American Journal of Emergency Medicine xxx (2014) xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Correspondence
Etiology and management of exercise-associated hyponatremic encephalopathy (EAHE) To the Editor,
The case report of Severac et al [1] describing a case of exerciseassociated hyponatremic encephalopathy (EAHE) brings to the reader's attention a condition that is considered one of the most important clinical problems in endurance exercise [2]. There is now a broad consensus as to the common underlying pathophysiologic process in this condition [2-5] and to the most appropriate diagnostic and treatment strategies [2,5]. The pathophysiology, especially in severe cases such as that reported, is typically dilutional, resulting from a combination of excess fluid consumption and failure to excrete that fluid load due to inappropriate arginine vasopressin secretion [2-5]. This is evidenced in this case by acute hyponatremia associated with hypotonicity and an aquaresis on recovery. To state as the authors do in their discussion that the pathophysiology includes “sodium depletion in sweat” risks perpetuating an unproven myth [5]. This matters because athletes may believe that salt supplementation is the answer to prevention [6] when the correct prevention strategy is proper fluid balance through drinking to thirst rather than a predetermined regime [2,5]. For the emergency practitioner, the key to the correct diagnostic and therapeutic path is to understand that EAHE is the clinical manifestations of acute cerebral edema consequent on water following the osmotic gradient into brain cells. Our anecdotal experience in treating such athletes is that abdominal pain is an infrequent symptom, unlike the authors' contention, whereas nausea and vomiting are common. These represent cerebral symptoms due to increased cerebral pressure. Once EAHE is diagnosed biochemically in an at-risk athlete, as occurred in this case, then the key clinical action is urgent administration of hypertonic saline. The formulation is less critical (concentrations between 3% and 20% have been used) than the need to deliver a bolus of sodium chloride with limited fluid. The aim is to acutely increase the serum sodium concentration by approximately 2 to 5 mmol/L, and this is usually achieved with the current recommended strategy of up to three 100-mL boluses of 3% saline given in short succession [5]. This rapidly reverses the cerebral cellular swelling and is a potentially lifesaving, time-critical intervention [7]. Because the
process of cellular swelling occurs rapidly in EAHE, the adaptation of cellular organic osmolite secretion does not take place as with chronic hyponatremia, so there is no risk of osmotic demyelination from rapid correction of the low blood sodium concentration [5]. We would strongly counsel against some of the strategies reported by Severac et al, such as the use of mannitol alone and the delay in treatment while a head computed tomographic scan or transcranial Doppler ultrasonography study is performed. Ian R. Rogers MB, BS Department of Emergency Medicine St John of God Murdoch Hospital & University of Notre Dame Murdoch, WA, Australia E-mail address: [email protected] Martin D. Hoffman MD Department of Physical Medicine & Rehabilitation Department of Veterans Affairs Northern California Health Care System & University of California Davis Medical Center Sacramento, CA USA http://dx.doi.org/10.1016/j.ajem.2014.02.049 References [1] Severac M, Orban JC, Leplatois T, et al. A case of near-fatal exercise-associated hyponatremia. Am J Emerg Med (2014). http://dx.doi.org/10.1016/j.ajem.2013.12. 041. [2] Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med 2008;18:111–21. [3] Rosner MH. Exercise-associated hyponatremia. Semin Nephrol 2009;29:271–81. [4] Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci USA 2005;102:18550–5. [5] Bennett BL, Hew-Butler T, Hoffman MD, et al. Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia. Wilderness Environ Med 2013;24:228–40. [6] Winger JM, Hoffman MD, Hew-Butler TD, et al. The effect of physiology and hydration beliefs on race behaviour and postrace sodium in 161-km ultramarathon finishers. Int J Sports Physiol Perform 2013;8:536–41. [7] Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med 2000;133:1010–1.
0735-6757/© 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Rogers IR, Hoffman MD, Etiology and management of exercise-associated hyponatremic encephalopathy (EAHE), Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.049
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Correspondence
Etiology and management of exercise-associated hyponatremic encephalopathy (EAHE) To the Editor,
The case report of Severac et al [1] describing a case of exerciseassociated hyponatremic encephalopathy (EAHE) brings to the reader's attention a condition that is considered one of the most important clinical problems in endurance exercise [2]. There is now a broad consensus as to the common underlying pathophysiologic process in this condition [2-5] and to the most appropriate diagnostic and treatment strategies [2,5]. The pathophysiology, especially in severe cases such as that reported, is typically dilutional, resulting from a combination of excess fluid consumption and failure to excrete that fluid load due to inappropriate arginine vasopressin secretion [2-5]. This is evidenced in this case by acute hyponatremia associated with hypotonicity and an aquaresis on recovery. To state as the authors do in their discussion that the pathophysiology includes “sodium depletion in sweat” risks perpetuating an unproven myth [5]. This matters because athletes may believe that salt supplementation is the answer to prevention [6] when the correct prevention strategy is proper fluid balance through drinking to thirst rather than a predetermined regime [2,5]. For the emergency practitioner, the key to the correct diagnostic and therapeutic path is to understand that EAHE is the clinical manifestations of acute cerebral edema consequent on water following the osmotic gradient into brain cells. Our anecdotal experience in treating such athletes is that abdominal pain is an infrequent symptom, unlike the authors' contention, whereas nausea and vomiting are common. These represent cerebral symptoms due to increased cerebral pressure. Once EAHE is diagnosed biochemically in an at-risk athlete, as occurred in this case, then the key clinical action is urgent administration of hypertonic saline. The formulation is less critical (concentrations between 3% and 20% have been used) than the need to deliver a bolus of sodium chloride with limited fluid. The aim is to acutely increase the serum sodium concentration by approximately 2 to 5 mmol/L, and this is usually achieved with the current recommended strategy of up to three 100-mL boluses of 3% saline given in short succession [5]. This rapidly reverses the cerebral cellular swelling and is a potentially lifesaving, time-critical intervention [7]. Because the
process of cellular swelling occurs rapidly in EAHE, the adaptation of cellular organic osmolite secretion does not take place as with chronic hyponatremia, so there is no risk of osmotic demyelination from rapid correction of the low blood sodium concentration [5]. We would strongly counsel against some of the strategies reported by Severac et al, such as the use of mannitol alone and the delay in treatment while a head computed tomographic scan or transcranial Doppler ultrasonography study is performed. Ian R. Rogers MB, BS Department of Emergency Medicine St John of God Murdoch Hospital & University of Notre Dame Murdoch, WA, Australia E-mail address: [email protected] Martin D. Hoffman MD Department of Physical Medicine & Rehabilitation Department of Veterans Affairs Northern California Health Care System & University of California Davis Medical Center Sacramento, CA USA http://dx.doi.org/10.1016/j.ajem.2014.02.049 References [1] Severac M, Orban JC, Leplatois T, et al. A case of near-fatal exercise-associated hyponatremia. Am J Emerg Med (2014). http://dx.doi.org/10.1016/j.ajem.2013.12. 041. [2] Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med 2008;18:111–21. [3] Rosner MH. Exercise-associated hyponatremia. Semin Nephrol 2009;29:271–81. [4] Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci USA 2005;102:18550–5. [5] Bennett BL, Hew-Butler T, Hoffman MD, et al. Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia. Wilderness Environ Med 2013;24:228–40. [6] Winger JM, Hoffman MD, Hew-Butler TD, et al. The effect of physiology and hydration beliefs on race behaviour and postrace sodium in 161-km ultramarathon finishers. Int J Sports Physiol Perform 2013;8:536–41. [7] Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med 2000;133:1010–1.
0735-6757/© 2014 Elsevier Inc. All rights reserved.
Please cite this article as: Rogers IR, Hoffman MD, Etiology and management of exercise-associated hyponatremic encephalopathy (EAHE), Am J Emerg Med (2014), http://dx.doi.org/10.1016/j.ajem.2014.02.049
