This document discusses primary open-angle glaucoma (POAG), including its definition, risk factors, prevalence, characteristics, symptoms, signs, progression, evaluations methods, and treatment options. POAG is the most common type of glaucoma, has no known cause but may be genetic or due to poor circulation. Treatments include pharmaceutical options like beta-blockers, prostaglandins, and surgery. The goal of treatment is to lower intraocular pressure to prevent further optic nerve damage and vision loss.

1. • Classification Of Glaucoma
• Investigations and VF defects
• PACG

2. Primary Open Angle Glaucoma
POAG
Brig Junaid Afsar Khan
CMH LMC

3. Learning Objectives
By the end of this session the students will be able to
• Describe the clinical features of POAG
• Learn the treatment of POAG

4. DEFINITION
(Also called Chronic Simple Glaucoma)
Is a generally bilateral though not symmetrical disease,
characterized by:
• An adult Onset
• IOP > 21 mm of mmHg at some point
• Open Angle
• Glaucomatous Cupping
• Visual Field Loss

5. Open Angle Glaucoma
•Obstruction at the level of the trabecular
meshwork
• Progressive loss of visual field over
time from periphery to center
•Optic disc (‘cupping’) due to retinal
ganglion cell death
• Open anterior chamber angle
• Majority of patients have IOP > 21
mmHg, asymptomatic

8. AETIOLOGY
• Unknown, but may be genetic.
• Degenerative changes in the extracellular matrix
of the trabecular meshwork.
OR
• due to poor circulation that can produce chronic
ischemia to the Optic Nerve Head.

9. Open Angle Glaucoma
Aka: chronic simple glaucoma (CSG)
and primary open angle glaucoma (POAG)
Risk Factors
IOP Diabetes
Age Myopia
Race Gender
Family history Cardiovascular disease
Central corneal thickness

10. POAG: OTHER RISK FACTORS
Factor Relative Risk
Age >40) 2
African-American vs.
Caucasian
4
Family history (1° relative) 2–4
Myopia 1.5–3
Decreased corneal thickness 3
History of trauma
History of steroid use
Primary Open-Angle Glaucoma

11. POAG: PREVALENCE BY AGE, GENDER, AND
RACE
Primary Open-Angle Glaucoma

12. POAG: PREVALENCE RELATED TO AGE
Primary Open-Angle Glaucoma

13. Screening for POAG =
IOP measurements
+
Optic disc evaluation
+
Visual field testing
Primary Open-Angle Glaucoma

14. POAG: CHARACTERISTICS
• Most common type of glaucoma
• Bilateral but not always symmetric
• Characteristic optic nerve and visual field damage
• Adult onset
• Open, normal-appearing anterior chamber angles
• Absence of secondary causes
Types of Glaucoma

15. SYMPTOMS
Most patients are asymptomatic and unaware of any vision
problem
However…..

16. …in advanced disease, some patients may note :
• decreased vision
• variety of visual problems, such as with night driving,
• fluctuating vision with reading or close work, and while
going from brightly lit to dim environments

17. SIGNS
• Optic disc cupping and loss of retinal nerve fiber layer
• Visual field loss
• Afferent pupil defect
• Elevated intraocular pressure IOP

18. SIGNS…
• Measurement of IOP
(TONOMETRY)

19. POAG: PROGRESSION
• Asymptomatic in early stages
• Often marked visual loss has occurred when patient presents with
vision symptoms
• Can result in blindness
Types of Glaucoma

20. GLAUCOMA:
VISUAL FIELD CHANGES
• Nasal field loss
• Paracentral field loss
• Midperipheral field loss
Introduction

21. Primary Open-Angle Glaucoma
Pattern of retinal nerve fibers

22. Primary Open-Angle Glaucoma
C:D ratio = 0.3

23. Primary Open-Angle Glaucoma
Healthy neuroretinal rim

24. Primary Open-Angle Glaucoma
Thinning neuroretinal rim, elongated cup

25. Primary Open-Angle Glaucoma
Groove or wedge defect in nerve fiber layer

26. Primary Open-Angle Glaucoma
Healthy, symmetric optic nerves

27. Primary Open-Angle Glaucoma
C:D ratio = 0.9 C:D ratio = 0.7

28. Primary Open-Angle Glaucoma
Extensive glaucomatous damage

29. Primary Open-Angle Glaucoma
Flame-shaped disc hemorrhage

30. Year 1 Year 12
Primary Open-Angle Glaucoma
PROGRESSIVE NEURAL TISSUE LOSS

31. Primary Open-Angle Glaucoma
Evaluating optic disc

32. Confocal scanning laser
ophthalmoscopy
OPTICAL NERVE IMAGING: EXAMPLES
OF NEW TECHNOLOGIES
Primary Open-Angle Glaucoma
Optical coherence
tomography
Scanning laser
polarimetry

33. Primary Open-Angle Glaucoma
Automated perimetry

34. Primary Open-Angle Glaucoma
Normal visual field

35. Primary Open-Angle Glaucoma
Nasal visual field and midperipheral vision loss

36. Progression of glaucomatous cupping
a. Normal (c:d ratio 0.2)
b. Concentric enlargement
(c:d ratio 0.5)
c. Inferior expansion with
retinal nerve fibre loss
e. Advanced cupping with nasal
displacement of vessels
f. Total cupping with loss of
all retinal nerve fibres
d. Superior expansion with
retinal nerve fibre loss

37. Early visual field defects
• Small arcuate scotomas
• Tend to elongate circumferentially
• Isolated paracentral scotomas
• Nasal (Roenne) step

38. Progression of visual field defects
• Formation of arcuate defects
• Enlargement of nasal step
• Development of temporal wedge
• Peripheral breakthrough
• Appearance of fresh arcuate
inferior defects

39. Advanced visual field defects
• Development of ring scotoma • Peripheral and central spread
• Residual temporal island
• Residual central island

41. Visual field test results over time: progressive scotoma
Primary Open-Angle Glaucoma

44. TREATMENT OF PRIMARY
OPEN ANGLE GLAUCOMA

45. BASELINE EVALUATION
• VISUAL ACUITY AND REFRACTIVE STATE
• SLIT LAMP BIOMICROSCOPY
• APPLANATION TONOMETRY
• GONIOSCOPY
• OPHTHALMOSCOPY
• PERIMETRY

46. TREATMENT GOALS
• TARGET PRESSURE
• IOP LEVEL IDENTIFIED BELOW WHICH FURTHER
OPTIC DISC DAMAGE IS UNLIKELY
• MONITORING
• OPTIC NERVE
• VISUAL FIELDS

47. MODALITIES OF TREATMENT OF
POAG
• Pharmacological Treatment
• Non Pharmacological Treatment
- Surgical Management
- Role of Lasers
- Role of Cryotherapy

48. Anti Glaucoma Drugs
• Beta-blockers
• Sympathomimetics
• Miotics
• Prostaglandin Derivatives
• Carbonic Anhydrase Inhibitors
• Hyperosmotic Agents

49. SURGICAL MANAGEMENT

50. Filtration procedures
Partial thickness Full thic
Trabeculectomy

51. Decreased VA is the common symtom of POAG
True OR False
False
POAG is usually asymptomatic

52. Next Lecture
Secondary Glaucomas

53. Beta Blockers
• Non selective:
Equipotent to beta-1 and beta-2 receptors
• Cardioselective:
More potent at beta-1 than beta-2 receptors

54. Beta Blockers
Mechanism of Action
Beta blockers reduce the
aqueous production by competing
with catecholamines at adrenergic
receptors thereby blocking them.

55. Beta Blockers
•Non selective:
Timolol (0.25%-0.5%)
Levobunolol (0.5%)
•Cardioselective:
Betaxolol (0.5%)

56. Beta Blockers
(Side Effects)
• Cardiovascular
• Hypotension
• Bradycardia
• Bronchospasm
• Bronchial Asthma
• COPD
• Drug Interaction
• Calcium Channel
antagonists
• Quinidine
• Miscellaneous
• Sleep Disorders
• Decreased Libido
• Fatigue and depression
• Skin rashes
• Headache and Nausea
• Aggravation of
Myasthenia Gravis

57. Sympathomimetics
• Adrenaline (0.5%,1%,2%)
• Dipivefrin (0.1%)
• Brimonidine (0.2%)
• Apraclonidine (0.5%, 1%)
These increase aqueous outflow through their beta-agonist
action

58. Miotics
• Pilocarpine (1%, 2%, 3%, 4%)
drops, gel, oculoserts
• Carbachol (3%)
Act by contracting the longitudinal muscle of the ciliary body
and mechanically pulling on the trabecular meshwork, thereby
opening it

59. Prostaglandin Derivatives
• Unoprostone
• Latanoprost
• Bimatoprost
Increase the Uveo-scleral outflow

60. Carbonic Anhydrase Inhibitors
• SYSTEMIC PREPARATIONS:
• Acetazolamide (tablets, sustained-release capsules,
powder)
• Dichlorphenamide tablets
• Methazolamide tablets
• TOPICAL PREPARATIONS
• Dorzolamide
• Brinzolamide

61. Carbonic Anhydrase Inhibitors
Mechanism of Action
Reduce the production of the aqueous

62. Hyperosmotic Agents
• Glycerol
• Isosorbide
• Mannitol
Act by increasing Osmolarity of blood, thereby creating an
osmotic gradient between blood and vitreous so that fluid is
drawn from eye, reducing pressure