Major Haemorrhage

Major haemorrhage is life-threatening blood loss requiring activation of a massive transfusion protocol, damage control resuscitation, and urgent identification and control of the bleeding source.

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Key Facts

Major haemorrhage is defined as loss of >1 blood volume in 24h, >50% blood volume in 3h, or bleeding rate >150mL/min Massive transfusion protocol (MTP): Provides pRBC, FFP, and platelets in a 1:1:1 ratio — reduces mortality Tranexamic acid 1g IV within 3 hours reduces death from bleeding by ~30% (CRASH-2 and WOMAN trials) O-negative blood should be immediately available; switch to crossmatched blood as soon as possible Target fibrinogen >1.5g/L: Give cryoprecipitate (2 pools = 10 units) if low Permissive hypotension (SBP 80-90): Limit crystalloid; avoid dilutional coagulopathy — does NOT apply to head injuries Point-of-care coagulation testing (TEG/ROTEM) guides targeted blood product replacement Calcium replacement: Citrate in blood products chelates calcium — give calcium chloride 10mL 10% IV per 4 units blood

Overview

Key Facts

Major haemorrhage is one of the most time-critical emergencies in medicine. A structured approach with early activation of the massive transfusion protocol, damage control resuscitation, and rapid source control saves lives.

Epidemiology

Major haemorrhage occurs in trauma, obstetrics (postpartum haemorrhage), gastrointestinal bleeding, surgical complications, and ruptured aortic aneurysms. Haemorrhage is the leading cause of preventable death in trauma. In the UK, massive transfusion protocols are activated thousands of times annually.

Aetiology

  • Trauma: Solid organ injury (liver, spleen), vascular injury, pelvic fracture, long bone fractures
  • Obstetric: Postpartum haemorrhage (uterine atony, placenta praevia, abruption, uterine rupture)
  • GI: Variceal bleeding, peptic ulcer, aorto-enteric fistula
  • Surgical: Post-operative bleeding, vascular surgery complications
  • Vascular: Ruptured AAA, aortic dissection
  • Coagulopathy: Anticoagulant-related, DIC, haemophilia

Pathophysiology

Massive blood loss leads to the lethal triad: hypothermia (from exposure and cold fluids), acidosis (from tissue hypoperfusion and anaerobic metabolism), and coagulopathy (from dilution, consumption, and hypothermia). This creates a vicious cycle where coagulopathy worsens bleeding, which worsens acidosis and hypothermia. Damage control resuscitation aims to break this cycle.

Clinical Presentation

Clinical Features of Major Haemorrhage

  • Tachycardia (earliest sign), hypotension, tachypnoea
  • Cold, pale, clammy peripheries; prolonged capillary refill
  • Altered mental status (confusion → unconsciousness)
  • Oliguria/anuria
  • Visible external bleeding or signs of internal bleeding (abdominal distension, chest drain output, PV bleeding)

Shock Index

  • Shock index = HR/SBP: Normal <0.7; >1.0 indicates significant haemorrhage

Red Flags

  • Patient not responding to initial resuscitation — ongoing uncontrolled haemorrhage
  • Coagulopathic bleeding (oozing from multiple sites, surgical wounds, IV sites) — DIC or consumptive coagulopathy
  • Chest drain output >1500mL initially or >200mL/hr for 2-4h — thoracotomy indication
  • Massive PPH (>1000mL) — activate obstetric haemorrhage protocol

Differential Diagnosis

SourceKey FeaturesInvestigation
Intra-abdominalDistension, peritonism, post-opFAST, CT, laparotomy
ThoracicChest drain output, haemothoraxCXR, CT, thoracotomy
PelvicPelvic fracture, perineal bleedingX-ray, CT, pelvic binder, IR
GIHaematemesis, melaena, rectal bleedingOGD, CT angiography
Obstetric (PPH)Post-delivery, uterine atonyClinical, bimanual compression
RetroperitonealBack pain, shock, stable abdomenCT
CoagulopathyOozing from multiple sitesCoag screen, TEG/ROTEM

Diagnosis / Investigation

Bedside

  • ABCDE assessment: Simultaneous assessment and resuscitation
  • FAST USS: Free fluid in abdomen/pelvis, haemothorax
  • ABG/VBG: Hb, pH, base deficit, lactate, Ca²⁺, K⁺
  • Point-of-care coagulation (TEG/ROTEM): Guide blood product therapy in real-time

Bloods

  • Group and crossmatch: Urgent — 6 units minimum; O-neg until available
  • FBC: Hb (may be normal initially in acute haemorrhage), platelets
  • Coagulation: PT, APTT, fibrinogen (target >1.5g/L)
  • U&Es, LFTs: Organ function
  • Lactate: Tissue perfusion (serial monitoring)
  • Calcium: Ionised Ca²⁺ — citrate in blood products causes hypocalcaemia

Imaging

  • CXR: Haemothorax, mediastinal widening
  • CT (with contrast): Identify bleeding source — CT angiography for active extravasation
  • CT angiography: Vascular injury, aortic pathology

Special Tests

  • Interventional angiography: Diagnostic and therapeutic embolisation
  • OGD: Upper GI bleeding source identification and treatment

Management

Non-pharmacological

  • Activate massive transfusion protocol (MTP): Single phone call activates blood bank to release packs
  • Haemorrhage control: Direct pressure, tourniquet (extremity), pelvic binder, splints
  • Warm patient: Warm fluids (Level 1 rapid infuser), blankets, warm theatre (>24°C)
  • Two large-bore IV cannulae or central access: Rapid infusion capability

Pharmacological

  • Tranexamic acid 1g IV over 10 min (then 1g over 8h in trauma; or additional 1g in PPH) — within 3 hours
  • Blood products (1:1:1 ratio):
    • pRBC: Restore oxygen-carrying capacity
    • FFP: Replace clotting factors (target PT/APTT <1.5× normal)
    • Platelets: Target >75 × 10⁹/L (>100 if head injury)
    • Cryoprecipitate: Target fibrinogen >1.5g/L (give 2 pools = 10 units)
  • Calcium chloride 10mL 10% IV: Give per 4 units blood (prevent citrate-induced hypocalcaemia)
  • Permissive hypotension: Limit crystalloid to 1-2L initially; target SBP 80-90 (NOT in TBI)
  • Reversal agents (anticoagulant-related bleeding):
    • Warfarin: Vitamin K 5-10mg IV + PCC (Beriplex 25-50 IU/kg)
    • Dabigatran: Idarucizumab 5g IV
    • Factor Xa inhibitors: Andexanet alfa (if available) or PCC

Surgical/Interventional

  • Damage control surgery: Control haemorrhage and contamination; temporary closure
  • Interventional radiology: Embolisation (pelvic, hepatic, splenic bleeding)
  • Emergency thoracotomy: Penetrating chest trauma with cardiac arrest
  • Emergency laparotomy: Abdominal haemorrhage in unstable patient
  • Endoscopy: GI bleeding — clip, injection, banding

Referral Criteria

  • Activate MTP — call blood bank (usually single-number activation)
  • Surgical source not controlled — urgent surgical team
  • Interventional radiology — if available, for angiographic embolisation
  • Massive PPH — obstetric team, anaesthetist, consider cell salvage

Prognosis

  • Mortality from major haemorrhage: Varies widely by cause — trauma ~40% for class IV shock, PPH ~1%
  • 1:1:1 transfusion ratio: PROPPR trial showed improved haemostasis; trend towards reduced mortality
  • Tranexamic acid within 1 hour: Reduces bleeding death by ~30% (CRASH-2)
  • Damage control resuscitation: Has transformed survival from haemorrhagic shock
  • Complications of massive transfusion: Hypocalcaemia, hyperkalaemia, hypothermia, TRALI, TACO, transfusion reactions

Other Relevant Information

Massive Transfusion Protocol — Typical Pack

ComponentAmount per Pack
Packed red blood cells4-6 units
Fresh frozen plasma4 units
Platelets1 adult dose
Cryoprecipitate2 pools (10 units)
Tranexamic acid1g IV

Targets During Major Haemorrhage

ParameterTarget
Hb>70-80 g/L
Platelets>75 × 10⁹/L (>100 if head injury)
Fibrinogen>1.5 g/L
PT/APTT<1.5× normal
Ionised calcium>1.0 mmol/L
pH>7.2
Temperature>35°C
LactateFalling

Key Haemorrhage Trials

TrialFinding
CRASH-2 (2010)TXA within 3h reduces bleeding death in trauma
WOMAN (2017)TXA reduces death from PPH
PROPPR (2015)1:1:1 ratio improves haemostasis vs 1:1:2
HALT-IT (2020)TXA did NOT reduce mortality in GI bleeding