Severe Exercise-Associated Hyponatremia in a Collegiate American Football Player

Introduction

Dehydration is a common problem in athletes that can adversely affect performance and health (³). Loss of fluid from sweat, urine production, and insensible losses during exercise can result in dehydration without adequate access to fluids (³). In response to fluid loss, the body uses several potent mechanisms, including both osmoregulatory thirst and hypovolemic thirst, to stimulate free water intake by the athlete (⁷). However, before the development of thirst, many athletes preemptively consume extra fluids during training or competition in attempts to “avoid dehydration” (¹⁰). Some athletes consume exaggerated amounts of hypotonic fluids in excess of actual fluid loss, and effectively dilute total body solute when the kidneys are unable to manage the excess fluid (⁵). This is a “voluntary” hypervolemic hyponatremic state defined as exercise-associated hyponatremia (EAH) (⁷).

EAH is classically reported in endurance and ultraendurance athletes including ultramarathoners, triathletes, and marathoners (⁷). A small number of cases have been reported in high school, collegiate, and professional level American football players (^4,6,7). We report a case of severe EAH in a National Collegiate Athletic Association (NCAA) Division III collegiate football player and review pearls and pitfalls in diagnosis and management.

Case Report

A healthy African-American/Black 21-year-old male NCAA Division III football defensive back presented with a chief complaint of emesis that developed during a competition. Ambient temperature during the game was between 79°F and 82°F with 40% to 50% humidity. In the fourth quarter, he left the game with generalized leg muscle cramping and, shortly after, developed multiple episodes of nonbloody, nonbilious emesis. Upon initial evaluation by the athletic training staff, he admitted to a headache. He denied trauma to the head during or before the game. He also denied any visual disturbance, difficulty with balance, or dizziness. The athletic training staff on the sidelines monitored him with no major changes in his clinical status; however, he did not return to the game.

Malaise, intermittent cramping, and nausea persisted for 2 h. Due to the concerns about possible heat illness, he was empirically cooled in the training room with an ice bath by the athletic training staff. Shortly thereafter, a team physician was contacted to evaluate him.

At that time, he continued to mention persistent nausea and vomiting. He denied any other gastrointestinal or genitourinary symptoms. He again denied any trauma to the head or abdomen and noted that he was feeling well before the game. He denied any medication, alcohol, supplement, or recreational drug use. His medical, family, and social history was unremarkable.

On examination, his oral temperature taken after the ice bath was 100.0°F with a blood pressure of 130/66 mm Hg and a pulse of 72 bpm. His respiratory rate was 16 breaths per minute with an oxygen saturation of 97% while breathing ambient air. He was alert and oriented; however, he was in mild distress due to intermittent retching. His pupils were equal and reactive. Mucus membranes were moist. The first and second heart sounds were normal, without murmurs. Breath sounds were normal in both lungs, without wheezing or rales. Bowel sounds were present, and the abdomen was soft, nondistended, and nontender on palpation. He had no edema in his extremities. He had a normal gait and a complete neurologic examination was normal. The remainder of the examination was normal.

Due to persistent symptoms, he was transferred to the emergency department (ED) via private vehicle for further evaluation and treatment.

Laboratory testing performed in the ED revealed a serum sodium of 124 mmol/L (normal range, 135–145 mmol/L) (Table). The patient was given 2 L of normal saline by the ED staff and a repeat serum sodium approximately 2 hours later had increased to 131 mmol/L. His nausea, vomiting, and cramping had resolved, though a mild headache persisted. He was discharged with a recommendation to follow-up in primary care clinic.

Table: Basic Metabolic Panel.

The patient was seen for follow-up in sports medicine clinic 3 d after discharge and reported to be feeling well. His serum sodium was retested and had normalized to 138 mmol/L. Upon further discussion, the player admitted that he had been trying to “prevent dehydration” in anticipation of the predicted hot and humid game-time weather conditions. The night before the game, he consumed 5 L of water. Before the midday game, he consumed another 5 L of a hypotonic sports drink. He continued to drink hypotonic fluids (water and a sports drink) throughout the game.

Based on the 2015 International Exercise-Associated Hyponatremia Consensus Guidelines, he was diagnosed with severe EAH with symptoms of headache, vomiting, and low serum sodium (⁷). At the time of follow-up, he was no longer symptomatic and his sodium levels had returned to normal. Therefore, the patient was allowed to return to play without restrictions. He was instructed to avoid excessive intake of fluids, increase salt intake before games, and avoid nonsteroidal anti-inflammatory drugs (NSAIDs) before games. He participated fully and uneventfully in the remainder of the season.

Discussion

To the authors’ knowledge, EAH has only been previously reported once in an NCAA American rules football player and that case was associated with administration of hypotonic intravenous fluids (⁶). Symptomatic EAH is rarely reported in athletes who are not participating in “endurance” events but has been reported in high school (⁷) and professional football players (⁴), professional rugby players (⁸), a recreational tennis player (¹²), a Bikram yoga participant (¹¹), and a lawn bowler with a cystic fibrosis gene mutation (⁹).

EAH is used to describe hyponatremia occurring during or up to 24 hours after physical activity (⁷). Mild EAH is used to describe EAH with nonspecific signs and symptoms without clear signs of encephalopathy. Symptoms of mild EAH may include lightheadedness, dizziness, puffiness, nausea, and body weight gain above baseline (⁷). Severe EAH is characterized by neurological signs and symptoms that may include vomiting, headache, altered mental status, seizure, coma, and dyspnea or frothy sputum that can accompany noncardiogenic pulmonary edema (⁷). Of note, muscle cramping may be an underrecognized symptom of EAH and should not be used as a clinical sign of dehydration (²).

On examination, most patients with EAH will have physical examination findings of euvolemia or hypervolemia due to overconsumption of fluids. Hypovolemic EAH is less common and debate remains about the risk of this disease to the athlete. The clinical assessment (vital signs, weight change, and physical examination) should help the examiner determine the fluid status of the athlete (⁷). The management of the athlete with EAH in this article focuses on the euvolemic and hypervolemic athlete with EAH.

Although a serum osmolality, urine sodium, urine osmolality, or urine-specific gravity could have all helped diagnose free water excess in this scenario in the initial ED setting, none of these were performed and may have contributed to a missed diagnosis and delay in appropriate treatment (²). Obtaining a complete history of fluid intake can be informative in the initial diagnosis and management (⁷). Rapid determination of sodium levels is important but should not delay care (⁷). The history obtained in follow-up helped confirm the diagnosis of EAH.

The management of symptomatic EAH involves fluid restriction and oral administration of high-sodium concentrated fluids in mild cases of EAH and intravenous administration of hypertonic saline in severe cases of EAH (⁷). Treatment decisions are primarily based on severity of symptoms, not sodium levels alone. A 3% sodium chloride solution is the recommended first-line choice of hypertonic saline for severe EAH though comparable amounts of a more concentrated sodium-containing solution may be used as an alternative for treatment (⁷). Use of NSAID medications are thought to be a risk factor for development of EAH and should be avoided in endurance competitions or those who have a history of EAH (⁷).

In this case, the administration of normal saline is not a recommended treatment strategy for severe EAH since this includes administration of unnecessary free water (⁷). In addition, a rectal temperature is recommended over an oral temperature to rule out exertional heat illness which was not performed in this case (¹).

Summary

Medical providers who treat athletes in the acute setting should be familiar with symptoms, diagnosis and treatment of EAH. Although many endurance and ultraendurance athletes are receiving education and advice on avoiding EAH, nonendurance athletes may be at risk of EAH due to improper hydration strategies and should be cautioned against excessive fluid intake (⁷).