Disseminated intravascular coagulation

Incidence
Age
Sex
Geography
Aetiology	- release of coagulant material /diffuse endothelial damage/generalized platelet aggregation -> activation of cagulation cascade -> widespread generation of fibrin within blood vessels - activation of monocyte with release of tissue factor and cytokines may be involved - consumption of platelets and coagulation factors, and secondary activation of fibrinolysis to produce FDPs may contribute to coagulation defect by inhibiting fibrin polymerization Causes - malignant disease - septicaemia, e.g. Gram-negative or meningococcal - haemolytic transfusion reactions - obstetric causes - abruptio placentae, amniotic fluid embolism - trauma, burns, surgery - malaria - snake bite
Presentation	- patient acutely ill and shocked - varies from no bleeding at all to complete haemostatic failure with widespread haemorrhage - bleeding from mouth, nose, venepuncture sites; may be widespread ecchymoses - thrombotic events due to vessel occlusion by fibrin and platelets; skin and kidneys are most commonly involved
Investigations	Severe cases with haemorrhage - PT, APTT, and TT very prolonged; fibrinogen level markedly reduced - high levels of FDPs - severe thrombocytopenia - blood film - fragmented red blood cells Mild cases without bleeding - increased synthesis of coagulation factors and platelets -> normal PT, APTT, TT and platelet counts - FDPs elevated
Macro
Micro
Staging
Serum Markers
Management	- treat underlying cause - maintenance of blood volume and tissue perfusion - transfusions of platelet concentrates, FFP, cryoprecipitate and red cell concentrates in patients who are bleeding
Prognosis
Complications

Haematology

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