Objective: The COVID-19 pandemic is affecting humankind in unprecedented and monumental ways. Healthcare professionals (HCPs) have had to deal with traumatic and complex situations at work. However, the current understanding of the emotional effects on HCPs and their vulnerability during the pandemic is limited. We investigated the effects of HCPs’ viral epidemic-related stress, professional quality of life (ProQOL), depression, and anxiety on their health-related quality of life (HRQOL). Methods: We recruited a convenience sample of 60 HCPs at two tertiary hospitals in provinces P and Y, Republic of Korea. We analyzed their demographics, viral epidemic-related distress, ProQOL (compassion satisfaction, burnout, and secondary traumatic stress), depression, anxiety, and HRQOL through self-reported questionnaires. Results: Burnout had a significant direct effect on depression, anxiety, physical health, and psychological HRQOL and indirectly affected all subcategories of HRQOL. Viral epidemic-related stress had no significant direct effect on any variable, but indirectly affected all subcategories of HRQOL. Depression and anxiety were endogenous variables (mediators). Depression was a pathway that directly and significantly affected all subcategories of HRQOL. Burnout had the most significant effect on physical health and psychological HRQOL, whereas depression had the greatest effect on social relationships and environmental HRQOL. Conclusion: Low compassion satisfaction caused burnout in HCPs, and burnout was significantly associated with depression, anxiety, and HRQOL. Furthermore, HRQOL showed a greater response when affected by indirect burnout through depression and anxiety than when directly affected by burnout.

Introduction. Dysfunction in the renin-angiotensin-aldosterone system (RAAS) has been observed in patients with coronavirus disease 2019 (COVID-19). It is presumed that the effect of reducing interleukin-6 (IL-6) levels by angiotensin II receptor blockers (ARBs) by RAAS modulation. We investigated changes in angiotensin II and IL-6 levels in four COVID-19 patients treated with ARBs. Case Presentation. Cases 1 and 2 were who had not received ARBs before and were newly administered ARBs. Case 3 restarted ARBs after discontinuation for 7 days, and case 4 received an increased dose of ARBs. The mean in angiotensin II levels (607.5 pg/mL, range: 488–850 pg/mL, reference   range < 100   pg / mL ), C-reactive protein (CRP) (10.58 mg/dL, range 4.45-18.05 mg/dL), and IL-6 (55.78 pg/mL, range: 12.86–144.82 pg/mL, reference   range < 7   pg / mL ) was observed at the admission in all patients. Upon clinical improvement, the mean decrease in CRP (1.02 mg/dL, range 0.06-3.78 mg/dL) and IL-6 (5.63 pg/mL, range 0.17-20.87 pg/mL) was observed in all patients. Conversely, angiotensin II levels gradually increased. Conclusion. This report supports the potential benefit of ARBs to improve the clinical outcomes of COVID-19 patients by controlling RAAS dysfunction.

Several studies on the treatment of coronavirus disease (COVID-19) are being conducted, and various drugs are being tried; however, the results have not been uniform. Steroids have been widely used in the treatment of COVID-19, but their effects are controversial. As immunosuppressive and anti-inflammatory agents, steroids are considered to reduce lung damage by regulating various inflammatory responses. We report a case of severe acute respiratory syndrome coronavirus-2 pneumonia manifesting as a cryptogenic organizing pneumonia-like reaction and discuss its treatment, clinical course, and favorable outcomes after steroid administration.

Studies on inflammatory markers, endothelial activation, and bleeding during extracorporeal membrane oxygenation (ECMO) are lacking. Blood samples were prospectively collected after ECMO initiation from 150 adult patients who underwent ECMO for respiratory failure between 2018 and 2021. After excluding patients who died early (within 48 h), 132 patients were finally included. Their tumor necrosis factor-alpha (TNF-α), tissue factor (TF), soluble thrombomodulin (sTM), and E-selectin levels were measured. A Cox proportional hazards regression model was used to estimate the hazard ratio for hemorrhagic complications during ECMO. The 132 patients were divided into hemorrhagic (n = 23, H group) and non-complication (n = 109, N group) groups. The sequential organ failure assessment score, hemoglobin level, and ECMO type were included as covariates in all Cox models to exclude the effects of clinical factors. After adjusting for these factors, initial TNF-α, TF, sTM, E-selectin, and activated protein C levels were significantly associated with hemorrhagic complications (all p < 0.001). TNF-α, TF, and E-selectin better predicted hemorrhagic complications than the model that included only the aforementioned clinical factors (clinical factors only (area under the curve [AUC]: 0.804), reference; TNF-α (AUC: 0.914); TF (AUC: 0.915); E-selectin (AUC: 0.869)). Conclusions: TNF-α levels were significantly predictive of hemorrhagic complications during ECMO.

Background: Recently, the use of extracorporeal membrane oxygenation (ECMO) in noncardiac surgery, such as thoracic surgery, has increased. However, there have been no studies on the mortality and incidence of intraoperative cardiac arrest with or without ECMO during thoracic surgery. Methods: Between January 2011 and October 2018, 63 patients received ECMO support during thoracic surgery. All patients who applied ECMO from starting at any time before surgery to the day of surgery were included. Patients were divided into the emergency ECMO group and the non-emergency ECMO group according to the timing of ECMO. We compared the factors related to 30 day mortality using Cox regression analysis. Results: The emergency ECMO and non-emergency ECMO groups comprised 27 and 36 patients, respectively. On the operation day, cardiopulmonary resuscitation (CPR) was a very important result, and only occurred in the emergency ECMO group (n = 20, 74.1% vs. 0%, p < 0.001). The most common cause of ECMO indication was the CPR in the emergency ECMO group and respiratory failure in the non-emergency ECMO group. There were significant differences in 30 day mortality between the emergency ECMO group and the non-emergency ECMO group (n = 12, 44.4% vs. n = 3, 8.3%, p = 0.001). The Kaplan–Meier analysis curve for 30 day mortality showed that the emergency ECMO group had a significantly higher rate of 30 day mortality than the non-emergency ECMO group (X2 = 14.7, p < 0.001). Conclusions: A lower incidence of intraoperative cardiac arrest occurred in the non-emergency ECMO group than in the emergency ECMO group. Moreover, 30 day mortality was associated with emergency ECMO.