This is a corrected version of the article that appeared in print.
Am Fam Physician. 2023;107(3):253-262
Patient information: See related handout on glaucoma, written by the authors of this article.
Author disclosure: No relevant financial relationships.
Glaucoma is a group of eye disorders characterized by progressive deterioration of the optic nerve that can lead to vision loss. Primary open-angle glaucoma (POAG) is the most common form in the United States. The risk of POAG increases with age, family history of glaucoma, type 2 diabetes mellitus, hypotension, hypothyroidism, obstructive sleep apnea, cardiovascular disease, and myopia. Up to one-half of patients are undiagnosed because a diagnosis often requires monitoring over years to document changes suggesting POAG. These include a cup-to-disc ratio of 0.3 or greater, intraocular pressure greater than 21 mm Hg on tonometry, nerve fiber layer defects identified on optical coherence tomography, and reproducible visual field defects. Topical intraocular pressure–lowering medications and selective laser trabeculoplasty are first-line treatments for POAG. Although POAG screening in the general adult population is not recommended, primary care physicians can help decrease POAG-related vision loss by identifying patients with risk factors and referring them for evaluation by an eye specialist. Medicare covers evaluations in patients at high risk. Primary care physicians should encourage medication adherence and identify barriers to treatment. The other type of glaucoma is angle-closure glaucoma, in which the flow of aqueous humor is obstructed. Angle-closure glaucoma can occur acutely with pupillary dilation and is an ophthalmologic emergency. The goal of treatment for acute angle-closure glaucoma is to reduce intraocular pressure quickly with medications or surgery, then prevent the recurrence of the obstruction to aqueous flow by a definitive ophthalmologic procedure.
Glaucoma is a group of eye disorders characterized by progressive deterioration of the optic nerve head and retinal nerve fiber layer (i.e., the portion of the optic nerve that runs through the retina). Without treatment, this neural deterioration can result in vision loss.
|Clinical recommendation||Evidence rating||Comments|
|Reducing intraocular pressure is the only treatment proven to stop or slow the progression of vision loss in primary open-angle glaucoma.3,5,9,18,24,25||A||Multiple randomized controlled trials, practice guidelines, and a Cochrane review|
|Selective laser trabeculoplasty is a first-line treatment for primary open-angle glaucoma.28||B||Multicenter randomized controlled trial comparing selective laser trabeculoplasty with standard medical therapy for patients with primary open-angle glaucoma|
|There is insufficient evidence to recommend screening for glaucoma in the general adult population.5,9||C||U.S. Preventive Services Task Force evidence review and practice guidelines from the American Academy of Ophthalmology|
|Primary care physicians should ask patients about barriers to adhering to their glaucoma medication and encourage the use of automated reminders.3,34,35||C||Narrative reviews and cohort studies|
There are two forms of glaucoma: primary open-angle glaucoma (POAG), in which the outflow tract is anatomically open, and angle-closure glaucoma (ACG), in which the outflow of aqueous humor from within the eye is obstructed.1–5 POAG in adults is the focus of this article because it is the most common form of glaucoma in the United States.1–3 Table 1 provides a glossary of terms related to the evaluation and treatment of patients with glaucoma.1–6
|Glaucoma suspect||Patients with eye findings that could indicate an increased risk of developing glaucoma; includes patients with an elevated intraocular pressure and a normal optic disc, retinal nerve fiber layer, and visual fields; may also include patients with an isolated suspicious optic nerve head (i.e., large cup-to-disc ratio > 0.3), retinal nerve fiber layer, or visual fields without elevated intraocular pressure|
|Gonioscopy||Measuring the angle between the iris and cornea using special lenses and slit lamp (http://www.gonioscopy.org/basic-exam-techniques.htm)|
|Lamina cribrosa||Highly organized, sieve-like structure at the opening in the sclera through which axons of the retinal ganglion cells pass from the retina to form the optic nerve; there are hundreds of openings through which roughly 1 million to 2 million nerve fibers, grouped into bundles, exit the eye, and when these axons bend and pass through the lamina cribrosa, they are sensitive to damage|
|Neuroretinal rim||Dense packing of nerve fibers and glial cells inside the optic disc, usually pink in color; damage with loss of the cells results in thinning of the rim, which is a cardinal feature of glaucoma; this thinning can happen diffusely, making the central portion of the optic disc (optic cup) appear larger, or focally, which appears as notching on the side of the rim|
|Ocular hypertension||Elevated intraocular pressure; greater than 21 mm Hg|
|Optic disc/optic nerve head||Oval structure in the posterior fundus where axons of retinal ganglion cells converge and exit the eye; some distinguish the optic nerve head as the three-dimensional structure where this occurs, whereas others use these terms interchangeably|
|Optical coherence tomography||Technique to provide cross-sectional images of the retina by measuring and analyzing patterns of reflected infrared light; this is analogous to ultrasonography using sound waves to visualize biologic structures and enables detailed, quantitative information about the optic nerve head, retinal nerve fiber layer, and other structures (https://www.ncbi.nlm.nih.gov/books/NBK554044/figure/ch3.Fig15)|
|Pachymetry||Measuring corneal thickness; patients with thinner corneas are at higher risk of developing glaucoma|
|Perimetry||Visual field testing; can be performed roughly by confrontation; most often done by automatic static perimetry in which the patient pushes a button when a light stimulus is presented somewhere in their visual field (https://www.youtube.com/watch?v=npwVkITgvKQ)|
|Physiologic cup||Short, funnel-shaped depression at the center of the optic nerve, where vessels can be viewed; typically paler than the surrounding neuroretinal rim; enlargement in the cup (i.e., cupping) is a cardinal feature in glaucoma; progressive cupping of the optic disc is a result of compression, stretching, and remodeling of the connective tissue of the lamina cribrosa; the cup-to-disc ratio is the vertical diameter of the cup expressed as a fraction of the vertical diameter of the disc, which is abnormal if > 0.3|
|Tonometry||Measurement of intraocular pressure; most commonly done by applanation tonometry, where intraocular pressure is determined by measuring the force required to flatten a portion of the cornea; indentation tonometry measures the force required to press into the cornea; primary care tonometry can be performed with a tonometer (requires topical anesthetic) or iCare|
Primary Open-Angle Glaucoma
ANATOMY AND PATHOPHYSIOLOGY
Aqueous humor is produced by the ciliary body and flows through the pupil and into the anterior chamber (Figure 1).7 The fluid drains primarily through the trabecular meshwork into the venous circulation. The balance between the rate of aqueous humor production and the rate of outflow determines intraocular pressure (IOP). Normal IOP varies with blood pressure, respiration, and time of day (lower in the evening).1–4
An elevated IOP is an important risk factor for glaucoma and can damage retinal cell axons when they pass out of the eye to form the optic nerve.1–10 However, some patients have a normal IOP and develop glaucomatous eye damage anyway. There are also patients with an elevated IOP who never develop eye damage; therefore, the pathophysiology of glaucoma is only partially understood.
The cause of POAG is multifactorial. The biomechanical theory states that there is resistance to aqueous outflow even though no obstruction is clinically identifiable, and the resulting IOP elevation directly damages the optic nerve head. The vascular theory states that decreased blood flow in vessels surrounding the optic nerve head results in ischemic damage. In the neurodegenerative theory, the cause is the primary deterioration of the optic nerve head, possibly due to autoimmunity, loss of neurotrophic factors, or failure of cellular repair mechanisms. An association with dementia has been noted in support of a neurodegenerative etiology.2,3,5,11
Glaucoma is second only to cataracts as the top cause of blindness worldwide and is the leading cause of blindness among people of African descent in the United States. The estimated prevalence of glaucoma in people older than 40 years is 3.5%, which increases with age. This prevalence is expected to increase from approximately 60 million people worldwide to 112 million by 2040 (estimates for the United States are 3 million and are expected to increase to 6 million by 2050). Up to 50% of people with glaucoma are undiagnosed, and this proportion is likely higher in medically underserved populations.4,12
POAG accounts for approximately 75% of glaucoma cases in the United States.4,12 The prevalence of POAG in people of African and Hispanic descent in the United States is at least threefold higher than in non-Latino White people.2,3,5,13,14 The reasons behind this association are unclear and complex, and warrant more study because there are also socioeconomic factors that influence access to care and the detection and treatment of glaucoma.5,15–17
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