Acute Hypopituitarism Caused By Sellar Hematoma Immediately Following Pituitary Surgery: Clinical and Biochemical Characteristics

Presentation Number: FRI 549
Date of Presentation: April 1st, 2016

Nadine El Asmar*1, Katia Elsibai2, Ribal Al-Aridi2, Warren Selman3 and Baha M Arafah1
1UH Cleveland Medical Center/Case Western Reserve University, Cleveland, OH, 2UH Case Medical Center/Case Western Reserve University, Cleveland, OH, 3UH Case Medical Center, Cleveland, OH

Abstract

Background and Objectives: Although often minimal and clinically unrecognized, postoperative sellar hematoma can develop after resection of pituitary tumors and other sellar masses such a Rathke’s Cleft Cyst (RCC) as a result of continued oozing at the surgical site. The hematoma can, at times be large enough to create a mass effect that might impair pituitary function. The clinical and biochemical features of sellar hematoma have not been previously examined and are the main goals of this investigation.

Methods:  Records of all 399 patients who had pituitary surgery over 10 years by one surgeon were reviewed. The standard protocol in all patients who have pituitary surgery is to frequently monitor ACTH, cortisol, and prolactin levels during the first 48 postop hrs (1, 2). Glucocorticoids (GC) are administered only when cortisol levels are <10 ug/dL on multiple occasions during the first 24 postop hrs.

Results: Sellar hematoma was suspected clinically (increasing headaches, visual impairment, fatigue and mental status alteration) and confirmed by imaging studies 1.5-8 days postop in 23 patients (18/279 with macroadenomas; 5/92 with RCC and in 0/28 with microadenomas). The remaining 376 patients did not have clinically significant symptoms and maintained normal HPA function. Although ASA/NSAID were discontinued > a week before surgery, patients who had hematomas were more likely (P<0.001) to have used such drugs than others who did not have the complication (6/23 Vs 21/348). All 23 patients had intact HPA function before the onset of symptoms as evidenced by appropriately elevated ACTH and cortisol levels. At diagnosis, ACTH (8.9±7ng/L) and cortisol (4.6±3.6ug/dL) levels were lower (p<0.005) than those obtained 24 hrs earlier (18.9±11.1 and 18.4±6.6; respectively). Cortisol levels were <5ug/dL in 15/23 and were 6-12.9ug/dL) in 8/23 patients. In contrast, prolactin levels increased (9.4±5.4 to 13±6.1 ug/L; P<0.001) over the same time period. Treatment with GC resulted in clinical improvement within 24-48 hrs in 19/23 patients while 4/23 also required surgical decompression. GC therapy was tapered and discontinued within 2 weeks and re-testing of HPA function shortly thereafter and again 3 months later showed normal HPA function in 17/23 and impaired function in 6/23.

Conclusions: When large, postoperative sellar hematoma can lead to mass effect that causes headaches, visual symptoms and acute hypopituitarism manifesting initially as impaired HPA function. Prompt recognition and GC administration often lead to resolution of the clinical manifestations and recovery of pituitary function in most patients. The rapid onset and reversibility of hypopituitarism and the associated increase in serum prolactin levels suggest that compression of portal vessels and/or pituitary stalk by the hematoma is the dominant mechanism of pituitary dysfunction in this setting.


 

 

Nothing to Disclose: NE, KE, RA, WS, BMA