Search

Background: There are limited and partially contradictory data on the effects of airway pressure release ventilation (APRV) in COVID-19-associated acute respiratory distress syndrome (CARDS). Therefore, we analyzed the clinical outcome, complications, and longitudinal course of ventilation parameters and laboratory values in patients with CARDS, who were mechanically ventilated using APRV. Methods: Respective data from 4 intensive care units (ICUs) were collected and compared to a matched cohort of patients receiving conventional low tidal volume ventilation (LTV). Propensity score matching was performed based on age, sex, blood gas analysis, and APACHE II score at admission, as well as the implementation of prone positioning. Findings: Forty patients with CARDS, who were mechanically ventilated using APRV, and 40 patients receiving LTV were matched. No significant differences were detected for tidal volumes per predicted body weight, peak pressure values, and blood gas analyses on admission, 6 h post admission as well as on day 3 and day 7. Regarding ICU survival, no significant difference was identified between APRV patients (40%) and LTV patients (42%). Median duration of mechanical ventilation and duration of ICU treatment were comparable in both groups. Similar complication rates with respect to ventilator-associated pneumonia, septic shock, thromboembolic events, barotrauma, as well as the necessity for hemodialysis were detected for both groups. Clinical characteristics that were associated with increased mortality in a Cox proportional hazards regression analysis included age (hazard ratio [HR] 1.08, 95% confidence interval [CI] 1.04-1.1; P <.001), severe acute respiratory distress syndrome (HR 2.62, 95% CI 1.02-6.7; P =.046) and the occurrence of septic shock (HR 17.18, 95% CI 2.06-143.2; P =.009), but not the ventilation mode. Interpretation: Intensive care unit survival, duration of mechanical ventilation, and ICU treatment as well as ventilation-associated complication rates were equivalent using APRV compared to conventional LTV in patients with CARDS. [ABSTRACT FROM AUTHOR]

Background: Reactivation of viruses such as Epstein-Barr virus (EBV) and cytomegalovirus (CMV) are common in critically ill patients and have been described in patients with severe COVID-19. However, it is unclear whether these reactivations are associated with increased mortality and whether targeted treatments are beneficial. Methods: In a retrospective single-center cohort study, patients with severe COVID-19 treated on our intensive care unit (ICU) were screened for EBV and CMV reactivation as detected by polymerase chain reaction. If present, patient characteristics, temporal connections to severe acute respiratory syndrome coronavirus 2 diagnosis and corticosteroid use, the use of targeted treatments as well as the course of disease and outcome were analyzed. As control group, non-COVID-19 patients with sepsis, treated within the same time period on our ICU, served as control group to compare incidences of viral reactivation. Results: In 19 (16%) of 117 patients with severe COVID-19 treated on our ICU EBV reactivations were identified, comparable 18 (14%) of 126 in the non-COVID-19 control group (P=.672). Similarly, in 11 (9%) of 117 patients CMV reactivations were identified, comparable to the 16 (13%) of 126 in the non-COVID-19 sepsis patients (P=.296). The majority of EBV (58%) and CMV reactivations (55%) were detected in patients under systemic corticosteroid treatment. 7 (37%) of 19 patients with EBV reactivation survived the ICU stay, 2 (29%) of 7 patients with rituximab treatment and 5 (42%) of 12 patients without treatment (P=.568). Five (50%) of 10 patients with CMV reactivation survived the ICU stay, 5 (83%) of 6 patients with ganciclovir treatment and 0 of 4 patients without treatment (P=.048). Follow-up analysis in these patients showed that the initiation of treatment lead to decrease in viral load. Conclusion: Critically ill patients with COVID-19 are at a high risk for EBV and CMV reactivations. Whether these reactivations are a cause of hyperinflammation and require targeted treatment remains uncertain. However, in patients with clinical deterioration or signs of hyperinflammation targeted treatment might be beneficial and warrants further studying. [ABSTRACT FROM AUTHOR]