Search

Background This study assessed associations between processed electroencephalographic (pEEG) use during anesthesia, surgery- and anesthesia-related risk factors, and neurologic outcomes and mortality after cardiac surgery. Methods Drawing from the Society of Thoracic Surgeons Adult Cardiac Surgery Database and its Adult Cardiac Anesthesiology Section, we identified 42,932 records for elective, urgent, and emergency cardiac surgery procedures between July 1, 2017, to December 31, 2019. Using propensity score weighted regression analysis, we analyzed the associations between pEEG use during anesthesia on the primary outcome, postoperative delirium (POD), and secondary outcomes (stroke, encephalopathy, coma, and operative mortality). Results The rate of pEEG use during anesthesia use was 32.8% (n=14,086), and its use was not associated with decreased odds for POD (odds ratio [OR], 0.88; 95%CI, 0.78-1.02) or encephalopathy (OR, 0.85; 95%CI, 0.70-1.03). Intraoperative pEEG monitoring use was also not associated with increased odds for stroke (OR, 1.17; 95%CI, 0.97-1.42) or coma (OR, 1.44; 95%CI, 0.82-2.52). In contrast, pEEG use during anesthesia was associated with higher odds for operative mortality (OR, 1.23; 95%CI, 1.05-1.44). This association remained significant after adjusting for POD (OR: 1.21, 95%CI: 1.03-1.41), stroke (OR: 1.21, 95%CI:1.04-1.42), and encephalopathy (OR: 1.28, 95%CI: 1.07-1.52). Conclusions This large retrospective database study found no association between pEEG use during cardiac surgery and postoperative neurologic outcomes such as POD, stroke, encephalopathy, or coma. However, patients who underwent pEEG monitoring during anesthesia experienced higher mortality, even after adjustment for neurologic outcomes.

In this review, we discuss recent developments and trends in the perioperative management of thrombocytopenia.Large contemporary data base studies show that preoperative thrombocytopenia is present in about 8% of asymptomatic patients, and is associated with increased risks for bleeding and 30-day mortality. Traditionally specific threshold platelet counts were recommended for specific procedures. However, the risk of bleeding may not correlate well with platelet counts and varies with platelet function depending on the underlying etiology. Evidence to support prophylactic platelet transfusion is limited and refractoriness to platelet transfusion is common. A number of options exist to optimize platelet counts prior to procedures, which include steroids, intravenous immunoglobulin, thrombopoietin receptor agonists, and monoclonal antibodies. In addition, intraoperative alternatives and adjuncts to transfusion should be considered. It appears reasonable to use prophylactic desmopressin and antifibrinolytic agents, whereas activated recombinant factor VII could be considered in severe bleeding. Other options include enhancing thrombin generation with prothrombin complex concentrate or increasing fibrinogen levels with fibrinogen concentrate or cryoprecipitate.Given the lack of good quality evidence, much research remains to be done. However, with a multidisciplinary multimodal perioperative strategy, the risk of bleeding can be decreased effectively.

Background We examined how intercostal nerve block (ICNB) with standard bupivacaine and ICNB with extended-release liposomal bupivacaine, compared with thoracic epidural analgesia (TEA), were associated with postoperative opioid pain medication consumption and hospital length of stay (LOS) after thoracic surgery. Methods We studied 1935 patients who underwent thoracic surgery between January 1, 2010, and November 30, 2017, at a tertiary academic center. Primary and secondary outcomes were postoperative opioid consumption expressed as morphine milligram equivalents (MMEs) at 24, 48, and 72 hours after surgery, the LOS, and total MME consumption from surgery to discharge. Results Of these patients, 888 (45.9%) received TEA, 730 (37.7%) ICNB with standard bupivacaine, 127 (6.6%) ICNB with liposomal bupivacaine, and 190 (9.8%) no regional analgesia. Compared with epidural analgesia, in 2017, ICNB liposomal bupivacaine provided similar pain control in terms of MME consumption at 24 and 72 hours, but decreased MME consumption at 48 hours (odds ratio [OR] = 0.33; confidence interval [CI] = 0.14-0.81) and at discharge (OR = 0.28; CI = 0.12-0.68) and was associated with a higher likelihood for a shorter LOS (hazard ratio = 3.46; CI = 2.42-4.96). Compared with TEA, ICNB with standard bupivacaine and no regional analgesia use showed varying impact on MME consumption between 24 and 72 hours after surgery, and their use was not associated with a significantly reduced MME consumption at discharge but with a shorter hospital LOS. Conclusions Multimodal analgesia involving regional anesthetic alternatives to TEA could help manage postoperative pain in thoracic surgery patients.

A bedridden patient with empyema presented for thoracoscopic decortication. During the procedure, despite a post-tetanic count (PTC) of 0 via calibrated quantitative neuromuscular monitoring, persistent diaphragmatic movement impaired operating conditions, so rocuronium was re-dosed. After surgery, the patient had 0 PTC. Sugammadex was titrated to achieve baseline neuromuscular strength, monitoring the effect of each 200-mg dose. Ultimately, 1200 mg was required to achieve baseline strength. We describe monitor troubleshooting, considerations with unexpectedly deep neuromuscular blockade, the importance of routine quantitative neuromuscular monitoring, and one strategy for sugammadex reversal in patients with profound paralysis outside of the standard dosing guidelines.

Venous thromboembolism (VTE) is a significant problem in the perioperative period, increasing patient morbidity, mortality, and health care costs. It is also considered the most preventable of the major postoperative complications. Despite widespread adoption of prophylaxis guidelines, it appears that morbidity from the disease has not substantially changed within the past 2 decades. It is becoming clear that current prophylaxis efforts are not sufficient. Using more potent anticoagulants may decrease the incidence of VTE, but increase the risk for bleeding and infection. Much has been learned about the pathophysiology of venous thrombogenesis in recent years. Beyond the "traditional coagulation cascade," which anticoagulants modulate, there is a growing appreciation for the roles of tissue factor, monocytes, neutrophils, neutrophil extracellular traps, microvesicles, and platelets in thrombus initiation and propagation. These recent studies explain to some degree why aspirin appears to be remarkably effective in preventing thrombus propagation. Endothelial dysfunction, traditionally thought of as a risk factor for arterial thrombosis, plays an important role within the cusps of venous valves, a unique environment where the majority of venous thrombi originate. This suggests a role for newer treatment modalities such as statins. Not all patients have an equal likelihood of experiencing a VTE, even when undergoing high-risk procedures, and better tools are required to accurately predict VTE risk. Only then will we be able to effectively individualize prophylaxis by balancing the risks for VTE against the risks associated with treatment. Given the different cell types and pathways involved in thrombogenesis, it is likely that multimodal treatment regimens will be more effective, enabling the use of lower and safer doses of hemostatic modulating therapies such as anticoagulants, antithrombotics, and antiplatelet medications.

We present a case in which we electively used venovenous extracorporeal membrane oxygenation (VV-ECMO) to facilitate safe resection of a nearly obstructing airway tumor near the carina in a 37-year-old male. The patient was brought to the operating room and underwent bifemoral cannulation for VV-ECMO under light sedation while maintaining spontaneous ventilation. After VV-ECMO was initiated, general anesthesia was induced, and the tumor was resected via rigid bronchoscopy. After resection, the patient was intubated, weaned from ECMO, decannulated, awoken, extubated, and taken to the postanesthesia care unit for recovery.

Background Anesthesiologists administer excess supplemental oxygen (hyper-oxygenation) to patients during surgery to avoid hypoxia. Hyper-oxygenation, however, may increase the generation of reactive oxygen species and cause oxidative damage. In cardiac surgery, increased oxidative damage has been associated with postoperative kidney and brain injury. We hypothesize that maintenance of normoxia during cardiac surgery (physiologic oxygenation) decreases kidney injury and oxidative damage compared to hyper-oxygenation. Methods/design The Risk of Oxygen during Cardiac Surgery (ROCS) trial will randomly assign 200 cardiac surgery patients to receive physiologic oxygenation, defined as the lowest fraction of inspired oxygen (FIO2) necessary to maintain an arterial hemoglobin saturation of 95 to 97%, or hyper-oxygenation (FIO2 = 1.0) during surgery. The primary clinical endpoint is serum creatinine change from baseline to postoperative day 2, and the primary mechanism endpoint is change in plasma concentrations of F2-isoprostanes and isofurans. Secondary endpoints include superoxide production, clinical delirium, myocardial injury, and length of stay. An endothelial function substudy will examine the effects of oxygen treatment and oxidative stress on endothelial function, measured using flow mediated dilation, peripheral arterial tonometry, and wire tension myography of epicardial fat arterioles. Discussion The ROCS trial will test the hypothesis that intraoperative physiologic oxygenation decreases oxidative damage and organ injury compared to hyper-oxygenation in patients undergoing cardiac surgery. Trial registration ClinicalTrials.gov, ID: NCT02361944. Registered on the 30th of January 2015. Electronic supplementary material The online version of this article (doi:10.1186/s13063-017-2021-5) contains supplementary material, which is available to authorized users.

Human fibrinogen concentrate (HFC) is approved by the Food and Drug Administration for use at 70 mg/kg to treat congenital afibrinogenemia. We sought to determine whether this dose of HFC increases fibrinogen levels in the setting of high-risk bleeding associated with aortic reconstruction and deep hypothermic circulatory arrest (DHCA).This was a prospective, pilot, off-label study in which 22 patients undergoing elective proximal aortic reconstruction with DHCA were administered 70 mg/kg HFC upon separation from cardiopulmonary bypass (CPB). Fibrinogen levels were measured at baseline, just before, and 10 minutes after HFC administration, on skin closure, and the day after surgery. The primary study outcome was the difference in fibrinogen level immediately after separation from CPB, when HFC was administered, and the fibrinogen level 10 minutes following HFC administration. Additionally, postoperative thromboembolic events were assessed as a safety analysis.The mean baseline fibrinogen level was 317 ± 49 mg/dL and fell to 235 ± 39 mg/dL just before separation from CPB. After HFC administration, the fibrinogen level rose to 331 ± 41 mg/dL (P.001) and averaged 372 ± 45 mg/dL the next day. No postoperative thromboembolic complications occurred.Administration of 70 mg/kg HFC upon separation from CPB raises fibrinogen levels by approximately 100 mg/dL without an apparent increase in thrombotic complications during proximal aortic reconstruction with DHCA. Further prospective study in a larger cohort of patients will be needed to definitively determine the safety and evaluate the efficacy of HFC as a hemostatic adjunct during these procedures.

Erythropoiesis-stimulating agents, such as erythropoietin (EPO), can be used to treat preoperative anemia. Some studies suggest an increased risk of mortality and thrombotic events, and use in cardiovascular surgery remains off-label. This study compares outcomes in cardiac surgery patients declining blood transfusion who received EPO with a matched cohort who did not.After institutional review board approval, we conducted a retrospective review of all patients who decline blood transfusion who underwent cardiac surgery and received EPO between January 1, 2004, and June 15, 2015, at a single institution. Control patients who did not receive EPO and were not transfused allogeneic red blood cells perioperatively were identified during the same period. Two controls were matched to each EPO patient using an optimal matching algorithm based on age, date of surgery, gender, operative procedure, and surgeon. The European System for Cardiac Operative Risk Evaluation (EuroSCORE) and baseline characteristics remaining unbalanced in the matched cohorts were controlled for in assessing patient outcomes. The primary outcome was a composite of mortality and thrombotic events, and secondary outcomes included change in hemoglobin (Hb) from baseline to discharge, acute kidney injury (AKI), sternal wound infection, atrial fibrillation, time to extubation, intensive care unit, and hospital length of stay (LOS).Fifty-three patients who decline transfusion and received EPO were compared to 106 optimally matched control patients who did not receive EPO or red blood cell transfusion in the perioperative period. The median additive EuroSCORE was similar between the EPO and control group [6 (4, 9) vs 5 (3, 7), respectively; P = .39]. There was no difference in the primary outcome (P = .12) and mortality was zero in both groups. The EPO group had a higher mean preoperative Hb (13.91 g/dL vs 13.31; P = .02) and a smaller change in Hb from baseline (-2.65 vs -3.60; P = .001). The incidence of AKI (47.17% vs 41.51%; P = .49) was similar and there was no significant difference in all other outcomes, including time to extubation, hospital LOS, or intensive care unit LOS.In this retrospective matched cohort study of patients declining transfusion and receiving EPO matched to control patients, there were no clinically meaningful differences in the outcomes.

Background Intraoperative autologous platelet (PLT) collection as part of a multimodal blood conservation program carries a Class IIa recommendation from the Societies of Thoracic Surgeons and Cardiovascular Anesthesiologists, but achieving a suitable PLT yield limits its application. A novel, autologous, intraoperative, high-yield plateletpheresis collection program was established and retrospectively analyzed to identify potential improvements over previously reported plateletpheresis protocols. Study design and m-ethods Targeting complex cardiothoracic surgery patients without recent anti-PLT agents, thrombocytopenia, or severe anemia, the program aimed to achieve a PLT yield of at least one standard apheresis unit (3.0 × 10(11) ) within 60 to 90 minutes and using an automated plateletpheresis device (Trima, Terumo BCT). Anesthetized and invasively monitored patients underwent plateletpheresis via a large-bore, indwelling central line placed for the surgery. Collection-related data for quality control purposes and subsequent PLT transfusion requirements were analyzed and reported. Results Forty-two patients donated autologous PLTs between 2011 and 2012. PLT yield was 4.5 (3.9-5.0) × 10(11) , which significantly exceeds previously reported yields, and procedure duration was 53.2 (48.4-57.9) minutes. As anticipated, postcollection PLT count decreased from 268 (242-293) × 10(9) to 182 (163-201) × 10(9) /L; hypocalcemia was minimized by infusion of 1 g of CaCl2 . Autologous PLT yield was inversely correlated with allogeneic PLT use, and avoidance of allogeneic PLT transfusion was increased when the autologous yield was the equivalent of 2 or more apheresis units. Conclusion High-yield, intraoperative autologous PLT collection is achievable using an automated plateletpheresis device. Initial experience shows a reduction in reliance on allogeneic PLTs for complex cardiothoracic surgery.

Increased pulse pressure (PP) is an important independent predictor of cardiovascular outcome and acute kidney injury (AKI) after cardiac surgery. The objective of this study was to determine whether elevated baseline PP is associated with postoperative AKI and 30-day mortality after noncardiac surgery.We evaluated 9125 adult patients who underwent noncardiac surgery at Duke University Medical Center between January 2006 and December 2009. Baseline arterial blood pressure was defined as the mean of the first 5 measurements recorded by the automated record keeping system before inducing anesthesia. Multivariable logistic regression analysis was performed to determine whether baseline PP adjusted for other perioperative risk factors was independently associated with postoperative AKI and 30-day mortality.Of the 9125 patients, the baseline PP was40 mm Hg in 1426 (15.6%), 40-80 mm Hg in 6926 (75.9%), and80 mm Hg in 773 (8.5%) patients. The incidence of AKI was 19.8%, which included 8.4% (151 patients) and 4.2% (76 patients) who experienced stage II and III AKI, respectively. In the risk-adjusted model for postoperative AKI, elevated baseline PP was associated with higher odds for postoperative AKI (adjusted odds ratio [OR] for every 20 mm Hg increase in PP, 1.17; 95% confidence interval [CI], 1.10-1.25; P.0001). Also elevated baseline preoperative PP was significantly associated with mild (stage I; OR, 1.19; 95% CI, 1.11-1.27; P.0001), but not with more advanced stages of postoperative AKI or with an incremental risk for 30-day mortality.We found a significant association between elevated baseline PP and postoperative AKI in patients who underwent noncardiac surgery. However, elevated PP was not significantly associated with more advanced stages of postoperative AKI or 30-day mortality in these patients.

Cognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models. Pilot work identified blood injectate volumes necessary to provide similar mortality rates (20–25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naive rats were used as controls. Functional and cognitive outcome was assessed over 35 days. DB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB. Both SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.

Atrial tissue gene expression profiling may help to determine how differentially expressed genes in the human atrium before cardiopulmonary bypass (CPB) are related to subsequent biologic pathway activation patterns, and whether specific expression profiles are associated with an increased risk for postoperative atrial fibrillation (AF) or altered response to β-blocker (BB) therapy after coronary artery bypass grafting (CABG) surgery. Right atrial appendage (RAA) samples were collected from 45 patients who were receiving perioperative BB treatment, and underwent CABG surgery. The isolated RNA samples were used for microarray gene expression analysis, to identify probes that were expressed differently in patients with and without postoperative AF. Gene expression analysis was performed to identify probes that were expressed differently in patients with and without postoperative AF. Gene set enrichment analysis (GSEA) was performed to determine how sets of genes might be systematically altered in patients with postoperative AF. Of the 45 patients studied, genomic DNA from 42 patients was used for target sequencing of 66 candidate genes potentially associated with AF, and 2,144 single-nucleotide polymorphisms (SNPs) were identified. We then performed expression quantitative trait loci (eQTL) analysis to determine the correlation between SNPs identified in the genotyped patients, and RAA expression. Probes that met a false discovery rate < 0.25 were selected for eQTL analysis. Of the 17,678 gene expression probes analyzed, 2 probes met our prespecified significance threshold of false discovery rate < 0.25. The most significant probe corresponded to vesicular overexpressed in cancer – prosurvival protein 1 gene (VOPP1; 1.83 fold change; P = 3.47 × 10−7), and was up-regulated in patients with postoperative AF, whereas the second most significant probe, which corresponded to the LOC389286 gene (0.49 fold change; P = 1.54 × 10−5), was down-regulated in patients with postoperative AF. GSEA highlighted the role of VOPP1 in pathways with biologic relevance to myocardial homeostasis, and oxidative stress and redox modulation. Candidate gene eQTL showed a trans-acting association between variants of G protein-coupled receptor kinase 5 gene, previously linked to altered BB response, and high expression of VOPP1. In patients undergoing CABG surgery, RAA gene expression profiling, and pathway and eQTL analysis suggested that VOPP1 plays a novel etiological role in postoperative AF despite perioperative BB therapy.

Use of genetically manipulated mice facilitates understanding pathological mechanisms in many diseases and contributes to therapy development. However, there is no practical and clinically relevant mouse model available for spinal cord ischemia. This report introduces a simplified long-term outcome mouse model of spinal cord ischemia. Male C57Bl/6J mice were anesthetized with isoflurane and endotracheally intubated. The middle segment of the thoracic aorta was clamped for 0, 8, 10 or 12 min via left lateral thoracotomy. Rectal temperature was maintained at 37.0+/-0.5 degrees C. A laser Doppler probe was used to measure lumbar spinal cord blood flow during thoracic aorta cross-clamping. Open field locomotor function and rotarod performance were evaluated at 1h and 1, 3, 5, and 7 days post-injury. Surviving neurons in the lumbar ventral horn were counted at 7 days post-injury. Cross-clamping the middle segment of the thoracic aorta resulted in approximately 90% blood flow reduction in the lumbar spinal cord. Neurological deficit and neuronal cell death were associated with ischemia duration. Another set of mice were subjected to 10 min aortic clamping or sham surgery and neurological function was examined at 1h and 1, 3, 5, 7, 14, and 28 days. Four of 5 mice (80%) in the injured group survived 28 days and had significant neurological deficit. This study indicates that cross-clamping of the aorta via left thoracotomy is a simple and reliable method to induce spinal cord ischemia in mice allowing definition of long-term outcome.

Cognitive dysfunction is increasingly recognized as a significant long-term complication following subarachnoid hemorrhage (SAH), affecting up to 60% of survivors. We proposed to determine the incidence and explore potential mechanisms of cognitive dysfunction in a rat model. The effects of intracisternal blood, saline and sham injections were compared. At five weeks, Morris water maze escape latency (P=0.001) and swimming distance (P=0.001) were significantly different between groups, with increased latencies and distances recorded in the blood group in spite of increased swimming speed. The number of morphologically intact cortical (r=-0.75, P=0.0001) and hippocampal CA1 (r=-0.80, P

Cerebral vasculopathy may play an important role in the development of delayed cerebral ischemia following subarachnoid hemorrhage (SAH). Platelet-derived growth factor AB (PDGF-AB) and vascular endothelial growth factor (VEGF) released from blood clot may trigger vasculopathy in cerebral arteries. We compared arteriographic and histological response to injection of blood with PDGF-AB and VEGF in basilar artery over 3 days.A total of 55 male New Zealand white rabbits were used in this study. SAH was simulated by single injection of 1 ml of autologous blood, while 50 microg PDGF-AB, 100 microg VEGF, and 50 microg PDGF-AB/100 microg VEGF combined were given in autologous cerebrospinal fluid (CSF) into the cisterna magna. Eight rabbits served as controls, receiving arteriograms but no cisternal injections, and 13 rabbits received reinjections of CSF. Basilar artery diameter was measured arteriographically at baseline and 3 days after injection. Immunohistochemistry was performed to assess change in the basilar artery.Control groups showed significantly less (p0.0002) basilar artery narrowing than all treatment groups. Proliferating cell nuclear antigen (PCNA) was not significant for treatment groups compared to CSF reinject control. PCNA was significantly different for the no puncture group compared to the CSF reinject control. Von Willebrand Factor staining may indicate endothelial proliferation in the adventitia of SAH, VEGF, and PDGFAB/ VEGF combined groups. PDGF labeling was abundant for SAH, PDGF-AB, and PGDF-AB/VEGF combined.PDGF-AB/VEGF and VEGF cause narrowing of the basilar artery similar to cisternal blood clot at 3 days, and thus blood clot was not required to cause arteriographic changes consistent with cerebral vasculopathy.

f s o A67-YEAR-OLD WOMAN presented with progressive dyspnea limiting her ability to perform daily activities. er past medical history was significant for hyperlipidemia and ashimoto thyroiditis. Upon further workup, a transthoracic chocardiogram (TTE) was performed, which revealed severe itral regurgitation (MR) with mild tricuspid regurgitation TR). Subsequently, she was scheduled for mitral valve repair. After an uneventful induction of anesthesia, an intraoperative ransesophageal echocardiogram (TEE) was performed using a atrix array transducer and images acquired on an IE33 ultraound system (Philips Healthcare, Andover, MA). The examiation showed biatrial enlargement and prolapse of both the mitral nd tricuspid valves. The tricuspid annulus in diastole measured 4 m in the midesophageal 4-chamber view. The diagnosis of severe R and mild TR was confirmed. The surgeon proceeded as lanned with a mitral valve repair via a minimally invasive ort-access approach. After cardiopulmonary bypass (CPB), the TEE showed a atisfactory mitral repair. However, there was hemodynamic vidence of TR with right ventricular dysfunction and an unerfilled left ventricle. The central venous pressure was eleated; there were large “v” waves on the pressure waveform. lthough the echocardiographic examination clearly showed R, there was no clearly defined turbulent jet, and, therefore, he TR could not be quantified simply using the vena contracta, he proximal isovelocity surface area, or the jet area. The systolic flow across the tricuspid valve was laminar (Fig ) and had a low peak velocity of 0.9 m/s. Both hepatic venous

We are grateful to the STASH trial investigators for their eff orts to advance the use of simvastatin in subarachnoid haemorrhage from bench to bedside. The results of the STASH trial do not support the use of 40 mg simvastatin daily to decrease delayed cerebral infarction and to improve long-term clinical outcome. The investigators, therefore, concluded that patients with subarachnoid haemorrhage should not be treated routinely with simvastatin. Unfortunately, the STASH trial and a similar study by Wong and colleagues underway to evaluate a dose of simvastatin higher than that used in STASH were not designed to evaluate neurocognitive outcomes. Cognitive dysfunction, such as memory defi cits and executive dysfunction, is increasingly recognised as an important, and perhaps even the most prevalent, long-term complication of subarachnoid haemorrhage. We are also concerned that the length of the treatment period—up to 3 weeks—was not suffi cient to investigate potential benefi ts of simvastatin on outcomes after subarachnoid haemorrhage. The pathophysiology of subarachnoid haem or rhage is poorly understood, as is our understanding of the duration of action of underlying mechanisms. Ischaemic stroke (eg, delayed cerebral infarction after subarachnoid haemorrhage) results in microglial activation that might persist for several months, potentially increasing brain injury; and endothelial injury can be observed throughout the arterial tree for months after subarachnoid haemorrhage. In our opinion, it would be reasonable to continue treatment with simvastatin until the damaged thrombogenic and dysfunctional cerebrovascular endothelium has recovered fully and the neuroinfl ammatory responses have subsided. In fact, experimental studies that replicate cognitive decline in subarachnoid haemorrhage show that the benefi cial eff ects of simvastatin on regional cerebral blood fl ow, motor function, cognitive function, and neuroprotection are forfeited when simvastatin is stopped after 2 weeks of treatment. A sustained improvement in cognitive function and neuronal survival was shown only when simvastatin administration was extended for the duration of the study (6 weeks). Although the STASH trial investigators report that simvastatin at a dose of 40 mg for up to 3 weeks did not prevent delayed cerebral infarction, it is unclear whether longer use could improve long-term outcomes. Statins are well tolerated with long-term use. Perhaps it is time to depart from the 2–3 week cerebral vasospasm treatment paradigm, and extend the treatment period in clinical trials of interventions for subarachnoid haemorrhage. Otherwise, we risk false negatives and might prematurely discard potentially useful treatments.

Atrioesophageal fistula (AEF) is a rare complication after radiofrequency ablation for atrial fibrillation but is associated with high mortality, usually due to sepsis or neurologic injury. We report the case of a patient who presented with an AEF and dense neurologic deficits who had complete neurologic recovery after management with emergent surgical repair without the use of cardiopulmonary bypass and with implementation of postoperative hyperbaric oxygen therapy.

PURPOSE OF REVIEW To update the reader about clinical management strategies for separation from cardiopulmonary bypass. A number of new drugs are being introduced in clinical practice, with significant utility in operative patient management. Further, there is increased routine use of complex devices to achieve separation from or avoidance of cardiopulmonary bypass. RECENT FINDINGS Selected medical and device strategies from the most recent literature will be discussed. First, the rationale for selected innovative agents to achieve myocardial performance is reviewed in four perioperative settings: agents for the management of myocardial dysfunction, vasomotor dysfunction, pulmonary hypertension, and right ventricular failure. Second is an evaluation of less commonly considered aspects of mechanical device use in the context of failure to wean from cardiopulmonary bypass or use to avoid cardiopulmonary bypass. Three devices will be discussed: intra-aortic balloon pump, ventricular assist devices, and extracorporeal membrane oxygenation. SUMMARY As our pharmacological and technological armamentarium improve, our population ages and procedures are attempted on patients with increasing co-morbid conditions, it will be important to both utilize newer pharmacological agents and consider innovative uses for device implementation to achieve optimal perioperative outcomes.

Postoperative neurocognitive decline (POCD) is the most frequently reported form of brain injury in the cardiac surgery setting. Even though most patients recover over a period of several months, recovery is variable and often transient, and early decline may be a marker of neurocognitive dysfunction after several years. Recent studies, however, suggest that late neurocognitive decline after coronary artery bypass graft surgery may not be specific to the use of cardiopulmonary bypass. Large prospective, longitudinal trials with appropriate controls remain necessary to identify how patient characteristics, disease progression, and surgical and anesthetic technique contribute to aging-related neurocognitive decline. This article reviews the current literature on the etiology of POCD following cardiac surgery, discusses strategies to reduce patient risk, and provides some insight into some controversies that merit continued investigation.

Postoperative atrial fibrillation (AF) is a potentially life-threatening complication after coronary artery bypass graft (CABG) surgery. Genetic predisposition may predict risk for developing postoperative AF.Study subjects underwent CABG surgery with cardiopulmonary bypass at Duke University Medical Center. In a discovery cohort of 877 individuals from the Perioperative Genetics and Safety Outcomes Study, we performed a genome-wide association study using a logistic regression model with a covariate adjustment for AF risk index. Single-nucleotide polymorphisms (SNPs) that met a P5 × 10(-5) were further tested using a replication dataset of 304 individuals from the CATHeterization GENetics biorepository, followed by meta-analysis. Potential pathways related to postoperative AF were identified through gene enrichment analysis using the top genome-wide association study SNPs (P10(-4)).Nineteen SNPs met the a priori defined discovery threshold for replication, but only 3 met nominal significance (P.05) in the CATHeterization GENetics group, with only one-rs10504554, in the intronic region in lymphocyte antigen 96 (LY96)-showing the same direction of the effect for postoperative AF (odds ratio [OR] 0.48, 95% CI 0.34-0.68, P = 2.9 × 10(-5) vs OR 0.55, 95% CI 0.31-0.99, P = .046) and strong overall association by meta-analysis (meta-P = 4.0 × 10(-6)). Gene enrichment analysis highlighted the role of LY96 in pathways of biologic relevance to activation and modulation of innate immune responses. Our analysis also showed potential association between LY96 and nuclear factor κ-B interaction and postoperative AF through their relevance to inflammatory signaling pathways.In patients undergoing CABG surgery, we found genetic polymorphisms in LY96 associated with decreased risk of postoperative AF.

Object The efficacy of nimodipine was examined in a murine model of subarachnoid hemorrhage (SAH). End points included the diameter of the lumen of the middle cerebral artery (MCA) and behavioral outcome. An apolipoprotein E (apoE)–mimetic peptide, acetyl-AS-Aib-LRKL-Aib-KRLL-amide, previously shown to have promise in this model was tested both alone and in combination with nimodipine. The effects of carboxyamidotriazole (CAI), a non–voltage-gated calcium channel blocker, were explored using the same animal paradigm. Methods Experimental SAH was induced in male C57B1/6J mice. For 3 days postoperatively, behavioral analyses were performed. In the first experiment, the mice were treated with vehicle or with low- or high-dose CAI for 3 days. In the second experiment, the mice were treated with vehicle, high- and low-dose nimodipine, and/or the apoE-mimetic peptide. On postoperative Day 3 each mouse was killed and perfused. Following this, the right MCA was removed and its lumen measured. Mice that received nimodipine demonstrated significant behavioral improvements when compared with vehicle-treated mice, but there was no clear dose-dependent effect on MCA diameter. Administration of the apoE-mimetic peptide was associated with improved functional performance and a significant reduction in vasospasm. Mice that received high-dose CAI performed worse on functional tests, despite a significant increase in the diameters of their MCA lumina. Conclusions These results demonstrate a dissociation between vasospasm and neurological outcomes that is consistent with findings of previous clinical trials.

Thromboembolic stroke is the most common severe complication following coil embolization of intracerebral aneurysms, with a 5% incidence of permanent deficits. Despite heparin anticoagulation, rescue therapy with the platelet glycoprotein IIb/IIIa receptor antagonist abciximab may be required. However, we describe a failure of abciximab rescue therapy and discuss the importance of monitoring the variable individual response to abciximab. Two patients underwent stent-assisted cerebral aneurysm coil embolization complicated by thromboembolic stroke. In one patient, abciximab rescue therapy failed and was associated with a poor neurological outcome. Thromboelastography (TEG® model 5000; Haemoscope, Skokie, IL) and platelet aggregometry suggested inadequate platelet inhibition, although other tests of platelet function suggested adequate inhibition. We describe a failure of regular-dose abciximab rescue therapy for thromboembolic stroke-complicating stent-assisted cerebral aneurysm coil embolization. The use of TEG to individualize abciximab dosing in this setting may improve patient outcome, as it tracks a pattern of coagulation consistent with the clinical picture.

A 79-YEAR-OLD man underwent an off-pump coronary artery bypass graft procedure for recent-onset exertional angina and significant multivessel disease. After a positive stress test, cardiac catheterization revealed an ejection fraction of 60%, 50% to 75% stenosis of the left anterior descending, 50% stenosis of the proximal left circumflex, and 100% occlusion of the right coronary artery. He was scheduled for elective off-pump coronary artery bypass surgery. On the day of surgery, after induction of anesthesia, a routine preprocedure transesophageal echocardiographic (TEE) study confirmed normal ventricular and valvular function. Specifically, no intracardiac shunt was detected with color-flow Doppler. After left internal mammary artery (LIMA) and endoscopic saphenous vein harvesting, the LIMA was grafted to the left anterior descending and veins were grafted to the posterior diagonal, the first diagonal and the obtuse marginal arteries. The patient tolerated the procedure well without complication. A postprocedure TEE study was again unremarkable and chest closure commenced. As the sternal wires were pulled together, a steady trickle of air bubbles was noted in the left atrium passing through the left ventricle into the aorta (Fig 1). This did not coincide with any intravascular injections, and no air was detected in the right heart. From where was the air coming?