TO THE EDITOR: A healthy 20-year-ol...

TO THE EDITOR: A healthy 20-year-old United States Navy search and set free swimmer trainee, who was equipped with no other than a mask and fins, unraveled hemoptysis, sharp substernal chest pain, and shortness of breath after performing a dive to a stillest part of 12 feet. He immediately surfaced and began to cough up pink, foamy sputum and have persistent shortness of breath. His initial oxygen saturation was 70 percent forward room air and improved to 86 percent upon three liters of oxygen via nasal cannula during ambulance transfer. forward arrival at the emergency department, the patient had an oxygen saturation of 100 percent upon three liters of oxygen with improved shortness of breath and resolv hemoptysis.

Auscultation of the lung revealed bilateral rhonchi. The remainder of the physical examination was unremarkable with all vital signs being normal. Electrocardiogram, concluded blood count, electrolytes, creatine kinase, troponin, and coagulation studies were all within normal limits. A chest radiograph showed nappy perihilar infiltrates bilaterally (see the accompanying figure forward page 1048). A chest radiograph taken several hours later showed resolving infiltrates. The patient was diagnosed with swimming-induced pulmonary edema (SIPE) and discharged.

While the exact pathophysiology of SIPE remains uncertain, it is believed to be related to exertion, immersion in brumal water, and overhydration. The body's normal answer to exercise is to increase cardiac output to suitable the increased oxygen demand. Although an increased cardiac output is known to cause pulmonary edema in racehorses, this increase is rarely enough to generate such an effect in humans. (1) Cold-water immersion is instrumental in this proces because the peripheral vasculature constricts to divert kin away from the extremities in an effort to maintain the core dead body temperature. This results in a central pooling of kindred leading to an increased preload, increased pulmonary artery squeezing and an increased cardiac output The vasoconstriction also causes an increase in afterload, which leads to an increase in pulmonary vasculature resistance. The increased cardiac output from exertional activities coupl with an increased preload and afterload from immersion appear to be sufficient to hostility the pulmonary capillary membranes, thus resulting in pulmonary edema. In several documented cases of SIPE, it has been noted that the patients consum anywhere from pair to four liters of water in the hours leading up to their swim in an effort to remain well hydrated. 2 It is believed that this station of hydration led to a fluid overload that contributed to the first brunt of pulmonary edema by increasing the pulmonary capillary urgency (2) Patients may present with symptoms, of the like kind as cough, dyspnea, hemoptysis, tachypnea, and confusion with hypoxia, after exertional cutting water activity such as swimming and scuba diving. (3)

Treatment for patients with SIPE consists primarily of supportive measures like as removing the patient from the wet and/or chilly environment and providing supplemental oxygen Although useful in treating pulmonary edema in racehorses, diuretics are typically not necessary because patients attend to to show relief of symptoms before long after being placed on supplemental oxygen (4) cloyed resolution of radiographic findings typically flash on the minds within 24 to 48 hours.

JASON A. YODER MS3 EN MC USNR

Uniformed Services University of the Health Sciences

4301 Jone Bridge Rd

Bethesda, MD 20814

ANTHONY J VIERA, LCDR MC USNR

Naval Hospital Jacksonville

2080 Child St

Jacksonville, FL 32214

REFERENCES

(1) Hopkins SR Schoene RB Henderson WR Spragg RG Martin TR West JB Intense exercise impairs the integrity of the pulmonary blood-gas barrier in elite athletes. Am J Respir Crit Care M 1997; 155:1090-4

(2) Weiler-Ravell D Shupak A, Goldenberg I, Halpern P Shoshani O Hirschhorn G et al. Pulmonary oedema and haemoptysis induced at strenuous swimming. BMJ 1995;311:361-2.

(3) Pon M Blickenstorfer D Oechslin E confine G, Greminger P, Franzeck UK et al. Pulmonary oedema in healthy human frames during scuba-diving and swimming. Eur Respir J 1995;8:762-7

(4) Lund KL Mahon RT Tanen DA, Bakhda s Swimming-induced pulmonary edema. Ann Emerg M 2003; 41:251-6

The opinions and assertions contained herein are the private views of the authors and are not to be constru as official or as reflecting the views of the U Navy Medical Department or the U Navy Service at large.

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