Intracranial Pressure and Cerebral Hemodynamic in Patients with Cerebral Tumors: A Randomized Prospective Study of Patients Subjected to Craniotomy in Propofol-Fentanyl, Isoflurane-Fentanyl, or Sevoflurane-Fentanyl Anesthesia

Background: A critical point during craniotomy is opening of dura, where a high intracranial pressure (ICP) results in swelling of cerebral tissue. Controlled studies concerning ICP, degree of dural tension, and degree of cerebral swelling are therefore warranted.

Methods: In an open-label study, 117 patients with supratentorial cerebral tumors were randomized to propofol-fentanyl (group 1), isoflurane-fentanyl (group 2), or sevoflurane-fentanyl anesthesia (group 3). Normo- to moderate hypocapnia was applied, with a target level of arterial carbon dioxid tension of 30-40 mmHg. Mean arterial blood pressure was stabilized with intravenous ephedrine (2.5-5 mg) if necessary. Subdural ICP, mean arterial blood pressure, cerebral perfusion pressure (CPP), arteriovenous oxygen difference (AVDo2), internal jugular vein oxygen saturation were monitored before and after a 10-min period of hyperventilation, and the carbon dioxide reactivity was calculated. Furthermore, the tension of dura before and during hyperventilation and the degree of cerebral swelling during hyperventilation and after opening of the dura were estimated by the neurosurgeon.

Results: No differences were found between groups with regard to demographics, neuroradiologic examination, positioning of the head, and time to ICP measurement. Before and during hyperventilation, ICP was significantly lower and mean arterial blood pressure and CPP significantly higher in group 1 compared with groups 2 and 3 (P < 0.05). The tension of dura before and during hyperventilation was significantly lower in group 1 compared with group2 (P < 0.05), but not significantly different from group 3. In group 1, cerebral swelling after opening of dura was significantly lower compared with groups 2 and 3 (P < 0.05). Furthermore, AVDo2 was significantly higher and jugular vein oxygen saturation and carbon dioxide reactivity were significantly lower in group 1 compared with groups 2 and 3 (P < 0.05). No significant differences with regard to ICP, CPP, AVDo2, carbon dioxide reactivity, and jugular vein oxygen saturation were found between patients anesthetized with isoflurane and sevoflurane.     

The effects of isoflurane and desflurane on intracranial pressure,cerebral perfusion pressure,and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors

BACKGROUND: Desflurane is a volatile anesthetic agent with low solubility whose use in neurosurgery has been debated because of its effect on intracranial pressure and cerebral blood flow. The purpose of this study was to determine the variations on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as well as on cerebral arteriovenous oxygen content difference (AVDo(2)) in normocapnic patients scheduled to undergo removal of supratentorial brain tumors with no evidence of mass effect during anesthesia with isoflurane or desflurane. METHODS: In 60 patients scheduled to undergo craniotomy and removal of supratentorial brain tumors with no evidence of midline shift, anesthesia was induced with intravenous fentanyl, thiopental, and vecuronium and was maintained with 60% nitrous oxide in oxygen. Patients were assigned to two groups randomized to receive 1 minimum alveolar concentration isoflurane or desflurane for 30 min. Heart rate, mean arterial pressure, intraparenchymal ICP, and CPP were monitored continuously. Before and after 30 min of continuous administration of the inhaled agents, AVDo(2) was calculated. RESULTS: There were no significant differences between groups in heart rate, mean arterial pressure, ICP, and CPP. ICP measurements throughout the study did not change within each group compared to baseline values. Mean arterial pressure decreased significantly in all patients compared to baseline values, changing from 105 +/- 14 mmHg (mean +/- SD) to 85 +/- 10 mmHg in the isoflurane group and from 107 +/- 11 mmHg to 86 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). CPP also decreased within each group compared with baseline values, changing from 95 +/- 15 mmHg to 74 +/- 11 mmHg in the isoflurane group and from 95 +/- 16 mmHg to 74 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). Cerebral AVDo(2) decreased significantly in both groups throughout the study, changing from 2.35 +/- 0.77 mm to 1.82 +/- 0.61 mm (mmol/l) in the isoflurane group (P < 0.05) and from 2.23 +/- 0.72 mm to 1.94 +/- 0.76 mm in the desflurane group (P < 0.05), without differences between groups. CONCLUSIONS: The results of this study indicate that there are no variations on ICP in normocapnic patients undergoing removal of supratentorial brain tumors without midline shift, as they were anesthetized with isoflurane or desflurane. CPP and cerebral AVDo(2) decreased with both agents.     

The effects of indomethacin on intracranial pressure and cerebral haemodynamics in patients undergoing craniotomy: a randomised prospective study

We compared the effects of indomethacin (bolus of 0.2 mg.kg-1 followed by an infusion of 0.2 mg.kg-1.h-1) and placebo on intracranial pressure and cerebral haemodynamics in 30 patients undergoing craniotomy for supratentorial brain tumours under propofol and fentanyl anaesthesia. Indomethacin was given before induction of anaesthesia and the infusion was terminated after opening of the dura. Subdural intracranial pressure was measured through the first burr hole and before opening the dura. Cerebral blood flow velocity, cerebral perfusion pressure, jugular bulb oxygen saturation, arterio-venous oxygen difference and carbon dioxide reactivity were measured; dural tension and the degree of brain swelling were estimated. Before induction of anaesthesia, indomethacin administration was associated with a significant decrease in cerebral blood flow velocity compared with placebo. After induction of anaesthesia, cerebral blood flow velocity and mean arterial blood pressure decreased significantly in both groups. Indomethacin was not associated with a decrease in intracranial pressure. There were no differences in cerebral perfusion pressure, dural tension or degree of brain swelling between the two groups. Carbon dioxide reactivity measured after induction of anaesthesia was significantly lower in the indomethacin group (p < 0.05). After removal of the bone flap, no significant difference in carbon dioxide reactivity was observed. We suggest that these findings are explained by propofol-induced cerebral vasoconstriction.     

Effect of alfentanil on intracranial pressure during propofol-fentanyl anesthesia for craniotomy. A randomized prospective dose-response study

BACKGROUND: The effect of alfentanil on intracranial pressure (ICP) in patients with supratentorial cerebral tumors has only been sparsely examined and with somewhat contradictory results. METHODS: Thirty-one patients were anesthetized with propofol and fentanyl. After removal of the bone flap a bolus-dose of alfentanil 10 (group 1), 20 (group 2), or 30 microg kg(-1) (group 3) was administered followed by an infusion of 10, 20, or 30 microg.kg(-1).h(-1) to patients in groups 1, 2, and 3, respectively. A control group received no alfentanil. Subdural ICP, mean arterial blood pressure (MAP), and cerebral perfusion pressure (CPP) were monitored and arterial and jugular bulb blood were sampled before and every minute for 5 min after the bolus administration of alfentanil and again after 5 min of hyperventilation to be able to calculate cerebral arterio-venous oxygen content difference (AVDO2) and carbon dioxide reactivity (CO2-reactivity). Results: No changes in subdural ICP or AVDO2 from alfentanil in the study period were observed within the groups. However, alfentanil decreased MAP and CPP. The maximum CPP decrease (mean value of each group) was 4 mmHg, 8 mmHg, and 18 mmHg in groups 1, 2, and 3, respectively. There was no difference between groups as regards the CO2-reactivity. Conclusion: We conclude that administration of alfentanil to propofol-fentanyl anesthetized patients with supratentorial cerebral tumors decreases MAP and CPP in a dose-related way, but does not influence subdural ICP, AVDO2 or the CO2-reactivity.     

The Effects of Isoflurane and Desflurane on Intracranial Pressure, Cerebral Perfusion Pressure, and Cerebral Arteriovenous Oxygen Content Difference in Normocapnic Patients with Supratentorial Brain Tumors

Background: Desflurane is a volatile anesthetic agent with low solubility whose use in neurosurgery has been debated because of its effect on intracranial pressure and cerebral blood flow. The purpose of this study was to determine the variations on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as well as on cerebral arteriovenous oxygen content difference (AVDo2) in normocapnic patients scheduled to undergo removal of supratentorial brain tumors with no evidence of mass effect during anesthesia with isoflurane or desflurane.

Methods: In 60 patients scheduled to undergo craniotomy and removal of supratentorial brain tumors with no evidence of midline shift, anesthesia was induced with intravenous fentanyl, thiopental, and vecuronium and was maintained with 60% nitrous oxide in oxygen. Patients were assigned to two groups randomized to receive 1 minimum alveolar concentration isoflurane or desflurane for 30 min. Heart rate, mean arterial pressure, intraparenchymal ICP, and CPP were monitored continuously. Before and after 30 min of continuous administration of the inhaled agents, AVDo2 was calculated.

Results: There were no significant differences between groups in heart rate, mean arterial pressure, ICP, and CPP. ICP measurements throughout the study did not change within each group compared to baseline values. Mean arterial pressure decreased significantly in all patients compared to baseline values, changing from 105 +/- 14 mmHg (mean +/- SD) to 85 +/- 10 mmHg in the isoflurane group and from 107 +/- 11 mmHg to 86 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). CPP also decreased within each group compared with baseline values, changing from 95 +/- 15 mmHg to 74 +/- 11 mmHg in the isoflurane group and from 95 +/- 16 mmHg to 74 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). Cerebral AVDo2 decreased significantly in both groups throughout the study, changing from 2.35 +/- 0.77 mm to 1.82 +/- 0.61 mm (mmol/l) in the isoflurane group (P < 0.05) and from 2.23 +/- 0.72 mm to 1.94 +/- 0.76 mm in the desflurane group (P < 0.05), without differences between groups.     

Optimal reverse trendelenburg position in patients undergoing craniotomy for cerebral tumors

OBJECT: To the authors' knowledge, repeated measurements of intracranial pressure (ICP), cerebral perfusion pressure (CPP), and the degree of dural tension during different positions on the operating table (reverse Trendelenburg position [rTp]) have not been studied in patients undergoing craniotomy. METHODS: In the present study 53 patients with supratentorial cerebral tumors who underwent craniotomy in the supine position were included. Subdural ICP, mean arterial blood pressure (MABP), CPP, and jugular bulb (JB) pressure were recorded, and the degree of dural tension was analyzed while patients were in the neutral operating position and at 5, 10, and 15 degrees rTp. The optimal operating position was defined as the one at which subdural ICP was as low as possible, and CPP was greater than or equal to 60 mm Hg or as high as possible. Subdural ICP, MABP, and JB pressure decreased significantly after each 5 degrres change in rTp compared with the preceding position. Dural tension decreased significantly up to 10 degrees rTp, but was unchanged at 15 degrees rTp. At 5 degrees rTp CPP remained unchanged, but it decreased significantly during 10 and 15 degrees rTp. The optimal position in the majority of patients was determined to be 15 degrees rTp. CONCLUSIONS: Before opening the dura mater for craniotomy, repeated measurements of ICP and CPP, in the neutral position and at 5, 10, and 15 degrees rTp, provide valuable information regarding the optimal level of ICP and CPP.     

Cerebrovascular carbon dioxide reactivity during general anesthesia: a comparison between sevoflurane and isoflurane

We compared cerebrovascular carbon dioxide reactivity during the administration of sevoflurane and isoflurane anesthesia by measuring cerebral blood flow velocity (CBFV) as an indirect measurement of cerebral blood flow. Thirty patients, 20-70 yr old, undergoing lower abdominal surgery and without known cerebral or cardiovascular system disease, were randomly assigned to either sevoflurane or isoflurane treatment groups. Anesthesia was induced with thiopental 5 mg/kg IV and maintained with either sevoflurane or isoflurane in 67% nitrous oxide and oxygen. The CBFV and pulsatility index (PI) of the left middle cerebral artery were monitored with transcranial Doppler. The P(ETCO)2 was increased stepwise from 20 to 50 mm Hg by changing the respiratory rate with a constant tidal volume. At every 5-mm Hg stepwise change in P(ETCO)2, CBFV and PI were recorded. CBFV increased with increasing P(ETCO)2. CBFV was significantly smaller in the isoflurane group at P(ETCO)2 = 20-40 mm Hg than in the sevoflurane group. The rate of change of CBFV with changes in CO2 was larger in the isoflurane group than in the sevoflurane group. PI was constant over time and was not different between groups. In conclusion, hypocapnia-induced reduction of intracranial pressure might be more effective during the administration of isoflurane than sevoflurane. IMPLICATIONS: Changes in cerebral blood flow caused by the changes of carbon dioxide tension are greater during the administration of isoflurane anesthesia compared with sevoflurane anesthesia. Attempts to decrease intracranial pressure by decreasing carbon dioxide tension may be more successful during isoflurane than sevoflurane anesthesia administration.     

The effects of sevoflurane and isoflurane on intracranial pressure and cerebral perfusion pressure after diffuse brain injury in rats

Twenty-four adult male Wistar rats, weighing 220 to 290 g, were anesthetized with 30 mg/kg intraperitoneal sodium thiopental, then underwent a tracheostomy. After diffuse impact-acceleration brain injury (BI) was induced, each rat was paralyzed and mechanically ventilated with 30% O2 in nitrous oxide (N2O). The rats were assigned randomly to two groups, each of which received one of the two volatile anesthetic agents, sevoflurane or isoflurane. The anesthetics were administered at 0.5, 0.75, 1.0, and 1.25 minimal alveolar concentration (MAC) for 30 minutes each, respectively, and anesthesia was maintained at 0.75 MAC during the last hour of the study period. Intracranial pressure (ICP), mean arterial pressure (MAP), rectal and intrahemispheric temperatures, and end-tidal volatile anesthetic concentrations were monitored continuously throughout the 3 hours, with measurements recorded every 15 minutes. At baseline, there were no significant differences between the two groups regarding the monitored physiologic values. In the sevoflurane group, MAP fell significantly after 45 minutes, and a similar change was observed in the isoflurane group after 30 minutes (P < .05, P < .01, and P < .001, respectively). Intracranial pressure increased significantly at 45 minutes in the sevoflurane group (P < .01) and remained elevated from 60 minutes until the end of the study period (P < .01, P < .001). Although ICP increased in the isoflurane group, the change was not significant. Cerebral perfusion pressure (CPP) decreased in parallel with MAP, with the reduction in the sevoflurane group being more pronounced than that in the isoflurane group. The results demonstrated that, under the conditions of diffuse BI, animals that were anesthetized with sevoflurane had higher ICP and lower CPP levels than those anesthetized with isoflurane.     

Continuous monitoring of cerebral oxygenation in acute brain injury: assessment of cerebral hemodynamic reserve

A new index of cerebral hemodynamics, cerebral hemodynamic reserve (CHR), was evaluated in 12 comatose adults with severe, acute, traumatic, diffuse swelling of the brain, who underwent continuous monitoring with a fiberoptic catheter of the saturation difference in arteriojugular oxyhemoglobin. CHR was assessed as the ratio of changes in global cerebral oxygen extraction to changes in cerebral perfusion pressure (CPP) as a result of spontaneous increases in intracranial pressure (ICP). During the course of hyperventilation (Pco2 in the range of 20 mm Hg) for ICP control below 20 mm Hg, 34 observations were made over the initial 48 hours postinjury. Despite normal CPP, in 25 of the observations (73.5%), ICP elevations to the range of 20 mm Hg were associated with compromised CHR, as evidenced by decreases in jugular oxygenation directly attributed to the ICP increases. In the remaining nine observations (26.5%), CHR was preserved, as evidenced by no changes or increases in jugular oxygenation when ICP increased. The CHR improved on the second day, suggesting an improved tolerance of the cerebral hemodynamics to ICP increases. Before the ICP elevations, in most of the observations, the global cerebral blood flow was estimated as being optimally decreased (by hypocapnia), in relation to cerebral oxygen consumption. This was reflected by the occurrence of baseline normalized cerebral oxygen extraction. It is concluded that in this group of patients, under circumstances of profound hyperventilation, ICP elevations within the normal CPP range may result in decreased cerebral oxygenation, even when the normal CPP would imply otherwise. It is suggested that CHR assessment may provide information regarding the status of intracranial "tightness," insofar as cerebral circulation and oxygenation are concerned.     

The effects of 10 degrees reverse Trendelenburg position on subdural intracranial pressure and cerebral perfusion pressure in patients subjected to craniotomy for cerebral aneurysm

The aim of the current study was to examine the effects of 10 degrees reverse Trendelenburg position (rTp) on subdural intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dural tension. Additionally, the relationship between preoperative Hunt and Hess (H and H) grade and the subdural ICP in patients scheduled for cerebral aneurysm surgery was investigated. Twenty-eight consecutive patients with a cerebral aneurysm were subjected to craniotomy in propofol/fentanyl or propofol/remifentanil anesthesia. Subdural ICP was measured after opening of the bone flap and exposure of dura. After reference measurements of subdural ICP and mean arterial blood pressure (MABP), the measurements were repeated during 10 degrees rTp. No significant differences between the anesthetic groups were disclosed. During 10 degrees rTp, a significant decrease in MABP, ICP, and jugular bulb pressure was observed whereas CPP remained unchanged. In H and H 0 patients (unruptured aneurysm), the ICP decreased from 2.9 +/- 2.6 mmHg to 0.4 +/- 2.2 mmHg at 10 degrees rTp. In H and H I to II patients, the ICP decreased from 9.3 +/- 3.8 mmHg to 4.6 +/- 3.3 mmHg at 10 degrees rTp. A significant difference in the mean baseline subdural ICP and DeltaICP (change in ICP) was found between patients with unruptured aneurysm and patients with subarachnoid hemorrhage (H&H I and II). Furthermore, the relationship between the subdural ICP at neutral position and DeltaICP was significant. In patients without intracranial hypertension, 10 degrees rTp decreases subdural ICP and dural tension in patients with ruptured as well as patients with unruptured cerebral aneurysm; CPP is unchanged.     

Reverse Trendelenburg position reduces intracranial pressure during craniotomy.

Cerebral swelling and herniation pose serious surgical obstacles during craniotomy for space-occupying lesions. Positioning patients head-up has been shown previously to reduce intracranial pressure (ICP) in neurotraumatized patients, but has not been investigated during intracranial surgery. The current study examined the effects of 10-deg reverse Trendelenburg position (RTP) on ICP and cerebral perfusion pressure (CPP). Forty adult patients subjected to craniotomy for supratentorial tumors were given standardized propofol-fentanyl-cisatracurium general anesthesia and were moderately hyperventilated. In 26 of 40 patients with expected poor clinical outcome, an additional catheter was placed in the internal jugular bulb to determine internal jugular bulb pressure (JBP). ICP was determined by subdural measurement using a 22-gauge needle advanced through the dura after removal of the bone flap. ICP was referenced to the level of the dural incision. ICP, mean arterial blood pressure, and CPP were compared with repeat measurements 1 minute after RTP. The tension of the dura was graded qualitatively by the surgeon by digital palpation and was compared to post-RTP. ICP decreased from 9.5 mm Hg to 6.0 mm Hg ( P <.001; all values are median) within 1 minute after 10-deg RTP. Mean arterial blood pressure decreased from 82.0 mm Hg to 78.5 mm Hg ( P <.001). CPP was unchanged (70.5 mm Hg versus 71 mm Hg after RTP), whereas JBP decreased from 8 mm Hg to 4 mm Hg ( P <.001). High initial ICP was correlated to the greatest magnitude of decrease in ICP. No significant correlation was found between change in ICP and change in JBP. Intracranial pressure after RTP resulted in decreased tension of the dura. RTP appears to be an effective means of reducing ICP during craniotomy, thereby reducing the risk of cerebral herniation. CPP is not affected. Studies over longer periods of time are warranted, however.     

Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.     

Differential effects of hyperventilation on cerebral blood flow velocity after tourniquet deflation during sevoflurane, isoflurane, or propofol anesthesia

The purpose of this study was to compare the degree of increase in middle cerebral artery (MCA) blood flow velocity after tourniquet deflation when modulating hyperventilation during orthopedic surgery under sevoflurane, isoflurane, or propofol anesthesia. Twenty-four patients undergoing elective orthopedic surgery were randomly divided into sevoflurane, isoflurane, and propofol groups. Anesthesia was maintained with sevoflurane, isoflurane, or propofol administration with 33% oxygen and 67% nitrous oxide at anesthetic drug concentrations adequate to maintain bispectral values between 45 and 50. A 2.0-MHz transcranial Doppler probe was attached to the patient’s head at the temporal window, and mean blood flow velocity in the MCA (V _mca) was continuously measured. The extremity was exsanguinated with an Esmarch bandage, and the pneumatic tourniquet was inflated to a pressure of 450 mmHg. Arterial blood pressure, heart rate, V _mca and arterial blood gases were measured every minute for 10 min after release of the tourniquet in all three groups. Immediately after tourniquet release, the patients’ respiratory rates were increased to tightly maintain end-tidal carbon dioxide (PetCO₂) at 35 mmHg. No change in partial pressure of carbon dioxide in arterial blood (PaCO₂) was observed pre- and posttourniquet deflation in any of the three groups. Increase in V _mca in the isoflurane group was greater than that in the other two groups after tourniquet deflation. In addition, during the study period, no difference in V _mca after tourniquet deflation was observed between the propofol and sevoflurane groups. Hyperventilation could prevent an increase in V _mca in the propofol and sevoflurane groups after tourniquet deflation. However, hyperventilation could not prevent an increase in V _mca in the isoflurane group.     

Newer inhalation anaesthetics and neuro-anaesthesia: what is the place for sevoflurane or desflurane?

The effects on cerebral circulation and metabolism of sevoflurane and desflurane are largely comparable to isoflurane. Both induce a direct vasodilation of the cerebral vessels, resulting in a less pronounced decrease in cerebral blood flow compared to the decrease in cerebral metabolism. This direct vasodilation seems to be dose-dependent and more pronounced for desflurane > isoflurane > sevoflurane. Many reports suggest luxury perfusion at high concentrations of desflurane. Sevoflurane maintains intact cerebral autoregulation up to 1.5 MAC. Desflurane induces a significant impairment in autoregulation, with a completely abolished autoregulation at 1.5 MAC. Both sevoflurane and desflurane (up to 1.5 MAC) maintain normal CO(2) regulation. As to their effect on final intracranial pressure (ICP), both sevoflurane and desflurane revealed no increases in ICP. However, compared to intravenous hypnotics, subdural ICP is higher with volatiles because of their tendency to increase cerebral swelling after dura opening (isoflurane > sevoflurane). Several case reports have noted seizure-like movements, as well as EEG recorded seizures during induction of sevoflurane anesthesia. Especially, in children during inhalational induction with hyperventilation at a high sevoflurane concentration, severe epileptiform EEG with a hyperdynamic response were observed, which urges for caution using inhalational sevoflurane induction in children for neurosurgical procedures. Neuroprotective properties (reduced neuronal death either by necrosis or apoptosis) have been attributed to all volatile agents. However, these neuroprotective effects have been described in experimental or animal models, so their possible effect on humans remains to be proven.     

Effects of 0.5 and 1.0 MAC isoflurane,sevoflurane and desflurane on intracranial and cerebral perfusion pressures in children

BACKGROUND: Isoflurane has been a commonly used agent for neuroanesthesia, but newer agents, sevoflurane and desflurane, have a quicker onset and shorter emergence from anesthesia and are increasingly preferred for general pediatric anesthesia. But their effects on intracranial pressure (ICP) and cerebral perfusion pressure (CPP), especially in pediatric patients with already increased ICP, have not been well documented. METHODS: We studied 36 children scheduled for elective implantation of an intraparenchymal pressure device for 24 h monitoring for suspected elevated ICP. After a standardized intravenous anesthesia, the patients were moderately hyperventilated with 60% nitrous oxide (N2O) in oxygen. The patients were then randomized to receive 0.5 and 1.0 MAC of isoflurane (Group I, n = 12), sevoflurane (Group S, n = 12) or desflurane (Group D, n = 12) in 60% N2O in oxygen. Respiratory and hemodynamic variables, ICP and CPP were recorded at baseline and after exposure to a target level of test drug for 10 min or until CPP fell below 30 mmHg (recommended lower ICP level is 25 mmHg in neonates, rising to 40 mmHg in toddlers). RESULTS: When comparing baseline values with values at 1.0 MAC, mean arterial pressure (MAP) decreased (P < 0.001) in all groups, with no differences between the groups. ICP increased (P < 0.001) with all agents, mean +2, +5, and +6 mmHg in Group I, S and D, respectively, with no differences between the groups. Regression analyzes found no relationship between baseline ICP and the increases in ICP from baseline to 1.0 MAC for isoflurane or sevoflurane. However, increased baseline ICP tended to cause a higher ICP increase with 1.0 MAC desflurane; regression coefficient +0.759 (P = 0.077). The difference between regression coefficients for Group I and Group D were not significant (P = 0.055). CPP (MAP-ICP) decreased (P < 0.001) in all groups, mean -18, -14 and -17 mmHg in Group I, S and D, respectively, with no significant difference between the groups. CONCLUSIONS: 0.5 and 1.0 MAC isoflurane, sevoflurane and desflurane in N2O all increased ICP and reduced MAP and CPP in a dose-dependent and clinically similar manner. There were no baseline dependent increases in ICP from 0 to 1.0 MAC with isoflurane or sevoflurane, but ICP increased somewhat more, although statistically insignificant, with higher baseline values in patients given desflurane. The effect of MAP on CPP is 3-4 times higher than the effect of the increases in ICP on CPP and this makes MAP the most important factor in preserving CPP. In children with known increased ICP, intravenous anesthesia may be safer. However, maintaining MAP remains the most important determinant of a safe CPP.     

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.     

Propofol versus isoflurane anesthesia under hypothermic conditions: effects on intracranial pressure and local cerebral blood flow after diffuse traumatic brain injury in the rat

BACKGROUND: The aim of this study was to compare the cerebral protective effects of two known protective anesthetics, isoflurane and propofol, when these were used in combination with moderate hypothermia (33-34 degrees C) after diffuse traumatic brain injury (TBI) in the rat. We assessed cerebral protection by measuring local cerebral blood flow (LCBF), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and intracranial pressure (ICP). METHODS: Sixteen female Wistar rats weighing 275 to 350 g were anesthetized and subjected to an accelerated-impact weight-drop model of diffuse TBI. Hypothermia (33-34 degrees C) was induced 45 minutes after TBI (baseline), and was maintained for 180 minutes. The isoflurane group (n = 8) received 70% N(2)O in O(2), and isoflurane at 0.9 +/- 0.04%. The propofol group (n = 8) received 70% N(2)O in O(2) and a propofol infusion (12 mg/kg/hr). LCBF was measured by laser Doppler flowmeter. MABP, ICP, and brain and rectal temperatures were measured every 15 minutes from baseline through 180 minutes. Blood gas and hematocrit testing was also done at baseline and every 60 minutes thereafter to assess the animals' physiological state. RESULTS: In the isoflurane group, MABP and CPP decreased significantly from baseline to 180 minutes (p < 0.05 and p < 0.01, respectively), and MABP was significantly lower than the pressure in the propofol group from 45 minutes through 180 minutes (p < 0.05, p < 0.01). ICP and LCBF remained unchanged in this group. In the propofol group, from baseline to 180 minutes, CPP increased to maximum 120 +/- 8 mmHg at 75 minutes from 98 +/- 5 mmHg (p < 0.05) and ICP fell from 18 +/- 2 mmHg to 7 +/- 1 mmHg (p < 0.01); and the latter was significantly lower than ICP in the isoflurane group (p < 0.05, p < 0.01, p < 0.001). LCBF in this group was significantly higher than LCBF in the isoflurane group in the last 30 minutes of the experiment (p < 0.05). The propofol group showed no change in MABP over the course of the experiment. CONCLUSION: In the clinical setting, propofol anesthesia may be better for use in combination with hypothermia in cases of traumatic brain injury, as it reduces ICP and increases CPP under these conditions.     

The comparative effects of desflurane and isoflurane on lumbar cerebrospinal fluid pressure in patients undergoing craniotomy for supratentorial tumors

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 (PaCO(2), 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.     

Pour ou contre les halogénés en neuroanesthésie pour chirurgie intracrânienne

Isoflurane, desflurane and sevoflurane all preserve cerebrovascular carbone dioxide (CO₂) reactivity. They are all concentration-dependant cerebral vasodilatators and decrease cerebral metabolism. Sevoflurane induces the smallest cerebral vasodilatation and preserve cerebral autoregulation up to 1.5 CAM, compared to isoflurane and desflurane which impair it upon 1 CAM. Propofol has been compared to inhaled agents. Propofol preserve cerebrovascular CO₂ reactivity, blood flow-metabolism coupling, cerebral autoregulation and has no vasodilatation effect. None of the three inhaled agents induce any clinical relevant increase of intracranial pressure (ICP), but studies were conducted in patients without any intracranial hypertension (ICHT). However, compared to propofol, ICP and brain swelling were higher with inhaled agents, more with isoflurane compared to sevoflurane. Finally, neuroprotective properties have been described in experimental model for all the inhaled agents but clinical proofs are still lacking. In conclusion, for intracranial surgery without any ICHT inhaled agents can be used as a maintenance anesthetic with a preference for sevoflurane. In case of ICHT or a risk of ICHT during the surgery, propofol is preferred for it slightest effect on ICP and cerebral hemodynamic.     

The effect of isoflurane on cerebrospinal fluid pressure in patients undergoing neurosurgery

Ten patients with intracerebral tumours (TC) and 13 patients with subarachnoid haemorrhage (SAH) from a ruptured cerebral arterial aneurysm were studied before intracranial surgery, and during a 3-h postoperative period. Cerebrospinal fluid pressure (CSFP) determined by an intraventricular (TC group) or intraspinal (SAH group) catheter, and mean arterial blood pressure (MABP) were recorded under neurolept anaesthesia (control) followed by isoflurane inhalation. These two measurements were performed during normocapnia. A third measurement was made during hypocapnia, with unchanged isoflurane concentration. After the experimental period, isoflurane remained the main anaesthetic agent throughout the surgical procedure. After recovery from anaesthesia, the patients were monitored with CSFP and blood pressure during the first postoperative hours, and the quality of breathing was assessed by hourly blood-gas analyses. The results show that isoflurane causes a 10-14% reduction of MABP with no further changes during hyperventilation. Mean CSFP increased 27% in the TC group, and 12% in the SAH group after isoflurane induction and decreased from these levels by 29% during hyperventilation in both groups. Consequently, the impact on cerebral perfusion pressure (CPP) by isoflurane was a 19% and 21% mean decrease in the TC and SAH group, respectively. Controlled hyperventilation reduced this effect by partially restoring control CPP values, with 8% and 14% increase, respectively. In the postoperative follow-up, all patients had normal breathing and blood pressure with low values of CSFP. It is concluded that isoflurane can be used in intracranial surgery with adequate safety if combined with controlled hyperventilation.