Monitored anesthesia care (MAC) is an anesthesia technique combining local anesthesia with parenteral drugs for sedation and analgesia. The use of MAC is increasing for a variety of diagnostic and therapeutic procedures in and outside of the operating room due to the rapid postoperative recovery with the use of relatively small amounts of sedatives and analgesics compared to general anesthesia. The purposes of MAC are providing patients with safe sedation, comfort, pain control and satisfaction. Preoperative evaluation for patients with MAC is similar to those of general or regional anesthesia in that patients should be comprehensively assessed. Additionally, patient cooperation with comprehension of the procedure is an essential component during MAC. In addition to local anesthesia by operators or anesthesiologists, systemic sedatives and analgesics are administered to provide patients with comfort during procedures performed with MAC. The discretion and judgment of an experienced anesthesiologist are required for the safety and efficacy profiles because the airway of the patients is not secured. The infusion of sedatives and analgesics should be individualized during MAC. Many procedures in and outside of the operating room, including eye surgery, otolaryngologic surgery, cardiovascular procedures, pain procedures, and endoscopy are performed with MAC to increase patient and operator satisfaction.
Numerous factors are associated with mortality after hip fracture surgery in elderly patients. The aim of this study was to investigate whether preoperative C-reactive protein (CRP) was an independent risk factor for 1-year mortality after hip fracture surgery in the elderly. The electronic medical records of 772 elderly patients (age ≥ 65 years) undergoing hip fracture surgery from May 2003 to November 2011 were reviewed retrospectively. The patients comprised a high CRP group (>10.0 mg/dL) and low CRP group (≤10.0 mg/dL), based upon preoperative CRP levels. The overall 1-year mortality was 14.1%; the value was significantly higher in the high CRP group than in the low CRP group (31.8% vs 12.5%; P < 0.001). On binary logistic regression, body mass index (odds ratio [OR], 0.93; 95% confidence interval [CI], 0.88–0.99; P = 0.025), history of malignancy (OR, 2.59; 95% CI, 1.47–4.57; P = 0.001), American Society of Anesthesiologists physical status (ASA PS) class 3–4 (OR, 1.96; 95% CI, 1.25–3.07; P = 0.003), preoperative albumin (OR, 0.39; 95% CI, 0.25–0.61; P < 0.001), preoperative CRP > 10.0 mg/dL (OR, 2.04; 95% CI, 1.09–3.80; P = 0.025), postoperative intensive care unit (ICU) admission (OR, 2.29; 95% CI, 1.15–4.59; P = 0.019), and creatinine on the second postoperative day (OR, 1.20; 95% CI, 1.00–1.45; P = 0.048) were independent predictors of 1-year mortality after hip surgery. Male gender and low preoperative hemoglobin were associated with in-hospital mortality, whereas delayed surgery and femoral neck fracture were related to the 6-month mortality. Low preoperative albumin and low body mass index predicted the 6-month and 1-year mortality. An increased preoperative CRP level, particularly >10.0 mg/dL, was associated with the 1-year mortality after hip fracture surgery in the elderly. In addition, a history of malignancy, high ASA PS score, and postoperative ICU admission were related to mortality after hip fracture.
BackgroundIschemia and the following reperfusion damage are critical mechanisms of spinal cord injury. Statins have been reported to decrease ischemia–reperfusion injury in many organs including the spinal cord. Anti-oxidative effect is one of the main protective mechanisms of statin against neuronal death and cytotoxicity. We hypothesized that statins’ anti-oxidative property would yield neuroprotective effects on spinal cord ischemia–reperfusion injuryMethodsPrimary cultured spinal cord motor neurons were isolated from Sprague–Dawley rat fetuses. Ischemia–reperfusion injury model was induced by 60 min of oxygen and glucose deprivation (OGD) and 24 h of reoxygenation. Healthy and OGD cells were treated with simvastatin at concentrations of 0.1, 1, and 10 μM for 24 h. Cell viability was assessed using water-soluble tetrazolium salt (WST)-8, cytotoxicity with LDH, and production of free radicals with DCFDA (2′,7′-dichlorofluorescein diacetate).ResultsOGD reduced neuronal viability compared to normoxic control by 35.3%; however, 0.1–10 μM of simvastatin treatment following OGD improved cell survival. OGD increased LDH release up to 214%; however, simvastatin treatment attenuated its cytotoxicity at concentrations of 0.1–10 μM (p < 0.001 and p = 0.001). Simvastatin also reduced deteriorated morphological changes of motor neurons following OGD. Oxidative stress was reduced by simvastatin (0.1–10 μM) compared to untreated cells exposed to OGD (p < 0.001).ConclusionsSimvastatin effectively reduced spinal cord neuronal death and cytotoxicity against ischemia–reperfusion injury, probably via modification of oxidative stress.
cris.nih.go.kr identifier: KCT0001410.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.