PRIMARY OPEN ANGLE

GLAUCOMA (POAG)

Eye Department
PMC-AJK
 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