Disseminated intravascular coagulation (DIC) is an acquired, life-threatening systemic disorder characterized by widespread activation of the coagulation cascade, resulting in excessive thrombin generation, fibrin formation, and microvascular thrombosis. The pathological process leads to simultaneous consumption of platelets and coagulation factors, producing a paradoxical state of both thrombosis and bleeding.

DIC is not a primary disease but a secondary complication of various underlying conditions, including severe infections, malignancies, trauma, and obstetric complications. The imbalance between procoagulant and anticoagulant mechanisms overwhelms the body's compensatory systems, resulting in disseminated fibrin deposition and subsequent organ dysfunction.

DIC may present as:

• Acute (overt) DIC – rapid onset, severe bleeding and organ failure

• Chronic (non-overt) DIC – slower progression, often associated with malignancy

Etiology and Risk Factors

DIC develops secondary to conditions that trigger systemic inflammation and coagulation activation. Common risk factors include:

1. Infectious Causes

• Severe sepsis and septic shock

• Bacterial infections (especially Gram-negative organisms)

• Viral infections (e.g., severe COVID-19)

2. Malignancies

• Acute promyelocytic leukemia (APL)

• Advanced solid tumors

3. Obstetric Complications

• Abruptio placentae

• Retained dead fetus syndrome

• Amniotic fluid embolism

• Severe preeclampsia/eclampsia

4. Trauma and Tissue Injury

• Major trauma

• Severe burns

• Extensive surgery

5. Other Causes

• Massive transfusion

• Severe liver disease

• Pancreatitis

• Snake envenomation

Pathophysiology

The pathogenesis of DIC involves:

1. Excessive activation of the coagulation cascade

2. Increased thrombin production

3. Fibrin deposition in microvasculature

4. Platelet consumption

5. Depletion of clotting factors

6. Secondary activation of fibrinolysis

This results in:

• Microvascular thrombosis

• Tissue ischemia

• Multi-organ dysfunction

• Bleeding due to consumption coagulopathy

Clinical Manifestations

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

Bleeding Manifestations

• Petechiae and purpura

• Oozing from venipuncture sites

• Gastrointestinal bleeding

• Hematuria

• Intracranial hemorrhage (severe cases)

Thrombotic Complications

• Renal cortical ischemia

• Hepatic dysfunction

• Pulmonary embolism (rare but possible)

• Digital ischemia

• Microvascular thrombosis leading to organ failure

Systemic Features

• Shock

• Coma or delirium

• Focal neurological deficits

• Acute kidney injury

⚠ Clinical manifestations often reflect both the underlying disorder and DIC itself.

Diagnostic Criteria

Diagnosis is based on clinical suspicion supported by laboratory findings. The International Society on Thrombosis and Haemostasis (ISTH) scoring system is commonly used.

Typical laboratory findings include:

• Prolonged prothrombin time (PT)

• Prolonged activated partial thromboplastin time (aPTT)

• Thrombocytopenia

• Decreased fibrinogen level

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

ISTH scoring system incorporates:

• Platelet count

• Elevated fibrin markers

• Prolonged PT

• Fibrinogen level

A cumulative score ≥5 suggests overt DIC.

Investigations

Essential investigations include:

• Complete blood count (CBC)

• Platelet count

• Peripheral blood smear (may show schistocytes)

• PT and INR

• aPTT

• Serum fibrinogen

• D-dimer

• Liver function tests

• Renal function tests

• Blood cultures (if infection suspected)

Continuous monitoring is required for:

• PT

• INR

• aPTT

• Platelet count

• Fibrinogen levels

Management

Management focuses primarily on treating the underlying cause while providing supportive therapy.

Non-Pharmacological and Supportive Management

1. Immediate and appropriate treatment of the underlying condition:

   • Antibiotics for sepsis

   • Chemotherapy for leukemia (especially APL)

   • Surgical evacuation in retained products of conception

   • Surgical debridement of necrotic tissue

2. Blood Component Therapy (for bleeding patients):

   • Platelet transfusion for significant thrombocytopenia with bleeding

   • Fresh frozen plasma (FFP) for clotting factor deficiency

   • Cryoprecipitate for hypofibrinogenemia

For multifactor deficiency or liver disease:

• FFP 10–15 mL/kg until bleeding is controlled

⚠ CAUTION:

• Platelet transfusion is contraindicated in non-bleeding patients unless platelet count is critically low.

• Severe DIC with multiorgan dysfunction requires management in an Intensive Care Unit (ICU).

Pharmacological Management

• Anticoagulation (e.g., low-dose heparin) may be considered in selected patients with predominant thrombotic manifestations and no active bleeding.

• Antithrombin concentrates (in selected cases)

• Recombinant thrombomodulin (used in some settings)

• Vitamin K in cases with concomitant deficiency

Use of anticoagulants must be individualized based on bleeding risk.

Complications

• Multiorgan failure

• Acute kidney injury

• Severe hemorrhage

• Intracranial bleeding

• Limb ischemia

• Mortality rates range from 20% to 50% depending on cause and severity

Prevention

Prevention involves:

• Early identification and management of sepsis

• Appropriate obstetric care

• Prompt treatment of malignancies

• Careful monitoring in high-risk patients

• Rational transfusion practices

Prognosis

Prognosis depends on:

• Underlying cause

• Severity of coagulation activation

• Timeliness of intervention

• Presence of organ dysfunction

Acute DIC associated with sepsis carries a poorer prognosis compared to chronic DIC associated with malignancy.

Keywords

Disseminated intravascular coagulation; DIC; Coagulopathy; Sepsis; Thrombosis; Fibrinolysis; Platelet consumption; Intensive care; Hematology; Shock; Organ failure

(Vancouver Style)

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