Hemoptysis During Swimming

Case Report

A 25-y-old male military officer was transferred to the emergency department of our hospital after an episode of hemoptysis. He denied smoking or having any significant medical history. For the past month, he had participated in the Special Forces’ Basic Underwater Demolition (BUD) training. During a nightly 2-h vigorous-intensity swimming session in the pool that did not involve diving or wearing a wetsuit, the officer complained of coughing, dyspnea, and chest tightness, which prompted him to withdraw from the exercise. On evaluation by the nearby medical staff, he had hemoptysis, tachypnea, and elevated blood pressure and heart rate. He received supplementary oxygen until his arrival at the hospital. On presentation, his blood pressure and heart rate were normal, and his respiratory rate was 25 breaths/min. Supplementary oxygen administration was briefly discontinued, and his oxygen saturation was 97% on room air. On chest auscultation, fine crackles in the right lower anterior and lateral chest were noted. Basic laboratory tests showed leukocytosis (13,700/microliter) and elevated concentrations of serum aspartate concentration (476 U·L^–1) and alanine (193 U·L^–1) aminotransferases, creatine phosphokinase (12,775 U·L^–1), high-sensitive cardiac troponin (318 ng·L^–1), and C-reactive protein (25 mg·L^–1) levels. His serum creatinine levels were within the normal range with no evidence of myoglobinuria. A chest radiograph demonstrated pulmonary infiltrates in the right middle lung field. Further imaging evaluation using chest computed tomography revealed diffuse ground-glass opacities affecting all pulmonary lobes, especially the right and left upper lobes and the middle lobe (Figure 1). His electrocardiogram and echocardiogram showed no pathologic findings.

Figure 1.

Chest computed tomography of the patient at admission demonstrating diffuse peripheral ground-glass opacities in all pulmonary lobes.

What is the diagnosis? How would you treat this patient?

Diagnosis

Swimming-induced pulmonary edema (SIPE).

Management and Outcome

The above-mentioned findings and patient's history were compatible with SIPE accompanied by exertional rhabdomyolysis owing to the history of prolonged strenuous exercise and the marked acute elevation in serum creatine phosphokinase level. The patient was admitted for monitoring and treated with intravenous fluids, inhaled β₂ agonists, and oxygen therapy. No episodes of hemoptysis were observed during his stay. Almost complete resolution of the ground-glass opacities (Figure 2) and normalization of his laboratory tests were noted after 5 d. A follow-up echocardiogram and a subsequent exercise stress test also were normal. The patient was discharged with a recommendation to abstain from swimming and strenuous exercise for 2 wk, and he was informed about the risk of recurrence.

Figure 2.

Chest computed tomography of the patient on the fifth day of hospitalization showing near-complete resolution of the infiltrates.

Discussion

SIPE is a form of hemodynamic pulmonary edema that occurs during exertional water sport activity, mostly in young and healthy individuals. The most common symptoms are dyspnea and cough, with occasional frothy sputum or hemoptysis. Risk factors include older age, female sex, the presence of an underlying cardiac disease (eg, systemic or pulmonary hypertension, subclinical coronary artery disease, or left ventricular hypertrophy), strenuous swimming in cold water, tight full-length wetsuits, overhydration before swimming, and history of a previous SIPE episode. ¹

The pathogenesis of the disease is yet to be fully understood. The predominant theory implicates the combined effect of central redistribution of blood due to the compressive forces exerted on the body during water immersion and peripheral vasoconstriction induced by exposure to lower temperatures and tight wetsuits leading to increased cardiac preload and afterload. In addition to this, an increase in sympathetic tone and an elevation of cardiac output are observed during intense exercise. The combination of the above-mentioned events results in a rise in mean pulmonary artery pressure as well as pulmonary artery wedge pressure. Subsequently, the elevation of hydrostatic pressure in pulmonary capillaries may cause both transudative edema and microscopic ruptures in the capillary-alveolar barrier leading to increased permeability to proteins and red blood cells.^1,2

The effect of blood pooling caused by immersion is observed during both surface and underwater swimming because buoyancy caused by the upward force of the liquid on the body counteracts gravity and thereby reduces the gradient for extravasation, which leads to fluid retention in the circulation. In addition to this, the pressure gradient between the alveoli and the mouth during head-out water immersion results in negative alveolar pressure, which promotes extravasation of fluid from the pulmonary vasculature to the alveoli. ³ Another mechanism for the occurrence of SIPE is the magnitude of the immersion-induced changes in lung function. A greater decrease in expiratory reserve volume, vital capacity, and overall compliance of the respiratory system, accompanied by an increase in inspiratory reserve volume, contributes to higher work of breathing and individual susceptibility to SIPE. ⁴

Older people with underlying cardiovascular diseases may already have elevated pulmonary capillary pressure before immersion, and even small increases after immersion could precipitate fluid transudation. ¹ In young, otherwise healthy individuals, overhydration before swimming seems to be an important risk factor, increasing central blood volume and cardiac preload, thus predisposing to elevated pulmonary pressures and capillary fracture.^5,6 Finally, the presence of a tight wetsuit around the thoracic cavity, besides increasing the total pressure gradient that counteracts extravasation and promotes central blood pooling, ³ could raise inspiratory resistance and lead to more negative alveolar pressure and subsequent alveolar edema. ²

Treatment is mainly supportive, including immediate removal from the water, placement in a warm environment, and removal of the wetsuit. Administration of supplemental oxygen, diuretics, and β₂ agonists may be considered. The recurrence rate of SIPE is high, reaching up to 40%. To prevent future episodes, individuals are advised to avoid exposure to cold water, appropriately warm up, and not overhydrate before water immersion. A thorough diagnostic cardiac and pulmonary workup to investigate for an underlying heart disease or pulmonary hypertension as the cause of the episode is also warranted. ⁷ Premedication with sildenafil, a selective inhibitor of phosphodiesterase-5 that reduces pulmonary vascular pressure and resistance, may effectively prevent SIPE in susceptible individuals without cardiac or pulmonary comorbidities. ⁸

Although the incidence of SIPE in recreational swimmers and athletes is 0.4% ⁹ and 1.4%, ¹⁰ respectively, much higher values of 2.8% ¹¹ and 5% ¹² have been reported for US BUD/SEAL trainees. Military special forces’ trainees may be particularly prone to SIPE due to their frequent engagement in strenuous combat swimming in cold environments and their practice of exceeding their limits in order to complete the training, thus ignoring milder symptoms until the condition becomes fully overt. Underlying cardiovascular disease is infrequent in this population, further evidenced by the absence of brain natriuretic peptide elevation in BUD/SEAL SIPE cases. ¹³ In contrast, overhydration is frequently advised in high-intensity training sessions to avoid heat injury, but this practice could predispose to SIPE if it precedes water immersion activities such as long swims or dives. This was first highlighted by a study ⁵ describing a mass occurrence of SIPE during a 2.4-km open sea swimming race in a military training program. Thirty swimmers had been instructed to drink approximately 5 L of water during the last 2 h preceding the swim to avoid dehydration. They did not wear wetsuits, and measured water temperature was 23⁰C. Eight swimmers (26.6%) developed symptoms compatible with SIPE, and 5 of them quit the race due to the severity of symptoms. Advising potential BUD training candidates to hydrate aggressively, as seen on several military websites,^14,15 may further increase the occurrence of SIPE among trainees. Therefore, raising awareness of the possible risk of overhydration is of great importance. Military medical personnel responsible for healthcare during swimming training sessions should be aware of the risk factors, symptoms, signs, and treatment of SIPE in order to offer preventive advice and also immediate management if needed.