Application of practice guidelines to anesthesiology.
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Anesthesiology↗
Biomedical subjects
F Dexter
Publications and source records attributed to F Dexter.
Comparison of the effects of propofol and pentobarbital on neurologic outcome and cerebral infarct size after temporary focal ischemia in the rat.
BACKGROUND: Although propofol is known to have effects on cerebral physiology similar to the barbiturates, a direct comparison of the relative effects of these drugs on outcome from cerebral ischemia has not been performed. The authors postulated that pentobarbital or propofol would yield similar effects on neurologic and histologic outcome from temporary focal ischemia in the rat. METHODS: Wistar rats were anesthetized with sufficient doses of pentobarbital (n = 20) or propofol (n = 20) to cause electroencephalographic burst suppression. The middle cerebral artery was then occluded for 75 min. Animals were awakened 4-6 h after onset of reperfusion and allowed to recover for 1 week. Neurologic function and infarct size were then assessed. RESULTS: Relevant physiologic values were similar between groups during ischemia and early reperfusion. No difference between groups was observed for severity of hemiparesis (P = 0.10). Total cerebral infarct volumes (median +/- quartile deviation) were similar for the two groups (pentobarbital = 190 +/- 36 mm3; propofol = 200 +/- 24 mm3, P = 0.35). CONCLUSION: Neurologic and histologic outcome were similar in pentobarbital or propofol anesthetized rats undergoing temporary focal cerebral ischemia and a 1-week recovery interval.
Anesthetics, Intravenous↗
Research synthesis of controlled studies evaluating the effect of hypocapnia and airway protection on cerebral outcome.
Hyperventilation is a standard method of treating patients with intracranial hypertension. I reviewed all the relevant peer-reviewed literature to identify the documented benefits of hyperventilation as treatment for cerebral disease. Studies were identified by searches of the Medline database between 1966 and September 1996, interviews with experts, and reviews of reference lists. Retained manuscripts reported results of a human or animal controlled trial that tested effect of hyperventilation and/or systemic hypocapnia on mortality, histopathology, or neurologic examination. Studies could be either randomized or observational and need not have been blinded. I found that for no clinical studies of cerebral disease, other than in acute head injury patients, was there any suggestion of a clinical benefit from hyperventilation. Three controlled, observational studies examined effects of airway management and ventilatory support in head-injured patients. These studies found that maintaining such patients hypocapnic, versus spontaneously breathing without ventilatory support, decreased mortality. However, by design the studies could not establish whether hypocapnia itself contributed to the decreased mortality. Two clinical studies examined the effect of PaCO2 itself in patients with head injury. In both, hypocapnic patients did not have better neurologic outcome. In conclusion, securing the airway and supporting ventilation probably reduces mortality in unconscious, neurosurgical patients. However, there are virtually no clinical data that hypocapnia improves outcome in patients with cerebral disease.
Animals↗
High-dose fentanyl does not adversely affect outcome from forebrain ischemia in the rat.
Fentanyl citrate has properties, including agonism of the mu-opioid receptor and proconvulsant activity, that theoretically could pose adverse effects in ischemic brain. This study examined the effects of high-dose fentanyl on outcome in rats subjected to transient near-complete forebrain ischemia. Rats were anesthetized with halothane and surgically prepared for ischemia. In one group (fentanyl; n = 15), intravenous fentanyl (400 micrograms/kg followed by an infusion of 16 micrograms/kg/min for 20 min) was administered and halothane was discontinued. In the remaining rats (control: n = 15), halothane administration was continued and no fentanyl was given. Following 10 min of bilateral carotid artery occlusion and profound systemic hypotension, animals were maintained normocapnic, normothermic, and mildly hyperoxemic for 8 h. Four days later, histologic and neurologic outcomes were assessed. In another group of rats also administered halothane (uncontrolled recovery; n = 15), no attempt was made to control physiologic variables during recovery from ischemia. Fentanyl caused preischemic evidence of epileptoid activity but decreased the percentage of neurons that died in the CA1 sector of the hippocampus relative to control (p = 0.0005). Damage in the cortex or caudoputamen was not different from that in the control group. Rats with an uncontrolled recovery had decreased damage in the cortex (p = 0.005) and caudoputamen (p = 0.00015) relative to control. In this model of forebrain ischemia, fentanyl caused no worsening of histologic damage in the cortex or caudoputamen and decreased hippocampal CA1 injury despite major electroencephalographic activation in the immediate preischemic period.
Anesthesia↗
Anesthesia providers' interventions during cataract extraction under monitored anesthesia care.
In 1993 Medicare paid more money to anesthesia providers for cataract surgery than for any other surgical procedure. Patients undergoing cataract surgery often receive monitored anesthesia care (MAC). Thus, cuts in anesthesia payments from Medicare for cataract surgery may be forthcoming. If few interventions were being done after a retrobulbar block was placed, then a registered nurse might be a safe alternative to an anesthesia provider to monitor the patient. The goal of this study was to describe interventions of anesthesia providers during cataract extraction after the placement of a retrobulbar block. Anesthetic records were reviewed for 560 consecutive cases of cataract extraction using MAC at a large tertiary medical center. Anesthesia providers performed interventions (e.g., administration of drugs) on 33% of patients after the retrobulbar block was in place (95% confidence bound, < 36%). In conclusion, insufficient evidence exists for managed care organizations or other groups to justify a change in practice toward a registered nurse monitoring patients undergoing cataract extraction with a retrobulbar block. Furthermore, until a prospective randomized study has been done, such organizations lack justification for decreasing the amount of time that anesthesia providers spend caring for such patients undergoing cataract extraction.
Cataract Extraction↗
Ethanol-induced changes in prostaglandin E concentration in the intact cerebral cortex of preterm and near-term fetal sheep.
Ethanol-induced changes in fetal prostaglandin E (PGE) concentration may play a role in the toxic effects of prenatal ethanol exposure. Using the novel technique of in utero microdialysis, the present study tested the hypothesis that acute ethanol exposure changes PGE concentration in the intact cerebral cortex of preterm (93 +/- 1 days of gestation) and near-term (124 +/- 1 days of gestation; term, approximately 147 days) fetal sheep. Fetal sheep were surgically instrumented with a microdialysis probe placed in the parasagittal parietal cortex. Three days later, the effects of maternal infusion of 1 g of ethanol/kg maternal body weight on preterm (n = 6) and near-term (n = 7) fetal cerebral cortical and plasma PGE concentrations were determined. In the preterm fetal cerebral cortex, PGE concentration was increased after ethanol infusion in all six animals studied. The median peak increase was 160% with a 95% confidence interval of 115 to 784%. There was considerable variation in the time of occurrence, magnitude, and duration of this increase. In the near-term fetal cerebral cortex, an increase in PGE concentration was observed after ethanol infusion in 5 of the 7 animals studied, whereas a decrease in PGE concentration was observed in the other two animals. Overall, ethanol did not increase significantly near-term fetal cerebral cortical PGE concentration. For both age groups, ethanol infusion had no effect on fetal plasma PGE concentration. These data indicate that ethanol can affect PGE production in the fetal cerebral cortex and that this effect seems to be gestational-age-dependent.
Animals↗
Assessment of primary and salvage lateral mass screw insertion torque in a cadaveric model.
This study was performed to determine the insertion torques of three types of lateral mass screws and to explore their relationship to bone mineral density (BMD). The peak insertion torque of primary articular screws was measured, and the holes were then stripped by overtightening. Larger diameter "salvage" screws were placed in the stripped holes, and peak insertion torque was measured. Peak primary screw insertion torque and BMD were positively correlated (r = 0.48, p = 0.00001). The ratio of salvage to primary screw insertion torque varied significantly among the systems (p = 0.0003). The positive correlation between BMD and primary screw peak insertion torque confirms the importance of bone density for satisfactory screw purchase. The large variation in the ratio of salvage to primary screw insertion torque among systems may be due to differences in primary and salvage screw design.
Bone Density↗
Flumazenil does not affect the increase in rat hippocampal extracellular glutamate concentration produced during thioacetamide-induced hepatic encephalopathy.
Hepatic encephalopathy (HE) is a neuropsychiatric disorder that often occurs as a consequence of acute or chronic liver failure. Previous reports have suggested that alterations in amino acid neurotransmission, particularly glutamate, may play an important role in the pathogenesis of HE. The objectives of the present study were to test the hypothesis that extracellular glutamate concentration is increased during HE, and to determine if flumazenil, a benzodiazepine antagonist, alters the extracellular concentration of glutamate during HE. The experimental approach involved using microdialysis probes to measure rat hippocampal extracellular glutamate concentration. HE was brought about as a result of thioacetamide-induced liver failure. Thioacetamide produced behavioral and metabolic effects, such as somnolence, hyperventilation and hyperammonemia, consistent with stage three HE. Comparison with saline-treated rats demonstrated that HE was associated with a significant increase (p = 0.010) in extracellular hippocampal glutamate concentration. Administration of flumazenil caused a transient increase in arousal level, but did not affect the increase in glutamate concentration (p = 0.93). These results corroborate the theory that glutamate neurotransmission is altered during HE and suggest that the flumazenil arousal of HE rats is not mediated by a change in extracellular glutamate concentration.
Animals↗
Application of cost-utility and quality-adjusted life years analyses to monitored anesthesia care for sedation only.
STUDY OBJECTIVE: To determine how much society should spend to decrease anxiety lasting for the duration of a surgical case. DESIGN: Indications for monitored-anesthesia care (MAC) include: (1) management of an unstable patient, (2) possible induction of general anesthesia, (3) need for the patient to be unconscious for part of the case, and (4) provision of sedation and/or analgesia. The first three indications facilitate quality surgical care. However, MAC solely to decrease anxiety has been criticized on economic grounds. Although MAC for these cases may improve the patient's experience during surgery, it does not facilitate safer surgery. I limited my theoretical analysis to (1) MAC for sedation only and (2) procedures that have an equal outcome with or without an anesthesiologist. Cost-utility analyses compare costs and benefits of technologies by using a common measure of health outcomes. The quality adjusted life year (QALY) gives the expected life years gained from a procedure, with each year weighted to reflect quality of life in that year. Quality of life generally ranges from zero (dead) to one (healthy without distress). Technologies costing more than $75,000 per QALY are usually considered too expensive to justify. I used a deliberately absurd, one unit change in quality of life to calculate the maximum hourly cost of MAC, which lets the cost per QALY be less than $75,000. MEASUREMENTS AND MAIN RESULTS: Hourly cost must be less than $8.56 per hour. Current Medicare reimbursement corresponds to $876,000 per QALY. CONCLUSION: MAC for sedation only is a very expensive technology compared with other medical interventions.
Ambulatory Surgical Procedures↗
Application of prediction levels to OR scheduling.
Many perioperative managers record operating room times (ORTs) and use average ORTs to facilitate scheduling of elective surgical procedures. A second statistic, the upper 95% prediction level (ie, 95% chance the next ORT will be less than the upper prediction level) can be calculated from previous ORTs and used in scheduling elective procedures. The author used eight elective surgical procedures to test a distribution-free method for calculating ORT upper prediction levels. Upper prediction levels can provide perioperative managers better knowledge than average ORTs to facilitate decision making during the scheduling of elective surgical procedures. This method can be used to find upper prediction levels for any desired measure of procedure duration (eg, surgeon, scheduled procedure-specific times).
Appointments and Schedules↗
Magnesium sulfate adversely affects fetal lamb survival and blocks fetal cerebral blood flow response during maternal hemorrhage.
Magnesium sulfate is commonly used in high-risk pregnancies, even though its actions in the fetus during maternal/fetal stress are not completely understood. The present study tested the hypothesis that magnesium sulfate alters the fetal cerebral blood flow response to hypoxemia produced during maternal hemorrhage. It was conducted in instrumented near-term fetal lambs at 123 days of gestation. Experimental treatment involved four periods of maternal hemorrhage over a 60-min period during fetal infusion of 0.25 g (n = 5) or 0.30 g (n = 6) magnesium sulfate, or normal saline (n = 11). The level of fetal cerx500l blood flow was determined using radiolabeled microspheres. For all three treatment groups, maternal hemorrhage produced fetal hypoxemia and some fetal demise. During fetal infusion of saline, 1 of 11 (9%) of the fetuses died; with the 0.25-g magnesium sulfate regimen, 1 of 5 (20%) died; and with the 0.30-g magnesium sulfate regimen, 3 of 6 (50%) of the fetuses died. Magnesium sulfate caused an increase in the proportion of fetal death produced by maternal hemorrhage (P < 0.05). Among surviving fetuses, hemorrhage-induced hypoxemia increased fetal cerebral blood flow during saline infusion. In contrast, infusion of magnesium sulfate had an inhibitory effect on this compensatory increase in fetal cerebral blood flow (P = 0.003). These data indicate that, in the sheep, magnesium sulfate increases fetal mortality and inhibits the compensatory increase in fetal cerebral blood flow during maternal hemorrhage-induced fetal hypoxemia.
Animals↗
The effects of plasma and brain magnesium concentrations on lidocaine-induced seizures in the rat.
Lidocaine and MgSO4 are often coadministered to patients with pregnancy-induced hypertension. This study examined whether MgSO4 alters the lidocaine-seizure threshold in the rat and, if so, whether systemic MgSO4 administration is as effective as intracerebroventricular MgSO4 infusion. In Experiment 1, rats were administered 50% MgSO4 or 0.9% NaCl intravenously (IV) (20 microL/h) for 5 days. In Experiment 2, rats were administered 0.9% NaCl, 0.8% MgSO4, or 2.0% MgSO4 (10 microL/h) via intracerebroventricular infusion for 24 h. All rats then underwent continuous IV lidocaine infusion until onset of electroencephalographic seizures. In Experiment 1, plasma [Mg2+] was greater in the MgSO4 group (5.1 +/- 1.5 mg/dL vs 1.8 +/- 0.3 mg/dL) but neither the dose of lidocaine required to induce seizures (MgSO4 = 19 +/- 2 mg/kg; saline = 23 +/- 5 mg/kg) nor brain [Mg2+] (MgSO4 = 794 +/- 17 micrograms/g; saline = 788 +/- 33 micrograms/g) were changed. In Experiment 2, intracerebroventricular MgSO4 increased both brain [Mg2+] (2% MgSO4 = 923 +/- 79 micrograms/g; saline = 788 +/- 35 micrograms/g) and the lidocaine seizure dose (2% MgSO4 = 39 +/- 7 mg/kg; saline = 26 +/- 3 mg/kg). Although intracerebroventricular administration of MgSO4 produces an anticonvulsant effect, chronic hypermagnesemia does not alter whole brain [Mg2+] and therefore offers no protection from lidocaine-induced seizures in this model.
Animals↗
Theoretical assessment of normobaric oxygen therapy to treat pneumocephalus.
BACKGROUND: Pneumocephalus has been linked to several clinical conditions, including headache, lethargy, and even brain herniation or death. The effects of different normobaric oxygen concentrations and durations of therapy on the rate of air absorption were examined. METHODS: An existing mathematical model of inert gas absorption was used. The model accounts for the major phenomena that determine absorption of bubbles, including surface tension, pressure dependence of bubble size, and removal of gases to the surrounding tissue. Sensitivity analysis tested reliability of our results. RESULTS: Times for a 50-ml air collection to have been absorbed were 5.8, 1.9, and 0.6 weeks at an FIO2 of 0.21, 0.4, and 1.0 respectively. Thirty percent and 72% of the air was absorbed in 2 days at an FIO2 of 0.4 and 1.0, respectively. The percent decrease in time for absorption achieved by increasing the FIO2 from 0.21 was nearly identical for different volumes of air. The benefit of increasing the FIO2 decreased with progressive increases in the FIO2. Increasing the FIO2 from 0.21 to 0.4 caused the time to total air absorption to decrease by 67%. In contrast, increasing the FIO2 from 0.8 to 1.0 caused the time to total air absorption to decrease by an additional 3%. CONCLUSIONS: Based on mathematical model predictions, an FIO2 of 0.4 or 1.0 for at least 1 week or 2 days, respectively, will significantly decrease the time for absorption of a pneumocephalus.
Humans↗
Rapid rewarming causes an increase in the cerebral metabolic rate for oxygen that is temporarily unmatched by cerebral blood flow. A study during cardiopulmonary bypass in rabbits.
BACKGROUND: Jugular venous hemoglobin desaturation during the rewarming phase of cardiopulmonary bypass is associated with adverse neuropsychologic outcome and may indicate a pathologic mismatch between cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2). In some studies, rapid rewarming from hypothermic cardiopulmonary bypass results in greater jugular venous hemoglobin desaturation. The authors wished to determine if rewarming rate influences the temperature dependence of CBF and CMRO2. METHODS: Anesthetized New Zealand white rabbits, cooled to 25 degrees C on cardiopulmonary bypass, were randomized to one of two rewarming groups. In the fast group (n = 9), aortic blood temperature was made normothermic within 4 min. In the slow group (n = 9), aortic blood temperature was made normothermic over 25 min. Cerebral blood flow (microspheres) and CMRO2 (Fick) were determined at baseline (25 degrees C), and at brain temperatures of 28 degrees, 31 degrees, 34 degrees, and 37 degrees C during rewarming. RESULTS: Systemic physiologic variables appeared similar between groups. At a brain temperature of 28 degrees C, CMRO2 was 47% greater in the fast rewarming group than in the slow group (2.2 +/- 0.5 vs. 1.5 +/- 0.2 ml O2.100 g-1. min-1, respectively; P = 0.01), whereas CBF did not differ (48 +/- 18 vs. 49 +/- 8 ml.100 g-1.min-1, respectively; P = 0.47). Throughout rewarming, CBF increased as a function of brain temperature but was indistinguishable between groups. Cerebral metabolic rate for oxygen differences between groups decreased as brain temperatures increased. CONCLUSIONS: Cerebral venous hemoglobin desaturation with rapid rewarming is caused by an increase in CMRO2 that is temporarily greater than the increase in CBF. This mismatch may indicate a transient abnormality in flow-metabolism coupling, or the effect of temperature gradients on oxygen transfer from hemoglobin to brain.
Animals↗
Electroencephalographic burst suppression is not required to elicit maximal neuroprotection from pentobarbital in a rat model of focal cerebral ischemia.
BACKGROUND: Barbiturates have previously been demonstrated to reduce focal cerebral ischemic brain damage. However, the dose of drug required to elicit maximal neuroprotection has not been defined. The authors' hypothesized that doses of pentobarbital substantially lower than those required to cause electroencephalographic burst suppression would result in maximal magnitudes of reduction of cerebral infarct volume. METHODS: Wistar rats underwent 90 min of filament occlusion of the middle cerebral artery while either awake (control), or anesthetized with intravenous sodium pentobarbital administered to preserve an active electroencephalogram (15-23 mg.kg-1.h-1) or a pattern of burst suppression (45-60 mg.kg-1.h-1; n = 17). During ischemia and for the first 6 h of recirculation, brain temperature was rigorously controlled at 38.0 +/- 0.2 degrees C. Rats were allowed a recovery interval of 7 days after which neurologic function and cerebral infarct volume were assessed. In nonischemic rats undergoing a similar anesthetic protocol, the cerebral metabolic rate of glucose utilization was measured at each anesthetic depth. RESULTS: Relevant physiologic values were similar between groups. Total infarct volume (mean +/- SD) was smaller in the active electroencephalogram group than in the control group (124 +/- 68 mm3 versus 163 +/- 66 mm3; P < 0.05). Increasing the dose of pentobarbital (burst suppression) did not further decrease infarct volume (128 +/- 54 mm3). Neurologic score and infarct volume were positively correlated (P < 0.001). Cerebral metabolic rate of glucose utilization was reduced by 56% in the burst suppression group versus 43% in the active electroencephalogram pentobarbital group (P < 0.001). CONCLUSIONS: Sodium pentobarbital administered at either dose (active electroencephalogram or burst suppression) resulted in an approximately equal to 25% reduction of cerebral infarct size, indicating that burst suppression is not required to elicit maximal neuroprotective efficacy.
Animals↗
Applications of information systems to operating room scheduling.
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Appointments and Schedules↗
Somatosensory evoked potentials correlate with neurological outcome in rabbits undergoing cerebral air embolism.
BACKGROUND AND PURPOSE: Somatosensory evoked potentials (SSEPs) have been used as an outcome measure in models of cerebral air embolism despite the lack of studies correlating SSEPs with other measures of neurological injury. We examined the relationship between SSEPs and neurological impairment in the setting of cerebral air embolism. METHODS: Anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 microL/kg of air into the internal carotid artery. SSEPs were recorded at intervals for the subsequent 2 hours. After the final recording the anesthetic was discontinued, and the animals recovered. Animals were neurologically evaluated at 3 and 24 hours after cerebral air embolism on a scale of zero (normal) to 97 (coma) points. RESULTS: There was a clear relationship between the dose of air and 2-hour SSEP amplitude (P = .00003). SSEP amplitudes at 2 hours were inversely correlated with neurological impairment scores at 3 hours (r = -0.71, P < .0001). SSEP amplitudes at 2 hours were less in animals that died (11 +/- 16%; n = 9) than in those that survived to 24 hours (53 +/- 20%; n = 9) (P = .0008). CONCLUSIONS: These results support SSEPs as an index of neurological impairment in this model of cerebral air embolism.
Animals↗
Heparin reduces neurological impairment after cerebral arterial air embolism in the rabbit.
BACKGROUND AND PURPOSE: Neurological injury after cerebral air embolism may be due to thromboinflammatory responses at sites of air-injured endothelium. Because heparin inhibits multiple thromboinflammatory processes, we hypothesized that heparin would decrease neurological impairment after cerebral air embolism. METHODS: To first establish a dose of air that would cause unequivocal neurological injury, anesthetized New Zealand White rabbits received either 0, 50, 100, or 150 microL/kg of air into the internal carotid artery (n = 5 in each group). One hour later, anesthesia was discontinued. Animals were neurologically evaluated at 24 hours with the use of a scale ranging from 0 (normal) to 97 (coma) points. In a subsequent experiment, anesthetized rabbits received either heparin (n = 17) or saline (n = 15) 5 minutes before air injection (150 microL/kg). Heparin was given as a 200-IU/kg bolus and followed by a constant infusion of 75 IU.kg-1.h-1 for 2 hours. Equal volumes of saline were given to control rabbits. Two hours later, anesthesia was discontinued. Animals were neurologically evaluated 24 hours after air embolism. RESULTS: There was a monotonic relationship between dose of air and severity of neurological impairment at 24 hours (P = 1.1 x 10(-7)). Animals receiving 150 microL/kg of air were unequivocally injured (score, 60 +/- 16). In the second experiment, heparin animals had significantly less neurological impairment at 24 hours (34 +/- 14) than saline controls (52 +/- 8) (P = .0013). CONCLUSIONS: When given prophylactically, heparin decreases neurological impairment caused by severe cerebral arterial air embolism.
Animals↗