A pediatric case developing critical abdominal distension caused by a combination of humidified high-flow nasal cannula oxygen therapy and nasal airway

Abstract Background We describe a pediatric patient who suffered from critical abdominal distention caused by a combination of humidified, high-flow nasal cannula (HHFNC) oxygen therapy and nasal airway. Case presentation A 21-month-old boy with a history of chronic lung disease was admitted to the intensive care unit (ICU). Immediately after admission, his airway was established using a tracheal tube and mechanical ventilation was started. Five days after the commencement of mechanical ventilation, finally, his trachea was extubated. Immediately after extubation, HHFNC therapy at 20 L/min with an FiO2 of 0.35 was applied. However, severe stridor was observed, then a nasal airway was placed in the left nostril. However, he became restless. Critical abdominal distention was observed. A subsequent chest X-ray revealed that the nasal airway was placed too deeply, and the gastrointestinal air was severely accumulated. Immediately, the nasal airway was removed, and HHFNC flow was reduced to 10 L/min. Frequent suctioning and continuous gastric drainage were required, which achieved gradual improvement of respiratory condition. Conclusions We need to recognize that HHFNC therapy is one of the positive pressure ventilation system. Therefore, HHFNC therapy might cause the similar adverse events to noninvasive pressure ventilation

急性呼吸促迫症候群の病態におけるヒストン修飾酵素Setdb2の重要な役割

Introduction: Acute respiratory distress syndrome (ARDS) is a severe hypoxemic respiratory failure with a high in-hospital mortality. However, themolecular mechanisms underlying ARDS remain unclear. Recent findings have indicated that the onset of severe inflammatory diseases, such as sepsis, is regulated by epigenetic changes. We investigated the role of epigenetic changes in ARDS pathogenesis using mouse models and human samples. Methods: Acute respiratory distress syndrome was induced in a mouse model (C57BL/6 mice, myeloid cell or vascular endothelial cell [VEC]–specific SET domain bifurcated 2 [Setdb2]–deficient mice [Setdb2ffLyz2Cre+ or Setdb2ffTie2Cre+], and Cre− littermates) by intratracheal administration of lipopolysaccharide (LPS). Analyses were performed at 6 and 72 h after LPS administration. Sera and lung autopsy specimens from ARDS patients were examined. Results: In the murine ARDS model, we observed high expression of the histone modification enzyme SET domain bifurcated 2 (Setdb2) in the lungs. In situ hybridization examination of the lungs revealed Setdb2 expression in macrophages and VECs. The histological score and albumin level of bronchoalveolar lavage fluid were significantly increased in Setdb2ffTie2Cre+ mice following LPS administration compared with Setdb2ffTie2Cre- mice, whereas there was no significant difference between the control and Setdb2ffLyz2Cre+ mice. Apoptosis of VECs was enhanced in Setdb2ffTie2Cre+ mice. Among the 84 apoptosis-related genes, the expression of TNF receptor superfamily member 10b (Tnfrsf10b) was significantly higher in Setdb2ffTie2Cre+ mice than in control mice. Acute respiratory distress syndrome patients' serum showed higher SETDB2 levels than those of healthy volunteers. SETDB2 levels were negatively correlated with the partial pressure of oxygen in arterial blood/fraction of inspiratory oxygen concentration ratio. Conclusion: Acute respiratory distress syndrome elevates Setdb2, apoptosis of VECs, and vascular permeability. Elevation of histone methyltransferase Setdb2 suggests the possibility to histone change and epigenetic modification. Thus, Setdb2 may be a novel therapeutic target for controlling the pathogenesis of ARDS.権利情報：© 2023 The Author(s). Published byWolters Kluwer Health, Inc. on behalf of the American College of Sports Medicine. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal