Risk factors of emergency reoperations

Background@#Emergency reoperation is considered to be a quality indicator in surgery. We analyzed the risk factors for emergency reoperations. @*Methods@#Patients who underwent emergency operations from January 1, 2017, to December 31, 2017, at our hospital were reviewed in this retrospective study. Multivariate logistic regression was performed for the perioperative risk factors for emergency reoperation. @*Results@#A total of 1,481 patients underwent emergency operations during the study period. Among them, 79 patients received emergency reoperations. The variables related to emergency reoperation included surgeries involving intracranial and intraoral lesions, highest mean arterial pressure ≥ 110 mmHg, highest heart rate ≥ 100 /min, anemia, duration of operation ＞120 min, and arrival from the intensive care unit (ICU). @*Conclusions@#The type of surgery, hemodynamics, hemoglobin values, the duration of surgery, and arrival from ICU were associated with emergency reoperations.

Retrospective investigation of anesthetic management and outcome in patients with deep neck infections

BACKGROUND: Although incidence of deep neck infection has decreased after the introduction of antibiotics and improvement of oral hygiene, the disease may remain serious to anesthesiologists and patients, especially relative to postoperative prognosis and airway management. The objective of this study is to clarify clinical characteristics and consider anesthetic implications. METHODS: This study reviews the experience of 116 patients that received operations for deep neck infections 1997–2017 in a university hospital. Variables included in data were age, sex, lesion, etiology, underlying disease, result of culture, anesthetic techniques, C-reactive protein level, and a variety of scores including ASA physical status, APACHE II, and SOFA. Scores were analyzed statistically to elucidate prognostic ability, and influences on intubation. RESULTS: The following background variables were associated postoperative complication; age, presence of diabetes, hypertension, and infectious disease, extended space and use of N2O. APACHE II ≥ 7 and SOFA ≥ 3 were revealed to be associated with postoperative complication. The following background variables were associated with difficult intubation: date of surgery ≤ 2009, non-otolaryngology department, and submental space. CONCLUSIONS: This study revealed the possibility that the preoperative evaluation, including the determination of scoring system, may be useful in predicting outcome and making a clinical decision of airway management in deep neck infections.

Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

Blood cells are transported into the brain and are thought to participate in neurodegenerative processes following hypoxic ischemic injury. We examined the possibility that transient forebrain ischemia (TFI) causes the blood-brain barrier (BBB) to become permeable to blood cells, possibly via dysfunction and degeneration of endothelial cells in rats. Extravasation of Evans blue and immunoglobulin G (IgG) was observed in the hippocampal CA1-2 areas within 8 h after TFI, and peaked at 48 h. This extravasation was accompanied by loss of tight junction proteins, occludin, and zonula occludens-1, and degeneration of endothelial cells in the CA1-2 areas. Iron overload and mitochondrial free radical production were evident in the microvessel endothelium of the hippocampus before endothelial cell damage occurred. Administration of deferoxamine (DFO), an iron chelator, or Neu2000, an antioxidant, blocked free radical production and endothelial cell degeneration. Our findings suggest that iron overload and iron-mediated free radical production cause loss of tight junction proteins and degeneration of endothelial cells, opening of the BBB after TFI.

Induction of the unfolded protein response and cell death pathway in Alzheimer's disease, but not in aged Tg2576 mice

The endoplasmic reticulum (ER) stress results from disrupted protein folding triggered by protein mutation or oxidation, reduced proteasome activity, and altered Ca2+ homeostasis. ER stress is accompanied by activation of the unfolded protein response (UPR) and cell death pathway. We examined if the UPR and cell death pathway would be activated in Alzheimer's disease (AD). RT-PCR experiments revealed increased splicing of X-box binding protein-1 (XBP-1), an UPR transcription factor, in AD compared with age-matched control. Among target genes of XBP-1, expression of protein disulfide isomerase (PDI), but not glucose-regulated protein 78 (GRP78), was increased in AD, suggesting disturbed activation of the UPR in AD. C/EBP homologous protein (CHOP), caspase-3, caspase-4, and caspase-12, downstream mediators of cell death pathway, were activated in AD. Neither the UPR nor cell death pathway was induced in aged Tg2576 mice, a transgenic mouse model of Alzheimer's disease that reveals both plaque pathology and some cognitive deficits. The present study suggests that disturbed induction of the UPR and activation of the pro-apoptotic proteins contribute to neuropathological process in AD irrespective of amyloid beta and senile plaque.