Surg Neurol 1991;36:83-90
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Temporary Clipping in Aneurysm Surgery: Technique and Results F a d y T . C h a r b e l , M . D . , J a m e s I. A u s m a n ,
M.D., Ph.D., Fernando
Ghaus M. Malik, M.D., Manuel Dujovny,
M.D., and James
G. Diaz, M.D.,
Ph.D.,
Sanders, M.D.
Henry Ford Neurosurgical Institute, Detroit, Michigan
Charbel FT, AusmanJI, Diaz FG, Malik GM, Dujovny M, Sanders J. Temporary clipping in aneurysm surgery: technique and results. Surg Neurol 1991;36:83-90. The use of temporary clipping has become an established tool in the armamentarium of the aneurysm surgeon. Our experience with 62 consecutive patients is presented, detailing operative protocols and results. Twenty-two had unruptured aneurysms (35%), 15 were grade I (24%), 16 grade II (25%), five grade III (8%), and four grade IV (7%). The aneurysms were mainly located in the middle cerebral artery (29 patients) and the anterior communicating artery (13 patients). Eleven of our 62 patients (17%) developed a new, persistent postoperative deficit. However, in only one case (2%) was temporary clipping felt to be implicated in the development of the deficit. In three other patients (5%), the effect of temporary clipping, although unlikely, could not be excluded. Overall, 92% of our patients with temporary clipping had good to excellent outcome, with 3% mortality and 5% morbidity. We believe that temporary clipping is a safe procedure that contributes significantly to a better outcome. KEYWORDS: Aneurysm clip; Cerebral arteries; Cerebral aneurysm; Brain retractor
Temporary clipping of intracranial vessels in aneurysm surgery was introduced by Pool [36] and Pool and Housepian [37] in 1960. Suzuki has popularized this technique in Japan; however, it has been slowly accepted in other countries. It became our practice to use temporary clips electively on the afferent and efferent vessels of aneurysms since 1982. This has been particularly useful during surgery on giant aneurysms and during immediate surgery, when dissection of the aneurysm is often difficult and the incidence of rerupture is high during the dissection and clip application [7]. The focus of this paper is to highlight the safety of temporary clipping utilizing cerebral protective agents and normotension,
Address reprint requests to:James I. Ausman, M.D., Ph.D., Henry Ford Neurosurgical Institute, 2799 West Grand Boulevard, Detroit, Michigan 48202. Received March 13, 1990; accepted January 15, 1991.
© 1991 by ElsevierSciencePublishingCo., Inc.
emphasizing its importance in reducing intraoperative aneurysm rupture with its associated increase in morbidity and mortality.
Materials and Methods This article retrospectively reviews surgical results with temporary clipping in our patients from 1982 through 1987. Grading of patients was based on the H u n t and Hess classification [22]. The operative protocol is illustrated in Table 1. After premedication, anesthesia is induced with fentanyl, pentothal, isoflurane, and 50% N 2 0 and 50% 0 2. Recently, we have used vecuronium, a short-acting, nondepolarizing muscle relaxant, as it causes minimal cardiovascular changes and does not, like succinylcholine, release potassium from denervated muscle and ischemic tissue. At the time of the craniotomy, furosemide 40 mg is given followed by mannitol 50 g 5 minutes later to increase brain "slackness." Arterial PCO2 is kept at 30 torr. Either spinal drainage or opening of the cisterns and lamina terminalis is used to remove cerebrospinal fluid (CSF); spinal drainage is preferred. From 100 to 200 mL of CSF is removed routinely through the spinal drain to provide brain relaxation after the dura mater is opened. Thirty minutes prior to temporary clipping, 2 5 - 7 5 g of mannitol is given intravenously to increase cerebral blood flow and decrease viscosity [9]. Approximately 5 minutes prior to temporary clipping, the patient is given pentothal 3 - 5 mg/kg and lidocaine 1.5 mg/kg intravenously. This is repeated every 1 5 - 2 0 minutes if temporary vascular occlusion extends beyond that time. In addition, the nitrous oxide is turned off during temporary clipping [18,41]. Blood pressure is maintained in a normotensive range as determined by preoperative measurements. Recently, we have discontinued the use of lidocaine because o f evidence that it may not be an effective brain protective agent [43]. Our strategy for aneurysm surgery is to isolate the proximal vessel to the aneurysm first to gain proximal control and then the distal vessel before clipping the aneurysm. For internal carotid aneurysms, we will dissect and isolate the proximal internal carotid either intracra0090-3019/91/$3.50
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Charbel et al
niaUy or in the neck. Temporary clips are then loaded and trial mock applications or occlusions are made at each site. The distal internal carotid is exposed. Then the base and neck of the aneurysm are dissected. Two suckers are ready for use, a microsucker and one large # 11, in case of intraoperative rupture. If the aneurysm appears difficult to isolate, the temporary clipping regimen will be instituted, and rapid dissection of the aneurysm is completed and the permanent clip applied. For middle cerebral aneurysms, proximal vessel isolation begins with the internal carotid artery, then the middle cerebral artery (MCA). For anterior communicating aneurysms, isolating the ipsilateral A 1 is achieved followed by both A2s and contralateral A 1. Temporary clip application should avoid compression of perforating vessels and leave major important or collateral channels open to continue perfusion of local areas. Sugita or Yasargil temporary clips (Downs, Aesculap) were used for temporary vascular occlusion. The measured blade pressure was 4 0 - 8 0 g, depending upon the size of the particular artery to be occluded. For small vessels Kleinert-Kutz clips (Weck) were applied. Usually, for a vessel of 2.0 mm or less, like the distal MCA or anterior cerebral artery, 40-g-force temporary clips are sufficient for occlusion [ 13]. Larger vessels (ie, intracranial internal carotid, vertebral, basilar, or M 1 middle cerebral) require 80-g-force temporary clips. If the vessels still appear to be patent while working on the aneurysm, we apply a second temporary clip in tandem with the first. If symptomatic postoperatively, the patients are given volume expanders, and cardiac output is maximized based on optimal pulmonary capillary wedge pressure and the Starling curve. If necessary, hypertension is also
induced in an attempt to overcome ischemic deficits secondary to documented segmental arterial narrowing. The hematocrit is also kept in the range of 30-32. Postoperatively, our asymptomatic aneurysms are kept euvolemic and normotensive, monitored primarily with CVP rather than a Swan-Ganz catheter. Hemodilution is reserved for patients with significant subarachnoid hemorrhage in whom we feel there is a relatively high likelihood to develop ischemia and in patients exhibiting ischemia. Angiography was performed in all patients postoperatively to assess clip placement, to evaluate deficits postoperatively, and to help differentiate segmental arterial narrowing versus vessel thrombosis. Patients were assessed on clinical outcome based on a scale used by the International Cooperative Study and, recently, by Jabre and Symon [23]. Excellent outcome applies to patients with full recovery. Patients with mild neurological deficit but who are able to lead an independent life are classified as good outcome. Patients with fair outcome are unable to return to social life although capable of self-care. Poor applies to patients incapable of self-care.
Results Temporary clipping was used in 62 patients operated on between 1982 and 1987. There were 23 men and 39 women, with an average age of 45 years and 42 years, respectively. Unruptured aneurysms were encountered in 22 patients (35%), while the other 40 patients were in the following grades: I, 15 patients (24%); II, 16 patients (26%); III, five patients (8%); and IV, four patients (7%).
Table 1. Temporary Clipping." Operative Protocol 1o-30 man: Mannitol 25-75g IV To-S rain: Penlolhsl 3-5 mgJkg IV ± Lidoceine 1,5 mg/kg IV ± Oilentln
Inducllon Fonianyl Pontolhal Isoflurane Muscle Relexani Vacuronlurn Succinyi-Choilne Oexemeth|sone Codeine Olycopyprolsie
10 mg IV 60 mg IM 0.2 mg IM
PRE-OPERATIVELY
N O: SO% 0 2 : 50% ANESTHESIA
Open Spinal Grain
I'o i N20 Turn
(FwU~l(~!~nilde ) 40 mg ,VJ
Spinel Drain Positioning
Open Clslern~s)
fi;P2~2,;--
_
OURAL OPENING
N
NORMOTENSION
Pa CO2 30mm Hg
_.1.
TEMPORARY CLIPPING = TO
. . . .
~
off
TO + 1S-20 man: Penlothal
_* Lldocldne
Temporary Clipping
Surg Neurol 1991;36:83-90
Table 2. AnatomicDistribution of Aneurysms 29 13 4 4 3 3
Middle cerebral artery Anterior communicating artery Posterior communicating artery Carotid ophthalmic bifurcation Terminal carotid bifurcation Posterior inferior cerebellar artery Anterior cerebral artery Pericallosal artery Anterior choroidal artery Posterior cerebral artery Vertebral artery
Giant aneurysms, defined as greater than 2.5 cm, comprised 32% of our series overall and half (11 patients) of our unruptured aneurysms. The aneurysms were mainly found on the MCA in 29 patients (47%) and the anterior communicating artery (ACoA) in 13 patients (21%). Aneurysms in other locations are shown in Table 2.
85
around the aneurysm during temporary clipping, probably from collaterals. The patient had a 15-minute temporary vascular occlusion time to allow for permanent clipping of the aneurysm followed by a distal STA-MCA bypass to a branch of the MCA, which arose from the waist of the aneurysm. Temporary clip time for the distal bypass was 35 minutes. The patient awoke from surgery with a right hemiparesis and mild expressive dysphasia, and improved at the time of discharge with only a mild hemiparesis. The postoperative angiogram disclosed excellent filling of the bypass. The second patient with a permanent deficit was a 54year-old man with a grade II right MCA aneurysm (30 mm) that had ruptured 4 days previously. The aneurysm ruptured intraoperatively, and temporary vascular occlusion was performed proximal and distal to the aneurysm for 50 minutes. The patient awoke with a left hemiparesis. The postoperative angiogram revealed a kink produced in the parent vessel by the permanent clip. At the time of discharge the hemiparesis had not changed. Thus, in this case, another explanation for the permanent deficit besides temporary clipping can be found.
Middle Cerebral Artery Aneurysms T h e r e were 29 patients requiring temporary clipping for MCA aneurysms. Twenty-five were electively clipped, four after intraoperative aneurysm rupture. Fourteen of the patients had giant MCA aneurysms, of which eight were clipped following subarachnoid hemorrhage. The median temporary clipping time of patients without deficit was 13 minutes. Those with new postoperative deficits had longer median temporary clipping times (Table 3). Six of the 11 patients in grade 0 had transient postoperative deficit sometimes associated with lengthy clipping and additional procedures, such as MCA reconstruction (two patients) and superficial temporal artery to middle cerebral artery (STA-MCA) bypass (two patients). However, none of these deficits persisted. N o n e of the grade III and IV patients had increased postoperative deficits. Two patients had a persistent new postoperative deficit (Table 4). A 51-year-old woman had a grade I left MCA aneurysm that was 25 mm in size. Two days after subarachnoid hemorrhage she had some mild bleeding
T a b l e 3.
MCA Aneurysms: Temporary Clip Times
No. of patients Median clip time (min) Range (min)
No. deficits
Temporary deficit
Permanent deficit
Total
17
12
2
29
13 1-50
24 1-155
33 15-50
14 1-155
Anterior Communicating Artery Aneurysms There were 13 patients who had temporary clipping for AcoA aneurysms. In all patients from this group, the temporary vascular occlusion was performed electively. The aneurysms ranged in size from 4 mm to 15 mm. Seven patients (54%) developed new immediate postoperative deficits. All but two patients (15%) had complete resolution of these new deficits at the time of discharge. The median temporary occlusion time for all the patients in this group was 16 minutes (Table 5). Patients with no or temporary postoperative deficits had a median occlusion time of 16 minutes. The predominant new postoperative deficits encountered were confusion and m e m o r y disturbance in all seven of the patients in this group. In two patients, problems with short-term memory persisted (Table 4). The first of these two patients was a 55-year-old woman, grade 0, with a 15-mm ACoA aneurysm. The dissection was difficult and required temporary clipping of both right and left A1 and A2 arterial segments. The total temporary occlusion time was 16 minutes. The patient awoke with a mild m e m o r y disturbance that had partially resolved by the time o f discharge with only a slight decrease in short-term memory. The other patient was a 63-year-old man, grade I, with a 4-mm ACoA aneurysm that was 5 days posthemorrhage. The aneurysm was difficult to dissect and required temporary occlusion times of 8, 6, and 18 minutes, with approximately 5 minutes of reperfusion between each clip time. The patient awoke with confu-
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Charbel et al
Table 4. Persistent Postoperative Deficits
Age (yr)//sex
Grade
SAH to surgery (days)
Aneurysm location
Side/size
Temporary clip time
Intraop rupture
1
MCA
51 F
I
2
L/25 m m
2
MCA
54 M
II
4
R/30 m m
3
ACoA
55 M
0
--
15 m m
4
ACoA
63 M
I
5
5
Carotid ophthalmic
79 F
0
--
L/40 m m
6
Carotid ophthalmic
44 M
I
2
R/50 m m
7
43 F
0
--
L/30 m m
10 min
No
8
Internal carotid bifurcation PCA
60 F
II
2
R/5 m m
15 min
Yes
9
PICA
54 F
0
--
L/40 m m
9 min
No
10
PICA
50 M
I
8
R/10 m m
35 min
No
11
PICA
78 F
II
1
R/10 m m
30 min
No
4 mm
Persistent postop deficit
15 min, 35 min EC-IC bypass to branch from aneurysm waist 50 min
Yes
Mild hemiparesis, word searching
Yes
16 min
No
Hemiparesis, angio: p e r m a n e n t clip kinked M C A Short-term memory disturbance Short-term memory disturbance
8 6 18 Total 16 7 10 4 4 Total 12
min min min 32 min min min min min min 41 rain rain
No
No
Loss of vision os
No
Decrease in peripheral vision od Loss of vision os L superior quadrantanopsia Mild dysmetria, mild ataxia Decreased R gag Decreased R gag, expired 2 m o postop from p n e u m o n i a
Permanent deficit caused by temporary clip No
No
Unlikely but possible Unlikely but possible
No
No
No
Unlikely but possible No No Yes
Abbreviations: ACoA, anterior communicating artery; EC-IC, extracranial-intracranial bypass; F, female; L, left; M, male; MCA, middle cerebral artery; PCA, posterior communicating artery; PICA, posterior inferior cerebellar artery; R, right; SAH, subarachnoid hemorrhage.
sion that had resolved to a mild short-term memory disturbance at the time of discharge. In summary, after temporary vascular occlusion, 4 2 % o f the patients had a new immediate postoperative deficit that persisted in only 17%. Analyzing the patients with persistent new postoperative deficits, in only one case could it be attributed with reasonable certainty to temporary clipping. In another three patients, although another mechanism was available to explain the deficit, the role of temporary clipping could not be definitely ignored even though unlikely (Table 4).
Discussion Proper clip placement under controlled circumstances is the desire o f every neurosurgeon operating on a
cerebral aneurysm, particularly one that has recently ruptured. At our institution it is our policy to operate on patients with ruptured aneurysms immediately. The dissection necessary for proper visualization o f the neck is often difficult and there is the risk o f intraoperative rupture. In 1960, Pool [36], and Pool and Housepian [37] reported the routine use of temporary clipping and hypothermia in 23 patients with ACoA aneurysms. H e credits Jefferson in 1928 as the first to use temporary clips in aneurysm surgery, utilizing a modified Michel clip. Suzuki and Yoshimoto [49] have long been major proponents of temporary clipping and, in 1973, presented results of 215 cases using temporary vascular occlusion. This represented 79% o f their aneurysm cases. Suzuki et al [48] used hypothermia for cerebral
Temporary Clipping
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Table 5. Anterior Communicating Artery Aneurysms: Temporary Clip Times No. deficits No. of patients Median clip time (min) Range Imin)
Temporary deficit
6
7
16 6-23
16 5-32
Permanent deficit 2 24 16-32
Total l3 16 5-32
protection and reported relative safety with temporary vascular occlusion. The maximum safe limits of temporary vascular occlusion in this series at 26°C was 48.5 minutes for bilateral A1 occlusion, 30 minutes at the M1 portion, and 82 minutes on the dominant A1. In 1979 Suzuki and Yoshimoto [49] presented another paper on the usefulness of temporary clipping with cerebral protection using mannitol with normothermia and normotension. Their maximum safe occlusion times under these circumstances were 65 minutes for bilateral A1, 65 minutes at the M1 segment, and 80 minutes at the dominant A1. They discontinued using hypothermia as a major cerebral protective maneuver in aneurysm surgery because it was time consuming and had the added risk of cardiac arrhythmias, hypotension, acidosis, and coagulopathy [24]. In 1983 Ljunggren et al [27] reported 16 patients who underwent early surgery for 10 MCA and six ACoA aneurysms. Ten of the 16 patients had intraoperative rupture of the aneurysm. Temporary clipping was done under normotensive blood pressure, with the systolic pressure never falling below 90 mm Hg. N o cerebral protective agents were given routinely; however, six patients had variable amounts of mannitol preoperatively and postoperatively. Their average temporary clip time in the MCA group was 12.75 minutes, with a median time of 8.5 minutes. Maximum occlusion time in their group without immediate postoperative deficit was 30 minutes. The average temporary clipping time in the ACoA group was 10 minutes, with a median time o f 10 minutes. Maximum occlusion time in this group was 15 minutes without any new immediate postoperative deficits. Jabre and Symon [23] presented their experience with 66 patients, with an overall mortality of 6.1%. They used moderate hypotension during aneurysm dissection with a mean blood pressure of around 70 mm Hg. N o cerebral protective agents were given during temporary clipping. More recently Momma et al [34] reported monitoring patients during the time of temporary vascular occlusion using central conduction time measurements. The largest group studied had ACoA aneurysms, o f which there were 22 cases. In addition, there were 16 cases of MCA aneurysms. The average temporary clipping time in the ACoA group
87
was 7 minutes, with a median time of 5 minutes. Maximum occlusion time without any new immediate postoperative deficit was 24 minutes. The average temporary clipping in the MCA group was 8 minutes, with a median time of 6 minutes. The maximum occlusion time without any immediate postoperative deficit was 8 minutes. The development of temporary clips has undergone major technical advances over the years. With the use of scanning electron and transmission microscopy [10-14,17,38], the blade pressure of temporary clips has been adjusted allowing for minimal vessel damage at the site of temporary occlusion. Sugita et al [46] felt the temporary clips should have a pressure less than 80 g at the blade tip to minimize vessel wall damage. At our institution, we use Sugita and Yasargil temporary clips with a closing force of 4 0 - 8 0 g. For small vessels, K l e i n e r t - K u t z clips are used. It has been our practice to use cerebral protective agents during the time of temporary vascular occlusion, as detailed in Table 1. Suzuki and Yoshimoto [49] have been major proponents of the cerebral protective effect of mannitol in prolonging safe temporary vascular occlusion. Seki et al [42], using a canine model, have shown that mannitol will increase regional cerebral blood flow to moderately ischemic areas. Little [26] has shown that mannitol improved microcirculation in ischemic areas of the cat. Recently, Meyer et al [29] reported that mannitol was "beneficial in stabilizing zones of moderate ischemia (ischemic penumbras), presumably by reducing cytotoxic edema that, as a result, improved cerebral blood flow." Pentothal is given just prior to temporary vascular occlusion. We give 3 to 5 mg/kg intravenously, and this is repeated every 1 5 - 2 0 minutes during the time of temporary vascular occlusion. The cerebral protective effects of barbiturates are represented extensively in the literature [19,20,28,31,33,35]. It is reported to cause inhibition of synaptic transmission in the socalled activation arm of cerebral metabolism [2]. Barbiturates have been shown to reduce the cerebral metabolic rate by approximately 50% [2,3,32,44,45,51]. Studies indicate that maximal effect of barbiturates is reached when the electroencephalogram becomes flat, and at that point no further cerebral protection is offered by additional barbiturates [32,33]. We agree with Michenfelder [30] that a "sleep dose" (3-5 mg/ kg) of thiopental is all that is necessary for cerebral protection to the ischemic area and that the washout of thiopental will be delayed in the ischemic areas as a result of the temporary vascular occlusion. Initially, we also used lidocaine, 1.5 mg/kg intravenously, given at the time of thiopental administration just prior to temporary vascular occlusion, and this was repeated every 1 5 - 2 0 minutes. Lidocaine delays
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the rise in extracellular potassium by partially blocking the sodium channels-known as the membrane stabilizing effect. Lidocaine can further reduce cerebral metabolism by inhibiting electrocortical activity, resulting in decreased 02 and glucose c o n s u m p t i o n - k n o w n as a barbiturate-like effect [ 4 - 6 ] . Evans et al [15], utilizing low doses of lidocaine in an air embolism ischemia modeJ in cats, found that it achieved both a reduction in neural decrement and an increase in recovery of neural function when assessed by measuring the SSER. However, more recent experimentation in an MCA focal ischemia model in cats failed to demonstrate any protective effect o f lidocaine, even when used in doses sufficient to suppress or flatten the electroencephalogram, as evidenced by histological and histochemical methods o f assessment o f the areas of neuronal alteration [43]. We have, therefore, discontinued the use o f lidocaine in our brain protection regimen. An important tenet in our approach to temporary vascular occlusion is to maintain normal blood pressure rather than induce hypotension [ 16]. Studies measuring retractor pressure on the cerebral cortex have shown increased local ischemia and infarction in animals maintained at hypotensive blood pressures [1,8,21, 25,39,40,47,50]. Therefore, in order to increase collateral perfusion of temporarily ischemic areas, one would want to maintain a normal or increased blood pressure during that time rather than induce relative hypotension. Intraoperative rupture of an aneurysm prior to proximal and distal control is disastrous and has been shown to triple operative morbidity and mortality [7]. The dissection o f proximal and distal vessels during this time is often done hastily and with poor visualization, contributing to the disruption of perforators and small cortical vessels. In addition, brain retraction under these circumstances is often precipitous, and a number of investigators have demonstrated the development of tissue ischemia under and adjacent to the retractor, especially with increasing retractor pressure, prolonged retraction, and hypotension [1,21,25,29,39,40]. With regard to thrombosis secondary to temporary clipping, we have two patients that could theoretically fit into this category: one with a giant carotid bifurcation aneurysm and a postoperative angiogram showing occlusion o f the ipsilateral anterior cerebral artery. The patient, however, did not develop a deficit. The temporary clip time was 13 minutes. The other patient had a posterior inferior cerebellar artery aneurysm and developed an occlusion of the vertebral artery at the level of the atlas. The temporary clip time was 30 minutes. T h e patient developed lower cranial nerve dysfunction and died of pneumonia. It is difficult to recommend safe time units for
Charbel et al
temporary vascular occlusion. Reviewing our data, we find that, in general, the patients with new and persistent postoperative deficits had longer temporary vascular occlusion times. However, we had a patient with a temporary clip time o f 110 minutes with no immediate postoperative deficit, while another patient with a temporary clip time of only 5 minutes developed a new deficit. Suzuki and co-workers [48,49] found similar "unpredictable" occurrences. The data of Momma et al [34] would also support this finding. With these reservations in mind, we can state that in our experience, using normothermia, normotension, and the above-mentioned brain protection protocol, temporary clipping can be used in the MCA up to 24 minutes without risk of permanent deficit, and in A1 bilaterally up to 16 minutes. As for aneurysms in other locations, smaller patient numbers preclude us from generating significant data.
Conclusion We had 62 patients from 1982 to 1987 who underwent temporary vascular occlusion during aneurysm surgery. A majority of our patients were grades 0 to II, representing 85 % of the total. The two largest groups in our series were the patients with MCA and ACoA aneurysms. Temporary clipping is o f undisputed value in preventing intraoperative rupture in patients with aneurysm surgery. This can result in decreased mortality and morbidity. Thus, in our experience, the rationale for brain protective agents and normotension appears justifiable. Among our patients, 26 (42%) developed a new immediate postoperative deficit. At the time o f discharge, all but 11 (17%) patients had had complete resolution o f these deficits. We carefully examined this group of 11 patients for all the potential causes of the persistent deficit. There was only one case (2%) in which temporary clipping was strongly implicated in the development of these persistent deficits and three other patients in whom the effect of temporary clipping, although very unlikely, could not be excluded (5%). T h e r e were two deaths in our series, establishing a mortality rate o f 3%. In two (3%) cases, vessel thrombosis did occur in which temporary clipping may have contributed, with only one persistent morbidity. In conclusion, temporary clipping, by decreasing our morbidity and mortality in aneurysm surgery, has become a standard technique in our pursuit for improving the outcome o f patients undergoing craniotomy and clipping of cerebral aneurysms. This work was supported in part by the Harris Foundation.
T e m p o r a r y Clipping
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44.
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tion in the repair of intracranial aneurysms. J Neurosurg 1968;28:14-9. Jabre A, Symon L. Temporary vascular occlusion during aneurysm surgery. Surg Neurol 1987;27:47-63. Kwak R, Okudaira Y, Suzuki J, Watabe Y. Problems in hypothermic anesthesia for direct surgical treatment of intracranial aneurysms, with special reference to ventricular fibrillation. Brain Nerve (Tokyo) 1972;24:403-10. Laha RK, Dujovny M, Rao S, Barrionuevo PJ, Bunegin L, Hellstrom HR, Albin MS, Taylor FH. Cerebellar retraction: significance and sequelae. Surg Neurol 1979;12:209-15. Little JR. Modification of acute focal ischemia by treatment with mannitol. Stroke 1978;9:4-9. Ljunggren B, Saveland H, Brandt L, Kagstrom E, Rehncrrona S, Nilsson PE. Temporary clipping during early operation for ruptured aneurysm: preliminary report, Neurosurgery 1983;12:525-30. McDermott MW, Durity FA, Borozny M, Mountain MA. Temporary vessel occlusion and barbiturate protection in cerebral aneurysm surgery. Neurosurgery 1989;25:54-62. Meyer F, Anderson R, Sundt T Jr, Yaksh T. Treatment of experimental focal cerebral ischemia with mannitol. J Neurosurg 1987;66:109-15, Michenfelder JD. Cerebral preservation for intraoperative focal ischemia. Clin Neurosurg 1985;32:105-13. Michenfelder JD, Milde JH. Cerebral protection by anesthetics during ischemia. Resuscitation 1975;4:219-23. MichenfelderJD, MildeJH. Influence of anesthetics on metabolic, functional and pathological responses to regional cerebral ischemia. Stroke 1975;6:405-10. Michenfelder JD, Milde JH, Sun& T Jr. Cerebral protection by barbiturate anesthesia. Arch Neurol 1976;33:345-50. Momma F, Wang A, Symon L. Effects of temporary arterial occlusion on somatosensory evoked responses in aneurysm surgery. Surg Neurol 1987;27:343-52. Moseley JI, Laurent JP, Molinari GF. Barbiturate attenuation of the clinical course and pathologic lesions in a primate stroke model. Neurology 1975;25:870-4. PoolJL. Aneurysms of the anterior communicating artery: bifrontal craniotomy and routine use of temporary clips. J Neurosurg 1961;18:98-111. PoolJL, Housepian E. Temporary clip occlusion of major cerebral arteries during intracranial aneurysm surgery. Surg Forum 1960;10:791-4. Richling B, Gottfried G, Lametschwandmer A, Scheiblbrander W. Endothelial lesions after temporary clipping: a comparative study. J Neurosurg 1979;51:654-61. Rosenorm J, Diemer N. Reduction of regional cerebral blood flow during brain retraction pressure in the rat. J Neurosurg 1982;56:826-9. Rosenorm J, Diemer N. The risk of cerebral damage during graded brain retractor pressure in the rat. J Neurosurg 1985;60:608-11. Sakabe T, Tsutsui T, Maekawa T, lshikawa T, Takeshita H. Local cerebral glucose utilization during nitrous oxide and pentobarbital anesthesia in rats. Anes 1985;63:262-6. Seki H, Yoshimoto T, Ogawa A, Suzuji J. Effect of mannitol on rCBF in canine thalamic ischemia-an experimental study. Stroke 1983;14:46-50. Shokunbi MT, Gelb AW, Peerless SJ, Meruart M, Floyd P. An evaluation of the effect of lidocaine in experimental focal ischemia. Stroke 1986;5:962-6. Siesjo B. Cerebral circulation and metabolism. J Neurosurg 1984;60:883-908.
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45. Smith AL, HoffJT, Nielsen SL, Larson CP. Barbiturate protection in acute focal cerebral ischemia. Stroke 1974;5:1-7. 46. Sugita K, Hirota T, Iguchi I, Mizutani T. Comparative study of the pressure of various aneurysm clips. J Neurosurg 1976;44: 723-7. 47. Sugita K, Kobayashi S, Takemae T, Matsuo K, Yokoh A. Direct retraction method in aneurysm surgery. J Neurosurg 1980;53:417-9. 48. Suzuki J, Kwak R, Okudaira Y. The safe time limit of temporary clamping of cerebral arteries in direct surgical treatment of intracranial aneurysms under moderate hypothermia. In: Suzuki J,
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ed. Cerebral aneurysms. Sendal, Japan: Neuron Publishing Co, 1979:325-9. 49. Suzuki J, Yoshimoto T. The effect of mannitol in prolongation of permissible occlusion time of cerebral arteries: clinical data of aneurysm surgery. In: Suzuki J, ed. Cerebral aneurysms. Sendai, Japan: Neuron Publishing Co, 1979:330-7. 50. Yokoh A, Sugita K, Kobayashi S. Intermittent versus continuous brain retraction. J Neurosurg 1983;58:918-23. 51. Yonas H, Dujovny M, Nelson D, Lipton SD, Segal R, Agdeppa D, Mazel M. The controlled delivery of thiopental and delayed cerebral revascularization. Surg Neurol 1981;15:27-34.
83
Temporary Clipping in Aneurysm Surgery: Technique and Results F a d y T . C h a r b e l , M . D . , J a m e s I. A u s m a n ,
M.D., Ph.D., Fernando
Ghaus M. Malik, M.D., Manuel Dujovny,
M.D., and James
G. Diaz, M.D.,
Ph.D.,
Sanders, M.D.
Henry Ford Neurosurgical Institute, Detroit, Michigan
Charbel FT, AusmanJI, Diaz FG, Malik GM, Dujovny M, Sanders J. Temporary clipping in aneurysm surgery: technique and results. Surg Neurol 1991;36:83-90. The use of temporary clipping has become an established tool in the armamentarium of the aneurysm surgeon. Our experience with 62 consecutive patients is presented, detailing operative protocols and results. Twenty-two had unruptured aneurysms (35%), 15 were grade I (24%), 16 grade II (25%), five grade III (8%), and four grade IV (7%). The aneurysms were mainly located in the middle cerebral artery (29 patients) and the anterior communicating artery (13 patients). Eleven of our 62 patients (17%) developed a new, persistent postoperative deficit. However, in only one case (2%) was temporary clipping felt to be implicated in the development of the deficit. In three other patients (5%), the effect of temporary clipping, although unlikely, could not be excluded. Overall, 92% of our patients with temporary clipping had good to excellent outcome, with 3% mortality and 5% morbidity. We believe that temporary clipping is a safe procedure that contributes significantly to a better outcome. KEYWORDS: Aneurysm clip; Cerebral arteries; Cerebral aneurysm; Brain retractor
Temporary clipping of intracranial vessels in aneurysm surgery was introduced by Pool [36] and Pool and Housepian [37] in 1960. Suzuki has popularized this technique in Japan; however, it has been slowly accepted in other countries. It became our practice to use temporary clips electively on the afferent and efferent vessels of aneurysms since 1982. This has been particularly useful during surgery on giant aneurysms and during immediate surgery, when dissection of the aneurysm is often difficult and the incidence of rerupture is high during the dissection and clip application [7]. The focus of this paper is to highlight the safety of temporary clipping utilizing cerebral protective agents and normotension,
Address reprint requests to:James I. Ausman, M.D., Ph.D., Henry Ford Neurosurgical Institute, 2799 West Grand Boulevard, Detroit, Michigan 48202. Received March 13, 1990; accepted January 15, 1991.
© 1991 by ElsevierSciencePublishingCo., Inc.
emphasizing its importance in reducing intraoperative aneurysm rupture with its associated increase in morbidity and mortality.
Materials and Methods This article retrospectively reviews surgical results with temporary clipping in our patients from 1982 through 1987. Grading of patients was based on the H u n t and Hess classification [22]. The operative protocol is illustrated in Table 1. After premedication, anesthesia is induced with fentanyl, pentothal, isoflurane, and 50% N 2 0 and 50% 0 2. Recently, we have used vecuronium, a short-acting, nondepolarizing muscle relaxant, as it causes minimal cardiovascular changes and does not, like succinylcholine, release potassium from denervated muscle and ischemic tissue. At the time of the craniotomy, furosemide 40 mg is given followed by mannitol 50 g 5 minutes later to increase brain "slackness." Arterial PCO2 is kept at 30 torr. Either spinal drainage or opening of the cisterns and lamina terminalis is used to remove cerebrospinal fluid (CSF); spinal drainage is preferred. From 100 to 200 mL of CSF is removed routinely through the spinal drain to provide brain relaxation after the dura mater is opened. Thirty minutes prior to temporary clipping, 2 5 - 7 5 g of mannitol is given intravenously to increase cerebral blood flow and decrease viscosity [9]. Approximately 5 minutes prior to temporary clipping, the patient is given pentothal 3 - 5 mg/kg and lidocaine 1.5 mg/kg intravenously. This is repeated every 1 5 - 2 0 minutes if temporary vascular occlusion extends beyond that time. In addition, the nitrous oxide is turned off during temporary clipping [18,41]. Blood pressure is maintained in a normotensive range as determined by preoperative measurements. Recently, we have discontinued the use of lidocaine because o f evidence that it may not be an effective brain protective agent [43]. Our strategy for aneurysm surgery is to isolate the proximal vessel to the aneurysm first to gain proximal control and then the distal vessel before clipping the aneurysm. For internal carotid aneurysms, we will dissect and isolate the proximal internal carotid either intracra0090-3019/91/$3.50
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Surg Neurol 1991;36:83-90
Charbel et al
niaUy or in the neck. Temporary clips are then loaded and trial mock applications or occlusions are made at each site. The distal internal carotid is exposed. Then the base and neck of the aneurysm are dissected. Two suckers are ready for use, a microsucker and one large # 11, in case of intraoperative rupture. If the aneurysm appears difficult to isolate, the temporary clipping regimen will be instituted, and rapid dissection of the aneurysm is completed and the permanent clip applied. For middle cerebral aneurysms, proximal vessel isolation begins with the internal carotid artery, then the middle cerebral artery (MCA). For anterior communicating aneurysms, isolating the ipsilateral A 1 is achieved followed by both A2s and contralateral A 1. Temporary clip application should avoid compression of perforating vessels and leave major important or collateral channels open to continue perfusion of local areas. Sugita or Yasargil temporary clips (Downs, Aesculap) were used for temporary vascular occlusion. The measured blade pressure was 4 0 - 8 0 g, depending upon the size of the particular artery to be occluded. For small vessels Kleinert-Kutz clips (Weck) were applied. Usually, for a vessel of 2.0 mm or less, like the distal MCA or anterior cerebral artery, 40-g-force temporary clips are sufficient for occlusion [ 13]. Larger vessels (ie, intracranial internal carotid, vertebral, basilar, or M 1 middle cerebral) require 80-g-force temporary clips. If the vessels still appear to be patent while working on the aneurysm, we apply a second temporary clip in tandem with the first. If symptomatic postoperatively, the patients are given volume expanders, and cardiac output is maximized based on optimal pulmonary capillary wedge pressure and the Starling curve. If necessary, hypertension is also
induced in an attempt to overcome ischemic deficits secondary to documented segmental arterial narrowing. The hematocrit is also kept in the range of 30-32. Postoperatively, our asymptomatic aneurysms are kept euvolemic and normotensive, monitored primarily with CVP rather than a Swan-Ganz catheter. Hemodilution is reserved for patients with significant subarachnoid hemorrhage in whom we feel there is a relatively high likelihood to develop ischemia and in patients exhibiting ischemia. Angiography was performed in all patients postoperatively to assess clip placement, to evaluate deficits postoperatively, and to help differentiate segmental arterial narrowing versus vessel thrombosis. Patients were assessed on clinical outcome based on a scale used by the International Cooperative Study and, recently, by Jabre and Symon [23]. Excellent outcome applies to patients with full recovery. Patients with mild neurological deficit but who are able to lead an independent life are classified as good outcome. Patients with fair outcome are unable to return to social life although capable of self-care. Poor applies to patients incapable of self-care.
Results Temporary clipping was used in 62 patients operated on between 1982 and 1987. There were 23 men and 39 women, with an average age of 45 years and 42 years, respectively. Unruptured aneurysms were encountered in 22 patients (35%), while the other 40 patients were in the following grades: I, 15 patients (24%); II, 16 patients (26%); III, five patients (8%); and IV, four patients (7%).
Table 1. Temporary Clipping." Operative Protocol 1o-30 man: Mannitol 25-75g IV To-S rain: Penlolhsl 3-5 mgJkg IV ± Lidoceine 1,5 mg/kg IV ± Oilentln
Inducllon Fonianyl Pontolhal Isoflurane Muscle Relexani Vacuronlurn Succinyi-Choilne Oexemeth|sone Codeine Olycopyprolsie
10 mg IV 60 mg IM 0.2 mg IM
PRE-OPERATIVELY
N O: SO% 0 2 : 50% ANESTHESIA
Open Spinal Grain
I'o i N20 Turn
(FwU~l(~!~nilde ) 40 mg ,VJ
Spinel Drain Positioning
Open Clslern~s)
fi;P2~2,;--
_
OURAL OPENING
N
NORMOTENSION
Pa CO2 30mm Hg
_.1.
TEMPORARY CLIPPING = TO
. . . .
~
off
TO + 1S-20 man: Penlothal
_* Lldocldne
Temporary Clipping
Surg Neurol 1991;36:83-90
Table 2. AnatomicDistribution of Aneurysms 29 13 4 4 3 3
Middle cerebral artery Anterior communicating artery Posterior communicating artery Carotid ophthalmic bifurcation Terminal carotid bifurcation Posterior inferior cerebellar artery Anterior cerebral artery Pericallosal artery Anterior choroidal artery Posterior cerebral artery Vertebral artery
Giant aneurysms, defined as greater than 2.5 cm, comprised 32% of our series overall and half (11 patients) of our unruptured aneurysms. The aneurysms were mainly found on the MCA in 29 patients (47%) and the anterior communicating artery (ACoA) in 13 patients (21%). Aneurysms in other locations are shown in Table 2.
85
around the aneurysm during temporary clipping, probably from collaterals. The patient had a 15-minute temporary vascular occlusion time to allow for permanent clipping of the aneurysm followed by a distal STA-MCA bypass to a branch of the MCA, which arose from the waist of the aneurysm. Temporary clip time for the distal bypass was 35 minutes. The patient awoke from surgery with a right hemiparesis and mild expressive dysphasia, and improved at the time of discharge with only a mild hemiparesis. The postoperative angiogram disclosed excellent filling of the bypass. The second patient with a permanent deficit was a 54year-old man with a grade II right MCA aneurysm (30 mm) that had ruptured 4 days previously. The aneurysm ruptured intraoperatively, and temporary vascular occlusion was performed proximal and distal to the aneurysm for 50 minutes. The patient awoke with a left hemiparesis. The postoperative angiogram revealed a kink produced in the parent vessel by the permanent clip. At the time of discharge the hemiparesis had not changed. Thus, in this case, another explanation for the permanent deficit besides temporary clipping can be found.
Middle Cerebral Artery Aneurysms T h e r e were 29 patients requiring temporary clipping for MCA aneurysms. Twenty-five were electively clipped, four after intraoperative aneurysm rupture. Fourteen of the patients had giant MCA aneurysms, of which eight were clipped following subarachnoid hemorrhage. The median temporary clipping time of patients without deficit was 13 minutes. Those with new postoperative deficits had longer median temporary clipping times (Table 3). Six of the 11 patients in grade 0 had transient postoperative deficit sometimes associated with lengthy clipping and additional procedures, such as MCA reconstruction (two patients) and superficial temporal artery to middle cerebral artery (STA-MCA) bypass (two patients). However, none of these deficits persisted. N o n e of the grade III and IV patients had increased postoperative deficits. Two patients had a persistent new postoperative deficit (Table 4). A 51-year-old woman had a grade I left MCA aneurysm that was 25 mm in size. Two days after subarachnoid hemorrhage she had some mild bleeding
T a b l e 3.
MCA Aneurysms: Temporary Clip Times
No. of patients Median clip time (min) Range (min)
No. deficits
Temporary deficit
Permanent deficit
Total
17
12
2
29
13 1-50
24 1-155
33 15-50
14 1-155
Anterior Communicating Artery Aneurysms There were 13 patients who had temporary clipping for AcoA aneurysms. In all patients from this group, the temporary vascular occlusion was performed electively. The aneurysms ranged in size from 4 mm to 15 mm. Seven patients (54%) developed new immediate postoperative deficits. All but two patients (15%) had complete resolution of these new deficits at the time of discharge. The median temporary occlusion time for all the patients in this group was 16 minutes (Table 5). Patients with no or temporary postoperative deficits had a median occlusion time of 16 minutes. The predominant new postoperative deficits encountered were confusion and m e m o r y disturbance in all seven of the patients in this group. In two patients, problems with short-term memory persisted (Table 4). The first of these two patients was a 55-year-old woman, grade 0, with a 15-mm ACoA aneurysm. The dissection was difficult and required temporary clipping of both right and left A1 and A2 arterial segments. The total temporary occlusion time was 16 minutes. The patient awoke with a mild m e m o r y disturbance that had partially resolved by the time o f discharge with only a slight decrease in short-term memory. The other patient was a 63-year-old man, grade I, with a 4-mm ACoA aneurysm that was 5 days posthemorrhage. The aneurysm was difficult to dissect and required temporary occlusion times of 8, 6, and 18 minutes, with approximately 5 minutes of reperfusion between each clip time. The patient awoke with confu-
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Charbel et al
Table 4. Persistent Postoperative Deficits
Age (yr)//sex
Grade
SAH to surgery (days)
Aneurysm location
Side/size
Temporary clip time
Intraop rupture
1
MCA
51 F
I
2
L/25 m m
2
MCA
54 M
II
4
R/30 m m
3
ACoA
55 M
0
--
15 m m
4
ACoA
63 M
I
5
5
Carotid ophthalmic
79 F
0
--
L/40 m m
6
Carotid ophthalmic
44 M
I
2
R/50 m m
7
43 F
0
--
L/30 m m
10 min
No
8
Internal carotid bifurcation PCA
60 F
II
2
R/5 m m
15 min
Yes
9
PICA
54 F
0
--
L/40 m m
9 min
No
10
PICA
50 M
I
8
R/10 m m
35 min
No
11
PICA
78 F
II
1
R/10 m m
30 min
No
4 mm
Persistent postop deficit
15 min, 35 min EC-IC bypass to branch from aneurysm waist 50 min
Yes
Mild hemiparesis, word searching
Yes
16 min
No
Hemiparesis, angio: p e r m a n e n t clip kinked M C A Short-term memory disturbance Short-term memory disturbance
8 6 18 Total 16 7 10 4 4 Total 12
min min min 32 min min min min min min 41 rain rain
No
No
Loss of vision os
No
Decrease in peripheral vision od Loss of vision os L superior quadrantanopsia Mild dysmetria, mild ataxia Decreased R gag Decreased R gag, expired 2 m o postop from p n e u m o n i a
Permanent deficit caused by temporary clip No
No
Unlikely but possible Unlikely but possible
No
No
No
Unlikely but possible No No Yes
Abbreviations: ACoA, anterior communicating artery; EC-IC, extracranial-intracranial bypass; F, female; L, left; M, male; MCA, middle cerebral artery; PCA, posterior communicating artery; PICA, posterior inferior cerebellar artery; R, right; SAH, subarachnoid hemorrhage.
sion that had resolved to a mild short-term memory disturbance at the time of discharge. In summary, after temporary vascular occlusion, 4 2 % o f the patients had a new immediate postoperative deficit that persisted in only 17%. Analyzing the patients with persistent new postoperative deficits, in only one case could it be attributed with reasonable certainty to temporary clipping. In another three patients, although another mechanism was available to explain the deficit, the role of temporary clipping could not be definitely ignored even though unlikely (Table 4).
Discussion Proper clip placement under controlled circumstances is the desire o f every neurosurgeon operating on a
cerebral aneurysm, particularly one that has recently ruptured. At our institution it is our policy to operate on patients with ruptured aneurysms immediately. The dissection necessary for proper visualization o f the neck is often difficult and there is the risk o f intraoperative rupture. In 1960, Pool [36], and Pool and Housepian [37] reported the routine use of temporary clipping and hypothermia in 23 patients with ACoA aneurysms. H e credits Jefferson in 1928 as the first to use temporary clips in aneurysm surgery, utilizing a modified Michel clip. Suzuki and Yoshimoto [49] have long been major proponents of temporary clipping and, in 1973, presented results of 215 cases using temporary vascular occlusion. This represented 79% o f their aneurysm cases. Suzuki et al [48] used hypothermia for cerebral
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Table 5. Anterior Communicating Artery Aneurysms: Temporary Clip Times No. deficits No. of patients Median clip time (min) Range Imin)
Temporary deficit
6
7
16 6-23
16 5-32
Permanent deficit 2 24 16-32
Total l3 16 5-32
protection and reported relative safety with temporary vascular occlusion. The maximum safe limits of temporary vascular occlusion in this series at 26°C was 48.5 minutes for bilateral A1 occlusion, 30 minutes at the M1 portion, and 82 minutes on the dominant A1. In 1979 Suzuki and Yoshimoto [49] presented another paper on the usefulness of temporary clipping with cerebral protection using mannitol with normothermia and normotension. Their maximum safe occlusion times under these circumstances were 65 minutes for bilateral A1, 65 minutes at the M1 segment, and 80 minutes at the dominant A1. They discontinued using hypothermia as a major cerebral protective maneuver in aneurysm surgery because it was time consuming and had the added risk of cardiac arrhythmias, hypotension, acidosis, and coagulopathy [24]. In 1983 Ljunggren et al [27] reported 16 patients who underwent early surgery for 10 MCA and six ACoA aneurysms. Ten of the 16 patients had intraoperative rupture of the aneurysm. Temporary clipping was done under normotensive blood pressure, with the systolic pressure never falling below 90 mm Hg. N o cerebral protective agents were given routinely; however, six patients had variable amounts of mannitol preoperatively and postoperatively. Their average temporary clip time in the MCA group was 12.75 minutes, with a median time of 8.5 minutes. Maximum occlusion time in their group without immediate postoperative deficit was 30 minutes. The average temporary clipping time in the ACoA group was 10 minutes, with a median time o f 10 minutes. Maximum occlusion time in this group was 15 minutes without any new immediate postoperative deficits. Jabre and Symon [23] presented their experience with 66 patients, with an overall mortality of 6.1%. They used moderate hypotension during aneurysm dissection with a mean blood pressure of around 70 mm Hg. N o cerebral protective agents were given during temporary clipping. More recently Momma et al [34] reported monitoring patients during the time of temporary vascular occlusion using central conduction time measurements. The largest group studied had ACoA aneurysms, o f which there were 22 cases. In addition, there were 16 cases of MCA aneurysms. The average temporary clipping time in the ACoA group
87
was 7 minutes, with a median time of 5 minutes. Maximum occlusion time without any new immediate postoperative deficit was 24 minutes. The average temporary clipping in the MCA group was 8 minutes, with a median time of 6 minutes. The maximum occlusion time without any immediate postoperative deficit was 8 minutes. The development of temporary clips has undergone major technical advances over the years. With the use of scanning electron and transmission microscopy [10-14,17,38], the blade pressure of temporary clips has been adjusted allowing for minimal vessel damage at the site of temporary occlusion. Sugita et al [46] felt the temporary clips should have a pressure less than 80 g at the blade tip to minimize vessel wall damage. At our institution, we use Sugita and Yasargil temporary clips with a closing force of 4 0 - 8 0 g. For small vessels, K l e i n e r t - K u t z clips are used. It has been our practice to use cerebral protective agents during the time of temporary vascular occlusion, as detailed in Table 1. Suzuki and Yoshimoto [49] have been major proponents of the cerebral protective effect of mannitol in prolonging safe temporary vascular occlusion. Seki et al [42], using a canine model, have shown that mannitol will increase regional cerebral blood flow to moderately ischemic areas. Little [26] has shown that mannitol improved microcirculation in ischemic areas of the cat. Recently, Meyer et al [29] reported that mannitol was "beneficial in stabilizing zones of moderate ischemia (ischemic penumbras), presumably by reducing cytotoxic edema that, as a result, improved cerebral blood flow." Pentothal is given just prior to temporary vascular occlusion. We give 3 to 5 mg/kg intravenously, and this is repeated every 1 5 - 2 0 minutes during the time of temporary vascular occlusion. The cerebral protective effects of barbiturates are represented extensively in the literature [19,20,28,31,33,35]. It is reported to cause inhibition of synaptic transmission in the socalled activation arm of cerebral metabolism [2]. Barbiturates have been shown to reduce the cerebral metabolic rate by approximately 50% [2,3,32,44,45,51]. Studies indicate that maximal effect of barbiturates is reached when the electroencephalogram becomes flat, and at that point no further cerebral protection is offered by additional barbiturates [32,33]. We agree with Michenfelder [30] that a "sleep dose" (3-5 mg/ kg) of thiopental is all that is necessary for cerebral protection to the ischemic area and that the washout of thiopental will be delayed in the ischemic areas as a result of the temporary vascular occlusion. Initially, we also used lidocaine, 1.5 mg/kg intravenously, given at the time of thiopental administration just prior to temporary vascular occlusion, and this was repeated every 1 5 - 2 0 minutes. Lidocaine delays
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the rise in extracellular potassium by partially blocking the sodium channels-known as the membrane stabilizing effect. Lidocaine can further reduce cerebral metabolism by inhibiting electrocortical activity, resulting in decreased 02 and glucose c o n s u m p t i o n - k n o w n as a barbiturate-like effect [ 4 - 6 ] . Evans et al [15], utilizing low doses of lidocaine in an air embolism ischemia modeJ in cats, found that it achieved both a reduction in neural decrement and an increase in recovery of neural function when assessed by measuring the SSER. However, more recent experimentation in an MCA focal ischemia model in cats failed to demonstrate any protective effect o f lidocaine, even when used in doses sufficient to suppress or flatten the electroencephalogram, as evidenced by histological and histochemical methods o f assessment o f the areas of neuronal alteration [43]. We have, therefore, discontinued the use o f lidocaine in our brain protection regimen. An important tenet in our approach to temporary vascular occlusion is to maintain normal blood pressure rather than induce hypotension [ 16]. Studies measuring retractor pressure on the cerebral cortex have shown increased local ischemia and infarction in animals maintained at hypotensive blood pressures [1,8,21, 25,39,40,47,50]. Therefore, in order to increase collateral perfusion of temporarily ischemic areas, one would want to maintain a normal or increased blood pressure during that time rather than induce relative hypotension. Intraoperative rupture of an aneurysm prior to proximal and distal control is disastrous and has been shown to triple operative morbidity and mortality [7]. The dissection o f proximal and distal vessels during this time is often done hastily and with poor visualization, contributing to the disruption of perforators and small cortical vessels. In addition, brain retraction under these circumstances is often precipitous, and a number of investigators have demonstrated the development of tissue ischemia under and adjacent to the retractor, especially with increasing retractor pressure, prolonged retraction, and hypotension [1,21,25,29,39,40]. With regard to thrombosis secondary to temporary clipping, we have two patients that could theoretically fit into this category: one with a giant carotid bifurcation aneurysm and a postoperative angiogram showing occlusion o f the ipsilateral anterior cerebral artery. The patient, however, did not develop a deficit. The temporary clip time was 13 minutes. The other patient had a posterior inferior cerebellar artery aneurysm and developed an occlusion of the vertebral artery at the level of the atlas. The temporary clip time was 30 minutes. T h e patient developed lower cranial nerve dysfunction and died of pneumonia. It is difficult to recommend safe time units for
Charbel et al
temporary vascular occlusion. Reviewing our data, we find that, in general, the patients with new and persistent postoperative deficits had longer temporary vascular occlusion times. However, we had a patient with a temporary clip time o f 110 minutes with no immediate postoperative deficit, while another patient with a temporary clip time of only 5 minutes developed a new deficit. Suzuki and co-workers [48,49] found similar "unpredictable" occurrences. The data of Momma et al [34] would also support this finding. With these reservations in mind, we can state that in our experience, using normothermia, normotension, and the above-mentioned brain protection protocol, temporary clipping can be used in the MCA up to 24 minutes without risk of permanent deficit, and in A1 bilaterally up to 16 minutes. As for aneurysms in other locations, smaller patient numbers preclude us from generating significant data.
Conclusion We had 62 patients from 1982 to 1987 who underwent temporary vascular occlusion during aneurysm surgery. A majority of our patients were grades 0 to II, representing 85 % of the total. The two largest groups in our series were the patients with MCA and ACoA aneurysms. Temporary clipping is o f undisputed value in preventing intraoperative rupture in patients with aneurysm surgery. This can result in decreased mortality and morbidity. Thus, in our experience, the rationale for brain protective agents and normotension appears justifiable. Among our patients, 26 (42%) developed a new immediate postoperative deficit. At the time o f discharge, all but 11 (17%) patients had had complete resolution o f these deficits. We carefully examined this group of 11 patients for all the potential causes of the persistent deficit. There was only one case (2%) in which temporary clipping was strongly implicated in the development of these persistent deficits and three other patients in whom the effect of temporary clipping, although very unlikely, could not be excluded (5%). T h e r e were two deaths in our series, establishing a mortality rate o f 3%. In two (3%) cases, vessel thrombosis did occur in which temporary clipping may have contributed, with only one persistent morbidity. In conclusion, temporary clipping, by decreasing our morbidity and mortality in aneurysm surgery, has become a standard technique in our pursuit for improving the outcome o f patients undergoing craniotomy and clipping of cerebral aneurysms. This work was supported in part by the Harris Foundation.
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