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Studies have demonstrated that low serum albumin levels are associated with a high postoperative complication rate after microvascular free flap reconstruction. The aim of this study was to investigate whether perioperative albumin supplementation reduced the postoperative complications of microvascular free flap reconstruction in oral and maxillofacial tumor resections.Patients who underwent microvascular free flap reconstruction during oral and maxillofacial tumor resections from January 2012 to December 2017 were enrolled in this retrospective study. The predictor variable was perioperative albumin supplementation. The primary outcome variables were surgery-associated postoperative complications, including local and systemic complications. The secondary outcome variables were the total duration of hospital stay, postoperative ICU admission rate, duration of ICU stay, and mortality during hospitalization.In total, 315 patients met the criteria. Patients with serum albumin supplementation showed a lower rate of surgery-associated local complications (6.5 vs 21.6%) with an adjusted odds ratio (OR) of 0.24 (95% confidence interval (CI), 0.12 to 0.49, P.001). The average postoperative hospital stay was significantly shortened for patients with albumin supplementation (12.56 ± 4.23 vs 15.34 ± 5.24 days, P.001). However, albumin supplementation had no effect on systemic complications.The results of this study suggest that perioperative albumin supplementation is associated with a decreased risk of local complications, shortened hospital stay, and decreased need for crystalloid infusion in patients who underwent oral and maxillofacial tumor resections with microvascular free flap reconstruction.

Sevoflurane is commonly used in clinical anesthesia. However, some reports indicated that Sevoflurane could induce mitochondrial injury and neuroapoptosis. Although the mechanism remains unclear, evidence points to the increase of intracellular calcium after administration of Sevoflurane. Herein, we sought whether the increment of intracellular Ca2+ caused by Sevoflurane administration could induce mitochondrial injury and apoptosis in primary neurons of the hippocampus. Fluo-4-acetoxymethyl ester Ca2+ probe was used for measuring intracellular Ca2+ concentrations. LDH assay, CCK-8 assay, and Western blotting were performed to confirm Sevoflurane-induced neuroapoptosis. ROS, mPTP, and ATP production were assayed to reveal mitochondrial injury. Our results indicated that Sevoflurane increased intracellular Ca2+ and neuronal death. Sevoflurane also elevated ROS and the opening of mPTP, and decreased ATP production in neurons. The expression of cytochrome c, cleaved caspase-9, cleaved caspase-3, and the ratio of Bax/Bcl-2 were also increased. By using calcium channel blocker Nimodipine, the increase of intracellular Ca2+ was attenuated, and the death rate of neurons, the ROS and opening of mPTP, decreased ATP production, the expressions of cytochrome c, cleaved caspase-9, cleaved caspase-3 and the ratio of Bax/Bcl-2 were alleviated. Our study suggested that Sevoflurane could increase intracellular Ca2+ to induce mitochondrial injury and mitochondria-mediated neuroapoptosis in neurons.