Fatal water intoxication
- 1Department of Histopathology, Torbay Hospital, Lawes Bridge, Torquay, Devon, TQ2 7AA, UK; desmond.farrell{at}sdevonhc-tr.swest.nhs.uk
- 2Department of Clinical Chemistry, Torbay Hospital
Water intoxication can occur in a variety of different clinical settings but is generally not well recognised in the medical literature. The condition may go unrecognised 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.
Postmortem serum samples are unsuitable for sodium measurement because concentrations decrease after death and there is considerable individual variation. However, vitreous sodium concentrations are stable in the early postmortem period, and the concentration in vitreous humour is similar to that found in normal serum.1 Studies have shown that abnormal vitreous humour sodium concentrations had corresponding antemortem hyponatraemia or hypernatreamia.2
Self induced water intoxication is known to psychologists, but there is a paucity of information and little awareness of this life threatening problem in the professional literature.3 The initial symptoms associated with this condition are very similar to psychosis, with inappropriate behaviour, delusions, hallucinations, confusion, and disorientation.4 If untreated, the symptoms may progress from mild confusion to acute delirium, seizures, coma, and death, as occurred in this case.
Fatal water intoxication has been described in several different clinical situations. The most common of these is psychogenic polydipsia (compulsive water drinking), which is sometimes associated with either mental illness or mental handicap.4,5 The condition has also been described in young army recruits of good health who developed hyponatraemia after apparent overhydration following heat related injuries.6 The most common symptoms suffered by this group were changes in mental status, emesis, nausea, and seizures. Accidental water intoxication has been described as a result of excessive water intake after an episode of gastroenteritis,7 and an iatrogenic case has occurred after gastric lavage.8 Forced water intoxication is a recognised form of child abuse, which commonly leads to brain damage and is sometimes fatal.9
In conclusion, we wish to highlight an unusual cause of death that may go unnoticed without an appropriate clinical history and relevant postmortem biochemical investigations. Both clinicians and pathologists need to be aware of this condition, which may manifest itself as a psychotic illness and so go unrecognised in its early stages. Early detection is crucial to prevent fatal complications.
