What is coagulopathy?

What is Coagulopathy?

Coagulopathy is a disorder of blood clotting characterized by impaired clot formation that can manifest as either excessive bleeding or, less commonly, abnormal thrombosis, resulting from dysfunction of coagulation factors, platelets, or fibrinolytic pathways. 1, 2

Core Definition and Clinical Manifestations

Coagulopathy represents a pathological state where the normal hemostatic mechanisms fail to maintain appropriate blood clotting. 3 The condition presents clinically as:

• Bleeding manifestations: Oozing from mucosal surfaces, venipuncture sites, or surgical wounds 4
• Laboratory abnormalities: Prolonged prothrombin time (PT), elevated partial thromboplastin time (PTT), decreased platelet counts, and reduced fibrinogen levels 1
• Impaired thrombin generation: The fundamental defect underlying coagulopathic bleeding 1

Pathophysiologic Mechanisms

Coagulopathy develops through multiple interconnected pathways that vary by clinical context:

In Trauma and Massive Hemorrhage

Early acute traumatic coagulopathy occurs in approximately one-third of severely injured patients upon hospital admission and represents a distinct entity from disseminated intravascular coagulation. 1, 4

The pathophysiology involves:

• Bleeding-induced shock: Tissue hypoperfusion triggers activation of anticoagulant pathways 1, 4
• Tissue injury-related thrombin-thrombomodulin complex generation: Activates protein C anticoagulant pathways 1, 4
• Endothelial glycocalyx degradation: Elevated syndecan-1 levels correlate with coagulopathy severity 1, 4
• Activation of fibrinolytic pathways: Hyperfibrinolysis particularly in obstetric hemorrhage and cardiopulmonary bypass 1

The "Lethal Triad" Components

Three environmental factors critically worsen coagulopathy:

1. Hypothermia: Severely impairs platelet function and coagulation enzyme activities, with effects underestimated by standard laboratory testing performed at 37°C 1, 2

2. Acidosis: Even slight pH decreases (7.4 to 7.0) reduce prothrombin activation by 70%, severely compromising both coagulation enzymes and platelet function 1, 2

3. Dilution: Large volume crystalloid, colloid, or blood product infusion dilutes coagulation factors and platelets 1, 4

Dilutional Coagulopathy

All patients receiving massive transfusion are at risk of dilutional coagulopathy, which reduces platelets, fibrinogen, and other coagulation factors when volume replacement uses red cells, crystalloids, and plasma expanders without sufficient fresh frozen plasma and platelets. 1

The severity depends on both volume and type of fluids infused. 1

Consumptive Coagulopathy

Some patients develop hemostatic failure without significant dilution through consumption of coagulation factors and platelets. 1 This occurs particularly in:

• Obstetric hemorrhage (placental abruption, amniotic fluid embolus) 1
• Cardiopulmonary bypass 1
• Massive trauma with head injury 1
• Sepsis 1

Diagnostic Criteria for Severe Coagulopathy

A PT ratio >1.2 or PT >15.5 seconds indicates severe coagulopathy with significantly higher mortality and transfusion requirements. 2, 4

Additional diagnostic parameters include:

• Platelet count <100,000/μL (severe coagulopathy threshold; <50,000/μL strongly associated with microvascular bleeding) 1, 2, 4
• **Fibrinogen <1.0 g/L** (insufficient in massive hemorrhage; target >1.5 g/L recommended) 1, 4
• Markedly elevated D-dimer (3-4 fold increase indicates increased thrombin generation) 2, 4
• Thromboelastography (TEG): Provides superior bedside functional assessment compared to standard coagulation tests 2, 4

Important caveat: Standard coagulation tests may underestimate the actual extent of coagulopathy because they don't reflect in vivo coagulation on cell membranes and are performed at 37°C rather than the patient's actual body temperature. 1

Clinical Contexts Where Coagulopathy Develops

Trauma-Associated Coagulopathy

Present in 25-36% of trauma victims upon emergency department admission, correlating with injury severity and associated with mortality beyond that expected from injury alone. 1

Sepsis-Associated Coagulopathy

Ranges from subclinical hypercoagulability to acute disseminated intravascular coagulation with widespread microvascular thrombosis and consumption of platelets and coagulation proteins. 5

Massive Hemorrhage in Surgery

Frequently combines surgical bleeding (from recognizable anatomic sources) with coagulopathic bleeding (from impaired thrombin generation). 1

Intensive Care Unit Coagulopathies

Related to systemic diseases, autoimmune dysfunction, acute infection, organ dysfunction, therapeutic medications, or medical treatments. 3

Clinical Significance and Outcomes

Coagulopathy upon hospital admission significantly increases the incidence of multiple organ failure and death compared to patients with similar injury patterns without coagulopathy. 1

The condition represents:

• Leading cause of potentially preventable death in trauma (uncontrolled post-traumatic bleeding) 1
• Primary cause of early in-hospital mortality within 48 hours of admission 1
• Fatal in approximately 30% of severe upper gastrointestinal bleeding cases in liver disease 1

Key Clinical Pitfall

The terminology surrounding coagulopathy creates confusion because the same designation may represent two clinically distinct presentations—bleeding or thrombosis—depending on circumstances. 6 In acute trauma and massive hemorrhage contexts, coagulopathy primarily manifests as excessive bleeding, not thrombosis, despite laboratory evidence of increased thrombin-generating potential in vitro. 7