European journal of anaesthesiology
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The prevalence of chronic postsurgical pain (CPSP) is a critical medical problem with economic implications. Its prevalence after gastrointestinal surgery is not well documented, particularly when a laparoscopic approach is used. ⋯ The incidence of CPSP after laparoscopic colorectal surgery (17%) is similar to those reported in the literature after laparotomy. Risk factors are redo surgery for postoperative peritonitis, IBD and preoperative pain.
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Renal failure affects the pharmacology of nondepolarizing neuromuscular blockers making recovery of neuromuscular function unpredictable. Sugammadex antagonises rocuronium-induced neuromuscular blockade by encapsulating rocuronium, creating a stable complex molecule that is mainly excreted by the kidneys. Previous studies suggest that sugammadex is effective in reversing moderate neuromuscular block in the presence of renal failure, but no data are available regarding reversal of profound neuromuscular block in patients with renal failure. ⋯ In patients with renal failure, sugammadex (4 mg kg) effectively and safely reversed profound rocuronium induced neuromuscular block, but the recovery was slower than healthy patients.
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Opioid analgesia not only reduces inhalational anaesthetic requirements but may also induce delayed hyperalgesia, with potential effects on the minimum alveolar concentration (MAC) of inhalational anaesthetics. ⋯ Tramadol-induced hyperalgesia in the rat lasted for several weeks and was associated with an increase in the MAC of sevoflurane. Prior administration of ketamine blocked both phenomena.
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Myopathies are generally considered to increase the risk for succinylcholine-induced hyperkalaemia and may affect the duration of action of neuromuscular blockers. Centronuclear (myotubular) myopathy (CNM) is congenital and produces various degrees of muscular weakness and associated complications such as respiratory failure. The effects of succinylcholine and the potentially lethal consequences of hyperkalaemia on patients with CNM are unknown due to its rarity. One source of information is the dog, as CNM occurs naturally in dogs. Because of its remarkable similarity with the disease in man, canine CNM can serve as a model to further our knowledge of the effects of succinylcholine. ⋯ CNM did not exacerbate the increase in blood potassium that is ordinarily seen with succinylcholine. Recovery from succinylcholine was nearly 50% longer in dogs with CNM. Although our sample size is too small to evaluate the incidence of succinylcholine-induced hyperkalaemia, extrapolation of these findings suggests that increased duration of action should be expected if succinylcholine is given to a patient with autosomal-recessive CNM.