Exertional Dysnatremia in Collapsed Marathon Runners A Critical ...

Clinical Chemistry / Dysnatremia in Collapsed Marathon Runners

Exertional Dysnatremia in Collapsed Marathon Runners A Critical Role for Point-of-Care Testing to Guide Appropriate Therapy Arthur J. Siegel, MD,1,6 Pierre d’Hemecourt, MD,2,6 Marvin M. Adner, MD,3 Terry Shirey, PhD,4 Jeffrey L. Brown, PsyD,1,6 and Kent B. Lewandrowski, MD5,6 Key Words: Dysnatremia; Encephalopathy; Exercise-associated hyponatremia; Inappropriate antidiuresis DOI: 10.1309/AJCP30OGLSLWLEIY

Abstract Dysnatremia may cause life-threatening encephalopathy in marathon runners. Hypernatremia and exercise-associated hyponatremia (EAH) may manifest with mental status changes and, if untreated, progress to coma and death. We reviewed the on-site blood sodium testing and treatment in collapsed runners at the finish-line medical tent at the Boston marathons from 2001 through 2008. Dysnatremia was diagnosed in 429 (32.5%) of 1,319 collapsed runners. Hypernatremia was present in 366 (27.7%) and hyponatremia in 63 (4.8%). Hypernatremic runners unable to drink fluids were treated with intravenous normal (0.9%) saline. Hyponatremic runners with seizures or coma received intravenous hypertonic (3%) saline. Sixteen runners with EAH able to drink a concentrated oral hypertonic solution recovered within 30 minutes. Based on on-site sodium testing, dysnatremic runners were treated with appropriate intravenous fluids according to validated standards of care. Hyponatremic runners able to drink an oral hypertonic solution recovered promptly.

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Am J Clin Pathol 2009;132:336-340 DOI: 10.1309/AJCP30OGLSLWLEIY

Exertional dysnatremia may result in life-threatening encephalopathy in collapsed marathon runners.1 As opposite disorders of body fluid homeostasis, hypernatremia and exercise-associated hyponatremia (EAH) may manifest similarly with confusion and disorientation and may progress, if untreated, to coma and death. On-site whole blood Na+ testing was introduced at the finish-line medical tent of the Boston marathon in 2001 to provide rapid diagnosis for emergency triage to appropriate treatment.2,3 Administration of intravenous normal (0.9%) saline, which is appropriate for hypernatremia, may induce seizures in cases of EAH, which will respond to hypertonic (3%) saline.4-6 In contrast with these evidence-based treatments,7-9 there is no consensus for management of the more prevalent cases of delirium due to EAH, which may progress to seizures following continued intake of hypotonic fluids. Concentrated broth as an oral hypertonic solution was used for runners able to drink fluids beginning in 2005, with results reported herein.

Materials and Methods Heparinized blood samples were obtained from collapsed runners in the finish-line medical tent at the Boston marathons from 2001 to 2008 for point-of-care testing using Nova analyzers (Nova Biomedical, Waltham, MA). In addition to intravenous normal (0.9%) and hypertonic (3%) saline for hypernatremia and life-threatening EAH encephalopathy, respectively, concentrated broth (4 bouillon cubes in 4 oz of water representing approximately 9% saline) as an oral hypertonic solution was administered to hyponatremic runners with delirium who were able to take fluids by mouth. © American Society for Clinical Pathology

Clinical Chemistry / Original Article

Blood Na+ testing before and after treatment was performed on 3 runners in 2008.

Results Dysnatremia (Na+ >145 mEq/L [145 mmol/L] or 150 mmol/L Subtotal No. with hyponatremia 130-135 mmol/L 150 mEq/L stable enough for discharge [150 mmol/L]); treat until condition stable enough for discharge

Severe Vomiting, seizures, obtundation, respiratory distress, coma Emergent IV hypertonic (3%) saline (100-mL bolus); repeat after 5 min if no response pending transfer to hospital

IV, intravenous. * Oral hypertonic saline was the initial treatment for runners with exercise-associated hyponatremia who were able to drink fluids by mouth. Positive clinical responses (as described) precluded the risk of progression and the need for IV hypertonic saline.

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© American Society for Clinical Pathology

Clinical Chemistry / Original Article

Based on these promising if anecdotal observations in initial cases, we undertook blood Na+ testing following oral hypertonic treatment as an objective outcome measure. Three cases in 2008 showed essentially normal Na+ values concurrent with a positive clinical response (Table 2). All runners so treated were discharged directly from the medical tent with written instructions to limit intake of hypotonic fluids until the onset of urination and to eat salty snacks. No cases required intravenous hypertonic saline or hospital transfer or exhibited delayed recurrence of symptoms. Table 3 summarizes these interventions. These findings support treatment with hypertonic fluids for EAH encephalopathy by the oral or intravenous route according to the clinical manifestations and severity. Lifethreatening cases with seizures or coma were treated with intravenous (3%) saline, and runners with mental status changes but able to drink fluids were treated safely and effectively with concentrated oral solutions. The positive clinical response relates to a prompt increase in the blood Na+ level, which reverses the osmotic gradient for the flow of water into brain cells. This can be achieved by using various concentrations of hypertonic saline as demonstrated in events in London, England (2%), and Cape Town, South Africa (5%).15,16 This treatment should be given as soon as possible after the diagnosis is confirmed to decrease acute cerebral edema before progression to brainstem compression. The paradox that hypertonic salt solutions are efficacious for treating EAH encephalopathy but that supplemental salt intake is apparently without value for prevention of EAH warrants explanation.17 The pathophysiology of inappropriate antidiuresis reconciles this apparent contradiction, under which the renal clearance of free water is limited, while additional salt is excreted in concentrated urine.18 The view in some sports medicine circles that salt supplements make avid drinking safe may well be incorrect. EAH may occur when the intake of hypotonic fluids exceeds total losses, including a reduced capacity of the kidneys to excrete free water. Recent reports indicate that the risk for EAH remains despite guidelines advising especially slower runners and walkers to drink only to thirst.19 Life-threatening cases, including fatalities, continue to occur despite evidence-based support for emergency treatment with hypertonic saline.20-23 On-site point-of-care electrolyte testing is an essential prerequisite to managing dysnatremia in competitive endurance athletic events. Limitations of this study include those inherent in descriptive studies in which the findings are applicable only to the specific race and demographics of the runners involved. Conclusions should also be considered as preliminary in view of the small sample. The incidence and severity of EAH may vary from year to year in a given race and between venues.23 An algorithm based on these considerations could provide

medical teams at other races with a platform to compare with their experiences. Oral hypertonic treatment for mild to moderate EAH encephalopathy deserves systematic study based on these promising if preliminary findings. From 1McLean Hospital, Belmont, MA; 2Boston Children’s Hospital, Boston, MA; 3Metro West Medical Center, Framingham, MA; 4Nova Biomedical, Waltham, MA; 5Massachusetts General Hospital, Boston; and 6Harvard Medical School, Boston. Address reprint requests to Dr Lewandrowski: Clinical Chemistry, Gray 5, Massachusetts General Hospital, Fruit St, Boston, MA 02114.

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DOI: 10.1309/AJCP30OGLSLWLEIY

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Siegel et al / Dysnatremia in Collapsed Marathon Runners

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