The Letter to the Editor of Dr Lipman demonstrates an unfortunate persistent confusion about potential dangers from exercise-related dehydration and the appropriate management of exercise-associated hyponatremia (EAH). We welcome the opportunity to respond to this letter with hopes that readers will be enlightened to nearly 40 years of evidence and that we can provide further support for our position in the WMS Practice Guideline on Treatment of Exercise-Associated Hyponatremia. 1
Dr Lipman seems to express 2 primary concerns with our EAH Practice Guideline. One of his issues is that he believes there is the potential for “grave consequences” from delay in treating an athlete’s hypovolemia out of concern that the athlete might have EAH. In his proposed algorithm, he recommends provision of 1 to 2 L of intravenous normal saline (NS) or NS with 5% dextrose in athletes who have symptoms suggestive of EAH and also display signs and symptoms of severe dehydration. He emphasizes symptom recognition in the diagnosis of dehydration. However, the clinical assessment of dehydration in athletes has been shown to be unreliable. 2 More importantly, as far as we know, there is no documentation in the scientific literature linking exercise-related dehydration to life-threatening conditions. 3 Endurance athletes have been shown to have body mass losses of 8% or greater without significant clinical symptomatology or adverse consequences.4,5 In most cases, such levels of dehydration are not hazardous and rarely require intravenous rehydration if oral fluids can be tolerated. Furthermore, a recent evidence-based review revealed that it is transient postural hypotension that is the most common etiology for why endurance athletes receive postevent medical attention. 6 This is caused by lower extremity pooling of blood once the athlete stops moving and the resultant impairment of cardiac baroreceptor reflexes. These athletes present with lightheadedness, dizziness, or syncope, which has historically been managed as dehydration or hyperthermia by race event medical providers. 6 The perception that heat exhaustion is caused by dehydration and that the levels of dehydration observed in endurance sports must be treated immediately with intravenous fluids has been termed the “dehydration myth” and was noted to have been “relentlessly perpetuated” well over a decade ago. 3 Unfortunately, it appears that the confusion continues to be perpetuated.
The second primary concern expressed in the letter of Dr Lipman appears to be that he believes that when point-of-care testing of serum sodium is not available, the literature does not support our recommendations and grading relative to the use of intravenous hypertonic saline (HTS) over NS in the treatment of presumed EAH. In this regard, he also indicates we do not provide ample evidence to support the concern we raise about treating EAH with intravenous NS. We believe that in Dr Lipman’s review of the 4 references we cite to support our position, he has unfortunately arrived at faulty conclusions. We will critically reexamine and clarify the findings of those papers that support our position.
The earliest report that we reference in support of treating EAH with HTS and the potential risk of treatment with NS was that of Frizzell et al. 7 This report is of 2 overhydrated ultramarathon runners with symptomatic EAH. One received intravenous NS, and was hospitalized for 5 days with 36 hours in a semicomatose state. The other runner received intravenous 3% HTS and was fully alert in 3 hours and discharged after 8 hours. Although not definitive proof of the effectiveness of HTS, this is early suggestive evidence. We disagree with Dr Lipman’s conclusion that the report indicates “severe EAH resolves with both NS and HTS” as we do not find a 5-day hospitalization with prolonged impairment of central nervous system function to be an acceptable outcome.
The second cited publication describes 7 marathon runners with symptomatic EAH. 8 For the 1 patient who died, the diagnosis of EAH was unsuspected, and the patient therefore did not receive treatment for EAH. In contrast, all 6 patients who were correctly diagnosed and treated with 3.3% HTS survived. We accept that, at best, this report suggests that there might be potential value of HTS in the treatment of EAH. We also agree that the additional 2 cases of EAH noted to have survived after receiving intravenous NS do not support that premise. But we do not agree with Dr Lipman’s conclusion that “HTS is beneficial for critical EAH, and mild EAH can be treated with either HTS or NS.” Rather, we would reserve such conclusion recognizing that some patients will survive despite inappropriate management.
The third cited publication describes a retrospective and prospective analysis of EAH treatment. 9 The retrospective analysis involved 11 overhydrated marathon runners with severe EAH (defined as blood sodium ≤125 mEq/L by the authors). They were all treated initially with intravenous NS. Five of these runners (blood sodium concentration range, 119–121 mEq/L) required hospitalization, with 3 requiring intubation. Two of these patients ultimately received HTS in the intensive care unit. Fortunately, all runners survived and were discharged several days later. The prospective treatment trial involved 4 cases of overhydrated marathon runners with severe EAH (blood sodium concentration range, 117–123 mEq/L) treated with 3% HTS. None required hospitalization, and the rate of blood sodium correction with HTS was shown to be more rapid than for those runners in the retrospective analysis who were treated with NS. Dr Lipman’s conclusion that “in critical EAH, NS had the same outcome as HTS therapy” is not supported given the extended hospitalization evident among those treated initially with NS.
The fourth cited publication describes 4 marathon runners who became unresponsive and were found to have EAH. 10 The 2 patients treated with intravenous NS died with evidence of cerebral edema on postmortem examinations. In contrast, in the 2 runners receiving 3% HTS, the treatment “resulted in rapid neurologic improvement without adverse effects.” Furthermore, the graphs provided in the publication that show the time course for treatment with HTS demonstrate that the resolution of neurological symptoms occurred in less than 2 hours after this treatment was initiated. Regarding the 2 patients treated with NS, the article has an unfortunate typographical error (indicating the infusion was initially “at 150 mL/,” denominator not provided), but it is understood that the infusion rate was 150 mL/h (Art Siegel, MD, personal communication, June 4, 2013). Dr Lipman’s conclusion that “severe EAH requiring intubation has a dismal prognosis” is unsupported given that runners with EAH who were treated with HTS had good outcomes and those who were treated with NS did not. Furthermore, his conclusion that “it is unknown what effect 150 mL of NS had on the hyponatremic state or clinical condition” seems to result from misinterpretation of the paper.
In addition to these 4 reports demonstrating the potential adverse consequences of intravenous NS hydration and benefits from HTS in athletes with EAH, another early case report provides further support for our concern about the potential dangers of intravenous NS hydration in EAH. 11 This case was of a runner who was taken to a hospital after arriving at 70 km in a 90-km ultramarathon with confusion. Presuming she was dehydrated, she was given 1 L of intravenous NS. She subsequently suffered a grand mal epileptic seizure and lapsed into coma. Her serum sodium concentration was found to be 115 mEq/L, and she was found to have neurogenic (noncardiac) pulmonary edema.
Given the supporting evidence for adverse consequences from intravenous NS hydration in athletes with EAH, the evidence that HTS is effective in treating EAH, and the finding that there is no evidence for life-threatening conditions from exercise-related dehydration resulting in a need for intravenous rehydration, we stand by our recommendation that “hypotonic or isotonic fluid intake should be restricted in known or suspected EAH until urination begins.” A recommendation grade 1A is supported as there is overwhelming evidence from the series of observational studies we cite to support this recommendation. We also believe that our recommendation for the use of HTS rather than NS in symptomatic confirmed or suspected EAH is well supported from the publications described above.
With regard to Dr Lipman’s proposed algorithm for treatment of EAH without point-of-care confirmation, we can agree that the right and left sides of his treatment scheme are consistent with our position. It is the central portion of the algorithm outlining treatment for the athlete who is symptomatic for EAH and dehydration with intravenous infusion of 1 to 2 L of NS where we strongly disagree. The cases described above demonstrating the adverse consequences of such treatment provide the support for our stance.
Finally, we would like to make it clear to your readers that a Letter to the Editor does not undergo peer review. We have expressed our concern to the Editor and asked that Dr Lipman’s contradictory algorithm not be published without peer review given that a published algorithm becomes easy for a reader to use without scrutinizing the accompanying text. We hope that the readers of your journal will closely review our response before accepting this algorithm.