Occasionally massive hemolysis may occur Electrolyte abnormalities that occur after massive aspiration in laboratory animals rarely achieve clinical significance in human victims However, infants and toddlers may ingest large amounts of water during submersion events, and if fresh water, may lead to symptomatic dilutional hyponatremia Even small (1 to mL/kg) quantities of fresh water cause disruption of surfactant, a rise in surface tension in the lungs, and alveolar instability Capillary and alveolar membrane damage allows fluid to leak into the alveoli, with subsequent pulmonary edema Aspiration of salt water (osmolality greater than normal saline) does not denature surfactant but creates an osmotic gradient for fluid to accumulate in the lungs, which dilutes surfactant Both fresh- and saltwater aspiration decrease pulmonary compliance, increase airway resistance and pulmonary artery pressure, and diminish pulmonary flow As nonventilated alveoli are perfused, an intrapulmonary shunt develops, leading to a fall in partial pressure of arterial oxygen (PaO2 ) Tissue hypoxia then leads to metabolic acidosis The victim is usually able to correct a rise in partial pressure of arterial carbon dioxide (PaCO ) Aspiration of bacteria, gastric contents, and foreign materials may cause additional trauma to the lungs Hypoxemia results in loss of consciousness If anoxia ensues, irreversible central nervous system (CNS) damage begins after to minutes Fear or cold may trigger the diving reflex (commonly encountered in infancy), which shunts blood to the brain and heart primarily and affords several minutes of additional perfusion Cold water is relatively protective of the CNS, but probably only if immersion hypothermia develops very rapidly or before compromise of oxygenation Hypothermia is more rapid in the victim who is younger (because of greater surface area:volume ratio) or is struggling in or swallowing icy water If laryngospasm or aspiration occurs before a fall in core body temperature and cerebral metabolic rate, protection is probably minimal Cardiovascular effects are primarily those expected with myocardial ischemia, severe systemic acidosis, hypothermia, and intravascular volume changes After aspiration of fresh water, the transient rise in intravascular volume later contributes to problems of cerebral and pulmonary edema Clinical Recognition In the first moments after rescue, the appearance of the child who has drowned may range from nearly normal to apparently dead Body temperature may be low, even in warm water Respiratory efforts may be absent, irregular, or labored, with pallor or cyanosis, retractions, grunting, and cough productive of pink, frothy material The lungs may be clear, or there may be rales, rhonchi, and wheezing Infection may develop as a consequence of aspirated mouth flora or organisms in stagnant water, but this is not usually important in the first 24 hours Respiratory function may improve spontaneously or deteriorate rapidly as pulmonary edema and small airway dysfunction worsen Deterioration may also occur slowly over 12 to 24 hours Intense peripheral vasoconstriction and myocardial depression may produce apparent or actual pulselessness The child may be alert and normal or have any level of CNS compromise Superficial evidence of head trauma may be noted if the submersion episode was a secondary event Head CT most typically shows diffuse loss of gray–white differentiation and/or bilateral basal ganglia edema/infarction Triage Considerations Outcome depends on the duration of submersion, the degree of pulmonary damage by aspiration, the effectiveness of initial resuscitative measures, and the degree of hypothermia Many children with submersion injuries are salvageable, and all should receive the benefit of excellent cardiopulmonary resuscitation (CPR), without delay, at the scene They should be given oxygen as needed if hypoxemia is present with an oxygen saturation of