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      Hyponatremia among Runners in the Boston Marathon

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          Abstract

          Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors. Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia. Of 766 runners enrolled, 488 runners (64 percent) provided a usable blood sample at the finish line. Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less). On univariate analyses, hyponatremia was associated with substantial weight gain, consumption of more than 3 liters of fluids during the race, consumption of fluids every mile, a racing time of >4:00 hours, female sex, and low body-mass index. On multivariate analysis, hyponatremia was associated with weight gain (odds ratio, 4.2; 95 percent confidence interval, 2.2 to 8.2), a racing time of >4:00 hours (odds ratio for the comparison with a time of <3:30 hours, 7.4; 95 percent confidence interval, 2.9 to 23.1), and body-mass-index extremes. Hyponatremia occurs in a substantial fraction of nonelite marathon runners and can be severe. Considerable weight gain while running, a long racing time, and body-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids ingested, and use of nonsteroidal antiinflammatory drugs were not. Copyright 2005 Massachusetts Medical Society.

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          Most cited references 17

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          Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners.

           J Varon,  J C Ayus,  A Arieff (2000)
          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. Case series. 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.
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            Hyponatremia in ultradistance triathletes.

            Hyponatremia ([plasma sodium] <135 mmol x L(-1)) is a potentially serious complication of ultraendurance sports. However, the etiology of this condition is still uncertain. This observational cohort study aimed to determine prospectively the incidence and etiology of hyponatremia in an ultradistance triathlon. The subjects consisted of 605 of the 660 athletes entered in the New Zealand Ironman triathlon (3.8-km swim, 180-km cycle, and 42.2-km run). Subjects were weighed before and after the race. A blood sample was drawn for measurement of plasma sodium concentration after the race. Complete data on pre- and postrace weights and plasma sodium concentrations were available in 330 race finishers. Postrace plasma sodium concentrations were inversely related to changes in body weight (P = 0.0001). Women (N = 38) had significantly lower plasma sodium concentrations (133.7 vs 137.4 mmol x L(-1); P = 0.0001) than men (N = 292) and lost significantly less relative weight (-2.7 vs -4.3%; P = 0.0002). Fifty-eight of 330 race finishers (18%) were hyponatremic; of these only 18 (31%) sought medical care for the symptoms of hyponatremia (symptomatic). Eleven of the 58 hyponatremic athletes had severe hyponatremia ([plasma sodium] < 130 mmol x L(-1)); seven of these 11 severely hyponatremic athletes were symptomatic. The relative body weight change of the 11 severely hyponatremic athletes ranged from 2.4% to +5%; eight (73%) of these athletes either maintained or gained weight during the race. In contrast, relative body weight changes in the 47 athletes with mild hyponatremia ([plasma sodium] 130-134 mmol x L(1)) were more variable, ranging from -9.25% to +2.2%. Hyponatremia is a common biochemical finding in ultradistance triathletes but is usually asymptomatic. Although mild hyponatremia was associated with variable body weight changes, fluid overload was the cause of most (73%) cases of severe, symptomatic hyponatremia.
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              Exercise-associated hyponatremia in marathon runners: a two-year experience.

              This study was conducted to better define the pathophysiology, risk factors, and therapeutic approach to exercise-associated hyponatremia. Medical records from all participants in the 1998 Suzuki Rock 'N' Roll Marathon who presented to 14 Emergency Departments (EDs) were retrospectively reviewed to identify risk factors for the development of hyponatremia. Hyponatremic patients were compared to other runners with regard to race time and to other marathon participants seen in the ED with regard to gender, clinical signs of dehydration, and use of nonsteroidal anti-inflammatory drugs (NSAIDs). An original treatment algorithm incorporating the early use of hypertonic saline (HTS) was evaluated prospectively in our own ED for participants in the 1999 marathon to evaluate improvements in sodium correction rate and incidence of complications. A total of 26 patients from the 1998 and 1999 marathons were hyponatremic [serum sodium (SNa) < or =135 mEq/L] including 15 with severe hyponatremia (SNa < or = 125 mEq/L). Three developed seizures and required intubation and admission to an intensive care unit. Hyponatremic patients were more likely to be female, use NSAIDS, and have slower finishing times. Hyponatremic runners reported drinking "as much as possible" during and after the race and were less likely to have clinical signs of dehydration. An inverse relationship between initial SNa and time of presentation was observed, with late presentation predicting lower SNa values. The use of HTS in selected 1999 patients resulted in faster SNa correction times and fewer complications than observed for 1998 patients. It is concluded that the development of exercise-associated hyponatremia is associated with excessive fluid consumption during and after extreme athletic events. Additional risk factors include female gender, slower race times, and NSAID use. The use of HTS in selected patients seems to be safe and efficacious.
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                Author and article information

                Journal
                New England Journal of Medicine
                N Engl J Med
                Massachusetts Medical Society
                0028-4793
                1533-4406
                April 14 2005
                April 14 2005
                : 352
                : 15
                : 1550-1556
                Article
                10.1056/NEJMoa043901
                15829535
                © 2005
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