Presentation on Primary Angle Closure Glaucoma

1. PRIMARY ANGLE CLOSURE
GLAUCOMA
SARAL LAMICHHANE
MBBS IV Year/Roll-61

2. Introduction
Glaucoma refers to a group of disorders
characterized by progressive optic neuropathy
resulting to characteristic visual field defects;
raised Intraocular Pressure(IOP) being the most
important risk factor.
 Normal Tension Glaucoma(NTG/LTG) also exist
 Normal IOP = 10 – 21 mmHg
(Mean: 162.5 mmHg)

3. Classification:
1) Congenital & Developmental Glaucoma
2) Primary Adult Glaucoma:
(No obvious systemic/ocular cause of rise in IOP)
a) Primary Open Angle Glaucoma (POAG)
b) Primary Angle Closure Glaucoma (PACG)
c) Primary Mixed Mechanism Glaucoma
3) Secondary Glaucoma:
(Rise of IOP with some primary ocular or systemic disease)

4. Primary Angle Closure Glaucoma
Primary glaucoma in which rise in Intraocular
Pressure (IOP) occurs due to blockage of aqueous
humor outflow by closure or narrower angle of
the anterior chamber.
Predisposing Risk Factors:
1) Anatomic Factors:
- Hyperopic eye
- Iris-lens diaphragm placed anteriorly
- Narrow angle of anterior chamber
- Plateau Iris Configuration

5. 2) General Factors:
- Age: 5th Decade onwards
- Sex: Females > Males
- Rainy Season
- Family History
- Race (Caucasians, South East Asians)
- Heredity: Family history
Precipitating factors:
- Dim illumination
- Emotional Stress
- Use of mydriatics: Atropine, Tropicamide, Cyclopentolate

8. • Aqueous humor secretion from Non-pigmented
epithelium of Ciliary processes Posterior Chamber
Pupil Anterior Chamber:
• Conventional (Trabecular) Pathway: 90%
Trabecular Meshwork Canal of Schlemm
Collector Channels Episcleral Vessels
• Uveoscleral Pathway:
Trabecular Meshwork Ciliary body
Suprachoroidal space Venous Drainage

9. Mechanism:
 Relative Pupil Block
- Iris bombe formation
- Appositional Angle Closure
- Synechial angle closure
Plateau Iris Configuration
- Anteriorly positioned ciliary
displacing the iris anteriorly
Phacomorphic mechanism
- Abnormal lens

10. Symptoms:
• Eye redness
• Eyeache
• Headache
• Nausea/Vomiting
• Blurring of vision
• Colored halos
Signs:
• Circumcorneal congestion
• Corneal edema, hazy cornea
• Very shallow anterior chamber
(Eclipse Sign)
• Iridocorneal angle closure as
seen in gonioscopy
• Raised Intraocular pressure
• Reduced visual acuity
• Vertically oval & mid-dilated
pupil

11. Progression
 Primary Angle Closure Suspect:
• No clinical signs/symptoms
• Irido-trabecular contact in greater than 2700
• Intraocular Pressure (IOP) Normal
• No Peripheral Anterior Synechiae (PAS)
• Optic disc & Visual Field Normal

12. Angle Closure:
• Irido-trabecular contact in greater than 2700
• Mild clinical symptoms/signs
• IOP may or may not be raised
• PAS may or may not be present
• Optic disc & Visual Field Normal

13. Acute Angle Closure:
• Typical clinical symptoms/signs present
• Irido-trabecular contact greater than 2700
• IOP raised
• PAS present
• Optic disc & Visual field normal

14. Angle Closure Glaucoma:
• Typical clinical symptoms/signs present
• Irido-trabecular contact greater than 2700
• IOP raised, PAS formed
• Optic Nerve shows glaucomatous damage
• Characteristic visual field defect

15. Optic Nerve Changes
• Glaucomatous cupping:
Increase in Cup : Disc ratio  0.6
Normal CDR = 0.3-0.4
• Cup Asymmetry:
CDR difference > 0.2 in two eyes
• Neuroretinal rim thinning: Cup to Disc distance
ISNT Rule- Thickness of Inferior rim> Superior rim
> Nasal rim> Temporal rim
Thinning usually in same sequence

19. • Bayonetting Sign:
Z shaped bending of vessels at the margin
• Disc hemorrhages: flame shaped
• Lamellar dot sign: pores in lamina cribrosa slit
shaped & visible upto disc margin
• Peripapillary chorioretinal atrophy

22. Visual Field Defect
• Isopter contraction
• Baring of blind spot
• Paracentral Scotoma
• Siedel’s Scotoma
• Superior Arcuate or Bjerrum’s Scotoma
• Inferior Arcuate or Bjerrum’s Scotoma
• Ring or Double Arcuate Scotoma
• Roenne’s central nasal step
• Tubular Vision

26. Diagnosis
• History: Symptoms
• Clinical Examination: Signs
• Diagnostic tests:
–Tonometry: IOP measurement
–Gonioscopy: Angle structures
–Slit lamp biomicroscopy
–Ultrasonic biomicroscopy
–Fundoscopy
–Visual Field Analysis

27. Management
Principle:
Immediate medical therapy (Lower IOP)
Definitive treatment
Prophylaxis of fellow eye
Long term glaucoma surveillance and IOP
management of both eyes

28. Immediate medical therapy:
• Intravenous line access
• Systemic hyperosmotic agents:
Mannitol 20% iv 1g/kg within 30-45 mins
Glycerol oral 1g/kg of 50% solution in lemon juice
• Systemic Carbonic Anhydrase Inhibitors:
Acetazolamide 500mg oral stat followed by 250 mg tds
• Analgesics/Antiemetics

29. • Topical Antiglaucoma medication:
Beta- Blockers:
Timolol 0.5%, Betaxolol 0.5%, Levobunalol 0.5%
Prostaglandin analogue:
Latanoprost (0.005%), Bimatoprost
Alpha-1 Adrenergic agonist:
Brimonidine (0.1-0.2%)
Pilocarpine 2% qid after 1 hour
• Steroid eye drops: Anti inflammatory

30. Definitive treatment:
Peripheral iridotomy
LASER Iridotomy
Trabeculectomy (Filtration Surgery)
Fellow Eye Prophylaxis:
Pilocarpine eye drops 1drop QID
Prophylactic LASER Iridotomy

33. Take home message…..
 Glaucoma as a disease affecting optic nerve,
Raised IOP as a risk factor only.
 Pupillary block mechanism of PACG.
4 stages of progression: PACS, AC, AAC, PACG.
Optic Nerve Damage & Visual Field Defects must
be present in PACG.
Immediate therapy with Mannitol and Topical
Antiglaucoma: B-blockers, PG Analog, Pilocarpine
Definitive treatment- Iridotomy, Trabeculectomy

34. Thank You!!!!