FRI349 Atypical Timing: Transient Diabetes Insipidus After Pituitary Apoplexy
Authors: Rivera Nazario Ivan A , Santiago Carrion Ada M , Torres Marina Torres , Cruz Alegyari Figueroa , Ortiz Yineli , Velez Alexandra Aponte , Vazquez Angelica , Sola Sanchez Ernesto J , Mangual Garcia Michelle M 
Published: October 2023

Disclosure: I.A. Rivera Nazario: None. A.M. Santiago Carrion: None. M.T. Torres: None. A. Figueroa Cruz: None. Y. Ortiz: None. A. Aponte Velez: None. A. Vazquez: None. E.J. Sola Sanchez: None. M.M. Mangual Garcia: None.

Pituitary apoplexy results from acute hemorrhage or infarction of the pituitary gland. Also, an adenoma that can develop transient or permanent pituitary hormone deficiency. Posterior pituitary function is nearly always preserved due to alternate blood supply. Most cases presenting among the fifth or sixth decade. Few cases of transient Diabetes Insipidus (DI) have been described in literature, approximately 4% of patients, making this an uncommon complication of this condition. Hereby, we describe a young male with sudden onset headache due to pituitary apoplexy with transient DI. A 33-year-old man without past medical history, presented to the emergency room with the chief complain of sudden severe headache. Physical examination without altered consciousness, visual impairment or meningeal irritation. Initial head CT was negative, except for findings of muscle spasms. Patient was discharged home with muscle relaxant and NSAIDs. Ten days later, patient continued with worsening headache, not responding to medical therapy. On reevaluation, brain MRI identified a pituitary macroadenoma, measuring 2.2 cm, with mass effect, suprasellar extension impinging the pituitary stalk, prechiasmatic optic nerves and cavernous sinus extension. Blood tests showed Na 139 mEq/L, K 4.1 mmol/L and adequate renal function. Pituitary function test consistent for hypopituitarism with free T4 0.39 ng/dL, TSH 0.084 mIU/mL, cortisol 0.19 mcg/dL, ACTH 9.39 ng/mL, GH &lt;0.1 ng/mL, IGF-1 22.8 ng/mL and prolactin 1.52 ng/mL; except normal FSH, LH and testosterone levels. After four months of apoplectic episode, he developed polyuria and polydipsia. Brain MRI with residual sellar mass of 1.2 cm with resolution of mass effect. Visual field charting was normal. Blood tests showed Na 139 mEq/L, K 4.1 mmol/L and adequate renal function. Started on hydrocortisone and levothyroxine replacement. Diagnosis of DI was suspected, but he refused water deprivation test or DDAVP therapy. During follow-up, patient was found with serum osmolality 288 mOsm/kg, urine osmolality 202 mOsm/kg and 4.6 L 24-hour urine collection. Three months later serum osmolality was 294 mOsm/kg, urine osmolality of 383 mOsm/kg with resolution of polyuria and polydipsia. This case presents a delayed onset of transient DI treated in a conservative way. In documented cases average onset was a period of 2 weeks with resolution in 2 months. Etiology most likely due to compression or destruction of the pituitary gland or stalk impeding transit of ADH from hypothalamus to the neurohypophysis. Transient impairment of the ADH secretion is rare in pituitary apoplexy deserving evaluation in this clinical scenario. When seen, it has been related to glucocorticoid use. This is an example of an atypical pituitary disorder requiring prompt recognition to prevent further complications.

Presentation: Friday, June 16, 2023