Hyperlactemia Predicts Surgical Mortality in Patients Presenting With Acute Stanford Type-A Aortic Dissection.

OBJECTIVE: Inspired by the limited facility of the Penn classification, the authors aimed to determine a rapid and optimal preoperative assessment tool to predict surgical mortality after acute Stanford type-A aortic dissection (AAAD) repair. DESIGN: Patients who underwent an attempted surgical repair of AAAD were determined using a de-identified single institution database. The charts of 144 patients were reviewed retrospectively for preoperative demographics and surrogates for disease severity and malperfusion. Bivariate analysis was used to determine significant (p≤0.05) predictors of in-hospital and 1-year mortality, the primary endpoints. Receiver operating characteristic curve generation was used to define optimal cut-off values for continuous predictors. SETTING: Single center, level 1 trauma, university teaching hospital. PARTICIPANTS: The study included 144 cardiac surgical patients with acute type-A aortic dissection presenting for surgical correction. INTERVENTIONS: Surgical repair of aortic dissection with preoperative laboratory samples drawn before patient transfer to the operating room or immediately after arterial catheter placement intraoperatively. MEASUREMENTS AND MAIN RESULTS: The study cohort comprised 144 patients. In-hospital mortality was 9%, and the 1-year mortality rate was 17%. Variables that demonstrated a correlation with in-hospital mortality included an elevated serum lactic acid level (odds ratio [OR] 1.5 [1.3-1.9], p<0.001), a depressed ejection fraction (OR 0.91 [0.86-0.96], p = .001), effusion (OR 4.8 [1.02-22.5], p = 0.04), neurologic change (OR 5.3 [1.6-17.4], p = 0.006), severe aortic regurgitation (OR 8.2 [2.0-33.9], p = 0.006), and cardiopulmonary resuscitation (OR 6.8 [1.7-26.9], p = 0.01). Only an increased serum lactic acid level demonstrated a trend with 1-year mortality using univariate Cox regression (hazard ratio 1.1 [1.0-1.1], p = 0.006). Receiver operating characteristic analysis revealed optimal cut-off lactic acid levels of 6.0 mmol/L and 6.9 mmol/L for in-hospital and 1-year mortality, respectively. CONCLUSION: Lactic acidosis, ostensibly as a surrogate for systemic malperfusion, represents a novel, accurate, and easily obtainable preoperative predictor of short-term mortality after attempted AAAD repair. These data may improve identification of patients who would not benefit from surgery.

The Left Atrial Appendage, Including LAA Occlusion Devices Line Watchman, Amulet, and Lariat.

Atrial fibrillation is a very common arrhythmia whose prevalence is expected to increase significantly as the population ages. The associated stroke risk is a major cause of morbidity and mortality. Stroke prevention by anticoagulation carries its own risks, leading to the search for alternative strategies. Multiple techniques have been developed to exclude the left atrial appendage (the main source of thromboembolism in atrial fibrillation) from the circulation. Such techniques offer the hope of stroke prevention without the risks of anticoagulation. This article describes the percutaneous approaches being currently performed in the United States. Particular emphasis is placed on the use of transesophageal echocardiography to guide these procedures.

Feasibility of left atrial appendage device closure following chronically failed surgical ligation.

BACKGROUND: Incomplete surgical left atrial appendage occlusion (S-LAAO) with a narrow neck has been shown to predict an increased rate of embolic stroke. Patients with a previously attempted S-LAAO were systematically excluded from all clinical trials of LAA closure devices. OBJECTIVE: The purpose of this study was to evaluate the feasibility of Watchman LAA device closure for patients referred with chronically incomplete S-LAAO. METHODS: A prospective single-arm feasibility cohort evaluated only subjects undergoing Watchman LAA closure following incomplete S-LAAO. Patients referred and implanted were followed in the Vanderbilt LAA Registry. Preprocedure computed tomographic angiography and transesophageal echocardiography (TEE) were performed to evaluate suitability for closure, with 45-day follow-up TEE postimplant. RESULTS: All attempted LAA closures after incomplete S-LAAO were successful (n = 6). Mean age was 76.3 ± 7 years. Mean CHADS2Vasc score was 3.8 ± 0.8, and HAS-BLED score was 3.5 ± 0.5. At 45-day follow up, all subjects had complete device seal with no thrombus on device and had transitioned to clopidogrel plus aspirin. Three subjects had narrow ostial necks with a maximum diameter ≤9 mm. In all cases, the 4.7-mm Watchman access sheath was able to cross the ostial stricture. Mean occluder size implanted was 28 ± 4 mm. Mean LAA dimension by TEE in the 45° and 135° views for depth was 31 mm and ostial diameter was 11 × 16 mm, below the minimum Watchman indication for use of 17 mm. No major intraoperative complications occurred. CONCLUSION: Watchman LAA closure seems to be feasible in patients with chronically incomplete S-LAAO, including subjects with a narrow neck ≤9 mm in width.

Incorrect Diagnosis of Type A Aortic Dissection Attributed to Motion Artifact During Computed Tomographic Angiography: A Case Report.

Early diagnosis of aortic dissection is important to reduce mortality, with surgical management representing standard treatment. Current methods of diagnosing type A aortic dissection include computed tomography angiography (CTA), magnetic resonance imaging, catheter-based arteriography, and transesophageal echocardiography. While each method has merits, there exists potential for false-positive findings. We present a case of a patient who was diagnosed with type A aortic dissection by CTA, but was found to not have an aortic dissection by transesophageal echocardiography under general anesthesia, preventing an unnecessary sternotomy. The echocardiographic findings suggested CTA artifact.

Complete Neurologic Recovery From Extreme Hypoglycemia Secondary to Cardiogenic Liver Failure: A Case Report.

Cardiogenic shock from acute severe mitral valve regurgitation can cause acute liver failure due to hypoperfusion. Impaired liver glycogenesis can then lead to profound hypoglycemia. The time frame for restoring normoglycemia without neurologic sequelae is not clearly established in humans. Thus, the clinical decision to provide further resuscitation in the setting of extreme hypoglycemia mainly depends on the patient's overall clinical condition, provider opinion, and/or institutional practice. Here, we report a case where the patient made complete neurologic recovery from extreme hypoglycemia (<5 mg/dL by central laboratory testing) secondary to acute cardiogenic shock and liver failure.

The Risk of Oxygen during Cardiac Surgery (ROCS) trial: study protocol for a randomized clinical trial.

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.

Hemodynamic instability in patients undergoing pulmonary embolectomy: institutional experience.

OBJECTIVES: Acute pulmonary embolism is a major cause of morbidity and mortality in patients presenting for emergent cardiac surgery with overall mortality ranging from 6% to as high as 85%. While the initial focus of treatment is nonsurgical or percutaneous interventions, surgical treatment continues to be a treatment for patients with refractory thrombus burden or cardiogenic shock. Our institution regularly performs surgical pulmonary embolectomy with improved outcomes compared to current reports. We thus performed a retrospective analysis of outcomes of pulmonary embolectomy patients and anesthetic management. DESIGN: A retrospective review of 40 patients undergoing emergent pulmonary embolectomy over a 4 year period (2008-2012) at our institution was performed to assess for a 2nd period of critical instability. SETTING: The study was conducted at a tertiary, level 1, trauma university medical center. PARTICIPANTS: The study was performed through chart review of patient hospital records. INTERVENTIONS: No interventions were performed. MEASUREMENTS: Anesthetic records were reviewed along with echocardiographic records and surgical reports to assess cardiac function, need for emergent cardiopulmonary bypass, and degree of patient morbidity. CONCLUSIONS: A total of 40 patients were studied. Hemodynamic instability occurred in 12.5% of patients at time of induction requiring emergent cardiopulmonary bypass. Another 17% of patients who remained stable following induction developed subsequent instability requiring emergent cardiopulmonary bypass during pericardial opening or manipulation which has not been previously reported. One patient died during hospitalization. Patients who required emergent bypass following induction of general anesthesia tended to receive higher doses of induction drugs than the other groups. In patients who needed emergent bypass during pericardial manipulation there were no identifiable factors suggesting that these patients remain at risk despite a stable post-induction course.

Anesthetic management and outcomes for patients with pulmonary hypertension and intracardiac shunts and Eisenmenger syndrome: a review of institutional experience.

STUDY OBJECTIVE: To propose a set of recommendations for the perioperative management of patients with Eisenmenger syndrome and similar physiology, based on 20 years of experience at a single institution. DESIGN: Retrospective study of institutional outcomes of Eisenmenger syndrome patients and patients with balanced or fixed right-to-left intracardiac shunts with pulmonary hypertension undergoing noncardiac surgery. SETTING: Single center, university-affiliated hospital. MEASUREMENTS: Measurements included data from patients with Eisenmenger syndrome or similar physiology, shunt direction, right ventricular systolic pressure, congestive heart failure classification, noncardiac surgery, type of anesthesia, echocardiographic and catheterization data, mortality within 30 days of surgery, choice of monitoring, and vasopressor use. MAIN RESULTS: 33 patients with Eisenmenger syndrome or similar physiology undergoing 53 general, regional and/or monitored anesthetic procedures were identified. Significant systemic arterial hypotension occurred in 14 individuals (26%) and oxygen desaturation in 9 (17%) patients. Administration of an intravenous (IV) vasopressor agent during induction significantly decreased the incidence of hypotension. The type of IV induction agent did not influence hemodynamic alterations, though patients who received propofol experienced a trend towards increased hypotension (83% of pts) when a vasopressor was not used. Inhalational induction, regardless of vasopressor use, was more likely to result in hypotension (60% of pts). The 30-day mortality was 3.8% (two pts). Both patients had minor elective procedures with monitored anesthesia care (MAC). CONCLUSIONS: Hypotension is more common in patients with Eisenmenger syndrome and similar physiology when a vasopressor is not used during the peri-induction period, regardless of induction agent. Etomidate tended to have better hemodynamic stability than other induction agents. The use of a vasopressor is recommended. We present general recommendations for anesthesiologists and strongly recommend use of a vasopressor before or during induction to reduce hypotension along with complete avoidance of inhalational induction. Further, MAC anesthesia has been associated with perioperative and 30-day mortality.