Hydration issues in the endurance athlete are centered on the two components of the extracellular fluid compartments, total body sodium balance and water balance. Exercise-associated hyponatremia (EAH) is defined by serum sodium ([Na+]) concentration <135 millimoles per liter (mmol/L) occurring during or up to 24 hours after physical activity and is severe if <125 mmol/L.1 It is clinically divided into asymptomatic or symptomatic, whereby the latter is often seen with [Na+] <128 mmo/L.2Dehydration is defined as a deficit in total body water (TBW) with accompanying disruption of metabolic processes and typically results in hypernatremia. Changes in TBW can be best measured in a lab using deuterium oxide; however changes in body weight have been used as a practical surrogate measure with dehydration being defined as body weight loss >3%.3 This is estimated to be about 5% TBW.1 Dehydration must be distinguished from hypovolemia, which pertains to a reduction in plasma volume. Less common electrolyte abnormalities include hypernatremia and hypomagnesmia.1
The etiology of EAH has been described through two generalized models: dilutional and depletional.1,2 The dilutional model proposes that sustained overhydration with hypotonic fluids in the setting of impaired water clearance though inappropriate arginine vasopressin (AVP) secretion results in euvolemic or hypervolemic hyponatremia and is associated with weight gain. The depletional model proposes that excessive loss of under-replaced solute (sodium and potassium) occurs through sweat or impaired renal retention resulting in hypovolemic hyponatremia and is associated with weight loss. It is widely accepted that EAH is multifactorial and is predominately caused by dilutional mechanisms. Thus, when weight is gained during an endurance event, there is greater likelihood that an athlete will be hyponatremic.3 Excessive water loss through hypotonic sweat is the primary cause of dehydration in endurance athletes.
Epidemiology including risk factors and primary prevention
Guidelines in the past for ad libitum fluid intake were aimed at preventing rapid and severe dehydration in extreme conditions. It is now known that the single most important risk factor for EAH is sustained, excessive fluid (water, sports drinks, or other hypotonic fluid) intake in excess of water loss through sweat, respiratory and renal excretion resulting in a positive fluid balance.1 Prevention is primarily aimed at organized educational programs advising athletes to drink to thirst and monitor their body weight. Pre-event sodium supplementation has proven to have little to no role in prevention.2
Other risk factors include weight gain during exercise, exercise duration >4 hours (i.e., slow pace), event inexperience or inadequate training, high or low body mass index (BMI), and readily available fluids.1 The use of non-steroid anti-inflammatory drugs (NSAIDs) has also been a proposed risk factor presumably due to potentiation of renal water retention.4,5,6 Incidence is greater in females compared to males; however, when adjusting for BMI and racing time, the apparent sex difference is not significant.1
Asymptomatic EAH rates range from 0% to 51%. Symptomatic EAH is considerably rarer, with severe complications representing <1% of all EAH cases. There have been 14 reported deaths since 1981.1 More recently, there have been 3 deaths in American football players encouraged to drink copious volumes of hypotonic fluids to relieve exercise-associated muscle cramps (EAMC). It is now recognized EAMC reflects neurological fatigue rather than dehydration and electrolyte imbalances.1
Dilutional hyponatremia results from total body water expansion relative to total body exchangeable sodium.1 Osmotic gradients result in water shifting into the intracellular compartment leading to cellular edema. Symptoms result from pathologic central nervous system (CNS) tissue expansion and become life threatening with elevated intracranial pressures.
The excretory rate of the kidneys is between 800-1000 milliliters/hour (mL/h) in the normal resting adult and the athlete loses about 500 ml/h during exercise. Thus, fluid consumption at a rate of 1.5 liters/hour (L/h) theoretically should prevent overhydration.2
Osmoreceptors within the circumventricular organ of the brain lack a blood-brain barrier and are in communication with blood and baroreceptors (carotid and aortic arch), thus act as physiological sensors to regulate plasma osmolality and volume by coordinating thirst and AVP secretion.1
AVP is synthesized in the hypothalamus, stored in the posterior pituitary gland, and acts at the V2 receptor in the collecting ducts of the kidney to open aquaporin channels thus reabsorbing water. Non-osmotic AVP secretion or Syndrome of Inappropriate Antidiuretic Hormone (SIADH) may occur during exercise due to stimuli including elevated body temperature, volume contraction, hypoglycemia, interleukin-6 (IL-6) release, and nausea or vomiting.1,2
Osmotic inactivation and/or impaired mobilization of osmotically inactive sodium stores has also been theorized to play a role in the development of hyponatremia during endurance events.3
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Serum [Na+] is not always a good predictor of symptoms. Asymptomatic EAH is a biochemical finding and athletes may only experience mild transient complaints that are typical of any endurance event. Mild symptomatic EAH may present with non-specific signs and symptoms such as light headedness, dizziness, nausea, bloating, puffiness, and/or increase in body weight.1,2 These athletes usually do not improve in the Trendelenburg position; however, they do not have signs of encephalopathy. Serum [Na+] levels should be measured as they may acutely progress to severe EAH or life-threatening exercise-associated hyponatremic encephalopathy (EAHE). EAHE is characterized by headache, vomiting, altered sensorium, seizures, dyspnea or frothy sputum (non-cardiogenic pulmonary edema), decorticate posturing or mydriasis (signs of brainstem herniation), and/or coma as sequelae of cerebral edema and brainstem herniation.1
Dehydration levels greater than 8% may cause athletes to experience severe thirst and dry mouth. If the level of dehydration reaches 15-20%, serious health consequences such as tachycardia, hypotension, and even death may result.7
Specific secondary or associated conditions and complications
Athletes with asymptomatic EAH are at risk for developing delayed-onset symptomatic EAH up to 24 hours after the event.
A secondary complication of symptomatic EAH is CNS-triggered non-cardiogenic pulmonary edema, which may require supplemental oxygen or intubation if adequate oxygen saturation is not maintained.
Performance decrements and cardiovascular strain have been documented when baseline body fluid volume decreases are >2%.
2. ESSENTIALS OF ASSESSMENT
Evaluation should include history of present illness, past medical history (with attention to hypertension, diabetes, hyperlipidemia, heart failure, chronic liver or kidney disease, and/or neurologic insults), supplements or medications (with attention to diuretics, antihistamines, anti-hypertensives, lithium, and NSAIDs), pre- and post-race weight, amount of fluid and food ingested during the event and what type, urine production (clear or dark and amount), vomiting or diarrhea, shortness of breath, history of problems in past races, and amount of training prior to current event.
Physical exam focuses on the central nervous system, pulmonary system, and cardiovascular system. Assessment of vital signs is essential. Tachycardia and hypotension are associated with dehydration, whereas vital signs (including body temperature) are usually not grossly abnormal in hyponatremia. A rectal temperature should be obtained to most accurately measure core body temperature in cases of suspected concomitant exertional heat-related illness as this may impact initial treatment protocol.8Basic cardiopulmonary exams may provide important information. Unconscious patients should be assessed for abnormal posturing and pupillary responses. In the conscious athlete, a brief mental status exam can be performed if there is question for altered sensorium. Evaluate for peripheral and pulmonary edema. Weight gain or loss can be used to assess water balance and may provide indication of serum [Na+]. Physical signs of dehydration include dry mucous membranes, poor skin turgor, sunken eyes, and delayed capillary refill.
Presentation of EAH varies depending on severity, ranging from asymptomatic to seizures to coma. Dehydration also has a wide range in presentation including mental status changes (confusion, behavioral changes including increased aggression).9
On-site serum [Na+] can be rapidly obtained within minutes using the i-STAT® handheld blood analysis system. Medical teams at most endurance events are equipped with i-STAT® analyzers and accompanying testing cartridges. Depending on which cartridges are available, renal function labs may also be obtained which can provide information on hydration status. There may be, however, instances where patients are suspected for having EAH and serum [Na+] cannot be obtained (see treatment section for management in this circumstance). Glucometers can rapidly determine blood glucose levels providing important information considering [Na+] is artificially lowered (i.e., pseudohyponatremia) by hyperglycemic states and must be corrected using correction factors.10 Other causes of pseudohyponatremia include hyperlipidemia and hyperproteinemia, both of which need to be determined through laboratory blood panels.10 In the hospital setting, serum and urine osmolality should be obtained. As stated earlier, deuterium oxide is used to measure changes in TBW but is not practical for onsite testing.
Neuroimaging such as computerized tomography (CT) of the brain may be obtained once an athlete with EAHE is at an advanced medical care facility, however this must not interrupt acute treatment.1
Supplemental assessment tools
Athletes should obtain their baseline event-day weight as it acts as a surrogate measurement of body fluid balance. Lack of weight loss or weight gain during an endurance event is a positive indicator of fluid overload and possible hyponatremia.1 Some weight loss (1.5-2.5 kilograms) is expected during an endurance race, but should not exceed 2% of body weight as this increases the risk for dehydration.11 If pre-race weight is not obtained, the history of the athlete’s normal weight is a good substitute.
Early predictions of outcomes
Severity of initial presenting symptoms and not absolute serum [Na+] can predict outcome and should guide therapy.1 Any athlete suspected for EAH should have rapid determination of serum [Na+]. With appropriate recognition and management, the vast majority of asymptomatic or mildly symptomatic EAH or dehydration cases resolve without long-term sequelae. For both EAH and dehydration, loss of consciousness or disorientation suggests more severe abnormalities and should be acted upon emergently.
Social role and social support system
Athletes with asymptomatic EAH or those treated for mild symptomatic EAH should be discharged from the event’s medical assessment area with a companion to monitor for the development of neurological symptoms that would prompt immediate medical attention.1
Extreme environmental temperatures can affect the likelihood of developing either dehydration or EAH. Cold may elevate the osmotic set-point for secretion of AVP, especially when age >65 years.12 Non-acclimatized athletes may require hydration beyond thirst drive in temperatures >38ºC to improve performance and prevent dehydration.12 Prolonged exercise in warmer climates has suggested excessive-sodium losses as the primary mechanism for EAH, however evidence to date is limited.2
Good Samaritan laws vary among states, however generally only cover doctors who are also bystander fans. Physicians might be participating and can help out in an emergency on the course if Good Samaritan laws are in place. If a doctor is an official race event volunteer, then additional malpractice insurance should be obtained. Recently insurance policies have been developed specifically for volunteer medical teams.
3. REHABILITATION MANAGEMENT AND TREATMENTS
Available or current treatment guidelines at different disease stages
Treatment should be determined by the degree of neurological impairment and not simply the [Na+], because both the magnitude and rate of development of hyponatremia influence brain edema.1 Onsite treatment guidelines for hyponatremia are now organized by whether serum [Na+] has or has not been confirmed by measurement and whether the athlete is asymptomatic, symptomatic, or in severe EAHE.1,2
Onsite treatment of EAH confirmed by [Na+] measurement:
- Asymptomatic EAH or mild EAH with non-neurological symptoms:
- Restrict hypotonic or isotonic fluid intake until onset of urination.
- May provide oral hypertonic saline solutions such as salty soup or snacks, especially in those with [Na+] <130 mmol/L.
- Observe for 60 minutes until symptoms resolve.
- Educate on neurologic signs and symptoms of EAH and advise to seek immediate medical attention.
- Discharge from medical area with a companion.
- Severe EAH or EAHE:
- Emergent treatment with IV hypertonic saline (100 mL 3% bolus) to decrease intracranial pressure.
- May give up to 3 boluses at 10 minute intervals.
- Stabilize for transfer to acute care facility.
- Onsite treatment suspected EAH not confirmed by [Na+] measurement:
- Consider differential diagnosis and weigh risk versus benefit of fluid restriction.
- Empiric treatment is recommended if clinical suspicion is high.
- If encephalopathy develops, rapid infusion of IV hypertonic saline should be initiated emergently as this is not associated with negative consequences if EAHE is wrongly assumed.
Coordination of care
It is critical that medical personnel in emergency transport services are aware of the athlete’s diagnosis, prior treatments, and the importance of avoiding isotonic or hypotonic fluid resuscitation which would worsen hyponatremia. The patient may need management in an intensive care unit (ICU) if they do not improve.
Measurement of treatment outcomes
There are no current guidelines necessitating ongoing [Na+] measurement during management for EAH as treatment is dictated primarily by symptoms, however this may be practiced in asymptomatic or mild symptomatic EAH athletes before discharge to ensure [Na+] is at least >130 mmol/L.
Patient & family education
Prevention through education is the main goal and requires broad programs targeted to athletes, coaches, trainers, and parents emphasizing the importance of appropriate hydration practices, recognition of EAH signs and symptoms, and urgency of therapy.1 They must understand that excessive fluid intake will not prevent muscle cramps and exertional heat stroke. This education, along with management protocols, must also reach onsite, emergency, and hospital medical personnel.
Some practical recommendations from the International Marathon Director’s Association include:12
- Drink to thirst. Obey the body’s natural physiological cues.
- Water, sodium, and glucose should be available at fluid replacement stations spaced 1.6 km (minimum) to 5 km (maximum) apart.
- Calibrated scales along a marathon course should be at the discretion of the medical team and weight loss of >4% or any weight gain constitutes justification for medical consultation.
- Sports drinks contain less sodium than body fluids and can worsen EAH.13
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
A few simple facts:
- Risk factors for EAH:
- Excessive drinking
- Low body weight
- >4 hours of exercise / slow pace
- Female (due to average lower body weight and longer participation times)
- Inexperience racer
- Extreme heat or cold
- How much should you drink? No more than 500-1200 mL/h, depending on training level and environmental factors, but thirst is the best gauge for hydration.
- Consumption of sports drinks can worsen EAH.13
4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
Cutting edge concepts and practice
The increasing usage of i-STAT® handheld blood analysis systems has advanced onsite care of EAH by improving its early recognition. Recent evidence suggests that some athletes mobilize sodium stores more than others, yet this is not well understood.3
5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Gaps in the evidence-based knowledge
Current controversy exists over the hypovolemic variant of EAH, particularly the contribution of sodium loss through hypotonic sweat and role of brain naturietic peptide in urinary sodium losses. Current guidelines are to treat these individuals with IV hypertonic saline bolus, followed by IV normal saline to replete volume.1 Other areas of future investigation include the role of diet, success of the “drink to thirst” strategy, recurrence rates of EAH, long-term health implications, possible genetic markers, the role of NSAIDs, investigating alternative treatments for mild EAH, and the variability in [Na+] and body weight days leading up to an event and at event start.1
- Hew-Butler T, Rosner MH, Fowkes-Godek S. Statement of the third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clin J Sport Med. 2015;25(4):303-320.
- Krabak BJ, Parker KM, DiGirolamo A. Exercise-associated collapse: is hyponatremia in our head? PM R. 2016;8:S61-S68.
- Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: Evidence from 2,135 weighed competitive athletic peformances. Proc Natl Acad Sci U S A. 2005;102:18550-18555.
- Page AJ, Reid SA, Speedy DB, Mulligan GP, Thompson J. Exercise-associated hyponatremia, renal function, and nonsteroidal antiinflammatory drug use in an ultraendurance mountain run. Clin J Sport Med. 2007;17(1):43-48.
- Speedy DB, Noakes TD, Schneider C. Exercise-associated hyponatremia: a review. Emerg Med. Mar 2001;13(1):17-27.
- Irving RA, Noakes TD, Buck R, et al. Evaluation of renal function and fluid homeostasis during recovery from exercise-induced hyponatremia. J Appl Physiol. 1991;70(1):342-348.
- Noakes TD. Dehydration during exercise: what are the real dangers? Clin J Sport Med. 1995;5(2): 123-128.
- O’Connor FG and Casa DJ. Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on July 20, 2016.)
- Speedy DB, Noakes TD, Rogers IR, et al. Hyponatremia in ultradistance triathletes. Med Sci Sports Exerc. 1999;31(6):809-815.
- Sterns RH. Causes of hyponatremia in adults. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on July 20, 2016.)
- O’Toole ML, Douglas PS, Laird RH, Hiller DB. Fluid and electrolyte status in athletes receiving medical care at an ultradistance triathlon. Clin J Sport Med. 1995;5(2):116-122.
- Hew-Butler T, Verbalis JG, Noakes TD. Updated fluid recommendation: position statement from the International Marathon Medical Directors Association (IMMDA). Clin J Sport Med. 2006;16(4):283-292.
- Cohen D. The truth about sports drinks. BMJ. 2012;345:e4737.
Danz M, Pöttgen K, Tönjes PM, et al. Hyponatremia among triathletes in the ironman European championship. New Engl J Med. 2016;374:997-998.
Godek SF, Bartolozzi AR, Peduzzi C, et al. Fluid consumption and sweating in National Football League and collegiate football players with different access to fluids during practice. J Athl Train. 2010;45(2):128-135.
Thomas DT, Erdman KA, Burke LM. Position of the Academy of Nutrition and Dietetics, Dieticians of Canada, and the American College of Sports Medicine: nutrition and athletic performance. J Acad Nutr Diet. 2016;116(3):501-528.
Zambraski EJ. The renal system. In: Tipton CM, ed. ACSM’s Advanced Exercise Physiology. Philadelphia, Baltimore: Lippincot Williams & Wilkins; 2006.
Original Version of the Topic:
Robert Irwin, MD, Michelle D. Francavilla, MD. Hydration Issues in the Athlete and Exercise Associated Hyponatremia. Publication Date:2012/12/28.
Richard G. Chang, MD
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Jameel J Khan, MD
Nothing to Disclose