Headache and Diplopia in a 41-Year-Old Man

Mousa Abujbara, MD

Disclosures

February 06, 2017

Once recognized, effective treatment of pituitary tumor apoplexy requires prompt administration of high-dose corticosteroids. Steroids should be administered in supraphysiologic doses to not only replace endogenous hormone deficiency during a stressful condition but also to take advantage of its anti-inflammatory effect by decreasing swelling on parasellar structures. The definitive treatment for pituitary tumor apoplexy is emergent surgical decompression. Transsphenoidal resection is the most common approach in this situation. In cases where significant extension of hemorrhage into the brain parenchyma beyond the diaphragma sella is present, an intracranial approach may be preferred. In a minority of cases, conservative medical therapy is an acceptable alternative; examples of this include patients who are poor surgical candidates and selected patients who present with isolated meningismus or ophthalmoplegia and show significant improvement with steroid administration. Medical management includes monitoring of endocrine, neurologic, and ophthalmologic function combined with hormone replacement.

With prompt recognition, timely surgery, and proper medical management, most patients with pituitary tumor apoplexy improve.[6] Ophthalmoplegia is usually the first symptom to resolve. Less readily restored is the optic nerve defect, resulting in decreased visual acuity and restricted visual fields. More than half of patients, however, have permanent hormone deficiencies resulting from pituitary injury and require hormone replacement. One study showed that maintenance steroid, thyroid hormone, and testosterone replacement was essential postoperatively in 82%, 89%, and 64% of patients, respectively.[7]

Following immediate administration of high-dose corticosteroids, the patient in this case underwent an emergent transsphenoidal resection. An infarcted adenoma was identified, with extensive areas of hemorrhage and necrosis consistent with apoplexy. Resolution of the headache and improvement of visual and extraocular function were noted 24 hours after surgery. An endocrinology evaluation was completed, and the patient was confirmed to have hypopituitarism. Two weeks following surgery, his ophthalmoplegia and visual field deficits had completely resolved. Pharmacologic management of the patient's hypopituitarism included replacement therapy with corticosteroids, levothyroxine, and testosterone.

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