PEDIATRICS Vol. 100 No. 6 December 1997,
p. e4
ELECTRONIC ARTICLE:
Hyponatremic Seizures Secondary to Oral Water Intoxication in
Infancy: Association With Commercial Bottled Drinking Water
Robert C. Bruce* and
Robert M. Kliegman
From the * Wilkinson Medical Clinics, SC, Oconomowoc, Wisconsin,
and the Department of Pediatrics, Medical College of Wisconsin,
Milwaukee, Wisconsin.
ABSTRACT
- CASE REPORTS
- DISCUSSION
- ABBREVIATIONS
- REFERENCES
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 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.1,13 Less
frequently, water in other forms such as juice, soda, or tea has been
implicated.12,16 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 1
On 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 <2 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 
4.5 mEq/L. After >45 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 hospitalization.
Additional history revealed that the infant's 22-year-old mother had
been buying cow-milk formula and supplementing feedings with bottled
drinking water for several days. The mother and child had been living
with the mother's aunt, who was taking an active role in child care
and expressed concern over the lack of time the mother spent with her
infant. Despite eligibility for financial assistance through the Aid
for Families with Dependent Children program, none had been sought.
Both care givers related that the particular bottled water product was
inexpensive and labeled in such a way that it seemed to contain
nutrients adequate for use as an infant feeding supplement.
Case 2
On December 8, 1993, a 56-day-old African-American infant was
brought to the emergency department at Children's Hospital of Wisconsin for evaluation after a brief seizure. With the exception of
symptoms of upper respiratory tract infection for several days, he had
been in good health. His rectal temperature was 37.8°C; respirations,
52/min; heart rate, 152/min; and blood pressure, 94/58 mm Hg. The
infant appeared alert, healthy, and in no distress. Funduscopic
examination was normal, and pupils were equal and reactive. There were
no focal neurologic findings, and capillary refill time was <2
seconds. Weight was 4.26 kg (25%); length, 57.5 cm (50%), and
occipitofrontal circumference, 38.5 cm (50%).
At the time of admission, the serum sodium concentration was 121 mEq/L;
chloride, 87 mEq/L; potassium, 4.8 mEq/L; bicarbonate, 21.3 mEq/L;
creatinine, 0.3 mg/dL (26.5 mmol/L); and blood urea nitrogen, <2 mg/dL
(0.7 mmol/L). Urine specific gravity was <1.005. Computed tomographic
imaging of the head performed within 2 hours of the initial sodium
measurement was normal.
The infant and his 16-year-old mother had been living with the
mother's parents. His mother related supplementing feedings of soy
formula (obtained through participation in the Women, Infants, and
Children Supplemental Feeding Program [WIC]) with bottled drinking
water since the onset of cold symptoms. Daily feedings consisted of
three bottles of formula and three bottles of drinking water. The
drinking water was viewed in this case as a safe and economical form of
clear liquid to assist in the relief of cold symptoms. His mother
stated the label on the bottle depicted a product specially made for
infants (Fig 1).
Fig. 1.
The bottled water product fed to the two infants
discussed in the case reports.
[View Larger Version of this Image (106K GIF file)]
Intravenous fluid therapy consisted initially of 0.9% saline, then 5%
dextrose in 0.45% saline, at a rate of 200 mL/kg/day. Diuresis at a
rate >5 mL/kg/h was accompanied by a weight loss of 140 g. Within
9 hours, the serum sodium concentration had returned to 136 mEq/L (rate
of return 1.4 mEq/h). The patient was discharged home in good
condition, after dietary counseling, <24 hours after admission.
Before we began the records review, the two cases associated with
bottled drinking water were reported to the Food and Drug Administration (FDA) and the local health department.
Using the Children's Hospital of Wisconsin IDX computer system, our
medical records department conducted a search for all patients 1 year
of age admitted with the diagnosis of hyponatremia and seizure over the
10-year period from January 1984 through March 1994. Cases were
included if the initial serum sodium concentration was 130 mEq/L and
if there was no history of chronic illness. Two patients were excluded,
one with panhypopituitarism and the other with cystic fibrosis. We
retrospectively reviewed the remaining records and recorded all
pertinent clinical, laboratory, and demographic information. Excess
total body water was calculated using body weight, serum sodium
concentration, and age-specific estimations of normal total body
water20 to approximate the volume of solute-free water
necessary to cause water intoxication and hyponatremic
seizures.21 Significant trends in age distribution and
correlations between age and various clinical observations
were measured (t test and 
2 analyses).
Demographic and Historical Data
Twenty-five consecutive additional cases of hyponatremic
seizures treated previously at our institution were identified (N = 27). The mean age of all cases was 4.8 ± 2.9 months, with a male-to-female ratio of 1:1. Twenty-one infants were <6 months of age
and 6 were older (P = .002). In 22 cases (82%),
infants were being cared for by single parents. Nine of the 27 (33%)
infants had no siblings, 18 (67%) had at least one other sibling, and 12 (44%) had two or more siblings. Twenty-six families (96%)
qualified for financial compensation through government programs;
however, 35% of these families were not making full use of these
resources. The rate of immunization for all infants was 48% (13 of
27).
There was documentation of feedings of at least one form of solute-free
water (alone or in addition to formula feedings) in all cases.
Seventeen infants (63%) were fed straight tap water, and four (15%)
were given sugar water (apparently mixed at home). Four infants (15%)
were fed tea, soda, or Kool-Aid. Seven infants (26%) were being fed
with overly dilute formula by parents who admitted doing so either
because they ran out of formula or wished to save money. The parents of
two infants claimed they had been given feeding instructions, each from
a different health care provider by telephone, which included feeding
solute-free water. Three infants were fed water in an attempt to
provide relief of upper respiratory symptoms. Eleven patients (41%)
were reportedly being fed some form of excess water on a regular basis;
4 (15%) were fed excess water acutely in addition to daily excess
water; and 12 (44%) reportedly became water-intoxicated acutely
(within a 24-hour period) without a history of regular feedings of
excess solute-free water. There were no other cases of hyponatremic
seizures and water intoxication associated with feedings of commercial bottled drinking water.
Clinical Data
The mean serum sodium concentration was 121 ± 4 mEq/L (113 to 127 mEq/L). Prolonged seizures (
15 minutes) occurred in 48% of
cases (13 of 27), and 9 infants (33%) required mechanical ventilation. Eight of the infants (30%) had seizures with focal characteristics. None of the infants >6 months of age required ventilatory support, and
only 1 had a prolonged seizure. The mean body temperature on admission
(including 4 infants with fever) was 36.4 ± 1.4°C. Serum sodium
levels returned to normal within a mean time interval of 11.3 ± 5.7 hours (mean rate of return 1.6 ± 0.7 mEq/h). Mean total body
water excess was 592 ± 209 mL (556 ± 212 mL for infants <6
months, 720 ± 147 mL for those older; P, not
significant). The mean length of hospitalization was 4.4 ± 2.9 days, and no neurologic deficits were evident at the time of hospital
discharge.
DISCUSSION
These examples illustrate a well-described spectrum of symptoms
that characterize water intoxication, consisting of altered mental
status (typically irritability or somnolence), hypothermia, edema, and
seizure.1,12 Symptoms are preceded by a rapid
fall in serum sodium concentration to 125 mEq/L and result from an acute overload of solute-free water substantial enough to increase total body water by 7% to 8% or more.22 Reported time
intervals over which infants have been fed water in excess sufficient
to precipitate hyponatremic seizures have varied from 90 minutes to 48 hours.1,14 The subsequent rapid fall in serum sodium concentration is thought to result in physiologic dysfunction at the
neuron level, which in turn leads to varying degrees of clinical
neurologic dysfunction.23 Twelve of the infants in our
series underwent cranial computed tomographic imaging, 8 of whom had
acute hyponatremia. The absence of radiographic evidence of cerebral
edema in all cases studied lends support to the theory that ion
gradient disturbances are at least as important as cellular swelling in
causing neurologic dysfunction during water intoxication.
Various physiologic mechanisms have been proposed to explain why young
infants, particularly those <6 months of age, are at risk for
developing water intoxication. Immature renal function in infancy is
thought to be a significant factor. Children <1 year of age have a
relatively low glomerular filtration rate, and although urine output
may exceed baseline rates in water-intoxicated infants, they are less
able to excrete free water per unit time than are older children and
adults.22 The hunger drive of infancy has also been
described as a powerful mechanism predisposing young infants to
overfeeding with water, overriding any innate tendency to select a diet
with higher solute content, which might otherwise serve as a protective
homeostatic mechanism.2,13 Others have hypothesized that
excess secretion of antidiuretic hormone is an important factor, but
the brisk diuresis of dilute urine that invariably accompanies recovery
of normal serum sodium levels has been cited as evidence against this
theory.2,18 Fortunately, despite the use of many different
therapeutic interventions, prompt return of sodium levels and full
restoration of neurologic function have been the rule in cases reported
previously of hyponatremic seizures associated with oral water
intoxication in infancy.1,13
A wide range of ingested volumes of water and times over which the
ingestion occurred has been reported.1,13 The
accuracy of dietary histories, often a nebulous combination of chronic as well as acute ingestions in the same patient, is confounded additionally by retrospective analysis. Although adequate neurologic homeostasis can be maintained in chronically hyponatremic patients, such infants may be especially prone to developing symptomatic hyponatremia after a relatively small increment in total body water.23 In calculating excess total body water in our
patients,24 we found that an infant who ingests from 260 to
540 mL of solute-free water may become symptomatic over a relatively
short period.
Once considered a rare clinical entity, oral water intoxication is
being reported with increasing frequency in the United States,
especially in urban settings. Poverty, care giver inexperience, lack of
proper instruction by health care providers, or a combination of these
factors has been implicated in virtually all reported cases.1 These associations characterize the patients in
our series as well. Some have identified an association of infantile water intoxication with families receiving infant formula through the
WIC.1,11,12 Cases of corruption of the WIC reimbursement procedures by grocery store operators, whereby other products have been
substituted for infant formula, have been described.11 In
other cases, it has been stated that the standard allotments of formula
provided through WIC may be inadequate for some infants by the time
they reach 4 to 6 months of age.1 Previous reports of cases
clustered during the summer months have led to speculation that
elevated ambient temperatures (resulting in diaphoresis and increase
thirst)8 and the absence of school lunch programs (representing additional financial stress caused by an increase in
money spent on food for families with school-age children)1 are contributing factors. Elsewhere, researchers in the area of child
development have described excess water drinking as a marker of care
taker interaction disturbance,25 and cases of water intoxication in infants have been associated with abusive as well as
psychologically unstable care givers.1,2,4 In offering explanations for why water intoxication in infants is being reported with increasing frequency, some have addressed the issue of infant formulas and their sodium content. Changes in most infant formulas in
recent years have resulted in a lower sodium content, which theoretically may make diluted formula a more potent inducer of water
intoxication.18
Since our initial report of the two infants who became ill after
bottled water feedings, the FDA has recommended that the labels on
infant drinking water products display a reminder that the product is
not to be used as an electrolyte solution.26 Although the
products are so labeled, the warning print is generally extremely
small, and some stores continue to stock bottled water products for
infants next to oral electrolyte solutions. An added concern, which is
beyond the scope of this report, is that these products tend to have
fluoride added without FDA regulation.
Although specific recommendations exist with regard to proper
mixing of infant formula, health care providers must continue to
reiterate these guidelines and the hazards of deviations from them,
especially for infants of families living under financial stress. To
date, no specific guidelines exist to assist parents in knowing how
much water to feed their infants. The calculation of excess total body
water provides only an approximation. Moreover, there was no
statistical correlation between excess total body water and patient
age. Therefore, the available data provide only a crude estimate of the
volume necessary to cause symptomatic hyponatremia in any given infant.
We conclude that commercially available bottled water products marketed
specifically for use in infants represent a potential threat to the
health of the children most likely to suffer from water intoxication.
With their packaging and relatively affordable price, these products
might be misused as feeding supplements by some parents with limited
financial resources. An awareness of these facts is essential to the
proper labeling of bottled water products and to educating the care
givers of young infants at risk. We must continue to inform the care
givers of infants in our clinics of the hazards of feeding excessive
amounts of this or any other form of solute-free water to young
infants.
FOOTNOTES
Received for publication Apr 4, 1997; accepted Jul 11, 1997.
Reprint requests to (R.C.B.) 950 Bartlett Dr, Oconomowoc, WI
53066.
ABBREVIATIONS
WIC, Women, Infants, and Children Supplemental
Feeding Program.
FDA, Food and Drug Administration.
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Pediatrics (ISSN 0031 4005). Copyright ©1997 by the American Academy of Pediatrics
