Recognizing and Intervening in Pituitary Apoplexy

Elizabeth Zink, MS, ACNP, CCRN, CNRN

Disclosures

Topics in Advanced Practice Nursing eJournal. 2005;5(4) 

In This Article

Case Study

A 75-year-old man with a history of hypertension presented to the emergency department with complaints of 2 days of fatigue, acute confusion, acute loss of vision in the left eye, vomiting, fever of 102.7 degrees, and severe headache. Neurologic examination revealed a left cranial nerve III palsy (dilated pupil, inability to move affected eye medially or upward) including ptosis (drooping of the affected eyelid), a cranial nerve IV palsy (inability to move the affected eye downward), right temporal visual field loss, severe visual loss in the left eye with light perception only, and left afferent pupillary defect (a weak or absent consensual pupillary response in the opposite eye when a light is directly shown on the diseased eye).

An emergency CT scan without contrast revealed a hyperdense mass in the area of the pituitary gland and optic chiasm (Figure 1). A follow-up MRI was immediately obtained and confirmed the existence of a pituitary macroadenoma with acute hemorrhage (Figure 2). The MRI findings also showed that the tumor was displacing the optic chiasm, explaining the acute visual field changes. Because of the patient's acute visual loss, neurosurgeons performed an emergency transsphenoidal resection.

Figure 1.

Initial CT scan.

Figure 2.

Initial MRI scan.

Postoperative care was provided in a neurosciences intensive care unit, where the patient complained of double vision (diplopia). Neurologic examination revealed a residual left cranial nerve III palsy, left cranial nerve IV palsy, and a right inferior quadrantanopia (loss of vision in the right inferior quarter of the visual field). Hormone replacement was initiated with hydrocortisone. Pathologic evaluation revealed a macroadenoma.

On the second postoperative day, a neuro-ophthalmologist reported resolution of diplopia and the patient denied any further visual changes. The neuro-ophthalmologist verified resolution of cranial nerve deficits and recommended computerized visual field examination as a follow-up diagnostic test to confirm resolution of visual field deficits. A full endocrinology evaluation was also completed, and the patient was found to have hypopituitarism. Pharmacologic management of the patient's hypopituitarism included a slow tapering of hydrocortisone, initiation of levothyroxine, and testosterone replacement therapy.

This patient demonstrates a classic presentation of pituitary apoplexy that was recognized, evaluated, and treated quickly, resulting in a favorable functional outcome.

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