ANGLE CLOSURE GLAUCOMA

Introduction
Of the nearly 67 million patients with glaucoma worldwide, it has been
estimated that one half are affected by angle-closure glaucoma. Primary angleclosure glaucoma (PACG) has been called the most common form glaucoma in
the world, and the leading cause of bilateral blindness. Occurring less often in
the West, it is predominant form of glaucoma in East Asia. PACG is responsible
for 91% of the bilateral blindness inChina and affects over 1,5 million Chinese.
The modern history of PACG goes back almost 150 years. In 1856, von
Graefe performed an iridectomy on a staphylomatous eye and demonstrated the
first cure for acute inflammatory glaucoma. However, the pathophysiology of
primary angle closure and how the iridectomy brought about this cure remained
in question for another century. In 1873, Leber wrote that aqueous was secreted
from the ciliary processes, traveled through the pupil, and entered into the
anterior chamber. He felt that the forward movement of the iris could lead to
elevated IOP and angle-closure glaucoma. In the later part of the 19th century,
Weber and later Priestly Smith hypothesized that angle-closure occured as a
result of swelling of the cilliary processes, which pushed the iris forward over the
trabecular meshwork. In 1920, Edward Curran proposed the mechanism of
pupillary block and the importance of an iridectomy in breaking this impeded
aqueous flow. His initial observations and theories on PACG were finally accepted
in 1951, following papers and presentations by Joseph Haas, Harold Scheie, and
Paul Chandler, confirming the principle of relative pupillary block. Advances in
gonioscopy prior to 1940, by Barkan, Trantus, Koeppe, Salzmann, and Troncoso
further helped define and distinguish the angle-closure glaucomas. The
developmentof the Goldmann lens in 1938 allowed more universal use of
gonioscopy, further advancing our knowledge and understanding of the anterior
chamber angle.
The angle-closure glaucomas include a large and diversified group of
diseases, which are unified by the presence of peripheral anterior synechiae
and/or iridotrabecular apposition. Their presentation can be acute, with profound
symptoms, or chronic, with asymptomatic visual loss. The physician must identify
the anatomic changes that have occurred and the underlying pathophysiology
that has precipitated these changes in order to initiated the appropriate therapy
for each type of angle-closure glaucoma. Early diagnosis and treatment in most
forms of angle-closure glaucoma can be invaluable, if not curative, and so
understanding and identifying the various forms of pathophysiology is essential if
proper treatment is to be initiated. Also, screening patients at greatest risk for
angle closure can be beneficial in reducing the number of patients developing
these diseases and reduce the risk of blindness.
Any discussion of angle-closure glaucoma is constrained by the lack of
uniform terminology in describing the various disease entities, especially primary
angle closure. Traditionally, the angle-closure glaucomas are broken down into 2
main categories : primary and secondary angle closure. Each category is further
divided by the symptomatology, etiology, and duration of each of the disease.

Often, each entity ends in glaucoma, even though in some cases glaucomatous
visual field loss or glaucomatous optic neuropathy has not occurred. Recent
trends have been to separate the various diseases depending on whether
glaucomatous optic nerve damage is or is not present. This trend is seen
especially with primary angle closure, where researchers have attempted to
make its terminology more similar to that used with primary open-angle disease.
In primary angle closure, there is no underlying pathology; there is only an
anatomic predisposition. In secondary angle closure, an underlying pathologic
cause, such as an intumescent lens, irirs neovascularization, corneal endothelial
migration, or epithelial downgrowth, initiates the angle closure.
Pathogenesis and Pathyphysiology of Angle Closure
Angle closure is defined by the apposition of the peripheral iris to the
trabecular meshwork and the resulting reduced drainage of aqueous humor
through the anterior chamber angle. In considering the underlying pathogenesis
of angle closure, it is important to assess the relative and absolute size and
position of each of the anterior segment structures and the pressure gradients
between the posterior and anterior chambers. Conceptually, the mechanism of
angle closure falls into 2 categories (table 5-1) :
Mechanisms that push the iris forward from behind
Mechanisms that pull the iris forward into contact with the trabecular
meshwork
Pupillary block
Pupillary block is the most frequent cause of angle closure and is the
underlying cause of most cases of primary angle closure. The flow of aqueous
from the posterior chamber through the pupil is impeded, and this obstruction
creates a pressure gradient between the posterior and anterior chambers,
causing the peripheral iris to bow forward against the trabecular meshwork (fig
5-1). Absolute pupillary block occurs when there is no movement of aqueous
through the pupil as a result of 360 of posterior synechiae (secluded pupil).
These posterior synechiae can form between the iris and the crystalline lens, an
intraocular lens, capsular remnants, and/or the vitreous face. Relative pupillary
block occurs when there is restricted movement of aqueous through the pupil
because of iris contact with the lens, intraocular lens, capsular remnants,
anterior hyaloid, or vitreous space-occupying substance (air, silicone oil).
Relative and absolute pupillary block are broken by an unobstructed peripheral
iridectomy.
Table 5-1
Underlying Mechanisms of Angle Closure
Iris pushed forward from behind, into the angle :
Relative pupillary block
Absolute pupillary block
Aqueous misdirection-malignant glaucoma
Ciliary body swelling, inflammation, or cysts
Anteriorly located ciliary processes (plateau iris configuration/syndrome)
Choroidal swelling, serous or haemorrhagic choroidal detachments or

effusions
Posterior segments tumors or space-occupying lesions (silicone oil, gas
bubble)
Contracting retrolental tissue (retinopathy of prematurity)
Anteriorly displaced lens
Encircling retinal bands/buckles
Iris pulled forward into contact with the angle :
Contraction of inflammatory membrane or fibrovascular tissue
Migration of corneal endothelium {iridocorneal endothelial (ICE) syndrome}
Fibrous in growth
Epithelial down growth
Iris incarceration in traumatic wound or surgical incision

Angle closure without pupillary block

Angle closure may occur without pupillary block. Iridotrabecular
apposition, or synechiae, can result from the iris and/or lens being pushed,
rotated, or pulled forward for a variety of reasons, as outlined in table 5-1. Each
of these underlying mechanisms can usually be identified by a comprehensive
examination, including gonioscopy. Many patients may present with multiple
underlying causes for their angle closure.
Lens-induced angle-closure glaucoma