Glaucoma

Introduction

Glaucomas are ocular disorders that lead to an optic neuropathy characterized by changes in the optic nerve head (optic disc) that is associated with loss of visual sensitivity and field.

• There are two major types of glaucoma: primary open-angle glaucoma (POAG) or ocular hypertension, which accounts for most cases and is therefore the focus of this chapter, and closed-angle glaucoma (CAG). Either type can be a primary inherited disorder, congenital, or secondary to disease, trauma, or drugs.
• In POAG, the specific cause of optic neuropathy is unknown. Increased intraocular pressure (IOP) was historically considered to be the sole cause. Additional contributing factors include increased susceptibility of the optic nerve to ischemia, excitotoxicity, autoimmune reactions, and other abnormal physiologic processes.
• Although IOP is a poor predictor of which patients will have visual field loss, the risk of visual field loss increases with increasing IOP. IOP is not constant; it changes with pulse, blood pressure, forced expiration or coughing, neck compression, and posture. IOP demonstrates diurnal variation with a minimum pressure around 6 pm and a maximum pressure upon awakening.

Clinical Presentation

POAG is slowly progressive and is usually asymptomatic until onset of substantial visual field loss. Central visual acuity is maintained, even in late stages.

• Patients with CAG typically experience intermittent prodromal symptoms (eg, blurred or hazy vision with halos around lights and, occasionally, headache). Acute episodes produce symptoms associated with a cloudy, edematous cornea; ocular pain; nausea, vomiting, and abdominal pain; and diaphoresis.

Diagnosis

POAG is confirmed by the presence of characteristic optic disc changes and visual field loss, with or without increased IOP. Normal tension glaucoma refers to disc changes, visual field loss, and IOP less than 21 mm Hg (2.8 kPa). Ocular hypertension refers to IOP greater than 21 mm Hg (2.8 kPa) without disc changes or visual field loss.

• CAG is usually visualized by gonioscopy. IOP is generally markedly elevated (e.g., 40–90 mm Hg [5.3–12 kPa]) when symptoms are present. Additional signs include hyperemic conjunctiva, cloudy cornea, shallow anterior chamber, and occasionally edematous and hyperemic optic disc.

Treatment Of Ocular Hypertension and Open-Angle Glaucoma

Goal of Treatment: The goal is to preserve visual function by reducing IOP to a level at which no further optic nerve damage occurs.

• Treat ocular hypertension if the patient has a significant risk factor such as IOP greater than 25 mm Hg (3.3 kPa), vertical cup: disc ratio greater than 0.5, or central corneal thickness less than 555 µm. Additional risk factors to be considered include family history of glaucoma, black race, severe myopia, and presence of only one eye. The goal of therapy is too lower IOP by 20% to 30% from baseline to decrease the risk of optic nerve damage.
• Treat all patients with elevated IOP and characteristic optic disc changes or visual field defects. An initial target IOP reduction of 30% is desired in patients with POAG.
• Initiate drug therapy in a stepwise manner, starting with lower concentrations of a single well-tolerated topical agent. Historically, β-blockers (e.g., timolol) where the treatment of choice provided no contraindications existed.
• Newer agents are also suitable for first-line therapy. Prostaglandin analogs (eg, latanoprost, bimatoprost, and travoprost) offer once-daily dosing, better IOP reduction, good tolerance, and, recently, availability of lower-cost generics. Brimonidine and topical CAIs are also suitable for first-line therapy.
• Pilocarpine and dipivefrin, a prodrug of epinephrine, are used as third-line therapies because of adverse events or reduced efficacy as compared with newer agents.
• Carbachol, topical cholinesterase inhibitors, and oral CAIs (e.g., acetazolamide) are used as last-resort options after failure of less toxic options.
• Optimal timing of laser trabeculoplasty or surgical trabeculectomy is controversial, ranging from initial therapy to after failure of third- or fourth-line drug therapy. Antiproliferative agents such as fluorouracil and mitomycin C are used to modify the healing process and maintain patency.

TREATMENT OF CLOSED-ANGLE GLAUCOMA

Acute CAG with high IOP requires rapid reduction in IOP. Iridectomy is the definitive treatment producing a hole in the iris that permits aqueous humor flow to move directly from the posterior to the anterior chamber.

• Drug therapy of an acute attack typically consists of an osmotic agent and secretory inhibitor (e.g., β-blocker, α2 -agonist, latanoprost, or CAI), with or without pilocarpine.
• Osmotic agents are used to rapidly decrease IOP. Examples include glycerin, 1 to 2 g/kg orally, and mannitol, 1 to 2 g/kg IV.
• Although traditionally the drug of choice, pilocarpine use is controversial as initial therapy. Once IOP is controlled, pilocarpine should be given every 6 hours until iridectomy is performed.
• Topical corticosteroids can be used to reduce ocular inflammation and synechiae.

Topical Drugs Used in the Treatment of Open-Angle Glaucoma

Betaxolol: Relative β1 -selective, Solution 0.5 One drop twice a day OR

Levobunolol: Nonselective Betagan Solution 0.25, 0.5 One drop twice a day OR

Dipivefrin: Epinephrine prodrug Propine Solution 0.1 One drop twice a day

Systemic Acetazolamide Tablet 125 mg, 250 mg 125–250 mg two to four times a day

Combinations Timolol– dorzolamide, Solution Timolol 0.5% dorzolamide 2% One drop twice daily