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

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Ophthalmology PPT 44 Primary Angle Closure Glaucoma 1 Lecture Notes




Department of

Ophthalmology



Objectives

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

to :

? Define primary angle closure glaucoma.

? Understand the pathophysiology and the risk

factors.

? Be able to classify primary angle closure

glaucoma.

? Understand the fundamentals of managing

primary angle closure glaucoma


DEFINITION

? Primary angle closure glaucoma is a type of

primary glaucoma(with no obvious systemic or

ocular cause) characterized by

occludable/closed angles leading to

obstruction of aqueous outflow resulting in

rise of intra ocular pressure, optic nerve

damage and visual field defects.

ANGLE OF ANTERIOR CHAMBER

? STRUCTURES

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




DRAINAGE OF AQUEOUS HUMOR

PRIMARY ANGLE CLOSURE

GLAUCOMA

EPIDEMIOLOGY

? PACG is the major cause of glaucoma blindness

worldwide.

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

? Gender :- F > M, 4 : 1

? Race :-seen commonly in South-East Asian

population, Chinese and Eskimos

? Heredity :- mostly sporadic but may be inherited

AD/AR

? first degree relatives are at increased risk.

? Refractive error :- more common in

hypermetropes
Ocular risk factors

1. Shallow anterior chamber both

centrally and peripherally.

2. Decreased anterior chamber volume.

3. Short axial length of the globe.

4. Small corneal diameter.

Ocular risk factors

5.Decreased posterior corneal radius of

curvature

6.Anterior position of the lens with respect to

the ciliary body.

7.Increased curvature of the anterior surface &

thickness of lens


PATHOGENESIS

? It is incompletely understood.

? 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

lens or microspherophakia))

? 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

iris rests posteriorly on the anterior lens capsule.

Anterior Iris Bowing

Simultaneous dilatation of the pupil renders the peripheral

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

Posterior Chamber to increase & peripheral iris bows

anteriorly


Iridocorneal contact

Eventually the iris touches the posterior corneal surface,

obstructing the angle and the IOP rises.

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

Precipitating factors

1. Factors that produce mydriasis

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

? Mydriatic agents :

? cyclopentolate, tropicamide, atropine, homatropine.

? Antipsychotic agents

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

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

? Antiparkinsonian agents : Trihexyphenidryl

? Antispasmolytics : Propantheline ,Dicyclomine

? Sympathomimetic agents : Adrenaline (epinephrine),

ephedrine, phenylephrine.


CLASSIFICATION

A. Primary angle-closure disease

? Irido-trabecular contact is the final common pathway of

angle closure disease, obstructing aqueous outflow

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

Angle closure suspect
Intermittent (sub acute) angle closure
Acute angle closure
Chronic angle closure
Absolute angle closure
New classification of PACG

qPrimary angle closure suspect/PACS

Has occludable/narrow angles
qPrimary angle closure/PAC

Has occludable/narrow angles +

High IOP/Peripheral anterior synechiae/

Excessive trabecular meshwork

pigmentation
qPrimary angle-closure glaucoma/PACG

PAC+ Optic disc changes+ Visual field

defects

Gonioscopic grading of Angle

closure

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

Scheie's.

? Shaffer's grading

Grade Angle width configuration

Chances of

Structures visible

closure

IV

35?-45?

Wide open

Nil

SL,TM,SS,CBB

I I

20?-35?

Open angle

Nil

SL,TM,SS

I

20?

Moderately open Possible

SL,TM

I

10?

Very narrow

Highly likely

SL only

0

0?

Closed

Closed

None


---------
Grade
IV

II

II

I
0

Van Herrick's grading


Tests for Angle closure

? Eclipse test : uses flash light to make a rough

assessment of angle depth

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

than 8mm Hg after one hour suggests PAC

?Mydriatic provocative test: Not preferred now

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

Glaucomatous halos remain intact , whereas

halos due to cataract are broken up into segments



PRIMARY ANGLE CLOSURE GLAUCOMA SUSPECT

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

an anatomically predisposed

eye.

? Symptoms :- absent
? Signs :

? Axial AC depth is < normal

& iris lens diaphragm is

convex

? Close proximity of the iris

to the cornea

? Gonioscopy :- occludable

angle(grade 1 or 0)

without indentation in at

least 3 quadrants.


?Clinical course without

treatment may be:

IOP may remain normal

Acute or sub acute angle

closure may ensue

Chronic angle closure may

develop, without acute or

sub acute stages.

? Treatment
? 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:-

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

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

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


INTERMITTENT(SUBACUTE)PRIMARY ANGLE CLOSURE

GLAUCOMA

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

any recognizable symptoms.

? Occurs in a predisposed eye with an occludable angle in

association with intermittent pupillary block.

? Precipitating factors :- physiological mydriasis , or

physiological shallowing of AC when patient assumes a

prone or semi prone position ;emotional stress.

? Symptoms

? Characteristic h/o transient blurring of vision with haloes

around lights

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

physiological miosis.

? Signs

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

narrow.

? Clinical course

? Without treatment is variable

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

? Treatment:- Prophylactic laser PeripheraI Iridotomy(PI)


ACUTE PRIMARY ANGLE CLOSURE GLAUCOMA

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

closure of the angle.

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

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

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

? IOP > 21 mmHg plus three of the following

findings:

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

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

pupil

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

decreased axoplasmic outflow)

? Constricted visual fields

? MANAGEMENT

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

attack-- main priorities.

? A. Immediate medical treatment

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

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

contraindications)

3.Topical

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

Timolol (if there is no contraindication).

4. Analgesia and emetics as required.


? B. Subsequent medical treatment

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%)

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

Timolol 0.5% b.d.,

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

glycerol.

? Surgical options in resistant cases include lens extraction,

goniosynechiolysis, trabeculectomy and cycloablation.

? Findings suggestive of previous episodes of acute

angle closure glaucoma

? Descemets Membrane folds

? Fine pigment granules on corneal endothelium

? Peripheral anterior synechiae

? Posterior synechiae

? Glaucomflecken

? Sectoral/generalized iris atrophy

? Fixed and semi dilated pupil

? Optic nerve cupping &/or pallor

? Gonioscopy shows narrow angle

or PAS

? Visual field loss
Chronic angle closure glaucoma

? Visual Acuity is normal unless damage is

advanced.

? Anterior chamber is shal ower in pupil ary

block than non-pupil ary block.

? Optic nerve signs depend on severity of

damage.

? IOP elevation may be only intermittent.

? Gonioscopic abnormalities-Peripheral

Anterior Synechiae, narrow angle,

pigmentation of Schwalbe's line.

Treatment of chronic angle closure

? Medical treatment is similar to that of POAG

? Prostaglandin/Prostamides

Latanoprost, Bimatoprost, Travoprost

? Beta blockers

Timolol maleate, Betaxolol

? Carbonic anhydrase inhibitors

Dorzolamide, Brinzolamide

? Sympathomimetics

Brimonidine, Apraclonidine

? Parasmpathomimetics

Pilocarpine

? Oral carbonic anhydrase inhibitors

Acetazolamide, Methazolamide


Treatment of chronic angle closure

? Laser Peripheral Iridotomy (PI) in affected eye

along with Prophylactic PI in fellow eye

Laser Peripheral Iridotomy

? Complications of laser therapy
1. Bleeding
2. IOP elevation
3. Iritis
4. Corneal burns
5. Lens opacities
6. Glare and diplopia
? Surgical treatment

Trabeculectomy (filtering surgery) is the

surgical procedure of choice

? Success:- 87- 100 % with multiple operations

? Complications:-

? Flat AC, hypotony

? Bleb related infections

? Cyclodialysis

? PATIENTS REQUIRE REGULAR AND LIFE LONG

FOLLOW UP

Absolute glaucoma

? Is the final/last stage of PACG

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

anterior ciliary veins

?Cornea gradually becomes hazy, insensitive

with bullous keratopathy and filamentary

keratitis

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

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

Management of absolute glaucoma

? Cycloablation/destruction of the secretory

ciliary epithelium

q Cyclophotocoagulation
q Cyclocryotherapy
q Cyclodiathermy
? Rarely
? Retrobulbar alcohol injection
? Enucleation of eyeball
Complications

? Corneal ulceration
? Staphyloma formation (Ciliary/Equatorial)
? Atrophic bulbi (Shrunken eye)

Conclusion

? Primary angle closure glaucoma is a

potentially sight threatening condition,

characterized by occludable anterior chamber

angles.

? Obstruction of aqueous outflow results in rise

of intra ocular pressure, optic nerve damage

and visual field defects.

? Management may include medical, laser

and/or surgical modalities.

This post was last modified on 07 April 2022