Hyponatremic Seizures Secondary to Oral Water Intoxication in Infancy: Association With Commercial Bottled Drinking Water

Abstract

ABSTRACT. In recent years, hyponatremic seizures resulting from water intoxication have been reported in the United States with an increasing frequency that some have likened to an epidemic.1 Infants of parents living in poverty and uninformed of the risks of feeding fluids other than infant formula to their babies are particularly at risk.1-12 Young infants with vomiting and diarrhea are especially prone to developing hyponatremia if fed fluids lacking sufficient sodium, but even those who are otherwise well may develop symptomatic hyponatremia as a result of being fed excess solute-free water. Most often tap water, either in the form of supplemental feedings or overly dilute formula, has been given in excessive amounts over relatively short periods of time.1-11,13-16 Less frequently, water in other forms such as juice, soda, or tea has been implicated. 12,16 -19 This report includes the cases of two infants treated at our institution for hyponatremic seizures and water intoxication after being fed with the same bottled drinking water product marketed for use in infants. The medical records of all infants <1 year of age admitted to our institution over 10 years with the diagnosis of hyponatremic seizures were also reviewed. CASE REPORTS Case 1On October 7, 1993, a 55-day-old African-American infant was brought to the emergency department at a local hospital for evaluation of new onset "eye twitching." En route to the hospital, she began to have generalized tonic-clonic seizure. Her rectal temperature was 35.6°C; heart rate, 180; and blood pressure, 90/50 mm Hg. Pupils were equal and reactive, and funduscopic examination was normal. Edema was noted in the periorbital and gluteal regions. All four extremities were moving rhythmically, and deep tendon reflexes were symmetrically hyperactive. Capillary refill time was Ͻ2 seconds, and the infant was acyanotic. Weight was 4.77 kg (50%); length, 52.0 cm (10%); and occipitofrontal circumference, 36.0 cm (10%).Laboratory analysis revealed serum sodium of 116 mEq/L; chloride 85, mEq/L; potassium, 5.6 mEq/L; bicarbonate, 16 mEq/0; glucose, 151 mg/dL (8.4 mmol/L); total calcium, 8.2 mg/dL (2.1 mmol/L); phosphate, 6.2 mg/dL (2.0 mmol/L); creatinine, 0.4 mg/dL (35.4 mmol/L); and blood urea nitrogen, 7 mg/dL (2.5 mmol/L). Blood gas analysis showed metabolic acidosis with base excess Ϫ4.5 mEq/L. After Ͼ45 minutes of seizure activity, treatment with lorazepam (0.13 mg/kg), phenytoin (20 mg/kg), and phenobarbital (20 mg/kg) provided control of seizures but resulted in respiratory depression. Urine output exceeded 6 mL/kg/h over the next 8 hours and was accompanied by a weight loss of 180 g and resolution of edema. With intravenous administration of 0.9% saline at a rate of 100 mL/kg/day, the serum sodium concentration returned to 138 mEq/L within 20 hours (a rate of 1.0 mEq/h); the metabolic acidosis also resolved. Clinical improvement within 24 hours was accompanied by a weight loss of 350 g. The infant was discharged in good condition, on formula feedings, after a 5-day hosp...

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