1. PRIMARY OPEN ANGLE GLAUCOMA PROF.DR.ÖZCAN OCAKOĞLU

2. WHAT IS GLAUCOMA? GLAUCOMA IS A DISEASE OF THE OPTIC NERVEOPTIC NERVE IT IS CAUSED BY PROGRESSIVE OPTIC NERVE DAMAGE GLAUCOMA CAN PROGRESS TO TOTAL LOSS OF VISION AND CAN CAUSE IRREVERSIBLE BLINDNESSIRREVERSIBLE BLINDNESS

3. WHAT CAUSES GLAUCOMA? GLAUCOMA IS USUALLY, BUT NOT ALWAYS, ASSOCIATED WITH ELEVATED INTRAOCULAR PRESSURE (IOP)INTRAOCULAR PRESSURE THE ELEVATED IOP LEADS TO DAMAGE OF THE OPTIC NERVE

4. WHAT IS THE IOP? THE PRESSURE INSIDE THE EYEBALL IS TERMED ”INTRAOCULAR PRESSURE (IOP)” IOP CAN BE MEASURED SEVERAL TECHNIQUES AS MILLIMETERS OF MERCURY (mmHg) NORMAL EYE PRESSURE RANGES FROM 10 to 21 mmHg ELEVATED IOP IS USUALLY “GREATER THAN 21 mmHg”

5. ANTERIOR CHAMBER IS FILLED WITH “AQUEOUS HUMOR” THIS FLUID IS PRODUCED BY THE PROCESSUS CILIARIS WHICH IS A PART OF CILIARY BODY THE AQUEOUS HUMOR THEN FLOWS THROUGH THE PUPIL AND LEAVES THE TRABECULAR MESHWORK (TM) TM IS LOCATED AT THE ANTERIOR CHAMBER ANGLE WHICH IS LOCATED BETWEEN THE CORNEA AND ROOT OF THE IRIS. HOW DOES IOP OCCUR? Inflow rate is 2 µl/min

6. OPEN ANTERIOR CHAMBER ANGLE NARROW OR CLOSED ANGLE ANTERIOR CHAMBER ANGLE?

7. OUTFLOW PATHWAYS NORMAL EYES SCHLEMM CHANNELSCHLEMM CHANNEL TRABECULAR MESHWORK Outflow rate is 2 µl/min TRADITIONAL PATHWAY TRABECULUM, SCHLEMM CHANNEL- INTRASCLERAL COLLECTORS-VEIN SYSTEM UVEOSCLERAL PATHWAY SPACES WITHIN LONGITIDUNAL FIBERS OF CILIARY MUSCLES AT CILIARY BODY

8. IS AN IMBALANCE BETWEEN THE INFLOW AND OUTFLOW OF AQUEOUS HUMOR. THE CAUSE OF THE HIGH IOP RAISING THE IOP!!

9. MORHOLOGICAL EFFECT OF ELEVATED IOP INCREASED IOP DAMAGES RETINAL GANGLION CELLS AND THEIR AXONS THE RESULT OF GLAUCOMATOUS PROCESS IS EXCAVATION OF OPTIC DISC AND EVENTUALLY OPTIC ATROPHY

10. FUNCTIONAL EFFECT OF ELEVATED IOP (VISUAL FIELD DEFECTS)

11. IOP RELATED OTHER CONDITIONS OCULAR HYPERTENSION  IN SOME CASES, GLAUCOMA MAY NOT OCCUR IN THE EYES WITH ELEVATED IOP (Increased IOP but no disease)  OHT IS USUALY CAUSED BY THICKER CORNEA THAN NORMAL VALUE NORMOTENSIVE GLAUCOMA  IN SOME CASES, GLAUCOMA MAY OCCUR IN THE EYES WITH NORMAL IOP  THIS FORM OF GLAUCOMA IS CAUSED BY POOR REGULATION OF BLOOD FLOW TO THE OPTIC NERVE

12.  PRIMARY GLAUCOMAS  THE PATHOLOGY IS ONLY LOCATED INSIDE THE EYE (ON FOCUSED TM)  THE MOST COMMONEST TYPE OF GLAUCOMA  PRIMARY OPEN ANGLE GLAUCOMA  PRIMARY ANGLE CLOSED GLAUCOMA  SECONDARY GLAUCOMAS  CONGENITAL (OR PEDIATRIC) GLAUCOMAS WHAT ARE THE DIFFERENT TYPES OF GLAUCOMA?

13. PRIMARY OPEN ANGLE GLAUCOMA INCREASED IOP (USUALLY > 22 MMHG, RELATED CCT) OPEN ANTERIOR CHAMBER ANGLE VISUAL FIELD ABNORMALITIES CUPPING AND ATROPHY OF THE OPTIC DISC SLOWLY, LONG TERM, INSIDIOUS DISEASE !

14. RESISTANCE POINTS AGAINST OUTFLOW GLAUCOMATOUS EYE SCHLEMM CHANNELSCHLEMM CHANNEL MAIN RESISTANCE POINTS AGAINST TO AQUEUS FLOW 1-INTERNAL WALL OF SCHLEMM CHANNEL 2-JUXTACANALICULAR PART OF TRABECULAR MESHWORK NORMAL EYE

15. INCREASED IOP CORNEAL THICKNESS THINNER THAN THE NORMAL (CCT< 500 MICRONS) GENETIC (POZITIVE FAMILY HISTORY) AGE AND RACE (OVER 40’S, BLACKS) WHAT ARE THE RISK FACTORS?

16. NO SYMPTOMS !!!= Thief of vision RARELY, SOME PATIENTS COMPLAINT HEADACHE, NEAR READING DISTURBANCES, HAZINESS OF VISION,DARK ADAPTATION PROBLEMS BUT NO SYMPTOM DIRECTLY RELATED POAG IN EARLY STAGE, VISUAL FIELD DEFECTS IS THE ONLY SYMPTOM, BUT THE PATIENTS DOES NOT FEEL THESE DEFECTS THUS, ANNUAL ROUTINE EXAMINATION IS ESSENTIAL FOR EARLY DIAGNOSIS. A tonometer measures pressure inside the eye to detect glaucoma. Visual field test. This test measures your side (peripheral) vision. It helps your eye care professional tell if you have lost side vision, a sign of glaucoma.

17. THE DIAGNOSE OF GLAUCOMA TONOMETRY PACHYMETRYGONIOSCOPY OPHTHALMOSCOPY PERIMETRY

18. TONOMETRY TONOMETRY IS A METHOD TO MEASURE THE PRESSURE INSIDE THE EYEBALL SEVERAL TYPES OF TONOMETERS ARE AVAILABLE FOR THIS TEST, THE MOST COMMON BEING THE APPLANATION TONOMETER

19. PACHYMETRY PACHYMETRY DETERMINES THE CENTRAL CORNEAL THICKNESS (CCT). NORMAL CENTRAL CORNEAL THICKNESS IS VARIABLE 500-520 MICRONS CCT MAY BE EFFECTED MEASURING IOP THINNER CORNEA (CCT < 500  m) CAN GIVE FALSELY LOW PRESSURE READINGS SEVERE GLAUCOMA PATIENTS MAY BE FAILED DIAGNOSE A THICK CORNEA (>600  m) CAN GIVE FALSELY HIGH PRESSURE READINGS UNNECESSARY TREATMENTS!

20. GONIOSCOPY  GONIOSCOPY IS PERFORMED TO CHECK THE DRAINAGE ANGLE OF AN EYE (ACA)  A SPECIAL CONTACT LENS (GONIOLENS) IS USED  THIS TEST DETERMINES THE ANGLES WHICH ARE OPEN, NARROWED, OR CLOSED  OPEN ANGLE: LONG TERM,SLOWLY, INSIDIOUS DISEASE  CLOSE (OR NARROWED): RISK OF ACUT GLAUCOMA CRISIS

21. VISUAL FIELD TESTING VF TESTING TO CHECK THE PATIENTS PERIPHERAL VISION TPYCALLY BY USING AN AUTOMATED VISUAL FIELD MACHINE THIS TEST IS DONE TO RULE OUT ANY VISUAL DEFECTS DUE TO GLAUCOMA NORMAL VF EARLY STAGE MODERATE STAGEEND STAGE

22. OPTIC NERVE HEAD EXAMINATION OPTIC NERVE HEAD IS EXAMINED WITH OPHTHALMOSCOPICALLY FOR GLAUCOMATOUS CHANGES CUPPING, WHICH IS AN EXCAVATION OF THE OPTIC DISC, CAN BE CAUSED BY INCREASED INTRAOCULAR PRESSURE. NORMAL OPTIC DISCGLAUCOMATOUS OPTIC DISCS

23. GENERAL TREATMENT OPTIONS FOR GLAUCOMA THE GOAL OF GLAUCOMA TREATMENT IS REDUCE THE PRESSURE BEFORE GLAUCOMATOUS LOSS OF VISION MOST CASES CAN BE CONTROLLED WELL WITH TREATMENTS, THEREBY PREVENTING FURTHER LOSS OF VISION EARLY DIAGNOSIS AND TREATMENT IS THE KEY TO PRESERVING SIGHT IN PEOPLE WITH GLAUCOMA

24. THE THERAPIES AIMED INCREASING OUTFLOW GOALS OF GLAUCOMA TREATMENT THE THERAPIES AIMED DECREASING AQUEOS PRODUCTION MEDICAL TREATMENT LASER TEDAVISI SURGICAL TREATMENT LASER TREATMENT

25. CHOLINERGICS PILOCARPINE PROSTAGLANDINS LATANOPROST TRAVOPROST BIMATOPROST MEDICAL THERAPY ADRENERGIC ANTAGONISTS (BETA BLOCKERS) NONSELECTIVE TIMOLOL, LEVOBUNOLOL, CARTEOLOL (ISA+), METIPRANOLOL SELECTIVE BETAXOLOL ADRENERGIC AGONISTS (SELECTIVE ALPHA-2 AGONISTS) APRACLONIDINE BRIMONIDINE CARBONIC ANHYDRASE INHIBITORS SYSTEMIC ACETOZOLAMIDE TOPICAL DORZOLAMIDE BRINZOLAMIDE AQUEUS SUPPRESANTS OUTFLOW FACILITATIVE DROGS FIXED COMBINATIONS TIMOLOL MALEAT + DorzolamideLatanoprost +  COSOPT XALACOM + Travoprost DOUTRAV

26. LASER THERAPY LASER TRABECULOPLASTY (SLT/ALT) LT IS PERFORMED ONLY IN EYES WITH OPEN ANGLES.  MICROSCOPIC LASER BURNS TO THE ANGLE ALLOW FLUID TO BETTER EXIT THE DRAINAGE CHANNELS.BURNS LT DOES NOT CURE GLAUCOMA BUT IS OFTEN DONE TO DECREASING NUMBER OF ANTIGLAUCOMATOUS EYE DROPS LASER TRABECULOPLASTY ALT BURNSSLT BURNS

27. LASER CYCLOPHOTOCOAGULATION  THIS THERAPY DESTROYS CILIARY BODY THEREBY REDUCING PRODUCTION OF AQUEOUS HUMOR  THIS TYPE OF THERAPY MAY BE DANGEROUS BECAUSE OF THE RISK OF PHITISIS BULBI  GENERALLY RESERVED FOR PATIENTS SUUFERING FROM SEVERE FORMS OF GLAUCOMA WITH POOR VISUAL ACUITY AND SERIOUS EYE PAIN

28. SURGICAL THERAPY SHUNT (IMPLANT) SURGERY (AHMED GLAUCOMA VALV) FILTRATION SURGERY (TRABECULECTOMY) NON PENETRATING SURGERY

29. TRABECULECTOMY  TRABECULECTOMY IS THE MOST COMMONLY PERFORMED GLAUCOMA SURGERY  THE AIM IS TO CREATE AN OPENING BETWEEN ANTERIOR CHAMBER AND THE SPACE UNDER CONJUNCTIVA  THE SURGERY PRODUCES A NEW DRAINAGE PATHWAY FOR AQUEOUS HUMOR TO EXIT THE EYE THEREBY LOWERING THE EYE PRESSURE

30. AQUEOUS SHUNT DEVICES (GLAUCOMA IMPLANTS OR TUBES)  THE ARTIFICIAL DRAINAGE DEVICES IS USED TO LOWER THE EYE PRESSURE.  THEY CONTAIN A TUBE ATTACHED TO A RESERVOIR (OR PLATE)  THE RESERVOIR IS PLACED BENEATH THE CONJUNCTIVA, TUBE IS INSERTED ANTERIOR CHAMBER  GENERALLY, IT USES TO TREAT THE DIFFICULT GLAUCOMA CASES AQUEOUS PASSES THE INSIDE TUBE LUMEN AND COLLECTS UNDER THE RESERVOIR