Drowning is a major global health problem, with significant mortality and morbidity in children.^1,2 Children younger than 14 years of age comprise about 20% of all drowning victims. One in every five emergency department (ED) visits for submersion-related injuries results in death secondary to drowning, and it is the most preventable cause of unintentional injury in children.³

Drowning is the leading cause of death in children from 1 to 4 years of age and the second leading cause of death from unintentional injuries worldwide in children from 1 to 14 years of age.⁴ The most common site of occurrence is backyard swimming pools.

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  Males are more likely to drown than females, in all age groups, with the highest rate being in the newborn to 4-year-old age group.^{5–7, 8,9}

  
  
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  African-American children are three times more likely to drown compared to Caucasian children.

  
  
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  Poverty, low parental education level, number of children in the family, and ethnicity have also been associated with an increased risk of drowning.⁷

  
  
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  The majority of drowning-related deaths (98.1%) occur in low- and middle-income countries as compared to high-income countries.⁵

  
  
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  Children are specifically at increased risk by seas/oceans, lakes, streams, swimming pools, and bathtubs, and specific cases have also been reported involving wells, cisterns, buckets, spas, and garden ponds.¹⁰

In the past, there have been a number of terms associated with drowning that have caused much confusion when labeling the official cause of injury or death.¹¹ Therefore in 2002, the World Congress on Drowning and the World Health Organization published the following consensus definition for drowning.^4,12

“Drowning is a process resulting from primary respiratory impairment from submersion/immersion in a liquid medium.”⁴ Drowning outcomes have been classified as: “death,” “morbidity,” and “no morbidity.” These patient outcomes can be further categorized as “moderately disabled,” “severely disabled,” “vegetative state/coma,” and “brain death.”

According to the advisory statement recommendations presented by The International Liaison Committee on Resuscitation, outdated and nonspecific terminology including “dry drowning,” “wet,” “active,” “silent,” “secondary,” and “near drowning” should no longer be utilized.¹³

The drowning process is comprised of a continued series of events beginning from the point when the victim’s airway is submerged under the liquid surface. This results in a lack of oxygen and a failure to exhale carbon dioxide causing hypoxemia, hypercapnia, and acidosis.¹⁴ The pathophysiology behind this process is complex and can be variable depending on the influence of different factors including drowning medium, medium temperature, associated trauma, and patient-specific factors, among others (Table 137-1). The primary insult, however, almost always, irrespective of the influencing variables, is hypoxia.

The main organs that are affected are the pulmonary, neurologic, cardiac, and renal systems.

PULMONARY

After the patient is submerged, he or she aspirates a small amount of water causing a reflex laryngospasm and subsequent apnea. This leads to hypoxia and loss of consciousness. Once unconscious, most patients will further aspirate more water. Approximately 10% of patients will maintain laryngospasm, leading to what was previously described as “dry drowning.”¹⁵

Freshwater and saltwater cause different pathophysiologic effects on the pulmonary system that ultimately still lead to the same resulting hypoxia. Aspirated freshwater causes surfactant to wash out, thus altering the surface tension properties of the alveolus. The alveoli collapse, preventing ventilation, and this creates an intrapulmonary shunt. Some of the fluid diffuses into the cell walls of the alveoli, leading to cell rupture and edema. Most water, however, is absorbed into the plasma volume. This subsequently leads to a ventilation–perfusion (V/Q) mismatch from alveolar collapse and shunting (Fig. 137-1).^15,16

Saltwater inhalation also causes V/Q mismatch, but via a different mechanism. The aspirated hypertonic saltwater pulls fluid from the plasma into the alveolar spaces, causing pulmonary edema. The fluid-filled alveoli are thus not ventilated, creating an intrapulmonary shunt (Fig. 137-2).¹⁴

Regardless of whether the event occurred in freshwater or saltwater, the end result is pulmonary edema with a decrease in pulmonary compliance. This leads to an increased V/Q mismatch resulting from intrapulmonary shunting. These processes result in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

NEUROLOGIC

Primary central nervous system (CNS) injury is associated with tissue hypoxia and ischemia. Decreased ventilation causes hypoxemia, which in turn causes cardiopulmonary arrest. This leads to decreased cerebral blood flow. The combination of hypoxemia and decreased cerebral perfusion rapidly leads to ischemia. The neuronal cell destruction that occurs with ischemia subsequently causes cerebral edema and increased intracranial pressure (ICP). Progressive rise in ICP within the first 24 hours after drowning may be reflective of the severity of the neurologic insult rather than its cause.¹⁷ But despite a number of trials in the previous decades, monitoring of ICP following drowning has not proven to influence or improve management and therefore is not recommended.^18–20 The presence of pupillary reactivity and motor activity on initial examination in the ED may help predict patient survival. However, these findings have not been shown to assist in the differentiation of neurologically intact versus vegetative state survivors.²¹ An electroencephalogram (EEG) can be helpful in these patients.²² Predictors of poor outcome based on EEG findings include burst suppression, generalized suppression, status epilepticus, and nonreactivity.^23,24 An MRI is better than a CT scan in ascertaining the degree of brain swelling and edema.²³ With cases of brain injury, tight glycemic control should be maintained.²⁵ For children who remain comatose after cardiopulmonary resuscitation (CPR) for 12 to 24 hours, hypothermia has been suggested, but there is a lack of definitive scientific evidence supporting this practice.²⁵ The data on long-term neurological outcome in drowning patients is also scarce, but studies suggest that gross neurological examination at the time of discharge from the hospital in young children does not reveal all the possible sequelae related to hypoxic brain injury.²⁵ Approximately 10% of drowning survivors will suffer severe neurologic sequelae with a degree of neurocognitive dysfunction. Therefore, long-term neurological and neuropsychological follow-up of drowned resuscitated children is strongly recommended.^25,26