PATHOPHYSIOLOGY OF HYPONATREMIA AFTER TRANSSPHENOIDAL PITUITARY SURGERY

Hyponatremia after pituitary surgery is presumed to be due to antidiur esis; however, detailed prospective investigations of water balance th at would define its pathophysiology and true incidence have not been e stablished. In this prospective study, the authors documented water ba lance in patients for 10 days after surgery, monitored any sodium dysr egulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituit ary damage with water balance dysfunction. Ninety-two patients who und erwent transsphenoidal pituitary surgery were studied. To evaluate pos terior pituitary damage, a questionnaire was completed immediately aft er surgery in 61 patients. To examine the osmotic regulation of vasopr essin secretion in normonatremic patients, water loads were administer ed 7 days after surgery. Patients were categorized on the basis of pos toperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% r emained normonatremic. Plasma arginine vasopressin (AVP) was not suppr essed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower d ietary sodium intake, and had similar fluid intake and cortisol and at rial natriuretic peptide (ANP) levels compared with normonatremic pati ents. Normonatremia, hyponatremia, and diabetes insipidus were associa ted with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hypona tremia after transsphenoidal surgery is complex. It is initiated by pi tuitary damage that produces AVP secretion and dysfunctional osmoregul ation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include no natrial natriuretic peptide-related excess natriuresis, inappropriatel y normal fluid intake and thirst, as well as low dietary sodium intake . Patients should be monitored closely for plasma sodium, plentiful di etary sodium replacement, mild fluid restriction, and attention to sym ptoms of hyponatremia during the First 2 weeks after transsphenoidal s urgery.