Poag 28.04.16 - dr.a.r.rajalakshmi
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Transcript of Poag 28.04.16 - dr.a.r.rajalakshmi
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Primary Open angle Glaucoma
Dr. AR Rajalakshmi
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• Glaucoma – Overview• POAG clinical features• Management
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DEFINITION
• Glaucoma is a chronic, progressive optic neuropathy caused by a group of ocular conditions which lead to damage of the optic nerve with loss of visual function.
• The most common risk factor known is a raised intraocular pressure.
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PATHOGENESIS
• MECHANICAL changes due to the rise of intraocular pressure and
• VASCULAR perfusion of the optic nerve head.
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MECHANICALmechanical pressure
on the lamina cribrosa
mechanical pressure on the lamina
cribrosa
altering capillary blood flow
backward displacement and compaction of the laminar plates narrows the openings through which the axons pass
GANGLION CELL DEATH
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VASCULAR
rise in intraocular pressure
mechanical pressure on the lamina cribrosa
decrease the capillary blood
flow
mechanical compression of vessels at the
lamina cribrosa
GANGLION CELL DEATH
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Diagnosis
combination of clinical signs—characteristic changes in• the optic nerve head• abnormalities in the visual field• rise in intraocular pressure
• The type of glaucoma is determined by the status of the anterior chamber angle as determined by gonioscopy
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Optic nerve head changes
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OPTIC NERVE HEAD – EARLY SIGNS
Increase in vertical c:d > 0.5
Asymmetry between the two optic nerve heads of more than 0.2
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Baring of circumlinear blood vessel
Splinter haemorrhages
Retinal nerve fibre layer defect
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OPTIC NERVE HEAD – LATE CHANGES
MARKED CUPPING POLAR NOTCHING
Nasalisation of vessels
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Peripapillary changes
Loss of NRR & disc pallor
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VISUAL FIELD• Portion of space in which objects are simultaneously
visible to the steadily fixating eye.
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Visual field examination
Screening tests …• Confrontational visual field testing • Amsler grid (assesses the central 10° the visual
field ) .
Quantitative measurements using manual or automated perimetry
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DISTRIBUTION OF RETINAL NERVE FIBRES
BJERRUM’S AREA : an arcuate area extending above and below the blind spot , 10 to 25 ̊from fixation
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Visual field defects• Relative paracentral scotoma
• Roenne’s nasal step
• Seidel scotoma
• Arcuate scotoma
• Double arcuate / ring scotoma
• End stage / near total field defect
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• RELATIVE PARACENTRAL SCOTOMA – areas where smaller / dimmer objects are not visualised by patient but larger & brighter objects are seen
• SEIDEL SCOTOMA• starts at the poles of the
blind spot , arches over the macular area without reaching the horizontal meridian nasally
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ARCUATE SCOTOMA • Starts at superior or inferior
poles of blind spot • Arches over macular area • Ends as a horizontal line
nasally • Does not cross the
horizontal divide of visual field
DOUBLE ARCUATE / RING SCOTOMA • Two arcuate scotomas
expand to involve the peripheral visual field
• Central(tubular vision ) and temporal islands of vision are left
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ROENNE’S NASAL STEP • Appearance of a horizontal
shelf in the nasal visual field.
• Caused by asymmetrical nerve fibre loss at the poles
END STAGE / NEAR TOTAL FIELD DEFECT• Small island of temporal
vision
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Intraocular pressure
• IOP > 21mmHg on more than one occasion
• Circadian Variation > 8mmHg
• Asymmetry in IOP between 2 eyes of more than 5 mmHg
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GAT
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Different types of tonometers
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Gonioscopy
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Grading of anglesvan HerickShaffer systemSpaethScheie
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Schaffer’s grading
Grade 0
Grade 1
Grade 2
Grade 3
Grade 4
Grade 4 (35–45°) is the widest angle, the ciliary body can be visualized. Grade 3 (25–35°) is an open angle, scleral spur is visible. Grade 2 (20°) is an angle in which the trabeculum but not the scleral spur can be seen. Grade 1 (10°) is a very narrow angle in which only the Schwalbe line and perhaps the top of the trabeculum can be identified. Slit angle is one in which there is no obvious iridocorneal contact but no angle structures can be identified. Grade 0 (0°) is closed due to iridocorneal contact.
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Classification of the Glaucomas
• Open angle• Angle closure
• Primary• Secondary
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Open-angle glaucomas Primary open-angle glaucoma (POAG)
Not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow or damage to optic nerve;usually associated with elevated I O P
Normal-tensionglaucoma ( NTG)
Considered in continuum of POAG; terminology often used when I O P is not elevated
Juvenile open-angleglaucoma (JOAG)
Terminology often used when open-angle glaucoma diagnosed at young age (typically 4-35 years of age)
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Ocular hypertension
Normal optic disc and visual field associated with elevated I O P
Glaucoma suspect Suspicious optic disc or visual field regardless of I O P
Secondary open angleglaucoma
Increased resistance to trabecular meshwork outflow associated with other conditions (eg, pigmentary glaucoma, phaco-lytic glaucoma, steroid-induced glaucoma, exfoliation syndrome, angle-recessionglaucoma)Increased post-trabecular resistance to outflow secondary to elevatedepiscleral venous pressure (eg, carotid cavernous sinus fistula)
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POAG
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DEFINITION
IOP > 21 mmHg Open angle of normal appearance
Visual field lossGlaucomatous disc damage
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RISK FACTORS • Genetics- multifactorial & polygenic – long arm of
chromosome 1 • Age : 6th-7th decade , rare before 40 yrs of age • Sex : Both sexes equally affected • Race: Blacks > Whites• Family history: siblings 10% risk, offspring-4 %• Diabetes mellitus • Ocular associations
– Myopia ,CRVO, RRD, RP • ↑ steroid responsiveness
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Pathogenesis
Direct damage by pressure Ischemia
Interference withaxoplasmic flow
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SYMPTOMS
• Insidious Onset/Nonspecific • ‘Asymptomatic’ most of the time • Painless Progressive Loss of Vision• Dull Headache / eye pain• Difficulty in Near Work • Constant pressure on ciliary muscle • Frequent change in presbyopic correction• Difficulty in vision more at night (dark adaptation delay )• Dark areas (scotomas) in field of vision
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Diagnosis
CLASSICAL TRIAD
• RAISED IOP • OPTIC NERVE HEAD CUPPING• VISUAL FIELD DEFECTS
• On Gonioscopy - the angle should be ‘normal’ and ‘open’
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Management
Principle:• Determine TARGET PRESSURE - the range of
IOP at which there is no further progression of glaucomatous damage.
• Parameters to document:• Baseline IOP at which damage occurred• Extent/severity of damage• Associated risk factors
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Treatment
• Medical• LASER• Surgery
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MEDICAL MECHANISM
• Decreased aqueous production
• Increased facility of outflow (trabecular / uveoscleral)
• Intraocular osmotic fluid reduction
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LASER THERAPY
Argon laser trabeculoplastySelective laser trabeculoplasty
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Surgical
TRABECULECTOMY• Involves creation of
fistula between angle of anterior chamber and sub Tenon’s space
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NORMAL TENSION GLAUCOMA• Definition:
– Typical glaucomatous optic disc cupping – Visual field loss– A mean IOP ≤ 21mm of Hg on diurnal testing – Open angles– Absence of any contributing ocular / specific
systemic disorders
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EPIDEMIOLOGY• NTG accounts for 30% of the Glaucomas• Age – significantly older than POAG• Gender – females ≥ males – 2:1• Race – Japan • Family history – POAG is greater in families
of patients of NTG
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PATHOGENESIS
• Controversy
• Vascular insufficiency
• Decreased optic disc resistance
• Optic nerve compression by normal carotid
arteries
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CLINICAL FEATURES• IOP
• In high teens • Wide diurnal and postural IOP fluctuations• Night and early morning spikes
• Visual field changes • Closer to fixation• Deeper• Steeper• Localised
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CLINICAL FEATURES • Splinter hemorrhage• Acquired optic disc pits • Focal notching
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CLINICAL FEATURES • OTHERS • Peripheral vasospasm on cooling • Migraine • Nocturnal hypotension• Reduced blood flow in ophthalmic & posterior ciliary
arteries • Paraprotienaemias and presence of serum auto
antibodies
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TREATMENT OF NTG• Lower IOP by 30% • Betaxolol- Increases the pulsatile ocular blood flow to the
optic nerve• Brimonidine 0.2%:Neuroprotective• Prostaglandin analogues –
• Latanoprost: 0.005% once daily• Bimatoprost: 0.03%• Travoprost: 0.004%
• Dorzolamide• Improves blood flow and velocity in the vicinity of optic nerve
• Calcium channel Blockers
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OCULAR HYPERTENSION
• Definition:– IOP 22mm of Hg or greater– Normal optic disc– Normal Visual Fields– Open angle– Absence of any ocular or systemic disorder
contributing to elevated IOP
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RISK FACTORS• Increasing age• Retinal nerve fibre layer defects • Optic nerve head morphology
– Higher vertical C/D ratio• Elevated IOP• Peripapillary changes • Central corneal thickness • Positive family history -first degree relative• High Myopia
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MANAGEMENT
• 20% IOP reduction• Medical
Other modalities less frequently• LASER• Surgery
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• POAG clinical features• ONH changes in POAG• Visual field defects in POAG• Management