Studies on post-operative water and elsctrolyte disturbances in patients with craniopharyngioma
A variety of water and electrolyte disturbances have been described in the literature as a complication of the abnormalities of the central nervous system. These disturbances are still considered to be one of the most difficult areas in
the management of these patients, mainly because of insufficient knowledge concerning their pathogenesis and pathophysiology.
Among 20 patients who had a radical removal of a craniopharyngioma from 1950 to 1962 at the Children's Hospital Medical Center in Boston, Massachusetts 15 showed electrolyte disturbances as fellows: 5 had transient hypernatremia,3 had transient hyponatremia, 3 had transient hyper and hyponatremia, and there were 4 cases of chronic hypernatremia. The following investigations were undertaken in 20 patients to study some of the factors affecting pathogensis and pathophysiology of these
In all cases, balance studies were done to measure daily weight, intake and output of water and electrolyte, serum chemistries, and, during the first week, hourly specific gravity of the urine which had been collected through an indwelling catheter. Thereafter voided urinary specimens were used while studies were continued from two weeks to two months post-operatively.
In some patients, further metabolic studies were carried out using a low Na intake of 10 mEq/day and/or a high K intake of 80-150mEq/day. Also studies were done on the effects of acute water loading of 20ml/kg/day, with or without cortisone premedication, and chronic water loading in which the daily intake was increased by one liter every 4 days. In the latter group the patients were on a fixed solute and calorie intake.
Pre-and post-operatively, the clinical observations and the results of studies of the renal and endocrine functions were examined for correlation with the electrolyte disturbances.
Summary of the Results:
1) In 4 of the 5 patients with transient hypernatremia. the development of hypernatremia was associated with a loss of water and body weight, as the result of decreased ADH output and of a transient disturbance in water intake, either due to disturbed thirst or inadequate supply of water.
The 5th patient developed a transient hypernatremia, not associated with the water loss but with water retention and weight gain and an inappropriate secretion of aldosterone.
2) 3 patients developed transient hyponatremia, which was associated with water retention and weight gain, as the result of an inappropriate ADH secretion.
3) In 3 patients who had developed transient hyper & hyponatremia, the development of hypernatremia was associated with loss of water as the result of decreased ADH output and inadequate water intake. The hyponatremia was associated
with water retention, as the result of an inappropriate ADH secretion.
4) In 2 of 4 patients with chronic hypernatremia, the development of hypernatremia was associated with loss of water and body weight due to decreased ADH output and inadequate water intake. The chronic state of hypernatremia seemed to be maintained due to a combination of decreased ADH activity and a persistant loss of thirst.
In the other 2 patients, the developement of hypernatremia was associated with a transient, inappropriate secretion of aldosterone in the early post operative period. Subsequently the aldosterone activity returned to normal, but the state of hypernatremia persisted despite loll Na intake, high K intake, or chronic water loading, suggesting the "resetting of osmoreceptors" to a higher threshold.
5) Determinations of other electrolytes showed no significant disturbances except for the serum Cl, which showed pattern of changes similar to those of the serum Na
6) In all patients, there was a disturbance in the ADH output postoperatively, either a transient or persistant loss of ADH. As judged by the specific gravity of the hourly voided urine, the loss of ADH was never complete in any single day, even with a large volume of urine.
7) In 4 patients, who underwent acute water loading test, all skewed impaired ability to excrete the excess water and this was not corrected by use of cortisone or thyroid medication. Impaired renal function and dehydration seemed to play an important role in this disturbed water excretion. A Possible role of decreased secretion of growth hormone was also discussed.
8) No significant correlation can be established between the above mentioned electrolyte disturbances, the pre- & post-operative clinical findings, and renal & endocrine functions, except that, in 4 cases showing a hypothalamic lesion at the
time of the surgery, all developed chronic hypernatremia along with the clinical signs of hypothalamic damage, such as loss of thirst, fluctuation in vital signs, personality changes and obesity.