Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Comparative StudyDifficult tracheal intubation is more common in obese than in lean patients.
Whether tracheal intubation is more difficult in obese patients is debatable. We compared the incidence of difficult tracheal intubation in obese and lean patients by using a recently validated objective scale, the intubation difficulty scale (IDS). We studied 134 lean (body mass index, <30 kg/m2) and 129 obese (body mass index, >or=35 kg/m2) consecutive patients. The IDS scores, categorized as difficult intubation (IDS >or=>5) or not (IDS <5), and the patient data, including oxygen saturation (SpO2) while breathing oxygen, were compared between lean and obese patients. In addition, risk factors for difficult intubation were determined in obese patients. The IDS score was >or=5 in 3 lean and 20 obese patients (P = 0.0001). A Mallampati score of III-IV was the only independent risk factor for difficult intubation in obese patients (odds ratio, 12.51; 95% confidence interval, 2.01-77.81), but its specificity and positive predictive value were 62% and 29%, respectively. SpO2 values noted during intubation were (mean +/- SD) 99% +/- 1% (range, 91%-100%) and 95% +/- 8% (range, 50%-100%) in lean and obese patients, respectively (P < 0.0001). We conclude that difficult intubation is more common among obese than nonobese patients. None of the classic risk factors for difficult intubation was satisfactory in obese patients. The high risk of desaturation warrants studies to identify new predictors of difficult intubation in the obese. ⋯ We report a difficult intubation rate of 15.5% in obese patients and 2.2% in lean patients. None of the risk factors for difficult intubation described in the lean population was satisfactory in the obese patients. We also report a high risk of desaturation in obese patients with difficult intubation.
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Anesthesia and analgesia · Aug 2003
Neurotrophic factors can partially reverse morphological changes induced by mepivacaine and bupivacaine in developing sensory neurons.
Both bupivacaine and mepivacaine induce morphological changes in growing neurons. We designed this study to investigate the role of some neurotrophic factors (NTFs) in supporting developing neurons exposed to the deleterious effects of these drugs. Dorsal root ganglia were isolated from chick embryos and exposed to either bupivacaine or mepivacaine. After 60 min of exposure, the culture media were replaced with fresh culture media free from local anesthetics. NTFs-brain-derived NTF, glial-derived NTF, or neurotrophin-3-were added to the replacement media, and the cells were examined up to 48 h after the washout. The growth cone collapse assay was applied by a quantitative method of assessment. When the replacement media were not supported by any NTF, the growth cone collapse values were significantly larger than the control values at 20 h after the washout of mepivacaine and 48 h after the washout of either bupivacaine or mepivacaine (P < 0.05). However, when any of the NTFs were used, the collapsing activity was significantly attenuated, and growth cone collapse values showed no statistically significant differences in comparison with the control values at these time points (P > 0.05). We conclude that several NTFs support the recovery of neurons after exposure to local anesthetics. The supporting effects of NTFs on the reversibility of mepivacaine-induced collapse tended to be more obvious than those seen after the bupivacaine washout. ⋯ Three neurotrophic factors (NTFs) can partially support the reversibility of mepivacaine- and bupivacaine-induced growth cone collapse in growing primary cultured sensory neurons. The effect of NTFs is more apparent after mepivacaine than after bupivacaine washout.
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Anesthesia and analgesia · Aug 2003
Clinical TrialThe effects of large-dose propofol on cerebrovascular pressure autoregulation in head-injured patients.
In healthy individuals, cerebrovascular pressure autoregulation is preserved or even improved when propofol is infused. We examined the effect of an increase in propofol plasma concentration on pressure autoregulation in 10 head-injured patients. Using target-controlled infusions, the static rate of autoregulation was determined at a moderate (2.3 +/- 0.4 microg/mL) and a large (4.3 +/- 0.04 microg/mL) plasma target concentration of propofol. Using norepinephrine to control cerebral perfusion pressure, transcranial Doppler measurements from the middle cerebral artery were made at a cerebral perfusion pressure of 70 and 85 mm Hg at each propofol concentration. Middle cerebral artery flow velocities at the large propofol concentration were significantly lower than at the moderate concentration, without any concurrent increase in arterio-jugular difference in oxygen content, a finding compatible with maintained flow-metabolism coupling. Despite this, static rate of autoregulation decreased significantly from 54% +/- 36% to 28% +/- 35% (P = 0.029). Our data suggest that after head injury, the cerebrovascular effects of propofol are different from those observed in healthy individuals. We propose that large doses of propofol should be used cautiously in head-injured patients, because there is the potential to increase the injured brain's vulnerability to secondary insults. ⋯ Propofol is used for sedation and control of intracranial pressure in head-injured patients. In contrast to previous data from healthy individuals, we show a deterioration of cerebrovascular pressure autoregulation with fast propofol infusion rates after head injury. Large propofol doses may increase the injured brain's vulnerability to secondary insults.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialEphedrine fails to accelerate the onset of neuromuscular block by vecuronium.
The onset time of neuromuscular blocking drugs is partially determined by circulatory factors, including muscle blood flow and cardiac output. We thus tested the hypothesis that a bolus of ephedrine accelerates the onset of vecuronium neuromuscular block by increasing cardiac output. A prospective, randomized study was conducted in 53 patients scheduled for elective surgery. After the induction of anesthesia, the ulnar nerve was stimulated supramaximally every 10 s, and the evoked twitch response of the adductor pollicis was recorded with accelerometry. Patients were maintained under anesthesia with continuous infusion of propofol for 10 min and then randomly assigned to ephedrine 210 microg/kg (n = 27) or an equivalent volume of saline (n = 26). The test solution was given 1 min before the administration of 0.1 mg/kg of vecuronium. Cardiac output was monitored with impedance cardiography. Ephedrine, but not saline, increased cardiac index (17%; P = 0.003). Nonetheless, the onset of 90% neuromuscular block was virtually identical in the patients given ephedrine (183 +/- 41 s) and saline (181 +/- 47 s). There was no correlation between cardiac index and onset of the blockade. We conclude that the onset of the vecuronium-induced neuromuscular block is primarily determined by factors other than cardiac output. The combination of ephedrine and vecuronium thus cannot be substituted for rapid-acting nondepolarizing muscle relaxants. ⋯ Ephedrine increased cardiac index but failed to speed onset of neuromuscular block with vecuronium. We conclude that ephedrine administration does not shorten the onset time of vecuronium.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe effect of mixing lidocaine with propofol on the dose of propofol required for induction of anesthesia.
Lidocaine is used to reduce pain associated with propofol injection, either mixed with propofol or preceding it as a separate injection. The addition of lidocaine to propofol causes destabilization of the emulsion and reduces anesthetic potency in rats and humans. We conducted a randomized double-blinded study on 67 patients to assess the effect of mixing lidocaine with propofol on the dose of propofol required for the induction of anesthesia. Patients in Group S (n = 32) received IV lidocaine 0.2 mg/kg followed by an infusion of propofol whereas those in Group M (n = 35) received IV normal saline (placebo) followed by an infusion of a freshly prepared mixture of propofol 1%/lidocaine 1% in 10:1 volume ratio. The infusion was stopped when the subjects lost consciousness, as detected by the syringe-drop method. There was no statistically significant difference between the two groups in the mean (95% confidence interval) doses of propofol required for loss of consciousness: 2.0 (1.8-2.2) mg/kg for Group S versus 1.9 (1.7-2.0) mg/kg for Group M (P = 0.206). Mixing 20 mg of lidocaine with 200 mg of propofol is unlikely to affect the dose of propofol required for the induction of anesthesia. ⋯ Adding lidocaine to propofol destabilizes the propofol emulsion. A randomized double-blinded trial found no statistically significant difference in the doses of propofol required for the induction of anesthesia whether administered as a freshly prepared propofol 1%/lidocaine 1% 10:1 mixture or as a separate injection after a dose of lidocaine.