PRIMARY OPEN ANGLE GLAUCOMA

PROF.DR.ÖZCAN OCAKOĞLU

HISTORICAL ASPECTSTHE 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

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”

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.

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

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

GLAUCOMASECONDARY 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

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

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!!

OUTFLOW PATHWAYS AND RESISTANCE POINTS

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.

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.

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

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

TonoPen XL Applanation Tonometer

                                                                                 

TonoPen XL Applanation Tonometer

                                                                                 

TonoPen XL Applanation Tonometer

                                                                                 

APPLANATION TONOMETRY

SCHIOTZ TONOMETER

PERRKINS HAND HELD TONOMETER

TONOPEN XL

NON CONTACT TONOMETER

THE TECHNIQUES OF

IOP MEASUREMENTS

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 !!

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

VISUAL FIELD TESTINGVF 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

NORMAL VF

AUTOMATED VISUAL FIELD ANALYZER

DIFFERENT STAGES OF GLAUCOMATOUS VISUAL FIELD

DEFECTS

EARLY STAGE MODERATE STAGE END STAGE

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

FUNDOSCOPIC CHANGES

NORMAL OPTIC DISC

GLAUCOMATOUS OPTIC DISCS

CONFOCAL SCANNING LASER OPHTHALMOSCOPY

HEIDELBERG RETINA TOMOGRAPHY

NORMAL OD GLAUCOMATOUS OD

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

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

•CHOLINERGICS•PILOCARPINE

•PROSTAGLANDINS•LATANOPROST•TRAVOPROST•BIMATOPROST

MEDICAL THERAPY

•ADRENERGIC ANTAGONISTS(BETA BLOCKERS)•NONSELECTIVE

TIMOLOL, LEVOBUNOLOL, CARTEOLOL (ISA+), METIPRANOLOL

•SELECTIVEBETAXOLOL

•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

+

Dorzolamide Latanoprost

+

COSOPT XALACOM

+

Travoprost

DOUTRAV

LASER THERAPYLASER 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

DIODE LASER CYCLOPHOTOCOAGULATION

SURGICAL THERAPY

SHUNT (IMPLANT) SURGERY(AHMED GLAUCOMA VALV)

FILTRATION SURGERY

(TRABECULECTOMY)

NON PENETRATING SURGERY

TRABECULECTOMY

NON PENETRATING SURGERY

AHMED GLAUCOMA VALVE