primary open angle glaucoma
DESCRIPTION
PRIMARY OPEN ANGLE GLAUCOMA. PROF.DR.ÖZCAN OCAKOĞLU. 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 ”. - PowerPoint PPT PresentationTRANSCRIPT
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PRIMARY OPEN ANGLE GLAUCOMA
PROF.DR.ÖZCAN OCAKOĞLU
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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
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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”
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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.
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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
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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
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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
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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!!
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OUTFLOW PATHWAYS AND RESISTANCE POINTS
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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.
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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.
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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
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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
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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
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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 !!
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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
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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
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NORMAL VF
AUTOMATED VISUAL FIELD ANALYZER
DIFFERENT STAGES OF GLAUCOMATOUS VISUAL FIELD
DEFECTS
EARLY STAGE MODERATE STAGE END STAGE
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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
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FUNDOSCOPIC CHANGES
NORMAL OPTIC DISC
GLAUCOMATOUS OPTIC DISCS
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CONFOCAL SCANNING LASER OPHTHALMOSCOPY
HEIDELBERG RETINA TOMOGRAPHY
NORMAL OD GLAUCOMATOUS OD
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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
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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
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•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
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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
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DIODE LASER CYCLOPHOTOCOAGULATION
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SURGICAL THERAPY
SHUNT (IMPLANT) SURGERY(AHMED GLAUCOMA VALV)
FILTRATION SURGERY
(TRABECULECTOMY)
NON PENETRATING SURGERY
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TRABECULECTOMY
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NON PENETRATING SURGERY
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AHMED GLAUCOMA VALVE