Early air transport after thoracic surgery might be safe: A retrospective observational study in the French Caribbean.

Objective: The objective of this study was to determine the incidence of early air transport (EAT) morbidity after transpleural surgery. We compared our cohort with our patients not requiring air transport. Methods: This was a retrospective observational study, in the Thoracic and Cardiovascular Surgery Department of the University Hospital of Martinique over 40 months. We included all of the files (national and local database, and systematic postoperative consultation) of patients operated on for thoracic surgery or distinguished transpleural surgical intervention, whatever their geographical origin. Patients from another French department benefited from EAT. The complications were classified according to Clavien-Dindo before or after the EAT. Diagnostic criteria were chest pain, dyspnea, and abnormal chest radiograph. Continuous variables are presented as mean, median, and SDs. Discrete variables are presented as n (%). Results: Of 491 patients operated on, 315 were transpleural surgeries, and 99 patients benefited from EAT. There were 55% resections, a percent predicted of forced expiratory volume in 1 second, and an average preoperative Tiffeneau ratio of respectively, 86% and 78. One complication was found: a pneumothorax in an emphysematous patient, 15 days after the flight, who had an index of prolonged air leak >10. The mean time between surgery and flight was 7.2 days (σ = 4.5), and 3.3 days (σ = 2.9) between removal of the last drain and flight. The morbidity of EAT after transpleural surgery was 1%. The 2 cohorts of "EAT" and "Locals" patients were statistically comparable, particularly in morbidity. Conclusions: EAT appears to be safe after transpleural surgery, following usual criteria for hospital discharge. It would be interesting to study, on a larger scale, the effect of IPAL as an independent risk factor (in case of high IPAL > 10) as well as pathologies that modify transpleural pressures restrictive ventilatory defect.

Bothrops lanceolatus snake venom impairs mitochondrial respiration and induces DNA release in human heart preparation.

INTRODUCTION: Envenomations by Bothrops snakebites can induce overwhelming systemic inflammation ultimately leading to multiple organ system failure and death. Release of damage-associated molecular pattern molecules (DAMPs), in particular of mitochondrial origin, has been implicated in the pathophysiology of the deregulated innate immune response. OBJECTIVE: To test whether whole Bothrops lanceolatus venom would induce mitochondrial dysfunction and DAMPs release in human heart preparations. METHODS: Human atrial trabeculae were obtained during cannulation for cardiopulmonary bypass from patients who were undergoing routine coronary artery bypass surgery. Cardiac fibers were incubated with vehicle and whole Bothrops lanceolatus venom for 24hr before high-resolution respirometry, mitochondrial membrane permeability evaluation and quantification of mitochondrial DNA. RESULTS: Compared with vehicle, incubation of human cardiac muscle with whole Bothrops lanceolatus venom for 24hr impaired respiratory control ratio and mitochondrial membrane permeability. Levels of mitochondrial DNA increased in the medium of cardiac cell preparation incubated with venom of Bothrops lanceolatus. CONCLUSION: Our study suggests that whole venom of Bothrops lanceolatus impairs mitochondrial oxidative phosphorylation capacity and increases mitochondrial membrane permeability. Cardiac mitochondrial dysfunction associated with mitochondrial DAMPs release may alter myocardium function and engage the innate immune response, which may both participate to the cardiotoxicity occurring in patients with severe envenomation.

Colour Doppler ultrasound after major cardiac surgery improves diagnostic accuracy of the pulmonary infection score in acute respiratory failure: A prospective observational study.

BACKGROUND: Postoperative pneumonia is a frequent complication after cardiac surgery, and its diagnosis is difficult. Little is known about the diagnostic accuracy of lung ultrasound (LUS) in the detection of pneumonia in cardiac surgical patients. The substitution of chest radiography by colour Doppler LUS (LUS-sCPIS) in the simplified clinical pulmonary infection score (sCPIS) could improve the diagnosis of pneumonia following cardiac surgery. OBJECTIVE: The aim of this study was to compare the diagnostic accuracy of LUS-sCPIS and of sCPIS alone in the detection of postoperative pneumonia after cardiac surgery. DESIGN: A prospective study of diagnostic accuracy. SETTING: A Surgical Intensive Care Unit of a French University Hospital. PATIENTS: Fifty-one patients with acute respiratory failure within 72 h after cardiac surgery were enrolled between January and May 2015. MAIN OUTCOME MEASURE: The two index tests, LUS-sCPIS and sCPIS, were calculated for all patients at the onset of acute respiratory failure. The reference standard for the diagnosis of pneumonia was based on the consensus of three physicians, blind to the sCPIS and LUS-sCPIS data, based on a posthoc review of all the clinical, radiological and microbiological evidence. The diagnostic accuracy of LUS-sCPIS was compared with that of sCPIS in the detection of postoperative pneumonia. RESULTS: Pneumonia was diagnosed in 26 out of 51 patients. The LUS-sCPIS detected the presence of pneumonia with a sensitivity of 92% (95% CI 0.85 to 0.99) and a specificity of 68% (95% CI 0.55 to 0.81). The sCPIS detected the presence of pneumonia with a sensitivity of 35% (95% CI 0.22 to 0.48) and a specificity of 84% (95% CI 0.74 to 0.94). The area under the curve (AUC) of LUS-sCPIS at 0.80 (95% CI 0.69 to 0.91) was higher than the AUC of sCPIS at 0.59 (95% CI 0.47 to 0.71; P = 0.0008). CONCLUSION: Compared with sCPIS, LUS-sCPIS improved diagnostic accuracy in the detection of postoperative pneumonia in patients with acute respiratory failure after cardiac surgery. It could be a useful bedside tool to guide pneumonia management. TRIAL REGISTRATION: Clinicaltrials.gov identifier: NCT03279887.