Objective: To study the mechanism of direct lung injury by seawater and explore its possible management.
Methods: To exclude the interference of hypoxia and acidosis during the study of seawater-induced direct lung injury, 18 normal hybrid dogs were randomly assigned into group A (with all lung lobes perfused with seawater), group R (with the right lung lobe perfused with seawater) and group D (with the diaphragmatic lobe of lung perfused with seawater), with 6 dogs in each group. The changes in blood gas dynamics, blood gas acid-base status and electrolytes, along with the histological changes in the lung tissues were comparatively analyzed between the 3 groups. Bronchial microscope was employed to observe the continuous changes in the bronchioles before and after seawater perfusion in group D, and the concentration of the bronchoalveolar fluid and blood LDH-L and ALP levels were tested.
Results: The values of PaO(2), PaCO(2), pH, actual bicarbonate (AB), base excess (BE), tidal volume, and respiration rate in groups A and R were significantly different from those in group D (P < 0.01), and in groups A and R, the above measurements at every stage after seawater perfusion were significantly different from those before perfusion (P < 0.01). In group D, however, blood gas dynamics, blood gas acid-base status and electrolytes changed little after seawater perfusion (P > 0.05). In all the groups, obvious lung tissue injuries were observed under optical microscope after seawater perfusion. Observation with electron microscope revealed injuries to type II alveolar epithelial cells, broadened respiratory mucosa, and platelet adherence. Bronchial microscope in group D presented the bronchus filled with bronchoalveolar fluid, and blood LDH-L and ALP levels kept rising significantly (P < 0.01). Within 4 h after seawater perfusion, no pathological changes were seen in the lung tissues without direct contact with seawater.
Conclusions: Seawater inspiration and retention in the lungs may lead to severe direct lung injury, and is the primary factor responsible for acute lung injury after drowning in the sea.
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