ISSN 2398-2969      

Drowning/near drowning

icanis

Synonym(s): Immersion Syndrome, Submersion Injury, Secondary Drowning


Introduction

  • Drowning is defined as death from asphyxia while submerged or within 24 hours of submersion.
  • Immersion syndrome results in immediate death upon contact with cold water.
  • Submersion describes a patient who experiences some water-related distress sufficient to require medical care. Submersion injuries can result in one of three outcomes:
    • Death within 24 hours of submersion (drowning)
    • Temporary survival (near drowning), or
    • Water rescue (save).
  • New recommendations by the American Heart Association include the use of the term submersion victim instead of near-drowning victim.
  • Secondary drowning refers to death from complications of submersion more than 24 hours after submersion.

Pathogenesis

Etiology

  • The majority of submersion accidents (~90%) result in pulmonary fluid aspiration.
  • The saline content of the aspirated fluid plays a role in the pathology produced.
    • Fresh water aspiration:
      • Fresh water dilutes surfactant and creates alveolar collapse and atelectasis. This increases ventilation-perfusion mismatch Ventilation-perfusion mismatching and intrapulmonary shunt, which results in hypoxemia.
      • Water is rapidly absorbed from the alveoli into the bloodstream, expanding the intravascular free water volume.
      • This volume expansion does not typically cause electrolyte imbalances.
    • Salt water aspiration:
      • The presence of salt water in alveoli does not disturb surfactant production by Type II pneumocytes or inactivate surfactant. Therefore, atelectasis is not a main feature of salt water aspiration.
      • The increased osmolarity of salt water causes fluid movement from the intravascular space into the alveoli, which can result in decreased circulating blood volume, hypotension, alveolar flooding, and hypoxemia.
  • Submersion accidents can also occur without aspiration of significant volumes of water (~10% of the time).
    • Minute amounts of water drawn into the mouth may cause severe laryngospasm. Hypoxemia may result from persistent laryngospasm. Further attempts to breathe may result in negative pressure pulmonary edema Lung: pulmonary edema secondary to laryngospasm and glottis closure.

Predisposing factors

General
  • Breakdown of safety precautions:
    • Unlocked or malfunctioning safety fences.
  • Climate:
    • Periods of warm weather during the winter may increase the chances of falling through ice covered lakes or rivers.
  • Pre-existing illness:
  • Poor judgement.
  • Lapse in supervision.
  • Inability to swim.

Pathophysiology

  • In all submersion injuries, the sequence of events starts with panic and air hunger caused by breath holding.
  • Reflex inspiratory efforts cause the patient to swallow water into the stomach and small amounts into the lungs. The aspiration of water causes laryngospasm leading to asphyxia.
  • Loss of consciousness causes muscles to relax and allows water to enter into the lungs.
    • The presence of fresh water in the lungs results in loss of surfactant causing atelectasis Lung: atelectasis , intrapulmonary shunt and ventilation/perfusion mismatch Ventilation-perfusion mismatching , which ultimately lead to systemic hypoxemia.
    • The presence of salt water in the lungs results in fluid movement from the intravascular space into the alveoli, which can result in decreased circulating blood volume, hypotension, alveolar flooding, and hypoxemia.
  • Non-cardiogenic pulmonary edema can also result from alterations in pulmonary capillary permeability, increased pulmonary resistance due to airway obstruction from laryngospasm, bronchoconstriction, inhaled particulate matter, or inhaled gastric contents.
  • Evolving hypoxemia causes neuronal ischemic injury and eventually leads to circulatory collapse, myocardial damage, dysfunction of multiple organ systems, and further ischemic brain injury.
    • The detrimental effects on the cardiovascular system are primarily due to hypoxemia rather than hypovolemia or hypervolemia.

Timecourse

  • Acute - animals can be dead within minutes from the time of submersion.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Harries M (2003) ABC of resuscitation: Near drowning. Brit Med J 327 (7427), 1336-1338 PubMed.
  • Bierens J J L M, Knape J T A & Gelissen H P M M (2002) Drowning. Current Opinion in Crit Care (6), 578-586 PubMed.
  • Grenfell R (2002) Drowning management and prevention. Australian Family Physician 31 (12), 990-993 PubMed.
  • Ibsen L M & Koch T (2002) Submersion and asphyxial injury. Crit Care Med 30 (11), S402-408 PubMed.
  • Sachdeva R C (1999) Near Drowning. Critical Care Clinics 15 (2), 281-296 PubMed.

Other sources of information

  • Macintire D K, Drobatz K J, Haskins S C, Saxon W D (2005) Near Drowning. In: Manual of Small Animal Emergency and Critical Care Medicine. Eds D K Macintire, K J Drobatz, S C Haskins, and W D Saxon. Lippincott Williams and Wilkins, Philadelphia, PA. pp 408-409.
  • Powell L L (2004) Accidental Drowning and Submersion Injury. In:T extbook of Respiratory Disease in Dogs and Cats.Ed L G King. Saunders, St. Louis, MO. pp 484-486.
  • McCullough S (2002) Near Drowning. In: The Veterinary ICU Book. Eds W E Wingfield and M Raffe. Teton New Media, Jackson Hole, WY. pp 577-581.
  • Martin L (2001) Near Drowning. In: Critical Care and Emergency Medicine Veterinary Secrets. Ed W E Wingfield. Hanley & Belfus, Philadelphia, PA. pp 187-189

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