Julie B. Weeks

Manual In-line Stabilization Increases Pressures Applied by the Laryngoscope Blade during Direct Laryngoscopy and Orotracheal Intubation

Background:Manual in-line stabilization (MILS) is recommended during direct laryngoscopy and intubation in patients with known or suspected cervical spine instability. Because MILS impairs glottic visualization, the authors hypothesized that anesthesiologists would apply greater pressure during intubations with MILS than without. Methods:Nine anesthetized and pharmacologically paralyzed patients underwent two sequential laryngoscopies and intubations, one with MILS and one without, in random order. A transducer array along a Macintosh 3 laryngoscope blade continuously measured applied pressures, and glottic view was characterized. Results:With MILS, glottic visualization was worse in six patients, and intubation failure occurred in two of these six patients. Maximum laryngoscope pressure at best glottic view was greater with MILS than without (717 ± 339 mmHg vs. 363 ± 121 mmHg, respectively; n = 8; P = 0.023). Other measures of pressure application also indicated comparable increases with MILS. Conclusion:Pressures applied to airway tissues by the laryngoscope blade are secondarily transmitted to the cervical spine and result in cranio-cervical motion. In the presence of cervical instability, impaired glottic visualization and secondary increases in pressure application with MILS have the potential to increase pathologic cranio-cervical motion.

Comparative Effects of Propofol, Pentobarbital, and Isoflurane on Cerebral Blood Flow and Blood Volume

While intravenous and volatile anesthetics have widely differing effects on cerebral blood flow (CBF), clinical studies suggest that the relative differences in their effects on intracranial pressure (ICP) may be smaller. Because acute changes in ICP are determined primarily by changes in cerebral blood volume (CBV), we compared the impact of propofol, pentobarbital, and isoflurane on CBF and CBV in rats. Equipotent doses of the three agents were determined by tail-clamp studies. Animals were then anesthetized with propofol (20 mg/kg load, 38 mg.kg-1.h-1 infusion), pentobarbital (30 mg/kg load, 20 mg.kg-1.h-1 infusion), or isoflurane 1.6-1.8%. Two hours later, CBF and CBV were measured using 3H-nicotine as a CBF tracer, and 14C-dextran and 99mTc-labeled red cells as markers for cerebral plasma and red blood cell volumes (CPV and CRBCV), respectively. Total CBV was the sum of CPV and CRBCV. CBF was 2.0-2.6 times greater with isoflurane than with propofol or pentobarbital (137 vs. 67 and 52 ml.100 g-1.min-1, respectively). By contrast, while CBV was greater in the isoflurane group than in either the propofol or pentobarbital groups, the magnitude of the intergroup differences were much smaller (propofol = 2.49 +/- 0.28 ml/100 g; pentobarbital = 2.27 +/- 0.15 ml/100 g; isoflurane = 2.77 +/- 0.24 ml/100 g, mean +/- SD). These results suggest that the simple measurement of CBF may not adequately describe the cerebrovascular effects of an anesthetic, at least with respect to predicting the magnitude of the agents likely effects on ICP.

Hyperglycemia in Patients Undergoing Cerebral Aneurysm Surgery: Its Association With Long-term Gross Neurologic and Neuropsychological Function

OBJECTIVE To evaluate whether elevated intraoperative blood glucose concentrations are associated with an increased risk of long-term neurologic dysfunction in patients at risk for ischemic brain injury. PATIENTS AND METHODS Data from 1000 patients were retrieved from the Intraoperative Hypothermia for Aneurysm Surgery Trial database. All patients were recruited between February 2000 and April 2003, and underwent surgery for aneurysm clipping within 14 days of subarachnoid hemorrhage. Gross neurologic and neuropsychological function was evaluated at 3 months after surgery using certified observers and standardized assessment instruments. Intraoperative blood glucose concentrations, measured once when the aneurysm clip was placed, were correlated with neurologic outcome using both univariable and multivariable logistic regression analyses. RESULTS Blood glucose concentrations at the time of aneurysm clipping ranged from 59 to 331 mg/dL. At 3 months after surgery, those with blood glucose concentrations of 129 mg/dL or more (upper 2 quartiles) were more likely to have impaired cognition (P=.03). Those with glucose concentrations of 152 mg/dL or more (upper quartile) were more likely to experience deficits in gross neurologic function assessed by the National Institutes of Health Stroke Scale (P<.05), but not other scoring scales. Length of stay in intensive care units was longer in those with glucose concentrations of 129 mg/dL or more, but there was no difference among glucose groups in the duration of overall hospital stay or the fraction of patients discharged to home. CONCLUSION In patients at high risk for ischemic brain injury, intraoperative hyperglycemia, of a magnitude commonly encountered clinically, was associated with long-term changes in cognition and gross neurologic function.

Microwave fixation for the determination of cerebral blood volume in rats.

The cerebral blood volume (CBV) is sensitive to changing hydrostatic pressures. Thus, measurement methods that rely on removing tissue from unfixed brain may lead to underestimates of the CBV due to the loss of blood from the tissue. In situ fixation of tissue before removal may offer improved accuracy. We employed a triple-label method to measure simultaneously whole brain CBF and CBV in halothane-anesthetized Sprague–Dawley rats, which were then killed either by focused microwave irradiation (≈8 kW of incident power × 770 ms) or by decapitation. CBF was measured with [3H]nicotine while the CBV was determined as the sum of the cerebral red cell volume (CRCV—measured with 99mTc-labeled red cells) and the cerebral plasma volume (CPV—measured with [14C]dextran). Animals were studied during hypocarbic (Paco2 ≈ 25 mm Hg), normocarbic, or hypercarbic (Paco2 ≈ 70 mm Hg) conditions. Added studies were performed to verify that the microwave irradiation scheme used was capable of fixing previously administered tracers in place, and also halting the entry of tracer given after irradiation. Results indicate that the method of killing had no effects on CBF measurements, as assessed either by absolute values during normocarbia or responsiveness to changing Paco2. However, all three volume measurements made using nondiffusible tracers (CRCV, CPV, and CBV) were significantly lower in animals killed by decapitation. Furthermore, CO2 responsiveness for all three variables (as assessed by the slope of the Paco2/volume) was not evident in decapitated animals. We conclude that in situ fixation offers significant advantages when examining the cerebral distribution space of nondiffusible tracers.

The Influence of Intravascular Volume Expansion on Cerebral Blood Flow and Blood Volume in Normal Rats

Background: Intravascular volume expansion can increase cerebral blood flow (CBF) in patients with cerebral ischemia. However, the changes in CBF produced by volume expansion in the normal brain remain the subject of debate, and the changes on cerebral blood volume (CBV; one determinant of intracranial pressure) have not been described. The effects of acute nondilutional volume expansion on cardiac output (CO), CBF, and CBV in normal rats were examined. Methods: Normocarbic, normothermic halothane/N2Oanesthetized rats were given 0, 6,12, 24, or 36 ml of a bloodhetastarch mixture (n=6 for each group). When volume loading was completed, 3H-nicotine was used to measure CBF, while99mTc-labeled red cells and 14C-dextran were used to measure cerebral red cell and plasma volumes. Animals were killed by microwave irradiation (8KW X 770 msec). In different animals, cardiac output (CO) was measured by thermodilution during the infusion of 36 ml of blood-hetastarch. Results:Central venous pressure (CVP) increased from 3.9 ± 0.7 mmHg (mean ± SD) in control animals to 13.0 ± 2.0 mmHg in rats given 36 ml of blood. Cardiac output increased to 138 ± 11% of control. There were no changes in arterial Hct or mean arterial pressure. There were no significant changes in CBF (which varied from 127 ± 22 ml·100 g-1·min-1 in controls to 102 ± 14 after the infusion of 36 ml). However, CBV increased in a linear fashion with increasing CVP, from 2.96 + 0.57 ml/100 g in control conditions to 4.47 ± 0.83 ml/100 g after the infusion of 36 ml of blood/hetastarch. Conclusions:In normal brain, CBF does not change during volume expansion, in spite of an increase in CO. This contradicts earlier studies, the results of which indicate an independent role for cardiac output in CBF control. Cerebral blood volume increased in proportion to CVP, suggesting simple passive venous distention. Whether this could increase ICP and compromise cerebral perfuslon remains unclear.

The Role of Electrode Size on the Incidence of Spreading Depression and on Cortical Cerebral Blood Flow as Measured by H2 Clearance

Cerebral blood flow was measured by the H2 clearance method 30 and 60 min after the implantation of 300, 250, 125, or 50 μm diameter platinum–iridium electrodes 2 mm deep into the right parietal cortex of normothermic, normocarbic halothane-anesthetized rats. Another group of animals had 50 μm electrodes inserted 1 mm. In all animals, the presence or absence of a wave of spreading depression (SD) was noted at the time of implantation, with recordings made with glass micropipettes. H2 flow values were compared with those measured in gray matter from the same anatomical region (but from different rats), using [3H]nicotine. The incidence of SD ranged from 60% following insertion of 300 μm electrodes to 0% with 50 μm electrodes. H2 clearance flows also varied with electrode size, from 77 ± 21 ml 100 g−1 min−1 (mean ± standard deviation) with 300 μm electrodes to 110 ± 31 and 111 ± 16 ml 100 g−1 min−1 with 125 and 50 μm electrodes, respectively (insertion depth of 2 mm). A CBF value of 155 ± 60 ml 100 g−1 min−1 was obtained with 50 μm electrodes inserted only 1 mm. Cortical gray matter blood flow measured with [3H]nicotine was 154 ± 35 ml 100 g−1 min−1. When the role of SD in subsequent flow measurements was examined, there was a gradual increase in CBF between 30 and 60 min after electrode insertion in those animals with SD, while no such change was seen in rats without SD. These results indicate that the choice of electrode size and implantation depth influences the measurement of CBF by H2 clearance. CBF values equivalent to those obtained with isotopic techniques can be acutely obtained with small (50 μm diameter) electrodes inserted 1 mm into the cortex. While the occurrence of SD does influence CBF in the period immediately after implantation, a relationship between electrode size and measured flow is present that is independent of SD.

Effect of Nitrous Oxide on Neurologic and Neuropsychological Function after Intracranial Aneurysm Surgery

Background:Laboratory studies suggest that nitrous oxide augments brain injury after ischemia or hypoxia. The authors examined the relation between nitrous oxide use and outcomes using data from the Intraoperative Hypothermia for Aneurysm Surgery Trial. Methods:The Intraoperative Hypothermia for Aneurysm Surgery Trial was a prospective randomized study of the impact of intraoperative hypothermia (temperature = 33°C) versus normothermia (temperature = 36.5°C) in patients with aneurysmal subarachnoid hemorrhage undergoing surgical clipping. Anesthesia was dictated by a limited-options protocol with the use of nitrous oxide determined by individual anesthesiologists. All patients were assessed daily for 14 days after surgery or until hospital discharge. Neurologic and neuropsychological testing were conducted at 3 months after surgery. Outcome data were analyzed via both univariate tests and multivariate logistic regression analysis correcting for factors thought to influence outcome. An odds ratio (OR) greater than 1.0 denotes a worse outcome in patients receiving nitrous oxide. Results:Outcome data were available for 1,000 patients, of which 373 received nitrous oxide. There was no difference between groups in the development of delayed ischemic neurologic deficit. At 3 months after surgery, there were no significant differences between groups in any outcome variable: Glasgow Outcome Score (OR, 0.84; 95% confidence interval [CI], 0.63–1.14; P = 0.268), National Institutes of Health Stroke Scale (OR, 1.29; 95% CI, 0.96–1.73; P = 0.087), Rankin Disability Score (OR, 0.84; 95% CI, 0.61–1.15; P = 0.284), Barthel Activities of Daily Living Index (OR, 1.01; 95% CI, 0.68–1.51; P = 0.961), or neuropsychological testing (OR, 1.26; 95% CI, 0.85–1.87; P = 0.252). Conclusions:In a population of patients at risk for ischemic brain injury, nitrous oxide use had no overall beneficial or detrimental impact on neurologic or neuropsychological outcomes.

A Focal Cryogenic Brain Lesion Does Not Reduce the Minimum Alveolar Concentration for Halothane in Rats

BackgroundA focal cortical cryogenic brain injury has been reported to reduce the brain pentobarbital concentrations needed to prevent movement in response to pain in rats. This occurred despite any apparent behavioral changes in the awake animals. To determine whether this was true with other anesthetics, the authors determined the minimum alveolar concentration (MAC) for halothane in normothermic, normocarbic ventilated Sprague-Dawley rats previously subjected to a freezing injury of the parietal cortex. MethodsInjury was produced in halothane-anesthetized rats by applying a cold (–70° C), 4-mm-diameter brass rod to the exposed dura for 5 or 15 s. Animals then were studied 3 days after injury, a time when cerebral metabolism in the Ipsilateral hemisphere reaches a minimum. Minimum alveolar concentration was determined using a tail-clamp stimulus, combined with end-tidal anesthetic sampling. In addition, exploratory activity was measured by the open field test just before MAC determination, and spontaneous nocturnal motility was monitored by an electronic motion sensor during the night before testing. ResultsIn normal animals subjected only to preparatory surgery, MAC was 1.10 ± 0.07% (mean ± SD). Almost identical values were found in rats subjected to 5− and 15-s cryogenic injuries (1.11 ± 0.07% and 1.08 ± 0.06%, respectively). There were no intergroup differences in open field test results or in spontaneous nocturnal activity. ConclusionsThese results indicate that a focal cortical brain injury that has no obvious neurologic or behavioral effects in the awake rat does not alter halothane requirements.

The influence of halothane, isoflurane, and pentobarbital on cerebral plasma volume in hypocapnic and normocapnic rats

Cerebral blood volume (CBV = cerebral plasma volume [CPV] + cerebral red cell volume [CRBCV]) is one determinant of intracranial pressure. In an effort to quantitate the effects of anesthetics and PaCO2 on CBV, the authors measured cerebral plasma volume (CPV) in normocapnic (PaCO2 approximately 42 mmHg) and hypocapnic (PaCO2 approximately 22 mmHg) rats receiving 1 MAC doses of isoflurane or halothane, or given an approximately equivalent dose of pentobarbital. All animals were paralyzed, their lungs mechanically ventilated, and body temperature kept normal throughout the study. CPV was measured using 14C-labeled dextran, a large (70,000 molecular weight [M.W.]), nondiffusible compound that was given intravenously and allowed to circulate for approximately 5 min. The experiments then were terminated by freezing the brains in situ with liquid N2 poured into a funnel affixed to the exposed calvarium. Isotope concentrations in solubilized brain and in plasma were determined by scintillation counting, and CPV was calculated as the ratio between these values. CPV during both hypocapnic and normocapnic pentobarbital anesthesia was less than with either volatile agent. During normocapnia, CPV for pentobarbital = 2.1 +/- 0.26 ml/100 g (mean +/- SD, n = 8), compared with 2.96 +/- 0.44 ml/100 g (n = 9) and 3.06 +/- 0.44 ml/100 g (n = 9) for halothane and isoflurane, respectively. There were no differences in CPV between the two volatile agents during normocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

A Comparison of the Effects of Halothane, Isoflurane, and Pentobarbital Anesthesia on Intracranial Pressure and Cerebral Edema Formation Following Brain Injury in Rabbits

To evaluate the impact of anesthetics on the evolution of a cerebral injury, 33 rabbits were subjected to a cryogenic brain lesion, followed by 10 h of anesthesia with 1 MAC halothane or isoflurane (n = 11 each) or with an equipotent dose of pentobarbital (n = 11). The lungs were ventilated to a PaCO2 = 30-35 mmHg with O2/air and normothermia was maintained. Intracranial pressure (ICP), mean arterial pressure (MAP), central venous pressure (CVP), arterial blood gases, and pH, osmolality, and other blood chemistries were recorded. Fifteen minutes after surgery, a left parietal injury was produced with liquid N2. A MAP greater than 70-75 mmHg was maintained throughout the study, using angiotensin II as needed, and CSF was removed if severe intracranial hypertension (ICP greater than 30 mmHg) threatened to reduce cerebral perfusion pressure (CPP = MAP-ICP) below 40 mmHg. 10 h after injury, the animals were killed, and edema formation assessed by: A) the wet weight of the two hemispheres; B) water content (%H2O; wet-dry weight) of the posterior aspect of the hemispheres; and C) specific gravity (SpGr) of tissue samples taken adjacent to and distant from the lesion. Animals given pentobarbital had higher MAPs until 3 h after the lesion had been induced. There were no subsequent intergroup differences in MAP, and no differences at any time in CVP, PaO2, PaCO2, pH, total fluids, or urine output. ICP increased in all animals, but with no significant intergroup differences (ICP in halothane animals was numerically lower). There were no clear differences in the incidence of ventricular drainage (1 halothane, 5 isoflurane, 3 pentobarbital; P = 0.16). In spite of CSF drainage and angiotensin, CPP