Timing of Aneurysm Surgery 9783110858853, 9783110101560

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Timing of Aneurysm Surgery

Timing of Aneurysm Surgery Edited by L. M. Auer

w DE

G

Walter de Gruyter Berlin-New York 1985

Prof. Dr. med. Ludwig M. Auer Universitätsklinik für Neurochirurgie Landeskrankenhaus A-8036 Graz

This book contains 233 illustrations and 129 tables.

CIP-Kurztitelaufnahme

der Deutschen

Bibliothek

Timing of aneurysm Surgery / ed. by L. M. Auer. — Berlin ; New York : de Gruyter, 1985. ISBN 3-11-010156-4 (Berlin ...) ISBN 0-89925-071-8 (New York) NE: Auer, Ludwig M. [Hrsg.]

Library of Congress Cataloging in Publication

Data

Main entry under title: Timing of aneurysm surgery. Includes bibliographies and indexes. 1. Brain — Blood vessels — Surgery. 2. Intracranial aneurysms — Surgery. I. Auer, Ludwig, M., 1948. 1929 - . [DNLM: 1. Cerebral Aneurysm — surgery. WL 355 T583] RD594.2.T56

1985

617'.481

85-10443

ISBN 0-89925-071-8 (U.S.)

© Copyright 1985 by Walter de Gruyter & Co., Berlin 30. All rights reserved, including those of translation into foreign languages. No part of this book may be reproduced in any form - by fotoprint, microfilm or any other means - nor transmitted nor translated into a machine language without written permission from the publisher, Typesetting and Printing: Buch- und Offsetdruckerei Wagner GmbH, Nördlingen. — Binding: Dieter Mikolai, Berlin. - Cover design: Rudolf Hübler. - Printed in Germany. The quotation of registered names, trade names, trade marks, etc. in this copy does not imply, even in the absence of a specific statement that such names are exempt from laws and regulations protecting trade marks, etc. and therefore free for general use. 3 11 010156 4 Walter de Gruyter • Berlin • New York 0-89925-071-8 Walter de Gruyter, Inc., New York

Introduction

One major problem in the discussion of " a c u t e " or " e a r l y " versus " l a t e " aneurysm surgery is still the definition itself. On going through the present material one can say that many authors mean an interval of 72 hours from SAH when they talk about "early/acute", others, however, understand an interval of 7 days. It has therefore been proposed that all data presented in future should be subdivided according to the day of operation after SAH. This makes evaluation of smaller series very difficult and further suggests the use of subdivision into days 0—3, 4—7 and later than 7. When the first collection of data from early operated patients was tried in 1 9 8 1 * the vast majority of patient-series was provided by Japanese Centres. Since 1981, a remarkable trend towards early admission and operation can be observed among European Neurosurgical Centres while most American colleagues have been hesitant to operate early. Data in this volume are based on experiences with 9300 patients harbouring ruptured cerebral aneurysms, about 3000 among them operated early, i. e. within 72 hours after SAH. New grading scales are under discussion to describe the clinical picture and prognosis with lower interobserver-variability; they are modifications of the Hunt and Hess scale used in combination with the Glasgow coma score. Moreover, the additional use of CT-data for further improvement of prognostic power has been discussed, bearing in mind the disadvantage of making a simple grading scale too complex. However, one important note has found wide agreement: the need to indicate the time period after SAH at which the patient has been graded, e. g. by indicating the day after SAH (day of bleeding day 0). In accordance with earlier observations, these present studies reconfirm the unchanged incidence of angiographic vasospasm in around 6 0 % of an unselected consecutive patient series; about half of them, i. e. 3 0 % of all patients, suffer from ischaemic neurological deficits of delayed onset. A high correlation has again been found between the amount of subarachnoid blood accumulation and the incidence of angiographic vasospasm as well as delayed inschaemia; the latter was 10 times more frequent in patients with severe SAH than in patients with thin localized SAH. Computerized tomography (CT) allowed the distinction between early and late occurrence of hypodense lesions; frequent postoperative C T controls have therefore been recommended for better detection of delayed inschaemia and other events. * Aneurysm Surgery in the Acute Stage (Hrsg.: L. M . Auer, F. Heppner, L. Symon) Acta Neurochir. 63 (1982).

VI

Introduction

Widely differing classification systems are still being used to describe the extent of SAH. Most of them could finally be compressed into 3—4 categories: it can be proposed to uniformly use scales which are in accordance with the admittedly rough description of "mild", "moderate" and "severe" besides "absent", i. e. " n o " SAH. This would facilitate future comparisons of different series. As a new aspect, the value of early CT in all patients with SAH from a ruptured aneurysm is discussed as a prognostic tool not only with respect to delayed ischaemia, but also with respect to comatose patients. In the latter group, CT distinguishes between patients with fatal bleeding into deep structures and those with a better prognosis such as patients with a subdural haematoma, acute hydrocephalus and severe SAH without intracerebral bleeding. Cerebral blood flow (CBF) has again been convincingly demonstrated as prognostically powerful for the occurrence of delayed ischaemic complications; both the absolute resting CBF-values and the autoregulatory capacity served as indicators. Subarachnoid haemorrhage can thus be recommended as an indication for CBF measurements in clinical routine. An increasing trend has been noticed to accept early operation as a measure against the threat of rebleeding. There is, however, little accordance as to whether all patients should undergo early operation, or only those in good clinical condition. The latter opinion is widespread, although data indicate that acute operation is more beneficial for poor-grade patients. In a non-randomised historical comparison, a better outcome after early versus late surgery was not apparent in all studies; if an improvement in prognosis by early operation was observed, it seemed more prominent in patients with higher preoperative Hunt and Hess grades. One likely explanation for differing results between several authors could be the experience in early surgery. When a centre compares the outcome of the first series of acutely operated patients with a previous series after delayed surgery, then a higher rate of complications during early surgery might jeopardize a benefit of the acute procedure by replacing morbidity from spasm by surgical morbidity. In neuropsychological tests, some of the postoperative problems reported by neurologically intact patients with normal CT were found to be purely psychological difficulties in managing the psychotrauma of undergoing surgery to the brain. On average, early operation was considered more difficult than later surgery. One frequent argument against early surgery is the risk of encountering brain swelling. Some of the following contributions indicate, however, that brain swelling is a rare event in the first 3 days after SAH; apparent brain swelling on opening of the dura is mostly reversed by CSF-drainage, and operation can be continued with a slack brain. Intraoperative aneurysmal rupture turned out to be not more frequent in the

Introduction

VII

early (day 0—3) than in later stages. It is also noteworthy that early operation of technically difficult aneurysms did not seem to be combined with a higher risk, as shown by several groups who have not applied any selection criteria for early interventions with respect to technical difficulty. At present, there is little accordance as regards the help or need of CSF-drainage during and after early aneurysm operation; however, the lowest incidence of shuntdependent hydrocephalus has been observed in series with intra- and postoperative drainage. Extensive evacuation of subarachnoid blood has not proven more effective in preventing delayed ischaemic symptoms from vasospasm, than incomplete, gentle evacuation of major clots in the cisterns. One of the major concerns for those colleagues who operate early, has become the timing of surgery in patients admitted on days 4—7 after SAH. This concern is based on earlier reports indicating a higher surgical risk on days 4—7 compared to days 0—3. In the present series, the surgical risk of operation on day 1—3 seemed not higher compared to day 4—7 and there was no difference in outcome when the preoperative Hunt and Hess grades were I or II; grades III—IV patients ran a higher risk on days 4—7 compared to days 1 - 3 . However, this statement is limited by the fact that all of the series were either following unspecified selection criteria, or did not clearly separate operations on days 4—7 from those on day 8 or later. In order to know definitively better, whether there is a difference in outcome between patients operated during the first 3 days, and those operated on days 4—7, a comparative description of unselected groups of patients would be required; outcome would have to be related to the clinical grade on the day of SAH in all patients, and all kinds of preoperative mortality would have to be included. These criteria have been considered in the International Cooperative Study on Aneurysm Surgery, the data from which can be expected in the near future. The studies presented here show uniformly, that patients in Hunt and Hess grades I—II can be safely operated on days 4 - 7 , if no impending complications from vasospasm are detected. The aim of preventing vasospasm by early evacuation of subarachnoid blood has not been convincingly reached. The incidence of delayed ischaemic symptoms after early surgery remains around 20—30% on average. However, in most recent series where early surgery was combined with pharmacological prevention of vasospasm by administration of a calcium-antagonist of the dihydropyridine-type, delayed ischaemic symptoms appeared in only a few percent of patients. Although these observations were made in uncontrolled studies, it appears that this approach deserves attention as an important step forward in the control of secondary brain lesions from aneurysm rupture. First data were obtained with a transcranial doppler technique for noninvasive detection of vasospasm. Moreover, analysis of evoked potentials and measurement of CBF appeared helpful. Under the control of these

VIII

Introduction

technical aids, preventive calcium antagonist treatment could be individually adapted to the patients' requirements in the future. What remains to be done? The most important factor in the management of patients with ruptured cerebral aneurysms has remained the most important problem for the majority of centres: a minor proportion of patients with minor S AH (warning leak) are diagnosed as such, only some of the patients with ruptured aneurysms arrive in a neurosurgical departmant, and only a small part is admitted early. Thus, what remains to be done after controlling the main secondary risk factors — rebleeding and vasospasm — is the organisation of referral to neurosurgery early after warning bleeding. Helicopter transport has proven helpful in geographically difficult areas. With more accurate analysis of the history of acutely admitted patients it becomes apparent that at least 10% suffer a recurrent bleeding within 48 hours. From the present knowledge it would thus appear that referral to neurosurgery should be achieved within the first 24 hours after SAH. Several authors in this volume show that the organisation of such early diagnosis and operation is possible without objective difficulties. Graz, July 1985

L. M. Auer

Contents

The Problem of Grading Scales A Proposal for Grading of Subarachnoid Haemorrhage due to Aneurysm Rupture (K. Sano, A. Tamura) Standardized Clinical Grading of Patients with Subarachnoid Haemorrhage: A Uniform International System? (G.M.Teasdale, K.W.Lindsay, G.Allardyce, S. Dharker, P. Ward) Prognostic Factors of Ruptured Intracranial Aneurysms — New Clinical Grading - (N. Yasui, S. Kawamura, H. Ohta, A. Suzuki, H. Kamiyama, I. Sayama) Computerized Tomography Early Computed Tomography for Prediction of Vasospasm after Aneurysmal Rupture: Experience with 364 Cases (A. Pasqualin, P. Cavazzani, R. Scienza, L. Rosta, R. Da Pian) Prognostic Evaluation of SAH on the Basis of Computer Tomographic Findings (W. Mauersberger, H. Hochbaum) Value of Early Computed Tomography after Aneurysm Rupture (F. Troisi, S. Acampora, G. Profeta, E. Scarano) Cerebral Blood Flow Preoperative Assessment of Cerebrovascular Reactivity Following Subarachnoid Haemorrhage — Clinical Correlations (J. D. Pickard, D. H. Read, A. H. J. Lovick) Cerebral Blood Flow in the Prediction of Vasospasm after Subarachnoid Haemorrhage (N.W.C. Dorsch, J. S.Compton) Mean Cerebral Blood Flow (m-CBF) and Cerebral Oxygen Utilization ( C M R 0 2 ) in Patients with Ruptured Intracranial Aneurysm at the Acute Stage (T. Hotta, J. Nakagawara, T. Shimada, T. Sasaki, S. Sato, T. Hyogo, S. Ogasawara, H. Ohmachi, K. Suematsu, J. Nakamura) The Usefulness of Noninvasive rCBF Measurement in the Treatment of Patients after Subarachnoid Haemorrhage (SAH). A 5 Year Review (A. Brawanski, A. Maximilian, M. R. Gaab) The Negative Angiogram Subarachnoid Haemorrhage with Negative Panangiography (G. HaenselFriedrich, H. Friedrich, S. Herbold, H. Vogelsang)

3

9

15

23 33 39

47 53

61

71

81

X

Contents

Spontaneous Subarachnoid Haemorrhage of Unknown Origin — A Prospective Study (G. Boné, L. M. Auer, G. Papaefthymiou, G. Ladurner, G. Schneider, H. Lechner) Timing of Surgery and Results Treatment of Ruptured Intracranial Aneurysms at the Acute Stage — Operative Timing and Results (N. Yasui, A. Suzuki, H. Ohta, H. Kamiyama, S. Kawamura) Current Results and Future Problems in Early Aneurysmal Surgery (K. Hashi, K. Sakatani, S. Ogawa, N . Hara, K. Murao) Early Surgery for Intracranial Aneurysms: Influence of Clinical and Operative Findings on Final Results (R. Da Pian, A. Pasqualin, R. Scienza, P. Cavazzani) Early Surgical Management Within 72 Hours after Subarachnoid Haemorrhage (185 Cases of Ruptured Intracranial Aneurysms) (K. Watanabe, K. Kikuchi, T. Matsuzaki, M . Suzuki) Experience in Aneurysm Surgery: Early Versus Late Surgery (H. Friedrich, V. Seifert, D. Stolke) Postoperative Course Following Acute and Delayed Operation on Cerebral Aneurysm. A Consecutive Series of 175 Operations (H. R. Eggert, J. Gilsbach) Timing of Operation after Subarachnoid Haemorrhage since the Introduction of C T (H. Sano, T. Kanno, K. Katada, N . Ishiyama, Y. Katou) Management Mortality Related to the Timing of Surgery for Anterior Circulation Aneurysms (B. Weir, K. Petruk, L. Disney, M. Grace) Results of Early Surgery for Ruptured Intracranial Aneurysm (N. F. Kassell, H. P. Adams, D.J.Boarini, G. A. Kongable, J. C. Torner) The Comatose Patients at the Acute Stage - A Surgical Taboo? (L. M . Auer) . . Acute Subdural Haematomas Following Spontaneous Rupture of Intracranial Aneurysms (L. Russegger, K. Twerdy, H. Kostron) The Treatment of Intraventricular Haemorrhage from Ruptured Aneurysm (V. V. Dolenc) Large Volume SAH — An Indication for Early Surgery? (G. Algers, A. Forssell, C. von Essen) What Does Full Recovery after Acute Aneurysm Operation Mean? A Psychological Study (S. Auer, B. Gallhofer, L . M . Auer) Rate and Causes of Mortality Related to the Timing of Open Surgery in Ruptured Supratentorial Aneurysms (Series of 143 Cases Operated by 5 Neurosurgeons) (B. Pertuiset, J. P. Sichez, A. Sermet, H. Nakano) Timing of Surgery, Operative Mortality, and Follow-up Results in Cases with Subarachnoid Haemorrhage due to Aneurysm Rupture (K. Sano) Aneurysm Surgery on the 4th—7th Day after SAH (A. Perneczky, W. Th. Koos) Timing of Surgery for Ruptured Cerebral Aneurysms (I. Saito, H. Segawa, I. Nagayama, K. Kitamura)

89

97 107 115

125 133 143 153 165 177 183 195 203 207 211

217 227 237 241

Contents

Timing of Operation with Regard to Four Different Stages (S.Kwak, E. Morikawa, T. Morimoto) Operative Outcome as Related to Time of Invervention. Analysis of Surgical Results in 891 Cases of Intracranial Aneurysm (F.Koschorek, E.Kraus, F. Scheil, H. Biinning) Timing of Aneurysm Surgery from View of a General Hospital (Review of 330 Cases) (G. Perneczky, G. Kleinpeter, H. R Ammerer, H. Brenner, F. Bock) . . . Overall Results from 141 " G o o d R i s k " Patients with Ruptured Cerebral Aneurysm Submitted to a "Delayed Surgery" Protocol. With a Note on " M e d i u m Level" Versus "High Level" Management (C. Testa, A. Andreoli, A. Arista, P. Limoni, F. Tognetti) The International Cooperative Study on the Timing of Aneurysm Surgery (N. F. Kassell, J . C. Torner, J . A. Jane) Ruptured Intracranial Aneurysms: A Review of Our New Experience (C. Cecotto, F. De Nardi, P. P. Janes, R. Giacomini) Is Early Operation for Ruptured Cerebral Aneurysm Justified? (H.Arnold, N . Freckmann, H. D. Herrmann) Contribution to indications for the Operation of Intracranial Saccular Aneurysms at the Acute Stage (M. Brnobic, P. Miklic, M. Scap, V. Brinar) Surgery of Ruptured Intracranial Aneurysms. Factors Influencing the Outcome (J. Ugrinovski, S. Jovkovski, K. Lozance, I. Pangovski, M . Vrcakovski) . Technical Aspects of Surgical Treatment Practical Clinical Applications of Modern Physiological Concepts in Aneurysm Surgery (L. Symon) Intraoperative Aneurysm Rupture (D. Samson, H. Batjer) Direct Surgical Approach to Infraclinoidal Aneurysms (A. Perneczky, E. Knosp, Th. Czech) Acute Aneurysm Surgery, Disturbed CSF-Circulation, Intracranial Pressure and Hydrocephalus (L. M . Auer, M. Mokry) The Value of CSF Drainage During Aneurysm Surgery and Prevention of the Development of Hydrocephalus (V. V. Dolenc) Pitfalls in Aneurysm Surgery — Management of Aneurysm Rupture (N. Yasui, A. Suzuki, H. Ohta, H. Kamiyama, K. Kitami) "Scavengery Surgery" for Subarachnoid Haemorrhage (I) — A Surgical Technique of Subarachnoid Clot Removal (T. Kawase, R. Shiobara, S. Toya, Y.Miyahara) "Scavengery Surgery" for Subarachnoid Haemorrhage (II) — Continuous Ventriculo-Cisternal Perfusion using Artificial Cerebrospinal Fluid with Urokinase (R. Shiobara, T. Kawase, S. Toya, K. Ebato, Y. Miyahara) Further Trial of Cisternal Clot Removal for Severe Subarachnoid Haemorrhage (K. Hashi, I. Aoyama, K. Nin, K. Shimotake)

XI

253

261 267

271 277 279 283 287 293

303 313 323 331 343 349

357

365 373

XII

Contents

Intermittent Versus Continuous Brain Retractor Pressure as Protective Procedure against Ischaemic Brain Cell Damage (J. Rosenorn, N. H. Diemer) . . . . The Effect of Hypotensive Agents on Regional Cerebral Blood Flow and Intracranial Pressure in Baboons with Space Occupying Lesions (Z. Czernicki, A. Hartmann, C. Buttinger, F. Trtinjak) Diagnosis and Timecourse of Vasospasm The Role of the Intracerebral Monoamine Systems in the Development of Vasospasm Following an Experimental Subarachnoid Haemorrhage (N. A. Svendgaard, J. Brismar, T. J. Delgado, N. H. Diemer) Serial Biochemical Changes in the Cerebrospinal Fluid during the Early Stage of Subarachnoid Haemorrhage: Relationship with Cerebral Vasospasm (A. Pasqualin, C. Vivenza, P. Rizzotti, C. Cocco, P. Cavazzani, R. Da Pian) . . . Cerebral Vasospasm and Aneurysm Surgery. A Review (U. Ebeling, H.J. Reulen Evaluation and Prediction of the Vasospasm Severity Following a Ruptured Supratentorial Aneurysm from Angiography, Clinical Grade and Somatosensory Evoked Potentials (B. Pertuiset, J. P. Sichez, F. Lille, P. Hazeman, H. Nakano, E. Chaumier) Correlation of the Middle Cerebral Artery Flow Velocity with the Clinical Course and CT-Visualized Subarachnoid Blood in Patients after Aneurysmal Subarachnoid Haemorrhage (R. W. Seiler, R. Aaslid, P. Grolimund) Time Course of Cerebrovascular Spasm in Early Aneurysm Operation: Transcranial Doppler Findings (A. Härders, J. Gilsbach) Course of Vasospasm Following Subarachnoid Haemorrhage: Serial Angioraphy, Its Relation to Timing and Perioperative Care (C. A. Miller, C. D. Hunt, W. E. Hunt) Clinical Features of Cerebral Vasospasm Following Early Surgery for Intracranial Aneurysm (A. Pasqualin, P. Cavazzani, R. Scienza, C. Licata, R. Da Pian) Is It Possible to Prevent or to Treat Vasospasm? (N. Yasui, A. Suzuki, H. Ohta, H. Kamiyama, K. Kitami, S. Kawamura, H. Nishimura)

381

385

393

403 411

421

429 437

445 451 461

Prevention and Treatment of Vasospasm Ca 2 + Homeostasis, Ca 2 + Entry Blockers, and Brain Ischaemia (B.K.Siesjö, T. Wieloch) 471 The Cerebrovascular Effect of Nimodipine (L. M. Auer, M. Mokry, E. Pöllauer) 481 Prevention and Treatment of Vasospasm and cerebral Ischaemia after SAH by Early Surgery and Nimodipine (A. J. M. Van der Werf, J. J. R. Dreissen, L. M. Hageman, K. W. Albrecht) 489 Acute Aneurysm Surgery and Preventive Nimodipine Control the Problem of Symptomatic Vasospasm (L.M.Auer, B.Ljunggren, L.Brandt, H.Säveland, J. Gilsbach, A. Härders, H. J. Reulen, U. Ebeling, U. Gröger, F. Oppel) 493

Contents

Prevention of Delayed Ischaemic Deficit and Improvement of Outcome by Acute Aneurysm Surgery and Nimodipine — Analysis of an Unselected Consecutive Series of Patients (L. M. Auer) Results of Early Aneurysm Operation and Intravenous Nimodipine (L. Brandt, B. Ljunggren, H. Säveland, P. E. Nilsson, K. E. Andersson, E. Vinge) Treatment of Subarachnoid Haemorrhage Following Aneurysm Rupture Without Specific Drug Therapy, with Antifibrinolytic Agents Alone and in Combination with Nimodipine: A Comparative Study (C. Sprung, E. Kazner) Clinical Experiences in the Prevention of Ischaemic Neurological Deficits after Subarachnoid Haemorrhage with Nimodipine (D. K. Böker, E. Kazner, C. Sprung, D. Adelt, H. P. Ammerer, R. Karnick, H. Baumann, J. A. Grotenhuis, H.Jaksche, A.R.Istaitih, H.J.Klein, G.Langelaar, L.Russegger, W. Sachsenheimer, G. Schackert, J. Schramm) Report of the Canadian Nimodipine Trial Examining Use of Nimodipine in Poor Grade Aneurysm Patients (L. Disney, B. Weir, K. Petruk, M. Grace) . . . Surgical Results of Ruptured Aneurysms Related to Timing (with Special Reference to Nimodipine) (H. Kostron, L. Russegger, V. Grunert) Experience with Nimodipine in Combination with Postoperative Hypertensive, Hypervolemic Treatment in the Management of Ruptured Intracranial Aneurysms (H. Baumann, M. Samii, R. Ramina, A. Seperhnia, P. Gürtner). . . Intraarterial Treatment of Cerebral Vasospasm after Subarachnoid Haemorrhage with Nimodipine (D. K. Böker, L. Solymosi) Appearance of Cerebral Vasospasm after Break of Nimotop-Prophylaxis and Their Treatment (Case Report) (H. P. Ammerer, G. Perneczky, F. Bock) . . . . Perioperative Management Regimen of Patients with Aneurysmal Subarachnoid Haemorrhage (S. Finn, C. A. Miller, S. Stephensen, W. E. Hunt) Prevention of Postoperative Vasospasm by Cisternal Irrigation (I. Saito, H. Segawa, I. Nagayama, H. Nihei) Prevention of Delayed Ischaemia by Radical Removal of Subarachnoid Clots Immediately after Rupture of Cerebral Aneurysms (M. Taneda) Hypervolemic Haemodilution Therapy for Patients with Symptomatic Vasospasm after Early Surgery of Cerebral Aneurysms (J. Nakagawara, J. Nakamura, R. Takeda, T. Usami, M. Nishiya, W. Ide, M. Shitamichi, Y. Okada, S. Fukuoka, I. Hashimoto, K. Suematsu) Experimental and Clinical Study in the Use of Intrathecal Alpha-Tocopherol in Vasospasm (Y. Kato, H. Sano, K. Katada, T. Kanno) Problems of Organisation, Transport and Preoperative Management A Functioning Model of Prompt Diagnostic Management and Treatment of SAH Due to a Ruptured Aneurysm (V. V. Dolenc, T. Kregar, J. Voncina) . . . .

XIII

503

515

523

535 545 551

561 567 575 579 587 595

601 615

629

XIV

Contents

Early Transportation, Organisation of Diagnosis and Operation at the Acute Stage (L. M. Auer, G. Papaefthymiou, H. Tritthart) Experiences on Emergency Management of SAH During the Last Thirty Years at Cardarelli Hospital, Naples (F. Troisi, G. Profeta, S.Acampora, R. De Falco) From Admission to Postoperative Management (J. Gilsbach, H. R. Eggert, A. Härders) Risk of Rebleeding During Angiography in Patients with Subarachnoid Haemorrhage at the Peracute Stage (M.Taneda, T.Sakamoto, N.Shimada, S. Hiraga, A. Kim) Intra-Angiographical Aneurysmal Rupture as a Rare Complication of Early Angiography (R. Preger, F. Assad) Rebleeding Attack of Cerebral Aneurysms — Clinical Significance of Early Aneurysmal Rebleeding (N. Yasui, A. Suzuki, H. Ohta, H. Kamiyama, S. Kawamura) Arterial Hypotension Following Acute Aneurysmal Subarachnoid Haemorrhage (K. Kataoka, M. Taneda) List of Contributors Authors Index Subject Index

635

641 645

653 657

665 673 679 681 683

The problem of grading scales

A Proposal for grading of subarachnoid haemorrhage due to aneurysm rupture K. Sano, A. Tamura

Summary This is a proposal to the W.F.N.S. Committee on Grading, and a modification of Hunt's (1974) and Teasdale's (1983) gradings. The Glasgow Coma Scale (GCS) is used to express levels of consciousness. Grade I: Grade II:

G C S : 15. Neurologically intact (except for cranial nerve palsy). G C S : 15. Neurologically intact (except for cranial nerve palsy) with neck stiffness, headache, or both. Grade III: G C S : 1 3 - 1 4 . III a : Without focal neurological deficit. III b : With focal neurological deficit. Grade IV: G C S : 8—12. With or without focal neurological deficit. Grade V: G C S : 3 - 7 . Unresponsive coma with or without abnormal posturing. Correlation between this grading system and the patient's outcome is tested and discussed.

Despite the advances in investigation techniques such as computed tomography (CT), etc., the management of individual patients with subarachnoid haemorrhage (SAH) due to aneurysm rupture still depends greatly on assessment of the patient's clinical condition. This is because the likely outcome is closely related to the severity of the patient's clinical state [3, 9]. Several systems for grading patients with SAH have been proposed; among them Botterells [1], Nishiokas [7], and Hunts [2, 3] have been used in many neurosurgical centres. Because of observer variability in either of these systems [6], the World Federation of Neurosurgical Societies appointed the Committee on Standardization of Grade of Subarachnoid Haemorrhage (Chairman, C . G . D r a k e ) in 1983. This is a proposal to the Committee. The present grading system (tab. 1) is based on Hunts grading, that of Teasdale et al. [10] and the discussion at the Meeting held on February 15, 1984, in Tokyo, with some 11 Japanese neurosurgeons and Prof. Teasdale.

4 Table 1 I II III

IV V

K. Sano, A. Tamura Grade GCS: 15. Neurologically intact (except for cranial nerve palsy). GCS: 15. Neurologically intact (except for cranial nerve palsy) with neck stiffness, headache, or both. GCS: 13-14. Ilia: without focal neurological deficit. IIIb: with focal neurological deficit. GCS: 8 - 1 2 , with or without focal neurological deficit. GCS: 3 - 7 . Unresponsive coma with or without abnormal posturing.

[GCS: Glasgow Coma Scale] Table 2

Status on Admission and Outcome at Discharge Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

42 9 3 1 6

Total

61

Table 3

IV 12-8

V 7-3

Total

20 9 2 1 10

1 5 3 1 5

1 1 2 2 25

64 24 10 5 46

42

15

31

149

IV 12-8

V 7-3

Total

Status on Admission and Outcome (6 months postop.) Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

38 4 1 0 7

23 4 0 1 9

1 4 4 0 5

2 0 2 1 26

64 12 7 2 47

Total

50

37

14

31

132

IV 12-8

V 7-3

Total

Table 4

Preoperative Status and Outcome at Discharge Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

42 9 2 0 2

21 10 1 0 5

0 5 5 2 5

0 0 2 2 10

63 24 10 4 22

Total

55

37

17

14

123

A proposal for grading of subarachnoid haemorrhage due to aneurysm rupture Table 5

Preoperative Status and Outcome (6 months postop.) Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

42 3 1 0 3

Total

49

Table 6

IV 12-8

V 7-3

Total

20 4 0 0 4

1 5 5 0 5

0 0 1 1 11

63 12 7 1 23

28

16

13

106

IV 12-8

V 7-3

Total

Postoperative Vasospasm and Outcome at Discharge Preoperative Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

1 0 2 0 1

4 4 1 0 1

0 3 3 1 2

0 0 1 1 2

5 7 7 2 6

Total

4

10

9

4

27

Table 7

Postoperative Vasospasm and Outcome (6 months postop.) Preoperative Grade GCS

I, II 15

III 14-13

IV 12-8

V 7-3

Total

Good recovery Moderately disabled Severely disabled Vegetative Dead

1 0 1 0 2

5 2 0 0 1

1 2 4 0 2

0 0 1 1 2

7 4 6 1 7

Total

4

8

9

4

25

Table 8

Cases without Postoperative Vasospasm and Outcome at Discharge Preoperative Grade GCS

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

41 9 0 0 1

Total

51

IV 12-8

V 7-3

Total

17 5 0 0 4

0 2 2 1 3

0 0 1 1 8

58 16 3 2 16

26

8

10

95

5

6 Table 9

K. Sano, A. Tamura Cases without Postoperative Vasospasm and Outcome (6 months postop.) Preoperative Grade GCS

IV 12-8

V 7-3

15 2 0 0 3

0 3 1 0 3

0 0 0 0 9

56 8 1 0 16

20

7

9

81

I, II 15

III 14-13

Good recovery Moderately disabled Severely disabled Vegetative Dead

41 3 0 0 1

Total

45

Total

In this grading, the Glasgow Coma Scale (GCS) [5] is used to express the level of consciousness because of its internationality, although Japanese neurosurgeons are more familiar with the so-called Japan Coma Scale [8] which is well correlated with the GCS. In the following tables 2 - 5 , the correlation between the grading of the patient's condition or the GCS on admission or just before surgery of aneurysms and the outcome of patients at discharge or 6 months after surgery is tested using the recent cases that were admitted within one week after SAH and in which the GCS was described. In the tables 6—9, the correlation between the preoperative grading and the outcome is checked in the cases with or without postoperatively developed symptomatic vasospasm. The numbers in these tables are numbers of patients. The outcome is tentatively expressed by the Glasgow Outcome Scale [4], Grade III in these tables is not divided into IIIa and Hit, because IIIb cases are small in number. Grades I and II are put together in these tables, since statistical analysis (the U-test) of the outcome in the author's series revealed no significant difference between these two [9]. As can be seen in the tables, the proposed grading system shows a good correlation with the outcome of the patient. The correlation is better in the preoperative grading than in the grading on admission. This is understandable because the patient's condition may change in the course of hospitalization. Symptomatic cerebral vasospasm developed postoperatively in 7.3% (4/55) of Grades I and II patients, 27.0% (10/37) of Grade III patients, 52.9% (9/17) of Grade IV patients, and in 28.6% (4/14) of Grade V patients, and worsened the outcome. This new grading system is clear in its description of the patient's condition, it results in less observer variability, and may be useful prognostically.

A proposal for grading of subarachnoid haemorrhage due to aneurysm rupture

7

References [1] Botterell, E . H . , W.M.Lougheed, J . W . S c o t t et al.: Hypothermia and interruption of carotid or carotid and vertebral circulation, in the surgical treatment of intracranial aneurysms. J . Neurosurg. 13 (1956) 1 - 4 2 . [2] Hunt, W. E., R. M . Hess: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J . Neurosurg. 2 8 (1968) 1 4 - 2 0 . [3] Hunt, W. E., E.J.Kosnik: Timing and perioperative care in intracranial aneurysm surgery. Clin. Neurosurg. 21 (1974) 7 9 - 8 9 . [4] Jennett, B., M . Bond: Assessment of outcome after severe brain damage. Lancet, i (1975) 4 8 0 - 4 8 4 . [5] Jennett, B., G.Teasdale: Aspects of coma after severe head injury. Lancet, i (1977) 8 7 8 - 8 8 1 . [6] Lindsay, K. W., G. M . Teasdale, R. P. Knill-Jones: Observer variability in assessing the clinical features of subarachnoid haemorrhage. J . Neurosurg. 58 (1983) 5 7 - 6 2 . [7] Nishioka, H.: Report on the cooperative study of intracranial aneurysms and subarachnoid haemorrhage. VII, Pt. 1. Evaluation of the conservative management of ruptured intracranial aneurysms. J . Neurosurg. 25 (1966) 574—592. [8] Ohta, T., S. Waga, H. Handa et al.: New grading of level of disordered consciousness. Neurol. Surg. 2 (1974, Japanese) 623-627. [9] Sano, K.: Cerebral vasospasm and aneurysm surgery. Clin. Neurosurg. 30 (1983) 13-58. [10] Teasdale, G., R. P. Knill-Jones, K.W.Lindsay: Neurosurgical Forum, letters to the Editor, Response. J . Neurosurg. 5 9 (1983) 5 5 0 - 5 5 1 .

Standardized clinical grading of patients with subarachnoid haemorrhage: A uniform international system? G. M. Teasdale, K. W. Lindsay, G. Allardyce, S. Dharker, P. Ward

Summary A scale for assessing patients with a recent subarachnoid haemorrhage has been constructed using the Glasgow Coma Scale and a simple assessment of the presence or absence of meningism. It was derived by redefining and amalgamating previous methods and is capable of being used more consistently by different observers. A retrospective study suggests that it may classify patients more appropriately in respect of prognosis than previous scales. We suggest that the scale could form the basis of a uniform, international method of grading.

Introduction Many studies emphasise that the clinical state of a patient with a recent subarachnoid haemorrhage has a powerful bearing on the prognosis. As well as being important in comparing results in different series, the relationship between initial severity and outcome is also vital when relating previous results to the management of a new patient. Unfortunately, many different scales and grading methods have been used and even the most popular of these give very variable results when a patient is assessed by different doctors. [3]

The Derivation and Definition of a New Scale Most scales are based on information about the patient's neurological condition and about symptoms or signs of meningism. Some included also such factors as blood pressure and age but there is general agreement that these should be considered separately. The Glasgow Coma Scale is now used widely in neurosurgical departments to assess the level of consciousness, the most important aspect of the neurological condition in acute brain damage. The finding that the Glasgow Coma Scale [6] was more consistent than other methods in the assessment of patients with

10

G. M . Teasdale, K. W. Lindsay , G. Allardyce, S. Dharker, P. Ward

a ruptured aneurysm [4] stimulated us to define a scale that would be compatible with the main existing systems but which, by sharpening the definition of each grade, would be more consistent and more useful [7]. As a result of experience and of discussions with Japanese neurosurgeons, we have modified slightly our initial suggestion. The proposed scale is shown in table 1. The new scale was derived primarily from the two most popular previous systems, the scale used in the cooperative study described by Nishioka et al. [5] and the Hunt and Hess method [1]. However, because of the variations between these scales, the new scale differs from each in important detail. Table 1 Grade

Glasgow C o m a Scale*

Headache/Neck Stiffness

I

15

0

II

15

Present

III

13/14

IV

8-12

V

0.05

Discussion Our data strongly suggest a high risk of vasospasm for patients with consistent or thick blood depositions in the subarachnoid space, with a clinical deterioration of 47%, and an additional 28% of angiographical spasm only. This relationship between the amount of subarachnoid blood and the development of vasospasm has been stressed by others before [1, 2, 6, 10, 16, 18], although large series of patients studied with early CT scans have rarely been reported [6, 9]. Our findings have been indirectly confirmed by experimental studies which have proved that degradation products from the blood play a primary role in the mechanism of vessel narrowing, possibly through lipid peroxidation [13] and/or other mechanisms [3, 5, 7, 8, 12, 14, 15]. In an attempt to better define a CT scan picture at high risk for spasm, we have investigated the morphology of the blood distribution in the cisterns, and we have concluded that depositions only in the frontal interhemispheric fissure bear a low risk of spasm, and multiple depositions represent a high risk of spasm. Based on our data, the persistence of cisternal hyperdensity in the CT scan many days after SAH probably increases the risk of spasm.

Early computed tomography for prediction of vasospasm

31

The definition of a CT scan " a t risk" for vasospasm (consistent or thick cisternal deposition, distributed in multiple cisterns, and persisting for many days after SAH) may give practical advantages such as the proper selection of patients with regard to timing of surgery, closer observation and possibility of prophylactic treatment in patients " a t risk", and more adequate evaluation of different therapeutical modalities in patients uniformly at risk for vasospasm. In conclusion, while angiography remains the main diagnostic test for vasospasm, in our experience CT scan may predict the evolution of SAH toward vasospasm indirectly improving the management of this serious complication.

References [1] Davis, J . M., K. R. Davis, R. M . Crowell: Subarachnoid haemorrhage secondary to ruptured intracranial aneurysm: prognostic significance of cranial CT. AJR 134 (1980) 711—715. [2] Fisher, C. M., J . P. Kistler, J . M . Davis: Relation of cerebral vasospasm to subarachnoid haemorrhage visualized by computerized tomographic scanning. Neurosurgery 6 (1980) 1—9. [3] Handa H., K.Osaka, S.Okamoto: Breakdown products of erythrocytes as a cause of cerebral vasospasm, in Wilkins R . H . (ed.): Cerebral Arterial Spasm pp. 1 5 8 - 1 6 4 . Williams and Wilkins, Baltimore/London 1980. [4] Hirata Y., Y. Matsukado, A. Fukumura: Subarachnoid enhancement secondary to subarachnoid haemorrhage with special reference to the clinical significance and pathogenesis. Neurosurgery 11 (1982) 3 6 7 - 3 7 1 . [5] Lye R . H . , K.S.Paul, C.M.Forster, E.T.Whalley et al.: Effect of fibrin-fibrinogen degradation products on human basilar artery preparations. Possible role in the etiology of cerebral arterial spasm. J . Neurosurg. 56 (1982) 3 3 9 - 3 4 3 . [6] Mizukami M., T. Takemae, T. Tazawa et al.: Value of computed tomography in the prediction of cerebral vasospasm after aneurysm rupture. Neurosurgery 7 (1980) 583—586. [7] Ohta T., H. Kajikawa, Y. Yoshikawa et al.: Cerebral vasospasm and haemoglobins: clinical and experimental studies. In Wilkins R. H. (ed.): Cerebral Arterial Spasm, pp. 1 6 6 - 1 7 2 . Williams and Wilkins, Baltimore/London 1980. [8] Osaka

K.:

Prolonged

vasospasm

produced

by the breakdown

products

of

erythrocytes.

J . Neurosurg. 4 7 (1977) 4 0 3 - 4 1 1 . [9] Pasqualin A., L. Rosta, R. Da Pian et al.: Prediction of vasospasm in patients with subarachnoid haemorrhage: the role of C T scan. Presented at the International Symposium on Cerebrovascular Diseases. Gardone Riviera, Italy, July 1981. [10] Saito I., T. Shigeno, K.Aritake et al.: Vasospasm assessed by angiography and computerized tomography. J . Neurosurg. 5 1 (1979) 4 6 6 - 4 7 5 . [11] Saito I., Y. Ueda, K. Sano: Significance of vasospasm in the treatment of ruptured intracranial aneurysms. J . Neurosurg. 4 7 (1977) 4 1 2 - 4 2 9 . [12] Sasaki T., S.Murota, S.Wakai et al.: Evaluation of prostaglandin biosynthetic activity in canine basilar artery following subarachnoid injection of blood. J . Neurosurg. 55 (1981) 7 7 1 - 7 7 8 . [13] Sasaki T., T. Tanishima, T. Asano et al.: Significance of lipid peroxidation in the genesis of chronic vasospasm following rupture of an intracranial aneurysm. Acta Neurochir., Suppl.28 (1979) 536-540. [14] Shigeno T., I. Saito, K. Sano et al.: Roles of subarachnoid blood clots and norepinephrine in cerebral vasospasm. In: Aneurysm Surgery in the Acute Stage (L. M . Auer, F. Heppner, L. Lymon eds.) Acta Neurochir. 63 (1982) 2 7 7 - 2 8 0 .

32

A. Pasqualin, P. Cavazzani, R. Scienza, L. Rosta, R. Da Pian

[15] Sonobe M., J. Suzuki: Vasospasmogenic substance produced following subarachnoid haemorrhage, and its fate. Acta Neurochir. 44 (1978) 97-106. [16] Suzuki J., S. Komatsu, T. Sato et al.: Correlation between CT findings and subsequent development of cerebral infarction due to vasospasm in subarachnoid haemorrhage. Acta Neurochir. 55 (1980) 63-70. [17] T. Tazawa, M . Mizukami, T. Kawase et al.: Relationship between contrast enhancement on computed tomography and cerebral vasospasm in patients with subarachnoid haemorrhage. Neurosurgery 12 (1983) 643-648. [18] Yamamoto 1., M. Hara, K. Ogura et al.: Early operation for ruptured intracranial aneurysms: Comparative study with computed tomography. Neurosurgery 12 (1983) 169-174.

Prognostic evaluation of SAH on the basis of computer tomographic findings W. Mauersberger, H. Hochbaum

Summary The CT results of 109 patients with SAH showed that the bleeding could be demonstrated in 83.5% of the cases. Patients who were admitted to hospital in a bad clinical situation showed in a great percentage of the cases an intracerebral bleeding with a space-occupying character. The postoperative morbidity and mortality are going to be essentially influenced by the intensity of the SAH, the development of ischaemic infarction and the presence of intracerebral and intraventricular bleeding. The development of malabsorption hydrocephalus does not seem to have an important role in defining the prognosis of the patient with SAH because it was also seen in cases with a very good outcome. Although the direct demonstration of aneurysms by means of Ct is only possible in exceptional cases, valuable additional information could be presented through the direct demonstration of bleeding, infarction areas and cerebrospinal fluid spaces [1-4, 6, 7], In this presented work it is intended to throw light on the question as to how far the results of CT studies can give a statement on the prognosis of patients with SAH after rupture of intracranial arterial aneurysms [1],

Material and Methods We reviewed the results of CT studies of 109 patients (including operated and nonoperated cases), who were treated for ruptured aneurysms between 1979 and 1983. CT's were done in the first 72 hours after the bleeding as well as later follow-up examinations in most of the cases. The distribution of the bleeding in the basal cisterns as well as in the cortical sulci was examined during our evaluation. We rated the extent of the bleeding, in a grossly quantitative way according to the following system. Mild, moderate and severe bleeding were denoted as 1,2 and 3

34

W. Mauersberger, H. Hochbaum

points respectively so as to establish a bleeding score in every patient. The presence of cerebral and intraventricular bleeding was also examined and similarly graded in 3 classes. Cases which showed evidence of infarction or disturbance of CSF circulation were additionally interpreted.

Results SAH occurred most frequently during the fourth and sixth decades of life. Females were more often affected than males. Aneurysms of the anterior communicating artery were the most commonly present with 37.6% and were followed by those of the middle cerebral artery (26.6%) and of the internal carotid artery (23.9%). Vertebrobasilar-aneurysms were found in 8 cases (7.3%) and multiple aneurysms in 5 patients (4.6%). According to the classification of Hunt and Hess, 69 patients (63.3%) were evaluated at the time of admission as grades I and II, 21% (n = 23) were admitted as grade III and 15.6% (n = 17) as grade IV- or V-patients. In 83.5% (n = 91) of the cases there was evidence of bleeding in the CT. No correlation between the intensity of bleeding into the subarachnoidal space and the neurological state of the patients at the time of admission could be observed. The bleeding score in grades I and II patients was 3.1, in grade III patients 6.2, in grade IV patients 2.0 and in grade V patients 4.1 (tab. 1). The neurological state of the patients was obviously influenced by the presence and extension of the accompanying intracerebral bleeding, which occurred only in 26.0% (n = 18) of grade I or II patients, in 30.3% (n = 7) in grade III patients and Table 1

Clinical grade at admission I + 11

CT normal CT pathological "bleeding score" SAH basal cisterns + + + ++ + Intracer. haemorrhage + + + ++ + Intravent. haemorrhage

III

V

IV

%

n

%

n

%

n

%

n

16 53

23.4 76.6

1 22

4.4 95.6

1 2

33.3 66.6

14

6.2

3.1 13 11 2

18.8 15.9 2.9

7 10 1 14

10.1 14.5 1.4 20.2

-

4.1

2.0

7 5 5

30.4 21.7 26.0

1 1 5 8

4.3 4.3 21.7 34.8

-

100

2

66.6

1 1

33.3 33.3

1 3 2

7.1 21.3 14.2

1 9 3

7.1 64.3 21.4

P r o g n o s t i c e v a l u a t i o n of S A H

35

in 64.7% (n = 11) in grades IV and V patients. Intracerebral bleeding with a distinct space-occupying character was seen in 1.4% (n = 1) of grades I and II patients, the incidence was raised to 2 1 . 7 % (n = 5) in grade III patients and to 5 9 % (n = 10) in grades IV and V patients. Intraventricular bleeding was seen in only 20.3% (n = 14) of grade I or II patients. The incidence increased to 34.8% (n = 8) in grade III patients and to 2 3 . 5 % (n = 4) in grades IV and V patients. Late follow-up examinations showed that the development of infarctions as a result of vasospasm was seen in 13% of patients with a special predominance in grade IV or V patients (21.4%) as compared to grades I and II patients (8.7%) (tab.2). Concerning the results, it was established that patients with the best outcome (those who were able to return back to their original work) showed a lower bleeding score (2.2) than those who had a postoperative disability to work (3.3) and those who were bedridden and needed specialized nursing care (5.1). The unfavourable results were proportional to the presence and severity of the accompanying intracerebral or intraventricular bleeding and consequently the prognosis of these patients was determined in proportion to the severity of the existing bleeding. Intracerebral bleeding of moderate and severe degrees has seen in 74.8% of cases who died or those who needed postoperatively specialized nursing care. In patients with moderate and good outcomes the incidence was 3 3 . 4 % . Intracerebral bleeding with a space-occupying character was not seen in patients with a very good outcome and only in 14.3% of the patients with good results. Table 2

A = full w o r k i n g c a p a c i t y (22 patients), B = limited w o r k i n g capacity (7 patients), C = c a r i n g for self ( 1 2 patients), D = b e d r i d d e n (23 patients), E = d e c e a s e d (45 patients) A

B

n

%

6 3

D

C

E

n

%

n

%

%

27.3

2

28.6

3

25.0 7

30.4

5

11.1

13.6

-

1

8.3 2

8.7

13

28.9

8.7

5

n

%

n

S A H basal cisterns

+ + + ++ +

1

"bleeding score"

4.5

-

1

2.2

14.3

-

-

2

3.3

4.0

5.1

11.1 4.2

Intracerebr. heamatoma

+

3

13.6

+ + ++ +

1

4.5

-

-

-

1 -

28.6 -

-

-

2

8.7

1

2.2

1

8.3 2

8.7

8

17.8

-

-

28.9

2

OO

2

13

2

16.7 7

30.4

15

33.3

1

14.3

5

41.7 6

26.1

16

35.6

14.3

1

8.3

1

4.3

3

4.3

1

8.3

1

4.3

6

13.4

14.3

Intraventr. haemorrhage

2

9.1

Hydrocephalus

3

13.6

-

Infarction -unilocular

-

-

1

-mulitlocular

-

-

-

-

36

W. Mauersberger, H. Hochbaum

Intraventricular bleeding was demonstrated in only 9.1% of the patients with a very good outcome. The incidence was 16.7% in intermediate outcome patients, 30.4% in unfavourable outcome patients and 33.3% in patients who subsequently died. Infarctions as a result of vasospasm were not seen in very good outcome patients, on the other hand they were seen in 21.1% of cases who died. Hydrocephalus, due to either occlusion of CSF pathways or disturbances of CSF absorption, was seen in 3 patients (13.6%) of the good outcome group. With intermediately good outcome patients the incidence was raised to 41% (n = 5) and was observed in 35.6% (n = 16) of the cases who died.

Discussion On the basis of the above results, it could be established that the prognosis of SAH as a result of rupture of intracranial arterial aneurysms is not only correlated to the age factor and the co-existence of other diseases but also largely dependent on the bleeding itself and it's secondary implications on the brain substance. While the neurological state of the patients at the time of admission was not found to be closely related to the intensity of bleeding into the basal cisterns and cortical fissures, it was definitely correlated to the presence and extension of the accompanying intracerebral bleeding. The results of treatment are determined, apart from the neurological state on admission to the hospital, by the intensity of subarachnoidal bleedings, the occurrence of rupture into the ventricular system and by secondary development of ischaemic infarctions as a result of vasospasm. Although the development of hydrocephalus according to our results was most commonly seen in patients with an unfavourable outcome, it was also seen in patients with a very good postoperative outcome. Our results show that CT examination not only demonstrates the presence of an already existing SAH in most of the cases but also allows an accurate evaluation of the prognosis.

References [1] Bell, B. A., B.E.Kendall, L. Symon: Computed tomography in aneurysmal subarachnoid haemorrhage, J. of Neurol., Neurosurg. and Psych. 43 (1980) 522-524. [2] Van Gijn, J., K.J.van Dongen: Computed tomography in the diagnosis of subarachnoid haemorrhage and ruptured aneurysm. Clin. Neurol. Neurosurg. 82 (1980) 11—24.

Prognostic evaluation of SAH

37

[3] Grote, E.: Value of CAT in pre- and postoperative management of cerebral aneurysms. In: Cerebral Aneurysms. Advances in diagnosis and treatment, pp. 190—195. (H. W. Pia, C. Langmaid, J. Zierski, Edts.) Springer, Berlin - Heidelberg - New York 1979. [4] Kazner, E., W. Lanksch: CAT findings in cerebral aneurysms and subarachnoid haemorrhage. In: Cerebral Aneurysms. Advances in diagnosis and treatment, pp. 184—190. (H. W. Pia, C. Langmaid, J. Zierski, Edts.) Springer, Berlin - Heidelberg — New York 1979. [5] Hunt, W. E., R. M. Hess: Surgical risk related to time of intervention in the repair of intracranial aneurysms. J.Neurosurg. 28 (1968) 14-18. [6] Mauersberger, W., E. Lins: Supplementation of conventional radiographic techniques by computer tomography in cases of subarachnoid haemorrhage (SAH). Acta Neurochir. 63 (1982) 3 1 - 3 5 . [7] Weisberg, L. A.: Computed tomography in aneurysmal subarachnoid haemorrhage. Neurology (Minneap.) 29 (1979) 802-808.

Value of early computed tomography after aneurysm rupture F. Troisi, S. Acampora, G. Profeta, E. Scarano

The diagnostic value of computed tomography (CT) in cases of ruptured aneurysm has already been emphasized in many studies [1, 3, 5, 6, 9, 10, 11] Most investigations, however, have concerned the relationship between CT findings and prediction of vasospasm [1, 6, 10, 11]. These authors have indicated one week as the mean interval between the subarachnoid haemorrhage (SAH) and the CT. The purpose of this study is to analyse the CT findings within the first hours after SAH and discuss surgical problems. The CT scan, in fact, shows the responsible lesion of acute deterioration in patients with a ruptured intracranial aneurysm, such as an intracerebral haematoma (ICH), figure 1, intraventricular haemorrhage (IVH), figure 2, hydrocephalus (HYD), figure 3, or an infarcted zone, figure 4. Particularly in these severe cases an earlier diagnosis mean that difficult therapeutic decisions have to be made. In our Department the patients with an intracranial ruptured aneurysm come early after SAH. They were rapidly submitted to CT scan und angiography, and they were also operated, if necessary.

Clinical Material Sixty-five patients (31 men and 34 women) between the ages of 10 and 74 years, admitted to the Department of Neurosurgery of the Cardarelli Hospital, Naples, during a 5-month period, were included in this study. CT scans were performed within two days after SAH. The presence of an aneurysm as the source of the haemorrhage was confirmed by cerebral angiography. In the 65 patients 74 saccular aneurysms and two associated arterio-venous malformations were found. Seven patients had multiple aneurysms (10.7%). Thirty-seven patients presented with expansive lesions (tab. 1), 24 of them an intracerebral haematoma, 8 an intracerebral haematoma with an intraventricular haemorrhage, 3 an intraventricular haematoma and 2 an acute hydrocephalus.

40

F. Troisi, S. A c a m p o r a , G. Profeta, E. Scarano

fcfc Fig. 1

a) Recent SAH and parenchymal h a e m o r r h a g e into the right temporal lobe. b) Aneurysm of the right middle cerebral artery and angiographical appearance of an intracerebral h a e m a t o m a .

Fig. 2

Intraventricular h a e m o r r h a g e and ventricular enlargement.

In the remaining 28 patients the CT scan (tab. 2) showed the aneurysm itself (fig. 5) either directly or through contrast enhancement (four cases), the quantity of blood in the basal cisterns or cerebral fissures (17 cases) and the appearance of vasospasm (7 cases). 8 ' * We presume t h a t in three patients there was a previous subarachnoid haemorrhage, while in the remaining f o u r an early vasospasm was likely.

Value of early computed tomography after aneurysm rupture

41

Fig. 3

Recent SAH and early hydrocephalus due to acute blockage in cerebrospinal fluid circulation. a) Ventricular enlargement with appearance of haemorrhage in the Illrd ventricle and in the occipital horns of lateral ventricles. b) Haemorrhage into the interpeduncular cisterns and the cisterna ambiens.

Fig. 4

Ischaemic lesion in the frontal lobes, especially on the right side, due to vasospasm with appearance of recent SAH, (anterior communicating artery aneurysm).

Table 1

CT findings of expansive lesions due to aneurysmal rupture

Location

Aneurysm

ICH

ICH-IVH

IVH

HYD

ACA-ACoA ICA MCA VBS

33 21 15 5

9 5 10

7

2 1

1

Total

74

24

1 8

1 3

2

42

Fig. 5

F. Troisi, S. Acampora, G. Profeta, E. Scarano

Aneurysm of the bifurcation of the left carotid artery.

Table 2

CT findings of no expansive lesions due to aneurysmal rupture

Location

Aneurysm

AA

ESA

VS

ACA-ACoA ICA MCA VBS

33 21 15 5

1 3

7 6 1 3

4 2 1

Total

74

4

17

7

As we included in this study patients with a ruptured intracranial aneurysm admitted soon after the subarachnoid haemorrhage, we found many IV and V grades patients (more than 50%).

Discussion and Conclusion According to our own experience, we think that CT scan is necessary not only for a rapid and complete diagnosis but also because it helps towards an appropriate therapeuthic management in patients with intracranial ruptured aneurysms. Therefore it is advisable to perform the CT scan within 24-48 hours following subarachnoid haemorrhage. In patients of grades I and II according to Hunt and Hess it is very important to quantify the amount of blood in the basal cisterns and cerebral fissures. In fact if blood is present in a small quantity, arteriography and operation may be programmed, but if blood is considerable, arteriography and operation must be accomplished with 72 hours from the ictus.

Value of early computed tomography after aneurysm rupture

43

In grade III patients with much blood in the cisterns, monitoring of intracranial pressure (ICP) and eventually ventricular drainage with a Beckers system [2, 7, 8] are to be performed in an emergency. As soon as intracranial pressure decreases, operation is possible. In grades IV and V patients treatment varies according to the C T findings: a) Considerable quantity of blood in subarachnoid cisterns: monitoring of intracranial pressure is necessary and eventually ventricular drainage; b) > 3 0 ml. intraparenchymal haematoma: arteriography in emergency; c) < 3 0 ml. intraparenchymal haematoma: monitoring of intracranial pressure; d) intraventricular haemorrhage or intracerebral and intraventricular haemorrhages: monitoring of intracranial pressure and intraventricular drainage. In the cases in which there is also obesity, severe cardiopathy, diabetes, a very high pressure, absence of spontaneous respiration, arteriography is contraindicated. In any case the C T scan is to be repeated after three and seven days. In conclusion, as our experience is based on a large number of patients with severe intracranial aneurysm rupture, only for a half of them has surgical treatment been possible. For the remaining cases we tried a diagnostic and therapeuthic management according to the C T findings and clinical conditions.

Summary The diagnostic value of computed tomography in cases of ruptured aneurysms has already been suggested, but these authors indicate one week as the mean interval between the subarachnoid haemorrhage and the computed tomography. The purpose of this study is to analyse the C T findings within the first hours after subarachnoid haemorrhage and discuss surgical problems. Sixty-five patients between the ages of 10 and 74 years were included in this study. C T scan were performed within two days after subarachnoid haemorrhage. The presence of an aneurysm as the source of the haemorrhage was confirmed by cerebral angiography. In 4 9 % of the patients an intracerebral haemorrhage, in 16% an intraventricular haemorrhage and in 3 % an acute hydrocephalus was found. The surgical procedures in an emergency (haematoma evacuation, monitoring of intracranial pressure, ventricular drainage with a Becker's system and so on) were discussed.

44

F. Troisi, S. Acampora, G. Profeta, E. Scarano

References [1] Auer, L. M.: Acute surgery of cerebral aneurysms and prevention of symptomatic vasospasm. Acta Neurochirurg. 69 (1983) 273-281. [2] Genovese M., G. Profeta et al.: L'emorragia intracerebrale profonda con inondazione ventricolare. Rass. Int. Clin. Ter. 62(10) (1982) 678-683. [3] Gurushinghe, N.T., A.E.Richardson: The value of computerized tomography in aneurysmal subarachnoid haemorrhage. J.Neurosurg. 60 (1984) 763-770. [4] Kosteljanetz, M.: CSF dynamics in patients with subarachnoid and/or intraventricular haemorrhage. J.Neurosurg. 60 (1984) 940-946. [5] Ladurner, G. et al.: Computertomography in subarachnoid haemorrhage and aneurysm. In: Aneurysm Surgery in the Acute Stage (L. M. Auer, F. Heppner, L. Symon eds.) Acta Neurochirurg. 63 (1982) 17-22. [6] Mizukami, M. et al.: Value of computed tomography in the prediction of cerebral vasospasm after aneurysm rupture. Neurosurgery 7 (6) (1980) 583-586. [7] Profeta, G. et al.: Ematomi intracerebrali profondi. Nuove prospettive chirurgiche. Atti del III Congr. Naz. di Neuroradiologia, Bari, 1983. [8] Profeta, G. et al.: Drenaggio attraverso il ventricolo di ematomi profondi inoperabili. Rivista di Neurobiologia 12(2-3) (1983) 153-161. [9] Profeta G., F. Troisi et al.: Comparazione dei risultati chirurgici degli aneurismi arteriosi sacculari in epoca pre- e post-microscopica. Rass. Int. Clin. Ter. 64(6) (1984) 366-370. [10] Saito I. et al.: Vasospasm assessed by angiography and computerized tomography. J. Neurosurg. 51 (1979) 466—475. [11] Sano H. et al.: Prospection of chronic vasospasm by CT findings. In: Aneurysm Surgery in the Acute Stage (L. M. Auer, F. Heppner, L. Symon eds.) Acta Neurochirurgica 63 (1982) 2 3 - 3 0 .

Cerebral blood flow

Preoperative assessment of cerebrovascular reactivity following subarachnoid haemorrhage - Clinical correlations J. D. Pickard, D. H. Read, A. H.J. Lovick

Summary Measurement of the intraoperative response to Halothane-induced hypotension reveals those patients at greatest risk of developing late cerebral ischaemia following cerebral aneurysm surgery after subarachnoid haemorrhage. A preoperative test has been devised to assess cerebrovascular autoregulation and the results related to the postoperative outcome. Cerebral blood flow was estimated using a modification of the intravenous 1 3 3 Xenon technique. Arterial blood pressure and end-tidal carbon dioxide were monitored. Following baseline estimations, arterial blood pressure was reduced by 3 0 % using Trimetaphan. In 35 patients where cerebral blood flow did not fall with hypotension, there was a 9% incidence of delayed cerebral ischaemia but in 26 patients where cerebral blood flow fell with hypotension there was a 4 2 % incidence of delayed cerebral ischaemia. This preoperative test of cerebrovascular autoregulation appears to give the same prognostic clues as does the intraoperative measurement of autoregulatory capacity.

Introduction Delayed cerebral ischaemia following subarachnoid haemorrhage may be the result of interplay between many different factors. Such delayed ischaemic episodes may reflect the inability of part of the cerebral circulation in some individuals to compensate for periods of hypotension or hypoxia. Such deficits may be reversed sometimes by raising the patient's blood pressure and expanding his blood volume [4, 10]. Measurements of cerebral blood flow have revealed that the ability of the cerebral circulation to compensate for changes in arterial blood pressure (autoregulation of CBF is impaired in both man and primate following a recent subarachnoid haemorrhage [6, 7]. Where CBF falls significantly with carotid clamping, the probability that such a patient will sustain an ischaemic episode after carotid ligation is increased considerably. We have shown previously that patients with impaired autoregulation to moderate intraoperative hypotension induced with Halothane have an increased risk of developing postoperative neurological deficits

48

J. D. Pickard, D. H. Read, A. H. J. Lovick

of late onset and these findings have been confirmed by other workers [1, 7]. We have now developed a preoperative test of cerebrovascular reactivity [8, 9] to see if this correlates with the intraoperative measurement of autoregulatory capacity and the postoperative outcome.

Clinical material and methods The intravenous 1 3 3 Xenon injection method for the measurement of cerebral blood flow was adapted originally to be used intraoperatively [11]. Analysis of the head clearance curve was restricted to the period between one and three minutes after the start of the curve and initial slope analysis used for CBF computation for three reasons: 1. physiological parameters could not be considered to remain constant over longer time periods 2. a bicompartmental model is probably not valid for the sick brain 3. such a time period combined with pulse height analysis minimise the problem of scattered radiation from the airways. N o attempt at estimation of regional cerebral blood flow was made — our previous primate studies had provided the justification for that simplification. The changes in cerebrovascular reactivity after subarachnoid haemorrhage are present globally in the brain although, of course, such changes may be more marked focally. We have subsequently modified and extended this technique in order to measure the cerebrovascular reactivity in patients preoperatively and details have been published elsewhere [5, 8]. Early attempts to measure cerebral blood flow in confused patients following subarachnoid haemorrhage were not entirely successful, mainly because such patients would not tolerate the use of a face mask in order to sample end-tidal 1 3 3 Xenon and C 0 2 concentrations. Arterial 1 3 3 Xenon concentration has been estimated by the clearance from the right lung [2, 3, 8], 61 patients with proven subarachnoid Neurosurgeon had made the decision to usual clinical and radiological criteria. except one patient in grade four on the

haemorrhage have been studied once the operate on the patient on the basis of their All patients were in grades one to three Hunt-Hess Scale.

The code of practice of the local Ethical Committee was followed throughout during the performance of these tests. A Neuro-anaesthetist and a senior Neurosurgical nurse were present at all times during the tests. Arterial blood pressure and E C G were measured and end tidal C 0 2 obtained from a fine catheter placed in the postnasal space following a nasal spray with local anaesthetic. Following at least two estimations of cerebral blood flow to establish baseline values, the patients were sedated with intravenous Diazemuls — the level of sedation

Preoperative assessment of cerebrovascular reactivity

49

was adjusted so that the patient was still able to respond readily to verbal commands. Following a further estimation of cerebral blood flow, the patient was tilted to approximately 30° head-up and the mean arterial blood pressure reduced to 70% of the control value with an intravenous infusion of Trimetaphan. Cerebral blood flow was again measured.

Results Cerebral blood flow There were two patterns of response of cerebral blood flow to hypotension (tab. 1). In Group A when mean arterial blood pressure fell from 101 to 70 mmHg, cerebral blood flow was maintained. In Group B with a similar fall in mean arterial blood pressure, cerebral blood flow fell from 62 ± 2 mls/100g/min to 43 ± 2 mls/100g/ min. There was no difference in baseline flows between the two groups. Table 1

Preoperative cerebrovascular reactivity test Hypotension

Control

Pco2 Group A Group B

mmHg 46 ±2 43 ±2

MABP mmHg 101 ± 4 105 ± 3

CBF ml/100g/min 58 ± 4 62 ± 2

Pco2

MABP mmHg 70 ± 3 71 ± 4

mmHg 45 ± 2 41 ± 2

CBF ml/100g/min 62 ±6 43+2

(mean ± S.E.M.)

Postoperative course New neurological deficits were classified as to whether they were present immediately on reversal of anaesthesia or were delayed in onset postoperatively (tab. 2). Immediate deficits occurred in both groups and there was no statistically significant difference in their incidence. However, the incidence of delayed cerebral ischaemia was much greater in Group B than in Group A patients. Furthermore, in four Table 2

Incidence of postoperative deficits None

Group A (n = 35) Group B (n = 26)

Immediate

Delayed Mild

57%

31%

6%

38%

23%

15%

NS

Hydrocephalus Severe 3% 27% 42% PC0.01

6% 4%

50

J . D. Pickard, D . H . Read, A. H . J . Lovick

patients with an immediate deficit in Group B, this deficit progressed resulting either in severe disability or death. There was no significant difference in the incidence of hydrocephalus between the two groups.

Discussion These results confirm our earlier findings using intraoperative measurements of cerebral blood flow and its response to halothane-induced hypotension. As arterial blood pressure is reduced with Halothane in the normal individual, there is an early increase in cerebral blood flow reflecting the direct cerebral vasodilatatory effects of halothane. This phenomenon is not seen with Trimetaphan. Hence the normal response to hypotension seen in Group A patients is for cerebral blood flow to remain unchanged. It should be stressed that the aim of our study was to determine whether a given patient was able to autoregulate with a modest fall in arterial blood pressure. It was not our aim to establish the systemic arterial blood pressure at which cerebral blood flow would inevitably fall. We were not able to make the distinction between true impairment of autoregulation (linear decrease of CBF with progressive hypotension) and upward shift of the lower limit of autoregulation: more estimations at different levels of arterial blood pressure would be required. In summary, this preoperative test of cerebrovascular reactivity is feasible within the clinical context of patients with subarachnoid haemorrhage and appears to give the same clues as does the intraoperative measurement of autoregulatory capacity.

Acknowledgments We are very grateful to the Chest, Heart & Stroke Association for their generous support of this work and to M r . Jason Brice, Mr. John Garfield and the staff of the Wessex Neurological Centre for their enthusiastic co-operation with this study.

References [1] Farrar, J . K., F. W. G a m a c h e , G . G . F e r g u s o n et al.: Effects of profound hypotension on cerebral blood flow during surgery for intracranial aneurysms. J . N e u r o s u r g . 5 5 ( 1 9 8 1 ) 8 5 7 - 8 6 4 . [2] Jaggi, J . L . , W. D. Obrist: External monitoring of the lung as a substitute for end-tidal

133

Xenon

133

Xenon

sampling in non-invasive C B F studies: preliminary findings. r C B F Bull. 2 ( 1 9 8 1 ) 2 5 - 2 8 . [3] Jaggi, J . L., W. D. Obrist: External monitoring of the lung as a substitute for end-tidal sampling in non-invasive C B F studies. J . C B F . M e t a b . 3 Suppl. 1 ( 1 9 8 3 ) 1 2 3 - 1 2 4 . [4] Kosnik, E. J . , W. E. Hunt: Post-operative hypertension in the management of patients with intracranial arterial aneurysms. J . Neurosurg. 4 5 ( 1 9 7 6 ) 1 4 8 - 1 5 4 .

Preoperative assessment of cerebrovascular reactivity

51

[5] Lovick, A. H.J., J. D. Pickard, B.A. Goddard: Prediction of late ischaemic complications after cerebral aneurysm surgery — use of a mobile microcomputer system for the measurement of pre-, intra-, and post-operative cerebral blood flow. In: Aneurysm Surgery in the Acute Stage (L. M. Auer, F. Heppner, L. Symon, eds.) Acta Neurochirur. 63 (1982) 3 7 - 4 2 . [6] Pickard, J. D., D. P.J. Boisvert, D. I. Graham et al.: Late effects of subarachnoid haemorrhage on the response of the primate cerebral circulation to drug-induced changes in arterial blood pressure. J. Neurol. Neurosurg. Psychiat. 42 (1979) 899-903. [7] Pickard, J.D., M.Matheson, J.Patterson et al.: Prediction of late ischaemic complications after cerebral aneurysm surgery by the intra-operative measurement of cerebral blood flow. J. Neurosurg. 53 (1980) 305-308. [8] Pickard, J . D . , D . H . Read, A. H.J. Lovick: Use of cerebral blood flow measurements in the prediction of delayed cerebral ischaemia following subarachnoid haemorrhage. In Cerebral Blood Flow & Metabolism Measurement. A. Hartmann, S. Hoyer. Springer Berlin/Heidelberg, pp. 149-152, 1985. [9] Read, D . H . , A . H . J . Lovick, J. D. Pickard: A pre-operative test of cerebrovascular autoregulation following subarachnoid haemorrhage. Brit. J. Anaesth. 55 (1983) 918. [10] Symon, L.: Disordered cerebrovascular physiology in aneurysmal subarachnoid haemorrhage. Acta Neurochir. 41 (1978) 7 - 2 2 . [11] Wyper, D. J., J . D . Pickard, U. Acar: Monitoring cerebral blood flow during intracranial operations: an intravenous injection method. Neurol. Res. 1 (1979) 3 1 - 3 7 .

Cerebral blood flow in the prediction of vasospasm after subarachnoid haemorrhage N. W. C. Dorsch, J. S. Compton

Summary Ninety-one patients had CBF studied once or more after a recent SAH. The results confirmed previous reports of a low flow generally, lower flow in patients with vasospasm or hydrocephalus, and reduced flow on the side of a unilateral aneurysm. In predicting future spasm, blood flow studies had value in two ways. A fall in blood flow from before to shortly after the operation was a sign of future trouble. In preoperative testing, if the ISI value in a study within two days of haemorrhage was outside the limits of the lower half of the normal range, i.e. showing either ischaemia or relative hyperaemia, then that indicated a considerably greater risk of spasm than if this flow was in the lower half of the normal range.

Introduction Cerebral blood flow (CBF) has been studied in patients with subarachnoid haemorrhage (SAH) for over a decade; its value so far has been mainly as a clinical research tool, showing overall changes of flow in groups of patients. There is evidence that, in general, SAH patients have a lower flow than normal, and flow is reduced still further in patients with symptomatic vasospasm, or with hydrocephalus or other cause of raised intracranial pressure [1—3]. More recently, attempts have been made to predict vasospasm in individual patients. Most of these have concentrated on showing impaired circulatory regulation to changes in blood pressure or carbon dioxide [4]. Some of the manoeuvres needed for such testing may be dangerous, but one successful application has been to measure flow changes with hypotension during aneurysm surgery [5]. In another report [6], flow was measured both before and shortly after operation; if there was a fall in CBF between the two studies, recovery was more likely to be complicated than if the flow increased.

54

N. W. C. Dorsch, J. S. Compton

Material and Methods Measurements of CBF in aneurysm patients were made using a 16-channel N o v o cerebrograph, mainly with intravenous administration of isotope. In view of potential inaccuracies in compartmental analysis, owing to changes in partition coefficients in ischaemic brain [7], most of the analysis has been done using the Initial Slope Index (ISI). In three years, 91 patients with subarachnoid haemorrhage have been studied. Each patient had between 1 and 10 studies, for a total of 224. In most cases the haemorrhage was due to an aneurysm, although this was not confirmed in some who died before angiography could be done. The flow studies were carried out as soon as possible after the haemorrhage, and within two days in 32 cases. Delays in the other patients were due mainly to late referral. There was in the group a higher proportion than expected of patients in a poor clinical grade or with spasm, as there was some selection of which patients to study. Of the 90 patients, 47 developed vasospasm (including a few who had signs when first studied); this was confirmed by angiography in over half.

Results General From the first study done on all 91 patients, a mean value of ISI of 43.33 (SD 10.98) was obtained. This was significantly lower than stated normal values of 51.5 ± 6.75 (t = 7.10; p < 0 . 0 0 1 ) . There was a poor but significant (r = - 0 . 5 2 , p < 0 . 0 0 1 ) correlation between individual values and the patient's clinical grade at the time. These results confirm those of other reports [1, 3]. Thirty-three patients had more than one study and a proven aneurysm on one side. In their initial study there was no difference between mean ISI on the side of the ruptured aneurysm (43.12, SD 11.97), and that on the other side (mean 44.20, SD 10.63). At the time, up to two weeks later, of maximum difference between the two sides, flow was in nearly all cases lower on the aneurysm side, with ISI 4 2 . 0 7 ± 10.73, than on the opposite side where ISI was 48.39 ± 11.22 (t = 6.40; p0.5

56

N. W. C. Dorsch, J. S. Compton

T h e C B F results of these patients were analysed in two ways: Effect of Surgery As reported by Symon et al. [6], the course following aneurysm surgery can be seen to differ, depending on whether flow rises or falls after operation. In 14 patients a C B F study was done within two days before operation, and another within 2 4 hours after. Seven of these patients had a rise in ISI between the two studies (by a mean of 1 2 . 1 ) ; there was no postoperative spasm in this group, and their eventual outcome was good, with a mean G . O . S . score of 7 . 6 . In the other seven, flow was lower postoperatively than before (mean fall of ISI 13.7). Only one of these patients had a completely uneventful course; all the others developed postoperative vasospasm, and three remained severely disabled (fig. 1).

Results of First Flow Study If the ISI values in the initial study are looked at in the two groups overall, little difference is seen. T h e mean value in the 19 patients with later spasm was 4 2 . 8 9 , with SD 1 4 . 7 6 , while the 13 non-spasm patients had flows of 4 6 . 9 2 ± 7 . 8 7 (t = 1 . 0 2 ; p > 0 . 3 ) .

+ 20 15

10

•

I

•

5

CHANGE OF ISI

o 5

10 15

20 25 30 3 5 I— Fig. 1

Plot of change in SCF (postoperative ISI value minus preoperative) against outcome (G.O.S. Score, 8 = dead, 1 = full recovery) in 1 4 patients. • — = early and ultimate outcome scores on one patient.

Cerebral blood flow in the prediction of vasospasm 10

57

Later spasm No spasm

Number of Patients

I 30

20

I 40

I 50

60

70

80

ISI Fig. 2

Histogram of ISI values in early CBF study on 32 patients. Number of patients with no spasm = 13; number with later spasm = 19.

It is only when individual values are looked at more closely that differences emerge. In figure 2 the flows are seen arranged in histogram form; it is then evident, with some overlap, that in those who did not develop spasm the ISI values were largely in the range of 40—50, while most results were either above or below that range in the patients with later spasm. The actual values for the studies as are shown in table 2, and a significant difference between the two groups can be seen. These results may be compared with the normal range for ISI (mean ± 2 X S.D.) of 38—65. Fifteen patients had an initial study with ISI in the lower half of this range, between 38 and 51.5; five of them (33%) later developed spasm. By contrast, 17 ISI's were outside this range, either above or below, and there was later vasospasm in 14 (82%) of this group (x 2 = 7.94; p < 0 . 0 0 5 ) . Breaking these figures down further, the ISI was below 34 in seven patients, all of whom developed symptomatic spasm, below 40 in eleven patients with 8 2 % later spasm, and above 51.5, the centre of the normal range, in nine, with spasm developing in 7 8 % . Table 2

Comparison of values of ISI in 32 patients having early CBF study

ISI

20-30

30-40

40-50

50-60

60-70

70-80

Total

Later spasm N o spasm

6 0

3 2

3 8

6 2

0 1

1 0

19 13

x 2 = 12.69; p = 0.025

58

N. W. C. Dorsch, J. S. Compton

Discussion Some of the results presented here are in agreement with many previous authors — there is a generally low flow in patients with SAH, differences between the sides occur with unilateral aneurysms, flow falls further as spasm develops, and increases with recovery or with hypertensive treatment [6], and there is improvement after drainage or shunting for hydrocephalus [10]. The results add weight to the previous reports, and validate the technique as used in this group of patients with ruptured aneurysms. Much more important is the fact that CBF studies can be used, with a significant degree of certainty, to predict which patients are going to develop symptomatic vasospasm. The more accurate technique for this presented above is to note changes in blood flow after aneurysm surgery compared with before; a fall in flow indicates that there is a risk of spasm later. In this small series there was only one false positive result, and no false negatives. However, like the technique of assessing autoregulation during surgery, it gives no preoperative warning of trouble. It is still useful, as it can indicate which patients should be treated vigorously with volume loading or induced hypertension; the treatment can be started before symptoms develop, and may even prevent clinical deterioration. Although it is rather less accurate in prediction, the absolute level of flow in the first posthaemorrhage study, done before two days, may be even more useful in clinical management. A patient whose ISI is outside the lower half of the normal range has a much higher risk of developing vasospasm; to our knowledge, this risk when the flow is high has not been reported previously. The main value of this assessment is that it can give an indication of risk before one is committed to surgery on an individual patient. Depending on one's surgical philosophy, such an indicator can be used in two ways in a patient shown to be at risk of vasospasm: either the operation can be delayed until the phase of spasm has passed and the patient recovered; or the patient may be submitted to very early surgery, both so that subarachnoid clots can be washed out and so that hypertensive therapy can be started more safely afterwards. The reason for the apparent hyperaemia in some patients, and their greater likelihood of later vasospasm, is unknown. A possible explanation is a reactive hyperaemia in response to the presence of blood, or loss of vasomotor regulation, prior to the onset of spasm. Further investigation is in progress to determine whether this phenomenon is associated with the abnormal cortical enhancement seen in some patients on C T scanning, which is another indicator of probable future spasm [11].

Cerebral blood flow in the prediction of vasospasm

59

References [1] Gelmers, H. J., J . W. F. Beks, H. L. Journée: Regional cerebral blood flow in patients with subarachnoid haemorrhage. [2] Meyer, C. H. A., D. Lowe, M. Meyer et al.: Subarachnoid haemorrhage: Older patients have a low cerebral blood flow. Brit. Med. J . 285 (1982) 1 1 4 9 - 1 1 5 3 . [3] Géraud, G., M . Trémoulet, A. Güell et al.: The prognostic value of CBF measurement in subarachnoid haemorrhage: Use of naloxone in focal ischaemia. J . Cereb. Blood Flow Metabolism 3 (suppl.l) (1983) 3 1 - 3 2 . [4] Heilbrun, M . P., J . Olesen, N.A.Lassen: Regional cerebral blood flow studies in subarachnoid haemorrhage. J.Neurosurg. 3 7 (1972) 3 6 - 4 4 . [5] Pickard, J . D . , M.Matheson, J.Patterson et al.: Prediction of late ischaemic complications after cerebral aneurysm surgery by the intraoperative measurement of cerebral blood flow. J. Neurosurg. 53 (1980) 3 0 5 - 3 0 8 . [6] Merory, J., D . J . T h o m a s , P. R. D. Humphrey et al.: Cerebral blood flow after surgery for recent subarachnoid haemorrhage. J . Neurol. Neurosurg. Psychiatry 43 (1980) 214—221. [7] Teasdale, G., D. Mendelow: Cerebral blood flow measurements in clinical neurosurgery. J . Cereb. Blood Flow Metabolism 1 (1981) 3 5 7 - 3 5 9 . [8] Jennett, B., J . Snoek, M . R. Bond et al.: Disability after severe head injury: Observations on the use of the Glasgow Outcome Scale. J . Neurol. Neurosurg. Psychiatry 44 (1981) 2 8 5 - 2 9 3 . [9] Brawanski, A., M . R. Gaab, J . Bockhorn et al.: Atraumatic rCBF measurement: An aid in the timing of surgery and the management of spasm following subarachnoid haemorrhage. In: Aneurysm Surgery in the Acute Stage (L.H.Auer, F.Heppner, L.Symon, eds.) Acta Neurochir. 63 (1982) 43-51. [10] Hartmann, A., E. Alberti, D. Lange: Effects of CSF drainage on CBF and CBV in subarachnoid haemorrhage and communicating hydrocephalus. Acta Neurol. Scand. 56 (Suppl. 64) (1977) 334-335. [11] Hirata, Y., Y. Matsukado, A.Fukumura: Subarachnoid enhancement secondary to subarachnoid haemorrhage with special reference to the clinical significance and pathogenesis. Neurosurgery 11 (1982) 3 6 7 - 3 7 1 .

Mean cerebral blood flow (m-CBF) and cerebral oxygen utilization (CMR02) in patients with ruptured intracranial aneurysm in the acute stage T. Hotta, J . Nakagawara, T. Shimade, T. Sasaki, S. Sato, T. Hyogo, S. Ogasawara, H. Ohmachi, K. Suematsu, J . Nakamura

Summary Thirty preoperative and 76 postoperative serial measurements of mean CBF (mCBF) and C M R 0 2 were performed to investigate the changes of m-CBF and C M R 0 2 following subarachnoid haemorrhage. All of 30 patients who had m-CBF and C M R 0 2 measurements preoperatively underwent aneurysm surgery within 3 days from the last haemorrhage. During the aneurysm surgery, brain vessel C 0 2 reactivity was evaluated by estimation of the changes in 0 2 content of the juvlar bulb venous blood (Pj0 2 ) corresponding to changes in the C 0 2 content of arterial blood (PaC0 2 ). At the acute stage of subarachnoid haemorrhage from an intracranial aneurysm, mCBF and C M R 0 2 correlated well with the severity of the clinical grades of Hunt and Hess. The higher the clinical grade, the greater the reductions in m-CBF and C M R 0 2 . The C 0 2 reactivity of the brain vessels also correlated well with the clinical grade. In high grade patients the C 0 2 reactivity was significantly reduced. The m-CBF early postoperatively (from 3 to 5 days) was also significantly increased in the high graded patients (7/? in grade III, Vw in grade IV).

Introduction The timing of aneurysm surgery, particularly in high grade patients, is still most controversial. But due to the recent improvement in operative procedures and the development of some regimens for the management of vasospasm following subarachnoid haemorrhage, early operation (within 3 days from SAH) of patients in good clinical condition has become acceptable. However, early operation of patients in a poor clinical condition is still controversial because of high mortality and morbidity postoperatively. Nevertheless, it is well known that the conservative treatment of high grade patients has a high risk of rebleeding, progressive brain

62

T. Hotta et al.

damage due to an existing haematoma, and developing cerebral ischaemia following vasospasm [12]. Serial measurements of CBF in the investigation of ruptured aneurysm patients has been reported previously [1, 11, 15, 16]. But the majority of reports are concerning brain ischaemia due to vasospasm [7, 8, 10, 13, 15]. The recognition of the pathophysiological condition and its changes in the acute stage of ruptured aneurysm patients has a very important meaning for their efficient treatment [5, 20]. This study was performed to estimate the serial changes of m-CBF and C M R 0 2 and to evaluate the surgical effect on m-CBF and C M R 0 2 during the acute pre- and postoperative periods. The C 0 2 reactivity of the brain vessels during operation was also estimated for the purpose of suitable anaesthaesie of patients with ruptured aneurysm at the acute stage.

Clinical Material and Methods This series consists of 36 patients with ruptured aneurysm operated within 3 days after subarachnoid haemorrhage. Patients were graded according to five clinical conditions described by Hunt and Hess without consideration of systemic disease. Thirty patients (6 in Gr. I, 15 in Gr. II, 9 in Gr. Ill) underwent serial measurements of mean CBF and C M R 0 2 during both pre- and postoperative periods. In six patients with grade grade IV m-CBF and C M R 0 2 were measured early postoperatively. In these cases, 23 cases (12 in Gr. I & II, 11 in Gr. Ill & IV) underwent estimation of the C 0 2 reactivity of the brain vessels during aneurysm clipping surgery. Measurement of the mean CBF was performed by the Xe-133 inhalation method using a cerebrograph made by Novo-Industries (Denmark) equipped with 32 detectors. The mean CBF was culculated by the initial slope index value of 7 detectors which are mounted near the Sylvian and the Rolandic areas on both side. Another 9 values on each side mounted frontally inferior temporally, and posteriorly were neglected because of the possibility of contamination, cross talk, and the influence of extracranial tissue. Our controlled m-CBF value was 55 ± 5 ml/ 100 gr/min. C M R 0 2 was measured by estimating the difference between the 0 2 content the of arterial blood (Pa0 2 ) sampled from pedic or radial artery and the 0 2 content of venous blood (Pj0 2 ) sampled from juvlar bulb. Sampling of blood was done immediately before CBF measurement. Our controlled C M R 0 2 was 3.4 ± 0.4 ml/ 100 gr/min. The C 0 2 reactivity of the brain vessel was estimated by the changes of P j 0 2 accompanying changes of PaCO z (range from 25 to 43 mmHg) under controlled ventilation during the clipping operation of the cerebral aneurysm.

Mean cerebral blood flow (m-CBF) and cerebral oxygen utilization ( C M R 0 2 )

63

Results The m-CBF and C M R 0 2 value in each grade examined within 3 days after SAH is shown in Table 1. In grade I patients m-CBF and C M R 0 2 are 46.5 ± 4.2 ml/100 gr/ min. and 2.77 ± 0.3 ml/100 gr/min. respectively. In grade II patients m-CBF is 37.2 ± 4.0 ml/100 gr/min. and C M R 0 2 is 2.32 ± 0.4 ml/100 gr/min. In grade III patients m-CBF is 27.0 ± 5.1 ml/100 gr/min. with 1.78 ± 0.3 ml/100 gr/min. C M R 0 2 . These were statistically significant when tested by the unpaired t-test. Table 1

Preoperative CBF and C M R 0 2 values within 3 days after subarachnoid haemorrhage Number of patients

Grade I

Grade II

Grade III

6

15

9

age

40.8 ± 10.0

47.6 ± 13.2

56.8 ± 11.7

PaC02 mmHg

CBF

CMRO2

%

ml/100g/min

ml/lOOg/min

35.5 ± 0.8

39.5 ± 5.3

46.5 ± 4.2

2.77 ± 0.3

PcO.OOl

P13 days after SAH

Fig. 2

C T finding a n d interval f r o m S A H .

Subarachnoid haemorrhage with negative panangiography

85

CT-scan findings suggest that the presence of detectable blood in the subarachnoid space of patients is less than that noted in series with haemorrhage due to ruptured aneurysms. The incidence of hydrocephalus was also low; only 2 patients required shunt surgery subsequently. vasospasm verified by second angiogram No. 12

10

6-

wLi

1 2 3 4 5 6 7 8 910,,12 14 li 13

Fig. 3

>14

>22 days after SAH

Time of angiography.

2 0 patients had normal angiographic findings. 16 patients showed evidence of vasospasm but only 2 of them deteriorated clinically due to severe spasm. In a further 15 patients the angiographic findings were normal except for the fact that not all the major intracranial vessels were sufficiently demonstrated. Table 3 Angiographic findings

No. of patients

Normal

20

Normal except of one or more inadequately demonstrated basal arteries due to

15

variatons (reangiography) Arteriosclerosis

16

(generalized atheromatous plaques) Evidence of vasospasm

16

(verified by normal second angiogram) Vasospasm suspected (patient refused reangiography)

4

86

G. Haensel-Friedrich, H . Friedrich, S. H e r b o l d , H . Vogelsang

Most of these patients had a second angiography, but an aneurysm could not be revealed in any of these cases. Additional spinal angiograms were performed in 2 patients whose symptoms were highly suspicious of a spinal vascular malformation but with negative results. 4 patients had a negative myelography.

Treatment All patients were treated with bedrest, antihypertensive drugs, analgetics and sedation. We neither used antifibrinolytic agents nor Ca-antagonists.

Results Patients with untreated aneurysms run a high risk of recurrent bleeding within 6 weeks after their initial haemorrhage. In contrast, only one of our 71 patients rebled so far, the shortest follow-up time being 8 months and the longest 5 years. This young lady had been discharged from hospital 30 days after haemorrhage with normal panangiography (14. 1. 1981). In the taxicab which was to take her home she suffered a second haemorrhage, caused by an aneurysm of the right carotid artery, which could only be demonstrated on the second emergency angiogram (13. 2. 1981).

Fig. 4

a) First angiogram after SAH; b) Second angiogram after rebleeding.

Subarachnoid haemorrhage with negative panangiography

87

Follow-up results Table 4 Outcome

N o . of patients

Returned to full activity

35

Retired (due to age)

19

Retired (before SAH)

8

Retired due to SAH

3

Unable to work but independent

3

Totally dependent

1

Unemployed

2

Total

71

On follow-up examination 41 of 71 patients were symptomfree, 23 complained of recurrent headache, 19 of physical fatigue, 9 of mental fatigue and 15 of reduced concentration. Most patients were afraid of a second haemorrhage although they had been informed about the low risk of rebleeding in such cases on discharge. Only 4 patients showed residual neurological symptoms, 1 of them had a severe hemiparesis due to vasospasm, another a slight hemiparesis, the third slight ataxia and the fourth dysphasia. At follow-up examination 35 out of 71 patients had returned to as full activity as before SAH, 19 had retired due to age, 8 had already retired before SAH and only 3 because of complaints due to SAH. 3 patients are still unable to work but independent, 2 of them because of psychiatric diseases like depression unrelated to SAH. Only one patient with severe hemiparesis is totally dependent and housebound.

Conclusion From our study it is evident that patients with SAH of unknown aetiology do not differ regarding age, sex and neurological symptoms from those with SAH due to aneurysms. However, most patients do not exceed the grade I and II according to the Hunt and Hess Scale on admission, as compared to patients with bleeding from aneurysms. In contrast to haemorrhage from an aneurysm, the risk of rebleeding is low in patients with SAH of unknown origin as can be seen from our cases and from the literature. Our results suggest that repeating a complete panangiographic study is not routinely justified [4]. On the other hand angiography of specific vessels should be repeated if they have been inadequately demonstrated at the first study. We repeat angiography after 3—4 weeks if vasospasm was evident on the first angiogram.

88

G. Haensel-Friedrich, H. Friedrich, S. Herbold, H. Vogelsang

Therapy of SAH of unknown aetiology consists of sedation, analgetics and hypertensive agents. Antifibrinolytic drugs are not indicated according to the results in the literature [2], Table 5 Andreoli

Hayward

Beguelin

Own study

Period

1979

1974-1976

1977-1981

1979-1983

No. of patients

38

51(41)

42

71

Mean age

49.7

47.5

43.8

49.5

Diagnostic

Panangiography

Panangiography

CT

CT

C T pneumence-

panangiography

panangiography

procedures

phalography Rebleeding

2

0

1*

1

Died

2

0

5**

0

Mean follow-up

2 years ( 0 )

3 Vi months—

1—5 years

8 months-5 years

37

71

2Vi years

time Still alive

36

41

*Also second angiography negative **Vasospasm while treated with antifibrinolytics

Any specific therapy does not exist, but early mobilisation is recommended to avoid thromboembolic complications. In summary, we may conclude that the prognosis of SAH of unknown aetiology is better by far than that of SAH due to a vascular malformation.

References [1] Andrioli, G. C., G. Salar, L. Rigobello: Subarachnoid haemorrhage of unknown aetiology. Acta Neurochir. 4 8 (1979) 2 1 7 - 2 2 1 . [2] Beguelin, M . D., R. Seiler: Subarachnoid haemorrhage with normal cerebral panangiography. Neurosurg. 13 (4) (1983) 4 0 9 - 4 1 1 . [3] Edner, G., D. M . C. Forster, L. Steiner et al.: Spontaneous healing of intracranial aneurysms after subarachnoid haemorrhage. J . Neurosurg. 4 8 (1978) 4 5 0 - 4 5 4 . [4] Forster, D. M . C., L. Steiner, S. Hakanson et al.: The value of repeat pan-angiography in cases with unexplained subarachnoid haemorrhage. J . Neurosurg. 4 8 (1978) 7 1 2 - 7 1 6 . [5] Hayward, R. D.: Subarachnoid haemorrhage of unknown aetiology. J. Neurol. Neurosurg. Psychiat. 4 0 (1977) 9 2 6 - 9 3 1 . [6] Saks, A. L., G. E. Perret, H. B. Locksley et al. (Eds.): Intracranial aneurysms and subarachnoid haemorrhage. A cooperative study. J . B. Lippincott Comp., Philadelphia 1969. [7] Standness, B., A. Heilo: Subarachnoid haemorrhage of unknown aetiology. J . Oslo City Hospital, 3 0 (1980) 1 5 1 - 1 5 2 . [8] West, H. H.: Normal cerebral arteriography in patients with spontaneous subarachnoid haemorrhage. Neurology (Minneap.) 2 7 (6) (1977) 5 9 2 - 5 9 4 .

Spontaneous subarachnoid haemorrhage of unknown origin — a prospective study G. Bone, L. M. Auer, G. Papaefthymiou, G. Ladurner, G. Schneider, H. Lechner

Summary Twentysix patients with subarachnoid haemorrhage (SAH) of unknown origin were investigated with regard to spontaneous course and clinical outcome. These data were compared with those of 83 patients with SAH due to a ruptured aneurysm. The patients with SAH of unknown origin showed less severe neurological symptoms on admission. The occurrence of mild signs of bleeding on C T and negative CT findings respectively were more common in patients with SAH of unknown origin. Full recovery was more common in SAH of unknown origin. It may be concluded that patients with SAH of unknown origin have a better clinical course and outcome with a lower frequency of rebleeding, and less neurological deficit in the acute period, as well as less disability in the follow-up period, than patients with aneurysmal SAH.

Introduction The incidence of subarachnoid haemorrhage (SAH) among neurological and psychiatric patients can be estimated in epidemiological studies with 0.5% [15, 12]. In the majority of cases the aetiology can be clearly defined. Malformations of the cerebral vessels — arterial aneurysms and angiomas represent more than 5 0 % [5,11] of sources of haemorrhage. However, after exclusion of other sources of bleeding like haemorrhagic diathesis [11, 7], there remain a number of patients with SAH of unknown origin. Estimates of the frequency of "idiopathic" SAH have ranged widely [5, 6, 7, 9, 11], and this group of patients has not always received adequate attention. By contrast, in patients with SAH of known origin the conditions for clinical course and prognostic criteria have been well defined [2, 5, 8]. To see whether SAH of unknown origin follows the same pattern as aneurysmal haemorrhage, it was interesting to investigate and define the spontaneous course and longterm prognosis of SAH of unknown origin.

G. Bone, L. M. Auer, G. Papaefthymiou, G. Ladurner, G. Schneider, H. Lechner

90

Patients and Material Twentysix patients (12 female, 14 male) with S.AH of unknown origin were investigated, admitted to one of the two departments of the University Hospital of Graz between 1979 and 1984. Their age varied between 17 and 66 years, mean age 50 years. The time interval between SAH and admission was less than 72 hours. The clinical and neurological symptoms were graded according to the scale of Hunt and Hess. Subarachnoid haemorrhage was confirmed by lumbar puncture and CT. Four vessel angiography was performed in all patients within twelve hours after admission. Also the haematological parameters were normal. These 26 patients with SAH of unknown origin were compared with 83 patients with SAH caused by ruptured intracranial aneurysm. The degree of SAH in the CT was expressed as mild with a thin localized layer in the CT, moderate with a thick layer in two of three subarachnoid compartments (basal cisterns, sylvian fissures, interhemispheric space) or one subarachnoid compartment and cortical surface, severe with thick layers in all three subarachnoid compartments or two and the cortical surface. The clinical course and recovery were classified on the last day of hospital stay as full recovery, mild, moderate and severe residual symptoms. The results of the follow-up investigations after a time interval between six months and four years were divided in to groups of "excellent results with full recovery" — the patient can lead an independent life, returning to normal activities, without deficits, "fair", with residual neurological or intellectual impairment and " p o o r " with dependence of the patient on nursing care.

Results Clinical findings Neurologically, the grading in accordance with the scale of Hunt and Hess was I in 12 of the 26 patients, II in 6 patients and III in 5 patients. There were 2 cases with grades IV, and 1 with grade V. Grade I was more often found in SAH of unknown origin, than in aneurysmal SAH (tab. 1). Table 1

Neurological symptoms grading (Hunt and Hess)

SAH

Number

I

II

III

IV

V

21

25

13

9

6

5

2

1

of Patients Aneurysm

83

15

Of unknown origin

26

12"

**P19.2 ±

U . l

I 10

10

20

30

10 W

60

70

80(0

20

30

10 50

60

70

80 10

20

30

10 50

60

70

80

years

Fig. 2

Sex and age distribution of patients.

Postoperative course f o l l o w i n g acute and delayed operation %

acconpanying

145

diseases

60-. •>010 10»0-

10 hypertension

%

No of

SAH

I D d ] üb dD LO hi'.i rl

V«]:;(U 1 .Jr

before

operation

luri/^

diab.mell. alcohol

other

n o

ycv BOVO60So-

'10¡0¿010-

first SAM Fig. 3

second SA1I

third SAH

fourth .SAII

Relative incidence of accompanying diseases and number of S A H before operation.

transcranial Doppler sonography [4], and by cerebral blood flow measurements [11] it seemed advisable to distinguish between 3 groups of patients (fig. 1). The " a c u t e " group (n = 84) consisted of patients operated on within 72 hours following their last S A H . The "subacute" group included 51 patients operated on between the fourth and 21st day, whereas 40 patients, w h o were operated on later than 3 weeks following their last S A H , were included in the " d e l a y e d " group. The groups were rather similar in terms of sex, age distribution (fig. 2), accompanying diseases, number of SAHs (fig. 3) and location of aneurysms (fig. 4). Preoperatively, the majority of patients in the "acute" and "subacute" groups were classified as grade III, according to Hunt and Hess [7] (fig. 4). Intracerebral haematomas, including 4 ventricular haemorrhages, occurred slightly more often in the " a c u t e "

group. Other pre-operative complications

of

S A H , such as hy-

drocephalus and brain infarction, were more frequent in the " d e l a y e d " group (fig. 5).

146

H. R. Eggert, J . Gilsbach

%

location of

aneurysms

50. to30 20-

10ICA

MCA

ACoA

Ilk ACA

JDÌD

Vert./Bas. multiple

70-

60504030-

2010-

IV grading before Fig. 4

(HUNT/HESS) surgery

Location of aneurysms and grade before surgery.

Results Intraoperative complications Rupture of the aneurysms before clipping, occlusion or stenosis of major or perforating arteries, major bleeding due to rupture of the aneurysm as well as incomplete clipping of the aneurysm were considered as intraoperative complications. These complications did not occur more frequently in acute operations than in delayed procedures (fig. 5). Rupture of the aneurysm did not influence the final outcome. Temporary clipping of feeding arteries was not regarded as a complication and did not influence the postoperative course. Furthermore, in patients in whom induced hypotension was applied, the final outcome did not differ from that in those

Postoperative course following acute and delayed operation %

prroperut ivc

comp 1 i c a t t o n s

ED

i ntmccrebra 1 hcnitoon

%

i n t r a o p e r a t i ve

of

147

SAM

i n i ' a r c t ion

hydroccphn I us

comp I i c a t i ono

80-1

K Fig. 5

Milli

I

o c c i u s j on oT a r t e r i e s

major b l e c d i nft

incompleto clippinft

Lan temporary clippirvî

i nduced h y p o t e n s i on

Preoperative complications of SAH and intraoperative complications.

cases where it was not used. Nevertheless, it could not be excluded that induced hypotension could cause additional postoperative deficits in some patients of the "acute" and "subacute" groups [5]. Postoperative complications Comparing the frequency of postoperative complications and the outcome on discharge, it has to be noted that patients following an operation in the acute stage remained in the neurosurgical clinic nearly twice as long as the patients in the "delayed" group (tab. 1). A similar incidence of general complications, such as postoperative haematomas and infections, occurred among the groups. Hydrocephalus was observed more often in the "acute" group, even when the preoperative incidence of hydrocephalus was taken into consideration. While postoperative brain infarction, confirmed by CT scans, was not observed in the "delayed" group, it occurred most often in the "subacute" group. However, considering the total incidence of brain infarction, it happened least frequently in the "acute" group. The postoperative course was considered a complicated one if postoperative complications or additional postoperative deficits had a major influence on the duration of stay in the neurosurgical clinic. A complicated postoperative course in this sense was observed more frequently in the "delayed" group than in the "acute" group. The most striking observation was the rather high incidence of

148 Table 1

H. R. Eggert, J. Gilsbach Incidence of postoperative complications Acute

Subacute

Delayed

18.6 ± 10.3

12.6 ± 7.3

9.8 ± 6.3

Immediate

10%

10%

40%

Delayed

13%

8%

5%

Infarction

6%

8%

-

Recurrent SAH

-

4%

3%

Postoperative haemorrhage

1%

-

3%

Subdural haematoma

1%

2%

-

Postoperative neurosurgical care

Additional p. o. deficit

Epidural haematoma

2%

4%

3%

Infection

5%

2%

3%

Hydrocephalus

19%

4%

5%

4%

2%

5%

Pulmonary embolism

1%

-

5%

Other complications

4%

6%

8%

23%

29%

35%

6%

8%

5%

Complications of CSF shunts

Complicated course Death

immediate additional postoperative deficits in the "delayed" group (tab. 1, fig. 6). This additional postoperative deficit consisted of mental impairment as well as of neurological deficits. While motor deficits disappeared quite considerably during hospitalization, most of the mental deficits were still observed on discharge of the patients from the neurosurgical clinic. In the "acute" group immediate additional postoperative deficits did not have a higher incidence than in the "delayed" group and the rate of early regression of these deficits was constantly higher in this group. On the other hand, delayed postoperative deficits appeared to be most prominent following acute operations and consisted mainly of motor deficits. This secondary impairment had to be regarded in most cases as a delayed ischaemic deficit due to vasospasm. On discharge there were no major differences in mental or neurological deficits among the three groups (fig. 6).

Outcome on discharge The outcome of the patients on discharge from the neurosurgical clinic was graded in accordance with the Glasgow outcome scale [8]. Major differences were obtained in the group of severely disabled patients, who were more frequently found among the patients operated on at a delayed stage (fig. 7). This is probably due to the significantly shorter observation time of these patients. The most common reason for designating patients to outcome group 2 or 3 was a psychoorganic syndrome, which extended from slight retardation to a severe amnestic syndrome (fig. 8). In the

Postoperative course following acute and delayed operation I

149

psvchoorganic syndrome

80' 70605010-

30 20-

10

motor d e f i c i t

60-,

50 4030 20

rii

10

•li

Bun.

aphasia 70-, 60-

bO10

5020 10-rrm

I

preoperative

Fig. 6

msD

postoperative

delayed

e a r l y regression

-Ml

on discharge

Incidence and evolution of mental and neurological deficits.

delayed group patients were designated more frequently to group 2 or 3 because of major neurological deficits. The mortality rate was similar in all three groups (fig. 7, tab. 2). However, in the acute and subacute groups death usually had to be attributed to SAH or to intraoperative complications, whereas in the delayed group death was due to pulmonary complications.

H . R . Eggert, J . Gilsbach

150

SU-, 10-

302010good recovery ( 1 ) Fig. 7

moderate disability (?)

severe disability (3)

vegetative ( '! )

wm=n dead ( 5 )

O u t c o m e on discharge according to Glasgow outcome scale.

80-, 70605040302010-

psychoor^ni c syndrome Fig. 8

kU m

aphasia

motor d e f i c i t

Reasons for arranging patients in outcome groups 2 or 3 .

Table 2

Causes of death Acute

Subacute

Delayed

Infarction

3

1

-

4

(2.3%)

Recurrent SAH

-

2

-

2

(1.1%)

Hypertensive

1

-

-

1

(0.6%)

1

-

2

3

(1.7%)

-

1

-

1

(0.6%)

11

(6.3%)

haemorrhage Pulmonary embolism Pneumonia

5

(6.0%)

4

(7.8%)

2

(5.0%)

Postoperative course following acute and delayed operation

151

Discussion A comparison of the intraoperative and postoperative course and the outcome of patients operated on at different times following SAH is of value in that it makes it possible to differentiate between operative trauma and the natural course of SAH. As our results reveal, acute surgery on ruptured cerebral aneurysms is at least no more disadvantageous to the patients than delayed operation, under the given local preconditions. If the rates of mortality and morbidity due to recurrent bleeding and vasospasm during the waiting period in delayed operations is taken into consideration, the acute operation is evidently more favourable than the subacute and delayed operation. The lower total rate of infarction in patients operated in the acute stage indicates that it is possible to prevent ischaemic deficits by early cleaning of the subarachnoid space and by consistently applied postoperative hypervolemia and normo- or hypertension [2, 9, 14]. In most cases the postoperative course seemed to be predominantly ruled by the operative trauma and less influenced by the SAH when the appropriate postoperative treatment was applied. Only in few cases was there a progressive downhill course which was probably due to the SAH observed. Trying to find out the basic reason for a complicated postoperative course will in some cases be a rather subjective attempt. Death and a complicated course were observed most often as a consequence of inappropriate intraoperative or postoperative management (table 3). Inappropriate intraoperative management consisted of incomplete clipping, occlusion of perforating or other arteries, as well as induced hypotension, followed by severe additional deficits. Postoperative management was considered inappropriate if deficits or death occurred from the lack of postoperative hypervolemia and normo- or hypertension. Although this estimation might to some Table 3

Estimated reasons for a complicated postoperative course and fatal outcome Acute compi, po. course

Accomp. disease Preop. compi. of SAH SAH/intracerebral haematoma Intraoperative management Postoperative management Postop. compi.

9% -

17%

Subacute death

20%

compi, po. course

death

compi, po. course

death

_

-

-

-

6%

-

12% 18%

-

11%

-

12%

-

35%

-

43%

40%

50%

25%

40%

17%

4%

Delayed

-

17%

75% -

25%

-

24%

-

-

100%

152

H. R. Eggert, J . Gilsbach

extent be speculative, it reveals the areas in which we are still learning so that the results of operations on ruptured aneurysms in the acute stage may be improved in the future.

References [1] Dolenc, V., M . Fettich, M. Korsic et al.: Blood Clot Evacuation in Aneurysm Surgery in the Acute Stage (Arguments pro and con). Acta Neurochir. 63, (1982) 1 0 5 - 1 0 9 . [2] Gianotta, S. L. G. W. Kindt: Total Morbidity and Mortality Rates of Patients with Surgically Treated Intracranial Aneurysms. Neurosurg. 4 (1979) 1 2 5 - 1 2 8 . [3] Gilsbach, J., H. R. Eggert: Early Operations on Ruptured Aneurysms. In: Advances in Neurosurgery 11 (Jensen, Brock, Klinger, eds). Springer-Verlag, Berlin - Heidelberg 1983. [4] Härders, A., J . Gilsbach: Transkranielle Dopplersonographie in der Neurochirurgie. Ultraschall 5, 1984. In press. [5] Hitchcock, F. R., S. A. Tsementzis, A. A. Dow: Short- and Long-Term Prognosis of Patients with a Subarachnoid Haemorrhage in Relation to Intra-Operative Period of Hypotension. Acta Neurochir. 70 (1984) 2 3 5 - 2 4 1 . [6] Hori, S., J.Suzuki: Early Intracranial Operations for Ruptured Aneurysms. Acta Neurochir. 4 6 (1979) 9 3 - 1 0 4 . [7] Hunt, W. E., R. M. Hess: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J . Neurosurg. 28 (1968) 1 4 - 2 0 . [8] Jennet, B., M . Bond: Assessment of outcome after severe brain damage. A practical scale. Lancet 1 (1975) 4 8 0 - 4 8 4 . [9] Kassell, N . F . , S . J . Peerless, O.J.Durward et al.: Treatment of Ischemic Deficits from Vasospasm with Intravascular Volume Expansion and Induced Arterial Hypertension. Neurosurg. 11 (1982) 337-343. [10] Ljunggren, B., L.Brandt, E. Kagström et al.: Results of early operations for ruptured aneurysms. J . Neurosurg. 54 (1981) 4 7 3 - 4 7 9 . [11] Meyer, C. A., D. Lowe, M . Meyer et al.: Progressive Change in Cerebral Blood Flow during the First Three Weeks after Subarachnoid Hemorrhage. Neurosurg. 12 (1983) 5 8 - 7 6 . [12] Sano, K., I.Saito: Timing and Indication of Surgery for Ruptured Intracranial Aneurysms With Regard to Cerebral Vasospasm. Acta Neurochir. 4 1 (1978) 4 9 - 6 0 . [13] Suzuki, I., T. Onuma, T. Yoshimoto: Results of Early Operations on Cerebral Aneurysms. Surg. Neurol. 11 (1979) 4 0 7 - 4 1 2 . [14] Wilkins R. M.: Attempted Prevention or Treatment of Intracranial Arterial Spasm: A Survey. Neurosurgery 6 (1980) 1 9 8 - 2 1 0 . [15] Yasui, N., Z . I t o , M . Ohta et al.: Surgical Problems and Pathophysiology in Severe Cases with Ruptured Aneurysms in the Acute Stage. Acta Neurochir. 63 (1982) 1 6 3 - 1 7 4 .

Timing of operation after subarachnoid haemorrhage since the introduction of C T H. Sano, T. Kanno. K. Katada, N. Ishiyama, Y. Katou

Summary The mortality is statistically better in early operation within 24 hours especially in grade IV. The incidence of symptomatic vasospasm is statistically better in early operation within 24 hours especially in grade III. The patient's outcome is statistically better after early operation within 24 hours, especially in grade IV and less so in grade III. Rebleeding occurred often within 6 hours. Therefore, cases of grades I and II are an indication for early operation in order to prevent rebleeding. Cases of grades III and IV are also an absolute indication for early operation within 24 hours after SAH. The severely in ill patient needs the earlier operation. 24 hours after SAH is an optimal time to treat SAH.

Introduction With the advent of the operative microscope the operation of intracranial aneurysms has become safe and further advances in the clinical outcome have occurred with the introduction of computed tomography into the diagnostic procedures. C T has considerably helped us in noting the following features in patients with aneurysmal rupture [1, 8] [1] presence of hydrocephalus [2] in assessing the amount of haematoma in the basal cistern, its grading and subsequent prospective cerebral vasospasm preoperatively [3] occurrence of cerebral infarction secondary to vasospasm [4] also to note how much brain damage has occurred postoperatively. With the above features in view we analysed patients with aneurysms treated in our University Hospital since Sept. 1976 based on timing of the operation, neurological grading (Hunt and Hess) [3, 4] C T grading of haematoma in the basal cistern [8], incidence of symptomatic vasospasm and the clinical outcome in the patients.

Material and methods 381 aneurysm cases were treated in our University Hospital from September 1976 to August 1982; 254 cases of which were operated by the same Neurosurgeon. 61

154

H . S a n o , T. K a n n o . K. K a t a d a , N . I s h i y a m a , Y. K a t o u

cases which were treated conservatively, because of age or severe grading etc., were evaluated separately. Therefore 315 cases made up the material for this study. Operative timing was classified as follows, within 24 hours, 24—48 hours, 2—3 days, 3—14 days, and more than 2 weeks after SAH. The Hunt and Hess grading system [3,4] was used for neurological grading. In cases with early operation a decision was taken just before surgery. In cases with delayed operation the operative decision was taken at admission. Grade IV was divided into grade IVa and grade IVb; Grade IVa meant stupor or semicoma without herniation signs and grade IVb meant semicoma with herniation signs. -Grade IV included only grade IVa since grade IVb was classified into grade V. The location and volume of the haematoma was evaluated by CT findings, especially haematoma in the basal cistern which was classified into 5 grades [8]. (fig. 1) Grade 4 + : severe haematoma fills the basal cistern from the parasellar to sylvian, ambient and quadrigeminal cistern, and the CT number is over 70. The haematoma margin must be sharp. In grade 3 + : considerable haematoma is in the parasellar sylvian and ambient cistern but not in the quadrigeminal cistern. The CT number is over 60. In grade 2 + : a moderate haematoma exists in the parasellar and partially in the Sylvian fissure, but not in the ambient cistern. The CT number is about 50. In grade 1 + : there is a minimal haematoma in the parasellar only. The CT number is about 40. In grade 0: the haematoma is undetectable in the basal cistern by CT. Postoperatively, if the patient develops hemiplegia or if deterioration in conscious level is noticed then the CT would be repeated. If CT shows a low density area in relation to the arterial territory, that would indicate the

G R A D E of HEMATOMA in the BASAL CISTERN SEVER

!4+l

1

MUCH 13-fi

¡MODERATE 12+) LITTLE 11+1

LOCATION of HEMATOMA

PARASaXA CISTERN PREBONTINE

AMBIENT QUADRIGEMINAL

Fig. 1

G r a d e of h a e m a t o m a in t h e basal cistern. L o c a t i o n a n d v o l u m e of t h e h a e m a t o m a w e r e e v a l u a t e d by C T findings a n d classified i n t o 5 grades.

155

Timing of operation after the introduction of CT

occurrence of symptomatic vasospasm. The patients' outcomes were classifield into 6 degrees as follows: Excellent: almost the same state before SAH, Good: Patient recovers enough to do his daily activity as well as return to work though not of the same grade as before, Fair: self care with mild neurological deficit, Poor: Dependent, Vegetative, Dead. The correlation was evaluated statistically between the mortality rate and the incidence of symptomatic vasospasm as compared with the timing of surgery in each neurological grade. The incidence of symptomatic vasospasm was compared in cases of early operation within 24 hours after SAH with the other cases. Mortality, incidence of symptomatic vasospasm and outcome were studied statistically in cases of early operation within 24 hours after SAH and compared with the other cases.

Results The patient's number was shown according to his neurological grading and timing of operation (tab. 1). 82 cases were operated within 24 hours after SAH, comprising of 2 cases of grade I, 13 cases of grade II, 23 cases of grade III, 21 cases of grade IV and 23 cases of grade V. There were 8 cases operated on from 24 hours to 48 hours after SAH. There were 7 cases operated on from 2 days to 3 days after SAH. There were 15 cases operated on from 4 days to 2 weeks. There were 142 cases operated on after 2 weeks of SAH, comprising of 18 cases of nonruptured, 54 cases of grade I, 46 cases of grade II, 17 cases of grade III and 7 cases of grade IV. There were 61 cases not operated on because of grade, age and/or occurrence of rebleeding while awaiting surgery comprising of one case of non ruptured aneurysm, 3 cases of grade 1,15 cases of grade II, 10 cases of grade III, 19 cases of grade IV, 13 cases of grade V. Mortality was studied according to the neurological grading and timing of the operation, (tab. 2) 28 out of 82 cases (34%) died after early operation within 24 hours after SAH in which 26 cases were in grades IV and V. 3 out of 8 cases (38%)

Table 1

Total number of cases - Tabulated according to neurological grading and timing of surgery

Neur. grade - 2 4 hs

- 4 8 hs

Timing of Surgery - 3 ds —2 ws

Nonrup. Gr. Gr. Gr. Gr. Gr.

I II III IV V

Total

18 2 13 23 21 23 82

1 3 4

6 1

3 6 3 3

8

7

15

Conser.

Total

1

19

2ws—

54 46 17 7

3 15 10 19 13

63 80 62 55 36

142

61

315

156 Table 2

H . Sano, T. Kanno. K. Katada, N . Ishiyama, Y. K a t o u Mortality rate - Tabulated as per neurological grading and timing of surgery

N e u r . grade

Timing of Surgery - 2 4 hs

- 4 8 hs

Gr.I

%

%

Gr. II

Vl3

- 3 ds

Total ( % )

—2 ws

Nonrupt.

0/l8

Gr. Ill

Va

Gr. IV

%i

Gr. V

•%3

Total ( % )

2%2

Table 3

2ws—

%

% (

Vi Vi

%

0%)

%o(

%4

%

Vi

°/l7

Vi

%

y.?

Vn(

y»

(38%)

Vi ( 1 4 % )

(27%)

4/i5

6%)

"/36 ( 3 6 % )

% (34%)

0%)

( 6%)

4/65

3/H2

(2%)

(82%)

3»/2Ì4

(15%)

Incidence of s y m p t o m a t i c vasospasm versus neurological grading and H a e m a t o m a in the basal cisterns

N e u r . grade

Grade of h a e m a t o m a in the basal cistern 0

1

2

3

Vi

Gr. I

Vu

Vu

Gr. II

Va

%i

% %

Gr. Ili

l/9

V»

6/l5

Gr. IV

%

Vu

5/l2

Vis ( 8 . 9 % )

%8 ( 1 4 . 6 % )

14 /

Total ( % )

2 /72(2.8%)

Total ( % ) 4 2 /57(

34

3.5%)

"/« (16.9%)

% % (41.2%)

7/io

10/52

(19.2%)

%

(24.4%)

(70%)

operated on from 24 to 48 hours after SAH died. One out of 7 cases (14%) operated on the 3rd day after SAH died. 4 out of 15 cases (27%) operated on from 4 days to 2 weeks died. 3 out of 142 cases (2%) operated on after 2 weeks of SAH died. Out of a total of 254 cases 39 died (15%) and the maximum was within the 1st 24 hours after SAH and those too who had been in grade V. The incidence of symptomatic vasospasm was studied according to the neurological grading and timing of surgery (tab. 3). The incidence of symptomatic vasospasm was 1 2 % (7/59) in cases operated within 24 hours. It was 3 8 % (3/8) in cases operated on the next day, 4 3 % (3/8) in cases operated on the 3rd day, 4 0 % (6/15) in cases operated on on 4 days to 2 weeks, 8 % (11/142) in cases operated after 2 weeks, 1 3 % (30/231) in total. Correlation of the incidence of symptomatic vasospasm, neurological grading and grade of haematoma in the basal cistern was examined, although cases of grade V were excluded because they might have died before the occurrence of vasospasm, (tab. 4) Symptomatic vasospasm occurred in 2 out of 57 cases of neurological grade I (3.5%), 11 out of 65 cases of grade II (16.9%), 10 out of 52 cases of grade III (19.2%) and 11 out of 45 cases of grade IV (24.4%). However, symptomatic vasospasm occurred in 2 of 72 cases (2.8%) of CT grade 0 of haematoma in the basal cistern, 4 in 45 cases (8.9%) of CT grade I, 7 in 48 cases (14.6%) of CT grade 2, 14 in 34 cases (41.2%) of CT grade 3, 7 in 10 cases (70%) of CT grade 3.

Timing of operation after the introduction of CT Table 4

Incidence of symptomatic vasospasm according to the timing of surgery and neurological grading

Neur. grade - 2 4

hs

- 4 8 hs

Timing of Surgery —3 ds —2 ws

Gr. I Gr. II Gr. III Gr. IV

% >/,3 y23

'/j

3

%!

'/4

°/i

Total (%)

% (12%)

% (38%)

Vi (43%)

Table 5

157

/s

Total (%) 2ws—

% % % %

%o( 3%) '/« (14%) 10 /i2 (19%) 9 /36 (25%)

Î/54 4

/4
4 weeks

4 patients

9%

PCoA

8

> 1 year

1 patient

2%

BA

3

Table 2

Grading of patients operated for ruptured aneurysm (45)

Hunt and Hess

Glasgow outcome

(preoperative)

(at discharge)

I

1 7 patients

I

18 patients

II

1 0 patients

II

1 0 patients

III

1 2 patients

III

7 patients

IV

6 patients

IV

4 patients

V

0 patient

V

6 patients

Overall surgical mortality: 1 3 . 3 %

Experiences with Nimodipine

565

Six our of fourty-five operated patients died (13.3%) Mortality in grade I patients was zero. One 70 year old grade II patient perished due to postoperative delayed ischaemic deficit. Furthermore we lost one 60 year old grade III patient due to pulmonary embolism. Of the remaining six patients in grade IV, four of them unfortunately died due to DID.

Results of our previous series In our previous series of seventy patients we operated on most ruptured aneuysms after the second week following SAH. Nimodipine was then not available and we did not use postoperative hypertensive, hypervolemic treatment. Twelve grades I to III patients were operated during the first 72 hours after aneurysmal rutpure. In those patients we had good results comparably to our present series. We lost five patients on whom we operated between days 4 and 7 following SAH due to postoperative vasospasm. Another three patients died after late surgery with signs of a delayed ischaemic deficit. An additional three good risk patients were lost waiting for late surgery. They died from a second fatal bleeding. Such fatalities have not occurred in our present series.

Conclusion Based on our experience during the last 15 months of aneurysm surgery, mostly in the acute stage, combining treatment with Nimodipine and postoperative hypertensive and hypervolemic treatment, we are inclined to believe this to be a safe and effective measure to anticipate the symptoms of vasospasm and to prevent patients from a second, probably fatal bleeding. By such a strategy of management in the last 15 months we could achieve results in grades I to III patients similar to those which are known to compliment late surgery. Grade IV patients managed by the same regime did not apparently derive a significant benefit from this therapy, four out of these six having died. It will have to be seen if such management, perhaps with some modification, could be found useful in this desperate group.

Acknowledgements The authors wish to thank Dr. W. Freise for his assistance at evaluation patient data, and Dr. K. E. Turel for reviewing the manuscript. We gratefully acknowledge Bayer Pharmaceutical for providing us with Nimodipine free of charge.

566

H. Baumann, M . Samii, R. Ramina, A. Sepehrnia, P. Gürtner

References [1] Allen, G.S., et al.: Cerebral arterial spasm - a controlled trial of Nimodipine in patients with subarachnoid hemorrhage. The New England Journal of Medicine, 3 0 8 No. II (1983) 6 1 9 - 6 2 4 . [2] Auer, L . M . , B. Ljunggren, et al.: Verhinderung zerebraler Infarkte infolge arterieller Spasmen durch akute Aneurysmachirurgie und prophylaktische Anwendung von Nimodipin bei Patienten mit SA Blutung. Presented at Satellit Symposium during 35th annual meeting of Deutsche Gesellschaft für Neurochirurgie, Hannover 1984. [3] Drake, C.G.: Management of Cerebral Aneurysm. Stroke, 12, No. 3, (1981) 2 7 3 - 2 8 3 . [4] Flamm, E. S.: Parausrgical Treatment of Aneurysms. Clin. Neurosurg. 24 (1976) 2 4 0 - 2 4 7 . [5] Higuchi, H., Y. Nagamine, H. Satoh: Direct operation on intracranial aneurysms within 4 8 hours of subarachnoid haemorrhage-correlation between ct findings and vasopsasm, pp. 4 3 6 ^ 1 4 1 . Modern Neurosurgery Springer, Berlin-Heidelberg, 1983. [6] Hunt, W. E., Kosnik, E . J . : timing and perioperative care in intracranial aneurysm surgery. Clin. Neurosurg. 2 1 (1973) 7 9 - 8 9 . [7] Hunt, W. E., C. A. Miller: The results for early operation for aneurysm. Clin. Neurosurg. 2 4 (1977) 208-215. [8] Kassel, N. F., S . J . Peerless, et al.: Reversal of ischaemic deficits by induced arterial hypertension. Presented at second international workshop on cerabral vasospasm. Amsterdam July 11—14, 1979. [9] Kazner,

E.,

Ch. Sprung,

et

al.:

Klinische

Erfahrungen

in

der

Prophylaxe

ischaemischer

neurologischer Defizite nach SA Blutung mit Nimodipin. Presented at Satellit Symposion during 35th annual meeting of Deutsche Gesellschaft für Neurochirurgie, Hannover, 1984. [10] Koos, W.T., A. Perneczky, et al.: Behandlung ischaemischer neurologischer Defizite infolge zerebraler Vasospasmen nach SA Blutung mit Nimodipin. Presented at Satellit Symposion during 35th annual meeting of Dt. Ges. f. Neurochir. 1984. [11] Ljunggren, B., H.Säveland, L.Brandt: Causes of unfavorable outcome after early aneurysm operation. Neurosurg. 13, No. 6 (1983) 6 2 9 - 6 3 3 . [12] Ojeman, R. G.: Surgical management of cerebral desease, p. 128. Williams & Wilkins, Baltimore London 1983. [13] Pakarinen, S.: Incidence, aethiology and prognosis of primary subarachnoid haemorrhage. Acta Neurol. Scand. 42 (suppl.29)

(1967) 1 - 1 2 8 .

[14] Peerless, S . J . : Pre- and postoperative management of cerebral aneurysms. Clin. Neurosurg. 26 (1979) 2 0 9 - 2 3 1 . [14a] Reimann, I.V., U.Klotz: Clinically important interactions of Cimetidine. Inn. Med. 1 (1983) 31-40. [15] Saito, I., K. Aritake, K. Sano: Early operation on ruptured aneurysms. Result of 120 cases operated on within one week after SAH. Modern Neurosurgery, pp. 424—435, Springer, Berlin - Heidelberg, 1982. [16] Shepard, R. H.: Ruptured cerebral aneurysm. Early and late prognosis with surgical treatment. J . Neurosurg. 5 9 (1983) No. 6: 1 - 1 5 . [17] Suzuki, J.: Cerebral aneurysms. Experience with 1000 directly operated cases. Tokyo, Neuron. 1979. [18] Troupp, H.: The management of intracraniel arterial aneurysms in the acute stage. Adavances and technical standards in Neurosurg, pp. 3 5 - 4 5 , Springer, Wien 1976. [19] Vapalahti, M., B. Ljunggren, et al.: Early aneurysm operation and outcome in two remote Scandinavian populations. J . Neurosurg, 60 (1984) 1 1 6 0 - 1 1 6 2 . [20] Weir, B.: Medical aspects of the preoperative management of aneurysms, a review. Le Journal Canadien des Ciences Neurologiques. 6, No. 4 (1979) 4 4 1 ^ 1 5 0 . [21] Winn, H. R., A. E. Richardson, J . A. Jane: The long term prognosis in untreated cerebral aneurysms. Ann. Neurol. 1 (1977) 3 5 8 - 3 7 0 . [22] Yasargil, M . G.: Microsurgery, Vol II, p. 3 3 8 , Thieme, Stuttgart - New York, 1984.

Intraarterial treatment of cerebral vasospasm after subarachnoid haemorrhage with Nimodipine D. K. Böker, L. Solymosi

Summary Four cases of angiographically proven vasospasm after spontaneous subarachnoid haemorrhage are reported. In three cases the spasm was symptomatic. Vasospasm appeared preoperatively and postoperatively in two cases each. All cases were treated by perfusion of the internal carotid artery with Nimodipine (Bay e 9736) at a dosage of 0.2 mg/h for 90 minutes. Resolution of the spasm could be demonstrated angiographically. There were no side effects attributable to this form of treatment. Thus, we feel that there might arise new possibilities for intervention in selected cases of cerebral vasospasm.

Introduction Cerebral vasospasm after spontaneous subarachnoid haemorrhage is a problem that is still today responsible for quite a large proportion of unsatisfactory outcomes. The mechanism of spasm induction is not yet fully understood, but there seems to be a new promising approach to treatment and prevention of cerebral angiospasm using the calcium antagonist Nimodipine (Bay e 9736) [5]. So far experiences exist with oral, intravenous and topical application of Nimodipine, showing under experimental conditions [2, 6, 7] a dilatation of pial arteries and in clinical studies a reduction in spasm-related complications [1, 3]. Until now there has been only one communication on intraarterial application of Nimodipine in humans. Grotenhuis, et al. [4] reported of intraarterial slow bolus injections of Nimodipine, but there was no convincing effect with regard to the solution of angiospasm. Perfusion of the cerebral arteries immediately after angiographic demonstration of vasospasm might be a more effective form of treatment. Therefore, it seems justified to report briefly our experiences in four such cases and to describe the technique.

Case reports Case 1 A 46-year old female suffered from spontaneous subarachnoid haemorrhage 9 days before she was transferred to this hospital. Neurological examination of the somnolent, but cooperative patient revealed a moderate right-sided hemiparesis.

568

Fig. 1 a, b)

D. K. Böker, L. Solymos

Case 1: Left-sided carotid angiogram, a.p. and lateral view: Lobated aneurysm oa anterior communicating artery. Marked spasm in segments Ai and M 1 ; and in the supraclinoidal portion of the internal carotid artery. Delayed filling of anterior cerebral arteries.

There were no reflex differences detectable, nor disturbances of sensitivity. Cerebral angiography performed on the same day disclosed an aneurysm of the anterior communicating artery. There was also diffuse severe spasm of the internal carotid arteries, middle cerebral arteries, and anterior cerebral arteries, bilaterally (figs. 1 a, b). Injection of the vertebral artery showed, filling of both anterior cerebral arteries by anastomoses via the posterior pericallosal arteries. This opening of collateral circulation might perhaps indicate that the spasm had been present already for a somewhat longer time. As the hemiparesis had appeared only a few hours before, we decided to try a treatment of the angiospasm by intraarterial perfusion of the internal carotid artery with Nimodipine. A 3-French lysis catheter was placed with its tip into the left internal carotid artery through a 7-French angiography catheter. Nimodipine was applied by constant perfusion at a dosage of 0.2 mg/h for 90 minutes. During treatment the angiography catheter remained with its tip in the thoracal aorta. After treatment a control angiography was performed. It showed almost complete disappearance of the spasm (figs. 2 a, b). But as the aneurysm had also enlarged, the patient was operated on immediately after. Postoperatively Nimodipine treatment was continued by intravenous administration for 8 days. Neurological deficits disappeared totally within one week. Control angiography three weeks after surgery showed correct clipping of the aneurysm. There was no angiospasm The patient was discharged without neurological deficits.

Intraarterial treatment of cerebral vasospasm

Fig. 2 a, b)

569

Case 1: Control angiogram after intraarterial Nimodipine treatment. Increase of caliber of the left internal carotid artery, external carotid not bent altered. Increase of size of the aneurysm. Better orthograde filling of anterior cerebral arteries. Posterior communicating artery now identifyable.

Case 2 A 42-year old male underwent surgery for a supracolinoidal aneurysm of the right internal carotid artery. There were no neurological deficits pre- and immediately postoperatively. On the 11th postoperative day he developed a slight left-sided hemiparesis. Nimodipine was given orally at a dosage of 180 mg per day. Despite this treatment the paresis became worse during the following two days and was almost complete on the third day. CT scan did not reveal any sign of cerebral infarction, but angiography demonstrated severe spasm of the right internal carotid artery and to a lesser extent of the right anterior cerebral artery (fig. 3 a). We began initially treatment of spasm with intravenous applicatiou of Nimodipine at a dosage of 2 mg/h; After 30 minutes we performed a control angiography which showed no alterations as compared to the pre-treatment angiograms. Therefore we started an intraarterial perfusion according to the schedule described above. Another angiographic control after 90 minutes showed that the spasms had almost disappeared (fig. 3 b). Only in the direct vicinity of the clip there was further constriction of the carotid artery. A 13 days intravenous treatment with Nimodipine at a dosage of 2 mg/h and five days of oral treatment followed. Neurological deficits improved and although at the end of treatment there was still a slight left-sided hemiparesis, the patient is not disabled.

570

D. K. Boker, L. Solymos

»

S I

*

Fig. 3 a, b)

'

'

¡mm

Right-sided carotid angiogram a) supradinoidal aneurysm being clipped. Marked spasm of the A j and M 2 segments as well as supradinoidal segment of the internal carotid. Control angiogram; b) after intraarterial Nimodipine treatment. Resolution of the spasm, increase in caliber of internal carotid and their branches. In the direct vicinity of the clip no effect.

Case 3 This 45-year old woman experienced spontaneous subarachnoid haemorrhage three days before she was transferred to our clinic. On the morning of transmission she had developed severe rightsided hemiparesis. An immediately performed angiography disclosed an aneurysm of the anterior communicating artery. There was severe spasm of the left supradinoidal carotid artery and of the left-sided anterior and middle cerebral arteries in the A] and Mi section, respectively. Because the paresis had developed only a few hours before and because of the severity of the spasm we decided to perform a perfusion of the left carotid artery with Nimodipine according to the schedule described in case 1. For technical reasons we could not perform a control angiography after 90 minutes of intraarterial treatment. But as early as during intraarterial application of Nimodipine a slight improvement of the hemiparesis occurred. There were no side effects which could be attributed to the intraarterial perfusion. After one week of intravenous application of the calcium antagonist neurological records of the patient were normal.

Intraarterial treatment of cerebral vasospasm

571

Case 4 This 32-year old female underwent surgery for an aneurysm of a small branch of the left middle cerebral artery, three days after subarachnoid haemorrhage. Neurological records were normal pre- and postoperatively. For prevention of angiospasm intravenous Nimodipine treatment was started the day before the operation and continued five days postoperatively at a dosage of 2 mg/h. The following two days 240 mg/day were given orally, then the dose was reduced at a rate of 60 mg/day. With the beginning of dose reduction the patient complained of headache but neurological record remained normal. On the 10th postoperative day a control angiography was performed. It showed complete clipping of the aneurysm. But there was marked spasm of the left supraclinoidal carotid artery and the left Aj and M j sections, respectively (fig. 4 a). According to the schedule described above we started a perfusion of the left internal carotid with Nimodipine at 0.2 mg/h. Control angiography after 90 minutes documented a good, but not complete solution of the spasm (fig. 4 b). Intravenous application of Nimodipine (2 mg/h) for another 5 days, followed by 7 days of oral treatment was performed thereafter. Immediately after intraarterial perfusion headache had disappeared, and the patient remained free of signs or symptoms. She could be discharged without any complaints.

Fig. 4 a, b)

Angiogram after clipping of an aneurysm of a small branch of ACM. Lateral view a) Marked spasm of the supraclinoidal carotid; b) Angiogram after intraarterial Nimodipine treatment. Increase of caliber of the carotid artery. Same angiographic phase as in Fig. 4 a: increased cerebral perfusion.

572

D. K. Boker, L. Solymos

Discussion The calcium antagonist Nimodipine provides a promising approach to the treatment of cerebral vasospasm after spontaneous subarachnoid haemorrhage. Intravenous or oral application can be performed as routine treatment. Topical application during surgery usually results in an impressive dilatation of spastic vessels. Wie decided to try an intraarterial treatment in our first and third case because of the severity of the spasm and because paresis had occurred in both cases only a few hours before. In the first case, filling of terminal branches of the anterior cerebral arteries via anastomoses to the posterior pericallosal arteries seemed to indicate an important reduction in orthograde blood flow in the anterior cerebral arteries, which was also a reason for our decision. The effect of the treatment was rather impressive, but one will also have to assume, that it might sometimes be of high risk: not only the spasm disappeared, but the size of the aneurysm also increased considerably. The second and the fourth cases were postoperative ones. In the second case it is remarkable, that signs of a vasospasm appeared as late as 11 days after surgery. Oral Nimodipine treatment had no effect, and an immediate benefit of intravenous treatment was not detectable after 30 minutes. But the resolution of spasm after intraarterial treatment was nearly complete. The constriction of the carotid artery in the immediate vicinity of the clip suggests that this might be due to the clip, being positioned too close to the carotid wall. In the fourth case headache appeared at the time of dose reduction, on the 8 th postoperative day. After intracranial perfusion, which resulted in an incomplete solution of the spasm, headache disappeared. Thus one can assume that the headache was due to vasospasm, which might have been caused by dose reduction of Nimodipine. Perhaps development of spasm could have been prevented by a more prolonged intravenous application of Nimodipine. In our third case we could not perform a control angiography, which was a severe draw-back. But as the neurological deficit of the patient became better during treatment, we feel that the spasm must have been resolved, at least to some extent. In conclusion, we found intraarterial perfusion with Nimodipine in the treatment of cerebral vasospasm easy to perform in combination with angiography. There were no side-effects attributable to the technique. But as the aneurysm may also increase in size during this treatment, it would probably be better restricted to the treatment of postoperative vasospasm. At least, one should be prepared for immediate surgery. Further investigations will have to be made to judge the real value of this treatment protocol, but we feel that in selected cases there might arise new possibilities for the treatment of cerebral vasospasm.

Intraarterial treatment of cerebral vasospasm

573

References [1] Allen, G. S., H. S. Ahn, T. F. Preziosi, et al.: Cerebral arterial spasm, a controlled trial of nimodipine in patients with subarachnoid haemorrhage. New Engl. J. Med. 308 (1983) 619-624. [2] Auer, L. M.: Pial arterial and venous reaction to intravenous infusion of nimodipine in cats. J. Neurol. Sei. 26 (1982) 213-218. [3] Auer, L.M., H.Ito, A.Suzuki, et al.: Prevention of symptomatic vasospasm by topically applied nimodipine. In: Aneurysm Surgery in the Acute Stage (L. M. Auer, F. Heppner, L. Symon, eds). Acta Neurochir. 63 (1982) 297-302. [4] Grotenhuis, J. A., W. Bettag, B.J. O. Fiebach, et al.: Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH. A preliminary report. J. Neurosurg. 61 (1984) 231-240. [5] Kazda, S., R. Towart, Nimodipine: A new calcium antagonistic drug with a preferential cerebrovascular action. In: Aneurysm Surgery in the Acute Stage (L. M . Auer, F. Heppner, L. Symon, eds). Acta Neurochir. 63 (1982) 259-265. [6] Tanaka, K., F. Gotoh, F. Muramatsu, et al.: Effect of nimodipine, a calcium antagonist, on cerebral vasospasm after subarachnoid haemorrhage in cats. Drug Res. 32 (1982) 1529—1534. [7] Voldby, B., M . Buhl., O . F . Petersen, et al.: Modification of cerebral vasospasm by intraventricular administration of a calcium antagonist in the dog. Acta Neurochir. 59 (1981) 287.

Appearance of cerebral vasospasm after break of Nimotop-prophylaxis and their treatment (case report) H. P. Ammerer, G. Perneczky, F. Bock

Summary 60 patients were treated with Nimotop® after SAH during the last 18 months. Out of this material four cases were selected, where vascular spasm occurred after changing from intravenous to oral therapy. Since there is still discussion going on about the given evidence of an open study it seems legitimate to use special cases for the discussion of the therapy plan.

Methods The patients had been selected according to the references of a joint study. The SAH had to date back no longer than four days and the clinical status should not exceed grade 3 of the Hunt and Hess-Scale. Up to the present only intravenous application was used. The dosage varied between 2 mg/h at the beginning of the study and 4—5 mg/h in our last patients. This therapy was given for at least 10 days and at least 6 days postoperatively. Afterwards the patient had to take Nimotop orally for 5 days (140 mg/d). We have seen that spasms do still occur and we could not find a statistically striking difference compared with the time before this treatment. Given account of the changes in operating-technique, intensiv-care, fluctuation of the surgeons and, last but not least, the drastic change in timing of the operation, the occurrence of spasm after SAH seems to be the least variable. Out of 60 patients treated with Nimodipine, 6 suffered vasospasm with neurological symptoms. Four were selected where the symptoms of cerebral hypoxemia occurred in a temporal connection with changes in the therapy (fig. 1). The first patient, female, age fifty, showed an aneurysm of the internal carotid artery plus a smaller one of the M.C.A. Nimodipine was started intravenously four days after bleeding. Both aneurysms were operated on the fifth day without complications. Therapy was converted to oral application after 12 days. Up to this time the patient was without any

H + H Scale

1 2 3 4

case 1 50 a

i

J

i

i j

i i i i i i

i i

-L-l d 20

10 /Nimotop

3 mg/h

2mg/h"

H + H

case 2

A6a i i I i i i i i i i i i

d

20

10 /

Nimotop

2 mg/h

|

/

3 mg/h

case 3 61 a

i i i i

i 20

10 /

case

i

U

a

Nimotop 2 mg/h

|

/

3

m

9/h

¿ i l

j Fig. 1

I d 20

10 Ni motop

A mg/h

k mg/h

Line shows deterioration of patients (Hunt and Hess-scale) after break of nimodipine-therapy. Only case 3 and 4 improved.

intravenous

neurological symptoms. But now she deteriorated within hours to grade four (HuntHess-Scale). Even a renewed intravenous application of now 2 mg/h was not successful. At the present she is apallic and needs nursing. The second presented case suffered subarachnoid haemorrhage from a tumour. Histology showed a metastasis of a melanoma of alveolar type. The CT-Scan could not exclude the existence of an aneurysm. 13 days after SAH the therapy was discontinued after the operation by mistake. Again diffuse spasm occurred and resulted in a right hemiparesis and mother aphasia. We did not succeed with a second attempt.

Appearence of cerebral vasospasms

Fig. 2

577

Spasm after changing intravenous to oral therapy (case 3). 12 th day after SAH.

In the third case, female, age 61, Nimodipine was started on the day of the bleeding. Angiograms showed an aneurysm of the left M.C.A. without spasm. The clinical situation was excellent after operation until we switched to oral therapy. Dysphasia occurred on the same day and ended in complete motor aphasia and hemiparesis on the day after. Angiography showed spasm on the left side (fig. 2) and intravenous Nimodipine 3 mg/h was started again. Within hours the situation improved dramatically and the symptoms disappeared completely after two days. The angiograms were also normal again (fig. 3). We had another case with a similar course. But there we did not document angiographically (case 4). All four patients showed the same onset of spasm after changing to oral therapy. Two of them improved. These last two cases seem to indicate the effectiveness of the drug. But we should be aware that all spasm occurred between days 12 and 14 after SAH. The correlation could be due to the time plan of our study. Even if the disappearence of symptoms is striking; there are spontaneous remissions. What should be again discussed is the

578

Fig. 3

H. P. Ammerer, G. Perneczky, F. Böck

Normal angiogram after renewed intravenous therapy (case 3) 14 th day after SAH.

use of oral and the duration of intravenous therapy if we believe in the benefits of this drug. At the present we think that intravenous application should last for 14 days at least and than dosage should be gradually decreased. Oral application does not seem to be useful.

References [1] Allen, G. S., et al.: Cerebral Arterial Spasm. A controlled trial of Nimodipine patients with SAH. New Engl. J. Med. 308 (1983) 619-624. [2] Auer, L.M., L. Ito, A.Suzuki, et al.: Prevention of symptomatic vasospasm by topically applied nimodipine. In: Aneurysm Surgery in the Acute Stage (L. M. Auer, F. Heppner, L. Symon, eds). Acta Neurochir. 63 (1982) 297-302. [3] Ammerer, H. P., R. Karnik. G. Perneczky.: Erfahrungen mit Nimodipine und Prostaglandin bei akuten Subarachnoidalblutungen. In: Der zerebrale Angiospasmus. (G. Voth, ed.), pp. 429—436, de Gruyter Verlag, Berlin - New York 1984. [4] Kazner, E., et al.: Clinical Experiences in the Prevention of Ischemic Neurological Deficits after SAH with Nimodipine. In Press.

Perioperative management regimen of patients with aneurysmal subarachnoid haemorrhage S. Finn, C. A. Miller, S. Stephensen, W. E. Hunt

Summary A perioperative management regimen of aneurysmal subarachnoid haemorrhage is described, based on experience with 32 patients. The main techniques involved were pain control, strict regulation of blood chemistries and blood gases and invasive monitoring including use of arterial lines and Swan-Ganz catheters. Most important was the correlation between pulmonary wedge pressure and ischaemic neurological deficit. Increasing pulmonary wedge pressure pressure was associated with reversal of neurological deficits on numerous occasions.

Introduction Cerebral infarction, presumably the direct result of vaso-constrictive arteriopathy (VA), is the important cause of morbidity and mortality in aneurysmal subarachnoid haemorrhage (SAH). If rebleeding can be prevented, the management of the haemodynamic crisis becomes the most critical factor in treatment. Based on theoretical considerations, the work of others and our clinical experience [1, 3—7] we think that, at present, systemic haemodynamic factors are more important in preventing infarction than the measures designed to prevent or reverse the VA. Our experience in manipulation of blood volume and blood pressure (BP) appears to have a favourable effect on the incidence of neurological deficits and has clearly been shown to reverse deficits in some cases [2]. Some of the theoretical bases for the phenomena we are about to report are understood, but other factors which we do not yet understand also seem to be operative. In 1976, Kosnik and Hunt reported the effect of volume expansion and hypertension in reversing neurological deficits following SAH [2]. We at first used systemic arterial pressure (SAP) and central venous pressure (CVP) as indicators of adequate perfusion and blood volume. We noted that CVP could be low with little or no change in SAP. We speculated that cardiac output (CO), peripheral resistance and rheologic factors might be operative and therefore began the use of the Swan-Ganz (S-G) catheter to obtain more data. The therapeutic responses reported here are based on clinical neurological observations by trained personnel. While these are

580

S. Finn, C. A. Miller, S. Stephensen, W. E. Hunt

preliminary observations, we believe that the clinical responses to our protocol are sufficiently encouraging to warrant reporting at this time.

Method Patients admitted to the Ohio State University Hospitals with suspected SAH are continuously monitored with an automatic blood pressure cuff. Having established the diagnosis by C T scan (or failing this, by lumbar puncture), an angiogram is performed. Some patients are operated on immediately, some are managed conservatively for a relatively long period of time. In either case, the patient is placed in the neurosurgical intensive care unit where an arterial line and a S-G catheter are inserted. BP; CVP and pulmonary wedge pressure (PWP) are recorded hourly. C O ; electrolytes, glucose, BUN and arterial blood gases (ABG) are measured at least every 6 hours. The fundamental goal is to optimize cerebral perfusion, while minimizing the chance of re-rupture of the aneurysm. Pain control is important. We use 25 mg of meperidine every 2 hours intravenously for 24—48 hours and as needed thereafter. This helps control hypertension, tachycardia, and restlessness. The low dose does not cause depression of the level of consciousness or affect pupillary responses. Blood chemistries and ABG's are strictly regulated. Most important, there is strict control of blood volume and arterial BP. We perceive 4 clinical situations: 1. In patients with recently ruptured aneurysms awaiting surgery, we maintain the PWP at normal for that patient ( 1 0 - 1 2 torr in patients with no cardiac disease) and maintain the BP below 130/90 with analgesics or sodium nitroprusside. 2. In patients with recently ruptured aneurysms who develop increased neurological deficits, we at once increase the PWP until the deficit resolves. BP is increased if increasing the PWP is ineffective. 3. In patients who have a clipped aneurysm, we maintain the PWP between 1 2 - 1 4 torr and allow the blood pressure to rise to 1 5 0 or 160/90 before instituting hypotensive treatment. 4. In patients with a clipped aneurysm who develop neurological deficits, we increase the PWP by rapid volume expansion until the deficit resolves or the C O begins to decline. If needed, we may also increase the BP with dopamine. Volume expansion is accomplished primarily with hetastarch, but also fresh frozen plasma (FFP) and packed red cells (PRC) depending on the haematocrit. Two special situations will modify the management. In unrepaired aneurysms with preexisting hypertension, we attempt to lower the BP by about 2 5 % of its premorbid level. With preexisting heart disease, the PWP is governed by optimal CO.

Perioperative management regimen

581

The S-G catheter is changed every 5—7 days. It is removed when the patient can tolerate a normal PWP without neurological deficits. We have had no complications related to its use.

Case report This case report illustrates the main features of our care of these patients. A 41 year old white male presented to OSU Hospital 12 hours after sudden severe headache which awakened him from sleep. There was associated vomiting and photophobia. The neurological exam was normal, the neck stiff. The basal cisterns were opacified in the CT scan. The diagnosis was SAH. Hunt/Hess grade II, post haemorrhage day (PHD) 0. Immediate arteriography revealed an anterior communicating artery aneurysm. The patient, was operated at once and the aneurysm clipped (fig. 1). The first 3 postoperative days (POD) were uneventful. He was

PHD 0 Fig. 1

PHD 1

CT scans on PHD 0 and PHD/POD 1. The aneurysm clip is seen in the upper right scan.

582

S. Finn, C. A. Miller, S. Stephensen, W. E. Hunt

extubated 12 hours postoperatively (POD/PHD 1). The S-G catheter was removed on POD/PHD 3. On POD/PHD 4 he developed a mild left hemiparesis (fig. 2). CVP was 6 cm of H 2 0 , but SAP was unchanged. A 3 0 0 ml bolus of hetastarch was given at once and the S-G catheter was re-inserted. Following this fluid bolus, PWP was 12 torr and C O was 9.3 1/min. After a total of 7 5 0 ml of hetastarch, the PWP had risen to 14—16 torr, C O and CVP were unchanged and the hemiparesis resolved. C T scan showed a lucent region in the medial right frontal lobe without displacement of ventricles or the midline structures. On POD/PHD 5, the PWP dropped to 4 torr without change in CVP, SAP or C O . He developed an increasing left hemiparesis. One liter of hetastarch and 5 0 0 ml of PRC's were given PWP rose to 16—22 torr with arrest of the progressive hemiparesis.

4

5

6

7

POST H E M O R R H A G E DAY (PHD) Fig. 2

Graph of PWP, CVP and systolic blood pressure (SBP) versus PHD. Haematocrit and strength are graphed at the top. 1 is normal strength, 4 is hemiplegia. Note that on P H D 5 a left hemiparesis occurred when the P W P dropped but CVP and SBP were unchanged.

Perioperative management regimen

583

PHD 6 Fig. 3

CT scan on PHD 6 shows a lucency in medial right frontal lobe, unchanged from the scan on PHD 5. This radiographic picture was associated with both normal strength and hemiplegia depending on the PWP.

During the night PWP drifted down to 12 torr. Two hours later a profound left hemiplegia, with drowsiness and disorientation developed (fig. 2). CO was 10.9 1/ min. CT scan showed the same radiolucent lesion of the right medial frontal lobe (fig. 3). The patient was intubated and given 500 ml hetastarch, 1 liter FFP and 1 liter PRC's until his PWP was greater than 18 torr. He was digitalized and dopamine was started to maintain BP above 160 torr systolic. Over the next 8 hours, he again became able to move his left side. By POD/PHD 7, he had only a mild hemiparesis. PWP was maintained between 18—20 torr. On the evening of POD/PHD 8 and the morning of POD/PHD 9 his PWP dropped to 14^-17 torr for a period of 10 hours, and shortly thereafter, he again developed a dense left hemiplegia (fig.4). CO was 10.4 1/min and CVP was 10-14 cm of H 2 0 . Two liters of fluid were given. The hemiplegia resolved to a minimal hemiparesis when the PWP was 2 0 - 2 2 torr.

584

S. Finn, C . A. Miller, S. Stephensen, W. E. H u n t 27.4

8

31.9

9

POST HEMORRHAGE DAY (PHD) Fig. 4

P H D 7 - 1 0 . O n P H D 9, a left hemiplegia occurred. After the PWP d r o p p e d to 1 4 - 1 7 torr for a period of 10 hours. An P H D 10, a left hemiplegia recurred when the PWP fell to 15 torr. SBP did not change and C V P w a s increased at the time. Increasing the PWP with rapid v o l u m e e x p a n s i o n p r o m p t l y reversed the neurological deficit.

On POD/PHD 10, his PWP dropped to 15 torr and left hemiplegia developed for the fourth time (fig. 4). CVP was 20 cm of H 2 0 and CO was 10.9 1/min. Fluid was given until the PWP was 21—25 torr. The hemiparesis again became minimal. Over the next two days, PWP exceeded 21 torr. On POD/PHD 12 his strength was normal. He was extubated on POD/PHD 13. Over the next 3 days, the PWP was gradually allowed to fall without recurrent neurological deficit. On POD/PHD 16, the Swan-Ganz catheter was removed. He was subsequently monitored with CVP readings and transferred to the regular ward on POD/PHD 18. During this time he lost 3.1 kg. Serum sodium ranged between 131—135 mEq/1 except for one occasion on POD/PHD 5 when it was 128 mEq/1. The haematocrit ranged between 27.5—36.8%. He has made a full recovery.

Perioperative management regimen

585

Discussion It would appear from these observations that, aside from MAP, the PWP provides the closest correlation with the appearance of a neurological deficit and its reversal. The PWP, furthermore, may vary independently of the CVP. The second most reliable observation in assuring optimal cerebral perfusion is the CVP. 0 2 , C 0 2 , sugar and osmolality are also important but are more obvious. The haematocrit could be of particular importance, but very difficult to keep steady. We emphasize that blood volume, CVP and PWP may drop remarkably without this being detected on routine evaluation of blood pressure, pulse and respiration. It is clear from clinical responses that these factors are critical. If they are allowed to fall far below normal characteristics, the chance of an ischaemic crisis is greatly increased. If a developing neurological deficit is recognized early and appropriate correction is made, reversal of that deficit has been seen repeatedly. This occurred in 15 of 32 patients treated with our regimen and in all cases the treatment was effective. As to the role of PWP, we doubt that it has a direct influence on cerebral perfusion, but must reflect other phenomena, perhaps reflex neurogenic, perhaps systemic endocrine, perhaps changes in viscosity, in volume or other unknown factors. These questions remain to be answered. The purpose of this communication is purely to indicate that the above manipulations, through whatever mechanism, have repeatedly been observed to reverse neurological deficits in patients with VA following SAH. We are therefore pursuing this line of clinical observation in attempting to answer some of the questions raised by the gratifying clinical response described.

Conclusion 1. Systemic hemodynamics are important in the treatment of cerebral ischaemia following SAH. 2. Adequate analgesia is essential to achieve hemodynamic stability in these patients. 3. Blood chemistries and ABG's should be strictly controlled. 4. BP, and especially CVP, must be maintained but may be normal even in the face of an ischaemic neurological deficit. 5. Ischaemic neurological deficit was most closely correlated with PWP. Increasing the PWP was seen to reverse the neurological deficit on numerous occasions.

586

S. Finn, C. A. Miller, S. Stephensen, W. E. Hunt

References [1] Kassell, N. F., S . J . Peerless, Q . J . Durward, et al.: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 11, No. 2 (1982) 337-343. [2] Kosnik, E . J . , W . E . H u n t : Postoperative hypertension in management of patients with intracranial arterial aneurysms. J.Neurosurg. 45 (1976) 1 4 8 - 1 5 4 . [3] Maroon, J . C., P. B. Nelson: Hypovolemia in patients with subarachnoid haemorrhage: Therapeutic implications. Neurosurgery, 4, No. 3 (1979) 2 2 3 - 2 2 6 . [4] Pritz, M . B.: Treatment of cerebral vasospasm. Usefulness of Swan-Ganz catheter monitoring of volume expansion. Surg. Neurol. 2 1 (1984) 2 3 9 - 2 4 4 . [5] Rosenwasser, R. H., T. E.Delgado, W. A.Buchheit, et al.: Control of hypertension and prophylaxis against vasospasm in cases of subarachnoid haemorrhage: A preliminary report. Neurosurgery, 12, No. 6 (1983) 6 5 8 - 6 6 1 . [6] Wood, J . H . , F. A. Simcone, R. E. Kron, et al.: Rheological aspects of experimental hypervolemic hemodilution with low molecular weight dextran: Relationships of cortical blood flow, cardiac output and intracranial pressure to fresh blood viscosity and plasma volume. Neurosurgery, 11, No. 6 (1982) 7 3 9 - 7 5 3 . [7] Wood, J . H., L. L. Snyder, F. A. Simeone: Failure of intravascular volume expansion without hemodilution to elevate cortical blood flow in region of experimental focal ischemia. J . Neurosurg. 56 (1982) 8 0 - 8 1 .

Prevention of postoperative vasospasm by cisternal irrigation I. Saito, H. Segawa, I. Nagayama, H. Nihei

Summary Cisternal irrigation is used for washing out the subarachnoid blood clots for the prevention of postoperative vasospasm. A pair of silicone tubes are inserted into the cisterns, one in the prechiasmatic cistern and the other in the sylvian fissure. From a bottle at 15—20 cm above the patient's head, 500 ml of Saline or Ringer-Lactate solution with 24.000 units of Urokinase and 40 mg of Gentamycin is dripped through one tube and drained from the other. A total of 1.500 ml of fluid per day is used for continuous irrigation postoperatively. Of 25 cases submitted to this cisternal irrigation 6 (24%) developed postoperative vasospasm. In these cases, vasospasm did not develop in the internal carotid artery or the main portion of the middle cerebral artery. When vasospasm developed, it was restricted to the peripheral branches of the cerebral arteries only. When compared with previous cisternal drainage methods, this cisternal irrigation appears to be a more effective procedure for the prevention of postoperative vasospasm.

Introduction One of the most important purposes of early operation on a ruptured cerebral aneurysm is to wash out the subarachnoid clots for the prevention of vasospasm. Between 1974 and 1983, a total of 98 cases with ruptured aneurysm were operated on within 3 days after SAH. The subarachnoid clots were suctioned as well as possible during surgery and washed out with CSF for several days postoperatively through a drain inserted in the basal cistern. Of these 98 cases, 34 (34.7%) showed symptomatic vasospasm postoperatively (tab. 1). The incidence of vasospasm in the natural course of SAH was also calculated. Of 120 cases in which surgery was not performed until the 3rd week and survived the second week after SAH, 54 cases (45%) showed vasospasm. When these two groups are compared, cases operated on within 3 days after SAH showed vasospasm less often than cases in the natural course of SAH. However, there was no statistical difference in the incidence of vasospasm between the two groups. On the other hand, in cases operated on within

588 Table 1

I. Saito, H. Segawa, I. Nagayama, H. Nihei Did a washout of the cisternal clots by early surgery and cisternal drainage prevent the development of postoperative vasospasm?

cases showing postoperative vasospasm

34

cases operated on days 0 , 1 , 2 after SAH

98

VS cases showing preoperative vasospasm

54

cases remeining through the 2nd week after SAH

Table 2

120

Subarachnoid blood clots on CT and development of vasospasm Vasospasm slight preop. CT

blood

(+)52

clots

(-)

4

postop. CT

(+)

narrowing

( + ) 31

16

7

8

( - ) 21 (-) 4

0

5

16

0

0

4

(-)

(In 56 cases submitted to surgery on days 0, 1 & 2 of SAH) - Nov. '82 -

3 days after SAH, the relationship between subarachnoid clots on pre- and postoperative C T scans and the development of vasospasm was examined (tab. 2). In 5 2 cases with subarachnoid clots on the preoperative CT, 21 cases displayed no blood clots on the postoperative C T and died not develop symptomatic vasospasm. Only 5 of these 2 1 cases showed any narrowing of the cerebral artery on postoperative angiograms, and in these cases, the narrowing was slight. These results seem to suggest that when cisternal clots are completely removed during early surgery or washed out through cisternal drainage, it is possible to prevent the development of vasospasm [8, 10]. Since last year, we have been trying a new cisternal irrigation system for more efficient washout of cisternal clots and vasoactive substances. In this paper, this cisternal irrigation system is detailed and its efficacy for prevention of vasospasm is discussed.

Materials and methods Our system of cisternal irrigation is illustrated in figure 1. A pair of silicone tubes are inserted into the cisterns, one in the prechiasmatic cistern and the other on the lateral side of the carotid artery or in the sylvian fissure. From a bottle at 15—20 cm above the head of the patient ( 3 0 - 4 0 cm above the bed), 5 0 0 ml of Saline or RingerLactate solution with 2 4 . 0 0 0 units Of urokinase and 4 0 mg of Gentamycin is

Prevention of postoperative vasospasm by cisternal irrigation |Cisternal

589

Irrigation

BT 2

A

30 40 cm

Fig. 1

Our cisternal irrigation system. 1. a bottle with 5 0 0 ml of Saline or Ringer-Lactate, 2 4 . 0 0 0 units of Urokinase and 4 0 mg of Gentamycin. 2. a capsule for control of intracranial pressure.

dripped through one catheter and drained from the other. Irrigation continues for as long as 15 days, using 1 5 0 0 ml of Saline per day. Up to now, a total of 2 5 cases operated on within 4 days after SAH have been submitted to this cisternal irrigation (tab. 3). The grade of the patients at operation is classified according to Hunts system without his original modifications [2]. A high density area (HDA) on the preoperative C T are divided into three categories; localized, diffuse thin and diffuse thick. "Localized" means on the C T the HDA is located in the basal cistern and/or in the unilateral sylvian fissure. "Diffuse t h i n " means that HDA occupies the bilateral sylvian fissures and the basal cistern but is very thin and shows a faint density. Finally, "diffuse thick" represents a diffuse and voluminous deposit of blood clots in all the cisterns.

Results The cases are summarized in table 3. Irrigation continued for as long as 15 days. In cases which showed an early disappearance of the cisternal clots on C T , irrigation was stopped after a short period. On the other hand, it was carried out for a long period in cases in which cisternal clots were persistent or vasospasm was identified on an angiogram. Actually, an average of 1 3 5 0 ml of saline or Ringer-Lactate solution was dripped and the drained fluid including saline, CSF, cisternal clots and their degenerative substances amounted to 1 4 5 0 ml daily.

590

I. Saito, H. Segawa, I. Nagayama, H. Nihei

Table 3

Summary of cases

case

location 1

op.

of AN

day

grade

pre-op. 2

cisternal

post-op. 3

final

CT

irrigation

vasospasm

outcome

13 days

(-)

dependent independent

1. 2.

63 F

Lt MCA

0

V

localized with ICH

56 M

Lt PICA

0

IV

diffuse thin

3.

61 F

RTMCA

0

V

diffuse thin with ICH 15 days

(-) M2

4.

39 M

Rt ICA

2

II

diffuse thick

5 days

independent

5.

60 M

AcoA

0

III

diffuse thick

10 days

(-)

independent

6.

41 F

RtMCA

0

III

diffuse thick

7 days

(-) A1-A2

7.

55 F

Lt M C A

1

II

diffuse thick

8 days

independent A l , M l distal died

8.

50 M

RtICA

1

I

localized

7 days

27 M

AcoA

2

II

localized

3 days

(-)

independent

9.

independent

10.

43 M

AcoA

0

II

diffuse thin

14 days

(")

11.

64 M

AcoA

1

III

diffuse thick

14 days

12.

58 F

AcoA

2

III

diffuse thin

11 days

13.

53 F

Lt M C A

3

II

localized

11 days

14.

52 F

AcoA

1

III

localized with IVH

2 days

5 days

15.

53 F

Lt ICA

0

III

localized

12 days

16.

AcoA

0

12 days

AcoA

3

II II

diffuse thin

17.

49 F 57 M

18.

58 M

AcoA

2

IV

diffuse thick

11 days

19.

40 F

AcoA

1

II

diffuse thin

11 days

20.

55 F

RtMCA

1

II

localized

8 days

21.

55 M

RtMCA

1

I

diffuse thin

8 days

22.

54 F

RtICA

1

II

diffuse thin

2 days

23.

56 M

LtMCA

1

IV

diffuse thick

12 days 11 days

diffuse thin

24.

56 F

AcoA

0

II

diffuse thin

25.

41 M

AcoA

0

II

localized

1

2

3

9 days

5 days

(")

died

independent

(")

died

(-) M2,M3

independent

(-)

independent

(-) A l , 2, M 2

independent

Al, M2

independent

(-)

independent

(")

independent

died dependent

(-)

independent

(-)

independent

(-)

independent

(")

independent

(-) (")

independent independent

location of AN = location of ruptured aneurysm. MCA = middle cerebral artery. PICA = vertebral-posterior inferior cerebellar artery. ICA = internal carotid artery. AcoA = anterior communicating artery. pre-op. C T = distribution of cisternal clots on preoperative CT. See text. ICH = intracerebral haematoma. post-op. vasospasm = location of postoperative vasospasm on angiograms. M 2 , M 3 = M 2 or M 3 portion of the middle cerebral artery. M, distal = distal part of M j portion of the middle cerebral artery. A,, A 2 = A, or A2 portion of the anterior cerebral artery.

As shown in table 3, of 2 5 cases submitted to the cisternal irrigation, 6 ( 2 4 % ) demonstrated postoperative vasospasm. It was noted that the vasospasm which developed in these cases was not diffuse but localized. The internal carotid artery or the M j portion of the middle cerebral artery did not demonstrate vasospasm. Postoperative vasospasm was sometimes seen in the M 2 or M 3 portion of the middle cerebral artery or the A 2 portion of the anterior cerebral artery. These results are due

Prevention of postoperative vasospasm by cisternal irrigation

Fig. 2

591

CTs and angiograms of case 23. upper left and centre: CTs on day 1 showed a diffuse thick deposit of cisternal clots, upper right: angiogram on day 1 revealed ruptured 1CA; aneurysm (one arrow) and unruptured MCA; aneurysm (two arrows). lower left and centre: a small amount of residual clots were shown in the bilateral sylvian fissures and the ambient cistern on CTs obtained on day 5 (4th postoperative day). lower right: vasospasm was not identified on angiogram carried out on day 7 (6th postoperative day).

592

I. Saito, H. Segawa, I. Nagayama, H. Nihei

to the fact that the saline fluid is effective in carrying the blood clots away from the area between the prechiasmatic cistern and the sylvian fissure, whereas irrigation was not so effective in washing blood clots out of the posterior part of the sylvian fissure, the subarachnoid space of the cerebral convexity and the interhemispheric fissure. In the final outcome at 6 months after SAH, 3 out of 6 cases showing postoperative vasospasm died; one (case 3 in table 3) due to severe preoperative brain damage (grade V), one (case 7) to a haemorrhage in the brain stem on the 9th postoperative day and the last (case 13) to DIC 4 months after SAH. There was no death due to large cerebral infarction and oedema secondary to severe vasospasm. No severe meningitis occurred as a complication of this cisternal irrigation in any of these 25 cases. An illustrative case (case 23 in table 3). A grade IV patient with a internal carotid aneurysm and unruptured middle cerebral aneurysm showed a diffuse thick deposit of subarachnoid clots on the preoperative CT (upper portion of fig. 2). Operation on the aneurysm was performed on day 1, through a craniotomy fashioned in the left frontal region. After clipping the aneurysm, one tube was inserted into the prechiasmatic cistern and the other into the left sylvian fissure. The cisternal irrigation was carried out continuously for 12 days. The CT on the 4th postoperative day (day 5 after SAH) showed that most of the cisternal clots had been cleared and a small number of residual clots in the left sylvian fissure (lower portion of fig. 2). In this case, no vasospasm developed.

Discussion When compared with the incidence of vasospasm in the natural course of SAH [54 (45%) out of 120 cases] or in cases submitted to early surgery and when the previous cisternal drainage method was utilized [34 (34.7%) out of 98 cases], postoperative vasospasm developed less often in cases undergoing this cisternal irrigation system [6 (24%) out of 25 cases]. The causes of vasospasm are not yet definitely known. The correlation between the existence of cisternal clots surrounding the cerebral arteries and the development of vasospasm was first suggested by observations during aneurysm surgery [3, 8, 9] and later confirmed by CT and angiograms [1, 5, 6]. Furthermore, as we have reported [8, 10], there was a possibility that vasospasm could be prevented by early surgery when the cisternal clots were washed out completely. However, as others have also documented [7], it is not always feasible to remove cisternal clots sufficiently by surgery, particularly blood clots in the interhemispheric fissure of the posterior half of the insular cistern. Our previous cisternal drainage method in

Prevention of postoperative vasospasm by cisternal irrigation

593

which residual blood clots were drained with CSF from the basal cisterns for several postoperative days was not always efficient enough to prevent postoperative vasospasm. Kaneko, et al. [4] reported that postoperative vasospasm was prevented or weakened by irrigation of the basal cisterns with fluids. They inserted a pair of silicone catheters into the basal cistern and repeatedly injected 500—1.000 ml of saline or lactate Ringer's solution through one of these catheters twice a day for 7 days postoperatively. In our method, one tube was inserted into the sylvian fissure and Saline or RingerLactate solution was continuously dripped from the level of 15—20 cm above the patient's head through the tube. Urokinase was also used for more effective washout of blood clots. Urokinase was first used in cases with intraventricular haematoma in our clinic. It was not easy to remove intraventricular haematomas through a ventricular catheter. However, it was noted that intraventricular clots were more voluminously drained when a small amount of saline with Urokinase was injected into the ventricle. There were no unfavourable side-effects in cases undergoing an application of Urokinase. Although this cisternal irrigation was tried, blood clots were not always cleared from the slyvian fissure of the operated side or the cisterns contralateral to the surgery. However, vasospasm did not develop often in such cases. It can be said that vasospasm is prevented by saline solutions which dilute vasoactive substances released from the blood clots surrounding the cerebral arteries. It is now supposed that prevention of vasospasm can be obtained by washing out cisternal clots or diluting vasoactive substances with fluid through irrigation even when the washout of cisternal clots is not complete. When compared with previous cisternal drainage methods, this system of cisternal irrigation is expected to be a more effective procedure for the prevention of postoperative vasospasm.

References [1] Fisher, C . M . , J.P.Kistler, J . M . D a v i s : Relation of cerebral vasospasm to subarachnoid haemorrhage visualized by computerized tomographic scanning. Neurosurgery 6 ( 1 9 8 0 ) 1 - 9 . [2] Hunt, W. E.: Grading of risk in intracranial aneurysms. In: Recent Progress in Neurological Surgery. K. Sano, S.Ishii (eds.), pp. 1 6 9 - 1 7 5 . Excerpta Medica, Amsterdam 1 9 7 4 . [3] Johnson, R . J . , J . M . P o t t e r , R. C . R e i d : Arterial spasm in subarachnoid haemorrhage; mechanical considerations. J . Neurol. Neurosurg. Psychiatry. 2 1 ( 1 9 5 8 ) 6 8 . [4] Kaneko, M . , Y. Hosaka, H. Koga: Experience of per-acute operation for severe type of ruptured intracranial aneurysm. Application of repeated irrigation of basal cistern. Neurol. Med. Chir. (Tokyo) 2 0 ( 1 9 8 0 ) 9 1 5 - 9 2 1 . [5] Katada, K., T. Kanno, K. Sano: Computed tomography of ruptured cerebral aneurysms in the acute stage. Neurol. Surgery (Tokyo) 5 ( 1 9 7 7 ) 9 5 5 - 9 6 3 .

594

I. Saito, H. Segawa, I. Nagayama, H. Nihei

[6] Mizukami, M., T. Takemae, T. Tazawa, et al.: Value of computed tomography in the prediction of cerebral vasospasm after aneurysm rupture. Neurosurgery 7 (1975) 583-586. [7] Mizukami, M., T. Kawase, T. Usami, et al.: Prevention of vasospasm by ealy operation with removal of subarachnoid blood. Neurosurgery 10 (1982) 301-307. [8] Saito, I., Y. Ueda, K. Sano: Significance of vasospasm in the treatment of ruptured intracranial aneurysms. J. Neurosurg. 47 (1977) 412-429. [9] Saito, I., K. Sano: Vasospasm following rupture of cerebral aneurysm. Neurol, med. Chir. (Tokyo) 19 (1979) 103-107. [10] Sano, K., I. Saito: Early operation and washout of blood clots for prevention of cerebral vasospasm. In: Cerebral Arterial Spasm, pp. 510-513. R.H.Wilkins (ed.). Williams & Wilkins Co, Baltimore 1979.

Prevention of delayed ischaemia by radical removoal of subarachnoid clots immediately after rupture of cerebral aneurysms M . Taneda

Summary The effect of removal of subarachnoid blood clots on the prevention of delayed ischaemic deficit was evaluated in 2 4 2 patients with ruptured supratentorial aneurysms, which were clipped within 48 hours after subarachnoid haemorrhage (SAH) via a pterional approach. They were all classified preoperatively in grades 1 to 4 according to the system of Hunt and Hess. Severe delayed ischaemia which caused permanent disability or death occurred in 32 (30.8%) of 104 group A patients in whom blood clots only adjacent to the aneurysms were removed. It occurred in 17 (13.3%) of the other 138 group B patients in whom subarachnoid clots were more radically removed along the arteries around which the arachnoid membrane could be opened as extensively as possible at least by way of a unilateral pterional approach. In group B, the clots around the middle cerebral artery (MCA) ipsilateral to approach were most extensively removed up to the distal portion beyond the trifurcation. The incidence of delayed ischaemia in the area of the M C A ipsilateral to approach was 2 2 . 1 % in group A and 5 . 8 % in group B. Its incidence in the area of the other arteries than the M C A ipsilateral to approach was 8.7% in Group A and 6.5% in Group B. The results in this study indicate that extensive removal of subarachnoid clots minimizes the incidence of delayed ischaemia due to vasospasm.

Introduction It has been strongly suggested that the extravasated blood in the subarachnoid space is related to the occurrence of vasospasm [1, 8]. The purpose of this study is to access the efficacy of removal of subarachnoid blood clots on the prevention of a delayed ischaemic deficit due to vasospasm.

596

M. Taneda

Material and methods Patients selected for this study were hospitalized and examined by angiography within 24 hours of subarachnoid haemorrhage (SAH). They were 2 4 2 consecutive patients with ruptured non-giant aneurysms arising from the anterior circulation, except those of the distal anterior cerebral artery. All aneurysms were obliterated within 48 hours of SAH through a pterional approach. The patients were preoperatively classified neurologically in grades 1 to 4 according to the system of Hunt and Hess [3], and were classified into two groups according to the extent of removal of subarachnoid bloods clots. In 104 patients in group A, subarachnoid blood clots lying around the aneurysms and in the cisterns adjacent to them were removed. On the other hand, in 138 patients in group B, subarachnoid clots were removed extensively. The arachnoid membrane was invariably opened as extensively as possible via a unilateral pterional approach to remove the clots around the arteries. The arteries around which the arachnoid membrane could be opened by way of this approach included all bilateral trunks of the cerebral arteries of the carotid system, as well as the insular segments of the middle cerebral artery (MCA) on the side of approach. Therefore, the artery around which the clots were invariably removed radically up to the distal segment in group B was the M C A on the side ipsilateral to the approach. The clinical condition and age distribution of the patients are shown in table 1. Delayed ischaemic symptoms due to vasospasm were diagnosed by angiography. If the arterial calibre was less than half that observed on the angiogram performed within 24 hours of SAH, and the distribution of vasospasm corresponded to the clinical smyptoms, ischaemia due to vasospasm was considered to be responsible for the clinical deterioration. Outcomes were determined 6 months after SAH. The patients who had returned to full previous activity with or without minor neurological deficits were classified as having a good outcome. The patients who were unable to return to their previous activity or had died were classified as having a bad outcome.

Results The results are summarized in table 1. The incidence of delayed ischaemia that was responsible for a bad outcome (severe ischaemia) was 3 0 . 8 % (32 of 104 patients) in group A, as opposed to 12.3% (17 of 138 patients) in group B. The incidence of severe delayed ischaemia which occurred in the area of the M C A on the side of surgical approach was 22.1% in group A, as opposed to 5 . 8 % in group B. The incidence of severe delayed ischaemia which

Prevention of delayed ischaemia by radical removal of subarachnoid clots Table 1

597

Summary of patient population and results of two different treatments Treatment Group

Condition and Results A No. of cases

B 104

138

age less than 70 No. %

91

No. %

13

No. % No. % No. %

29

115 87.5

83.8

70 or more 23 12.5

16.7

grade 1 & 2 3 4

32 27.9

44

23.2 55

42.3 31

39.8 51

29.8

severe delayed ischaemia total

37.0

32 No. 30.8 % including the territory of MCA ipsilateral to the approach No. 23 % 22.1 excluding the territory of MCA ipsilateral to the approach No. 9 % 8.7

17

good

90

12.3 8 5.8 9 6.5

outcome

bad

No. % No. %

49 47.1 55

65.2 48

52.9

34.8

occurred in the area of other arteries than the MCA on the side of the surgical approach was 8.7% in group A, as opposed to 6.5% in group B. The outcome was good in 49 of 104 patients (57.1%) in group A, as opposed to 90 of 138 patients (65.2) in group B.

Discussion Although it has been proposed that removal of subarachnoid clots prevents delayed ischaemia due to vasospasm [4, 5, 6], it has not been decided how extensively the clots should be removed. Vasospasm is usually more severe on the side of the brain

598

M.Taneda

ipsilateral to the aneurysm not located on the midline [2, 9], As surgical approach is usually made on the side ipsilateral to aneurysms, it seems to be most effective for the prevention of delayed ischaemia to remove the subarachnoid clots around the arteries on the side of surgical approach. Actually, the incidende of severe delayed ischaemia was reduced from 22.1% to 5.8% in the area of the MCA ipsilateral to the approach by removing the clots radically. In a few cases with aneurysms located on the MCA or internal carotid artery (ICA), however, delayed ischaemia may occur not only in the area of the MCA ipsilateral to location of aneurysms, but also in the area of the other arteries. If an aneurysm is located on the anterior communicating artery, delayed ischaemia may occur bilaterally. The occurrence of severe delayed ischaemia w«is 8.7% in the area of the other arteries than the MCA ipsilateral to the approach, if clots were not removed, as indicated in this study. Removal of clots along the trunks of cerebral arteries up to the contralateral trifurcation of the MCA reduced this rate to 6.5%. However, this is higher than the incidence of delayed ischaemia in the area of the MCA around which clots were removed more radically. Although it is worth trying extensive removal of clots lying in the hemisphere contralateral to the approach along the trunks of cerebral arteries to obtain a 2.2% reduction in the incidence of delayed ischaemia, it is theoretically desirable to remove more clots along all arteries up to peripheral portion for a further decrease in its occurrence. Otherwise, delayed ischaemia may occur in the area of the artery around which the clots were not removed up to distal portion [7]. Accordingly, more extensive removal of clots prevents delayed ischaemia more effectively. However, aneurysm surgery at the acute stage is not always easy, and how extensively to remove the clots depends on the skill of each surgeon. The most important surgical technique is how to operate on acute cases without forceful brain retration. Usually, the author does not use retractors to expose the MCA and ICA ipsilateral to the approach. Another important technique is how to remove the clots with minimum mechanical stimuli to the arteries or with minimum injury to the brain. For this, the subarachnoid clots are removed by a sharp flow of saline ejected through a small and fine needle.

References [1] Fisher, C. M., J. P. Kistler, J. M . Davis: Relation of cerebral vasospasm to subarachnoid haemorrhage visulaized by computerized tomographic scanning. Neurosurgery 6 (1980) 1 - 9 . [2] Fisher, C. M., G. H. Robertson, R. G. Ojemann: Cerebral vasospasm with ruptured saccular aneurysm — the clinical manifestations. Neurosurgery 1 (1977) 245-248. [3] Hunt, W. E., R. M . Hess: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J. Neurosurg. 28 (1968) 14-20.

Prevention of delayed ischaemia by radical removal of subarachnoid clots

599

[4] Mizukami, M., T. Kawase, T. Usami, et al.: Prevention of vasospasm by early operation with removal of subarachnoid blood. Neurosurgery 10 (1982) 301-307. [5] Saito, I., Y. Ueda, K. Sano: Significance of vasospasm in the treatment of ruptured intracranial aneurysms. J. Neurosurg. 47 (1977) 412-429. [6] Taneda, M.: Effect of early operation for ruptured aneurysms on prevention of delayed ischemic symptoms. J. Neurosurg. 57 (1982) 622-628. [7] Taneda, M., A. Wakayama, K. Ozaki, et al.: Biphasic occurrence of delayed ischemia after early aneurysm surgery. Case report. J. Neurosurg. 58 (1983) 440—442. [8] Wilkins, R. H.: The role of intracranial arterial spasm in the timing of operations for aneurysms. Clin. Neurosurg. 24 (1977) 185-207. [9] Wilkins, R . H . , J.A.Alexander, G . L . O d o m : Intracranial arterial spasm: a clinical analysis. J. Neursorug. 29 (1968) 121-134.

Hypervolemic haemodilution therapy for patients with symptomatic vasospasm after early surgery of cerebral aneurysms J. Nakagawara, J. Nakamura, R. Takeda, T. Usami, M. Nishiya, W. Ide, M. Shitamichi, Y. Okada, S. Fukuoka, I. Hashimoto, K. Suematsu

Summary All 78 patients with ruptured cerebral aneurysms were operated on within 72 hours of rupture and treated postoperatively with hypervolemic haemodilution therapy during the period of 1983—1984. Five percent human albumin (1.0—1.5 g/kg/min) and 1 0 % glycerol (1000—1600 ml/day) were administered intravenously to maintain a mean CVP of 10 to 15 c m H 2 0 , and mean haematocrit values of 3 0 % to 3 3 % . Blood-contaminated CSF was drained continuously (150—200 ml/day for about two weeks postoperatively) from the basal cisterns to remove the subarachnoid blood and to control the ICP. Measurements of the CBF, cerebral metabolic rate of oxygen ( C M R 0 2 ) , delivery of oxygen (D-0 2 ) and oxygen extraction fraction (OEF) were carried out during the treatment. Patients with cerebral vasospasm showed significant reductions in CBF and D - 0 2 and an elevation of OEF. A critical CBF level of about 25 ml/100 g/min (45% of normal value) was noted in patients who developed neurological symptoms with low density areas in the CT scan. With the introduction of profound haemodilution, the progression of cerebral vasospasm was not always accompanied by a reduction in CBF. The relationship between preoperative grades and postoperative results was analyzed. Patients in grades II and III showed greater improvement in comparison with those treated without this regimen. These results suggest that hypervolemic haemodilution therapy improves cerebral perfusion and reduces the incidence and the size of cerebral infarction during the period of cerebral vasospasm.

Introduction It is well known that recurrent bleeding and cerebral infarction due to severe vasospasm are two major prognostic factors in the management of patients with

602

Nakagawara, Nakamura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

subarachnoid haemorrhage from ruptured cerebral aneurysms. With the introduction of microsurgical techniques, operation at the acute stage on cerebral aneurysms have been recommended for the prevention of rebleeding and the removal of subarachnoid clots to prevent cerebral vasospasm. Despite recent improvements in microsurgical techniques, severe vasospasm and associated delayed neurological deficits still lead to unacceptable morbidity and mortality [1, 11, 16]. Intravascular volume expansion [12, 15] and induced hypertension have become popular adjuncts to the treatment of neurological deficits associated with vasospasm. These therapeutic techniques are thought to increase regional cerebral blood flow (CBF), thus improving cerebral tissue oxygenation [2, 8]. This seems to be due to the impairment of autoregulation in the ischaemic brain [8, 10, 12]. However, Wood and Simeone [18—20] have suggested that in the absence of an elevated blood pressure, neither intravascular volume expansion nor augmentation of cardiac output, without haemodilution, is capable of raising regional cerebral blood flow in the ischaemic brain. High haematocrit levels increase the blood viscosity, and thus, decrease cerebral blood flow [3, 4, 17, 19]; therefore, intravascular volume expansion appears to require concomitant haemodilution for the improvement of collateral perfusion to ischaemic regions of the brain. Starting in 1983, all patients (78 cases) surgically treated for cerebral aneurysm in the acute stage were also treated with hypervolemic haemodilution therapy. The purpose of this paper is to evaluate cerebral blood flow and metabolic changes following induced haemodilution during the period of vasospasm. In addition, the 78 patients were analyzed for postoperative results.

Clinical materials and methods Seventy-eight patients with ruptured cerebral aneurysms, including 16 cases with multiple aneurysms, were operated on within 72 hours of rupture. Fifty-three were female and 25 were male; their ages ranging from 18 to 72 years with an average age of 50 years. The preoperative neurological grades (Hunt and Hess, without consideration of other systemic diseases or preoperative vasospasm) and the number of patients were as follows: 1-13, 11-29, 111-23, IV-10 and V-3. Postoperatively, all patients were treated with hypervolemic haemodilution therapy. Five percent human albumin (1.0-1.5 g/kg/day) and 10% glycerol (1000-1600 ml/day) were administered intravenously to maintain a mean central venous pressure (CVP) of 10 to 15 c m H 2 0 , and mean haematocrit values between 30% and 33%. Blood-contaminated cerebrospinal fluid (CSF) was drained continuously (150—200 ml/day for about two weeks postoperatively) from the basal cisterns to remove the subarachnoid blood and to control the intracranial pressure (ICP).

Hypervolemic haemodilution therapy

603

The cerebral blood flow (CBF) and cerebral oxygen metabolism were monitored in all patients using the Xenon-133 inhalation technique (Novo cerebrograph®). Hemispheric CBF (mean r-CBF) values were calculated with initial slope analysis (Fourier method); the normal mean r-CBF in our laboratory is 55 ± 7.0 (S.D.) ml/ 100 g/min. The following metabolic information was calculated: Cerebral metabolic rate of oxygen (CMR0 2 ) = CBFx(Ca0 2 -Cj0 2 ). Delivery of oxygen (D-0 2 ) = CBFxCa0 2 Oxygen extraction fraction (OEF) = C M R 0 2 / D - 0 2 = ( C a 0 2 - C j 0 2 ) / C a 0 2 Where C a 0 2 ; arterial 0 2 content (vol%) C j 0 2 ; jugular 0 2 content (vol%) The arterial and jugular blood 0 2 content ( C a 0 2 and Cj0 2 ) were determined by using the following procedure: Small polyethylene catheters were introduced into the brachial artery and the internal jugular vein (superior bulb) to monitor arterial blood pressure and to collect arterial and jugular venous blood for blood gas analysis. Heparinized blood samples were analyzed immediately for pH, oxygen tension (P0 2 ) and carbon dioxide tension (PC0 2 ) on an ABL-2 acid-base laboratory® (Radiometer). The haemoglobin concentration (Hb) and oxygen saturation (Sa0 2 ) were measured on a Haemoximeter® (Radiometer).

Results Volume expansion without haemodilution for severe symptomatic vasospasm In the previous surgical treatment for ruptured cerebral aneurysms, postoperative hypervolemia was mainly produced by the transfusion of blood (either whole blood or packed red blood cells) and Rheomacrodex® to maintain a CBP of 10 to 15 c m H 2 0 , and mean haematocrit values of about 40%. However, in the patients with severe symptomatic vasospasm, mean CBF and D - 0 2 decreased rapidly in accordance with the progression of cerebral vasospasm (fig. 1). A critical CBF level of about 25 ml/100 g/min was noted in patients who developed neurological symptoms with expanding low density areas in the CT scan. A good outcome was not obtained in these patients. OEF schowed a gradual elevation in patients with the progression of the vasospasm (fig. l a , b).

604

Fig. 1

Nakagawara, Nakaraura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

CBF and cerebral 0 2 metabolism using hypervolemic therapy without haemodilution (Ht at about 40%) for symptomatic vasospasm. A critical CBF level of about 25 ml/100 g/min was noted in those patients who developed neurological symptoms with expanding low density areas in the CT scan.

Haemodynamic changes following induced haemodilution applied after the onset of the vasospasm To investigate haemodynamic changes following the application of induced haemodilution after the onset of the vasospasm, hypervolemic haemodilution therapy was started 5 to 7 days after haemorrhage in 4 patients who exhibited vasospasm. With the introduction of this therapy, the progression of cerebral vasospasm was not accompanied by reductions in CBF, D - 0 2 or C M R 0 2 (tab. 1 A). One patient, during the period of severe vasospasm (11 days after haemorrhage), was treated with whole blood transfusion which resulted in an elevated haematocrit value; a reduction in CBF to a value less than the ciritical flow level was seen and cerebral infarction was produced (tables 1—8, fig. 2).

Hypervolemic haemodilution therapy

Fig. 2

605

CBF and cerebral 0 2 metabolism using hypervolemic therapy with and without haemodilution during vasospasm. Haemodilution was started 6 days after haemorrhage. Until the 9th day, the progression of vasospasm was not accompanied by a reduction in CBF, D-O z or CMR0 2 . Whole blood transfusion from the 9th day caused an immediate decline in the CBF, D - 0 2 and C M R 0 2 .

Measurement of cerebral blood flow and cerebral oxygen metabolism in postoperative hypervolemic haemodilution therapy Patients without cerebral vasospasm (fig. 3 a, b) A marked increase in CBF and D - 0 2 was noted postoperatively in the patients without vasospasm. CMRO2 increased gradually for about two months unaffected by the more rapid increase of CBF and D - 0 2 . At about two weeks after operation, some cases showed hyperperfusion and a large increase in D - 0 2 accompanied by a reduction in OEF (fig. 3 b). Patients with non-symptomatic vasospasm (fig. 3 c, d, e) Postoperatively, a reduction in D - 0 2 was noted in accordance with the progression of cerebral vasospasm. However, the change in CBF was variable with some cases

606

Nakagawara, Nakamura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

showing minimal or no decrease owing to the introduction of profound haemodilution (fig. 3 c). C M R 0 2 showed minimal reduction, in spite of the reduced D - 0 2 , due to the elevation of OEF.

a . T.T.26F A (GrfyADL

Fig. 3

Ó 1W2W

1M

Ó 1W2W

1M~

b. H.T. 18M Lt-Ai (GrU) ADLI

2M

2M

Ó 1W2W

Ó 1W2W

1M

1M

C. C . 0 . 3 8 F Rt-IC-PC ( G r I ) ADLI

2M Ó1W2W

1M~

2M Ó 1W2W

1M~

CBF and cerebral 0 2 metabolism using postoperative hypervolemic haemodilution therapy: patients without cerebral vasospasm (a, b), patients with non-symptomatic vasospasm (c, d, e), patient with symptomatic vasospasm (f).

Hypervolemic haemodilution therapy Table 1

607

Haeraodynamic changes - Hypervolemia during vasospasm

Age/ /Sex

Case

F

A) N.W.

H&H Grade

Ht

Gr H

36 -

CBF mi/IOOg/min 33

Delivery of 0 2 CMR02 mi/1009/min mi/l00g/min

26.7—28.7

3.94-4.00

1.99-2.00

23.6-35.5

3.63-4.28

1.90-1.93

27.1-28.6

4.14-3.99

1.57-1.71

34.0-39.4

4.90-4.95

2.26-2.42

28.7-22.8

4.00-3.77

2.00-1.62

(Day6)(Day9)

I.K.

63 F

Gr n

38 -

31

(Day7)(Day8)

K.M.

69 F

Gr H

35 -

30

(Day6)(Day10) T.F.

45 F

34 -

Gr I

30

(Day5)(Day6) B)

N.W.

48 F

Gr H

33 -

38

(Day9)(Day11) B) : with whole blood transfusion

A): with haemodilution Table 2

Operative results (6 months follow-up) - Haemodilution therapy

A c t i v i t i e s o f daily life ( A D L ) *

H & H Grade

I

n

I

1/

V

Gr

I

10

1

1

O

1 •

II

22

2

2

1

I

13

4

2

1

w

1

1

2

2

V

O

O

O

O

3 ;

3

46

8

7

4

13

78

(59%)

(10%)

(9%)

(5%)

(17%)

I n 1 V V

Normal life U n a s s i s t e d life Partially a s s i s t e d Totally assisted Dead

• a • X

29

CO

ADL*

13

CM

Total

Total

23 10

Complicated operation Vasospasm (VS) General complication Primary d a m a g e + V S

608

Nakagawara, Nakamura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

Table 3

Comparison of operative results (Grades II and III)

H &H Grade

Number of patients

I

n

1

N

V

54

33

4

5

2

10

(61%)

(7%)

(9%)

(4%)

(19%)

21

2

2

1

2

(76%)

(7%)

(7%)

(3%)

(7%)

22

4

11

6

16

(37%)

(7%)

(19%)

(10%)

(27%)

13

4

2

1

3

(57%)

(17%)

(9%)

(4%)

(13%)

1977-1981*

Grade H

**

1983-1984

1977-1981*

Grade 1

1983-1984

**

A D L

29

59

23

* without hypervolemic haemodilution ** with hypervolemic haemodilution

Table 4

Unfavourable events in relation to outcome in Grade III patients

Unfavourable events Uneventful

Total(%) 5

2 2

oo

10 (43%) 4 (17%)

OOO

Symptomatic vasospasm Transient (TIA. RIND) Permanent

5

A D L (6 month) I n IV v 0 0 0 0 0 1

Surgical trauma Deficits

0

0

0

0

1

1

Persistent hemorrhage Deficits

0

0

1

1

0

2

General complication Total

0 13

0

0

0

1

1 23

Angiographic vasospasm

11

4

1

1

1

18 (78%)

0 1

Hypervolemic haemodilution therapy

609

The disappearance of cerebral vasospasm was indicated by the increase in CBF, D - 0 2 , C M R 0 2 and the normalization of OEF (about 40%). During the vasospasm, these patients showed no abnormal neurological manifestations with minimal or no low density areas on the CT scan. The recovery was excellent at the time of discharge.

Patient with symptomatic vasospasm (fig. 3 f) Very large reductions in CBF and D - 0 2 followed the progression of cerebral vasospasm, although the haematocrit level was maintained at about 30%. In spite of the elevation of OEF, a marked reduction in C M R 0 2 was associated with deterioration of neurological symptoms and multiple low density areas in the CT scan. However, the size of the infarcted areas produced by the severe vasospasm was relatively small, and the recovery of CBF, D - 0 2 and C M R 0 2 was observed in accordance with the disappearance of vasospasm. In this patient, marked improvement of the neurological symptoms was noted by the 3 month follow-up.

Operative results with postoperative hypervolemic haemodilution therapy The results of the surgical series, using postoperative hypervolemic haemodilution therapy, are shown in table 2. The total operative mortality rate was 17%. In the 65 patients who were in grades I to III, the mortality rate was 9%. The operative mortality rate was higher in patients with higher preoperative grades. Death caused by cerebral infarction due to severe vasospasm was noted in only one patient in grade III and two in grade IV. Other causes of death were massive haematoma in 3 patients (grade V), complicated operation in 4 and general complications in 3. The relationship between preoperative grades and postoperative results was evaluated (tab. 3). Patients in grades II and III treated with hypervolemic haemodilution therapy (1983—1984) showed greater improvement in comparison with similar patients treated without this regimen (1977-1981). The therapeutic efficacy of hypervolemic haemodilution therapy for cerebral vasospasm was investigated; unfavourable events in relation to the final outcome were classified and presented in table 4 for Grade III patients. The occurrence of late angiographic vasospasm was not obviously reduced in these patients. Of the 14 patients with symptomatic vasospasm, 10 had transient ischaemic symptoms (TIA or RIND) and 4 developed permanent neurological deficits. Of the 4 patients with permanent neurological deficits, the activities of daily life (ADL) at the 6 month follow-up was II in 2 patients, III in 1 and V (dead) in 1. The patients with symptomatic vasospasm showed good recovery and a low mortality rate.

610

Nakagawara, Nakamura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

Discussion The cerebral blood flow (CBF) in patients with subarachnoid haemorrhage (SAH) has been measured by many investigators [5—9]. It has been reported that the CBF decreased in patients with severe brain damage or hydrocephalus following SAH, as well as in patients with cerebral vasospasm. There has been controversy over whether angiographic vasospasm reduces CBF or not; however, delayed ischaemic neurological deficits followed by severe vasospasm was associated with the reduction in CBF [5, 7, 8, 14]. The critical flow level for adequate cerebral function during cerebral vasospasm was suggested by several clinical studies. Ishii [8] reported that all patients with diffuse severe vasospasm (i. e., arterial diameter reduced to less than half of its normal value) showed focal areas of CBF reduced below 30 ml/100 g/min in addition to a reduction in mean CBF. Kawase and Mizukami [9] observed that neurological symptoms might be developed in patients with a mean r-CBF below 55% of the normal value; a mean r-CBF below 40% or regional CBF below 35% could produce cerebral infarction. In our observations, a critical CBF level of about 25 ml/100 mg/ min (45% of normal value) was noted in patients who developed neurological symptoms with low density areas in the CT scan. Intravascular volume expansion or hypervolemia is currently a common adjunct to the treatment for focal cerebral ischaemia [2, 10, 15]. Its clinical use is designed to improve cerebral perfusion for the reversal of neurological deficits associated with vasospasm. According to the experimental studies of Wood and Simeone, intravascular volume expansion without haemodilution failed either to increase CBF to ischaemic regions of the brain or to reduce the size of the cerebral infarction. In addition, a significant inverse correlation between CBF and haematocrit values was found in ischaemic animals [20]. Therefore, intravascular volume expansion appears to require associated haemodilution for the improvement of collateral perfusion to the ischaemic regions of the brain. According to our investigation, induced haemodilution applied after the onset of vasospasm did not significantly raise the calculated oxygen transport (D-0 2 ) to the ischaemic brain (tab. 1 A). However, the augmentation in CBF may be the dominant factor affecting oxygen transport in the ischaemic brain; because a vicious circle, ending in cerebral infarction, will be started by hypoperfusion less than the critical flow level. The reduction in oxygen transport associated with vasospasm appears to produce cerebral metabolic failure. Both arterial and jugular venous blood samples were collected in the present study, allowing metabolic events to be taken into consideration. The elevated OEF in patients with cerebral vasospasm represents oxygen transport (D-0 2 ) insufficient to meet metabolic demands (CMR0 2 ). Montgomery and Grubb [13] reported the

Hypervolemic haemodilution therapy

611

same observation using a single photon detector system. In patients with nonsymptomatic vasospasm (treated with hypervolemic haemodilution therapy), C M R O z showed minimal reduction with the elevation of OEF in spite of the reduction in D - 0 2 during the progression of cerebral vasospasm. In patients with symptomatic vasospasm, the very large reductions in CBF and D - 0 2 were followed by a marked reduction in C M R 0 2 coupled with an elevation of OEF. At this stage, the elevation of OEF would imply the occurrence of cerebral vasospasm associated with SAH. A large cerebral infarction caused by hypoperfusion due to vasospasm will show a reduction of OEF below the normal limit because of the reduced oxygen requirement in the damaged tissue. With haemodilution therapy, the mechanism of improvement in the CBF was probably due to increased perfusion pressure across the constricted conductance vessels. In the arteries larger than arterioles, blood flow is generally influenced by the haematocrit value, the main determinant of whole blood viscosity. In the microcirculation, blood flow is relatively less influenced by haematocrit; the haematocrit within the microvasculature may be as small as one-half of the haematocrit in the peripheral blood. In the normal circulation, the arterial pressure falls very slightly in the large and medium sized arteries because their resistance to

Fig. 4

Hypothetical diagram of blood pressure and local vascular resistance during the period of vasospasm in comparison with normal circulation.

612

Nakagawara, Nakamura, Takeda, Usami, Nishiya, Ide, Shitamichi, Okada, Fukuoka

flow is small; however, it falls rapidly in the small arteries and arterioles, which are the main sites of the vascular resistance influenced by the haematocrit value, according to the Hagen-Poiseuile equation (R = 8 |xL/jtr4). For the same reason as above, diffuse constriction of conductance vessels, during vasospasm, may cause an increase in local vascular resistance coupled with a reduction in perfusion pressure in the arterial tree distal to the vasospasm (fig. 4). Therefore, the reduction in blood viscosity induced by haemodilutation may decrease local vascular resistance not only in the small arteries and arterioles but in the conductance constricted vessels. Hypervolemic haemodilution therapy was designed to increase perfusion pressure across the constricted vessels and other collateral pathways for the improvement of CBF in the ischaemic regions of the brain. Further studies of CBF and cerebral metabolism during SAH and vasospasm are necessary to establish adequate management for postoperative cerebral vasospasm; intravascular volume expansion induced by haemodilution will then become a more effective adjunct in the prevention of ischaemic deficits.

References [1] Auer, L. M . : Acute surgery of cerebral aneurysms and prevention of symptomatic vasospasm. Acta Neurochir. 6 9 (1983) 2 7 3 - 2 8 1 . [2] Giannotta, S. L., J . E. McGillicuddy, G. W. Kindt: Diagnosis and treatment of postoperative cerebral vasospasm. Surg. Neurol. 8 (1977) 2 8 6 - 2 9 0 . [3] Gottstein, U.: Cerebral blood flow, C M R O z and C M R of glucose in patients with hypo- and hyperchromic anemia and polycythemia: the effect of hemodilution on CBF, C M R and hematocrit. In: Cerebral vascular disease, J . S. Meyer, H. Lechner, M . Reivich (eds.), pp. 2 2 5 - 2 2 9 , Vol 2. Excepta Medica, Amsterdam 1978. [4] Grotta, J . , R. Ackerman, J . Correia, et al.: Whole blood viscosity parameters and cerebral blood flow. Stroke 13 (1982) 2 9 6 - 3 0 1 . [5] Grubb, R. L., M . E. Raichle, J . D. Eichling, et al.: Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. J . Neurosurg. 4 6 (1977) 4 4 6 ^ 1 5 3 . [6] Grubb, R. L.: Cerebral haemodynamics and metabolism in subarachnoid haemorrhage and vasospasm. In: Cerebral arterial spasm. R . H . Wilkins (ed.), pp. 3 4 1 - 3 4 9 . Williams & Wilkins, Baltimore, 1980. [7] Heilbrun, M.P., J.Olesen, N.A.Lassen: Regional cerebral blood flow studies in subarachnoid hemorrhage. In: R.H.Wilkins (ed.), pp.314—319, Cerebral arterial spasm. Williams & Wilkins, Baltimore 1980. [8] Ishii, R.: Regional cerebral blood flow in patients with ruptured intracranial aneurysms. J . Neurosurg. 50 (1979) 5 8 7 - 5 9 4 . [9] Kawase, T., M . Mizukami, T. Tazawa, et al.: Critical flow levels in cerebral ischemia -

II.

Vasospasm following subarachnoid haemorrhage. Brain Nerve (Tokyo) 33 (1981) 6 1 - 6 9 . [10] Kosnik, E. J., W. E. Hunt: Postoperative hypertension in the management of patients with intracranial arterial aneurysms. J . Neurosurg. 45 (1976) 1 4 8 - 1 5 4 . [11] Ljunggren, B., H.Saveland, L.Brandt: Causes of unfavourable outcome after early aneurysm operation. Neurosurgery 13 (1983) 6 2 9 - 6 3 3 .

Hypervolemic haemodilution therapy

613

[12] Maroon, J. C., P. B. Nelson: Hypovolemia in patients with subarachnoid haemorrhage: therapeutic implications. Neurosurgery 4: 223-226, 1979. [13] Montgomery, E. B., R. L. Grubb, M. E. Raichle: Cerebral haemodynamics and metabolism in postoperative cerebral vasospasm and treatment with hypertensive therapy. Ann. Neurol. 9: 502—506, 1981. [14] Pitts, L.H., P. Macpherson, D.J. Wyper, et al.: Effects of vasospasm on cerebral blood flow after subarachnoid hemorrhage. In: R. H. Wilkins (ed.), Cerebral arterial spasm: proceeding of the second international workshop. Baltimore: Williams 8C Wilkins, 1980, pp. 333-337. [15] Pritz, M.B., S.L.Giannotta, G.W.Kindt, et al.: Treatment of patients with neurological deficits associated with cerebral vasospasm by intravascular volume expansion. Neurosurgery 3 (1978) 364-368. [16] Taneda, M.: Effect of early operation for ruptured aneurysms on prevention of delayed ischaemic symptoms. J. Neurosurg. 57 (1982) 622-628. [17] Thomas, D. J., C. H. du Boulay, J. Marshall, et al.: Prevention of stroke - the viscosity factor. In: Cerebral vascular disease, Vol 2: J.S.Meyer, H.Lechner, M.Reivich (eds.), p p . 2 1 1 - 2 1 5 . Excepta Medica, Amsterdam 1979. [18] Wood, J . H . , L.L.Snyder, F.A.Simeone: Failure of intravascular volume expansion without haemodilution to elevate cortical blood flow. In: Region of experimental focal ischaemia. J. Neurosurg. 56 (1982) 8 0 - 9 1 . [19] Wood, J . H . , F.A.Simeone, E.A.Fink, et al.: Hypervolemic haemodilution in experimental focal cerebral ischaemia: Elevation of cardiac output, regional cortical blood flow, and ICP after intravascular volume expansion with low molecular weight dextran. J. Neurosurg. 59 (1983) 502-509. [20] Wood, J . H . , F.A.Simeone, R.E.Krön, et al.: Rheological aspects of experimental hypervolemic haemodilution with low molecular weight dextran: relationship of cortical blood flow, cardiac output, and intracranial pressure to fresh blood viscosity and plasma volume. Neurosurgery 11 (1982) 739-753.

Experimental and clinical study in the use of intrathecal alpha-tocopherol in vasospasm Y. Kato, H. Sano, K. Katada, T. Kanno

Vasospasm is one of the continuing problems in aneurysm surgery. Recently it has been reported that the incidence of the symptomatic vasospasm could be forecast by C T findings [8]. Many methods have been tried to overcome this problem of vasospasm. Free radical injury after subarachnoid haemorrhage has been reported to be one of the causes of chronic vasospasm [1, 2, 3 , 5 , 7]. As a-tocopherol is one of the free radical scavengers, we studied both experimentally and clinically the role of a-tocoperhol in preventing chronic vasospasm by intrathecal administration.

Experimental study Material and method Twenty adult dogs have been used in this study. In ten dogs subarachnoid haemorrhage was induced by injecting 5 ml of its own arterial blood mixed with 2 ml of normal saline into the cisterna magna. In the other ten dogs the same amount of blood mixed with 2 ml of a-tocopherol containing 100 mg was injected into the cisterna magna. Tyamiral N a was injected intravenously following injection of atropine 0.25 mg intramuscularly for anaesthesia, vertebral artery was exposed and a 0.8 mm cutdown tube was inserted into the vertebral artery, 5 ml of 6 5 % angiog r a p h y was injected into the vertebral artery by hand. Vertebral angiogram was taken before and 24 hours after inducing subarachnoid haemorrhage. The size of the basilar artery and posterior cerebral artery were measured from each angiogram. The constriction ratio was calculated as follows. Constriction ratio =

Arterial diameter of post SAH-primary diameter

primary diameter of the artery The animal's neurological status was monitored as follows, stage 0: the same condition as before SAH stage 1: moving actively stage 2: sitting only stage 3: lying down

616

Y. Kato, H. Sano, K. Katada, T. Kanno

After the completion of the study, the animals were sacrificed and pathological examination was done to study the arterial changes microscopically.

Results Angiographic findings In the SAH group the arterial diameter became narrow after SAH. (fig. 1) Constriction ratio = - 1 8 . 0 5 12.55% ( N = 10) In the PCA constriction ratio = - 1 7 . 7 4 7 . 7 2 % (N = 10)

Fig. 1

Angiographic findings in S A H group. Arteries became narrow 30 minutes after making SAH, dilated 4 hours after S A H and then again narrowed 24 hours afterwards.

Fig. 2

Angiographic findings in a-tocopherol group. Arteries dilated 24 hours after making SAH.

Study in the use of intrathecal alpha-tocopherol in vasospasm

617

On the other hand, in the a-tocopherol group the arterial diameter became rather dilated (fig. 2) and the constriction ratio was shown from —14.3% to 25.8%. In the PCA the constriction ratio was 7.05% to 17.86% (N = 10) and in the basilar artery it was 16.74 23.07% (N = 10) (fig. 3) Animals' neurological status The animals' neurological status were monitored and compared with the amount of SAH. In the experimental group which use a-tocopherol 7 dogs were in stage 1 and 3 dogs were in stage 2 after SAH. While in the control groups 6 animals were in stage 3, 3 in stage 2, 1 in stage 1. Therefore, the neurological status was fairly good in a-tocopherol group, even when the amount of SAH is more than in the control group, where even a small amount of SAH has led to a poor neurological status (fig. 4).

SAH SAH + a — T o c o p h e r o l

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1

Measurement of diameters BA and PCA before and after SAH. Constriction ratio w a s positive in a - t o c o p h e r o l group while it negative in S A H . It w a s statistically significant.

Fig. 4

Animal's condition and h a e m a t o m a volume. T h e neurological status w a s fairly g o o d in a tocopherol group even w h e n the a m o u n t of S A H is m o r e as compared t o control group w h e n even a small a m o u n t of S A H has lead to p o o r neurological status.

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Histopathological findings Each case was examined pathologically which showed endothelial degeneration and oedema, constriction of internal lamina, and oedema and vascular degeneration of media in the SAH group. But only mild constriction of elastica lamina was found in SAH with the a-tocopherol group. The intima and media were fairly intact (fig. 5, tab. 1).

Clinical study Material and method 4 1 5 cases of cerebral aneurysms had been operated from September 1 9 7 6 to December 1982, which included 63 cases of cerebral aneurysms, with the intrathecal use of a-tocopherol since April 1981. Every ase except four patients over 7 0 years old or in grade V in which manitol was not effective was operated immediately on admission to hospital within 2 4 hours. But the cases who came more than 3 days after onset were operated in the delayed stage after day 14. 100 mg of a-tocopherol was introduced intrathecally via a drainage tube in cases of early operation or via a spinal tap every day until day 16 in cases who had much haematoma in the basal cistern shown by C T findings. If a case had some neurological deficit like

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Table 1

Histopathological findings Histopathological changes of arterial wall were more frequent in S A H group than a - t o c o p h e r o l group

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