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

TREATMENT

MEDICAL 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

Parasympathomimetics

Non selective agonists

Prostamides

• Drugs increasing UVEOSCLERAL OUTFLOW

Alpha-2-agonists

PG & 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 POAG

Indications:

• 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