Respiratory failure and ischemic neurologic injury are the threats to life after submersion although associated injuries are occasionally present. Older victims who are not immediately unconscious may panic, struggle in the water, hold their breath, or hyperventilate. Once under water, involuntary breathing resumes at a break point determined by the PaO2 or PaCO2. This soon leads to vomiting and aspiration of water and emesis. "Dry drowning" without aspiration results from laryngospasm and glottal closure. Whatever the mechanism, the final common pathway is profound hypoxemia.

Initial hypoxemia results from flooding of alveoli and impairment of gas exchange. Although both seawater and fresh water wash surfactant out of alveoli, fresh water also changes the surface tension properties of surfactant. Surfactant loss leads to atelectasis, ventilation perfusion mismatch, and breakdown of the alveolar capillary membrane.4 Hypoxemia follows aspiration of small amounts of water and is seen experimentally with aspiration of 2.2 mL/kg of either fresh water or saltwater. Contributing to pulmonary injury may be aspiration of bacteria, algae, sand, particulate matter, emesis, and chemical irritants. Noncardiogenic pulmonary edema results from direct pulmonary injury, surfactant loss, inflammatory contaminants, and cerebral hypoxia.

Poor perfusion and hypoxemia lead to metabolic acidosis in a majority of patients, yet perhaps as a result of the young age of most victims, the cardiovascular status is remarkably stable. Blood volume shifts depend on the nature and quantity of the fluid aspirated, although life-threatening changes are unusual in resuscitated patients, because most human drowning victims aspirate quantities of water below those which produce significant disturbances. Electrolyte abnormalities in near-drowning patients are seldom significant, and hematologic values are usually normal, although the clinician occasionally will see hemoconcentration or hemolysis that results in anemia. Rarely, disseminated intravascular coagulation will occur.

Renal function is usually adequate, although proteinuria may occur, and hemoglobinuria can follow hemolysis. Acute tubular necrosis can result from hypoxia or myoglobinuria.

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