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Primary Open Angle Glaucoma

Primary Open-Angle Glaucoma (POAG) is characterized by a gradual increase in intraocular pressure without an obvious cause, leading to optic nerve damage and potential vision loss. Risk factors include age, family history, race, and certain health conditions, while the pathogenesis involves decreased aqueous outflow and mechanical stress on retinal ganglion cells. Clinical features include asymptomatic progression, specific visual field defects, and characteristic changes in the optic nerve head.

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6 views25 pages

Primary Open Angle Glaucoma

Primary Open-Angle Glaucoma (POAG) is characterized by a gradual increase in intraocular pressure without an obvious cause, leading to optic nerve damage and potential vision loss. Risk factors include age, family history, race, and certain health conditions, while the pathogenesis involves decreased aqueous outflow and mechanical stress on retinal ganglion cells. Clinical features include asymptomatic progression, specific visual field defects, and characteristic changes in the optic nerve head.

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vakulareddy80
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© © All Rights Reserved
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PRIMARY OPEN-ANGLE

GLAUCOMA (POAG)

Roll no:
62
Introduction
:
❖ POAG, is a type of primary glaucoma where there is no
obvious systemic or ocular cause of rise in intraocular
pressure (IOP).
❖ POAG is also known as “chronic simple glaucoma of adult
onset” is typically characterised by:
➢ Slowly progressive raised IOP (>21mm Hg) associated
with,
➢ Open normal appearing anterior chamber angle,
Etiopathogenesi
s:
Etiopathogenesis of POAG is not known exactly. Some of known are :
A. Predisposing and risk factors
-These include the following:
1. Intraocular pressure (IOP)
2. Family history (Heredity) : POAG has ‘Polygenic inheritance’
approx 2 dozen loci have been identified for POAG,out of which
only been genes • Myocilin C (MYOC),
havethree
cloned:
• Optineurin (OPTN), and
• WD repeat domain 36 (WDR
3. Age
4.Race - POAG more common, develops
earlier and more severe in ‘black people'than in whites.
5. Myopes - are more predisposed than normal
6. CentralCornealThickness(CCT)
7. Diabetics
8. Cigarette smoking
9. High Blood Pressure
10.Thyrotoxicosis
11.Corticosteroid responsiveness
B. Pathogenesis of rise in IOP:
It is certain that the rise in IOP occurs due to ‘decrease in
aqueous outflow facility’.
Recently, it has been proposed that reduced aqueous outflow facility
occurs due to “failure of aqueous outflow pump mechanism” leads
to trabecular meshwork stiffening and apposition of Schlemm’s canal
wall. Such changes occurs due to age-related causes:
➔ Thickening and sclerosis of trabecular meshwork with faulty
collagen tissue, leads to failure of active pump mechanism.
➔ Narrowing of intertrabecular spaces.
➔ Deposition of amorphous material in ‘juxtacanalicular space’.
➔ Collapse of Schlemm's canal and absence of giant vacuoles in cells.
C. Pathogenesis of glaucomatous optic
neuropathy:
It has now been recognised that ‘progressive optic
neuropathy’ results from depth of retinal ganglion cells (RGCs)
in a typical pattern which results in characteristic optic disc
appearance and specific visual field defects.

Factors involved in etiology of retinal ganglion cell death can be


grouped as:
I. Primary insults:
1. Raised intraocular pressure (Mechanical theory)
- Raised IOP causes mechanical stretch on lamina cribrosa leads to
axonal deformation and ischemia by altering capillary blood flow.
As a result, Neurotrophins (growth factors) not able to reach
2. Pressure independent factors (Vascular insufficiency
theory):

-Factors affecting vascular perfusion of optic nerve head in


absence of raised IOP have been implicated in glaucomatous
optic neuropathy
in patients with normal tension glaucoma (NTG). Factors includes :
i. Failure of autoregulatory mechanism of blood flow
ii. Vasospasm:
- Is another mechanism affects vascular perfusion of optic nerve
head.
iii. Systemic hypotension
iv. Other factors:
II. Secondary insults (Excitotoxicity theory).

Neuronal degeneration is believed to driven by toxic


factors such as glutamate, oxygen-free radicals or nitric oxide
which are released when RCGs undergoes death due to 1o insults.
Like wise, 2o insults leads tocontinued damage-mediated
apoptosis, even after primary insults has been controlled .
Clinical
Features
SYMPTOMS:
- Asymptomatic.
- Non-specific symptoms:
1.Headache and eye ache.
2. Difficulty in reading and close work.
3. Delayed dark adaptation.
4. Scotoma (defect in the visual field).
5. Significant loss of vision and
blindness.
SIGNS:

I. Anterior segment signs

II. Intraocular-pressure changes

III. Glaucomatous optic nerve head


changes

IV. Visual field defects.

V. Anterior segment signs:


-Ocular examination including ‘Slit lamp
biomicroscopy’ reveals Normal anterior
segment.
- In late stages, pupil reflex becomes
II. Intraocular-pressure changes:

-Different patterns of
diurnal variation of IOP
are –
● Morning rise in IOP- 20% of
cases
● Afternoon rise in IOP- 25%
cases
● Biphasic rise in IOP- 55%
cases.

-Variation in IOP of over 5mm Hg is


suspicious & over 8mm Hg is diagnostic of
III. Glaucomatous optic nerve head changes:

Examination techniques:
-Best technique is Slit-lamp biomicroscopic examination to
have a stereotypic view of optic disc with contact or noncontact lenses.

Recording and documentation techniques:


- Serial hand drawings & optic disc imaging.

Optic disc imaging techniques includes:


➔ Confocal scanning laser topography(CSLT)
➔ Optical coherent tomography (OCT)
➔ Scanning laser polarimetry,
i.e. nerve fibre analyser (NFA).
Glaucomatous changes in optic disc:

A. Early glaucomatous changes: should be suspected if


fundus ex. reveals one or more of following signs:

• Vertical oval cup

• Asymmetry of the cups

• Large cup, with cup: disc ratio >0:4

• Splinter hemorrhages

• Pallor areas on the disc

• Atrophy of retinal nerve fibre layer(RNFL).


B. Advanced glaucomatous changes in the
optic disc:

1.Marked cupping (cup size 0.7-0.9)

2.Thinning of ‘neuro-retinal
rim'(NRR). Normally, thickest to thinnest
parts of NRR of optic disc are-
inf,sup,nas,temporal(ISNT rule).

3. Nasal shifting of retinal vessels.


Have appearance of broken off at margin is an
imp sign (Bayonetting sign).

4. Pulsations of retinal arterioles.


C. Glaucomatous optic atrophy:

- As the damage progresses, all the


neural tissue of the disc is destroyed and optic
nerve head appears ‘white & deeply
excavated’(hollowing).
IV. Visual field defects:

Visual field defects appear only after about 40% of axons have
been damaged & subsequently field defects usually run parallel to changes
at optic nerve head and continue to progress if IOP is not controlled.

Anatomical basis of field defects:

A. Distribution of retinal nerve fibres:


• Fibres from nasal half of retina as SRF & IRF.
• Fibres from macular area come

horizontally as ‘Papillomacular bundle’


(PMB).
• Fibres from temporal retina SAF & IAF.
B. Arrangement of nerve fibre within optic nerve head:
-The nerve fibres originating from periphery of retina lie deep in
retina but occupy most peripheral(superficial) part of optic disc.

-While, fibres originating closer to nerve head lie superficially in


retina & occupy more central(deep) portion of disc.

➔ Superior & inferior arcuate nerve


fibres (SAF & IAF).
➔ Macular fibres.
Nomenclature of glaucomatous field defects:

Visual field defects in glaucoma are initially observed in


“Bjerrum’s area” i.e. 10-20 degrees from fixation and correlates with
optic disc changes.

1. Isopter contraction.
- earliest visual field defect occurs in glaucoma.
2. Baring of blind spot.
3. Small wing-shaped paracentral scotoma.
4. Seidel’s scotoma.
5. Arcuate or Bjerrum's scotoma.

6. Ring or double arcuate


scotoma.

7. Roenne’s central nasal step.

8. Peripheral field defects.

9. Advanced glaucomatous field


defects.
THANK
YOU

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