Disseminated intravascular coagulation (DIC)

Learning outcome

1. Describe the causes, pathophysiology, clinical and laboratory features of disseminated intravascular coagulation (DIC)

Pathophysiology

Disseminated intravascular coagulation (DIC) is a complex haemorrhagic disorder caused by uncontrolled activation of the coagulation cascade, usually upon inappropriate release of tissue factor (TF). Other factors such as bacterial components, snake venom and products of conception may also activate the coagulation cascade. As described in earlier sections, TF is expressed by endothelial cells but is not normally found in circulation. In DIC, excessive release of TF into the circulation may occur in response to inflammatory cytokines e.g. sepsis, or following endothelial damage, e.g. trauma.

This leads to diffuse thrombosis of small blood vessels and excessive utilisation of coagulation factors and platelets in the micro-thrombi formation. Fibrinolysis is also activated to break-down the fibrin that has been laid down from the intravascular coagulation, leading to generation of fibrin degradation products. The subsequent reduction in coagulation factors and platelets result in failure of haemostasis and diffuse bleeding.

The following video helps explain the process of DIC.

Causes of DIC

Many conditions may precipitate DIC, either by release of procoagulants into the blood stream or by extensive endothelial damage. Common causes include;

1. Sepsis, especially from gram-negative septicaemia and meningococcal septicaemia
2. Trauma and massive bleeding
3. Obstetrical accidents – abruptio placenta, amniotic fluid embolism, septic abortions
4. Haemolytic blood transfusion reactions
5. Acute promyelocytic leukemia
6. Carcinoma e.g. carcinoma of pancreas
7. Snake bite

Clinical features

The two main manifestation of DIC are;

1. Bleeding due to depletion of coagulation factors and thrombocytopenia
2. Multi-organ damage due to ischaemia caused by diffuse intravascular thrombosis

Bleeding is usually generalised. Patient may develop ecchymoses, haematomas, gastrointestinal bleeding, haematuria, ocular and intracranial bleeding. There may be prolonged bleeding from venipuncture sites, excessive bleeding at operation sites and uterine bleeding in case of obstetrical accidents.

Laboratory features

Characteristic laboratory features include;

1. Prolonged APTT and PT due to depletion of coagulation factors
2. Prolonged TT as a result of reduced fibrinogen
3. Low fibrinogen due to excessive conversion to fibrin and incorporation into intravascular thrombi and subsequent fibrinolysis
4. Positive fibrin degradation products and d-dimers caused by plasmin activity that degrades fibrin (fibrinolysis)
5. Low platelets due to trapping of platelets in the intravascular thrombi
6. Fragmented red cells (schistocytes) caused by red cells having to pass through the fibrin meshwork of intravascular thrombi

Management

Basic principles of management include

1. Treating the precipitating cause
2. Replacement therapy – red cell, platelet and plasma infusions, fibrinogen containing cryoprecipitate
3. Anticoagulation and anti-fibrinolytics in selected cases