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Glaucoma - Angle closure

Definition
  • Group of diseases in which there is reversible (appositional) or adhesional (synechial) closure of the anterior-chamber angle. 
  • Prolonged or repeated contact between the peripheral iris and the trabecular meshwork may lead to peripheral anterior synechiae and functional damage to the trabecular meshwork. 
  • The angle closure may or may not be associated with elevated intraocular pressure (IOP) or glaucomatous optic neuropathy, and may occur in an acute or chronic form.
Risk Factors
  • Female
  • Hyperopia
  • Shallow peripheral anterior chamber
  • Second eye having angle closure
  • Inuit / Asian ethnicity
  • Age
  • FHx
Differential diagnosis
  • Open angle glaucoma
  • Other optic neuropathy
  • Eye trauma
  • Keratitis
  • Conjunctivitis
  • Corneal ulcer
  • Episcleratitis / Scleratitis
Epidemiology
  • The number of people affected by glaucoma in the world is approximately 45 million. 
    • One third are from primary angle-closure glaucoma (PACG). [2] 
  • Half of cases leading to blindness are estimated to result from PACG. [3]
  • 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 US, but up to 50% of glaucoma cases in Asian populations. 
  • Among the white population in Europe and the US, the estimated prevalence of PACG is 0.04% to 0.4%. [15] [16] 
  • The prevalence of PACG in the Inuit population is estimated at 2.65% to 4.8%. [11] [12] [13] [14]
  • Women are 2 to 4 times more likely to have ACG than men. [4] 
  • Acute ACG is most common between the ages of 55 and 65 years. [17]
Aetiology 
  • Angle closure can be primary, secondary to another eye disease, or drug induced.
  • Eye diseases that can cause ACG include ectopia lentis due to Weill-Marchesani syndrome, and neovascularisation of the iris secondary to diabetic retinopathy.
  • Sulfa-containing drugs can cause ACG by causing supraciliary body effusions.
Clinical features
  • 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.
  • halos around lights 
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • aching eye or brow pain
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • headache
    • A deep, dull, periocular ache may be present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • nausea, vomiting
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • reduced acuity
    • Present in the acute and sub-acute forms but usually not with the chronic form of angle closure.
  • eye redness
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • elevated intraocular pressure (IOP)
    • In healthy eyes, IOP is generally 10 to 21 mmHg. In acute attacks, IOP rises rapidly to relatively high levels, typically above 40 mmHg.
  • corneal oedema
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure
  • fixed dilated pupil
    • Iris ischaemia may cause the pupil to remain permanently fixed and dilated.
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure.
  • blurred vision
    • Present in the acute and sub-acute forms but not with the chronic form of angle closure
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 commonest reason is relative pupillary block
      • other reasons include plateau iris syndrome, enlarged or anteriorly displaced lens, and malignant glaucoma
    • Mechanisms that pull the iris into contact with the TM 
      • e.g., contraction of inflammatory membrane as in uveitis
      • fibrovascular tissue as in iris neovascularisation
      • 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 and/or obstructed that aqueous outflow from the eye is impaired, and intraocular pressure (IOP) rises. [18]
  • 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.
Investigations
  • Gonioscopy
    • Definitive test for diagnosing angle closure.
      • trabecular meshwork is not visible in angle closure, because the peripheral iris is in contact with it
    • Gonioscopy of both eyes should be performed on all patients in whom angle closure is suspected.
    • 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.
    • It is also important for the detection of plateau iris and other specific anatomical configurations.
    • It may be therapeutic in breaking the attack of acute angle closure.
  • Fundoscopy
  • Automatic static perimetry
    • Identifies the presence, and quantifies the amount, of glaucomatous visual field loss during initial diagnosis and subsequently during follow-up care.
Management

a) conservative

b) medical
  • The immediate goal of treatment is to relieve the acute symptoms and decrease intraocular pressure (IOP). 
    • This is usually achieved with medical therapy. [25] 
    • 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. [28] 
    • Alpha-agonists reduce IOP by around 26% within 2 hours post-dose. [28] 
    • Carbonic anhydrase inhibitors, topical beta-blockers, or alpha-2 adrenergic may be used as first-line therapies either alone but more typically in combination..
  • In patients in whom angle closure is thought to be secondary to pupillary block or plateau iris syndrome, cholinergic agents (such as pilocarpine)[C Evidence] should be started after IOP decreases to <40 mmHg. [28] 
    • They 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. 
    • They are therefore contraindicated in these cases. [29]
  • If these medical treatments are unsuccessful or if pressures are exceedingly high, hyper-osmotic agents should be used.
    • 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.
  • 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.
  • If IOP remains elevated following these measures, it is lowered in a fashion similar to open-angle glaucoma with IOP-lowering medications, and if these are ineffective, then IOP-lowering surgery. [24]
  • Topical ophthalmic prostaglandin analogues work by increasing aqueous outflow. 
    • They reach peak effectiveness 10 to 14 hours after administration, so they are not used during acute attacks, [28] and are the most potent IOP-lowering agents available and should be used first line. [43] [44] 
    • 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 systemic use, and should be reserved for patients with glaucoma refractory to other medical treatment. [28]
  • Uncommonly IOP remains elevated despite all these measures, and in this case IOP-lowering surgery, such as trabeculectomy, is indicated. [45]
c) surgical
  • Definitive surgical treatment is aimed at achieving a persistently open angle.
    • Laser peripheral iridotomy (LPI), sometimes followed by argon laser peripheral iridoplasty (ALPI), is usually successful. [24] [30] [31] [32] [B Evidence]
    • 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 trabecular meshwork (TM), resulting in opening or widening of the angle. [31] [32] [33] [34] [35] 
    • LPI is indicated in all eyes with angle closure and usually in fellow eyes as well. [25] [36]
  • If residual angle closure occurs in the presence of patent LPI, then further laser surgery should be performed. 
    • 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. [37]
Prognosis
  • Acute angle closure
    • After the resolution of the acute episode, eyes should be assessed for degree of angle closure, the presence of peripheral anterior synechiae (PAS), degree of cataract, and optic disc and visual field damage. 
    • Intraocular pressure (IOP) should be checked multiple times to detect asymptomatic rise in IOP. 
    • The second eye should be assessed and treated to prevent attack.[6]
    • The prognosis is favourable 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 then in Asians. [40] [42]
  • Chronic angle-closure glaucoma
    • With control of the IOP, progressive visual deterioration can be prevented. 
    • The efficacy of peripheral iridotomy for disease control depends on both the underlying mechanism and the stage of the disease when diagnosed. [49]
    • Greater extent of PAS, a higher presenting IOP, and a larger cup-to-disc ratio are all predictors of poor pressure control following iridotomy. [50]
    • 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. [51]
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