Ocular

Pathology 2
Lecture 2 Primary Open Angle
Glaucoma (POAG)
MSc Hala Abu Zahou
Definition:
• Glaucoma is a GROUP of ocular disorders where vision can be lost due to
damage to the optic nerve (ON). These group of diseases show
common features:

• Structural changes: At the optic nerve head (ONH).

• Functional changes: Causing typical patterns of visual field loss.

• Associated with raised IOP: BUT NOT NECESSARILY.

May be due to primary or secondary disease mechanisms.

GLAUCOMA:
• Glaucoma is the leading cause of irreversible blindness worldwide.
Glaucoma can cause blindness if left untreated. And unfortunately, approximately 10% of people with
glaucoma who receive proper treatment still experience loss of vision.
• Typically has no symptoms (until late STAGES)
Usually, no pain is associated with increased eye pressure.
• Up to 50% of glaucoma cases are undiagnosed.
• Visual loss is usually permanent.
• There is NO CURE – i.e. treatment is lifelong.
Glaucoma is not curable, and vision loss cannot be regained. With medication and/or surgery, it is
possible to halt further loss of vision. Since glaucoma is a chronic condition, it must be monitored for
life.
• There are various RISK FACTORS.
Everyone is at risk for glaucoma from babies to senior citizens. Yes, older people are at a higher risk
for glaucoma, but babies can be born with glaucoma.
Structural changes: • These occur at the Optic Nerve
Head (ONH).

•Progressive loss of retinal

ganglion cells (RGC)→ loss of the
retinal nerve fiber layer results
in diffuse or notching (thinning)
of the neuro‐retinal rim
especially to the optic disc margin
– ↑ cupping of optic disc
• Note the loss of the neuro
retinal rim allowing the blood
vessels to “disappear”
ISNT RULE
• The ISNT rule
refers to how the optic nerve is
supposed to look in a normal eye
• Normally the neuro‐retinal rim is
thickest inferiorly and thinnest
temporally.
• With glaucoma, you begin to see
vertical thinning, with atrophy
along the inferior and superior
rims.
Functional changes:
➢Purpose of VF testing:
1. Detect field defects due to retinal pathology.
2. GLAUCOMA.
3. Optic nerve and visual pathway pathology (neurological fields).
4. Monitor pathological changes.
➢Typical patterns of visual field loss in glaucoma include:
– Enlarged blind spot
– Nasal step
– Arcuate scotomas
However, ... may have 40‐50% loss of RGC before field defect detected
an OCT is often best used to disclose early glaucomatous changes.
Visual Fields Dimensions

Normal (peripheral) visual field dimensions

– monocular
‐Nasal 50‐60
‐Superior 60‐70
‐Inferior 70‐80
‐Temporal 90‐100

Normal (peripheral) visual field dimensions

– binocular
‐Horizontal 200
‐Vertical 110
Spatial localisation with VF
‐Fovea projects straight ahead

‐Nasal retina projects temporally

‐Temporal retina projects nasally

‐Superior retina projects inferiorly

‐Inferior retina projects superiorly

Glaucomatous visual field defects
3. IOP:

• The disease MAY be associated with raised IOP BUT NOT NECESSARILY

– IOP may be raised (= > 21mm Hg)

...or...
– IOP may be normal (= < 21mm Hg)
• Glaucoma not necessarily caused by ↑ IOP
... but …
• Lowering of IOP usually helps to slow disease progression.
Aqueous dynamics:
• You should know that:
• Aqueous humour is a thin, transparent fluid.
• Provides oxygen and nutrients to non-vascularised tissues of the
anterior chamber.
• Removes waste products
• Provides a clear media for light to pass through to the retina
•Maintains intra‐ocular pressure (IOP) to maintain shape of the globe.
Aqueous dynamics:

• Produced in the ciliary body/processes

• Passes into posterior chamber
• Through pupil
• Into Anterior chamber
•Towards anterior angle of eye (angle be
tween iris & cornea)
➢ IOP controlled by balance between
aqueous production & outflow.
What is normal IOP?
IOP = 10‐21mmHg.
• IOP > 21mm Hg = suspicious
• Difference of IOP between eyes = suspicious

• Normal diurnal fluctuation – IOP typically highest in the Morning

on waking.
– Fluctuation in normal eyes about 5mmHg.
– Fluctuation in glaucoma and Ocular hypertension (OHT)
is much greater ± 15mmHg.
Classification:
❖Primary open angle glaucoma (POAG).
– Not associated with any other ocular disease.
– Most common type.
Types of POAG
• Chronic open angle (COAG)
• High tension >21mmHg.
• Normal / low tension (NTG/LTG) ≤ 21mmHg
❖Closed angle Glaucoma.
❖ Secondary Glaucoma.
❖Congenital Glaucoma.
POAG / COAG:
• Glaucoma is caused by increased resistance to aqueous outflow
(↓ outflow).
And many studies found that this is could be due to:
• Trabecular meshwork obstruction or loss of function.
• Changes to functioning of the Schlemm canal.
• Metabolism.
• Abnormal immunologic processes.
Risk factors:
➢ Most important:
• ↑IOP
• OHT (Ocular hypertension)
• ↑ Age
Risk ↑ with every decade over 40
• Ethnicity
African or Hispanic
• Family history
A glaucoma gene has been identified
• Glaucoma suspect
Risk factors
➢ Moderate importance:
• Myopia
- Some changes can imitate glaucoma….
- >6D
• Diabetes
• Previous eye injury
Investigation:
• History
– Signs, symptoms, risk factors
• Examination
– VA
– Pupils
– Slit lamp‐ anterior segment, IOP (tonometry), gonioscopy, iris and lens
– Pachymetry
– Posterior fundus ‐ optic disc (C/D ratio, NRR, notching, drance HB)
– VF’s & RNFL (OCT)
– Colour vision
– Fundus photography
– Water drinking test (WDT)
Treatment:
• There is NO cure for glaucoma and treatment is usually lifelong.
• The decision to treat is based on:
➢ Level of IOP
➢ Presence of risk factors
➢ Degree of changes both in structural and functional
– Optic disc haemorrhage
– Cupping
– Visible NFL defects

AIM of treatment is to prevent further optic nerve and VF damage.

Effect of medication on aqueous humour:
IOP is a balance between aqueous production and aqueous outflow
• Some medications stimulate or increase uveoscleral outflow.
• Some medication decrease aqueous production.
Aims when using medication is to:
1. Reduce IOP by 20‐30%.
2. Use lowest concentration and as infrequent possible.
3. Use drug with least level of side effects.
Types of medication:
• Beta blockers (↓ aqueous production)
– has cardiac and breathing side effects, dry eyes
• Alpha‐2 agonists ( ↓aqueous production & ↑ uveoscleral outflow)
– causes red eyes and stings when used, dry mouth
• Prostaglandin analogues (↑ uveoscleral outflow)
– Ocular side effects include change in iris colour, increase lash growth, red eyes
• Carbonic anhydrase inhibitors (↓ aqueous production)
– Tingling in fingers and toes, gastric upsets, allergic conjunctivitis
• Miotics (↑ outflow)
– Brow aches, accommodation spasms, reduce VA in dim light

Combination drugs – Greater effect in lowering IOP, combines 2 drugs easier to use.
Laser treatment:
Argon laser trabeculoplasty (ALT)
• Uses thermal energy to open the trabecular meshwork.
• Successful in patients with POAG, Pseudoexfoliation (PXF) and pigment
dispersion syndrome (PDS).
• Affect is not permanent and not repeatable.
Selective laser trabeculoplasty (SLT)
• Light energy.
• Selectively targets the pigmented trabecular meshwork cells
• It is a gentler laser
• Can be repeated.
• Peripheral iridotomy (PI) for ACG
Surgical: Trabeculectomy
• Trabeculectomy is usually advised for patients with glaucoma
that continues to progress despite use of medications and/or
treatments.

• Provides an alternative method for filtration of aqueous humour.

• It has many complications such as Chorio-retinal Folds and

Bleb Leak
Surgical: Molteno
/ baerveldt
/ Ahmed tube
 GLAUCOMA
Let’s putting it all together
IOP
• What is classed as abnormal IOP ?
• Which of the IOP readings below could indicate glaucoma? Why?

16 A 18 17 A 21 23 A 22
IOP can not diagnose glaucoma on its own.
What else do you need?

A. Visual field defect

B. Optic disc cupping
C. Thinning of RFNL
D. All the above
Cup disc
ratio (C/D
ratio)
• Divide the disc in tenths
• Compare horizontal & vertical diameter of
cup to disc
 • IS THERE A DEFECT?
VF Analysis • It is important to Remember the nerve fibre
layout & their projection