The term “glaucoma” refers to a group of disorders that share common phenotypes. There are over 20 different subtypes of glaucoma. The glaucomas are defined by a characteristic loss of retinal ganglion cell axons leading to a progressive optic neuropathy that is related to intraocular pressure (IOP). If untreated, glaucoma can cause visual disability and even blindness. Although elevated intraocular pressure (IOP) is no longer formally part of the definition, it is recognized as the major risk factor for progression of the disease.

The subtypes of glaucoma are categorized into open-angle glaucoma (OAG) or closed-angle glaucoma (CAG). The “angle” refers to the iridocorneal (iris-cornea) junction at the periphery of the anterior chamber (Fig. 1). The angle is the site of drainage for aqueous humor. OAGs and CAGs are further subclassified into ‘primary,’ when the cause of the dysfunctional IOP is unknown, or ‘secondary,’ when the cause of the elevated IOP is the result of a known disease process. Furthermore, glaucomas are classified by their onset – acute or chronic. The most common form of glaucoma in the United States is Primary Open-Angle Glaucoma (POAG).

With approximately three million Americans affected by glaucoma it is the second leading cause of blindness in the United States. Although it affects people of all ages, it is 6 times more common in those over 60 years of age than those 40 years of age. Annual medical costs for glaucoma services to glaucomatous patients and glaucoma suspects totals over 2.86 billion dollars.

Aqueous humor is a clear fluid that circulates in the anterior chamber of the eye to provide nutrients and remove metabolic waste from the avascular structures of the eye – namely the lens, cornea, and trabecular meshwork. The balance of aqueous secretion and drainage determines the IOP. Aqueous humor is produced by the ciliary processes, which are located behind the iris, through active secretion, ultrafiltration, and diffusion. Aqueous circulates within the posterior chamber, travels through the pupil, and exits the eye through the angle via one of two pathways (Fig. 1): (1) the conventional pathway through the trabecular meshwork, canal of Schlemm, intrascleral channels, and then episcleral and conjunctival veins; or (2) the uveoscleral pathway, through the ciliary body face, choroidal vasculature, and vortex or scleral veins. The conventional pathway is responsible for the majority of outflow, especially in older adults. CAG results from physical obstruction of these drainage tissues by approximation of the iris and cornea (Fig. 2). OAG occurs when aqueous drainage is impaired by increased resistance to aqueous drainage that is intrinsic to the outflow pathways (Fig. 3). Although it is possible that overproduction of aqueous humor could lead to an elevated IOP, all studies have shown that the pathophysiology is poor aqueous drainage. The average IOP is approximately 16 mmHg (2 mmHg standard deviation). An elevated IOP is defined as a value that is 2SD above the average (i.e., greater than 20 mmHg). There is a form of OAG, named “low-” or “normal-tension glaucoma,” in which damage occurs within the average range (11–21 mmHg). Although IOP reduction is often effective treatment for this type of glaucoma, other etiologic factors such as vasospasm or ischemia are thought to have a larger role in the pathophysiology.

Vision loss from chronic glaucoma is usually painless and slowly progressive. Peripheral vision is usually affected first, and the deficits may be asymmetric. This results in delays in realization of vision loss.

Acute angle closure and a few secondary glaucomas present with symptoms, most commonly painful red eye, blurred central vision, and rapid progression of visual loss. The presence of non-visually related symptoms are due to the rapid change in IOP causing immediate ischemic compromise of several ocular tissues – principally, the cornea and optic nerve.

Diagnosis of glaucoma requires a complete history and ocular examination including measurement of IOP, assessment of the anterior chamber angle by gonioscopy, quantification of vision loss by visual field testing, and examination of the ocular fundus for signs of optic neuropathy such as cupping (Fig. 4). Gonioscopy is examination of the iridocorneal angle with a slit-lamp and contact lens containing mirrors to visualize the angle. Measurement of an elevated IOP identifies a significant risk-factor but is neither necessary nor sufficient for the diagnosis of glaucoma. Visual field defects and optic nerve defects characteristic of glaucoma are strong support for the diagnosis but other causes of optic neuropathy such as optic neuritis need to be excluded.

To date, lowering IOP is the only clinically proven treatment for the glaucomas. Glaucoma suspects may also be treated depending on the presence of high risk characteristics and the individual risk aversion of the patient. The treatment approach differs between CAG and OAG. CAG treatment requires laser or surgery to bypass the mechanical blockage. OAG can be treated with topical medications, laser, and/or incisional surgery. Topical medication may decrease aqueous production or increase aqueous drainage. Laser trabeculoplasty attempts to enhance the drainage function of the trabecular meshwork. Laser peripheral iridotomy creates a secondary pathway to allow aqueous to bypass a potential blockage; in doing so, equalization of the pressure gradient between the spaces anterior and posterior to the iris often allows the angle to deepen. Laser iridoplasty directly alters the angle anatomy by moving the iris away from the drainage structures. Glaucoma that is refractory to the above treatments may require cyclodestructive procedures to destroy the ciliary body and decrease aqueous production. Incisional operations such as trabeculectomy and glaucoma drainage implant devices create a new pathway to drain aqueous from the anterior chamber to the subconjunctival space.

Many lasers are used in glaucoma management. Their use has increased because their less invasive nature and generally lower rates of complications appeal to surgeons. The most commonly used lasers are argon, diode, and neodymium:yttrium-aluminum-garnet (Nd:YAG). The argon laser (488–514 nm) has a thermal effect on tissues, which either results in coagulation or vaporization depending upon the power settings used. The diode laser (810 nm) also has a photocoagulative effect. The Nd:YAG laser (1,064 nm) has a coagulative effect when used in a continuous-wave mode. The short-pulsed q-switched Nd:YAG has a photodisruptive effect on tissues, which has an explosive effect. Other lasers have a photoablative effect that results in excision of tissue without any damage to the adjacent tissue. Photoablation has more applications for the cornea, but is also used in glaucoma. Besides the type of effect observed on tissues, different lasers may be used because they specifically target a certain type of tissue or because they have a desirable depth of penetration.

Iridotomy is the creation of a microscopic hole through the iris that provides an alternate route for aqueous to enter the anterior chamber (Fig. 5). Laser iridotomy is preferred over surgical iridotomy because it is safer, equally effective, and preferred by patients; however, surgical iridectomy serves as second-line treatment if laser iridotomy is unable to be performed (e.g. a patient who is unable to maintain position in the laser). The popularity of this established technological advancement is evidenced by utilization statistics. Although the total number of laser iridotomies and surgical iridectomies has increased in proportion to the aging population, the ratio of laser iridotomies to surgical iridectomies performed has increased from 15:1 in 1995 to 52:1 in 2004. The procedure is treatment for all forms of CAG that involve pupillary block. Patients with easily occludable angles may also require the procedure.

Argon laser peripheral iridoplasty is the delivery of thermal energy that causes circumferential contraction of the iris away from the trabecular meshwork. Laser iridoplasty is a treatment for certain closed-angle glaucomas, and is often attempted when laser iridotomy fails or is not indicated because the pathophysiology does not involve pupillary block.