Water intoxication can occur in a variety of different clinical settings but is generally not well recognized in the medical literature. The condition may go unrecognized in the early stages when the patient may have symptoms of confusion, disorientation, nausea, and vomiting, but also changes in mental state and psychotic symptoms. Early detection is crucial to prevent severe hyponatraemia, which can lead to seizures, coma, and death.
The patient reported here was a 64 year old woman with a known history of mitral valve disease but no other relevant past history. On the evening before her death, she began compulsively drinking water in vast quantities, estimated at between 30 and 40 glasses, and this was interspersed with episodes of vomiting. She became hysterical and also distressed, shouting that she had not drunk enough water. She declined medical attention but continued to drink water after she had gone to bed. She later fell asleep and died some time later.
A postmortem examination was carried out six hours later. The pituitary and adrenal glands were normal and there was no evidence of a bronchial tumour. There were bilateral pleural effusions of 200 ml on each side and the cut surfaces of the lungs (568 g and 441 g) exuded frothy pink fluid. The heart (461 g) showed evidence of mitral valve disease and left ventricular hypertrophy. Within the stomach there was 800 ml of watery fluid and the intra-abdominal organs were generally wet.
Postmortem toxicology was negative. A sample of vitreous humour showed a sodium concentration of 92 mmol/litre (serum reference range, 132–144). Potassium, urea, and glucose were all within the serum reference ranges. Blood cortisol was raised, excluding an addisonian crisis.
The cause of death was given as hyponatraemia as a result of acute water intoxication.
Water intoxication provokes disturbances in electrolyte balance, resulting in a rapid decrease in serum sodium concentration and eventual death. The development of acute dilutional hyponatraemia causes neurological symptoms because of the movement of water into the brain cells, in response to the fall in extracellular osmolality. Symptoms can become apparent when the serum sodium falls below 120 mmol/litre, but are usually associated with concentrations below 110 mmol/litre. Severe symptoms occur with very low sodium concentrations of 90–105 mmol/litre. As the sodium concentration falls, the symptoms progress from confusion to drowsiness and eventually coma. However, the rate at which the sodium concentration falls is also an important factor, and the acute intake of large volumes of water over a short period of time, as occurred in this case, would have produced a rapid drop in serum sodium, which was fatal.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770067/
