• blood-brain barrier
• brain cell swelling
• osmolality
• hyperglycaemia
• insulin
• isotonic saline

Carlotti et al¹ state that fluid and electrolyte management might contribute to the development of cerebral oedema in hyperglycaemia. There is a simple rule of thumb, formulated by Katz, which may help calculate water and electrolyte deficits and predict the changes in sodium levels which accompany changes in glucose levels,² namely that a decrease of 0.29 mmol/l in serum sodium may be expected for every 1.0 mmol/l increment in serum glucose.

This may be explained as follows: hyperglycaemia causes an osmotic movement of water out of the cells, which leads to hyponatraemia by dilution. Thus, at presentation, the patient is usually severely dehydrated intracellularly. However, the serum sodium is lower than would be expected because of this dilution of the extracellular fluid. When the patient is treated with insulin, glucose enters the cells, taking water with it, leading to a relative concentration of the extracellular fluid, and thereby a rise in serum sodium. This rise may be predicted and calculated using Katz’s formula.²

Carlotti et al also comment on the report of Glaser et al that the chance of cerebral oedema during treatment is increased in children who present with high initial serum urea levels and when there is a lack of an increase in serum sodium levels during treatment.³ This increased risk may be explained by the fact that the urea level rises in proportion to the degree of dehydration. …