Management of Dilutional Coagulopathy
Dilutional coagulopathy should be prevented through early infusion of fresh frozen plasma (FFP) during massive hemorrhage resuscitation, with aggressive warming, correction of acidosis, and maintenance of fibrinogen levels above 1.5 g/L. 1
Understanding Dilutional Coagulopathy
Dilutional coagulopathy occurs when volume replacement with red cells, crystalloid, and plasma expanders is performed without sufficient infusion of FFP and platelets, leading to reduced platelets, fibrinogen, and other coagulation factors. 1 This is distinct from consumptive coagulopathy and represents a preventable complication of massive hemorrhage management. 1
Immediate Assessment and Monitoring
Laboratory Evaluation
- Obtain baseline coagulation studies including PT, aPTT, and Clauss fibrinogen (not derived fibrinogen, which is misleading). 1
- Fibrinogen level is more sensitive than PT and aPTT for detecting developing dilutional coagulopathy. 1
- Consider near-patient testing with thromboelastography (TEG) or thromboelastometry (ROTEM) if available. 1
Critical Thresholds
- Fibrinogen levels below 1 g/L are usually insufficient in massive hemorrhage; target levels above 1.5 g/L. 1
- Platelet count below 50 × 10⁹/L is strongly associated with hemostatic compromise and microvascular bleeding; maintain minimum target of 75 × 10⁹/L. 1
Prevention Strategy
Early Component Therapy
The cornerstone of preventing dilutional coagulopathy is early infusion of FFP during resuscitation. 1 This should begin before significant dilution occurs, not after coagulopathy develops.
Resuscitation Principles
- Use warmed blood and blood components for fluid resuscitation. 1
- Establish largest bore IV access possible, including central access. 1
- Blood availability hierarchy: O-negative/O-positive (quickest), group-specific, then cross-matched. 1
Active Management
Temperature Control
Active warming is required to prevent hypothermia-induced coagulopathy; target normothermia with core temperatures between 36-37°C. 1 Hypothermia below 34°C is associated with greater than 80% independent risk of mortality after controlling for shock, coagulopathy, and injury severity. 1
- Remove wet clothing immediately. 1
- Increase ambient temperature. 1
- Use forced air warming devices. 1
- Warm all transfused fluids. 1
Physiologic Correction
Once bleeding control is achieved, aggressively normalize blood pressure, acid-base status, and temperature, but avoid vasopressors. 1 Acidosis markedly attenuates thrombin generation and platelet function. 2
Component Therapy Targets
- Maintain platelet count ≥75 × 10⁹/L during active bleeding. 1
- Maintain fibrinogen ≥1.5 g/L (higher levels likely improve hemostasis further). 1
- Transfuse RBC, FFP, and platelets early, preferably in 1:1:1 ratio. 2
Clinical Decision Points
When to Escalate to Damage Control
Employ damage control surgery in patients presenting with deep hemorrhagic shock, signs of ongoing bleeding, and coagulopathy. 1
Additional triggers include:
- Temperature ≤34°C 1
- pH ≤7.2 1
- Inaccessible major anatomic injury 1
- Need for time-consuming procedures with suboptimal resuscitation response 1
Post-Resuscitation Care
Critical Care Monitoring
Following massive hemorrhage treatment, admit to critical care for monitoring of coagulation, hemoglobin, blood gases, and wound drain assessment. 1
Thromboprophylaxis
Commence standard venous thromboprophylaxis as soon as bleeding is controlled, as patients rapidly develop a prothrombotic state. 1 Temporary inferior vena cava filtration may be necessary. 1
Common Pitfalls
- Do not rely on derived fibrinogen values—they are misleading. 1
- Do not delay FFP infusion until coagulopathy develops—prevention is key. 1
- Do not use vasopressors during active resuscitation. 1
- Do not overlook hypothermia prevention—it profoundly impairs coagulation. 1, 2
- Do not assume normal coagulation tests exclude coagulopathy in trauma—activation of anticoagulant pathways may occur without abnormal tests. 1