PRIMARY OPEN ANGLE GLAUCOMA

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

2. HISTORICAL ASPECTS • THE GLAUCOMA TERM IS DERIVED FROM THE OLD GREEK WORD “GLAUKOS” WHICH MEANS “GREYISH-BLUE” • HIPPOCRATES DEFINED GLAUCOMA AS “A DISEASE OF THE ELDERLY PATIENTS IN WHICH THE PUPILLA BECOMES BLUE”. • A PERSON WITH A SWOLLEN CORNEA AND A RAPIDLY DEVELOPING CATARACT AND CHRONIC (LONG-TERM) ELEVATED PRESSURE INSIDE THE EYE c. 460 BC–c. 380 BC

3. WHAT IS THE INTRAOCULAR PRESSURE? • PRESSURE INSIDE THE EYE IS TERMED ”INTRAOCULAR PRESSURE (IOP)” • EYE PRESSURE IS MEASURED IN MILLIMETERS OF MERCURY (mmHg) • “NORMAL EYE PRESSURE” IS NOT A STABLE NUMBER(S), IT RANGES FROM 10 to 21 mmHg • ELEVATED IOP IS AN EYE PRESSURE OF “GREATER THAN 21 mmHg”

4. WHAT IS GLAUCOMA? • CURRENTLY, GLAUCOMA IS DEFINED AS “A PROGRESSIVE OPTIC NEUROPATHY WHICH CAUSES PERMANENT BLINDNESS BY DAMAGING THE OPTIC NERVE AND THE PERIFERIC VISUAL FIELD” • GLAUCOMA AFFECTS 3% OF THE SOCIETY AND THE SECOND FREQUENT REASON OF PERMANENT BLINDNESS (ESPECIALLY IN DEVELOPED COUNTRIES). • THE PREVALANCE IS HIGHER IN ELDERLY POPULATION.

5. CLASSIFICATION OF GLAUCOMA • VARIOUS CLASSIFICATIONS ARE AVAILABLE. • MANY CLASSIFICATIONS ARE BASED ON ETIOLOGY, ANATOMY AND CLINICAL PRESENTATION. • CLASSIFICATION BY THE TIME OF ONSET IS AS; • CONGENITAL GLAUCOMAS • ACQUIRED GLAUCOMAS • PRIMARY GLAUCOMAS • SECONDARY GLAUCOMAS

6. CLASSIFICATION OF THE ACQUIRED GLAUCOMAS • PRIMARY OPEN ANGLE GLAUCOMA • NORMAL PRESSURE GLAUCOMA • OCULAR HYPERTENSION • PRIMARY ANGLE CLOSURE GLAUCOMAS • ACUTE ANGLE CLOSURE GLAUCOMA • SUBACUTE ANGLE CLOSURE GLAUCOMA • SECONDARY OPEN ANGLE GLAUCOMAS • PSEUDOEXFOLIATION GLAUCOMA • PIGMENTARY GLAUCOMA • PHACOLYTIC GLAUCOMA • SECONDARY TO OCULAR INFLAMMATION • SECONDARY TO HIGH EPISCLERAL VENOUS PRESSURE • SECONDARY TO STEROID THERAPY • SECONDARY ANGLE CLOSURE GLAUCOMAS • DUE TO PERIPHERAL ANTERIOR SYNECHIAE • SWOLLEN LENS OR PUPILLARY SECLUSION ANTERIOR MOVEMENT OF THE IRIS-LENS DIAPHRAGM • NEOVASCULAR GLAUCOMA • PLATEAU IRIS SYNDROME

7. PRIMARY OPEN ANGLE GLAUCOMA • POAG IS DESCRIBED AS OPTIC NERVE DAMAGE FROM MULTILP POSSIBLE CAUSES THAT IS CHRONIC AND PROGRESSES OVER TIME • A LOSS OF OPTIC NERVE FIBERS IS CHARACTERISTIC OF THE DISEASE • POAG CHARACTERISTICS ARE OPEN ANTERIOR CHAMBER ANGLE, HIGH INTRAOCULAR PRESSURE IN THE EYE ,VISUAL FIELD ABNORMALITIES AND CUPPING AND ATROPHY OF THE OPTIC DISC

8. POAG CAUSES ? • THE EXACT CAUSE OF POAG IS UNKNOWN • THE MOST IMPORTANT (AND WELL KNOWN) CAUSE OF POAG IS INCREASED IOP • THE CAUSE OF THE HIGH IOP IS GENERALLY ACCEPTED TO BE BECAUSE OF AN IMBALANCE IN THE PRODUCTION AND DRAINAGE OF FLUID IN THE EYE (AQUEOUS HUMOR) • THE FLUID IS CONTINUALLY BEING PRODUCED BUT CANNOT BE DRAINED BECAUSE OF THE IMPROPERLY FUNCTIONING DRAINAGE CHANNELS (CALLED TRABECULAR MESHWORK) RAISING THE IOP!!

9. OUTFLOW PATHWAYS AND RESISTANCE POINTS

10. THE BASIS OF THE GLAUCOMATOUS DAMAGE IS THE LOSS OF RETINAL GANGLION CELLS. THE GANGLION CELLS CONSTITUTING THE RETINAL NERVE FIBER LAYER AND THEIR AXONS DIE DURING THE GLAUCOMATOUS DAMAGE PROCESS. GLAUCOMATOUS DAMAGE

11. SYMPTOMS • MOST CASES ARE ASYMPTOMATIC UNTIL THE VISUAL FIELD ABNORMALITIES BECOME PROMINENT AND AFFECT CENTRAL VISION. • THUS, ANNUAL ROUTINE EXAMINATION IS ESSENTIAL FOR EARLY DIAGNOSIS.

12. THE EVALUATION OF GLAUCOMA PATIENTS • VISUAL ACUITY (BEST CORRECTED) • BIOMICROSCOPY (CLUES TO SPESIFIC DIAGNOSIS...) • MEASUREMENT OF INTRAOCULAR PRESSURE • APPLANATION TONOMETRY (GOLDMANN) • NONCONTACT TONOMETRY • PACHYMETRY (CENTRAL CORNEAL THICKNESS) • EVALUATION OF THE ANTERIOR CHAMBER ANGLE (GONIOSCOPY) • VISUAL FIELD TESTING • FUNDUSCOPY

13. TONOMETRY • TONOMETRY IS A METHOD USED TO MEASURE THE PRESSURE INSIDE THE EYE • BECAUSE IOP VARIES FROM HOUR TO HOUR IN ANY INDIVIDUAL (DIURNAL VARIATION), MEASUREMENTS MAY BE TAKEN AT DIFFERENT TIMES OF DAY (MORNING AND NIGHT) • A DIFFERENCE IN PRESSURE BETWEEN MORNING AND NIGTH OF 5 mmHg OR MORE MAY SUGGEST GLAUCOMA • A DIFFERENCE IN PRESSURE BETWEEN THE TWO EYES OF 3 mmHg OR MORE MAY SUGGEST GLAUCOMA

14. APPLANATION TONOMETRY PERRKINS HAND HELD TONOMETER THE TECHNIQUES OF IOP MEASUREMENTS SCHIOTZ TONOMETER TONOPEN XL NON CONTACT TONOMETER

15. PACHYMETRY • NORMAL CENTRAL CORNEAL THICKNESS IS VARIABLE 500-520 MICRONS • 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 !!

16. GONIOSCOPY • GONIOSCOPY IS PERFORMED TO CHECK • THE DRAINAGE ANGLE OF AN EYE • A SPECIAL CONTACT LENS(GONIOLENS) • IS PLACED ON THE EYE • THIS TEST IS IMPORTANT TO • DETERMINE IF THE ANGLES ARE OPEN, • NARROWED, OR CLOSED • OPEN ANGLE: LONG TERM,SLOWLY, INSIDIOUS DISEASE • CLOSE(OR NARROWED): RISK OF ACUT GLAUCOMA CRISIS SL:SCHWALBE’S LINE TM:TRABECULAR MESHWORK SS:SCLERAL SPUR CBB:CILIARY BODY BAND

17. VISUAL FIELD TESTING • VF TESTING TO CHECK THE PATIENTS PERIPHERAL VISION • TYPCALLY BY USING AN AUTOMATED VISUAL FIELD MACHINE • THIS TEST IS DONE TO RULE OUT ANY VISUAL DEFECTS DUE TO GLAUCOMA • VF DEFECTS MAY NOT BE APPERENT UNTIL OVER 40% OF THE OPTIC NERVE FIBER LAYER HAS BEEN LOST • VF TESTING MAY NEED TO BE REPEATED • A LOW RISK OF GLAUCOMATOUS DAMAGE, THE TEST MAY BE PERFORMED ONCE A YEAR • A HIGH RISK OF GLAUCOMATOUS DAMAGE, TEST MAY BE PERFORMED AS FREQUENTLY AS EVERY 2 MONTHS

18. DIFFERENT STAGES OF GLAUCOMATOUS VISUAL FIELD DEFECTS AUTOMATED VISUAL FIELD ANALYZER NORMAL VF MODERATE STAGE END STAGE EARLY STAGE

19. OPTIC NERVE HEAD EXAMINATION • EACH OPTIC NERVE HEAD IS EXAMINED FOR ANY DAMAGE OR ABNORMALITIES • THIS MAY REQUIRE DILATION OF THE PUPILS TO ENSURE AN ADEQUATE EXAMINATION OF THE OPTIC NERVES • FUNDUS PHOTOGRAPHS,WHICH ARE PICTURES OF YOUR OPTIC DISC ARE TAKEN FOR FUTURE REFERENCE AND COMPARISON • DIFFERENT IMAGING STUDIES MAY BE CONDUCTED TO DOCUMENT THE STATUS OF OPTIC NERVE AND TO DETECT CHANGES OVER TIME

20. FUNDOSCOPIC CHANGES NORMAL OPTIC DISC GLAUCOMATOUS OPTIC DISCS

21. CONFOCAL SCANNING LASER OPHTHALMOSCOPY GLAUCOMATOUS OD NORMAL OD HEIDELBERG RETINA TOMOGRAPHY

22. PEOPLE CAN HAVE OPTIC NERVE DAMAGE WITHOUT HAVING ELEVATED IOP THE MAIN REASON OF THIS CONDITION IS VASCULAR INSUFFICIENCY (OCULAR ISCHEMIA?) PEOPLE CAN HAVE ELEVATED PRESSURES WITHOUT SIGNS OF OPTIC NERVE DAMAGE OR VISUAL FIELD LOSS THEY ARE CONSIDERED AS A RISK FOR GLAUCOMA THESE PEOPLE ARE KNOWN AS GLAUCOMA SUSPECT TWO DIFFERENT SITUATION NORMAL TENSION (OR LOW TENSION) GLAUCOMA OCULAR HYPERTENSION

23. GENERAL TREATMENT OPTIONS FOR GLAUCOMA THE GOAL OF GLAUCOMA TREATMENT IS REDUCE THE PRESSURE BEFORE IT CAUSES GLAUCOMATOUS LOSS OF VISION • MEDICAL THERAPY • LASER THERAPY • SURGICAL THERAPY

24. 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 • CHOLINERGICS • PILOCARPINE • PROSTAGLANDINS • LATANOPROST • TRAVOPROST • BIMATOPROST AQUEUS SUPPRESANTS OUTFLOW FACILITATIVE DROGS FIXED COMBINATIONS TIMOLOL MALEAT + + + Dorzolamide Latanoprost Travoprost   COSOPT XALACOM DOUTRAV

25. LASER THERAPY • LASER TRABECULOPLASTY • ARGON LASER TRABECULOPLASTY (ARGON LASER) • SELECTIVE LASER TRABECULOPLASTY (ND:YAG) • CYCLOPHOTOCOAGULATION • TRANSSCLERAL (ND:YAG, DIODE) • TRANSPUPILLARY (ARGON) • TRANSVITREAL (DURING VITRECTOMY) • ENDOSCOPIC (ARGON) ARGON LASER TRABECULOPLASTY DIODE LASER TRANSSCLERAL CYCLOPHOTOCOAGULATION

26. DIODE LASER CYCLOPHOTOCOAGULATION

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

28. TRABECULECTOMY

29. NON PENETRATING SURGERY

30. AHMED GLAUCOMA VALVE