Pituitary apoplexy

Tarakad S Ramachandran MD (Dr. Ramachandran of SUNY Upstate Medical University has no relevant financial relationships to disclose.)
Matthew Lorincz MD PhD, editor. (Dr. Lorincz of the University of Michigan receives salary support from Wilson Therapeutics AB for performing UWDRS examinations in a clinical trial.)
Originally released August 5, 1994; last updated August 25, 2015; expires August 25, 2018

Overview

Acute pituitary apoplexy typically begins with sudden severe headache, followed over 24 to 48 hours by nausea, vomiting, visual disturbance, and a variety of other neurologic symptoms, including meningeal irritation, fever, clouding of consciousness, or coma. The diagnosis is often missed in the early stages. The importance of a high index of suspicion leading to correct diagnosis and early surgery cannot be overemphasized. CT and MRI of the brain are helpful in making the diagnosis of pituitary apoplexy. It is well known that pituitary apoplexy can result in remission of acromegaly with normalization of growth hormone levels and in partial or complete anterior or posterior, or both, pituitary insufficiency.

Key points

 

• Pituitary apoplexy is a clinical concept and applies only to symptomatic cases.

 

• Rare cases present with coagulation necrosis of the pituitary without massive hemorrhage.

 

• Visual loss from chiasmal compression of more than 24 hours is usually irreversible.

 

• Rathke cleft cyst apoplexy closely resembles the clinical syndrome of pituitary tumor apoplexy and should be treated as a distinct entity.

 

• Estimation of pituitary hormone levels after pituitary apoplexy is a must, and appropriate hormone replacement therapy should be instituted as needed.

Historical note and terminology

Pituitary apoplexy is a frequently catastrophic, potentially fatal syndrome that typically follows hemorrhage into a macroadenoma of the pituitary gland. No subtype of adenoma confers a higher risk of apoplexy (Biousse et al 2001). It may occur within a normal or adenomatous gland (Semple et al 2005). This results in injury to the secretory tissues of the pituitary itself and compression of neighboring neural and vascular structures, including hypothalamus. Rarely, hemorrhage into nonadenomatous tissue is responsible (Fernandez-Real et al 1995).

The frequent occurrence of hemorrhagic foci in adenomas of the adenohypophysis had been long recognized pathologically. Bailey first described the clinical syndrome of apoplexy in a case of fatal hemorrhage into a growth hormone-secreting posterior pituitary adenoma (Bailey 1898). Bleibtreu reported a similar early case of fatal apoplexy in a young acromegalic (Bleibtreu 1905). Both patients presented with symptoms of sudden severe headache, vomiting, ophthalmoplegia, and coma—the hallmarks of pituitary apoplexy. The syndrome was not widely recognized and named until 1950 (Brougham et al 1950).

It is important to note that the term pituitary apoplexy is a clinical concept and applies only to symptomatic cases. It defines a clinical syndrome and not simply the occurrence of hemorrhage into an adenoma, which is a common and frequently subclinical process. Some cases present with coagulation necrosis of a pituitary adenoma without massive hemorrhage.

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