Abstract Disseminated intravascular coagulation (DIC) is a contradictory process involving both coagulation and anticoagulation. It is caused by numerous diverse factors. The coagulation process is initiated by the formation of prothrombin activator via either the extrinsic or intrinsic pathway of coagulation. In DIC the inhibitory mechanisms that normally localise coagulation are overwhelmed by the massive systemic activation of the coagulation process. The result is widespread thrombosis, with end-organ ischaemia and dysfunction causing the prominant symptoms. Thrombosis is often overshadowed by generalised bleeding. Haemorrhage is caused by the combination of consumption of coagulation factors, reduced fibrinogen levels, thrombocytopaenia and circulation of fibrin degradation products (FDPs) acting as anticoagulants. Excessive fibrinolysis is activated in response to the widespread formation of thrombi. Manifestations of DIC are wide and varied. These may be thrombotic, haemorrhagic or mixed. The disorder can occur in the acute or chronic form. The most dominating specific sign of DIC is profuse diverse bleeding from unrelated sites. Effective care of the patient with DIC is enhanced by a thorough understanding of its pathophysiology and clinical manifestations. Patients are frequently acutely ill with multiple organ failure. Early diagnosis and reversal of the cause are crucial. Therapy is highly individualised depending on cause, manifestations and haemodynamic status. If haemorrhage predominates, selective replacement therapy is recommended based on laboratory and clinical response. However, the regimes of both aggressive replacement therapy and anticoagulation with heparin remain highly controversial. There is a lack of published information and further research is needed in this area.