Definitions

Traditionally, the terminology describing submersion injuries has been confusing and impractical. In the past, drowning referred to death within 24 hours of suffocation from submersion in a liquid, whereas near-drowning described victims who survived at least 24 hours past the initial event regardless of the outcome. In 2005 the World Health Organization (WHO) published a new policy defining drowning to clarify documentation and to better track submersion injuries worldwide. Drowning was defined as “the process of experiencing respiratory impairment from submersion/immersion in liquid.” Furthermore, the WHO policy stated, “Drowning outcomes should be classified as: death, morbidity, and no morbidity. … the terms wet, dry, active, passive, silent, and secondary drowning should no longer be used.”⁴ The term near-drowning should not be used, and the association of the term drowning with a fatal outcome should be abandoned.

Immersion syndrome refers specifically to syncope resulting from cardiac dysrhythmias on sudden contact with water that is at least 5° C lower than body temperature. The risk is proportional to the difference between body temperature and water temperature. Wetting of the face and head before entrance into the water may prevent the inciting sequence of events. Putative mechanisms for the syndrome are vagal stimulation leading to asystole and ventricular fibrillation secondary to QT prolongation after a massive release of catecholamines on contact with cold water. The resultant loss of consciousness leads to secondary drowning.²

Risk Factors

Age, gender, and race affect incidence of drowning. Toddlers and older teenagers are at greatest risk of death by drowning, with annual incidences of 2.46 and 1.47 per 100,000, respectively.¹ Boys account for almost 80% of victims older than 1 year.¹ Black males between 15 and 19 years of age have the highest annual incidence of drowning mortality (3.92 per 100,000), and black children between the ages of 5 and 14 years drown at nearly three times the rate of white children of the same age.^1,7,12 The risk of death by drowning within the American Indian population is twice as high as it is for the white population.¹

Ethanol consumption in proximity with water is a major risk factor for submersion injury or death. Acute ethanol intoxication may be a contributing factor in 30 to 50% of drownings among adults and adolescents.⁸ In one study of boating fatalities, most of which were due to drowning, an association was established between blood ethanol concentration (BEC) and risk of death from drowning while using watercraft. Odds ratios of fatality from drowning followed a trend from 2.8 for a BEC of 1 to 49 mg/dL to 37.4 for a BEC of 150 mg/dL or greater compared with sober case controls.¹⁴

Drowning in the United States follows clear temporal patterns. Two thirds of pediatric deaths occur between May and August, and most submersion injuries occur on weekends between noon and 8 PM.⁸ Submersion victims older than 20 years are most often participating in water sports or using watercraft.

The relationship between swimming ability and the risk of drowning is unclear. No direct evidence exists to suggest that inexperienced swimmers are more likely to drown. On the contrary, skilled swimmers have greater exposure to water and may be more prone to submersion incidents.¹⁵

Numerous medical conditions confer an increased likelihood of drowning or submersion injury. Seizure disorders increase the chance of drowning among children and adolescents nearly 20 times.¹⁶ Autism and other developmental and behavioral disorders increase risk in children as well.^17–19 Prolonged QT syndrome is also a risk factor for drowning. Laboratory studies show that immersion in cold water extends the QT interval. Interrogation of the automated internal cardiac defibrillator of a 12-year-old girl with prolonged QT syndrome who had a cardiac arrest on diving into the ocean revealed immediate further prolongation of the QT interval, followed by a premature ventricular complex and subsequent ventricular tachycardia within 5 seconds.^20,21 This phenomenon may account for a significant proportion of immersion syndrome events and otherwise unexplained submersion injuries.

Pathophysiology

Unexpected submersion triggers breath-holding, panic, and a struggle to surface. Air hunger and hypoxia develop, and the victim begins to swallow water. As breath-holding is overcome, involuntary gasps result in aspiration. The quantity of fluid aspirated, rather than the composition, determines subsequent pulmonary derangement.

The historical emphasis on pathophysiologic differences between freshwater and saltwater aspiration with respect to resultant electrolyte imbalance, hemolysis, and fluid compartment shifting was based on animal studies conducted in the early 20th century. Subsequent investigations revealed that significant intravascular abnormalities do not occur until the amount of aspirated water exceeds 11 mL/kg of body weight; autopsy studies show that most drowning victims aspirate less than 4 mL/kg.²² In one review of the hospital treatment of 91 submersion victims, no patient required emergent intervention for a significant electrolyte abnormality.²³ Aspiration of 1 to 3 mL/kg of either fresh water or salt water destroys the integrity of pulmonary surfactant, leading to alveolar collapse, atelectasis, noncardiogenic pulmonary edema, intrapulmonary shunting, and ventilation-perfusion mismatch.² Profound hypoxia and metabolic and respiratory acidoses ensue, leading to cardiovascular collapse, neuronal injury, and ultimately death.

The classic hypothesis was that 10 to 15% of drowning victims die without aspiration of a significant amount of water. Death from such dry drowning putatively results from severe laryngospasm causing hypoxia, convulsion, and death without entry of fluid into the lungs. An exhaustive review of the literature failed to corroborate this hypothesis.²⁴ Dry drownings more appropriately reflect deaths from causes other than simple submersion.

Many factors may influence the pathophysiologic sequence of events in submersion injury and affect the chance of survival, including age, water temperature, duration and degree of hypothermia, diving reflex, and effectiveness of resuscitative efforts. Because of a lower ratio of body mass to surface area, children have hypothermia more quickly and to a greater degree after immersion in cold water than adults do. Hypothermia lowers cerebral metabolic rate and is neuroprotective to some extent for victims of submersion injury.²⁵ Despite dramatic case reports of patients surviving prolonged submersion in cold water with full neurologic recovery, hypothermia is generally a poor prognostic finding. Cold-water immersion speeds the development of exhaustion, altered consciousness, and cardiac dysrhythmia. The diving reflex may also play a protective role in infant and child submersions. Activation of the diving reflex by fear or immersion of the face in cold water shunts blood centrally to the heart and brain. Apnea and bradycardia ensue, prolonging the duration of submersion tolerated without central nervous system damage.²⁶

Symptoms and Signs

Many submersion injuries are witnessed. Toddler drownings are an important exception, however, often occurring because of a lapse in supervision. On occasion, the history of coughing, choking, or vomiting in a patient found near a body of water suggests the diagnosis. Signs of pulmonary injury may be obvious in a submersion victim who is hypoxic, cyanotic, and in obvious respiratory distress or arrest. More subtle clues, such as increased respiratory rate and audible rhonchi, rales, or wheezes, should alert the clinician to evolving respiratory compromise. Submersion victims swallow a significantly greater volume of water than is aspirated, and gastric distention from positive-pressure ventilation during rescue is common. As a result, 60% of patients vomit after a submersion event.² Aspiration of gastric contents greatly compounds the degree of pulmonary injury and increases the likelihood that acute respiratory distress syndrome will ensue. In addition, aspiration of particulate contaminants such as mud, sewage, and bacteria may obstruct the smaller bronchi and bronchioles and greatly increase the risk of infection (both bacterial and fungal in nature).²⁷

Victims with central nervous system injury may present with symptoms ranging from mild lethargy to coma with fixed and dilated pupils. Central nervous system injury results from the initial hypoxic or ischemic insult and from the cascade of reperfusion injury that follows reestablishment of cerebral blood flow after an arrest. The release of inflammatory mediators and the generation of oxygen free radicals in the postresuscitative period contribute to cytotoxic cerebral edema, compromise of the blood-brain barrier, and increased intracranial pressure. Cerebral arteriolar vasospasm and enhanced platelet aggregation impede cerebral perfusion at the macrocirculatory and microcirculatory levels.²⁶

Cardiac dysrhythmias may incite a submersion injury or develop as its consequence. Hypoxemia, acidosis, and, potentially, hypothermia are the primary factors responsible for dysrhythmias ranging from ventricular tachycardia and fibrillation to bradycardia-asystole. Electrolyte disturbances are rarely significant enough to be dysrhythmogenic.²³