RESUMEN
This study aims to resolve the unmet need for ventilator surge capacity by developing a prototype device that can alter patient-specific flow in a shared ventilator setup. The device is designed to deliver a predictable tidal volume (VT), requiring minimal additional monitoring and workload. The prototyped device was tested in an in vitro bench setup for its performance against the intended use and design criteria. The ventilation parameters: VT and airway pressures, and ventilation profiles: pressure, flow and volume were measured for different ventilator and device settings for a healthy and ARDS simulated lung pathology. We obtained VTs with a linear correlation with valve openings from 10 to 100% across set inspiratory pressures (IPs) of 20 to 30 cmH2O. Airway pressure varied with valve opening and lung elastance but did not exceed set IPs. Performance was consistent in both healthy and ARDS-simulated lung conditions. The ventilation profile diverged from traditional pressure-controlled profiles. We present the design a flow modulator to titrate VTs in a shared ventilator setup. Application of the flow modulator resulted in a characteristic flow profile that differs from pressure- or volume controlled ventilation. The development of the flow modulator enables further validation of the Individualized Shared Ventilation (ISV) technology with individualization of delivered VTs and the development of a clinical protocol facilitating its clinical use during a ventilator surge capacity problem.
Asunto(s)
Diseño de Equipo , Pulmón , Respiración Artificial , Síndrome de Dificultad Respiratoria , Volumen de Ventilación Pulmonar , Ventiladores Mecánicos , Humanos , Respiración Artificial/instrumentación , Respiración Artificial/métodos , Síndrome de Dificultad Respiratoria/terapia , Síndrome de Dificultad Respiratoria/fisiopatología , Pulmón/fisiopatología , PresiónRESUMEN
The COVID-19 pandemic has resulted in an increased need for ventilators. The potential to ventilate more than one patient with a single ventilator, a so-called split ventilator setup, provides an emergency solution. Our hypothesis is that ventilation can be individualized by adding a flow restrictor to limit tidal volumes, add PEEP, titrate FiO2 and monitor ventilation. This way we could enhance optimization of patient safety and clinical applicability. We performed bench testing to test our hypothesis and identify limitations. We performed a bench testing in two test lungs: (1) determine lung compliance (2) determine volume, plateau pressure and PEEP, (3) illustrate individualization of airway pressures and tidal volume with a flow restrictor, (4a) illustrate that PEEP can be applied and individualized (4b) create and measure intrinsic PEEP (4c and d) determine PEEP as a function of flow restriction, (5) individualization of FiO2. The lung compliance varied between 13 and 27 mL/cmH2O. Set ventilator settings could be applied and measured. Extrinsic PEEP can be applied except for settings with a large expiratory time. Volume and pressure regulation is possible between 70 and 39% flow restrictor valve closure. Flow restriction in the tested circuit had no effect on the other circuit or on intrinsic PEEP. FiO2 could be modulated individually between 0.21 and 0.8 by gradually adjusting the additional flow, and minimal affecting FiO2 in the other circuit. Tidal volumes, PEEP and FiO2 can be individualized and monitored in a bench testing of a split ventilator. In vivo research is needed to further explore the clinical limitations and outcomes, making implementation possible as a last resort ventilation strategy.
Asunto(s)
COVID-19 , Respiración Artificial , Humanos , Pandemias , Respiración con Presión Positiva , SARS-CoV-2 , Volumen de Ventilación Pulmonar , Ventiladores MecánicosRESUMEN
PURPOSE: With the rising incidence of failed bariatric procedures, the importance of revisional surgery has been increasing. These revisional procedures come with a higher risk of complications leading to longer hospital stays. We believe though that enhanced recovery after revisional bariatric surgery is possible and needs to be advocated. MATERIALS AND METHODS: We retrospectively analyzed our laparoscopic conversions of failed gastric banding and failed Mason gastroplasty to Roux-en-Y gastric bypass. A total of 321 patients was included in the study, from February 2010 until December 2019. The primary endpoints were length of stay (LoS), in-hospital complication rate, and early readmission rate (< 30 days). Logistic regression was used to investigate the impact of several independent variables on complication and readmission rates. RESULTS: Fifty-four patients were male and 267 female. The mean age was 44.2 years and mean BMI at the time of conversion was 37.9 kg/m2. We converted 273 failed adjustable gastric bandings (85,0%) and 48 failed Mason gastroplasties (15.0%). The main reason for conversion was the recurrence of obesity. A mean LoS of 2.10 days was calculated. We had an overall in-hospital complication rate of 3.73% and the overall early readmission rate was 3.43%. The odds ratio for LoS on early readmission is 1.52 (p=0.0079; CI 95% [1.12-2.07]). CONCLUSION: The above data imply that the implementation of advanced ERAS principles for revisional surgery in our center is safe and does not lead to a higher risk of early readmission.
Asunto(s)
Cirugía Bariátrica , Derivación Gástrica , Gastroplastia , Laparoscopía , Obesidad Mórbida , Adulto , Femenino , Humanos , Masculino , Obesidad Mórbida/cirugía , Complicaciones Posoperatorias/epidemiología , Complicaciones Posoperatorias/cirugía , Reoperación , Estudios RetrospectivosRESUMEN
AIMS: Cardiovascular complications, including myocarditis, are observed in coronavirus disease 2019 (COVID-19). Major cardiac involvement is a potentially lethal feature in severe cases. We sought to describe the underlying pathophysiological mechanism in COVID-19 lethal cardiogenic shock. METHODS AND RESULTS: We report on a 48-year-old male COVID-19 patient with cardiogenic shock; despite extracorporeal life support, dialysis, and massive pharmacological support, this rescue therapy was not successful. Severe acute respiratory syndrome coronavirus 2 RNA was detected at autopsy in the lungs and myocardium. Histopathological examination revealed diffuse alveolar damage, proliferation of type II pneumocytes, lymphocytes in the lung interstitium, and pulmonary microemboli. Moreover, patchy muscular, sometimes perivascular, interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, were seen in the cardiac tissue. The lymphocytes 'interlocked' the myocytes, resulting in myocyte degeneration and necrosis. Predominantly, T-cell lymphocytes with a CD4:CD8 ratio of 1.7 infiltrated the interstitial myocardium, reflecting true myocarditis. The myocardial tissue was examined for markers of ferroptosis, an iron-catalysed form of regulated cell death that occurs through excessive peroxidation of polyunsaturated fatty acids. Immunohistochemical staining with E06, a monoclonal antibody binding to oxidized phosphatidylcholine (reflecting lipid peroxidation during ferroptosis), was positive in morphologically degenerating and necrotic cardiomyocytes adjacent to the infiltrate of lymphocytes, near arteries, in the epicardium and myocardium. A similar ferroptosis signature was present in the myocardium of a COVID-19 subject without myocarditis. In a case of sudden death due to viral myocarditis of unknown aetiology, however, immunohistochemical staining with E06 was negative. The renal proximal tubuli stained positively for E06 and also hydroxynonenal (4-HNE), a reactive breakdown product of the lipid peroxides that execute ferroptosis. In the case of myocarditis of other aetiology, the renal tissue displayed no positivity for E06 or 4-HNE. CONCLUSIONS: The findings in this case are unique as this is the first report on accumulated oxidized phospholipids (or their breakdown products) in myocardial and renal tissue in COVID-19. This highlights ferroptosis, proposed to detrimentally contribute to some forms of ischaemia-reperfusion injury, as a detrimental factor in COVID-19 cardiac damage and multiple organ failure.