|Swimming-induced pulmonary edema|
Pulmonary oedema of immersion|
|Classification and external resources|
Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).
SIPE usually occurs during exertion in conditions of water immersion, such as swimming and diving. With the recent surge in popularity of triathlons and swimming in open water events there has been an increasing incidence of SIPE. It has been reported in scuba divers, apnea (breath hold) free-diving competitors combat swimmers, and triathletes. The causes are incompletely understood at the present time.
Signs and symptoms
As with other forms of pulmonary edema, the hallmark of SIPE is a cough which may lead to frothy or blood-tinged sputum. Symptoms include:
- Shortness of breath out of proportion to effort being expended.
- Crackles, rattling or ‘junky’ feelings deep in the chest associated with breathing effort – usually progressively worsening with increasing shortness of breath and may be cause for a panic attack
- Cough, usually distressing and productive or not of a little pink, frothy or blood-tinged sputum (hemoptysis)
The wetsuit may feel as though it is hindering breathing ability.
It has been described in scuba divers, long distance swimmers, and breath-hold diving.
The mechanisms by which SIPE occurs are controversial, and likely multiple factors are required for the phenomenon to manifest.
- 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)
- Cold water may cause peripheral vasoconstriction and other neuro-humoral changes that contribute to central shift of the blood volume
- Wetsuits may add additional extrinsic compression to the extremities.
- Increased pressure somewhere in the pulmonary circulation (pulmonary artery hypertension, left heart diastolic dysfunction) leads to increased pressure gradient across the pulmonary capillaries
- Capillary stress from oxidative or physical injury leads to breach
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.
- 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.
- Avoidance of excessive pre-swim hydration is advisable
- Nifedipine or sildenafil 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 has generally been reported to be conservative, though deaths have been reported.
- Removal from water
- Diuretics and / or Oxygen when necessary
- Episodes are generally self-limiting in the absence of other medical problems 
SIPE is estimated to occur in 1-2% of competitive open-water swimmers, with 1.4% of triathletes, 1.8% of combat swimmers and 1.1% of divers and swimmers reported in the literature.
Most of the medical literature on the topic comes from case series in military populations and divers, and an epidemiological study in triathletes. 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. A study in SIPE-susceptible individuals during submersion in cold water showed that pulmonary artery and pulmonary artery wedge pressures were higher than in non-susceptible people. These pressures were reduced by sildenafil. SIPE may also be a cause of death during triathlons.
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