Anesthesiology
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To assess the patterns of injury and liability associated with monitored anesthesia care (MAC) compared with general and regional anesthesia, the authors reviewed closed malpractice claims in the American Society of Anesthesiologists Closed Claims Database since 1990. ⋯ Oversedation leading to respiratory depression was an important mechanism of patient injuries during MAC. Appropriate use of monitoring, vigilance, and early resuscitation could have prevented many of these injuries. Awareness and avoidance of the fire triad (oxidizer, fuel, and ignition source) is essential to prevent on-the-patient fires.
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Developmental differences in responses to acute and chronic nerve injury have received minimal attention. This study examines developmental differences in behavioral responses to a proximal (closer to the spinal cord) (L5 and L6 spinal nerve root ligation) or to a more distal (closer to peripheral innervation) (partial sciatic nerve ligation) nerve injury in rats paralleling the infant to young adult human. ⋯ These data suggest that resolution of sensitization to A-fiber input occurs more rapidly in young animals. In addition, distal injury has less of a sensitizing effect on A-fiber input than proximal injury in the younger animals. The authors speculate that neuroimmune responses, especially at the site of injury, are developmentally regulated and less likely to produce chronic pain when injury occurs at a young age.
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Although intrathecal administration of midazolam, a water-soluble imidazobenzodiazepine derivative, has been found to produce analgesia, how it exerts this effect at the neuronal level in the spinal cord is not fully understood. ⋯ Midazolam reduced excitatory synaptic transmission by acting on the gamma-aminobutyric acid type A/benzodiazepine receptor in interneurons, leading to a decrease in the excitability of spinal dorsal horn neurons. This may be a possible mechanism for the antinociception by midazolam in the spinal cord.
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Spinal prostaglandins seem to be important in the early pathogenesis of experimental neuropathic pain. Here, the authors investigated changes in the expression of cyclooxygenase and nitric oxide synthase (NOS) isoforms in the lumbar, thoracic, and cervical spinal cord and the pharmacologic sensitivity to spinal prostaglandin E2 (PGE2) after L5-L6 spinal nerve ligation (SNL). ⋯ The increased expression of cyclooxygense-2, neuronal NOS, and inducible NOS and the enhanced sensitivity to PGE2 in spinal segments affected by SNL support the hypothesis that spinal prostanoids play an early pathogenic role in experimental neuropathic pain.
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Partial sciatic nerve ligation (PSNL) produces axonal damage, a local inflammatory response, and wallerian degeneration. Cytokines secreted near the site of nerve injury are thought to play important roles in development and maintenance of central sensitization and neuropathic pain. Injection of clonidine at the site and time of nerve injury slows the development of PSNL-induced hypersensitivity and reduces local cytokine expression by actions on alpha2 adrenoceptors. The current study tested whether clonidine would have a similar effect in established nerve injury. ⋯ These data suggest that perineural clonidine acts on alpha2 adrenoceptors to reduce hypersensitivity in established nerve injury, likely by an immunomodulatory mechanism, and may be effective in patients in the weeks after nerve injury.