Journal of anesthesia
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Journal of anesthesia · Jan 2006
Review Meta AnalysisThe benefits of adding epidural analgesia to general anesthesia: a metaanalysis.
The purpose of this metaanalysis was to determine the benefits of postoperative epidural analgesia in patients operated on under general anesthesia. By searching the American National Library of Medicine's Pubmed database from 1966 to July 10, 2004, 70 studies were identified. These included 5402 patients, of which 2660 had had epidural analgesia. ⋯ It also reduces the first 24-h morphine consumption, OR = -13.62 mg (95%CI = -22.70, -4.54, P = 0.003), and improves the forced vital capacity (FVC), OR = 0.23 l (95%CI = 0.09, 0.37, P = 0.001) at 24 h. A thoracic epidural containing a local anesthetic reduces the incidence of renal failure: OR = 0.34 (95%CI = 0.14, 0.81, P = 0.01). Epidural analgesia may thus offer many advantages over other modes of postoperative analgesia.
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The epidural administration of local anesthetics can provide anesthesia without the need for respiratory support or mechanical ventilation. Nevertheless, because of the additional effects of epidural anesthesia on motor function and sympathetic innervation, epidural anesthesia does affect lung function. These effects, i.e., a reduction in vital capacity (VC) and forced expiratory volume in 1 s (FEV(1.0)), are negligible under lumbar and low thoracic epidural anesthesia. ⋯ In chronic obstructive pulmonary disease (COPD) patients, the use of thoracic epidural anesthesia has raised concerns about respiratory insufficiency due to motor blockade, and the risk of bronchial constriction due to sympathetic blockade. However, even in patients with severe asthma, thoracic epidural anesthesia leads to a decrease of about 10% in VC and FEV(1.0) and no increase in bronchial reactivity. Overall, epidural administration of local anesthetics not only provides excellent anesthesia and analgesia but also improves postoperative outcome and reduces postoperative pulmonary complications compared with anesthesia and analgesia without epidural anesthesia.
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Ischemic neuronal injury is characterized by early death mediated by excitotoxicity and by delayed death caused by apoptosis. Current evidence indicates that volatile agents, barbiturates, and propofol can protect neurons against ischemic injury caused by excitotoxicity. In the case of volatile agents and propofol, neuroprotection may be sustained if the ischemic insult is relatively mild; however, with moderate to severe insults, this neuronal protection is not sustained after a prolonged recovery period. ⋯ Cerebral ischemia is characterized by continued neuronal loss for a long time after the initial ischemic insult. Therefore, in investigations of cerebral ischemia, the duration of the recovery period should be taken into consideration in the analysis of the neuroprotective effects of anesthetic agents. A combination of different approaches that target specific stages of the evolution of ischemic injury may be required for sustained neuroprotection.
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Journal of anesthesia · Jan 2005
ReviewDrugs to facilitate recovery of neuromuscular blockade and muscle strength.
Several drugs that quicken recovery from neuromuscular blockade caused by vecuronium in anesthetized patients are reviewed. Ulinastatin, a protease inhibitor, is thought to promote the release of acetylcholine at the neuromuscular junction and increases hepatic blood flow and urine volume. For this reason, ulinastatin quickens recovery from neuromuscular blockade in anesthetized patients receiving vecuronium. ⋯ Therefore, recovery from neuromuscular blockade is hastened. Nicorandil enhances membrane K+ conductance in skeletal muscle and increases contraction of the skeletal muscle. Thus, nicorandil quickens recovery from neuromuscular blockade.