DIC Summary

Definition

  • Acquired coagulopathy syndrome
  • Widespread inappropriate fibrin deposition
  • Consumption of platelets & coagulation factors
  • Leads to thrombosis and bleeding

Common Causes

  • Sepsis/severe infection
  • Major trauma/burns
  • Malignancies (AML, adenocarcinoma)
  • Obstetric complications
  • Severe organ failure

Clinical Features

  • Bleeding: From ≥3 unrelated sites
  • Thrombosis: Ischemic signs
  • Organ dysfunction: Multi-organ failure

Key Lab Findings

  • ↓ Platelets, ↓ Fibrinogen
  • ↑ PT/PTT, ↑ D-dimer/FDP
  • ↑ Thrombin time
  • ↓ Coagulation factors

Management

  • Treat underlying cause
  • Replacement therapy (FFP, platelets)
  • Consider heparin in thrombotic DIC
  • Caution with antifibrinolytics

Replacement Criteria

  • Active bleeding
  • Invasive procedure needed
  • High bleeding risk
  • Documented deficiencies

Critical Points

  • Always treat underlying cause first
  • Heparin contraindicated in bleeding
  • Avoid antifibrinolytics generally
  • FFP preferred over cryoprecipitate

Disseminated Intravascular Coagulation (DIC)

Acquired coagulopathy syndrome characterized by widespread thrombosis and consumption coagulopathy

Overview

Disseminated intravascular coagulation (DIC) is an acquired syndrome characterised by activation of coagulation pathways, resulting in formation of intravascular thrombi and depletion of platelets and coagulation factors. Thrombi may lead to vascular obstruction/ischaemia and multi-organ failure. Spontaneous bleeding may occur.

Clinical Emergency: DIC is a life-threatening condition requiring immediate identification and management of both the coagulopathy and underlying cause.

Causes

Disease states that trigger systemic activation of coagulation may lead to DIC. Causes include:

Infection & Trauma

  • Sepsis/severe infection
  • Major trauma or burns

Malignancies

  • Acute myelocytic leukaemia
  • Metastatic mucin-secreting adenocarcinoma

Obstetric Disorders

  • Amniotic fluid embolism
  • Eclampsia
  • Abruptio placentae
  • Retained dead fetus syndrome

Organ Failure

  • Severe pancreatitis
  • Acute hepatic failure

Vascular Disorders

  • Kasabach-Merritt syndrome
  • Giant haemangiomas
  • Large aortic aneurysms

Toxic/Immunological Reactions

  • Blood transfusion reaction
  • Haemolytic reactions
  • Organ transplant rejection
  • Snake bite

Pathophysiology

Disseminated intravascular coagulation (DIC) is characterised by a widespread inappropriate intravascular deposition of fibrin with consumption of coagulation factors and platelets.

Mechanism

Initial Trigger

  • Release of procoagulant material into circulation
  • Widespread endothelial damage
  • Platelet aggregation

Coagulation Cascade

  • Increased thrombin activity overwhelms natural anticoagulants
  • Deposition of fibrin in microcirculation
  • Widespread platelet aggregation
  • Interference with fibrin polymerisation

Consumption and Fibrinolysis

  • Intense fibrinolysis stimulated by vascular thrombi
  • Release of fibrin degradation products (FDPs)
  • FDPs interfere with fibrin polymerisation
  • Combined action of thrombin and plasmin causes:
    • Depletion of fibrinogen and coagulation factors
    • Thrombocytopenia from platelet consumption

Clinical Features

Common findings include thrombosis, bleeding, or both. In general, ischaemic findings are considered earlier signs of DIC, while bleeding findings are late overt signs. Bleeding from at least three unrelated sites is typical.

Haemorrhagic Features

Cutaneous Bleeding

  • Petechiae/ecchymosis
  • Oozing at wound or venepuncture sites

Mucosal Bleeding

  • Bleeding from ears, nose or throat
  • Haematuria
  • Haemoptysis
  • Gastrointestinal bleeding

Serious Bleeding

  • Intracranial bleeding
  • Retroperitoneal bleeding

Ischaemic Features

Systemic Ischemia

  • Oliguria
  • Hypotension/tachycardia
  • Circulatory collapse
  • Delirium/coma

Cutaneous Ischemia

  • Purpura fulminans
  • Gangrene
  • Acral cyanosis

Laboratory Findings

Initial Laboratory Investigations

Test Finding in DIC Significance
Platelet count Thrombocytopenia Platelet consumption
Fibrinogen Low levels Consumption by thrombosis
PT/PTT Prolonged Factor depletion
D-dimer/FDPs Elevated Enhanced fibrinolysis

Additional Tests

Coagulation Tests

  • Thrombin time (TT): Prolonged
  • Coagulation factors: Low levels (V, VIII, X, XIII)
  • Antithrombin III: Decreased
  • Protein C/S: Decreased

Blood Film

  • Schistocytes (fragmented RBCs)
  • Thrombocytopenia
  • Microangiopathic changes

Management

Primary Goal: Treatment of the underlying disorder. Active treatment of the underlying disorder stops the triggering process.

Restoration of Physiological Coagulation Pathways

Normal coagulation can be restored by inhibition of overactive coagulation pathways and enhancement of suppressed anticoagulation systems.

Heparin Therapy

  • Inhibits coagulation cascade
  • Prevents further thrombogenesis
  • Enhances effect of antithrombin III
  • Requires normal antithrombin III levels

Indications for Heparin

  • Dominant thrombotic symptoms
  • No significant bleeding evidence
  • Chronic DIC presentation
  • Contraindicated in high bleeding risk

Replacement Therapy

Replacement of platelets and coagulation factors is indicated only in patients:

  • With active bleeding
  • Requiring an invasive procedure
  • At risk for bleeding complications
  • With documented deficiency of platelets and/or coagulation factors

Blood Products

  • Fresh Frozen Plasma (FFP): Preferred - provides balanced coagulation factors and inhibitors
  • Platelet concentrates: For thrombocytopenia
  • Cryoprecipitate: Alternative source of fibrinogen
  • Fibrinogen concentrates: Specific replacement

Replacement Guidelines

  • FFP: 15-20 mL/kg
  • Platelets: 1 unit/10kg (target >50×10⁹/L)
  • Cryoprecipitate: If fibrinogen <1.0 g/L
  • Monitor response with repeat coagulation tests

Antifibrinolytic Agents

Use with extreme caution: Antifibrinolytic agents inhibit fibrinolytic pathways and may worsen thrombosis.

Agents

  • Aminocaproic acid
  • Tranexamic acid

Limited Indications

  • Severe refractory bleeding
  • Hyperfibrinolysis with acute promyelocytic leukemia
  • Other cancer-associated hyperfibrinolysis
  • Only after hematology consultation

Monitoring and Prognosis

Monitoring Parameters

Laboratory Monitoring

  • Platelet count (4-6 hourly initially)
  • PT/PTT, fibrinogen, D-dimer
  • Complete blood count
  • Renal and hepatic function

Clinical Monitoring

  • Vital signs and organ perfusion
  • Bleeding manifestations
  • Thrombotic complications
  • Organ function assessment

Prognosis

  • Mortality rate: 30-80% depending on underlying cause
  • Worst prognosis with sepsis and multi-organ failure
  • Better outcomes with early recognition and treatment
  • Chronic DIC may have better prognosis than acute DIC