Water Intoxication

It is a term which has been used in the past to describe a syndrome in which water is retained in the body in excess of electrolytes. Severe cases are uncommon but significant dilution of body fluids by excess water is frequently observed and, also, frequently misdiagnosed. Actually, there are several syndromes to which the above definition might apply, in all of which serum hypotonicity is characteristic. These include: 1) water retention, 2) primary sodium depletion and 3) symptom-less hypotonicity or asymptomatic hyponatremia in which the cause is unknown (61c). Primary water retention will be discussed here.

Many clinical states may be associated with a reduced ability to excrete water, e.g., organic renal disease, reflex renal ischemia, hypotension and peripheral circulatory failure. Oliguria and water retention may follow trauma and perhaps other forms of stress. The surgical patient is liable to water retention and intoxication if an excessive amount of sodium free water is administered. It has been suggested that anuric patients metabolize large amounts of fat and that this endogenously produced water in-creases body water even if external water and electrolyte balance remain constant. Some surgical patients likewise metabolize considerable amounts of fat. The majority of cases of water intoxication result when excessive fluids are given parenterally or per-rectum, occasionaly from oral intake.

The clinical symptoms of acute water intoxication, ac-cording to Wynn, usually begin suddenly with mental disturbances: “Strange behavior, loss of attention, confusion, staring, aphasia, incoordination and sleepiness are interspersed with periods of violent behavior, shouting delirium and extreme muscular weakness.” Subsequently, convulsions and coma are observed. In cases of insidious onset, lethargy, prostration, muscle weakness, sleepiness, apathy and disorientation are prominent findings. Occasionally there is anorexia, nausea and vomiting. Signs of water intoxication are largely the reverse of those of sodium depletion. There is gain in weight, normal tissue turgor and elasticity, normal tension of the eyeballs, warm moist skin, normal pulse and normal or slightly elevated blood pressure. Muscle strength is reduced. In coma, plantar reflexes are extensor in type.

Laboratory findings include reduction of hemoglobin and serum protein concentration, reflecting the increase in extracellular fluid and blood volume. An increase in red cell volume is indicated by a decrease in mean corpuscular hemoglobin concentration. Serum sodium and chloride are reduced; serum potassium is low or normal. Serum bicarbonate is moderately reduced and blood urea nitrogen is usually low unless anuria has been a feature of the condition. The sodium and chloride concentration of the urine may be quite high despite the low serum concentration.