Primary open angle glaucoma (poag)

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

3. poag K/a Chronic simple glaucoma Most prevalent of all glaucoma Affects both sexes equally

4. 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

5. Risk factors IOP Age Race Family history Diabetes Mellitus Myopia

6. Pathophysiology

7. 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

8. 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

9. 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

10. 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

11. 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

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

13. 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

14. Bayonetting Parapapillary atrophy Lamellar-dot sign

15. 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

16. anderson’s criteria On static perimetry , glaucomatous field loss is considered significant if: Analysis of glaucoma hemi-field test is abnormal in 2 consecutive occasion 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% P attern standard deviation (PSD) should have a probablity of < 5% confirmed on two consecutive tests

17. Visual field abnormalities Initially observed in Bjerrum area, 10- 25° from fixation Correlate with abnormalities seen on optic nerve head Field defects: 1. P aracentral 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

18. Grading of glaucomatous damage MILD DAMAGE Minimal cupping Nasal step / paracentral step MD < -6dB

19. MODERATE DAMAGE Thinning of NRR Arcuate scotoma MD < -12dB

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

21. END STAGE Gross cupping Small residual field

22. TREATMENT

23. 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

24. Target IOP depends upon IOP at which damage has occurred Severity of Visual Field damage Rate of progression of damage Age and Life Expectancy

25. 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

26. I Line II Line III Line

27. 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

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

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

30. Surgery in poag Indications: Failure of medical therapy Anticipated progressive damage or intolerably high IOP Combined with cataract procedure ( phacotrabeculectomy ) Primary therapy

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

32. 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