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CLINICAL INVESTIGATION
Year : 2009  |  Volume : 53  |  Issue : 1  |  Page : 44-51 Table of Contents     

Subdural Pressure and Brain Condition During Propofol Vs Isoflurane - Nitrous Oxide Anaesthesia in Patients Undergoing Elective Supratentorial Tumour Surgery


1 Assistant Professor, Neuro ICU and Pain Clinic, Bangur Institute of Neurosciences & Psychiatry,Kolkata, India
2 Professor, Department of Neuro Anaesthesiology, Neuro ICU and Pain Clinic, Bangur Institute of Neurosciences & Psychiatry,Kolkata, India

Date of Web Publication3-Mar-2010

Correspondence Address:
Bibhukalyani Das
Professor, Department of Neuro Anaesthesiology, Neuro ICU and Pain Clinic, Bangur Institute of Neurosciences & Psychiatry,Kolkata
India
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PMID: 20640077

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Total intravenous anaesthesia has received much importance than inhalational anaesthesia in neuroanaesthetic practice. In an effort to determine whether any important clinical differences occur, studies concerning intracranial pressure (ICP), degree of dural tension and degree of brain swelling during intravenous and inhalational based anaes­thesia are warranted like the present one.
A total of 68 patients were assigned randomly to one of two groups. In Group-I(n=34), anaesthesia was induced with propofol (1-3mg.kg -1 ) and maintained with propofol (6-10mg.kg -1 .hr -1 ) and fentanyl (2-3mcg.kg -1 .hr -1 ). In Group­ II (n=34), anaesthesia was induced with propofol (1-3mg.kg -1 ) but maintained with isoflurane, nitrous oxide and fentanyl (2-3mcg.kg -1 .hr -1 ). Moderate hypocapnia was applied to maintain arterial carbon dioxide around 30mmHg. Mean arterial blood pressure was stabilized with phenylephrine whenever necessary. Subdural intracranial pressure, mean arterial pressure, cerebral perfusion pressure were monitored before and after 10min period of hyperventila­tion. Furthermore, the tension of dura before and after of hyperventilation and the degree of brain swelling after opening of dura were also estimated by the neurosurgeon.
No differences were found between the groups with regards to demographics, neuroradiologic diagnosis, posi­tion of head and time of ICP measurement. Before hyperventilation, both ICP and dural tension were significantly lower in Group I compared with Group-II (P<0.05). But after hyperventilation there was no significant difference of ICP and dural tension in between groups. The degree of brain swelling after opening of dura was similar in both groups. There was a positive correlation between measured ICP and brain swelling score.

Keywords: Subdural pressure, Cerebral perfusion pressure, Propofol, Isoflurane- nitrous oxide, Hyperventilation, Supratentorial tumour


How to cite this article:
Santra S, Das B. Subdural Pressure and Brain Condition During Propofol Vs Isoflurane - Nitrous Oxide Anaesthesia in Patients Undergoing Elective Supratentorial Tumour Surgery. Indian J Anaesth 2009;53:44-51

How to cite this URL:
Santra S, Das B. Subdural Pressure and Brain Condition During Propofol Vs Isoflurane - Nitrous Oxide Anaesthesia in Patients Undergoing Elective Supratentorial Tumour Surgery. Indian J Anaesth [serial online] 2009 [cited 2013 May 20];53:44-51. Available from: http://www.ijaweb.org/text.asp?2009/53/1/44/60256


   Introduction Top


Major goals of neurosurgical anaesthesia are main­tenance of haemodynamic stability, sufficient cerebral perfusion pressure, relaxed brain to facilitate neurosur­gical resection and avoidance of agents or procedures that increase intracranial pressure (ICP).

There has been long standing controversy regard­ing use of inhalational or intravenous anaesthetic agent for intracranial procedure. Total intravenous anaesthe­sia has always received much importance to avoid ce­rebral vasodilating effect of nitrous oxide (N 2 O) and volatile agents. But so far no study comparing intrave­nous with volatile based anaesthesia has been able to demonstrate major outcome difference [1],[2] . However most ofthese studies examined a heterogenous patient population and ICP measured bydifferent techniques.

Several experimental and clinical studies of cere­bral haemodynamics including cerebral blood flow (CBF), cerebral metabolism for oxygen (CMRO 2 ), ICP have been conducted during isoflurane [3],[4] , propofol [5][6],[7] anaesthesia. Only few comparative studies of ICP are available. In one prospectivetrial, where three anaes­thetic techniques (isoflurane-N 2 O, N 2 O-fentanyl, propofol-fentanyl) were used for elective supratento­rial craniotomy, epidural ICP was measured through burrhole.Though ICP did not differ significantly, more patients with isoflurane- N 2 O group had ICP greater than 24mmHg as compared to other two groups [1] .Other studies monitoring lumbar cerebrospinal fluid (CSF) pressure demonstrated conflicting results, either no dif­ference of ICP during propofol versus thiopentone­isoflurane anaesthesia [2] or significantly lower ICP dur­ing propofol compared to isoflurane [8] .

During craniotomy one of the most critical point is opening of dura where a high ICP may cause some degree of brain swelling [9] . Subdural ICP measurement after removal of bone flap is a regional estimateof ICP which is influenced by presence of space occupying lesion (SOL) [10] and gravity [11] . In one study, thelevel of subdural ICP and intraventricular pressure correlated well with the dural tension and the degree of brain swell­ing after opening of dura, estimated by neurosurgeons, blinded to the level of ICP [12] . In a recent trial, subdural ICP and incidence of brain swelling after opening of dura were significantly lower during propofol anaes­thesia when compared to isoflurane and sevoflurane. [13]

The primary goal of present study was to detect any difference insubdural ICP occured during propofol versus isoflurane-nitrous oxide anaesthesia along with the effect of hyperventilation in patients undergoing elec­tive craniotomy for supratentorial tumour. Degree of dural tension and brain swelling after openingof the dura were also studied as secondary objectives.


   Methods Top


The study was undertaken at Bangur Institute of Neuroscience and Psychiatry after approval of the pro­tocolby local ethical committee. It was a prospective randomized trial. Verbal and written consent was taken from all patients.

Sixty eight patients of age 18 to 65 years, of either sex, American Society of Anesthesiologists physical status I and II, GlasgowComa Scale (GCS) of 15 un­dergoing elective craniotomy for supratentorial tumour resection were randomly allocated in one of the two groups. Group I- Propofol (n= 34), Group II­I soflurane-nitrousoxide (n=34).

Patients diagnosed as having supratentorial tumour with midline shift of less than 10mm (revealed by cere­bral computed tomography or magnetic resonance im­aging) were included in this study. Medically controlled hypertension or diabetes mellitus were also included.

Patients were excluded if they suffered from ischaemic heart disease, congestive heart failure, renal or hepatic dysfuntion, or severe chronic respiratory dis­ease.


   Anaesthesia And Monitoring Top


The patients were premedicated with 150mg oral ranitidine one hour prior to anaesthesia. Preoperative corticosteroid, anticonvulsant, antihypertensive were administered as usual. Monitoring before induction con­sisted of automated noninvasive blood pressure, con­tinuous electrocardiogram and pulse oximetry. After induction of anaesthesia, a radial artery catheter was inserted with zero pressure adjustment at mid-axillary line for continuous blood pressure monitoring and blood sampling. Urine output and rectal temperature were continuously monitored throughout the procedure. In­spired and end-tidaloxygen, carbon dioxide, nitrous oxide and isoflurane were measured. Lungs were mechanically ventilated to maintain an arterial blood car­bon-dioxide tension between 30-40 mmHg and inspira­tory peak pressure less than 20cm of H 2 O. Train of­ four was used to monitor muscular relaxation which was achieved by acontinuous infusion of atracurium. The anaesthetic procedures were as follows.

Group-I : Propofol

Anaesthesia was induced with 1-3mg.kg -1 propofol over 1min and 2-4 mcg.kg -1 fentanyl. Lidocaine 1mg.kg -1 was administered over 1 minute followed by muscle relaxation with 0.5mg.kg -1 atracurium. After 3 minutes of mask ventilation with 100% oxygen, tra­chea was intubated. Lungs were mechanically venti­lated with oxygen in air (fraction of oxygen 0.5). Anaesthesia was maintained with infusion of propofol (6­10mg.kg -1 .hr -1 ) and fentanyl (2-3mcg.kg. -1 hr -1 ). Rate of propofol infusion was adjusted to maintain adequate depth of anaesthesia. Just before skin incision of scalp, fentanyl 1mcg.kg -1 was supplemented. Infusion rate of propofol and fentanyl were kept unchanged during ICP measurement and during estimation of dural tension.

Group-II:Isoflurane-nitrous oxide

Anaesthesia was induced with 1-3 mg.kg -1 propofol over 1min and 2-4mcg.kg -1 fentanyl. Lidocaine 1mg.kg -1 was administered over 1minute followed by muscle relaxation with 0.5mg.kg -1 atracurium. After 3 minutes of mask ventilation with 100% oxygen, tra­chea was intubated. Lungs were mechanically venti­lated with 50% nitrous oxide in oxygen (fraction of oxygen 0.5). Isoflurane was added to the inspired gas mixture and concentration was increased in 0.2% in­crements for maintaining adequate depth of anaesthe­sia. Fentanyl infusion was administered (2-3mcg.kg -1 .hr­1 ) as in Group-I. Just before skin incision of scalp fen­tanyl 1mcg.kg -1 was supplemented. Infusion rate of fen­tanyl and percentage of isoflurane were kept unchanged during ICP measurement and during estimation of du­ral tension.

Intravenous phenylephrine was administered if systolic blood pressure decreased greater than 20mmHg of baseline inspite of normal saline infusion. Mannitol 0.75gm.kg -1 was administered to all patients while mak­ing first burr hole.

Subdural Intracranial Pressure measurement, Es­timation of Duraltension and Brain swelling:

After removal of bone flap, a 22G/0.8mm venflon cannula was placed under dura and connected to a pressure transducer system via a polyethylene catheter. Zero level of ICP was adjusted with the transducer kept at the levelof orbitomeatal line. After 1minute of stabilization mean valueof subdural pressure was used as an estimate of ICP. After initial measurement of ICP, pulmonary ventilation was increased by 30% (increas­ing rate and tidal volume) for 10min. Subdural ICP was again measured at 11 th min after first measurement. Cerebral perfusion pressure (CPP) was calculated as the difference between mean arterial pressure (MAP) and ICP.

Estimation of dural tension was made in a scale of four, using tactile evaluation by neurosurgeon. Neurosurgeons were blinded to anaesthetic technique. The tension was categorized as follows: (1) very slack (2) normal (3) increased tension (4) pronounced in­creased tension. The degree of brain swelling was evaluated by then eurosurgeon after opening of the dura. Degree of swelling was estimated and categorized as follows (1) no swelling, excellent operating condition (2) minimum swelling (3) moderate swelling and (4) pronounced swelling of the brain.


   Statistical Analysis Top


Based on a previous study of ICP, given a mini­mal detectable significant difference of 3.5mmHg, ex­pected SD 5.0mmHg, power of 0.80, and a statistical significance levelof P<0.05, the total sample size (num­ber of patients) was calculated to be 68. Data within groups were tested for normal distribution. Two sample t-test was applied for parametric data (ICP, MAP, CPP). Chi-square test was used for analysis of demo­graphic data, localization, size and histopathologic di­agnosis of the tumours, preoperative drug administra­tion between the groups. Difference in dural tension and brain swelling were tested by chi-square test in 2x4 tables. For correlation, Pearson product moment correlation and line arregression were performed. Data were expressed as mean ±SD. P<0.05 was consid­ered statistically significant.


   Results Top


A total of 68 patients were enrolled in the study with equal number of 34 patients in each group. De­mographic data are shown in [Table 1]. There were no significant differences between the groups in terms of age, sex, weight and ASA grading.

Clinical data including time interval between in­duction and ICP measurement and vasopressor admin­istration are shown in [Table 2]. There were no differ­ence in neurological diagnosis (site, type and size of tumour) and number of patients taking antihyperten­sive or anticonvulsant. The number of patients requir­ing blood pressure support, differed significantly be­tween groups and total dose of vasopressor used also was significantly higher in propofol group than isoflurane-nitrousoxide group.

After removal of bone flap subdural ICP, MAP were measured and CPP was derived and are summa­rized in [Table 3]. Before hyperventilation, there was no significant difference of MAP and CPP in between groups but subdural ICP was significantly lower in propofol group than isoflurane-nitrous oxide group. After hyperventilation ICP decreased significantly in isoflurane-nitrous oxide group. Difference in PaCO 2 (before and after hyperventilation) was greater in propofolgroup but reduction in ICP after hyperventi­lation was significantly smaller as compared to isoflurane-nitrous-oxide group.

The dural tension before and after hyperventilation as estimated by neurosurgeon, are shown in [Table 4].

Before hyperventilation, dural tension was significantly higher in isoflurane-nitrous oxide group but after hy­perventilation there was no significant difference in be­tween groups. Degree of brain swelling after opening of dura, as shown in [Table 5], was similar in both groups.

There was a positive correlation between mea­sured ICP and brain swelling score as well as neuro­logical data (tumoursize and midline shift) and brain swelling score.


   Discussion Top


Different anaesthetic agents have different effects on cerebral haemodynamics. For example, propofol decreases CBF, ICP and may decrease cerebral per­fusion pressure via its effects on blood pressure. [14] Isoflurane appears to produce moderate increase in CBF and pronounced decrease in cerebral metabo­lism. An increase in ICP caused by it may be mild and can be prevented by hypocapnia [15] . Several groups have shown that it can increase ICP or decrease cerebral perfusion pressure in neurosurgical patients. [16],[17],[18] Nitrous oxide is also a potent vasodilator and can increase CBF and ICP when given either alone or in combination with a volatile agent. [19],[20],[21] But this increase can be attenuated by prior administration of thiopentone and hypocap­nia [22] . Opioids are assumed to have no important ef­fects as long as ventilation is controlled. Recently sufentanil, alfentanil and fentanyl have been reported to increase ICP and CBF [23],[24] although this has not been observed uniformly [25] and all three drugs have been used successfully in neuroanaesthesia.

Despite these concerns, there is no clinical evi­dence that one particular anaesthetic management regi­men is superior to other. The few available compara­tive trials suggest no important difference between propofol versus isoflurane, nitrous oxide versus no ni­trous oxide. [2],[26],[27] In the current study, we found that subdural ICP and the degree of dural tension were sig­nificantly lower during propofol anaesthesia as com­pared to isoflurane-nitrous oxide anaesthesia but after hyperventilation there was no statistical difference be­tween two groups. Both before and after hyperventila­tion, a significantly lower CPP was found in propofol group. A significant difference was found regarding phe­nylephrine administration with regard to number of pa­tients and total dose requirement.

In comparative studies of lumbar CSF pressure in patients without space occupying lesion subjected to desflurane, isoflurane, sevoflurane and propofol ana­esthesia, a higher CSF pressure was found during vola­tile anaesthesia compared with propofol anaesthesia [8],[16] . In another study of lumbar CSF pressure in neurosur­gical patients subjected to either propofol-fentanyl or thiopental- isoflurane-fentanyl anaesthesia, no signifi­cant difference of lumbar CSF pressure was recorded [2] .

Subdural pressure is more accurate as a regional estimate [10],[11] compared with lumbar CSF pressure mea­surement because tumour or cerebral edema localized close to craniotomy increases subdural pressure more than lumbar CSF pressure. In addition, obliteration of CSF pathway caused by tumour makes lumbar CSF pressure less reliable. No significant difference in epi­dural ICP was recorded in another comparative study of propofol and isoflurane-nitrous oxide anaesthetized patients. [1] In principle, their findings corroborate with those of current study. Methodologic differences in ICP monitoring might explain the comparatively lower ICP values in our study.

In this study, brain swelling after opening of dura was similar in both groups. Neurosurgeons were blinded to anaesthetic technique. In another study no differ­ence was mentioned regarding brain swelling between isoflurane-N 2 O and propofol/fentanyl group [1] . How­ever, a significant correlation was found between brain swelling score and ICP.

In clinical studies, cerebral autoregulation is pre­served with propofol but is impaired during 1.5 MAC isoflurane. [28],[29] As such, a higher CPP during isoflurane ­nitrous oxide anaesthesia should elicit a decrease in ICP. The question of whether cerebral autoregulation influ­ences ICP is further complicated by the fact that cere­bral autoregulation is impaired or abolished in patients with cerebral tumours. [30] In this study, isoflurane ad­ministration was restricted to well defined and low MAC level (1 MAC) and maintenance doses of propofol and fentanyl were well defined. Accepted mean arterial blood pressure reduction was 20%, oth­erwise vasopressor was administered.

In this study, the decrease in ICP after hyperven­tilation averaged 1.5mmHg in the propofol group but 3mmHg in isoflurane-N 2 O group. The significantly greater decrease in ICP during isoflurane-nitrous ox­ide anaesthesia may be due to better carbon dioxide responsiveness. This is in agreement with other clinical studies indicating a preserved carbon dioxide reactiv­ity during anaesthesia with isoflurane [4],[31] but decreased carbon dioxide reactivity during anaesthesia with propofol. [32],[33]

It is tempting to conclude that one anaesthetic regi­men is better than other. Each anaesthetic has advan­tages and disadvantages. As noted, isoflurane and ni­trous oxide are vasodilators and both can increase ICP. In contrast, total intravenous anaesthesia consisting of propofol and fentanyl (without nitrous oxide) should reduce CBF and ICP. But combination of low dose isoflurane with nitrous oxide and fentanyl might cause an intermediate increase in CBF and ICP because concentration of either drug can be decreased than con­centration of any agent when using alone to provide an anaesthetic plane required for surgical resection. None of the anaesthetic was associated with any intra opera­tive difficulties.

We designed the current trial in such a manner that the subject population was as uniform as possible and we restricted the trial to patients with known su­pratentorial tumours with midline shift less than 10mm. Although supratentorial surgery in patients with large tumour might reveal differences, in this study, any sig­nificant difference in subdural ICP and brain condition for surgery after hyperventilation was not revealed in both groups. Limitation of the study were firstly inabil­ity to estimate carbon dioxide reactivity, inability to define absolute end points of anaesthesia in both groups in absence of anaesthetic depth monitor.

The current study indicates that during craniotomy for supratentorial cerebral tumours, subdural ICP is lower in patients anaesthetized with propofol than isoflurane-nitrous oxide. After hyperventilation, there were no significant difference of ICP and dural tension. Degree of brain swelling after opening of dura was simi­lar in both groups. CPP was higher, may be due to better preservation of carbon dioxide responsiveness in isoflurane-nitrous oxide group as compared with propofol group. These results support the view that despite their cerebrovascular effects, institution of hyperventilation makes both anaesthetic regimens equally acceptable for intracranial tumour surgery.



 
   References Top

1.Todd MM, Warner DS, Sokoll MD, et al. Aprospective, comparative trial of three anesthetics for elective su­pratentorial craniotomy.Propofol/ Fentanyl, Isoflurane/ Nitrous Oxide, and Fentanyl/Nitrous Oxide.Anesthesi­ology1993;78: 1005-20.  Back to cited text no. 1      
2.Ravussin P, Tempelhoff R, Modica PA, Bayer-Berger MM. Propofol vs thiopenthal-isoflurane for neurosur­gical anesthesia: Comparison of hemodynamics, CSF pressure and recovery. J Neurosurg Anesthesiol 1991; 3:85-95.  Back to cited text no. 2      
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7.Oshima T, Karasawa F, Satoh T. Effects of propofol on cerebral blood flow and the metabolic rate of oxygen in humans.Acta Anaesthesiol Scand 2002;46: 831-35.  Back to cited text no. 7      
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9.Bundgaard H, Landsfeldt U, Cold GE. Subdural moni­toring of ICP during craniotomy: Thresholds of cere­bral swelling/ herniation. ActaNeurochir Suppl (Wien) 1998;71:276-8.  Back to cited text no. 9      
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11.Bundgaard H, Cold GE. Studies of regional subdural pressure gradients during craniotomy. Br J Neurosurg 2000;14:229-34.  Back to cited text no. 11      
12.Cold GE, Tange M, Jensen TM, Ottesen S. Subdural pressure measurement during craniotomy: Correlation with tactile estimation of dural tension and brain her­niation after opening of dura. Br J Neurosurg 1996; 10:69-75.  Back to cited text no. 12      
13.PetersenKD, Landsfeldt U, Cold GE,et al. Intracanial pressure and cerebral hemodynamic in patients with cerebral tumors. ARandomized prospective studyof patients subjected to craniotomy in propofol- fenta­nyl, isoflurane- fentanyl, sevoflurane-fentanyl anes­thesia.Anesthesiology2003; 98: 329-36.  Back to cited text no. 13      
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15.Grosslight K, Foster R, Colohan AR, Bedford RF. Isoflurane for neuroanesthesia: Risk factors for in­creases in intracranial pressure.Anesthesiology1985; 63:533-36.  Back to cited text no. 15      
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23.Marx W, Shah N, Long C, Arbit E, Galcich J, Mascott C, Mallya K, Bedford R. Sufentanil, alfentanil and fentanyl : Impact on cerebrospinal fluid pressure in patients with brain tumors. J NeurosurgAnesth 1989;1: 3-7.  Back to cited text no. 23      
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26.Lampe GH,WaukIZ, Donegan JH, PittsLH, Jackler RK, Litt LL, Rampil IJ, Eger EI. Effect on outcome of pro­longed exposure of patients to nitrous oxide. Anesth Analg1990;71: 586-90.  Back to cited text no. 26      
27.Grundy BL, Pashayan AG, Mahla ME, Shah BD. Three balanced anaesthetic techniques for neuroanaesthesia: Infusion of thiopental sodium with sufentanil or fenta­nyl comparedwithinhalation of isoflurane.JClinAnesth 1992;4:372-77.  Back to cited text no. 27      
28.Van Hemelrijck J, Fitch W, Mattheussen M, Van Aken H, Plets C, Lauwers T. Effect of propofol on cerebral circulation and auto-regulation in the baboon. Anesth Analg1990;71: 49-54.  Back to cited text no. 28      
29.Strebel S, Lam AM, Matta B, Mayberg TS, Aaslid R, Newell DW. Dynamicand static cerebral autoregulation during isoflurane, desflurane, and propofol anesthesia. Anesthesiology1995;83: 66-76.  Back to cited text no. 29      
30.Endo H, Larsen B, Lassen LA. Regional cerebral blood flow alterations remote from the site of intracranial tu­mors.JNeurosurg1977;46: 271-81.  Back to cited text no. 30      
31.Inada T, Shingu K, Uchida M, Kawachi S, Tsushima K, Niitsu T. Changes in the cerebral arteriovenous oxygen content difference by surgical incision are similar dur­ing sevoflurane and isoflurane anaesthesia. Can J Anaesth1996;43: 1019-24.  Back to cited text no. 31      
32.Harrison JM,Girling KJ, Mahajan RP.Effects of target­controlled infusion of propofol on the transient hyperaemic response and carbon dioxide reactivity in the middlecerebralartery.Br JAnaesth1999; 83: 839-44.  Back to cited text no. 32      
33.CenicA, GraenRA, Howard-Lech VL. LeeTY, GelbAW. Cerebral blood volume and blood flow at varying arte­rial carbon dioxide tension levels in rabbits during propofol anesthesia. AnesthAnalg 2000; 90: 1376-83.  Back to cited text no. 33      



 
 
    Tables

  [Table 2], [Table 2], [Table 3], [Table 4], [Table 5]



 

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