Decision Making in Emergency Critical Care

SECTION 12 - Environmental Critical Care


Samuel Gerson and Jose Evangelista III


The International Liaison Committee on Resuscitation defines drowning as primary respiratory impairment caused by submersion or immersion in liquid.1 Updated terminology separates the event into fatal or nonfatal drowning, discouraging the use of ambiguous terms such as near drowning or dry versus wet drowning.2 Worldwide, drowning accounts for an estimated 388,000 annual deaths, represents 7% of all injury-related fatalities, and is the leading cause of death among young males.3 In the United States, drowning causes roughly 10 fatalities per day and ranks fifth among leading causes of death from unintentional injury.4 It is estimated that for every drowning fatality, four nonfatal drowning victims are treated in an emergency department with more than 50% requiring hospital admission; this is compared to a 6% admission rate for all unintentional injuries.5


The major pathophysiologic event in drowning is hypoxia secondary to aspiration. Following submersion/immersion, the victim typically passes through the following stages within minutes6; breath holding → laryngospasm → aspiration → hypoxia with loss of consciousness and apnea → cardiac arrest. The clinical presentation of drowning results from dysfunction in multiple organ systems including the cardiovascular, pulmonary, and neurologic. As tissue hypoxia and acidemia increase, cardiac rhythm most often progresses from sinus tachycardia, to sinus bradycardia, to pulseless electrical activity (PEA), and eventually to asystole as the terminal event.7 Regardless of whether salt water or fresh water enters the lung, the resulting injuries are the same: surfactant washout and dysfunction, increased permeability of the alveolar–capillary membrane, decreased lung compliance, and ventilation/perfusion ratio mismatching from areas of unventilated dead space.8 Depending on the amount of fluid aspirated, pulmonary manifestations range from minor respiratory complaints to fulminant noncardiogenic pulmonary edema consistent with acute respiratory distress syndrome (ARDS).

Neurologic status of the drowning victim depends on the degree and duration of hypoxia prior to successful resuscitation and ranges from awake and alert to comatose in the acute setting.9 Irreversible brain injury develops within 4 to 10 minutes of tissue hypoxia at normal body temperature, followed by cerebral edema and elevated intracranial pressure (ICP).10 Hypothermic exposure at the time of drowning may be protective by reducing cerebral oxygen consumption and delaying neuronal death for up to an hour or more.11 Permanent neurologic sequelae in survivors may vary from minor disorders in memory, movement, and coordination to a more devastating persistent vegetative or comatose state.9


During the primary response to a drowning incident, respondents should initiate cardiopulmonary resuscitation in a person submerged <60 minutes without clear signs of death.12 Because respiratory failure is the primary cause of cardiac arrest in drowning, resuscitation begins with rescue breaths or bag–valve–mask (BVM) ventilations in keeping with the traditional protocol of airway, breathing, and circulation (ABC).13 Providing supplemental oxygen at the highest flow rate available is a critical early action, preferably through a nonrebreather face mask at 15 L/min in the awake, alert patient. If passive measures fail to correct hypoxia, continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP) may be effective and prevent the need for invasive airway management.14However, early intubation and mechanical ventilation with positive end-expiratory pressure (PEEP) is indicated for worsening oxygenation despite noninvasive support or for deterioration of respiratory drive or neurologic status with a goal of maintaining oxygen saturation above 92%.8 While many drowning accidents involve trauma, cervical spine injuries are rare, and immobilization should only be implemented for cases in which head or neck injury is suspected.15

For drowning victims who suffer cardiac arrest, PEA or asystole is managed as per standard advanced cardiovascular life support (ACLS) algorithms. Prompt defibrillation is indicated for rare cases of ventricular fibrillation.16 As in all hypothermic cases, rewarming the patient to a core temperature above 32°C is essential to optimize resuscitation efforts and prevent dysrhythmias. While there is some debate regarding the duration of resuscitation, most experts agree that efforts should be halted when the patient is rewarmed and is asystolic >20 minutes.12

After initial stabilization is achieved and the primary survey completed, further evaluation typically includes chest radiography and arterial blood gas measurements. Lung ultrasound also provides a rapid and effective bedside tool to diagnose, quantify, and monitor pulmonary edema in drowning victims.17 In patients who remain unresponsive without a clear cause, toxic/metabolic investigation and head/neck imaging are warranted. Use of a validated grading system (See Literature Table for additional details) helps to guide intervention and disposition in the emergency department.13,18

  • Grade 1:No lung findings, normal arterial oxygenation → observation for 6 hours
  • Grade 2:Scattered pulmonary crackles, stabilized with low flow oxygen → admit for extended observation or discharge if signs of clinical improvement after 6 hours
  • Grades 3 to 6:Acute pulmonary edema with or without hypotension → ICU admission



In drowning victims who require invasive mechanical ventilation, guidelines recommended for ARDS patients (lung-protective ventilation) should be followed:19

  • Set tidal volumes <6 mL/kg
  • Adjust PEEP to optimize alveolar recruitment
  • Maintain low plateau pressures
  • Minimize suctioning to prevent hypoxia and elevated airway pressures
  • Do not attempt to wean prior to 24 hours on mechanical ventilation

Prophylactic antibiotics for pneumonia are advised in cases of exposure to polluted sources; however, they are not routinely indicated for the majority of drowning victims.20,21 Given the substantially increased risk for translocation of bacteria in the lung in cases of water aspiration (and lung injury), obtaining blood cultures early in the clinical course may be of significant clinical utility. Early respiratory cultures may have diminished utility and are not generally recommended. Glucocorticoids have not been proven to reduce pulmonary injury from drowning, but may be beneficial for bronchospasm poorly controlled by inhaled bronchodilators.20,22 Exogenous surfactant and inhaled liquid perfluorocarbon use remain controversial, but may be considered in cases that are refractory to standard therapy.23,24Finally, extracorporeal membrane oxygenation (ECMO) is indicated with severe ARDS when pulmonary exchange is inadequate to maintain oxygenation.25,26


In the hypotensive patient, conservative fluid management is recommended to avoid volume overload that could worsen cardiac and pulmonary function.27 Bedside echocardiography is a useful tool to monitor volume status, identify cardiogenic shock, and guide the use of cardioactive or vasopressor medications.28 Acute renal failure is uncommon but may result from prerenal (hypovolemia, shock) or renal (anoxic renal tubular injury, rhabdomyolysis) etiologies.29


Therapeutic hypothermia in drowning victims is neuroprotective and is supported by extrapolation from randomized clinical trials in cardiac arrest patients,30,31 and from case reports on drowning.25,32While initial resuscitation efforts may require rewarming of a hypothermic patient, core temperature should be maintained at 32°C to 34°C for 24 hours in comatose patients who regain spontaneous circulation. Tight control of blood glucose, arterial oxygenation, and carbon dioxide levels is essential to prevent increases in brain metabolism.33 Neurologic monitoring techniques—including EEG, MRI, and cerebral biomarkers—provide useful prognostic tools, but have not yet demonstrated an impact on clinical decision-making.34 Seizures are common after anoxic brain injury and warrant treatment with antiepileptic medications; however, prophylactic anticonvulsants are not currently proven or recommended in drowning victims.35 Finally, aggressive control of ICP in case reports of pediatric drowning has produced disappointing results and is not considered a management priority.36


In the United States, drowning ranks fifth among leading causes of death from unintentional injury.4 Management of the downing victim requires careful evaluation of pulmonary status with use of lung-protective strategies when mechanical ventilation is indicated, conservative fluid management, and consideration of ECMO support in severe cases.



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8.Gregorakos L, Markou N, Psalida V, et al. Near-drowning: clinical course of lung injury in adults. Lung. 2009;187:93–97.

9.Conn AW, Montes JE, Barker GA, et al. Cerebral salvage in near drowning following neurological classification by triage. Can Anaesth Soc J. 1980;27:201–210.

10.Smith ML, Auer RN, Siesjo BK. The density and distribution of ischemia brain injury in the rat following 2–10 min of forebrain ischemia. Acta Neuropathol. 1984;64(4):319–332.

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17.Laursen CB, Davidsen JR, Madsen PH. Utility of lung ultrasound in near-drowning victims. BMJ Case Rep. 2012;21:2012.

18.Szpilman D, Bierens JJ, Handley AJ, et al. Drowning. N Engl J Med. 2012;366(22):2102–2110.

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22.Towards evidence base emergency medicine: best BETs from the Manchester Royal Infirmary: corticosteroids in the management of near-drowning. Emer Med J. 2001;18:465–466.

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24.Gauger PG, Pranikoff T, Schreiner RJ, et al. Initial experience with partial liquid ventilation in pediatric patients with acute respiratory distress syndrome. Crit Care Med. 1996;24:16–22.

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27.Wiedemann HP, Wheeler AP, Bernad GR, et al. Comparison of two fluid management strategies in acute lung injury. N Engl J Med. 2006;354(24):2564–2575.

28.Perera P, Mailhot T, Riley D, et al. The Rush exam: rapid ultrasound in shock in the evaluation of the critically ill. Emerg Med Clin North Am. 2010;28(1):29–56.

29.Spicer ST, Quinn D, Nyi Nyi NN, et al. Acute renal impairment after immersion and near drowning. J Am Soc Nephrol. 1999;10:382–386.

30.Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurological outcome after cardiac arrest. N Engl J Med. 2002;346(8):549–556.

31.Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of- hospital cardiac arrest with induced hypothermia. M Engl J Med. 2002;346(8):557–563.

32.Hein OV, Triltsch A, von Buch C. Mild hypothermia after near drowning in twin toddlers. Crit Care. 2004;8(5):R353–R357.

33.Warner D, Knape J. Recommendations and consensus brain resuscitation in the drowning victim. In Bierens JJLM, ed. Handbook on Drowning: Prevention, Rescue, and Treatment. Berlin: Springer-Verlag; 2006:436–439.

34.Topjian AA, Berg RA, Bierens JJLM, et al. Brain resuscitation in the drowning victim. Neurocrit Care. 2012;17:441–467.

35.Abend NS, Topjian A, Ichord R, et al. Electroencephalographic monitoring during hypothermia after pediatric cardiac arrest. Neurology. 2009;72(22):1931–1940.

36.Dean JM, McComb JG. Intracranial pressure monitoring in severe pediatric near- drowning. Neurosurgery. 1981;9(6):627–630.