Anesthesiology
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Intraoperative hypotension (IOH) is a common side effect of general anesthesia and has been reported to be associated with adverse perioperative outcomes. These associations were found using different definitions for IOH. It is unknown whether the incidences of IOH found with those different definitions are comparable. The authors aimed to describe the relation between the chosen definition and incidence of IOH. ⋯ There is no widely accepted definition of IOH. With varying definitions, many different incidences can be reproduced. This might have implications for previously described associations between IOH and adverse outcomes.
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Editorial Comment
The impact of lack of standardized definitions on the specialty.
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Sexual dysfunction due to ejaculatory and genital pain after groin hernia surgery may occur in approximately 2.5% of patients. However, the specific psychosexological and neurophysiologic characteristics have not been described, thereby precluding assessment of pathogenic mechanisms and treatment strategies. ⋯ Postherniotomy ejaculatory pain and pain-related sexual dysfunction is a specific chronic pain state that may be caused by pathology involving the vas deferens and/or nerve damage. Therapeutic strategies should therefore include neuropathic pain treatment and/or surgical exploration.
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Current evidence indicates that p38 mitogen-activated protein kinase activation in spinal microglia contributes to the development of neuropathic pain. However, how nerve injury activates p38 in spinal microglia is incompletely unknown. Nerve injury-induced ectopic spontaneous activity is essential for the generation of neuropathic pain. The authors examined whether peripheral neural activity is necessary for p38 activation in spinal microglia. ⋯ After nerve injury, activity in the peripheral nerve is required for the induction but not the maintenance of p38 activation in spinal microglia.
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Chronic pain conditions may result from peripheral nerve injury, chronic peripheral inflammation, or sensory ganglia inflammation. However, inflammatory processes may also contribute to peripheral nerve injury responses. To isolate the contribution of local inflammation of sensory ganglia to chronic pain states, the authors previously developed a rat model in which long-lasting pain is induced by inflaming sensory ganglia without injuring the neurons. This results in prolonged mechanical pain, local increases in proinflammatory cytokines, increased neuronal hyperexcitability, and abnormal spontaneous activity. ⋯ Neuronal inflammation per se, in the absence of nerve injury, causes large increases in Na channel density and enhanced excitability. The unusual finding of increased K current may reflect regulation of excitability in the face of such large increases in Na current.