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Purpose of Review: Cerebral ischemia plays a major role in the pathophysiology of the injured brain, including traumatic brain injury and subarachnoid hemorrhage, thus improvement in outcome may necessitate monitoring and optimization of cerebral blood flow (CBF). To interpret CBF results in a meaningful way, it may be necessary to quantify cerebral autoregulation as well as cerebral metabolism. This review addresses the recent evidence related to the changes in CBF and its monitoring/management in traumatic brain injury., Recent Findings: Recent evidence on the management of patients with traumatic brain injury have focused on the importance of cerebral autoregulation in maintaining perfusion, which necessitates the measurement of CBF. However, adequate CBF measurements alone would not indicate the amount of oxygen delivered to neuronal tissues. Technologic advancements in measurement devices have enabled the assessment of the metabolic state of the cerebral tissue for the purpose of guiding therapy, progress as well as prognostification., Summary: Current neurocritical care management strategies are focused on the prevention and limitation of secondary brain injury where neuronal insult continues to evolve during the hours and days after the primary injury. Appropriately chosen multimodal monitoring including CBF and management measures can result in reduction in mortality and morbidity.

Purpose of Review: This review will examine the recent literature on anesthesia and monitoring techniques in relation to cerebral autoregulation. We will discuss the effect of physiologic and pharmacological factors on cerebral autoregulation alongside its clinical relevance with the help of new evidence., Recent Findings: Intravenous anesthesia, such as combination of propofol and remifentanil, provides best preservation of autoregulation. Among inhaled agents sevoflurane appears to preserve autoregulation at all doses, whereas with other agents autoregulation is impaired in a dose-related manner., Summary: Intraoperative cerebral autoregulation monitoring is an important consideration for the patients with neurologic disease. Transcranial Doppler based static autoregulation measurements appears to be the most robust bedside method for this purpose.

Background: Lactic acidosis is considered an early sign of propofol infusion syndrome. In this study, we investigated the changes in lactate and pH with propofol versus volatile anesthesia (VA) of long duration., Methods: Demographic and intraoperative data were recorded retrospectively from the anesthesia records of patients who underwent elective spine surgery longer than 8 h. Propofol patients were matched 1:2 to VA patients, based on anesthesia time (AT) (+/-30 min) and blood loss (BL) (+/-500 mL)., Results: Of 246 patients identified, 50 received propofol (AT = 10 +/- 2 h, BL = 1955 +/- 1409 mL) and were matched to 100 VA cases (AT = 10 +/- 1 h, BL = 1801 +/- 1543 mL), and of those, 40 and 72 patients, respectively, had complete lactate data at baseline and at 8 h after anesthesia and were included in the main analysis. The propofol group received 8.8 +/- 2 mg x kg(-1) x h(-1) of propofol. The VA group age was older than the propofol group (58 +/- 12 vs 51 +/- 15 yr, respectively, P = 0.002), but there was no difference between the groups in gender, ASA grade, intraoperative hemodynamic variables, and use of vasopressors. After 8 h, the VA group had a larger increase in arterial lactate from baseline compared with the propofol group (change from baseline: propofol, 0.48 +/- 0.72 mmol/L; VA, 1.2 +/- 1.2 mmol/L, P = 0.001)., Conclusions: During prolonged spine surgery >8 h, VA was associated with higher serum lactate, when compared with propofol infusion. Prospective studies are needed to elucidate the exact mechanisms and clinical implications of this finding.

Patients with refractory seizures may undergo awake craniotomy and cortical resection of the seizure area, using intraoperative functional mapping and electrocorticography (ECoG). We used dexmedetomidine in 6 patients, transitioning successively from the asleep-awake-asleep method, through a combined propofol/dexmedetomidine sedative infusion, to dexmedetomidine as the only sedation. Initial experience with the asleep-awake-asleep method in 2 patients was successful with the replacement of propofol/laryngeal mask anesthesia, 20 to 30 minutes before ECoG testing, by dexmedetomidine infusion, maintained at 0.2 mcg kg-1 h-1 throughout neurocognitive testing. Propofol anesthesia was reintroduced for resection. One patient received combined dexmedetomidine (0.2 mcg kg-1 h-1) and propofol (200 mcg kg-1 min-1) infusions for sedation. Both infusions were stopped 15 minutes before ECoG. Subsequently, they were restarted and the epileptic foci resected. Three patients received dexmedetomidine as the sole sedative agent, together with scalp block local anesthesia, and incremental boluses totaling 150 to 175 mcg of fentanyl per case. Dexmedetomidine was started with 0.3 mcg kg-1 boluses and maintained with 0.2 to 0.7 mcg kg-1 h-1for craniotomy, testing, and resection. The infusion was paused for 20 minutes in 1 patient to allow improvement in neurocognitive testing. This occurred within 10 minutes. All patients enjoyed good hemodynamic control, with blood pressure maintained within 20% of initial values, and made uneventful recoveries. The surgical conditions were all reported as favorable. Dexmedetomidine can be used singly for sedation in awake craniotomy requiring ECoG. Individual dose ranges vary, but a bolus of 0.3 mcg kg-1 with an infusion of 0.2 mcg kg-1 min-1 is a good starting point, allowing accurate mapping of epileptic foci and subsequent resection.

The pharmacologic profile of the alpha-2 agonist dexmedetomidine (Dex) suggests that it may be an ideal sedative drug for deep brain stimulator (DBS) implantation. We performed a retrospective chart review of anesthesia records of patients who underwent DBS implantation from 2001 to 2004. In 2003, a clinical protocol with Dex sedation for DBS implantation was initiated. Demographic data, use of antihypertensive medication, and duration of mapping were compared between patients who received Dex (11 patients/13 procedures) and patients who did not receive any sedation (controls: 8 patients/9 procedures). There were no differences in severity of illness between the two groups. Dex provided patient comfort and surgical satisfaction with mapping in all cases, and significantly reduced the use of antihypertensive medication (54% in the Dex group, versus 100% in controls, P = 0.048). In DBS implantation, sedation with Dex did not interfere with electrophysiologic mapping, and provided hemodynamic stability and patient comfort. Routine use of Dex in these procedures may be indicated.

We conducted a retrospective cohort study in children <13 yr with traumatic brain injury (TBI) at a Level 1 pediatric trauma center to describe risk factors for intraoperative hypotension (IH) during emergent decompressive craniotomy. Between 1994 and 2004, 108 children underwent emergent decompressive craniotomy for TBI. Overall, 56 (52%) patients had IH. Independent risk factors for IH were each 10 mL estimated blood loss/kg (ARR 1.15 95% CI 1.08-1.22), each mm of computed tomography (CT) midline shift (ARR 1.04 95%CI 1.01-1.07), each 10 mL of CT lesion volume (ARR 1.03 95%CI 1.01-1.05), and emergency department (ED) hypotension (5/5 patients with ED hypotension had IH). CT midline shift > or =4 mm predicted IH (ARR 1.67 95% CI 1.06-2.63), independent of blood loss. IH occurred frequently during emergent decompressive craniotomy in children with TBI. ED hypotension, blood loss, CT lesion volume, and CT midline shift predicted IH. Anesthesiologists can expect children with preoperative CT midline shift > or =4 mm to have IH during this procedure.

The purpose of the study was to compare cerebral autoregulation (CA) and CO2 reactivity (CO2R) between the anterior and posterior circulation under sevoflurane anesthesia. We studied 9 adult ASA physical status I patients (22-47 yr) scheduled for elective orthopedic surgery. Blood flow velocity in the middle cerebral artery (Vmca) and in the basilar artery (Vba) were measured using transcranial Doppler ultrasonography. For CA testing, arterial blood pressure was increased using phenylephrine infusion. CA was quantified with the autoregulatory index (ARI). CO2R was investigated at PaCO2 of 30 +/- 2.8 mm Hg, 39.4 +/- 2.6 mm Hg, and 48.7 +/- 2.8 mm Hg. Linear regression analysis was used for CO2R. We found ARI was preserved in both arteries: ARImca (middle cerebral artery) = 0.72 +/- 0.2; ARIba (basilar artery) = 0.66 +/- 0.2; P = 0.5. With regard to CO2R, Vmca increased with slope of 1.7 cm/s/mm Hg PaCO2, Vba increased with slope of 1.5 cm/s/mm Hg PaCO2; P = 0.83. Absolute Vmca was higher compared with Vba; P < 0.05. We conclude that in healthy individuals under 0.5 MAC of sevoflurane and small-dose remifentanil: 1) mean flow velocities of BA are less than those of MCA; 2) autoregulation and CO2R are preserved in the basilar artery and are similar to those of MCA.

We describe the incidence and etiology of fever and the relationship between fever characteristics and outcome in children with severe traumatic brain injury (TBI). We conducted a retrospective study of children <14 years and with Glasgow Coma Scale (GCS) score of <9 admitted to a level I pediatric trauma center intensive care unit (PICU) between 1998 and 2003. We examined whether fever characteristics were associated with poor outcome (hospital discharge GCS score <13 and discharge disposition of either death or discharge to a skilled nursing facility). PICU length of stay (LOS) and hospital LOS were also examined. Data are presented as means and medians (SD), and P < 0.05 reflects significance. Ninety-three records were reviewed. Patients were 5.7 (SD 4.1) years old, 70% were male, and the average admission GCS score was 5. Mortality rate was 14%. Forty-eight (52%) patients had fever, and 23 (48%) of those patients had infectious fever. Each additional febrile episode was associated with a twofold higher risk of patients having a hospital discharge GCS score of <13 (odds ratio 2.4, 95% confidence interval 1.2-5.0) and having a 0.4-day longer PICU LOS (P < 0.001). Patients with infectious fever had a 0.9-day longer PICU LOS (P < 0.001). Patients with any fever in the PICU had an increased HLOS (0.9 days; P < 0.001). Our data suggest that in severe pediatric TBI, both fever and infection were common, and both were associated with longer LOS. Patients with higher fever burden had poor hospital discharge GCS score.

Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.

Blindness caused by ischemic optic neuropathy in the hospital setting occurs perioperatively and in critically ill patients, but its etiology remains ill defined. We describe four critically ill patients who developed blindness within 1 mo of one another. Three cases occurred outside of the operative arena. Potential risk factors for the development of ischemic optic neuropathy, such as use of vasopressors, venous congestion, and hypotension, are described.

Systemic lupus erythematosus is a multifactorial autoimmune disease of complex etiology, which may be associated with cognitive dysfunction, seizures, and headache. The authors present an unusual presentation of systemic lupus erythematosus complicated by global cerebral edema and subarachnoid hemorrhage secondary to rupture of a cerebral aneurysm. The complicated patient management issues are discussed.

Background: The relationship between systolic blood pressure and outcome in children after severe traumatic brain injury (TBI) is unclear. We examined the relationship between age-appropriate systolic blood pressure (AASBP) percentile and outcome after severe pediatric TBI., Methods: We examined the association between AASBP percentiles and outcome in 172 children younger than 14 years of age with a Glasgow Coma Scale score < 9. Outcome was evaluated using discharge Glasgow Outcome Scale score. Poor outcome was defined as a Glasgow Outcome Scale score < 4., Results: Poor outcome was associated with AASBP < 75th percentile (odds ratio, 4.2; 95% confidence interval, 2.1-8.3). Patients with systolic blood pressure (SBP) > or = 90 mm Hg and AASBP < 75th percentile had a higher odds for poor outcome compared with patients with SBP > or = 90 mm Hg and AASBP > or = 75th percentile (odds ratio, 3.5; 95% confidence interval, 1.7-7.3). CONCLUSION AASBP < 75th percentile was associated with poor outcome after severe pediatric TBI, even when SBP was > or = 90 mm Hg.

In adults, the lower limit of cerebral autoregulation (LLA) is generally considered to be a mean arterial pressure (MAP) of 60 mmHg. The LLA in healthy children has not been identified. The aim of this report is to describe the LLA in anesthetized children and relate it to age. Static cerebral autoregulation testing was performed in children 6 months to 14 years of age during <1 MAC sevoflurane anesthesia. Mean middle cerebral artery flow velocities (Vmca) were continuously measured using transcranial Doppler ultrasonography. MAP was increased with infusion of intravenous phenylephrine incrementally titrated to the greater of either: 1) 20% above baseline MAP or 2) 80 mmHg (<9 years), 90 mmHg (9-14 years). The LLA was defined by the point where the two linear regression lines fitting the Vmca/MAP crossed. The lower limit reserve (LLR) and autoregulatory reserve (ARR%) were defined as follows: LLR=Baseline MAP-LLA; ARR (%)=(LLR/Baseline MAP)x100. There were 13 subjects <2 years of age (group 1), 13 subjects 2 to 5 years of age (group 2), 14 subjects 6 to 9 years of age (group 3), and 13 subjects 10 to 14 years of age (group 4). Older children (groups 3 and 4) had a higher baseline MAP compared with younger children (groups 1 and 2) (82 +/- 10 mmHg vs. 70 +/- 10 mmHg, respectively; P=0.0001). However, there was no difference in LLA (59 +/- 17 mmHg vs. 60 +/- 8 mmHg; P=0.6) between older and younger children. Consequently, the LLR was greater in older children compared with younger children (25 +/- 12 mmHg vs. 12 +/- 10 mmHg, respectively; P=0.0007). Similarly, the ARR was significantly higher in older children compared with younger children (30% +/- 16% vs. 16% +/- 12%; P=0.002). In this study, we found no age-related differences in the LLA. Older children had a greater LLR and ARR compared with young children. The baseline MAP in young children may rest close to the LLA. These findings may have implications for managing hemodynamics in anesthetized children at risk for secondary brain injury.

Background: The potential benefit of propofol dose regimens that use physiologic pharmacokinetic modeling to target the brain has been demonstrated in animals, but no data are available on the rate of propofol distribution to the brain in humans. This study measured the brain uptake of propofol in humans and the simultaneous effects on electroencephalography, cerebral blood flow velocity (V(mca)), and cerebral oxygen extraction., Methods: Seven subjects had arterial and jugular bulb catheters placed before induction. Electroencephalography and V(mca) were recorded during induction with propofol while blood samples were taken from both catheters for later propofol analysis. Brain uptake of propofol was calculated using mass balance principles, with effect compartment modeling used to quantitate the rate of uptake., Results: Bispectral index (electroencephalogram) values decreased to a minimum value of approximately 4 at around 7 min from the onset of propofol administration and then slowly recovered. This was accompanied by decreases in V(mca), reaching a minimum value of approximately 40% of baseline. Cerebral oxygen extraction did not change, suggesting parallel changes in cerebral metabolism. There was slow equilibrium of propofol between the blood and the brain (t(1/2keo) of 6.5 min), with a close relation between brain concentrations and bispectral index, although with considerable interpatient variability. The majority of the decreases in V(mca), and presumably cerebral metabolism, corresponded with bispectral index values reaching 40-50 and the onset of burst suppression., Conclusion: Description of brain distribution of propofol will allow development of physiologic pharmacokinetic models for propofol and evaluation of dose regimens that target the brain.

Implications: Transesophageal echocardiography may be useful in guiding detection and removal of thorax penetrating objects and for the monitoring of complications after removal of such objects.

Implications: The effects of inhaled nitric oxide (INO) on cerebrovascular hemodynamics are not well established. We report no adverse cerebral effects with INO therapy in a child with traumatic brain injury.

The authors present the case of an anemic 22-month-old child undergoing lower extremity surgery in whom the lower limit of cerebral autoregulation was shifted to the right.

The authors examined the relationship between fibrin degradation products (FDP) and outcome in children with isolated head injury by reviewing the records of 69 children who met the following criteria: (1) less than 16 years of age; (2) diagnosis of isolated head injury and (3) FDP levels. Outcome was evaluated using the following Glasgow Outcome Scale (GOS): 1 = death; 2 = vegetative state; 3 = functionally impaired; 4 = minimal dysfunction; 5 = premorbid level of functioning. Poor outcome was defined as GOS 1-3. Twenty-nine of 33 patients with FDP > 1000 (g/mL had GOS scores < 4 compared to 4/36 patients (11%) with FDP < 1000 microg/mL (Fisher's Exact Probability Test P < .0001). When stratified by GCS, no other prognosticator of outcome was needed when GCS was < 7 and > 12. In patients with GCS 7-12, however, 4/6 with FDP >1000 microg/mL had a poor outcome and all 12 patients with FDP < 1000 microg/mL had a good outcome (P = .004). The authors conclude that FDP > 1000 microg/mL predicts poor outcome in children with isolated head injury. Fibrin degradation products are a strong independent prognosticator of outcome in children when GCS is between 7 and 12.

Background: Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia., Methods: Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation., Results: The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg., Conclusions: Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.

The lower-limb venous return, assessed by the peak systolic venous velocities (PSVV) of the left common femoral vein, was recorded at different stages of operation for five patients undergoing major gynecologic operative laparoscopy. The average baseline PSVV was 23.1 cm/s. After positioning the patient in the Trendelenburg position, the PSVV increased to an average of 31.5 cm/s; this was a statistically significant increase. Creation of the pneumoperitoneum changed the waveform from a normal phasic pattern to a dampened, continuous, monophasic waveform. The average PSVV was reduced to 15.9 cm/s; this dampening was statistically significant. Further dampening was evident 1 hour intraoperatively, and the flow became intermittent, with cycles of dampened flow followed by periods of absent flow; these changes in PSVV were not statistically significant. Calf compressors did not increase the femoral PSVV at the beginning of operation, nor at I hour intraoperatively; the decrease was not statistically significant. After release of the pneumoperitoneum, the baseline waveform pattern and velocity returned. The Trendelenburg position used for gynecologic operative laparoscopy was associated with a statistically significant increase in the lower-limb PSVV. This increase did not fully counteract the dampening effect of a pneumoperitoneum on lower-limb PSVV. The authors' study did not support the benefit previously reported on the use of pneumatic calf compressors. The authors therefore recommend continuing the practice of antithrombotic measures for patients undergoing gynecologic operative laparoscopy.

Although injury to the brain and spinal cord can have varied etiology and mechanisms, the common pathway appears to be mediated by occurrence of ischemia and secondary injury. Because the pathophysiology in traumatic brain injury is heterogeneous, improvement in outcome will come from better diagnosis and monitoring, so that targeted therapy can be tailored to the individual patient. This review focuses on traumatic injury to the brain and spinal cord, and highlights recent developments in this area.

Unlabelled: The conventional wisdom that neurosurgical patients experience minimal postoperative pain and require little analgesia has been challenged. To address this, we reviewed our anesthesia and postanesthesia care unit (PACU) records for 1995 and compared pain management in patients undergoing major intracranial and selected extracranial procedures. We recorded patient weight, operative time, time in the PACU, intraoperative and postoperative opioid use, PACU pain scores, and level of consciousness in patients who had undergone open fixation of mandible or maxilla (Group E), clipping of aneurysms or excision of tumors (Group I), or lumbar laminectomy (Group L). Group I (n = 78) patients received less fentanyl in the operating room (0.016 microg x kg(-1) x min(-1) versus 0.023 microg x kg(-1) x min(-1) for Group E [n = 134] and 0.023 microg x kg(-1) x min(-1) for Group L [n = 21]; P < 0.05), received less morphine in the PACU (0.0004 vs 0.0013 vs 0.0015 mg kg(-1) x min(-1); P < 0.005), reported lower pain scores (0.76 vs 2.5 vs 2.4; P < 0.05), and spent less time in the PACU (89.5 vs 109 vs 105 min; P < 0.05) than Group E or L patients. Our results were similar when only patients with Glasgow Coma Scale scores > or = 14 were used in a subset analysis. We conclude that patients suffer less pain and use fewer opioids in the PACU after intracranial surgery than after facial reconstruction or lumbar laminectomy. Our results confirm that the average craniotomy patient has less postoperative pain than patients who undergo other surgical procedures, although patients who undergo frontal craniotomy may require more aggressive pain management., Implications: This study compares the pain report and analgesic use in patients after intracranial versus extracranial surgery. The results confirm the commonly held but recently challenged belief that neurosurgery patients suffer less pain postoperatively than other patients. In this study, we found that most patients report minimal pain after intracranial surgery but that a small subset of patients, many of whom have undergone frontal craniotomies, require aggressive treatment of postoperative pain.

Unlabelled: This study examined the concentration-related effects of sevoflurane and isoflurane on cerebral physiology and plasma inorganic fluoride concentrations. Middle cerebral artery flow velocity (Vmca), intracranial pressure (ICP), electroencephalogram (EEG) activity, and jugular bulb venous oxygen saturation were measured, and cerebral perfusion pressure (CPP) and estimated cerebral vascular resistance (CVRe) were calculated at baseline and at 0.5, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC) sevoflurane (n = 8) or isoflurane (n = 6). Mannitol 0.5-0.75 g/kg was given before dural incision, and blood was sampled for plasma inorganic fluoride during surgery and for up to 72 h postoperatively. Both sevoflurane and isoflurane decreased Vmca (to 31 +/- 12 - 36 +/- 14 cm/s, mean +/- SD), did not significantly alter ICP (13 +/- 9 - 15 +/- 11 mm Hg), and did not cause epileptiform EEG activity. With sevoflurane, decreased Vmca was accompanied by decreased CPP and unchanged CVRe at 0.5 MAC, and unchanged CPP and increased CVRe at 1.0 and 1.5 MAC. Plasma inorganic fluoride was 39.0 +/- 12.9 microM at the end of anesthesia (3.2 +/- 2.0 MAC hours) with sevoflurane, similar to the value (36.2 +/- 3.9 microM) for 3.7 +/- 0.1 MAC hours sevoflurane in patients not receiving mannitol. Decreased Vmca during sevoflurane presumably results from decreased cerebral metabolic rate, with CVRe changing secondarily in accord with CPP. Plasma inorganic fluoride does not seem to be altered by mannitol-induced diuresis., Implications: In neurosurgical patients, sevoflurane decreased middle cerebral artery flow velocity and caused no epileptiform electroencephalogram activity and no increase of intracranial pressure or plasma inorganic fluoride. These effects are suitable for neurosurgery. Two other possible effects of sevoflurane, i.e., increased cerebrospinal fluid volume and/or intracranial elastance, may not be suitable for neurosurgery and warrant further study.

The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. Four groups (E-H) received the same treatment; in addition, head trauma was delivered using a weight-drop device to the left cranium (2 h after ethanol treatment in the acute ethanol groups). To assess the influence of acute plus chronic alcohol and whether the glutamate antagonist ketamine can modify the neurologic outcome following head trauma, two additional head trauma groups were studied: group I received both acute and chronic ethanol treatment and group J received acute ethanol (1.5 g/kg) IP plus ketamine (180 mg/kg). Neurologic assessment was performed at 1, 2, 4, 8, 10, and 24 hours after head trauma or sham trauma in all animals who survived the treatment (omitted in group J animals while still under the anesthetic influence of ketamine). At the end of 24 hours, or at the time of death, the animals were decapitated. Specific gravity was determined from brain tissues adjacent to the injury and the contralateral hemispheres and the volume of hemorrhagic necrosis was quantified. None of the rats in the sham trauma groups died or had neurologic deficits. Of the head trauma groups, the mortality in animals that received 3 g/kg of ethanol and the animals that received acute plus chronic ethanol treatment was 100% before the end of 24 hours. Fifty percent of the animals receiving low-dose acute ethanol treatment (1.5 g/kg) died before 24 hours. In contrast, the mortality in the other groups was only 30% (p < 0.05). The neurologic severity score was significantly higher (greater neurological deficit) in the surviving animals that received acute ethanol treatment at 10 and 24 hours than in rats receiving no ethanol or chronic ethanol treatment. Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.

Background: Accuracy of jugular venous oxygen saturation (SjvO2) measurement depends on sampling of cerebral venous outflow blood not contaminated by systemic venous blood. The influence of the rate of blood withdrawal has not been determined., Methods: The authors examined the effect of withdrawing blood at different rates from jugular venous bulb catheters (JVBC) on SjvO2 in 10 mechanically ventilated patients undergoing neurosurgical procedures. All patients received a standardized anesthetic consisting of propofol, fentanyl, vecuronium, and isoflurane. Routine monitors included electrocardiograph (ECG), invasive blood pressure, pulse oximetry, and a JVBC. During a period of stable anesthetic and surgical conditions, JVBC blood samples were drawn at 2, 4, and 10 ml/min using a calibrated pump (Harvard Pump model 900, Harvard Apparatus, South Natick, MA) during mild and moderate hypocapnia (arterial carbon dioxide tension [PaCO2], 26.0 +/- 0.5 and 33.0 +/- 0.5 mmHg)., Results: Faster rates of withdrawal (10 and 4 ml/min vs. 2 ml/min) resulted in significantly higher SjvO2 values at both levels of PaCO2 (66.0 +/- 3% and 61.2 +/- 3% vs. 56.9 +/- 3% at PaCO2 = 26.0 +/- 0.5 mmHg, and 75.0 +/- 3% and 71.3 +/- 3% vs. 68.0 +/- 3% at PaCO2 = 33.0 +/- 0.5 mmHg, respectively; P < 0.01)., Conclusions: The authors conclude that the SjvO2 values measured with intermittent sampling are affected by the rate of withdrawing blood from JVBC, probably as a result of extracranial contamination. They recommend blood samples should be drawn slowly.

We designed the present study to determine whether the minimum alveolar concentration (MAC) for isoflurane is decreased after closed head trauma (CHT) in rats and, if so, whether the decrease of MAC is related to the severity of neurological impairment following CHT. Isoflurane MAC was determined in 36 Sprague-Dawley rats. Then, at time = 0 h, animals were grouped. Group 1 (n = 8) received no CHT, group 2 (n = 14) received moderate CHT, and group 3 (n = 14) received severe CHT. Neurological severity score (NSS, 0 = no deficit and 25 = maximal impairment) and MAC were determined at 1, 4, 24, and 48 h. In groups 1 and 2, isoflurane MAC at 1, 2, 24, and 48 h (1.0-1.1 +/- 0.8-1.2%, median +/- range) was not significantly different from baseline (1.0-1.1 +/- 1.0-1.1%). In group 3, isoflurane MAC at 1, 2, 24, and 48 h (0.4 +/- 0.2-0.5%) was decreased as compared to baseline (1.1 +/- 1.0-1.1%). In group 2, NSS at 1 h was 18 +/- 11-21 and improved by 48 h to 9 +/- 4-15. In group 3, NSS at 1 h was 24 +/- 22-25 and was not significantly different from NSS at 48 h (24 +/- 24-25). Thus, moderate CHT does not significantly alter isoflurane MAC, whereas severe CHT equivalent to a Glasgow Coma Scale score of 3 to 6 significantly decreases isoflurane MAC.