Download MBBS Ophthalmology PPT 46 Primary Angle Closure Glaucoma 3 Lecture Notes

PRIMARY ANGLE CLOSURE

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GLAUCOMA

Acknowledgement

? Figures and photographs

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Courtesy : Kanski's Clinical Ophthalmology

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Learning Objectives

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

to :

? Define primary angle closure glaucoma.

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? Understand the pathophysiology and the risk

factors.

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? Be able to classify primary angle closure

glaucoma.

? Understand the fundamentals of managing

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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

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? STRUCTURES

? Schwalbe's line
? Trabecular meshwork

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? 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

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Ocular risk factors

1. Shallow anterior chamber both

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centrally and peripherally.

2. Decreased anterior chamber volume.

3. Short axial length of the globe.

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4. Small corneal diameter.

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Ocular risk factors

5.Decreased posterior corneal radius of

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curvature

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.

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

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lens or microspherophakia))

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

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

iris rests posteriorly on the anterior lens capsule.

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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

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Iridocorneal contact

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Eventually the iris touches the posterior corneal surface,

obstructing the angle and the IOP rises.

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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

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? Antidepressants

? Tricyclic agents: amitriptylene ,imipramine
? Non-tricyclic agents: fluoxetine

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? Antiparkinsonian agents : Trihexyphenidryl

? Antispasmolytics : Propantheline ,Dicyclomine

? Sympathomimetic agents : Adrenaline (epinephrine),

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ephedrine, phenylephrine.


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CLASSIFICATION

A. Primary angle-closure disease

? Irido-trabecular contact is the final common pathway of

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angle closure disease, obstructing aqueous outflow

1. New classification
Primary angle closure suspect/PACS

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

Angle closure suspect

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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

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Has occludable/narrow angles
qPrimary angle closure/PAC

Has occludable/narrow angles +

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High IOP/Peripheral anterior synechiae/

Excessive trabecular meshwork

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pigmentation
qPrimary angle-closure glaucoma/PACG

PAC+ Optic disc changes+ Visual field

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defects

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Gonioscopic grading of Angle

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closure

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

Scheie's.

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? Shaffer's grading

Grade Angle width configuration

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Chances of

Structures visible

closure

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IV

35?-45?

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Wide open

Nil

SL,TM,SS,CBB

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I I

20?-35?

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Open angle

Nil

SL,TM,SS

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I

20?

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Moderately open Possible

SL,TM

I

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10?

Very narrow

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Highly likely

SL only

0

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0?

Closed

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Closed

None

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---------
Grade
IV

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II

II

I

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0

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Van Herrick's grading

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Tests for Angle closure

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? Eclipse test : uses flash light to make a rough

assessment of angle depth

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

than 8mm Hg after one hour suggests PAC

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?Mydriatic provocative test: Not preferred now

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

Glaucomatous halos remain intact , whereas

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halos due to cataract are broken up into segments

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PRIMARY ANGLE CLOSURE GLAUCOMA SUSPECT

? Also known as Latent PACG
? Essentially, the term implies

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an anatomically predisposed

eye.

? Symptoms :- absent

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? Signs :

? Axial AC depth is < normal

& iris lens diaphragm is

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convex

? Close proximity of the iris

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to the cornea

? Gonioscopy :- occludable

angle(grade 1 or 0)

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without indentation in at

least 3 quadrants.

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?Clinical course without

treatment may be:

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IOP may remain normal

Acute or sub acute angle

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closure may ensue

Chronic angle closure may

develop, without acute or

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sub acute stages.

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

5 years is about 50 %.

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

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

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

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

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INTERMITTENT(SUBACUTE)PRIMARY ANGLE CLOSURE

GLAUCOMA

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

any recognizable symptoms.

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? Occurs in a predisposed eye with an occludable angle in

association with intermittent pupillary block.

? Precipitating factors :- physiological mydriasis , or

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physiological shallowing of AC when patient assumes a

prone or semi prone position ;emotional stress.

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? Symptoms

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? Characteristic h/o transient blurring of vision with haloes

around lights

? Ocular discomfort or frontal headache

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? Attacks are recurrent and are usually broken after 1-2 hrs by

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

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? Some eyes develop an acute attack
? Others chronic angle closure

? Treatment:- Prophylactic laser PeripheraI Iridotomy(PI)

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ACUTE PRIMARY ANGLE CLOSURE GLAUCOMA

? Sight threatening emergency

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? Painful loss of vision due to sudden and total

closure of the angle.

? VA usually 6/60-Hand Movements.

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? 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:

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? Periorbital or ocular pain
? Diminished vision
? Specific history of rainbow haloes with blurred vision

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? IOP > 21 mmHg plus three of the following

findings:

? Ciliary flush (perilimbal conjunctival hyperemia)

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? Corneal edema (epithelial,stromal)
? Shallow anterior chamber

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Findings during an acute attack of angle-closure glaucoma

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

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pupil

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

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decreased axoplasmic outflow)

? Constricted visual fields

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? MANAGEMENT

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

attack-- main priorities.

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? A. Immediate medical treatment

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

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posteriorly.

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

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

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contraindications)

3.Topical

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

Timolol (if there is no contraindication).

4. Analgesia and emetics as required.

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? B. Subsequent medical treatment

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

fellow eye.

Topical steroids (prednisolone 1% or dexamethasone 0.1%)

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

Timolol 0.5% b.d.,

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

? If the above measures fail:

? Laser iridotomy or iridoplasty after clearing corneal oedema with

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glycerol.

? Surgical options in resistant cases include lens extraction,

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goniosynechiolysis, trabeculectomy and cycloablation.

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? Findings suggestive of previous episodes of acute

angle closure glaucoma

? Descemets Membrane folds

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? Fine pigment granules on corneal endothelium

? Peripheral anterior synechiae

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? Posterior synechiae

? Glaucomflecken

? Sectoral/generalized iris atrophy

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? Fixed and semi dilated pupil

? Optic nerve cupping &/or pallor

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? Gonioscopy shows narrow angle

or PAS

? Visual field loss

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Chronic angle closure glaucoma

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? Visual Acuity is normal unless damage is

advanced.

? Anterior chamber is shal ower in pupil ary

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block than non-pupil ary block.

? Optic nerve signs depend on severity of

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damage.

? IOP elevation may be only intermittent.

? Gonioscopic abnormalities-Peripheral

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Anterior Synechiae, narrow angle,

pigmentation of Schwalbe's line.

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Treatment of chronic angle closure

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? Medical treatment is similar to that of POAG

? Prostaglandin/Prostamides

Latanoprost, Bimatoprost, Travoprost

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? Beta blockers

Timolol maleate, Betaxolol

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? Carbonic anhydrase inhibitors

Dorzolamide, Brinzolamide

? Sympathomimetics

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Brimonidine, Apraclonidine

? Parasmpathomimetics

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Pilocarpine

? Oral carbonic anhydrase inhibitors

Acetazolamide, Methazolamide

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Treatment of chronic angle closure

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? 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
2. IOP elevation

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

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? Surgical treatment

Trabeculectomy (filtering surgery) is the

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surgical procedure of choice

? Success:- 87- 100 % with multiple operations

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? Complications:-

? Flat AC, hypotony

? Bleb related infections

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? Cyclodialysis

? PATIENTS REQUIRE REGULAR AND LIFE LONG

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FOLLOW UP

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Absolute glaucoma

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? Is the final/last stage of PACG

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

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anterior ciliary veins

?Cornea gradually becomes hazy, insensitive

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with bullous keratopathy and filamentary

keratitis

?Anterior chamber is very shallow/flat

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Clinical features of absolute glaucoma

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

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Management of absolute glaucoma

? Cycloablation/destruction of the secretory

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ciliary epithelium

q Cyclophotocoagulation
q Cyclocryotherapy
q Cyclodiathermy

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? Rarely
? Retrobulbar alcohol injection
? Enucleation of eyeball

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Complications

? Corneal ulceration
? Staphyloma formation (Ciliary/Equatorial)

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? Atrophic bulbi (Shrunken eye)

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Conclusion

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? Primary angle closure glaucoma is a

potentially sight threatening condition,

characterized by occludable anterior chamber

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angles.

? Obstruction of aqueous outflow results in rise

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of intra ocular pressure, optic nerve damage

and visual field defects.

? Management may include medical, laser

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and/or surgical modalities.

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