Primary angle closure glaucoma

Primary angle closure glaucoma

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  By Mutahir Shah M PhilVision Sciences Pakistan Institute of Community Ophthalmology Primary Angle Closure Glaucoma
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  Structure of NormalAngle on Gonioscopy
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  Introduction to PACG The term ‘angle closure’ refers to occlusion of the trabecular meshwork by the peripheral iris (iridotrabecular contact – ITC), obstructing aqueous outflow.  Angle closure can be primary, when it occurs in an anatomically predisposed eye, or secondary to another ocular or systemic factor.  PACG may be responsible for up to half of all cases of glaucoma globally,  A particularly high prevalence in individuals of Far Eastern descent.  It is typically associated with greater rapidity of progression and visual morbidity than POAG.
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  Classification  Association ofInternational Glaucoma Societies classify PACG in the following types.  Primary angle closure suspect (PACS)  Primary angle closure (PAC)  Primary angle-closure glaucoma (PACG)
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  Primary angle closuresuspect (PACS)  Gonioscopy shows posterior meshwork ITC in three or more quadrants but no PAS.  Many patients with less ITC have evidence of intermittent angle closure, and a lower threshold for diagnosis such as two quadrants of ITC, pigment smudging(blurred or indistinct) or even a very narrow angle approach (perhaps 20° or less – may be justified.  Normal IOP, optic disc and visual field.  No peripheral anterior synechiae (PAS).  The risk of PACG at 5 years may be around 30%.
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  (A) On gonioscopyonly a double Schwalbe line and part of the non-pigmented trabecular meshwork are visible (B) pigment smudging of the non-pigmented meshwork seen on indentation gonioscopy; © sparsely pigmented Schwalbe line
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  Primary angle closure(PAC)  ITC in three or more quadrants, with glaucomatous optic neuropathy.  Optic nerve damage from an episode of severe IOP elevation, such as acute angle closure, may not appear as typical glaucomatous cupping.
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  Primary angle-closure glaucoma (PACG) Gonioscopy shows three or more quadrants of ITC with raised IOP and/or PAS or excessive pigment smudging on the TM.  Normal optic disc and field.  Some authorities further classify PAC into non- ischaemic and ischaemic, the latter showing anterior segment evidence of prior substantial IOP elevation such as iris changes or glaukomflecken (see Fig. ).
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  Risk Factors  Age. The average age of relative pupillary block is about 60 years at presentation.  Non-pupillary block forms of primary angle closure tend to occur at a younger age.  Gender.  Females are more commonly affected than males.  Race.  Particularly prevalent in Far Eastern and Indian Asians; in the former non-pupillary block is relatively more significant.  Family history.  Genetic factors are important but poorly defined, with an increased prevalence of angle closure in family members.
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   Refraction.  Eyeswith ‘pure’ pupillary block are typically hypermetropic.  Although this is not as clear-cut with non-pupillary block, which can occur in myopic eyes.  Up to one in six patients with hypermetropia of one dioptre or more are primary angle closure suspects, so routine gonioscopy should be considered in all hypermetropes.  Axial length.  Short eyes tend to have a shallow AC eyes with nanophthalmos have a very short eye with a proportionally large lens and are at particular risk.
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  Diagnosis  Symptoms:  MostPatients are asymptomatic including a majority of those with intermitently or chronically Elevated IOP  Blurred Vision (smoke filled Room)  Color halos around light (Rainbow around light) due to corneal epithelial corneal oedema.  Frontal, Ocular /periocular pain and Headache.  Nausea ,Vomiting  Precipitating factors include watching television in a darkened room.  Pharmacological Mydriasis, Acute emotional stress, semiprone position, etc
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  Signs  Acute PrimaryAngle Closure  VA is usually 6/60 to HM.  The IOP is usually very high (50–100 mmHg).  Conjunctival hyperaemia with violaceous circumcorneal injection.  Corneal epithelial oedema (Fig. 10.60A  The AC is shallow, and aqueous flare is usually present.  An unreactive mid-dilated vertically oval pupil is classic  The fellow eye typically shows an occludable angle; if not present, secondary causes should be considered.
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  Fig. Shallow anteriorchamber . (B) Corneal epithelial oedema, with very numerous tiny epithelial cysts; (C) mid- dilated vertically oval pupil
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  Chronic Presentation  VAis normal unless damage is advanced.  The AC is usually shallower in relative pupillary block than non-pupillary block.  IOP elevation may be only intermittent.  ‘Creeping’ angle closure is characterized by a gradual band-like anterior advance of the apparent insertion of the iris.  It starts in the deepest part of the angle and spreads circumferentially.  Intermittent ITC may be associated with the formation of discrete PAS, individual lesions having a pyramidal (‘saw-tooth’) appearance.
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  Resolved APAC  Early: low IOP (ciliary body shutdown and effect of intensive treatment), folds in Descemet membrane if IOP has reduced rapidly ,  optic nerve head congestion,  choroidal folds.  Late:  Iris atrophy with a spiral-like configuration,  glaukomflecken (white foci of necrosis in the superficial lens) and other forms of cataract,  irregular pupil due to iris sphincter/dilator damage and posterior synechiae ;  the optic nerve may be normal or exhibit varying signs of damage, including pallor and/or cupping .
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  Resolved acute primaryangle closure. (A) Stromal corneal oedema and folds in Descemet membrane; (B) glaukomflecken, spiral-shaped atrophic iris, dilated pupil and posterior synechiae; (C) optic atrophy – combined pallor and cupping
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  DD of PACG Lens-induced angle closure due to a swollen or subluxated lens.  Malignant glaucoma, especially if recent intraocular surgery.  Other causes of secondary angle closure, with or without pupillary block; see below.  Neovascular glaucoma may occasionally cause the sudden onset of pain and congestion.  Hypertensive uveitis, e.g. iridocyclitis with trabeculitis (particularly herpetic including cytomegalovirus), glaucomatocyclitic crisis (Posner–Schlossman syndrome).  Scleritis (rarely episcleritis) with or without angle closure.  Pigment dispersion.
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  Investigation  Anterior segmentOCT  Anterior chamber depth measurement  Biometry if lens extraction is considered.  Posterior segment ultrasonography in atypical cases to exclude causes of secondary angle closure  Provocative testing  Pharmacological mydriasis probably discriminates poorly.  It carries a small risk of precipitating APAC in susceptible patients without a patent iridotomy.  Dark room/prone provocative test (DRPPT):  the patient sits in a dark room, face down for one hour without sleeping (sleep induces miosis).  The IOP is checked (immediately after the test, as IOP can normalize very rapidly), and an IOP rise of 8 mmHg or more is frequently taken as being of significance