Stroke is a leading cause of morbidity and mortality in the United States and occurs in the perioperative period. The authors studied the incidence, predictors, and outcomes of perioperative stroke using the American College of Surgeons National Surgical Quality Improvement Program.
Data on 523,059 noncardiac, nonneurologic patients in the American College of Surgeons National Surgical Quality Improvement Program database were analyzed for the current study. The incidence of perioperative stroke was identified. Logistic regression was applied to a derivation cohort of 350,031 patients to generate independent predictors of stroke and develop a risk model. The risk model was subsequently applied to a validation cohort of 173,028 patients. The role of perioperative stroke in 30-day mortality was also assessed.
The incidence of perioperative stroke in both the derivation and validation cohorts was 0.1%. Multivariate analysis revealed the following independent predictors of stroke in the derivation cohort: age ≥ 62 yr, history of myocardial infarction within 6 months before surgery, acute renal failure, history of stroke, dialysis, hypertension, history of transient ischemic attack, chronic obstructive pulmonary disease, current tobacco use, and body mass index 35-40 kg/m² (protective). These risk factors were confirmed in the validation cohort. Surgical procedure also influenced the incidence of stroke. Perioperative stroke was associated with an 8-fold increase in perioperative mortality within 30 days (95% CI, 4.6-12.6).
Noncardiac, nonneurologic surgery carries a risk of perioperative stroke, which is associated with higher mortality. The models developed in this study may be informative for clinicians and patients regarding risk and prevention of this complication.
"Age ≥ 62 year, history of myocardial infarction within 6 months before surgery, acute renal failure, history of stroke, dialysis, hypertension, history of transient ischemic attack, chronic obstructive pulmonary disease, current tobacco use, and body mass index 35-40 kg/m2 are known as independent predictors of stroke . The complexity of the surgical procedure and surgery induced hypercoagulable status also influence the incidence of stroke . The management of stroke involves a decision regarding the quickest suitable revascularization metod. "
[Show abstract][Hide abstract] ABSTRACT: Perioperative ischemic stroke is an uncommon event associated with significant morbidity and mortality. The complexity of the surgical procedure and surgery induced hypercoagulable status also influence the incidence of stroke. The management of stroke involves a decision regarding the quickest suitable revascularization method. Endovascular mechanical thrombectomy, such as intra-arterial mechanical thrombectomy (IAMT), can restore vascular patency of the vessels, providing an alternative or synergistic method to restore blood flow. Although, there are no recommended treatment guidelines, IAMT is eligible to be a treatment of choice for perioperative ischemic stroke. We experienced a case of a patient who demonstrated hemiplegia and aphasia, the early symptom of acute ischemic stroke, in the post-anesthesia care unit and performed IAMT successfully. Thus we report the case with a review of the relevant literature.
Korean journal of anesthesiology 05/2014; 66(5):402-6. DOI:10.4097/kjae.2014.66.5.402
"Ischemic injury to neuronal cells might occur in the perioperative period during major cardiovascular but also non-cardiac surgical procedures . Against current dogma that carbon monoxide (CO) is poisonous, particularly to the brain, emerging data suggest that at low doses CO provides potent neuroprotection by its anti-inflammatory and anti-apoptotic properties , . "
[Show abstract][Hide abstract] ABSTRACT: Carbon monoxide (CO) is an accepted cytoprotective molecule. The extent and mechanisms of protection in neuronal systems have not been well studied. We hypothesized that delivery of CO via a novel releasing molecule (CORM) would impart neuroprotection in vivo against ischemia-reperfusion injury (IRI)-induced apoptosis of retinal ganglion cells (RGC) and in vitro of neuronal SH-SY5Y-cells via activation of soluble guanylate-cyclase (sGC).
To mimic ischemic respiratory arrest, SH-SY5Y-cells were incubated with rotenone (100 nmol/L, 4 h) ± CORM ALF186 (10-100 µmol/L) or inactivated ALF186 lacking the potential of releasing CO. Apoptosis and reactive oxygen species (ROS) production were analyzed using flow-cytometry (Annexin V, mitochondrial membrane potential, CM-H2DCFDA) and Western blot (Caspase-3). The impact of ALF186± respiratory arrest on cell signaling was assessed by measuring expression of nitric oxide synthase (NOS) and soluble guanylate-cyclase (sGC) and by analyzing cellular cGMP levels. The effect of ALF186 (10 mg/kg iv) on retinal IRI in Sprague-Dawley rats was assessed by measuring densities of fluorogold-labeled RGC after IRI and by analysis of apoptosis-related genes in retinal tissue.
ALF186 but not inactivated ALF186 inhibited rotenone-induced apoptosis (Annexin V positive cells: 25±2% rotenone vs. 14±1% ALF186+rotenone, p<0.001; relative mitochondrial membrane potential: 17±4% rotenone vs. 55±3% ALF186+rotenone, p<0.05). ALF186 increased cellular cGMP levels (33±5 nmol/L vs. 23±3 nmol/L; p<0.05) and sGC expression. sGC-inhibition attenuated ALF186-mediated protection (relative mitochondrial membrane potential: 55±3% ALF186+rotenone vs. 20±1% ODQ+ALF186+rotenone, p<0.05). ALF186 protected RGC in vivo (IRI 1255±327 RGC/mm(2) vs. ALF186+IRI 2036±83; p<0.05) while sGC inhibition abolished the protective effects of ALF186 (ALF186+IRI 2036±83 RGC/mm(2) vs. NS-2028+ALF186+IRI 1263±170, p<0.05).
The CORM ALF186 inhibits IRI-induced neuronal cell death via activation of sGC and may be a useful treatment option for acute ischemic insults to the retina and the brain.
PLoS ONE 11/2013; 8(4):e60672. DOI:10.1371/journal.pone.0060672 · 3.23 Impact Factor
"Stroke, an ischemic cerebral injury, is a leading cause of morbidity and mortality in the Western world and may occur in the perioperative period . Perioperative stroke is primarily associated with major cardiovascular procedures but has also been reported after non-cardiac surgery, occurring with an incidence of 0.1% . Pre-clinical evaluation of many neuroprotective strategies showed only modest or inconsistent tissue protection . "
[Show abstract][Hide abstract] ABSTRACT: Ischemia and reperfusion injury (I/R) of neuronal structures and organs is associated with increased morbidity and mortality due to neuronal cell death. We hypothesized that inhalation of carbon monoxide (CO) after I/R injury ('postconditioning') would protect retinal ganglion cells (RGC).
Retinal I/R injury was performed in Sprague-Dawley rats (n = 8) by increasing ocular pressure (120 mmHg, 1 h). Rats inhaled room air or CO (250 ppm) for 1 h immediately following ischemia or with 1.5 and 3 h latency. Retinal tissue was harvested to analyze Bcl-2, Bax, Caspase-3, HO-1 expression and phosphorylation of the nuclear transcription factor (NF)-κB, p38 and ERK-1/2 MAPK. NF-κB activation was determined and inhibition of ERK-1/2 was performed using PD98059 (2 mg/kg). Densities of fluorogold prelabeled RGC were analyzed 7 days after injury. Microglia, macrophage and Müller cell activation and proliferation were evaluated by Iba-1, GFAP and Ki-67 staining.
Inhalation of CO after I/R inhibited Bax and Caspase-3 expression (Bax: 1.9±0.3 vs. 1.4±0.2, p = 0.028; caspase-3: 2.0±0.2 vs. 1.5±0.1, p = 0.007; mean±S.D., fold induction at 12 h), while expression of Bcl-2 was induced (1.2±0.2 vs. 1.6±0.2, p = 0.001; mean±S.D., fold induction at 12 h). CO postconditioning suppressed retinal p38 phosphorylation (p = 0.023 at 24 h) and induced the phosphorylation of ERK-1/2 (p<0.001 at 24 h). CO postconditioning inhibited the expression of HO-1. The activation of NF-κB, microglia and Müller cells was potently inhibited by CO as well as immigration of proliferative microglia and macrophages into the retina. CO protected I/R-injured RGC with a therapeutic window at least up to 3 h (n = 8; RGC/mm(2); mean±S.D.: 1255±327 I/R only vs. 1956±157 immediate CO treatment, vs. 1830±109 1.5 h time lag and vs. 1626±122 3 h time lag; p<0.001). Inhibition of ERK-1/2 did not counteract the CO effects (RGC/mm(2): 1956±157 vs. 1931±124, mean±S.D., p = 0.799).
Inhaled CO, administered after retinal ischemic injury, protects RGC through its strong anti-apoptotic and anti-inflammatory effects.
PLoS ONE 09/2012; 7(9):e46479. DOI:10.1371/journal.pone.0046479 · 3.23 Impact Factor
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