History and Examination
A 27-year-old previously healthy National Football League player had a seizure following the first day of minicamp practice. His spouse witnessed the player experiencing a generalized tonic-clonic seizure, accompanied by incontinence and loss of consciousness. She called 911, and upon arrival the paramedics found the patient to be confused, disoriented, combative, and diaphoretic. His initial examination in the field revealed blood pressure of 114/60 mm Hg, pulse rate of 68 beats/min, respiratory rate of 24 breaths/min, and a Glasgow coma score of 11. Electrocardiogram (ECG) interpretation confirmed normal sinus rhythm with no acute changes. Pulse oximeter reading on room air revealed an oxygen saturation of 93% and finger stick blood sugar was 47 g/dL. He was placed on oxygen at 6 L/min by nasal cannula and transported to the local emergency room.
Initial emergency room examination revealed blood pressure of 128/72 mm Hg, pulse rate of 80 beats/min, respiratory rate of 20 breaths/min, and rectal temperature of 99.4°F. The player was comatose and unresponsive to verbal commands; he did respond by withdrawal to painful stimuli applied to the left leg and both arms, but not to the right leg. Pupils were equal size, dilated, and not reactive to light, with a normal fundoscopic examination result. Results of ear, nose, and oral examinations were normal. His neck was supple, without rigidity, thyromegaly, adenopathy, or masses. Cardiopulmonary, abdominal, genitourinary, and rectal examination results were also normal. His extremities had normal color and temperature, symmetric pulses and reflexes, and no peripheral edema. A skin examination revealed no rashes, petechiae, or lesions, but he did have a few contusions on the extensor surfaces of his arms consistent with normal contact during football practice.
Repeat ECG was normal. Portable chest radiograph result was normal except for a possible left upper lobe infiltrate. Arterial blood gas was as follows: pH 7.41, pO2 155 mm Hg, and pCO2 41 mm Hg on 4 L/min by nasal cannula. Complete blood count showed hemoglobin 15.6 g/dL, hematocrit 46%, and leukocyte count 8700/mL with 74% neutrophils. He was given 1 mg of intravenous (IV) phenytoin. Blood chemistries revealed Na 116 mmol/L, K 3.4 mmol/L, Cl 81 mmol/L, CO2 24 mmol/L, blood urea nitrogen (BUN) 8 mg/dL, creatinine 0.8 mg/dL, and glucose 114 mg/dL. Toxicology screen was negative. Head CT scan revealed a low attenuation lesion of the left parietal lobe suggestive of a possible early infarct; there were no masses or hemorrhage (Fig. 1). He was given IV normal saline with 40 meq/L of KCl at 200 mL/h and lorazepam, 2 mg IV, for control of agitation and combativeness. He was transferred to the neurologic intensive care unit (NICU) with diagnoses of encephalopathy, hyponatremia, new-onset tonic-clonic seizure disorder, possible left parietal lobe infarct, possible left upper lung infiltrate, or aspiration.
According to the athletic trainer, the player had been in the league for 5 years as a journeyman tight end and had no known previous significant injuries or illnesses. This was the first day of the first two-a-day minicamp sessions for the team; the high ambient temperature was 74°F, and it was a sunny day with little cloud cover. The player did not appear to have sustained a significant blow to the head during the two practice sessions. Following the afternoon session, the player complained of feeling ill, with nausea, excessive fatigue, and a diffuse headache. He drank three 20-oz bottles of a sports drink, after which he had significant emesis but felt improved. He went home without being weighed and was encouraged to consume sports drinks as tolerated. Over the evening, his wife reported that he complained of increasing headache and nausea and was becoming increasingly disoriented prior to having the seizure. She reported that he was using an over-the-counter supplement for weight loss and was drinking up to 3 gallons of water every day because that is what he was advised to do growing up in Texas and throughout his college and professional football career.
The player had his preparticipation evaluation 5 months earlier, at which time his only complaint was frequent sinus infections, which were usually treated with amoxicillin and pseudoephedrine/guaifenesin. He was 6 feet 3 inches tall, 289 pounds, with blood pressure of 130/82 mm Hg and pulse rate of 76 beats/min; the remainder of the examination was normal. At that time, he was advised by the coaching staff to lose 25 pounds prior to the start of minicamp. His update examination 2 months earlier revealed his weight to be 267 pounds with 22% body fat; blood work revealed hemoglobin 16 g/dL, hematocrit 49%, leukocyte count 5800/mL, platelet count 224,000/uL, Na 147 mmol/L, K 3.9 mmol/L, Cl 103 mmol/L, CO2 28 mmol/L, BUN 25 mg/dL, creatinine 1.5 mg/dL, glucose 87 mg/dL, and thyroid-stimulating hormone 1.21 uU/mL.
Hospital Course and Treatment
At the time of admission to the NICU he remained disoriented, with slurred speech and purposeless thrashing movements; he followed simple commands, withdrew from pain, and moved all extremities but with only limited movement of his right leg. As sedation weaned, the player remained disoriented and extremely combative. Given his muscle mass and strength and concern for the safety of the patient and medical staff he was sedated with IV propofol on an as-needed basis.
Additional hospital laboratory testing revealed the following: erythrocyte sedimentation rate 1, Mg 1.5 mg/dL, prothrombin time 14.6 seconds, partial thromboplastin time 26 seconds, and measured serum osmolarity of 244. His total body water excess was calculated as 10.6 L, or 23.3 pounds (Table 1).
It was uncertain if the hyponatremia was acute or chronic. Given the potential for serious adverse effects of rapid correction of chronic hyponatremia, it was the opinion of the nephrologists to correct the serum sodium to 125 mmol/L then slowly increase to normal over 48 hours. The patient was treated with various IV fluids (Table 2), with close monitoring of intake, output, and serum and urine electrolyte concentrations and osmolarity. The patient remain disoriented, confused, and extremely combative, requiring propofol every 2 to 3 hours. Approximately 12 hours after admission to the NICU he began to move his right leg spontaneously. His status remained unchanged until 28 hours after his seizure when he awoke alert and oriented, lucid, with no memory of the recent events, including minicamp practice. At that time, the results of his physical examination and neurologic examination were entirely normal; he remained stable and was discharged 2 days after admission.
Electroencephalography (EEG) was performed with sedation and revealed slow background activity with continuous slow activity in the left temporal lobe suggestive of mild diffuse encephalopathy and left temporal lobe dysfunction. Neurology consultation recommended treatment of his seizure disorder with phenytoin, IV bolus of 500 mg and 1000 mg followed by an oral dose of 300 mg at night. Repeat CT scan of the brain day 1 was normal, and MRI of the brain with extratemporal lobe epilepsy protocol on day 2 was normal. He experienced no further seizures. Phenytoin, 300 mg at night, was continued at discharge; follow-up EEG 2 weeks later was normal, and the phenytoin was discontinued 1 month after discharge. He has remained seizure-free 7 years following this episode.
For empiric treatment of the lung infiltrate he was begun on clindamycin, 900 mg IV every 8 hours. He remained afebrile without cough, sputum production, or dyspnea, and pulmonary examination continued to be normal with good air entry and no wheezes, rales, or rhonchi. Repeat portable chest radiograph on day 1 and posteroanterior and lateral views on day 2 were normal. He was discharged home off antibiotics with no development of pulmonary symptoms.
The player did admit to drinking 2 to 3 gallons of water every day because he had been taught that “water is the best replacement fluid.” The supplement that he was using contained papaya, garlic, valvarine, corn spice, magnesium oxide, and magnesium carbonate. Although this likely did not contribute to his metabolic disturbance, he was advised against using over-the-counter supplements for weight loss. He was encouraged to consume sports drinks in addition to water and to increase salt intake. He also underwent nutritional counseling for appropriate diet to assist with weight maintenance and for optimal football performance. Following hospital discharge he gradually resumed aerobic and weight training exercises and returned to full activity without restriction 4 weeks after discharge. He has had no further medical problems.
The dilemma of management of this case of hyponatremia was determining the correct etiology. Because of the history of chronic voluntary water over-consumption, use of an unknown over-the-counter supplement for weight loss, significant sweat losses during practice, and episodes of emesis, it was uncertain if hyponatremia was acute or chronic. Hyponatremia may have occurred at least partially as a result of sodium losses through sweat, emesis, and supplement use. An increase in free water through voluntary hyperhydration or due to a syndrome of inappropriate antidiuretic hormone secretion from the lung lesion or brain lesion may also have contributed to the hyponatremia. Seizure secondary to hyponatremia may occur due to absolute serum sodium concentration or due to a rapid change in serum sodium concentration. Correction of chronic hyponatremia with a rapid increase in serum sodium may result in further seizure activity or central pontine myelinolysis, in which the patient remains in a chronic vegetative state. Hence, the rationale for attempting to correct the serum sodium to 125 mmol/L, to prevent further seizures, followed by slowly correcting the sodium level over 48 hours.
The etiology and management of acute hyponatremia due to overhydration has been reviewed by Noakes . In his report, patients either diurese spontaneously within the first hour or 2 of exercise cessation with urine rates of up to 600 mL/h for many hours thereafter, accompanied by a reduction in the severity of symptoms; or they show scanty urine production without clinical improvement and may only start the to increase urine outputs in response to a diuretic challenge with IV furosemide. Hypertonic 3% saline, 100 mL/h IV, has been used with success in severely symptomatic patients and should also be considered. Thus, most patients with the mild form of this condition should recover spontaneously if given nothing other than supportive care and perhaps furosemide if the onset of their diuresis is delayed.
This 27-year-old previously healthy professional football player developed a tonic-clonic seizure and delirium due to acute hyponatremia. This appears to be the first case of hyponatremia in an American football player. Hyponatremia was due to acute water intoxication; sodium losses through sweat and emesis may have partially contributed. There may have also been some contribution from renal dysfunction and diuresis due to his supplement use. Proper education regarding appropriate type and volume of fluid consumption, additional dietary salt intake, general nutrition, and close monitoring of body weight should prevent this disorder. The CT scan and chest radiograph findings appear to have been artifacts, but complicated the treatment of this patient. Because of these radiographic findings and the history of chronic excessive water consumption, the patient was treated as having chronic hyponatremia. In retrospect, he should have been treated as having acute hyponatremia with water restriction, and possibly diuretics or IV 3% saline.