J. Carlos Ayus, MD; Joseph Varon, MD; Allen I. Arieff, MD
Presented in part at the annual meeting of the American Society of Nephrology, Miami, Florida, 4 November 1999, and published as an abstract in J Am Soc Nephrol. 1999; 10:119A.
Acknowledgments: The authors thank Dr. J. Gary Grant for his invaluable contribution to the database and Dr. David E. King for analysis of the neuroradiologic studies.
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Current Author Addresses: Drs. Ayus and Varon: Baylor College of Medicine, 4 Brompton Court, Houston, TX 77024.
Dr. Arieff: University of California, San Francisco, School of Medicine, 299 South Street, Sausalito, CA 94965.
Author Contributions: Conception and design: J.C. Ayus, J. Varon, A.I. Arieff.
Analysis and interpretation of the data: J.C. Ayus, J. Varon, A.I. Arieff.
Drafting of the article: J.C. Ayus, A.I. Arieff.
Critical revision of the article for important intellectual content: J.C. Ayus, A.I. Arieff.
Final approval of the article: J.C. Ayus, J. Varon, A.I. Arieff.
Provision of study materials or patients: J.C. Ayus, J. Varon, A.I. Arieff.
Collection and assembly of data: J.C. Ayus, A.I. Arieff.
Noncardiogenic pulmonary edema is often associated with increased intracranial pressure and can be the initial manifestation of hyponatremic encephalopathy. Marathon runners tend to develop conditions that lead to hyponatremia.
To describe the development and treatment of noncardiogenic pulmonary edema in marathon runners that was associated with hyponatremic encephalopathy.
One university hospital and two community hospitals.
Seven healthy marathon runners who had a history of nonsteroidal anti-inflammatory drug use. The runners collapsed after competing in a marathon and were hospitalized with pulmonary edema.
Plasma sodium levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or computed tomographic scans of the brain.
Patients had nausea, emesis, and obtundation. The mean (±SD) plasma sodium level was 121 ± 3 mmol/L, and oxygen saturation was less than 70%. Electrocardiograms and echocardiograms were normal. Chest radiographs showed pulmonary edema with a normal heart. Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated. Scanning of the brain showed cerebral edema. All patients were intubated and mechanically ventilated. Treatment with intravenous NaCl, 514 mmol/L, increased plasma sodium levels by 10 mmol/L in 12 hours. Pulmonary and cerebral edema resolved as the sodium level increased. One patient had unsuspected hyponatremic encephalopathy and died of cardiopulmonary arrest caused by brainstem herniation. All six treated patients recovered and were well after 1 year of follow-up.
In healthy marathon runners, noncardiogenic pulmonary edema can be associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed and can be successfully treated with hypertonic NaCl.
J. Carlos Ayus, Joseph Varon, Allen I. Arieff. Hyponatremia, Cerebral Edema, and Noncardiogenic Pulmonary Edema in Marathon Runners. Ann Intern Med. 2000;132:711–714. doi: 10.7326/0003-4819-132-9-200005020-00005
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Published: Ann Intern Med. 2000;132(9):711-714.
Endocrine and Metabolism, Fluid and Electrolyte Disorders, Nephrology, Neurology.
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