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Thromboembolic disease and anticoagulation

Thromboembolic disease and anticoagulation. Venous thromboembolism. DVT PE A Leading cause of morbidity and mortality. Natural History of DVT. Rare under 16 years Annual incidence 30/100,000 40 years Annual incidence 90/100,000 60 years Annual incidence 260/100,000 80 years.

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Thromboembolic disease and anticoagulation

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  1. Thromboembolic disease and anticoagulation

  2. Venous thromboembolism DVT PE A Leading cause of morbidity and mortality

  3. Natural History of DVT Rare under 16 years Annual incidence 30/100,000 40 years Annual incidence 90/100,000 60 years Annual incidence 260/100,000 80 years

  4. Natural History of DVT >80% of symptomatic DVT are proximal 20% of isolated calf will spread proximally PE usually arises from proximal DVT Most patients with proximal DVT have asymptomatic PE and visa versa

  5. Natural History of DVT 10% of symptomatic PE are fatal 30% of untreated symptomatic non-fatal PE will have a fatal recurrence

  6. Pathogenesis Virchow’s Triad: Venous stasis Endothelial changes (damage) Hypercoagulability

  7. Risk Factors for DVT Previous VTE Age Pregnancy Obesity Inherited Thrombophilia Malignancy Oestrogens Immobility Trauma Surgery Antiphospholipid antibodies

  8. Diagnosis of DVT Clinical assessment alone is unreliable Differential of red, tender, swollen leg: Cellulitis, ruptured bakers cyst, haematoma, superficial thrombophlebitis

  9. Diagnosis of DVT Venography – gold standard but expensive and invasive Venous Doppler ultrasonography – Non-invasive, check for compressibility of veins For proximal 97% sensitive 94% specific May repeat at 1 week if negative D-Dimer AND clinical risk score

  10. Compression US of the right leg in a patient with and a patient without common femoral vein thrombus. Note that a vein with acute thrombus demonstrates no intraluminal echoes. Thrombus is only detected by lack of compression. In contrast, a normal vein is easily compressible.

  11. Diagnosis of PE Clinically: Pleuritic chest pain SoB Syncope Haemoptysis Palpitations Tachycardia

  12. Diagnosis of PE Oxygen saturation; EGC; CXR Pulmonary angiogram – gold standard but expensive and invasive

  13. Diagnosis of PE V/Q scan: Normal perfusion excludes but only 40% have so need to compare with ventilation Mismatched defect Important to combine result with clinical findings (and possibly D Dimer)

  14. Ventilation / Perfusion ScansA. Very Low Probability of Pulmonary EmbolismB. High Probability of Pulmonary Embolism

  15. Diagnosis of PE Helical (spiral) CT Contrast used to visualise Pulmonary arteries Fewer technical failures and may diagnose other pathology Does NOT exclude if negative CT but high clinical probability

  16. Spiral CT for diagnosing pulmonary embolism. The blood clot (thrombus) can be seen as spots where the contrast medium (bright white in this picture) is missing.

  17. Treatment of VTE Heparin (followed by warfarin) Low molecular weight (occasionally unfractionated) Increases action of Antithrombin on Xa (and IIa) Overlap for 2 days with INR>2 on warfarin NB renal function Side effects: Bleeding, HIT, osteoporosis.

  18. Heparin Unfractionated bolus then continuous infusion monitor with APTT (ratio 1.5-2.5) reversal by stopping infusion and (if needed) Protamine sulphate can be hard to anticoagulate some infants due to low antithrombin levels Low molecular weight less monitoring once or twice daily administration more reliable pharmacokinetics (NB renal excretion) anti-Xa levels - 4h post dose if monitoring needed eg in renal disease Treatment 0.5-1; Prophylaxis 0.1-0.3 IU/ml

  19. II, VII, IX, X, protein C and S are vitamin K dependent. NB C and S fall first so overlap with heparin (Warfarin induced skin necrosis) Monitor by INR INR= (Patient PT/Control PT)ISI (ISI=international sensitivity index of reagent) Warfarin

  20. Near patient testing………………….

  21. Treatment of VTE Warfarin INR 2-3 usually for 3-6 months Long term considered if unprovoked event and/or recurring or severe risk factors (eg antiphospholipid syndrome or malignancy)

  22. Pre treatment counselling Drug interactions (Amiodarone) Yellow books Anticoagulation clinic

  23. Treatment of bleeding/excess anticoagulation on warfarin INR 3-6 (target 2.5); INR 4-6 (target 3.5) Reduce dose or stop; restart when INR<5 INR 6-8 No or minor bleeding Stop warfarin; restart when INR<5

  24. Treatment of bleeding/excess anticoagulation on warfarin INR>8; No or minor bleeding Stop warfarin; restart when INR<5 If other risks for bleeding give 0.5-2.5mg vitamin K orally

  25. Treatment of bleeding/excess anticoagulation on warfarin Major bleeding Stop warfarin Give Prothrombin complex concentrate Give 5mg vitamin K oral or i.v. PCC – II; VII; IX; X – discuss dose with haematologist DO NOT USE FFP IF PCC AVAILABLE UNLESS IT IS CONTRAINDICATED

  26. Other anticoagulant agents Aspirin Clopidogrel Abciximab NSAIDS Fibrinolytics

  27. Thrombophilia screening Remember patient risk factors and FBC Factor V Leiden (V resistant to cleavage by Protein C) Prothrombin gene G20210A variant (high II) Low Antithrombin, protein C, protein S

  28. Thrombophilia screening Antiphospholipid antibodies Anticardiolipin antibodies Lupus anticoagulant Anti-Beta2 glycoprotein I antibodies High homocysteine

  29. Questions

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