Download managing Secondary angle-closure Glaucomas

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ONLINE SURVEY
Managing Secondary
Angle-closure
Glaucomas
Early recognition and treatment of the cause promote resolution.
By Oluwatosin Smith, MD
U
nlike primary angle-closure glaucoma, secondary angle-closure glaucoma (SACG) occurs as
a sequel to a wide range of ocular and some
systemic conditions. Many forms of SACG have
been described at length and are well documented, but
some new causative entities have been reported. The
occurrence of SACG can be broadly divided into disease in the presence (relative or absolute) or absence of
pupillary block leading to an elevation in IOP.
Figure 1. Neovascular glaucoma after central retinal vein
occlusion.
46 Glaucoma today SEPTEMBER/October 2012
“Unlike primary angle-closure
glaucoma, secondary angleclosure glaucoma occurs as a
sequel to a wide range of ocular
and some systemic conditions.”
PATHOPHYSIOLOGIC CONSIDERATIONS
Pupillary block can be relative, as in phacomorphic
glaucoma, where a large or intumescent cataract
pushes the iris forward, closing the angle. Pupillary
block also occurs in eyes with pseudoexfoliation and
weak zonules, ectopia lentis, Marfan syndrome, and
microspherophakia, where the anteriorly subluxated
lens can narrow or close the angle. If not carefully
evaluated, patients may be misdiagnosed with acute
primary angle-closure glaucoma instead of acute angle
closure secondary to the lens’ subluxation. The cause
of this error includes neglected history or signs of ocular trauma.1
Absolute pupillary block may result from the formation of 360º of posterior synechiae between the
iris and any structure that lies posterior to it (eg, lens,
lens capsule, anterior vitreous phase, and rarely, the
IOL), thus trapping aqueous in the posterior chamber.
This situation can occur in uveitic eyes or those with
inflammation after ocular surgery. Aqueous misdirection syndrome that traps fluid in the vitreous cavity
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can also cause the anterior chamber to become shallow and the angle to close.
In the absence of pupillary block, the angle can close
due to the formation of a vascular inflammatory or
hemorrhagic membrane, leading to peripheral anterior
synechiae (Figure 1). Additional causes are epithelial
downgrowth, fibrous ingrowth, or the migration of
corneal endothelial cells (ie, iridocorneal endothelial
syndrome). SACG can also result from the anterior
displacement of the lens-iris diaphragm due to swelling and inflammation of the ciliary body, contracting
retrolental tissue (eg, retinopathy of prematurity),
or a scleral buckle; anterior rotation of the lens-iris
diaphragm, as induced by topiramate; and choroidal
effusion or detachment (eg, uveal effusion syndrome,
postoperative finding in nanophthalmic eyes).
DIFFERENTIATION, DIAGNOSIS, AND
TREATMENT
Properly managing SACG entails determining the
cause of the angle closure, which dictates the specific
treatment modality to be instituted. Early detection
of the underlying pathology and prompt treatment
are therefore imperative for a successful outcome.
Except when membrane formation disrupts the angle
anatomy, treating the cause of SACG generally leads to
its resolution. A carefully obtained history—including
a review of systems, past ocular history, past medical
history, past surgical history, list of medications, and
family history—is sometimes required to elucidate the
possible causative or inciting agent.
An assessment of the patient’s general appearance
and a thorough eye examination to look for signs of
prior trauma, evidence of uveitis, a disparity in the
“The presence of a bilateral
secondary angle closure raises the
possibility of drug-induced SACG
or the presence of uveal effusion
syndrome.”
anterior chamber depth between eyes, the presence
of choroidal effusion, etc., facilitate a proper diagnosis.
An initial approach is to determine whether or not
the patient is in pupillary block. Absolute pupillary
block with iris bombé and peripheral narrowing of
the anterior chamber, angle closure, and elevated IOP
can easily be remedied by a laser peripheral iridotomy
(LPI). In certain instances, however, the development
of chronic angle closure will necessitate additional
glaucoma surgery.
The presence of a bilateral secondary angle closure
raises the possibility of drug-induced SACG or the
presence of uveal effusion syndrome. Early identification of either problem can spare the patient unwarranted surgical intervention. The list of drugs that can
induce secondary angle closure continues to grow,
but the culpability of sulfa derivatives like topiramate
has been well documented. Other causative conditions or medications described include Campylobacter
jejuni infections, buproprion HCl (Wellbutrin;
GlaxoSmithKline), and methazolamide2,3 (Figure 2).
Conservative management with IOP-lowering medication, topical or systemic steroids, and cycloplegics
should resolve the problem after cessation of the
Figure 2. Secondary angle closure after use of topiramate.
SEPTEMBER/October 2012 Glaucoma today 47
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inducing agent or treatment of the possible cause.4
Miotics such as pilocarpine can exacerbate SACG
caused by medication and uveal effusion syndrome
with worsening of the angle closure.4 Peripheral iridotomy or iridoplasty is not warranted in these cases
and should be avoided.4 In certain instances, drainage
of ciliochoroidal effusion may be indicated.4,5
By and large, SACG is managed through the treatment of its causative factors after the physician
addresses acute elevations of IOP. Depending on the
cause, intervention may involve removing a large intumescent or subluxated lens, treating choroidal swelling
or effusion and removing the causative agent, or treating chronic uveitis. An LPI will suffice in some cases.
In contrast, neovascular glaucoma, endothelial downgrowth, fibrous ingrowth, and iridocorneal endothelial
syndrome are a lot harder to manage; distortion of
or permanent damage to the anterior chamber angle
requires the creation of an alternate drainage pathway,
more commonly a glaucoma drainage device.6
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IATROGENIC CONSIDERATION
The advent of Descemet stripping endothelial keratoplasty
introduced new sources of SACG.
In these cases, pupillary block
can be caused by the presence of
air anterior to the iris or, more
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commonly, by the migration of
air behind the iris resulting in extensive iridocorneal
adhesions.7 The IOP usually rises during the first few
postoperative days. This spike can initially be managed medically, but a cycloplegic agent may also be
required, depending on the clinical scenario. In the
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“Properly managing SACG entails
determining the cause of the
angle closure, which dictates the
specific treatment modality to be
instituted.”
presence of extensive and persistent iridocorneal adhesion, medical management can fail to remedy the air
posterior to the iris, in which case surgical intervention will be required.7 In cases of pupillary block, an
LPI is warranted to break the attack. Regardless, when
indicated, surgical intervention requires reformation of
the angle, removal of the air, and a surgical peripheral
iridotomy if the causative mechanism was pupillary
block.
CONCLUSION
SACGs are generally easy to treat if the physician
recognizes the causative factor or mechanism early.
A thorough history and astute examination facilitate
proper diagnosis and, thus, decisions on treatment.
Correct diagnosis and appropriate treatment choices
early on can spare patients unwarranted procedures
and potentially save their sight in the long run. n
Oluwatosin Smith, MD, is in practice with
Glaucoma Associates of Texas in Dallas. She
acknowledged no financial interest in the
product or company mentioned herein.
Dr. Smith may be reached at (214) 360-0000;
[email protected].
1. Luo L, Li M, Zhong Y, et al. Evaluation of secondary glaucoma associated with subluxated lens misdiagnosed
as acute primary angle-closure glaucoma [published online ahead of print January 3, 2012]. J Glaucoma.
doi:10.1097/IJG.0b013e318241b85b.
2. Mukherji S, Ramanathan S, Tarin S. Uveal effusion associated with Campylobacter jejuni infection presenting
as bilateral angle closure glaucoma. J Glaucoma. 2011;20(9):587-588.
3. Kwon SJ, Park DH, Shin JP. Bilateral transient myopia angle-closure glaucoma, and choroidal detachment
Direct link: https://www.research.net/s/GT5
induced by methazolamide [published online ahead of print July 12, 2012]. Jpn J Ophthalmol. doi:10.1007/
s10384-012-0159-y.
Have you personally encountered a patient with
secondary angle-closure glaucoma after Descemet
stripping endothelial keratoplasty?
Yes
No
4. van Issum C, Mavrakanas N, Schutz JS, Shaarawy T. Topiramate-induced acute bilateral angle closure and
myopia: pathophysiology and treatment controversies. Eur J Ophthamol. 2011; 21(4):404-409.
5. Parikh R, Parikh S, Das S, Thomas R. Choroidal drainage in the management of acute angle closure after
topimarate toxicity. J Glaucoma. 2007;16(8):691-693.
6. Assaad MH, Baerveldt G, Rockwood EJ. Glaucoma drainage devices: pros and cons. Curr Opin Ophthalmol.
1999;10(2):147-153.
7. Lee JS, Desai NR, Schmidt GW, et al. Secondary angle closure caused by air migrating behind the pupil in
Descemet stripping endothelial keratoplasty. Cornea. 2009;28(6):652-656.
48 Glaucoma today SEPTEMBER/October 2012