Primary Open angle Glaucoma

Dr. AR Rajalakshmi

• Glaucoma – Overview• POAG clinical features• Management

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.

PATHOGENESIS

• MECHANICAL changes due to the rise of intraocular pressure and

• VASCULAR perfusion of the optic nerve head.

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

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

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

Optic nerve head changes

OPTIC NERVE HEAD – EARLY SIGNS

Increase in vertical c:d > 0.5

Asymmetry between the two optic nerve heads of more than 0.2

Baring of circumlinear blood vessel

Splinter haemorrhages

Retinal nerve fibre layer defect

OPTIC NERVE HEAD – LATE CHANGES

MARKED CUPPING POLAR NOTCHING

Nasalisation of vessels

Peripapillary changes

Loss of NRR & disc pallor

VISUAL FIELD• Portion of space in which objects are simultaneously

visible to the steadily fixating eye.

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

DISTRIBUTION OF RETINAL NERVE FIBRES

BJERRUM’S AREA : an arcuate area extending above and below the blind spot , 10 to 25 ̊from fixation

Visual field defects• Relative paracentral scotoma

• Roenne’s nasal step

• Seidel scotoma

• Arcuate scotoma

• Double arcuate / ring scotoma

• End stage / near total field defect

• 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

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

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

Intraocular pressure

• IOP > 21mmHg on more than one occasion

• Circadian Variation > 8mmHg

• Asymmetry in IOP between 2 eyes of more than 5 mmHg

GAT

Different types of tonometers

Gonioscopy

Grading of anglesvan HerickShaffer systemSpaethScheie

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.

Classification of the Glaucomas

• Open angle• Angle closure

• Primary• Secondary

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)

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)

POAG

DEFINITION

IOP > 21 mmHg Open angle of normal appearance

Visual field lossGlaucomatous disc damage

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

Pathogenesis

Direct damage by pressure Ischemia

Interference withaxoplasmic flow

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

Diagnosis

CLASSICAL TRIAD

• RAISED IOP • OPTIC NERVE HEAD CUPPING• VISUAL FIELD DEFECTS

• On Gonioscopy - the angle should be ‘normal’ and ‘open’

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

Treatment

• Medical• LASER• Surgery

MEDICAL MECHANISM

• Decreased aqueous production

• Increased facility of outflow (trabecular / uveoscleral)

• Intraocular osmotic fluid reduction

LASER THERAPY

Argon laser trabeculoplastySelective laser trabeculoplasty

Surgical

TRABECULECTOMY• Involves creation of

fistula between angle of anterior chamber and sub Tenon’s space

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

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

PATHOGENESIS

• Controversy

• Vascular insufficiency

• Decreased optic disc resistance

• Optic nerve compression by normal carotid

arteries

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

CLINICAL FEATURES • Splinter hemorrhage• Acquired optic disc pits • Focal notching

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

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

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

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

MANAGEMENT

• 20% IOP reduction• Medical

Other modalities less frequently• LASER• Surgery

• POAG clinical features• ONH changes in POAG• Visual field defects in POAG• Management