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(BQ) Part 1 book Critical care of the stroke patient has contents: Intracranial pressure monitoring in cerebrovascular disease, cerebral blood flow, antivirus therapy in cerebrovascular disease, anagement of lumbar drains in cerebrovascular disease,... and other contents.
Critical Care of the Stroke Patient Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:13 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:13 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 Critical Care of the Stroke Patient Edited by Stefan Schwab Professor and Director, Department of Neurology, University of Erlangen-Nuremberg, Erlangen, Germany Daniel Hanley Jeffrey and Harriet Legum Professor and Director, Division of Brain Injury Outcomes, The Johns Hopkins Medical Institutions, Baltimore, MD, USA A David Mendelow Professor of Neurosurgery, Institute of Neuroscience, University of Newcastle Upon Tyne, Newcastle Upon Tyne, UK Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:13 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 University Printing House, Cambridge CB2 8BS, United Kingdom Cambridge University Press is part of the University of Cambridge It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning and research at the highest international levels of excellence www.cambridge.org Information on this title: www.cambridge.org/9780521762564 © Cambridge University Press This publication is in copyright Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press First published 2014 Printing in the United Kingdom by TJ International Ltd Padstow Cornwall A catalogue record for this publication is available from the British Library Library of Congress Cataloguing in Publication data Critical care of the stroke patient / edited by Stefan Schwab, Daniel Hanley, A David Mendelow Includes bibliographical references and index ISBN 978-0-521-76256-4 (hardback) I Schwab, S (Stefan), editor of compilation II Hanley, D F (Daniel F.), editor of compilation III Mendelow, A David., editor of compilation [DNLM: Stroke – therapy Critical Care – methods WL 356] ISBN 978-0-521-76256-4 Hardback Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate Every effort has been made in preparing this book to provide accurate and up-to-date information which is in accord with accepted standards and practice at the time of publication Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved Nevertheless, the authors, editors and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation The authors, editors and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:13 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 Contents List of contributors Section Monitoring Techniques Intracranial pressure monitoring in cerebrovascular disease page viii Anthony Frattalone and Wendy C Ziai Cerebral blood flow 20 Rajat Dhar and Michael C Diringer Brain tissue oxygen monitoring in cerebrovascular diseases 37 Klaus Zweckberger and Karl L Kiening Cerebral microdialysis in cerebrovascular disease 44 Paul M Vespa Ultrasound and other noninvasive techniques used in monitoring cerebrovascular disease 54 Guănter Seidel Scales in the neurointensive care unit 66 Elise Rowan and Barbara A Gregson Section Interventions Antiedema therapy in cerebrovascular disease 79 81 Dimitre Staykov and Juărgen Bardutzky Decompressive surgery in cerebrovascular disease 90 Katayoun Vahedi and Franc¸ois Proust v Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:27 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 vi Contents 9a Neuroradiologic intervention in cerebrovascular disease 19 103 Neuroradiological interventions in cerebrovascular disease: intracranial revascularization 243 Sandeep Ankolekar and Philip Bath Olav Jansen and Soenke Peters 9b Blood pressure management in acute ischemic stroke 120 Section Critical Care of Intracranial Hemorrhage 255 Martin Radvany and Philippe Gailloud 10 The use of hypothermia in cerebrovascular disease 20 129 11 External ventricular drainage in hemorrhagic stroke 21a Management of acute hypertensive response in the ICH patient 12 Management of lumbar drains in cerebrovascular disease 21b Respiratory care of the ICH patient 13 Intravenous and intra-arterial thrombolysis for acute ischemic stroke 158 21c Nutrition in the ICH patient Decompressive surgery and hypothermia 21d Management of infections in the ICH patient 167 21e Management of cerebral edema in the ICH patient 22a Surgery for spontaneous intracerebral hemorrhage 22b Minimally invasive treatment options for spontaneous intracerebral hemorrhage 16 Critical care of basilar artery occlusion 194 22c Image-guided endoscopic evacuation of spontaneous intracerebral hemorrhage 335 Justin A Dye, Daniel T Nagasawa, Joshua Perttu J Lindsberg, Tiina Sairanen, and R Dusick, Winward Choy, Isaac Yang, Paul Heinrich P Mattle 17 329 Andrew Losiniecki and Mario Zuccarello 190 H Bart van der Worp and Stefan Schwab 320 A David Mendelow, Barbara A Gregson, and Patrick Mitchell M Hemmen Space-occupying hemispheric infarction: clinical course, prediction, and prognosis 315 Neeraj S Naval and J Ricardo Carhuapoma 169 179 306 Edgar Santos and Oliver W Sakowitz Rainer Kollmar, Patrick Lyden, and Thomas 15 297 Dimitre Staykov and Juărgen Bardutzky Martin Koăhrmann and Stefan Schwab 14 286 Omar Ayoub and Jeanne Teitelbaum Dimitre Staykov and Hagen B Huttner Section Critical Care of Ischemic Stroke 274 Wondwossen G Tekle and Adnan I Qureshi 145 Mahua Dey, Jennifer Jaffe, and Issam A Awad 257 Corina Epple and Thorsten Steiner Dan Holmes, Sara Pitoni, Louise Sinclair, and Peter J D Andrews Management of intracranial hemorrhage: early expansion and second bleeds M Vespa, and Neil A Martin Critical care of cerebellar stroke 206 23 Tim Nowe and Eric Juăttler Intraventricular hemorrhage 348 Wendy C Ziai and Daniel Hanley 18 Rare specific causes of stroke Alexander Beck, Philipp Goălitz, and Peter D Schellinger 226 24 Interventions for cerebellar hemorrhage Jens Witsch and Eric Juăttler Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:27 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 363 Contents 25 Interventions for brainstem hemorrhage 32 378 33 26 Surgery for arteriovenous malformations 385 Radiation therapy for arteriovenous malformations 34 387 394 Oliver Ganslandt, Sabine Semrau, and Reiner 28 Management of cavernous angiomas of the brain Section Critical Care of Cerebral Venous Thrombosis Medical interventions for subarachnoid hemorrhage Craniotomy for treatment of aneurysms 423 437 Arnd Doărfler Ischemic brain damage in traumatic brain injury (TBI): extradural, subdural, and intracerebral hematomas and cerebral contusions 501 515 447 517 A David Mendelow Index Endovascular interventions for subarachnoid hemorrhage 499 421 Patrick Mitchell 31 Identification, differential diagnosis, and therapy for cerebral venous thrombosis Section Vascular Disease Syndromes Associated With Traumatic Brain Injury Joji B Kuramatsu and Hagen B Huttner 30 490 400 36 29 Management of cardiopulmonary dysfunction in subarachnoid hemorrhage Jose´ M Ferro and Patrı´cia Canha˜o Mahua Dey and Issam A Awad Section Critical Care of Subarachnoid Hemorrhage 480 Jan-Oliver Neumann and Oliver W Sakowitz 35 Fietkau Management of metabolic derangements in subarachnoid hemorrhage Kara L Krajewski and Oliver W Sakowitz A David Mendelow, Anil Gholkar, Raghu Vindlacheruvu, and Patrick Mitchell 27 464 Rajat Dhar and Michael C Diringer Berk Orakcioglu and Andreas W Unterberg Section Critical Care of Arteriovenous Malformations Management of vasospasm in subarachnoid hemorrhage The color plate section can be found between pages 252 and 253 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:27 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 538 vii Contributors Peter J D Andrews Department of Anaesthesia, Critical Care & Pain Medicine, University of Edinburgh, and Consultant, Critical Care, Western General Hospital, Lothian University Hospitals Division, Edinburgh, Scotland, UK Sandeep Ankolekar Division of Stroke, University of Nottingham, Nottingham, UK Issam A Awad Section of Neurosurgery and Neurovascular Surgery Program, Division of Biological Sciences and the Pritzker School of Medicine, The University of Chicago, Chicago, IL, USA Omar Ayoub Assistant Professor of Neurology, Stroke, and Neurocritical Care, Jeddah, Saudi Arabia Philip Bath Division of Stroke Medicine, University of Nottingham, Nottingham, UK Juărgen Bardutzky Department of Neurology, University of Freiburg, Freiburg, Germany Alexander Beck Department of Neurology, Friedrich-AlexanderUniversity of Erlangen-Nuremberg, Erlangen, Germany viii Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:12:41 GMT 2015 http://ebooks.cambridge.org/ebook.jsf?bid=CBO9780511659096 Cambridge Books Online © Cambridge University Press, 2015 272 Chapter 20: Management of intracranial hemorrhage [60] Huttner HB, Schellinger PD, Hartmann M, et al Hematoma growth and outcome in treated neurocritical care patients with intracerebral hemorrhage related to oral anticoagulant therapy Comparison of acute treatment strategies using vitamin K, fresh frozen plasma, and prothrombin complex concentrates Stroke 2006;37:1465–70 [61] Steiner T, Freiberger A, Griebe M, et al International normalised ratio normalisation in patients with coumarin-related intracranial haemorrhages – the INCH trial: a randomised controlled multicentre trial to compare safety and preliminary efficacy of fresh frozen plasma and prothrombin complex – study design and protocol Int J Stroke 2011;6(3):271–7 [62] Boeer A, Voth E, Henze T, Prange HW Early heparin therapy in patients with spontaneous intracerebral haemorrhage J Neurol Neurosurg Psychiatry 1991;54:466–7 [63] Eckman MH, Rosand J, Knudsen KA, Singer DE, Greenberg SM Can patients be anticoagulated after intracerebral hemorrhage? A decision analysis Stroke 2003;34:1710–11 [64] Greenberg SM, Eng JA, Ning M, Smith EE, Rosand J Hemorrhage burden predicts recurrent intracerebral hemorrhage after lobar hemorrhage Stroke 2004;35:1415–20 [65] Majeed A, Kim Y, Roberts R, Holmström M, Schulman S Optimal timing of resumption of wafarin after intracranial hemorrhage Stroke 2010;41:2860–6 [66] Connolly SJ, Ezekowitz MD, Yusuf S, et al Dabigatran versus warfarin in patients with atrial fibrillation N Engl J Med 2009;361:1139–51 [67] Wallentin L, Yusuf S, Ezekowitz MD, et al Efficacy and safety of dabigatran compared with warfarin at different levels of international normalised ratio control for stroke prevention in atrial fibrillation: an analysis of the RE-LY trial Lancet 2010;376:975–83 [68] Steiner T, Bohm M, Dichgans M, et al Recommendations for the emergency management of complications associated with new direct oral anticoagulants (doac) apixaban, dabigatran, and rivaroxaban Clinical Res Cardiol 2013;102:399–412 [69] Zhou W, Schwarting S, Illanes S, et al Hemostatic therapy in experimental intracerebral hemorrhage associated with the direct thrombin inhibitor dabigatran Stroke 2011;42:3594–9 [70] Patel MR, Mahaffey KW, Garg J, et al Rivaroxaban versus warfarin in nonvalvular atrial fibrillation N Engl J Med 2011;365:883–91 [71] Eerenberg ES, Kamphuisen PW, Sijpkens MK, Meijers JC, Buller HR Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate a randomized, placebocontrolled, crossover study in healthy subjects Circulation 2011: 124 [72] Leissinger CA, Blatt PM, Hoots WK, Ewenstein B Role of prothrombin complex concentrates in reversing warfarin anticoagulation: a review of the literature Am J Hematol 2008;83:137–43 [73] van Ryn J, Stangier J, Haertter S, et al Dabigatran etexilate – a novel, reversible, oral direct thrombin inhibitor: interpretation of coagulation assays and reversal of anticoagulant activity Thromb Haemost 2010;103(6):1116–27 [74] van Ryn J, Stangier J, Haertter S, et al Dabigatran etexilate – a novel, reversible, oral direct thrombin inhibitor: interpretation of coagulation assays and reversal of anticoagulant activity Thromb Haemost 2010;103:1116–27 [75] Piriyawat P, Morgenstern LB, Yawn D, Hall CE, Grotta JC Treatment of acute intracerebral hemorrhage with e-aminocaproic acid – a pilot study Neurocritical Care 2004;1:47–51 [76] Vujkovac B, Sabovic M Treatment of subdural and intracerebral haematomas in a haemodialysis patient with tranexamic acid Nephrol Dial Transplant 2000;15:107–9 [77] Carhuapoma JR, Barrett RJ, Keyl PM, Hanley DF, Johnson RR Stereotactic aspiration-thrombolysis of intracerebral hemorrhage and its impact on perihematoma brain edema Neurocrit Care 2008;8:322–9 [78] Morgan T, Zuccarello M, Narayan R, et al Preliminary findings of the minimally-invasive surgery plus rtPA for intracerebral hemorrhage evacuation (MISTIE) clinical trial Acta Neurochir Suppl 2008;105:147–51 [79] The Medicines Company Clevidipine in the treatment of patients with acute hypertension and intracerebral hemorrhage (accelerate) http://clinicaltrialsgov/show/ NCT00666328; Acess date: 16.3.2009 [80] Lyden PD, Shuaib A, Lees KR, et al Safety and tolerability of nxy-059 for acute intracerebral hemorrhage: The chant trial Stroke 2007;38:2262–9 [81] Wang J, Tsirka SE Tuftsin fragment 1–3 is beneficial when delivered after the induction of intracerebral hemorrhage Stroke 2005;36:613–18 [82] Lee ST, Chu K, Jung KH, et al Memantine reduces hematoma expansion in experimental intracerebral hemorrhage, resulting in functional improvement J Cereb Blood Flow Metab 2006;26:536–44 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:15 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.025 Cambridge Books Online © Cambridge University Press, 2015 Chapter 20: Management of intracranial hemorrhage [83] Lee ST, Chu K, Sinn DI, et al Erythropoietin reduces perihematomal inflammation and cell death with enos and stat3 activations in experimental intracerebral hemorrhage J Neurochem 2006;96:1728–39 [84] Sinn DI, Kim SJ, Chu K, et al Valproic acid-mediated neuroprotection in intracerebral hemorrhage via histone deacetylase inhibition and transcriptional activation Neurobiol Dis 2007;26:464–72 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:15 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.025 Cambridge Books Online © Cambridge University Press, 2015 273 Cambridge Books Online http://ebooks.cambridge.org/ Critical Care of the Stroke Patient Edited by Stefan Schwab, Daniel Hanley, A David Mendelow Book DOI: http://dx.doi.org/10.1017/CBO9780511659096 Online ISBN: 9780511659096 Hardback ISBN: 9780521762564 Chapter 21a - Management of acute hypertensive response in the ICH patient pp 274-285 Chapter DOI: http://dx.doi.org/10.1017/CBO9780511659096.026 Cambridge University Press 21a Management of acute hypertensive response in the ICH patient Wondwossen G Tekle and Adnan I Qureshi Introduction Pathophysiology About 37000 to 52400 people in the United States suffer from intracerebral hemorrhage (ICH) every year (1) Hypertension is the most important risk factor for spontaneous ICH accounting for about 60–70% of cases (2) Broderick et al showed hypertension was the primary cause of ICH in 72% of the 188 patients evaluated in the study (3) Risk of ICH is increased in certain populations of hypertensive patients who are noncompliant with antihypertensive medication, are aged 55 years or younger, or are cigarette smokers Hispanics, African Americans, Native Americans, and those of Asian ancestry have higher incidence of ICH related to hypertension (4–6) Nearly two-thirds of hypertensive patients have uncontrolled blood pressure (BP) (greater than 140/90 mmHg) at admission (7) Control of BP among patients with chronic hypertension reduces the incidence of intracerebral hemorrhage (8–10) Elevated BP, termed as acute hypertensive response (AHR), is observed in over 60% of patients coming to the ER (11) A large and nationally representative survey (12) showed that over 75% of ICH patients had systolic blood pressure (SBP) > 140 and 20% greater than 180 mmHg at presentation Patients with stroke and high initial BP are at a 1.5–5.0-fold increased risk of death or dependency and clinical deterioration (13, 14) Cerebral autoregulation is a mechanism by which the brain maintains its normal blood flow despite fluctuations in cerebral perfusion pressure (CPP) over a range of mean arterial blood pressure (MAP) changes ranging from 60 to 150 mmHg (15) Pre-capillary arterioles in the brain are responsible for autoregulation, constricting during elevated BP and dilating during hypotension to maintain constant cerebral blood flow CPP is the difference between MAP and intracranial pressure, and the normal range of CPP is around 60– 100 mmHg During chronic hypertension, the autoregulation curve (Fig 21a.1) shifts to the right in order to maintain normal flow under higher systemic BP (16) The arterioles of small and medium size adapt to the persistently elevated systemic BP, which presumably results in structural changes in the walls of these small vessels and reduction in their baseline caliber Such changes likely stiffen the vessels and decrease their compliance, resulting in degenerative changes in arterioles and making them prone to rupture Breakage of elastic lamina, lipohyalinosis, granular or vesicular cellular degeneration, fibrinoid necrosis of the subendothelium with focal dilatations (microaneurysms) in the walls of cerebral vessels are among the main pathologic processes leading to vascular rupture in most cases of hypertension-related ICH (17,18) Critical Care of the Stroke Patient, ed Stefan Schwab, Daniel Hanley, and A David Mendelow Published by Cambridge University Press © Cambridge University Press 2014 274 Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:45 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.026 Cambridge Books Online © Cambridge University Press, 2015 CBF ml/100 mg/min Chapter 21a: Management of acute hypertensive response in the ICH patient 100 90 80 70 60 50 40 30 20 10 0 50 10 0 15 20 MAP mmHg 25 CBF = cerebral blood flow; MAP = mean arterial pressure Normotensive Hypertensive Fig 21a.1 Cerebral autoregulation in normotensive and chronically hypertensive patients Degeneration of smooth muscle cells may be the result of prolonged tension or spasm of the arterial wall as a result of longstanding hypertension (15) Most bleeding in hypertension-related ICH occurs at or near the bifurcation of small arterioles, ranging between 50 and 700 µm in diameter Rationale for treatment of AHR in acute ICH Elevated SBP after ICH is associated with hemorrhage growth and poor outcome (19,20), although the cause and effect relationship is unclear SBP reduction may reduce the rate of hematoma expansion; however, conclusive evidence is still lacking As a result, controversy remains on what should be the ideal goal of treatment for the AHR Two recently concluded multicentre clinical trials documented the safety and tolerability of early and aggressive reduction of BP in acute phase of ICH (21,22) Large phase III trials are being planned to answer the bigger question of whether or not such treatments improve outcome Some of the crucial pathophysiologic and prognostic considerations pertaining to management of AHR in ICH are based on the effect of SBP reduction on regional cerebral blood flow (rCBF) and metabolism, hematoma expansion, peri-hematoma edema, and ultimately, clinical outcome Regional cerebral blood flow and metabolism in ICH Evidence suggests that SBP reduction in acute ICH may be tolerated because of reduced metabolism (hibernation) (23) and preserved autoregulation (24,25) in the perihematoma region Qureshi et al described three phases for CBF and metabolic changes in the perihematoma region (23) Hibernation is seen during the first 48 hours whereby a reduction in rCBF and metabolism occurs in both ipsilateral and contralateral hemispheres Reperfusion phase occurs between 48 hours and 14 days, and consists of a heterogeneous pattern of blood flow, including areas of normal, hypo- and hypercerebral perfusion Finally, normalization phase comes after 14 days and a normal blood flow pattern is restored except in the non-viable tissue Powers et al found that there was no change in both global and peri-hematoma rCBF and autoregulation was preserved in small- and medium-sized hematomas when MAP was reduced by a magnitude of 15% from baseline value (24) Zazulia et al demonstrated decreased rCBF Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:45 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.026 Cambridge Books Online © Cambridge University Press, 2015 275 276 Chapter 21a: Management of acute hypertensive response in the ICH patient and oxygen extraction fraction (OEF) (26) using positron emission tomography (PET) scan in acute phase of ICH Multiple other magnetic resonance imaging (MRI) and PET-based studies (27–30) have confirmed the absence of ischemia in the perihematomal tissue The mechanism underlying reduction in rCBF and metabolism in the peri-hematoma is unclear; although direct inhibition of mitochondrial function has been proposed (31–33) Some studies (34–37) suggested that an ‘ischemic penumbra’ may be seen when the hematoma is large and associated with elevated ICP (38) While local microvascular compression and impaired autoregulation are thought to be some of the mechanisms involved to create such an ischemic zone (34–36), it is arguable that decreasing BP could potentially impair rCBF and lead to further tissue ischemia In the setting of increased ICP after ICH, elevated BP may be helpful to maintain adequate cerebral perfusion pressure (CPP) Hematoma expansion and peri-hematoma edema Early elevation of SBP in ICH patients is associated with hematoma expansion (37,39,40) and peri-hematoma brain edema formation (41) Chen et al (42) observed a persistent elevation of BP in six of their eight patients before hematoma expansion Broderick et al (43) also recorded a SBP of at least 195 mmHg during the first hours after symptom onset in five out of six patients with hematoma expansion In one observational study, hematomas enlarged in 9% of patients with systolic blood pressure maintained below 150 mmHg and in 30% of those with systolic blood pressure maintained at less than 160 mmHg or a higher threshold (44) Yet, it remains unclear whether elevated systolic BP contributes to hemorrhage expansion or elevation in SBP occurs in response to increased ICP from hemorrhage growth (44) Some prospective studies of ICH growth did not find an independent association between clinical variables such as hypertension and ICH expansion (45,46) The Recombinant Activated Factor VII Intracerebral Hemorrhage Trial (FAST) found that baseline BP was associated with ICH growth in univariate but not multivariate analyses (47) In a study of patients with ischemic stroke (48), persistently elevated SBP was associated with formation of cerebral edema, although the prognostic value of relative peri-hematomal edema remains controversial (49) The Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT) (21) showed early intensive BP-lowering treatment attenuated hematoma growth over 72 hours in patients with ICH, but there were no appreciable effects on perihematomal edema Highlights of ATACH and INTERACT trials on safety and tolerability of early and aggressive reduction of BP in acute ICH The ATACH (50) was a traditional phase I, dose escalation, multicentre prospective study that recruited patients with ICH and SBP >170 mmHg who present to the emergency department within hours of symptom onset Intravenous nicardipine was administered to reduce SBP to three different target SBP tiers of 170– 200 mmHg, 140–170 mmHg, and 110–140 mmHg in the first, second, and third cohorts of patients respectively Primary outcomes of interest were: (1) treatment feasibility (achieving and maintaining the systolic blood pressure goals for 18–24 hours); (2) neurologic deterioration within 24 hours; and (3) serious adverse events within 72 hours ATACH found that the proportions of neurologic deterioration and serious adverse events were below the prespecified safety thresholds, and the 3-month mortality rate was lower than expected in all SBP tiers The INTERACT trial recruited 404 patients with CTconfirmed ICH and elevated SBP (150–220 mmHg) and randomly assigned to an intensive (target SBP 150 mmHg, then consider aggressive reduction of BP with continuous intravenous infusion, with frequent BP monitoring every minutes If SBP is >180 mmHg or MAP is >130 mmHg and there is evidence of or suspicion of elevated ICP, then consider monitoring ICP and reducing BP using intermittent or continuous intravenous medications to keep cerebral perfusion pressure >60 to 80 mmHg If SBP is >180 mmHg or MAP is >130 mmHg and there is no evidence of or suspicion of elevated ICP, then consider a modest reduction of BP (e.g MAP of 110 mmHg or target BP of 160/90 mmHg) using intermittent or continuous intravenous medications to control BP, and clinically re-examine the patient every 15 minutes SBP indicates systolic blood pressure; MAP, mean arterial pressure Reproduced with permission [54] Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:45 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.026 Cambridge Books Online © Cambridge University Press, 2015 277 278 Chapter 21a: Management of acute hypertensive response in the ICH patient and the EUSI guidelines (55) should be followed Great caution is advised about lowering BP too aggressively without concomitant management of cerebral perfusion pressure Frequent or continuous BP monitoring is necessary in all patients with ICH Even though BP can be monitored adequately with an inflatable cuff in most patients with acute hypertensive response, intra-arterial monitoring should be considered in patients who require frequent titration with intravenous antihypertensive agents and in patients whose neurological status is deteriorating ICP monitoring may be necessary in patients with a suspected increased ICP, to measure and preserve cerebral perfusion pressure during systemic BP lowering Patients with a poor level of consciousness, midline shift, or compression of basal cisterns on computed tomographic scan may be considered for ICP monitoring when being treated with antihypertensive agents The AHA guideline also recommends BP management tailored to the individual patient factors such as pre-morbid BP, presumed cause of hemorrhage, age, and elevated ICP MAP should be maintained between 90 and 130 mmHg As there is no evidence-based guideline on how low the BP can be in ICH, particularly those with no history of chronic hypertension, it is recommended that SBP be maintained above 90 mmHg in all cases of ICH (57) The European Union Stroke Initiative (EUSI) BP management recommendation (55) takes into account the patient’s premorbid BP status, and it is summarized as follows: Patients with known hypertension or signs of chronic hypertension (e.g electrocardiogram or retinal changes), an upper limit of SBP of 180 mmHg and a diastolic BP of 105 mmHg, and target BP is 160/ 100 mmHg (or MAP 120 mmHg) Patients without known history of hypertension, the upper limits are 160/95 mmHg, and the target BP is 150/90 mmHg (or MAP 110 mmHg) The mean BP reduction should always be limited to 70 mmHg by titrating the MAP The consensus to keep CPP >70 mmHg is derived from experience in traumatic brain injury and ICH which suggests that maintaining CPP >60 mmHg is associated with better outcome (58,59) The Brain Trauma Foundation (60) recommends maintaining cerebral perfusion pressure >70 mmHg to enhance perfusion to ischemic regions of the brain after severe traumatic injury However, it is worth noting that this global measure of CPP can underestimate the localized pressure, perfusion, and autoregulatory changes in focal ICH Until more sensitive measures based on direct local blood flow and metabolism parameters are discovered for routine clinical use, the standard CPP measurement should be utilized Antihypertensive agents and regimens The goal of pharmacologic reduction of AHR should be to achieve good BP control without promoting cerebral vasodilatation and increased cerebral blood volume (CBV) The agents that are recommended by the ASA for acute hypertensive response are either intravenous or transdermal agents with rapid onset and short duration of action to allow precise titration Table 21a.2 summarizes some of the characteristics of these agents Indirect comparisons suggest that intermittent intravenous bolus regimens of anti-hypertensives produce more variable BP control than continuous infusion regimens (63) A multicentre prospective observational study (63) reported the use of intravenous labetalol, hydralazine, and/or nitroprusside for maintaining BP >160/ 90 mmHg within 24 hours of symptom onset among patients with ICH Low rates of neurological deterioration and hematoma expansion were observed in treated patients Patients treated within hours of symptom onset were more likely to be functionally independent at month than patients who were treated between and 24 hours Another study (78) evaluated the tolerability and safety of intravenous nicardipine infusion within 24 hours of symptom onset to reduce and maintain MAP Target by 10 mmHg or less MAP > Target by more than 10 mmHg Repeat reading every minutes for 15 minutes No change Repeat reading after minutes No change Increase infusion by increments of 1−1.5 mg/h every 15 minutes to bring the MAP to the target range Increase infusion by increments of 2.5 mg/h every 15 minutes to bring the MAP to the target range If after stabilization of the target range, the MAP becomes less than the target range: MAP > Target by 10 mmHg or less Repeat reading every minutes for 15 minutes No change MAP > Target by more than 10 mmHg Repeat reading after minutes No change Decrease infusion by decrements of mg/h every 15 minutes to bring the MAP to the target range, or until medication is discontinued Decrease infusion by decrements of 2.5 mg/h every 15 minutes to bring the MAP to the target range Fig 21a.2 Nicardapine infusion protocol deterioration and hematoma expansion were observed among treated patients Recently, INTERACT and ATACH trials also showed the feasibility and tolerability of IV nicardipine and other anti-hypertensive infusion protocols Figure 21a.2 shows nicardipine infusion protocol used by our centre Management of hypertension with oral medications in the immediate post-ICH period A number of clinical trials have shown the benefit of treating hypertension in the immediate post-stroke Downloaded from Cambridge Books Online by IP 216.195.11.197 on Thu Nov 05 23:26:45 GMT 2015 http://dx.doi.org/10.1017/CBO9780511659096.026 Cambridge Books Online © Cambridge University Press, 2015 Chapter 21a: Management of acute hypertensive response in the ICH patient Clinical diagnosis of acute stroke Reduce BP if > 185/110 mmHg using short acting IV medications* Ischemic stroke Candidate for thrombolysis Reduce BP if >185/110 mmHg using short-acting IV medication a Emergent computed tomographic scan Not a candidate for thrombolysis Reduce BP if >220/120 mmHg using short-acting IV medication Avoid and treat hypotension (180 mmHg or MAP>130 mmHg using short-acting IV medication; ICP monitoring recommended to maintain CPP >60 mmHg b Intracerebral hemorrhage Do not suspect high ICP Reduce BP if SBP>180 mmHg or MAP>130 mmHg using short-acting IV medication Monitor neurological examination every 15 minutes b Treat with thrombolysis Maintain BP