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Letters to the Editor

The Presented Evidence to Support Symptomatic Hypovolemic-Associated EAH Is Not Convincing

Hoffman, Martin D. MD, FACSM; Weiss, Robert H. MD

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Current Sports Medicine Reports: 11/12 2017 - Volume 16 - Issue 6 - p 464-466
doi: 10.1249/JSR.0000000000000420
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Deaths from exercise-associated hyponatremia (EAH) have been reported in association with various endurance competitions and activities (1,4,8). Unfortunately, at least four deaths from EAH since 2014 make it evident that the condition remains of concern (2,8,9,12). Dilutional hyponatremia from sustained overhydration in conjunction with impaired water clearance from nonosmotic secretion of arginine vasopressin is known to be the primary pathophysiology for symptomatic EAH (4). While EAH has been well documented in hypovolemia (6,11), symptomatic EAH is largely, if not exclusively, dilutional in nature (7,11).

Ongoing concern about EAH is supported by a recent case report published in this journal (3) of a man who developed hyponatremic encephalopathy during a 1200-km cycling event. A unique aspect of this report is that the authors retrospectively examined the trajectories of select biomarkers during recovery to conclude that they provide “clear evidence for volume depletion as the primary pathophysiological mechanism for the development of severe, symptomatic EAH” in this case. Their conclusion was based on an elevated blood urea nitrogen (BUN) on admission, downward trajectories during recovery of serum potassium, serum calcium, serum total protein, BUN, hemoglobin and hematocrit, and an increase in mean corpuscular volume (MCV) during recovery.

While a case of symptomatic hypovolemic EAH would be worthy of being reported, we are not convinced that the authors provide adequate support for the claim that the subject of their report was hypovolemic. The authors provide no data on the usual assessment measures for hydration status. Assessment of hypovolemia (synonymous in internal medicine and nephrology practice with decreased total body salt and water) is a clinical exercise of evaluating mucus membranes, skin turgor, and most importantly, orthostatic blood pressure. In the exercise setting, change in body mass is another measure that may be useful for assessment of hydration status, though it must be recognized that body mass loss is required during exercise to maintain euhydration due to the effects of body mass change from substrate use, release of water bound with muscle and liver glycogen, and production of water during substrate metabolism (5–7,10). While the ratio of BUN to creatinine is a marginally useful measure of prerenal azotemia (which does not necessarily indicate hypovolemia but more commonly indicates decreased “effective arterial volume”), the BUN in isolation is not useful for the diagnosis of hypovolemia. Elevated BUN concentrations may serve as a nonspecific indicator of increased protein catabolism, high dietary protein intake, kidney disease, hypermetabolic state (e.g., hyperthyroid) and gastrointestinal bleeding. Thus, an elevated BUN without additional findings is insufficient for making a diagnosis of hypovolemia.

We also are not convinced that the biochemical trajectories during recovery reported by Hew-Butler et al. (3) are adequate to support a diagnosis of hypovolemia given how the recovery trajectories they present are nearly identical to a case of symptomatic dilutional EAH we have previously reported. This case involved a 161-km ultramarathon competitor who progressively overhydrated (he had gained 2.4% of his body mass from immediately before the race start to 126 km, based on accurate measurement techniques) before dropping out and later seizing. After field treatment with two 100-mL boluses of 3% hypertonic saline, his admission serum sodium concentration was 122 mmol/L.

The time course during recovery of select biomarkers for our case are shown in Figures 1–3. These figures are arranged for easy comparison with those figures provided by Hew-Butler et al. As is evident, the time course for each biomarker was strikingly similar to those presented by Hew-Butler et al. Given that our case of dilutional hyponatremia displayed the same biomarker recovery trajectories as the case reported by Hew-Butler et al., we question if their subject was hypovolemic based on only the information they have provided in their report. While indeed there may be a volume depletion variant of symptomatic EAH, critical examination of the evidence provided by Hew-Butler et al. does not support such a diagnosis in their case.

Figure 1
Figure 1:
Recovery trajectories of serum concentrations of sodium ([Na+]), potassium ([K+]), creatine kinase ([CK]), and calcium ([Ca++]) during the hospitalization of an ultramarathon runner for dilutional EAH previously reported (7).
Figure 2
Figure 2:
Recovery trajectories of serum total protein, BUN, whole blood hemoglobin concentrations, and hematocrit during the hospitalization of an ultramarathon runner for dilutional EAH previously reported (7).
Figure 3
Figure 3:
Recovery trajectory of blood MCV during the hospitalization of an ultramarathon runner for dilutional EAH previously reported (7).

Martin D. Hoffman, MD, FACSM
Department of Physical Medicine and Rehabilitation
Department of Veterans Affairs
Northern California Health Care System
University of California Davis Medical Center
Sacramento, CA
Ultra Sports Science Foundation
El Dorado Hills, CA
mdhoffman@ucdavis.edu
Robert H. Weiss, MD
Departments of Medicine
Department of Veterans Affairs
Northern California Health Care System, and
Division of Nephrology
Department of Internal Medicine
University of California Davis Medical Center
Sacramento, CA

The authors declare no conflicts of interest.

This material is the result of work supported with resources and the use of facilities at the VA Northern California Health Care System. The contents reported here do not represent the views of the Department of Veterans Affairs or the United States Government.

References

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