Anesthesia and analgesia
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Anesthesia and analgesia · Jul 2003
Case ReportsAllodynia after acute intrathecal morphine administration in a patient with neuropathic pain after spinal cord injury.
Acute intrathecal administration of relatively small doses of opioids may precipitate neuropathic pain and allodynia in those with spinal cord injury.
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For more than a century, Mayo Clinic has used various communication strategies to optimize the efficiency of physicians. Anesthesiology has used colored wooden tabs, colored lights, and, most recently, a distributed video paging system (VPS) that was near the end of its useful life. A computer-based anesthesiology paging system (CAPS) was developed to replace the VPS. The CAPS uses a hands-off paradigm with ubiquitous displays to inform the practice where personnel are needed. The system consists of a dedicated Ethernet network connecting redundant central servers, terminal servers, programmable keypads, and light-emitting diode displays. Commercially available hardware and software tools minimized development and maintenance costs. The CAPS was installed in >200 anesthetizing and support locations. Downtime for the CAPS averaged 0.144 min/day, as compared with 24.2 min/day for the VPS. During installation, neither system was available and the department used beepers for communications. With a beeper, the median response time of an anesthesiologist to a page from a beeper was 2.78 min, and with the CAPS 1.57 min; this difference was statistically significant (P = 0.021, t(67) = 2.36). We conclude that the CAPS is a reliable and efficient paging system that may contribute to the efficiency of the practice. ⋯ Mayo Clinic installed a computer-based anesthesiology paging system (CAPS) to inform operating suite personnel when assistance is needed in procedure and recovery areas. The CAPS is more reliable than the system it replaced. Anesthesiologists arrive at a patient's bedside faster when they are paged with the CAPS than with a beeper.
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Anesthesia and analgesia · Jul 2003
Peripheral antihyperalgesic and analgesic actions of ketamine and amitriptyline in a model of mild thermal injury in the rat.
In this study, we examined antihyperalgesic and analgesic actions after local peripheral administration of ketamine and amitriptyline in a rat model of mild thermal injury. Exposure of the hindpaw to 52 degrees C for 45 s under anesthesia produced a subsequent thermal hyperalgesia lasting at least 2 h. The local peripheral administration of ketamine (100-1000 nmol) 15 min before the thermal injury produced an antihyperalgesic effect when injected into the ipsilateral paw, whereas amitriptyline produced both antihyperalgesic (300 nmol) and analgesic (1000 nmol) effects. Administered after the thermal injury, ketamine had no effect, whereas amitriptyline retained its analgesic but not its antihyperalgesic effect. Amitriptyline (300 and 1000 nmol) produced an analgesic action when administered into the normal nonsensitized hindpaw. Both drugs increase paw volume, particularly at larger doses; biogenic amines are not involved in the action of amitriptyline, as was shown previously for ketamine. These results indicate that (a) ketamine produces antihyperalgesia, but not analgesia, when administered locally with a mild thermal injury model; (b) amitriptyline produces both antihyperalgesia and analgesia when administered locally; and (c) the increase in paw volume produced by these drugs occurs by different mechanisms. ⋯ This study examines the pain-relieving properties of the local peripheral administration of ketamine and amitriptyline, two drugs in current clinical use, in a thermal injury model of hyperalgesia and demonstrates both antihyperalgesic and analgesic properties. These observations provide support for their potential use as local (e.g., topical) analgesics.
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Anesthesia and analgesia · Jul 2003
Anesthetic sensitivities to propofol and halothane in mice lacking the R-type (Cav2.3) Ca2+ channel.
Because inhibition of voltage-dependent Ca(2+) channels can be a mechanism underlying general anesthesia, we examined sensitivities to propofol and halothane in mice lacking the R-type (Ca(v)2.3) channel widely expressed in neurons. Sleep time after propofol injection (26 mg/kg IV) and halothane MAC(RR) and MAC (50% effective concentrations for the loss of the righting reflex and for the tail pinch/withdrawal response, respectively) were determined. Significantly shorter propofol-induced sleep time (291.6 +/- 16.8 s versus 344.4 +/- 12.1 s) and larger halothane MAC(RR) (1.11% +/- 0.04% versus 0.98% +/- 0.03%) were observed in Ca(v)2.3 channel knockouts (Ca(v)2.3(-/-)) than in wild-type (Ca(v)2.3(+/+)) litter mates. To investigate the basis of the decreased anesthetic sensitivities in vivo, field excitatory postsynaptic potentials and population spikes (PSs) were recorded from Schaffer collateral CA1 synapses in hippocampal slices. Propofol (10-30 micro M) inhibited PSs by potentiating gamma-aminobutyric acid-ergic inhibition, and this potentiation was markedly smaller at 30 micro M in Ca(v)2.3(-/-) mice, possibly accounting for the decreased propofol sensitivity in vivo. Halothane (1.4%-2.2%) inhibited field excitatory postsynaptic potentials similarly in both genotypes, whereas 1%-2% halothane depressed PSs more in Ca(v)2.3(-/-) mice, suggesting the postsynaptic role of the R-type channel in the propagation of excitation and other mechanisms underlying the increased halothane MAC(RR) in Ca(v)2.3(-/-) mice. ⋯ Because inhibition of neuronal Ca(2+) currents can be a mechanism underlying general anesthesia, we examined anesthetic sensitivities in mice lacking the R-type (Ca(v)2.3) Ca(2+) channels both in vivo and in hippocampal slices. Decreased sensitivities in mutant mice imply a possibility that agents blocking this channel may increase the requirements of anesthetics/hypnotics.
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Anesthesia and analgesia · Jul 2003
Comment Letter Comparative StudyRemifentanil manual versus target-controlled infusion.