IPE: Healthy or Not, Here I Come!

A specific case series in Navy SEALS reported an incidence as high as 5%, and other literature reviews similarly report higher incidences in highly trained endurance athletes.  A common predisposing factor is an overhydration in anticipation of an endurance event which effectively mimics fluid overload when combined with immersion physiology as discussed below.  Why female sex is a risk factor is poorly understood, and the female predominance is more apparent in divers than in endurance athletes.  Other less frequently implicated risk factors include asthma, diabetes, and medications such as beta-blockers.    

Immersion physiology

Shifts in cardiovascular physiology can be surprisingly drastic even with wading in knee-deep water.  Even more profound shifts occur with immersion to the neck as seen in surface swimming or complete immersion as seen in diving.  Immersion to the neck, for instance, causes a near-immediate shift of ~700cc of blood towards the central circulation with correspondent rapid changes in cardiac filling pressures.  Additionally, when immersed, a small pressure gradient exists between the water surface and lung such that negative airway pressures are established.  In cold water, vasoconstriction leads to elevated pressures at the level of the pulmonary capillary, and this pressure change is exacerbated further with intense exercise.  Collectively, the centralization of blood volume, negative airway pressures, and increased pulmonary capillary pressures create a physiologic pre-disposition to capillary leak and accumulation of transudative alveolar fluid.   

Consistent with this understanding of physiologic changes, individuals with underlying cardiac disease are indeed at higher risk for IPE even though, as mentioned, otherwise healthy individuals can also be affected. Underlying hypertension is a risk factor for IPE and is associated with recurrent IPE.  The recurrence rate is reported at 30% though this is likely an underestimation since many individuals do not return to the swimming or diving activity that caused the initial IPE episode.  Interestingly, some case series suggest the common development of hypertension in the years following an IPE event in individuals who were normotensive at the time of the initial episode.  The discussion spurred here addresses the possibility that these individuals have an underlying hyperactive vasoconstrictor response which predisposed them to both IPE and hypertension.     

Distinction from other dive injuries 

While not relevant for triathletes and surface swimmers, other types of dive injuries can broaden the differential diagnosis for SCUBA divers.  Decompression sickness (DCS), arterial gas embolism (AGE), and IPE are all diving-related processes that require careful differentiation.  This differentiation is important as emergent hyperbaric oxygen therapy is indicated in the treatment of DCS and AGE whereas it is not indicated and could be detrimental in cases of IPE.  Depth and duration are important features of taking a dive history as both are direct factors in the development of DCS, or the bends.  In parsing out IPE and AGE though, timing is arguably the most important feature.    

DCS vs. IPE:

DCS can affect the pulmonary system in what is referred to as “the chokes”, giving a recently surfaced diver cough, frothy sputum, dyspnea, and hypoxemia.  Symptoms alone of pulmonary DCS and IPE can be nearly indistinguishable, but the timing of symptoms can be used to differentiate the two.  DCS is inherently a disease of decompression and therefore occurs after a period of breathing compressed gas at depth.  DCS symptoms will occur most commonly within 1-3 hours after surfacing from a dive and nearly exclusively within 24 hours, while IPE symptoms will develop at depth or even pre-dive while at the surface. 

AGE vs. IPE:

Symptoms of AGE on the other hand (i.e. unconsciousness, hemiplegia, cardiac arrest), will occur instantly upon surfacing from a dive or at most within 5-10 minutes of surfacing and are usually accompanied by a history of a rapid ascent.  While it would be uncommon for an AGE to purely affect the pulmonary system, AGE and IPE can be difficult to distinguish.  Timing of onset of symptoms again can be helpful, as it would be unlikely for AGE symptoms to occur at depth.  Another feature that can make differentiating these diagnoses particularly difficult is that both AGE and IPE can present with a history of a rapid ascent.  Symptoms of IPE at depth will not uncommonly and understandably induce panic and lead to a rapid ascent which is conversely more classic for AGE.  Timing is again paramount as IPE symptoms will have occurred just prior to the rapid ascent vs. after in the case of AGE (*If the patient is able to provide this much detail in history).     

In a devastating but fascinating scenario, IPE developed at depth can create an oxygen requirement.  As the dyspneic diver aborts their dive and ascends the water column due to symptoms, the partial pressure of inspired O2 decreases (depending on initial depth, this can be 4-5 fold) such that hypoxemia gets worse and the diver can even lose consciousness and drown.  This loss of consciousness upon ascent can make these cases indistinguishable from AGE and the limited history at presentation may never allow for true differentiation.  Even independent from cases like this where IPE could be mistaken for AGE, IPE is thought to be under-reported as a relevant factor in swimming and diving-related drownings.   

Treatment and return to the water

Analogous to descent as a treatment for altitude-related illness, patients should be removed from the water as quickly as possible and in cold water cases, be kept warm upon removal.  Chest radiography will demonstrate pulmonary edema.  In addition to respiratory derangements, patients will typically be hypertensive and complain of extreme fatigue at the time of presentation.  Treatment for IPE is otherwise supportive and typically will be identical to other cases of pulmonary edema ranging from supplemental oxygen to mechanical ventilation.  Non-invasive positive pressure ventilation (NIPPV) may be appropriate in many cases.  Admission may obviously be required.  Patients recover quickly, at most within 1-2 days.  Reversible pathology such as Takotsubo’s cardiomyopathy can be a predisposing factor, so echocardiography should be a part of a patient’s evaluation after presenting with IPE. 

Patients who have had an episode of immersion pulmonary edema are at risk to have subsequent episodes, and as such, must be educated about this risk prior to returning to any swimming or diving activities.  Risks and benefits should be thoroughly discussed, and shared decision-making can be employed to determine whether any return to water-based activities is worth the risk to the patient.  Sildenafil has been demonstrated in a case-control study as a potential prophylactic measure to reduce IPE risk.  If desired, dive medicine specialists can be found here who can facilitate this conversation.    

De-Brief

• IPE can affect those who are predisposed as well as young and otherwise healthy individuals and can be fatal in severe cases

• Patients who’ve had a case of IPE are at risk for subsequent events with return immersion activities

• Coldwater and vigorous exercise in water are risk factors for IPE

• Centralization of blood volume and increased pulmonary capillary pressure predispose an individual to the capillary leak and alveolar fluid accumulation which manifests as IPE

• • In divers, the timing of onset of symptoms is the most important feature to differentiate IPE from other dive injuries such as DCS or AGE.

• Treatment for IPE is consistent with that of all pulmonary edema cases

References:

1. Hageman SM, Chakraborty RK, Murphy-Lavoie HM. Immersion Pulmonary Edema. [Updated 2021 Jul 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.
2. Manish Kumar & Paul D. Thompson (2019) A literature review of immersion pulmonary edema, The Physician and Sportsmedicine, 47:2, 148-151, DOI: 10.1080/00913847.2018.1546104
3. Moon RE, Martina SD, Peacher DF, Potter JF, Wester TE, Cherry AD, Natoli MJ, Otteni CE, Kernagis DN, White WD, Freiberger JJ. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016 Mar 8;133(10):988-96. doi: 10.1161/CIRCULATIONAHA.115.019464. Epub 2016 Feb 16. PMID: 26882910; PMCID: PMC5127690.
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6. Volk C, Spiro J, Boswell G, Lindholm P, Schwartz J, Wilson Z, Burger S, Tripp M. Incidence and Impact of Swimming-Induced Pulmonary Edema on Navy SEAL Candidates. Chest. 2021 May;159(5):1934-1941. doi: 10.1016/j.chest.2020.11.019. Epub 2020 Nov 25. PMID: 33245874.