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Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
Resuming anticagulation in intracerebral hemorrhage patients
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Resuming anticagulation in intracerebral hemorrhage patients

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  • The “spot sign” (arrow), contrast extravasation after contrast-enhanced computed tomography, is associated with a high risk of hematoma expansion.
  • Transcript

    • 1. ‫بسم ا الرحمن الرحيم‬ ‫1‬
    • 2. • .Should anticoagulation be resumed after cerebral hemorrhage? An everyday story Moataz Fatthy MSc 2
    • 3. 3
    • 4. AGENDA…• Rationale• Risk factor• Risk Stratification• Complications• Management 4
    • 5. 5
    • 6. • The most feared and the most deadly complication of oral anticoagulant therapy• Anticoagulant therapy during and after anticoagulation-associated ICH. 6
    • 7. • Unfortunately, little evidence from clinical trials on which to base the decision.• Nevertheless, the potential benefit of resuming anticoagulation outweighs the considerable risk. 7
    • 8. Please pick your poison (Franklin michota , MD) 8
    • 9. • narrow therapeutic window• vary considerably in dose- response from patient to patient• subject to significant interactions with other drugs and with foods.• monitored with laboratory testing• good patient compliance• patient education is essential. 9
    • 10. • Warfarin has a striking effect on the incidence and outcomes of ICH.• While the overall incidence of ICH in the general population is approximately 25 per 100,000 person-years• The incidence in patients on warfarin is exponentially higher, at 2 to 3 per 100 per year, and appears to be increasing. 10
    • 11. • In addition, once ICH occurs, the risk of death is up to twice as high in those on warfarin• The bulk of this effect is likely due to a higher risk of ongoing bleeding after the event. 11
    • 12. 12
    • 13. 13
    • 14. Risk factors for intracerebral hemorrhageduring warfarin anticoagulationFirmly established riskfactors Possible risk factors• Advancing age (especially • Concomitant use of aspirin >75 years) • Cerebral amyloid angiopathy• Hypertension (especially • Asian or Mexican-American ethnicity systolic blood pressure >160 • Tobacco smoking mmHg) • Heavy alcohol consumption• History of cerebrovascular • Leukoaraiosis detected by brain disease CT/MRI• Intensity of anticoagulation • Microbleeds by T2*-weighted MRI 14
    • 15. 15
    • 16. • A population-based study has reported a four-fold increase in the incidence of warfarin-associated ICH during the 1990s due to the increasing use of warfarin in elderly patients• Antiplatelet therapy with aspirin increases ICH risk by about 40 percent 16
    • 17. • Dual antiplatelet therapy with aspirin plus clopidogrel increases the risk of ICH twofold compared with aspirin• Combining adjusted-dose warfarin with aspirin appears to double the ICH risk compared with similar intensities of warfarin anticoagulation without aspirin. 17
    • 18. 18
    • 19. Suggested patient risk stratification for arterialor venous thromboembolism 19
    • 20. INDICATION FOR VITAMIN K ANTAGONIST MECHANICAL HEART ATRIAL VENOUS VALVE FIBRILLATION THROMBOEMBOLISM Recent event (within 3 Any mitral valve prosthesis CHADS2 score ≥ 5 months( Older prosthetic aortic Recent stroke or transient Severe thrombophilia (low valve ischemic attack (within 3 protein C, protein S, orHigh risk Recent stroke or transient months( antithrombin level; ischemic attack (within 6 Rheumatic valvular heart antiphospholipid antibody ( months disease syndrome; multiple ( abnormalities Venous thromboembolic Bileaflet aortic valve event in the past 3 to 12 prosthesis and one of the months following: Nonsevere thrombophilic Atrial fibrillation CHADS2 score 3 or 4 conditions (eg, Prior stroke or transient heterozygous factor IIModerate risk Prior stroke or transient ischemic attack mutation( Hypertension ischemic attack Recurrent venous Diabetes thromboembolism Congestive heart failure Active cancer (treated Age over 75 within 6 months, or ( palliative treatment Bileaflet aortic valve CHADS2 score ≤ 2 and no Single venous prosthesis without atrial thromboembolic event >Low risk prior stroke or transient fibrillation, and with no 12 months ago and no ischemic attack 20 other stroke risk factors other risk factors
    • 21. INDICATION FOR VITAMIN K ANTAGONIST MECHANICAL HEART ATRIAL VENOUS VALVE FIBRILLATION THROMBOEMBOLISM Recent event (within 3 Any mitral valve prosthesis CHADS2 score ≥ 5 months( Older prosthetic aortic Recent stroke or transient Severe thrombophilia (low valve ischemic attack (within 3 protein C, protein S, orHigh risk Recent stroke or transient months( antithrombin level; ischemic attack (within 6 Rheumatic valvular heart antiphospholipid antibody ( months disease syndrome; multiple ( abnormalities 21
    • 22. INDICATION FOR VITAMIN K ANTAGONIST MECHANICAL HEART ATRIAL VENOUS VALVE FIBRILLATION THROMBOEMBOLISM Venous thromboembolic Bileaflet aortic valve event in the past 3 to 12 prosthesis and one of the months following: Nonsevere thrombophilic Atrial fibrillation CHADS2 score 3 or 4 conditions (eg, Prior stroke or transient heterozygous factor IIModerate risk Prior stroke or transient ischemic attack mutation( Hypertension ischemic attack Recurrent venous Diabetes thromboembolism Congestive heart failure Active cancer (treated Age over 75 within 6 months, or ( palliative treatment 22
    • 23. INDICATION FOR VITAMIN K ANTAGONIST MECHANICAL HEART ATRIAL VENOUS VALVE FIBRILLATION THROMBOEMBOLISM Bileaflet aortic valve CHADS2 score ≤ 2 and no Single venous prosthesis without atrial thromboembolic event >Low risk prior stroke or transient fibrillation, and with no 12 months ago and no ischemic attack 23 other stroke risk factors other risk factors
    • 24. 24
    • 25. Extracranial bleeding leads Intracranial bleeding such asto death or disability in only ICH leads to death or3% of cases disability 76% of cases 25
    • 26. Higher risk of expansion 26
    • 27. • Unfortunately, continued bleeding is common after ICH.• In patients In warfarin-associated ICH, up to 50% of patients who present within 3 hours of symptom onset, 25% of hematomas expand more than 30% over the first hour, and another 12% expand this amount over the next 24 to 48 hours or may be longer.• Over 70% of patients presenting acutely develop at least some amount of expansion within 24 hours. 27
    • 28. Higher risk of expansion• A large hematoma volume on presentation• Early presentation, especially within 3 hours (??undergo computed tomography (CT( while still bleeding(• Higher INR is a significant predictor, not just of higher risk, but also of a more delayed expansion.• Certain radiographic findings indicate higher risk. One is the “spot sign,” ie, contrast extravasation after contrast-enhanced CT.• Apparently, the more spots present, and the denser the contrast, the greater the risk “spot-sign score” 28
    • 29. The “spot sign” (arrow), contrast extravasation after contrast-enhanced computed tomography, is associated with a high risk of hematoma expansion. GOLDSTEIN J N , GREENBERG S M Cleveland Clinic Journal of Medicine 2010;77:791-799
    • 30. 30
    • 31. In the acute phase.. In the chronic phase.. ? ? 31
    • 32. In the acute phase.. In the chronic phase..• how does the risk of further • how does the risk of bleeding (hematoma recurrent hemorrhage expansion) compare with compare with the excess the short-term risk of risk of thromboembolism if thromboembolism? the patient does not resume anticoagulation therapy? 32
    • 33. • Anticoagulant reversal should be the Acute phase primary consideration in the first 24 management hoursHeparin or LMWH is recommended72 hours after ICH is diagnosedNot underweight (< 50 kg),Normal renal function (creatinine clearance > 30mL/minute/1.73 m2)Normal platelet function.Does not have coagulopathy.warfarin-related ICH has concomitant DVTor PE (ie, < 4weeks old), then caval interruption therapy would beindicated. 33
    • 34. • Anticoagulant reversal should be the Acute phase primary consideration in the first 24 management hoursLines of reversalVitamin K 5 to 10 mg intravenouslyProthrombin complex concentrates 10 to 50 U/kgRecombinant factor VIIa 40 to 80 μg/kgFresh frozen plasma 10 to 50 U/kg. 34
    • 35. There are few relevant guidelines for the reversal ofanticoagulation in patients with AAICH, and expert opinionon this subject differs • PCC, recombinant factor VIIa, or fresh frozen plasma given with intravenous vitamin K were advocated in the 2008 American College of Chest Physicians Guidelines for patients with life-threatening bleeding such as intracranial hemorrhage 35
    • 36. There are few relevant guidelines for the reversal ofanticoagulation in patients with AAICH, and expert opinionon this subject differs • Replacement of the vitamin K-dependent factors to correct the INR and the administration of intravenous vitamin K. PCCs were considered a reasonable alternative to FFP. Recombinant factor VIIa was not routinely recommended as a sole agent for reversal 36
    • 37. • Other guidelines have • PCC preparations are not suggested using various readily available in combinations of vitamin emergency departments K, FFP, PCC, and at most United States recombinant factor VIIa hospitals; their use is often restricted to hematology specialists, reducing their immediate availability. 37
    • 38. Chronic phase managementEvaluations of patients for their risk of thrombosis in light of theiroriginal indication for oral anticoagulant therapy.The risk of ICH is related to the intensity of anticoagulation, a lowertarget international normalized ratio may be the best compromise,depending on the patient.Alternatively, antiplatelet therapy alone may offer some benefit with lessrisk of ICH 38
    • 39. Whether and when to resume anticoagulation ? • Old Dilemma • A new trend 39
    • 40. Old Dilemma• ICH in patients with atrial fibrillation, the risk of thromboembolism would need to exceed 7% per year to justify restarting anticoagulation after deep ICH,and no risk level was high enough to justify restarting anticoagulation after lobar ICH.• The American Heart Association comments that for nonvalvular atrial fibrillation, long-term anticoagulation should be avoided after spontaneous lobar ICH, but that antiplatelet agents may be considered.• The decision to restart anticoagulation may also be a function of whether the underlying risk factor is a temporary or long term one . 40
    • 41. Old DilemmaClearly, the risk is high on the first day, but small after thefirst few days. • A history of embolic stroke with atrial fibrillation, should be restarted on warfarin after 10 to 14 days, depending on the risk of thromboembolism and ICH recurrence. 41
    • 42. Old Dilemma • The American College of Chest Physicians recommends starting prophylactic-dose heparin the day after an ICH, with no clear guidance on restarting warfarin. 42
    • 43. Old Dilemma • The American Heart Association suggests that, in patients with a very high risk of thromboembolism for whom restarting warfarin is considered, warfarin may be restarted 7 to 10 days after ICH onset. 43
    • 44. A new trend• The decision to resume • Patients determined to be anticoagulation after at high risk of anticoagulant-associated thrombosis and low risk intracranial hemorrhage of rebleeding are the best should be based on the candidates for resuming risk of rebleeding vs the anticoagulation. risk of thrombosis. 44
    • 45. INDICATION FOR VITAMIN K ANTAGONIST MECHANICAL HEART ATRIAL VENOUS VALVE FIBRILLATION THROMBOEMBOLISM Recent event (within 3 Any mitral valve prosthesis CHADS2 score ≥ 5 months( Older prosthetic aortic Recent stroke or transient Severe thrombophilia (low valve ischemic attack (within 3 protein C, protein S, orHigh risk Recent stroke or transient months( antithrombin level; ischemic attack (within 6 Rheumatic valvular heart antiphospholipid antibody ( months disease syndrome; multiple ( abnormalities Venous thromboembolic Bileaflet aortic valve event in the past 3 to 12 prosthesis and one of the months following: Nonsevere thrombophilic Atrial fibrillation CHADS2 score 3 or 4 conditions (eg, Prior stroke or transient heterozygous factor IIModerate risk Prior stroke or transient ischemic attack mutation( Hypertension ischemic attack Recurrent venous Diabetes thromboembolism Congestive heart failure Active cancer (treated Age over 75 within 6 months, or ( palliative treatment Bileaflet aortic valve CHADS2 score ≤ 2 and no Single venous prosthesis without atrial thromboembolic event >Low risk prior stroke or transient fibrillation, and with no 12 months ago and no ischemic attack 45 other stroke risk factors other risk factors
    • 46. Suggested risk stratification for recurrent intracranial hemorrhage Cerebral amyloid angiopathy or lobar intracranial hemorrhageHigh risk Microbleeds on magnetic resonance imaging Hypertensive vasculopathy or deep intracranial hemorrhage with any of the : following Normal international normalized ratio at theModerate risk time the hemorrhage is diagnosed Patient not compliant with the dosing and monitoring of vitamin K antagonist therapy Patient not compliant with antihypertensive therapy Hypertensive vasculopathy or deepLow risk intracranial hemorrhage in a compliant patient 46
    • 47. Suggested risk stratification for recurrent intracranial hemorrhage Cerebral amyloid angiopathy or lobar intracranial hemorrhageHigh risk Microbleeds on magnetic resonance imaging 47
    • 48. Suggested risk stratification for recurrent intracranial hemorrhage Hypertensive vasculopathy or deep intracranial hemorrhage with any of the : following Normal international normalized ratio at theModerate risk time the hemorrhage is diagnosed Patient not compliant with the dosing and monitoring of vitamin K antagonist therapy Patient not compliant with antihypertensive therapy 48
    • 49. Suggested risk stratification for recurrent intracranial hemorrhage Hypertensive vasculopathy or deepLow risk intracranial hemorrhage in a compliant patient 49
    • 50. RISK OF ICH RISK OF THROMBOEMBOLISM High Moderate LowHigh Do not resume Do not resume Do not resume Individualized IndividualizedModerate Do not resume approach approachLow Resume Resume Do not resume 50
    • 51. How to avoid …• Good control of warfarin intensity and limiting the use of aspirin, will reduce the risk of ICH.• Blood pressure control is especially important for avoiding ICH. The use of warfarin in elderly patients should go hand in hand with aggressive blood pressure management.• If patients on long-term warfarin have a history of falls, risk factor screening/intervention program for reducing the risk of falls may be of value. 51
    • 52. Take home message• Pick up your poison• ICH is the nightmare• Acute management includes anticoagulant reversal and should be the primary consideration in the first 24 hours• Patients determined to be at high risk of thrombosis and low risk of rebleeding are the best candidates for resuming anticoagulation.• Consider INR control ,BP control, patients with recurrent falls and other anticoagulation methods with higher compliance 52
    • 53. 53

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