BASICS

DESCRIPTION

• A diverse group of neurodegenerative eye diseases that result in a typical excavated appearance of the optic nerve (ON)

• Associated with midperipheral and central visual field defects with the intraocular pressure (IOP) as a major risk factor

• Glaucomas are divided into open-angle glaucoma (OAG) types if the trabecular meshwork can be visualized, or closed-angle glaucoma if the meshwork cannot be visualized.

• OAG is further subdivided into primary OAG if there are no other ocular or systemic diseases present. Secondary OAG if associated with an ocular cause (i.e., exfoliative or pigmentary glaucoma) or a systemic disease (i.e., amyloidosis).

EPIDEMIOLOGY

Incidence

• 2 million patients in the USA (50% undetected)

• Glaucoma is the second leading cause of blindness in the USA.

Prevalence

10 million patients at risk as ocular hypertensives (elevated IOP with normal ONs and visual fields)

RISK FACTORS

• High IOP (major risk factor)

• Old age

– 40–49 years = 0.22% prevalence

– 80 years = 14% prevalence

• African American—3 times increased prevalence (vs. Caucasians) and more severe disease

• Family history (5–19% increased risk)

• Migraine headaches, myopia, hypertension

GENERAL PREVENTION

Screening for glaucoma is most effective if aimed at high-risk groups: elderly and African Americans

PATHOPHYSIOLOGY

• Final pathway is damage to the retinal ganglion cells.

• 1 Million ganglion cells in each ON

• Ganglion cell axon travels from the retina to the lateral geniculate body of the thalamus.

• 2 General theories of glaucoma ON damage: (1) VASCULAR—abnormality of blood flow damages ganglion cells. (2) MECHANICAL—weakness of lamina cribrosa (specialized connective tissue at the level of the ON canal) causes damage to the ganglion cell axons.

ETIOLOGY

• IOP is the most significant and treatable risk factor.

• Degree of glaucomatous ON damage is directly related to the IOP level.

• IOP 25–29 mm Hg = 7% prevalence ON damage.

• IOP 35–39 = 52% prevalence ON damage

ON damage can occur at normal IOP (>21 mm Hg): Baltimore Eye Study demonstrated that 50% of all OAG patients had screening IOPs of <21 mm Hg.

DIAGNOSIS

HISTORY

OAG is a diagnosis based on exam of the ON.

PHYSICAL EXAM

• A dilated stereoscopic exam is the most accurate.

• Important ON findings: large cup/disc ratio (decreased ganglion cell axons), ON asymmetry, progressive cup enlargement, neural rim notching, vertical cup enlargement, regional ON pallor, splinter disc hemorrhage, enlarged ON pit

DIAGNOSTIC TESTS & INTERPRETATION

Visual Field Tests

• Corroborates the clinical exam findings of ON damage (Superior ON damage causes inferior visual field changes.)

• Nonglaucomatous optic neuropathies: lack of correlation of visual field changes with ON damage.

• Glaucomatous optic neuropathies: the site and extent of the disc damage correlates with the severity and location of visual field loss.

Follow-up & special considerations

• Early glaucoma ON damage can have a “normal visual field” (preperimetric glaucoma).

• Postmortem studies showed that 50% of ganglion cells can be lost prior to abnormalities in the visual field.

Imaging

Initial approach

Serial, stereoscopic optic disc photography is the most accurate method of diagnosis and follow-up.

Follow-up & special considerations

Newer imaging techniques may improve clinical assessments (scanning laser polarimetry, confocal scanning laser tomography, optical coherence tomography).

DIFFERENTIAL DIAGNOSIS

• OAG is a diagnosis of exclusion.

• Optic disc pallor in excess of excavation suggests a nonglaucomatous optic neuropathy.

• Nonglaucomatous optic neuropathy may include intermittent angle-closure glaucomas, anterior ischemic optic neuropathies (giant cell arteritis), compressive optic neuropathies, congenital ON colobomas, and dominant ON atrophy.

TREATMENT

ADDITIONAL TREATMENT

General Measures

• IOP reduction to prevent further optic disc damage and visual loss is the goal of treatment.

• Treatment options either lower aqueous production or increase aqueous outflow to decrease IOP.

• 3 Main treatment categories:

– Topical medications (β-blockers, prostaglandins analogs, alpha-agonists, cholinergic agonists, carbonic anhydrase inhibitors [topical or oral])

– Office laser procedures (laser trabeculoplasty)

– Operating room incisional surgeries

COMPLEMENTARY & ALTERNATIVE THERAPIES

OAG Treatment Trials

• Studies demonstrating that lowering IOP slowed ON damage

– Ocular Hypertensive Treatment Trial: patients with IOP 24–32 mm Hg with normal ON and visual fields treated with standard medicines versus observation showed 9.5% of observed group versus 4.5% of medically treated group developed OAG (1)[A].

– Collaborative Normal Tension Glaucoma Study: showed that a 30% IOP reduction of an initially normal IOP (<21 mm Hg), prevented or delayed OAG progression in 80% or patients in 5 years (2)[A].

– Advanced Glaucoma Intervention Study: showed that patients with advanced visual field loss who had IOP controlled (<18 mm Hg) 100% of office visits had no progression of visual field loss. Patients with IOP >18 mm Hg at 50% of office visits had significant worsening of visual field (3)[A].

• Studies comparing patient outcomes with different treatment protocols

– Glaucoma Laser Trial: compared argon laser trabeculoplasty with standard topical medicines for lowering IOP in newly diagnosed, untreated OAG patients. 2-year results demonstrated no major differences in terms of visual acuity or visual field changes (4)[A].

– Collaborative Initial Glaucoma Treatment Study: showed that newly diagnosed OAG patients randomized to initial treatment with medications and lasers versus surgical trabeculectomy had similar 5-year visual field outcomes (5)[A].

– Tube Versus Trabeculectomy Study: compared OAG patient outcomes who had prior eye surgery (glaucoma or cataract surgery) and were randomized to glaucoma drainage implant surgery (Baerveldt) or trabeculectomy. The 3-year clinical outcomes were similar (6)[A].

ONGOING CARE

PROGNOSIS

• Patients with worse visual field loss and ON damage at diagnosis have a higher risk of blindness.

• Early diagnosis and effective IOP-lowering treatment are critical to visual field preservation.

• Some patients with OAG progress despite IOP lowering and require more aggressive treatment.

• Close monitoring and follow-up of all patients with OAG are critical to preserve vision.

• Overall quality of life issues are critical to the treatment of patients with glaucoma.

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