Major haemorrhage is a time-critical emergency requiring early recognition, rapid haemorrhage control, balanced blood-product resuscitation and coordinated multidisciplinary care.
Approximately 4,700 cases of traumatic major haemorrhage are reported annually in England and Wales. Outside major trauma centres, gastrointestinal bleeding is also extremely common, with an estimated patient presenting to a United Kingdom hospital approximately every six minutes.
Although dramatic external bleeding is usually easy to recognise, significant internal haemorrhage may initially be clinically subtle. Emergency clinicians must therefore maintain a high index of suspicion and activate the local major haemorrhage protocol early when life-threatening bleeding is suspected.
Major haemorrhage may be defined as life-threatening bleeding that is likely to require massive transfusion.
Traditional definitions include:
These definitions are difficult to calculate during active resuscitation. Most local major haemorrhage protocols therefore use a combination of suspected ongoing bleeding and physiological deterioration, such as:
Clinical judgement remains essential. The protocol should be activated before profound cardiovascular collapse develops.
Major haemorrhage should be considered early in patients with:
A useful approach when searching for the source of bleeding is:
Blood on the floor and four more
This prompts consideration of:
The alternative mnemonic SCALPeR may also be used to structure the search for occult blood loss.
Hypotension is often a late sign of haemorrhagic shock. Equally, the absence of tachycardia does not exclude significant blood loss.
Some patients with severe haemorrhage may develop:
The initial response to volume loss is usually vasoconstriction and tachycardia. This may subsequently be followed by vagally mediated bradycardia, which may still be reversible.
Bradycardia should not automatically be interpreted as evidence of irreversible or terminal shock.
Older adults may have severe haemorrhage despite apparently acceptable observations. They may have limited cardiovascular reserve, take rate-limiting medication or fail to mount a typical tachycardic response.
In older trauma patients, a systolic blood pressure below 110 mmHg or a heart rate above 90 beats per minute may represent significant physiological deterioration.
Pregnancy produces major physiological changes that can mask blood loss.
Increased circulating blood volume, vascularity and cardiac output mean that more than 35% of the circulating blood volume may be lost before classic signs of haemorrhagic shock become apparent.
Anticoagulant and antiplatelet medication can increase the severity and duration of bleeding. Emergency clinicians should establish:
Reversal should follow local guidance and, where appropriate, early haematology advice.
Investigations should occur alongside resuscitation and must not delay definitive haemorrhage control.
Focused assessment with sonography in trauma may identify free intraperitoneal or pericardial fluid.
It has good specificity but insufficient sensitivity to exclude intra-abdominal bleeding. A negative scan must not be used as a rule-out test when clinical concern remains high.
Whole-body trauma computed tomography may identify otherwise occult injuries and sources of haemorrhage in sufficiently stable patients.
An unstable patient with an obvious surgical source should not experience a harmful delay while awaiting computed tomography.
An elevated lactate may indicate impaired tissue perfusion. A lactate level above 4 mmol/L is associated with increased mortality.
Serial lactate measurement and lactate clearance can help assess the response to resuscitation, although treatment should be guided by the overall clinical picture.
A low haemoglobin concentration may support the diagnosis, but a normal initial haemoglobin does not exclude major haemorrhage.
During acute blood loss, whole blood is lost. The haemoglobin concentration may remain normal until fluid shifts, resuscitation or haemodilution occur.
Blood should be obtained early for:
Where possible, group-and-save and cross-match samples should be collected before donor blood is administered.
Once major haemorrhage is suspected, the immediate question should be:
Who can definitively stop the bleeding?
Call for senior help immediately.
Depending on the source, this may include:
Definitive haemorrhage control must occur in parallel with resuscitation.
These may include:
Adequate vascular access is essential. Two large-bore peripheral cannulas are generally preferable initially. In profound shock, intraosseous access or central venous access may be required, provided this does not delay blood-product administration or definitive haemorrhage control.
Damage-control resuscitation aims to control bleeding while preventing or correcting physiological deterioration.
Its principal components are:
Permissive hypotension attempts to balance tissue perfusion against the risk of:
A mean arterial pressure of approximately 65 mmHg may be a reasonable initial target in selected adults until bleeding is controlled.
However, the target must be individualised. Permissive hypotension is generally inappropriate in patients requiring higher cerebral or uteroplacental perfusion pressures, including those with:
Permissive hypotension is also not routinely practised in children, as hypotension frequently represents a pre-arrest state.
Some patients require abbreviated life-saving surgery focused solely on rapid control of bleeding and contamination.
Definitive reconstruction may be delayed until:
The Emergency Department team should involve the relevant surgical specialty early and avoid unnecessary delays to theatre or interventional radiology.
Large-volume crystalloid resuscitation should be avoided in major haemorrhage.
Crystalloid administration can contribute to:
When critical bleeding is suspected, blood should be replaced with appropriately balanced blood products through the local major haemorrhage protocol.
Activation alerts the transfusion laboratory and facilitates the rapid release of:
Emergency group O blood may be immediately available in the resuscitation area. Group-specific or fully cross-matched blood should replace emergency blood as soon as it is safe and available.
Fresh frozen plasma and cryoprecipitate may require thawing. Early activation is therefore essential.
A nominated member of the resuscitation team should coordinate communication with the transfusion laboratory using closed-loop communication.
The ideal blood-product ratio is not definitively established.
British Society for Haematology guidance supports an initial red blood cell to fresh frozen plasma ratio of approximately:
Some local protocols use an initial ratio of:
This is commonly described as a 1:1:1 strategy.
Fixed-ratio resuscitation provides an appropriate starting point. Subsequent treatment should be guided by:
Tranexamic acid should be given as early as possible in significant traumatic bleeding and within three hours of injury.
A commonly used adult regimen is:
The mortality benefit is greatest when treatment is given early and diminishes as the three-hour point approaches.
Tranexamic acid is not routinely recommended for gastrointestinal bleeding.
The HALT-IT trial demonstrated no mortality benefit and identified potential harm, including an increased risk of thromboembolic events and seizures.
Red blood cells restore oxygen-carrying capacity and circulating volume.
Emergency group O negative or group O positive blood may be used according to the patient’s age, sex and local transfusion policy.
Fresh frozen plasma contains all soluble coagulation factors.
An adult treatment dose is approximately 15 mL/kg, often equivalent to three or four units.
Platelets support primary haemostasis and clot formation.
They should be administered according to the major haemorrhage protocol, platelet count, clinical bleeding and viscoelastic testing where available.
Cryoprecipitate contains:
It is commonly administered when fibrinogen is reduced or when significant ongoing bleeding suggests fibrinogen depletion.
Stored blood products contain citrate. During rapid or massive transfusion, citrate binds ionised calcium and may produce clinically important hypocalcaemia.
Hypocalcaemia can cause:
Ionised calcium should be measured repeatedly using blood-gas analysis.
Calcium replacement should follow the local major haemorrhage protocol. Calcium chloride is often preferred during profound haemorrhagic shock because it contains more elemental calcium than calcium gluconate, but it should ideally be administered through reliable venous access because extravasation may cause tissue injury.
In major haemorrhage, untreated hypocalcaemia is generally more dangerous than cautious calcium replacement.
Rapid administration of older stored red blood cells may cause hyperkalaemia, particularly in:
Potassium should be monitored on serial blood gases.
Rapid administration of unwarmed blood can produce severe hypothermia. Blood warmers and rapid infusers must be correctly connected, powered and checked during use.
Potential complications include:
These diagnoses can be difficult to recognise during active haemorrhage. Any unexplained deterioration should prompt reassessment.
The lethal triad consists of:
These processes amplify one another and are associated with poor outcomes. Prevention should begin immediately rather than waiting until all three are established.
Hypothermia impairs platelet function and reduces the activity of coagulation enzymes.
Actions include:
Acidosis usually reflects inadequate tissue perfusion and ongoing shock.
Severe acidosis reduces the effectiveness of the coagulation system and contributes to haemodynamic deterioration.
Management should focus on:
The definitive treatment for haemorrhage-related metabolic acidosis is restoration of tissue perfusion and control of bleeding.
Coagulopathy in major haemorrhage is multifactorial and may result from:
A normal initial coagulation screen does not exclude evolving coagulopathy.
Conventional coagulation tests:
A prothrombin time or activated partial thromboplastin time greater than 1.5 times normal supports the diagnosis of coagulopathy. However, blood-product administration should not be delayed while waiting for laboratory confirmation in a patient with critical ongoing bleeding.
Thromboelastography and rotational thromboelastometry may provide more immediate information regarding:
These tests may support targeted administration of plasma, platelets, cryoprecipitate or antifibrinolytic therapy.
Acute traumatic coagulopathy may develop early after severe injury, independently of dilution, hypothermia and acidosis.
It is associated with:
Management remains centred on:
Major haemorrhage resuscitation can rapidly become chaotic. Clear allocation of roles improves safety.
Useful roles include:
Closed-loop communication should be used throughout.
The team must maintain an accurate record of:
Blood-product traceability is a legal requirement. Documentation must continue when the patient moves from the Emergency Department to theatre, interventional radiology or intensive care.
The major haemorrhage protocol should be formally stood down when:
The transfusion laboratory should be informed immediately so that unused blood products can be safely returned and laboratory staff can resume routine activity.
When faced with major haemorrhage:
Major haemorrhage is a time-critical emergency in which early recognition and decisive action save lives.
The Emergency Department team should:
Regular multidisciplinary simulation and major haemorrhage “fire drills” can identify system weaknesses and improve staff familiarity with the local protocol before the next critical case occurs.