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Giuseppe Micieli Dip . Neurologia d’Urgenza IRCCS Istituto Neurologico C Mondino Pavia

Manifestazioni cliniche di sanguinamento: Il sanguinamento cerebrovascolare. Giuseppe Micieli Dip . Neurologia d’Urgenza IRCCS Istituto Neurologico C Mondino Pavia . Cerebrovascular Disease Stroke Subtypes. Hemorrhagic stroke (17%). Ischemic stroke (83%). Lacunar small vessel

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Giuseppe Micieli Dip . Neurologia d’Urgenza IRCCS Istituto Neurologico C Mondino Pavia

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  1. Manifestazioni cliniche di sanguinamento: Il sanguinamento cerebrovascolare Giuseppe Micieli Dip. Neurologia d’Urgenza IRCCS Istituto Neurologico C Mondino Pavia

  2. Cerebrovascular DiseaseStroke Subtypes Hemorrhagic stroke (17%) Ischemic stroke (83%) Lacunar small vessel disease (25%) Intracerebral hemorrhage (59%) Atherothrombotic disease (20%) SAH (41%) Embolism (20%) Cryptogenic (30%) Albers GW et al. Chest. 1998;114:683S-698S. Rosamond WD et al. Stroke. 1999;30:736-743.

  3. Hypertension Hematologic disorders Thrombocytopenia Platelet dysfunction Coagulopathies Blood vessel abnormalities Arteriovenus malformation Aneurism Moyamoya disease Amyloid angiopathy Tumors Primary brain tumor(much less common than metastatic tumor) Metastatic brain tumor(melanoma, choriocarcinoma, thyroid carcinoma, renal cell carcinoma, bronchogenic carcinoma, breast carcinoma) Drugs Illicit drugs(cocaine, amphetamine) Over-the-counter medications(phenylpropanolamine) Prescription medications(warfarin, aspirin, TPA, heparin) Possible causes of spontaneous nontraumatic ICH

  4. Quality-of-care indicators and accepted reasons for nontreatment Neurology 2005;65:360–365

  5. ICH afterthrombolysis IH1: smallpetechiae IH2: more confluentpetechiae PH1: haematoma in <30% of the infarcted area; slight space-occupyingeffect PH2: dense haematoma >30% of the infarcted area; substantial space-occupyingeffect

  6. ICH: epidemiology and relationship with antithrombotic treatment Nicolini A et al. Haematologica 2002;87:948-956

  7. Volume of haemorrhage, AC and AP use Stead LG et al. Clin Neurol Neurosurg 2009

  8. AP or OA therapy effect on unfavorable outcome and in-hospital mortality Saloheimo P et al. Stroke 2006;37:129-133

  9. ICH: stima della frequenza assoluta • FA: 0.3-0.6% • CVD: 0.4-1.0% • FA: 0.3% • CVD: 0.4% • FA: 0.2% • CVD: 0.3% 0.15 % 0.5-1.0% Hart RG et al. Stroke 2005;36:1588-1593

  10. Da soli o in associazione?

  11. Rates of CNS bleeding during antiplatelet therapy with ASA and Clopidogrel Hart RG et al. Stroke 2005;36:1588-1593

  12. MATCH: life-threatening and major bleeding Life threatening: any fatal bleeding event, or a drop in haemoglobin of 5g/d, or significant hypotension with the need of inotropes (hemorrhagic shock) or, symptomatic intracranial haemorrhage, or requiring transfusion of  4 units of RBC or equivalent amount of whole blood Major bleeding:significantly disabling (with persistent sequelae), or intraocular bleeding leading to significant loss of vision or, requiring transfusion of  3 units of RBC or equivalent amount of whole blood Diener HC, et al. Lancet 2004;364:331-337

  13. CHARISMA: Overall Population Safety Results *Adjudicated outcomes by intention to treat analysis ICH= Intracranial Hemorrhage Bhatt DL, Fox KA, Hacke W, et al. NEJM 2006 – In press

  14. ASA and ER-Dipyridamole versus Clopidogrel for recurrent stroke: primary and secondary outcomes Sacco R et al. NEJM 2008;359:1-14

  15. Prasugrel vs Clopidogrelin Acute CoronarySyndromes Wiviott SD et al. NEJM 2007;357:2001-2015

  16. Platelet antiaggregants and anticoagulants within 48 hours of acute ischemic stroke Coull BM et al, Stroke 2002

  17. SPREAD: Terapia anticoagulante in prevenzione secondaria 2003 2007 (&2010) Raccomandazione 10.12 Grado D In pazienti con qualunque eziologia cardioembolica, escludendo i casi a rischio emboligeno molto elevato, qualora vi sia una lesione estesa alla TC a 48 ore, è indicato procrastinare di almeno 14 giorni l’inizio del trattamento anticoagulante, per il maggior rischio di trasformazione emorragica sintomatica. Qualora una TC abbia documentato una lesione minore del 30% dell’emisfero colpito senza trasformazione emorragica in forma di ematoma, il trattamento può essere iniziato precocemente. • Raccomandazione 10.10 • Grado D  • In pazienti con qualunque etiologia cardioembolica, in assenza delle controindicazioni elencate al Capitolo 5, è indicato iniziare il trattamento anticoagulante orale tra 48 opre e 14 giorni tenendo conto di: • Gravità clinica • Estensione della lesione alle • neuroimmagini • Comorbosità cardiologica • (definita anche con • ecocardiografia)

  18. ECASS study: ICH following thrombolysis Derex L, Nighoghossian N. JNNP 2008;79:1093-1099

  19. Thrombolysis-related ICH Acute Myocardial Infarction: 0.6% Pulmonary Embolism: 3% Ischaemic Stroke*: 6-11% Intravenous thrombolytic therapy 6% Intra-arterial thrombolytic therapy 11% * ICH in brain areas outside the vascular distribution of the ischaemic stroke: 20% Mac Carron MO & Nicol JAR, Lancet Neurology 2004;3(8):484

  20. Tissue Plasminogen Activator – Possible Reasons for Temporal Restriction rt-PA Multi-tasking:Additional physiological functions of tPA turn deleterious in the ischemic setting tPA , a neurotoxic agent: Endogenous glutamate can cause neurotoxicity, e.g. under ischemic conditions; tPA is able to aggravate this toxicity. Benchenane et al, Trends Neurosci 27: 155 (2004) Second Generation: Recombinant Proteins Cleavage rt-PA ogen Plasmin Plasmin Fibrin

  21. Caso clinico: maschio, 71 anni, emiparesi sinistra, esordita da circa 45’ Plavix 75 mg cp 1 cp dopo pranzo Cardioaspirin 100 mg cp 1 cp dopo cena Torvast 10 mg cp 1 cp alla sera Triatec 5 mg cp 1 cp al mattino Bisoprololo 2.5 mg cp 1 cp al mattino Dopo circa 2 h dalla trombolisi

  22. AP treatment and thrombolysis:distribution of the mRS scores at 3 months Diedler J et al. Stroke 2010;41:288-294

  23. AP treatment and thrombolysis:causes of death Diedler J et al. Stroke 2010;41:288-294

  24. Cerebral microbleeds • Prevalence: • No CVD: 4.7% • Ischemic CVD: 40% • Ischemic CVD with cerebral microangiopathy: 57% • Hemorrhagic CVD:68% • Location: • Cortical-subcortical area Koennecke HC, Neurology 2006;66(2):165

  25. Leukoaraiosi e ICH TAO-relata • Presenza: • OR: 12.9 (95%CI: 2.8-59.8) • Grado 3-4: • OR: 24.9 (95% CI: 4.5-137.4) Valori espressi in n(%) Smith EE et al, Neurology 2002

  26. Anticoagulant-related ICH Hart R, Stroke 1995;26:1471

  27. Anticoagulant-related ICH Anticoagulation toconventional intensitiesincreases the risk of intracranial hemorrhage7- to 10-fold, to an absolute rate of nearly 1%/y for many stroke-prone patients. Most (70%) anticoagulant-related intracranial hemorrhages areintracerebral hematomas(approximately 60% are fatal); the bulk of the remainder are subdural hematomas. Predictorsof anticoagulant-related intracerebral hematoma are advanced patientage (>75 yrs), race, prior ischemic stroke, hypertension (systolic BP >160 mmHg), intensity of anticoagulation, concomitant use of antiplatelet drug, and cerebral amyloid angiopathy. In approximately half of anticoagulated patients with intracerebral hematoma the bleeding evolves slowly over 12 to 24 hours, and emergency reversal of anticoagulation is crucial Hart R mod, Stroke 1995;26:1471

  28. Kaplan-Meier estimate of rate of hemorrhage expansion Flibotte Neurology, 2004;63(6):1059

  29. The increasing incidence of anticoagulant-associated intracranial haemorrhage 1988 1993-1994 1999 All ischemic stroke NA 140.0 (133.2-146.8) 142.6 (135.8-149.3) Cardioembolic stroke NA 31.1 (27.9-34.3) 30.4 (27.3-33.5) Cardioembolic ischemic stroke due to AF NA 22.0 (19.3-24.8) 20.6 (18.1-23.2) All ICH 16.5 (14.1-18.9) 22.1 (19.4-24.8) 24.6 (21.8-27.4) AAICH 0.8 (0.3-1.3) 1.9 (1.1-2.7) 4.4 (3.2-5.5) Flaherty ML et al. Neurology 2007;68:116-121

  30. Racial/ethnic differences in the risk of ICH among patients with AF Shen A Y-J et al. J Am Coll Med 2007;50:309-315

  31. Predittori di ICH durante TAO Età Fang MC et al, Ann Intern Med 2004

  32. Predittori di ICH durante TAOIpertensione arteriosaPROGRESS trial • Il rischio assoluto passava da 0.6%/anno a 0.3%/anno e 0.2%/anno rispettivamente Pressione arteriosa sistolica Chapman N et al, Stroke 2004

  33. Rischio emorragico e valori di INR Aumento rischio ICH di 2-5 volte, direttamente correlato ai valori di INR. Buona parte delle ICH occorrono, tuttavia, con INR in range terapeutico 40% Cantalapiedra A et al, J Thromb Thrombolysis 2006

  34. Risk analysis of thrombo-embolic and recurrent bleeding events in AC-related ICH Recurrent ICH: 8/108 pts (before restarting OAC) TE risk: 0,66/1000 pts-day at risk (8/11590 pts-day) De Vleeschouwe S et al, Acta Chir Bel 2005;105:268-274

  35. Discontinued anticoagulation for intracranial haemorrhage In a patient who is taking warfarin and experiences an intracranial haemorrhage, warfarinshould be stoppedand its effects reversed fully with vitamin K orally, subcutaneously or intravenously and clotting factor replacement. Thetiming of recommencinganticoagulation will depend on therisk of embolisationand on therisk of rebleeding. It is possible to resume warfarin therapy quite early, even within the first 7-14 days, without high risk of recurrent bleeding in patients with a high risk of re-embolisation and a small intracranial bleed.

  36. Avoiding CNS bleeding during antithrombotic therapy Hart RG et al. Stroke 2005;36:1588-1593

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