Author: Wayne Wen Tao Kark / Editor: Adrian Boyle / Reviewer: Robert Hirst / Codes: ACCS LO 2, EnvC5, RP8, SLO1, SLO2, SLO3, SLO4 / Published: 29/02/2020


Drowning is the process of experiencing respiratory impairment from submersion/immersion in liquid.

‘Submersion’ refers to the airway going below the level of the surface of the liquid and ‘immersion’ refers to liquid being splashed across a person’s face.

Terms such as ‘near drowning’, ‘wet drowning’, ‘dry drowning’, whilst used historically are no longer used. Terms describing outcomes have been simplified to no morbidity, morbidity, and death. Drowning may be further classified as cold-water (<20˚C) and warm-water (>20˚C).


The World Health Organisation (WHO) recorded 409,272 deaths from unintentional drowning worldwide in the year 2000 (excluding cataclysms, water and other transport accidents, assault and suicide). This is an accidental drowning rate of 6.8 per 100,000, making drowning the second highest cause of death from injury, after road traffic injuries.

International data may drastically underestimate drowning figures, even for high-income countries, as intentional drowning deaths and drowning deaths due to natural disasters are not coded in mortality data. In addition, there are large variations between countries in the quality and means of data collection1

Young children are particularly at risk of drowning, as they are unaware of dangers and are less able to escape from water once submerged. Even relatively small bodies of water (e.g bathtubs, buckets) pose a risk. These cases are preventable by continuous supervision of young children, and preventing unintentional access to water (e.g fencing around pools). Non-accidental injury should be considered in young children who drown at home or in shallow water2.

Amongst adults, men account for 81% of deaths by drowning, with peak incidence in men aged 20-29, although rates of drowning are nearly as high in men aged 30-692.

Physiological responses in drowning

Airway Protection

The usual response to submersion is a voluntary breath hold, to prevent aspiration of water. Voluntary apnoea results in progressive hypercapnia, acidosis and hypoxia which, together with feedback signals from the respiratory muscles, stimulates the respiratory centres and eventually forces the individual to take involuntary breaths.

Reflex laryngospasm may also occur, preventing further penetration of water into the lungs. The degree and duration of laryngospasm is highly variable. Prolonged hypoxia is usually associated with relaxation of the vocal cords and passage of some water into the lower airways, but tight laryngospasm can persist beyond cardiac arrest. The volume of fluid aspirated is usually small (<4mL/kg fluid) but results in significant hypoxia.

Diving Reflex

The mammalian diving reflex, seen predominantly in infants when the face contacts cold water, is thought to have a protective role. Apnoea, bradycardia and peripheral vasoconstriction occur. This reduces cardiac output (and myocardial oxygen demands) and conserves oxygen, while maintaining perfusion of the brain and vital organs. This helps prevent hypoxic damage during the early stages of submersion, and may account for improved survival rates following prolonged submersion in cold water in young children.

Cardiovascular Effects

The hydrostatic pressure of water on the body, when immersed, results in increased venous return and an increase in cardiac output. Loss of this pressure effect when exiting the water causes a sudden loss of peripheral resistance and venous pooling. This causes hypotension and circulatory collapse. Patients should be extricated from the water in a horizontal position, if possible, to counteract this effect.


Drowning injuries result from impaired lung function and gas exchange. This leads to hypoxia and acidosis, which causes secondary damage to other organs.

Respiratory complications

Submersion in water interrupts normal respiration, resulting in a progressive hypoxia, hypercapnia and acidosis. If prolonged, this may lead to loss of consciousness.

Aspiration of even small amounts (1-3mL/kg) of fluid significantly impairs gas exchange. Aspirated water dilutes and inactivates surfactant, making the alveoli prone to collapse. Atelectasis and reduced lung compliance produce a ventilation-perfusion mismatch

Aspirated water also causes direct lung injury, particularly if the water is contaminated (eg dirt, sand or gastric contents.) Damage to the alveolar basement membrane may result in acute respiratory distress syndrome (ARDS)

Learning Bite

Small amounts of fluid inactivate surfactant and impair gas exchange.

Fresh water and Salt water

Early work in animal models showed pathological differences between fresh and salt water aspiration. Systemic uptake of aspirated fresh water (hypotonic) caused haemodilution and hypervolaemia. In turn, haemodilution caused haemolysis and electrolyte disturbances which were thought to predispose to cardiac arrhythmias. In contrast, aspiration of salt water led to uptake of electrolytes and loss of protein rich serum into the hypertonic environment of the alveoli, causing pulmonary oedema and hypovolaemia.

It is unclear, however, whether these effects are clinically important. Recent studies show that, because of the relatively small volumes of aspiration seen in drowning cases, clinically significant fluid and electrolyte shifts are unlikely to occur. The management of fresh and salt water drowning is the same.

Learning Bite

There is no practically important difference in the way that fresh and salt water drowning cases should be managed.

Cardiovascular complications

Cardiac ischaemia or arrhythmias may occur during drowning. Hypoxaemia combines with increased demands on the myocardium (increased cardiac output combined with increased systemic vascular resistance due to peripheral vasoconstriction). Volume and electrolyte disturbances may further contribute to cardiovascular instability


Pneumonia is a common complication in drowning victims, resulting from aspiration of water and contaminants during submersion, or secondary infection during recovery. These patients are often infected with unusual bacteria, such as Aeromonas sppBurkholderia pseudomalaeiChromobacterium sppPseudomonas speciesand Leptospirosis.


Rapid onset hypothermia is protective. Several case reports show survival despite prolonged periods of submersion in ice cold water (over one hour). Hypothermia slows metabolism and reduces oxygen consumption; helping to reduce the inflammatory response. However, unless the onset of hypothermia is rapid, significant injury may develop before the body cools.

Effects of hypoxia and hypoperfusion

Asphyxia and aspiration cause hypoxaemia, while cardiovascular instability results in hypoperfusion of vital organs. This combination of hypoxia and hypoperfusion (ischaemia) results in metabolic acidosis and cell death. Neurological damage is usually the main problem in patients that survive drowning. However, damage is not limited to the brain. Myocardial infarction, rhabdomyolysis, acute tubular necrosis and DIC are common complications of drowning.

Associated injuries

There is a high incidence of associated injuries in victims of drowning. Head and cervical spine injuries are particularly common in patients rescued from shallow water.


Initial assessment should aim to identify respiratory compromise and other end-organ damage. Symptoms and signs of aspiration include dyspnoea, cough, retrosternal discomfort, tachypnoea and audible crackles on chest auscultation. Look for evidence of any precipitating causes (eg seizure, arrhythmias, myocardial infarction, stroke) and associated injuries (e.g. head or spinal injuries)

Investigations of victims of drowning should include:

  • Arterial blood gases (ABG) should be taken in all patients with a significant history of submersion. Low PaO2is an early indicator of aspiration. Patients may remain asymptomatic despite significant hypoxia and pulse oximetry may be inaccurate due to peripheral vasoconstriction.
  • CXR may show fluffy shadowing resulting from aspiration, atelectasis, or developing pulmonary oedema / ARDS
  • ECG and cardiac monitoring
  • Core temperature measurement using a low-reading thermometer. Consider continuous monitoring if hypothermic
  • Check electrolytes and BM
  • Consider blood culture in patients with significant aspiration, as this may be required to guide the choice of antibiotics if infection develops
  • Consider X-rays or CT-imaging where there is a suspicion of head, neck or spinal injuries.

Risk Stratification

There have been several attempts to identify reliable prognostic indicators. These aim to distinguish between those who will survive with little long-term disability from those who have established brain injury, or who are unlikely to survive.

95% of patients rescued from drowning with a pulse survive without long-standing sequelae. However, mortality amongst those found in cardiac arrest is 93%3. Of those resuscitated, only 7-11% make a partial or full recovery. Delayed CPR or prolonged cardiac arrest are associated with a poor chance of recovery.

Outcome is almost entirely determined by the duration of submersion. Known submersion <10 minutes is a good prognostic factor and >25 minutes is a poor prognostic factor. Prolonged submersion in cold or icy water with no sequelae is rare, but possible. Other factors associated with increased morbidity and mortality include a low Glasgow Coma Score (GCS), lack of pupillary response, acidosis & hypotension. However, most studies on the subject are based on weak evidence, and most prognostic tools lack validation4.

Learning Bite

There are no prognostic features that reliably predict a poor outcome after drowning.

The initial management of drowning follows the ATLS principles of Airway with cervical spine control, Breathing and Circulation.


Spinal injury should be considered in all cases of drowning, especially in patients recovered from shallow water or those with evidence of head injury. However, retrospective analyses, although limited, suggest the incidence of in-water cervical spine injury is low (<0.5%)5.

Appropriate spinal precautions should be taken. Patients should be lifted out of the water in a horizontal position to prevent venous pooling and sudden cardiovascular collapse.

Airway and Breathing

Early, effective maintenance of airway and ventilation prevents cardiac arrest and improves neurological outcome. Attempting to drain water from the lungs is ineffective.

All drowning patients, except those with normal oxygenation, normal saturations and normal auscultation, should receive supplemental oxygen, as significant hypoxia may develop without dyspnoea. The goal is to deliver the highest concentration of oxygen possible.

An arterial blood gas (ABG) can help determine management; a falling PaO2 suggests developing acute respiratory distress syndrome (ARDS) which may require assisted ventilation.

Patients who are asymptomatic and have no evidence of respiratory compromise (no CXR changes or hypoxia on ABG) after six hours can be safely discharged home. All symptomatic patients should be admitted for observation.

Patients should have high-flow oxygen delivered by facemask at rate of 15 litres per minute, aiming for oxygen saturations of 92-98%. Patients protecting their airway who are conscious may benefit from a trial of non-invasive ventilation, using either CPAP or BiPAP. Patients with significant respiratory compromise or reduced GCS may require early intubation & mechanical ventilation. Bronchospasm may be treated with nebulised bronchodilators.

Ventilation strategies vary, but the aim is to maintain oxygenation while minimising ventilator associated lung injury. Inspired O2 concentration (FiO2) should ideally be maintained below 0.50, as higher concentrations cause absorption atelectasis and have a direct toxic effect on lung parenchyma.

PEEP should be maintained at a minimum of 5cm H2O to prevent shear stress from the repeated opening and closing of alveoli. This can be increased to maximise oxygen delivery, as long as cardiac output is not compromised. Low tidal volume ventilation (6ml/kg) should be considered. There is currently insufficient evidence to support a target PaCO2. PEEP support should be left unchanged for at least 48-hours to permit adequate surfactant regeneration & ensure alveolar recruitment before weaning is attempted. Early weaning may cause the return of pulmonary oedema, a prolonged stay, and further morbidity6.

Several experimental techniques have been suggested to improve ventilation, including proning the patient, intratracheal administration of surfactant, and nitric oxide inhalation. Evidence is poor for these, and further studies are required. Studies have demonstrated little benefit from steroids.

Learning Bite

Patients who are asymptomatic and have no evidence of respiratory compromise (no CXR changes or hypoxia on ABG) after six hours can be safely discharged home. All symptomatic patients should be admitted for observation.


The management of cardiac arrest follows ALS guidelines. Pulses may be difficult to feel in hypothermic patients. Hypovolaemia is the usual cause of shock in these patients, and may necessitate fluid resuscitation. Electrolyte disturbances, though uncommon, should be corrected.

Hypotension is usually correctable with oxygenation, crystalloid infusion, and restoration of normal body temperature. Vasopressors should only be used in refractory hypotension after a trial with crystalloids.


Drowning injuries are often associated with hypothermia. Severe hypothermia (body temperature <30˚C) may be associated with marked depression of critical body functions and rewarming measures should be implemented. Hypothermia is associated with prolonged exposure and carries a poor prognosis. In rare cases, hypothermia may confer neuroprotection to those falling into icy water.


Bacterial colonisation at the site of the drowning is usually not sufficient to promote pneumonia in the immediate post-drowning period. Pneumonia is often misdiagnosed due to early radiographic appearances and the presence of mild fever & leucocytosis, which are usually a physiological response to the drowning event.

There is no good evidence to support the routine use of prophylactic antibiotics. The incidence of ventilator-associated pneumonia can be 34-52%7, and treatment should be initiated as per local protocol. Treatment should ideally be guided by culture results. The microorganisms encountered in salt-water drowning are often part of the human oropharyngeal flora or Enterobacteriaceae8, although freshwater drownings are associated with more atypical organisms.

Acute Kidney Injury

Acute kidney injury, resulting from hypovolaemia, hypoxaemia, rhabdomyolysis, and lactic acidosis may result following drowning9.

Neurological complications

Brain injury results from hypoxia and ischaemia, so management focuses on maintaining oxygenation and cerebral perfusion. Secondary brain injury may be reduced by preventing hyperthermia (maintaining a core body temperature <36˚C) following cardiac arrest, controlling seizures promptly with benzodiazepines, and maintaining tight glycaemic control.

Raised intracranial pressure following drowning is a poor prognostic indicator. However, attempts at management of ICP or specific neuro-resuscitative pharmacological treatments (e.g. barbiturates, calcium channel antagonists, antioxidants) have shown little benefit in improving outcomes.

Key Learning Points

  • Patients should be extracted from the water in a horizontal position to prevent cardiovascular collapse. Level 5 evidence, Grade C recommendation.
  • The initial management of fresh and salt-water drowning is the same. Level 5 evidence, Grade C recommendation.
  • Submersion <10 minutes is a good prognostic factor and >25 minutes is a poor prognostic factor. Level 1 evidence, Grade B recommendation.
  • The initial management of drowning follows the ATLS principles. Level 5 evidence, Grade D recommendation.
  • The volume of fluid aspirated is usually small (<4mls/kg). Attempting to drain water from the lungs is ineffective. Level 5 evidence, Grade C recommendation.
  • Management of hypoxaemia and circulatory failure is key to the management of drowning. Level 4 evidence, Grade B recommendation.
  • Check an arterial blood gas on all patients with a history of submersion, as a surprising degree of hypoxia may be present in an asymptomatic individual. Level 5 evidence, Grade D recommendation.
  • Remember to look for evidence of precipitating causes and associated injuries and manage appropriately. Level 4 evidence, Grade B recommendation.
  • Patients who are asymptomatic and have no evidence of respiratory compromise (no chest x-ray changes or hypoxia on ABG) after 6 hours can be safely discharged home. All symptomatic patients should be admitted for observation. Level 5 evidence, Grade D recommendation.
  • Pneumonia following drowning may involve unusual pathogens. Level 5 evidence, Grade D recommendation.
  • Steroids have not been shown to be effective in drowning. Level 4 evidence, Grade C recommendation.
  • Consider child abuse in young children who are drowned in bath tubs, buckets or shallow water. Level 5 evidence, Grade D recommendation.
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