coenzymes required for DNA synthesis. PK: absorbed in proximal small bowel, stored mainly in liver and excreted renally. | Folate-deficiency megaloblastic anaemia; prevention in pregnancy and high-risk situations. A common adult therapeutic dose is 5 mg orally daily for about 4 months, longer if the cause persists. Prevention doses differ and must follow national policy. | Untreated vitamin B12 deficiency unless B12 is also corrected. Hypersensitivity is rare. | Antifolate medicines such as methotrexate, trimethoprim and some anticonvulsants have clinically important interactions; folate may alter anticonvulsant concentrations. | Usually well tolerated. Rare rash, bronchospasm or anaphylaxis. Main danger is masking haematological signs of B12 deficiency while neurological injury progresses. | Establish cause of macrocytosis. Check B12 before folate alone where feasible. Monitor Hb, MCV and clinical response. Teach duration and dietary sources without implying diet alone treats severe deficiency. |
| Vitamin B12 Hydroxocobalamin or cyanocobalamin | PD: cofactor for DNA synthesis, myelin maintenance and methylmalonate metabolism. PK: dietary B12 requires intrinsic factor and terminal ileum; IM treatment bypasses absorption. Large hepatic stores mean deficiency develops slowly. | Confirmed deficiency due to pernicious anaemia, gastric/ileal disease, malabsorption or poor intake. Common IM regimens use 1 mg doses frequently during loading then maintenance every 2–3 months for irreversible causes; exact preparation and neurological involvement determine schedule. | Hypersensitivity to cobalamin/cobalt. Use clinical caution in severe anaemia because rapid marrow response may change potassium. | Chloramphenicol may blunt haematological response. Metformin and prolonged acid suppression can contribute to deficiency. | Injection pain, rash, itching. Rare anaphylaxis. Hypokalaemia can occur during brisk correction of severe deficiency. | Assess paraesthesia, gait, cognition, glossitis and diet. Obtain diagnostic bloods before treatment where feasible, but do not delay urgent treatment for neurological disease. Monitor Hb/reticulocyte response and neurological recovery. Lifelong treatment may be needed. |
| Epoetin alfa and related ESAs | PD: activate erythropoietin receptors on marrow progenitors, increasing RBC production. PK: given IV or SC; response takes days to weeks, so it is not emergency correction. | Selected CKD anaemia and chemotherapy-associated anaemia. Dosing is indication- and product-specific, often weight-based or fixed at intervals. Titrate to the lowest dose that reduces transfusion need; do not chase a normal Hb. | Uncontrolled hypertension; pure red-cell aplasia due to anti-EPO antibodies. Caution with malignancy, seizure disorder and thrombosis risk. | No dominant CYP interactions, but ineffective without adequate iron; combined prothrombotic risks matter clinically. | Hypertension, headache, influenza-like symptoms, vascular-access thrombosis. Serious: stroke, myocardial infarction, venous thrombosis, seizures and rare pure red-cell aplasia. | Correct iron/folate/B12 deficiency first. Check BP, Hb trend, rate of rise and iron status. Withhold/adjust only by protocol. Teach that benefit is delayed and thrombosis symptoms require urgent care. |
| Filgrastim | PD: recombinant G-CSF stimulates neutrophil precursors. PK: SC/IV; clearance rises as neutrophils recover. | Selected chemotherapy-associated neutropenia, stem-cell mobilisation and severe chronic neutropenia. A common starting regimen is 5 micrograms/kg/day SC or IV, adjusted to indication and counts. | Hypersensitivity to product. Caution in sickle cell disease, myeloid malignancy and splenic disease. | Lithium can increase neutrophil release. Timing close to cytotoxic chemotherapy is protocol-dependent. | Bone/muscle pain, fever, headache. Serious: splenic rupture, acute respiratory distress, capillary-leak syndrome and sickle crisis. | Monitor CBC and ANC. Assess fever and infection despite treatment. Report left upper-quadrant/shoulder pain, respiratory distress or sudden hypotension urgently. |
| Hydroxyurea | PD: inhibits ribonucleotide reductase; in sickle cell disease raises fetal haemoglobin, reduces sickling and improves red-cell hydration. PK: well absorbed orally, widely distributed, partly metabolised and renally eliminated. | Disease modification in sickle cell disease; specialist malignant indications. Sickle cell therapy often starts around 15 mg/kg once daily in adults, with lower starting doses in renal impairment and gradual titration to tolerated response under protocol. | Severe marrow suppression. Avoid or use only specialist guidance in pregnancy/breastfeeding; counsel about reproductive risk. Caution in renal/hepatic impairment. | Other marrow suppressants increase cytopenia. Some antiretroviral combinations increase toxicity; coordinate HIV care. | Nausea, skin/nail pigmentation, mouth ulcers. Serious: neutropenia, thrombocytopenia, severe anaemia, leg ulcers and infection. | Baseline and regular CBC with differential/reticulocytes, renal/liver tests and pregnancy assessment. Teach daily adherence, handling precautions, contraception discussion and prompt reporting of fever or bleeding. |
Anticoagulants
Anticoagulants prevent formation and extension of fibrin-rich clots. They are high-alert medicines. Choice depends on indication, pregnancy, kidney/liver function, bleeding risk, monitoring access, cost, adherence and availability of reversal.
| Medicine | Pharmacodynamics and pharmacokinetics | Indications and common adult dosage examples | Contraindications and precautions | Interactions | Side effects and serious adverse effects | Monitoring and nursing care |
|---|---|---|---|---|---|---|
| Unfractionated heparin | PD: binds antithrombin, rapidly inactivating thrombin IIa and factor Xa. PK: IV effect is immediate; SC slower. Short, dose-dependent half-life; cleared by cellular and renal mechanisms. | VTE treatment, ACS, procedures and prophylaxis. A common VTE regimen is 80 units/kg IV bolus then 18 units/kg/hour, adjusted by aPTT/anti-Xa protocol. Prophylaxis is often 5,000 units SC every 8–12 hours. Protocols vary. | Active major bleeding, previous immune HIT, severe thrombocytopenia, recent high-risk CNS/eye surgery. Caution with neuraxial procedures, uncontrolled hypertension and ulcers. | Antiplatelets, NSAIDs, thrombolytics and other anticoagulants increase bleeding. IV nitroglycerin may reduce heparin effect in some cases. | Bleeding, bruising, injection reaction. Serious: HIT with thrombosis, anaphylaxis, hyperkalaemia and osteoporosis with prolonged use. | Use independent double-check for infusion. Monitor aPTT/anti-Xa per protocol, CBC, platelets, bleeding and infusion pump. Protamine reverses much of effect. Avoid IM injections and document exact stop time. |
| Enoxaparin LMWH | PD: enhances antithrombin inhibition of factor Xa more than IIa. PK: predictable SC bioavailability, peak about 3–5 hours, mainly renal clearance. | VTE prophylaxis often 40 mg SC once daily; treatment often 1 mg/kg SC every 12 hours or indication-specific alternative. Reduce/modify in severe renal impairment and special populations. | Active major bleeding, immune HIT history, severe thrombocytopenia. Caution with renal impairment, extreme weight and neuraxial anaesthesia. | Additive bleeding with NSAIDs, antiplatelets and other anticoagulants. | Bleeding, injection-site bruising, thrombocytopenia. Serious: HIT, spinal/epidural haematoma and hyperkalaemia. | Check weight, creatinine/CrCl, CBC and platelets. Routine aPTT is not useful. Inject into rotated abdominal sites; do not massage or expel the prefilled syringe air bubble unless instructed. Protamine reversal is incomplete. |
| Warfarin | PD: inhibits vitamin K epoxide reductase, reducing synthesis of II, VII, IX, X and proteins C/S. PK: oral, highly protein-bound, hepatic CYP metabolism; delayed onset/offset because circulating factors must turn over. | Mechanical heart valves and selected AF/VTE indications. Start dose varies, commonly 2–5 mg once daily, then adjust strictly to INR target. Acute VTE usually requires overlap with a rapid anticoagulant until therapeutic criteria are met. | Pregnancy except rare specialist circumstances, active major bleeding, inability to monitor, recent high-risk surgery. Caution in liver disease, malnutrition, falls and poor adherence. | Numerous: many antibiotics/antifungals, amiodarone and alcohol may increase INR; enzyme inducers may reduce it. NSAIDs/antiplatelets increase bleeding. Major changes in vitamin K intake alter effect. | Bleeding and bruising. Serious: intracranial haemorrhage, skin necrosis, purple-toe syndrome and fetal harm. | Monitor INR, CBC, bleeding, diet/illness/medicine changes. Give at same time; verify tablet strength. Vitamin K reverses slowly; major bleeding may require PCC or plasma per protocol. Carry anticoagulant card. |
| Apixaban | PD: directly inhibits factor Xa. PK: rapid oral absorption; hepatic CYP3A4/P-gp handling plus renal/fecal clearance; half-life about 12 hours. | AF stroke prevention often 5 mg twice daily with reduction only when criteria are met. Acute VTE often 10 mg twice daily for 7 days, then 5 mg twice daily. Confirm indication and current label. | Active major bleeding, significant hepatic coagulopathy. Caution in severe renal impairment, pregnancy and neuraxial procedures. | Strong combined CYP3A4/P-gp inhibitors increase levels; inducers reduce effect. NSAIDs/antiplatelets increase bleeding. | Bleeding, nausea, anaemia. Serious: intracranial/GI bleeding and spinal haematoma. | No routine INR. Monitor CBC, renal/liver function, bleeding and adherence. Short half-life makes missed doses important. Specific reversal availability varies. |
| Rivaroxaban | PD: direct factor Xa inhibitor. PK: oral, partly CYP3A4/P-gp and renal clearance; higher treatment doses require food for reliable absorption. | Acute VTE commonly 15 mg twice daily with food for 21 days, then 20 mg once daily with food; prophylaxis and AF doses differ and require renal review. | Active major bleeding, significant hepatic coagulopathy. Caution/avoidance thresholds vary with renal function and indication. | Strong CYP3A4/P-gp inhibitors/inducers alter exposure; additive bleeding with NSAIDs/antiplatelets. | Bleeding, anaemia, GI symptoms. Serious: major bleeding and spinal/epidural haematoma. | Confirm phase of VTE therapy to prevent 15 mg/20 mg error. Give specified doses with food. Monitor CBC, renal/liver function and adherence; INR is not a monitoring test. |
| Dabigatran | PD: direct thrombin inhibitor. PK: prodrug absorbed orally, P-gp substrate, predominantly renal elimination. | Selected AF and VTE. A common adult regimen is 150 mg twice daily; for VTE it follows 5–10 days of parenteral anticoagulation. Age, renal function and bleeding risk may require a different dose. | Active major bleeding, mechanical heart valve, severe renal impairment. Caution with oesophageal/GI disease and neuraxial procedures. | P-gp inhibitors raise and inducers lower levels. Other antithrombotics increase bleeding. | Dyspepsia, abdominal discomfort, bleeding. Serious: major haemorrhage and spinal haematoma. | Check renal function. Swallow capsules whole and store exactly as directed because moisture affects stability. Do not use INR to quantify effect. Idarucizumab may reverse effect where available. |
Safe Subcutaneous LMWH Administration
- Verify product, strength, indication, weight, renal function, platelet count and last dose.
- Inspect for active bleeding and excessive bruising; coordinate timing with procedures.
- Select and rotate an abdominal site away from umbilicus, scars, wounds and bruises.
- Clean and dry skin; pinch a fold. Insert at the angle recommended for the patient/device.
- Do not expel the air bubble from a prefilled syringe unless manufacturer instructions say so.
- Inject slowly; withdraw and apply gentle pressure if needed. Do not rub.
- Document drug, dose, time, site and assessment.
Heparin-Induced Thrombocytopenia
Immune HIT causes a substantial platelet fall and paradoxical venous or arterial thrombosis, commonly 5–10 days after exposure or sooner after recent exposure. New thrombosis, skin necrosis or systemic reaction after a bolus are warning signs. Stop all heparin sources including flushes, notify urgently, assess clinical probability and prepare a protocol-selected non-heparin anticoagulant. Do not substitute LMWH or start warfarin alone during acute HIT.
Anticoagulant Reversal
| Agent | Reversal/management principle | Critical nursing responsibilities |
|---|---|---|
| UFH | Stop infusion; protamine dose is based on recent heparin exposure. | Record last hours of dosing; monitor for hypotension, bradycardia and anaphylactoid reaction during slow protamine administration. |
| LMWH | Withhold; protamine gives incomplete reversal; specialist advice. | Record last dose, renal function, weight and bleeding severity; routine aPTT may be misleading. |
| Warfarin | Vitamin K restores synthesis slowly; major bleeding often requires 4-factor PCC or plasma where PCC unavailable. | Check INR/bleeding, prepare product, repeat INR, monitor volume overload with plasma and thrombosis after reversal. |
| Dabigatran | Idarucizumab where available; supportive/source control and specialist guidance. | Confirm last dose and renal function; collect directed tests without delaying life-saving action. |
| Factor Xa inhibitors | Andexanet alfa where available or PCC-based protocol; supportive/source control. | INR is unreliable; report exact medicine, last dose, renal/liver function and interacting drugs. |
Antiplatelets and Thrombolytics
| Medicine | PD/PK | Indications and dosage examples | Contraindications/interactions | Side effects/adverse effects | Nursing monitoring |
|---|---|---|---|---|---|
| Aspirin | Irreversibly inhibits platelet COX-1 and thromboxane A2 for platelet lifespan. Rapid oral absorption; hepatic metabolism and renal excretion. | ACS loading commonly 150–300 mg chewed, then maintenance often 75–100 mg daily. Stroke protocols vary. Not for routine primary prevention without individual assessment. | Active bleeding, aspirin allergy, some asthma, severe ulcer disease. NSAIDs, anticoagulants, steroids and alcohol increase bleeding. Ibuprofen timing may interfere with antiplatelet action. | Dyspepsia, bruising, bronchospasm. Serious: GI/intracranial bleeding, anaphylaxis, renal injury and salicylate toxicity. Avoid in children with viral illness except specialist use. | Confirm indication and dose; assess bleeding, allergy/asthma and GI history. In ACS, chewing speeds absorption. Teach not to self-add NSAIDs. |
| Clopidogrel | Prodrug irreversibly blocks platelet P2Y12 ADP receptor; requires hepatic CYP activation. Effect lasts platelet lifespan. | ACS/PCI loading commonly 300–600 mg, then 75 mg daily; stroke and peripheral arterial indications vary. | Active bleeding. CYP2C19 inhibitors may reduce activation; other antithrombotics/NSAIDs increase bleeding. | Bleeding, bruising, diarrhoea, rash. Rare serious thrombotic thrombocytopenic purpura and severe neutropenia. | Do not stop after coronary stenting without cardiology instruction. Monitor bleeding and CBC when indicated. Fever, neurological change and thrombocytopenia require urgent review. |
| Alteplase | Recombinant tissue plasminogen activator converts fibrin-bound plasminogen to plasmin. Very short plasma half-life; systemic fibrinolytic effect persists. | Selected acute ischaemic stroke: 0.9 mg/kg IV, maximum 90 mg; 10% bolus then remainder over 60 minutes. STEMI/PE regimens differ and are protocol-specific. | Active bleeding, previous intracranial haemorrhage and other condition-specific exclusions; recent surgery/trauma, anticoagulation and uncontrolled BP require strict screening. Antithrombotics increase bleeding. | Bleeding, orolingual angioedema. Serious: intracranial haemorrhage, systemic haemorrhage and reperfusion arrhythmia in MI. | Confirm last-known-well, imaging and exact weight. Independent dose check. Frequent neurological/BP/bleeding observations. Avoid unnecessary punctures. Stop/escalate for headache, vomiting, acute hypertension or deficit. |
| Tenecteplase | Modified tPA with greater fibrin specificity and longer half-life, allowing a single IV bolus. | Weight-tiered STEMI dosing; selected stroke protocols use 0.25 mg/kg IV bolus, maximum 25 mg. Indication and regulatory/local guidance must be verified. | Same major bleeding exclusions as thrombolysis; medication errors arise because MI and stroke doses differ. | Major/intracranial bleeding, angioedema, reperfusion arrhythmias. | Verify indication-specific dose and vial concentration with an independent checker; monitor as for thrombolysis. |
Haemostatic Medicines and Blood Products
| Medicine | PD/PK | Indications and dosage examples | Contraindications/interactions | Side/adverse effects | Nursing responsibilities | |
|---|---|---|---|---|---|---|
| Tranexamic acid | Competitive lysine analogue blocks plasminogen binding and reduces fibrin breakdown. Oral/IV; mainly renal elimination. | PPH: 1 g IV over 10 minutes within 3 hours of birth, repeat 1 g after 30 minutes if bleeding continues or within 24 hours if it restarts. Trauma: commonly 1 g IV over 10 minutes then 1 g over 8 hours within 3 hours of injury. Other uses vary. | Active intravascular clotting; caution in renal impairment, seizures and selected urinary-tract bleeding. Other prothrombotic therapy requires assessment. | Nausea, diarrhoea. Rapid IV causes hypotension. Serious: seizures, visual disturbance and thrombosis. | Give early only for correct indication; adjust renal dose, infuse at correct rate and continue definitive haemorrhage control/resuscitation. | |
| Vitamin K Phytomenadione | Supports hepatic gamma-carboxylation of factors II, VII, IX, X and proteins C/S. Effect requires new factor synthesis and is not immediate. | Deficiency, neonatal prophylaxis and warfarin reversal. Dose and route vary widely—from low oral/IV doses for excessive INR without bleeding to higher IV doses with factor replacement for major bleeding. | Hypersensitivity. IV route requires caution; avoid unnecessary large doses when rapid re-anticoagulation is needed. | Antagonises warfarin. Broad-spectrum antibiotics and cholestasis may contribute to deficiency. | Injection reaction, flushing, taste change. Rare severe anaphylactoid reaction with IV use. | Verify route and urgency; administer IV slowly as product directs. Monitor INR response; remember it does not replace factors immediately. |
| Desmopressin | V2-receptor agonist releases endothelial von Willebrand factor and factor VIII; also produces antidiuresis. Renal elimination. | Selected type 1 von Willebrand disease, mild haemophilia A and uraemic platelet dysfunction. Common haemostatic dose 0.3 micrograms/kg IV diluted and infused over 15–30 minutes; intranasal products differ. | Hyponatraemia, significant polydipsia; caution in young children, cardiac/renal disease and repeated dosing. | Other hyponatraemia-causing drugs increase risk. | Headache, flushing, tachycardia. Serious: water intoxication, hyponatraemia, seizures and thrombosis. | Restrict fluid as prescribed; monitor sodium, fluid balance, weight and neurological state. Tachyphylaxis limits repeated dosing. |
Blood Components and Their Use
| Component | Content/action | Indication and dose principle | Contraindications/cautions | Adverse effects | Nursing responsibilities |
|---|---|---|---|---|---|
| Red-cell concentrate | Raises oxygen-carrying capacity; does not replace platelets or clotting factors. | Clinically significant symptomatic anaemia or acute blood loss. Adults often receive one unit then reassessment when not massively bleeding; paediatric volume is weight-based. | Avoid using solely as volume expansion. Caution heart/renal failure and chronic transfusion. | Haemolysis, allergy, fever, overload, lung injury, infection and iron overload. | Compatibility and bedside ID; baseline/interval observations; assess Hb and symptoms; use slower rate/diuretic plan when ordered for overload risk. |
| Platelets | Provides functional platelets. | Selected thrombocytopenia or platelet dysfunction with bleeding, high risk or procedure. Dose depends on adult therapeutic unit or paediatric weight. | Not routine in immune HIT/TTP without severe bleeding or specialist indication. | Fever, allergy, bacterial sepsis, alloimmunisation, lung injury. | Check indication/count; transfuse promptly; monitor reaction and post-count when ordered. |
| Fresh frozen plasma | Multiple coagulation factors. | Bleeding with multiple-factor deficiency or selected urgent reversal. Common dose around 10–15 mL/kg, guided by protocol and response. | Not a routine volume expander or nutrition source. | Allergy/anaphylaxis, overload and lung injury. | ABO compatibility, thawing/transport time, volume assessment and coagulation response. |
| Cryoprecipitate | Concentrated fibrinogen, VIII, XIII and von Willebrand factor. | Bleeding with low fibrinogen; dose based on fibrinogen level, weight and protocol. | Do not use when a safer specific factor concentrate is indicated/available. | Allergy, fever, infection and thrombosis. | Check fibrinogen before/after and monitor bleeding/reaction. |
| Factor concentrates/PCC | Replace one or several factors rapidly. | Haemophilia, von Willebrand disease or urgent warfarin reversal; units are indication and weight-based. | Thrombosis risk; product-specific hypersensitivity. | Thrombosis, inhibitor formation and rare allergy. | Verify exact product, factor units, reconstitution, lot, rate and response. |
Safe Blood Transfusion Procedure
| No. | Action | Rationale |
|---|---|---|
| 1 | Confirm prescription, component, indication, consent, compatibility sample and patent IV access. | Ensures the product corrects a defined need and that the patient is prepared. |
| 2 | Label the pre-transfusion sample at the bedside after positive identification. | Prevents wrong-blood-in-tube errors. |
| 3 | Inspect the component for identity, integrity, unusual colour, clots, expiry and transport conditions. | Damaged or contaminated products must not be infused. |
| 4 | Two authorised trained staff perform the final bedside match of patient, wristband, prescription, group, compatibility label, component number and expiry. | The bedside check is the last defence against fatal ABO mismatch. |
| 5 | Record baseline temperature, pulse, respiration, BP, oxygen saturation and relevant examination. | Provides comparison for early reaction detection. |
| 6 | Use an approved blood set and only compatible fluid. Begin at prescribed rate and observe closely in the early phase. | Severe reactions often begin soon after exposure. |
| 7 | Repeat observations at policy intervals and whenever symptoms develop; complete within the permitted time. | Early recognition and stopping reduce harm. |
| 8 | Document product/number, volume, times, observations, response and any reaction. | Ensures traceability, handover and haemovigilance. |
Transfusion Reactions and Emergency Response
| Reaction | Recognition | Immediate management |
|---|---|---|
| Acute haemolytic | Fever, chills, anxiety, chest/back pain, dyspnoea, hypotension, dark urine, bleeding or shock. | Stop transfusion; new tubing with compatible fluid; ABC support; call clinician/blood bank; recheck identity; send bag/samples; monitor urine/shock. |
| Febrile non-haemolytic | Temperature rise and chills without haemolysis. | Stop and assess; exclude haemolysis and bacterial contamination before labelling benign. |
| Allergy/anaphylaxis | Itching/urticaria or wheeze, angioedema, hypotension and collapse. | Stop; emergency anaphylaxis protocol and airway/circulation support. |
| Bacterial sepsis | High fever, rigors, vomiting, severe hypotension and shock. | Stop; cultures, sepsis resuscitation and prescribed antibiotics urgently; send component for investigation. |
| TACO | Dyspnoea, hypertension, crackles, raised JVP, pulmonary oedema. | Stop/slow as directed, sit upright, oxygen, urgent review and prescribed diuretic; monitor balance. |
| TRALI | Acute hypoxaemia and bilateral infiltrates without circulatory overload. | Stop, urgent respiratory support and blood-bank notification; diuretics are not automatic. |
Universal response: Stop the transfusion immediately, keep IV access with compatible fluid through new tubing, assess and support ABC, call for help, recheck identity, notify the blood bank and follow the reaction protocol. Never restart without authorised direction.
Comprehensive Nursing Care Plan
| Nursing problem | Expected outcome | Interventions with rationale | Evaluation |
|---|---|---|---|
| Risk for bleeding | No major bleeding; stable haemodynamics/Hb. | Inspect skin, gums, urine, stool, wounds and neurological state; trend labs; avoid unnecessary punctures/IM injections; prevent falls; apply prolonged pressure; maintain reversal plan. | No new bleeding, stable trends, patient names warning signs. |
| Ineffective tissue perfusion related to anaemia/blood loss | Improved alertness, perfusion and activity tolerance. | Monitor ABC, pallor, capillary refill, chest pain, dyspnoea, consciousness and urine output; control bleeding; give prescribed haematinic/component; reassess response. | Symptoms and observations improve; laboratory response appropriate. |
| Risk for thrombosis | No DVT, PE, stroke or device thrombosis. | Assess limbs, respiratory and neurological state; verify doses; mobilise/hydrate as prescribed; use mechanical prophylaxis correctly; never massage suspected DVT. | No thrombotic signs; prevention delivered consistently. |
| Activity intolerance | Safe graded activity with manageable fatigue. | Cluster care, allow rest, assist mobilisation, monitor exertional symptoms and treat cause. | Increasing activity without syncope, severe dyspnoea or chest pain. |
| Knowledge deficit | Patient explains purpose, dose, monitoring, interactions and emergencies. | Teach-back; written plan; demonstrate injection if relevant; specific missed-dose advice; review OTC/herbal products and follow-up. | Accurate return demonstration and explanation. |
Special Populations and Medication Errors
- Pregnancy: LMWH is preferred for many indications because it does not cross placenta; warfarin causes fetal harm except rare specialist circumstances. Plan delivery timing.
- Renal impairment: LMWH, dabigatran, several Xa inhibitors and tranexamic acid accumulate. Use calculated renal function, not serum creatinine alone.
- Liver disease: both bleeding and thrombosis occur; INR alone does not describe whole haemostasis.
- Common errors: confusing treatment and prophylaxis doses, wrong heparin concentration, using INR for DOACs, omitting renal review, wrong thrombolytic dose, treating every anaemia with iron and bypassing transfusion identity checks.
Patient Education
- Know generic name, purpose, dose, time and duration; keep an updated medicine list and anticoagulant card.
- Never double a missed dose unless the specific product instructions say so.
- Tell clinicians, dentists and pharmacists before procedures or new medicines.
- Avoid non-prescribed aspirin, ibuprofen, diclofenac and herbal remedies that may increase bleeding.
- Seek urgent care for haematemesis, melaena, red urine, uncontrolled bleeding, severe headache, weakness, collapse, major trauma or head injury.
- Seek urgent care for sudden dyspnoea, chest pain, haemoptysis, unilateral swollen leg or focal neurological deficit.
- Attend all laboratory and follow-up visits even when feeling well.
Uganda-Relevant Practice
- Investigate malaria, hookworm, nutritional deficiency, obstetric/menstrual loss, sickle cell disease, chronic infection and kidney disease as clinically relevant.
- Use current Uganda Clinical Guidelines and Essential Medicines and Health Supplies List for dose, level-of-care restriction and referral.
- Apply patient blood management: treat anaemia, minimise avoidable blood loss and use blood components for evidence-based indications.
- Refer early when coagulation monitoring, imaging, reversal agents, blood products or specialist/critical care are unavailable.
Revision Summary
- Confirm the cause before treating anaemia.
- Understand PD/PK to predict onset, clearance, interactions and reversal.
- Every hematological drug needs a specific indication, dose, contraindication screen and monitoring plan.
- HIT is thrombocytopenia with thrombosis: stop all heparin and obtain urgent specialist care.
- For a suspected transfusion reaction, stop the transfusion first and assess ABC.
Authoritative References
- Uganda Ministry of Health: Uganda Clinical Guidelines, 2023
- Essential Medicines and Health Supplies List for Uganda, 2023
- WHO Model List of Essential Medicines, 24th list, 2025
- WHO Patient Blood Management and Clinical Use of Blood
- American Society of Hematology VTE Guidelines
- American Society of Hematology HIT Guideline
Educational material; apply patient-specific prescriptions, current local protocols and specialist guidance.