RESUMO
BACKGROUND: Coronavirus disease 2019 (COVID-19) pneumonia can be associated with refractory respiratory failure requiring extracorporeal membrane oxygenation(ECMO). Although ECMO has helped many COVID patients, optimal management strategies for these patients remain unknown. METHODS: We conducted a retrospective review of all COVID patients requiring ECMO at our hospital. Six months into the pandemic, we changed our management strategy to focus on early mobilization. The early mobilization effort included tracheostomy within 48 h of cannulation, decreasing sedation, and an aggressive physical and occupational therapy program progressing toward early ambulation while on ECMO. The primary outcome measured was survival to discharge. The primary stratification was based on the mobilization strategy. RESULTS: From 2020 to 2021, 47 COVID patients have been supported with ECMO at our institution. Five are still in the hospital on ECMO. 39 (83%) were supported with venovenous ECMO while 8 (17%) were supported with venoarterial or a right ventricular assist device type configuration. All 47 (100%) were cannulated at bedside with transesophageal echocardiographic guidance. The average age was 47 ± 9 years; 36(77%) were male; and 20 (43%) were Hispanic. The median duration of support was 22 (11-44) days. Excluding those who remain in the hospital and on support, overall survival to discharge was 24/42 (57%). When stratified by mobilization strategy, early tracheostomy and mobilization were associated with significantly improved survival (74% [17/23] vs. 37% [7/19], p = .02). There were no changes in patient acuity or duration of support throughout the study period. CONCLUSION: In conclusion, early tracheostomy, decreased sedation, and aggressive mobilization of COVID-19 ECMO patients is associated with improved survival.
Assuntos
COVID-19 , Oxigenação por Membrana Extracorpórea , Insuficiência Respiratória , Humanos , Masculino , Adulto , Pessoa de Meia-Idade , Feminino , Oxigenação por Membrana Extracorpórea/efeitos adversos , Deambulação Precoce , COVID-19/terapia , Estudos Retrospectivos , Insuficiência Respiratória/terapiaRESUMO
BACKGROUND: Although several studies have characterized the risk of coinfection in COVID pneumonia, the risk of the bloodstream and respiratory coinfection in patients with COVID-19 pneumonia on extracorporeal membrane oxygenation (ECMO) supports severe acute respiratory distress syndrome (ARDS) is poorly understood. METHODS: This is a retrospective analysis of patients with COVID-19 ARDS on ECMO at a single center between January 2020 and December 2021. Patient characteristics and clinical outcomes were compared. RESULTS: Of 44 patients placed on ECMO support for COVID-19 ARDS, 30 (68.2%) patients developed a coinfection, and 14 (31.8%) patients did not. Most patients underwent venovenous ECMO (98%; 43/44) cannulation in the right internal jugular vein (98%; 43/44). Patients with coinfection had a longer duration of ECMO (34 [interquartile range, IQR: 19.5, 65] vs. 15.5 [IQR 11, 27.3] days; p = .02), intensive care unit (ICU; 44 [IQR: 27,75.5] vs 31 [IQR 20-39.5] days; p = .03), and hospital (56.5 [IQR 27,75.5] vs 37.5 [IQR: 20.5-43.3]; p = .02) length of stay. When stratified by the presence of a coinfection, there was no difference in hospital mortality (37% vs. 29%; p = .46) or Kaplan-Meier survival (logrank p = .82). Time from ECMO to first positive blood and respiratory culture were 12 [IQR: 3, 28] and 10 [IQR: 1, 15] days, respectively. Freedom from any coinfection was 50 (95% confidence interval: 37.2-67.2)% at 15 days from ECMO initiation. CONCLUSIONS: There is a high rate of co-infections in patients placed on ECMO for COVID-19 ARDS. Although patients with coinfections had a longer duration of extracorporeal life support, and longer length of stays in the ICU and hospital, survival was not inferior.
Assuntos
COVID-19 , Coinfecção , Oxigenação por Membrana Extracorpórea , Síndrome do Desconforto Respiratório , COVID-19/complicações , COVID-19/epidemiologia , COVID-19/terapia , Coinfecção/epidemiologia , Humanos , Síndrome do Desconforto Respiratório/epidemiologia , Síndrome do Desconforto Respiratório/etiologia , Síndrome do Desconforto Respiratório/terapia , Estudos RetrospectivosRESUMO
Machine learning techniques have been recently applied for discriminating between Viable and Non-Viable tissues in animal wounds, to help surgeons to identify areas that need to be excised in the process of burn debridement. However, the presence of outliers in the training data set can degrade the performance of that discrimination. This paper presents an outlier removal technique based on the Mahalanobis distance to improve the accuracy detection of Non-Viable skin in human injuries. The iteratively application of this technique improves the accuracy results of the Non-Viable skin in a 13.6% when applying K-fold cross-validation.
Assuntos
Aprendizado de Máquina , Pele , HumanosRESUMO
Previous studies have suggested that the heart may be capable of limited repair and regeneration in response to a focal injury, while other studies indicate that the mammalian heart has no regenerative capacity. To further explore this issue, we performed a series of superficial and transmural myocardial injuries in C57BL/6 and MRL/MpJ adult mice. At defined time intervals following the respective injury (days 3, 14, 30 and 60), we examined cardiac function using echocardiography, morphology, fluorescence-activated cell sorting for 5-bromo-2-deoxyuridine-positive cells and molecular signature using microarray analysis. We observed restoration of myocardial function in the superficial MRL cryoinjured heart and significantly less collagen deposition compared with the injured hearts of C57BL/6 mice. Following a severe transmural myocardial injury, the MRL mouse has increased survival and decreased ventricular remodeling compared with the C57BL/6 mouse but without evidence of complete regeneration. The cytoprotective program observed in the severely injured MRL heart is in part due to increased cellular proliferation, increased vasculogenesis, and decreased apoptosis that limits the extension of the injury. We conclude that MRL injured hearts have evidence of myocardial regeneration, in response to superficial injury, but the stabilized left ventricular function and improved survival observed in the MRL mouse following severe injury is not associated with complete myocardial regeneration.
Assuntos
Traumatismos Cardíacos/fisiopatologia , Miocárdio/metabolismo , Regeneração/fisiologia , Animais , Colágeno/metabolismo , Ecocardiografia , Citometria de Fluxo , Traumatismos Cardíacos/etiologia , Traumatismos Cardíacos/genética , Imuno-Histoquímica , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos MRL lpr , Miocárdio/patologia , Cadeias Pesadas de Miosina/genética , Cadeias Pesadas de Miosina/metabolismo , Cadeias Leves de Miosina/genética , Cadeias Leves de Miosina/metabolismo , Análise de Sequência com Séries de Oligonucleotídeos , Regeneração/genética , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Tempo , Transcrição Gênica , Remodelação Ventricular/genética , Remodelação Ventricular/fisiologia , Cicatrização/genética , Cicatrização/fisiologia , Ferimentos Penetrantes/complicaçõesRESUMO
Heart disease is a leading cause of death in newborns and in adults. Efforts to promote cardiac repair by introduction or recruitment of exogenous stem cells hold promise but typically involve isolation and introduction of autologous or donor progenitor cells. We have found that the G-actin-sequestering peptide thymosin beta4 promotes myocardial and endothelial cell migration in the embryonic heart and retains this property in postnatal cardiomyocytes. Survival of embryonic and postnatal cardiomyocytes in culture was also enhanced by thymosin beta4. We found that thymosin beta4 formed a functional complex with PINCH and integrin-linked kinase (ILK), resulting in activation of the survival kinase Akt/PKB, which was necessary for thymosin beta4's effects on cardiomyocytes. After coronary artery ligation in mice, thymosin beta4 treatment resulted in upregulation of ILK and Akt activity in the heart, enhanced early myocyte survival, and improved cardiac function. These findings suggest that thymosin beta4 promotes cardiomyocyte and endothelial migration, survival, and repair and may be a novel therapeutic target in the setting of acute myocardial damage.