Anesthesia and analgesia
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Anesthesia and analgesia · Mar 1998
Diabetes mellitus and difficult laryngoscopy in renal and pancreatic transplant patients.
Limited mobility of the cervical spine or temperomandibular joint may contribute to increased difficulty of laryngoscopy in patients who have severe diabetes mellitus. The frequency of difficult laryngoscopy in diabetics undergoing renal and/or pancreatic transplants has been reported to be as high as 32%. We retrospectively reviewed the anesthetic records of all adult patients who underwent renal and/or pancreatic transplant and endotracheal intubation from January 1, 1985 to October 31, 1995. Characteristics specifically reviewed included the presence of diabetes mellitus, type of organ donor, age, gender, body mass index, previous difficult laryngoscopy, known characteristics potentially related to difficult laryngoscopy, and degree of difficulty with laryngoscopy. Laryngoscopy was graded as easy, minimally to moderately difficult, and moderately to extremely difficult to perform. Factors associated with any degree of difficult intubation were univariately assessed by using Fisher's exact test. Of 725 patients, 15 (2.1%) were identified as having difficult laryngoscopies, although all underwent successful endotracheal intubations. Factors associated with difficult laryngoscopy were diabetes mellitus (P = 0.002) and characteristics known to be related to difficult laryngoscopy (P = 0.02). These findings confirm an increase in the frequency of difficult laryngoscopy in diabetic patients undergoing renal and/or pancreatic transplant, although no laryngoscopies were rated as moderately to extremely difficult. We conclude that the frequency of difficult laryngoscopy in these diabetic patients is much lower than previous reports have suggested. ⋯ Previous studies have suggested that airway management of many diabetic patients may be difficult. Our medical record review of patients with severe diabetes undergoing organ transplants showed that extraordinary techniques were not required to successfully manage their airways.
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Anesthesia and analgesia · Mar 1998
Propofol sedation produces dose-dependent suppression of lidocaine-induced seizures in rats.
The association of propofol with excitatory motor activity, such as myoclonic jerking and opisthotonus, in humans and in animals suggests that it may aggravate clinical seizure activity in some circumstances, although evidence suggests that under other circumstances, propofol inhibits seizure activity. In the current study, we assessed the effect of sedating doses of propofol on lidocaine-induced seizure activity in spontaneously breathing rats receiving no other anesthetics. Adult Sprague-Dawley male rats, 300-400 g, were divided into a control group and three experimental groups representing three graded levels of propofol sedation. The control rats then received a lidocaine infusion at the rate of 150 mg x kg(-1) x h(-1), resulting in a slow, progressive increase in systemic lidocaine concentrations. At the onset of electroencephalographic (EEG) seizure activity, arterial lidocaine concentrations were obtained. The treated rats received propofol according to three different dose schedules: Dose 1 = 10 mg x kg(-1) x h(-1) after a 2.5-mg/kg bolus; Dose 2 = 20 mg x kg(-1) x h(-1) after a 5-mg/kg bolus; Dose 3 = 40 mg x kg(-1) x h(-1) after a 10-mg/kg bolus. After 30 min, a steady level of sedation, dependent on the dose of propofol, was achieved. The lidocaine infusion was then started, and systemic lidocaine levels were obtained at the onset of EEG seizure activity. The lidocaine was continued until the onset of death by cardiac arrest. Plasma lidocaine was measured by gas chromatography. Analysis of variance and Dunnett's t-test were used for comparisons with the control values. Continuous propofol sedation increased the seizure dose of lidocaine from 37.7 +/- 3.5 mg/kg (mean +/- SEM) to 52.5 +/- 2.6 mg/kg (Dose 1, P < 0.05) and 67.9 +/- 8.6 mg/kg (Dose 2, P < 0.05), and completely abolished lidocaine seizures at Dose 3. The lethal dose of lidocaine, 89.4 +/- 10.5 mg/kg control versus 108.7 +/- 10.3 mg/kg (Dose 1), 98.3 +/- 10.1 mg/kg (Dose 2), and 93.5 +/- 10.4 mg/kg (Dose 3) did not differ among groups. The lidocaine levels at seizure threshold were increased in the propofol-treated rats: 16.9 +/- 0.5 microg/mL control versus 19.2 +/- 0.7 microg/mL (Dose 1, P = not significant) and 23.7 +/- 1.8 microg/mL (Dose 2, P < 0.05). Continuous propofol sedation in spontaneously breathing rats receiving no other anesthetics exerts a protective effect against lidocaine-induced seizures in a monotonic, dose-dependent fashion. The cardiac arrest dose of lidocaine is unaffected by propofol under these conditions. ⋯ The i.v. anesthetic drug propofol, given to rats to produce sedation, was found to suppress seizure activity caused by overdosage of the local anesthetic lidocaine.