Haemorrhage control and major haemorrhage protocol

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Major haemorrhage is a clinical state in which bleeding threatens life and demands coordinated transfusion and source control. Recognition combines mechanism, anatomical findings, pre-hospital loss, mental state, skin perfusion, pulse and pressure trends, lactate or base deficit and response to initial blood. No single activation score is universally decisive. Young or pregnant patients may compensate until sudden collapse, whereas beta-blockade, pacing and frailty can remove the expected tachycardia.

External control is immediate and mechanical. Apply direct pressure through an appropriate dressing, pack deep junctional wounds where trained, and use a commercial limb tourniquet for life-threatening extremity bleeding not controlled promptly. Place it proximal to the wound, not across a joint, tighten until bleeding stops and document the time. Do not repeatedly loosen it outside a controlled surgical plan. Splint long-bone fractures and use a pelvic binder correctly when pelvic bleeding is suspected.

Protocol activation creates a system rather than merely ordering red cells. One caller gives patient identifiers, location and anticipated urgency; transfusion prepares emergency or group-specific components; portering and laboratory teams sustain delivery and testing; a senior clinician coordinates blood, haemostatic therapy, warming and the route to haemorrhage control. Local packs differ, so clinicians must know component ratios, emergency-release procedure, cool-chain rules and explicit stand-down communication.

Resuscitation and haemostasis proceed together. Restrictive volume replacement during active bleeding avoids forcing blood pressure high before control, but targets change with traumatic brain injury, spinal cord injury, pregnancy and chronic hypertension. Blood components are preferred to large crystalloid volumes when available. Tranexamic acid acts on fibrinolysis and is time-dependent. Fibrinogen, platelet and plasma therapy follows the major-haemorrhage protocol and laboratory or viscoelastic results as these become available.

Temperature, calcium and acid-base physiology are active treatments. Fully expose only as needed, remove wet material, raise ambient temperature, use forced-air warming and pass blood through an approved warmer. Measure ionised calcium repeatedly because citrate load can produce hypotension and impaired clotting. Correcting hypoperfusion and haemorrhage is the main treatment for acidosis; bicarbonate does not replace flow. Mechanical ventilation and anaesthesia may worsen venous return, so coordinate induction with blood availability.

Definitive control depends on source and physiology. Thoracic bleeding may need thoracotomy, abdominal injury laparotomy or embolisation, pelvic bleeding binder plus packing, fixation or angioembolisation, and limb vascular injury immediate surgery. A stable or responding patient may undergo CT to map the source. A non-responder with a credible source usually needs the shortest route to an operating, interventional or hybrid environment with resuscitation continuing en route.

After apparent haemostasis, recurrent shock remains possible. Recheck wounds, drains, abdomen, pelvis and limb compartments; repeat blood gas, haemoglobin, platelets, coagulation, fibrinogen, calcium, potassium and temperature. Distinguish continued bleeding from transfusion reaction, tension pneumothorax, cardiogenic failure and vasoplegia. Once the major-haemorrhage protocol is stopped, ensure laboratory specimens, transfusion records, component traceability and a plan for thromboprophylaxis when bleeding risk permits.

Key points

Control visible catastrophic bleeding first with firm direct pressure, wound packing or an approved tourniquet; record tourniquet placement and application time clearly.
Search the chest, abdomen, pelvis, retroperitoneum and long bones for concealed loss; a small external wound does not explain away abnormal physiology.
Activate the major-haemorrhage protocol from clinical suspicion and response, not after laboratory confirmation, and state the delivery location and responsible clinician.
Use blood components in the locally specified balanced pack, minimise crystalloid during active bleeding and obtain rapid definitive source control through surgery, embolisation or both.
Give tranexamic acid as soon as possible: adult trauma regimen 1 g IV over 10 minutes then 1 g over 8 hours, with treatment started within 3 hours of injury.
Prevent the lethal physiology of coagulopathy by active warming, warmed blood, serial fibrinogen or viscoelastic assessment and repeated ionised-calcium measurement with protocol-led replacement.
Take samples before transfusion if this causes no delay, but never wait for a normal early haemoglobin, INR or platelet count before controlling obvious major bleeding.
Stand down the protocol explicitly once haemostasis and physiology are credible, notify transfusion, reconcile unused components and continue surveillance for recurrent bleeding and transfusion harm.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Compressible bleeding

Scalp and limb wounds, traumatic amputation and some junctional injuries cause visible loss that can often be reduced by pressure, packing or tourniquet.

Cavity haemorrhage

Thoracic, intraperitoneal and retroperitoneal injury can conceal litres of blood, with pelvic disruption, solid-organ damage and major vascular injury important causes.

Medication and disease

Anticoagulants, antiplatelet drugs, liver dysfunction, inherited bleeding disorders and frailty reduce haemostatic reserve or alter the expected physiological response.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Reduced oxygen delivery
Falling circulating volume and red-cell mass reduce cardiac output and tissue oxygen delivery, producing anaerobic metabolism, lactate accumulation and organ dysfunction.
2
Trauma-induced coagulopathy
Severe tissue injury and shock activate anticoagulant and fibrinolytic pathways; dilution, acidosis and consumption further reduce effective clot formation.
3
Hypothermia and calcium loss
Exposure and unwarmed infusion lower temperature, while citrate in blood components binds calcium; both impair coagulation and cardiac performance.
4
Reperfusion burden
Delayed restoration after profound shock can release acid and inflammatory mediators, causing vasodilatation, myocardial depression and multiple-organ injury despite later haemostasis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

External exsanguination

Persistent pooling, soaked dressings, spurting, amputation or expanding junctional haematoma requires pressure, packing or tourniquet without waiting for observations.

Compensated shock

Anxiety, tachypnoea, cool peripheries, delayed refill and narrow pulse pressure can precede hypotension, particularly in a young otherwise healthy adult.

Concealed source

Reduced breath sounds, abdominal distension, pelvic mechanism, perineal bruising or deformed femur suggests major internal loss even without external blood.

Transient responder

Brief improvement followed by recurrent tachycardia, hypotension or lactate rise strongly supports uncontrolled haemorrhage and should accelerate source control.

Developing coagulopathy

Diffuse wound ooze, line-site bleeding, low fibrinogen, falling platelets or abnormal viscoelastic clot formation indicates haemostatic failure requiring protocol-guided correction.

Transfusion reaction

New fever, rash, wheeze, haemoglobinuria, unexpected shock or respiratory deterioration during transfusion requires immediate component cessation, identity checks and transfusion-team support while resuscitation continues.

Red flags requiring action

Uncontrolled external bleeding, expanding swelling, traumatic amputation, suspected pelvic disruption or blood loss into chest or abdomen requires immediate haemorrhage-control action.
Altered mental state, cool mottled skin, delayed refill, tachypnoea, narrowing pulse pressure, rising lactate or base deficit may identify shock before systolic hypotension develops.
Recurrent instability after blood, continued drain or wound loss, falling fibrinogen, prolonged clot initiation or low ionised calcium indicates resuscitation failure and ongoing bleeding until proven otherwise.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line blood gasFirst stepFirst line
Why
Quantify perfusion and rapidly identify calcium, potassium and acid-base danger.
Interpretation and limitations
Trend lactate or base deficit and ionised calcium rather than relying on one value; improvement supports restored flow but does not prove anatomical haemostasis.
02
Group and crossmatch
Why
Provide compatible ongoing blood-component support.
Interpretation and limitations
Send a correctly labelled sample promptly; use emergency group O components according to local policy when delay is unsafe and switch to group-specific supply when authorised.
03
FBC and conventional coagulation
Why
Measure red cells, platelets and coagulation disturbance.
Interpretation and limitations
Early haemoglobin may be normal; repeat platelet count, prothrombin time, activated partial thromboplastin time and fibrinogen as bleeding and transfusion evolve.
04
Preferred viscoelastic testing when availablePreferred
Why
Guide targeted haemostatic replacement during active major bleeding.
Interpretation and limitations
Rapid clot initiation, strength and lysis patterns may support protocol-directed plasma, fibrinogen or platelet decisions, but sampling and interpretation must not delay source control.
05
Focused bedside imaging
Why
Direct immediate intervention when CT is unsafe.
Interpretation and limitations
Chest or pelvic radiography and eFAST can reveal actionable sites, yet negative ultrasound cannot exclude retroperitoneal or early abdominal bleeding.
06
Definitive contrast CTDefinitive
Why
Map bleeding and plan surgery or embolisation in a suitable responder.
Interpretation and limitations
Active arterial contrast extravasation, solid-organ injury and vascular disruption guide treatment; persistent non-response should bypass imaging that delays haemostasis.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Obstructive shock

Tension pneumothorax and tamponade cause hypotension with impaired venous return and demand immediate mechanical treatment rather than escalating transfusion alone.

Neurogenic shock

Spinal injury may cause hypotension, relative bradycardia and warm skin, but haemorrhage must still be actively excluded before attributing shock to sympathetic loss.

Cardiogenic shock

Myocardial contusion, infarction or pre-existing cardiac disease may produce pulmonary congestion, arrhythmia and poor response to volume despite no major bleeding source.

Septic or anaphylactic shock

Vasodilatation from infection, drug reaction or transfusion reaction can mimic worsening haemorrhage and is distinguished by timing, skin, airway and temperature features.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ImmediateStop accessible bleeding and activateFirst stepLife-threatening bleeding is seen or strongly suspected from mechanism and physiology.

1Apply direct pressure, haemostatic packing or a tourniquet as anatomically appropriate, splint long-bone injury and position a pelvic binder over the greater trochanters when indicated.
2Call the major-haemorrhage protocol with patient identifiers and location, obtain large-bore intravenous or intraosseous access and send urgent blood samples without delaying transfusion.
3Begin warmed blood-component support, administer timely tranexamic acid and prevent heat loss while the team identifies the likely internal source.
4Request senior trauma, anaesthetic, surgical, interventional-radiology and transfusion input early and select the shortest safe route to haemorrhage control.

02OngoingCorrect haemostatic physiologyBleeding continues while components and source-control capability are mobilised.

1Follow the local balanced component pack initially, avoiding large crystalloid loads that dilute clotting factors and increase oedema.
2Repeat blood gas, ionised calcium, temperature, full blood count, coagulation and fibrinogen or viscoelastic testing at protocol-defined intervals.
3Replace calcium, fibrinogen, plasma and platelets according to the major-haemorrhage algorithm and results, while warming every suitable infusion.
4Use response to each cycle to refine destination; persistent or transient response demands faster mechanical source control, not simply a larger transfusion.

03ResolutionStand down safelyBleeding is controlled and haemodynamics, perfusion and laboratory trends are stabilising.

1Announce protocol stand-down to transfusion and all clinical teams, return unused products under cool-chain rules and reconcile every unit administered.
2Continue surveillance for recurrent haemorrhage, hypocalcaemia, hyperkalaemia, hypothermia, lung injury, circulatory overload and haemolytic or allergic reaction.
3Review all lines, drains, wounds and compartments and repeat haemoglobin and coagulation testing according to loss, procedure and clinical course.
4Document source-control completion, future transfusion thresholds, anticoagulant plan and when mechanical then pharmacological thromboprophylaxis can safely begin.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Inhibits fibrinolysis and reduces bleeding mortality when used early in adults with active or suspected significant traumatic haemorrhage.

Tranexamic acid

Administer 1 g intravenously over 10 minutes, followed immediately by 1 g by intravenous infusion over 8 hours; start treatment as early as possible and no later than 3 hours after traumatic injury.

Avoid routine late administration beyond 3 hours unless hyperfibrinolysis is specifically diagnosed; use renal dose adjustment for maintenance exposure and do not let infusion delay operative or radiological haemostasis.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Exsanguination

Delay in recognising bleeding, protocol activation or definitive control causes cardiac arrest and death that blood-component replacement alone cannot prevent.

Dilutional coagulopathy

Large volumes of crystalloid or red cells without appropriate haemostatic support dilute platelets and coagulation factors and increase tissue oedema.

Transfusion complications

Hypocalcaemia, hypothermia, hyperkalaemia, acidosis, acute lung injury, circulatory overload and incompatible transfusion require active prevention and surveillance.

Compartment and organ injury

Ongoing tissue bleeding can create limb compartment syndrome, abdominal hypertension, renal failure, myocardial injury and secondary brain ischaemia.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record observations and perfusion response frequently, with serial lactate or base deficit rather than relying on blood pressure alone.
Measure temperature and ionised calcium during ongoing transfusion, replacing deficiencies under the local protocol and checking the response.
Repeat FBC, coagulation and fibrinogen or viscoelastic testing after resuscitation cycles and after source control.
Maintain accurate component traceability, estimated blood loss, tourniquet and binder timings, TXA time and cumulative crystalloid exposure.
After stand-down, watch for recurrent bleeding, compartment syndrome, transfusion-associated lung injury, overload, hyperkalaemia and acute kidney injury.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Pressure can precede hypotension

Compensation preserves systolic blood pressure at the cost of skin, renal and gut perfusion, so normal pressure does not exclude dangerous loss.

Blood is a bridge

Components restore oxygen carriage and clot substrates, but only mechanical or procedural haemostasis definitively ends blood loss.

Calcium is functional

Citrate-related hypocalcaemia impairs myocardial contraction and coagulation and can worsen apparent resistance to resuscitation.

Warm every stage

Preventing heat loss in the room, patient, infusions and transfers is more effective than attempting late correction of profound hypothermia.

Stand-down needs ownership

Uncommunicated cessation wastes scarce components and risks errors, while premature cessation leaves recurrent haemorrhage unsupported.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a low haemoglobin or abnormal INR before activating a clinically indicated protocol.
02
Covering a bleeding wound with repeated dressings without direct pressure, packing or tourniquet control.
03
Giving litres of cold crystalloid while blood and definitive haemostasis are available.
04
Counting red-cell units without monitoring temperature, calcium, fibrinogen, platelets and acid-base trends.
05
Interpreting brief pressure improvement as proof that internal bleeding has stopped.
06
Failing to notify transfusion explicitly when the protocol is complete or the patient changes location.