Too Much of a Good Thing

A 19-year-old female college student was brought to the emergency department by friends who stated that she had a generalized seizure and then became comatose at their sorority house. They denied that the patient had ingested drugs or alcohol, and did not think she had any chronic medical problem or took medication. Physical examination revealed an unresponsive young woman in mild respiratory distress. Pulse rate was 120 bpm, respiratory rate was 24 bpm, blood pressure was 115/82 mm Hg, temperature 97.6°F. Mucous membranes were moist, and pupils were equal at 5 mm and sluggishly reactive. The neck was supple. Bilateral crackles were heard on lung auscultation. Initial laboratory values included sodium 118 mmol/L, potassium 2.7 mmol/L, chloride 85 mmol/L, bicarbonate 18 mmol/L, glucose 112 mg/dL, urine pregnancy test negative, urine specific gravity 1.023. The patient was intubated without difficulty. At this point, one of her friends admitted that they had been participating in a sorority hazing ritual, in which the patient had been forced to drink more than six liters of tap water over several hours. She had vomited, and become confused before having the seizure. Although physicians following the doctrine of Paracelsus have long believed that even water must be toxic, the clinical manifestations of water intoxication were not described in detail until publication of the classic paper by Rowntree in 1923 (Arch Intern Med 1923;32:157). As Rowntree intuited, these signs and symptoms are caused by hyponatremic encephalopathy with increased intracerebral pressure, and consist of headache, blurred vision, tremor and twitching, nausea and vomiting, confusion, ataxia, seizure, coma, and death. Rowntree also suggested that the key factor in the development of this syndrome was not specifically the amount of water ingested or the rate at which it was consumed, but rather a situation in which water intake exceeded the body's ability to eliminate it. Water intoxication has been reported in a number of different settings. A typical description involves a psychiatric patient with psychogenic polydipsia who also may be taking one or several medications that impair excretion of free water by releasing or enhancing the action of antidiuretic hormone (Table 1). The military has reported cases of recruits who become hyponatremic after ingesting large amounts of water to produce a urine sample or to hydrate during exercise.Table 1: Drugs that Cause the Syndrome of Inappropriate Antidiuretic Hormone (SIADH)Symptomatic hyponatremia has occurred following aggressive hydration not only by marathon runners and triathletes, but also by individuals engaged in moderate recreational activities such as hiking. Because the club drug MDMA (“ecstasy”) facilitates the release of antidiuretic hormone, cerebral edema and near-fatal hyponatremic coma have been reported in young people who take that drug and then push fluids. Fraternity Cases In 2003, several cases of severe hyponatremic encephalopathy occurred in fraternity initiates who were forced to drink large quantities of water as part of hazing activities. With recent publicity about ethanol-related deaths in association with hazing, some fraternity members not schooled in the wisdom of Paracelsus have turned to water as a mistakenly safe alternative. In November, a Southern Methodist University junior was hospitalized for 11 days when he became comatose and developed pulmonary edema after ingesting three or four gallons of water along with hot sauce in a drinking contest. In March, a freshman at the State University of New York at Plattsburgh died after being fed large amounts of water through a funnel. A young woman fell into a coma after a hazing ritual in which she had to drink more than six liters of tap water over several hours The diagnosis of water intoxication can be missed initially because the signs and symptoms are similar to those of alternate possible conditions. Weakness, nausea and vomiting, tremor and confusion also can signify exacerbation of psychosis in the patient with psychogenic polydipsia, dehydration and heat illness in the endurance athlete, or drug effect in the MDMA abuser. It is important to measure serum electrolytes as soon as possible in these patients. Other important laboratory values to monitor include glucose, tests of renal and hepatic function, and serum osmolality. Urine should be checked for osmolality, urine sodium concentration, and specific gravity. Because endocrine disorders can cause hyponatremia, thyroid function tests and a morning cortisol level should be obtained. Increased creatinine kinase may reflect rhabdomyolysis, which has been associated with water intoxication. CT scan of the head may reveal intracerebral edema. The key diagnostic clinical and laboratory findings in pure water intoxication and water intoxication combined with the syndrome of inappropriate antidiuretic hormone (SIADH) are listed in tables 2 and 3.Table 2: Key Clinical and Laboratory Findings in Acute Water IntoxicationTable 3: Key Clinical and Laboratory Findings in Acute Water Intoxication with SIADHThe major controversy concerning the treatment of significant hyponatremia relates to the proper method and rate with which to increase the serum sodium level. Water restriction should suffice for the asymptomatic or minimally symptomatic patient. The hyponatremic patient with seizures or coma may require hypertonic (3%) saline. Unfortunately, there have been no clinical trials evaluating the optimal rate to administer hypertonic saline in these cases. Too rapid correction of low sodium levels has been associated with the rare but devastating complication of central pontine myelinolysis (CPM), which can cause a variety of delayed but persistent neurological deficits including quadriplegia and locked-in syndrome. Although some authors suggest that an increase of 2 mmol/L/hr in the serum sodium level is safe, at least one report describes fatal CPM after correction at this rate (Crit Care Med 1992;20:534). An increase of 0.5 mmol/L/hr seems acceptable, with a total correction of no more than 8 to 12 mmol/L over the first day. In a seizing hyponatremic patient, it may be necessary to increase serum sodium concentration at a rate of 1 to 2 mmol/L/hr for the first few hours only. Because individuals vary considerably in their response to saline administration, frequent measurement of serum sodium levels during the initial stages of correction is crucial.