Combining IL-6 and SARS-CoV-2 RNAaemia-based risk stratification for fatal outcomes of COVID-19.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic rapidly increases the use of mechanical ventilation (MV). Such cases further require extracorporeal membrane oxygenation (ECMO) and have a high mortality. OBJECTIVE: We aimed to identify prognostic biomarkers pathophysiologically reflecting future deterioration of COVID-19. METHODS: Clinical, laboratory, and outcome data were collected from 102 patients with moderate to severe COVID-19. Interleukin (IL)-6 level and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RNA copy number in plasma were assessed with ELISA kit and quantitative PCR. RESULTS: Twelve patients died or required ECMO owing to acute respiratory distress syndrome despite the use of MV. Among various variables, a ratio of oxygen saturation to fraction of inspired oxygen (SpO2/FiO2), IL-6, and SARS-CoV-2 RNA on admission before intubation were strongly predictive of fatal outcomes after the MV use. Moreover, among these variables, combining SpO2/FiO2, IL-6, and SARS-CoV-2 RNA showed the highest accuracy (area under the curve: 0.934). In patients with low SpO2/FiO2 (< 261), fatal event-rate after the MV use at the 30-day was significantly higher in patients with high IL-6 (> 49 pg/mL) and SARS-CoV-2 RNAaemia (> 1.5 copies/µL) compared to those with high IL-6 or RNAaemia or without high IL-6 and RNAaemia (88% vs. 22% or 8%, log-rank test P = 0.0097 or P < 0.0001, respectively). CONCLUSIONS: Combining SpO2/FiO2 with high IL-6 and SARS-CoV-2 RNAaemia which reflect hyperinflammation and viral overload allows accurately and before intubation identifying COVID-19 patients at high risk for ECMO use or in-hospital death despite the use of MV.

Environmental maintenance with effective and useful zoning to protect patients and medical staff from COVID-19 infection.

AIM: The coronavirus disease 2019 (COVID-19) pandemic has accelerated all over the world, and global health-care systems have become overwhelmed with potentially infectious patients seeking testing and care. It is essential to set up effective and useful zoning to prevent the spread of infection to and from medical staff or other patients with effective use of standard precautions with personal protective equipment (PPE). METHODS: We repurposed a general ward into an acute care unit for severe COVID-19 patients taking into consideration airflow, the direction of movement of medical staff, and prevention of the spread of infection to medical staff and other patients. We checked the daily condition and body temperature of all medical staff for 60 days. RESULTS: There was no evidence of COVID-19 infection in any medical staff or other patients during the period thanks to effective and useful zoning with PPE. CONCLUSION: Special wards and rooms should be set up for future protection of medical staff and other patients, and prevent the explosion of COVID-19 infection with effective and useful zoning with PPE.

Creating a new index to evaluate imbalance in medical demand and supply when disasters occur.

AIM: This study examines the use of the medical risk/resource ratio (RRR) and need for medical resources (NMR) as new indicators of the imbalance in medical demand and supply in disasters. These indicators are used to quantify the medical demand-supply imbalance per disaster base hospital, examine the demand-supply imbalance in the region, and verify the need for medical support. METHODS: We calculated the RRR of each disaster base hospital by dividing the revised estimate of the number of patients with the number of empty beds. We calculated the required number of hospital beds as the NMR to restore the RRR of each disaster base hospital to two. The RRR and NMR were combined, and prioritization for medical support was classified into three levels. RESULTS: The median RRR was 23 (range, 1-101), and the median NMR was 943 (range, 0-2,124). Fifteen hospitals had a medical support priority of 1, five hospitals had a priority of 2, and 13 hospitals had a priority of 3. CONCLUSION: The medical demand-supply imbalance and amount of medical support needed can be quantified using RRR and NMR, which allows examination of the priority level for medical support.

Adrenaline aggravates lung injury caused by liver ischemia-reperfusion and high-tidal-volume ventilation in rats.

BACKGROUND: We often administer adrenaline to improve hypotension of patients undergoing systemic inflammation that is not treated with volume resuscitation. The effects of adrenaline on injured lungs during shock status have not been elucidated. We previously demonstrated that hepatic ischemia-reperfusion followed by high-tidal-volume ventilation-induced systemic inflammation, hypotension, and lung injury in rats. Using this animal model, we investigated the effects of adrenaline on lung injury and hemodynamics. METHODS: Anesthetized rats were ventilated and underwent hepatic inflow interruption for 15 min twice. After the second liver ischemia-reperfusion, the tidal volume was increased to 24 ml · kg(-1) body weight from 6 ml · kg(-1), and 12 rats in each group were observed for 360 min after reperfusion with or without continuous intravenous adrenaline administration. Extra fluid was administered according to the decline in the arterial blood pressure. RESULTS: Adrenaline administration significantly reduced the volume of intravenous resuscitation fluid. The wet-to-dry weight ratio of the lungs was higher (7.53 ± 0.37 vs. 4.63 ± 0.35, P < 0.001), the partial oxygen pressure in arterial blood was lower (213 ± 48 vs. 411 ± 33, P = 0.004), and the tumor necrosis factor-α concentration in bronchoalveolar lavage (BAL) fluid was higher (10(2.64) ± 10(0.22) vs. 10(1.91) ± 10(0.27), P = 0.015), with adrenaline. Histopathological examinations revealed marked exudation in the alveolar spaces in rats receiving adrenaline. CONCLUSIONS: Continuous administration of adrenaline partially prevented a rapid decline in blood pressure but deteriorated lung injury in a rat model of liver ischemia-reperfusion with high-tidal-volume ventilation. A possibility that adrenaline administration aggravate ventilator-induced lung injury during systemic inflammation should be considered.