Presentation 2018

1. Primary Angle-
Closure Glaucoma
Presenter: Dr.Akhilesh Shrestha
Nepal Medical College
Jorpati,Attarkhel
Roll no:1590

2. Introduction
• Apposition of peripheral iris against the
trabecular meshwork>Closure of narrow angle
of anterior chamber>Obstruction Of Aqueous
Outflow
• Major cause of world glaucoma blindness is
PACG.
• Ophthalmic Emergency

3. Etiology
Predisposing
Factor
Anatomical
Factors
General Factors
Precipitating
Factor
Dim
illumination
Emotional
stress
Use of
Mydriatic drugs

4. Predisposing Factor
Anatomical Factor General Factor
1. Hypermetropic eyes with shallow
anterior chamber.
1.Age:common in 5th decade of life
2. Eyes in which iris-lens diaphragm is
placed anteriorly.
2.Sex: M:F=1:4
3. Eyes with narrow angle of anterior
chamber.
3. Personality: common in nervous
individuals with unstable vasomotor
system
4. Plateau iris configuration. 4. Season: Rainy
5. Family history: Believed to be inherited
6. Race: Caucasians=Accounts for about 6% of
all glaucomas and presents in 6th to 7th decade
Asians: Presents in the 5th to 6th decade and
accounts for 50% of primary adult glaucoma
More common in South-East Asians, Chinese
and Eskimos
Uncommon in Blacks

5. Pathogenesis
Pupillary
block
Mechanism-
70%
Phacomorphic
Mechanism-
20%
Plateau Iris
configuration
& Syndrome-
10%

6. Pupillary Block Mechanism
• Precipitating Factors: Consists Physiological Mydriasis,
Pharmacological Mydriasis/Miosis, Valsavla Manoevure
• Mydriasis:
Precipitating Factor>Mid Dilation of Pupil>apposition
between iris and lens>Relative Pupil Block>Aqueous
Collects in posterior chamber>Aqueous pushes peripheral
iris forming Iris Bombe result in Appositional Angle Closure
d/t Iridocorneal Contact>Further increase in pressure
converts to Synechial Angle Closure
• Miosis:
Constrict Ciliary Muscle > Zonules get relaxed > Lens
moves forward

7. Plateau Iris configuration And
Syndrome
• Plateau Iris configuration: Anterior chamber
angle is closed by pushing mechanism because of
the anterior positioned ciliary processes
displacing the peripheral iris anteriorly. Treated
By Iridotomy.
• Plateau Iris Syndrome: Occurs when acute angle
closure glaucoma occurs either spontaneously or
after pharmacological dilation inspite of
iridotomy. Treated by miotics and laser peripheral
iridoplasty.

8. Phacomorphic Mechanism
• Abnornal Lens causes
-Pupillary Block
-Push peripheral iris forward into angle
structures.

9. Classification Of Angle Closure
Glaucoma
(As per International society of Geographical and Epidemiological Ophthalmology)
• Primary Angle Closure Suspect
• Primary Angle Closure
- Acute - Sub-acute - Asymptomatic
• Primary Angle Closure Glaucoma

10. Primary Angle-Closure Suspect
• Symptoms: Absent and patient suspected on the basis of routine
ocular examination for other eye complaints, fellow eye present with
acute attack of PAC or Glaucoma screening programme.
• Signs:
1)Eclipse Sign: Decreased axial anterior chamber depth
2)Slit-Lamp Biomicroscopic Sign:
-Decreased axial anterior chamber depth
-Convex shaped iris lens diaphragm
-Close proximity of the iris to cornea in periphery
3)Van Herick Slit-Lamp Grading of the angle:Peripheral anterior
chamber depth is compared to the adjacent corneal thickness.
Grading
-Grade 4(Wide Open Angle):PACD=3/4 to 1CT
-Grade 3(Mild Narrow Angle):PACD=1/4 to 1/2CT
-Grade 2(Moderate Narrow Angle):PACD=1/4CT
-Grade 1(Extremely Narrow Angle):PACD<1/4CT
-Grade 0(Closed Angle):PACD=NIL

11. • Diagnostic Test(For confirmation)
-IOP measurement
-Goniscopy
-Ultrasonic Biomicroscopy
-Anterior Segment OCT
-Optic Disc Evaluation
-Visual Field Analysis
• Diagnostic Criteria
-Goniscopy: Irido-trabecular contact= >270 angle and no
peripheral synechia.
-IOP: Normal
-Optic Disc: No Glaucomatous Change
-Visual Field: Normal
• Impression: Angle at risk

12. MANAGEMENT
• Provocative Test: Not used currently
• Treatment:
-Prophylactic Laser Iridotomy: If Irido-trabecular
contact >270(Gonioscopy). If untreated rate of
conversion to PACG in next 5 years in 50%.
-Periodic Follow Up: Follow periodically and
educated about symptoms.

13. Primary Angle Closure
• Diagnostic Criteria
-Irido-trabecular contact: >270
-IOP elevated and/or Peripheral anterior
synechiae present
-Optic Disc: Normal
-Visual Field: Normal
• Impression: Angle is abnormal in i.e Function
(Elevated IOP)or structure(PAS+)
• Types:
-Acute - Sub-acute -Chronic

14. Sub-Acute Primary
Angle Closure
Acute Primary Angle
Closure
Symptoms -U/L Transient Blurring of Vision
few min to 1-2 hours
-Colored halos
-Headache
-Browache and eyeache on
affected eye.
-Attacks may self terminate d/t
physiological miosis.(Bright light,
sleep etc.)
-Recurrent attacks are not
uncommon but between attacks
patient is normal
-Pain:Acute attack characterized by
sudden onset of very severe pain,
radiates along branch of 5th Cranial
Nerve
-Nausea, vomiting and prostration a/w
pain
-Rapidly progressive impairment of
vision, redness, photophobia and
lacrimation develops in all cases
-5% patient give past history.

15. Sub-Acute Primary
Angle Closure
Acute Primary Angle Closure
Signs Eye is usually white and not
congested
-Transient rise of IOP: 40-50
mm Hg for 1-2 hours.
-Lids: Edematous
-Conjunctiva: Chemosed & congested
-Cornea: Edematous & insensitive
-Anterior Chamber: Very Shallow with aqueous
flare or cells.
-Angle of anterior Chamber: Grade 0
-Iris: Discolored
-Pupil: Semi-dilated,fixed and non-reactive to light
and accomodation.
-IOP: raised(40-70mm hg)
-Optic Disc: Edematous and hyperaemic
-Fellow eye: shallow anterior chamber and
occludable angle

16. Treatment of Sub-Acute Primary Angle
Closure
• Peripheral Laser Iridotomy

17. Treatment of Acute Primary Angle Closure
Immediate Medical therapy
to lower IOP
Definitive Therapy Prophlaxis of fellow eye
1)Systemic Hyperosmotics if
IOP>40mmHg
-IV mannitol(1gm/kg body
weight)-if nausea& vomit(+)
-Oral Hyperosmotics:
Glycerol+lemon juice
1)Laser Peripheral Iridotomy:
Done if <270
Prophylactic laser iridotomy or
surgical peripheral iridotomy
should be done ASAP as
chance of acute attack is 50%.
2)Systemic Carbonic
anhydrase Inhibitor
-Acetazolamide 500mg iv stat
followed by 250 mg tab TDS
2)Filtration Surgery: Done if
ITA>270 after max medical
therapy or if peripheral
iridotomy is not effective.
3)Topical antiglaucoma drugs
-B-blocker: 0.5% timolol
-PG analogue: latanoprost
-etc
3)Clear Lens Extraction By
Phacoemuslification with
intraocular lens implantation
4)Analgesics, antiemetics,
compressive goinoscopy
Long term glaucoma surveillance and IOP management to
prevent glaucomatous blindness. Eye treated with PI may
develop PACG or Filtration Surgery may fail5)Steroid:To reduce
Inflamation

18. Sequelae of Acute PAC
• Postsurgical acute PAC: Status after PI surgery
1)Normalized IOP: Eye quietens +/- marks of
acute attack
2)Raised IOP: Surgery Unsuccessful then treated
with Trabeculectomy.
• Spontaneous Angle Reopening: May occur in some
case. Treatment of choice: Laser PI
• Ciliary Body Shut Down
• Vogt’s Triad: Glaukomflecken
Patches of iris atrophy
Slightly dilated non-reacting pupil

19. Primary Angle Closure Glaucoma
• Considered Analogous to Chronic Primary Angle Closure Glaucoma
• Results d/t gradual synechial closure of the angle of anterior
chamber
• Presence of Optic Disc changes and field changes
• Diveded into Acute/Sub-acute/Chronic
• Acute/Sub-Acute similar features as in PAC
• Symptoms of Chronic PACG:
IOP: raised constantly
Eyeball: No congestion and painless
Optic Disc: Glaucomatous Cupping
Visual Field Defect: Same as POAG
Gonioscopy: >270 angle closure with PAS

20. • Diagnostic Criteria
1)Irido-Trabecular Contact: >270
2)PAS are formed
3)IOP: Elevated
4)Optic Disc: Glaucomatous Damage
5)Visual Field: Same as POAG
• Impression: Angle is abnormal in function(elevated IOP) and
structure (PAS+ve)
• Treatment
1)Laser Iridotomy +/- medical therapy initially
2)Trabeculectomy: Done if above treatment fails to control IOP
3)Prophylactic Iridotomy: Done in fellow eye

21. Absolute Primary Angle Closure
Glaucoma
• PACG if untreated enters the final phase of Absolute PACG.
• C/F:
1)Painful blind eye: Eye is painful, irritable and completely blind.
2)Peri-limbal Reddish Blue Zone with slight ciliary flush around
cornea
3)Caput Medusae: few seen in long standing cases.
4)Cornea: Early: Insensitive > Slowly turns hazy > may develop
epithelial bullae or filaments.
5)Anterior Chamber: Shallow
6)Iris: Atrophic
7)Pupil: Fixed and dilated
8)Optic Disc: Glaucomatous Optic Atrophy
9)IOP: High(Eyeball is tony hard)

22. Management
• Retrobulbar Alcohol Injection: Relives pain
1ml of 2% Xylocaine injected followed by 1ml
of 80% alcohol 5-10 min.It destroys the ciliary
ganglion
• Destruction of secretary ciliary epithelium:
Done via cyclotherapy or cyclodiathermy or
cyclocoagulation.
• Enucleation: Done when pain is not relived by
conservative method.

23. Complication
• Corneal Ulceration: d/t prolonged edema and
insensitivity.
• Stapyhloma Formation: Raised IOP= Sclera
becomes very thin and atrophic and bulges
out later in ciliary region or equatorial region.
• Atropic Bulbi: Later Ciliary body degenerates,
IOP falls and eyeball shrinks.