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    Angle-Closure Glaucoma

    Glaucoma

    Authors: Ani Khondkaryan, MD, and Brian A. Francis, MD, MS

    Introduction

    Acute angle closure is an urgent but uncommon dramatic symptomatic event with blurring of vision, painful red eye, headache, nausea, and vomiting. Diagnosis is made by noting high intraocular pressure (IOP), corneal edema, shallow anterior chamber, and a closed angle on gonioscopy. Medical or surgical therapy is directed at widening the angle and preventing further angle closure. If glaucoma has developed, it is treated with therapies to lower IOP.

    Chronic angle-closure glaucoma is diagnosed by noting peripheral anterior synechiae on gonioscopy, as well as progressive damage to the optic nerve and characteristic visual field loss. Chronic angle-closure glaucoma is treated with therapies to lower intraocular pressure.

    History and Exam

    Key Factors for Acute Angle-Closure Glaucoma

    • Presence of risk factors (eg, hyperopia, thick cataractous lens)
    • Halos around lights
    • Aching eye or brow pain
    • Headache
    • Nausea, vomiting
    • Reduced acuity
    • Eye redness
    • Closed angle on gonioscopy
    • Extremely elevated IOP
    • Corneal edema
    • Engorged conjunctival vessels
    • Fixed dilated pupil

    Key Factors for Chronic Angle-Closure Glaucoma

    • Presence of risk factors
    • Peripheral anterior synechiae on gonioscopy
    • Elevated IOP

    Diagnostic Tests

    First Tests to Order

    • Gonioscopy examination of anterior chamber angle
    • Slit-lamp examination
    • Automatic static perimetry

    Other Tests to Consider

    • Ultrasound biomicroscopy
    • Anterior segment optical coherence tomography (OCT) of angle
    • Evaluation of the optic nerve head by fundoscopy
    • Retinal OCT
    • Heidelberg retinal tomography
    • GDx Nerve Fiber Analyzer

    Treatment Options

    Acute—Initial Presentation

    • Dynamic gonioscopy
    • Oral carbonic anhydrase inhibitors and/or topical beta-blocker and/or topical alpha-2 agonist
    • Topical cholinergic agonists
    • Hyperosmotic agents
    • Laser peripheral iridotomy after acute attack resolved (once corneal edema resolves); may consider lens extraction after acute attack resolved

    Ongoing or Chronic Angle-Closure Glaucoma

    • Topical prostaglandin analog and/or topical beta-blocker and/or topical alpha-2 agonist
    • Carbonic anhydrase inhibitors
    • Lens extraction surgery
    • Trabeculectomy and/or tube shunt
    • Consider surgical lysis of goniosynechiae

    Definition

    Angle-closure glaucoma (ACG) is a group of diseases in which there is reversible (appositional) or adhesional (synechial) closure of the anterior-chamber angle. The angle closure may occur in an acute or chronic form. In the acute form, the IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork ™ by the iris via papillary block mechanism. The chronic form may develop after acute angle closure where synechial closure of the angle persists, or it may develop over time as the angle closes from prolonged or repeated contact between the peripheral iris and the TM, which often leads to peripheral anterior synechiae (PAS) and functional damage to the angle.

    Classification

    Clinical Classification  

    Classification of angle closure based on presence or absence of symptoms

    • Acute: abrupt onset of symptomatic elevation of IOP (> 21 mm Hg), resulting from total closure of the angle, which is not self-limiting.
    • Subacute (or intermittent): abrupt onset of symptomatic elevation of IOP resulting from total closure of the angle, which is self-limiting and recurrent.
    • Chronic: elevated IOP resulting from angle closure that is asymptomatic.

    Common Vignette 1

    A 50-year-old woman who has no eye symptoms is found during routine ophthalmic examination to have elevated IOP of 42 mm Hg in both eyes. Funduscopy shows that the optic nerve head appears normal with no evidence of glaucomatous neuropathy. Gonioscopy shows that the anterior chamber angles are closed for almost the full circumference.

    Common Vignette 2

    A 64-year-old woman presents to the emergency room with severe pain around her right eye of 4-hour duration, accompanied by blurred vision in the same eye. She is also nauseated. Examination shows a red right eye with edematous cornea and a wide pupil that is unresponsive to light. IOP is extremely elevated (60 mm Hg) only in the right eye. The anterior chamber angle is closed in both eyes.

    Other Presentations

    Patients may present with spontaneously resolving symptoms of intermittent ache and/or blurred vision with haloes around lights seen from one eye. Patients may also notice a change in vision, which may represent longstanding chronic progressive visual field loss.

    Epidemiology

    The number of people in the world affected by glaucoma is approximately 45 million. One third are from primary angle-closure glaucoma (PACG).

    • Half of cases leading to blindness are estimated to result from PACG.
    • The prevalence of PACG varies among different racial and ethnic groups. The highest rates are reported in Inuit and Asian populations, and lowest rates are reported in African and European populations. It is estimated that all forms of PACG account for about 10% of glaucoma cases in the U.S., but up to 50% of glaucoma cases in Asian populations. Among the white population in the U.S. and Europe the estimated prevalence of PACG is 0.04% to 0.4%. The prevalence of PACG in the Inuit population is estimated at 2.65% to 4.8%.
    • Women are 2 to 4 times more likely to have ACG than men.  
    • Acute ACG is most common between the ages of 55 and 65 years.  

    Etiology

    Angle closure can be primary, secondary to another eye disease, or drug induced. Eye diseases that can cause ACG, include a thick cataractous lens (phacomorphic glaucoma); ectopic lens (eg, in settings of trauma, as well as Marfan’s or Weill-Marchesani syndrome); neovascularization of the angle secondary to diabetic retinopathy or ocular ischemia; and tumors.

    Sulfa-containing drugs can cause ACG by causing supraciliary body effusions. This form of ACG has a distinctly different etiology and is not treated in the same fashion as PACG. It is unresponsive to laser peripheral iridotomy and is treated with topical steroids and discontinuation of the causative drug, as well as topical and systemic IOP lowering drugs.

    Pathophysiology

    Angle closure occurs when the peripheral iris is in contact with the trabecular meshwork (TM), either intermittently (appositional closure) or permanently (synechial closure).

    Specific mechanisms leading to angle closure can be divided into 2 categories:

    • Mechanisms that push the iris from behind. The most common reason is relative pupillary block, but other reasons include plateau iris syndrome, enlarged or anteriorly displaced lens, and malignant glaucoma.
    • Mechanisms that pull the iris into contact with the TM. Examples include contraction of inflammatory membrane as in uveitis, fibrovascular tissue as in iris neovascularization, or corneal endothelium as in iridocorneal endothelial syndrome.

    Chronic intermittent friction between the iris and the TM can lead to progressive dysfunction of the TM. With time, adhesions (synechiae) form between the iris and parts of the TM.

    • Eventually the TM is so dysfunctional or obstructed that aqueous outflow from the eye is impaired and IOP rises.  
    • Prolonged elevation of IOP leads anatomically to glaucomatous changes in the optic nerve head and loss of optic nerve axons and functionally to progressive loss of the visual field.
    • If untreated this process may progress to complete blindness.

    Angle closure is usually chronic and progressive, but uncommonly it manifests as an acute attack of complete closure with severe symptoms.

    Diagnostic Approach

    Acute ACG presents with a change in vision or with severe acute symptoms. Chronic ACG is often discovered incidentally during routine examination or during examination for another reason. ACG can also present with intermittent symptoms, change in vision, or severe acute symptoms such as pain in the affected eye, headache, and associated nausea or vomiting. Patients who are suspected of having ACG should be referred to ophthalmology care immediately.

    History

    • Acute ACG is suggested by pain in the affected eye, blurred vision, halos around lights seen from one eye, headache, and associated nausea or vomiting.
    • Many patients with chronic ACG are asymptomatic.
    • A history of ACG increases the risk of angle closure in the unaffected eye.
    • There may be intermittent ache and/or blurred vision with haloes around lights seen from one eye, which resolve spontaneously.
    • The patient may report a change in vision.
    • Some medications increase the risk of ACG, such as anticholinergic topical ocular medication (eg, pupil dilators) or systemic medication (eg, sulfonamides, topiramate, phenothiazines) because they induce angle narrowing.

    Examination

    • Visual acuity should be tested because it may be decreased.
    • Examination of the eye may show it to be red with vascular congestion, corneal edema, and a dilated unresponsive pupil.
    • The IOP may be raised above 21 mm Hg.

    Investigations

    • The optic nerve head should be investigated by slit-lamp examination or funduscopy, and may show typical changes of glaucoma such as a large optic cup and nerve fiber loss.
    • Gonioscopy of both eyes should be performed when angle closure is suspected. Gonioscopy refers to the technique used for viewing the anterior chamber angle of the eye for evaluation of angle structures. Special contact lenses (gonioscopy lenses) overcome the problem of total internal reflection of light rays from the chamber angle, and allow visualization of the angle using obliquely inclined mirrors. The angle can be closed even in the absence of any other symptoms or signs. If the clinician is uncertain about the gonioscopic findings, he/she can refer the patient for objective imaging of the angle either via ultrasound biomicroscopy or OCT.
    • Automatic testing of the visual field should be routinely done to assess the presence and extent of glaucomatous visual field loss.

    Objective quantitative assessment of optic nerve damage can be obtained by imaging machines, such as Heidelberg retinal tomography, OCT, and GDx nerve fiber analysis.

    Risk Factors

    Strong:

    • Female gender: Women are 2 to 4 times more likely to have ACG than men.
    • Hyperopia: The anterior chamber depth and volume are smaller in hyperopic eyes.
    • Shallow peripheral anterior chamber: Having smaller anterior segment dimensions is the main ocular risk factor for closure of the angle, with anterior chamber depth having the strongest correlation with angle closure and ACG.
    • Second eye having angle closure: Anatomic factors of both eyes are virtually always similar. An untreated fellow eye has a 40% to 80% chance of developing an acute episode of angle closure over the next 5 to 10 years.
    • Inuit and Asian ethnicity: Highest rates of ACG are reported in Inuit and Asian populations.

    Weak:

    • Advanced age: Acute ACG is most common between the ages of 55 and 65 years. The size of the lens increases progressively with age, thus crowding the region of the anterior chamber angle, making it shallower.
    • Family history: Family history has been suggested as a risk factor, but is not universally recognized.
    • Use of medications that induce angle narrowing: Anticholinergic topical pupil dilators (eg, cyclopentolate or atropine) or systemic medication (eg, sulfonamides, topiramate, phenothiazines)

    History and Exam

    Key diagnostic factors with common frequency:

    • Presence of risk factors: Key risk factors include female gender, Inuit or Asian ethnicity, hyperopia, use of medication that can induce angle narrowing, and shallow anterior chamber.

    • Elevated IOP: In healthy eyes, IOP is generally 10 to 21 mm Hg. In acute attacks, IOP rises rapidly to relatively high levels, typically above 40 mm Hg.

    • Present in the acute and subacute forms but not with the chronic form of angle closure:

      Halos around lights
      Aching eye or brow pain
      Deep, dull, periocular headache
      Nausea, vomiting
      Reduced acuity
      Eye redness
      Corneal edema
      Fixed dilated pupil. Iris ischemia may cause the pupil to remain permanently fixed and dilated.

    Other diagnostic factors:

    • Common:

      Incidental eye findings: In chronic disease, most patients are asymptomatic and ACG is incidentally detected as part of an ophthalmic examination.

      Blurred vision: In chronic disease, most patients are asymptomatic and ACG is incidentally detected as part of an ophthalmic examination.

    • Uncommon: Change in vision; in effect this is new recognition of longstanding chronic progressive visual field loss

    Diagnostic Tests

    First tests to order:

    • Gonioscopy:

      Definitive test for diagnosing angle closure; gonioscopy of both eyes should be performed on all patients in whom angle closure is suspected. It should also be performed prior to instilling dilating medications to rule out eyes susceptible to angle closure.

      If angle closure is present, compression (indentation) gonioscopy with a four-mirror or similar lens is particularly helpful to differentiate between appositional (reversible) closure versus synechial (irreversible) angle closure, as well as allow for assessing the extent of peripheral anterior synechiae.

      Gonioscopy is also important for the detection of plateau iris and other specific anatomic configurations.

      Gonioscopy may be therapeutic in breaking the attack of acute angle closure.

      Result: TM is not visible in angle closure because the peripheral iris is in contact with it.

    • Slit lamp examination:

      The best method of examining the optic disc is with the slit lamp combined with a high magnification posterior pole lens. The anterior chamber depth should be noted and the size of the phakic lens.

      Result: shallow anterior chamber; and signs of glaucoma: large optic cup, narrowing of the neuroretinal rim, splinter hemorrhage, nerve fiber loss

    • Automatic static perimetry:

      Identifies the presence, and quantifies the amount, of glaucomatous visual field loss during initial diagnosis and subsequently during follow-up care.

      Result: visual field defects

    Other tests to consider:

    • Ultrasound biomicroscopy:

      Can be ordered for objective documentation of angle closure when findings during physical examination (gonioscopy) are not clear

      Useful for demonstrating specific etiologies for angle closure such as plateau iris or supraciliary body fluid and for demonstrating dynamic changes in the angle during light and dark, and after other provocative tests and after treatment

      Result: closed angle; occludability of the angle in the dark vs. light; plateau iris or supraciliary body fluid

    • Anterior segment optical coherence tomography:

      Can be ordered for objective documentation of angle closure when findings during physical examination (gonioscopy) are not clear

      Useful for demonstrating dynamic changes in the angle during light and dark

      Less capable of defining specific etiologies for angle closure due to inability to image behind the iris

      Result: closed angle, occludability of the angle in the dark versus light

    • Retinal OCT:

      Can be used to assess loss of nerve tissue in and around the optic nerve objectively and quantitatively

      Result: quantifies neural tissue in and around the optic nerve

    • Heidelberg retinal tomography:

      Can be used to assess loss of nerve tissue in and around the optic nerve objectively and quantitatively

      Presents this in relation to a nomogram derived from healthy eyes

      Result: quantifies neural tissue in and around the optic nerve

    • GDx nerve fiber analyzer:

      Can be used to assess loss of nerve tissue in and around the optic nerve objectively and quantitatively

      Result: quantifies neural tissue in and around the optic nerve


    Differential Diagnosis

    Disease/Condition

    Differentiating Signs/Symptoms

    Differentiating Tests

    Open-angle glaucoma (primary and secondary)

    Clinically indistinguishable from chronic ACG.

    Gonioscopy shows an open angle.

    Other optic neuropathies (eg, compressive)

    Visual field defects are different from those of glaucoma.

    IOP is normal. Gonioscopy shows an open angle. Optic nerve atrophy (whitening of tissue) in contrast to loss of tissue and cupping.

    Eye trauma

    Acute red eye. Usually no nausea or vomiting. Hx of recent trauma.

    IOP usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal. There may be signs of trauma on eye exam and ocular adnexa (eyelid ecchymosis, hyphema, inflammation).

    Keratitis

    Acute red eye. Usually no nausea or vomiting.

    Conjunctival discharge. Signs of infectious infiltrate in the cornea.

    IOP usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

    Conjunctivitis, Acute

    Acute red eye. Usually no nausea or vomiting.

    Conjunctival discharge. Signs of infectious infiltrate in the cornea.

    IOP usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

    Corneal ulcer

    Acute red eye. Usually no nausea or vomiting.

    Recent foreign body, contact lens use, or known poor eye closure (eg, facial palsy).

    IOP usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

    Episcleritis or scleritis

    Acute red eye. Usually no nausea or vomiting.

    Known systemic disease, such as rheumatoid arthritis.

    IOP usually normal. Gonioscopy shows an open angle. The anterior chamber depth is usually normal.

    Chemical injury

    Acute red eye.

    History of exposure to chemicals.

    IOP may be elevated, but gonioscopy shows an open angle.

    Diagnostic Criteria

    Acute Angle-Closure Attacks

    Presence of at least 2 of the following symptoms:

    • Ocular or periocular pain
    • Nausea or vomiting
    • Antecedent history of intermittent blurring of vision with haloes

    Presenting IOP > 21 mm Hg

    Presence of at least 3 of the following signs:

    • Conjunctival injection
    • Corneal epithelial edema
    • Mid-dilated unreactive pupil
    • Shallow anterior chamber

    Chronic Angle-Closure Attacks  

    Developed for the use in prevalence surveys, it identifies 3 stages in the natural history of angle closure:

    • Primary angle-closure suspect: an "occludable angle" with normal IOP, optic disc, and visual field, without evidence of peripheral anterior synechiae (PAS)
    • Primary angle closure: an "occludable angle" with either raised IOP and/or primary PAS; optic disc and field normal
    • Primary angle-closure glaucoma: primary angle closure with evidence of glaucomatous damage to optic disc and visual field

    Diagnostic Guidelines

    Europe

    The effectiveness of the Heidelberg Retina Tomograph and laser diagnostic glaucoma scanning system (GDx) in detecting and monitoring glaucoma, Health Technology Assessment NHS R&D HTA Programme, 2011.

    North America

    • Comprehensive adult medical eye evaluation, American Academy of Ophthalmology, 2009.
    • Comprehensive adult eye and vision examination, American Optometric Association, 2005.
    • Primary angle closure, American Academy of Ophthalmology, 2009.

    Screening

    Which Population to Screen

    Glaucoma is the second leading cause of blindness around the world. Half of these cases are due to angle closure.  Because angle closure is potentially preventable, screening is immensely important.

    Everyone aged 40 years or older undergoing an eye examination, either routinely or for a specific reason, should be screened for angle closure.   

    Which Test to Use

    The definitive test for the identification of angle closure and eyes at risk is gonioscopy.

    Other methods to identify eyes at risk include ultrasound measurement of anterior chamber depth (ACD) and determining the ACD to axial length ratio. High frequency ultrasound (UBM) or anterior segment OCT may also be used to image the angle.

    Treatment Approach

    Initial Medical Management of Acute Episode

    The immediate goal of treatment is to relieve the acute symptoms and decrease IOP, which is usually achieved with medical therapy.  

    • Oral or topical carbonic anhydrase inhibitors, topical beta-blockers, and topical alpha-2 adrenergic agonists lower IOP through suppression of aqueous humor production.
    • Beta-blockers reduce IOP by around 20% to 30% within 1 hour of instillation.  
    • Alpha-agonists reduce IOP by around 26% within 2 hours post-dose.  
    • Carbonic anhydrase inhibitors, topical beta-blockers, or alpha-2 adrenergic agents may be used as first-line therapies either alone or more typically in combination.

    In patients where angle closure is thought to be secondary to pupillary block or plateau iris syndrome, cholinergic agents (such as pilocarpine). 1[C] Evidence should be started after IOP decreases to < 40 mm Hg.

    Cholinergic agents can paradoxically result in shallowing of the anterior chamber and narrowing of the angle in eyes with angle closure secondary to lens-induced mechanism or aqueous misdirection (malignant glaucoma). They are therefore contraindicated in these cases.  

    If these medical treatments are unsuccessful, hyperosmotic agents should be used. Hyperosmotic agents are also used initially when pressures are exceedingly high.

    Following resolution of the acute attack, definitive surgical treatment should be performed within 24 to 48 hours with the aim of achieving a persistently open angle.

    Definitive Surgical Management for Chronic ACG after Resolution of Acute Attack

    Definitive treatment is aimed at achieving a persistently open angle:

    • Laser peripheral iridotomy (LPI), where a laser is used to make an opening in the iris, is usually successful for acute angle-closure glaucoma (2[B] Evidence). LPI alleviates pupillary block by allowing aqueous to bypass the pupil. The pressure differential between anterior and posterior chambers is eliminated, and the iris loses its convex configuration and falls away from the TM, resulting in opening or widening of the angle. LPI is indicated in all eyes with primary angle closure and usually in fellow eyes as well, since the majority of fellow eyes will also develop glaucomatous changes (Bain 1957, Lowe 1962, Hyams 1975).
    • Laser iridoplasty or gonioplasty can be considered in the presence of a patent LPI with a residual appositional angle. An argon laser is used to place contraction burns in the peripheral iris over its entire circumference in order to pull the peripheral iris away from the TM.
    • If residual angle closure is attributable to the lens then lens then extraction surgery, with or without goniosynechialys, is considered (2[B] Evidence)
    • Cholinergic agents may be used if there is residual angle closure after laser treatment. These agents cause pupil constriction with thinning of the iris and its pulling away from the inner eye wall and TM, thus opening the angle.

    Persistently Elevated IOP in Patients with ACG Despite Surgery

    If IOP remains elevated following these measures in acute angle­-closure glaucoma, as well as in cases of chronic angle-closure glaucoma, it is lowered in a fashion similar to open-angle glaucoma with IOP-lowering medications, and if these are ineffective, then IOP-lowering surgery.

    Topical ophthalmic prostaglandin analogs work by increasing aqueous outflow.

    • They reach peak effectiveness 10 to 14 hours after administration, so they are not used during acute attacks.
    • As chronic therapy, however, they are the most potent IOP-lowering agents available and should be used first line.
    • Topical beta-blockers and alpha-2 adrenergic agonists may also be used. They are typically used alone or in combination at the discretion of the physician.

    Systemic carbonic anhydrase inhibitor chronic therapy is uncommonly used because of the many adverse effects of chronic systemic use, and should be reserved for patients with glaucoma refractory to other medical treatment.

    Uncommonly IOP remains elevated despite all these measures, and in this case IOP-lowering surgery, such as trabeculectomy or aqueous tube shunt implantation, is indicated.

    Treatment Options

    Acute

    Patient Group

    Tx Line

    Treatment

    Initial presentation

    First

    Dynamic gonioscopy to attempt to break angle closure

    First

    Carbonic anhydrase inhibitors and/or topical beta-blocker and/or topical alpha-2 agonist:

    Carbonic anhydrase inhibitors decrease aqueous humor formation and are used commonly as first-line therapy in combination with beta-blockers and alpha-2 agonists. Topical dorzolamide and brinzolamide are preferred over systemic acetazolamide and methazolamide. Topical beta-blockers lower IOP through suppression of aqueous humor production. Beta-blockers reduce IOP by around 20% to 30% within 1 hour of instillation.  Topical alpha-2 adrenergic agonists lower IOP through suppression of aqueous humor production. Alpha-agonists reduce IOP by around 26% within 2 hours postdose.

    Primary options:

    • Acetazolamide: 125-250 mg orally (immediate-release) up to four times daily, maximum 1000 mg/day; 250-500 mg intravenously every 2-4 hours, maximum 1000 mg/day
    • Betaxolol ophthalmic: (0.5%) 1-2 drops into the affected eye(s) twice daily
    • Brinzolamide ophthalmic: (1%) 1 drop into the affected eye(s) 2 or 3 times daily
    • Dorzolamide ophthalmic: (2%) 1 drop into the affected eye(s) twice or three times daily
    • Levobunolol ophthalmic: (0.25%) 1-2 drops into the affected eye(s) twice daily; (0.5%) 1-2 drops into the affected eye(s) once daily
    • Methazolamide: 50-100 mg orally twice or three times daily
    • Brimonidine ophthalmic: (0.1 to 0.2%) 1 drop into the affected eye(s) 3 times daily
    • Timolol ophthalmic: (0.25% or 0.5%) 1 drop into the affected eye(s) twice daily; (0.5% gel) 1 drop into the affected eye(s) once daily

    Adjunct

    Hyperosmotic agents:

    If there is failure of initial medical treatment or IOP is greater than 50 mm Hg, hyperosmotic agents are used to control acute episodes of elevated IOP. They are rarely administered for longer than a few hours because their effects are transient. They are indicated in patients when medical treatments are unsuccessful or if pressures are exceedingly high.

    • Primary option: glycerine, 1-2 g/kg/dose orally, repeat every 5 hours when required
    • Secondary option: mannitol, 1.5 to 2 g/kg/dose intravenously over 30 minutes

    Plus

    Laser peripheral iridotomy after acute attack resolved:

    Laser peripheral iridotomy (LPI)is usually successful. LPI alleviates pupillary block by allowing aqueous to bypass the pupil. The pressure differential between anterior and posterior chambers is eliminated, the iris loses its convex configuration and falls away from the TM, resulting in opening or widening of the angle. LPI is indicated in all eyes with angle closure and usually in fellow eyes since the majority of fellow eyes in patients with acute angle-closure glaucoma also develop glaucomatous changes.

    Ongoing

    Patient Group

    Tx Line

    Treatment

    Residual angle closure after laser peripheral iridotomy with elevated IOP

    First

    Topical prostaglandin analog and/or topical beta-blocker and/or topical alpha-2 agonist:

    These agents are typically used individually but may be used in combination as well. They may be used in refractory cases. Latanoprost has been associated with lower incidence of conjuctival hyperemia than other prostaglandin analogs. Topical ophthalmic prostaglandin analogs work by increasing aqueous outflow reaching peak effectiveness 10 to 14 hours after administration. They are the most potent IOP-lowering agents. Latanoprost and travoprost are preferred over bimatoprost. Topical beta-blockers lower IOP through suppression of aqueous humor production. Topical alpha-2 adrenergic agonists lower IOP through suppression of aqueous humor production. Topical cholinergic agonists may or may not need to be continued.

    Primary options:

    • Apraclonidine ophthalmic: (0.5%) 1-2 drops into the affected eye(s) three times daily
    • Betaxolol ophthalmic: (0.5%) 1-2 drops into the affected eye(s) twice daily
    • Bimatoprost ophthalmic: (0.03%) 1 drop into the affected eye(s) once daily at night
    • Latanoprost ophthalmic: (0.005%) 1 drop into the affected eye(s) once daily at night
    • Levobunolol ophthalmic: (0.25%) 1-2 drops into the affected eye(s) twice daily; (0.5%) 1-2 drops into the affected eye(s) once daily
    • Travoprost ophthalmic: (0.004%) 1 drop into the affected eye(s) once daily at night
    • Brimonidine ophthalmic: (0.1 to 0.2%) 1 drop into the affected eye(s) three times daily
    • Timolol ophthalmic: (0.25% or 0.5%) 1 drop into the affected eye(s) twice daily; (0.5% gel) 1 drop into the affected eye(s) once daily

     

     

    Carbonic anhydrase inhibitors:

    Carbonic anhydrase inhibitors decrease aqueous humor formation. Topical dorzolamide and brinzolamide are preferred over systemic acetazolamide and methazolamide. Systemic carbonic anhydrase inhibitor chronic therapy is uncommonly used because of the many adverse effects of systemic use, and should be reserved for patients with glaucoma refractory to other medical treatment.

    Primary options:

    • Brinzolamide ophthalmic: (1%) 1 drop into the affected eye(s) twice or three times daily
    • Dorzolamide ophthalmic: (2%) 1 drop into the affected eye(s) twice or three times daily

    Secondary options:

    • Acetazolamide: 125-250 mg orally (immediate-release) up to four times daily, maximum 1000 mg/day; 250-500 mg intravenously every 2-4 hours, maximum 1000 mg/day
    • Methazolamide: 50-100 mg orally twice or three times daily

     

    Adjunct (in cases of plateau iris)

    Argon laser peripheral iridoplasty (when there is a component of plateau iris):

    ALPI is a procedure during which contraction burns are placed in the peripheral iris with the aim of thinning it and pulling it away from the TM.

     

    Adjunct

    Lens extraction surgery:

    If residual angle closure is attributable to the lens pushing forward the iris, then lens extraction surgery with or without goniosynechialysis is considered.

     

    Adjunct

    Topical cholinergic agonists:

    Cholinergic agents may be used if there is residual angle closure after laser treatment. These agents cause pupil constriction with thinning of the iris and its pulling away from the inner eye wall and TM, thus opening the angle. Instillation frequency and concentration of pilocarpine is determined by response. Patients with heavily pigmented irides may require higher strengths. In acute attack 1% to 2% is the preferred solution. Stronger miotics may increase the pupillary block. Patients may be maintained on pilocarpine as long as IOP is controlled and no deterioration in visual fields occurs.

    Primary option: Pilocarpine ophthalmic (1-2%) 1 drop into the affected eye(s) up to 4 times daily

     

    Adjunct

    Trabeculectomy or tube shunt implantation:

    Uncommonly IOP remains elevated despite medical and surgical measures, and in this case IOP-lowering surgery, such as trabeculectomy or tube shunt implantation, is indicated.

     

    Emerging Therapies

    Emerging Surgical Treatment for Acute Angle Closure Attacks

    It has been suggested that an acute attack of angle closure can be terminated by surgical means such as an anterior chamber paracentesis to acutely lower IOP and break the cycle of rising IOP. It may also allow clearing of the corneal edema to facilitate LPI. Other reports recommend laser iridoplasty, corneal indentation, cataract or clear lens extraction.

    Emerging Surgical Treatment for Chronic Angle-Closure Glaucoma

    The treatment of chronic angle-closure glaucoma is similar to that of open-angle glaucoma. Recently developed procedures to treat chronic angle-closure glaucoma include the Ex-PRESS glaucoma implant, canaloplasty, trabectome, and trabecular micro-bypass stent. [Francis, et al 2011] [1398 Chai CL. 2010]

    Treatment Guidelines

    Asia

    Clinical practice guidelines: glaucoma, Singapore Ministry of Health, 2010. Evidence-based guidelines on the treatment of glaucoma. The goal of treatment is to maintain useful visual function and patient's quality of life by lowering IOP. Treatment options for lowering IOP are discussed.

    Europe

    The effectiveness of the Heidelberg Retina Tomograph and laser diagnostic glaucoma scanning system (GDx) in detecting and monitoring glaucoma, Health Technology Assessment NHS R&D HTA Programme, 2011.

    North America

    • Comprehensive adult medical eye evaluation, American Academy of Ophthalmology, 2009.
    • Comprehensive adult eye and vision examination, American Optometric Association, 2005.
    • Primary angle closure, American Academy of Ophthalmology, 2009.

    Prognosis

    Acute Angle Closure

    After the resolution of the acute episode, eyes should be assessed for degree of angle closure, the presence of PAS, degree of cataract, and optic disc and visual field damage. IOP should be checked multiple times to detect asymptomatic rise in IOP. The second eye should be assessed and treated to prevent attack.  

    The prognosis is favorable if the IOP can be controlled. IOP is reported to be controlled with laser peripheral iridotomy alone in 42% to 72% in whites, more often than in Asians.   

    Chronic Angle-Closure Glaucoma

    With control of the IOP, progressive visual deterioration can be controlled. The efficacy of peripheral iridotomy for disease control depends on both the underlying mechanism and the stage of the disease when diagnosed. 

    Greater extent of PAS, a higher presenting IOP, and a larger cup-to-disc ratio are all predictors of poor pressure control following iridotomy. 

    Once glaucomatous optic neuropathy has developed (defined as structural damage to the disc and/or visual field loss), virtually all cases (94% to 100%) will require further treatment to control IOP. 

    Monitoring

    Following iridotomy, patients may have an open anterior-chamber angle or an anterior-chamber angle with a combination of open sectors and areas occluded by irreversible iridotrabecular synechiae.

    After the acute episode of angle closure has been addressed, patients who are found to have glaucomatous optic neuropathy should be followed up periodically, probably every 3 to 6 months, similar to patients with primary open-angle glaucoma, to ensure IOP is controlled and there is no further glaucomatous progression of optic nerve or visual field changes.

    Patients who do not have glaucomatous optic neuropathy should be followed up periodically, approximately every 6 to 12 months, to detect further closure of the angle or elevation of IOP.

    Complications

    Complications

    Likelihood

    Timeframe

    Fellow eye attack:

    The fellow eye, which usually shares the anatomic predisposition for increased pupillary block, is at high risk for developing acute angle closure. An untreated fellow eye has a 40% to 80% risk of developing an acute attack. It is recommended that the contralateral eye be treated prophylactically with laser peripheral iridotomy if the chamber angle is found to be anatomically narrow (Bain 1957, Lowe 1962, Hyams 1975).

    High

    Variable

    Retinal vein occlusion:

    This complication may be prevented by prompt reduction of IOP. Once it occurs there is no specific immediate treatment.

    Medium

    Short-term

    Loss of vision:

    This complication may be prevented by prompt reduction of IOP.

    Medium

    Short-term

    Permanent decrease in visual acuity:

    Patients with primary angle-closure glaucoma (PACG) often present with higher IOP and more advanced visual field loss than those with primary open-angle glaucoma (POAG).  These finding suggest that PACG is a more IOP-dependent disease. Following successful treatment of acute primary angle-closure, there is some evidence that retinal nerve fiber layer thickness significantly decreases within 16 weeks after the attack. Adequate and prompt treatment with lowering of IOP will reduce the risk for permanent injury to the retinal ganglion cells and axons.

    Medium

    Variable

    Repeat episode of acute ACG:

    If the mechanism of angle closure was not eliminated, an acute episode can recur. The clinician should look for the specific mechanism of angle closure, and treat it accordingly. It is also important to verify that the peripheral iridotomy is patent.

    Low

    Variable

     

    Clinical Evidence References

    1[C]

    Intraocular pressure: there is poor-quality evidence that in people with angle closure glaucoma receiving acetazolamide, low dose pilocarpine, an intensive pilocarpine regimen, or pilocarpine ocular inserts all reduced intraocular pressures after 2 hours with no significant difference among groups. More info at BMJ Clinical Evidence.

    2[B]

    Symptom improvement and intraocular pressure: there is medium-quality evidence that for people with uniocular acute angle closure glaucoma, there is no significant difference between surgical iridectomy and laser iridotomy in improvements in intraocular pressure after 3 years. Poor-quality evidence has not shown whether surgical iridectomy is more effective than laser iridotomy in improving visual acuity at 3 years in people with uniocular acute angle closure glaucoma. More info at BMJ Clinical Evidence.

    Evidence Level A

    Systematic reviews (SRs) or randomized controlled trials (RCTs) of > 200 participants

    Evidence Level B

    Randomized controlled trials (RCTs) of < 200 participants, methodologically flawed RCTs of > 200 participants, methodologically flawed systematic reviews (SRs) or good quality observational (cohort) studies

    Suggested Reading

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