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cover story
Traumatic Angleclosure Glaucoma
A higher index of suspicion for this diagnosis is warranted when the patient
has predisposing risk factors for angle closure.
By Julia Song, MD
T
raumatic glaucoma occurs after an ocular injury,
whether it be blunt or penetrating trauma.
Acute blunt trauma can tear the ciliary body
and clog the trabecular meshwork with red
blood cells, pigment, or debris. Elevated IOP is usually
temporary and can be controlled medically. In the long
term, blunt trauma can result in angle-recession glaucoma (for more on this topic, read the article by Quang
Nguyen, MD, on page 37). Penetrating intraocular trauma can result in inflammation, bleeding, and elevated
IOP. This article focuses on the mechanisms of traumatic
angle-closure glaucoma (ACG).
CLASSIFICATION
Trauma resulting in ACG can be divided into two
categories: (1) secondary ACG with pupillary block
and (2) secondary glaucoma without pupillary block.
Previous pupillary block, hyperopia, nanophthalmia,1
cataract, the presence of a phakic IOL,2 iris transfixation
of a posterior chamber IOL,3 intracameral air (for the
treatment of a Descemet membrane detachment4 or
intracameral migration after vitreoretinal surgery5),
inflammation, peripheral anterior synechiae, or angle
recession can increase a patient’s risk toward developing ACG upon trauma. For example, angle closure in
an elderly Asian woman may direct the physician to a
preexisting occludable anterior chamber angle, whereas
a child who develops angle closure may have cilio­
choroidal edema.
It is important to determine the mechanism of the
angle closure, because the treatments of the two types
of ACG differ. Surgeons generally manage traumatic
pupillary-block ACG with a laser peripheral iridotomy
(LPI). In contrast, physicians usually treat nonpupillary-
“Patients with preexisting
occludable anterior chamber
angles can develop
pupillary-block glaucoma after
trauma.”
block ACG with mydriatics to relax the ciliary body and
allow the lens-iris diaphragm to move posteriorly.
PUPILLARY-BLOCK ACG
As stated, patients with preexisting occludable anterior chamber angles can develop pupillary-block glaucoma after trauma. Tse and colleagues reported ACG in
a 52-year-old woman who sustained blunt ocular trauma
and a periorbital hematoma.6 The patient underwent an
LPI and was found to have bilaterally shallow anterior
chambers. On the other hand, Kutner reported a case of
blunt trauma causing ciliary body edema in an 18-yearold that resolved with cyclopentolate.7 Ultrasound
biomicroscopy after blunt trauma displaces the anterior lens, with resultant transient myopia,8 increased
lens thickness (probably due to lens edema), choroidal
detachment, and ciliary body edema. Resolution reverses
the myopia.
Subluxated lenses or herniated vitreous can also cause
pupillary block. Sowka reported the case of a 72-year-old
pseudophakic man who, after blunt trauma, suffered a
posterior capsular rupture, which resulted in vitreous
prolapse, pupillary block, iris bombe, and ACG. He was
treated with cycloplegics as well as anti-inflammatory
agents and topical glaucoma medications and, subsequently, with a total of three LPIs.9
may/june 2012 Glaucoma today 35
cover story
(Courtesy of Heather Dealy, MD.)
Transvenous coil embolization, however, has also been
reported to produce pupillary-block glaucoma, causing a
cranial nerve III palsy and resultant mydriasis in a patient
already predisposed to narrow anterior chamber angles.18
Penetrating trauma can also cause ACG. In one report,
the formation of extensive anterior synechiae after the
inadvertent penetration of anesthetic agents into the
anterior chamber necessitated the implantation of a
glaucoma drainage device.19
Figure. Blood in Schlemm canal secondary to raised episcleral venous pressure.
Another cause of pupillary block is iatrogenic trauma
from laser treatment. Melamed and colleagues found
that, in patients with subluxated lenses, a YAG LPI produced further anterior tilting of the cataract and subsequent ACG.10 YAG iridotomy can also cause a posterior
dislocation of the lens and pupillary-block glaucoma.11
The mechanism most likely involves a shock-wave effect
and zonular rupture. YAG capsulotomy is another reported cause of the IOL’s anterior dislocation, with vitreous
herniation and resultant pupillary block.12 This type of
angle-closure attack is broken with pupillary dilation.
Some traumatic forms of ACG require more than
cycloplegia or LPI.13 In a case report by Netland et al,
trauma caused the crystalline lens’ dislocation into the
anterior chamber, which led to pupillary block that
necessitated a lensectomy and anterior vitrectomy.14
Patients predisposed to anteriorly displaced lenses
(Marfan syndrome, spherophakia, Weill-Marchesani syndrome, or homocystinuria) are at increased risk of traumatic dislocation of a phakic lens.
ADDITIONAL MECHANISMS
Orbital disorders, particular carotid-cavernous fistulas,
and embolization treatments have been associated with
ACG. The mechanism involves venous thrombosis and
stasis,15 concomitant exudative retinal detachment and
choroidal detachment,16 intraorbital engorgement,17
raised episcleral venous pressure, and blood in Schlemm
canal on gonioscopy (Figure). Embolization results in
increased superior ophthalmic venous pressure, choroidal transudation, the anterior displacement of the
lens-iris diaphragm, and nonpupillary-block glaucoma.
36 Glaucoma today may/june 2012
CONCLUSION
Blunt and penetrating trauma to the eye can result in
traumatic ACG. The mechanism appears to involve mass
effect (vitreous, lens) into the pupillary region, resulting
in pupillary block, or choroidal swelling and rotation of
the lens-iris diaphragm without pupillary block. A third
mechanism involves traumatic mydriasis or associated
cranial nerve palsy that results in a dilated pupil and subsequent pupillary-block glaucoma. Clinicians should have
a higher level of suspicion for ACG when the patient has
predisposing risk factors such as hyperopia, shallow anterior chambers, and a history of surgery. n
Julia Song, MD, is in private practice with
DrSongVision in Pasadena and Long Beach,
California. Dr. Song may be reached at
(562) 427-0700; [email protected].
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