Volume 1, Number 1, 1998 Asian Journal of OPHTHALMOLOGY
16
OPHTHALMOLOGY
IN VIEW
P
rimary angle closure glaucoma is a common disease that
is frequently seen by ophthalmologists in Asia. The problem
is made worse by late attendance, often days or weeks
after onset, and the consequent medical unresponsiveness of this
disease.
1
In Asia, the prevalence of primary angle closure glaucoma
can exceed that of primary open angle glaucoma, whereas the
reverse is true in many predominantly Caucasian countries.
2
The
chronic condition develops insidiously, the patient often being
unaware of the ocular problem until relatively late in the disease
process.
In acute angle closure glaucoma, the rise in intraocular pressure
is associated with infarction of the iris tissue and inflammation.
Oedema of the corneal epithelium is typically present, and can be
seen by the irregular scatter of light from the corneal surface (figure
1). In an acute attack, the pupil is mid-dilated. An oval appearance
results from sectorial infarction of the iris sphincter with spiralling
of the stromal fibres (figure 2).
Images of Primary Angle Closure
Glaucoma
Figure 1. Clinical appearance of acute angle closure glaucoma.
Figure 2. Characteristic oval, mid-dilated appearance of angle closure
glaucoma.
capsular region (figure 4). Another aspect of acute glaucoma in
Asian eyes is the frequency of very shallow anterior chamber, both
centrally and peripherally, which differs from the disease behaviour
described in a Caucasian population.
1
Glaucomflecken, virtually diagnostic of a previous attack of
angle closure glaucoma, are seen to have an irregular amoeboid
shape in high power view (figure 5).
2
A histological section of an
affected lens (figure 6) reveals foci of the epithelial cell necrosis.
The optic disc maintains a normal appearance at follow-up
provided the acute attack is rapidly controlled. If this is not achieved,
damage occurs resulting in visible optic atrophy and corresponding
field loss. Six months after an acute glaucoma attack, images of a
normal left and involved right eye show flat diffuse optic atrophy,
Figure 3. Features of the pupil and iris in angle closure glaucoma.
After an acute attack, the iris atrophy remains, and often
sphincter pupillae action is lost. The patient in figure 3 has had a
peripheral iridectomy; the pupil is irregular after sectorial infarction
of the iris with spiralling of the remaining viable fibres and
depigmentation secondary to atrophy of the iris stroma.
Raised intraocular pressure may cause necrosis of the anterior
lens epithelium. After an acute attack of angle closure glaucoma,
diffuse small white opacities are often seen in the anterior sub-
Asian Journal of OPHTHALMOLOGY Volume 1, Number 1, 1998
17
OPHTHALMOLOGY
IN VIEW
Figure 5. High power view of glaucomflecken.
Figure 6. Histological section of lens showing foci of epithelial cell
necrosis.
Figure 7. Six-month follow-up after acute closure glaucoma: involved right
eye (a) and normal left eye (b).
a b
Figure 8. Successful laser iridotomy.
Figure 4. Discrete, granular opacities (glaucomflecken) and corneal oedema.
Treatment for an eye with acute angle closure glaucoma
involves reducing the intraocular pressure as quickly as possible
by pharmacological means, after which a laser iridotomy is
performed (figure 8).
2
In medically unresponsive cases, laser
iridoplasty has been effective in stopping the acute attack, allowing
for a reduction in invasive surgery.
1
The long-term prognosis for
intraocular pressure control depends upon the extent of trabecular
meshwork damage from ischaemia or the formation of synechiae
during the acute attack.
2
The conversion rate to chronic angle
closure glaucoma is 32% over an average period of 18 months.
1
References
MMM
1. Wong JS, Chew PTK, Alsagoff Z, et al. Clinical course and
outcome of primary acute angle-closure glaucoma in Singapore.
Singapore Med J 1997;36:16-18.
2. Spalton DJ, Hitchings RA, Hunter PA. Atlas of Clinical
Ophthalmology, 2nd ed. London: Times Mirror International
Publishers Ltd., 1995.
indicating neuronal and vascular damage to the disc from the acute
attack (figure 7). If ocular pressure remains elevated, the optic
nerve takes on a cupped appearance indistinguishable from that
seen in open angle glaucoma. Acute infarction of the optic disc
may also occur resulting in an appearance of anterior ischaemic
optic neuropathy.
1
