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Pituitary Apoplexy Clinical Presentation

  • Author: Michael S Vaphiades, DO; Chief Editor: Hampton Roy, Sr, MD  more...
Updated: Mar 23, 2015


Patients may present with the following complaints[4] :



Clinical presentation is marked by headache in 95% of cases. The headache is sudden and postulated to result from stretching and irritation of the dura mater in the walls of the sella supplied by the meningeal branches of cranial nerve V. The headache also may result from irritation of the trigeminal nerve from the expanding mass. Frequently, it is retro-orbital in location and may be unilateral at onset, then becomes generalized.

Vomiting occurs in 69% of patients and often accompanies the headache. The mechanism is unclear but may be due to meningeal irritation or increased intracranial pressure.

Visual acuity defects (52%) and visual field defects (64%) result from upward expansion of the tumor, which compresses the optic chiasm, optic tracts, or optic nerve. The classic visual field defect is a bitemporal superior quadrantic defect. Optic tract involvement from a prefixed chiasm is less common and results in a contralateral homonymous hemianopia. Optic nerve compression from a postfixed chiasm is rare and may mimic optic neuritis with pain on eye movement, monocular visual acuity loss, and a central scotoma on visual field testing. See the image below.

Automated visual field showing a bitemporal field Automated visual field showing a bitemporal field defect due to compression of the optic chiasm from below.

Ocular paresis (78%) results from compression of the cavernous sinus, which makes cranial nerves III, IV, and VI vulnerable to compression. If consciousness is maintained, diplopia may be present. Of the cranial nerves, the oculomotor nerve (cranial nerve III) is involved most commonly, resulting in a unilateral dilated pupil, ptosis, and a globe that is deviated inferiorly and laterally.[5]

Less commonly, cranial nerve IV is involved. A fourth cranial nerve palsy typically manifests as vertical diplopia that worsens when the patient gazes in a direction opposite or tilts the head toward the direction of the hypertropic (affected) eye. It also is worsened by downgaze.

The sixth cranial nerve is least commonly involved, perhaps because of its sheltered position in the cavernous sinus. Its involvement produces horizontal diplopia, which results from inability to abduct the involved eye. By virtue of its existence in the cavernous sinus, the trigeminal nerve (cranial nerve V) involvement may produce facial pain or sensory loss.

Horner syndrome may develop from damage to the sympathetic fibers. Hemispheric deficits may also develop.

The carotid siphon may be compressed against the anterior clinoid process, leading to stroke and vasospasm from subarachnoid blood.

Leakage of blood and necrotic tissue into the subarachnoid space may lead to meningismus, stupor, and coma.

The cerebrospinal fluid frequently is marked by increased pressure and pleocytosis (even in the absence of hemorrhage), increased numbers of red blood cells, and xanthochromia.

Involvement of the hypothalamus may alter thermal regulation. Destruction of adenohypophyseal tissue may lead to endocrinologic deficiencies.

Pituitary apoplexy can occur in ectopic sites. Hori examined normal adult brains at autopsy and found ectopic pituitary cells in the leptomeninges of the peri-infundibular region in 75%.[6] He postulated that these cells may produce an ectopic pituitary adenoma. Ectopic pituitary adenomas commonly present late because they displace rather than invade vital nervous structures. They may be discovered only after the patient has pituitary apoplexy. Only one case of an ectopic pituitary adenoma that underwent apoplexy has been reported.



Predisposing factors of pituitary apoplexy include endocrine stimulation tests, bromocriptine treatment, head trauma, pregnancy, and pituitary irradiation.

Okuda reported one woman with a giant pituitary adenoma who underwent triple bolus stimulation test with luteinizing hormone-releasing hormone, thyrotropin-releasing hormone (THR), and insulin.[7] The patient became stuporous, and computerized tomography (CT) scan revealed pituitary and subarachnoid hemorrhage (SAH). The investigators theorized that TRH-induced vasospasm may be a causative factor.

Some associate apoplexy with administration of gonadotrophin-releasing hormone. Corticotropin-releasing hormone administration was associated with pituitary apoplexy in a patient with Cushing syndrome. In one study, bromocriptine therapy was associated with high T1 signal in the pituitary tumor on magnetic resonance imaging (MRI), but none of the patients studied had clinical evidence of pituitary apoplexy. Others associate pituitary apoplexy with long-term bromocriptine therapy.

Pituitary apoplexy can occur after head trauma. This probably results from shear forces applied to the pituitary stalk with contusion, hemorrhage, and infarction of the adenoma.

Pituitary apoplexy during induction chemotherapy for acute myeloid leukemia has been reported by Silberstein and colleagues.[8]

Apoplexy has been reported after cardiac bypass surgery by Thurtell and colleagues.[9]

Brar and Garg reported a case of pituitary apoplexy in a young man who ascended to high altitude gradually, even after proper acclimatization.[10]

Pituitary apoplexy has been reported in a patient with dengue fever and thrombocytopenia.[11] Kruljac et al reported a patient with pituitary metastasis presenting as ischemic pituitary apoplexy following heparin-induced thrombocytopenia.[12]

Apoplexy during pregnancy may be due to temporary enlargement of pituitary adenoma, which compromises the blood supply.

Sheehan syndrome refers to pituitary apoplexy of a nontumorous gland, presumably due to postpartum arterial spasm of arterioles supplying the anterior pituitary and its stalk.

In 1937, Sheehan reported 11 cases of women who died in the puerperium, all of whom had necrosis of the anterior pituitary gland (adenohypophysis). Nine of the 11 cases had severe hemorrhage at delivery. The other 2 cases had no hemorrhage but were gravely ill prior to delivery.

Usually, at least 1-2 liters of blood loss and hypovolemic shock are associated with a retained placenta. Sheehan syndrome occurs in 1-2% of women suffering significant postpartum hemorrhage.

Normally, the pituitary gland hypertrophies in pregnancy. This hypertrophy, combined with locally released factors, mediates vascular spasm and renders the pituitary more susceptible to infarction from compromised blood flow.

In Sheehan syndrome, inability to lactate after delivery due to prolactin deficiency occurs and amenorrhea due to gonadotrophin deficiency classically develops.

Also, after delivery, shaved pubic hair or axillary pubic hair fails to regrow, and waxy skin depigmentation develops.

Signs of hypothyroidism and hypoadrenalism may develop, and posterior pituitary (neurohypophysis) involvement with diabetes insipidus may occur. The less frequent involvement of the neurohypophysis probably stems from a difference in the anatomy of the vascular supply. The neurohypophysis contains an anastomotic ring of blood vessels that the adenohypophysis lacks.

The clinical presentation of acute pituitary apoplexy has only been reported in the literature in a minority of patients with Sheehan syndrome. The more commonly reported scenario is a woman who develops amenorrhea years later, with a diagnosis of Sheehan syndrome being made retrospectively.

However, Sheehan syndrome is a neurological emergency and is potentially lethal. The neuroimaging characteristics of Sheehan syndrome are distinctive. In pregnancy, the pituitary enlarges from diffuse nodular hyperplasia of prolactin secreting cells. On MRI, the normal pituitary gland is largest in the immediate postpartum period, measuring up to 11.8 mm in height and convex in appearance. The anterior pituitary is usually hyperintense on T1-weighted images in pregnant and postpartum women when compared to controls. After delivery, the size of the pituitary gland rapidly returns to normal beyond the first week postpartum.

The characteristic MRI finding in Sheehan syndrome is an enlarged pituitary gland bulging under the optic chiasm with peripheral enhancement surrounding an isointense gland; this characteristic MRI finding is called the "pituitary ring sign" (see Imaging Studies).[13]

Weisberg warns that radiotherapy is potentially hazardous in pituitary tumors with prior hemorrhagic, necrotic, or cystic changes.[14] Apoplexy may be precipitated in these cases.

Some believe that apoplexy is more prevalent in patients who produce excess pituitary hormones (eg, acromegaly, Cushing syndrome), perhaps because the tumor is fueled by the hormones. Others report that most pituitary tumors that undergo apoplexy are endocrinologically silent.

Ahmed and Semple reviewed the potential complications of pituitary apoplexy, one being mechanical occlusion of the internal carotid arteries in the cavernous sinus, and the other being vasospasm.[15] Both may result in brain ischemia.

Contributor Information and Disclosures

Michael S Vaphiades, DO Professor, Departments of Ophthalmology, Neurology, and Neurosurgery, Chief of Neuro-Ophthalmology and Electrophysiology Services, University of Alabama at Birmingham School of Medicine; Consulting Staff, Children's Hospital, Birmingham

Michael S Vaphiades, DO is a member of the following medical societies: American Academy of Neurology, North American Neuro-Ophthalmology Society, American Academy of Ophthalmology, American Osteopathic Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Edsel Ing, MD, FRCSC Associate Professor, Department of Ophthalmology and Vision Sciences, University of Toronto Faculty of Medicine; Consulting Staff, Hospital for Sick Children and Sunnybrook Hospital

Edsel Ing, MD, FRCSC is a member of the following medical societies: American Academy of Ophthalmology, American Association for Pediatric Ophthalmology and Strabismus, American Society of Ophthalmic Plastic and Reconstructive Surgery, Royal College of Physicians and Surgeons of Canada, Canadian Ophthalmological Society, North American Neuro-Ophthalmology Society, Canadian Society of Oculoplastic Surgery, European Society of Ophthalmic Plastic and Reconstructive Surgery, Canadian Medical Association, Ontario Medical Association, Statistical Society of Canada, Chinese Canadian Medical Society

Disclosure: Nothing to disclose.


Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

  1. Nawar RN, AbdelMannan D, Selman WR, Arafah BM. Pituitary tumor apoplexy: a review. J Intensive Care Med. 2008 Mar-Apr. 23(2):75-90. [Medline].

  2. Mohr G, Hardy J. Hemorrhage, necrosis, and apoplexy in pituitary adenomas. Surg Neurol. 1982 Sep. 18(3):181-9. [Medline].

  3. Kurisu K, Kawabori M, Niiya Y, Ohta Y, Mabuchi S, Houkin K. Pituitary apoplexy manifesting as massive intracerebral hemorrhage. Case report. Neurol Med Chir (Tokyo). 2012. 52(8):587-90. [Medline].

  4. Mou C, Han T, Zhao H, Wang S, Qu Y. Clinical features and immunohistochemical changes of pituitary apoplexy. J Clin Neurosci. 2009 Jan. 16(1):64-8. [Medline].

  5. Bahmani Kashkouli M, Khalatbari MR, Yahyavi ST, Borghei-Razavi H, Soltan-Sanjari M. Pituitary apoplexy presenting as acute painful isolated unilateral third cranial nerve palsy. Arch Iran Med. 2008 Jul. 11(4):466-8. [Medline].

  6. Hori A. Suprasellar peri-infundibular ectopic adenohypophysis in fetal and adult brains. J Neurosurg. 1985 Jul. 63(1):113-5. [Medline].

  7. Okuda O, Umezawa H, Miyaoka M. Pituitary apoplexy caused by endocrine stimulation tests: a case report. Surg Neurol. 1994 Jul. 42(1):19-22. [Medline].

  8. Silberstein L, Johnston C, Bhagat A, Tibi L, Harrison J. Pituitary apoplexy during induction chemotherapy for acute myeloid leukaemia. Br J Haematol. 2008 Oct. 143(2):151. [Medline].

  9. Thurtell MJ, Besser M, Halmagyi GM. Pituitary apoplexy causing isolated blindness after cardiac bypass surgery. Arch Ophthalmol. 2008 Apr. 126(4):576-8. [Medline].

  10. Brar KS, Garg MK. High altitude-induced pituitary apoplexy. Singapore Med J. 2012 Jun. 53(6):e117-9. [Medline].

  11. Kumar V, Kataria R, Mehta VS. Dengue hemorrhagic fever: A rare cause of pituitary tumor hemorrhage and reversible vision loss. Indian J Ophthalmol. Jul-Aug /2011. 59:311-2. [Medline].

  12. Kruljac I, Cerina V, Pecina HI, et al. Pituitary metastasis presenting as ischemic pituitary apoplexy following heparin-induced thrombocytopenia. Endocr Pathol. 2012 Dec. 23(4):264-7. [Medline].

  13. Vaphiades M. The "pituitary ring sign": An MRI sign of pituitary apoplexy. Neuro-ophthalmology. 2007. 31:111-6.

  14. Weisberg LA. Pituitary apoplexy. Association of degenerative change in pituitary ademona with radiotherapy and detection by cerebral computed tomography. Am J Med. 1977 Jul. 63(1):109-15. [Medline].

  15. Ahmed SK, Semple PL. Cerebral ischemia in pituitary apoplexy. Acta Neurochir. 2008. 150:1193-6.

  16. Chokyu I, Tsuyuguchi N, Goto T, Chokyu K, Chokyu M, Ohata K. Pituitary apoplexy causing internal carotid artery occlusion--case report. Neurol Med Chir (Tokyo). 2011. 51:48-51. [Medline].

  17. Madhusudhan S, Madhusudhan TR, Haslett RS, Sinha A. Pituitary apoplexy following shoulder arthroplasty: a case report. J Med Case Rep. 2011 Jul 5. 5:284. [Medline]. [Full Text].

  18. Mohindra S, Kovai P, Chhabra R. Fatal Bilateral ACA Territory Infarcts after Pituitary Apoplexy: A Case Report and Literature Review. Skull Base. 2010 Jul. 20(4):285-8. [Medline]. [Full Text].

  19. Briet C, Salenave S, Chanson P. Pituitary Apoplexy. Endocrinol Metab Clin North Am. 2015 Mar. 44(1):199-209. [Medline].

  20. Binning MJ, Liu JK, Gannon BS, Osborn AG, Couldwell WT. Hemorrhagic and nonhemorrhagic Rathke cleft cysts mimicking pituitary apoplexy. J Neurosurg. 2008. 108:3-8.

  21. Kaplun J, Fratila C, Ferenczi A, Yang WC, Lantos G, Fleckman AM. Sequential pituitary MR imaging in Sheehan syndrome: report of 2 cases. AJNR Am J Neuroradiol. 2008 May. 29(5):941-3. [Medline].

  22. Liu S, Wang X, Liu YH, Mao Q. Spontaneous disappearance of the pituitary macroadenoma after apoplexy: a case report and review of the literature. Neurol India. 2012 Sep-Oct. 60(5):530-2. [Medline].

  23. Bills DC, Meyer FB, Laws ER Jr, et al. A retrospective analysis of pituitary apoplexy. Neurosurgery. 1993 Oct. 33(4):602-8; discussion 608-9. [Medline].

  24. Thomason K, Macleod K, Eyres KS. Hyponatraemia after orthopaedic surgery - a case of pituitary apoplexy. Ann R Coll Surg Engl. 2009 Apr. 91(3):3-5. [Medline].

  25. Muthukumar N, Rossette D, Soundaram M, Senthilbabu S, Badrinarayanan T. Blindness following pituitary apoplexy: timing of surgery and neuro-ophthalmic outcome. J Clin Neurosci. 2008 Aug. 15(8):873-9. [Medline].

  26. Harrington DO, Drake NV. Chiasm. The Visual Fields, Text and Atlas of Clinical Perimetry. 1990. 290-6.

  27. Krisht AF, Tindall GT. Pituitary apoplexy. In: Clinical Decisions in Neuro-ophthalmology. 1999. 295-301.

  28. Rose-Innes AP. Sheehan syndrome. Gilman S, ed. Neurology Medlink. 2001.

Enhanced coronal CT showing large pituitary tumor with a "snowman" configuration and heterogeneous density (mixed signal) within the tumor indicative of pituitary apoplexy. Hemorrhage was confirmed at surgery.
Enhanced axial and coronal T1-weighted MRI of a typical large pituitary tumor with a "snowman" configuration (coronal) and marked enhancement with contrast. This tumor has not undergone apoplexy.
Enhanced T1-weighted axial and coronal MRI showing a large pituitary tumor that has recently undergone ischemic apoplexy showing a necrotic (hypointense) center and ring of gadolinium enhancement (hyperintense), ie, the "pituitary ring sign." There is a small area of hemorrhagic blush in the center of the necrosis.
Automated visual field showing a bitemporal field defect due to compression of the optic chiasm from below.
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