eMedicine Specialties > Emergency Medicine > Environmental

Near Drowning

Author: Michael J Verive, MD, Director, Pediatric Intensive Care, Department of Pediatric Critical Care, Mount Sinai Hospital; Program Director, Pediatric Intensive Care, Hope Children's Hospital
Contributor Information and Disclosures

Updated: Apr 29, 2009

Introduction

Background

Submersion injuries are a significant cause of death and disability in children, second only to unintentional trauma. At least one third of survivors sustain moderate to severe neurologic sequelae. Although no uniform classification for submersion injuries is noted, drowning is usually defined as death from asphyxia within 24 hours of submersion in water. Near drowning refers to survival (even if temporary) beyond 24 hours after a submersion episode.

Submersion injuries may be further classified as cold-water or warm-water injuries. 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. Some references include very-cold-water drowning, which refers to submersion in water at temperatures of 5°C or less.

Additional classification may include the type of water in which the submersion occurred, such as freshwater and salt-water submersion injury. However, the distinction between freshwater and salt-water submersion injury is primarily academic because initial treatment is not affected by water type.

Pathophysiology

Submersion injury occurs when a person is submerged in water, attempts to breathe, and either aspirates water (wet drowning) or has laryngospasm without aspiration (dry drowning). Although most patients with submersion injury have aspirated a small amount of water or gastric contents into their lungs, approximately 10-15% of patients have become asphyxiated without evidence of aspiration. The most important contributory factors to morbidity and mortality from near drowning are hypoxemia and a decrease in oxygen delivery to vital tissues. The pathophysiology of near drowning is intimately related to the multiorgan effects of hypoxemia. CNS damage may occur because of hypoxemia sustained during the drowning episode (primary injury) or may result from ongoing pulmonary injury, reperfusion injury, or multiorgan dysfunction (secondary injury), particularly with prolonged tissue hypoxia.



Although differences observed between freshwater and salt-water aspirations in electrolyte and fluid imbalances are frequently discussed, they are rarely of any clinical significance for people who have experienced near drowning. Most patients have fluid aspiration of less than 4 mL/kg. 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, rather than aspiration, is more likely to cause clinically significant electrolyte imbalances, including hyponatremia from ingestion of large volumes of fresh water (especially in children).

CNS effects

CNS injury remains the major determinant of subsequent survival and long-term morbidity in cases of near drowning. 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. However, submersion injuries that are associated with prolonged hypoxia or ischemia are likely to lead to both significant primary injury and secondary injury from reperfusion, sustained acidosis, cerebral edema, hyperglycemia, release of excitatory neurotransmitters, seizures, hypotension, and impaired cerebral autoregulation, especially in older patients who cannot rapidly achieve core hypothermia.

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, often presenting with signs and symptoms of hyperstimulation of the sympathetic nervous system (including tachycardia, hypertension, tachypnea, diaphoresis, agitation, muscle rigidity).

CNS infection, an uncommon but serious complication of near drowning, may result from unusual soil and waterborne bacteria and fungi, including Pseudallescheria boydii and Scedosporium apiospermum. These infections are usually insidious in onset, typically occurring more than 30 days after the initial submersion injury.

Pulmonary effects

Fluid aspiration of as little as 1-3 mL/kg can result in significantly impaired gas exchange, primarily secondary to altered surfactant function. Freshwater is considerably hypotonic relative to plasma and causes disruption of alveolar surfactant. Salt water, which is hyperosmolar, increases the osmotic gradient and therefore draws fluid into the alveoli, diluting surfactant (surfactant washout).

Altered surfactant volume, function, or both result in atelectasis and pronounced injury to the alveoli-capillary unit, resulting in lower functional residual capacity and pulmonary edema. Acute respiratory distress syndrome (ARDS) from altered surfactant function and neurogenic pulmonary edema is a common complication in survivors of submersion injury. Increased airway resistance secondary to plugging of the patient's airway with debris, as well as release of inflammatory mediators that result in vasoconstriction, may impair gas exchange.

Ventilator-associated lung injury (VALI) can further compromise noncompliant, edematous lung tissue. 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 cc/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. As with CNS infections, 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.

Cardiovascular effects

Hypovolemia is primarily due to fluid losses from increased capillary permeability. Profound hypotension may occur during and after the initial resuscitation period, especially when rewarming is accompanied by vasodilatation. 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.

Other effects

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

Frequency

United States

According to data from the 1997 National Center for Health Statistics, drowning is the second leading cause of injury-related deaths in children aged 1-14 years.1 In California, Arizona, and Florida, it is the number one cause of injury-related death. 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. The overall drowning and submersion injury death rate was 1.93 per 100,000 people for all age groups in 1995. Peak incidence of 3.22 per 100,000 injury deaths occurred in children younger than 4 years.

Mortality/Morbidity

More than 1500 children die in the United States each year from submersion injuries. For every drowning death in this country, an estimated 4 additional hospitalizations and 14 emergency department (ED) visits are due to submersion injuries. Approximately 1 in 8 males and 1 in 23 females experience some form of water-associated event but never seek medical attention.

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.

As early resuscitation is associated with improved outcomes, many studies have attempted to determine clinical, laboratory, or other variables to identify which patients would benefit from resuscitative efforts. Although no individual characteristics have been found to predict survivability, the Orlowski score has been found to identify the likelihood of neurologically intact survival. In using the Orlowski score, 1 point is given for each item; scores of 2 or less are associated with a 90% likelihood of complete recovery, and submersion-injury patients with scores of 3 or more have only a 5% chance of survival. The items in the Orlowski score are as follows:

  1. Age 3 years or older
  2. Submersion time of more than 5 minutes
  3. No resuscitative efforts for more than 10 minutes after rescue
  4. Comatose on admission to the emergency department
  5. Arterial pH of less than 7.10

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.

Sex

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.

Age

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.

Clinical

History

All aspects leading to the near-drowning episode should be determined. Rarely does a patient present with the classic "Hollywood scenario" of a novice swimmer stranded in water, frantically struggling and flapping his or her arms in desperation. Experienced snorkelers, for example, may experience syncope secondary to hypoxia after hyperventilating to drive off carbon dioxide, and deep-water divers may succumb to "shallow-water blackout" as they ascend.

Most persons are found after having been submerged in water for an unobserved period. Witnessed events may include experienced swimmers not resurfacing after a dive. Relevant factors include submersion time, associated trauma, drug or alcohol ingestion, type of water, amount of water contamination, water temperature, and attempted rescue maneuvers.

Medical history must be obtained to look for a secondary cause or causes of drowning, including one or more of the following:

  • Trauma (unintentional and intentional)
  • Seizures
  • Cardiac disease, dysrhythmias, and syncope
  • Exhaustion and hypothermia
  • Hypoglycemia
  • Alcohol and drug use

Physical

The clinical presentations of people who experience submersion injuries widely vary.

  • Asymptomatic, especially if brief, witnessed submersions with immediate resuscitation
  • Symptomatic
    • Cough
    • Dyspnea
    • Wheezing
    • Hypothermia
    • Bradycardia or tachycardia
    • Vomiting, diarrhea, or both
    • Anxiety
    • Altered mental status
  • Cardiopulmonary arrest
    • Cardiac arrhythmias (ventricular tachycardia, ventricular fibrillation, bradycardia)
    • Apnea
  • Death

Causes

Drowning and near-drowning events must be thought of as primary or secondary events. Secondary causes of drowning include seizures, head or spine trauma, cardiac arrhythmias, hypothermia, alcohol and drug ingestion, syncope, apnea, hyperventilation, suicide, and hypoglycemia. Causes grouped by age of persons follows:

  • In infants younger than 1 year
    • Bathtubs and buckets of water are the most common means of drowning.
    • Child abuse should be considered in all such cases.
  • In children aged 1-5 years: Residential swimming pools are the most common venue.
  • In young adults aged 15-19 years
    • Submersion injuries occur in ponds, lakes, rivers, oceans, and other natural bodies of water.
    • Injuries are frequently associated with boating, alcohol, or both.

More on Near Drowning

Overview: Near Drowning
Differential Diagnoses & Workup: Near Drowning
Treatment & Medication: Near Drowning
Follow-up: Near Drowning
References

References

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Further Reading

Keywords

near drowning, submersion injuries, water accidents, drowning, asphyxia, accidental drowning, aspiration, near-drowning accident, warm-water injuries, cold-water injuries, freshwater injury, salt-water injury, hyponatremia, hypoxia, ischemia, reperfusion, sustained acidosis, cerebral edema, hyperglycemia, hypothermia, ischemic brain injury, tachycardia, hypertension, tachypnea, atelectasis, acute respiratory distress syndrome, ventilator-associated lung injury, VALI, pneumonia, hypovolemia, rhabdomyolysis, acute tubular necrosis, disseminated intravascular coagulation, DIC, metabolic acidosis, GI injuries, ventricular tachycardia, ventricular fibrillation, bradycardia, seizures, head trauma, spine trauma, cardiac arrhythmias, hypothermia, alcohol ingestion, drug ingestion, syncope, apnea, hyperventilation, suicide, treatment, diagnosis

Contributor Information and Disclosures

Author

Michael J Verive, MD, Director, Pediatric Intensive Care, Department of Pediatric Critical Care, Mount Sinai Hospital; Program Director, Pediatric Intensive Care, Hope Children's Hospital
Michael J Verive, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Medical Association, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

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