Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1997
Randomized Controlled Trial Clinical TrialTeaching the use of fiberoptic intubation for children older than two years of age.
In 144 anesthetized children aged 2-9 yrs, the safety and feasibility of orotracheal fiberoptic intubation, with and without an airway endoscopy mask, were assessed and compared with laryngoscopic intubation. Eight anesthesia residents with experience in adult fiberoptic intubation, but who were beginners in pediatric anesthesia, participated in this study. In a randomized fashion, each resident intubated 18 children (6 in each group). The time (mean +/- SD) to achieve successful intubation was different for laryngoscopic and fiberoptic intubation (34 +/- 17 s and 80 +/- 39 s, respectively; P < 0.001). The use of the airway endoscopy mask further prolonged fiberoptic intubation (167 +/- 121 s, P < 0.001). Spo2 values remained >95% in all patients during conventional laryngoscopy and fiberoptic laryngoscopy with a mask, whereas Spo2 decreased below 95% in 2 of the 48 patients during fiberoptic intubation without a mask. Both patients promptly recovered during ventilation via a face mask. We conclude that teaching the use of fiberoptic intubation in healthy, anesthetized children aged 2-9 yrs is safe and feasible. ⋯ Fiberoptic intubation is a valuable technique of airway management. We studied the feasibility and safety of a training program that could be used for children more than 2 yrs old. This study demonstrates that fiberoptic intubation can be effectively practiced in pediatric patients without increased risk of side effects.
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Anesthesia and analgesia · Nov 1997
Randomized Controlled Trial Clinical TrialThe differential effects of prostaglandin E1 and nitroglycerin on regional cerebral oxygenation in anesthetized patients.
We evaluated the effects of prostaglandin E1 (PGE1) and nitroglycerin (NTG) on regional tissue oxygenation and use in the brain using near infrared spectroscopy (NIRS). Twenty-four patients who underwent elective cardiac surgery were randomly divided into two groups. The study was performed after the induction of anesthesia and before the start of the surgical procedure. After measuring arterial and jugular venous blood gases, cardiovascular hemodynamics, and relative cerebral oxyhemoglobin (HbO2), deoxyhemoglobin, and cytochrome aa3 at the baseline, PGE1 (n = 12) or NTG (n = 12) was infused intravenously at a rate of 0.3 g/kg or 5 g/kg, respectively. Thirty minutes after the start of drug infusion, administration of the drugs was stopped. Both PGE1 and NTG reduced mean arterial pressure to approximately 70% of the baseline value 10, 20, and 30 min after start of drug infusion (P < 0.05). Internal jugular venous pressure increased significantly during NTG but not during PGE1 infusion (P < 0.05). PGE1 increased HbO2 concentration, which was sustained for 30 min after discontinuing the drug. NTG increased HbO2 concentration, but this gradually returned to the baseline level after discontinuation of the drug. Baseline value of jugular oxygen saturation was 64.5% +/- 2.1%, and there was no significant changes during the infusion of PGE1 or NTG. These results demonstrate that both NTG and PGE1 increased cerebral oxygen saturation as measured by NIRS. This may be explained by local cerebral hyperemia without major alteration in flow/metabolism coupling of brain. The onset of this increase was slower and the duration of this effect after discontinuation of the drug was more prolonged with PGE1. These phenomena occurred despite the relatively similar time course of the effect of these two drugs on systemic hemodynamic values. ⋯ The cerebrovascular effects of vasodilators used for induced hypotension are not fully understood. In this study, we used near infrared spectrometry and jugular oxygen saturation measurement to assess the effects of prostaglandin E1 and nitroglycerin on cerebral perfusion. We found that nitroglycerin and prostaglandin E1 increase cerebral oxygen saturation as measured by near infrared spectrometry, but with different time courses. This information will hopefully help anesthesiologists to better maintain adequate regional cerebral oxygenation.
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Anesthesia and analgesia · Nov 1997
Risk factors for neurologic deterioration after revascularization surgery in patients with moyamoya disease.
To investigate the risk factors for postoperative neurological deterioration in patients with moyamoya disease, we retrospectively reviewed the perioperative course of 368 cases of revascularization surgery in 216 patients with this disease. Risk factors anecdotally associated with postoperative ischemic events were analyzed by comparing groups with or without a history of such events on the operative day. Ischemic events were noted in 14 cases (3.8%), 4 of which were defined as strokes and the others as transient ischemic attack (TIA). Postoperative neurological deterioration more often developed in patients who suffered from frequent TIAs, had precipitating factors for TIA, and underwent indirect nonanastomotic revascularization. The authors conclude that the incidence of postoperative ischemic events were related more to the severity of moyamoya disease and the type of surgical procedure than to other factors, including anesthetic management. ⋯ Although preventing stroke is the major concern for patients with moyamoya disease, risk factors for perioperative cerebral ischemia have not been clarified. We retrospectively analyzed the perioperative course in 368 cases with this disease and found that the severity of the disease and type of surgical procedure were major determinants of postoperative cerebral ischemia.
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Anesthesia and analgesia · Nov 1997
Effects of inhaled nonimmobilizer, proconvulsant compounds on desflurane minimum alveolar anesthetic concentration in rats.
Anesthetics depress the central nervous system, whereas nonimmobilizers (previously called nonanesthetics) and transitional compounds having the same physical properties (e.g., solubility in lipid) do not produce anesthesia (nonimmobilizers) or are less potent anesthetics than might be predicted from their lipophilicity (transitional compounds). Potential explanations for the absent or decreased anesthetic effect of nonimmobilizer and transitional compounds include the theories that the nonimmobilizers are devoid of anesthetic effect and that transitional compounds have a decreased capacity to produce anesthesia; that the effects of these compounds are not apparent because the concentrations examined are too low; or that anesthesia, or lack thereof, results from a balance between depression and excitation (all nonimmobilizer and transitional compounds produce convulsions). To examine these issues further, we tested the effect of various multiples of the convulsive 50% effective dose (ED50) of three nonimmobilizers and one transitional compound on the minimum alveolar anesthetic concentration (MAC) of desflurane in rats. The nonimmobilizer 2,3-dichlorooctafluorobutane (NI-1), from 0.7 to 1.1 times its convulsive ED50, increased the MAC of desflurane by 14%-27%, but at 1.6 times its convulsive ED50 caused no change in MAC; the nonimmobilizer 1,2-dichlorohexafluorocyclobutane (NI-2) did not change MAC at concentrations up to its convulsant ED50, but it increased MAC by 25% and 36% at 1.3 and 1.7 times its convulsant ED50, respectively. The nonimmobilizer flurothyl (NI-3) decreased the MAC of desflurane by 20% +/- 6% (mean +/- SD) at 0.5 times its convulsant ED50, but it caused no change at higher partial pressures (up to 7.8 times its convulsant ED50), and the transitional compound CF3CCl2-O-CF2Cl (T-1) significantly decreased MAC by 16% +/- 7% at 0.8 times its convulsant ED50, but the 6%-8% decreases in MAC at 0.4 and 1.6 times its convulsant ED50 were not significant. Thus, neither nonimmobilizer nor transitional compounds produced a consistent dose-related effect on the MAC of desflurane, and any changes were small. These results suggest that the excitation produced by transitional compounds or nonimmobilizers does not explain their limited ability or inability to produce anesthesia. The data are consistent with a decreased anesthetic efficacy of transitional compounds and the lack of efficacy of nonimmobilizers. ⋯ Inhaled compounds that do not cause anesthesia (nonimmobilizers) are used to test theories of anesthetic action. Their use presumes that a trivial explanation, such as cancelling stimulatory and depressant effects, does not explain the absence of anesthesia. The present results argue against such an explanation.
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Anesthesia and analgesia · Nov 1997
Quantitative differences in the production and toxicity of CF2=BrCl versus CH2F-O-C(=CF2)(CF3) (compound A): the safety of halothane does not indicate the safety of sevoflurane.
Carbon dioxide absorbents degrade both halothane and sevoflurane to toxic unsaturated compounds (CF2=CBrCl and CH2F-O-C[=CF2][CF3] [i.e., Compound A], respectively). Given the long history of safe administration of halothane, comparable toxicities of these degradation products would imply a similar safety of sevoflurane. We therefore examined CF2=CBrCl in the context of four issues relevant to previous studies of the toxicity of Compound A: 1) reactivity of the degradation product in vitro; 2) rate of its production in vitro; 3) its in vivo toxicity; 4) importance of the beta-lyase pathway to the toxicity in vivo. We found the following. 1) CF2=CBrCl is less reactive than Compound A, degrading in human serum albumin at one-fifth the rate of Compound A. 2) Over a 3-h period of "anesthesia," a standard circle system containing Baralyme (Allied Healthcare Products, Inc., St. Louis, MO) produces 30 times as much Compound A from a minimum alveolar anesthetic concentration (MAC) concentration of sevoflurane as CF2=CBrCl from a MAC concentration of halothane; with soda lime, the difference is 60-fold. Correcting for differences in uptake of halothane versus sevoflurane decreases the differences to 20-40 times. 3) For a 3-h administration to rats, the partial pressure of Compound A causing minimal renal injury or necrosis of half the affected tubule cells exceeds the partial pressure of CF2=CBrCl causing minimal injury or necrosis of half the affected tubule cells by a factor of approximately 4-6. Thus, the ratio of production (Item 2 above) to the partial pressure causing injury with CF2=CBrCl is approximately a quarter of that ratio for Compound A. 4) Compounds that block the beta-lyase pathway either do not change (acivicin) or decrease (aminooxyacetic acid; AOAA) renal injury from CF2=CBrCl in rats, whereas these compounds increase (acivicin) or do not change (AOAA) injury from Compound A. We conclude that the safety of halothane cannot be used to support the safety of sevoflurane. ⋯ Carbon dioxide absorbents degrade halothane and sevoflurane to unsaturated compounds nephrotoxic to rats. Relative to sevoflurane's degradation product, halothane's degradation product has less toxicity relative to production, less reactivity, and a different mechanism of injury. The clinical absence of halothane nephrotoxicity does not necessarily indicate a similar absence for sevoflurane.