Complications
Most late deaths and long-term sequelae of drowning are neurological in origin. Adequate oxygenation and cerebral perfusion post-rescue may prevent or limit neurological damage.[69] The likelihood of anoxic-ischaemic cerebral insult is low in grade 1 to 5 drownings, but high in grade 6 (cardiopulmonary arrest).
Cardiac dysfunction with low cardiac output is common immediately after severe drowning episodes, especially after the return of spontaneous circulation.[15] This may cause hypotension, which can be corrected with oxygenation, rapid crystalloid infusion, and restoration of normal body temperature. Vasopressors should only be used in refractory hypotension after a trial with crystalloids.
Bacterial colonisation at the site of the drowning (e.g., river, sea) is not generally sufficient to promote pneumonia in the immediate post-drowning period.[69] Pneumonia is often misdiagnosed because of the early radiographic appearance of water in the lungs, and the presence of leukocytosis and low-grade fever, which are physiological responses to the stress of the event. The incidence of ventilator-associated pneumonia increases to 34% to 52% in the third or fourth day of hospitalisation when pulmonary oedema is resolving.[70] Prophylactic antibiotics are not recommended.[71]
Electrolyte disturbances have been reported in the literature, primarily in patients who drowned in water with an abnormally high salt concentration, such as the Dead Sea. No study has found these disturbances to be clinically significant.[72]
Metabolic acidosis occurs in the majority of drowning patients transferred to the emergency department.[46] The acidosis should be corrected when pH is lower than 7.2, or bicarbonate is less than 12 mEq/L, despite adequate ventilatory support.
Acute kidney injury, resulting from hypovolaemic shock, hypoxaemia, rhabdomyolysis, and lactic acidosis, may occur secondary to drowning. In severe cases, patients may require haemodialysis.[73]
Use of this content is subject to our disclaimer