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Diagnostic yield and accuracy of CT angiography, MR angiography, and digital subtraction angiography for detection of macrovascular causes of intracerebral haemorrhage: prospective, multicentre cohort study. BMJ 2015; 351:h5762. 30. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure- lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet 2001; 358:1033. 31. Arima H, Chalmers J, Woodward M, et al. Lower target blood pressures are safe and effective for the prevention of recurrent stroke: the PROGRESS trial. J Hypertens 2006; 24:1201. 32. Zahuranec DB, Wing JJ, Edwards DF, et al. Poor long-term blood pressure control after intracerebral hemorrhage. Stroke 2012; 43:2580. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 24/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate 33. 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Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med 2016; 375:1033. 39. Arima H, Tzourio C, Anderson C, et al. Effects of perindopril-based lowering of blood pressure on intracerebral hemorrhage related to amyloid angiopathy: the PROGRESS trial. Stroke 2010; 41:394. 40. Chong BH, Chan KH, Pong V, et al. Use of aspirin in Chinese after recovery from primary intracranial haemorrhage. Thromb Haemost 2012; 107:241. 41. Flynn RW, MacDonald TM, Murray GD, et al. Prescribing antiplatelet medicine and subsequent events after intracerebral hemorrhage. Stroke 2010; 41:2606. 42. Viswanathan A, Rakich SM, Engel C, et al. Antiplatelet use after intracerebral hemorrhage. Neurology 2006; 66:206. 43. Biffi A, Halpin A, Towfighi A, et al. Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy. Neurology 2010; 75:693. 44. RESTART Collaboration. Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial. Lancet 2019; 393:2613. 45. Al-Shahi Salman R, Dennis MS, Sandercock PAG, et al. Effects of Antiplatelet Therapy After Stroke Caused by Intracerebral Hemorrhage: Extended Follow-up of the RESTART Randomized Clinical Trial. JAMA Neurol 2021; 78:1179. 46. Gaist D, Hald SM, Garc a Rodr guez LA, et al. Association of Prior Intracerebral Hemorrhage With Major Adverse Cardiovascular Events. JAMA Netw Open 2022; 5:e2234215. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 25/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate 47. Poli D, Antonucci E, Dentali F, et al. Recurrence of ICH after resumption of anticoagulation with VK antagonists: CHIRONE study. Neurology 2014; 82:1020. 48. Yung D, Kapral MK, Asllani E, et al. Reinitiation of anticoagulation after warfarin-associated intracranial hemorrhage and mortality risk: the Best Practice for Reinitiating Anticoagulation Therapy After Intracranial Bleeding (BRAIN) study. Can J Cardiol 2012; 28:33. 49. Vestergaard AS, Skj th F, Lip GY, Larsen TB. Effect of Anticoagulation on Hospitalization Costs After Intracranial Hemorrhage in Atrial Fibrillation: A Registry Study. Stroke 2016; 47:979. 50. Claassen DO, Kazemi N, Zubkov AY, et al. Restarting anticoagulation therapy after warfarin- associated intracerebral hemorrhage. Arch Neurol 2008; 65:1313. 51. Majeed A, Kim YK, Roberts RS, et al. Optimal timing of resumption of warfarin after intracranial hemorrhage. Stroke 2010; 41:2860. 52. Cannegieter SC, Rosendaal FR, Bri t E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation 1994; 89:635. 53. Murthy SB, Gupta A, Merkler AE, et al. Restarting Anticoagulant Therapy After Intracranial Hemorrhage: A Systematic Review and Meta-Analysis. Stroke 2017; 48:1594. 54. Biffi A, Kuramatsu JB, Leasure A, et al. Oral Anticoagulation and Functional Outcome after Intracerebral Hemorrhage. Ann Neurol 2017; 82:755. 55. Ivany E, Ritchie LA, Lip GYH, et al. Effectiveness and Safety of Antithrombotic Medication in Patients With Atrial Fibrillation and Intracranial Hemorrhage: Systematic Review and Meta- Analysis. Stroke 2022; 53:3035. 56. Pisters R, Lane DA, Nieuwlaat R, et al. A novel user-friendly score (HAS-BLED) to assess 1- year risk of major bleeding in patients with atrial fibrillation: the Euro Heart Survey. Chest 2010; 138:1093. 57. Donz J, Rodondi N, Waeber G, et al. Scores to predict major bleeding risk during oral anticoagulation therapy: a prospective validation study. Am J Med 2012; 125:1095. 58. Eckman MH, Rosand J, Knudsen KA, et al. Can patients be anticoagulated after intracerebral hemorrhage? A decision analysis. Stroke 2003; 34:1710. 59. Farmakis D, Davlouros P, Giamouzis G, et al. Direct Oral Anticoagulants in Nonvalvular Atrial Fibrillation: Practical Considerations on the Choice of Agent and Dosing. Cardiology 2018; 140:126. 60. Connolly SJ, Eikelboom J, Joyner C, et al. Apixaban in patients with atrial fibrillation. N Engl J Med 2011; 364:806. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 26/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate 61. Poli D, Antonucci E, Vignini E, et al. Anticoagulation resumption after intracranial hemorrhage in patients treated with VKA and DOACs. Eur J Intern Med 2020; 80:73. 62. Turagam MK, Osmancik P, Neuzil P, et al. Left Atrial Appendage Closure Versus Oral Anticoagulants in Atrial Fibrillation: A Meta-Analysis of Randomized Trials. J Am Coll Cardiol 2020; 76:2795. 63. Tzikas A, Freixa X, Llull L, et al. Patients with intracranial bleeding and atrial fibrillation treated with left atrial appendage occlusion: Results from the Amplatzer Cardiac Plug registry. Int J Cardiol 2017; 236:232. 64. Tzikas A. Left Atrial Appendage Occlusion with Amplatzer Cardiac Plug and Amplatzer Amulet: a Clinical Trials Update. J Atr Fibrillation 2017; 10:1651. 65. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2019; 50:e344. 66. Shoamanesh A, Selim M. Use of Lipid-Lowering Drugs After Intracerebral Hemorrhage. Stroke 2022; 53:2161. 67. Laufs U, Gertz K, Huang P, et al. Atorvastatin upregulates type III nitric oxide synthase in thrombocytes, decreases platelet activation, and protects from cerebral ischemia in normocholesterolemic mice. Stroke 2000; 31:2442. 68. Asahi M, Huang Z, Thomas S, et al. Protective effects of statins involving both eNOS and tPA in focal cerebral ischemia. J Cereb Blood Flow Metab 2005; 25:722. 69. Pezzini A, Grassi M, Iacoviello L, et al. Serum cholesterol levels, HMG-CoA reductase inhibitors and the risk of intracerebral haemorrhage. The Multicenter Study on Cerebral Haemorrhage in Italy (MUCH-Italy). J Neurol Neurosurg Psychiatry 2016; 87:924. 70. Rist PM, Buring JE, Ridker PM, et al. Lipid levels and the risk of hemorrhagic stroke among women. Neurology 2019; 92:e2286. 71. Ma C, Gurol ME, Huang Z, et al. Low-density lipoprotein cholesterol and risk of intracerebral hemorrhage: A prospective study. Neurology 2019; 93:e445. 72. Woo D, Deka R, Falcone GJ, et al. Apolipoprotein E, statins, and risk of intracerebral hemorrhage. Stroke 2013; 44:3013. 73. Amarenco P, Bogousslavsky J, Callahan A, et al. Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) Investigators. N Engl J Med 2006; 3555:549. 74. Amarenco P, Bogousslavsky J, Callahan A 3rd, et al. High-dose atorvastatin after stroke or transient ischemic attack. N Engl J Med 2006; 355:549. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 27/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate 75. Saliba W, Rennert HS, Barnett-Griness O, et al. Association of statin use with spontaneous intracerebral hemorrhage: A cohort study. Neurology 2018; 91:e400. 76. Ribe AR, Vestergaard CH, Vestergaard M, et al. Statins and Risk of Intracerebral Hemorrhage in Individuals With a History of Stroke. Stroke 2020; 51:1111. 77. Sanz-Cuesta BE, Saver JL. Lipid-Lowering Therapy and Hemorrhagic Stroke Risk: Comparative Meta-Analysis of Statins and PCSK9 Inhibitors. Stroke 2021; 52:3142. 78. Pandit AK, Kumar P, Kumar A, et al. High-dose statin therapy and risk of intracerebral hemorrhage: a meta-analysis. Acta Neurol Scand 2016; 134:22. 79. Tai SY, Lin FC, Lee CY, et al. Statin use after intracerebral hemorrhage: a 10-year nationwide cohort study. Brain Behav 2016; 6:e00487. 80. Westover MB, Bianchi MT, Eckman MH, Greenberg SM. Statin use following intracerebral hemorrhage: a decision analysis. Arch Neurol 2011; 68:573. 81. Haussen DC, Henninger N, Kumar S, Selim M. Statin use and microbleeds in patients with spontaneous intracerebral hemorrhage. Stroke 2012; 43:2677. 82. Romero JR, Preis SR, Beiser A, et al. Risk factors, stroke prevention treatments, and prevalence of cerebral microbleeds in the Framingham Heart Study. Stroke 2014; 45:1492. 83. Bai Y, Hu Y, Wu Y, et al. A prospective, randomized, single-blinded trial on the effect of early rehabilitation on daily activities and motor function of patients with hemorrhagic stroke. J Clin Neurosci 2012; 19:1376. 84. Selim M, Foster LD, Moy CS, et al. Deferoxamine mesylate in patients with intracerebral haemorrhage (i-DEF): a multicentre, randomised, placebo-controlled, double-blind phase 2 trial. Lancet Neurol 2019; 18:428. 85. Sreekrishnan A, Leasure AC, Shi FD, et al. Functional Improvement Among Intracerebral Hemorrhage (ICH) Survivors up to 12 Months Post-injury. Neurocrit Care 2017; 27:326. 86. Shah VA, Thompson RE, Yenokyan G, et al. One-Year Outcome Trajectories and Factors Associated with Functional Recovery Among Survivors of Intracerebral and Intraventricular Hemorrhage With Initial Severe Disability. JAMA Neurol 2022; 79:856. 87. Cumming TB, Thrift AG, Collier JM, et al. Very early mobilization after stroke fast-tracks return to walking: further results from the phase II AVERT randomized controlled trial. Stroke 2011; 42:153. 88. Foster L, Robinson L, Yeatts SD, et al. Effect of Deferoxamine on Trajectory of Recovery After Intracerebral Hemorrhage: A Post Hoc Analysis of the i-DEF Trial. Stroke 2022; 53:2204. 89. Saulle MF, Schambra HM. Recovery and Rehabilitation after Intracerebral Hemorrhage. Semin Neurol 2016; 36:306. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 28/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate 90. Delcourt C, Sato S, Zhang S, et al. Intracerebral hemorrhage location and outcome among INTERACT2 participants. Neurology 2017; 88:1408. 91. Kim KH, Kim HD, Kim YZ. Comparisons of 30-day mortalities and 90-day functional recoveries after first and recurrent primary intracerebral hemorrhage attacks: a multiple- institute retrospective study. World Neurosurg 2013; 79:489. 92. Pasi M, Casolla B, Kyheng M, et al. Long-term functional decline of spontaneous intracerebral haemorrhage survivors. J Neurol Neurosurg Psychiatry 2021; 92:249. 93. Planton M, Saint-Aubert L, Raposo N, et al. High prevalence of cognitive impairment after intracerebral hemorrhage. PLoS One 2017; 12:e0178886. 94. Banerjee G, Summers M, Chan E, et al. Domain-specific characterisation of early cognitive impairment following spontaneous intracerebral haemorrhage. J Neurol Sci 2018; 391:25. 95. Donnellan C, Werring D. Cognitive impairment before and after intracerebral haemorrhage: a systematic review. Neurol Sci 2020; 41:509. 96. Flaherty ML, Haverbusch M, Sekar P, et al. Long-term mortality after intracerebral hemorrhage. Neurology 2006; 66:1182. 97. Fogelholm R, Murros K, Rissanen A, Avikainen S. Long term survival after primary intracerebral haemorrhage: a retrospective population based study. J Neurol Neurosurg Psychiatry 2005; 76:1534. 98. Gonz lez-P rez A, Gaist D, Wallander MA, et al. Mortality after hemorrhagic stroke: data from general practice (The Health Improvement Network). Neurology 2013; 81:559. 99. Hansen BM, Nilsson OG, Anderson H, et al. Long term (13 years) prognosis after primary intracerebral haemorrhage: a prospective population based study of long term mortality, prognostic factors and causes of death. J Neurol Neurosurg Psychiatry 2013; 84:1150. Topic 129071 Version 14.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 29/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate GRAPHICS Medications and other substances that may increase the risk of bleeding or bruising Drug class or substance Mechanism Anticoagulants Interfere with clot formation (secondary hemostasis) Antiplatelet agents, including NSAIDs Interfere with platelet function (primary hemostasis) Glucocorticoids Interfere with vascular integrity Antibiotics Cause vitamin K deficiency, especially with longer use Some interfere with platelet function SSRIs Interfere with platelet function (primary hemostasis) Alcohol Complications of liver disease may affect clot formation and may cause thrombocytopenia May cause thrombocytopenia due to direct marrow toxicity Vitamin E Interferes with vitamin K metabolism in some individuals Garlic Interferes with platelet function in some individuals Gingko biloba Unknown This is a partial list that does not include drugs used for cancer therapy or drugs that alter the metabolism of anticoagulants. The magnitude of increased bleeding risk depends on many factors including the patient's other bleeding risk factors and the specific drug, dose, and duration of use. Fish oil is often cited, but bleeding risk does not appear to be increased. Refer to drug information monographs and UpToDate topics for further information. NSAIDs: nonsteroidal antiinflammatory drugs; SSRIs: selective serotonin reuptake inhibitors. Graphic 120264 Version 2.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 30/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Evaluating the underlying etiology of nontraumatic intracerebral hemorrhage This is an algorithm to guide etiologic testing; additional testing may be indicated for patients who develop new or worsening symptoms during recovery period. Refer to the UpToDate topic on secondary prevention and long-term prognosis of spontaneous intracerebral hemorrhage for additional details. ICH: intracerebral hemorrhage. Refer to the separate UpToDate table on clinical and neuroimaging features of intracerebral hemorrhage associated with underlying causes. Lobar or cortical ICH, evidence of multifocal superficial siderosis, age 55 years, and other sources for hemorrhagic features excluded. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 31/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Refer to the UpToDate topic on cerebral amyloid angiopathy for additional details. Graphic 132295 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 32/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Distinctive distribution of cerebral microbleeds (A-C) CMBs on T2*-weighted gradient echo MRI sequences suggestive of deep penetrating (hypertensive) vasculopathy. CMBs predominate in bilateral thalami (A), brainstem (B), and dentate nucleus of cerebellum (C). (D-F) CMBs on T2*-weighted gradient echo MRI sequences suggestive of cerebral amyloid angiopathy. CMBs predominate in cerebral hemispheres (D, E). Associated findings include lobar hemorrhage (D; arrow and thick arrow) and superficial siderosis (F; circles). CMB: cerebral microbleeds; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 33/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Graphic 132282 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 34/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Clinical and neuroimaging features of intracerebral hemorrhage associated with underlying causes Alternative Specifying ICH Characteristic Other associated features underlying feature underlying cause causes Basal ganglia or brainstem Deep perforating vasculopathy (HTN) CMBs in basal ganglia, thalamus, pons, cerebellar location nuclei Subcortical white matter lesions on MRI Deep perforating territory ischemic infarcts Clinical history of HTN or diabetes mellitus Lobar location Cerebral amyloid angiopathy Deep penetrating vasculopathy (HTN) Cortico-subcortical CMBs Convexal superficial siderosis Clinical history of cognitive impairment Intraventricular hemorrhage Arteriovenous malformation Deep penetrating vasculopathy (HTN) Flow voids within or adjacent to ICH Calcification within or adjacent to ICH Cavernous malformation Small ICH with adjacent calcification Cavernous malformation Deep penetrating vasculopathy (HTN) T2-weighted image hyperintensity at center on MRI Peripheral rim of T2*- weighted gradient echo image hypointensity on MRI Subarachnoid Ruptured cerebral Perimesencephalic SAH predominates over basal surfaces hemorrhage Basal cisterns aneurysm hemorrhage Clinical history of Non-aneurysmal SAH thunderclap headache Subarachnoid hemorrhage Reversible cerebral vasoconstriction Trauma Hemispheric or cortical ICH Clinical history of recurrent thunderclap headache Cerebral amyloid Convexity syndrome angiopathy Cerebral venous thrombosis https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 35/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Arteriovenous malformation Simultaneous Infective endocarditis Cerebral amyloid CMBs acute infarcts angiopathy Mycotic aneurysms (typically distal arterial locations) Deep penetrating vasculopathy (HTN) Systemic/cutaneous evidence of embolism New heart murmur Cerebral vasculitis Multifocal segmental narrowing on vascular imaging Clinical history of new persistent headaches Progressive cognitive or other neurologic impairment Prominent edema Cerebral sinus thrombosis Subacute ICH of other etiologies Edema/hemorrhage extends to cortical surface Venous flow void (eg, delta and empty-delta signs) Clinical history of seizure or progressive headache Tumor (primary/metastatic) Multifocal lesions Contrast enhancement Clinical history of new persistent headaches Clinical exam findings may be milder than imaging abnormalities Hemorrhagic transformation of (Cytotoxic) Edema appears in distribution of arterial territory infarct Arterial stenosis or occlusion proximal to territory of hemorrhage Clinical history of ischemic risk factors Flow voids Moyamoya Arteriovenous malformation Basal ganglia or hemispheric location Bilateral (but may be asymmetric) narrowing of distal internal carotid or https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 36/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate proximal anterior/middle cerebral arteries Clinical history of episodes of transient weakness with vigorous laughing/crying (Prominent cause of ICH and infarcts in children) ICH: intracerebral hemorrhage; HTN: hypertension; CMB: cerebral microbleeds; MRI: magnetic resonance imaging; SAH: subarachnoid hemorrhage. Graphic 132289 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 37/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Acute and subacute lobar hemorrhage Noncontrast head CT shows acute right parietal ICH (A). T2* susceptibility-weighted sequence on MRI performed one day later shows an acute ICH in the right frontal and parietal hemisphere (B) as well as a subacute hemorrhage in the left occipital lobe (thick arrow) and chronic ICH in right inferior parietal lobule (C; arrow). In addition, multiple microbleeds at cerebral corticomedullary junctions (B, C) are consistent with cerebral amyloid angiopathy. CT: computed tomography; ICH: intracerebral hemorrhage; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. Graphic 132283 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 38/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Excessive perihematomal edema in a patient with hemorrhagic lung metastasis Noncontrast head CT showing left frontal ICH surrounded by excessive volume of hypodense vasogenic edema (A, B). MRI performed one day later shows hyperintense vasogenic edema on T2*-weighted gradient echo image (C). Pre- (D) and post-contrast (E) T1-weighted MRI images demonstrate enhancement (arrows) consistent with underlying tumor. CT: computed tomography; ICH: intracerebral hemorrhage; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. Graphic 132284 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 39/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Hemorrhagic transformation of ischemic infarction Noncontrast head CT (A) shows heterogeneous hyperdensity within hypodense region involving right frontal and insular lobes. On subsequent MRI of the brain, FLAIR (B), T2* gradient recall echo (C), and DWI (D) sequences show hypointense ICH (thin arrows) and hyperintensities consistent with acute infarction in the distribution of the right middle cerebral artery (thick arrows). CT: computed tomography; MRI: magnetic resonance imaging; FLAIR: fluid-attenuated inversion recovery; DWI: diffusion-weighted imaging; ICH: intracerebral hemorrhage. Courtesy of Glenn A Tung, MD, FACR. Graphic 132275 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 40/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Enhancing intracranial vessels associated with ICH due to AVM Noncontrast head CT showing right posterior frontal ICH (A, B). T2- weighted MRI images (C, D) and post-contrast T1-weighted MRI image (E) show flow voids and focal enhancement (arrows), both suspicious for AVM nidus. Subsequent digital subtraction angiograms images (F, G) show both pial AVM nidus (thick arrows). https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 41/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate CT: computed tomography; ICH: intracerebral hemorrhage; MRI: magnetic resonance imaging; AVM: arteriovenous malformation. Courtesy of Glenn A Tung, MD, FACR. Graphic 132285 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 42/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Multifocal intracerebral hemorrhage from thyroid cancer Noncontrast head CT (A) shows multiple hyperdensities (arrows). T2*-weighted gradient echo MRI images show that some but not all lesions are hypointense hemorrhages (B, C). Pre- (D) and post-contrast (E) T1- weighted MRI images show contrast enhancement consistent with metastases. ICH: intracerebral hemorrhage; CT: computed tomography; MRI: magnetic resonance imaging. Courtesy of Glenn A Tung, MD, FACR. Graphic 132287 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 43/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Intraventricular hemorrhage due to ruptured periventricular arteriovenous malformation Noncontrast head CT (A) showing IVH. CT angiogram (B) showing abnormal tangle of vessels (circle) in the left perisplenial region. Digital subtraction angiogram (C) showing AVM nidus (circle). CT: computed tomography; IVH: intraventricular hemorrhage; AVM: arteriovenous malformation. Courtesy of Glenn A Tung, MD, FACR. Graphic 132281 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 44/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Goal blood pressure according to baseline risk for cardiovascular disease and method of measuring blood pressure Routine/conventional office blood pressure Unattended AOBPM, (manual measurement daytime ABPM, or home with stethoscope or blood pressure oscillometric device)* Higher-risk population 125 to 130/<80 120 to 125/<80 Known ASCVD Heart failure Diabetes mellitus Chronic kidney disease Age 65 years Calculated 10-year risk of ASCVD event 10% Lower-risk 130 to 139/<90 125 to 135/<90 None of the above risk factors All target ranges presented above are in mmHg. On average, blood pressure readings are 5 to 10 mmHg lower with digital, unattended, or out-of- office methods of measurement (ie, AOBPM, daytime ABPM, home blood pressure) than with routine/standard methods of office measurement (ie, manual auscultatory or oscillometric measurement), presumably due to the "white coat effect." However, it is critical to realize that this average difference in blood pressures according to the methodology of measurement applies to the population and not the individual. Some patients do not experience a white coat effect, and, therefore, there is some uncertainty in setting goals that are specific to the method of measurement. When treating to these goals, a patient may (inadvertently) attain a blood pressure below the given target. Provided the patient does not develop symptoms, side effects, or adverse events as a result of the treatment regimen, then reducing or withdrawing antihypertensive medications is unnecessary. Less aggressive goals than those presented in the table may be appropriate for specific groups of patients, including those with postural hypotension, the frail older adult patient, and those with side effects to multiple antihypertensive medications. AOBPM: automated oscillometric blood pressure monitoring; ABPM: ambulatory blood pressure monitoring; ASCVD: atherosclerotic cardiovascular disease; ACC/AHA: American College of Cardiology/American Heart Association. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 45/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Office blood pressure must be performed adequately in order to use such measurements to manage patients. Critical to an adequate office assessment of blood pressure are proper patient positioning (eg, seated in a chair, feet flat on the floor, arm supported, remove clothing covering the location of cuff placement) and proper technique (eg, calibrated device, proper-sized cuff). The average of multiple measurements should be used for management. Refer to UpToDate topics on measurement of blood pressure. Office readings should not be used to manage blood pressure unless it is performed adequately. Home blood pressure, like office blood pressure, must be performed adequately in order for the measurements to be used to manage patients. First, the accuracy of the home blood pressure device must be verified in the clinician's office. Second, the clinician should verify that the cuff and bladder that the patient will use are the appropriate size. Third, patients should measure their pressure after several minutes of rest and while seated in a chair (back supported and feet flat on the floor) with their arm supported (eg, resting on a table). Fourth, the blood pressure should be measured at different times per day and over multiple days. The average value of these multiple measurements is used for management. Home blood pressure readings should not be used to manage blood pressure unless it is performed adequately and in conjunction with office blood pressure or ambulatory blood pressure. The level of evidence supporting the lower goal in higher-risk individuals is stronger for some risk groups (eg, patients with known coronary heart disease, patients with a calculated 10-year risk 15%, chronic kidney disease) than for other risk groups (eg, patients with diabetes, patients with a prior stroke). Refer to UpToDate topics on goal blood pressure for a discussion of the evidence. Prior history of coronary heart disease (acute coronary syndrome or stable angina), prior stroke or transient ischemic attack, prior history of peripheral artery disease. In older adults with severe frailty, dementia, and/or a limited life expectancy, or in patients who are nonambulatory or institutionalized (eg, reside in a skilled nursing facility), we individualize goals and share decision-making with the patient, relatives, and caretakers, rather than targeting one of the blood pressure goals in the table. The 2013 ACC/AHA cardiovascular risk assessment calculator should be used to estimate 10-year cardiovascular disease risk. In the large subgroup of patients who have an initial (pretreatment) blood pressure 140/ 90 mmHg, but who do not have any of the other listed cardiovascular risk factors, some experts would set a more aggressive blood pressure goal of <130/<80 mmHg rather than those presented in the table. This more aggressive goal would likely reduce the chance of developing severe hypertension and ultimately lower the relative risk of cardiovascular events in these lower-risk patients over the long term. However, the absolute benefit of more aggressive blood pressure lowering in these patients is comparatively small, and a lower goal would require more intensive pharmacologic therapy and corresponding side effects. Graphic 117101 Version 3.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 46/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Considerations for individualizing antihypertensive therapy Indication or Antihypertensive drugs contraindication Compelling indications (major improvement in outcome independent of blood pressure) Heart failure with reduced ejection fraction ACE inhibitor or ARB, beta blocker, diuretic, aldosterone antagonist* Postmyocardial infarction ACE inhibitor or ARB, beta blocker, aldosterone antagonist Proteinuric chronic kidney ACE inhibitor or ARB disease Angina pectoris Beta blocker, calcium channel blocker Atrial fibrillation rate control Beta blocker, nondihydropyridine calcium channel blocker Atrial flutter rate control Beta blocker, nondihydropyridine calcium channel blocker Likely to have a favorable effect on symptoms in comorbid conditions Benign prostatic hyperplasia Alpha blocker Essential tremor Beta blocker (noncardioselective) Hyperthyroidism Beta blocker Migraine Beta blocker, calcium channel blocker Osteoporosis Thiazide diuretic Raynaud phenomenon Dihydropyridine calcium channel blocker Contraindications Angioedema Do not use an ACE inhibitor Bronchospastic disease Do not use a non-selective beta blocker Liver disease Do not use methyldopa Pregnancy (or at risk for) Do not use an ACE inhibitor, ARB, or renin inhibitor (eg, aliskiren) Second- or third-degree heart block Do not use a beta blocker, nondihydropyridine calcium channel blocker unless a functioning ventricular pacemaker Drug classes that may have adverse effects on comorbid conditions Depression Generally avoid beta blocker, central alpha-2 agonist Gout Generally avoid loop or thiazide diuretic Hyperkalemia Generally avoid aldosterone antagonist, ACE inhibitor, ARB, renin inhibitor Hyponatremia Generally avoid thiazide diuretic https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 47/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Renovascular disease Generally avoid ACE inhibitor, ARB, or renin inhibitor ACE: angiotensin-converting enzyme; ARB: angiotensin receptor blocker. A benefit from an aldosterone antagonist has been demonstrated in patients with NYHA class III-IV heart failure or decreased left ventricular ejection fraction after a myocardial infarction. Adapted from: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA 2003; 289:2560. Graphic 63628 Version 15.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 48/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Can anticoagulation be resumed after intracerebral hemorrhage*? ICH: intracerebral hemorrhage. Applicable only for patients with a persistent thromboembolic indication for anticoagulation. Timing of initiating/resuming medication depends on strength of indication and ICH features. Refer to the UpToDate topic on secondary prevention and long-term prognosis of spontaneous intracerebral hemorrhage for additional details. Cerebral vascular malformation, ruptured cerebral aneurysm or intracranial dissection, primary or metastatic tumor, cerebral venous thrombosis, cerebral vasculitis, or other cerebral vasculopathy. Refer to the UpToDate topic on secondary prevention and long-term https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 49/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate prognosis of spontaneous intracerebral hemorrhage for additional details. Examples include recurrent deep venous thrombosis or pulmonary embolus. Known bleeding diathesis, severe thrombocytopenia (<50,000/microL), abnormal liver or kidney function, or uncontrolled hypertension; patient prioritizes prevention of hemorrhagic over thromboembolic complications. Graphic 132293 Version 1.0 https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-secondary-prevention-and-long-term-prognosis/print 50/56 7/6/23, 12:54 PM Spontaneous intracerebral hemorrhage: Secondary prevention and long-term prognosis - UpToDate Comparison of the CHADS and CHA DS -VASc risk stratification scores for 2 patients with nonvalvular AF 2 2 Definition and scores for CHADS and Stroke risk stratification with the 2 CHA DS -VASc CHADS and CHA DS -VASc scores 2 2 2 2 2 Unadjusted [1] CHADS acronym Score CHADS acronym ischemic stroke rate (% per year) 2 2 Congestive HF 1 0 0.6 Hypertension 1 1 3.0 Age 75 years 1 2 4.2 Diabetes mellitus 1 3 7.1 Stroke/TIA/TE 2 4 11.1 Maximum score 6 5 12.5 6 13.0 Unadjusted ischemic stroke rate CHA DS -VASc acronym 2 2 [2] CHA DS -VASc acronym Score 2 2 (% per year) Congestive HF 1 0 0.2