Pituitary apoplexy

Douglas J Lanska MD FAAN MS MSPH (

Dr. Lanska of the University of Wisconsin School of Medicine and Public Health, the Medical College of Wisconsin, and IM Sechenov First Moscow State Medical University has no relevant financial relationships to disclose.

Originally released August 5, 1994; last updated November 24, 2019; expires November 24, 2022


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. A high index of suspicion is needed to establish the correct diagnosis and institute early surgery if needed. CT and MRI of the brain are helpful in making the diagnosis. Pituitary apoplexy can result in remission of acromegaly with normalization of growth hormone levels and with partial or complete pituitary insufficiency involving the anterior, posterior, or both aspects of the gland.

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 essential, and appropriate hormone replacement therapy should be instituted as needed.

Historical note and terminology

Pituitary apoplexy is a not infrequently catastrophic, and 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. American neurologist Pearce Bailey (1865-1922) first described the clinical syndrome of pituitary apoplexy in a case of fatal hemorrhage into a growth-hormone-secreting posterior pituitary adenoma (Bailey 1898; Pearce 2015).

American neurologist Pearce Bailey Image: Pearce Bailey (1865-1922)
German physician Leopold Bleibtreu reported a similar early case of fatal apoplexy in a young acromegalic (Bleibtreu 1905; Pearce 2015). 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).

Ischemic necrosis of the hyperplastic pituitary of pregnancy (Sheehan syndrome) is only rarely complicated by pituitary apoplexy (Sheehan and Summers 1949).

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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