Postoperative mortality after inpatient surgery: Incidence and risk factors

Karamarie Fecho1, Anne T Lunney1, Philip G Boysen1, Peter Rock2, Edward A Norfleet11Department of Anesthesiology, School of Medicine, University of North Carolina, Chapel Hill, NC, USA; 2Department of Anesthesiology, University of Maryland, Baltimore, MD, USAPurpose: This study determined the incidence of and identified risk factors for 48 hour (h) and 30 day (d) postoperative mortality after inpatient operations.Methods: A retrospective cohort study was conducted using Anesthesiology’s Quality Indicator database as the main data source. The database was queried for data related to the surgical procedure, anesthetic care, perioperative adverse events, and birth/death/operation dates. The 48 h and 30 d cumulative incidence of postoperative mortality was calculated and data were analyzed using Chi-square or Fisher’s exact test and generalized estimating equations.Results: The 48 h and 30 d incidence of postoperative mortality was 0.57% and 2.1%, respectively. Higher American Society of Anesthesiologists physical status scores, extremes of age, emergencies, perioperative adverse events and postoperative Intensive Care Unit admission were identified as risk factors. The use of monitored anesthesia care or general anesthesia versus regional or combined anesthesia was a risk factor for 30 d postoperative mortality only. Time under anesthesia care, perioperative hypothermia, trauma, deliberate hypotension and invasive monitoring via arterial, pulmonary artery or cardiovascular catheters were not identified as risk factors.Conclusions: Our findings can be used to track postoperative mortality rates and to test preventative interventions at our institution and elsewhere.Keywords: postoperative mortality, risk factors, operations, anesthesia, inpatient surger

Mechanism for resveratrol-induced cardioprotection against reperfusion injury involves glycogen synthase kinase 3β and mitochondrial permeability transition pore

Resveratrol pretreatment can protect the heart by inducing pharmacological preconditioning. Whether resveratrol protects the heart when applied at reperfusion remains unknown. We examined the effect of resveratrol on myocardial infarct size when given at reperfusion and investigated the mechanism underlying the effect. Isolated rat hearts were subjected to 30 min ischemia followed by 2 h of reperfusion, and myocardial samples were collected from the risk zone for Western blot analysis. Mitochondrial swelling was spectrophotometrically measured as a decrease in absorbance at 520 nm (A520). Resveratrol reduced infarct size and prevented cardiac mitochondrial swelling. Resveratrol enhanced GSK-3β phosphorylation upon reperfusion, an effect that was mediated by the cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) pathway. Resveratrol translocated GSK-3β from cytosol to mitochondria via the cGMP/PKG pathway. Further studies showed that mitochondrial GSK-3β was co-immunoprecipitated with cyclophilin D but not with VDAC (voltage dependent anion channel) or ANT (adenine nucleotide translocator). These data suggest that resveratrol prevents myocardial reperfusion injury presumably by targeting the mPTP through translocation of GSK-3β from cytosol to mitochondria. Translocated GSK-3β may ultimately interact with cyclophilin D to modulate the mPTP opening

NO mobilizes intracellular Zn2+ via cGMP/PKG signaling pathway and prevents mitochondrial oxidant damage in cardiomyocytes

Our aim was to determine if NO prevents mitochondrial oxidant damage by mobilizing intracellular free zinc (Zn2+)

Postconditioning prevents reperfusion injury by activating delta-opioid receptors. Anesthesiology 2008

Background: While postconditioning has been proposed to protect the heart by targeting the mitochondrial permeability transition pore (mPTP), the detailed mechanism underlying this action is unknown. The authors hypothesized that postconditioning stimulates opioid receptors, which in turn protect the heart from reperfusion injury by targeting the mPTP. Methods: Rat hearts (both in vivo and in vitro) were subjected to 30 min of ischemia and 2 h of reperfusion. Postconditioning was elicited by six cycles of 10-s reperfusion and 10-s ischemia. To measure nitric oxide concentration, cardiomyocytes loaded with 4-amino-5-methylamino-2=,7=-difluorofluorescein were imaged using confocal microscopy. Mitochondrial membrane potential was determined by loading cardiomyocytes with tetramethylrhodamine ethyl ester. Result