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MODERATOR – DR. O. P. GUPTA
PRIMARY OPEN ANGLE GLAUCOMA (POAG)
GLAUCOMA
Chronic, progressive optic neuropathy caused by a group of ocular conditions which lead to damage of the optic nerve with loss of visual function
IOP is the major risk factor
Normal tension glaucoma
POAG• K/a Chronic simple glaucoma
• Most prevalent of all glaucoma
• Affects both sexes equally
POAG• An IOP >21 mmHg
• Glaucomatous optic nerve damage
• An open anterior chamber angle
• Characteristic visual field loss
• Absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic neuropathy
RISK FACTORS
• IOP• Age
• Race
• Family history
• Diabetes Mellitus
• Myopia
PATHOPHYSIOLOGY
PATHOGENESIS OF GLAUCOMATOUS OPTIC NEUROPATHY
1. Ischaemic theory
Suggests that poor blood perfusion of ONH causes ischaemia and resultant loss of optic nerve fibre
2. Mechanical theory
Suggests that weakness of supporting tissues of optic nerve head makes it susceptible to mechanical deformation by IOP with resultant nerve fibre damage
3. Immune theory Increased incidence of paraproteinemia and auto
antibodies and antiglutathione S-transferace antibodies
Cause retinal ganglion cell apoptosis
4. Apoptotic theory
Genetically programmed destruction of retinal ganglion cells may play a part in the pathogenesis
CLINICAL FEATURES
• Usually asymptomatic until a significant visual field loss has occurred
• Eye ache, headache, haloes
• Delayed dark adaptation
• Frequent changes of presbyopic glasses
• Raised IOP & fluctuations in IOP
CHANGES IN IOP
• IOP >21 mm Hg on more than one occasion
• Circardian variation of IOP >8 mm Hg
• Asymmetry of IOP >5 mm Hg between two eyes
BASE LINE INFORMATION
• History: Ocular, Systemic, Family history, History of medication
• Pupillary reaction
• Slit lamp biomicroscopy: Anterior segment to r/o 2° causes- shallow anterior
chamber, pxf, inflammation Fundus evaluation to rule out lesions which can
cause visual field defects AT, DVT
• CCT > 555µm: false high IOP
< 540µm: false low IOP
• Gonioscopy
• Perimetry: Automatic static threshold perimetry
• Provocative Tests: Water drinking test
OPTIC NERVE HEAD CHANGES
• Asymmetry of CDR >0.2
• A localized notch or thinning of NRR.
• Enlarged CDR >0.5 in vertical axis
• Superficial disc hemorrhages
• Shift of vessels to nasal side
• Bayonetting
• Parapapillary atrophy
• Lamellar-dot sign
Non-specific signs of glaucomatous damage. (A) Inferior baring of circumlinear blood vessels; (B) inferior bayoneting; (C) collaterals; (D) loss of nasal neuroretinal rim; (E) lamellar dots; (F) disc haemorrhage
ANDERSON’S CRITERIA
On static perimetry, glaucomatous field loss is considered significant if:
1. Analysis of glaucoma hemi-field test is abnormal in 2 consecutive occasion
2. 3 contiguous non-edge points on the pattern deviation plot within Bjerrum area have a probability of < 5% of being in normal population, one of which have a probability of < 1%
3. Pattern standard deviation (PSD) should have a probablity of < 5% confirmed on two consecutive tests
VISUAL FIELD ABNORMALITIES• Initially observed in Bjerrum area, 10- 25° from fixation
• Correlate with abnormalities seen on optic nerve head
• Field defects:
1. Paracentral scotomas
2. Nasal step
3. Siedel scotoma
4. Arcuate scotoma
5. Double arcuate or ring scotoma
6. End-stage or near total defect with only a residual temporal island of vision
GRADING OF GLAUCOMATOUS DAMAGE
• MILD DAMAGE Minimal cupping Nasal step / paracentral
step MD < -6dB
• MODERATE DAMAGE Thinning of NRR Arcuate scotoma MD < -12dB
• SEVERE DAMAGE Marked cupping Extensive visual field loss
including defects within central 5 degree
MD > -12dB
• END STAGE Gross cupping Small residual field
TREATMENTMEDICAL MANAGEMENT
LASER
SURGICAL
PRINCIPLE OF TREATMENT
• Usually start with MEDICAL THERAPY.
• Before starting the treatment - Assess each eye individually, inform patients
• Start treatment in worse eye first
• Set TARGET PRESSURE
TARGET IOP DEPENDS UPON
• IOP at which damage has occurred
• Severity of Visual Field damage
• Rate of progression of damage
• Age and Life Expectancy
CLASSIFICATION• Drugs decreasing AQUEOUS PRODUCTION Beta-blockers Alpha-2-agonists CAI• Drugs increasing TRABECULAR OUTFLOW
ParasympathomimeticsNon selective agonistsProstamides
• Drugs increasing UVEOSCLERAL OUTFLOWAlpha-2-agonistsPG & PM
I Line II Line III Line
RATIONALE FOR DRUGS COMBINATIONS
• Do not combine drugs of same pharmalogical group
• More than two drugs usually not recommended
• If first line of drugs is not effective or tachyphylaxis occurs-change drug rather than adding another drug
LASERS IN POAG
• Outflow Enhancement • Laser Trabeculoplasty
• Inflow reduction• Cyclophotocoagulation (in end stage disease)
LASER TRABECULOPLASTY
• Uncontrolled glaucoma despite maximal tolerated medical therapy particularly in elderly
• Avoidance of polypharmacy
• Avoidance of surgery
• Poor compliance
SURGERY IN POAGIndications:• Failure of medical therapy
• Anticipated progressive damage or intolerably high IOP
• Combined with cataract procedure (phacotrabeculectomy)
• Primary therapy
• Penetrating filteration surgeries
• TRABECULECTOMY
• Nonpenetrating filteration surgery(NPFS)
• Deep Sclerectomy
• Viscocanalostomy
RECENT ADVANCES IN GLAUCOMA SURGERIES
I. The Ex-Press mini glaucoma shunt
II. Nonpenetrating Ab Externo Schlemm’s Canaloplasty
III. Ab Interno Devices: The Trabectome and Micro-bypass Stent
IV. The Gold Microshunt: A Suprachoroidal Device