Secondary Angle

Closure Part II
AAO READING SUBDIVISI GLAUKOMA
Secondary Angle Closure
Without Pupillary Block
Conditions Associated With a Pushing Mechanism

TUMOR

Tumors in the posterior segment of the eye or anterior uveal cysts

>>> Primary choroidal melanomas, ocular metastases, and retinoblastoma

Ocular tumors can also cause anterior segment neovascularization  angle

closure
 Malignant glaucoma

DEFINITION
Also called aqueous misdirection or ciliary block glaucoma is a
rare but potentially devastating form of glaucoma that usually presents following
ocular surgery in patients with a history of angle closure.

It can occur spontaneously in eyes with an open angle or following cataract

surgery or various laser procedures
 Malignant glaucoma

In malignant glaucoma, there is typically marked asymmetry between the affected anterior chamber and that of the
fellow eye.

Classically, the condition has been thought to result from anterior rotation of the ciliary body and posterior
misdirection of the aqueous, in association with a relative block to forward aqueous movement at the level of the lens
equator, vitreous face, and ciliary processes.

However, this historical explanation is a matter of controversy, and some have proposed that it is not physically
plausible but, rather, that malignant glaucoma may result from the simultaneous presence of several factors, including
a small, anatomically predis- posed eye, a propensity for choroidal expansion, and reduced vitreous fluid conductivity.
 Malignant glaucoma

Clinically, the anterior chamber is shallow or flat, with anterior displacement of the lens, IOL, or vitreous face.

Optically clear zones may be seen in the vitreous. Some experts argue this represents aqueous humor trapped in
the vitreous cavity; however, this is con- troversial.

In the early postoperative setting, malignant glaucoma is often difficult to dis- tinguish from choroidal effusion,
pupillary block, or suprachoroidal hemorrhage.

Often, the level of IOP, time frame following surgery, patency of an iridotomy, or presence of a choroidal effusion
.
or suprachoroidal hemorrhage helps the clinician make the appropriate diagnosis.

In some cases, the clinical picture is difficult to interpret, and surgical interven- tion may be required in order to
establish the diagnosis
 Malignant glaucoma

Figure 12. Ultrasound biomicroscopy (UBM) of an eye

Figure 13. UBM of an eye with acute primary angle
with malignant glaucoma. The lens–iris diaphragm is
closure. Pupillary block leads to forward bowing of
pushed forward, causing a uniform shallowing of the
the peripheral iris. The peripheral chamber is
anterior chamber (AC). The central portion of the
shallow, whereas the central chamber is relatively
anterior lens capsule (LC) is nearly in contact with the
deep by comparison. AC = anterior chamber; C =
cornea (C). Note ciliary body (CB) detachment, which
cornea; CB = ciliary body; I = iris; LC = lens
is commonly seen in malignant glaucoma. I = iris; PC
capsule; PC = posterior chamber; S = sclera.
= posterior chamber; S = sclera.
 Management

▰ Intensive cycloplegic therapy

▰ Aggressive aqueous suppression with b-adrenergic antagonists, a2-
adrenergic agonists, and carbonic anhydrase inhibitors;
▰ Dehydration of the vitreous with hyperosmotic agents.
▰ Definitive surgical treatment  pars plana vitrectomy with anterior hyaloido-
zonulectomy combined with iridectomy and an anterior chamber–deepening
procedure
 Uveal and ciliary body effusions

DEFINITION
Uveal effusion or uveal hemorrhage refers to fluid or blood in the potential space
between the uvea (choroid and ciliary body) and the sclera.

Etiology:
• certain sulfonamide medications
• Panretinal photocoagulation, inflammation, infection,
• Penetrating surgery, scleral buckle surgery,
• Trauma and tumor
• Retinal vein occlusion
• Uveal effusion syndrome.
 Uveal and ciliary body effusions

The suprachoroidal or supraciliary mass effect may result in secondary angle closure related to forward
displacement of the lens–iris interface.

In ad- dition, exudative retinal detachments can act as space-occupying lesions in the vitreous, which
may progressively push the retina forward toward the lens and cause angle closure.

Potential causes of exudative retinal detachment include retinoblastoma, Coats disease, metastatic
carcinoma, choroidal melanoma, suprachoroidal hemorrhage, choroidal effu- sion or detachment,
infections (eg, HIV), and subretinal neovascularization in age-related macular degeneration with
extensive effusion or hemorrhage.
 Vitreoretinal surgery

Scleral buckles (especially the encircling bands) used to repair retinal detachments can produce
shallowing of the anterior chamber angle and frank angle closure, often accom- panied by choroidal
effusion and anterior rotation of the ciliary body, causing a flattening of the peripheral iris with a relatively
deep central anterior chamber.

Vortex vein compres- sion may be responsible for the choroidal effusion. Usually, the anterior chamber
deep- ens with opening of the anterior chamber angle over days to weeks with medical therapy consisting
of cycloplegics, anti-inflammatory agents, b-adrenergic antagonists, carbonic anhydrase inhibitors,
and hyperosmotic agents.

If medical management is unsuccessful, laser iridoplasty, drainage of suprachoroidal fluid, or adjustment

of the scleral buckle may be required.

The scleral buckle can impede venous drainage by compressing a vortex vein and thus elevating
episcleral venous pressure and IOP. Such cases may respond only to moving the scleral buckle or
releasing tension on the encircling band. Iridectomy is usu- ally of no benefit in this condition.
 Vitreoretinal surgery

Result of injection of air,

Pars plana vitrectomy may lead
longacting gases or silicone oil
to angle closure
into the eye.

IOP may become elevated by The ciliary body is thickened and

an angle-closure mechanism rotated anteriorly, and, often, an
 Following panretinal anterior annular choroidal
photocoagulation detachment occurs.
 Vitreoretinal surgery

Pars plana vitrectomy may lead to angle closure as a result of injection of air, long- acting gases such as sulfur
hexafluoride and perfluorocarbon gases (perfluoropropane and perfluoroethane), or silicone oil into the eye.

These substances are less dense than water and rise to the top of the eye. An iridotomy may be beneficial and
should be located inferiorly to prevent obstruction of the iridotomy site by the gas or oil.

Eyes that have undergone complicated vitreoretinal surgery and have elevated IOP re- quire individualized
treatment plans. Therapeutic options include the following: removal of the silicone oil; release of the encircling
element; removal of expansile gases; and pri- mary glaucoma surgery, such as trabeculectomy, tube shunt surgery,
or a cyclodestructive procedure.

Following panretinal photocoagulation, IOP may become elevated by an angle-closure mechanism. The ciliary
body is thickened and rotated anteriorly, and, often, an anterior annular choroidal detachment occurs. Generally,
this secondary angle closure is self- limited, and therapy consists of temporary medical management with
cycloplegic agents, topical corticosteroids, and aqueous suppressants.
 Nanophthalmos

DEFINITION
Eye is normal in shape but unusually small, with a shortened axial
length (< 20 mm), a small corneal diameter, and a relatively large lens
for the volume of the eye. Thickened sclera may impede drainage from
the vortex veins.

Choroidal effusion may occur spontaneously and may induce angle

closure.
 Nanophthalmos

Laser iridotomy, laser peripheral iridoplasty, and medical therapy are the safest ways to manage IOP elevation in
these patients.

Surgery should be avoided if possible because of the high rate of complications. When intraocular surgery is
performed, prophylactic posterior sclerotomies may reduce the severity of intraoperative choroidal effusion.

If the angles remain compromised despite a patent iridotomy, lensectomy is an additional treat- ment option. In
such cases, a limited core vitrectomy is sometimes necessary to provide adequate anterior chamber depth for safe
lens removal. ‘

Many clinicians consider early lens extraction in patients with nanophthalmos to avoid the development of angle
closure. In such cases, the surgeon should consider prophylactic measures to reduce the risk for clinically
significant choroidal effusion, including sclerotomies, decompression of the eye with a Honan balloon, and
systemic hyperosmotic agents such as mannitol.
 Persistent fetal vasculature and retinopathy of
prematurity

The contraction of retrolental fibrovascular tissue seen in persistent fetal vasculature (PFV; formerly known as
persistent hyperplastic primary vitreous) and in retinopathy of prema- turity can cause progressive shallowing of the
anterior chamber angle with subsequent

angle closure. In PFV, the onset of this complication usually occurs at 3–6 months of age during the cicatricial phase
of the disease, although angle closure may occur later in child- hood. Cataractous swelling of the lens can also cause
angle closure. PFV is usually uni- lateral and often associated with microphthalmos and elongated ciliary processes.
These conditions are discussed in more detail in BCSC Section 6, Pediatric Ophthalmology and Strabismus, and
Section 12, Retina and Vitreous.
 Drug-induced secondary angle-closure glaucoma

Caused by Topiramate,
acetazolamide, methazolamide,
buproprion, and trimethoprim-
sulfamethoxazole
Cause a syndrome characterized
by acute myopic shift and acute
bilateral angle closure

Clinical Manifestation:
• Sudden bilateral vision loss with acute myopia
• Bilateral ocular pain
• Headache
• In myopia  a uniformly shallow anterior chamber with anterior
displacement of the iris and lens, microcystic corneal edema, elevated IOP
(40–70 mm Hg), a closed anterior chamber angle, and ciliochoroidal
effusion.
Drug-induced secondary angle-closure glaucoma

Figure 14. Topiramate-induced angle closure. A, B-scan ultrasonogram of an

eye with a very shallow anterior chamber (asterisk) and topiramate-induced
angle closure. The choroidal effusion is clearly evident (arrows). B,
Ultrasonographic view of an extremely shallow anterior chamber and closed
angle (asterisk). The posterior choroidal effusion is clearly visible (arrow).
Secondary Angle Closure
Without Pupillary Block
Conditions Associated With Combined Pushing and
Pulling or Other Mechanisms
 Ocular inflammation

▰ Released Fibrin and increased aqueous proteins posterior synechiae and

peripheral anterior synechiae
Ocular inflammation (cont.)

▰ Peripheral iris
edema
Ocular inflammation (cont.)

Secondary angle closure can occur as a result of ocular inflammation. Fibrin and in- creased aqueous
proteins released due to the breakdown of the blood–aqueous barrier may predispose to formation of
posterior synechiae (Fig 10-20) and PAS. If left untreated, these posterior synechiae can lead to a
secluded pupil, iris bombé, and secondary angle closure (Fig 10-21).
 Ocular inflammation (cont.)

Peripheral iris edema, organization of inflammatory debris in the angle, and bridging of the angle by large
keratic precipitates (seen in sarcoidosis) can accompany the ocular inflammation and lead to formation of
PAS. These PAS most often form in the inferior an- terior chamber angle, unlike the PAS in PAC, which
typically occur in the superior angle. The PAS are usually not uniform in shape or height, further
distinguishing inflammatory disease from PAC (Fig 10-22). In rare instances, ischemia secondary to
inflammation may cause rubeosis iridis and neovascular glaucoma.
Ocular inflammation can lead to the shallowing and closure of the anterior chamber angle by other
mechanisms as well, such as uveal effusion and subsequent anterior rota- tion of the ciliary body.
Significant posterior uveitis can cause massive exudative retinal detachment or choroidal effusions that
push the lens–iris interface forward, resulting in secondary angle closure. Treatment is primarily directed
at the underlying cause of the uveitis. Aqueous suppressants and corticosteroids are the primary agents
for reducing IOP and preventing synechial angle closure in this situation. Although prostaglandin ana-
logues can cause increased inflammation in some eyes, they may be considered if needed to control IOP.
Interstitial keratitis may be associated with open-angle glaucoma or angle closure. The angle-closure
component may be caused by chronic inflammation and PAS formation or by multiple cysts of the iris
pigment epithelium.
 Ocular inflammation (cont.)

Treatment:
▰ Underlying cause
▰ Aqueous suppressants and corticosteroids
▰ Prostaglandin analogues may be considered
 Shallow or flat anterior chamber after surgery

▰ Flat anterior chamber  PAS formation

▰ Hypotony after surgery and a flat chamber after cataract surgery or
filtering surgery indicates a leak
▰ Seidel test  repair leak

Flat chamber management:

▰ Re-form flat chamber within 24 hours after wound leak repair
▰ Observation + corticosteroid therapy for several days to prevent
synechiae
Thank You