PRIMARY ANGLE CLOSURE
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GLAUCOMAAcknowledgement
? Kanski's Clinical Ophthalmology (8th Edition).
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? Becker- Schaffer's Diagnosis and therapy ofThe Glaucomas (8th Edition).
? Comprehensive Ophthalmology (A.K.Khurana)
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(7th Edition).2
Learning Objectives
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? At the end of this class the students shal be ableto :
? 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 closureglaucoma.
? Understand the fundamentals of managing
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primary angle closure glaucoma
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Question? Which of the following medications is least
likely to be associated with the induction or
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aggravation of angle-closure glaucoma?
? a. pilocarpine.
? b. oral antihistamines.
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? c. cyclopentolate.? d. aspirin
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DEFINITION
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? Primary angle closure glaucoma is a type of
primary glaucoma(with no obvious systemic or
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ocular cause) characterized byoccludable/closed angles leading to
obstruction of aqueous outflow resulting in
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rise of intra ocular pressure, optic nerve
damage and visual field defects.
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5Video on applanation tonometry
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ANGLE OF ANTERIOR CHAMBER
? STRUCTURES
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? Schwalbe's line
? Trabecular meshwork
? Scleral spur
? Ciliary body band
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? Root of iris7
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
? Race :-seen commonly in South-East Asian
population, Chinese and Eskimos
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? Heredity :- Mostly sporadic
? 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
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volume.3. Short axial length of the globe.
4. Small corneal diameter.
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Ocular risk factors
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5.Decreased posterior corneal radius ofcurvature
6.Anterior position of the lens with respect to
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the ciliary body.
7.Increased curvature of the anterior surface &
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thickness of lens12
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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 anterior
chamber due to physiological degree of resistance at the pupil ,since the
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iris rests posteriorly on the anterior lens capsule.13
Anterior Iris Bowing
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Simultaneous dilatation of the pupil renders the peripheral
iris more flaccid. The pupil block causes the pressure in the
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Posterior Chamber to increase & peripheral iris bowsanteriorly
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Iridocorneal contact
Eventually the iris touches the posterior corneal surface,
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obstructing the angle and the IOP rises.
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Precipitating factorsFactors that produce mydriasis
? Dim illumination
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? Emotional stress(due to increased sympathetic tone)? Drugs
? Mydriatic agents :
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? cyclopentolate, tropicamide, atropine, homatropine.? Antipsychotic agents
? Phenothiazines: e.g., perphenazine ,fluphenazine
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? Anticonvulsants e.g., Topiramate16
? Antidepressants
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? Tricyclic agents: amitriptylene ,imipramine? Non-tricyclic agents: fluoxetine
? Antiparkinsonian agents : Trihexyphenidryl
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? Antispasmolytics : Propantheline ,Dicyclomine? Sympathomimetic agents : Adrenaline (epinephrine),
ephedrine, phenylephrine.
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CLASSIFICATION
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A. Primary angle-closure disease
? Irido-trabecular contact is the final common pathway of
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angle closure disease, obstructing aqueous outflow1. New classification
Primary angle closure suspect/PACS
Primary angle closure/PAC
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Primary angle-closure glaucoma/PACG2. Old classification
Angle closure suspect
Intermittent (sub acute) angle closure
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Acute angle closureChronic angle closure
Absolute angle closure
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New classification of PACGqPrimary angle closure suspect/PACS
Has occludable/narrow angles
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qPrimary angle closure/PACHas 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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19Gonioscopic grading of Angle
closure
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? Several grading systems :- Shaffer's, Spaeth's,
Scheie's.
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? Shaffer's gradingGrade Angle width configuration
Chances of
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Structures visible
closure
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IV35?-45?
Wide open
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Nil
SL,TM,SS,CBB
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I I20?-35?
Open angle
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Nil
SL,TM,SS
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I20?
Moderately open Possible
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SL,TM
I
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10?Very narrow
Highly likely
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SL only
0
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0?Closed
Closed
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None
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---------
Grade
IV
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IIII
I
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021
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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qFincham's Test: Also known as stenopaeic-slit test.Glaucomatous halos remain intact , whereas
halos due to cataract are broken up into segments
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PRIMARY ANGLE CLOSURE GLAUCOMA SUSPECT
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? Also known as Latent PACG
? Essentially, the term implies
an anatomically predisposed
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eye.
? Symptoms :- absent
? Signs :
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? Axial AC depth is < normal
& iris lens diaphragm is
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convex? Close proximity of the iris
to the cornea
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? Gonioscopy :- occludable
angle(grade 1 or 0)
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without indentation in atleast 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 ensueChronic 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
fellow eye should undergo prophylactic peripheral laser
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iridotomy (Laser PI)? If both eyes have occludable angles, laser PI may be done
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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
prone or semi prone position ;emotional stress.
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INTERMITTENT(SUBACUTE)PRIMARY ANGLE
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CLOSURE GLAUCOMA? 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
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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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INTERMITTENT(SUBACUTE)PRIMARY ANGLECLOSURE GLAUCOMA
? Clinical course
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? Without treatment is variable
? Some eyes develop an acute attack
? Others chronic angle closure
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? 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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30Findings during an acute attack of angle-closure glaucoma
? Two of the following symptom sets:
? Periorbital or ocular pain
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? Diminished vision? Specific history of rainbow haloes with blurred vision
? IOP > 21 mmHg plus three of the following
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findings:? Ciliary flush (perilimbal conjunctival hyperemia)
? Corneal edema (epithelial,stromal)
? Shallow anterior chamber
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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 fields32
? MANAGEMENT
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? Patient comfort ,lowering of the IOP and to break acuteattack-- 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
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fellow eye.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.
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? If the above measures fail:? Laser iridotomy or iridoplasty after clearing corneal oedema with
glycerol.
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? Surgery in resistant cases.
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? Findings suggestive of previous episodes of acute
angle closure glaucoma
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? Fine pigment granules on corneal endothelium? Peripheral anterior synechiae
? Posterior synechiae
? Glaucomflecken
? Sectoral/generalized iris atrophy
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? Fixed and semi dilated pupil35
Findings suggestive of previous episodes of
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acute angle closure glaucoma
? Optic nerve cupping &/or pallor
? Gonioscopy shows narrow angle or PAS
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? Visual field loss36
Chronic angle closure glaucoma
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? Visual Acuity is normal unless damage isadvanced.
? Anterior chamber is shal ower in pupil ary block
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than non-pupil ary block.
? Optic nerve signs depend on severity of 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
? Prostaglandin/Prostamides
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Latanoprost, Bimatoprost, Travoprost? Beta blockers
Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors
Dorzolamide, Brinzolamide
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Treatment of chronic angle closure
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? Sympathomimetics
Brimonidine, Apraclonidine
? 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
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along with Prophylactic PI in fellow eye40
Laser Peripheral Iridotomy
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? Complications of laser therapy1. Bleeding
2. IOP elevation
3. Iritis
4. Corneal burns
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5. Lens opacities6. Glare and diplopia
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? Surgical treatmentTrabeculectomy (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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42Absolute 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, insensitivewith bullous keratopathy
?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
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?High IOP
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Management of absolute glaucoma
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? Cycloablation/destruction of the secretory
ciliary epithelium
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q Cyclophotocoagulationq Cyclocryotherapy
q Cyclodiathermy
? Rarely
? Retrobulbar alcohol injection
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? Enucleation of eyeball45
Complications
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? Corneal ulceration
? Staphyloma formation (Ciliary/Equatorial)
? Atrophic bulbi (Shrunken eye)
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46Conclusion
? Primary angle closure glaucoma is a
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potentially sight threatening condition,characterized by occludable anterior chamber
angles.
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? 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
and/or surgical modalities.
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Question
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? Primary angle closure glaucoma occurs mostcommonly in patients with shallow anterior
chambers. Among the following, which does
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NOT contribute to a shallow anterior
chamber?
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? A) Mature lens? B) Hyperopia
? C) Ocular hypertension
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? D) Iris bomb?
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Question
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? With respect to angle-closure glaucoma, which of the
fol owing is true?
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? a. Men are at increased risk.? b. The anterior chamber depth increases with age,
predisposing to pupillary-block- induced angle-closure
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glaucoma.? c. Primary angle-closure glaucoma may occur in eyes with
any type of refractive error.
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? d. Family history, while important in open-angle glaucoma,
does not play a role in angle-closure glaucoma.
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