ACIOL = anterior chamber intraocular lens; CRVO = central ret i nal vein occlusion; IOP = intraocular pressure; PAS = peripheral anterior synechiae; PRP = panret i nal photocoagulation; RBCs = red blood cells; TM = trabecular meshwork; VEGF = vascular endothelial growth factor.

^aFor childhood glaucomas, see Chapter 11.

^bThe mechanism of primary angle closure usually involves pupillary block. Plateau iris configuration and syndrome are also usually accompanied by some degree of pupillary block. Those conditions can only be reliably diagnosed after an iridotomy is performed (see Chapter 9).

^cPhacomorphic glaucoma can be caused by pupillary block and non– pupillary block mechanisms.

IOP elevation is seen on clinical examination; and IOP elevation, if pre sent, cannot be attributed to the use of corticosteroids. OAG is classified as secondary when an abnormality is identified that has a putative role in the pathogenesis of the glaucoma.

In eyes that have POAG with elevated IOP, the etiology of the outflow obstruction is thought to be an abnormality in the extracellular matrix of the trabecular meshwork and in trabecular cells in the juxtacanalicular region or an abnormality in the function of the endothelial cells lining the inner wall of Schlemm canal (see Chapter 2). The term normaltension glaucoma is often used for eyes with POAG without known IOP elevation. The conceptual basis for this distinction and for the terminology itself is controversial and is discussed in greater detail in Chapter 7.

In angle closure, the peripheral iris partially or completely obstructs the trabecular meshwork. The obstruction may be caused either by appositional iridotrabecular contact or by adhesions, known as peripheral anterior synechiae (PAS), between the iris and the trabecular meshwork. When angle closure is pre sent in association with glaucomatous optic neuropathy, it is known as angle- closure glaucoma. Angle closure is classified as primary in the absence of an under lying disorder to explain the mechanism of iridotrabecular contact or secondary when the angle closure can be attributed to certain disease pro cesses (see Table 1-1). Globally, primary angle closure is a major public health prob lem.

Normal aqueous humor flow in the anterior segment is illustrated in Figure 1-2A. In primary angle closure (and in some forms of secondary angle closure), the flow of aqueous humor from the posterior to the anterior chamber is obstructed at the pupil (Fig 1-2B). The resulting pressure gradient pushes the peripheral iris forward into the anterior chamber angle. This is known as pupillary block angle closure.

In some forms of secondary angle closure and in plateau iris, the peripheral iris or the entire lens– iris interface is pushed forward, narrowing the iridocorneal angle (see Chapter 9 in this volume). This can result from an abnormality of the ciliary body, posterior segment tumors, hemorrhage, or other causes described in Chapter 10. In other forms of secondary angle closure, the peripheral iris is pulled forward, typically by contraction of a cellular, fibrovascular, or inflammatory membrane. These conditions are called non– pupillary block angle closure.

Combined- mechanism glaucoma refers to the condition in which an eye with glaucomatous optic neuropathy that has under gone successful treatment for angle closure with either laser iridotomy or removal of the crystalline lens continues to demonstrate reduced outflow fa cil ity and elevated IOP in the absence of PAS. This term can also be used when secondary causes of glaucoma play a role in the disease pro cess in an eye with previously diagnosed POAG or primary angle-closure glaucoma, for example, when a patient with POAG develops a central ret i nal vein occlusion and subsequent neovascular glaucoma. IOP elevation associated with uveitis may occur due to a combination of mechanisms, including inflammation of the trabecular meshwork, increased viscosity of aqueous humor due to the presence of cells and protein, corticosteroid use, and the presence of PAS.

As the leading cause of irreversible blindness in the world, glaucoma poses a significant public health prob lem. It has been estimated that by 2020, approximately 80 million people worldwide will have glaucoma, with 11.2 million bilaterally blind as a result. A meta- analysis estimated that the global prevalence is about 3.5% in the population aged 40–80 years. Because older age is a major risk factor for glaucoma and because life expectancies are increasing in most populations, the prevalence of glaucoma is expected to increase sharply in the coming de cades. (Note: The confidence intervals have been omitted around the estimated prevalence and incidence values in this chapter.)

The prevalence (total number of individuals with a disease at a specific time) and incidence (number of new cases that develop during a specific period) of POAG vary widely across population- based samples owing to differences in ethnic and racial repre sen ta tion (Fig 1-3). In the Baltimore Eye Survey, the prevalence of POAG among white individuals ranged from 0.9% in those aged 40–49 years to 2.2% in those aged ≥80 years, whereas the prevalence among black individuals ranged from 1.2% to 11.3%, respectively. The overall population-based prevalence was 4–5 times higher among black individuals than white individuals.

In the Rotterdam Study, a longitudinal population- based study of northern Eu ro pe ans, the observed prevalence was 1.1% among subjects ≥55 years of age. In the same study cohort, the incident risk of developing glaucoma at 10 years was 2.8%. In both the Baltimore Eye Survey and the Rotterdam Study, half of the subjects with glaucoma were unaware of their diagnosis.

The prevalence of glaucoma in the Barbados Eye Study (a predominantly African Ca rib bean population) was 7% in individuals ≥40 years, and the 4- year incidence of glaucoma was 2.2%. Again, older age was found to be a major risk factor for the prevalence and incidence of glaucoma.

The observed prevalence of OAG in the Los Angeles Latino Eye Survey (LALES), a longitudinal population- based study of Latinos (mostly Mexican ancestry) ≥40 years of age, was 4.7%, with 75% unaware of their diagnosis at baseline. The prevalence among those 80 years or older was nearly 22%. The 4- year incidence rate of OAG was 2.3%.