A Case of Water Intoxication with Prolonged Hyponatremia Caused by Excessive Water Drinking and Secondary SIADH
A 22-year-old man who was an inmate in a detention facility joined a game of ‘rock/paper/scissors’ with his roommates at 8:00 p.m. They made a rule that the loser of each game must drink a cup of water as a penalty by using a plastic cup with a capacity of 300 ml. That night, he lost the game again and again, and had to drink 20–22 cups of water during 25–28 games in total for the 3-hour game, indicating that he must have drunk at least 6 liters of water in 3 h. At 11:30 p.m., 3.5 h after beginning the penalty drinking, he showed restlessness and peculiar behavior, including speaking meaningless words. Because he also started vomiting and having convulsions soon thereafter, he was seen by a doctor in a clinic at the facility at midnight, and he was administered 100 mg phenobarbital intramuscularly.\nHowever, his condition was not improved by the treatment, and it progressively worsened, showing more serious signs such as incontinence of urine and feces, tonic convulsions, and consciousness disturbance. He was finally transferred to our hospital at 2:00 p.m., 18 h after the beginning of the penalty drinking. Clinical episodes which can cause SIADH, such as epilepsy, brain surgery history, head injury or a history of meningoencephalitis, were not seen in his past history.\nWhen he was hospitalized, he was in a coma (Japan Coma Scale; III-100). His height, body weight, blood pressure, pulse rate and body temperature were 167 cm, 49 kg, 140/90 mm Hg, 60 beats/min and 36.8°C, respectively. Edema was not present in his face or legs. The neurological examination showed no abnormality including enhanced or pathological tendon reflex. Muscle rigidity was slightly enhanced in the proximal portion of his extremities. The results of the laboratory tests on admission are summarized in table , and significant hyponatremia (120 mmol/l) was assumed to be the principle cause of the coma and/or other neurological abnormalities. A brain magnetic resonance imaging (MRI) study showed high-intensity signals in the perilateral ventricular region and brain white matter consistent with the development of brain edema, as shown in fig. . A chest X-ray showed no abnormalities, including alveolar shadow, pleural effusion, cardiomegaly and congestion (X-ray not shown).\nAlthough excess water drinking in the detention facility would have triggered the dilution of the patient's body fluid, it was not concluded that the temporal massive water drinking caused the prolonged dilution of body fluid until 15 h after the discontinuation of the water drinking. Indeed, his laboratory tests showed hypertonic urine (305 mosm/kg H2O), indicating the disturbance of free water excretion in response to the remarkable hyponatremia. This finding, taken together with the patient's decreased free water clearance, inhibition of the renin-aldosterone system and hypouricemia with elevated uric acid clearance led us to make a tentative diagnosis as secondary SIADH, and the diagnosis was confirmed later by the detection of an inappropriate elevation of the plasma ADH concentration.\nThe patient's clinical course and the changes in the laboratory findings are summarized in fig. . As an initial therapy for the severe hyponatremia, physiological saline was infused in combination with 40 mg furosemide twice a day. In addition, 6.6 mg dexamethasone was also administered for the reduction of the patient's brain edema. Because he showed systemic convulsions again on the 2nd day, an electroencephalogram was performed and showed a spike and wave pattern, suggesting the diagnosis of epilepsy. The convulsions disappeared after an administration of phenytoin.\nOn the 3rd day, his consciousness disturbance had almost disappeared, with an elevation of the serum sodium concentration (138 mmol/l). On admission, he showed elevated serum creatine phosphokinase (2,386 IU/l) and urine myoglobin (372.1 ng/ml) as well as muscle pain, which were consistent with rhabdomyolysis resulting from the recurrent convulsions and hyponatremia. Following the improvement of the hyponatremia, those abnormalities also disappeared by the 5th day. After confirmation of the disappearance of the brain high-intensity signals by MRI and the normalization of the disturbed free water clearance on the 5th day, the patient was discharged and he returned to the detention facility with no significant clinical signs on the 6th day.