Major haemorrhage and massive transfusion

Surgical approach (context-dependent: source control)

• Principle: stop the bleeding early (source control) while resuscitation runs in parallel
  • Trauma: damage control surgery (DCS) — rapid haemorrhage control (packing, vascular control/shunts, temporary closure), avoid definitive repair until physiology corrected
  • Pelvic trauma: pelvic binder, pre-peritoneal packing, external fixation, consider IR embolisation
  • Obstetrics: uterotonics → balloon tamponade → uterine artery ligation/B-Lynch → hysterectomy, consider IR
  • GI/vascular surgery: clamp/proximal control, packing, temporary shunts, endovascular options where feasible
• Minimise ongoing losses: avoid hypothermia, correct coagulopathy, limit crystalloid, permissive hypotension where appropriate (not TBI/pregnancy)

Anaesthetic management (generic for major haemorrhage scenarios)

• Type of anaesthesia: usually GA (unstable physiology, need for airway control, rapid surgery), regional generally avoided if active haemorrhage/coagulopathy/haemodynamic instability
  • If regional already in situ (e.g., epidural for labour): treat sympathectomy/hypotension aggressively, reassess coagulation before catheter removal
• Airway: cuffed ETT preferred (aspiration risk, ongoing resuscitation, need for controlled ventilation), SGA only as brief bridge in extremis
• Duration: variable (often 1–6+ hours), plan for prolonged resuscitation and ICU transfer
• Analgesia: procedure-dependent, often high pain burden (laparotomy/orthopaedic/obstetric) → multimodal but avoid NSAIDs if bleeding/renal risk, consider ketamine/opioid infusions
• Monitoring/Access: 2 large-bore peripheral cannulae + rapid infuser, early arterial line, consider central access for vasopressors/rapid infusion, urinary catheter, temperature monitoring

Definitions &amp, triggers

• Major haemorrhage: bleeding causing or likely to cause haemodynamic instability and/or requiring rapid blood component therapy, definitions vary by context
  • Common pragmatic triggers: ongoing blood loss &gt,150 mL/min, or &gt,50% blood volume in 3 h, or ≥4 units RBC in 1 h with ongoing bleeding, or anticipated need for massive transfusion
• Massive transfusion (adult): typically ≥10 units RBC in 24 h or ≥4 units in 1 h (with ongoing need) or replacement of ≥1 blood volume in 24 h
• Major Haemorrhage Protocol (MHP): pre-defined, logistics-focused system to deliver blood components rapidly with lab/POC guidance

Pathophysiology: lethal triad/tetrad

• Trauma/major bleeding coagulopathy is multifactorial: tissue injury + shock → endothelial dysfunction, anticoagulant pathway activation, hyperfibrinolysis, compounded by dilution, hypothermia, acidosis, hypocalcaemia
• Hypothermia: impairs platelet function and enzymatic coagulation, worsens acidosis and arrhythmia risk
• Acidosis: reduces coagulation factor activity, severe acidaemia reduces response to catecholamines and increases arrhythmia risk
• Hypocalcaemia: citrate from blood products chelates Ca2+ → myocardial depression, hypotension, coagulopathy, risk increased with rapid transfusion and liver dysfunction

Immediate management: structured approach

• Call for help early: senior anaesthetist, ODP, theatre coordinator, haematology/transfusion lab, ICU, activate MHP when criteria met
• A–E with simultaneous haemorrhage control: airway/oxygenation, ventilation, circulation with haemostatic resuscitation, disability, exposure/temperature
• Access/monitoring: two large-bore cannulae (14–16G) ± rapid infuser, arterial line early, consider central line, ECG, SpO2, EtCO2, invasive BP, temperature, urine output
• Blood sampling early and repeat: FBC, coagulation (PT/APTT), fibrinogen, group &amp, screen/crossmatch, VBG/ABG (Hb, lactate, base deficit), U&amp,E, Ca2+, use viscoelastic testing if available (TEG/ROTEM)
• Temperature management: forced-air warming, fluid/blood warmers, warm theatre, warmed irrigation, aim normothermia
• Permissive hypotension (selected trauma): target SBP ~80–90 mmHg until haemorrhage control if no TBI, avoid in pregnancy and TBI (maintain CPP)

Blood products: what they contain &amp, key practical points

• RBC: oxygen carrying, increases Hb, minimal coagulation factors/platelets, stored with additive solutions, risks include hypothermia, citrate load, hyperkalaemia (esp. older blood), dilutional coagulopathy
• FFP: replaces multiple coagulation factors, typical dose 15–20 mL/kg, takes time to thaw (unless pre-thawed), large volumes may cause TACO
• Cryoprecipitate: fibrinogen-rich (also FVIII, vWF, FXIII), used to treat hypofibrinogenaemia, typical adult initial dose often 2 pools (local policy) then guided by fibrinogen/viscoelastic tests
• Fibrinogen concentrate: rapid administration alternative to cryo (where available), dose guided by fibrinogen level/ROTEM (e.g., FIBTEM)
• Platelets: treat thrombocytopenia/platelet dysfunction, target thresholds depend on context (see below), remember dilution and hypothermia impair function
• Calcium: give IV calcium (chloride via central line or gluconate peripherally) guided by ionised Ca2+ during rapid transfusion

Transfusion strategy during MHP

• Aim: early balanced component therapy while awaiting results, then switch to goal-directed therapy using lab + viscoelastic testing
• Empirical ratios (adult trauma common approach): RBC:FFP approximately 1:1 (or 2:1 depending local protocol) with early platelets, avoid large volumes of crystalloid
• Fibrinogen is often the first factor to fall: replace early (cryo/fibrinogen concentrate) if low or if viscoelastic suggests poor clot firmness
• Tranexamic acid (TXA): give early in trauma and obstetric haemorrhage unless contraindicated, typical trauma dosing 1 g IV then 1 g over 8 h (local policy), benefit greatest if within 3 h of injury
• Targets (typical, follow local policy): Hb ~80–100 g/L (higher if ongoing shock/cardiac disease), platelets &gt,50 x10^9/L (≥100 if TBI/neuraxial/major surgery), fibrinogen &gt,1.5–2.0 g/L (obstetrics often ≥2.0 g/L), PT/APTT &lt,1.5x normal
• Consider cell salvage (if not contraindicated) and rapid infuser with warmed products, minimise iatrogenic blood loss (small sample tubes)

Choice of blood when urgent

• Hierarchy: crossmatched blood (best) → group-specific (ABO/RhD matched) → uncrossmatched emergency blood
• Emergency RBC: often group O, O negative for females of childbearing potential (local definitions vary) and when group unknown, O positive may be used for adult males/post-menopausal females to preserve O negative stocks
• FFP: ideally ABO compatible, AB plasma is universal donor plasma (limited supply), follow local transfusion lab guidance
• RhD and Kell considerations: avoid RhD positive to RhD negative females of childbearing potential, consider anti-D prophylaxis if exposed, Kell negative blood may be prioritised for females of childbearing potential (policy-dependent)

Adjuncts and special situations

• Prothrombin complex concentrate (PCC): rapid reversal of warfarin-associated bleeding (with IV vitamin K), may be used in DOAC-related bleeding per local guidance (often alongside specific antidotes)
• Specific anticoagulant reversal: dabigatran → idarucizumab, factor Xa inhibitors → andexanet alfa (where available) or PCC per protocol, always involve haematology
• Recombinant factor VIIa: not routine, consider only after surgical control, correction of fibrinogen/platelets, normothermia, pH &gt,7.2, Ca2+ normal, thrombosis risk
• Obstetric haemorrhage: early fibrinogen replacement and TXA, consider point-of-care testing, anticipate rapid deterioration, involve obstetrics/haematology/IR early
• Traumatic brain injury: avoid hypotension, aim adequate CPP, correct coagulopathy aggressively, higher platelet threshold commonly used

Complications of massive transfusion (must be able to list + manage)

• Coagulopathy: dilutional + consumption + trauma-induced, treat with balanced components + fibrinogen + platelets guided by tests
• Hypothermia: worsens bleeding and arrhythmias, active warming essential
• Electrolytes/acid-base: hypocalcaemia (citrate), hyperkalaemia (stored RBC), metabolic alkalosis late (citrate metabolism), acidosis from shock
• TRALI vs TACO: acute hypoxaemia after transfusion, TRALI is non-cardiogenic pulmonary oedema, TACO is volume overload—treat with diuresis/ventilation, stop transfusion and escalate
• Haemolytic transfusion reaction (ABO incompatibility): fever, hypotension, bleeding/oozing, haemoglobinuria, DIC, renal failure, stop transfusion, resuscitate, inform lab, send samples
• Dilutional thrombocytopenia/platelet dysfunction: anticipate and replace early in massive bleeding
• Hypomagnesaemia (citrate binding) and arrhythmias: consider checking Mg2+ if ongoing instability

Communication, documentation, and governance (UK practice)

• Use local MHP: clear roles (runner, documentation, transfusion liaison), timed cycles of product delivery, and explicit stop criteria
• Document: indication, units/components, times, patient ID checks, adverse events, lab results, calcium/TXA given, temperature, estimated blood loss, cell salvage volume
• Stop MHP promptly when bleeding controlled, avoid over-transfusion and iatrogenic complications

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