TBI Associated Coagulopathy 

Definition

TBI-associated coagulopathy refers to any abnormality in coagulation parameters (PT/INR, aPTT, platelet function, fibrinogen, or viscoelastic tests) occurring early after TBI, attributable directly to brain injury–induced pathophysiologic mechanisms.

Epidemiology & Clinical Importance

• Occurs in 25–60% of moderate–severe TBI
• Can be present on arrival to ED
• Strongly associated with:
• Progressive intracranial hemorrhage
• Raised ICP
• Need for neurosurgical intervention
• Increased mortality (2–4×)

Pathophysiology 

TBI-AC is multifactorial and evolves over time.

1. Tissue Factor (TF) Release – Initiating Event

• Brain tissue is rich in tissue factor
• TBI → disruption of blood–brain barrier → massive TF release
• TF activates extrinsic coagulation pathway
• Leads to thrombin burst

# Key exam line:

The brain is the most thrombogenic organ in the body.

2. Consumptive Coagulopathy

• Excess thrombin → widespread clot formation
• Consumption of:
• Fibrinogen
• Platelets
• Coagulation factors
• Results in secondary hypocoagulability

3. Hyperfibrinolysis 

• Endothelial injury → release of tPA
• Excess plasmin generation
• Rapid clot breakdown

Manifestations:

• Low fibrinogen
• Elevated D-dimer
• Poor clot strength on TEG/ROTEM

# Important:
Early TBI is often hyperfibrinolytic, later phases may become hypofibrinolytic / shutdown.

4. Protein C Pathway Activation

• Thrombin–thrombomodulin complex activates protein C
• Activated protein C:
• Inhibits factors Va and VIIIa
• Suppresses PAI-1 → ↑ fibrinolysis

This explains:

• Anticoagulation + hyperfibrinolysis simultaneously

5. Platelet Dysfunction (Even with Normal Count)

• Platelets become functionally impaired
• Poor aggregation and adhesion
• Not detected by routine platelet count

# Exam pearl:

Normal platelet count does NOT exclude platelet dysfunction in TBI.

6. Endothelial Glycocalyx Shedding

• Catecholamine surge → endothelial damage
• Loss of glycocalyx → auto-heparinization
• Results in endogenous anticoagulation

7. Secondary Aggravating Factors

These worsen but do not initiate TBI-AC:

• Hypothermia
• Acidosis
• Hemodilution
• Shock / hypoperfusion

Temporal Evolution of TBI-AC

Laboratory Findings

Conventional Tests

• ↑ PT / INR
• ↑ aPTT
• ↓ fibrinogen
• Platelet count: normal or ↓ (function impaired)

# Limitations:

• Poor sensitivity for early platelet dysfunction
• Delayed results

Viscoelastic Tests 

TEG / ROTEM findings:

• Prolonged R time → factor deficiency
• Reduced MA → platelet dysfunction
• Increased LY30 → hyperfibrinolysis

# Exam point:
Viscoelastic testing allows goal-directed transfusion in TBI.

Clinical Consequences

• Expansion of intracranial hematoma
• New hemorrhagic lesions
• Raised ICP
• Failure of surgical hemostasis
• Increased mortality

Management Principles (Guideline-Based, Exam-Focused)

1. Early Recognition

• Screen all moderate–severe TBI
• Do not wait for massive bleeding

2. Avoid Secondary Insults

• Maintain:
• Normothermia
• pH > 7.30
• Ionized calcium normal

3. Targeted Blood Component Therapy

4. Tranexamic Acid (TXA)

• Most effective if given within 3 hours
• Benefit seen mainly in:
• Mild–moderate TBI
• Hyperfibrinolytic states

# Avoid late indiscriminate use (risk of thrombosis).

5. Neurosurgical Considerations

• Correct coagulopathy before surgery
• Maintain platelets >100,000/µL for neurosurgery
• INR preferably <1.4

 Exam –

• TBI-AC is primary and brain-driven
• Can occur without systemic shock
• Platelet function matters more than count
• Early phase often hyperfibrinolytic
• Viscoelastic testing is superior to PT/INR
• Early TXA only — timing is critical