Delayed occurrence of diabetes insipidus following transsphenoidal surgery with radiological evaluation of the pituitary stalk on magnetic resonance imaging.

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Delayed occurrence of diabetes insipidus following transsphenoidal surgery with radiological evaluation of the pituitary stalk on magnetic resonance imaging.

World Neurosurg. 2017 Dec 08;:

Authors: Hayashi Y, Aida Y, Sasagawa Y, Oishi M, Kita D, Tachibana O, Ueda F, Nakada M

Abstract
INTRODUCTION: Diabetes insipidus (DI) is a major complication of transsphenoidal surgery (TSS). DI usually occurs within a couple of days after TSS. Delayed occurrence of postoperative DI is rarely observed and its developing mechanisms remain unknown. Methods Six patients were identified as having postoperative delayed DI, which was defined as DI that first occurred two or more weeks after TSS. They consisted of one male and five females, and their mean age was 38.3 (range: 10-76) years. Five patients were histologically diagnosed with Rathke cleft cyst (RCC), while one was RCC co-existed with prolactin-secreting adenoma. Sequential T1-weighted magnetic resonance imaging (MRI) was evaluated for hyperintensity (HI) in the pituitary stalk and the posterior lobe, indicating the location of antidiuretic hormone (ADH).
RESULTS: No patients had any DI before TSS. Delayed DI occurred two weeks to three months after TSS and persisted for two weeks to five months. T1-weighted MRI revealed that the HI in the posterior lobe became faint, but did not disappear after DI occurrence, and their intensities increased with recovery from DI. In contrast, the HI in the pituitary stalk was found faintly preoperatively and turned clear postoperatively, and decreased with recovery from DI. Their morphological patterns were dependent on DI duration.
CONCLUSION: In the delayed occurrence of DI, it was suggested that preoperative ADH transport was mildly congested, yet not completely blocked when DI manifested postoperatively. Gradual spreading of inflammation to the infundibulum after RCC removal was considered as one possible mechanism of this delayed DI development.

PMID: 29229338 [PubMed - as supplied by publisher]

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