Primary Angle-Closure Glaucoma

Robert J. Goulet III
Kathryn B. Freidl
L. Jay Katz



• Angle closure is defined by apposition of the iris against the trabecular meshwork. In acute primary angle closure, the intraocular pressure (IOP) rises rapidly due to a sudden increase in trabecular meshwork obstruction by the iris. Glaucomatous optic neuropathy can result from this event (acute primary angle-closure glaucoma).

• The most common cause is pupillary block.



• Primary angle closure incidence ranges from 4.7–15.5/100,000 people/year.

• Inuit > Asians > India/Thai/Malay > Europeans > African/Hispanic

• The fellow eye of a patient suffering an acute attack has a 40–80% chance of developing an acute attack within 5–10 years.


• Prevalence of angle-closure glaucoma in the US is 0.2%.

• Acute angle closure is rare, relative to chronic angle closure.


• Older age

• Female gender

• Race (see above)

• Hyperopia/shorter axial length/shallow

• anterior chamber

• Thick crystalline lens

• Family history


• Screening gonioscopy is necessary to identify patients at risk of having occludable angles.

• Provocative tests (stimulation of mydriasis), have not been shown to be accurately predictive of eyes at risk for acute angle closure.

• Peripheral iridotomy in eyes determined to have anatomically narrow angles can prevent acute attacks and resultant vision loss.


• Physical obstruction of the trabecular meshwork by the iris leads to decreased aqueous drainage and acute elevation of intraocular pressure. The following mechanisms can occur independently or in various combinations.

– Pupillary block: Iridolenticular touch causes resistance of aqueous flow from the posterior chamber to the anterior chamber. Elevated posterior chamber pressure causes the iris to bow forward and occlude the trabecular meshwork.

– Phacomorphic: Age-associated lens enlargement or lens dislocation can lead to pupillary block or anterior displacement of the iris. This is traditionally thought of as a secondary angle-closure mechanism but can contribute to primary angle closure.

– Plateau Iris: Anteriorly displaced ciliary processes push the peripheral iris forward resulting in narrowing of the anterior chamber angle.


• Not all eyes with narrow angles develop angle closure.

– In normal eyes, there appears to be a decrease in iris volume with mydriasis; it has been proposed that eyes prone to acute angle closure may experience an increase in iris volume with mydriasis.

– Additionally, eyes prone to angle closure may inadequately regulate choroidal thickness.

Clinically imperceptible changes in choroidal thickness may increase intraocular pressure, rotate the ciliary body–iris complex forward, and increase resistance at the iris–lens interface.


• Small anterior segment (Hyperopia, Nanophthalmos, Microphthalmos)

• Retinal vascular occlusion (as a result of elevated IOP)

• Ischemic optic neuropathy (as a result of elevated IOP)



• Presenting complaints include ocular pain, headache, blurred vision, halos around lights, nausea, and vomiting.

• Prior episodes of headache with blurred vision may signify previous angle-closure events.

• Ophthalmic and medical history should focus on contributory factors:

– Recent pharmacologic dilation

– Use of medicines with anticholinergic effects

– antihistamines, tricyclic antidepressants, MAO inhibitors

– Causes of ciliary body edema

Panretinal photocoagulation

Scleral buckle

Medications such as sulfonamides and topiramate


• Decreased visual acuity

• Mid-dilated pupil

• Relative afferent pupillary defect (RAPD)

• Elevated intraocular pressure

• Conjunctival injection

• Microcystic corneal edema

• Shallow anterior chamber with mild cell and flare

• Optic nerve swelling and hyperemia

• Retinal arterial pulsations

• Gonioscopy: Closed angle (perform indentation gonioscopy to differentiate between appositional and synechial angle closure)

• Signs of previous acute attack:

– Lower corneal endothelial cell count compared to the unaffected fellow eye

– Peripheral anterior synechiae (PAS)

– Anterior subcapsular lens opacities (glaukomflecken) secondary to ischemia

– Segmental iris atrophy with pigment release from focal iris stromal necrosis

– Dilated, irregular pupil from iris ischemia



Initial approach

• The diagnosis is made on clinical examination.

• Imaging of the anterior segment is useful in the setting of a patent peripheral iridotomy to delineate causes of non-pupillary block angle closure. One may use:

– Ultrasound biomicroscopy

– Optical coherence tomography

Follow-up & special considerations

• It is essential to evaluate the angle of the fellow eye. Iridotomy should be done in the fellow eye as soon as possible due to high risk of subsequent angle closure.

• Need to perform repeat gonioscopy following peripheral iridotomy to confirm narrow angle has resolved.

– If narrow angle is not resolved with peripheral iridotomy, anterior segment imaging is warranted.

Diagnostic Procedures/Other

Thymoxamine test: Thymoxamine is a selective alpha 1 adrenergic antagonist that blocks the iris dilator muscle, producing miosis. In normal eyes, IOP will not decrease with thymoxamine administration. In angle closure, thymoxamine causes the IOP to decrease as miosis removes iris from the outflow channel. Thymoxamine is not available in the US.


• Malignant glaucoma

• Secondary angle closure

• Glaucomatocyclitic crisis (Posner–Schlossman syndrome)

• Herpetic uveitis

• Pigmentary glaucoma

• Pseudoexfoliative glaucoma

• Neovascular glaucoma



First Line

Topical ocular hypotensives

– Pilocarpine should not be used as a first line agent for angle closure. Despite its miotic effect, pilocarpine may worsen angle closure due to anterior displacement of the lens-iris diaphragm. Additionally, the miotic response may be limited by iris ischemia.

– Aqueous suppressants

– β-blockers, alpha 2 agonists, carbonic anhydrase inhibitors

– Outflow facilitators

– Prostaglandins

– Steroids may be helpful in reducing any coincident or contributory inflammatory swelling.

Prednisolone, Durezol

Systemic carbonic anhydrase inhibitors

– Acetazolamide

– Diamox 125–250 mg PO q.i.d

– Diamox Sequels 500 mg PO b.i.d

– Diamox 500 mg IV b.i.d

– Do not exceed 1g in a 24-hour period.

– Contraindicated in severe renal disease, hepatic disease, severe pulmonary obstruction, and adrenocortical insufficiency.

– Methazolamide 50–100 mg PO b.i.d

Contraindicated in renal insufficiency.

Systemic hyperosmotic

– Mannitol 1.5–2 g/kg IV over 30 min period

20% solution (7.5–10 mL/kg)

15% solution (10–13 mL/kg)

Do not exceed 500mL in a 24-hour period.

Contraindicated in anuria, progressive renal failure, CHF, severe dehydration, or intracranial bleeding.

Second Line

• Analgesic and antiemetic medications can be used to control symptoms of acute IOP rise.

• Topical osmotic medications can temporarily dehydrate a swollen cornea to facilitate laser treatment.

– Glycerin (apply topical anesthetic first)

• Muro-128


General Measures

Compression gonioscopy may open the angle allowing trabecular flow.

Issues for Referral

Surgical intervention as listed below

Additional Therapies

Pilocarpine is not an alternative to iridotomy.


Intervention is dependent upon the underlying cause of angle closure. Medical management does not correct the pathology in this condition or decrease the risk of recurrent episodes. Laser or surgical intervention is required.

Pupillary Block:

– Peripheral laser iridotomy (with Argon or Yag laser) should be done as soon as possible.

– If attack is broken medically, one may consider waiting for corneal edema to clear to complete iridotomy.

– Surgical iridectomy should be considered when laser treatment cannot be accomplished.

– Argon laser peripheral iridoplasty may be used when angle closure is unresponsive to medical therapy, as an alternative to laser iridotomy, or if laser iridotomy fails.

– Goniosynechialysis

Plateau iris

– Argon laser peripheral iridoplasty

– Peripheral laser iridotomy should be performed in an attempt to eliminate any pupillary block component.

– Pilocarpine can place the iris on stretch and open the angle.

– Some cases may be responsive to surgical lens extraction.


– There is often an element of super-imposed pupillary block, so if possible, peripheral laser iridotomy should be preformed.

– Surgical lens extraction

• Trabeculectomy or glaucoma drainage device (i.e., tube shunt) placement may be necessary for inadequately controlled IOP after the above measures.



Laser peripheral iridotomy in fellow eye should be done as soon as possible.

Patient Monitoring

• The ischemia caused by acute angle closure may result in decreased aqueous production by the ciliary body. Rebound hypertension or recurrent angle closure may develop if the anatomical problem is not resolved. The patient should be monitored very closely to ensure stability of IOP and unimpeded flow of aqueous from the anterior chamber (open angle, filter, tube shunt, etc.).

• The patient will require life-time monitoring for the development or progression of glaucoma.

• A full examination, including visual fields and optic nerve head/nerve fiber layer imaging, should be completed to assess for glaucomatous changes. A dilated examination should be completed when deemed safe for the patient.


No dietary modifications are indicated.


The patient should be educated about the nature of his/her disease and concerning symptoms to monitor. Medications that may result in narrowing of the anterior chamber angle (see above) should be discussed with the patient.


• Prompt treatment with adequate IOP reduction minimizes resultant optic neuropathy.

• Continued elevation of intraocular pressure following laser PI may be due to peripheral anterior synechia, incomplete iridotomy, underlying open angle glaucoma, or secondary angle closure. Treat these appropriately.

• Primary angle-closure glaucoma is the leading cause of glaucomatous blindness worldwide.


• Ischemic optic neuropathy

• Retinal vascular occlusion

• Chronic angle closure (PAS)

• Trabecular meshwork injury

• Accelerated cataract progression

• Corneal decompensation


• Aptel F, Philippe D. Optical coherence tomography qualitative analysis of iris volume changes after pharmacologic mydriasis. Ophthalmology, 2010;117(1):3–10.

• Foster P, Low S. Primary angle closure glaucoma. In: Shaarawy TM, Shurwood MB, Hitchings RA, et al. Eds. Glaucoma, Vol I, Philadelphia: Elsevier; 2009: 327–337.

• Tarongoy P, Ho CL, Walton DS. Angle-closure glaucoma: The role of the lens in the pathogenesis, prevention, and treatment. Surv Ophthalmol 2009;54(2):211–225.

• Quigley HA. Editorial: The iris is a sponge: A cause of angle closure. Ophthalmology, 2010;116(1):1–2.

• Quigley HA. Angle-closure glaucoma-simpler answers to complex mechanisms: LXVI Edward Jackson Memorial Lecture. Am J Ophthalmol 2009;148(5):657–669. e1.



365.20 Primary angle-closure glaucoma, unspecified

365.22 Acute angle-closure glaucoma

365.61 Glaucoma associated with pupillary block

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Nov 9, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Primary Angle-Closure Glaucoma

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