A 68-year-old Caucasian female was referred to our glaucoma clinic by her cataract surgeon due to elevated IOP after cataract surgery. She recently had an uncomplicated cataract surgery in her left eye followed by cataract surgery in her right eye complicated by a posterior capsular tear requiring sulcus IOL placement and anterior vitrectomy. The postoperative course in the right eye was further complicated by an IOP of 58 mm Hg on post-op day 1 resulting in a chronically dilated pupil, cystoid macular edema (currently on ketorolac t.i.d.) and a retinal hole and horseshoe tear requiring panretinal photocoagulation. She had already been started on latanoprost for elevated IOP in both eyes postoperatively. She reported occasional headaches but denied vision changes, loss of peripheral vision or any neurologic symptoms.

THE OCULAR EXAM

Patient exam was remarkable for the following:

• Visual acuity: 20/40-1 OD, 20/20 -2 OS
• Pupils: Fixed dilated OD, no relative afferent pupillary defect (RAPD) OU
• IOP: 18 mm Hg OD (Tmax 54), 12 mm Hg OS (Tmax 23), on latanoprost OU

Anterior exam was significant for corneal endopigment and three-piece sulcus IOL with trace posterior capsular opacification OD and trace guttae and posterior chamber IOL OS. Gonioscopy was open OU with rare peripheral anterior synechiae OD, with 2-3+ posterior trabecular meshwork pigmentation OU. Posterior exam (performed with a 90-D lens) revealed 0.3 cup-to-disc ratio with intact rims OU with trace disc pallor, peripapillary atrophy, macular edema and horseshoe tear with surrounding laser OD and a normal posterior exam OS.

ADDITIONAL TESTING

Due to the patient’s previously elevated IOP, a corneal pachymetry, OCT of the retinal nerve fiber layer (RNFL) and Humphrey Visual Field (HVF) 24-2 were ordered. Pachymetry measurements demonstrated slightly thin corneas at 508 µm OD and 512 µm OS. RNFL thickness was full OD with thinning OS, specifically temporally and superotemporally (Figure 1). HVF 24-2 was reliable OU and remarkable for generalized depression OU on total deviation with the greyscale concerning for bitemporal defects respecting the vertical midline. Given the discordancy of findings — dense bitemporal visual field loss that respected the vertical midline in the absence of significant cupping and RNFL thinning — there was a high index of suspicion for a non-glaucomatous etiology for the patient’s clinical optic neuropathy; namely, compressive, nutritional or infectious causes.

ARRIVING AT THE DIAGNOSIS

Given the differential diagnosis, the following labs and imaging studies were ordered: rapid plasma reagin and fluorescent treponemal antibody absorption tests to evaluate for syphilis, angiotensin-converting enzyme to evaluate for sarcoidosis and vitamin B12 to evaluate for a nutritional deficiency. All laboratory studies were within normal limits. MRI of the brain/orbits showed a cystic and solid 3.0 x 3.8 x 3.1-cm sellar-suprasellar mass with enlargement of the sella and invasion of the cavernous sinus, partial encasement of the cavernous segment of the internal carotid arteries and uplifting of the optic chiasm (Figure 2). Differential diagnosis for the lesion includes craniopharyngioma and pituitary macroadenoma.

Given the above findings, the patient was referred to a local neurosurgeon for evaluation. We are continuing to follow her in glaucoma clinic for her ocular hypertension as well as for serial HVFs.

DISCUSSION

Bitemporal hemianopsia is the most common visual field defect in sellar lesions due to optic chiasm compression at the site of crossing of nasal optic nerve fibers, representing the temporal visual field.¹ In patients with bitemporal hemianopsia, visual acuity is usually preserved.¹ Sellar masses account for approximately 15% of all brain and central nervous system tumors.² Pituitary adenomas are the most common type of sellar and suprasellar masses, accounting for 85% in one study.³

The most common presenting symptoms of clinically non-functioning pituitary adenomas are visual field defects and headache, and typically surgical intervention is indicated in cases with visual field defects.⁴ Close ophthalmologic monitoring after treatment of these lesions is crucial as visual field defects can be the first sign of tumor recurrence.⁵

Our patient endorsed mild headaches but did not notice her visual field defects at presentation.

TAKE-HOME POINTS

When evaluating a patient for glaucomatous optic neuropathy, the clinician should complete a thorough clinical evaluation consisting of IOP measurement, gonioscopy, high-magnification examination of the optic nerve head (preferably with a 90-D or 78-D lens) as well as structural and functional assessments of the optic nerve head, such as OCT RNFL and HVF. Expected exam findings in a patient with glaucoma include optic nerve head cupping, a glaucomatous visual field defect, RNFL thinning and possibly elevated IOP. When a patient’s HVF does not correspond to the rest of the clinical exam and testing, further evaluation with appropriate labs and/or imaging to rule out non-glaucomatous causes of optic neuropathy is a crucial next step. OM

For additional images, see the online version of this article.

REFERENCES

1. Bresson D, Herman P, Polivka M, Froelich S. Sellar Lesions/Pathology. Otolaryngol Clin North Am. 2016;49:63-93.
2. Dolecek TA, Propp JM, Stroup NE, Kruchko C. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States in 2005-2009 [published correction appears in Neuro Oncol. 2013 May;15:646-647]. Neuro Oncol. 2012;14 Suppl 5(Suppl 5):v1-49.
3. Saeger W, Lüdecke DK, Buchfelder M, Fahlbusch R, Quabbe HJ, Petersenn S. Pathohistological classification of pituitary tumors: 10 years of experience with the German Pituitary Tumor Registry. Eur J Endocrinol. 2007;156:203-216.
4. Molitch ME. Nonfunctioning pituitary tumors and pituitary incidentalomas. Endocrinol Metab Clin North Am. 2008;37:151-171, xi.
5. Chiu EK, Nichols JW. Sellar lesions and visual loss: key concepts in neuro-ophthalmology. Expert Rev Anticancer Ther. 2006;6 Suppl 9:S23-S28.

About the Author

Barbara Smith, MD, is a resident physician in ophthalmology at the University of Tennessee Health Science Center, Hamilton Eye Institute, Memphis, Tenn. Email her at bdsmith@uthsc.edu.

Claire Kiernan, MD, is an assistant professor of ophthalmology at the University of Tennessee Health Science Center, Hamilton Eye Institute in Memphis, Tenn. Email her at ckierna2@uthsc.edu.