Etiology of Increased Plasma D-Dimers

Arterial Thromboembolic Disease

• Acute Limb Ischemia (see Acute Limb Ischemia)
• Atrial Fibrillation (AF) (see Atrial Fibrillation)
• Intracardiac Thrombus (see Intracardiac Thrombus)
• Ischemic Cerebrovascular Accident (CVA) (ee Ischemic Cerebrovascular Accident)
• Myocardial Infarction (MI) (see Coronary Artery Disease)

Venous Thromboembolic Disease

• Deep Venous Thrombosis (DVT) (see Deep Venous Thrombosis)
• Pulmonary Embolism (PE) (see Acute Pulmonary Embolism)

Renal

• Acute Kidney Injury (AKI) (see Acute Kidney Injury)
• Chronic Kidney Disease (CKD) with Cardiovascular Disease (see Chronic Kidney Disease)
• Nephrotic Syndrome (see Nephrotic Syndrome)
• Renal Vein Thrombosis (see Renal Vein Thrombosis)

Obstetric

• Pre-Eclampsia/Eclampsia (see Pre-Eclampsia, Eclampsia)
• Pregnancy (see Pregnancy)

Hyperfibrinolytic State (see Hyperfibrinolytic States)

Primary Hyperfibrinolytic States

• Alpha-2 Antiplasmin Deficiency (see Alpha-2 Antiplasmin Deficiency)
• Plasminogen Activator Inhibitor-1 (PAI-1) Deficiency (see Plasminogen Activator Inhibitor-1 Deficiency)

Secondary Hyperfibrinolytic States

• Cardiopulmonary Bypass (see Cardiopulmonary Bypass)
  • Coagulopathy after cardiopulmonary bypass is multi-factorial and may include a component of hyperfibrinolysis
• Cirrhosis (see Cirrhosis): due to decreased tPA clearance from the circulation and decreased alpha-2 antiplasmin synthesis by the liver
• Disseminated Intravascular Coagulation (DIC) (see Disseminated Intravascular Coagulation): due to release of tPA, resulting in the generation of plasmin at site of injury
  • Acute Promyelocytic Leukemia (APML) (see Acute Promyelocytic Leukemia)
  • Hemophagocytic Syndrome (see Hemophagocytic Syndrome)
  • Prostate Cancer (see Prostate Cancer)
    • DIC with secondary hyperfibrinolysis
    • Excessive production of urinary-type plasminogen activators by the malignant cells
    • Decreased alpha-2 antiplasmin synthesis
• Factor XI Deficiency (see Factor XI Deficiency): due to decreased thrombin synthesis, resulting in decreased activation of thrombin activatable fibrinolysis inhibitor (TAFI)
• Heat Stroke (see Heat Stroke)
• Hemophilia A (Factor VIII Deficiency) (see Hemophilia A): due to decreased thrombin synthesis, resulting in decreased activation of thrombin activatable fibrinolysis inhibitor (TAFI)
• Hemophilia B (Factor IX Deficiency) (see Hemophilia B): due to decreased thrombin synthesis, resulting in decreased activation of thrombin activatable fibrinolysis inhibitor (TAFI)
• Orthotopic Liver Transplantation (see Liver Transplant): due to decreased tPA clearance from the circulation and decreased alpha-2 antiplasmin synthesis (both of which occur during the anhepatic period of the transplant)
• Trauma
• Thrombolytics (see Thrombolytics): due to depletion of alpha-2 antiplasmin, plasminogen, and fibrinogen
  • Streptokinase (see Streptokinase)
  • Urokinase (see Urokinase)

Other

• Congestive Heart Failure (CHF) (see Congestive Heart Failure)
• Malignancy
• Sickle Cell Disease Vaso-Occlusive Crisis (see Sickle Cell Disease)
• Surgery: with tissue ischemic/necrosis
• Systemic Inflammatory Response Syndrome (SIRS)/Sepsis (see Sepsis)
• Venous Malformation

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References

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