Download MBBS Ophthalmology PPT 44 Primary Angle Closure Glaucoma 1 Lecture Notes

Department of

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Ophthalmology



Objectives

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? At the end of this class the students shal be able

to :

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? Define primary angle closure glaucoma.

? Understand the pathophysiology and the risk

factors.

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? Be able to classify primary angle closure

glaucoma.

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? Understand the fundamentals of managing

primary angle closure glaucoma

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DEFINITION

? Primary angle closure glaucoma is a type of

primary glaucoma(with no obvious systemic or

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ocular cause) characterized by

occludable/closed angles leading to

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obstruction of aqueous outflow resulting in

rise of intra ocular pressure, optic nerve

damage and visual field defects.

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ANGLE OF ANTERIOR CHAMBER

? STRUCTURES

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? Schwalbe's line
? Trabecular meshwork
? Scleral spur
? Ciliary body band
? Root of iris

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DRAINAGE OF AQUEOUS HUMOR

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PRIMARY ANGLE CLOSURE

GLAUCOMA

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EPIDEMIOLOGY

? PACG is the major cause of glaucoma blindness

worldwide.

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? Age :- Average age at presentation 50-60 yrs

? Gender :- F > M, 4 : 1

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? Race :-seen commonly in South-East Asian

population, Chinese and Eskimos

? Heredity :- mostly sporadic but may be inherited

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AD/AR

? first degree relatives are at increased risk.

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? Refractive error :- more common in

hypermetropes
Ocular risk factors

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1. Shallow anterior chamber both

centrally and peripherally.

2. Decreased anterior chamber volume.

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3. Short axial length of the globe.

4. Small corneal diameter.

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Ocular risk factors

5.Decreased posterior corneal radius of

curvature

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6.Anterior position of the lens with respect to

the ciliary body.

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7.Increased curvature of the anterior surface &

thickness of lens

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PATHOGENESIS

? It is incompletely understood.

? a. Iris?pupil obstruction (e.g., `pupil ary block')

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? b. Ciliary body anomalies (e.g., `plateau iris syndrome')
? c. Lens?pupil block (e.g., `phacomorphic block' (swollen

lens or microspherophakia))

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? Relative Pupillary block
? Normal y the pressure in the post. chamber exceeds that in the ant.

chamber due to physiological degree of resistance at the pupil ,since the

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iris rests posteriorly on the anterior lens capsule.

Anterior Iris Bowing

Simultaneous dilatation of the pupil renders the peripheral

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iris more flaccid. The pupil block causes the pressure in the

Posterior Chamber to increase & peripheral iris bows

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anteriorly


Iridocorneal contact

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Eventually the iris touches the posterior corneal surface,

obstructing the angle and the IOP rises.

(Figures and photographs- Courtesy : Kanski's Clinical Ophthalmology)

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Precipitating factors

1. Factors that produce mydriasis

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? Dim illumination
? Emotional stress(due to increased sympathetic tone)
? Drugs

? Mydriatic agents :

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? cyclopentolate, tropicamide, atropine, homatropine.

? Antipsychotic agents

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? Phenothiazines: e.g., perphenazine ,fluphenazine
? Anticonvulsants e.g., Topiramate
? Antidepressants

? Tricyclic agents: amitriptylene ,imipramine

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? Non-tricyclic agents: fluoxetine

? Antiparkinsonian agents : Trihexyphenidryl

? Antispasmolytics : Propantheline ,Dicyclomine

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? Sympathomimetic agents : Adrenaline (epinephrine),

ephedrine, phenylephrine.

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CLASSIFICATION

A. Primary angle-closure disease

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? Irido-trabecular contact is the final common pathway of

angle closure disease, obstructing aqueous outflow

1. New classification

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Primary angle closure suspect/PACS
Primary angle closure/PAC
Primary angle-closure glaucoma/PACG
2. Old classification

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Angle closure suspect
Intermittent (sub acute) angle closure
Acute angle closure
Chronic angle closure
Absolute angle closure

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New classification of PACG

qPrimary angle closure suspect/PACS

Has occludable/narrow angles

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qPrimary angle closure/PAC

Has occludable/narrow angles +

High IOP/Peripheral anterior synechiae/

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Excessive trabecular meshwork

pigmentation
qPrimary angle-closure glaucoma/PACG

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PAC+ Optic disc changes+ Visual field

defects

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Gonioscopic grading of Angle

closure

? Several grading systems :- Shaffer's, Spaeth's,

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Scheie's.

? Shaffer's grading

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Grade Angle width configuration

Chances of

Structures visible

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closure

IV

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35?-45?

Wide open

Nil

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SL,TM,SS,CBB

I I

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20?-35?

Open angle

Nil

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SL,TM,SS

I

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20?

Moderately open Possible

SL,TM

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I

10?

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Very narrow

Highly likely

SL only

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0

0?

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Closed

Closed

None

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---------
Grade
IV

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II

II

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I
0

Van Herrick's grading

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Tests for Angle closure

? Eclipse test : uses flash light to make a rough

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assessment of angle depth

? Provocative tests for PAC suspects
?Prone- darkroom test: An increase in IOP of more

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than 8mm Hg after one hour suggests PAC

?Mydriatic provocative test: Not preferred now

qFincham's Test: Also known as stenopaeic-slit test.

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Glaucomatous halos remain intact , whereas

halos due to cataract are broken up into segments

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PRIMARY ANGLE CLOSURE GLAUCOMA SUSPECT

? Also known as Latent PACG

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? Essentially, the term implies

an anatomically predisposed

eye.

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? Symptoms :- absent
? Signs :

? Axial AC depth is < normal

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& iris lens diaphragm is

convex

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? Close proximity of the iris

to the cornea

? Gonioscopy :- occludable

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angle(grade 1 or 0)

without indentation in at

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least 3 quadrants.


?Clinical course without

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treatment may be:

IOP may remain normal

Acute or sub acute angle

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closure may ensue

Chronic angle closure may

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develop, without acute or

sub acute stages.

? Treatment

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? Without treatment , risk of an acute pressure rise during the next

5 years is about 50 %.

? The need to treat is based on following criteria:-

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? If one eye has had acute or subacute angle closure, then

fellow eye should undergo prophylactic peripheral laser
iridotomy (Laser PI)

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? If both eyes have occludable angles, laser PI may be done


INTERMITTENT(SUBACUTE)PRIMARY ANGLE CLOSURE

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GLAUCOMA

? A form of pupillary block glaucoma, which may not have

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any recognizable symptoms.

? Occurs in a predisposed eye with an occludable angle in

association with intermittent pupillary block.

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? Precipitating factors :- physiological mydriasis , or

physiological shallowing of AC when patient assumes a

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prone or semi prone position ;emotional stress.

? Symptoms

? Characteristic h/o transient blurring of vision with haloes

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around lights

? Ocular discomfort or frontal headache
? Attacks are recurrent and are usually broken after 1-2 hrs by

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physiological miosis.

? Signs

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? During an attack , eye is usually white
? In between attacks, eye looks normal although the angle is

narrow.

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? Clinical course

? Without treatment is variable

? Some eyes develop an acute attack

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? Others chronic angle closure

? Treatment:- Prophylactic laser PeripheraI Iridotomy(PI)

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ACUTE PRIMARY ANGLE CLOSURE GLAUCOMA

? Sight threatening emergency
? Painful loss of vision due to sudden and total

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closure of the angle.

? VA usually 6/60-Hand Movements.
? IOP is usually very high (40?70 mmHg).

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Findings during an acute attack of angle-closure glaucoma
? Two of the following symptom sets:

? Periorbital or ocular pain
? Diminished vision

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? Specific history of rainbow haloes with blurred vision

? IOP > 21 mmHg plus three of the following

findings:

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? Ciliary flush (perilimbal conjunctival hyperemia)
? Corneal edema (epithelial,stromal)
? Shallow anterior chamber
Findings during an acute attack of angle-closure glaucoma

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? Anterior chamber cell and flare
? Mid-dilated ,vertically oval and sluggishly reactive

pupil

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? Closed angle on gonioscopy
? Hyperemic and swollen optic disc(due to

decreased axoplasmic outflow)

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? Constricted visual fields

? MANAGEMENT

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? Patient comfort ,lowering of the IOP and to break acute

attack-- main priorities.

? A. Immediate medical treatment

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1. Patient should lie supine to allow the lens to shift

posteriorly.

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2. Acetazolamide 500 mg orally(if there is no vomiting).

or I.V Mannitol 20% 1-2 g/kg over 1 hour (rule out

contraindications)

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3.Topical

Prednisolone or dexamethasone q.i.d (if AC reaction)

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Timolol (if there is no contraindication).

4. Analgesia and emetics as required.

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? B. Subsequent medical treatment

Pilocarpine 2% q.i.d. to the affected eye and 1% q.i.d. to the

fellow eye.

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Topical steroids (prednisolone 1% or dexamethasone 0.1%)

q.i.d. if the eye is acutely inflamed.

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Timolol 0.5% b.d.,

and oral acetazolamide 250 mg q.i.d. may be required.

? If the above measures fail:

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? Laser iridotomy or iridoplasty after clearing corneal oedema with

glycerol.

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? Surgical options in resistant cases include lens extraction,

goniosynechiolysis, trabeculectomy and cycloablation.

? Findings suggestive of previous episodes of acute

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angle closure glaucoma

? Descemets Membrane folds

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? Fine pigment granules on corneal endothelium

? Peripheral anterior synechiae

? Posterior synechiae

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? Glaucomflecken

? Sectoral/generalized iris atrophy

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? Fixed and semi dilated pupil

? Optic nerve cupping &/or pallor

? Gonioscopy shows narrow angle

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or PAS

? Visual field loss
Chronic angle closure glaucoma

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? Visual Acuity is normal unless damage is

advanced.

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? Anterior chamber is shal ower in pupil ary

block than non-pupil ary block.

? Optic nerve signs depend on severity of

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damage.

? IOP elevation may be only intermittent.

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? Gonioscopic abnormalities-Peripheral

Anterior Synechiae, narrow angle,

pigmentation of Schwalbe's line.

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Treatment of chronic angle closure

? Medical treatment is similar to that of POAG

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? Prostaglandin/Prostamides

Latanoprost, Bimatoprost, Travoprost

? Beta blockers

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Timolol maleate, Betaxolol

? Carbonic anhydrase inhibitors

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Dorzolamide, Brinzolamide

? Sympathomimetics

Brimonidine, Apraclonidine

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? Parasmpathomimetics

Pilocarpine

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? Oral carbonic anhydrase inhibitors

Acetazolamide, Methazolamide

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Treatment of chronic angle closure

? Laser Peripheral Iridotomy (PI) in affected eye

along with Prophylactic PI in fellow eye

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Laser Peripheral Iridotomy

? Complications of laser therapy
1. Bleeding

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2. IOP elevation
3. Iritis
4. Corneal burns
5. Lens opacities
6. Glare and diplopia

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? Surgical treatment

Trabeculectomy (filtering surgery) is the

surgical procedure of choice

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? Success:- 87- 100 % with multiple operations

? Complications:-

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? Flat AC, hypotony

? Bleb related infections

? Cyclodialysis

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? PATIENTS REQUIRE REGULAR AND LIFE LONG

FOLLOW UP

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Absolute glaucoma

? Is the final/last stage of PACG

? Clinical features:

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? Painful blind eye
?Perilimbal reddish blue zone, due to dilated

anterior ciliary veins

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?Cornea gradually becomes hazy, insensitive

with bullous keratopathy and filamentary

keratitis

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?Anterior chamber is very shallow/flat
Clinical features of absolute glaucoma

? Iris is usually atrophic

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?Pupil is fixed and dilated
?Glaucomatous optic atrophy of the optic disc
?High IOP

Management of absolute glaucoma

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? Cycloablation/destruction of the secretory

ciliary epithelium

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q Cyclophotocoagulation
q Cyclocryotherapy
q Cyclodiathermy
? Rarely
? Retrobulbar alcohol injection

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? Enucleation of eyeball
Complications

? Corneal ulceration
? Staphyloma formation (Ciliary/Equatorial)

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? Atrophic bulbi (Shrunken eye)

Conclusion

? Primary angle closure glaucoma is a

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potentially sight threatening condition,

characterized by occludable anterior chamber

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angles.

? Obstruction of aqueous outflow results in rise

of intra ocular pressure, optic nerve damage

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and visual field defects.

? Management may include medical, laser

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and/or surgical modalities.