Citation

Kong KW, Meng Y, Deng XM. Acad. J. Naval Med. Univ. 2023; 44(3): 349-355.

Copyright

(Copyright © 2023, Hai jun jun yi da xue xue bao bian ji bu)

DOI

10.16781/j.CN31-2187/R.20220375

PMID

unavailable

Abstract

Drowning is an important public health safety issue and is one of the most common causes of accidental death. Lungs are one of the main organs damaged after drowning. Inhalation of seawater or freshwater will directly damage lung tissue, and induce oxidative stress and inflammatory responses to further aggravate lung damage. Nearly 1/3 of patients eventually progress to acute respiratory distress syndrome. The combined effect of pathological changes such as alveolar surfactant disruption, altered alveolar epithelial structure and function and increased pulmonary capillary permeability ultimately leads to decreased lung compliance, increased intrapulmonary shunt, atelectasis and pulmonary edema. However, because seawater is a hypothermic and hypertonic liquid and contains a large number of bacteria, it produces more intense damaging stimulation in the lungs and alveoli. Therefore, the course of acute respiratory distress syndrome induced by seawater drowning is more rapid and the mechanism is more complex. This article reviews the research progress on the mechanism of seawater drowning-induced lung injury in order to provide new ideas for its treatment.

Language: zh

Keywords

drowning; acute respiratory distress syndrome; inflammation; oxidative stress; seawater