Symptomatic Exercise-associated Hyponatremia Research Articles

Oral Hypertonic Saline Is Effective in Reversing Acute Mild-to-Moderate Symptomatic Exercise-Associated Hyponatremia.

To determine whether oral administration of 3% hypertonic saline (HTS) is as efficacious as intravenous (IV) 3% saline in reversing symptoms of mild-to-moderate symptomatic exercise-associated hyponatremia (EAH) in athletes during and after a long-distance triathlon. Noninferiority, open-label, parallel-group, randomized control trial to IV or oral HTS. We used permuted block randomization with sealed envelopes, containing the word either "oral" or "IV." Annual long-distance triathlon (3.8-km swim, 180-km bike, and 42-km run) at Mont-Tremblant, Quebec, Canada. Twenty race finishers with mild to moderately symptomatic EAH. Age, sex, race finish time, and 9 clinical symptoms. Time from treatment to discharge. We successfully randomized 20 participants to receive either an oral (n = 11) or IV (n = 9) bolus of HTS. We performed venipuncture to measure serum sodium (Na) at presentation to the medical clinic and at time of symptom resolution after the intervention. The average time from treatment to discharge was 75.8 minutes (SD 29.7) for the IV treatment group and 50.3 minutes (SD 26.8) for the oral treatment group (t test, P = 0.02). Serum Na before and after treatment was not significantly different in both groups. There was no difference on presentation between groups in age, sex, or race finish time, both groups presented with an average of 6 symptoms. Oral HTS is effective in reversing symptoms of mild-to-moderate hyponatremia in EAH.

Exercise-Associated Hyponatremia.

Exercise-associated hyponatremia (EAH) refers to below-normal serum sodium concentrations [Na+] that develop during exercise. The pathogenesis of EAH is best described as a spectrum ranging between profound polydipsia to modest sweat sodium losses with hypovolemia and relative dilution. Non-osmotic arginine vasopressin (AVP) remains the unifying pathogenic stimulus to abnormal renal water retention in acute symptomatic EAH. Cases of hyponatremia are mostly reported after endurance sports, but are also observed after shorter duration events and in team sport athletes. The signs and symptoms of EAH are vague, and include bloating, vomiting, headache, and altered mental status. A diagnosis of EAH can only be confirmed by a blood test, whereas signs/symptoms guide the most appropriate treatment strategy. Mild-to-moderate EAH (without encephalopathy) can be treated with either fluid restriction or an oral bolus of a hypertonic saline solution. Severe EAH (with encephalopathy) is a life-threatening emergency and should be urgently treated with intravenous 100 mL boluses of 3% saline until the resolution of encephalopathy symptoms. The prevention of EAH is evolutionarily rooted in preventing overdrinking during exercise. Drinking according to the dictates of thirst is the most individualized strategy to prevent life-threatening dysnatremia during exercise, regardless of sport.

Predicted Risk for Exacerbation of Exercise-Associated Hyponatremia from Indiscriminate Postrace Intravenous Hydration of Ultramarathon Runners

BackgroundAsymptomatic or mildly symptomatic exercise-associated hyponatremia (EAH) can be exacerbated by aggressive hydration. ObjectiveThis work predicts the percentage of athletes at risk for exacerbation of EAH from indiscriminate hydration after an ultramarathon. MethodsPostrace serum sodium, creatinine, creatine kinase (CK), and urea nitrogen concentrations were determined for 161-km ultramarathon participants. Body mass was measured prior to and immediately after the race. Incidents when serum CK was > 20,000 U/L or creatinine ≥ 1.5 times estimated baseline were considered to be “at risk for receiving I.V. hydration” if presenting to a hospital. Those with EAH without body mass loss during the race were considered “overhydrated” and “at risk for EAH exacerbation.” ResultsAmong 627 finishers, 16 (2.6%) were at risk for EAH exacerbation. Considering 421 observations at risk for receiving I.V. hydration, 16 (47.1%) of the 34 observations with EAH were at risk for EAH exacerbation. Among those at risk for receiving I.V. hydration and with EAH, serum urea nitrogen and creatine concentration as a multiple of estimated baseline were lower (p < 0.05) for those at risk for EAH exacerbation, compared with those without overhydration, but there were no clinically useful laboratory findings to distinguish these two groups due to considerable overlap of values. ConclusionsWhether in the field or hospital setting, I.V. hydration of an athlete after an ultramarathon carries a notable risk for exacerbating EAH, so clinicians should use caution when hydrating athletes after endurance events.

Body Mass Changes Across a Variety of Running Race Distances in the Tropics.

BackgroundCurrent literature evaluating body mass (BM) changes across a variety of running race distances is limited. The primary objective of this study was to profile the range of BM changes across race distances. The secondary objective was to evaluate the prevalence of exercise-associated hyponatremia (EAH) in runners admitted to the on-site medical tent following participation of race events of different distances.MethodsA total of 1934 runners across seven footrace categories (10-, 21-, 25-, 42-, 50-, 84-, and 100-km) were included in the study. One thousand eight hundred eighty-seven runners had their BM measured before and after each race. Blood sodium concentrations were measured from the remaining 47 symptomatic runners admitted to the on-site medical tents and did not complete the race.ResultsIn terms of hydration status, 106 (6 %) were overhydrated, 1377 (73 %) were euhydrated, and 404 (21 %) were dehydrated. All race distances exhibited similar percentage of overhydrated runners (5 % in 10 km, 3 % in 21 km, 5 % in 25 km, 6 % in 42 km, 8 % in 50 km, 7 % in 84 km, and 6 % in 100 km). Forty-seven runners were admitted to the medical tents. Eight (17 %) were diagnosed with EAH (4 from 42 km, 2 from 84 km, 2 from 100 km), 38 (81 %) were normonatremic, and 1 (2 %) was hypernatremic. The % ΔBM across all races ranged from −8.0 to 4.1 % with a greater decrement noted in the 42-, 50-, 84-, and 100-km categories.ConclusionsApproximately 3–8 % runners had increased post-race BM, suggesting overhydration regardless of race distance. Symptomatic EAH was seen at race distances at or above 42 km, where BM changes demonstrated the widest range of values.

How common is symptomatic hyponatremia in endurance athletes?

Evidence-Based Answer Symptomatic exercise-associated hyponatremia (EAH) as seen in 0% to 1.1% of endurance athletes, typically manifesting as neurologic symptoms ranging from dizziness, headache, and lethargy to seizures and death (SOR C, cohort studies).

Exercise-Associated Hyponatremia in an Ultra-Endurance Mountain Biker

Symptomatic exercise-associated hyponatremia (EAH), which is relatively common among marathon runners, is an uncommon event among ultra-endurance athletes. A 44-year-old man presented to the emergency department with increased thirst after successfully completing a 100-mile mountain bike race in Leadville, Colorado. Initial laboratory tests revealed a blood sodium level of 116 mEq/L. The primary etiologic factor in EAH is fluid consumption in excess of fluid losses in prolonged exertion. Early diagnosis and management is crucial to prevent cerebral and pulmonary edema.

Use of Hypertonic Saline in the Treatment of Exercise-associated Hyponatremia: Setting the Record Straight

The use of hypertonic saline in symptomatic exercise-associated hyponatremia (EAH) is a topic of great debate. Many unnecessary deaths from this condition have occurred because of failure of many in the exercise community to understand the proper use of this life-saving therapy. Dr. Ayus's group have been the pioneers in the use of hypertonic saline in the treatment of EAH. A landmark paper appearing in the Annals of Internal Medicine (2000) originally outlined its use in marathon runners with EAH presenting with non-cardiogenic pulmonary edema.1 They systematically used hypertonic saline to treat six runners with hyponatremic encephalopathy. His group went on to introduce the novel concept of using a 100 cc bolus of 3% NaCl for this condition2,3 and he was the first in the world to treat EAH this way in 2005 in a marathon in Cape Town, South Africa.4 In our recent paper,5 it appears that credit has not been given fully to Dr. Ayus and his colleagues. It is imperative that recognition be given to those who have done the original work and it is our hope that this sets the record straight. Tamara Hew-Butler, DPM, PhD Systematic Inflammation Laboratory Phoenix, AZ Timothy D. Noakes, MB ChB, MD, DSc University of Cape Town Cape Town, South Africa Arthur J. Siegel, MD Harvard Medical School Boston, MA

Hyponatremia Among Runners in the Zurich Marathon

Hyperhydration and exercise-associated hyponatremia (EAH) are critical issues during endurance events. We studied a cohort of marathon runners to examine EAH's prevalence in a marathon with a short time limit and to investigate underlying mechanisms that may be responsible for its development. Observational cohort study. 2006 Zurich Marathon (cool and rainy weather, time limit of 5 hours). 167 marathon runners were recruited the month before the race. Body mass, plasma sodium, and osmolality were measured just before the start and immediately after the race. Fluid intake during the race was ascertained by a recall questionnaire. Five subjects (3 %) developed asymptomatic EAH, and no symptomatic EAH was found. Body mass change during the race correlated similarly with postrace sodium levels (r = -0.72, P < 0.0001) and with sodium change during the race (r = -0.66, P < 0.0001). Postrace sodium levels correlated significantly with sodium change during the race (r = 0.74, P < 0.0001). Fluid intake correlated significantly (r = -0.43, P < 0.0001) with plasma sodium change between the start and finish of the race. Postrace sodium levels and postrace osmolality were significantly correlated (r = 0.68, P < 0.0001). In this study we observed a relatively low incidence of EAH in subjects running the marathon in around 2.5 to 5 hours and in a cool environment. Plasma sodium change during the race and postrace sodium levels correlated with body mass change. There was also a direct correlation between fluid intake and plasma sodium change during the race.

Exercise-Associated Hyponatremia: Role of Cytokines

Exercise-associated hyponatremia (EAH) has emerged in recent years as a life-threatening complication of endurance sports that may lead to fatal cerebral and pulmonary edema. Defined as a serum sodium concentration <135 mEq/L (1 mEq/L = 1 mmol/L), symptomatic EAH is a dilutional hyponatremia with abnormal fluid retention mediated by decreased urine production, which is a variant of the syndrome of inappropriate antidiuretic hormone secretion. Strategies for prevention and treatment must take into account the pathophysiology underlying this dominant clinical paradigm. Beyond educating runners to drink moderately, monitoring changes in body weight during endurance sports may facilitate the early detection of positive fluid balance characteristic of symptomatic cases. Rapid diagnosis by point-of-care testing indicates the need for fluid restriction in mild cases and emergent treatment with hypertonic (3%) NaCl to reverse acute hypotonic encephalopathy. The efficacy of arginine vasopressin V 2 receptor antagonists warrants study as an alternative treatment to loop diuretics for volume overload in these patients. Nonosmotic stimulation of arginine vasopressin secretion may be mediated in part by enhanced release of muscle-derived interleukin-6 during glycogen depletion, linking exertional rhabdomyolysis to the pathogenesis of EAH.