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Drowning

  • Author: G Patricia Cantwell, MD, FCCM; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Jul 05, 2016
 

Background

Drowning remains a significant worldwide public health concern, ranking as the third leading cause of unintentional injury death and accounting for 7% of all injury-related deaths. It is a major cause of disability and death, particularly in children. At least one third of survivors sustain moderate-to-severe neurologic sequelae.[1]

Exact definitions of drowning have varied widely.[2] Drowning was previously defined as death secondary to asphyxia while immersed in a liquid, usually water, or within 24 hours of submersion.

At the 2002 World Congress on Drowning held in Amsterdam, a group of experts suggested a new consensus definition for drowning in order to decrease the confusion over the number of terms and definitions (>20) that have appeared in the literature.[3]  This group developed a uniform definition that allowed more accurate analysis and comparison of studies, enabled researchers to draw more meaningful conclusions from pooled data, and improved the ease of surveillance and prevention activities.

The consensus definition states that drowning is a process resulting in primary respiratory impairment from submersion in a liquid medium. Implicit in this definition is that a liquid-air interface is present at the entrance to the victim's airway, which prevents the individual from breathing oxygen. The terms "wet drowning", "dry drowning", "active or passive drowning", "near-drowning", "secondary drowning", and "silent drowning" may be noted in historical references, yet they have been abandoned in favor of the general term "drowning." Terms describing outcomes were simplified to death, morbidity, or no morbidity.[3]

Drowning usually occurs silently and rapidly. The classic image of a victim helplessly gasping and thrashing in the water is infrequently reported. The more ominous scenario of a motionless individual floating in the water or quietly disappearing beneath the surface is more typical.

Drowning may be further classified as cold-water or warm-water injury. Warm-water drowning occurs at water temperatures of 20°C or higher, and cold-water drowning occurs at water temperatures of less than 20°C. Although ice-cold water has been reported to be protective, especially in young children,[4] prolonged immersions can nullify the effect of temperature on survivability.[5] Hypothermia occurs commonly in drowning and is usually secondary to conductive heat loss during submersion, not synonymous with cold-water drowning.

Additional classification may include the type of water in which the submersion occurred, such as freshwater and saltwater, or natural bodies of water versus man made. Although initial treatment of submersion victims is not affected by the type of water, serum electrolyte derangements may be related to the salinity of the water (particularly if large amounts of water are ingested), while long-term infectious complications are primarily related to whether the victim was submersed in a natural or a man-made body of water.[6]

Immediate threats include effects on the central nervous and cardiovascular systems (see Workup). Thus, the most critical actions in the immediate management of drowning victims include prompt correction of hypoxemia and acidosis (see Treatment).

The degree of CNS injury depends on the severity and duration of hypoxia. Posthypoxic cerebral hypoperfusion may occur. Long-term effects of cerebral hypoxia, including vegetative survival, are the most devastating (see Treatment).

Prevention is key for reducing morbidity and mortality from drowning. Community education is the key to prevention.

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Etiology

Drowning may be a primary event or may be secondary to events such as the following:

  • Seizures
  • Head or spine trauma
  • Cardiac arrhythmias
  • Hypothermia
  • Alcohol and drug ingestion
  • Syncope
  • Apnea
  • Hyperventilation
  • Suicide
  • Hypoglycemia

Causes tend to vary with the person’s age.

Infants

Infants most often drown in bathtubs or buckets of water. Most of these victims drown during a brief (< 5 min) lapse in adult supervision.

Bathtub and pail drownings may represent child abuse; carefully examine the child for other evidence of injury, review the child's history for previous events, and review the details of the incident very carefully with the child's parent or guardian.[24, 25]

Children aged 1-5 years

Residential swimming pools are the most common venue.[25, 26, 27] The US Consumer Product Safety Commission reports that a swimming pool is 14 times more likely than a motor vehicle to be involved in the death of a child younger than 5 years.

Many residential pools have no physical barrier between the pool and the home. Open gates are involved in up to 70% of drownings in cases involving fenced-in pools. Pools may also be accessed through unlocked windows when the pool area abuts the house.[28]

A study from Australia on drowning in water tanks[29] and one from Bangladesh on drowning in ditches, canals, and ponds[30] illustrate that water exposure is both culturally and geographically related. Limiting access to such areas is an important target for prevention strategies.

Young adults aged 15-19 years

Young adults typically drown in ponds, lakes, rivers, and oceans. Approximately 90% of drownings occur within 10 yards of safety. Cervical spine injuries and head trauma, which result from diving into water that may be shallow or contain rocks and other hazards, have been implicated.

Alcohol and, to a lesser extent, other recreational drugs are implicated in many cases. Australian, Scottish, and Canadian data showed that 30-50% of older adolescents and adults who drowned in boating incidents were inebriated, as determined by blood alcohol concentrations.

All age groups

Any of the following may lead to drowning episodes in people of any age:

  • Seizure disorder
  • Myocardial infarction (MI) or syncopal episode
  • Poor neuromuscular control, such as that seen with significant arthritis, Parkinson disease, or other neurologic disorders
  • Major depression/suicide
  • Anxiety/panic disorder
  • Diabetes, hypoglycemia
  • Water sports hazards, especially with personal watercraft
  • Poor judgment and substance abuse (alcohol or other recreational drugs) in conjunction with boat operation
  • Cervical spine injury and head trauma associated with surfing, water skiing, and jet skiing
  • Scuba diving accidents and other injuries (eg, bites, stings, lacerations)

A study by the European Alliance Against Depression reviewed gender-specific suicide methods in 16 European countries.[31] They found that women were more likely to choose drowning as a suicide method. They suggested that gender-specific prevention strategies should be developed.

Natural disasters

Drowning is a well-recognized complication of natural disasters, such as hurricanes and earthquakes, which produce tidal waves (tsunamis) and flooding. A study of loss of life from Hurricane Katrina analyzed 771 fatalities. Most involved elderly individuals and were caused by drowning due to the direct physical impact of flooding. Mortality was highest near severe levee breaches where water was moving at rapid velocity and in areas with increased water depth.[32]

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Epidemiology

United States statistics

While drowning deaths have shown a gradual decline, from 2005-2014, there were an average of 3,536 fatal unintentional drownings (non–boating related) annually in the United States, which is about 10 deaths per day.[33] An additional 332 drowning deaths occurred each year in boating-related incidents.[34]

Drowning is the sixth leading cause of accidental death for people of all ages and the second leading cause of death for children aged 1-14 years, after motor vehicle collisions.[1, 35, 36] This averages out to about 10 deaths per day in the United States.

Approximately one quarter of these deaths occur in children 14 years of age or younger. Four times as many children receive emergency department care for nonfatal injuries for every child that dies. A bimodal distribution of deaths is observed, with an initial peak in the toddler age group and a second peak in adolescent to young adult males. Fifteen percent of children admitted for drowning die in the hospital.

Drownings tend to occur most frequently on weekends (40%) in the summertime months (May through August). Drownings are seen more commonly in rural areas and in the southern and western United States (62%).[37] In California, Arizona, and Florida, drowning is the number one cause of injury-related death.

Morbidity from submersion occurs in 12-27% of survivors aged 1-14 years. Preschool-aged boys are at greatest risk of submersion injury. A survey of 9,420 primary school children in South Carolina estimated that approximately 10% of children younger than 5 years had an experience judged a "serious threat" of drowning.

In 2008, the US Lifesaving Association reported more than 70,000 rescues from drowning at beach venues.[38] California alone reports approximately 25,000 ocean rescues on its beaches each year. More than 4.5 million preventive actions, including moving swimmers from areas of rip currents and other hazards, were reported during this same period of time. Approximately 1 in 8 males and 1 in 23 females experience some form of water-associated event but never seek medical attention.

International statistics

Annually, an estimated 372,000 people die from drowning, which accounts for drowning to be a major public health problem worldwide. Global estimates of drowning are likely a significant underestimation of the actual public health impact. No annual international incidence of associated neurological injury has been reported.[1]

Several of the most densely populated nations in the world fail to report nonfatal drowning incidents. This, along with the fact that in many instances no attempt is made to resuscitate at the scene[39] and that many cases are never brought to medical attention, renders accurate worldwide incidence approximation and classification virtually impossible.[40] The overall incidence of drowning has an estimated range of 20-500 times the rate of fatal drowning.

British data suggest that approximately 10% of drownings in the United Kingdome occur in the domestic setting, most frequently during baths, in water-filled containers both indoors and outdoors, and in garden ponds.[41] Structures overhanging water posed a particular risk. Young children (< 5 years) and older adults were shown to be at highest risk.[41, 42, 43]

The drowning site appears to be a function of availability. In areas of the world where bathing occurs in nearby streams, rivers, and lakes, data collected suggest that the incidence is[39, 44] more similar to that found in industrialized nations in the adolescent and young adult groups (aged 15-24 y), where most incidents occur in natural bodies of water.

Hong et al suggest that this risk is due not only to rural residence and lower socioeconomic status but also to the education level of parents, which would suggest that targeted public health intervention strategies might prove to be effective in decreasing this incidence.[44, 45]

Boating and related water sports, combined with alcohol consumption, increase both the likelihood and severity of submersion injuries. Risk-taking behaviors, especially in males, are similarly associated with increased morbidity and mortality.

An Australian study that focused on drowning risks at surf beaches found that in the 204 individuals studied, adolescent and adult males spent longer amounts of time in the water, were more likely to use surfing equipment, were more likely to consume more alcoholic beverages, and spent more time in deeper water. The authors hypothesized that over-representation of males in drowning statistics is in part a function of this greater exposure to deeper waters further from shore.[46]

Males also generally feel more confident about their swimming abilities and their ability to return to shore if caught in a rip current.[47]

The authors found no gender difference in the likelihood of holding a first aid qualification, cardiopulmonary resuscitation (CPR) certification, or prior swimming lesson participation. They suggested that larger, controlled studies should address the role of overconfidence, self-rated versus measured swimming competency, surf experience, ability to judge swimming conditions, and the use of flotation devices in relation to drowning risk.[47]

This later study provided somewhat different data from that in a previous, smaller 2008 study by Morgan et al that indicated no difference in gender or age on likely surf-drowning risk, including preexisting medical conditions, presence of drugs or alcohol, or the likelihood of swimming without a buddy or in rip current conditions.[48]

Scuba diving accounts for an estimated 700-800 deaths per year; etiologies include inadequate experience/training, exhaustion, panic, carelessness, and barotrauma.[49] Denoble et al studied 947 recreational diving accidents from 1992-2003, during which 70% of the victims drowned. Drowning was usually secondary to a disabling injury, equipment problems, problems with air supply, and cardiac events in these individuals.[50]

A 2009 Western Australian study reviewed 24 diving fatalities and found that the lack of formal certification (30%) was associated with the breach of safety practices.[51] The authors noted that shore dives or dives from private crafts were fatal 3 times as often as dives from commercial boats. These researchers also found that dive depth, ignoring a preexisting medical condition, nonadherence to the buddy system, poorly planned dives, and the lack of establishment of positive buoyancy when in distress contributed to diving fatalities. Only twice was faulty equipment the cause, once during scuba and once during a "hookah" dive (ie, with surface-supplied air). Seventy percent occurred during the day. Twenty five percent involved tourists.[51]

A study of 19 reported fatalities in Australia in 2008 concluded that the causes of death included apnoeic hypoxia, trauma, and cardiac related issues. The study concluded that trauma from a marine creature, snorkeling or diving alone, apnoeic hypoxia, and preexisting medical conditions were factors in several deaths.[52]

A Danish occupational medical study of 114 drowning fatalities in the period 1989-2005 among fishing industry seamen found that approximately one half of the deaths occurred during vessel disasters in rough weather, with capsizing and foundering, or collisions. One third occurred during other occupational accidents that caused the victim to go overboard. One third occurred when the victim underwent difficult disembarkation during nighttime hours in foreign ports or was intoxicated.[53]

A Swedish study emphasized the contribution of alcohol and drugs to drowning deaths and the importance of considering such information in developing prevention programs. Although the number of drowning deaths has significantly decreased, men and middle aged and older people had a higher incidence. Among women, suicidal drowning was common.[54]

A Canadian study of drowning during work-related and recreational helicopter crashes over water found that educational strategies to increase survival likelihood included wearing survival gear during the trip, prior escape training, ensuring that crew and passengers possessed appropriate knowledge of escape routes, and assuming appropriate crash positioning. They suggested that companies using helicopter transport over water should focus on regular and repeated safety training and improvement in safety measures on helicopters.[55]

Accidental death, such as drowning, complicate tourism in many countries.[56, 57] An Australian study found accidental drowning to be the cause of approximately 5% of all deaths in the 1068 visitor deaths reviewed.[58]

Race-related demographics

Between 2000 and 2007, the rate of fatal accidental drowning for African Americans across all ages was 1.3 times that of whites; for Native Americans and Alaskan Natives, this rate was 1.7 times that of whites.[35] However, the relative rates vary with age. African-American children aged 0-4 years exhibit a lower rate of drowning (2.32 per 100,000), probably secondary to less pool access. In older pediatric age groups, the incidence is 2-5 times higher.

In indigenous children and teenagers in the United States and Canada, injuries account for 71% of childhood deaths. In Alaska, drowning is the leading cause of death among indigenous children.

Focused interventions have targeted indigenous groups in Alaska. Over a 20-year period (1982-84 vs 2002 vs 2004), the age-adjusted mortality rate declined 28%, compared with a 5% decline for the United States as a whole. This author suggests that developmentally and culturally appropriate interventions and community-based educational interventions, such as a requirement for wearing personal flotation devices, 4-sided fencing of pools, and the prohibition of alcohol sale to minors, can be highly effective.[59]

Between 1994 and 2005, drowning rates demonstrated an increase among white males 65 years and older and middle-aged white females (45-64 y) but showed a decrease in black boys, adolescents, and young adult males (5-24 y), black girls and adolescents (5-14 y), and white adolescents and young women (15-24 y).[60]

Sex- and age-related demographics

Males are approximately 4 times more likely than females to have submersion injuries. This rate is consistent with increased risk-taking behavior in boys, especially in adolescence. Males are also 12 times more likely than females to be involved in a boat-related drowning; alcohol use is frequently a contributing factor. Only in bathtub incidents do girls predominate in incidence.

A bimodal age distribution is noted in persons with a submersion injury. Children younger than 4 years and adolescents aged 15-19 years are at highest risk. This bimodal distribution is predominantly observed in males, who have a much higher incidence of submersion injuries during adolescence than females do. Most toddlers drown in swimming pools and bathtubs, whereas most adolescents drown in natural bodies of water.

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Pathophysiology

The most important contributory factors to morbidity and mortality from drowning are hypoxemia and acidosis and the multiorgan effects of these processes. Central nervous system (CNS) damage may occur because of hypoxemia sustained during the drowning episode (primary injury) or may result from arrhythmias, ongoing pulmonary injury, reperfusion injury, or multiorgan dysfunction (secondary injury), particularly with prolonged tissue hypoxia.

After initial breath holding, when the victim's airway lies below the liquid's surface, an involuntary period of laryngospasm is triggered by the presence of liquid in the oropharynx or larynx. At this time, the victim is unable to breathe in air, causing oxygen depletion and carbon dioxide retention. As the oxygen tension in blood drops further, laryngospasm releases, and the victim gasps, hyperventilates, possibly aspirating variable amounts of liquid. This leads to further hypoxemia.

Lunetta et al reviewed the autopsies of 578 individuals who had apparently drowned and found evidence of water in the lungs of 98.6% of those studied. As they noted, active ventilation while submerged is required to aspirate water, as water does not passively flow into the lungs once the victim is dead.[7]

Depending upon the degree of hypoxemia and resultant acidotic change in acid-base balance, the person may develop myocardial dysfunction and electrical instability, cardiac arrest, and CNS ischemia.[8] Asphyxia leads to relaxation of the airway, which permits the lungs to take in water in many individuals, although most patients aspirate less than 4 mL/kg of fluid.

Fluid aspiration of at least 11 mL/kg is required for alterations in blood volume to occur, and aspiration of more than 22 mL/kg is required before significant electrolyte changes develop. Ingestion of large volumes of freshwater, rather than aspiration, is the likely cause of clinically significant electrolyte disturbances, such as hyponatremia, in children after drowning.

Approximately 10-15% of individuals maintain tight laryngospasm until cardiac arrest occurs and inspiratory efforts have ceased. These victims do not aspirate any appreciable fluid (previously referred to as "dry drowning") (see the chart below).

Mechanism of hypoxia in submersion injury. Mechanism of hypoxia in submersion injury.

In young children suddenly immersed in cold water (< 20°C), the mammalian diving reflex may occur and produce apnea, bradycardia, and vasoconstriction of nonessential vascular beds with shunting of blood to the coronary and cerebral circulation.

Pulmonary effects

The target organ of submersion injury is the lung. Aspiration of as little as 1-3 mL/kg of fluid leads to significantly impaired gas exchange. Injury to other systems is largely secondary to hypoxia and ischemic acidosis. Additional CNS insult may result from concomitant head or spinal cord injury. The period of hypoxia/hypoxemia is initially limited to the duration of hypopnea or apnea and may resolve with initial rescue efforts. 

Patients with prolonged hypoxic episodes are prone to alveolar fluid aspiration resulting in vagally mediated pulmonary vasoconstriction, hypertension, and fluid-induced bronchospasm. Freshwater moves rapidly across the alveolar-capillary membrane into the microcirculation. Freshwater is considerably hypotonic relative to plasma and causes disruption of alveolar surfactant. Destruction of surfactant produces alveolar instability, atelectasis, and decreased compliance, with marked ventilation/perfusion (V/Q) mismatching. As much as 75% of blood flow may circulate through hypoventilated lungs.

Saltwater, which is hyperosmolar, increases the osmotic gradient and therefore draws fluid into the alveoli, diluting surfactant (surfactant washout). Protein-rich fluid then exudes rapidly into the alveoli and pulmonary interstitium. Compliance is reduced, the alveolar-capillary basement membrane is damaged directly, and shunting occurs. This results in rapid development of serious hypoxia.

The distinction between submersion fluid type is primarily academic and mostly connotes epidemiologic significance. Hypoxia serves as the primary insult and, with alveolar aspiration, culminates in surfactant disruption, alveolar collapse and derecruitment, intrapulmonary shunting, increased pulmonary vascular resistance, and ventilation-mismatch. These processes result in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS).

Pulmonary hypertension may be exacerbated by inflammatory mediator release. In a minor percentage of patients, aspiration of vomitus, sand, silt, stagnant water, and sewage may result in occlusion of bronchi, bronchospasm, pneumonia, abscess formation, and inflammatory damage to alveolar capillary membranes.

Postobstructive pulmonary edema following laryngospasm and hypoxic neuronal injury with resultant neurogenic pulmonary edema may also occur. ARDS from altered surfactant effect and neurogenic pulmonary edema often complicate management.

Commonly, these edematous, noncompliant lungs may be further compromised by ventilator-associated lung injury (VALI). Newer modes of ventilation, including high-frequency oscillatory ventilation and airway pressure release ventilation, or an open-lung approach that limits tidal volumes to 6-8 mL/kg while using positive end-expiratory pressure (PEEP) to support optimal respiratory compliance, can help support oxygenation and ventilation with less risk of VALI than is associated with older methods of ventilation.

Pneumonia is a rare consequence of submersion injury and is more common with submersion in stagnant warm and fresh water. Uncommon pathogens, including Aeromonas, Burkholderia, and Pseudallescheria, cause a disproportionate percentage of cases of pneumonia. Because pneumonia is uncommon early in the course of treatment of submersion injuries, the use of prophylactic antimicrobial therapy has not proven to be of any benefit.

Chemical pneumonitis is a more common sequela than pneumonia, especially if the submersion occurs in a chlorinated pool or in a bucket containing a cleaning product.

Central nervous system effects

Hypoxic-ischemic brain injury is a foreboding sequelae of asphyxial cardiac arrest associated with drowning. The degree of CNS injury remains the major determinant of subsequent survival and long-term morbidity in cases of drowning. Two minutes after immersion, a child will lose consciousness. Irreversible brain damage usually occurs after 4-6 minutes. Most children who survive are discovered within 2 minutes of submersion. Most children who die are found after 10 minutes.

The areas of high risk in the brain are the metabolically active subcortical tissues and those with watershed perfusion. Global brain injury occurs in cases of hypoxemia and low-flow states resulting in energy failure, lipid peroxidation, free radical production, inflammatory processes, and release of excitotoxic neurotransmitters. Neuronal and glial functions are disrupted. Asphyxial cardiac arrest results in the development of microinfarctions as well as selective neuronal injury.[9, 10]

Primary CNS injury is initially associated with tissue hypoxia and ischemia. If the period of hypoxia and ischemia is brief or if the person is a very young child who rapidly develops core hypothermia, primary injury may be limited, and the patient may recover with minimal neurologic sequelae, even after more prolonged immersion.

In contrast, drowning that is associated with prolonged hypoxia or ischemia is likely to lead to both significant primary injury and secondary injury, especially in older patients who cannot rapidly achieve core hypothermia. Sources of secondary injury include the following:

  • Reperfusion
  • Sustained acidosis
  • Cerebral edema
  • Hyperglycemia
  • Release of excitatory neurotransmitters
  • Seizures
  • Hypotension
  • Impaired cerebral autoregulation

Although cerebral edema is a common consequence of prolonged submersion (or submersion followed by prolonged circulatory insufficiency), retrospective reviews and animal studies have not demonstrated any benefit from the use of intracranial pressure monitoring with diffuse axonal injury. However, as submersion injuries may be associated with trauma (especially to the head, neck, and trunk), focal or persistent neurologic deficit may indicate mass lesions or other injury amenable to surgical intervention.

Autonomic instability (diencephalic/hypothalamic storm) is common following severe traumatic, hypoxic, or ischemic brain injury. These patients often present with signs and symptoms of hyperstimulation of the sympathetic nervous system, including the following:

  • Tachycardia
  • Hypertension
  • Tachypnea
  • Diaphoresis
  • Agitation
  • Muscle rigidity

Autonomic instability has also been found to present as takotsubo stress-induced cardiomyopathy, with associated electrocardiographic changes, apical ballooning on echocardiogram, and elevated serum troponin levels.[11]

Seizures may be the result of acute cerebral hypoxia, but they may also be inciting events that lead to loss of consciousness and inability to protect the airway.

Cardiovascular effects

Drowning may result in an acute asphyxial cardiac arrest, which emanates from hypoxemia that precedes the development of ischemia. This scenario results from initial cessation of gas exchange followed by worsening hypoxia and eventual cardiac arrest. Hypoxemia is the overriding insult.

Hypovolemia may be due to fluid losses from increased capillary permeability. Profound hypotension may take place during and after the initial resuscitation period, especially when rewarming is accompanied by vasodilatation. It is important to remain cognizant that many patients present with hypothermia due to prolonged submersion times rather than true cold-water submersion.

Myocardial dysfunction may result from ventricular dysrhythmias, pulseless electrical activity (PEA), and asystole due to hypoxemia, hypothermia, acidosis, or electrolyte abnormalities (less common). In addition, hypoxemia may directly damage the myocardium, decreasing cardiac output.

Pulmonary hypertension may result from the release of pulmonary inflammatory mediators, increasing right ventricular afterload and thus decreasing both pulmonary perfusion and left ventricular preload. However, although cardiovascular effects may be severe, they are usually transient, unlike severe CNS injury.

Primary arrhythmias, including long-QT syndromes (particularly type I) and catecholaminergic polymorphic ventricular tachycardia (CPVT), may predispose patients to fatal arrhythmias during swimming. Sudden, severe cardiovascular collapse in otherwise healthy patients with brief, witnessed immersion may be the result of existing cardiac conduction defects and may not represent secondary effects of immersion injury.[12] Swimming may serve as an arrhythmogenic trigger and result in the diving reflex, which can lead to autonomic instability. The diving reflex is elicited by contact of the face with cold water and consists of breath-holding, bradycardia, and intense peripheral vasoconstriction. The exertion associated with swimming may additionally result in predisposition to syncopal events.

Infection

Infection in the sinuses, lungs, and CNS, as well as other less common sites, may result from unusual soil and waterborne bacteria, amebas, and fungi, including Pseudallescheria boydii and Scedosporium apiospermum,Naegleria, Balamuthia, as well as Burkholderia and Aeromonas organisms, and newly discovered human pathogens (Francisella philomiragia).[6, 13, 14, 15, 16, 17, 18, 19] These infections are usually insidious in onset, typically occurring more than 30 days after the initial submersion injury. P boydii‒complex infections are difficult to treat and are often fatal.[15, 20, 21]

Several investigators have suggested that the finding of evidence of seawater organisms, such as bioluminescent bacteria and plankton DNA, or normal inhabitants of the trachea in the bloodstream may be utilized as an additional indicator to support the conclusion of death by drowning in bodies discovered in aquatic environments.[22, 23]

Other effects

The clinical course may be complicated by multiorgan system failure resulting from prolonged hypoxia, acidosis, rhabdomyolysis, acute tubular necrosis, or the treatment modalities. Disseminated intravascular coagulation (DIC), hepatic and renal insufficiency, metabolic acidosis, and GI injuries must be considered and appropriately managed.

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Prognosis

Patients who are alert or mildly obtunded at presentation have an excellent chance for full recovery. Patients who are comatose, those receiving CPR at presentation to the emergency department (ED), or those who have fixed and dilated pupils and no spontaneous respirations have a poor prognosis. In a number of studies, 35-60% of individuals needing continued CPR on arrival to the ED die, and 60-100% of survivors in this group experience long-term neurologic sequelae.

Pediatric studies indicate that mortality is at least 30% in children who require specialized treatment for drowning in the pediatric intensive care unit (PICU). Severe brain damage occurs in an additional 10-30%.

The neuroprotective effects of cold-water drowning are poorly understood. Intact survival of comatose patients after cold-water submersion is still quite uncommon.

Hypothermia profoundly decreases the cerebral metabolic rate, but neuroprotective effects seem to occur only if the hypothermia occurs at the time of submersion and only if very rapid cooling occurs in water with a temperature of less than 5°C (eg, if the individual broke through ice into the water).

Morbidity and death from drowning are caused primarily by laryngospasm and pulmonary injury, resulting hypoxemia and acidosis, and their effects on the brain and other organ systems. A high risk of death exists secondary to the subsequent development of acute respiratory distress syndrome (ARDS).

The adult mortality rate is difficult to quantify because of poor reporting and inconsistent record keeping. Thirty-five percent of immersion episodes in children are fatal; 33% of episodes result in some degree of neurologic impairment, with 11% resulting in severe neurologic sequelae.

Anecdotal reports of survival are noted in children with moderate hypothermic submersion (core temperature < 32°C), but most persons experiencing cold-water submersion do not develop hypothermia rapidly enough to decrease cerebral metabolism before severe, irreversible hypoxia and ischemia occur.

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Patient Education

Prevention strategies are of paramount importance. Community education is vital in promoting water safety, injury prevention, and CPR initiatives. Unfortunately, community activism often occurs only following a tragic death or injury.

Toddlers must not be allowed near bathrooms or buckets of water without immediate adult supervision. Children must never swim alone or unsupervised, and children younger than 4 years and any children who are unable to swim must be closely monitored by a responsible adult. Adults must be well aware of their own and their children's swimming limits.

Appropriate barriers must be used around pools, wading pools, and other water-containing devices at home. The US Consumer Product Safety Commission has published model regulations regarding pool fencing. Homeowners can stress that all caregivers know CPR, have immediate access to a poolside phone, and ensure their children know how to call 911. Most pool-related drownings occur within the first 6 months of pool exposure. Additionally, the absence of proper pool fencing is reported to increase the odds of pool-related drowning by three to fivefold.[28]

Children must be taught safe conduct around water and during boating and jet- or water-skiing. Use of alcohol or other recreational drugs is not appropriate when swimming or engaging in other water sports, as well as when operating or riding in motorized watercraft. Appropriate boating equipment should be used, including personal flotation devices, and all boaters must understand weather and water conditions.

Parents are strongly urged to learn CPR and water safety training in case rescue and resuscitation are needed. A 1990 study found that 86% of pool owners supported voluntary CPR training, while 40% of those surveyed supported mandatory training.[61] The American Academy of Pediatrics updated the policy statement in 2010, focusing on water safety as well as drain-entrapment hazards, dangers of inflatable pools, and benefits of swimming lessons.[62]

For patient education information, see the Public Health Center and Environmental Exposures and Injuries Center, as well as Cardiopulmonary Resuscitation (CPR) and Drowning.

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Contributor Information and Disclosures
Author

G Patricia Cantwell, MD, FCCM Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical Care Medicine, University of Miami Leonard M Miller School of Medicine/ Holtz Children's Hospital, Jackson Memorial Medical Center; Medical Director, Palliative Care Team, Holtz Children's Hospital; Medical Manager, FEMA, South Florida Urban Search and Rescue, Task Force 2

G Patricia Cantwell, MD, FCCM is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Michael J Verive, MD, FAAP Pediatrician, UP Health System Portage

Michael J Verive, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, Society for Pediatric Sedation

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, Education Officer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H Director, PENN Travel Medicine; Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania, University of Pennsylvania School of Medicine

William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center

Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

James Martin, MD Fellow, Department of Emergency Medicine, Division of Hyperbaric Medicine, Hospital of the University of Pennsylvania

Disclosure: Nothing to disclose.

Robert L Norris, MD Professor, Department of Surgery, Chief, Division of Emergency Medicine, Stanford University Medical Center

Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM Professor of Emergency Medicine, Education Officer, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine; Medical Director, Fast Track, Department of Emergency Medicine

Suzanne Moore Shepherd is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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