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PRIMARY OPEN ANGLE GLAUCOMA PROF.DR.ÖZCAN OCAKOĞLU.

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Presentation on theme: "PRIMARY OPEN ANGLE GLAUCOMA PROF.DR.ÖZCAN OCAKOĞLU."— Presentation transcript:

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 BC460 BC380 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 SECONDARY OPEN ANGLE GLAUCOMAS PSEUDOEXFOLIATION GLAUCOMA PIGMENTARY GLAUCOMA PHACOLYTIC GLAUCOMA SECONDARY TO OCULAR INFLAMMATION SECONDARY TO HIGH EPISCLERAL VENOUS PRESSURE SECONDARY TO STEROID THERAPY PRIMARY ANGLE CLOSURE GLAUCOMAS ACUTE ANGLE CLOSURE GLAUCOMA SUBACUTE ANGLE CLOSURE GLAUCOMA 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 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) POAG CAUSES ? RAISING THE IOP!!

9 OUTFLOW PATHWAYS AND RESISTANCE POINTS

10 GLAUCOMATOUS DAMAGE 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.

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 TonoPen XL Applanation TonometerTonoPen XL Applanation Tonometer TonoPen XL Applanation TonometerTonoPen XL Applanation Tonometer TonoPen XL Applanation TonometerTonoPen XL Applanation Tonometer APPLANATION TONOMETRY SCHIOTZ TONOMETER PERRKINS HAND HELD TONOMETER TONOPEN XL NON CONTACT TONOMETER THE TECHNIQUES OF IOP MEASUREMENTS

15 PACHYMETRY NORMAL CENTRAL CORNEAL THICKNESS IS VARIABLE 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 SL:SCHWALBE’S LINE TM:TRABECULAR MESHWORK SS:SCLERAL SPUR CBB:CILIARY BODY BAND 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

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 NORMAL VF AUTOMATED VISUAL FIELD ANALYZER DIFFERENT STAGES OF GLAUCOMATOUS VISUAL FIELD DEFECTS EARLY STAGE MODERATE STAGEEND 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 HEIDELBERG RETINA TOMOGRAPHY NORMAL OD GLAUCOMATOUS OD

22 NORMAL TENSION (OR LOW TENSION) GLAUCOMA 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 OCULAR HYPERTENSION TWO DIFFERENT SITUATION

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

24 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

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 SHUNT (IMPLANT) SURGERY (AHMED GLAUCOMA VALV) FILTRATION SURGERY (TRABECULECTOMY) NON PENETRATING SURGERY

28 TRABECULECTOMY

29 NON PENETRATING SURGERY

30 AHMED GLAUCOMA VALVE


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