Traditionally, the terminology describing drowning 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. The World Health Organization (WHO) published a new policy defining drowning to clarify documentation and to better track drowning injuries worldwide. Drowning was defined as “the process of experiencing respiratory impairment from submersion/immersion in liquid.” Furthermore, the WHO policy states, “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.” Also, the term near-drowning should not be used, and the associated 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.

Each year an estimated 360,000 people die of drowning worldwide, a rate of approximately 40 individuals an hour, most of whom are children. Low- and middle-income countries account for more than 90% of all drowning deaths and a disproportionate share of years of life lost. Drowning is among the top ten causes of mortality for children and young people worldwide.

In the United States, drowning is the tenth most common cause of unintentional death, accounting for 3709 deaths (1.1 per 100,000) in 2017. Among children 1 to 4 years old, drowning is the leading cause of injury mortality; for 5- to 9-year-olds, it is second only to motor vehicle crashes.

The incidence of drowning with nonfatal outcomes is not well documented. The Centers for Disease Control and Prevention (CDC) estimates that for every child who dies by drowning in the United States, another five receive emergency department (ED) care for a drowning event, and half of these children require hospitalization. Among all age groups, an estimated one to four hospitalizations secondary to nonfatal drownings occur for every drowning death. The economic implications of drowning injuries are profound. In Australia, drowning-related injuries have the highest average lifetime cost ($40,000 USD per patient) of any injury type.

Drownings occur in domestic settings such as swimming pools, hot tubs, bathtubs, large buckets, and rainwater tanks and in all forms of natural bodies of water. A review of all drowning deaths among individuals younger than 20 years old in the United States during a 1-year period revealed that 55% of infants younger than 1 year old drown in bathtubs, and nearly 16% drown in large household buckets. Most (56%) children 1 to 4 years old drown in artificial pools, whereas most (63%) deaths among older children occur in natural bodies of fresh water.

Because of natural disasters, the incidence of drowning injuries and fatalities is rising. In disasters such as floods and tsunamis, older populations are disproportionately affected. A study from hurricane Katrina found that 49% of fatalities were in people 75 years old or older.

Age, gender, and race affect incidence of drowning. Toddlers (1–3 years old) and those over 80 years old are at greatest risk of death by drowning, with annual incidences of 2.5 and 2.1 per 100,000, respectively. Males account for almost 75% of victims. Indigenous American and Alaska Native children between 1 and 4 years old have the highest annual incidence of drowning mortality (3.8 per 100,000), and black teenagers between 11 and 12 years old drown in swimming pools at ten times the rate of white children of the same age. The risk of death by drowning for all ages of the American Indigenous and Alaska Native population is 80% higher than the United States population as a whole. ^,

Ethanol consumption in proximity with water is a major risk factor for drowning. Acute ethanol intoxication may be a contributing factor in up to 50% of drownings among adults and adolescents. The risk of death from drowning while using watercraft is directly proportional to an operator’s blood ethanol concentration (BEC). The odds ratios of fatality from drowning follow 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.

Drowning in the United States is seasonal, with most occurring during the summer months. Two-thirds of pediatric deaths occur between the months of May and August. Drowning injuries are 48% more likely to occur on weekends than weekdays and drowning victims older than 20 years old 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 time in water and may be more prone to drowning incidents.

Numerous medical conditions confer an increased likelihood of drowning injury. Seizure disorders increase the chance of drowning among children and adolescents nearly 20-fold and longitudinal studies of patients with epilepsy found that 10% of deaths were due to drowning. Autism and other developmental and behavioral disorders increase risk in children as well. Immersion in cold water extends the QT interval, thus increasing the risk of dysrhythmias in individuals with baseline prolonged QT syndrome.

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 system derangement.

The pathophysiologic differences between freshwater and saltwater aspiration with respect to resultant electrolyte imbalance, hemolysis, and fluid compartment shifting do not occur until the amount of aspirated water is significantly more than the typical drowning victim aspirates. In one review of the hospital treatment of drowning victims, no patient required emergent intervention for a significant electrolyte abnormality. Aspiration of 1 to 3 mL/kg of either fresh water or saltwater destroys the integrity of pulmonary surfactant, leading to alveolar collapse, atelectasis, noncardiogenic pulmonary edema, intrapulmonary shunting, and ventilation-perfusion mismatch. Profound hypoxia and metabolic and respiratory acidosis 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 purportedly 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. Dry drownings more appropriately reflect deaths from other causes (e.g., fatal cardiac dysrhythmias and severe hypothermia) than from simple submersion.

Many factors may influence the pathophysiologic sequence of events in drowning and affect the chance of survival, including age, water temperature, duration and degree of hypothermia, diving reflex, and effectiveness of resuscitative efforts. Children have a lower ratio of body mass to surface area and, therefore, develop 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. 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 , an involuntary physiologic response to cold submersion that includes apnea, bradycardia, and increased peripheral vascular resistance, may play a protective role in infant and child submersions. The diving reflex works to shunt blood centrally to the heart and brain, thereby prolonging the duration of submersion tolerated without central nervous system (CNS) damage. The evidence to date, however, has not shown a clear correlation between outcome and water temperature.

Many drowning episodes are witnessed. Toddler drownings are an important exception, however, often occurring because of a lapse in supervision. Signs of pulmonary injury may be obvious in a drowning victim who is hypoxic, cyanotic, and in respiratory distress or arrest. More subtle clues, such as increased respiratory rate and audible rhonchi, rales, or wheezes on pulmonary auscultation, should alert the clinician to evolving respiratory compromise. Drowning 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 soon after a drowning event. Aspiration of gastric contents greatly compounds the degree of pulmonary injury and increases the likelihood that acute respiratory distress syndrome (ARDS) will ensue. In addition, aspiration of particulate contaminants such as mud, algae, sewage, and bacteria may obstruct the smaller bronchi and bronchioles and greatly increase the risk of infection (both bacterial and fungal in nature).

Victims with CNS injury may present with symptoms ranging from mild lethargy to coma with fixed and dilated pupils. CNS injury results from the initial hypoxic or ischemic insult and from the cascade of reperfusion injury that follows reestablishment of cerebral blood flow after a cardiopulmonary arrest. The release of inflammatory mediators and the generation of oxygen free radicals in the post-resuscitative period contribute to cytotoxic cerebral edema, compromise of the blood-brain barrier, and increased intracranial pressure.

Cardiac dysrhythmias may incite drowning or develop as a 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.

Other clinical sequelae of drowning may include acute renal injury, which is present on admission in approximately 50% of patients as the result of lactic acidosis; prolonged hypoperfusion; and, in some instances, rhabdomyolysis. Hypothermia-related coagulopathy or disseminated intravascular coagulation (DIC) may occur.

Many factors help predict patients who will survive a drowning injury neurologically intact. Hypoxia, which is usually dependent on submersion time, is the most important factor related to outcome and subsequent quality of life in drowning victims. Drowning victims who arrive in the ED alert with normal hemodynamics are unlikely to experience neurologic impairment. Victims younger than 3 years old, submersion for longer than 5 to 10 minutes, and initiation of cardiopulmonary resuscitation (CPR) more than 10 minutes after rescue portend a poor prognosis. Adverse neurologic findings on initial presentation do not preclude full neurologic recovery, although in general, patients whose duration of submersion or resuscitation exceeds 10 minutes have an unfavorable outcome. With the exception of victim age, however, such measurements are often unknown or inaccurately estimated at the time of a patient’s arrival in the ED. On arrival, objective findings associated with an unfavorable prognosis include hypothermia, severe acidosis, unreactive pupils, a Glasgow Coma Scale score of 3, and asystole or the need for ongoing CPR. Neurologically intact survival is reported for individual patients even with several of these factors present; however, none of the proposed scoring systems using combinations of these variables has 100% predictive power.

Children who present with an abnormal head computed tomography (CT) scan (e.g., intracranial bleed, cerebral edema) within the first 24 hours have a nearly 100% mortality rate. Furthermore, an abnormal head CT scan at any time is associated with poor outcome (persistent vegetative state (PVS), post-coma unresponsiveness (PCU) or death).