An acute or chronic multisystem disorder caused by simultaneous activation of the coagulation and fibrinolytic pathways. It is a clinical and laboratory diagnosis.
- Cancer (especially adenocarcinoma)
- Obstestric issues (eg: placental abruption)
- Intravascular Haemolysis (ABO-incompatible transfusion)
2 main forms of presentation
- "Acute Bleeders": Haemorrhage, petechiae, ecchymoses;
- "Chronic Clotters": Venous or Arterial Thromboembolic events
- Heparin-induced thrombocytopenia (heparin-PF4 antibodies)
- Thrombotic thrombocytopenic purpura
Bloods (NB: can be normal in chronic disease)
Full Blood Count:
Full Blood Count:
- Hb: decreased or still normal in an acute bleed.
- WCC: raised if sepsis is a cause
- ^ Thrombin
- ^ PT (INR) and aPTT
- ^ Pro-coagulants (VII, X, V, and II)
- ^ Anti-coagulants (antithrombin, protein C, and protein S)
- Fibrinogen: can be low, normal or elevated (its an acute phase reactant)
- D-Dimer: High
- Smear: microangiopathic changes, schistocytes, helmet cells
- 20% have associated hepatic and renal dysfunction.
The 3 C's
- Cause: Treat underlying cause
- Complications: Educate and monitor for haemorrhage or VTE
- Coagulation is not routinely done, options are:
- Bleeding/High Risk: Fresh Frozen Plasma, Cryoprecipitate.
- Thromboembolism: consider anti-coagulation in peri-op state.
- Relative contraindications: Tranexamic Acid, Prothrombin Complex Concentrates
Antithrombin III in severe sepsis, JAMA, 2001:
- Randomized Control Trial
- 2314 patients with sepsis to antithrombin or placebo and found no difference in mortality
love to show off?
- Rare, Life-threatening
- Extensive tissue thrombosis and hemorrhagic skin necrosis
- Due to protein C deficiency:
- Inherited: homozygous or compound heterozygous
- Acquired: post-menigococcal infection
An acute or chronic multisystem disorder that often occurs in the critically unwell. Clinical and laboratory diagnosis that requires urgent discussion with Senior Colleagues.