Cerebral Protection in Cerebrovascular and Aortic Surgery PDF
Preview Cerebral Protection in Cerebrovascular and Aortic Surgery
Cerebral Protection in Cerebrovascular and Aortic Surgery J. Ennker . J. S. Coselli T. Treasure Editors Cerebral Protection in Cerebrovascular and Aortic Surgery Springer Editors address: J. EnnkerM.D. Heart Institute LahrIBaden Hobergweg7 D-77933 Lahr Germany Joseph S. Coselli, M.D. 6560 Fannin, =IF 1144 Houston, TX 77030 USA T. Treasure, M.D., MS, FRCS St. George Hospital Dept. of Cardiothoracic Surgery Blackshow Road London SW17 OQT Great Britain ISBN-13: 978-3-642-95989-9 e-ISBN-13: 978-3-642-95987-5 001: 10.1007/978-3-642-95987-5 Die Deutsche Bibliothek - CIP-Einheitsaufnahme Cerebral protection in cerebrovascular and aortic surgery / J. Ennker ... ed. - Darmstadt: Steinkopff ; New York: Springer, 1997 NE: Ennker, Jiirgen [Hrsg.] This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplica tion of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from SteinkopffVeriag. Violations are liable for prosecution under the German Copy right Law. © 1997 by Dr. Dietrich SteinkopffVeriag GmbH & Co. KG, Darmstadt Softcover reprint of the hardcover 1s t edition 1997 Medical Editor: Beate Riihlemann - English Editor: James C. Willis - Production: Heinz J. Schafer Cover Design: Erich Kirchner, Heidelberg The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Typesetting: Typoservice, Griesheim Preface The contributions in this book were originally presented in a symposium held in October 1995, at the SchloBhotel Blihlerhohe in Baden-Baden, on the theme about "Cerebral Pro tection in Cerebrovascular and Aortic Surgery". The symposium was planned to combine the experience of prominent authorities in cerebral physiology, neurology and neurosurgery with the experience of international surgeons operating on the diseased aorta and its supraaortic vessels. The first part focuses on cerebral monitoring, cerebral physiology and neurological disorders after operations on the aorta and its supraaortic vessels. The second part concentrates on the surgical techniques and corresponding results of some of the most experienced surgeons from leading centers of the world. The protection of the brain from hypoxic or ischemic injury is a major chaIlenge during repair of aortic arch aneurysms and operations on the supraaortic vessels. Operations in this difficult field pose one of the most complicate technical challenges in surgery today. The first successful replacement of an aortic arch aneurysma was carried out by DeBakey in 1957 (1) with an aortic homograft. For many years after this pioneering oper ation morbidity and mortality for the treatment of aortic pathology in the transverse arch location have remained unacceptably high. The early operations were carried out with one of the foIlowing two methods. One method was to establish circulation to the brachio cephalic vessels by placement of temporary bypass grafts originating off the proximal ascending aorta to be taken down at the completion of arch replacement. The second technique employed direct anteg rade perfusion through the brachiocephalic vessels with the aid of cardiopulmonary bypass. In 1975, Griepp and coworkers (2) reported that the use of profound hypothermia and circulatory arrest for cerebral protection during aortic surgery provided a far simpler and safer technique for repair of aortic arch pathology. With popularization of profound hypothermia and deep circulatory arrest the results of aortic arch surgery improved. Nevertheless, in case of arrest times exceeding 60 minutes the inci dence of neurological disorders and cerebral injury increased. This phenomenon was con firmed in clinical series by Griepp et a\. 1991 (3) and supported by E. S. Crawford and coworkers in 1993 (5). In an effort to prolong the safe period of hypothermic circulatory arrest Veda and associates (6) reported the use of continuous retrograde cerebral perfusion via the superior vena cava in 1990. This technique was first described by Ochsner and Mills in 1980 (4) who instaIled retrograde perfusion for treatment of massive air embolism occurring during cardiopulmonary bypass. In 1982, Lemole and coworkers published a technique of intermittent retrograde cerebral perfusion during profound hypothermia and circulatory arrest it. Today the technique of ante grade cerebral perfusion and the technique of retrograde cerebral perfusion are both in use. Among the most eminent surgeons of the antegrade perfusion technique are T. Kazui and J. Bachet who demonstrated their exceIlent results on neurologic outcome in their presentations. On the other hand J. CoselIi presented his results with no neurological complication using, retrograde cerebral perfusion. VI Preface --------------------------------------------------------------------------- To answer the question of which concept is best to protect the brain during operations on the aortic arch many new studies have to be performed. The questions of safe duration for brain perfusion, range of perfusion pressure or use of a cerebroplegia with antiischemic drugs, still have to be answered. We would like to thank the authors for their support and contributions. We are also indebted to Mrs. Ibkendanz and Mrs. Rtihlemann and others from the SteinkopffVerlag for assembling and publishing this book. Our special gratitude goes to our coworker Stefan Bauer for his support in organizing the symposium and his share in the production of the book. We hope that this book will serve as an useful synopsis of current knowledge of cerebral damage, cerebral protection and surgical management of pathology of the aortic arch and the supraaortic vessels. Lahr, December 1996 1. Ennker References 1. OeBakey ME, Cooley OA, Crawford ES, Morris GC (1957) Successful resection of fusiform aneurysm of the aortic arch with replacement by homograft. Surg Gynecol Obst 105: 656--{)64 2. Griepp RB, Stinson EB, Hollinsworth JF, Buehler 0 (1975) Prosthetic replacement of the aortic arch. J Thorac Cardiovasc Surg 70: 1051-1063 3. Griepp RB, Ergin MA, Lansman JL, Gall JO, Pogo G (1991) The physiology of hypothermic circulatory arrest. Semin Thorac Cardiovasc Surg 3: 188-193 4. Mills NL, Ochsner JL (1980) Massive air embolism during CPB: causes, prevention and management. J Thorac Cardiovasc Surg 80: 708-717 5. Svensson LG, Crawford ES, Rashkind SA et al. (1993) Deep hypothermia with circulatory arrest: deter minants of stroke and early mortality in 656 patients. J Thorac Cardiovasc Surg 106: 19-31 6. Veda Y, Miki S, Kusuhara K, Okita Y, Tahara T, Yamanaka K (1990) Surgical treatment of aneurysm of dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg (Torino) 31: 553-558 Contents Preface . ... . . .. .. . ....... ... . . .......... . .... . .. .. ..... V Protection, diagnosis and treatment of cerebral ischemia Neuroprotection in cerebral ischemia Paschen, W., K.-A. Hossmann ..... . . . . . ..... . . .. .. . . 3 PET, MRI, and MRS for imaging offunctional brain disorders Herholz, K., H. Lanfermann .... . .. . ...... . . .... .... . 11 Expression ofICAM-l and VCAM-l on endothelial cells after global cerebral ischemia and reperfusion in the rat Harringer, w., X.-M. You, G. Steinhoff, U. Linstedt, A. Haverich .......... 23 Cerebral protection during neurosurgical operations Hamer, J. . .... .. .. . . . . .. .. . . . . . ..... . .. . .. . . . .... . ... . . 27 Intensive care of acute ischemic stroke Hacke, w., S. Schwab, M. De Georgia 37 Cerebral protection in Cerebrovascular Surgery Anesthesia in cerebrovascular surgery Thiel, A., G. Hempelmann . . . . .. . . . .. ...... .. . . .. . ... . . .. .... 51 Neuromonitoring during carotid artery surgery: Somatosensory evoked potentials versus transcranial Doppler sonography Dinkel, M., H. Langer, H. Loerler, J. Pflumm, J. Schi.ittler, H. Schweiger 59 The choice of method for cerebral protection from ischemia in carotid endarterectomy Kazantchian, P.O., V A. Popov, T. V Rudakova ...... . ..... ... ...... 67 SEPs monitoring during carotid surgery: reliability and limitations Cirelli, M. R., F. Magnoni, L. Pedrini, M. D'Addato . . . . . . . . . . . . . . . . . . . 71 VIII Contents -------------------------------------------------------------- Effect of myocardial revascularization on the blood flow volume in carotid arteries Gagaev, Ao v., Ao L. Maximov, 1. Eo Soboleva, Eo V. Chebotar, Ao Ao Charov, Mo V. Riazanov, 1. Gagaeva 75 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Cerebral protection during simultaneous cerebrovascular and cardiac surgery using extracorporeal circulation for both procedures Finkbeiner, Y., Ao Schiessler, Jo Ennker 79 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Cerebral protection in the pediatric age group Studies of hypothermic circulatory arrest and low flow bypass as used for congenital heart surgery Jonas, Ro Ao 93 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Alteration of cerebral blood flow velocity (CBFV) in neonates and infants after cardiac surgery. Relation to occurrence of cerebral injury? Abdul-Khaliq, Ho, Ao Gamillscheg, F. Uhlemann, V. Alexi-Meskishvili, Yo Weng, Ro Hetzer, P. Eo Lange 103 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Change ofregional cerebral hemoglobin saturation (rS02) in children undergoing corrective cardiac surgery of congenital heart disease by means of high-flow cardiopulmonary bypass (CPB) Abdul-Khaliq, Ho, To Weipert, V. Alexi-Meskishvili, Yo Weng, Ro Hetzer, P. Eo Lange 113 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 The relation between arterial oxygen tension and cerebral blood flow during cardiopulmonary bypass Chow, Go, 1. Go Roberts, Po Fallon, Mo Onoe,Ao Lloyd-Thomas, Mo Jo Elliott, Ao Do Edwards, F. Jo Kirkham 119 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 00 0 0 0 0 0 0 0 0 0 0 0 0 Cerebral perfusion during low-flow cardiopulmonary bypass with circulatory arrest in rabbits - An experimental study for CPB in neonates Troitzsch, Do, So Vogt, Ao Peukert 125 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Neurophysiology, monitoring, cardiopulmonary bypass technique Cerebral protection in surgery ofthe aortic arch: The place of neurophysiologic monitoring Zickmann, Bo, K. Wulf, F. Dapper, Go Hempelmann 133 Neurophysiological consequences of circulatory arrest with hypothermia Treasure, To 143 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 _____________________________________________________________c ~o~n~te~n~ts IX Cerebral oxygenation during cardiac surgery Nollert, G., P. Mohnle, P. Tassani-Prell, M. Schmoeckel, A. Welz, B. Reichart 157 Cerebral ischemia and brain related complications after cardiac surgery Isgro, F., Ch. Schmidt, G. Grimm, W. Saggau ....................... 171 The role of cardiopulmonary bypass technique in cerebral protection Blauth, C. .............................................. 177 Cerebral protection in aortic arch surgery Antegrade versus retrograde cerebral perfusion - a review of the recent literature Ennker, J., A. St. Bauer ..................................... 187 Surgery of aortic arch aneurysm -A ten-year experience with cold cerebroplegia Bachet, J., D. Guilmet, G. Dreyfus, B. Goudot, A. Piquois .............. 193 Aortic arch surgery using antegrade selective cerebral perfusion Akashi, H., K. Tayama, S. Fukunaga, K. Kosuga, S. Aoyagi . . . . . . . . . . . . .. 203 Selective cerebral perfusion for brain protection during surgery of the aortic arch Kazui, T. ............................................... 211 Brain monitoring during retrograde cerebral perfusion in operations on the thoracic aorta Ehrlich, M., M. Grabenwoger, D. Luckner, F. Cartes-Zumelzu, P. Simon, G. Grubhofer, A. Lassnig, G. Laufer, E. Wolner, M. Havel .............. 219 Impact of antegrade perfusion in aortic arch surgery Kleine, P., C. Draeger, A. AIken, J. Laas .......................... 225 Hypothermic circulatory arrest through the left chest Coselli, J. S. ............................................ 229 Retrograde cerebral perfusion in surgery for aortic arch aneurysms Coselli, J. S. ............................................ 239 Chronic dissecting aneurysm of the innominate artery, surgical treatment under retrograde cerebral perfusion Camilleri, L., B. Legault, D. Carrie, I. Brazzalotto, P. Bailly, L. Boyer, Ch. de Riberolles ......................................... 251 Retrograde cerebral perfusion -An experimental study to evaluate brain perfusion in non-human primates Boeckxstaens, Chr. J., V. van Hoof, R. Vanmaele, W. J. Flameng . . . . . . . . . .. 255 Is there a conflict between clinical and experimental evidence on the benefit of retrograde cerebral perfusion? Treasure, T. ............................................. 273 Protection, diagnosis and treatment of cerebral ischemia · '··J~l~ Neuroprotection in cerebral ischemia W. Paschen, K.-A. Hossmann Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, KOIn, Germany Introduction The brain exhibits, in comparison with other organs, a high sensitivity to a critical reduc tion in blood flow. A few minutes after cessation of cerebral blood flow the tissue is depleted of primary and secondary energy compounds (glycogen, glucose and high energy phosphates such as adenosine triphosphate and phosphocreatine) due to the low energy reserves of the brain (34, 56). Such a situation occurs during cardiac arrest when blood flow to the brain stops completely. The occlusion of an intracerebral artery, in contrast, may cause a mild or severe reduction or even cessation of cerebral blood flow. The extent of this disturbance depends on the quality of collateral circulation and the local perfusion pressure. Whether these changes are critical for the survival of neurons depends on the duration and density of blood flow reduction. Different functions of neurons are affected at different threshold levels of cerebral blood flow: e.g., spontaneous electrical activity is already impaired when blood flow is reduced to about 60 % of control (26, 42), aerobic glucose metabolism is disturbed when blood flow is reduced to below 35 % of control (50), and at flow levels below about 20 % of control the tissue is depleted ofATP (50), the electrolyte homeostasis is disturbed (8-10), and cell death ensues unless blood flow is re established. Interestingly, protein synthesis is suppressed already at blood flow levels of about 55 to 60 % of control, i.e., at considerably higher flow levels than those below which disturbances in energy metabolism take place (38). In experimental studies, the strategy for protecting neurons from cell damage depends greatly on the model used for producing cerebral ischemia. The pathological process lead ing to ischemic cell death in models of focal and global cerebral ischemia is different from that occurring in permanent or reversible focal cerebral ischemia. Spreading depression for example, plays a major role in neuronal destruction in the penumbra of an ischemic focus (38) while after global cerebral ischemia spreading depression-like phenomena have not been observed, and the pathological process leading to ischemic cell damage is restricted to selectively vulnerable brain areas such as the hippocampal CAl-subfield where neuronal cell death occurs after a delay of about 3 days following cerebral ischemia (32). Exact knowledge of the pathological process leading to ischemic cell damage is the prerequisite for cause-related, direct therapeutical intervention. This paper, therefore, is designed to provide a comprehensive description of the pathophysiological and pathobiochemical disturbances induced by focal and global cerebral ischemia.
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