Drowning and Diving Accidents

Ian R. Grover

Accidental drowning occurs in all age groups, but is most common in children aged 1 to 4 years. Despite a recent decline in the number of deaths, drowning remains the second leading cause of injury-related death for children aged 1 to 14 years, and the sixth leading cause of accidental death for all age groups. In adults, alcohol is the most important single factor contributing to drowning incidents. US statistics from 2007 show there were 3,443 unintentional drowning-related deaths, and approximately 70,000 episodes of drowning where the victim survived. A recent decline in the number of fatalities may reflect better prevention because of enhanced private pool safety.

Previous reports and studies used conflicting nomenclature to refer to drowning victims. Cases were divided into freshwater and saltwater drowning, and they were also divided into drowning (victims died within 24 hours of the incident) and near-drowning (survived for at least 24 hours after the incident). In 2003, the American Heart Association published the “Recommended Guidelines for Uniform Reporting of Data From Drowning” that removes the different classifications and simplifies the reporting of drowning cases. Drowning is now defined as “a process resulting in primary respiratory impairment from submersion/immersion in a liquid medium.” Implicit in this definition is that a liquid/air interface is present at the entrance of the victim’s airway, preventing the victim from breathing air. The victim may live or die after this process, but whatever the outcome, he or she has been involved in a “drowning incident.”

PATHOPHYSIOLOGY

Historically, the pathophysiology of drowning was attributed to an electrolyte disturbance induced by aspiration of fluid. However, current data suggest aspiration-related hypoxemia as the major pathophysiologic abnormality. The earlier notion that death could result from drowning without aspiration was based on misinterpretation of seminal documents. In 10% to 15% of drowning cases, hypoxemia appeared to be secondary to simple asphyxia. In these cases, termed dry drowning, with little or no aspiration, the hypothesis was that reflex laryngospasm prevented aspiration. However, no experimental evidence supports this hypothesis. Most experts believe that dry drowning does not occur and that other causes for in-water fatalities should be sought, such as sudden cardiac death. The sine qua non of drowning is the aspiration of fluid.

The hypoxemia observed in drowning cases is related to aspiration. The exact volume of fluid aspirated by victims remains unclear but animal experiments that seem to duplicate human injury require fluid in the range of 1 to 10 mL/kg. The mechanism of hypoxemia depends on the nature of the fluid aspirated. In seawater aspiration, osmotic and irritative effects from sand, diatoms, algae, and other particles provoke an exudative response. This exudate fills alveoli and results in ventilation/perfusion () mismatch and hypoxemia. In freshwater aspiration, pulmonary surfactants are also lost from the lung, leading to focal collapse, () mismatch, and hypoxemia. When water is instilled into the trachea of experimental animals, pathologic studies reveal damage to alveolar and endothelial cells, as well as disruption of the capillary basement membrane.

CLINICAL MANIFESTATIONS

The clinical manifestations of drowning vary with the duration and severity of the hypoxemia. The neurologic presentation reflects the degree of cerebral anoxia. Pulmonary injury ranges from mild, manifesting as cough and mild shortness of breath, to severe, presenting with extreme dyspnea, pulmonary edema, and acute respiratory distress syndrome.

Laboratory studies generally reveal hypoxemia, metabolic acidosis, and, perhaps, superimposed respiratory acidosis. Minor changes in electrolytes are seen frequently; however, clinically significant alterations in serum sodium or potassium are distinctly unusual in drowning in either freshwater or seawater. Chest radiographs may display a spectrum of abnormalities, ranging from patchy infiltrates to dense pulmonary edema. Rarely, massive particulate aspiration can also occur. It has been hypothesized that the pulmonary edema occasionally seen in drowning victims is caused by negative pressure inspiration (attempting to breathe against a closed glottis) or to neurogenic factors.

MANAGEMENT

The management of drowning patients is mainly supportive. Arterial blood gases should be monitored frequently and mechanical ventilatory support should be instituted if acute respiratory failure and refractory hypoxemia develop. Patients with acute respiratory failure may require high ventilator pressures to provide adequate oxygenation and ventilation, reflecting the marked reduction in pulmonary compliance. The application of positive end–expiratory pressure (PEEP) during mechanical ventilation reduces morbidity and mortality. In most cases, ventilatory support is necessary for only a short time. Less invasive methods of ventilatory support such as nasal continuous positive airway pressure and bi-level positive airway pressure may reduce the need for intubation and the risks associated with mechanical ventilation. The routine administration of hypertonic or hypotonic intravenous fluids is not warranted. The use of antibiotics in the drowning victim is usually restricted to those who develop fever, new pulmonary infiltrates, or purulent secretions. Prophylactic antibiotics do not improve mortality or decrease morbidity. Most pulmonary infections in drowning victims are secondary to hospital-acquired organisms; prophylactic antibiotics may only select more resistant organisms. Rarely, the victim may aspirate water that is heavily contaminated with a known organism. Prophylactic antibiotics may be appropriate in this situation.

Routine bronchoscopy to search for particulate matter causing airway obstruction is generally unnecessary. Adrenocortical steroids are not indicated to treat the lung injury associated with near drowning. Experimental evidence strongly suggests that steroids do not improve the long-term outcome or short-term morbidity. One uncontrolled report (four cases), however, suggests high-dose steroids may be beneficial in drowning victims who present with pulmonary edema. The use of surfactants to treat drowning victims has been reported recently. It is unclear whether such therapy alters the outcome. In an experimental model, surfactant therapy did not offer any benefit over traditional supportive approach.

COMPLICATIONS

Pneumothorax, lung abscess, and empyema occasionally complicate the course in drowning patients if severe respiratory failure occurs. Hypothermia at the time of the immersion incident can also complicate the picture. Although renal failure and disseminated intravascular coagulation have been reported, they are probably sequelae of prolonged acidosis, hypoxemia, and hypotension, rather than specific complications of near drowning.

PROGNOSIS

The victim’s prognosis primarily depends on the extent and duration of the hypoxemic episode. Age and prior illnesses can be modifying factors. Epidemiologic data do not support the hypothesis that cold-water immersion improves the prognosis of the drowning victim. However, in rare, well documented cases, victims who fully recover after prolonged submersion in cold water have been reported. Many empiric studies have attempted to better define prognostic factors for the drowning victim. Unfortunately, no factors seem to be completely reliable. In general, patients who present with a normal chest radiograph or normal mental status are likely to survive without sequelae.

Most large studies indicate that 5% to 10% of all victims suffer varying degrees of permanent neurologic dysfunction, although some suggest a higher percentage with long-term neurologic sequelae. Not surprisingly, those who sustain a cardiorespiratory arrest persisting to the time of presentation in an emergency room have a poor chance of survival and a high incidence of neurologic sequelae. However, children who sustain a “cardiorespiratory arrest” that responds to first aid measures at the scene of the accident do not necessarily have a poor prognosis. In the late 1970s after a small experience of drowning victims with a high percentage of long-term neurologic sequelae, it was suggested that the incidence of neurologic dysfunction following near-drowning episodes could be lowered by aggressive attempts at cerebral salvage. This HYPER therapy included barbiturate coma, controlled hyperventilation, diuretics, paralysis, intentional hypothermia, and adrenocortical steroids. The rationale for this therapy was to lower intracranial pressure (ICP), reduce cerebral edema, and lower cerebral oxygen demand in order to prevent further (secondary) neurologic damage. This mode of therapy presumes that further damage occurs after the initial anoxic insult and that further damage can be prevented by these measures.

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