Disseminated intravascular coagulation (DIC)

Overview

Disseminated intravascular coagulation (DIC) is an acquired, life-threatening systemic disorder characterized by widespread activation of the coagulation cascade.

This causes:

• Excessive thrombin generation.

• Fibrin formation.

• Microvascular thrombosis.

• Consumption of platelets and coagulation factors.

The result is a paradoxical state of both thrombosis and bleeding.

DIC is not a primary disease but occurs as a secondary complication of underlying conditions.

Types of DIC

Acute DIC

• Rapid onset.

• Severe bleeding.

• Organ dysfunction.

• Commonly associated with sepsis, trauma, and obstetric emergencies.

Chronic DIC

• Slower progression.

• Often associated with malignancy.

Causes and risk factors

DIC develops due to conditions that trigger systemic inflammation and coagulation activation.

Infectious causes

• Severe sepsis and septic shock.

• Bacterial infections, especially Gram-negative organisms.

• Severe viral infections.

Malignancies

• Acute promyelocytic leukaemia (APL).

• Advanced solid tumours.

Obstetric causes

• Abruptio placentae.

• Retained dead fetus syndrome.

• Amniotic fluid embolism.

• Severe preeclampsia/eclampsia.

Trauma and tissue injury

• Major trauma.

• Severe burns.

• Extensive surgery.

Other causes

• Massive transfusion.

• Severe liver disease.

• Pancreatitis.

• Snake envenomation.

Pathophysiology

DIC involves:

• Excessive activation of the coagulation cascade.

• Increased thrombin production.

• Fibrin deposition in microvasculature.

• Platelet consumption.

• Depletion of clotting factors.

• Secondary activation of fibrinolysis.

This results in:

• Microvascular thrombosis.

• Tissue ischemia.

• Multi-organ dysfunction.

• Bleeding due to consumption coagulopathy.

Clinical presentation

Clinical features depend on the severity of DIC and the underlying disorder.

Bleeding manifestations

• Petechiae.

• Purpura.

• Oozing from venipuncture sites.

• Gastrointestinal bleeding.

• Haematuria.

• Intracranial haemorrhage in severe cases.

Thrombotic complications

• Renal cortical ischemia.

• Hepatic dysfunction.

• Digital ischemia.

• Microvascular thrombosis causing organ failure.

• Pulmonary embolism (rare but possible).

Systemic features

• Shock.

• Acute kidney injury.

• Coma.

• Delirium.

• Focal neurological symptoms.

Note:

• Clinical features are usually related to both DIC and the underlying disorder.

Diagnostic criteria

Diagnosis is based on clinical suspicion supported by laboratory findings.

The International Society on Thrombosis and Haemostasis (ISTH) scoring system may be used.

Findings supporting DIC include:

• Prolonged prothrombin time (PT).

• Prolonged activated partial thromboplastin time (aPTT).

• Thrombocytopenia.

• Reduced fibrinogen level.

• Elevated D-dimer or fibrin degradation products (FDPs).

ISTH scoring includes:

• Platelet count.

• Fibrin markers.

• PT prolongation.

• Fibrinogen level.

A cumulative score ≥5 suggests overt DIC.

Investigations

• Full blood picture (FBP/CBC).

• Platelet count.

• Peripheral blood smear (may show schistocytes).

• PT.

• International normalized ratio (INR).

• aPTT.

• Fibrinogen level.

• D-dimer.

• Liver function tests.

• Renal function tests.

• Blood cultures if infection is suspected.

Monitoring

Monitor:

• PT.

• INR.

• aPTT.

• Platelet count.

• Fibrinogen level.

Management of Disseminated intravascular coagulation (DIC)

Management focuses on rapid treatment of the underlying disorder and supportive care.

Treatment of underlying cause

Rapid and appropriate treatment includes:

• Antibiotics for infection.

• Surgical debridement of necrotic tissues.

• Chemotherapy for malignant causes.

• Evacuation of dead fetus.

Blood component therapy

For patients with bleeding or significant consumption:

• Platelet transfusion for thrombocytopenia.

AND

• Fresh frozen plasma (FFP) for coagulation factor depletion.

Additional supportive therapy:

• Cryoprecipitate may be considered for severe hypofibrinogenaemia.

For multifactor deficiency or significant bleeding:

• FFP 10–15 ml/kg until bleeding is controlled.

Important note

• Platelet concentrate is contraindicated in patients with DIC who are not bleeding unless there is a specific indication such as critically low platelet count.

• If DIC is severe enough to cause multiorgan dysfunction, management in an intensive care unit (ICU) is required.

Pharmacological management

Anticoagulation may be considered only in selected patients with predominant thrombotic manifestations and no active bleeding.

Options may include:

• Low-dose heparin in selected cases.

• Antithrombin concentrates in selected cases.

• Recombinant thrombomodulin where available.

• Vitamin K when deficiency is present.

Use of anticoagulants must be individualized based on bleeding risk and clinical condition.

Complications

• Multiorgan failure.

• Acute kidney injury.

• Severe haemorrhage.

• Intracranial bleeding.

• Limb ischemia.

• Death.

Prevention

Prevention involves:

• Early recognition and treatment of sepsis.

• Appropriate obstetric care.

• Prompt treatment of malignancies.

• Careful monitoring of high-risk patients.

• Rational transfusion practices.

Prognosis

Prognosis depends on:

• Underlying cause.

• Severity of coagulation activation.

• Timeliness of treatment.

• Presence of organ dysfunction.

Acute DIC associated with sepsis generally has a poorer prognosis compared with chronic DIC associated with malignancy.