Primary open angle glaucoma

1. MODERATOR – DR. O. P. GUPTA
PRIMARY OPEN ANGLE
GLAUCOMA (POAG)

2. GLAUCOMA
 Chronic, progressive optic neuropathy caused by a group
of ocular conditions which lead to damage of the optic
nerve with loss of visual function
 IOP is the major risk factor
 Normal tension glaucoma

4. POAG
• K/a Chronic simple glaucoma
• Most prevalent of all glaucoma
• Affects both sexes equally

5. POAG
• An IOP >21 mmHg
• Glaucomatous optic nerve damage
• An open anterior chamber angle
• Characteristic visual field loss
• Absence of signs of secondary glaucoma or a non-glaucomatous
cause for the optic neuropathy

6. RISK FACTORS
• IOP
• Age
• Race
• Family history
• Diabetes Mellitus
• Myopia

7. PATHOPHYSIOLOGY

10. PATHOGENESIS OF GLAUCOMATOUS OPTIC
NEUROPATHY
1. Ischaemic theory
Suggests that poor blood perfusion of ONH
causes ischaemia and resultant loss of optic nerve
fibre
2. Mechanical theory
Suggests that weakness of supporting tissues of
optic nerve head makes it susceptible to mechanical
deformation by IOP with resultant nerve fibre damage

11. 3. Immune theory
 Increased incidence of paraproteinemia and auto
antibodies and antiglutathione S-transferace
antibodies
 Cause retinal ganglion cell apoptosis
4. Apoptotic theory
Genetically programmed destruction of retinal
ganglion cells may play a part in the pathogenesis

12. CLINICAL FEATURES
• Usually asymptomatic until a significant visual field
loss has occurred
• Eye ache, headache, haloes
• Delayed dark adaptation
• Frequent changes of presbyopic glasses
• Raised IOP & fluctuations in IOP

13. CHANGES IN IOP
• IOP >21 mm Hg on more than one occasion
• Circardian variation of IOP >8 mm Hg
• Asymmetry of IOP >5 mm Hg between two eyes

14. BASE LINE INFORMATION
• History: Ocular, Systemic, Family history,
History of medication
• Pupillary reaction
• Slit lamp biomicroscopy:
 Anterior segment to r/o 2° causes- shallow anterior
chamber, pxf, inflammation
 Fundus evaluation to rule out lesions which can
cause visual field defects
 AT, DVT

15. • CCT > 555µm: false high IOP
< 540µm: false low IOP
• Gonioscopy
• Perimetry: Automatic static threshold perimetry
• Provocative Tests: Water drinking test

16. OPTIC NERVE HEAD CHANGES
• Asymmetry of CDR >0.2
• A localized notch or thinning of NRR.
• Enlarged CDR >0.5 in vertical axis
• Superficial disc hemorrhages
• Shift of vessels to nasal side

17. • Bayonetting
• Parapapillary atrophy
• Lamellar-dot sign

19. Non-specific signs of glaucomatous damage. (A) Inferior baring of circumlinear blood vessels;
(B) inferior bayoneting; (C) collaterals; (D) loss of nasal neuroretinal rim; (E) lamellar dots; (F)
disc haemorrhage

20. ANDERSON’S CRITERIA
On static perimetry, glaucomatous field loss is considered
significant if:
1. Analysis of glaucoma hemi-field test is abnormal in 2
consecutive occasion
2. 3 contiguous non-edge points on the pattern deviation
plot within Bjerrum area have a probability of < 5% of
being in normal population, one of which have a
probability of < 1%
3. Pattern standard deviation (PSD) should have a
probablity of < 5% confirmed on two consecutive tests

21. VISUAL FIELD ABNORMALITIES
• Initially observed in Bjerrum area, 10- 25° from fixation
• Correlate with abnormalities seen on optic nerve head
• Field defects:
1. Paracentral scotomas
2. Nasal step
3. Siedel scotoma
4. Arcuate scotoma
5. Double arcuate or ring scotoma
6. End-stage or near total defect with only
a residual temporal island of vision

24. GRADING OF GLAUCOMATOUS DAMAGE
• MILD DAMAGE
 Minimal cupping
 Nasal step / paracentral
step
 MD < -6dB

25. • MODERATE DAMAGE
 Thinning of NRR
 Arcuate scotoma
 MD < -12dB

26. • SEVERE DAMAGE
 Marked cupping
 Extensive visual field loss
including defects within
central 5 degree
 MD > -12dB

27. • END STAGE
 Gross cupping
 Small residual field

28. TREATMENT
MEDICAL MANAGEMENT
LASER
SURGICAL

29. PRINCIPLE OF TREATMENT
• Usually start with MEDICAL THERAPY.
• Before starting the treatment - Assess each eye
individually, inform patients
• Start treatment in worse eye first
• Set TARGET PRESSURE

30. TARGET IOP DEPENDS UPON
• IOP at which damage has occurred
• Severity of Visual Field damage
• Rate of progression of damage
• Age and Life Expectancy

31. CLASSIFICATION
• Drugs decreasing AQUEOUS PRODUCTION
Beta-blockers
Alpha-2-agonists
CAI
• Drugs increasing TRABECULAR OUTFLOW
Parasympathomimetics
Non selective agonists
Prostamides
• Drugs increasing UVEOSCLERAL OUTFLOW
Alpha-2-agonists
PG & PM

33. I Line II Line III Line

38. RATIONALE FOR DRUGS COMBINATIONS
• Do not combine drugs of same pharmalogical group
• More than two drugs usually not recommended
• If first line of drugs is not effective or tachyphylaxis occurs-
change drug rather than adding another drug

39. LASERS IN POAG
• Outflow Enhancement
• Laser Trabeculoplasty
• Inflow reduction
• Cyclophotocoagulation (in end stage disease)

40. LASER TRABECULOPLASTY
• Uncontrolled glaucoma despite maximal tolerated medical
therapy particularly in elderly
• Avoidance of polypharmacy
• Avoidance of surgery
• Poor compliance

41. SURGERY IN POAG
Indications:
• Failure of medical therapy
• Anticipated progressive damage or intolerably high IOP
• Combined with cataract procedure (phacotrabeculectomy)
• Primary therapy

42. • Penetrating filteration surgeries
• TRABECULECTOMY
• Nonpenetrating filteration surgery(NPFS)
• Deep Sclerectomy
• Viscocanalostomy

43. RECENT ADVANCES IN GLAUCOMA SURGERIES
I. The Ex-Press mini glaucoma shunt
II. Nonpenetrating Ab Externo Schlemm’s Canaloplasty
III. Ab Interno Devices: The Trabectome and Micro-bypass
Stent
IV. The Gold Microshunt: A Suprachoroidal Device