In this presentation, we will review glaucoma, which is one of the leading causes of blindness in the world. It is a disease of the eye that is best characterized as an optic neuropathy. We will review the two types, open-angle glaucoma and angle-closure glaucoma. The learning objectives of this presentation will be to review the anatomy of the angle; understand the etiology of open-angle versus angle-closure glaucoma; differentiate open-angle and angle-closure glaucoma clinically; briefly summarize the diagnostic approaches; and, finally, discuss the treatment options. We will briefly discuss the pathophysiology, epidemiology, clinical presentation, diagnosis, and treatment of open-angle and angle-closure glaucoma. To better understand the pathophysiology of glaucoma, let’s review the anatomy of the angle. The angle is the recess formed by the irido-corneal junction and contains the trabecular meshwork. This meshwork transmits aqueous fluid and allows it to drain the Schlemm’s canal into the venous system. Aqueous humor is produced by the ciliary body, flows through the pupil, drains through the anterior chamber angle, and exits the eye. This is illustrated in the diagram. The exact pathophysiology of open-angle glaucoma is not well understood. But it is thought to be due to decreased aqueous outflow and/or increased aqueous production. This results in increased intraocular pressure and subsequent optic nerve injury and axon loss. Angle-closure glaucoma results from narrowing or closure of the anterior chamber angle or iris root, with subsequent occlusion of the trabecular meshwork, obstruction of drainage of the aqueous fluid from the anterior chamber, and rapid elevation in the intraocular pressure. This also subsequently results in vision loss due to optic nerve injury. There are two types of angle-closure glaucoma, primary angle closure, which results from an atomic predisposition; and secondary angle closure glaucoma, which is due to uveitis, trauma, hemorrhage, vaso-proliferative retinopathy, or ocular syndromes. Both can result in acute-angle closure glaucoma. As mentioned earlier, glaucoma is the second leading cause of blindness in the world and the leading cause of blindness among African Americans. Open-angle glaucoma is most common in people of European or African descent and affects 44.7 million people worldwide. The risk factors include an age greater than 60 and the risk increases with age; African American race, in whom prevalence is three times higher as compared to Caucasians; a positive family history; elevated intraocular pressure; myopia; certain ocular conditions, such as pseudoexfoliation; and certain medical conditions, such as diabetes mellitus, hypertension, and cardiovascular disease. Angle-closure glaucoma is most common in people of Asian descent. Risk factors include an age greater than 40 or 50 years old; Asian or Inuit descent; female sex; a family history of angle-closure glaucoma; hyperopia; certain medications, such as over-the-counter decongestants, adrenergic agents, antipsychotics, antidepressants, and anticholinergic agents; and certain ocular conditions. Open-angle glaucoma is commonly asymptomatic, in spite of elevations in intraocular pressure. It is detected incidentally on ophthalmologic examination. It manifests initially as peripheral visual field loss. And visual acuity is preserved if the central vision is not affected. Central visual field loss is often a late manifestation of the disease. The mean progression rate from a full field of vision to blindness is approximately 25 years if untreated. But only a small minority actually progress to blindness. The clinical manifestations of angle-closure glaucoma are determined by the rapidity and degree of intraocular pressure elevation and angle closure. If the rise in intraocular pressure is slow, the patient may remain asymptomatic, as in chronic angle-closure glaucoma. A rapid elevation, however, as an acute-angle closure glaucoma, may result in reduced vision, halos around lights, headache, severe eye pain, nausea, and vomiting. This is considered a medical emergency. The science suggestive of acute-angle closure glaucoma include conjunctival injection, corneal edema or cloudiness, and a mid-dilated pupil that reacts poorly to light. These can be precipitated in the evening, as dim lights cause pupillary dilatation, blocking a narrow angle. Open-angle glaucoma is defined as an adult onset, chronic, generally bilateral and asymmetric disease. It is characterized by glaucomatous optic nerve damage. This is evidenced by thinning, cupping, or a notching of the disc and characteristic visual field deficits, namely an arcuate defect or a nasal step paracentral scotoma. There also has to be an open and normal appearing anterior chamber angle and absence of secondary causes. Diagnostic testing includes a fundoscopic examination, visual field testing with automated perimetry, and measurement of intraocular pressure by applanation tonometry. Normal intraocular pressure measures 80 to 21 millimeters of mercury. Elevated intraocular pressure is not diagnostic of open-angle glaucoma. About one third to one half of patients with visual field deficits have normal intraocular pressures. And greater than 90% of patients with elevated intraocular pressure have no optic nerve damage. However, patients with elevated intraocular pressure should be referred to an ophthalmologist, given a higher risk of developing glaucoma. All patients over the age of 40 should undergo screening for glaucoma, with a comprehensive eye exam, as should any patients with abnormal cupping or elevated intraocular pressure. All patients that present with signs or symptoms concerning for angle-closure glaucoma should undergo emergent ophthalmologic evaluation. This should be performed in both eyes and should include testing of visual acuity; a pupillary examination; measurement of intraocular pressure; visual field testing by confrontation and/or formal methods; an undilated fundoscopic examination, as dilating drops may exacerbate the symptoms; and a slit lamp exam to estimate the width of the angle. The gold standard for measuring the width of the angle is gonioscopy. However, this requires a special lens. The goal of therapy in open-angle glaucoma is to reduce the intraocular pressure and decrease the risk of progression to visual field loss and optic nerve changes. As open-angle glaucoma tends to be bilateral, but can be very asymmetric, monocular treatment may be indicated initially. There is no clear threshold for initiating treatment. However, following two instances of intraocular pressure greater than 25 millimeters of mercury, most ophthalmologists would initiate therapy. The types of therapy include pharmacologic therapy. There are topical agents that increase aqueous outflow, such as prostaglandins, alpha-adrenergic agonists, and cholinergic agonists. Those that decrease aqueous production, such as beta-blockers and carbonic anhydrous inhibitors and prostaglandins. Prostaglandins and beta-blockers are the first-line agents. And combining drugs from different classes can increase efficacy. Alternatively, there is laser therapy or trabeculopasty. This increases aqueous outflow and decreases intraocular pressure over a period of two years or less. However, more than one treatment is usually required in each eye. Surgery creates an alternative route for aqueous humor to drain. However, there’s a high risk of complication and failure related to scarring. Pharmacotherapy is the first line and surgical intervention is recommended only in patients that have advanced open-angle glaucoma and that have not responded to medications. The target intraocular pressure is greater than 25% to 30% below the initial intraocular pressure. And patients with open-angle glaucoma require lifetime monitoring, at least twice a year, and continuous therapy. In angle-closure glaucoma, outcomes depend on the rapidity of detection and initiation of treatment. Damage to the optic nerve can occur within hours of an acute-angle closure attack. An ophthalmologist should evaluate the patient within one hour of their presentation. If there is likely more than one-hour delay, the patient should be initiated unimpaired treatment. Pressure-lowering drops, including timolol maleate, apraclonidine, and pilocarpine should be administered, along with a systemic medication, acetazolamide. Eye pressure should be checked 30 to 60 minutes after administration of these medications. If the medical treatment is successful, the signs and symptoms should lessen or resolve. Peripheral iridotomy is the treatment of choice once the attack is broken. By laser or surgery, a tiny hole can be created in the peripheral iris to drain the aqueous humor. Prophylactic peripheral iridotomy should be performed if the fellow eye is found to have a narrow angle. Patients with narrow anterior chamber angles who are awaiting surgery, should be advised to avoid decongestants and anticholinergic medications. In summary, glaucoma is a leading cause of blindness in the world. But it’s preventable. It is characterized as an optic neuropathy. Open-angle glaucoma may be related to increased aqueous production or a decreased outflow, resulting in increased intraocular pressure and progressive peripheral visual field loss, followed by central field loss. Angle-closure glaucoma is due to narrowing or closure of the anterior chamber angle, resulting in intraocular pressure elevation, optic nerve injury, and vision loss. Acute angle-closure glaucoma is a medical emergency and must be treated within 24 hours to prevent permanent vision loss. Patients with glaucoma need to be monitored and treated lifelong. I hope you have found this presentation informative. I have included references for further exploration.