Table Of ContentCerebral 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.]
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© 1997 by Dr. Dietrich SteinkopffVeriag GmbH & Co. KG, Darmstadt
Softcover reprint of the hardcover 1s t edition 1997
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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.
