No abstract

The role of veno-venous extracorporeal membrane oxygenation therapy (V-V ECMO) in severe COVID-19 acute respiratory distress syndrome (ARDS) is still under debate and conclusive data from large cohorts are scarce. Furthermore, criteria for the selection of patients that benefit most from this highly invasive and resource-demanding therapy are yet to be defined. In this study, we assess survival in an international multicenter cohort of COVID-19 patients treated with V-V ECMO and evaluate the performance of several clinical scores to predict 30-day survival. Methods: This is an investigator-initiated retrospective non-interventional international multicenter registry study (NCT04405973, first registered 28 May 2020). In 127 patients treated with V-V ECMO at 15 centers in Germany, Switzerland, Italy, Belgium, and the United States, we calculated the Sequential Organ Failure Assessment (SOFA) Score, Simplified Acute Physiology Score II (SAPS II), Acute Physiology And Chronic Health Evaluation II (APACHE II) Score, Respiratory Extracorporeal Membrane Oxygenation Survival Prediction (RESP) Score, Predicting Death for Severe ARDS on V‑V ECMO (PRESERVE) Score, and 30-day survival. Results: In our study cohort which enrolled 127 patients, overall 30-day survival was 54%. Median SOFA, SAPS II, APACHE II, RESP, and PRESERVE were 9, 36, 17, 1, and 4, respectively. The prognostic accuracy for all these scores (area under the receiver operating characteristic—AUROC) ranged between 0.548 and 0.605. Conclusions: The use of scores for the prediction of mortality cannot be recommended for treatment decisions in severe COVID-19 ARDS undergoing V-V ECMO; nevertheless, scoring results below or above a specific cut-off value may be considered as an additional tool in the evaluation of prognosis. Survival rates in this cohort of COVID-19 patients treated with V‑V ECMO were slightly lower than those reported in non-COVID-19 ARDS patients treated with V-V ECMO.

Acute respiratory distress syndrome (ARDS) in COVID-19 patients is associated with poor clinical outcomes and high mortality rates, despite the use of mechanical ventilation. Veno-Venous Extracorporeal membrane Oxygenation (VV-ECMO) in these patients is a viable salvage therapy. We describe clinical outcomes and survival rates in 52 COVID-19 patients with ARDS treated with early VV-ECMO at a large, high-volume center ECMO program. Outcomes included arterial blood gases, respiratory parameters, inflammatory markers, adverse events, and survival rates. Patients’ mean age was 47.8 ± 12.1 years, 33% were female, and 75% were Hispanic. At the end of study period, 56% ( n = 29) of the patients survived and were discharged and 44% ( n = 23) of the patients expired. Survival rate was 75.0% (9 out of 12) in patients placed on ECMO prior to mechanical ventilation. Longer duration on mechanical ventilation prior to ECMO intervention was associated with a 31% (aOR = 1.31, 95% CI, 1.00–1.70) increased odds of mortality after adjusting for age, gender, BMI, number of comorbid conditions, and post-ECMO ventilator days. Early and effective ECMO intervention in critical ill COVID-19 patients might be a valuable strategy in critical care settings to increase their odds of survival.

Patients with congestive heart failure (CHF) frequently become anemic. In this review, we will examine the possible etiologies for anemia in heart failure, discuss the cardiovascular consequences of anemia, the effect of anemia on prognosis and exercise capacity, as well as the potential benefits of anemia treatment in this patient population. Etiology of anemia in CHFThe etiology of anemia in patients with congestive heart failure (CHF) is multifactorial and may result from any one or combination of the following factors: chronic disease state, malnutrition, hemodilution from volume overload, medical therapy such as angiotensin enzymeconverting (ACE) inhibition, or elevated cytokine production [1][2][3][4].Similar to the anemia of chronic disease, anemia in heart failure patients is characterized by normal red blood cell morphology and normal iron stores and may be in part mediated by the actions of pro-inflammatory cytokines [4]. Cytokines can reduce red blood cell volume by suppressing erythropoietin production and erythropoiesis in the bone marrow, reducing availability of tissue iron stores for incorporation into hemoglobin, and decreasing red blood cell survival time in the circulation. Pro-inflammatory cytokine activity is increased in patients with CHF in proportion to the severity of symptoms and is associated with increased mortality [5]. Whether cytokine activation is causally linked to anemia in patients with CHF is unknown.Heart failure results in decreased renal perfusion, which ultimately results in sodium retention and volume overload. Plasma volume is commonly increased above normal values even in non-edematous treated patients with CHF. Accordingly, hemodilution secondary to plasma volume expansion may also contribute to decreased hematocrit in patients with heart failure. A small