PRIMARY OPEN

ANGLE GLAUCOMA

PROF.DR.ZCAN OCAKOLU
HISTORICAL ASPECTS
THE GLAUCOMA TERM IS DERIVED FROM THE

OLD GREEK WORD GLAUKOS WHICH MEANS

GREYISH-BLUE

HIPPOCRATES DEFINED GLAUCOMA AS A c. 460 BCc. 380 BC

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

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
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
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
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!!

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








APPLANATION TONOMETRY



PERRKINS HAND
HELD TONOMETER

THE TECHNIQUES OF






IOP MEASUREMENTS


SCHIOTZ
TONOPEN XL
TONOMETER

NON CONTACT TONOMETER

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
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
SL:SCHWALBES LINE
DETERMINE IF THE ANGLES ARE
TM:TRABECULAR
MESHWORK OPEN,
SS:SCLERAL SPUR NARROWED, OR CLOSED
CBB:CILIARY BODY BAND OPEN ANGLE: LONG TERM,SLOWLY,
INSIDIOUS DISEASE
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
 DIFFERENT STAGES OF
GLAUCOMATOUS VISUAL FIELD
DEFECTS

AUTOMATED VISUAL FIELD ANALYZER

NORMAL VF 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

NORMAL OD GLAUCOMATOUS OD

HEIDELBERG RETINA TOMOGRAPHY

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

ISCHEMIA?)
 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
 MEDICAL THERAPY
AQUEUS OUTFLOW FACILITATIVE
DROGS
SUPPRESANTS
ADRENERGIC ANTAGONISTS CHOLINERGICS
(BETA BLOCKERS) PILOCARPINE
NONSELECTIVE PROSTAGLANDINS
TIMOLOL, LEVOBUNOLOL, LATANOPROST
CARTEOLOL (ISA+), METIPRANOLOL TRAVOPROST
SELECTIVE BIMATOPROST
BETAXOLOL
ADRENERGIC AGONISTS
FIXED COMBINATIONS
(SELECTIVE ALPHA-2 AGONISTS)
APRACLONIDINE TIMOLOL MALEAT
BRIMONIDINE
CARBONIC ANHYDRASE INHIBITORS + + +
SYSTEMIC
ACETOZOLAMIDE Dorzolamide Latanoprost Travoprost
TOPICAL
DORZOLAMIDE COSOPT XALACOM DOUTRAV
BRINZOLAMIDE
LASER THERAPY
LASER TRABECULOPLASTY
ARGON LASER TRABECULOPLASTY
(ARGON LASER)
SELECTIVE LASER ARGON LASER
TRABECULOPLASTY
TRABECULOPLASTY (ND:YAG)

CYCLOPHOTOCOAGULATION
TRANSSCLERAL (ND:YAG, DIODE)
TRANSPUPILLARY (ARGON)
TRANSVITREAL (DURING
VITRECTOMY)
ENDOSCOPIC (ARGON)
DIODE LASER TRANSSCLERAL
CYCLOPHOTOCOAGULATION
 DIODE LASER
CYCLOPHOTOCOAGULATION
SURGICAL THERAPY
FILTRATION NON PENETRATING
SURGERY SURGERY
(TRABECULECTOMY)

SHUNT (IMPLANT) SURGERY

(AHMED GLAUCOMA VALV)
TRABECULECTOMY
NON PENETRATING
SURGERY
AHMED GLAUCOMA VALVE