The rate of intestinal fluid absorption appeared to match the rate of oral fluid ingestion and there was

no evidence of fluid accumulation in the intestine with reverse sodium movement from the extracellular space into intestinal fluid. The results of this study are therefore at variance with the Priestley-Haldane hypothesis and suggest that reverse sodium movement did not contribute to the hyponatraemia induced by oral fluid overload in these subjects. Rather it appears that humans may have a limited capacity to excrete fluid at rates in excess of approximately 900 ml/h in response to higher rates of oral fluid intake. When the rate of intestinal fluid absorption matches the rate of fluid ingestion and exceeds the kidneys' maximum capacity for fluid excretion, the excess fluid accumulates in the extra- and intracellular fluid compartments, inducing the dilutional hyponatraemia of water intoxication. These findings may have relevance to other clinical conditions in which hyponatraemia develops in response to high rates of oral or intravenous fluid provision. (University of Cape Town Research Unit for Exercise Science and Sports Medicine) 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. The cause of death was given as hyponatraemia as a result of acute water intoxication. (D J Farrell and L Bower) Forced water intoxication is a new generally fatal syndrome of child abuse that occurs in children previously subjected to other types of physical abuse. (Arieff AI, Kronlund BA.) Hyponatremia, also called water intoxication, is generally the result of drinking excessive amounts of plain water which causes a low concentration of sodium in the blood. Once a rare occurrence at sporting events, it is becoming more prevalent as participation increases and more novice exercisers are entering endurance events. Prolonged and excessive sweating increases the risk that an athlete will alter the delicate balance of blood-sodium concentration. Because sodium is lost in sweat it is important for those exercising at high intensities for long periods of time to replace any loses. Research has found that long duration endurance events, such as the Ironman distance triathlons, often have finishers with low blood sodium concentrations. Those at most risk are those who are on the course the longest, because they tend to drink the most water during the event. Runners who drink extra fluids in the days before the race or those who stop at water stop during the race are also at increased risk of hyponatremia. In fact, a study published in the New England Journal of Medicine (April, 2005) found that 13 percent of Boston Marathon runners developed hyponatremia from drinking too much water. The early warning signs are often subtle and may be similar to dehydration and include nausea, muscle cramps, disorientation, slurred speech, and confusion. At this point, many athletes drink more water because they think they are dehydrated. Unfortunately, water alone will increase the problem of hyponatremia. At the most extreme an athlete may experience seizures, coma, or death. (Consensus Statement of the 1st International Exercise-Associated Hyponatremia, Consensus Development Conference, Cape Town, South Africa 2005. Clinical Journal of Sport Medicine. 15(4):208-213, July 2005.) Water intoxication assumes an important place because the role of tissue hydration has been well established in idiopathic epilepsy. In the latter disease it was shown by McQuarrie and Peeley (1931) that grand ma1 seizures can be precipitated in patients kept on a low mineral diet when their water intake was increased. (ERNST GELLHORN AND H. M. BALLIN) Contrary findings were reported by Underhill and Sallick (7), who, while agreeing that the blood became diluted and that the magnitude of the blood chloride reduction exceeded the degree of hemodilution, claimed that a large amount of chloride was lost in the urine. They concluded that "the loss of tissue salts with consequent disturbance of the water-salt equilibrium of the body constitutes an important factor in the mechanism of water intoxication." (FRANCIS SCOTT SMYTH, WILLIAM CALLAHAN DEAMER AND NILKANTH M. PHATAK)