What is Disseminated Intravascular Coagulation (DIC)?

What is Disseminated Intravascular Coagulation (DIC)?

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterized by widespread intravascular activation of coagulation with loss of localization, arising from various underlying diseases, which can originate from and cause damage to the microvasculature, leading to organ dysfunction if sufficiently severe. 1

Core Pathophysiologic Features

DIC represents a systemic coagulation disorder with three simultaneous, paradoxical processes:

• Widespread microvascular thrombosis occurs due to uncontrolled activation of the coagulation cascade, leading to fibrin deposition throughout the vasculature 2, 3
• Consumption coagulopathy develops as platelets and coagulation factors (including fibrinogen) are depleted through ongoing clot formation 1
• Life-threatening hemorrhage results from the depletion of clotting factors and platelets, creating a bleeding tendency despite the underlying prothrombotic state 2, 3

Essential Diagnostic Requirement

A mandatory condition for diagnosing DIC is the presence of an underlying disorder known to be associated with DIC - DIC is not a disease itself but rather a mechanistic process involved in disease progression 1

Critical Role of Endothelial Dysfunction

Endothelial injury is an essential component of DIC pathogenesis, though current diagnostic criteria focus primarily on coagulation abnormalities:

• Endothelial dysfunction precedes the coagulation disorder and represents a critical early event in DIC development 1
• The degree of endothelial involvement varies by underlying disease: highly significant in sepsis-induced coagulopathy, moderate in trauma-induced coagulopathy, and variable in hematologic malignancy-associated coagulopathy 1
• Endothelial damage converts the normally anticoagulant endothelium to a procoagulant state, exposing tissue factor and activating the coagulation cascade 4

Common Underlying Causes

The most frequent triggers of DIC include:

• Sepsis is the most common cause, with mortality of 24.8% in septic patients who develop DIC according to Japanese nationwide data 1, 5
• Malignancies, particularly pancreatic cancer and adenocarcinomas, pose particularly high risks 5
• Trauma with tissue injury and shock 5
• Obstetric complications including eclampsia, placental abruption, and amniotic fluid embolism 2, 3
• Acute liver failure through multiple mechanisms including decreased clearance of activated coagulation factors 5

Characteristic Laboratory Findings

The decompensated coagulation disorder in overt DIC is identified by:

• Thrombocytopenia from platelet consumption 1
• Prolonged prothrombin time reflecting consumption of coagulation factors 1
• Elevated fibrin-related markers (D-dimer, fibrin degradation products) indicating ongoing fibrin formation and breakdown 1
• Decreased fibrinogen levels in advanced cases, though fibrinogen may initially be normal or elevated as an acute phase reactant 1

Clinical Significance and Mortality

DIC remains a refractory condition with high mortality, making early detection critical:

• Early detection facilitates potential therapeutic approaches and improves outcome prediction in critically ill patients 1
• The International Society on Thrombosis and Haemostasis (ISTH) recommends screening for sepsis-induced coagulopathy (the compensated phase of DIC) in patients with sepsis 1, 5
• Organ dysfunction develops when microvascular thrombosis becomes sufficiently severe, representing the most serious complication beyond bleeding 1

Key Clinical Pitfall

The paradoxical nature of DIC creates diagnostic challenges: patients simultaneously have both thrombotic and bleeding tendencies, requiring careful assessment of the dominant clinical picture rather than assuming bleeding is the primary concern based on laboratory abnormalities alone 2, 3