Grand Rounds Anesthesia Aneurysm

for Intracranial Surgery

Ian A. Herrick, BSc, MD, FRCPC,* Adrian W. Gelb, MB, ChB, FRCPCT Department Canada.

of Anaesthesia,

Aneurysmal rupture represents the most common cause of subarachnoid hemorrhage. Approximately two-thirds of persons who experience a subarachnoid hemorrhage will die or become disabled. Although advances in neurosurgical techniques, neuroanesthetic management, and neuroradiology have resulted in great progress in reducing the operative risk for patients with intracranial aneurysms, the overall outcome following subarachnoid hemorrhage remains disappointing. This article provides an overview of some current concepts related to the perioperative management of patients with intracranial aneurysms, such as the risk and management of rebleeding and vasospasm, and considerations related to the timing of surgery. The anestheiic managemeni ofCthese patients is reviewed, emphasizing principles relating to the facilitation of surgery-by optimizing operative conditions and minimizing the risks of intraoperative aneurysmal rup-

*Assistant Professor tProfessor

and Chairman

Address correspondence to Dr. Herrick at the Department of Anaesthesia, University Hospital, P.O. Box 5339, London, Ontario, Canada N6A 5A5. Received for publication February 28, 1991; accepted for publication July 25, 1991. 0 1992 Butterworth-Heinemann J. Clin. Anesth.

4:73-85,

1992.

revised manuscript

‘u’niversity of -Western Ontario,

London,

Ontario,

ture or the aggravation of neurologic deficits-and to the provision of a smooth, stable recovery. Despite the disappointing overall prognosis following subarachnoid hemorrhage, adherence to these principles can optimize the outcome for those patients who reach the operating room. Keywords: Anesthesia, intracranial.

neurosurgical;

aneurysm,

Introduction it has been estimated that as many as 5 miiiion persons in the North American population have intracranial arterial aneurysms. 1 Subarachnoid hemorrhage (SAH) accounts for about 10% of strokes. Aneurysmal rupture is the most common cause of subarachnoid hemorrhage (80% to 90%), with an annual frequency of iO to i i per lUU,UUUpersons.is2 Oniy about one-third of persons who experience an aneurysmal SAH will recover without major disability. This high morbidity and mortality relates largely to the fact that many persons fail to reach the hospital in satisfactory condition. Despite advances over the past 30 years in perioperative management, including anesthesia, microsurgical techniques, and neuroradiology, outcome morbidity and mortality remain high even among patients who reach the hospital. This is due predominantly to rebleeding and cerebral vasospasm. This article reviews current concepts related to the perioperative management of patients with intracranial aneurysms, highlights controversial areas, and proJ. Clin. Anesth., vol. 4, January/February

1992

73

vides a clinical basis for anesthetic management that will provide patients who reach the operating room (OR) with the best prognosis for functional recovery.

Preoperative Considerations Patients who experience SAH are traditionally graded according to one of two systems; the or-igiual gr-ading system proposed by Botterell et al? in 1956 or a more _^^^_. -__l:~:_-c:..----,.“_A 1.. II.._& ..-J TT___L:ItXcZIILIII”UIIIL~LIOII p~“p”XW uy “UIIL nllu “C>S’ 111 1968 (Tabk I). The second classification system has subsequently been revised to include grade 0, reflecting patients with intracranial aneurysms who have not experienced SAH. Although surgical mortality rates vary somewhat among institutions, patients with a neurologic grade of 0 to 1 generally undergo surgical clipping with a low mortality rate (fl--.. _I-..-_ 1^_.._ 1____ :_.._“r:_..r_J :_ 11.0111 IYLIlCIIlld.

1v1a11y

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,,I

the context of both regional and global cerebral ischemia, but as yet none has demonstrated unequivocal efficacy.20

Calcium-Channel

Blocking

Drugs

nrnmicinrr cm-t=hrsI nrntw-rive At presm, the mnct drug is nimodipine, a calcium-channel blocking drug closely related to nifedipine. Like nifedipine, nimodipine’s predominant systemic effect is arterial vasodilation, with a much less pronounced effect on myocardial conduction. Nimodipine is a potent, relatively selective cerebral vasodilator.2”.Y’ Several sttrdies have demonstrated a significant improvement in outcome at 3 months following SAH in patients treated with nimodipine and a significant decrease in delayed neurologic deterioration due to vasospasm.22-zt Although nimodipine was originally believed to reverse or prevent vasospasm, recent evidence has demonstrated that despite a decreased occurrence of neurologic deterioration following nimodipine treatment, the occurrence of angiographic arterial narrowing does not appear to be decreased.gJ,2+ It has thus been suggested that nimodipine may exert its effect predominantly via a cellular cerebral protective mechanism rather than by directly reversing cerebral arterial narrowing. Nicardipine, another calcium-channel blocker closely related to nifedipine, also demonstrates important cerebrovascular vasodilatory effects. Although less intensively studied than nimodipine, this drug may prove useful in the treatment of cerebral vasospasm and its consequences.25 In light of recent reports of potential adverse inL.._

76

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J. Clin. Anesth., vol. 4, January/February 1992

teractions between calcium-channel antagonists a11d anesthetic drugs,Y6 concern has arisen regarding the impact of nimodipine and nicardipine on the management of anesthesia in patients presenting for aneurysm surgery. With the exception of a potential mild decrease in BP, which appears to be readily attenuated with volume loading, these drugs, based on preliminary investigations, have not been reported to have an adverse effect on the conduct of anesthesia.Y7,Y* At high doses, administered intravenously (IV), ninw dipine has been shown to have a more pronounced effect on arterial BP when combined with volatile anesthetic drugs.‘!’

Rebleeding Rebleeding from a ruptured aneurysm represents a J -_.,.n*_r:-- L”IIIp)IICdLI”n, ,.---l:--*:,.c. “__IU~ld”IC CLlU”, ment. Early operation offers several advantages, including prevention of rebleeding, opportunity to evacuate subarachnoid blood and decrease the risk of vasospasm, and facilitation of the treatment of vasospasm, if it develops, by decreasing the risk of rehl,,A;,m “ILLL4‘llg

.a~~rw-;-,t~c-i w;th ““&CL1h,,T\PrtPnr;.,PIh,,~~~,,~l~-~~ .n~y”““““‘“c’“,y~. V”IL-lll.L c&.7)LI”L‘cILLL4

therapy. decrease

Several reports of clinical series support a in the rate of rebleeding, with a comparable

Table 2.

aneurysm surgery:

Herrick

and Gelb

or superior outcome, in patients undergoing early operation and clipping, compared with those who have later surgery.3g-4L Support for early operation contrasts with traditional North American neurosurgical opinion, which favors delayed surgery (at least 1 week after SAH). Advantages associated with delayed aneurysm clipping include resolution of cerebral edema, thereby lessening the need for retraction and facilitating surgical exposure; stabilization of the aneurysm clot, thereby decreasing the risk of intraoperative rupture; and resolution of subarachnoid clot, thus facilitating surgical dissection. The International Cooperative Study on the Timing of Aneurysm Surgery34 reviewed data related to the timing of surgery and the outcome of 3,521 patients hospitalized within 3 days following SAH. These data were contributed by 213 neurosurgeons with a speciai interest in aneurysm surgery at 68 medicai centers in 14 countries. The results demonstrated that among patients who underwent surgery, postoperative results were superior with delayed surgery (11 to 14 days following SAH). Good-grade patients (alert) had a favorable outcome if surgery was done within 3 days of SAH or after day 11; however, mortality in this group was decreased only with later surgery. on planned surgical intervals and included those patients who did not undergo operations, were similar with regard to mortality (20%) and good outcome (60%) for patients with surgery planned for both the early (0 to 3 days) and late (11 to 14 days) intervals. T-h.= himheat A 11L “‘ ~“‘d’

mnrh;clit,r lll”l “‘U’L,

>nrl mnrtalitw c&l&U lll”l ‘“LA’,

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among patients who underwent operations 7 to 10 days after SAH (Table 2). Early operation significantly

Surgical and Management Outcome at 6 Months after SAH

Interval (days after SAH) 0 to 3 4 to 6 7to 10 11 to 14 15+

Overall Surgical Outcome (%)a Good Recovery 66 66 64 77 72

Overall Management Outcome (%)”

Mortality

Good Recovery

17 19 18 7 8

63 60 56 62 63

Mortality 20 24 28 21 20

includes all patientswho had surgery during each interval. bManagementoutcome includes all patients who had surgery planned for each interval (includingpatients who did not actuallyhave surgery). SAH = subarachnoidhemorrhage.

aSurgical outcome

Source: Modified from Kassell NF, Torner JC, Jane JA, Haley EC, Adams HP: The International Cooperative Study on the Timing of Aneurysm Surgery-surgical results. J Neurosurg 1990;73:37-47.

J.

Clin. Anesth., vol. 4, January/February 1992

77

decreased the risk of rebleeding, but this decrease in mortality was nullified by deaths due to cerebral ischemia. Early operation does not appear to decrease the risk of vasospasm and cerebral infarction as a cause of neuroiogic deterioration foiiowing SAH.5,,*Z Interestingly, the results also demonstrated a higher frequency of “tight” brains associated with earl? operation, although this was not believed to contribute significantly to the technical difficulty of the operation. The rate of intraoperative aneurysmal rupture was found to be the same regardless of the time interval in which surgery was performed.“1 Early operation remains a useful modality in the management of recent SAH, particularly among goodgrade patients, but these candidates must be carefully selected. Cerebral ischemia remains a leading cause of morbidity and mortality among these patients, reflecting the need to develop an effective regimen for rrre.i,=nt;nrr C>V nr the y’” ‘L”“LL5 “L VPI:P,-E;~~. I&V._, ‘“LLS ~,.>c~c~c,c,,\ v”“““y”““’ \,I ,\,--l,tef hmnitalilxa the _--- nerind r _---.,- -_vv r”“‘~-” tion, any neurologic deterioration associated with BP decreases, and preoperative blood volume and electrolyte status. An elevation of body temperature is common following SAH due to the presence of blood in the subarachnoid space. Even a one- or two-degree elevation in temperature increases cerebral oxygen (02) requirements and should be treated preoperatively. Pieoperative sedation is rarely necessary in these patients and can be associated with various problems. Depression of ventilation associated with opioids, barbiturates, and high doses of benzodiazepines may result in hypercapnia, with increases in CBF and ICP. Depression of the level of consciousness may hinder perioperative neurologic assessment. Preoperative anxiety is not a problem in patients with a depressed level of consciousness (grades 3-5), and hence sedation is not required. In the awake patient, a reassuring preoperative visit by the anesthesiologist will usuall) alleviate anxietv. If preoperative sedation is considered necessary. a small dose of benzodiazepine is probably the best choice, since these drugs, in IOU doses, provide anxioiysis with minimal sedation and impact on ventilation.

Adonitoring During anesthetic induction, heart rate (HR), ECG, BP, and oxygen saturation (pulse oximetry) should be monitored. Some controversy exists regarding the advantage of intra-arterial monitoring of BP during induction. While an intra-arterial cannula can often be placed under local anesthesia to afford continuous observation of the hemodynamic response to induc-

Anesthesia

tion, the pain and anxiety associated with preinduction instrumentation can sometimes cause adverse hemodynamic changes. Frequent noninvasive measurements of BP during induction represent a reasonable alternative. Following induction, other monitors can be established, including an intra-arterial cannula either before or following tracheal intubation. An esophageal or precordial stethoscope allows monitoring of ventilation, since the patient’s chest may not be accessible after surgical positioning. Since these procedures often last several hours, core temperature should be monitored. A urinary catheter should be placed, particularly if mannitol is to be administered. End-tidal carbon dioxide tension should be monitored continuously. Many clinicians find a central venous pressure line useful to monitor the adequacy of fluid replacement during and after the operation, as well as for easy, rapid titration of vasoactive drugs for reguiation of BP. Depending on the preoperative cardiac status of the patient, a pulmonary artery catheter may be indicated to assess fluid status and the hemodynamic response to volume expansion. Many surgeons use a lumbar drain, which is typically placed prior to surgical po&iuuing. Evoked potential monitoring has been shown to be .._-r.., ~..-:--..-_..-_...LISTILl ULII mg dlltS”l yam ^.._I^ sLl1gU-..r_-~_*__r:--_~_._-__ y I”1 UcXtsLLIIIgdU”tSlYitl effects associated with permanent or temporary vessel occlusion.50-S*

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The principles of anesthetic management of patients with cerebral aneurysms relate to the facilitation of surgery (optimizing conditions for brain retraction, exposure, and securement of the aneurysm), while minimizing the risk of intraoperative aneurysmal rupture or the aggravation of neurologic deficits, and to the provision of a smooth, stable recovery. These goals are accomplished by careful control of hemodynamics, optimization of ICP and cerebral compliance, and maintenance of adequate cerebral perfusion and 0, delivery. Anesthesia induction represents a critical period for the patient with an unsecured cerebral aneurysm. The goal is to achieve a smooth induction while maintaining a normal or slightly decreased aneurysmal transmural pressure. Preoxygenation via face mask using 100% 0, is provided. Opioids are often included in the induction sequence to attenuate the response to tracheal intubation. Although doses and individual preferences vary, commonly used opioids

for intracranial

aneurysm surgery: Herrick and Gelb

include fentanyl 2 to 10 kg/kg, sufentanil 0.5 to 1.0 kg/kg, and alfentanil 25 to 50 kg/kg. The use of sufentanil and alfentanil in neurosurgical patients has been the subject of some controversy due to reports of increases in CBF and ICP following administration of these drugs. 53-55Absolute increases in ICP reported in humans have been small, and other investigators56-59 have failed to confirm these flndings. Although debate continues regarding the safety of these drugs,60,6L our practice is to use fentanyl, sufentanil, or alfentanil according to the individual preference of the attending anesthesiologist, based on the belief that for patients undergoing aneurysm surgery, the beneficial hemodynamic profile of each of these drugs outweighs potential concerns regarding small increases in ICP.= IV thiopental sodium is the most commonly used induction drug. Other choices include methohexital, midazoiam, and etomidate. Common properties associated with these drugs-such as rapid loss of condecrease in CBF, ICP, and cerebral sciousness; metabolic rate for oxygen; and reasonable cardiovascular stability-make them appealing for use in neuroanesthesia. Each drug is associated with a mild (10% to 15%) BP decl-ease, which helps to offset the sympathetic response to intubation and decompresses the ^- ^.._..yJlll “- UUIIIIg -l..-:-_ pc”“U ,-.Z-rl ..71.,,rlJ 13 :, UCCI~:aJCU. J,.,,,““,~ d,,tJlll d W11KZ:ll LUL Propofol, recently released in North America, appears to offer similar advantages, although the effects of propofol on some neurologic variables have not been adequately investigated in patients with neurologic disease. Nnne nf rnmmnnlv A.“.&.. VI thP ll.C ~““““““‘ ,

IICP~ uuIu ~PIIT-~~IIE~-II~~I. .*.,-- V..ILIYII-U. hlnrk-.-..-.

ade drugs is known to cross the blood-brain barrier or to affect the neurovasculature directly. Changes in intracranial dynamics reflect either the systemic effects of the drug or the effect of interventions performed while the patient is under the influence of the drug. Succinylcholine is widely used to facilitate tracheal intubation. Although increases in ICP have been reported after succinylcholine administration,63,64 this effect has been attributed to afferent muscle spindle activity and can be attenuated by defasciculation.65 While controversy regarding the importance of these changes continues, the rapid onset of relaxation and excellent intubating conditions provided by succinylcholine may be clearly advantageous in some clinical circumstances. Nondepolarizing neuromuscular blocking drugs such as atracurium, vecuronium, and pancuronium also can be used to facilitate intubation. Atracurium and vecuronium have become very popular due to the lack of associated cardiovascular effects. Cardiovascular changes (primarily tachycardia) associated J. Clin. Anesth., vol. 4, January/February

1992

‘79

with pancuronium can be acceptably attenuated with induction doses of opioids. Laryngoscopy and intubation are extremely stimulating, and the associated sympathetic response can be devastating for patients with intracranial aneurysms. It is important to ensure that this response is adequately blocked prior to instrumenting the airway by achieving a deep level of anesthesia and complete neuromuscular blockade. Anesthesia can be deepened prior to laryngoscopy with an additional dose of opioid, thiopental sodium, and/or lidocaine 1 to 2 mg/ kg.66.67 The use of alpha- and/or beta-blocking drugs or direct vasodilators (e.g., sodium nitroprusside) also has been reported to provide some protection from the response to intubation,“8-7’) although the use of vasodilators may cause an increase in ICP. Gentle hyper-ventilation with isoflur-ane @or- to intubation is effective in attenuating the hemodynamic response. fl,---I_. -_. _:-_,_ .1_.._:_:-1__, 1-..+ ,. ____l. ..,,.. ,,____-1 LIeal 1y, IIU slllglr U1ug 15rueal, “UL* Cdlrlully p‘aL‘IIcU combination of IV and volatile anesthetic drugs can provide a smooth induction and stable hemodynamic and ICP conditions during intubation.

Maintenance

of Anesthesia

pental sodium, opioid, or inhalation drug. I‘he ideal level of hyperventilation for patients undergoing aneurysm surgery has not been established, and thus clinical practice varies among neuroanesthesiologists. Many neuroanesthesioiogists, including ourseives. prefer some degree of hyperventilation to offset the cerebrovascular effects of isoflurane (if used) and to supplement the effects of mannitol and CSF drainage. We are not aware of definitive evidence to support a particular preference within the spectrum from normocapnic ventilation to moderate hyperventilation (arterial carbon dioxide tension 25 to 30 mmHg). Fluids administered intraoperatively are govperned by maintenance requirements, blood loss, and urine output. Prior to securing the aneurysm, fluid administration should be restricted to maintenance requirements. Once the aneurvsm is clipped, fluid deficits and additional volume may be administered to achieve ,,,-1 -,:,*..:, :, rr.,% c ,.-* I. allu ,,lalllLd,,l /‘ \,\,‘ v 1D 111 UlC Li-1, 111#11,.,,-,I ll”, ,,,a1 _,._,.._ Idllfic;. ,,o,,,e evidence suggests that cerebral ischemia may be aggravated in the presence of hyperglycemia,“>m7” although the evidence is conflicting in some animal models of focal ischemia.7”.x’) Since the concern exists and there is no compelling reason in most patients to administer glucose,‘8 it is our practice to avoid solutions that contain dextrose. ic r.c>mmnnlv IMsnnitnl .~..~~~~~_.,~ _I -V....-AV._-,

An ideal anesthetic drug for aneurysm surgery should provide the capacity to lower BP rapidly and reversibly, allow control of ICP, protect against cerebral isrhemia, minimize the formation of vasogenic cerebral edema, and allow rapid emergence. Drugs frequently used to maintain anesthesia include nitrous oxide in oxygen (N,O/O,), an opioid such as fentanyl, and a volatile drug such as isoflurane. Prolonged neuromuscular blockade can be achieved with any of the nondepolarizing muscle relaxants. IV anesthesia using a continuous infusion of alfentanil has been reported to provide satisfactory anesthesia for neurosurgical patients, but the infusion must be terminated approximately 1 hour prior to the conclusion of surgery to avoid excessive postoperative somnolescence.7L Some reports have suggested that N,O may increase ICP via an increase in CBF.7Y-74 These findings remain controversial, and many anesthesiologists, including ourselves, continue to use N,O in neurosurgical patients without clinically apparent adverse effects. Michenfelder,7” however, has suggested, based on a review of the literature, that in patients with intracranial hypertension, it may be prudent to discontinue the use of N,O to reduce brain bulk. Painful stimuli, such as skull pin insertion, should be anticipated and hemodynamic responses prevented by deepening anesthesia with additional thio80

J. Clin. Anesth., vol. 4, January/February 1992

aciminicte~d UY----...Y &_-_y

intr~nrwr~. . . ... .._ rL’”

tively to decrease intracranial volume and facilitate brain retraction. ‘The timing of administration is influenced by its effects on intravascular volume and ICP. Mannitol causes an immediate increase in intr-avascular volume and CBF and a subsequent decrease in ICP due to its osmotic effects. The dose of mannitol varies from 0.25 to 1.0 g/kg according to surgical preference. Mannitol should be administered as the bone flap is turned to avoid the risk of tearing bridging veins due to premature shrinkage of the brain. Some investigators have recommended that it should be given only after the dura is opened, due to reports that the associated increase in intravascular volume combined with the decrease in ICP may increase transmural pressure and lead to aneurysmal rupture.8i Sometimes larger doses of mannitol (2.0 g/kg) are administered to increase CBF and provide cerebral protection during temporary arterial occlusion. Doses of mannitol in excess of 2 g/kg have been reported to affect electrolytes, resulting in a transient marked increase in serum potassium and a decrease in serum sodium.HY,X” Mannitol begins to lower intracranial volume and ICP within 4 to 5 minutes following administration and achieves a peak effect at about 45 minutes. Its effects can be augmented by the administration of furosemide 0.1 to 1 .O mg/kg IV, which decreases total

Anesthesia for intracranial anewysm surgery:

body water content, CSF production, and astroglial swelling. The use of a lumbar CSF drain also decreases intracranial volume and lessens the need for brain retraction. Lumbar drainage decreases the need for osmotic diuresis to achieve good operating conditions and has the advantage that no concomitant increase in intravascular volume occurs. Drainage of CSF is initiated only after the dura is opened, to prevent brain shifts due to the generation of pressure gradients. The rate of drainage should not exceed 5 ml/ min, to prevent reflex hemodynamic changes, which typically consist of hypertension and/or bradycardia.

Coniroiied iYypoiension Controlled hypotension is commonly used intraoperatively to decrease aneurysmal wall tension, making the aneurysm softer and more pliable at the time of surgical clipping. In addition, if premature rupture of the aneurysm occurs, blood loss is decreased and control of hemorrhage is easier to accomplish. Local hypotension can be achieved by occlusion of the aneurysm’s feeding vessel(s) with temporary clips. Aneurysms in the carotid circulation also can be temporarily decompressed by ipsilateral compression of the carotid artery in the neck. In many hospitals, temporary clips tend to be reserved primarily for giant fir mmnl;r~tHl -dnPllt-.lEmE r;zawn-xahle nfrl;n;r~l "1 L"lllyllLLLc._uCAn~""'~""'"' I UI"IU"Ic- rennrtc '"y""" "I L.I1111L_u1 series of aneurysms using temporary clips suggest that this technique will likely become more widespread.lj.84 The current common practice is to use pharmacologic drugs to decrease systemic BP. Sodium nitroprusside (SNP) is the most commonly used drug, although isoflurane also is popular.*5 The use of other drugs has been reported, but none has achieved the popularity of these two. 86,87Recent studies suggest that IV adenosine may represent a useful drug for the induction of hypotension, but use of this drug remains investigational at present.86 The safe limit of controlled hypotension has not been definitively established. Since cerebral autoregulation is maintained to an MAP of 50 mmHg, some clinicians argue that this limit should not be exceeded. In addition, since poor-grade aneurysm patients may not have intact autoregulation, some clinicians argue that a lower limit of 60 mmHg should be adopted. Other groups believe that most patients will tolerate a 10% to 20% decrease in CBF without detrimental derangement of cerebral function and advocate decreasing MAP to as low as 40 mmHg for short periods.87

Herrick

and Gelb

Limits of autoregulation are shifted to the right in patients with preexisting hypertension, so decreases in BP should be limited to no more than 40% of preoperative MAP in these patients.87 Severe, uncontrolled hypertension is a relative contraindication to the use of controlled hypotension. Other relative contraindications include cerebral atherosclerosis, atherosclerotic or valvular heart disease, and significant pulmonary, renal, or hepatic insufficiency.s7 Prior to the induction of hypotension, establishment of adequate intravascular volume is important. BP control is less stable in the face of hypovolemia, and oliguric hypotension is associated with more tissue dysfunction than drug-induced normovolemic hypotension. ‘The inspired oxygen concentration also should be increased during controlled hypotension to counter the concomitant increase in puimonary shunt associated with SNP and some other drugs, although this has not been reported in association with isoflurane-induced hypotension.88

Intraoperative Aneurysm Rupture Rupture of an intracranial aneurysm during anesthetic induction or prior to the commencement of surgery is typically a devastating event. In these circumstances, surgery is usually deferred to allow assessment of neurologic status (e.g., CT scan), prognosis, and control of ICP. If rupture of the aneurysm occurs following craniotomy, the primary therapeutic focus should be to achieve control of the hemorrhage, since, in general, the prognosis for patients who experience aneurysm rupture during surgery appears to relate to the rapidity with which hemostasis is achieved.sg Intraoperative aneurysm rupture is typically associated with marked brain swelling, which tends to be refractory to interventions such as mannitol and corticosteroids.90 Rapid induction of hypotension using isoflurane or SNP (if available) to achieve an MAP of 40 to 50 mmHg (or lower if necessary) effectively decreases the rate of hemorrhage, thereby facilitating surgical exposure of the aneurysm and hemostasis by application of temporary or permanent clips. Reduction in the rate of hemorrhage for aneurysms in the ~~ _.1_l _:__-_~l_rl-.- -I-- __._ L- __L:_-.-J l__. ---..-1 carouu cu-cuiauou also cau ue acmeveu uy mauua~ compression of the ipsilateral carotid artery. Blood loss should be replaced promptly using crystalloid initially and, if necessary, blood or colloid later.

Recovery At the termination of surgery, anesthetic drugs should be discontinued, the patient shodi be weii oxygenJ. Clin. Anesth., vol. 4, January/February

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81

and residual neuromuscular blockade should be reversed. Responses to placement of the head dressing, suctioning of the oropharynx, and extubation should be anticipated and attenuated. IV lidocaine 1.5 mg/kg or a small dose of opioid (e.g., fentanyl 0.5 to 1.0 kg/kg) administered prior to extubation may help to minimize coughing but will deepen anesthesia. Following successful clipping of the aneurysm, many anesthesiologists allow BP to increase to 10% to 20% above preoperative normotensive levels, but excessive increases should be avoided. Antihypertensive drugs such as SNP, hydralazine, beta blockers, and labetalol may be used effectively to control hemodynamic responses during and following emergence.9’-“9 The patient should be awake and responsive as soon as possible after the completion ,of surgery to Patient5 whu expel-ience allow neur-olugic a55~5sment. intraoperative complications such as aneurysmal rupe._-^ ,.--^__I. A_ -..e:,.-+_ .WlLll ...+L n I. ucpnaacu -1,.--,.““,.-I IC” I ^_._ 1 VI -r LU‘C “ 1 p” “‘-~‘du’ tJdL”C~~LS Cs1 consciousness preoperatively should remain intubated until their neurologic status is stable and an intact airway and adequate ventilation can be ensured. The fully monitored patient should be transferred to a recovery area staffed by personnel familiar with, and skilled in, the management of neurosurgical patients. Vital signs, including neurologic signs, should ated,

h,= and rhartprl yc nhwr\I,=4 v.,y.,. .-,_. -..._.*-. ._._- PITPI-v _.._‘,, 1; _.I rnin~~t~c .A& . ..-.- “. Tht:

tient should be placed in a 30-degree tion,

and

carefully codeine

supplemental

0,

should

head-up

be provided.

p2posi-

Small,

titrated doses of IV opioid or intramuscular may he given if analgesics arc reqllired.

Summary The treatment of patients with intracranial aneurysms who reach the OR presents a challenge to both the neurosurgeon and the anesthesiologist. Anesthetic management of these patients encompasses multifactorial concerns. In this article, we have attempted to outline aspects of perioperative management where consensus has been achieved, as well as to review areas where controversy continues to exist. The principles of anesthetic management for patients with intracranial aneurysms are similar to those associated with other areas of anesthesia: control of hemodynamics, optimization of the surgical field (cerebral and aneurysmal compliance), and maintenance of adequate tissue (cerebral) blood flow and oxygenation. With these principles in mind, we discussed rational approaches for the selection of anesthetic drugs and techniques, focusing on optimizing patient safety and outcome, while recognizing that individual preferences and practice styles vary widely.

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1992

Acknowledgments We gratefully acknowledge Ihe secretariat assistance C. llawke in the preparation of this manuscript.

of %I\.

References of intracranial 1. Kassell NF, I’orner JC: Epidemiology I& Anestheaol Clin 1982;20: 13-17. aneurysms. 2. Kajikawa H, Kajikawa M, Ohta T, Hirota N, Mori M: Overview of natural history of aneurysmal subarachnoid hemorrhage. Review of literature. In: Kikuchi H. Fukushima T, Watanabe K. eds. Intmcranic~l Amrysmc--Su~;ricul Timing and Techniques. Niigata, ,Japan: Nishimura (:o, 1986:54-62. 3. Botterell EH, Longhead WM, Scott _JW, C’andewatel. SL: Hypothermia and interruption ofcarotid or carotid and vertebral circulation in the surgical management oi~intracrand aneurysms.,/ Nrurosq 1956:13:1-42. 4. Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J :\~Puro.curg 1968;28: 14-20. in patients with %5 Maroon ,JS. Nelson PB: Hypovolemia subarachnoid hemorrhage: therapeutic implications. Neuro.tIc?;9en; 3979;4:22?-6. 6 Solomon RA. Post KD, McMurtry JG III: Depression of circulating blood volume in patients after subarachnoid hemorrhage: implications for the management of’ symptomatic vasospasm. Nruros~rgr~ 1984; 15:%4-6 I 7 Brazenor (;A, Chamberlain MJ, Gelb AW: Systemic hypovolemia after subarachnoid hemorrhage. 1 h’rlruorllr1:-:,.h r R,ACn,,A Re,‘,ST, D I\, \,d,LCIC,,J, UeUI”LU DC. 1x1. &flurar,e jung RS, “..:-....I vs. nitrous oxide: impact on cerebrospinal fluid pressure in anesthetized patients with brain tumors [Abstract]. J ,Veurosurg Anesth 1990:2:215. Archer DP, L.abrecque P, Tyler jL, Meyer E, Trop D: Cerebral blood volume is increased in dogs during administration of nitrous oxide or isoflurane. Anesthesiology 1987;67:642-8. Hansen TD, Warner DS, Todd MM, Vust LJ: Effects of nitrous oxide and volatile anaesthetics on cerebral blood flow. Ur J Anaesth 1989;63:290-5. Michenfelder JD: Anesthesia and the Brain. New York: Churchill Livingstone, 1988:59. Pulsinelli WA, Levy DE, Sigsbee B, Scherer P, Plum F: Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus. AmJ Med 1983;74:540-4. Lanier WL, Stangland KJ, Scheithauer BW, Milde JH, Michenfelder JD: ‘l‘he effects of dextrose and head position on neurological outcome after complete cermhml CL,, ‘&A ;.rhe,n;,> LaL.II._‘I.Iy

;., LII VW-;n,r>te~. y’ IIIIYC-_“.

,~uam;,,at;,,,, L‘ -...I...IYL.VLI