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Glaucoma
GLAUCOMA
Glaucoma is a group of disorders in which
there is damage to the optic nerve due
mainly to the effect of raised intraocular
pressure
GLAUCOMA
• Most types of glaucoma can be controlled
but rarely cured
• Poor control of glaucoma leads to blindness
Glaucoma
Intraocular pressure depends on the balance
between the production of aqueous and it’s
drainage
Aqueous is produced in the ciliary body
It flows from the posterior chamber through the
pupil into the anterior chamber
Aqueous is removed from the eye via the
trabecular meshwork in the anterior chamber
angle
Glaucoma
• Glaucoma is a form of optic neuropathy
• There is damage to the axons of the retinal
ganglion cells at the lamina cribosa or optic
nerve head
• This leads to changes at the optic disc –
cupping and visual field loss
• Optic disc cupping may be asymetrical
Visual Fields
• Glaucoma results in loss of visual field, and visual
acuity is only affected in the end-stage of
uncontrolled disease
• Diagnosis and/or progression of glaucoma is typically
assessed using static perimetry, such as the
Humphrey Visual Field Analyser
Humphrey visual fields
Normal visual field right eye
Superior arcuate field loss in the
left eye due to glaucoma
Humphrey visual fields
Glaucomatous field loss
Markedly restricted peripheral fields- tunnel vision-
left eye worse than right
Left eye normal. Right- marked superior
arcuate and lesser inferior arcuate field loss
Optic disc cupping
The optic nerve head (ONH), also known as the optic disc, is
made up of a pink neuroretinal rim and of a central pale
optic cup
The neuroretinal rim is made up of nerve fibres derived from
the nerve fibre layer of the retina, whereas the optic cup is
that part of the ONH which does not contain nerve fibres
In glaucoma, there is loss of nerve fibres, and therefore the
optic cup enlarges and the neuroretinal rim becomes
thinner, and this is known as pathological optic nerve
cupping or glaucomatous optic neuropathy
Some people have a large optic cup, but in the presence of a
healthy neuroretinal rim, and this is known as
physiological cupping
Look at optic discs with a direct ophthalmoscope
Normal disc on left and cupped disc on right
Note increased area of pallor and the bending of the blood vessels at the disc margin
in the cupped disc.
Examination of the glaucoma patient
• Visual acuity
• Visual fields – confrontation testing with
finger counting in four quadrants of each eye,
(not very useful, Humphrey visual fields much
better)
• Pupilary reactions – relative afferent pupilary
defect with marked optic nerve damage
Examination of the glaucoma patient
• Examination with light source looking at
anterior chamber depth
• Shine a light across the eye from the lateral
side
normal eye -- both sides of iris illuminated
shallow anterior chamber--
nasal side of iris not illuminated
Anterior chamber depth
Normal – note light
illuminating both sides of iris
Shallow – nasal side of iris is
in darkness
Measurement of intraocular pressure (IOP)
• Normal IOP is 10-20mm Hg
• It is usually measured with Applanation
tonometry
• Opticians often use puff tonometry
• Digital tonometry (using fingers to gauge
fluctuation) can only tell if pressures are very
high
Goldman tonometer
Local anaesthetic plus fluorescein
drops are instilled in the eyes.
The tonometer prism touches the
cornea
The dial is turned until the two green
semi circles just touch.
Intra ocular pressure is then read
measured in mmHg,
Patients must be warned not to rub
their eyes for 15 to 20 minutes after
drops are instilled
Primary open angle glaucoma (POAG) risk factors
• Raised intraocular pressure
• Affects 1 in 200 people over 40 years of age,
and 1 in 10 over 80 years of age
• More common and more severe in African
and Caribbean ancestry
• A primary family member with a history of
POAG is associated with increased risk of the
condition
Primary open angle glaucoma - symptoms
• It is a “silent” disease, and is therefore often
diagnosed quite late
• Visual acuity may only be lost at the end stage
of the disease whereas visual field has already
gradually been lost throughout the disease
process
• Treatment is aimed at stopping any further
damage to the optic nerve – previous damage
cannot be reversed
Primary open angle glaucoma-treatment
Treatment is to lower intraocular pressure
• Medical management by use of one or more anti-glaucoma
medications,
– Topical anti-glaucoma preparations
• Prostaglandin analogues ( increase outflow, of
aqueous)
• Beta-blockers (reduce production of aqueous)
• Alpha2-agonists (enhance outflow of aqueous)
• Carbonic anhydrase inhibitors (reduce production of
aqueous)
• Miotics/Parasympathomimetic agents (enhance
outflow of aqueous)
– Oral anti-glaucoma preparations
• Carbonic anhydrase inhibitors (for short-term use only)
Surgical management of POAG
Trabeculectomy
Reserved for a minority of cases where the
condition progresses in spite of maximal
tolerable topical therapy
Selective laser trabeculoplasty SLT
Both above procedures increase outflow of
acquous
Trabeculectomy
Note
1.cystic drainage bleb under upper lid
2.Peripheral iridectomy at 11oclock
Acute angle closure glaucoma
Symptoms
Ocular pain, often severe
Red eye
Blurred vision
Haloes around lights
Nausea/vomiting
Acute angle closure glaucoma
Signs
Dilated fixed pupil
Narrow anterior chamber angle
Hazy cornea due to oedema
Hard eye
Pupillary block
Acute angle closure
glauucoma
Red eye
Hazy oedematous cornea
Semi dilated pupil
Acute angle closure glaucoma
Patients with angle closure glaucoma need
urgent referral to an eye unit for treatment
If treatment is not started early permanent loss
of vision can ensue

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Glaucoma RCSI

  • 2. GLAUCOMA Glaucoma is a group of disorders in which there is damage to the optic nerve due mainly to the effect of raised intraocular pressure
  • 3. GLAUCOMA • Most types of glaucoma can be controlled but rarely cured • Poor control of glaucoma leads to blindness
  • 4. Glaucoma Intraocular pressure depends on the balance between the production of aqueous and it’s drainage Aqueous is produced in the ciliary body It flows from the posterior chamber through the pupil into the anterior chamber Aqueous is removed from the eye via the trabecular meshwork in the anterior chamber angle
  • 5. Glaucoma • Glaucoma is a form of optic neuropathy • There is damage to the axons of the retinal ganglion cells at the lamina cribosa or optic nerve head • This leads to changes at the optic disc – cupping and visual field loss • Optic disc cupping may be asymetrical
  • 6. Visual Fields • Glaucoma results in loss of visual field, and visual acuity is only affected in the end-stage of uncontrolled disease • Diagnosis and/or progression of glaucoma is typically assessed using static perimetry, such as the Humphrey Visual Field Analyser
  • 7. Humphrey visual fields Normal visual field right eye Superior arcuate field loss in the left eye due to glaucoma
  • 8. Humphrey visual fields Glaucomatous field loss Markedly restricted peripheral fields- tunnel vision- left eye worse than right Left eye normal. Right- marked superior arcuate and lesser inferior arcuate field loss
  • 9. Optic disc cupping The optic nerve head (ONH), also known as the optic disc, is made up of a pink neuroretinal rim and of a central pale optic cup The neuroretinal rim is made up of nerve fibres derived from the nerve fibre layer of the retina, whereas the optic cup is that part of the ONH which does not contain nerve fibres In glaucoma, there is loss of nerve fibres, and therefore the optic cup enlarges and the neuroretinal rim becomes thinner, and this is known as pathological optic nerve cupping or glaucomatous optic neuropathy Some people have a large optic cup, but in the presence of a healthy neuroretinal rim, and this is known as physiological cupping
  • 10. Look at optic discs with a direct ophthalmoscope Normal disc on left and cupped disc on right Note increased area of pallor and the bending of the blood vessels at the disc margin in the cupped disc.
  • 11. Examination of the glaucoma patient • Visual acuity • Visual fields – confrontation testing with finger counting in four quadrants of each eye, (not very useful, Humphrey visual fields much better) • Pupilary reactions – relative afferent pupilary defect with marked optic nerve damage
  • 12. Examination of the glaucoma patient • Examination with light source looking at anterior chamber depth • Shine a light across the eye from the lateral side normal eye -- both sides of iris illuminated shallow anterior chamber-- nasal side of iris not illuminated
  • 13. Anterior chamber depth Normal – note light illuminating both sides of iris Shallow – nasal side of iris is in darkness
  • 14.
  • 15. Measurement of intraocular pressure (IOP) • Normal IOP is 10-20mm Hg • It is usually measured with Applanation tonometry • Opticians often use puff tonometry • Digital tonometry (using fingers to gauge fluctuation) can only tell if pressures are very high
  • 16. Goldman tonometer Local anaesthetic plus fluorescein drops are instilled in the eyes. The tonometer prism touches the cornea The dial is turned until the two green semi circles just touch. Intra ocular pressure is then read measured in mmHg, Patients must be warned not to rub their eyes for 15 to 20 minutes after drops are instilled
  • 17. Primary open angle glaucoma (POAG) risk factors • Raised intraocular pressure • Affects 1 in 200 people over 40 years of age, and 1 in 10 over 80 years of age • More common and more severe in African and Caribbean ancestry • A primary family member with a history of POAG is associated with increased risk of the condition
  • 18. Primary open angle glaucoma - symptoms • It is a “silent” disease, and is therefore often diagnosed quite late • Visual acuity may only be lost at the end stage of the disease whereas visual field has already gradually been lost throughout the disease process • Treatment is aimed at stopping any further damage to the optic nerve – previous damage cannot be reversed
  • 19. Primary open angle glaucoma-treatment Treatment is to lower intraocular pressure • Medical management by use of one or more anti-glaucoma medications, – Topical anti-glaucoma preparations • Prostaglandin analogues ( increase outflow, of aqueous) • Beta-blockers (reduce production of aqueous) • Alpha2-agonists (enhance outflow of aqueous) • Carbonic anhydrase inhibitors (reduce production of aqueous) • Miotics/Parasympathomimetic agents (enhance outflow of aqueous) – Oral anti-glaucoma preparations • Carbonic anhydrase inhibitors (for short-term use only)
  • 20. Surgical management of POAG Trabeculectomy Reserved for a minority of cases where the condition progresses in spite of maximal tolerable topical therapy Selective laser trabeculoplasty SLT Both above procedures increase outflow of acquous
  • 21. Trabeculectomy Note 1.cystic drainage bleb under upper lid 2.Peripheral iridectomy at 11oclock
  • 22. Acute angle closure glaucoma Symptoms Ocular pain, often severe Red eye Blurred vision Haloes around lights Nausea/vomiting
  • 23. Acute angle closure glaucoma Signs Dilated fixed pupil Narrow anterior chamber angle Hazy cornea due to oedema Hard eye Pupillary block
  • 24. Acute angle closure glauucoma Red eye Hazy oedematous cornea Semi dilated pupil
  • 25. Acute angle closure glaucoma Patients with angle closure glaucoma need urgent referral to an eye unit for treatment If treatment is not started early permanent loss of vision can ensue