Abstract
To the Editor:
We appreciate that Spano et al 1 have brought to your readers’ attention an interesting case of symptomatic hyponatremia that was mistaken for high altitude cerebral edema. The case highlights the importance of recognizing overlapping signs and symptoms of exercise-associated hyponatremia (EAH) and acute altitude illness, as has been previously discussed.2,3 The Wilderness Medical Society Practice Guideline for treatment of EAH 3 goes a step farther to point out that EAH may also be mistaken for dehydration or heat illness as a result of a similar complex of signs and symptoms. In general, incorrect diagnoses delay the institution of proper treatment. In the case of EAH, a delay in proper treatment can result in disastrous neurological sequelae. Even more concerning, though, can be treatment that could make matters worse, as it was with the case described by Spano et al. 1
The case is that of a woman who had been hiking in the Sierra Nevada Mountains. During her second day, she experienced headache, nausea, vomiting, and diarrhea that was later followed by a grand mal seizure. She was incorrectly presumed to be suffering from high altitude cerebral edema and received at least 1.5 L of normal saline solution before recognition that she was hyponatremic. Isotonic and hypotonic fluids were continued after available physical examination and laboratory studies suggested that that she was hyponatremic and volume replete. Fortunately, it appears that likely effects from arginine vasopressin causing fluid retention had resolved, and her blood sodium was able to correct despite this intervention.
The current treatment recommendation for confirmed or suspected EAH is hypertonic saline solution rather than isotonic or hypotonic fluids. 3 The hypertonic saline solution may be given orally when the patient can take oral fluids, but should otherwise be given as a 100-mL intravenous bolus of 3% hypertonic saline solution, and repeated 2 additional times if needed.3,4 The rationale for concern about treating EAH with isotonic and hypotonic fluids has been extensively detailed. 5 Although Spano et al 1 comment that hypertonic saline solution has been used in the treatment of EAH, they lead the reader to believe that appropriate management of EAH is with isotonic fluids by the statements “normal saline therapy of symptomatic hypotonic hyponatremia can be effective [in this setting]” and “an initial normal saline bolus would be effective therapeutically in both hyponatremia and hypernatremia cases.” Furthermore, they cite one of our publications to support the use of normal saline solution in treating EAH. That paper referred to 2 ultramarathon runners with combined biochemical hyponatremia and rhabdomyolysis progressing to acute kidney injury who received intravenous normal saline solution. 6 We have discussed the importance of correctly balancing the contradictory interventions appropriate for EAH and acute kidney injury, and have recommended extreme caution in the use of intravenous normal saline solution as initial treatment when EAH may be a diagnosis. 3 ,5–8 Acute kidney injury, as might occur in a volume-depleted state or as a consequence of rhabdomyolysis, was not a concern in the case described by Spano et al, 1 so it cannot be used to rationalize use of isotonic and hypotonic fluids once the EAH diagnosis had been made.
The information provided in this case report suggests that the patient had overhydrated (“consumed liberal amounts of filtered water”) and was not dehydrated given her admission blood pressure (although orthostatic blood pressures, which would have been most useful in assessing volume status, are not reported) in the face of normal blood urea nitrogen and creatinine concentrations. Her symptom of nausea, a potent nonosmotic stimulus for secretion of arginine vasopressin, was also likely involved in the initial pathogenesis of her severe hyponatremia.3,4 Interestingly, it is conceivable that the underlying stimulus for her nausea was acute mountain sickness. We do not believe there is support for a depletional mechanism to have played a role, as was suggested by the authors. Although a depletional mechanism may be involved in the development of EAH under some circumstances, 7 as far as we are aware the severe symptomatic cases of EAH reported thus far in the literature have been associated with fluid overload without evidence for a depletional mechanism.4,7 The treatment for these cases of EAH should focus on elevating the blood sodium concentration rapidly to resolve cerebral edema, which can be achieved with a bolus of hypertonic saline solution without risk of osmotic demyelination or central pontine myelinolysis.3,4