Blood Products

Foundations and mechanisms

Conceptual classification of blood products

Blood products are biological pharmacological therapies used to restore oxygen carriage, haemostasis, oncotic pressure or specific plasma proteins. They are distinct from conventional drugs because efficacy and toxicity depend on donor biology, processing, storage lesion, immunological compatibility and recipient physiology. For anaesthetic practice, the core distinction is between cellular components, plasma-derived haemostatic components, and fractionated or recombinant products.

Product	Main therapeutic function	Typical adult unit content	Storage	Key pharmacology/physiology
Red cell concentrate	Oxygen carriage	~220–350 ml; haematocrit ~0.55–0.70	2–6°C; up to 35–42 days depending on additive solution	1 unit increases Hb by ~10 g/L in a 70 kg adult
Platelets	Primary haemostasis	Adult therapeutic dose: pooled or apheresis, ≥2.4 × 1011 platelets	20–24°C with agitation; usually 5–7 days	Raises platelet count by ~20–40 × 109/L
Fresh frozen plasma	Replacement of multiple coagulation factors	~200–300 ml/unit	Frozen ≤ −25°C; thawed shelf-life commonly 24 h	Dose 15–20 ml/kg; meaningful correction when PT/APTT >1.5 × normal
Cryoprecipitate	Fibrinogen-rich replacement	Adult dose: 2 pools; each pool usually 5 donor units	Frozen; use promptly after thawing	Contains fibrinogen, factor VIII, factor XIII, vWF, fibronectin
Prothrombin complex concentrate	Rapid vitamin K-dependent factor replacement	Factors II, IX, X ± VII; proteins C/S	Refrigerated or room temperature depending preparation	Warfarin reversal: typically 25–50 IU/kg plus vitamin K
Albumin	Colloid oncotic support, plasma exchange replacement	4–5% iso-oncotic; 20% hyperoncotic	Room temperature	Human plasma half-life ~16–20 days, but intravascular persistence depends on capillary leak

Red cells: oxygen delivery and storage lesion

The pharmacodynamic endpoint of red cell transfusion is improved systemic oxygen delivery, expressed as DO₂ = cardiac output × arterial oxygen content, where CaO₂ ≈ 1.34 × Hb × SaO₂ + 0.023 × PaO₂ in SI units. Thus transfusion chiefly augments the haemoglobin-bound component; dissolved oxygen remains negligible except during hyperbaric oxygenation. Normal adult haemoglobin is approximately 130–180 g/L in men and 115–165 g/L in women, but transfusion thresholds are determined by physiology rather than normality.

During refrigerated storage, red cells develop a storage lesion: depletion of ATP and 2,3-diphosphoglycerate, reduced deformability, potassium leak, phosphatidylserine exposure, free haemoglobin and microparticle accumulation. 2,3-DPG falls substantially within 1–2 weeks, shifting the oxyhaemoglobin dissociation curve left and impairing tissue unloading; it recovers after transfusion over approximately 24–72 h. Extracellular potassium may rise progressively, especially in irradiated or older units, and is relevant in neonates, massive transfusion and rapid central administration.

Haemostatic components: coagulation biology

Haemostasis requires adequate thrombin generation, fibrinogen substrate, platelet number/function, calcium, pH and temperature. Coagulation factor activity is usually adequate for surgical haemostasis when levels exceed approximately 30% of normal, but fibrinogen is the first factor to reach critically low concentrations during major haemorrhage. Normal fibrinogen is ~2.0–4.5 g/L; bleeding risk increases below 1.5–2.0 g/L, and many major haemorrhage protocols target ≥1.5 g/L, with obstetric haemorrhage often targeting ≥2.0 g/L because low fibrinogen predicts progression to severe postpartum haemorrhage.

FFP provides all soluble coagulation factors at roughly 1 IU/ml but is a dilute product, requiring large volumes to alter coagulation tests. A 15 ml/kg dose gives approximately 3–4 units in a 70 kg adult and increases factor levels by only ~20–30%. It is therefore inefficient for isolated fibrinogen deficiency and inappropriate for simple volume expansion. Cryoprecipitate is concentrated fibrinogen therapy; one adult dose commonly increases fibrinogen by ~0.5–1.0 g/L, depending on plasma volume and ongoing consumption.

Compatibility, immunology and modification

ABO compatibility is central because naturally occurring IgM anti-A or anti-B antibodies activate complement and can cause immediate intravascular haemolysis. Red cells must be ABO compatible with recipient plasma; group O red cells are used in emergencies, with O RhD-negative prioritised for females of childbearing potential. Plasma compatibility is reversed: donor plasma must not contain antibodies against recipient red cells, making AB plasma the universal plasma donor. RhD-negative recipients, particularly females of childbearing potential, should avoid RhD-positive red cells where possible because anti-D alloimmunisation may cause haemolytic disease of the fetus/newborn.

• Leucodepletion: reduces febrile non-haemolytic reactions, HLA alloimmunisation and CMV transmission risk; UK components are universally leucodepleted to <1 × 10⁶ leucocytes/unit.
• Irradiation: 25–50 Gy damages donor lymphocyte DNA, preventing transfusion-associated graft-versus-host disease; required in susceptible immunocompromised patients and after intrauterine transfusion.
• CMV-seronegative components: considered for intrauterine transfusion, neonates and selected profoundly immunocompromised patients, although leucodepletion markedly reduces risk.
• Washed components: remove plasma proteins, useful for recurrent severe allergic reactions or IgA deficiency with anti-IgA antibodies.

Quantitative triggers and major haemorrhage principles

Restrictive red cell transfusion is supported by landmark randomised data, notably the TRICC trial, which found a threshold of 70 g/L non-inferior or superior to 100 g/L in many critically ill patients. Current perioperative and critical care practice commonly uses Hb <70 g/L as a trigger in stable non-bleeding adults, <80 g/L in many patients with cardiovascular disease or major surgery, and higher targets only for active ischaemia or uncontrolled haemorrhage. Platelet thresholds are typically <10 × 10⁹/L prophylactically, <50 × 10⁹/L for invasive procedures or major bleeding, and <100 × 10⁹/L for neurosurgery or ocular posterior segment surgery.

In major haemorrhage, dilutional coagulopathy, hypothermia, acidosis and hypocalcaemia amplify trauma-induced coagulopathy. Citrate anticoagulant chelates ionised calcium; ionised Ca²⁺ should be maintained >1.0 mmol/L, ideally normal ~1.12–1.32 mmol/L. Massive transfusion protocols use early balanced component therapy, often approximating red cells:plasma:platelets of 1:1:1 or 2:1:1, informed by PROPPR trial data showing improved haemostasis and reduced death from exsanguination with 1:1:1 compared with 2:1:1, though overall mortality was similar. Viscoelastic testing guides mechanism-based replacement by identifying fibrinogen deficit, platelet contribution, thrombin generation failure and hyperfibrinolysis in real time.

Clinical assessment and investigations

Assessment of the requirement for blood products

Clinical assessment must define whether the problem is oxygen-carrying capacity, circulating volume, primary haemostasis, coagulation factor deficiency, or fibrinogen depletion. In anaesthesia and critical care, transfusion decisions should not be based on a single laboratory value: they integrate haemodynamic instability, rate of blood loss, tissue hypoxia, comorbidity, anticoagulant exposure, temperature, pH, calcium, and anticipated surgical bleeding.

Clinical problem	Key findings	Principal investigations	Common transfusion threshold
Red cell deficit	Dyspnoea, tachycardia, hypotension, angina, raised lactate, low ScvO2	Hb, arterial blood gas, lactate, ECG if ischaemic risk	Restrictive threshold Hb <70 g/L; target 70–90 g/L. Consider <80 g/L in acute coronary syndrome or symptomatic cardiovascular disease
Platelet deficit/dysfunction	Mucocutaneous bleeding, petechiae, oozing from lines; antiplatelet drugs, bypass, uraemia	Platelet count, blood film, TEG/ROTEM, drug history	<10 × 109/L prophylaxis; <50 × 109/L bleeding or major surgery; <100 × 109/L neurosurgery or posterior eye surgery
Coagulation factor deficiency	Diffuse surgical bleeding, liver disease, DIC, massive haemorrhage, warfarin	PT/INR, APTT, fibrinogen, TEG/ROTEM	FFP usually when bleeding with PT or APTT >1.5 × normal; dose 12–15 mL/kg
Hypofibrinogenaemia	Massive haemorrhage, obstetric haemorrhage, trauma, DIC	Clauss fibrinogen, FIBTEM A5/A10	Cryoprecipitate or fibrinogen concentrate if fibrinogen <1.5 g/L in major bleeding; in obstetric haemorrhage, <2.0 g/L predicts severe progression

NICE NG24 and UK transfusion guidance support restrictive red cell transfusion in stable non-bleeding adults, commonly at Hb 70 g/L with a post-transfusion target of 70–90 g/L. A single adult red cell unit typically raises Hb by approximately 10 g/L. In massive haemorrhage, laboratory thresholds lag behind physiology; activation criteria include loss of one blood volume in 24 h, 50% blood volume in 3 h, bleeding >150 mL/min, or anticipated requirement for >4 units red cells rapidly with shock. Early balanced resuscitation approximating red cells:plasma:platelets of 1:1:1 is informed by trauma data including PROPPR, which showed improved haemostasis and reduced exsanguination at 24 h compared with 1:1:2, though no significant 24 h or 30 day mortality difference.

Pre-transfusion investigations and compatibility testing

Before elective transfusion, obtain a correctly labelled group-and-screen sample. It determines ABO and RhD group and screens for clinically significant alloantibodies. If antibodies are present, antigen-negative compatible units are required and delays should be anticipated. Crossmatch may be electronic when the antibody screen is negative and local criteria are met; otherwise serological crossmatch is required. Sample validity is commonly 72 h if the patient has been transfused or pregnant within the preceding 3 months, because anamnestic alloantibody responses may emerge. In immediate life-threatening haemorrhage, group O RhD-negative red cells are used for females of childbearing potential; group O RhD-positive may be used for adult males or older females where stock conservation is necessary. FFP and platelets should be ABO-compatible where possible; plasma incompatibility risks haemolysis from donor anti-A or anti-B.

Investigation of bleeding phenotype

Standard coagulation tests assess plasma clot initiation under artificial conditions and poorly predict surgical bleeding, but remain essential for diagnosis and monitoring. PT/INR reflects extrinsic/common pathways and is prolonged in warfarin effect, vitamin K deficiency, liver disease and DIC. APTT reflects intrinsic/common pathways and is prolonged by unfractionated heparin, lupus anticoagulant, haemophilia and factor inhibitors. Clauss fibrinogen is preferred over derived fibrinogen in critical bleeding. Platelet count does not measure platelet function; consider platelet dysfunction with cardiopulmonary bypass, P2Y₁₂ inhibitors, aspirin, uraemia and hypothermia.

Viscoelastic haemostatic assays provide near-patient dynamic assessment of clot initiation, propagation, strength and fibrinolysis. TEG reaction time or ROTEM clotting time prolongation suggests factor deficiency or heparin effect; low maximum amplitude/maximum clot firmness reflects platelet-fibrin clot strength; isolated low FIBTEM amplitude indicates fibrinogen deficit; high lysis index reduction or maximum lysis suggests hyperfibrinolysis. Interpretation must be contextualised with temperature, pH and ionised calcium: hypothermia <35°C, pH <7.2 and ionised Ca²⁺ <1.1 mmol/L impair coagulation and reduce response to blood products. Citrate toxicity during massive transfusion causes hypocalcaemia; calcium chloride 10% 10 mL intravenously or calcium gluconate 10% 30 mL may be required, titrated to ionised calcium.

Presentation and investigation of transfusion reactions

Any deterioration during transfusion is a transfusion reaction until proven otherwise. Fever, rigors, hypotension, bronchospasm, urticaria, back or chest pain, haemoglobinuria, bleeding, hypoxaemia or shock require immediate cessation of the transfusion, maintenance of intravenous access with 0.9% saline, ABC assessment, and clerical identity check at the bedside.

Reaction	Typical presentation	Key investigations and interpretation
Acute haemolytic transfusion reaction	Minutes to hours; fever, flank pain, hypotension, DIC, haemoglobinuria; usually ABO incompatibility	Repeat group/crossmatch, direct antiglobulin test, plasma free Hb, LDH ↑, bilirubin ↑, haptoglobin ↓, urine Hb, FBC, coagulation, U&E
Febrile non-haemolytic reaction	Temperature rise ≥1°C with chills, no haemolysis or sepsis	Diagnosis of exclusion; check haemolysis screen and cultures if significant fever or rigors
Bacterial contamination	High fever, rigors, hypotension, shock; platelets highest risk due to room-temperature storage	Blood cultures from patient and residual component; send pack to transfusion laboratory
TRALI	Acute hypoxaemia and bilateral pulmonary oedema within 6 h, no circulatory overload	CXR infiltrates, PaO2/FiO2 ≤300 or SpO2 <90% on air; BNP not markedly raised; report for donor antibody investigation
TACO	Dyspnoea, hypertension, raised JVP, pulmonary oedema, positive fluid balance, often within 12 h	CXR oedema, BNP/NT-proBNP raised, echocardiography if unclear; improves with diuretics
Allergic/anaphylactic	Urticaria to bronchospasm, angio-oedema, shock; consider IgA deficiency	Serum tryptase at 1–2 h and baseline; IgA level and anti-IgA if severe recurrent reactions
Delayed haemolytic reaction	24 h to 28 days; falling Hb, jaundice, fever after prior sensitisation	DAT positive, new alloantibody, bilirubin/LDH ↑, inadequate Hb increment

Differential diagnoses during transfusion include progression of haemorrhagic shock, anaesthetic anaphylaxis, sepsis, myocardial ischaemia, pulmonary embolism, aspiration and fluid overload unrelated to transfusion. All serious reactions must be reported to the transfusion laboratory and haemovigilance system; the implicated component and giving set should be retained for investigation.

Management, pharmacology and procedures

Transfusion strategy and component prescribing

Blood product administration should be treated as a pharmacological intervention: prescribe a defined component, dose, rate, target endpoint and monitoring plan. Modern practice emphasises restrictive red cell transfusion, early haemostatic resuscitation in major bleeding, and avoidance of empiric “top-up” transfusion. UK guidance is broadly consistent with NICE NG24 and British Society for Haematology recommendations.

Product	Typical adult dose	Expected effect	Key indications
Packed red cells	1 unit then reassess	Hb rise approximately 10 g/L in a 70 kg adult	Symptomatic anaemia, major haemorrhage, Hb <70 g/L in stable non-bleeding patients; consider <80 g/L in acute coronary syndrome
Fresh frozen plasma	15–20 mL/kg	Replaces coagulation factors; meaningful effect usually if PT/APTT ratio >1.5	Major haemorrhage, DIC with bleeding, urgent warfarin reversal if PCC unavailable
Platelets	1 adult therapeutic dose	Increment 20–40 × 109/L	Bleeding with thrombocytopenia/platelet dysfunction; maintain >50 × 109/L, >100 × 109/L for neurosurgery/ocular surgery
Cryoprecipitate	2 pools in adults, or 5–10 mL/kg	Raises fibrinogen by approximately 0.5–1.0 g/L	Fibrinogen <1.5 g/L in bleeding; <2.0 g/L in obstetric haemorrhage often used as trigger
Fibrinogen concentrate	25–50 mg/kg	Rapid fibrinogen replacement; dose guided by Clauss fibrinogen or ROTEM FIBTEM	Acquired hypofibrinogenaemia where available; congenital fibrinogen deficiency

Major haemorrhage management

Management requires simultaneous haemorrhage control, resuscitation and correction of trauma-induced coagulopathy. Activate the major haemorrhage protocol early. Use group-specific blood as soon as available; until then use O negative red cells for females of childbearing potential and O positive may be acceptable for adult males or post-menopausal females depending on local policy. Avoid hypothermia, acidosis and hypocalcaemia, as these impair thrombin generation and platelet function.

• Red cell to plasma strategy: empirical balanced resuscitation commonly begins with 1:1 or 2:1 red cell:FFP, adding platelets early. The PROPPR trial showed 1:1:1 versus 2:1:1 did not significantly reduce 24-hour or 30-day mortality, but improved haemostasis and reduced exsanguination.
• Tranexamic acid: give 1 g IV over 10 minutes followed by 1 g over 8 hours, ideally within 3 hours of injury. CRASH-2 demonstrated reduced death due to bleeding; administration after 3 hours may increase bleeding mortality. WOMAN trial supports the same regimen in postpartum haemorrhage.
• Fibrinogen replacement: fibrinogen is often the first factor to reach critically low levels. Target >1.5 g/L in major bleeding and commonly >2.0 g/L in obstetrics.
• Calcium: citrate in blood products chelates ionised calcium. Monitor ionised Ca²⁺; maintain >1.1 mmol/L. Give calcium chloride 10% 10 mL IV centrally, or calcium gluconate 10% 30 mL IV peripherally, repeated according to ionised calcium.
• Temperature: warm all components through an approved blood warmer when rapid transfusion is required; target core temperature >36°C.

Adjunctive haemostatic pharmacology

Drug	Dose	Mechanism and caveats
Prothrombin complex concentrate	25–50 IU/kg depending on INR and product	Vitamin K-dependent factors II, VII, IX, X; first-line urgent warfarin reversal with vitamin K 5–10 mg IV. Thrombosis risk; not routine for trauma coagulopathy without VKA effect.
Vitamin K	5–10 mg IV slowly	Restores hepatic synthesis of factors II, VII, IX, X; onset 4–6 h, maximal 12–24 h. Anaphylactoid reactions are rare with slow IV administration.
Protamine	1 mg per 100 units unfractionated heparin given in previous 2–3 h; maximum usually 50 mg	Cationic protein complexes heparin. Excess protamine is anticoagulant; risks include hypotension, pulmonary vasoconstriction and anaphylaxis, especially after prior exposure or fish allergy.
Desmopressin	0.3 microgram/kg IV over 20–30 min	Releases endothelial vWF and factor VIII; useful in uraemic platelet dysfunction, mild haemophilia A and type 1 vWD. Risk hyponatraemia and tachyphylaxis.

Procedural aspects and modifications

Use positive patient identification at sampling and administration; wrong blood in tube remains a major preventable cause of fatal ABO-incompatible transfusion. Baseline observations should be recorded and repeated at 15 minutes after starting, then according to local policy. Blood should be started within 30 minutes of removal from controlled storage and usually completed within 4 hours. Red cells may be transfused via peripheral or central venous access using a 170–200 micron filter; no drugs should be co-administered through the same line, and 0.9% saline is the compatible crystalloid.

Special components include CMV-negative products for selected high-risk groups, irradiated cellular components to prevent transfusion-associated graft-versus-host disease in susceptible patients, and washed components for recurrent severe allergic reactions or IgA deficiency. Leucodepletion, universal in the UK, reduces febrile non-haemolytic reactions, CMV transmission and HLA alloimmunisation but does not prevent TA-GvHD.

Recognition and acute management of complications

Any suspected transfusion reaction mandates immediate cessation of the transfusion, maintenance of IV access with 0.9% saline, clerical check, ABC assessment, and notification of the transfusion laboratory. Return the implicated unit and administration set; send repeat group and screen, direct antiglobulin test, FBC, U&E, coagulation, bilirubin, LDH, haptoglobin, plasma free Hb, and blood cultures if sepsis is possible.

• Acute haemolytic reaction: fever, flank pain, hypotension, haemoglobinuria, DIC; usually ABO incompatibility. Treat shock, maintain urine output, manage DIC and critical care escalation.
• Febrile non-haemolytic reaction: exclude haemolysis/sepsis; treat with paracetamol if mild.
• Allergic/anaphylaxis: urticaria may respond to antihistamine; anaphylaxis requires IM adrenaline 500 micrograms of 1:1000, high-flow oxygen and fluids.
• TRALI: acute hypoxaemia and bilateral pulmonary infiltrates within 6 h, non-cardiogenic; supportive ventilation. Diuretics are not primary therapy.
• TACO: hydrostatic pulmonary oedema, hypertension, raised JVP/BNP; stop transfusion, sit upright, oxygen, diuretics. Risk is reduced by single-unit prescribing and slower rates.

Long-term follow-up includes documentation, haemovigilance reporting to SHOT where appropriate, investigation for alloantibodies, counselling after significant reactions, and review of ongoing transfusion requirements, including iron therapy, erythropoiesis-stimulating agents or definitive haemostatic/surgical management to reduce future exposure.

Exam controversies and advanced synthesis

Restrictive versus liberal red cell transfusion

The modern default is restrictive transfusion, because packed red cells are not a benign “oxygen drug”: they increase viscosity, reduce microvascular flow, impair immunomodulation, and expose patients to TACO, TRALI, haemolysis and infection risk. The landmark TRICC trial in ICU patients showed that a haemoglobin trigger of 70 g L^-1 was at least as safe as 100 g L^-1, with possible mortality benefit in younger and less severely ill patients. The FOCUS trial in high-risk hip fracture patients found no advantage to a liberal 100 g L^-1 strategy over a restrictive strategy around 80 g L^-1 or symptoms.

Clinical context	Common trigger/target	Exam nuance
Stable non-bleeding adult	Transfuse at Hb <70 g L-1; target 70–90 g L-1	Use single-unit transfusion and reassess; 1 adult unit raises Hb by approximately 10 g L-1.
Acute coronary syndrome or significant myocardial ischaemia	Often consider Hb <80–90 g L-1	Evidence is less secure; avoid automatic liberal transfusion but tolerate less anaemia.
Major haemorrhage	Do not wait for Hb alone	Hb is misleading during early bleeding; use physiology, estimated blood loss, shock and coagulation monitoring.
Traumatic brain injury	Usually avoid Hb <70 g L-1; many target 80–100 g L-1	Balance oxygen delivery against transfusion complications; evidence remains heterogeneous.

Massive haemorrhage: ratios versus goal-directed therapy

A common viva controversy is whether massive transfusion should be fixed-ratio or viscoelastic-guided. The PROPPR trial compared 1:1:1 versus 1:1:2 plasma:platelets:RBCs in severe trauma. Overall 24-hour and 30-day mortality were not significantly different, but 1:1:1 reduced exsanguination and improved haemostasis. This supports early balanced resuscitation, particularly before laboratory results are available. However, mature systems increasingly transition rapidly to goal-directed replacement using ROTEM/TEG, fibrinogen concentration, platelet count, PT/APTT and ionised calcium.

• Massive haemorrhage protocol: commonly defined as replacement of one blood volume in 24 h, >50% blood volume in 3 h, or >4 units RBC in 1 h with ongoing bleeding.
• Targets during active bleeding: Hb 70–90 g L^-1, platelets >50 × 10⁹ L^-1 or >100 × 10⁹ L^-1 in CNS/ocular bleeding, fibrinogen >1.5–2.0 g L^-1, PT/APTT ratio <1.5, ionised Ca²⁺ >1.0 mmol L^-1, temperature >35°C and pH >7.2.
• Fibrinogen first: fibrinogen is often the earliest coagulation factor to reach critically low levels; cryoprecipitate contains approximately 2 g fibrinogen per adult dose, whereas fibrinogen concentrate is typically dosed 25–50 mg kg^-1.
• Calcium: citrate toxicity from rapid plasma/platelet/RBC transfusion causes hypocalcaemia, hypotension and coagulopathy. Give calcium chloride 10% 5–10 mL IV centrally, or calcium gluconate 10% 10–30 mL IV peripherally, titrated to ionised calcium.

Plasma, platelets, PCC and cryoprecipitate: common pitfalls

Fresh frozen plasma is not a volume expander and should not be prescribed merely because the INR is mildly abnormal. It requires ABO compatibility, thawing time, and large volumes: typical dosing is 12–15 mL kg^-1. It is poor practice to “correct” an INR of 1.4 before a low-risk procedure in a non-bleeding patient. In contrast, major bleeding with prolonged PT/APTT requires early plasma or factor-specific therapy.

For warfarin-associated major bleeding, 4-factor prothrombin complex concentrate is preferred to FFP because it is rapid, low-volume and concentrated. Give vitamin K 5–10 mg IV concurrently because PCC has a finite duration, reflecting factor VII half-life of approximately 6 h. PCC dosing is commonly weight- and INR-based, often 25–50 IU kg^-1. It is not a general antidote for all DOAC bleeding; idarucizumab reverses dabigatran, and andexanet alfa reverses apixaban/rivaroxaban where available, though cost, thrombotic risk and outcome data remain controversial.

Albumin, crystalloids and the “colloid” controversy

Albumin is a blood product pharmacologically acting as a colloid oncotic agent, ligand carrier and endothelial glycocalyx modulator. The SAFE trial found 4% albumin and saline had similar 28-day mortality in general ICU patients, with possible harm in traumatic brain injury and possible benefit in sepsis. The ALBIOS trial did not show overall mortality benefit in severe sepsis, although subgroup signals persist. For Primary FRCA, the defensible position is: albumin is not a routine resuscitation fluid, may be useful in selected cirrhosis indications, large-volume paracentesis, hepatorenal syndrome and selected hypoalbuminaemic critical illness, but should not replace haemostatic resuscitation in bleeding.

Viva-level synthesis: product selection is physiology-driven

Problem	Best product or intervention	Rationale
Low oxygen-carrying capacity	RBC	Increases arterial oxygen content: CaO2 = 1.34 × Hb × SaO2 + 0.023 × PaO2.
Dilutional/consumptive coagulopathy with prolonged PT/APTT	FFP 12–15 mL kg-1	Replaces multiple coagulation factors but needs sufficient volume.
Hypofibrinogenaemia	Cryoprecipitate or fibrinogen concentrate	Target fibrinogen >1.5–2.0 g L-1; higher thresholds used in obstetric haemorrhage.
Thrombocytopenic bleeding	Platelets	Adult pool usually raises count by 20–40 × 109 L-1.
Warfarin major bleeding	4-factor PCC plus IV vitamin K	Rapid factor II, VII, IX, X replacement; vitamin K sustains reversal.

High-yield examination traps

• Do not confuse TRALI with TACO: both cause hypoxaemia within 6 h, but TRALI is non-cardiogenic permeability oedema often with hypotension/fever, whereas TACO has hypertension, raised JVP, positive fluid balance and responds to diuresis.
• Platelets are stored at 20–24°C, explaining higher bacterial contamination risk; RBCs are stored at 2–6°C for up to about 35 days depending on additive solution.
• Irradiated components prevent transfusion-associated graft-versus-host disease but do not prevent CMV transmission; CMV-negative or leucodepleted products are used for CMV risk reduction.
• In obstetric haemorrhage, a fibrinogen <2 g L^-1 predicts progression to severe haemorrhage; early fibrinogen replacement is often more important than escalating plasma alone.
• In massive transfusion, lethal coagulopathy is not corrected by products alone: simultaneously treat hypothermia, acidosis, hypocalcaemia and ongoing surgical bleeding.