Life-threatening hyponatremia in marathon runners: The Varon-Ayus syndrome revisited (original) (raw)
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Varon J: Life-threatening hyponatremia in marathon runners: The Varon-Ayus syndrome revisited
2020
Life-threatening hyponatremia can occur when sodium concentration falls to 125 mmol/L or less. Symptoms usually do not depend on the absolute sodium concentration but on the rate of fall. Estimates of mortality in acute hyponatremia are as high as 50%. Marathon runners are at particular risk of developing a syndrome which consists of severe hyponatremia, pulmonary edema and cerebral edema as originally described by Varon and Ayus. This syndrome, if not managed appropriately has a very high morbidity and mortality.
Exercise-Associated Hyponatremia and the Varon-Ayus Syndrome
2009
Endurance sports such as marathon running are increasingly popular, attracting both professional and recreational athletes. While most participants recognize that these events can result in health hazards, few consider death a likely outcome. Exercise associated hyponatremia can be a consequence for which fatal outcomes may occur. In some it is mild and without symptoms. However, in others it is of such severity that respiratory failure secondary to pulmonary edema, and possibly death may result. This article reviews new information regarding predisposing factors, treatment, and outcomes associated with exercise induced hyponatremia and the Varon-Ayus syndrome (hyponatremia, pulmonary edema and cerebral edema associated to marathon running).
Incidence of Hyponatremia During a Continuous 246-km Ultramarathon Running Race
Frontiers in Nutrition
The purpose of this observational study was to examine the incidence of exercise-associated hyponatremia (EAH) in a 246-km continuous ultra-marathon. Methods: Over 2 years, 63 male finishers of the annual Spartathlon ultra-marathon foot race from Athens to Sparta, Greece were included in the data analysis. A blood sample was drawn from an antecubital vein the day before the race as well as within 15 min post-race and analyzed for sodium concentration. During the second year of data collection, blood was also drawn at the 93-km checkpoint (n = 29). Height and weight were measured pre and post-race. Results: Mean race time of all subjects was 33 ± 3 h with a range of 23.5 and 36.0 h. Of the 63 finishers recruited, nine began the race with values indicative of mild hyponatremia. Seven runners were classified as hyponatremic at the 93-km checkpoint, three of whom had sodium levels of severe hyponatremia. After the race, 41 total finishers (65%) developed either mild (n = 27, 43%) or severe hyponatremia (n = 14, 22%). Mean change in bodyweight percentage and serum sodium from pre-race to post-race was −3.6 ± 2.7% (−2.5 ± 1.9 kg) and −6.6 ± 5.6 mmol•L −1 , respectively. Pre-race serum sodium level was not a significant predictor of post-race serum sodium levels (β = 0.08, R 2 = 0.07, P = 0.698), however, there was a significant negative association between change in bodyweight percentage and post-race serum sodium concentration (β = −0.79, R 2 = 0.29, P = 0.011). Conclusion: The incidence of EAH of 52 and 65%, when excluding or including these individuals with pre-race hyponatremia, was the highest reported in current literature.
Sodium status of collapsed marathon runners
Archives of pathology & laboratory medicine, 2005
Recommendations for prevention and treatment of medical emergencies in participants in marathon races center on maintenance of adequate hydration status and administration of fluids. Recently, new recommendations for fluid replacement for marathon runners were promulgated by medical and athletic societies. These new guidelines encourage runners to drink ad libitum between 400 and 800 mL/h as opposed to the previous "as much as possible" advice. To assess the sodium and hydration (plasma osmolality) status of collapsed marathon runners after the promulgation of new hydration guidelines. Plasma sodium and osmolality values of runners who presented to the medical tent at the finish line of the 2003 Boston Marathon were measured. Using reference ranges derived from the general population, of 140 collapsed runners, 35 (25%) were hypernatremic (sodium, >146 mEq/L) and 6 (12%) were hyperosmolar (osmolality, >296 mOsm/kg H(2)O), whereas 9 (6%) were hyponatremic (sodium, <...
Hyponatremia among Runners in the Boston Marathon
New England Journal of Medicine, 2005
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. methods 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.
Hyponatremia in Marathon Runners due to Inappropriate Arginine Vasopressin Secretion
The American Journal of Medicine, 2007
PURPOSE: Exercise-associated hyponatremia (EAH), as defined by a blood sodium concentration [Na ϩ ] less than 135 mmol/L, may lead to hypotonic encephalopathy with fatal cerebral edema. Understanding the pathogenetic role of antidiuresis may lead to improved strategies for prevention and treatment. METHODS: Normonatremic marathon runners were tested pre-and post-race for creatine kinase, interleukin-6, cortisol, prolactin, and arginine vasopressin. Similar testing also was carried out in runners with encephalopathy caused by EAH, including 2 cases with fatal cerebral edema. RESULTS: Normonatremic runners (n ϭ 33; 2001) with a mean 3% decrease in body weight showed a 40-fold increase in interleukin-6 (66.6 Ϯ 11.9 pg/mL from 1.6 Ϯ 0.5 pg/mL, P ϭ .001), which was significantly correlated with increases in creatine kinase (r ϭ 0.88, P ϭ Ͻ.0001), cortisol (r ϭ 0.70, P ϭ .0003), and prolactin (r ϭ 0.67, P Ͻ.007), but not arginine vasopressin (r ϭ 0.44, P ϭ .07). Collapsed runners with EAH (n ϭ 22; 2004) showed a mean blood urea nitrogen less than 15 mg/dL with measurable plasma levels of arginine vasopressin (Ͼ0.5 pg/mL) in 43% of cases. Two marathon runners with fatal cerebral edema additionally showed less than maximally dilute urines (Ͼ100 mmol/kg/H 2 O) and urine [Na ϩ ] greater than 25 mEq/L. CONCLUSIONS: Cases of EAH fulfill the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Runners with hypotonic encephalopathy at subsequent races were treated with intravenous hypertonic (3%) saline on the basis of this paradigm, which resulted in rapid clinical improvement without adverse effects. Release of muscle-derived interleukin-6 may play a role in the nonosmotic secretion of arginine vasopressin, thereby linking rhabdomyolysis to the pathogenesis of EAH.
Exercise-Associated Hyponatremia in Marathon Runners
Journal of Clinical Medicine
Exercise-associated hyponatremia (EAH) was first described as water intoxication by Noakes et al. in 1985 and has become an important topic linked to several pathological conditions. However, despite progressive research, neurological disorders and even deaths due to hyponatremic encephalopathy continue to occur. Therefore, and due to the growing popularity of exercise-associated hyponatremia, this topic is of great importance for marathon runners and all professionals involved in runners’ training (e.g., coaches, medical staff, nutritionists, and trainers). The present narrative review sought to evaluate the prevalence of EAH among marathon runners and to identify associated etiological and risk factors. Furthermore, the aim was to derive preventive and therapeutic action plans for marathon runners based on current evidence. The search was conducted on PubMed, Scopus and Google Scholar using a predefined search algorithm by aggregating multiple terms (marathon run; exercise; sport;...
Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia
Journal of Science and Medicine in Sport, 2013
Objectives: To determine more conclusively whether intravenous (IV) administration of 3% saline is more efficacious than oral administration in reversing below normal blood sodium concentrations in runners with biochemical hyponatremia. Design: Randomized controlled trial. Methods: 26 hyponatremic race finishers participating in the 161-km Western States Endurance Run were randomized to receive either an oral (n = 11) or IV (n = 15) 100 mL bolus of 3% saline. Blood sodium concentration (Na + ), plasma protein (to assess %plasma volume change), arginine vasopressin (AVP), blood urea nitrogen (BUN) and urine (Na + ) were measured before and 60 min following the 3% saline intervention. Results: No significant differences were noted with respect to pre-to post-intervention blood [Na + ] change between intervention groups, although blood [Na + ] increased over time in both intervention groups (+2 mmol/L; p < 0.0001). Subjects receiving the IV bolus had a greater mean (±SD) plasma volume increase (+8.6 ± 4.5% versus 1.4% ± 5.7%; p < 0.01) without significant change in [AVP] (−0.2 ± 2.6 versus 0.0 ± 0.5 pg/mL; p = 0.49). 69% of subjects completing the intervention trial were able to produce urine at race finish with a mean (±SD) pre-intervention urine [Na + ] of 15.2 ± 8.5 mmol/L (range 0-35; NS between groups). [BUN] of the entire cohort pre-intervention was 30.7 ± 10.5 mg/dL (range 13-50). Conclusions: No group difference was noted in the primary outcome measure of change in blood [Na + ] over 60 min of observation following a 100 mL bolus of either oral or IV 3% saline. Administration of an oral hypertonic saline solution can be efficacious in reversing low blood sodium levels in runners with mild EAH.
Hyponatremia and seizures in an ultradistance triathlete
The Journal of Emergency Medicine, 2000
Hyponatremia is being increasingly recognized as a complication of participation in ultra-endurance sports. Reported is the case of an Ironman triathlete who collapsed at the end of the race, having gained 5% in body weight. His serum sodium concentration at the finish was 116 mmol/L. After an Intensive Care Unit course complicated by recurrent seizures, he eventually made a complete neurologic recovery. The pathogenesis of hyponatremia and its management in such cases is discussed.
Medicina
Exercise-associated hyponatremia (EAH) is defined as a plasma sodium concentration of <135 mmol/L during or after endurance and ultra-endurance performance and was first described by Timothy Noakes when observed in ultra-marathoners competing in the Comrades Marathon in South Africa in the mid-1980s. It is well-established that a decrease in plasma sodium concentration <135 mmol/L occurs with excessive fluid intake. Clinically, a mild hyponatremia will lead to no or very unspecific symptoms. A pronounced hyponatremia (<120 mmol/L) will lead to central nervous symptoms due to cerebral edema, and respiratory failure can lead to death when plasma sodium concentration reaches values of <110–115 mmol/L. The objective of this narrative review is to present new findings about the aspects of sex, race location, sports discipline, and length of performance. The prevalence of EAH depends on the duration of an endurance performance (i.e., low in marathon running, high to very high ...