Pituitary apoplexy overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]
Overview
Pituitary apoplexy is bleeding into the pituitary gland. Pituitary gland is a small gland joined to the hypothalamus gland at the base of brain. The pituitary produces many of the hormones that control essential body processes. Pituitary apoplexy is most commonly associated with pituitary adenoma.
Historical Perspective
Pituitary apoplexy was first discovered by Pearce Bailey in the year 1898. In the year 1905, Leopold Bleibtreu recorded the postmortem examination of a 21-year-old acromegalic patient, in whom he discovered that the pituitary gland had been replaced by an old hemorrhage. The term pituitary apoplexy was coined by Brougham, Heusner and Adams in the year 1950.
Pathophysiology
Pituitary apoplexy is an acute clinical syndrome caused by hemorrhage and necrosis in the pituitary gland. Most commonly it is associated with pituitary adenoma.
Differentiating Pituitary apoplexy From Other Diseases
Pituitary apoplexy must be differentiated from other diseases that cause severe headache such as subarachnoid hemorrhage, meningitis, intracranial mass, cerebral hemorrhage, cerebral infarction, intracranial venous thrombosis, migraine, head injury, lymphocytic hypophysitis and radiation injury.
Epidemiology and Demographics
The worldwide prevalence of pituitary apoplexy is 6.2 per 100,000 persons. The incidence of pituitary apoplexy is 0.7 per 100,000 persons.[1]
Risk Factors
Common risk factors in the development of pituitary apoplexy include bleeding disorders, diabetes, use of a breathing machine, radiation to the pituitary gland, angiography, head injury, surgery, pituitary stimulation and pregnancy induced lactotroph hyperplasia.
Screening
There are no screening guidelines for pituitary apoplexy.
Natural History, Complication and Prognosis
If left untreated, pituitary apoplexy is an acute life threatening condition. Pituitary apoplexy may lead to sudden decline in pituitary hormone production. The most life threatening endocrinopathy is acute adrenal crisis. Complications of pituitary apoplexy include Vision loss, optic neuritis, Diplopia, Ptosis, Increased intracranial pressure, Hypothyroidism, Hypogonadism and Growth hormone deficiency. The prognosis of pituitary apoplexy depends upon presentation and initiation of therapy. Emergent application of medical and surgical treatment is associated with greater improvement in visual field defects, visual acuity, and diplopia. The outlook is good for people who are diagnosed early and treated. Patients require hormone(s) replacement therapy for life.
Diagnosis
Pituitary apoplexy diagnosis depend upon presentation. CT scan without contrast is the initial test of choice in emergency department patients who presents with sudden-onset severe headache, visual loss or ophthalmoplegia suggesting of pituitary apoplexy. CT scan can also help to differentiate; whether subarachnoid hemorrhage is arising from pituitary hemorrhage or an aneurysm. MRI is done if the CT scan is suspicious for pituitary apoplexy. MRI is more sensitive than CT scan. MRI is more accurate in distinguishing the soft tissues of the pituitary from the surrounding bony structures. MRI is also superior to CT scan for detecting ischemia and infarction in brain tissue.
Treatment
The optimal therapy for pituitary apoplexy depends upon presentation of patient. Emphasis is on early hemodynamic stabilization of the patient, with evaluation for signs of pituitary hormones deficiency. Life threatening hypopituitarism must be treated with replacement of hormones.
Surgery
Neurological decompression is done once the patient is hemodynamically stable. Surgery relieves pressure on the pituitary and improves visual field defects and ocular palsy. Early decompression has been associated with better visual and endocrine outcome.
References
- ↑ Fernandez A, Karavitaki N, Wass JA (2010). "Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK)". Clin Endocrinol (Oxf). 72 (3): 377–82. doi:10.1111/j.1365-2265.2009.03667.x. PMID 19650784.