Scuba diving is considered to be a safe sport when an individual is properly trained and takes appropriate precautions. However, there can be disastrous complications if circumstances are unfavorable or appropriate precautions are not taken. One such potential complication is immersion pulmonary edema. Immersion pulmonary edema (IPE) is used by many as an umbrella term for scuba divers’ pulmonary edema (SDPE) and swimming-induced pulmonary edema (SIPE). Both of these conditions share similar presenting symptoms, diagnostics, and treatment. Case studies from the 1980s to present time highlight differences in pathophysiology and certain predisposing factors. The pathophysiology is not completely understood, and both conditions are likely underdiagnosed since postmortem exams with pulmonary edema exhibit non-specific findings of heavy edematous lungs and frothy sputum in the airways. These same findings can be found following drowning and prolonged resuscitation efforts.
There are numerous predisposing factors to immersion pulmonary edema, for example, over-hydration, cold water, negative inspiratory pressure, asthma, diabetes, drugs (such as beta blockers), underlying cardiac pathology, physical exertion, previous episodes of IPE, systemic and pulmonary hypertension. Cold water is believed to be a major contributing factor to the underlying pathophysiology. However, there have been numerous case reports and studies with individuals diving in tropical waters of 30 to 35 C. The majority of the incidence of IPE in warm water was diving-related, but it has been seen with extreme exertion and overhydration in swimmers.
Based on case studies in Europe, IPE incidence is about 1.1%. When reviewing the literature, SIPE tends to occur more commonly in males in excellent physical condition without any comorbidities. It typically occurs in military or combat swimmers and triathletes, and it is associated with heavy physical exertion and possibly, increased airway resistance. SDPE, however, is seen more frequently in recreational divers, particularly middle-aged females and is commonly associated with underlying comorbidities like hypertension, ischemic heart disease and possibly transient reversible cardiomyopathies such as Takotsubo cardiomyopathy. Fatalities occur most commonly in females over the age of 50. There is a recurrence rate around 30%, although it is likely an underestimate as many people stop diving or they infrequently dive. Therefore, it is difficult to track recurrences. The overall incidence is difficult to assess because the number of fatalities attributed to IPE has been minimal and almost all were in-hospital deaths. This is likely due to the high reliance on bystander reporting of progression of symptoms and early signs since postmortem exam cannot distinguish IPE from other causes of death common in swimming and diving.
Many factors contribute to the hemodynamic and cardiorespiratory changes that induce leakage of fluid from the capillary into the interstitial space and eventually, into the alveolar airspace. IPE is likely due to stress failure secondary to increased pulmonary vascular resistance, transudative edema, and pulmonary capillary leak. With immersion, there is an increase in pulmonary and systemic arterial pressure caused by passive redistribution of venous blood from the extremities to the heart and pulmonary vessels. This increase in intrathoracic blood volume results in a measured decrease in vital capacity. Cold water will augment this further with a reduction in vital capacity to 91% of baseline and increased shunting centrally as a means of heat conservation. This cold water effect is primarily seen with exposure to the torso and limbs rather than the head. Extreme physical exertion will also increase peripheral vascular resistance (PVR) causing increased afterload as well as increased pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), and pre-load from redistribution of blood from peripheral to thoracic vessels which are augmented further in cold water immersion. The shunting of blood into the thoracic cavity leads to an increase in hydrostatic pressure in pulmonary capillaries. Increased pre-load, afterload, and hydrostatic pressure in combination with extreme demands on pulmonary capillaries can cause capillary rupture leading to pulmonary edema and hemoptysis. However, there have been cases of IPE in thermoneutral water in individuals who do not exert themselves. This suggests additional mechanisms such as impaired left ventricular function, reversible cardiomyopathies, high blood volume, or high venous tone. In one study, individuals who experienced SIPE were compared against controls measuring mean PAP, PAWP, and PVR during exercise in cold water before and after administration of sildenafil. There was a no statistical difference in PAWP and mean PAP between both groups following sildenafil administration suggesting a mechanism during exertion causing a limited increase in left ventricular stroke volume with a relatively greater rise in right ventricular stroke volume causing an increase in hydrostatic pressure and resultant pulmonary edema. Large, negative intrathoracic pressures generated during strenuous exercise, breathing against a closed glottis, or breathing with a malfunctioning regulator may also contribute in some cases. It is also believed that breathing dense gas results in decreased alveolar pressure and changes in capillary permeability contributing to the pulmonary edema. There is a neurogenic variant of pulmonary edema previously described in the literature with a rise in catecholamines causing increased pulmonary artery and wedge pressure along with peripheral vasoconstriction. A study monitoring hemodynamic response to immersion demonstrated a wide range of mean PAP and PAWP with some PAP values exceeding 40 mm Hg. A pulmonary capillary leak is believed to occur at PAWP 17 to 20 mm Hg. Individuals who have had an IPE event demonstrate an exaggerated vasoconstrictive response to cold. When tested in dry conditions, patients with a history of IPE do not exhibit abnormal pulmonary function tests, abnormal exercise capacity, or abnormal pulmonary arterial pressure in response or hypoxemia. Post IPE event evaluation reveals normal PAP, PAWP, echocardiography, lung volumes, spirometry, and diffusing capacity of the lungs for carbon monoxide. When compared to healthy individuals, those who have a history of IPE had no difference in forearm vascular resistance, left ventricular systolic and diastolic dysfunction, and plasma levels of vasoreactive hormones such as epinephrine, norepinephrine, or cortisol. This strongly suggests physical exertion and immersion in water, particularly cold water, precipitate IPE.
Symptoms typically start within 10 minutes of a swim and have been reported to start at various times throughout a dive; however, there is a worsening of symptoms upon ascent. IPE is believed to originate with myocardial ischemia beginning early in the session with decompensation when divers surface. Symptoms range widely from mild shortness of breath with frothy sputum to frank hemoptysis, hypoxemia, and death. Blood pressure is typically elevated, and patients complain of extreme fatigue.
IPE can be confirmed radiographically; although, it may be so mild that a CT is more a more definitive test. SDPE may have some transitory respiratory or cardiac disorders underlying it, so respiratory function tests and blood gases are indicated. A thorough cardiac investigation including troponins, CK-MB, BNP, serial ECG, and early echocardiogram is also important. Coronary artery assessments may be required, and cardiac pathology addressed. Abnormal cardiac tests should be repeated to demonstrate reversibility or if they are transitory, as seen with Takotsubo cardiomyopathy and reversible myocardial dysfunction. With IPE, BNP is typically high. Antidiuretic hormone (ADH) can be monitored by measuring copeptin (stable C-terminal domain of precursor hormone to ADH). Natremia and albuminuria were typically lower. Ischemia-modified albumin is typically elevated and decreases after normobaric oxygen treatment that reduced hypoxemia. Biomarkers are helpful in early diagnosis and distinction of IPE from decompression sickness.
Removal from the water will reverse the hydrostatic effect of immersion decreasing filling pressures. Keeping swimmers or divers warm after removal from the water will decrease vasoconstriction and central blood pooling. Patients should be kept upright if they are conscious. For most, a full recovery can be seen within a day or 2 with rest, normobaric oxygen for hypoxemia, and/or beta-mimetic therapy. In severe cases, there may be myocardial injury and or loss of consciousness which could result in aspiration or fatality.
IPE can co-exist or be mistaken for other diving-related diseases. These include pulmonary barotrauma and decompression sickness. While there is no known association between decompression illness and SDPE, there have been many cases of SDPE with symptoms beginning with ascent resulting in some confusion. There are a number of reasons ascent is associated with worsening of symptoms in IPE. Reasons include damage to pulmonary capillaries from increased pulmonary hypertension caused by pulmonary filtration of bubbles during decompression, hydrostatic positional effects causing negative inspiratory pressures, natural progression of the disease, expansion of intrathoracic gas redistributing pulmonary edema fluids (Boyle’s Law), or a decrease in pulmonary oxygen pressures during ascent (Henry’s law). It is critical to differentiate SDPE from decompression sickness and arterial gas embolism because a hyperbaric chamber is not indicated in SDPE and could potentially cause harm. In older swimmers and divers, reversible stress cardiomyopathies have been recorded which may explain recurrences triggered by the physiologic effects of immersion. Due to its similarity and potential overlap, aspiration pneumonitis should be excluded.
Upon removal from the water, there is typically a rapid improvement, although some patients need intensive resuscitation. There have been reports of unconsciousness and even death. With supportive treatment, there is complete resolution of symptoms and normalization of imaging and labs within a couple of days.
With a recurrence rate of 30% with immersion, underlying pathologies, and the potential for severe or fatal outcomes, a diagnosis and reversal of underlying causes of IPE should occur before participation in further diving, snorkeling, or energetic swimming. A delay in an investigation for underlying cardiac pathology such as reversible cardiomyopathies may result in normalization of the transitory anomalies. If these tests are performed many days after the event, they may be misleading, resulting in medical and cardiac “clearance to resume diving” with potentially unfortunate subsequent incidents and deaths. If individuals continue to dive and snorkel, there should also be an emphasis on limiting contributing factors by using thermal protection, not overhydrating, ensuring minimal equipment resistance, avoiding excessive exertion, avoiding beta-blockers or sympathomimetics, using companion divers, and always having emergency oxygen and medivac capability.