Major Haemorrhage

Introduction

Major haemorrhage is bleeding severe enough to threaten life through loss of circulating volume and oxygen-carrying capacity. It is defined operationally - loss of one blood volume within 24 hours (roughly 70 mL/kg in an adult), 50% of blood volume lost within 3 hours, ongoing bleeding at a rate exceeding 150 mL/min, or any bleeding causing haemodynamic instability - rather than by a single number, because the clinical picture matters more than a precise volume that is rarely known in real time.¹

Uncontrolled haemorrhage remains one of the leading causes of preventable death after trauma, and a major cause of death in obstetric, gastrointestinal and vascular emergencies. Survival depends on rapidly finding and controlling the source, correcting the physiological derangement caused by blood loss, and replacing what has been lost in a way that supports clotting rather than dilutes it - the modern approach known as damage control resuscitation.

This article covers the general principles that apply across causes; specific conditions such as ruptured AAA, upper GI bleeding and postpartum haemorrhage have their own detailed management covered elsewhere but follow the same resuscitation framework.

Two ideas run through everything that follows. First, resuscitation and source control happen in parallel, not sequentially - blood products are started while the surgical, endoscopic or interventional team is being mobilised, not after. Second, replacing lost blood with plasma-poor fluid (crystalloid, or red cells alone) worsens the coagulopathy that is already driving the bleeding, which is why the specific composition of what is transfused matters as much as the volume.

Recognition and classification

The body compensates for blood loss remarkably well before vital signs change, which is why relying on blood pressure alone dangerously underestimates early haemorrhage. Tachycardia, narrowing pulse pressure and a rising respiratory rate typically appear before hypotension.

Immediate management

In trauma, catastrophic external haemorrhage is controlled before airway - written as <C>ABC - because uncontrolled exsanguinating bleeding kills faster than an airway problem. In non-traumatic bleeding the same principle applies: control what can be controlled while resuscitating in parallel.

Control the source

• Direct pressure on an external wound, maintained continuously rather than checked repeatedly
• Tourniquet for catastrophic limb haemorrhage not controlled by pressure - applied proximal to the bleeding, tightened until bleeding stops, and the time of application recorded and never hidden under a dressing
• Haemostatic dressings packed into a wound cavity that cannot be adequately compressed externally
• Pelvic binder for suspected pelvic fracture with haemodynamic instability, applied at the level of the greater trochanters
• Early surgical, endoscopic or interventional radiology referral for internal bleeding that cannot be controlled at the bedside - definitive source control, not resuscitation alone, is what stops the patient dying

Resuscitate

1. Two large-bore IV cannulae (14-16G), or intraosseous access if IV access fails
2. Send bloods immediately - FBC, U&E, clotting, fibrinogen, group and save or crossmatch, and a venous or arterial lactate
3. Activate the major haemorrhage protocol as soon as major bleeding is suspected - do not wait for a crossmatch result
4. Give tranexamic acid 1 g IV over 10 minutes, then a further 1 g over 8 hours, within 3 hours of the bleed (trauma) or as per local protocol for other causes
5. Transfuse blood products in a balanced ratio rather than large volumes of crystalloid
6. Keep the patient warm - hypothermia worsens coagulopathy

The major haemorrhage protocol

Every UK hospital has a major haemorrhage protocol - a pre-agreed pathway that mobilises blood bank, porters, laboratory and clinical staff the moment it is activated, so that blood products arrive within minutes rather than being requested and awaited individually.

• Activation is typically a single phone call or emergency button, triggering the blood bank to issue emergency group O negative red cells immediately (O positive is acceptable in males and in females beyond childbearing age, to conserve the O negative supply)
• Group and save, then crossmatched blood as soon as the sample is processed, replacing the emergency-issue units
• Fixed-ratio blood component packs are typically dispensed - commonly around 1:1:1 red cells to FFP to platelets - to pre-empt the dilutional coagulopathy that follows resuscitation with red cells alone
• Cryoprecipitate if fibrinogen falls below the local threshold (commonly 1.5-2.0 g/L)
• Cell salvage where appropriate (for example major surgery, some obstetric haemorrhage) to return the patient's own shed blood
• Repeat bloods (FBC, clotting, fibrinogen, calcium, potassium, lactate) after each pack to guide further product administration - ideally supported by viscoelastic testing (ROTEM/TEG) where available, which gives a faster, more complete picture of coagulopathy than standard clotting tests

Damage control resuscitation

Damage control resuscitation is the modern approach to major haemorrhage, built on the recognition that aggressive crystalloid resuscitation dilutes clotting factors, worsens acidosis and disrupts early clot formation. Its three pillars are permissive hypotension, haemostatic resuscitation, and rapid definitive haemorrhage control.

• Permissive hypotension - in penetrating or blunt trauma without traumatic brain injury, targeting a lower systolic blood pressure (around 90 mmHg, or a palpable radial pulse) until the bleeding is surgically controlled, rather than normalising blood pressure with fluid that can dislodge a forming clot. This does not apply where a head injury is suspected, since cerebral perfusion pressure must be preserved
• Minimise crystalloid - large volumes dilute clotting factors and platelets and are avoided where blood products are available; a small bolus may still be used while awaiting blood if there is any delay
• Haemostatic resuscitation - replacing red cells, plasma and platelets together in balanced ratios rather than red cells alone, to avoid dilutional coagulopathy
• Correct the lethal triad - hypothermia, acidosis and coagulopathy potentiate each other in a vicious cycle; actively warm the patient and all infused fluids, and correct acidosis by treating its cause (adequate perfusion) rather than with bicarbonate alone

Complications of massive transfusion

Monitoring the response to resuscitation

Heart rate and blood pressure normalising is reassuring but not sufficient on its own - both can look acceptable while tissues remain under-perfused, particularly in a young patient who compensates well. Trending markers of tissue perfusion gives a more reliable picture of whether resuscitation is actually working.

• Serial lactate - a falling lactate over serial samples ('lactate clearance') is reassuring; a static or rising lactate despite apparent haemodynamic improvement suggests ongoing occult bleeding or inadequate perfusion
• Base excess/deficit on the blood gas - a worsening base deficit tracks with the severity and duration of shock
• Urine output - a reasonable surrogate for end-organ perfusion once a catheter is in place, though it lags behind acute changes
• Conscious level - improving alertness is a simple bedside sign of restored cerebral perfusion
• Repeat FBC, clotting and fibrinogen after each blood product pack, ideally guided by viscoelastic testing where available, to titrate further product replacement rather than transfusing on a fixed schedule alone

Non-traumatic major haemorrhage

The same principles of early recognition, source control and damage control resuscitation apply outside trauma, though the specific interventions differ by cause.

• Upper GI bleeding - resuscitate, correct coagulopathy (including reversing anticoagulants), and arrange urgent endoscopy; risk-stratify with the Glasgow-Blatchford score before endoscopy and the full Rockall score afterwards
• Ruptured abdominal aortic aneurysm - permissive hypotension while arranging immediate surgical or endovascular repair; aggressive fluid resuscitation before the aorta is controlled can worsen bleeding
• Postpartum haemorrhage - uterine massage, uterotonics (oxytocin, ergometrine, carboprost), tranexamic acid, and escalation to balloon tamponade or surgery if bleeding continues, run in parallel with major haemorrhage protocol activation
• Variceal bleeding - terlipressin and prophylactic antibiotics alongside resuscitation, with urgent endoscopic banding; over-transfusion above a conservative haemoglobin target can worsen portal pressure and rebleeding

Red flags

Prognosis

Outcome depends chiefly on how quickly the source of bleeding is controlled and how effectively coagulopathy is prevented rather than treated after the fact. Systems that activate a major haemorrhage protocol early, apply damage control resuscitation principles, and secure rapid surgical, endoscopic or interventional source control have measurably better survival than those relying on reactive, crystalloid-heavy resuscitation.