title: Post-operative diabetes insipidus after endoscopic transsphenoidal surgery.
abstract: Diabetes insipidus (DI) after endoscopic transsphenoidal surgery (ETSS) can lead to increased morbidity, longer hospital stays, and increased medication requirements. Predicting which patients are at high risk for developing DI can help direct services to ensure adequate care and follow-up. The objective of this study was to review our institution's experience with ETSS and determine which clinical/laboratory variables are associated with DI in this patient population. The authors wanted to see if there was an easily determined single value that would help predict which patients develop DI. This represents the largest North American series of this type. We retrospectively reviewed the charts of patients who had undergone ETSS for resection of sellar and parasellar pathology between 2006 and 2011. We examined patient and tumor characteristics and their relationship to postoperative DI. Out of 172 endoscopic transsphenoidal surgeries, there were 15 cases of transient DI (8.7%) and 14 cases of permanent DI (8.1%). Statistically significant predictors of postoperative DI (p < 0.05) included tumor volume and histopathology (Rathke's cleft cyst and craniopharyngioma). Significant indicators of development of DI were postoperative serum sodium, preoperative to postoperative change in sodium level, and urine output prior to administration of 1-deamino-8-D-arginine vasopressin. An increase in serum sodium of ≥2.5 mmol/L is a positive marker of development of DI with 80% specificity, and a postoperative serum sodium of ≥145 mmol/L is a positive indicator with 98% specificity. Identifying perioperative risk factors and objective indicators of DI after ETSS will help physicians care for patients postoperatively. In this large series, we demonstrated that there were multiple perioperative risk factors for the development of DI. These findings, which are consistent with other reports from microscopic surgical series, will help identify patients at risk for diabetes insipidus, aid in planning treatment algorithms, and increase vigilance in high risk patients.
authors.affiliation: Department of Neurosurgery, Detroit Medical Center, Wayne State University, 4160 John R Street, Suite 930, Detroit, MI, 48201, USA.
authors.forename: Matthew
authors.initials: M
authors.lastname: Schreckinger
authors.forename: Blake
authors.initials: B
authors.lastname: Walker
authors.forename: Jordan
authors.initials: J
authors.lastname: Knepper
authors.forename: Mark
authors.initials: M
authors.lastname: Hornyak
authors.forename: David
authors.initials: D
authors.lastname: Hong
authors.forename: Jung-Min
authors.initials: JM
authors.lastname: Kim
authors.forename: Adam
authors.initials: A
authors.lastname: Folbe
authors.forename: Murali
authors.initials: M
authors.lastname: Guthikonda
authors.forename: Sandeep
authors.initials: S
authors.lastname: Mittal
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Szerlip
mesh_terms: D001127:Arginine Vasopressin / Q000378:metabolism; D003894:Deamino Arginine Vasopressin / Q000378:metabolism; D003919:Diabetes Insipidus / Q000209:etiology* / Q000378:metabolism; D005260:Female; D006801:Humans; D008297:Male; D044583:Neuroendoscopy / Q000009:adverse effects*; D010911:Pituitary Neoplasms / Q000378:metabolism / Q000601:surgery; D012189:Retrospective Studies
chemical_list: D001127:Arginine Vasopressin; D003894:Deamino Arginine Vasopressin