Complex condition that describes the inappropriate activation of the clotting cascades, resulting in thrombus formation and subsequently leading to the depletion of clotting factors and platelets

Aetiology

• Causes include sepsis, obstetric emergencies, malignancy, hypovolaemic shock

Pathophysiology

• Arises because of systemic activation of coagulation either by release of procoagulant material, such as tissue factor, or via cytokine pathways as part of the inflammatory response
• Such systemic activation leads to widespread generation of fibrin and deposition in blood vessels, leading to thrombosis and multiorgan failure
• Due to the widespread coagulation activation there is consumption of platelets and coagulation factors, and secondary activation of fibrinolysis leading to production of FDPs and D-dimer
• These further contribute to the coagulation defect by inhibiting fibrin polymerization
• The consequences of these changes are a mixture of initial thrombosis, followed by a bleeding tendency due to consumption of coagulation factors and dysregulated fibrinolytic activation
  • Microvascular thrombus formation → end organ failure
  • Clotting factor consumption → bruising, purpura, generalised bleeding

Clinical presentation

• Patient is often acutely ill and shocked
• Clinical presentation varies from no bleeding at all to profound haemostatic failure with widespread haemorrhage

Symptoms

• Excessive bleeding e.g. epistaxis, gingival bleeding, haematuria, bleeding from cannula sites
• Fever
• Confusion
• Potential coma

Signs

• Petechiae
• Bruising