Managing functional visual field loss with low IOP

January 31, 2016

When visual field defects progress despite good IOP control, clinicians should look for other factors, according to Malik Y. Kahook, MD.

San Francisco-When visual field defects progress despite good IOP control, clinicians should look for other factors, according to Malik Y. Kahook, MD.

Dr. Kahook, chief of glaucoma services at the University of Colorado in Aurora, CO, discussed strategies for addressing normal or low-tension glaucoma here at the Glaucoma Symposium CME.

He defined low-tension glaucoma as chronic, progressive optic neuropathy with characteristic optic nerve head cupping, retinal nerve fiber layer thinning and functional visual field loss with an IOP of less than 22 mm Hg.

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Clinicians should still focus on lowering IOP in these patients, but also investigate other factors, Dr. Kahook said. These include vascular dysregulation, hypotension (particularly nocturnal), lamina cribrosa abnormalities, and autoimmune disorders.

Compared with patients with primary open-angle glaucoma, patients with low-tension glaucoma are more likely to have paracentral defects, nerve fiber layer hemorrhages, focal notches and peripapillary atrophy, he said.

The big question to answer in these patients is whether they have glaucoma or some other condition that mimics it, Dr. Kahook said.

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“When we have low-tension glaucoma, we have certain features that we look for to guide us toward imaging,” he said.

He listed the following glaucomatous etiologies: primary open-angle glaucoma with diurnal fluctuation of IOP; intermittent acute angle-closure glaucoma; underestimation of actual IOP; resolved corticosteroid-induced glaucoma; uveitic glaucoma; traumatic glaucoma; uveitic glaucoma/glaucomatocyclitic crisis (Posner-Schlossman); “burned out” pigmentary glaucoma, myopia with peripapillary atrophy, optic nerve coloboma or pits; and congenital disc anomalies/cupping.

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Dr. Kahook said compressive, metabolic, toxic, inflammatory or infectious optic neuropathy can mimic glaucoma. This includes pituitary adenoma, meningioma, empty sella syndrome, Leber heriditary optic atrophy, methanol optic neuropathy, optic neuritis, and syphilis.

What to rule out

 

Finally, he advised ruling out vascular injuries, including giant cell arteritis, non-arteritic anterior ischemic optic neuropathy, posterior ischemic optic neuropathy, central retinal artery occlusion and carotid/ophthalmic artery occlusion.

He described the following circumstances that suggest neurologic, cardiovascular, or autoimmune evaluation: pallor greater than cupping, non-retinal nerve fiber bundle visual field defect, cupping and visual field defects that do not correlate, vision worse than 20/20, horizontal over vertical cupping, color vision deficiencies, age less than 50 years and progression despite having achieved an IOP of 10 mm Hg.

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“If you see any of these, start thinking about imaging,” he said.

Clinicians should also watch for disc hemorrhages, Dr. Kahook said. He defined these as splinter or flame-shaped, perpendicular prelaminar hemorrhages that cross the peripapillary zone and extend to adjacent the superficial retinal nerve fiber layer.

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“Ninety-nine percent of the time I see a hemorrhage like this, if not more, it’s related to low-tension glaucoma,” he said.

In the presence of a disc hemorrhage, conditions to check include posterior vitreous detachment, diabetes and hypertension, he said.

Optic disc drusen, increased intracranial pressure, peripapillary choroidal neovascular membrane, ischemic optic neuropathy, he said.

When Dr. Kahook suspects glaucoma and finds a disc hemorrhage, he considers treating the patient for glaucoma. If the patient does have glaucoma with a disc hemorrhage, he monitors more closely and alters treatment to achieve a lower target IOP.

What are the red flags

 

He listed the following field defect red flags: defects that respect the vertical midline, defects that do not correlate with the nerve, rapid progression of visual defects and focal defects with a large “step-off.”

“Usually glaucoma is a smoother process that happens with the visual field defect,” he said.

When these flags pop up, he collaborates with the primary-care provider to consider sleep studies with 24-hour blood pressure checks, a diagnosis of hypertension, an autoimmune disease work up, and a history to determine whether vitamin deficiencies or toxic exposures could be responsible.

In collaboration with neuro-ophthalmologists or neurologist, he might consider magnetic resonance imaging of the orbit. He would go over these images with the radiologist as well as the patient.

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He also might check diurnal and nocturnal IOP. Two-thirds of glaucoma patients have their highest IOP outside clinic hours, especially at night, he said.

In an office visit, supine IOP is closer to peak IOP while supine at night; intraocular measurements in the sitting position during normal office hours don’t reflect the true range of an individual’s IOP or their peak IOP variation throughout the day, he said.

When a visual field defect progresses despite an IOP of less than 12 mm Hg, Dr. Kahook first ascertains that medication has been optimized, and that the patient is adhering, that there is no nocturnal hypotension.

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If he cannot determine an alternate cause, he presumes that a large component of the visual field defect is independent of IOP. So he might try any of the following: a trabeculectomy to get to single-digit IOP, complementary and alternative medicine such as Ginko biloba, changing the patient’s sleep position, an alpha-agonist, off-label memantine and calcium channel blockers.

He may also begin counseling the patient on how to live with low vision.

“That patient should be aware of what the future might hold,” he said.

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