P-46 A CASE OF PITUITARY APOPLEXY PRESENTING WITH OPHTHALMOPLEGIA
Authors: Sayim Kubra , Mert Meral , Cakır Ilkay , Ciftci Sema , Piskinpasa Hamide , Kasapoglu Melis Ozyazanlar , Saydam Simge 
Published: January 2025

Introduction

Pituitary apoplexy is a rare endocrinological emergency that may be life-threatening due to pituitary hormone deficiency or compression effect, if not treated appropriately. It usually develops secondary to acute ischemia or hemorrhage in the pituitary gland and presents with headache, vomiting, ophthalmoplegia, vision loss. In this case, we aim to present a case of pituitary apoplexy who applied to the emergency service with a complaint of vomiting, and developed ophthalmoplegia while hospitalized.

Clinical Case

A 76-year-old male patient applied to the emergency department with complaints of nausea and vomiting that had been continuing for the last week. At admission, physical examination, blood pressure and neurologic examination were normal. The laboratory tests were as follows: Glu:141 mg/dl, Cre:0,7 mg/dl, AST:25 U/L, ALT:13 IU/L, Na:118 mmol/L, K:3.0 mmol/L. He was admitted to the service in order to investigate hyponatremia and hypokalemia. On the first day of his hospitalization, restriction of upward sight in the right eye and ptosis developed. Cranial imaging with computerized tomography revealed a contrast-enhancing mass at the level of pituitary gland. A well-frameworked, 20 mm in diameter, hyperintens at T1-weighted images, with heterogeneous contrast enhancing lesion was reported in the contrast-enhanced pituitary MRI. Preliminary diagnosis were considered to be a bleeding cyst or pituitary apoplexy. Pituitary hormone tests were as follows: TSH:0.5 mIU/L (0.27-4.8), sT4: 1,38 ng/dL (0,79-1,59), sT3: 2.1 ng/L (2,04-4,4), FSH: 2.6 IU/L (1,5-12,4), LH: 0.87 IU/L (1,7-8,6), Total Testosterone: 0.4 ng/ml (2,8-8), PRL: 1 µg/dl (4,6-21,4), ACTH: 1,5 ng/L (7-63,2), Cortisol: 1.8 µg/dl (6-19), İGF-1: 53 mg/L (50-184). Hormone replacement with methylprednisolone 2x20 mg intravenous was started with the diagnosis of anterior pituitary insufficiency. The patient underwent to transphenoidal pituitary surgery for decompression, under a steroid cover. Hemodynamics remained stable following surgical intervention. Postop urinary output was also normal. But, right side ptosis continued after surgery. The patient was discharged with oral prednisolone 5 mg 1*1. Steroid was discontinued at the second week following surgery. The entire pituitary axis was determined to be intact at the first month. Pathology was reported as a large hemorrhagic infarction of the pituitary gland compatible with pituitary apoplexy. Consultations with Neurology and ophthalmology departments were done because of the persistence of right ptosis. No additional intervention was planned, follow-up was recommended. A significant improvement of ptosis was observed after a two months period.

Conclusion

Although the neurological signs and symptoms of pituitary apoplexy usually improves following accurate medical or surgical interventions in majority of patients, it should be kept in mind that it may take time for ptosis to recover after surgical decompression as in our case.Figure 1:Improvement in ptosis in the second month after surgery