Recovery parameters after sevoflurane and isoflurane anesthesia

Trauma patients who succumb to their injuries do so by one of several mechanisms discussed in this article. The most common include head injury, exsanguination, sepsis, and multiple organ failure. The article also discusses adverse consequences of hypothermia, including a model for calculating total heat loss.     

Gallstones and diabetes: a case-control study in a free-living population sample

Data on the association between cholelithiasis and diabetes often are controversial and are mostly based on autopsies or on hospital series. Therefore, we designed a case-control study to determine the prevalence of diabetes mellitus in a group of subjects with gallstones or having undergone cholecystectomy (cases) and compared these with a control group of subjects without gallstones, selected during an epidemiological study performed on a free-living population sample. The subjects were matched for sex, age, and body mass index. We enlisted 336 cases and 336 controls, aged 30 to 69 years. All subjects with fasting glycemic levels of < 140 mg/dL and without a documented history of diabetes were submitted to a simplified oral glucose tolerance test (OGTT). All subjects who underwent OGTT were classified according to the National Diabetes Data Group (NDDG) criteria. The prevalence of diabetes in the subjects affected by gallstone disease was significantly higher than that in controls (11.6% vs. 4.8%; odds ratio [OR], 2.55; 95% confidence interval [CI], 1.39-4.67). Diabetes was more frequent in subjects with gallstone disease than in the control group, even according to sex (18.3% vs. 9.9% for men: OR, 2.03; 95% CI, 0.99-4.2; 9.3% vs. 2.6% for women: OR, 3.85; 95% CI, 1.4-10.6). We conclude that an altered glucose metabolism may increase the risk of developing cholelithiasis in certain subjects.     

Waste gas exposure during desflurane and isoflurane anaesthesia

BACKGROUND: Currently, there are no data available concerning the occupational exposure to desflurane during general anaesthesia. This prospective, randomized study reports on occupational exposure to desflurane, compared to isoflurane, in a modern operation theatre (OT). METHODS: The study was performed in an OT equipped with a modern air-conditioning system and with a low-leakage anaesthesia machine connected to a central scavenging system. Trace concentrations of the anaesthetics were measured continuously by means of a photoacoustic infrared spectrometer during general anaesthesia in 30 patients undergoing eye surgery. Values were obtained within the breathing zone of the anaesthetist, the surgeon, the auxiliary nurse and at the mouth of the patient. RESULTS: Desflurane and isoflurane were administered with median (range) endtidal concentrations of 4.7 (3.8-10.3) vol% and 0.9 (0.6-1.4) vol%, respectively. The personnel-related median values of the average trace concentrations of desflurane and isoflurane were 0.5 (0.01-7.5) ppm and 0.2 (0.01-1.6) ppm, respectively. CONCLUSIONS: Occupational exposure to desflurane is low in the environment of a modern OT, even though it has to be administered in approximately 5-fold higher concentrations compared to isoflurane.     

Fatal hepatic necrosis after isoflurane anaesthesia

Several halogenated anaesthetic agents have been associated with hepatotoxicity. We report a case of fulminant, fatal hepatic necrosis after uneventful isoflurane anaesthesia in a patient without previous liver disease, who may have been sensitised by previous exposure to enflurane. Although no anti-trifluoroacetyl antibodies could be detected in the patient's serum, isoflurane hepatotoxicity seems very likely to be the reason for fulminant hepatic failure in this patient.     

The independent metabolic effects of halothane and isoflurane anaesthesia

Twelve healthy, unpremedicated women scheduled for total abdominal hysterectomy were given either isoflurane (n = 6) or halothane (n = 6) anaesthesia. They all received general anaesthesia for a period of 3 h, with surgery being carried out only in the last hour. The anaesthesia consisted of thiopentone, pancuronium and a mixture of oxygen-enriched air (FiO2 = 34%) supplemented with 1 MAC of either isoflurane or halothane. The patients were maintained normothermic, and with an arterial SaO2 above 95% throughout the period of the study. The following measurements were made before, during and after anaesthesia (with and without surgery): oxygen consumption (VO2), carbon dioxide production (VCO2); circulating concentrations of various hormones (insulin, growth hormone and cortisol); various metabolites; selected amino acids and albumin; forearm arterio-venous concentration difference of glucose, lactate, free fatty-acids and selected amino acids (four patients in each group). Whole body VO2 decreased significantly by over 20% during anaesthesia (with or without surgery), P < 0.05). Although the circulating concentration of most amino acids showed little or no change during anaesthesia alone, there was a tendency for the flux of most metabolites to decrease, and this persisted during surgery (P < 0.05). During anaesthesia alone there was a twofold reduction in the plasma cortisol concentration (P < 0.05), and a decrease in albumin concentration (P < 0.01). With the onset of surgery, plasma cortisol concentration increased rapidly (in association with several other hormones and metabolites) but hypoalbuminemia persisted.     

Reduction in post-intubation respiratory resistance by isoflurane and albuterol

PURPOSE: This study examined the bronchodilating effects of 0.6 MAC and 1.1 MAC isoflurane (ISF) on respiratory system resistance (Rrs) following tracheal intubation and determined whether albuterol supplements that effect. METHODS: Sixty-seven adult patients were anaesthetized with 2 micrograms.kg-1 fentanyl and 5 mg.kg-1 thiopentone and their tracheas intubated following administration of 1 mg.kg-1 succinylcholine. Respiratory system resistance was measured following intubation and the patients then randomized to receive either 1.1 MAC ISF in oxygen or 0.6 MAC ISF in 50% nitrous oxide and oxygen. Ten minutes later, Rrs was again measured. Patients were then further randomized to receive albuterol or a placebo using incremental doses of 2, 5, and 10 puffs (albuterol puff = 90 micrograms) delivered via a metered dose inhaler at ten minute intervals. RESULTS: Isoflurane at 1.1 MAC decreased post-intubation Rrs by 23 +/- 5% (mean +/- sem) whereas the decrease was only 7 +/- 5% for 0.6 MAC ISF (P < 0.01). Two puffs of albuterol resulted in a further decrease of 12 +/- 3% (mean +/- sem) in Rrs compared with a 2 +/- 4% decrease in the placebo groups (P < 0.05). Additional puffs of albuterol resulted in no further changes in Rrs. CONCLUSION: We conclude that following tracheal intubation the reduction in Rrs produced by ISF is highly concentration dependent. Albuterol results in a small further reduction in Rrs.     

Status asthmaticus treated with inhaled isoflurane and intravenous isoproterenol

We report the case of an 18-year-old man with status asthmaticus who was treated with inhaled isoflurane and intravenous isoproterenol. The patient was intubated and mechanical ventilation was began immediately after admission to the hospital. He received intravenous methylprednisolone and aminophyline, and frequent inhalation of isoproterenol aerosol. However, his respiratory status deteriorated: peak inspiratory pressure increased markedly, and right pneumothorax, right lower lobe atelectasis, and hypotension developed. He was then given isoflurane by inhalation and a continuous intravenous infusion of isoproterenol, which was followed by marked improvement in his respiratory and hemodynamic status. Isoflurane can be effective in patients with status asthmaticus, and it does not increase the arrhythmogenicity of catecholamines. Intravenous administration of isoproterenol can also be useful in the treatment of patients with status asthamticus. The combination of isoflurane with intravenous isoproterenol may be useful when status asthmaticus is hard to control with conventional therapy.     

Effect of isoflurane and sevoflurane on evoked potentials and EEG

Evoked potentials and EEG are used to monitor the central nervous system and the depth of anesthesia in anesthetized patients. In this study, we examined EEG, VEP, SEP and ABR at various concentrations of isoflurane or sevoflurane, and evaluated the influence of volatile agents and their usefulness for the monitoring of the depth of anesthesia. With increasing concentrations of isoflurane and sevoflurane, AE (frequency which account for 80% of total voltage) showed dose-related reduction and EEG showed a trend toward a slower wave and higher amplitude. With increasing concentrations of isoflurane and sevoflurane, P100 of VEP showed a significant dose-related reduction in its amplitude and increase in its latency. So we could not record P100 at the level of the anesthesia of 1.0 MAC with 66% N2O. N20 of SEP can be easily recorded at any depth of anesthesia. And the trend showed consistent dose-related changes in amplitude and latency. With increasing concentrations of isoflurane and sevoflurane, wave III and V of ABR increased significantly in latency, but the changes were very small. In conclusion, the effect of isoflurane and that of sevoflurane on evoked potentials and EEG are similar with each other and with other volatile agents. SEP is the most consistent and reliable factor to monitor the depth of anesthesia neurophysiologically.     

Gastric myoelectric and motor activity in dogs after isoflurane anesthesia

To characterize the effects of isoflurane on gastric motility, gastric electrical and contractile activities were assessed in six healthy adult dogs before and after recovery from anesthesia. Baseline recordings (fasting and fed state) were obtained in unanesthestized dogs 8 days after implantation of serosal electrodes and strain-gauge force transducers. After an overnight fast, dogs were anesthetized with 1.3 minimum alveolar concentration (MAC) isoflurane for 4.5 hours (approximately 6 MAC hours). No other anesthetic or sedative drugs were administered. During anesthesia, ventilation was mechanically controlled to maintain arterial carbon dioxide tension at 36 +/- 4 mm Hg. Gastric electrical and contractile activities (fasting and fed state) were recorded again 18 hours after recovery from isoflurane anesthesia. Recordings were analyzed to determine gastric slow-wave frequency, presence of slow-wave dysrhythmias, slow-wave propagation velocity, coupling of contractions to slow waves, a motility index based on relative contractile amplitudes, and onset and duration of contractions after a standardized meal. The only variable that was significantly decreased 18 hours after 6 MAC hours of isoflurane anesthesia was the gastric motility index during fasting-state phase III. This decrease was not apparent in the fed-state test periods. Our results suggest that, with the exception of gastric motility index during fasting-state phase III, variables for gastric electrical and contractile activities in dogs are unaffected by isoflurane 18 hours after anesthesia.     

Comparison of the amnesic effects of propofol and isoflurane anesthesia

Networks of interstitial cells of Cajal embedded in the musculature of the gastrointestinal tract are involved in the generation of electrical pacemaker activity for gastrointestinal motility. This pacemaker activity manifests itself as rhythmic slow waves in membrane potential, and controls the frequency and propagation characteristics of gut contractile activity. Mice that lack a functional Kit receptor fail to develop the network of interstitial cells of Cajal associated with Auerbach's plexus in the mouse small intestine and do not generate slow wave activity. These cells could provide an essential component of slow wave activity (for example, a biochemical trigger that would be transferred to smooth muscle cells), or provide an actual pacemaker current that could initiate slow waves. Here we provide direct evidence that a single cell, identified as an interstitial cell of Cajal by light microscopy, electron microscopy and expression of Kit mRNA, generates spontaneous contractions and a rhythmic inward current that is insensitive to L-type calcium channel blockers. Identification of the pacemaker of gut motility will aid in the elucidation of the pathophysiology of intestinal motor disorders, and provide a target cell for pharmacological treatment.     

Ventilatory responses to acute and sustained hypoxia during isoflurane anesthesia

In the awake state, isocapnic hypoxic ventilatory responses (HVRs) are biphasic, with an acute response within 5 min of hypoxic stimulation followed by a less pronounced sustained response. In this study, we investigated the influence of isoflurane anesthesia (end-tidal concentration 1.1 kPa) on acute and sustained isocapnic HVRs in eight healthy women at pulse oximetry arterial saturations of 75%-80%. The aims were to determine whether HVR (20 min of hypoxia) during anesthesia was biphasic and to quantify ventilatory responses. Pneumotachography and in-line infrared capnometry were used. A biphasic HVR was found both in awake and anesthetized patients. Of the subjects, six had decreased and two had increased acute and sustained isocapnic HVRs in the anesthetized, compared with the awake state, which resulted in an approximately 50% reduction in both acute and sustained HVRs. In addition, the ventilatory response pattern was altered by anesthesia. Awake HVR was accomplished by increased tidal volumes while respiratory rates were unchanged. The opposite occurred during anesthesia. The underlying mechanisms for this biological action of inhaled anesthetics remains to be elucidated. In conclusion, this study clearly demonstrates the persistence of hypoxic ventilatory sensitivity during clinical anesthesia. Implications: We studied the ventilatory effects of 20 min of breathing air with low oxygen content (hypoxic) in eight women, before and during anesthesia with inhaled isoflurane. We demonstrated a persistent but blunted hypoxic ventilatory response during clinical anesthesia.     

Biological monitoring during exposure to the anesthetics isoflurane and sevoflurane

Exposure to traces of inhaled anaesthetic agents may impair the health of the operating theatre personnel. Although no cause-effect relationship has been found, most public health authorities recommend various occupational exposure standards to minimize possible health risks. If metabolites of the substances are known, biological monitoring is an alternative to the monitoring of the operating theatre's air. The new anaesthetic agent Sevoflurane is considerably more transformed to fluoride than Isoflurane. Concerning fluoride there exist Biological Tolerance Values of 4.0-7.0 mg fluoride (F-) per gram creatinine (Crea). The aim of our study was to compare the fluoride excretion under the occupational exposure to sevoflurane and isoflurane. By the means of a direct-reading instrument trace concentrations of sevoflurane, isoflurane, and nitrous oxide were measured during 40 anaesthetic procedures. Urine samples were collected before (Z1) and after the workshift (Z2), and in the morning of the next day (Z3). The analysis was done by the means of an ionselective electrode. The personnel-related concentrations (median, range) were 0.50 (0.16-7.04) ppm isoflurance and 27.36 (5.87-467.10) ppm nitrous oxide, and 0.79 (0.15-1.95) ppm sevoflurane and 17.74 (2.45-84.20) ppm nitrous oxide. The resulting fluoride values presented at Z1, Z2, and Z3 as median (range) during exposure to isoflurane were 0.15 (0.11-0.53), 0.19 (0.11-0.53), 0.20 (0.11-0.31) mg F-/g Crea, and 0.15 (0.10-0.46), 0.22 (0.13-0.44), 0.23 (0.15-0.69) mg F-/g Crea during exposure to sevoflurance, respectively. The trace concentrations were clearly under 10 ppm for the volatile substances and 100 ppm for nitrous oxide. The values are comparable to data recorded under similar working conditions. The measured fluoride values were low and remained under the legal tolerance values. Under the described conditions potential health risks were low.     

Halothane and isoflurane alter calcium dynamics in rat cerebrocortical synaptosomes

An increase in synaptosomal Ca2+ triggers neurotransmitter release and volatile anesthetics have been shown to inhibit neurotransmitter release by inhibition of Ca2+ entry. We have examined the effect of isoflurane and halothane on the kinetics of increase and decrease of Ca2+ in rat cerebrocortical synaptosomes ([Ca2+]in). We have also used specific Ca2+ antagonists to examine the role of L-, N-, and P-type Ca2+ channels. Synaptosomal [Ca2+]in was measured spectrofluorometrically using fura-2 as a Ca2+ reporter; Ca2+ transients were initiated by depolarization with 40 mM KCl. We found that < or = 1 minimum alveolar anesthetic concentration halothane and isoflurane decreased peak [Ca2+]in by approximately 40%, that both anesthetics decreased the rate of [Ca2+]in increase and decrease, that specific voltage-dependent calcium channel antagonists had little effect on peak or plateau [Ca2+]in, and that the volatile anesthetics increased the permeability of synaptosomal membranes to Ca2+. These results suggest that the volatile anesthetics, at clinically relevant concentrations, can alter Ca2+ homeostasis in the synapse. IMPLICATIONS: Clinically relevant concentrations of halothane and isoflurane markedly depress K+-evoked increases in rat cerebrocortical synaptosomal calcium (Ca2+) unrelated to L-, N-, and P-type voltage-dependent calcium channels and increase the Ca2+ permeability of the synaptosomal membrane. These changes in Ca2+ dynamics could have profound effects on Ca2+ signaling in the synapse.     

Hepatocellular integrity during and after isoflurane and halothane anaesthesia in surgical patients

Subclinical disturbance in hepatocellular integrity, indicated by glutathione transferase Alpha (GSTA), has been associated with halothane, sevoflurane and propofol, but not with isoflurane anaesthesia. We anaesthetized 82 patients with isoflurane or halothane at 1 MAC for superficial surgery. GSTA concentration were measured with a sensitive time-resolved immunofluorometric assay in serum samples. GSTA concentrations increased from a baseline value of geometric mean 1.8 micrograms litre-1 (95% confidence intervals 1.4-2.2 micrograms litre-1) to a peak of 4.3 (3.3-5.7) micrograms litre-1 in the isoflurane group and from 2.1 (1.6-2.9) micrograms litre-1 to 6.2 (4.1-9.5) micrograms litre-1 in the halothane group. The change in GSTA was significant within groups but the difference between groups was not significant. Two patients exhibited an unexpectedly large increase in GSTA (peaks 370 and 620 micrograms litre-1) and a mild increase in alanine aminotransferase after halothane anaesthesia. We conclude that hepatocellular integrity was mildly disturbed after isoflurane and halothane anaesthesia but there was no difference between anaesthetics. Halothane anaesthesia may be associated with more advanced hepatocellular disturbance in some cases.     

Hypothermia eliminates isoflurane requirements at 20 degrees C

BACKGROUND: Hypothermia decreases anesthetic requirements, but the temperature that completely eliminates anesthetic needs has not been previously determined. METHODS: Eight female goats were anesthetized with isoflurane and catheters were placed in the femoral artery and cranial vena cava, after which the right carotid artery and external jugular vein were dissected free. Peripheral temperature was monitored in the rectum and core temperature in the vena cava. A thermistor was placed in the epidural space via a small burr hole to monitor brain temperature. Minimum alveolar concentration (MAC) for isoflurane was determined by eliciting gross, purposeful movement with a tail clamp. Cardiopulmonary bypass (CPB) was established using bubble oxygenators with venous blood drained from a jugular vein and arterial blood infused with a roller pump into the carotid artery. The animals were cooled to approximately 29 degrees C, and MAC redetermined, after which further cooling to 20 degrees C was accomplished. Isoflurane was eliminated, core and brain temperature adjusted in 2-3 degrees C increments, and the tail clamp applied until two temperatures were found that just permitted and just prevented movement. The animals were rewarmed, isoflurane added, and post-CPB MAC determined. RESULTS: At 38.5 degrees C, pre-CPB MAC was 1.3 +/- 0.1% (mean +/- SEM). At 29.0 degrees C, MAC was 0.7 +/- 0.1%, and the anesthetizing temperature was 20.1 +/- 0.6 degrees C. At 37.3 degrees C, post-CPB MAC was 1.0 +/- 0.1% (P < 0.05 vs. pre-CPB). CONCLUSIONS: These results confirm the rectilinear decrease in MAC seen in previous studies and establishes the anesthetizing temperature at 20 degrees C.     

Median nerve somatosensory evoked potentials during isoflurane anaesthesia

PURPOSE: The effect of isoflurane on the subcortical P14 component of the median nerve somatosensory evoked potential (SEP) is poorly known. We studied whether the P14 wave from the upper brainstem, recorded with a nasopharyngeal electrode, was attenuated at the isoflurane-induced EEG burst-suppression level. We also compared the effect of isoflurane on the P14, cervical N13 and cortical N20, N35 and N6, components. METHODS: Seventeen elective patients were anaesthetized with isoflurane. Somatosensory evoked potentials were recorded prior to anaesthesia, at 0.5 MAC and 1 MAC end-tidal isoflurane as well as at the level when EEG was in burst-suppression (mean 1.9 vol% end-tidal isoflurane). RESULTS: Isoflurane had varying effects on the subcortical components of median SEP. The amplitude of nasopharyngeal P14 was stable, but the mean latency increased from 14.4 +/- 1.2 msec at 0.5 MAC to 15.2 +/- 1.1 msec at burst-suppression level (P < 0.05). In contrast, the N13 neck response amplitude was attenuated from 3.3 +/- 0.6 microV to 2.6 +/- 0.5 microV (P < 0.005) without latency changes. The latency of the cortical N20 wave was increased from 19.7 +/- 1.1 msec at awake to 24.4 +/- 1.6 msec at burst-suppression level (P < 0.0001) and amplitude was reduced from 3.3 +/- 1.1 microV to 1.3 +/- 0.6 microV (P < 0.0001). The later cortical components were attenuated even during 0.5 MAC isoflurane and were not recordable during EEG burst-suppression. CONCLUSION: We conclude that P14 can reliably be recorded with nasopharyngeal electrodes during isoflurane anaesthesia, even during EEG burst-suppression, when the N20 wave is attenuated. In contrast, the middle-latency SEP components are sensitive to isoflurane anaesthesia.