Massive haemorrhage in theatre
- Crisis
When a patient bleeds heavily during surgery, the team stops the bleeding, replaces blood with balanced blood products and keeps the patient warm.
What it is
Massive haemorrhage is blood loss fast enough to threaten life: roughly the loss of a whole blood volume within a day, half of it within a few hours, or bleeding that needs rapid, repeated transfusion to keep the circulation going. In theatre it happens in trauma, obstetrics, vascular, liver and cancer surgery, or when a major vessel is injured. The patient falls into a vicious circle known as the lethal triad: hypothermia, acidosis and coagulopathy, each worsening the others; low ionised calcium from the citrate in stored blood makes it worse. Modern management is damage-control resuscitation: surgical control of bleeding as the priority, early activation of the hospital's massive transfusion protocol, blood products given in a balanced ratio close to whole blood (red cells, plasma and platelets around 1:1:1) instead of large volumes of crystalloid, early tranexamic acid, replacement of fibrinogen and calcium, and active warming. Until bleeding is controlled, a lower-than-normal blood pressure (permissive hypotension) may be accepted in selected trauma patients, but not with head or spinal cord injury.
How to recognise it
- Rapid blood loss in suction canisters, swabs and drapes, or a surgeon reporting uncontrolled bleeding.
- Tachycardia, falling blood pressure and pulse pressure, a shock index (heart rate over systolic pressure) above one.
- Falling end-tidal carbon dioxide and wide swings of the arterial trace with ventilation.
- Cold, pale peripheries, falling urine output and a rising lactate.
- Oozing from wounds and line sites, a sign that coagulopathy has begun.
Why it happens
- Loss of circulating volume lowers venous return, cardiac output and oxygen delivery, so tissues switch to anaerobic metabolism and lactic acidosis follows.
- Clotting factors and platelets are consumed and diluted by crystalloid and red cells alone.
- Hypothermia from exposure and cold fluids slows the clotting enzymes and platelet function.
- Acidosis further impairs clotting enzymes and heart contraction.
- Citrate in stored blood binds calcium, which is needed for clotting and for heart and vessel tone; stored blood can also raise potassium.
What to do at once
- Declare major haemorrhage and call for help — saying it aloud mobilises the team, the blood bank and a senior surgeon.
- Ask the surgeon for control: pressure, packing, clamps, damage-control surgery — no transfusion keeps up with uncontrolled bleeding.
- Activate the massive transfusion protocol and name a runner and a communicator — the blood bank prepares packs in a fixed ratio.
- Secure wide-bore venous access and an arterial line — flow depends on cannula size, and beat-to-beat pressure guides resuscitation.
- Give uncrossmatched group O red cells until group-specific blood arrives — delay costs more than the small risk of unmatched blood.
- Transfuse red cells, plasma and platelets in a balanced ratio through a rapid warmer — this replaces what is lost, not only the volume.
- Give tranexamic acid early — it blocks fibrinolysis and saves lives in trauma and postpartum bleeding.
- Replace calcium and fibrinogen guided by tests — citrate lowers calcium and fibrinogen falls first in heavy bleeding.
- Warm the patient and all fluids and correct acidosis — cold and acid stop clotting factors working.
- Send blood tests every half hour or so: blood count, coagulation, fibrinogen, gases, calcium, potassium — results steer the next packs.
The lethal triad and its fourth partner, and how each is fought
| Problem | Why it matters | What the team does |
|---|---|---|
| Hypothermia | Slows clotting enzymes and platelets | Fluid warmer, forced-air warming, warm theatre, cover the patient |
| Acidosis | Weakens clotting and heart contraction | Restore perfusion with blood, stop the bleeding |
| Coagulopathy | Bleeding becomes generalised | Balanced products, tranexamic acid, fibrinogen replacement |
| Low ionised calcium | Citrate binds calcium; vessels and clotting fail | Measure and replace calcium during transfusion |
Costly mistakes
- Activating the protocol too late, or waiting for laboratory results before giving plasma and platelets.
- Pouring in large volumes of crystalloid, causing dilution, cooling and tissue oedema.
- Forgetting calcium, so the patient stays hypotensive and coagulopathic despite products.
- Not warming fluids or the patient, allowing hypothermia to undo the transfusion.
- Forgetting to stand down the protocol once bleeding is controlled, wasting scarce blood.
Next step
- Once bleeding is controlled, stand down the massive transfusion protocol and switch to test-guided, targeted transfusion.
- Keep a senior anaesthetist and surgeon involved; consider interventional radiology or a return to theatre if bleeding restarts.
- Transfer to intensive care for monitoring of coagulation, potassium, calcium, lactate and temperature.
- Watch for transfusion reactions, circulatory overload, transfusion-related lung injury and acute kidney injury in the following hours and days.
- Record every product given with its unit identifiers, inform the patient and family, and debrief the team.
Test yourself
Think of the answer, then tap the question to see it.
What ratio of blood products is used in damage-control resuscitation for massive haemorrhage?
Red cells, plasma and platelets in a balanced ratio close to 1:1:1, which approximates whole blood, with limited crystalloid.
What are the three parts of the lethal triad in massive haemorrhage?
Hypothermia, acidosis and coagulopathy, each worsening the others; low ionised calcium from transfused citrate adds a fourth problem.
Why must calcium be monitored and replaced during massive transfusion?
The citrate used to store blood binds calcium; low ionised calcium impairs clotting, heart contraction and vascular tone.
In which patients is permissive hypotension contraindicated?
In traumatic brain injury and spinal cord injury, where low blood pressure reduces perfusion of the injured nervous tissue and worsens outcome.
Elsewhere in DurgiPedia
- Blood groups, transfusion and transfusion reactions
- Coagulation tests: PT/INR, aPTT and platelets
- Shock physiology
- Blood transfusion: bedside checks, monitoring and reactions
- Coagulation tests: PT/INR, aPTT, fibrinogen and D-dimer
- Shock: the clinical signs and the types
Connections
Educational content; it does not replace supervised training, your institution's protocols or the anaesthetist's or intensivist's decision. It contains no doses and no ventilator or infusion settings.
Sources: Massive Transfusion (StatPearls (NCBI Bookshelf), 2025); Permissive Hypotension (StatPearls (NCBI Bookshelf), 2024).
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Representative model, for educational purposes only.
