Case Presentation: A 65-year-old man with a history of bilateral retinal detachment, coronary artery disease, type 2 diabetes, hypothyroidism, and hypertension presented with several days of left eye pain, bitemporal headache and decreased vision. Vital signs were notable for fever (101.2F) and tachycardia (124 bpm). On physical exam, he was unable to open his left eyelid and had a fixed and dilated left pupil pointed downward and laterally, consistent with 3rd nerve palsy. Laboratory studies showed leukocytosis (13.1 K/uL) and an elevated CRP (10.5 mg/L); severely reduced serum prolactin at 1.3 ng/mL (normal 4.1 – 18.4 ng/mL), testosterone at 36.5 ng/dL (normal 193-740 ng/dL) and cortisol at 1.1 ug/dL (normal 6-18.4 ug/dL). FSH, LH, insulin-like growth factor 1, and thyroid studies were normal. Magnetic resonance imaging of the brain revealed pituitary enlargement, compatible with pituitary macroadenoma (2.0 x 1.0 cm) with abutment of the tumor on the optic chiasm on the right side. He was diagnosed with pituitary apoplexy and was started on dexamethasone, levothyroxine, and empiric antibiotics for suspected meningitis. The patient underwent transsphenoidal resection of the pituitary and continued to have left CN III palsy after surgery with improved vision after fixing his retinal detachment. He was discharged on decadron and has been kept on prednisone (for adrenal insufficiency) and testosterone replacement therapy. Biopsy demonstrated infarcted pituitary macroadenoma with hemorrhage and positive immunostaining for FSH and LH and MR post-surgery revealing a residual pituitary gland.
Discussion: Pituitary apoplexy is a condition in which a pituitary tumor spontaneously hemorrhages, and most often occurs in the 5th decade of life, predominantly in males. Due to the anatomy of the pituitary gland and its close proximity to the optic chiasm and pre-chiasmatal optic nerve, compression or displacement of the optic nerve/chiasm can result in bitemporal hemianopsia, or mixed visual field defects.[2] Diplopia with oculomotor palsy is often caused by tumor invasion of the cavernous sinus (CN III, IV or VI). Our patient had oculomotor symptoms of CN III palsy, likely resulting from the mass compressing the cavernous sinus, which lies superior to the pituitary gland. However, what was not explained by this pathology was his bilateral retinal detachments. Only very few case reports describe bilateral retinal detachments as a consequence of a pituitary microadenoma as well as possible link between hypercortisolism and subsequent retinal pathology. Prolactin, produced by the anterior pituitary, acts as a neuroprotective and pro-angiogenic agent and thus, lack of prolactin receptor leads to photoreceptor dysfunction and decreased synthesis of retinal neuroprotective molecules. Thus, we suspect that our patient was predisposed to bilateral retinal detachment from hypoprolactinemia leading to apoptosis of retinal cells and disruption of retinal structures.
Conclusions: Little is known about the consequences of hypoprolactinemia outside of the context of lactation. Yet, the growing body of literature suggests that there could be ramifications of hypoprolactinemia in non-lactating individuals. The challenge is that there is currently no guideline for prolactin replacement in these individuals and hospitalists are left without guidance. Further investigation into the clinical manifestations of hypoprolactinemia in non-lactating persons is warranted.