Take home: A reasonable goal for patients with low-tension glaucoma patients is an IOP that is 30% below the untreated baseline. However, some patients will continue to progress and may require single-digit target IOP goals.
Low-tension glaucoma is not such a distinct disorder that its pathogenesis differs from primary open-angle glaucoma. Instead, it represents a multifactorial disease entity along a continuum of IOP measurements, said David S. Greenfield, MD, professor of ophthalmology, co-director, Glaucoma Service, and director, Glaucoma Fellowship, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami.
Despite its many names—low-tension glaucoma, normal-tension glaucoma, low-pressure glaucoma, pseudoglaucoma, and soft glaucoma—patients can go blind without proper treatment and monitoring, Dr. Greenfield said.
The well-known Normal Tension Glaucoma Study provided valuable clinical pearls regarding low-tension glaucoma treatment, Dr. Greenfield said. This included the importance of confirming suspected visual field progression, examining for optic disc hemorrhages, inquiring about migraines, and realizing that not all patients will continue to progress. The study also revealed that a target intraocular pressure (IOP) 30% below the untreated baseline is achievable and will prevent progression in about 80% of patients.
“Twenty percent of patients will continue to progress despite low IOP targets,” Dr. Greenfield said. Clinicians should also be aware of the Low-Pressure Glaucoma Treatment Study (LoGTS), in which eyes randomized to brimonidine 0.2% were less likely to exhibit visual field progression and optic disc hemorrhage than eyes receiving timolol 0.5%. These findings occurred despite similar IOP levels in both groups during the course of the study.
In his hands, Dr. Greenfield takes a four-step approach to treating low-tension glaucoma. He will confirm whether there is visual field progression, exclude non-glaucomatous mechanisms of optic disc cupping (Figure 1), track the level of IOP responsible for progression, and then consider management either by surgery or nonsurgical methods.
When considering surgical treatment, clinicians should take into account who is progressing most quickly. Trabeculectomy is the preferred surgical approach, but it is critical to carefully select the patient population to avoid hypotony-related risks common in high myopes, those 90 years or older, and those on anti-coagulation therapy.
Although most of the time clinicians can prevent further visual field loss by achieving a single- digit target IOP, such a process is not effective for 15% of patients.
“Some eyes will continue to progress, prompting us to wonder what other factors could be at work,” he said. These include low nocturnal blood pressure, low ocular perfusion pressure (which has emerged in a number of studies as a risk factor), and low intracranial pressure. Figures 2 and 3 illustrate the importance of the translaminar pressure gradient in a patient who developed profound optic disc edema following surgical IOP lowering in the left eye and was subsequently diagnosed with pseudotumor cerebri (idiopathic intracranial hypertension). The optic nerve in the fellow eye was protected from optic disc edema due to elevated IOP. The optic disc edema resolved following administration of oral acetazolamide therapy.
In patients who continue to progress at very low levels of IOP, cranial neuroimaging, 24-hour ambulatory blood pressure monitoring, and sleep studies to exclude obstructive sleep apnea can be helpful. “Frequent monitoring is helpful to study the velocity of progression,” he said.
This article was adapted from Dr. Greenfield’s presentation at the American Academy of Ophthalmology annual meeting in Las Vegas in November 2015.
Presentation title: Robert N. Shaffer Lecture: Glaucoma at Low Tension: When Normal Isn't Good Enough