Journal of anesthesia
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Journal of anesthesia · Oct 2012
Prediction of volume responsiveness using pleth variability index in patients undergoing cardiac surgery after cardiopulmonary bypass.
The pleth variability index (PVI) is derived from analysis of the plethysmographic curve and is considered to be a noninvasive parameter for prediction of volume responsiveness. The aim of our prospective clinical study was to evaluate if volume responsiveness can be predicted by PVI in patients undergoing cardiac surgery after cardiopulmonary bypass. ⋯ For consideration of fluid responsiveness PVI is as accurate as SVV in patients after cardiopulmonary bypass. Methodological limitations such as instable cardiac rhythm after cardiopulmonary bypass and right- or left ventricular impairment seem to be responsible for low specificity and positive predictive values in both parameters PVI and SVV.
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Journal of anesthesia · Oct 2012
Randomized Controlled TrialIntravenous ketamine compared with diclofenac suppository in suppressing acute postoperative pain in women undergoing gynecologic laparoscopy.
We aimed to compare the analgesic effects of low-dose intravenous ketamine with the effects of diclofenac suppositories in acute postoperative pain management in women undergoing gynecologic laparoscopic surgery under general anesthesia. ⋯ Diclofenac 100-mg suppositories were more effective in suppressing acute pain than 0.15 mg/kg intravenous ketamine in women undergoing elective gynecologic laparoscopy, with fewer untoward complications.
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Journal of anesthesia · Oct 2012
Interleukin-18 levels reflect the long-term prognosis of acute lung injury and acute respiratory distress syndrome.
The purpose of this study was to investigate the relationship between the blood levels of interleukin (IL)-18 measured in the early stage of acute respiratory failure and the prognosis for patient survival. ⋯ The present data demonstrate an inverse correlation between serum IL-18 level and the P/F ratio, suggesting the possible involvement of IL-18 in the pathogenesis of respiratory failure in patients with ALI/ARDS. Early-stage serum IL-18, IL-12, and TNF-α levels appear to reflect the >60-day prognosis in patients with ALI/ARDS.
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Journal of anesthesia · Oct 2012
Case ReportsLife-threatening hemorrhagic shock after laparoscopic surgery: a case of postoperative thrombotic thrombocytopenic purpura.
We report the successful management of a female patient who developed postoperative thrombotic thrombocytopenic purpura (TTP) after an uneventful laparoscopic oophorocystectomy. The patient underwent uneventful laparoscopic surgery for ovarian cystoma. One hour after completion of surgery, the patient suddenly went into shock, with her blood pressure dropping to 60/40 mmHg. ⋯ TTP is an idiopathic disorder, known to be triggered by surgical trauma. Postoperative TTP is difficult to distinguish clinically from DIC because of its close similarity with the latter and subtle differences from other postoperative hematological complications. It is important to bear in mind the possibility of postoperative TTP in patients with unexplained hemorrhagic shock after uneventful surgery.
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Journal of anesthesia · Oct 2012
Propofol attenuates angiotensin II-induced vasoconstriction by inhibiting Ca2+-dependent and PKC-mediated Ca 2+ sensitization mechanisms.
Angiotensin II (Ang II)-induced vascular contraction is mediated by Ca(2+)-dependent mechanisms and Ca(2+) sensitization mechanisms. The phosphorylation of protein kinase C (PKC) regulates myofilament Ca(2+) sensitivity. We have previously demonstrated that sevoflurane inhibits Ang II-induced vasoconstriction by inhibiting PKC phosphorylation, whereas isoflurane inhibits Ang II-induced vasoconstriction by decreasing intracellular Ca(2+) concentration ([Ca(2+)](i)) in vascular smooth muscle. Propofol also induces vasodilation; however, the effect of propofol on PKC-mediated myofilament Ca(2+) sensitivity is poorly understood. The aim of this study is to determine the mechanisms by which propofol inhibits Ang II-induced vascular contraction in rat aortic smooth muscle. ⋯ These results suggest that the inhibitory effect of propofol on Ang II-induced vascular contraction is mediated by the attenuation of a Ca(2+)-dependent pathway and Ca(2+) sensitivity through the PKC signaling pathway.