Traditionally drowning has been defined as death due to suffocation within 24 hours of submersion in a liquid medium and near-drowning as survival for 24 hours or more following such an incident.¹ Considerable confusion has surrounded the use of these terms. In part this is because the distinction between drowning and near-drowning often cannot be made before 24 hours, making the terms clinically irrelevant. In addition it has been suggested that the use of a time limit for survival is not a scientific concept and is not in accordance with outcome parameters as used in the internationally accepted Utstein style.¹

To address this issue the Utstein Taskforce on Drowning was convened in Amsterdam as part of the 2002 World Congress on Drowning. The International Liaison Committee on Resuscitation (ILCOR) has since endorsed a review of the terminology and defines drowning in the following way:

Drowning. Drowning is 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. ²

The term submersion is generally accepted to indicate an incident in which the victim’s body is totally covered by water, while the term immersion refers to an incident in which the victim is only partially covered by water, although for drowning to occur the face and airway must at least be covered.²

ILCOR recommends that other terms such as dry drowning versus wet drowning, active versus passive versus silent drowning, secondary drowning and near drowning be abandoned.²

Epidemiology

In Australia drowning is a leading cause of accidental death in children. Its incidence peaks in early childhood and again in adolescence. Males outnumber females in both groups. Children under five years of age are the most vulnerable to drowning in Australia.³ In the period between 1 July 2008 and 30 June 2009 there were 302 drowning deaths in Australian waterways. Children aged 0-4 years accounted for 11% of deaths overall and 74% of deaths under the age of 14 years. 59% of drowning deaths in the 0–4 years age group occurred in swimming pools with around 84% of cases occurring from wandering or falling in.⁴

Risk groups for childhood drowning are children aged 0–4 years, children living in cities with high swimming pool to population ratios, children living in hot climates, children living in areas with lack of isolation pool fencing, and Indigenous children.⁵ More toddlers drown in swimming pools than from any other cause.⁶ Most children who drown in pools are out of sight for less than 5 minutes and are in the care of one or both parents.⁷ Around the home small children can also drown in baths, buckets, and garden ponds. Up to 8% of cases of drowning in small children in the domestic setting may be secondary to non-accidental injury.⁸

While pool-fencing legislation has proven to be effective in reducing the incidence of drowning in small children it has had little impact on rates of drowning in older children and adolescents. In this group alcohol, suicide, and risk-taking behaviours are important factors that lead to increased risk of drowning.⁸

Aetiology

Drowning is most commonly a primary event. In children it most often occurs when the victim is unable to rescue him or herself after entering the water, as in the case of a toddler falling into a swimming pool, or an infant drowning in a bath whilst unattended. In older children and adolescents fatigue while swimming may play a role, but drowning in these age groups is more likely to be secondary to other causes.

Drowning can occur secondarily to a number of underlying causes. These should be considered during assessment of the submersion victim. Individuals with seizure disorders have up to 19-times higher risk for drowning accidents, regardless of age.^3,^8,⁹ Prolonged QT-syndrome leading to dysrhythmia has been implicated as a significant cause of drowning, although the true incidence of this condition in drowned children is unknown. Ethanol is an important risk factor for drowning injury, particularly in adolescents. Elevated serum ethanol levels are documented in 10–50% of adolescent drownings.⁸ Head and cervical trauma from diving and boating-related accidents may also lead to drowning as a secondary event. Non-accidental injury is an important cause of drowning in infants and smaller children, particularly in events that occur in the home, such as in baths and buckets. Up to 8% of drownings presenting to tertiary paediatric centres may be attributed to child abuse.⁸

The immersion syndrome is sudden loss of consciousness secondary to a bradycardia, or tachyarrhythmia induced by contact with water at a temperature of at least 5°C below body temperature. This can lead secondarily to drowning. The immersion syndrome can occur in water with temperatures as warm as 31°C, although it is more likely to occur in much colder water. Wetting the face before entering the water may reduce its incidence.¹

Pathophysiology

The two most significant pathophysiological consequences of submersion are hypoxia from asphyxiation during the submersion itself, and aspiration of water into the lungs. It is the severity of the initial hypoxic insult that is the major determinant of outcome. If the initial hypoxic event is survived, the degree of hypoxic organ injury and pulmonary injury secondary to aspiration become the clinically important factors.

Much that is known about the sequence of events following submersion has come from animal models. Aspiration of water initially causes breath-holding or laryngospasm and the resultant asphyxiation leads to progressive hypoxia. Active and passive swallowing of water follows and, as hypoxia worsens, breath-holding and laryngospasm are terminated, resulting in aspiration of water into the lungs.¹

Anoxia lasting 1–3 minutes can shut down both the brain and the heart, causing loss of consciousness and hypoxic cardiac arrest. Rescue and early institution of cardiopulmonary resuscitation can salvage myocardial function, but the brain is more sensitive to hypoxic injury and it is the severity of this injury that determines outcome. Effects of hypoxia on other organ systems are delayed. Profound hypoxia can cause an acute respiratory distress syndrome, which develops within hours and further worsens hypoxic injury. Posthypoxic cerebral oedema is a major complication and can develop 6–12 hours following successful initial resuscitation from a serious submersion event. Most paediatric drowning deaths in hospital are due to hypoxic cerebral injury rather than pulmonary complications.⁸

The average volume of water aspirated in human drownings is 10–15 mL kg^–1. Aspiration of volumes as little as 1–3 mL kg^–1 of water can cause profound alterations in gas exchange and subsequent ventilatory abnormalities.¹⁰ Laryngospasm is thought to occur in 10–15% of drowning victims and a subset of patients who drown without evidence of significant aspiration of water at post-mortem, so-called dry-drowning, has been described. This concept has recently been questioned and it has been suggested that in these cases death has occurred prior to submersion.¹ Regardless of whether dry-drowning is a true clinical entity, or whether laryngospasm has occurred at the time of submersion, aspiration of water into the lungs remains a clinically important consideration in the management of all drowning victims.

Despite the large literature dedicated to the subject, there are no clinically or therapeutically important differences between drowning in fresh or salt water.^1,⁸ Pulmonary injury is related more to the amount of water aspirated than to the composition of the water itself. Both fresh and salt water cause loss of pulmonary surfactant, non-cardiogenic pulmonary oedema, impaired alveolar-capillary gas exchange, and increased intrapulmonary shunting with the potential for profound hypoxia.¹ Aspiration of water that is contaminated with particulate matter or bacteria can lead to complications from obstruction of small airways or increased risk of pulmonary infection, although neither is seen in the majority of patients.¹¹ If present, evidence of significant pulmonary injury due to aspiration will usually manifest or progress within hours of rescue. Delayed onset of respiratory distress and hypoxia, the so-called ‘delayed immersion syndrome’ or ‘secondary drowning’ has been refuted by recent evidence.⁸

Clinically significant electrolyte and fluid volume abnormalities are rarely seen in cases of drowning in humans despite being demonstrated in animal models.^1,^3,^8,¹¹ Occasionally a mild hyponatraemia, which self-corrects without specific therapy, is observed.⁸ Theoretical exceptions are drownings occurring in hypertonic solutions, such as the Dead Sea, or water contaminated with industrial waste.

Hypothermia is an important issue following drowning, particularly in small children who have a large body surface area to weight ratio. Cooling can occur at the time of submersion, but can also continue following rescue and during attempted resuscitation due to heat loss through evaporation. Hypothermia can confer some degree of protection from cerebral hypoxia, particularly in small children. Multiple case reports in the literature attest to intact survival of both children and adults following prolonged (>15 minutes) drownings in icy water (water temperature <10°C).¹² Profound hypothermia and subsequent intact survival has also been documented in children suffering drowning in non-icy water and in temperate climates.

The mechanisms of temperature drop and cerebral protection remain unclear. Surface cooling at the time of submersion is thought to be insufficient on its own to provide central cooling of a degree that confers cerebral protection. Other mechanisms of heat loss, such as via ingestion and/or aspiration of cold water, are not supported by quantitative evidence. Some authors suggest that core temperature drop is insufficient on its own to explain the cerebral protection afforded by hypothermia.¹³ The diving reflex, in which blood is shunted from the limbs and splanchnic circulation to the brain and heart alongside slowing of the heart rate and reduction of the basal metabolic rate, has been suggested as being an important mechanism for cerebral protection in children.¹³ There is little clinical evidence to indicate that the diving reflex is sufficiently active in humans, even small children, to confer any benefit on its own.^1,⁸ It is most likely that a combination of the effects of the diving reflex initially, followed by rapid and continued cooling, is what underlies the cerebral preservation that is sometimes seen in small children who suffer submersion and who are profoundly hypothermic.

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