![]() There is some debate around whether the different forms of IPE that occur in swimmers, scuba divers and breath-hold divers should be considered separately. This causes an increase in pressure gradients across pulmonary capillaries which can eventually cause a leakage of fluid into the air spaces in the lung. IPE occurs when immersion in water creates an extrinsic pressure on the body which can force blood away from the extremities into the chest. IPE was first documented in scuba divers in 1981 however, there is still a lack of understanding of its occurrence, risk factors, prognosis and preventative treatments, especially in open water swimmers. The risk of death is unknown due to difficulties differentiating between IPE and drowning for other reasons and the number of cases requiring hospital treatment is unclear due to the absence of an International Classification for Diseases (ICD) diagnosis code. It is thought that in most cases symptoms subside once the individual leaves the water however, IPE is potentially life threatening whilst a swimmer remains immersed and some IPE deaths in divers have been documented. IPE may affect people with no underlying health problems. SIPE is a type of immersion pulmonary oedema (IPE) that occurs when fluid accumulates in the lungs in the absence of water aspiration during surface or underwater swimming, causing acute shortness of breath and a cough productive of blood-tinged sputum. However, there is growing evidence that it is associated with a condition known as swimming-induced pulmonary oedema (SIPE). Open water swimming is a popular sport, with 842,500 participants in England in 2016. Further research should clarify the frequency of SIPE among recreational open water swimmers, confirm reported risk factors and explore others, explore long-term consequences and test interventions to prevent recurrences. SIPE may be an important public health problem affecting the growing number of recreational open water swimmers. Two very small uncontrolled studies of the effect of sildenafil for recurrence prevention were inconclusive. Two studies suggested that around 30% of people report recurrences of SIPE. The single small study of longer-term outcomes reported no difference between affected and unaffected swimmers. We found no studies that reported deaths from SIPE. Three studies suggested that SIPE symptoms usually resolve within 24 h, although a restrictive deficit in lung function persisted for a week in one small study. ![]() A third study reported that higher mean pulmonary artery pressures and pulmonary artery wedge pressures, and lower tidal volumes were associated with SIPE. One study found that hypertension, female sex, fish oil use, long course distance and another lower initial lung volumes and flows were risk factors for SIPE. One study reported that 1.4% of triathletes in the USA had experienced SIPE. Five studies, which differed from each other in case definition, swimming environment, population characteristics and denominators, reported an incidence of 0.01% of UK triathlons raced over 5 years in unspecified swimming environments (one study, not fully reported, of men and women of unspecified age) 0.5% of river races swum over 3 days in Sweden (one study, of men and women up to the age of 70) and 1.8–26.7% of time trials in the sea around Israel (three studies of male teenage military trainees). Quantitative synthesis was not possible because of study heterogeneity. Risk of bias was assessed by adapting existing quality assessment tools including those developed by the National Heart Lung and Blood Institute. We carried out a literature search using bibliographic databases and reference lists. The aim of this systematic review was to synthesise the evidence on SIPE incidence, prevalence, risk factors, short- and long-term outcomes, recurrence and effectiveness of interventions to prevent recurrences. Swimming-induced pulmonary oedema (SIPE) can affect people with no underlying health problems, but may be life threatening and is poorly understood.
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