MD Notes

creation date: 2026-04-05 23:54
tags: Pathologies

Disseminated Intravascular Coagulation

Background

Definitions

Disseminated intravascular coagulation (DIC) is a condition of disrupted hemostasis, wherein systemic activation of the coagulation processes result in the formation of microthrombi in small vessels throughout the body.

If not promptly identified and treated, organ dysfunction and depletion of clotting factors resulting in uncontrolled bleeding will occur.

Etiology

DIC is a secondary manifestation of underlying conditions.

Pregnancy-related causes:

Nonpregnancy-related causes:

  • Sepsis
  • Trauma
  • Cancer

Pathogenesis

DIC is characterized by abnormal activation of both coagulation and fibrinolysis resulting in ongoing systemic clot formation and subsequent breakdown.

Typical sequence of pathogenesis is as follows:

  1. Blood is exposed to normally protected procoagulants (eg. tissue factor)
  2. Coagulation cascade is activated causing formation of thrombi, consuming coagulation factors and platelets
  3. Fibrinolysis is activated at sites of thrombus formation
  4. Compensation occurs (synthesis of coagulation factors and platelets)

Compensation may be adequate or inadequate (often referred to as chronic and acute DIC, respectively). As thrombosis, reduced perfusion, and/or bleeding occurs, tissue or organ damage may result.

Clinical Presentation

Signs & Symptoms

Presentation varies based on the underlying etiology and severity.

Overt DIC
Overt fulminant DIC is more common in pregnancy as coagulation and fibrinolysis are both increased.

Overt bleeding and thrombosis are present:

  • Severe vaginal bleeding (note that concealed abruption is possible)
  • Diffuse oozing from skin (eg. at IV sites) or mucosa (eg. bladder catheter)
  • Signs of shock
  • Organ dysfunction (AKI, hepatic dysfunction, lung injury, neurologic dysfunction)

Latent and compensated activation of coagulation
Presents without obvious clinical symptoms and is often a chronic conditions.

  • Subtle hemostatic dysfunction
  • Increased thrombotic risk

History & Physical Exam

If unknown, a prenatal history of complications should be obtained.

If not pregnant or a non-pregnancy associated etiology is suspected, inquire about:

  • Cancer history
  • Trauma
  • Infection and possible source of sepsis

Risk Factors

Primary risk factor is the presence of pregnancy complication.

Diagnosis

Criteria

Diagnosis is made with a combination of clinical setting (eg. in pregnant patient with complication) and laboratory evidence of:

  • Thrombocytopenia
  • Coagulation factor consumption
  • Fibrinolysis (d-dimer)

Work-up

Initial laboratory workup

  • CBC (thrombocytopenia)
  • Coagulation studies (prolonged aPTT, PT, and TT)
  • Fibrinogen level (decreased)
  • D-dimer (elevated)
  • Liver function tests (normal with DIC; abnormal suggests liver pathology)
  • Thromboelastography (TEG)/rotational thromboelastometry (ROTEM)
  • BUN and creatinine (elevated with AKI)
  • Cultures if sepsis is suspected

Differential

Other causes of bleeding, especially around pregnancy, include:

  • Postpartum hemorrhage with dilutional coagulopathy
  • Primary thrombotic microangiopathy (eg. TTP)
  • von Willebrand disease

Other conditions in the setting of shock and elevated d-dimer include:

Red Flags / Complications

Management

Treatment of Underlying Cause and Supportive Measures

Treatment consist of management of underlying cause to eliminate stimulus for ongoing coagulation and thrombosis.

Additional supportive measures may be used:

  • Hemodynamic and/or ventilatory support
  • Aggressive hydration of acute hemolytic transfusion reaction
  • Blood product transfusion for severe bleeding

Systemic Therapies

Generally, systemic therapies are not used routinely.

Prevention/treatment of bleeding
Prophylactic administration of platelet and coagulation factors may be considered if patient is at high risk of bleeding and/or if platelet count is <10,000/mcL.

Patients who are bleeding or may be at risk (eg. surgery) with platelets <50,000/mcL should be given platelets:

  • 2 units/10 kg body weight

Patients with serious bleed and significantly prolonged PT, aPTT, or decreased fibrinogen should receive coagulation factor replacement:

  • Fresh Frozen Plasma (FFP)
  • Cyroprecipitate

Other considerations
Antifibrinolytic agents (eg. TXA, EACA, aprotinin) are contraindicated due to risk of thrombotic complications.

Prophylactic anticoagulation for thrombosis risk is also not indicated. Anticoagulation may be considered in the context of VTE treatment.

References

Tools / Guidelines

Additional Reading

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