Coagulation and Haemostasis
Haemostasis maintains blood fluidity while preventing bleeding through vascular, platelet, and coagulation factors working in concert. Primary haemostasis: Vascular spasm, platelet adhesion (glycoprotein Ib-von...
What matters first
Haemostasis maintains blood fluidity while preventing bleeding through vascular, platelet, and coagulation factors working in concert. Primary haemostasis: Vascular spasm, platelet adhesion (glycoprotein Ib-von...
DIC with bleeding and thrombosis
2 Feb 2026
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84 cited sources
Clinical board
A visual summary of the highest-yield teaching signals on this page.
Urgent signals
Safety-critical features pulled from the topic metadata.
- DIC with bleeding and thrombosis
- Massive transfusion with coagulopathy
- Thrombocytopenia <50 × 10⁹/L with bleeding
- INR >1.5 or APTT >45 seconds
Exam focus
Current exam surfaces linked to this topic.
- ANZCA Primary Written
- ANZCA Primary Viva
Content status and exam context
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Clinical explanation and evidence
Quick Answer
Haemostasis maintains blood fluidity while preventing bleeding through vascular, platelet, and coagulation factors working in concert. Primary haemostasis: Vascular spasm, platelet adhesion (glycoprotein Ib-von Willebrand factor interaction), activation (shape change, granule release), aggregation (GPIIb/IIIa-fibrinogen bridges) forming platelet plug. Secondary haemostasis: Coagulation cascade with amplification via positive feedback loops. Extrinsic pathway (PT/INR): Factor VIIa + Tissue Factor (TF) activate Factor X; Intrinsic pathway (APTT): Contact activation (XII → XI → IX + VIII) activates Factor X; Common pathway: Factor Xa + Va + Ca²⁺ + phospholipid (prothrombinase complex) converts prothrombin (II) to thrombin (IIa); thrombin converts fibrinogen (I) to fibrin (Ia) and activates XIII (cross-links fibrin). Regulation: Antithrombin (inhibits thrombin, Xa, IXa, XIa), Protein C/S (inactivate Va and VIIIa), Tissue Factor Pathway Inhibitor (TFPI inhibits VIIa-TF complex). Fibrinolysis: Plasminogen → plasmin (tPA, urokinase) degrades fibrin; regulated by PAI-1 and α2-antiplasmin. Anaesthetic implications: Coagulopathy from dilution (massive transfusion), consumption (DIC), hypothermia, acidosis (lethal triad); thrombocytopenia (TACO, HIT, ITP); drug effects (heparin, warfarin, DOACs). Viscoelastic testing (TEG/ROTEM): Rapid assessment of clot formation, strength, and fibrinolysis; guides goal-directed therapy. Indigenous populations have higher rates of thromboembolism and may have different clotting factor concentrations requiring careful thromboprophylaxis. [1-10]