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Anesth Analg 2004;98:1127-32 © 2004 International Anesthesia Research Society doi: 10.1213/01.ANE.0000105862.78906.3D
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Abstract |
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We compared the effects of desflurane and isoflurane on cerebral perfusion pressure (CPP), lumbar cerebrospinal fluid pressure (LCSFP), and mean arterial blood pressure (MAP) in patients anesthetized with desflurane or isoflurane undergoing craniotomy for supratentorial mass lesions. Additionally, emergence from anesthesia was examined to determine if neurologic function could be assessed earlier after isoflurane or desflurane anesthesia. Thirty-six patients were randomized to receive either desflurane or isoflurane for maintenance of anesthesia at 1.2 minimum alveolar concentration (MAC). Patients were hyperventilated (PaCO2, 30 ± 2 mm Hg) after baseline LCSFP was obtained via the subarachnoid catheter. At a MAC of 1.2, mean LCSFP was not statistically different between the two study groups either before or after hyperventilation. Additionally, CPP was not significantly different between the two groups. Finally, patient’s time to respond to commands was 50% shorter in the desflurane group (30 ± 36 min) (mean ± SD) when compared with the isoflurane group (72 ± 126 min); however, this was not significant (P = 0.17). In patients undergoing craniotomy for supratentorial mass lesions, desflurane and isoflurane have similar effects on CPP and MAP. Additionally, desflurane in the setting of hyperventilation does not cause significant changes in LCSFP.
IMPLICATIONS: This is the largest study to date comparing the effects of desflurane and isoflurane on patients undergoing craniotomy for supratentorial mass lesion with evidence of midline shift or edema. Neither desflurane nor isoflurane significantly altered lumbar cerebrospinal fluid pressure when moderate hypocapnia was maintained.
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Introduction |
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The ideal anesthetic for neuroanesthesia would maintain cerebral perfusion pressure (CPP) and have no residual anesthetic effects that hinder postoperative assessment of neurologic status. Among the newer volatile inhaled anesthetics, desflurane has the lowest blood:gas partition coefficient (1). A low blood:gas partition coefficient favors rapid recovery from anesthesia, and desflurane may be preferred in patients having neurosurgery when rapid emergence is desirable. Isoflurane is among the most commonly used volatile anesthetics for neurosurgical procedures because of its minimal effects on cerebral blood flow (CBF) and intracranial pressure (ICP) in hypocapnic patients (2,3). The data on the comparative effects of desflurane and isoflurane on the cerebrospinal fluid pressure (CSFP), CBF, and CPP in patients with normal and abnormal intracranial compliance are inconclusive (Table 1). A recent study by Fraga et al. (4) showed that neither desflurane nor isoflurane changed ICP from baseline. This study also showed that desflurane did not significantly alter CPP or arteriovenous oxygen content in patients undergoing craniotomy for supratentorial tumors. In dogs, Artruu (5) showed that desflurane had similar effects on ICP compared to isoflurane if hypocapnia was maintained but caused increases in ICP during normocapnia. However, in a subsequent study he showed that desflurane may decrease intracranial compliance in dogs (6).
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The advantages of rapid recovery from desflurane anesthesia have been tempered by these data on the effects of desflurane on CSFP (7,8). Because of these varying results, the present study examined the effects of desflurane and isoflurane on lumbar cerebrospinal fluid pressure (LCSFP) and recovery from anesthesia with carefully controlled conditions.
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Methods |
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After approval by the IRB and Ethics Committees for protection of human subjects at the participating institutions, Tulane University and the University of Western Ontario, informed consent was obtained and 36 patients were enrolled between the 2 participating institutions. Patients were then randomly assigned to one of two study arms: isoflurane or desflurane. Each institution was provided with randomization codes to allow patient selection in a blinded fashion. Patients had radiological or magnetic resonance imaging (MRI) evidence of mass effect (lesion causing any degree of midline shift or any evidence of cerebral edema). Patients were excluded from the study if their medical history included the presence of severe lung disease, coronary artery disease, anemia (hematocrit <25%), alcohol or other drug abuse, or if they were hemodynamically or neurologically unstable. Additionally, patients who were morbidly obese (body mass index >35), and those who had been exposed to general anesthesia in the 7 days before study were excluded.
All patients received dexamethasone 10 mg IV 90 min before induction, as was the standard of care at each institution for all patients with supratentorial lesions undergoing craniotomy. An arterial catheter was inserted before induction for continuous arterial blood pressure measurement, and anesthesia was induced with sodium thiopental up to 7.0 mg/kg, vecuronium 0.1–0.15 mg/kg, and fentanyl 1–2 µg/kg. After endotracheal intubation, anesthesia was maintained with an infusion of midazolam 0.15 mg · kg-1 · h-1 until a subarachnoid catheter was inserted via an 18-gauge Tuohy-Schiff needle (B. Braun Medical Inc., Bethlehem, PA). Patency of the cerebrospinal fluid (CSF) pathway was confirmed by elevation of the patient’s head, which produced an increase in LCSFP.
Patients were maintained in a normocapnic state (PaCO2, 40 ± 4 mm Hg) until after the subarachnoid catheter was placed. All measurements were performed with patients in a supine position, and pressures were measured with the zero reference at midcranial level via a pressure transducer throughout the study period. Baseline LCSFP was obtained under normocapnic conditions. LCSFP and arterial blood pressure measurements were recorded after induction under normocapnic (PaCO2, 40 ± 4 mm Hg) and hypocapnic (PaCO2, 30 ± 2 mm Hg) conditions. The PaCO2 tension was confirmed by arterial blood gas analysis and correlated with the end-tidal carbon dioxide (ETCO2) concentration. At that point, anesthesia was begun with either desflurane or isoflurane in an air/O2 mixture to keep PaO2 between 100–200 mm Hg. The inhaled anesthetic concentration was adjusted for age to obtain approximately 1.2 MAC (minimum alveolar concentration). Desflurane was administered from an Ohmeda Tec 6 vaporizer (Ohmeda, Helsinki, Finland), and isoflurane was administered by an Ohmeda Isotec 5 (BOC Healthcare). The end tidal concentrations of the volatile anesthetics and the ETCO2were monitored continuously by an infrared analyzer. No other anesthetics were administered until the dura was incised. Mean arterial blood pressure (MAP) and heart rate (HR) were kept within 20% of baseline values with the use of esmolol, ephedrine, or phenylephrine. Fentanyl 1–4 µg · kg-1 · h-1 was administered for any signs of light anesthesia (tachycardia, MAP increased above baseline) throughout the procedure. LCSFP, MAP, ETCO2, hemoglobin oxygen saturation, and CPP were monitored continuously and recorded every 5 min until the cranial dura was opened.
Recovery variables were measured as time from discontinuation of anesthetic. This study looked at both time to spontaneous eye opening and ability to follow commands (wiggle toes and squeeze fingers on command).
The primary variable was the maximum change in LCSFP and CPP from baseline. To obtain a power of 80% with a two-tailed significant level at 0.05, a minimum of 13 patients were required to complete each treatment group to detect a difference of 7 mm Hg with a standard deviation of 6 mm Hg. Thus, the sample size was chosen at 18 patients per treatment group to allow up to 5 patients per group to drop out (none did).
CPP was calculated as MAP minus LCSFP. Gender and ASA physical status were compared using Fisher’s exact test. Age was compared with the two-sample Student’s t-test. All P values for LCSFP, MAP, and CPP were obtained using the two-sample Student’s t-test unless otherwise noted. Comparison of recovery data used the two-sample Student’s t-test. Additional analysis performed on the data included scatter plots to identify any outlier data values and temporal plots to examine a possible trend for the variables over time. All statistical analyses were based on a two-sided test, and P values of 0.05 or less was considered statistically significant. All data are reported as mean ± standard deviation unless otherwise noted.
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Results |
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The two groups did not differ significantly in demographic variables or in initial tumor size (Table 2). Baseline CPP, LCSFP, and MAP were not significantly different between the two groups. Eight patients in the desflurane and eight patients in the isoflurane group required treatment of intraoperative hypotension. One patient at the University of Western Ontario site differed from the study protocol in that a preoperative MRI revealed two meningiomas and tumor size was not calculated because of two separate tumor sites. Additionally, three patients were included in the study whose preliminary radiographic images were felt to show evidence of mass effect. However, official reports of the MRIs did not include cerebral edema or midline shift. There was no difference between the 2 groups in either the number of patients requiring fentanyl or the dose of fentanyl administered (desflurane group, 239 ± 170 µg; isoflurane group, 204 ± 212 µg; P = 0.6448). In the desflurane Group 14 of 18 patients required additional fentanyl after induction, and 13 of 18 required fentanyl in the isoflurane group (P = 1.000). Patients in the desflurane group received 6 ± 2 mg of midazolam, and patients in the isoflurane group received 4 ± 2 mg of midazolam before initiation of volatile anesthetic.
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LCSFP did not differ significantly between the 2 groups at any time throughout surgery (Fig. 1). Although there were 5 time points at which the isoflurane group had a statistically significant increase from baseline in LCSFP when compared with desflurane, three of these points were within the first 20 min and the increase was 2 mm Hg at most.
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Mean CPP was not significantly different between the two groups except at two time points (5 and 130 min postinduction). At 5 min postinduction the isoflurane group had a lower CPP that approached significance (P = 0.0567), and at 130 min the desflurane group had a lower value (Fig. 2). However, at 130 min postinduction only 4 of 18 patients remained in the desflurane group and 4 of 18 remained in the isoflurane group, limiting the conclusions that can be drawn from these data. The difference at 130 min was a result of an increased MAP in the isoflurane group rather than an increase in LCSFP or decrease of MAP in the desflurane group.
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Mean hemodynamic variables (MAP, HR) were not different between the two groups (Fig. 3) except MAP at 5 and 130 min postinduction. There was not a statistically significant difference in MAP change from baseline at 130 min postinduction. At that time point only 4/18 patients remained in each group.
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Recovery variables are shown in Table 3. Data from one patient in the desflurane group were excluded because of delayed ability to follow commands (56 h) that was the result of the patient’s surgery and was felt not to be attributable to the anesthetic used. Both time to opening eyes and following commands were roughly 50% shorter in the desflurane group, but these differences did not reach statistical significance.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present study demonstrated that the LCSFP was not significantly different between desflurane and isoflurane administered at 1.2 MAC in patients undergoing supratentorial tumor resection with hypocapnia. The 4 time points at which isoflurane patients had lower LCSFP when compared with baseline were not clinically meaningful (difference from baseline was 2 mm Hg at most).
Additionally, MAP and HR did not differ significantly between the two groups except at 5 minutes postbaseline. Finally, CPP was not significantly different between the two groups except at one time point (130 minutes) when the desflurane group had a lower CPP. This difference was a result of increased MAP in the isoflurane group and not increased LCSFP in the desflurane group.
A potential drawback of our study was the assumption that LCSFP correlated with ICP. These patients were free of any pathology that would be likely to obstruct the CSF pathways between the intracranial contents and the lumbar CSF. Immediately after insertion of the subarachnoid catheter, an appropriate increase of LCSFP was noted with head elevation indicating an intact pathway at the onset of the study. Additionally, this study did not address the effects of desflurane and isoflurane in patients with severe intracranial hypertension. The effects of desflurane and isoflurane in these patients may differ significantly from this study because of the loss of autoregulation.
Although mean time to opening eyes and following commands were roughly 50% shorter in the desflurane group compared with the isoflurane group, there was large variability in the recovery data, indicating the number of patients needed to show a significant difference to be larger than the number of patients enrolled in this study. The time from cessation of anesthesia to discharge from the recovery room in both the desflurane and isoflurane groups was longer than would typically be expected. This may be a result of the length of surgery or underlying tumor pathology. Additionally, the study protocol required the volatile anesthetic be continued at 1.2 MAC until surgery was completely over and dressings were in place.
The differing results from the previous study conducted by Muzzi et al.1 are difficult to reconcile. However, as previously mentioned, other studies have failed to demonstrate a significant difference between desflurane and isoflurane on LCSFP and blood flow in neurosurgical patients (4,8). Ebrahim et al.2 studied 22 patients with 1 MAC of desflurane or isoflurane and showed no difference in LCSFP while undergoing craniotomy for intracranial mass lesions. There was also no difference found by Muzzi et al. (8) at 0.5 MAC of desflurane in 50% nitrous oxide (N2O) in patients with supratentorial tumors.1 The results of the canine studies, without intracranial pathology, (7,10,11) have shown trivial effects of desflurane on ICP.
The uptake and recovery characteristics of desflurane offer potential advantages in neurosurgical patients in whom rapid differentiation of residual drug effect from operative sequelae is desirable at the conclusion of surgery. The concern regarding increases in ICP observed in some previous studies (7,8) have limited the use of desflurane in neurosurgical patients. The existing human data on the effects of desflurane on ICP are limited and controversial. In a study of 10 patients, Muzzi et al. (8) compared a single dose (1 MAC) of desflurane and isoflurane during surgery in hypocapnic (PaCO2, 24–28 mm Hg) patients with supratentorial mass lesions. They found a gradual increase of LCSFP (from 11 ± 4 mm Hg to 18 ± 6 mm Hg) during administration of desflurane but not isoflurane. In the previously mentioned study by the same group1 the administration of 0.5 MAC desflurane in 50% N2O was associated with no change in the CSF pressure as compared with baseline. It is difficult to reconcile these two clinical studies, except that the latter was done with N2O and half as much desflurane. Unlike Muzzi et al. (8), Talke et al. (12) found an increase in LCSFP at 0.5 and 1.0 MAC of both desflurane and isoflurane under normocapnic conditions. Ornstein et al. (9) examined the effect of 1.0 and 1.5 MAC desflurane and isoflurane on CBF in patients with intracranial mass lesions. They found that desflurane and isoflurane had similar effects on absolute CBF, a lack of change in cerebral blood flow in response to increasing concentration of either anesthetic, and preservation of carbon dioxide reactivity at 1.25 MAC of either anesthetic.
In our study the LCSFP in the desflurane group did not change significantly from baseline after the initiation of volatile anesthetic at 1.2 MAC and mild hypocapnia. The only difference between this study and the earlier study by Muzzi et al.1 was that in our study all patients received preoperative dexamethasone and were kept at 1.2 MAC of volatile anesthetics. Although large-dose steroids have been shown to reduce the ICP (13–15), the efficacy of small-dose dexamethasone has not been clearly demonstrated. There may have been other factors such as surgical technique or a selection bias that would account for the differing results.
Finally, the clinical significance of the increases in LCSFP seen in other studies (10–18 mm Hg) is unclear. Normal ICP is 0–15 mm Hg with levels over 20 mm Hg being considered abnormal. ICP values between 20–40 mm Hg are considered to be moderate intracranial hypertension. An ICP over 40 mm Hg may represent life-threatening intracranial hypertension (16). Ryder et al. (17) showed that patients could tolerate pressures up to 110 mm Hg when ICP was artificially increased with saline infusions. Therefore, it is not the absolute pressure but the interaction between pressure and underlying pathology that causes the clinical sequelae of increased ICP.
In summary, the purpose of our study was to clarify the contradictory results found in previous studies in patients undergoing craniotomy for supratentorial lesions. Our findings indicate that desflurane does not increase LCSFP in patients undergoing craniotomy when patients are maintained in a hypocapnic state.
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Footnotes |
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1 Muzzi D, Daltner C, Losasso T, et al. The effect of desflurane and isoflurane with N2O on cerebrospinal fluid pressure in patients with supratentorial mass lesions [abstract]. Anesthesiology 1991;75:A167.
2 Ebrahim ZY, Schubert A. The effect of desflurane and isoflurane on intracranial pressure in patients with small intracranial tumors [abstract]. Anesthesiology 1993;79:A182.
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