The aetiology ofhypernarraemia was investigated since this condition, on occasions, can assume the role of the single most important life-threatening compor.ent of the clinical picture. A computer was programmed to extract, over a 12-rnth period, the results of all inpatients of the Royal Adelaide Hospital with hypernatraemia above or equal to 170 mM/1. Of the 14 cases found, 7 were medical and 7 surgical, and thc. case notes were reviewed critically. The highest level of serum sodium was 196 mM/1 and only 4 of the 14 patients survived. Some patients had more than one cause operating. Excessive input of sodium, as either saline or bicarbonate, was a probable factor in 5 patients. Much more common was excessive loss of water in all 14 patients. Insufficiently compensated loss of insensible water probably occurred in 10 patients with pyrexia, pneumonia and tracheotomy. Inadequately replaced loss of free water in the urine probably occurred in 10 patients due to osmotic diuresis (from hyperglycaemia, intravenous mannitol, gastric tube feeding and intravenous nutrition), chemical diuretics and traumatic diabetes insipidus. Of particular importance was the occurrence of marked hypernatraemia as a result of imbalanced nutrition in 7 patients (5 being on gastric and 2 on intravenous regimes). This potential hazard of assisted nutrition may not always be appreciated. In several instances hypernatraemia from dehydration was treated as for excess sodium intake. A plea for a more positive approach for recording cumulative balance of both water and electrolytes in serious cases was made. Examples of a relatively simple graphical means of doing this were presented and it was suggested that the clinical pathologist can play an important role in introducing such a system into the wards. The aetiology ofhypernarraemia was investigated since this condition, on occasions, can assume the role of the single most important life-threatening compor.ent of the clinical picture. A computer was programmed to extract, over a 12-rnth period, the results of all inpatients of the Royal Adelaide Hospital with hypernatraemia above or equal to 170 mM/1. Of the 14 cases found, 7 were medical and 7 surgical, and thc. case notes were reviewed critically. The highest level of serum sodium was 196 mM/1 and only 4 of the 14 patients survived. Some patients had more than one cause operating. Excessive input of sodium, as either saline or bicarbonate, was a probable factor in 5 patients. Much more common was excessive loss of water in all 14 patients. Insufficiently compensated loss of insensible water probably occurred in 10 patients with pyrexia, pneumonia and tracheotomy. Inadequately replaced loss of free water in the urine probably occurred in 10 patients due to osmotic diuresis (from hyperglycaemia, intravenous mannitol, gastric tube feeding and intravenous nutrition), chemical diuretics and traumatic diabetes insipidus. Of particular importance was the occurrence of marked hypernatraemia as a result of imbalanced nutrition in 7 patients (5 being on gastric and 2 on intravenous regimes). This potential hazard of assisted nutrition may not always be appreciated. In several instances hypernatraemia from dehydration was treated as for excess sodium intake. A plea for a more positive approach for recording cumulative balance of both water and electrolytes in serious cases was made. Examples of a relatively simple graphical means of doing this were presented and it was suggested that the clinical pathologist can play an important role in introducing such a system into the wards.