Staying Sufficiently Salty: Avoiding Exercise-associated Hyponatremia

Author: Calvin Tan

Edited by: Wesley Chan

Case:

You are the lead physician in the medical tent at the finish line of a single-stage, 24-hour, self-supported, 100-mile race. The only on-course support consists of simple tents every 20 or so miles with first aid supplies and water to refill hydration bladders. 

For the past 8 or so hours, runners have reached the finish line in various states of distress, and finally here, in the last hour of the day, the last few stragglers are coming in. Cots are being folded, and supplies are being put away when suddenly an athlete is carried into the tent by two volunteers.

The patient is a middle-aged male who just crossed the finish line then suddenly collapsed and has been unable to respond. From looking up his “bib” number, he has no declared medical problems, long-term medications, or allergies to medications.

You quickly complete your primary assessment of the patient and though he has decreased mental status, he is still protecting his airway. Breath sounds are normal bilaterally. Heart sounds are normal with pulses palpable throughout. The patient has reactive pupils, withdraws from pain, and has no abnormal posturing. 

What explains the patient’s symptoms? What is the pathogenesis of the disease? What is the next step?

Exercise-associated Hyponatremia

On November 3rd, 2020, our Wilderness EM Mini-Fellowship hosted a virtual journal club discussing the article:

Bennett BL, et al. Wilderness Medical Society Clinical Practice Guidelines for the Management of Exercise-associated Hyponatremia: 2019 Update. Wilderness Environ Med. 2020:31(1):50-62. [1]

Introduction:

Exercise-associated hyponatremia (EAH) is defined as serum sodium concentration below the normal reference range (135 mmol/L) that occurs up to 24 hours after prolonged activity. Patients with this condition can have symptoms ranging from asymptomatic to comatose. Because of this range, the true incidence of the disease is unknown, but studies conducted at individual endurance events have found the incidence to be as high as 50%. Most symptomatic cases are mild, and severe disease is quite rare.

Along with the uncertainty of disease incidence, the pathogenesis is still not fully understood. The best current explanation suggests a combination of excess hypotonic fluid intake, hypertonic fluid loss, endogenous vasopressin activity, and inadequate replenishment of sodium.

The 2019 update to the Wilderness Medicine Society Clinical Practice Guidelines offers expert opinion and a review of the literature to guide diagnosis, care, and interventions. While most cases are found in organized front- or backcountry events. The guidelines can also be applied should non-event-associated illness occur.

Pathophysiology:

The article points to overhydration with hypotonic solutions as the main driver of EAH. The hyponatremia is thought to be dilutional as the patient (runner, hiker, etc.) takes in fluids above the fluid losses from sweat, urine, and insensible losses. The strongest evidence to back this cause is a series of observations of overall weight gain when comparing pre- and post-exertional weights in endurance athletes who end up developing EAH; this suggests an overall gain in total body fluid.

However, this finding alone is not enough to explain the development of EAH. The article points out that while exercising individuals can lose anywhere from 1000-1500 mL/hour through renal excretion, sweat, and insensible losses depending on environmental factors, and many individuals who develop EAH do not drink over this maximal elimination rate. Therefore, it is likely that other factors are in play.

One of the main additional processes pointed to by the article is arginine vasopressin (AVP). AVP works at the distal tubules of the kidneys causing a net return of free water through increased expression of aquaporins in collecting duct cells (Figure 1). AVP secretion can be stimulated by physiologic conditions and factors often present during an activity such as exercise itself, pain, hypoglycemia, heat exposure, and NSAID use. 

Figure 1: AVP Pathway [2]

Risk Factors

Of the risk factors for EAH mentioned in the article, the biggest risk was associated with overhydration with hypotonic fluids. NSAID and diuretic use can also decrease GFR and limit electrolyte re-uptake respectively. As previously mentioned, NSAIDs are also implicated in the release of AVP.

Interestingly, although women were thought to have a higher incidence of EAH, the article states that after correcting for body mass index and exposure time, the effect of sex was not statistically significant to the likelihood of development of EAH. 

Recommendations

Prevention

The top level recommendation is for those patients who engaged in prolonged physical activity (greater than 4 hours) to avoid overhydration with hypotonic fluids (1A: strong recommendation, high-quality evidence). 

In the pre-exercise period, the recommendation is to increase participants’ and first responders’ education of risks associated with prolonged exercise – in this case, providing specific education on the risk factors as well as signs and symptoms of EAH (1C: strong recommendation, low-quality evidence). Suggested forms of education included videos, written handouts, and in-person briefings before an event. 

Additionally, there it is recommended to advise participants to drink to thirst as opposed to other experiential strategies such as drinking before experiencing thirst or drinking to an arbitrary, fixed amount (1C). The final preventative intervention suggested was making available supplemental sodium in the form of salty snacks or salt packets; this recommendation carried a lower rating because that it would likely not be enough to offset overhydration (2B: weak recommendation, moderate-quality evidence). Of note, the provision of oral sodium was also evaluated as a treatment for EAH and given the same rating due to unpredictable efficacy in increasing serum sodium (2B). Unlike water, electrolytes like sodium are dependent upon active transport to transit from the gastrointestinal (GI) lumen to the serum (Figure 2). 

Figure 2: GI Luminal H20 Exchange [3]

Assessment and Treatment

The other recommendations in the paper pertained to diagnosing and treating patients with EAH. The primary recommendation for assessment was to obtain a serum chemistry panel, if available, to make a definitive diagnosis of EAH (1A). Portable testing devices can be used for diagnosis as they are commercially available and often deployed at large events.

Figure 3. Example POC Device by Abbott Laboratories (no endorsement or financial relationship)

Unsurprisingly, another recommendation is that even in the absence of testing capabilities, history and symptomatology can be used to make the diagnosis (1C). Though EAH has a significant overlap of symptoms with hypernatremia as well as hyperthermia, key differentiators including fluid status (weight, presence of pulmonary edema) and temperature can be used to rule out other exertion-related etiologies.

Treatment recommendations include fluid restriction of patients suspected or diagnosed with EAH until urine production resumes as well as observation of symptomatic patients for at least an hour of treatment as further fluid absorption in the GI tract can continue to worsen the patient’s condition (1C). 

Lastly, in the rare cases of hypovolemic EAH, hypotonic IV solutions should still be avoided. Isotonic IV solutions can be used but should be restricted until the onset of urination similar to the oral fluid restriction strategy (1C). 

In patients with severe EAH, primary assessment should focus on neurologic and cardiac status as these patients can suffer from cerebral edema or non-cardiogenic pulmonary edema respectively (1A). Severe EAH can be treated with 100 mL boluses of hypertonic saline (1C). The strategy described in the article is 100 mL boluses every 10 minutes up to 3 times or until neurologic symptoms resolve. 

Figure 4. Possible historical and physical exam findings for exertional illnesses with proposed treatment approaches. [1]

Case Conclusion

You quickly complete your primary assessment of the patient and though he has decreased mental status, he is notably still protecting his airway. As an IV line is placed and a blood sample is taken, the rectal temperature registers at 98.1F. A few minutes later, the point of care testing unit returns a chemistry panel significant for sodium level of 127 mmol/L. 

You remember back to a guideline article you’d skimmed recently and remember hypertonic saline boluses were a suggested treatment for EAH. Treatment is initiated and after two 100 mL boluses, the patient begins to become more responsive and verbal. 

As you prepare to transfer the patient to a tertiary care center, an individual who identifies himself as the patient’s training partner appears. He states that they had completed shorter races in the past and did well with a fueling strategy of trying to take in at least 500 mL of water every hour along with salty snacks and gels they’d brought along. The pair separated just past the halfway mark as the patient began to have cramps and told his partner to go ahead. He states that he and the patient had planned their fueling and replacement strategy for only 16-17 hours of total exposure.

The patient is loaded into an emergency vehicle for transfer for further care. His training partner accompanies him in the vehicle, and the patient is noted to be progressively more verbal and aware. He states that he ran out of snacks and supplements around hour 20, but while trying to drag himself to the finish he felt fatigued and nauseous causing him to think he was dehydrated. So he had continued to drink water to try and stave it off. 

References: 

1.         1. Bennett BL, et al. Wilderness Medical Society Clinical Practice Guidelines for the Management of Exercise-associated Hyponatremia: 2019 Update. Wilderness Environ Med. 2020:31(1):50-62.
2.         2. Stockand JD. Vasopressin regulation of renal sodium excretion. Kidney Int. 2010;78(9):849-856.
3.         3. Hall JE, Guyton AC. (2011). Chapter 65. In Guyton and Hall textbook of medical physiology. Philadelphia, PA: Saunders/Elsevier.

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Wesley Chan

EM/IM Resident Class of 2024

Latest posts by Wesley Chan (see all)

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