Anesthesiology
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Randomized Controlled Trial Clinical Trial
Causes and prediction of maldistribution during continuous spinal anesthesia with isobaric or hyperbaric bupivacaine.
Many cases of cauda equina syndrome after maldistribution of local anesthetics during continuous spinal anesthesia have been reported. In experiments, a caudad route of catheter travel and the use of hyperbaric agents have been shown to induce these limited blocks. The aim of this clinical study was to verify this hypothesis and seek a predictive factor for the maldistribution of bupivacaine. ⋯ Hyperbaric solutions do not appear to be a clinical factor in the development of limited block. The principle factor causing the maldistribution of bupivacaine is the caudal orientation of the tip of the end-hole catheter rather than its level or the route of catheter travel.
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This study prospectively evaluated the ability of aspiration to detect intravascular placement of multiple-orifice epidural catheters. ⋯ Under the conditions of this study, which include using multiple-orifice catheters and dilute solutions of local anesthetic and opioid, aspiration and incremental drug injection alone safeguard against the risks of intravenously positioned local anesthetics. These results should not be extrapolated to other clinical settings without further study.
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Editorial Comment Review
Fast track cardiac surgery pathways: early extubation, process of care, and cost containment.
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A clinical bleeding diathesis is associated with hypothermia. Inhibition of platelet reactivity is the purported cause of this coagulopathy despite inconsistent evidence to support this hypothesis. To clarify the effect of temperature on intrinsic platelet function, platelet GPllb-IIIa activation and P-selectin expression were assessed under normothermic and hypothermic conditions in vitro. ⋯ Aggregation, fibrinogen binding, PAC-1 binding, and P-selectin antibody binding studies showed that platelet GPIIb-IIIa activation and alpha-granule release were enhanced at hypothermic temperatures. Thus hypothermia appears to increase the ability of platelets to respond to activating stimuli. The coagulopathy associated with hypothermia is not likely to be the result of an intrinsic defect in platelet function.