DROWNING AND NEAR-DROWNING



The pathophysiology of near-drowning in both freshwater and saltwater is similar. Survival de­pends on the pulmonary insult, the amount of hy­poxemic brain damage, and the degree of acidosis. A drowning victim responds initially by closing his glottis, and 10 per cent of drowned victims aspirate no fluid but die from asphyxia. The re­mainder aspirate fluid, develop pulmonary edema and intrapulmonary shunt, and may progress to profound hypoxemia accompanied by a clinical picture identical to the adult respiratory distress syndrome (ARDS). The quantity of aspirated fluid is rarely sufficient to produce a significant change in blood volume. Occasionally, however, near-drowning in hypotonic freshwater can cause tran­sient hypervolemia, whereas hypovolemia may follow hypertonic saltwater aspiration. Altera­tions in hematocrit or serum electrolytes are rarely life-threatening and not different with either salt- or freshwater near-drowning. Meta­bolic acidosis develops in 70 per cent of victims. Renal function remains normal in most, but some develop hemoglobinuria, albuminuria, or oliguria and acute tubular necrosis. The cardiovascular system displays remarkable stability, and altera­tions are primarily a consequence of hypoxemia or acidosis. The likelihood of neurological im­pairment depends on the duration of immersion and possibly the temperature of the water. Re­covery has been reported after submersion in very •cold water-for up to 4& miau-tss,This may be due partly to the diving reflex, which is initiated by facial immersion in cold water (<20°C) and results in severe bradycardia and the shunting of blood to the heart and brain in an attempt to limit hypoxic damage. Additionally, hypothermia low­ers 02 requirements and prolongs the tolerance of the brain and heart to severe hypoxemia.
The most decisive factor in the management of near-drowning victims is resumption of ventila­tion using mouth-to-mouth resuscitation. Even in victims with evident aspiration of fluid, time should not be wasted in attempting to drain liquid from the lungs, as large volumes are rarely aspir­ated. In the absence of an effective pulse, closed-chest cardiac resuscitation is required. Admission to hospital is imperative for all surviving victims because the patient’s clinical status may belie life-threatening hypoxemia, and supplemental 02 should be continued until the measurement of Pao2 indicates a satisfactory level. Intubation, me­chanical ventilation, and hemodynamic monitor­ing (as described in Chapter 22) will be required in patients who subsequently develop ARDS. Bronchodilators counteract bronchospasm, and bicarbonate administration is usually necessary to correct metabolic acidosis. Electrolyte disturb­ances, hemolysis,-and renal failure should be treated appropriately. Prophylactic steroid or an­tibiotic therapy is not indicated. Prognosis is good in patients who are alert or who have a blunted level of consciousness on admission to the emer­gency room, but poor in those in coma.