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Immersion Pulmonary Edema

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Other Names

  • Swimming-Induced Pulmonary Edema (SIPE)
  • Immersion Pulmonary Edema (IPE)

Background

  • This page refers to Immersion Pulmonary Edema (IPE), a phenomenon where pulmonary edema in swimmers and divers without an aspiration event.

History

  • First reported in scuba divers in 1981[1]

Epidemiology

  • Prevalence
    • Estimated to be about 1.8% to 5% in experienced combat swimmers[2]
    • In one study of open sea swimmers, 1.8% of young healthy men developed IPE (need citation)
    • In a survey of 1250 divers, 1.1% of respondents had symptoms consistent with IPE[3]
    • In a survey of USA triathlon participants, 1.4% of respondents recounted symptoms consistent with IPE[4]
  • More than 20 cases are reported annually among US Navy combat swimmers[5]

Pathophysiology

  • General
    • Overall, not well described in the literature
    • Presents with symptoms similar to pulmonary edema: cough, dyspnea, hemoptysis, without a history of aspiration
    • Similar to exertion-related pulmonary edema see in racehorses
    • Can occur in individuals without having pre-existing cardiac conditions

Etiology

  • Proposed mechanism
    • Stress failure of pulmonary capillaries due to redistribution of circulating fluid in central circulation
    • Increased pulmonary vasculature blood volume from water immersion, cold exposure and exercise
    • Reversible myocardial dysfunction may also play a role
  • Immersion
    • Increases cardiac output
    • Doubles pulmonary artery pressure
    • Blood is also redistributed from extremities to the thorax
  • Continuous negative airway pressure (breathing)
    • Immersed person breathes with continuous negative airway pressure equal to the vertical distance between the water surface and the lung centroid
    • Raised pulmonary capillary pressures and negative airway pressures set the stage for fluid transudation into the alveoli
    • However, usually additional factors are required to precipitate frank pulmonary edema.
  • Warm water immersion[4]
    • Hydrostatic effects of water compression immediately pushes as much as 700 mL of blood centrally
    • Increases cardiac output, heart size, cardiac filling pressures[6]
  • Cold water
    • Leads to vasoconstriction, increases pulmonary capillary pressure
  • Scuba diving
    • Ambient hydrostatic pressure increases at depth (e.g. 30 m of seawater, pressure is 4 bar)
    • This is less than the inspired O2 from the open circuit scuba system, leading to vasoconstriction
    • During ascent, head is above lung centroid with continuous negative airway pressure which can worsen IPE

Associated Conditions

  • Most patients with IPE are otherwise healthy
    • In one survey of patients, only 24% had an identifiable cardiopulmonary risk factor[7]

Risk Factors

  • Demographic
  • Sports
  • Swimming/ water factors
    • Strenuous swimming
    • History of IPE[2]
    • Cold water[9]
  • Occupational
    • Military/ Combat swimmers (e.g. Navy Seals)
  • Cardiopulmonary
  • Medications
  • Other
    • Overhydration or excessive fluid intake before swimming[11][12]
    • Physically trained individuals such as endurance athletes may be more vulnerable for unclear reasons[13]

Differential Diagnosis

Differential Diagnosis

Differential Diagnosis Dive Medicine

Clinical Features

  • History
    • Patients will not have a history of aspiration or laryngospasm
    • Onset is within 10 to 30 minutes of immersion
    • 90% have Cough, dyspnea and/or sputum production after cold water immersion[14]
    • Hemoptysis (50%)
    • Labored breathing
    • Frothy sputum
    • Weakness
    • Chest discomfort
    • Orthopnea
    • Loss of consciousness
    • Dizziness
  • Physical Exam
    • Hypoxia may be present (SpO2 < 92%)
    • Rales or ronchi may be heard
    • Heart sounds may include S3 or mitral rergutation
    • Bilateral inspiratory crackles

Evaluation

Radiographs

  • Standard Chest Radiograph
    • Often normal within 12-18 hours of the event
    • Findings include interstitial pulmonary edema, alveolar filling process
    • Also seen are cephalization, kerley B lines, ground glass opacities, infiltrates

CT

  • More sensitive than chest radiograph
    • However not needed to make diagnosis
  • Findings
    • Pleural effusion
    • Ground glass opacities

EKG

  • Findings
    • ST segment changes

Echocardiogram

  • Findings
    • Global or segmental hypokinesia
    • Reduced LV EF
    • LVH

Pulmonary Function Testing

  • Findings consistent with restrictive changes
    • Reduced FVC
    • Reduced FEV1[15]
    • Normal FEV1/FVC ratio
    • Reduced absolute FVC
    • Lower FEF25%-75%
    • Reduced diffusion capacity[16]

Laboratory

  • Arterial Blood gas
    • If obtained, ABG may reveal A-a gradient > 30
  • Cardiac biomarkers
    • May be elevated
  • Other labs which may be elevated
    • Copeptin
    • Brain natriuretic peptide (BNP)
    • Ischemia-modified albumin

Classification

  • Currently, there is no accepted classification system

Management

Nonoperative

  • Management is primarily supportive care
    • Remove from water
    • Remove cold clothing, place in warm environment
    • Remove wet suit if present
    • Consider Albuterol
  • Supplemental oxygen
    • Keep SpO2 > 92%
    • More severe cases may require invasive ventilation, hemodynamic support
  • Duration
    • Typically self limited, lasts 24-48 hours
  • Sildenafil[17]
    • Shown to decrease Mean Pulmonary Arterial Pressure (MPAP) and Pulmonary Artery Wedge Pressure (PAWP)
    • May prevent progression of pulmonary edema
    • Dosing is uncertain
  • Nifedipine
    • Used to prevent recurrence
    • No data to support at this time

Prevention

  • Prevention is key
    • Treat underlying conditions (i.e. LV dysfunction, hypertension)
    • Swim in tepid water
    • Avoid tight wet suits, hyperhydration
  • Diuretic
    • May help prevent IPE in some athletes
    • May also affect performance in other activities such as biking and running in triathlons
  • Cardiopulmonary risk factors
    • Testing/ screening should be performed in patients with risk factors
    • If present, avoid long swimming sessions

Rehab and Return to Play

Rehabilitation

  • No clear guidelines

Return to Play/ Work

  • Self limited condition typically resolves in 24 to 48 hours
    • Athletes should be seen by a physician prior to returning to swimming or diving

Complications and Prognosis

Prognosis

  • Recurrence
    • IPE tends to recur on exposure to similar conditions
    • Even in individuals without pre-existing risk factors[18]
    • Low lung volumes predict recurrence, but not severity[19]

Complications

  • Unknown

See Also

References

  1. ↑ Wilmshurst PT, Nuri M, Crowther A, et al. Cold-induced pulmonary edema in scuba divers and swimmers and subsequent development of hypertension. Lancet. 1989;1(8629):62–65.
  2. ↑ 2.0 2.1 Volk, Charles, et al. "Incidence and impact of swimming-induced pulmonary edema on Navy SEAL candidates." Chest 159.5 (2021): 1934-1941.
  3. ↑ Pons M, Blickenstorfer D, Oechslin E, et al. Pulmonary edema in healthy persons during scuba diving and swimming. Eur Respir J. 1995;8:762–767.
  4. ↑ 4.0 4.1 4.2 4.3 Miller CC III, Calder-Becker K, Modave F. Swimming-induced pulmonary edema in triathletes. The American Journal of Emergency Medicine. 2010;28(8):941–946.
  5. ↑ Mahon RT, Kerr S, Amundson D, et al. Immersion pulmonary edema in special forces combat swimmers. Chest. 2002;122:383–384.
  6. ↑ Arborelius, M., et al. "Hemodynamic changes in man during immersion with the head above water." (1972).
  7. ↑ 7.0 7.1 Carter EA, Koehle MS. Immersion pulmonary edema in Female Triathletes. Pulmonary Medicine. 2011;2011:1–4.
  8. ↑ Hampson NB, Dunford RG. Pulmonary edema of scuba divers. Undersea Hyperbaric Med. 1997;24(1):29–33.
  9. ↑ Ludwig BB, Mahon RT, Schwartzman EL. Cardiopulmonary function after recovery from swimming-induced pulmonary edema. Clin J Sport Med. 2006 Jul;16(4):348-51.
  10. ↑ Boussuges A, Pinet C, Thomas P, et al. Haemoptysis after breathhold diving. European Respiratory Journal. 1999;13(3):697–699.
  11. ↑ Yoder JA, Viera AJ. Management of swimming-induced pulmonary edema. Am Fam Physician. 2004 Mar 1;69(5):1046, 1048-9.
  12. ↑ Weiler-Ravell, D., et al. "Pulmonary oedema and haemoptysis induced by strenuous swimming." Bmj 311.7001 (1995): 361-362.
  13. ↑ Casey H, Dastidar AG, MacIver D. Swimming-induced pulmonary edema in two triathletes: a novel pathophysiological explanation. J R Soc Med. 2014;107:450–452.
  14. ↑ Henckes A. Pulmonary oedema in scuba-diving: frequency and seriousness about a series of 19 cases. Annales Françaises D’anesthésie Et De Réanimation. 2008;27(9):694–699.
  15. ↑ Peacher DF, Pecorella SRH, Freiberger JJ, et al. Effect of hyperoxia on ventilation and pulmonary hemo- dynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema. J Appl Physiol. 2010;109:68e78.
  16. ↑ Thorsen E, Skogstad M, Reed JW. Subacute effects of inspiratory resistive loading and head-out water immersion on pulmonary function. Undersea Hyperb Med. 1999;26:137–141.
  17. ↑ Moon RE et al. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016; CIRCULATIONAHA.115.019464.
  18. ↑ Edmonds C, Lippmann J, Lockley S, et al. Scuba divers’ pulmonary edema: recurrences and fatalities. Diving Hyperb Med. 2012;42 (1):40–44.
  19. ↑ Kumar, Manish, and Paul D. Thompson. "A literature review of immersion pulmonary edema." The Physician and Sportsmedicine 47.2 (2019): 148-151.
Created by:
John Kiel on 26 July 2022 14:34:26
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Last edited:
29 July 2022 18:19:16
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