Study design: Prospective, nonrandomized, observational cohort study. Objectives: To analyze procalcitonin (PCT) level in acute traumatic spinal cord injury patients with and without postoperative infectious complications, and to determine whether PCT is a prognostic parameter of infectious complications in the early postoperative period compared with other inflammatory markers. Setting: Spine center of Chongqing, China; Trauma center of Chinese People's Liberation Army, China. Methods: A total of 339 consecutive patients with acute spinal cord injury undergone surgery were evaluated. All patients underwent measurement of leukocyte count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and serum PCT preoperatively and 24-48 h postoperatively. Results: In all, 26 (7.7%) of 339 participants experienced postoperative infectious complication. Patients with infection exhibited significantly higher PCT and CRP levels compared with noninfection (both Po0.01). Multivariate logistic regression analysis showed that PCT and CRP levels were independent predicators for postoperative infection. The area under the receiver operating characteristics curve of PCT and CRP were 0.82 (95% confidence intervals (CI) 0.74-0.91) and 0.68 (95%CI, 0.57-0.78), respectively. A PCT cutoff of 0.1 ng ml À1 had a reasonable sensitivity of 92% to exclude an infection and antibiotics can be initially withheld. However, in patients with PCT level above 0.5 ng ml À1 , a rapid initiation of antibiotics may be warranted. Conclusions: Serum PCT is a more reliable biologic marker for the early prediction of postoperative infectious complications in patients with acute traumatic spinal cord injury compared with CRP. PCT can early identify postoperative infections for establishing effective antibiotic therapy.
Local anesthetics can cause severe toxicity when absorbed systemically. Rapid intravenous administration of lipid emulsion (LE) is the standard of care for severe local anesthetic systemic toxicity which can cause cardiovascular and central nervous system (CNS) injury. The biological mechanism by which LE alleviates CNS toxicity remains unknown and understudied. Previous research has suggested that local anesthetics cause an imbalance of excitatory and inhibitory transmission in the brain. Therefore, this study aimed to observe the effect of LE on glutamate‐ and GABA‐induced currents in CA1 pyramidal neurons after bupivacaine‐induced CNS toxicity. We further characterized post‐synaptic modifications in these cells to try to elucidate the mechanism by which LE mediates bupivacaine‐induced CNS toxicity. Sprague–Dawley rats received intravenous bupivacaine (1 mg kg −1 min −1 ) in either normal saline or LE (or LE without bupivacaine) for 5 min. An acute brain slice preparation and a combination of whole‐cell patch clamp techniques and whole‐cell recordings were used to characterize action potential properties, miniature excitatory, and inhibitory post‐synaptic currents, and post‐synaptic modifications of excitatory and inhibitory transmission in CA1 hippocampal pyramidal neurons. The expression level of GABAA receptors were assessed with western blotting, whereas H&E and TUNEL staining were used to assess cytoarchitecture and apoptosis levels respectively. Bupivacaine treatment significantly increased the number of observed action potentials, whereas significantly decreasing rheobase, the first interspike interval (ISI), and hyperpolarization‐activated cation currents (Ih) in CA1 pyramidal neurons. LE treatment significantly reduced the frequency of miniature inhibitory post‐synaptic currents and enhanced GABA‐induced paired pulse ratio with 50 ms interval stimulation in bupivacaine‐treated rats. Regulation of GABAA levels is a promising mechanism by which LE may ameliorate CNS toxicity after systemic absorption of bupivacaine.
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