Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2003
Clinical TrialPatient-controlled epidural analgesia in children: can they do it?
Extensive clinical experience and many studies support the use of i.v. patient-controlled analgesia (i.v. PCA) and regional anesthesia techniques for the treatment of postoperative pain in children. In contrast, little has been reported about the ability of children to use patient-controlled epidural analgesia (PCEA) or about the efficacy of this technique. We report a descriptive analysis of prospectively recorded data in 128 children (132 procedures) in whom PCEA was used for acute postoperative pain control. Satisfactory analgesia was obtained in 119 patients (90.1%) for up to 103 h with no episodes of desaturation and without clinical evidence of toxicity or serious adverse effects. Analgesia was satisfactory with the initial settings in 89 patients; in 38 others, this was achieved with changes in PCEA settings or solution. Five patients were switched to i.v. PCA because of inadequate analgesia. Eight patients with satisfactory analgesia were converted to i.v. PCA because of adverse effects. Children as young as 5 yr had the cognitive ability to understand and the willingness to use PCEA, consistent with reported use of i.v. PCA. Careful attention should be paid to the total hourly local anesthetic dose to avoid exceeding the recommended limits. Our prospectively collected data demonstrate that PCEA provides satisfactory analgesia with a small incidence of adverse side effects in children and should be considered along with other strategies in pediatric postoperative pain management. ⋯ A descriptive analysis of prospectively recorded data in 132 children receiving patient-controlled epidural analgesia for postoperative pain relief demonstrates satisfactory analgesia without serious toxicity or side effects in children as young as 5 yr. This modality should be considered as another strategy in pediatric postoperative pain management.
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Anesthesia and analgesia · Mar 2003
Postcardiac surgery complications: association of acute renal dysfunction and atrial fibrillation.
Postoperative creatinine increase is associated with adverse outcome after cardiac surgery. Although postoperative stroke and renal dysfunction are associated after cardiac surgery, suggesting a common systemic insult, a similar assessment of atrial fibrillation and renal dysfunction has not been performed. Therefore, we tested the hypothesis that patients with new-onset atrial fibrillation complicating coronary bypass surgery have a greater postoperative creatinine increase. Data were obtained for 453 elective coronary bypass surgery patients with no history of atrial fibrillation. Multivariate regression analyses of factors associated with peak fractional change in creatinine demonstrated a two-way interaction between age and atrial fibrillation (variable estimate, -1.1; P = 0.002). Similar results were obtained in a secondary multivariate model analyzing factors associated with peak postoperative creatinine (variable estimate, -0.01; P = 0.04). We confirmed our hypothesis that patients with new-onset atrial fibrillation are more likely to have acute renal dysfunction after cardiac surgery. The association of atrial fibrillation and creatinine increase diminishes with advancing age. These data are consistent with a common pathophysiology that contributes in an age-dependent fashion to the etiology of both acute renal dysfunction and atrial fibrillation after coronary bypass surgery. ⋯ We found an independent association between new-onset atrial fibrillation and postoperative creatinine increase that is influenced by age. The degree to which atrial fibrillation is associated with postoperative creatinine increase diminishes with advancing age. This interaction suggests that a common etiology for these two complications may be more important in younger patients.
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Anesthesia and analgesia · Mar 2003
Clinical TrialAn evaluation of the supraclavicular plumb-bob technique for brachial plexus block by magnetic resonance imaging.
Partly based on magnetic resonance imaging studies, the "plumb-bob" approach for brachial plexus block was designed to minimize the risk of pneumothorax. Nevertheless, the risk of pneumothorax has remained a concern. We analyzed magnetic resonance images from 10 volunteers to determine whether the risk of pneumothorax was decreased with this method. The recommended initial needle direction is anteroposterior through the junction between the lateral-most part of the sternocleidomastoid muscle and the superior edge of the clavicle. If the initial placement is not successful, the brachial plexus may be sought in sectors 20 degrees -30 degrees cephalad or caudad to the anteroposterior line in a sagittal plane through the insertion point. We found that the anteroposterior line reached the pleura in 6 of 10 volunteers without prior contact with the subclavian artery or the brachial plexus, but always with contact with the subclavian vein. To reach the middle of the brachial plexus, a mean cephalad redirection of the simulated needle by 21 degrees was required (range from 41 degrees cephalad to 15 degrees caudad in one case). We conclude that the risk of contacting the pleura and the subclavian vessels may be reduced by initially directing the needle 45 degrees cephalad instead of anteroposterior. If the brachial plexus is not contacted, the angle should be gradually reduced. ⋯ In magnetic resonance images of volunteers, simulated needle passes with the "plumb-bob" approach to the supraclavicular brachial plexus block were analyzed for precision and risk profile. To avoid needle contact with the lung, the subclavian vein, and the subclavian artery, our results suggest a change in the method's initial needle direction.
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Anesthesia and analgesia · Mar 2003
GABA(A) receptor blockade antagonizes the immobilizing action of propofol but not ketamine or isoflurane in a dose-related manner.
The enhancing action of propofol on gamma-amino-n-butyric acid subtype A (GABA(A)) receptors purportedly underlies its anesthetic effects. However, a recent study found that a GABA(A) antagonist did not alter the capacity of propofol to depress the righting reflex. We examined whether the noncompetitive GABA(A) antagonist picrotoxin and the competitive GABA(A) antagonist gabazine affected a different anesthetic response, immobility in response to a noxious stimulus (a tail clamp in rats), produced by propofol. This effect was compared with that seen with ketamine and isoflurane. Picrotoxin increased the 50% effective dose (ED(50)) for propofol by approximately 379%; gabazine increased it by 362%, and both antagonists acted in a dose-related manner with no apparent ceiling effect (i.e., no limit). Picrotoxin maximally increased the ED(50) for ketamine by approximately 40%-50%, whereas gabazine increased it by 50%-60%. The isoflurane minimum alveolar anesthetic concentration increased by approximately 60% with the picrotoxin and 70% with the gabazine infusion. The ED(50) for propofol was also antagonized by strychnine, a non-GABAergic glycine receptor antagonist and convulsant, to determine whether excitation of the central nervous system by a non-GABAergic mechanism could account for the increases in propofol ED(50) observed. Because strychnine only increased the immobilizing ED(50) of propofol by approximately 50%, GABA(A) receptor antagonism accounted for the results seen with picrotoxin and gabazine. We conclude that GABA(A) antagonism can influence the ED(50) for immobility of propofol and the non-GABAergic anesthetic ketamine, although to a different degree, reflecting physiologic antagonism for ketamine (i.e., an indirect effect via a modulatory effect on the neural circuitry underlying immobility) versus physiologic and pharmacologic antagonism for propofol (i.e., a direct effect by antagonism of propofol's mechanism of action). This study also suggests that the immobilizing action of isoflurane probably does not involve the GABA(A) receptor because antagonism of GABA(A) receptors for animals anesthetized with isoflurane produces results quantitatively and qualitatively similar to ketamine and markedly different from propofol. ⋯ IV picrotoxin and gabazine antagonized the immobilizing action of propofol in a dose-related manner, whereas antagonism of the immobilizing action of ketamine and isoflurane was similar, smaller than for propofol, and not dose-related. These results are consistent with a role for gamma-amino-n-butyric acid subtype A receptors in mediating propofol anesthesia but not ketamine or isoflurane anesthesia.