Lecture on Primary Open Angle Glaucoma For 4th Year MBBS Undergraduate Students By Prof. Dr. Hussain Ahmad Khaqan

1. Primary Open Angle Glaucoma
Prof. Dr. Hussain Ahmad Khaqan
 MD
 FRCS(Glasgow)
 FCPS(Ophth.)
 FCPS(Vitreo Retina)
 MHPE (KMU)
 CICO(UK)
 CMT(UOL)
 Fellowship in Medical Retina (LMU, Munich)
 Fellowship in Vitreo Retinal Surgery (LMU, Munich)
 Consultant Ophthalmologist & Retinal Surgeon
Professor of Ophthalmology
Lahore General Hospital, Lahore
Ameer Ud Din Medical College, Lahore
Post Graduate Medical Institute, Lahore
Shaukat Khanum Memorial Cancer Hospital & Research Centre ,Lahore

2. DEFINITION
• Age-related optic neuropathy characterized by
progressive optic nerve cupping, visual deficit
and gonioscopically open angles.

3. SYMPTOMS
• Usually asymptomatic until the later stages.
• Visual field defects.
• Tunnel vision and loss of central fixation typically do
not occur until late in the disease.
• Rarely, eye ache and haloes.

4. SIGNS CONTINUE..
• Intraocular pressure (IOP): IOP >21mmhg, often with
high diurnal variability.
• Gonioscopy: Normal-appearing, open anterior
chamber angle on gonioscopic evaluation. No
peripheral anterior synechiae (PAS).
• Transient corneal oedema.
• Disc changes
• Visual Field defects

5. Disc Hemorrhage
Figure: Optic nerve abnormalities Figure: Gonioscopy demonstrates open angle.

6. CAUSES
• Inflammatory
• Exfoliative
• Pigmentary
• Steroid-induced
• Angle recession
• Traumatic (as a result of direct injury, blood, or
debris)
• Episcleral venous pressure

7. RISK FACTORS
• The risk rises with IOP, increasing significantly at pressures over 24
mm Hg, and especially over 30 mm Hg.
• Age: increasing age (uncommon <40y).
• Ethnicity: African-Caribbean—more frequent, younger onset, more
severe.
• Central corneal thickness
• Diabetes
• Myopia (the disc is said to be more vulnerable due to the scleral
canal morphology).
• Hypertension or hypotension
• Family history: first-degree relative confers 1 in 8 risk; higher in
siblings.
• Steroid-induced IOP elevation: more common in primary open
angle glaucoma (POAG) and those with family history of primary
open angle glaucoma (POAG)

8. DIFFERENTIAL DIAGNOSIS
• Ocular hypertension: Normal optic nerve and visual field.
• Physiological optic nerve cupping
• Secondary open angle glaucoma
• Low tension glaucoma
• Optic atrophy
• Congenital optic nerve defects (e.g. , tilted discs, colobomas,
optic nerve pits)
• Optic nerve drusen

9. INVESTIGATIONS
• Complete ocular examination including visual acuity, pupillary
assessment.
• Baseline documentation of the optic nerves. May include
meticulous drawings, stereoscopic disc photos.
• Formal visual field testing (e.g. ,Humphrey automated visual
field/ Goldmann visual field tests).
• Measure central corneal thickness (CCT).
• Consider other laboratory work-up if required

10. TREATMENT
• Rigorous IOP-lowering commonly achieved with:
1. Medications
2. Laser: Argon laser trabeculoplasty (ALT) and selective
laser trabeculoplasty [SLT]
3. Glaucoma surgery.

11. MEDICATION
• Prostaglandin agonists (e.g. , latanoprost 0.005% q.h.s. , bimatoprost
0.01% or 0.03% q.h.s. , travoprost 0.004% q.h.s. , tafluprost 0.0015%
q.h.s.
• Beta-blockers (e.g., levobunolol or timolol 0.25% to 0.5% daily or b.i.d.)
• Selective α2-receptor agonists (brimonidine 0.1%, 0.15%, or 0.2% b.i.d. to
t.i.d.)
• Apraclonidine 0.5% or 1% may be used for short-term therapy (3 months)
• Topical carbonic anhydrase inhibitors (CAIs) (e.g. , dorzolamide 2% or
brinzolamide 1% b.i.d. to t.i.d.)
• Miotics (e.g. , pilocarpine q.i.d.)
• Sympathomimetic (dipivefrin 0.1% b.i.d. or epinephrine 0.5% to 2.0%
b.i.d.)
• Systemic carbonic anhydrase inhibitors (CAIs) (e.g. , methazolamide 25 to
50 mg p.o. b.i.d. to t.i.d. , acetazolamide 125 to 250 mg p.o. b.i.d. to
q.i.d. , or acetazolamide 500 mg sequel p.o. b.i.d.).