Swimming-induced pulmonary edema
Swimming induced pulmonary edema (SIPE) occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).[1]
SIPE usually occurs during heavy exertion in conditions of water immersion, such as swimming and diving. It has been reported in scuba divers,[2][3] apnea (breath hold) free-diving competitors[4][5] combat swimmers,[6][7] and triathletes.[1] The causes are incompletely understood at the present time.[1][8][9]
Signs and symptoms
As with other forms of pulmonary edema, the hallmark of SIPE is cough productive of pink, frothy or blood-tinged sputum. Symptoms include:
- Shortness of breath out of proportion to effort being expended.[1]
- Crackles, rattling or ‘junky’ feelings deep in the chest associated with breathing effort – usually progressively worsening with increasing shortness of breath.[1][6][7]
- Cough, usually distressing and productive of copious pink, frothy or blood-tinged sputum (hemoptysis)[1][2][3][4][5][6][7][8][9][10][11]
Risk factors
- Water immersion[9]
- Excessive pre-swim hydration[6]
- High blood pressure[1][3][10]
- Long course length in the case of triathlon (half ironman or greater)[1]
- Female gender[1][11]
- Antiplatelet agents such as aspirin and fish oil[1][5]
Mechanism
The mechanisms by which SIPE occurs are controversial, and likely multiple factors are required for the phenomenon to manifest.[1][8][9]
- Hydrostatic pressure from water immersion squeezes the extremities, and forces blood from the peripheral circulation (arms, legs) to the central circulation (heart, lungs, great vessels of the chest)[1][2][3][4][5][6][7][8][9][10][11]
- Cold water may cause peripheral vasoconstriction and other neuro-humoral changes that contribute to central shift of the blood volume[1][2][3][4][5][6][7][8][9][10][11]
- Wetsuits may add additional extrinsic compression to the extremities[1][6]
- Increased pressure somewhere in the pulmonary circulation (pulmonary artery hypertension, left heart diastolic dysfunction) leads to increased pressure gradient across the pulmonary capillaries[1][8][9]
SIPE is believed to arise from a “perfect storm” of some combination of these factors, which overwhelms the ability of the body to compensate, and leads to alveolar flooding.[1][8][9]
Prevention
With incidence reported to be in the range of 1-2 percent, most (greater than 98%) recreational swimmers do not appear to be at risk for SIPE.[1]
- Management of hypertension is likely to be important for hypertensive athletes. ACE inhibitors (particularly angiotensin II receptor antagonists) may be effective antihypertensive medications in this setting given their effect on diastolic relaxation, but rationale is theoretical and evidence of SIPE-related benefit is anecdotal.[12][13]
- Avoidance of excessive pre-swim hydration is advisable[8][9]
- Nifedipine[8] or sildenafil[14] could theoretically be beneficial due to their ability to modify pulmonary artery pressure, but any use for SIPE is investigational and these agents are not approved for this use.
Management
Management has generally been reported to be conservative, though deaths have been reported.[3]
- Removal from water[9]
- Observation[9]
- Diuretics and / or Oxygen when necessary[8]
- Episodes are generally self-limiting in the absence of other medical problems [8][9]
Epidemiology
SIPE is estimated to occur in 1-2% of competitive open-water swimmers, with 1.4% of triathletes,[1]1.8% of combat swimmers[7] and 1.1% of divers and swimmers[2] reported in the literature.
Research
Most of the medical literature on the topic comes from case series in military populations[6][7] and divers,[2][5][10][11] and an epidemiological study in triathletes.[1] A recent experimental study showed increased pulmonary artery pressure with cold water immersion, but this was done in normal subjects rather than in people with a history of SIPE.[15]
References
- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Miller III, Charles C.; Calder-Becker, Katherine; Modave, Francois (2010). "Swimming-induced pulmonary edema in triathletes". The American Journal of Emergency Medicine 28 (8): 941–6. doi:10.1016/j.ajem.2009.08.004. PMID 20887912.
- 1 2 3 4 5 6 Pons, M; Blickenstorfer, D; Oechslin, E; Hold, G; Greminger, P; Franzeck, UK; Russi, EW (1995). "Pulmonary oedema in healthy persons during scuba-diving and swimming". The European respiratory journal 8 (5): 762–7. PMID 7656948.
- 1 2 3 4 5 6 Henckes, A; Lion, F; Cochard, G; Arvieux, J; Arvieux, C (2008). "L'œdème pulmonaire en plongée sous-marine autonome : fréquence et gravité à propos d'une série de 19 cas" [Pulmonary oedema in scuba-diving: frequency and seriousness about a series of 19 cases]. Annales Françaises d'Anesthésie et de Réanimation (in French) 27 (9): 694–9. doi:10.1016/j.annfar.2008.05.011. PMID 18674877.
- 1 2 3 4 Liner, M. H.; Andersson, J. P. A. (2008). "Pulmonary edema after competitive breath-hold diving". Journal of Applied Physiology 104 (4): 986–90. doi:10.1152/japplphysiol.00641.2007. PMID 18218906.
- 1 2 3 4 5 6 Boussuges, A.; Pinet, C.; Thomas, P.; Bergmann, E.; Sainty, J-M.; Vervloet, D. (1999). "Haemoptysis after breath-hold diving". European Respiratory Journal 13 (3): 697–9. doi:10.1183/09031936.99.13369799. PMID 10232449.
- 1 2 3 4 5 6 7 8 9 Weiler-Ravell, D; Shupak, A; Goldenberg, I; Halpern, P; Shoshani, O; Hirschhorn, G; Margulis, A (1995). "Pulmonary oedema and haemoptysis induced by strenuous swimming". BMJ 311 (7001): 361–2. doi:10.1136/bmj.311.7001.361. PMC 2550430. PMID 7640542.
- 1 2 3 4 5 6 7 Adir, Y.; Shupak, A; Gil, A; Peled, N; Keynan, Y; Domachevsky, L; Weiler-Ravell, D (2004). "Swimming-Induced Pulmonary Edema: Clinical Presentation and Serial Lung Function". Chest 126 (2): 394–9. doi:10.1378/chest.126.2.394. PMID 15302723.
- 1 2 3 4 5 6 7 8 9 10 11 12 Koehle, Michael S; Lepawsky, Michael; McKenzie, Donald C (2005). "Pulmonary Oedema of Immersion". Sports Medicine 35 (3): 183–90. doi:10.2165/00007256-200535030-00001. PMID 15730335.
- 1 2 3 4 5 6 7 8 9 10 11 12 Yoder, JA; Viera, AJ (2004). "Management of swimming-induced pulmonary edema". American family physician 69 (5): 1046, 1048–9. PMID 15023003.
- 1 2 3 4 5 Wilmshurst, P; Nuri, M; Crowther, A; Webb-Peploe, MM (1989). "Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension". The Lancet 333 (8629): 62–5. doi:10.1016/S0140-6736(89)91426-8. PMID 2562880.
- 1 2 3 4 5 Coulange, M.; Rossi, P.; Gargne, O.; Gole, Y.; Bessereau, J.; Regnard, J.; Jammes, Y.; Barthélémy, A.; Auffray, J. P. (2010). "Pulmonary oedema in healthy SCUBA divers: new physiopathological pathways". Clinical Physiology and Functional Imaging 30 (3): 181–6. doi:10.1111/j.1475-097X.2010.00922.x. PMID 20141520.
- ↑ Little, W (2001). "Hypertensive pulmonary oedema is due to diastolic dysfunction". European Heart Journal 22 (21): 1961–4. doi:10.1053/euhj.2001.2665. PMID 11603900.
- ↑ Almuntaser, Ibrahim; Mahmud, Azra; Brown, Angie; Murphy, Ross; King, Gerard; Crean, Peter; Feely, John (2009). "Blood Pressure Control Determines Improvement in Diastolic Dysfunction in Early Hypertension". American Journal of Hypertension 22 (11): 1227–31. doi:10.1038/ajh.2009.173. PMID 19763121.
- ↑ Bussotti, M; Montorsi, P; Amato, M; Magini, A; Baldassarre, D; Tantardini, F; Veglia, F; Agostoni, P (2008). "Sildenafil improves the alveolar–capillary function in heart failure patients". International Journal of Cardiology 126 (1): 68–72. doi:10.1016/j.ijcard.2007.03.118. PMID 17490765.
- ↑ Wester, T. E.; Cherry, A. D.; Pollock, N. W.; Freiberger, J. J.; Natoli, M. J.; Schinazi, E. A.; Doar, P. O.; Boso, A. E.; Alford, E. L. (2008). "Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA". Journal of Applied Physiology 106 (2): 691–700. doi:10.1152/japplphysiol.91237.2008. PMID 19023017.
External links
- Calder-Becker, Katherine. "Swimming Induced Pulmonary Edema (SIPE)". Endurance Triathletes.
- Radiology Kerley's B and C lines - Swimming Induced Pulmonary Edema - MedPix Medical Image Database
