Transcript Glaucoma

Glaucoma
Intraocular pressure and aqueous
humor
• The intraocular pressure (IOP) of an eye is determined
by the balance of its aqueous production (which occurs
in the ciliary body) and its aqueous outflow (which occurs
through the angle of the eye) [link to anatomy lecture]
• The normal IOP is between 10 and 20 mmHg
Types of Glaucoma
• Narrow/closed angle glaucoma
– Attributable to restricted outflow of aqueous humor through the
eye’s outflow channel (the angle of the eye, which contains the
trabecular meshwork)
• Open angle glaucoma
– “A characteristic form of optic neuropathy, with some regard to
intraocular pressure (IOP)”
– this is the only definition which holds true for all types of open
angle glaucoma
Narrow/closed angle glaucoma
• In this type of glaucoma, the outflow channel for
aqueous humor is either dramatically reduced (when the
angle is narrow, but open) or blocked completely or
almost completely (when the angle is closed)
• Prevalence of 1 in 1000 persons over 40 years of age
• Risk factors for narrow/closed angle glaucoma
– Female gender
– Hypermetropia (these eyes are smaller, and have narrower
drainage angles)
History in Cases of Narrow/Closed
Angle Glaucoma
• Symptoms of raised IOP
– headache
– nausea
– vomiting
• Symptoms of corneal oedema (which occurs as a result
of raised IOP)
– reduced vision
– haloes
– photophobia
• Of note, the onset (i.e. suddenness) and the severity of
symptoms relate to the degree of angle
narrowing/closure and the consequential rise in IOP
Examination in Cases of
Narrow/Closed Angle Glaucoma
• Anterior segment
– Macroscopic
• hard, red eye
• cloudy cornea
• fixed, mid-dilated pupil
– Microscopic
• raised IOP (typically > 40 mmHg)
• some inflammatory cells in the anterior chamber
• shallow anterior chamber
• Posterior segment
– Typically a poor view
– Glaucomatous optic neuropathy, if the condition has
been present for some time
• ..
Angle closure
glaucoma
Note red eye, hazy cornea and
semi-dilated pupil
Management of Narrow/Closed
Angle Glaucoma
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The management of narrow/closed angle glaucoma is urgent, and involves 3 steps
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Step 1: Normalise IOP in the acute phase
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Lie the patient supine (to deepen the anterior chamber)
Instil pupil-constricting drops, pilocarpine, (these will open the angle, if scarring in the angle
has not yet occurred)
Topical steroids (to treat any inflammatory component)
Other topical anti-glaucoma medications, including:
• Beta-blockers
• Alpha agonists
• Prostoglandin analogues
Systemic anti-glaucoma agents:
• Oral
– Acetozolamide (reduces production of aqueous)
• Intravenous
– Acetozolamide
– Mannitol (a hyperosmotic agent)
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Which of these agents are required is a case-by-case decision based on the severity of the
particular case in question, and on the response to these measures by careful monitoring of
IOP
Management of Narrow/Closed
Angle Glaucoma
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Step 2: Manage the other eye
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Typically, the fellow eye will also suffer from, or be predisposed to, narrow/closed angle
glaucoma, and should be treated on its own merits
Usually, however, prophylactic measures are all that is required for the fellow eye, including:
• Pupil-constricting drops
• YAG iridotomy (see below)
Step 3: Prevent further episodes, and manage IOP in the long-term
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Create a pathway for the aqueous to flow directly from the posterior chamber (i.e. where the
aqueous is produced) to the angle of the eye, by creating a peripheral iridotomy with a YAG
laser (after the cornea has cleared); occasionally, a surgical iridectomy is required for this;
In a substantial proportion of cases, and because of damage to the drainage angle during the
acute episode, long-term anti-glaucoma measures will be required, including:
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Anti-glaucoma drops
Sometimes, glaucoma filtration surgery will be required
YAG iridotomy
Note red reflex coming through
iridotomy holes in iris
Red reflex also visible around pupil
due to iris atrophy
Opacity in pupil is posterior
capsular thickening post cataract
surgery. This is treated by cutting a
hole in the capsule with a Yag laser
Open Angle Glaucoma
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Congenital/infantile/paediatric
– 40% congenital, 55% within first 2 years of life
– congenital and infantile forms are attributable to developmental abnormality of
trabecular meshwork
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Acquired
– primary
– secondary
• To ocular abnormalities
– pseodoexfoliation
– pigment dispersion
– aniridia
• To ocular disease
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lens capsule perforation (lens-induced) [link]
phacomorphic [link]
trauma
uveitis
• To drugs
– Steroids, especially topical steroids
Congenital Glaucoma
• History
– There may be a family history of congenital glaucoma
• Examination
– Macroscopic
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Photophobia
Lacrimation
Blepharospasm
Buphthalmos (large cornea, > 12 mm in diameter)
– Microscopic
• Raised IOP
• Cupped discs (see below)
Picture of buphthalmos
Management of Congenital
Glaucoma
• The management is surgical, and will
consist of:
– Goniotomy or trabeculectomy
• Complications of surgery and co-existing ocular
pathology (e.g. cataracts) mean that the long-term
visual prognosis is poor in many cases
– Long-term anti-glaucoma drops may also be
required
Primary Open Angle Glaucoma
(POAG)
• “a characteristic form of optic neuropathy,
with some regard to intraocular pressure”
• Such a definition is required because
some patients can have glaucoma in the
presence of normal IOP (known as normal
tension glaucoma) and some people can
have high IOP but not develop glaucoma
(known as ocular hypertension)
POAG
• Affects 1 in 200 people over 40 years of
age, and 1 in 10 over 80 years of age
• It is a “silent” disease, and is therefore
often diagnosed quite late
• More common and more severe in black
people
• A family history of POAG is associated
with increased risk of the condition
History, Examination and
Investigations
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History
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In non-advanced disease, the patient is typically asymptomatic
There may be a family history of glaucoma
History of ocular trauma?
Examination
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IOP
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Look for ocular disease or abnormalities that can cause secondary glaucoma
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Pseuodexfoliation
Pigment dispersion
Swollen or perforated lens
Signs of trauma
Uveitis
Gonioscopy
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IOP is measured by Goldmann applanation tonometry, and should be corrected for corneal thickness
(thicker corneas yield higher readings, and thinner corneas yield lower readings)
This involves the use of a special lens to grade the degree to which the drainage angle is open
Investigations
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Visual field analysis (see below)
Neuro-imaging
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Very rarely indicated, and only where unexplained optic neuropathy is seen in conjunction with visual
field loss, but where a diagnosis of glaucoma is doubtful; in these circumstances, images of the optic
chiasm are advisable;
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
Diagram of view
through slit lamp of
tonometry
Undercorrected
Overcorrected
Correct pressure
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 fieldstunnel vision- left eye worse than right
Left eye normal. Right- marked superior
arcuate and lesser inferior arcuate field
loss
Diagnosis of Primary Open Angle
Glaucoma (POAG)
• The diagnosis of POAG is made on a case-by-case basis, based on
the following:
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Visual field
IOP
Appearance of optic nerve head (optic disc)
Family history
• Of these, the appearance of the optic nerve head is the most
important parameter
– 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
Normal disc on left and cupped disc on right
note increased area of pallour and the bending of the blood vessels at
the disc margin in the cupped disc.
Management of Primary Open
Angle Glaucoma
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The aim of management is to lower the IOP
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Medical management by use of one or more anti-glaucoma medications, and in the
context of regular IOP and ONH checks, and monitoring of visual fields
– Topical anti-glaucoma preparations
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Prostaglandin analogues (reduce production, and increase outflow, of aqueous)
Beta-blockers (reduce production of aqueous)
Alpha-agonists (enhance outflow of aqueous)
Carbonic anhydrase inhibitors (reduce production of aqueous)
Miotics (enhance outflow of aqueous)
– Oral anti-glaucoma preparations
• Carbonic anhydrase inhibitors (for short-term use only)
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Surgical management
– Trabeculectomy
– Reserved for a minority of cases where the condition progresses in spite of
maximal tolerable therapy
Trabeculectomy
Note
cystic drainage bleb
peripheral iridectomy
POAG
Uncontrolled glaucoma leads to blindness
POAG can be controlled but not cured
Any damage to the optic nerve prior to diagnosis
cannot be reversed
POAG needs lifelong follow up and treatment
Normal Tension Glaucoma
• Normal tension glaucoma simply refers to a
condition characterised by glaucomatous optic
neuropathy and loss of visual field, but in the
presence of normal IOP measurements
• If there is doubt about the diagnosis, neuroimaging of the optic chiasm should be
undertaken
• The management is precisely the same as that
of POAG, but aiming for a lower target IOP
Ocular Hypertension
• Ocular hypertension (OHT) is characterised by
high IOP, but in the absence of glaucomatous
optic neuropathy or field loss
• Patients with OHT are at increased risk of
developing glaucoma, and therefore should be
closely monitored
• There is some evidence to suggest that IOP
reduction in patients with OHT reduces the risk
of developing glaucoma
Secondary Glaucomas
• Pseudoexfoliaton (PXF)
– A condition common amongst those of Scandinavian
origin or descent, and therefore common in Irish
people
– Characterised by the accumulation of grey-white
basement membrane material on the pupil edge and
on the lens capsule
– If pseuodoexfoliation causes glaucoma, it is known as
glaucoma capsulare
– PXF also causes cataract
– Glaucoma capsulare is managed in precisely the
same manner as POAG
Pseudoexfoliation
Note white deposit on anterior lens capsule at periiphery and also
just outside the margin of the pupil before it was dilated.
Pigment Dispersion Syndrome
• Characterised by dispersion of pigment throughout the
anterior segment
– Pigment on the corneal endothelium (known as Krukenberg’s
spindle)
– Pigment on the anterior lens surface (known as Scheie’s stripe)
– Loss of pigment from the iris, with consequential iris
transillumination
• When pigment dispersion syndrome causes glaucoma, it
is known as pigmentary glaucoma
• Pigmentary glaucoma is managed in precisely the same
way as POAG
Pigment Dispersion
Syndrome
Note pigment on corneal
endothelium
Aniridia
• Congenital absence of the iris
– Associated with foveal hypoplasia
– Glaucoma typically develops in late childhood
– Managed in the same way as POAG, but the
need for surgery is likely
Glaucoma secondary to ocular
disease
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Lens-induced glaucoma [link]
Phacomorphic glaucoma [link]
Uveitis [link]
Trauma
– Blunt trauma can cause damage to the drainage
angle (known as angle recession), which can cause
glaucoma at the time of injury, or months or years
later
• The management of all secondary glaucomas
involves the treatment of the underlying cause
(e.g. treating the inflammation if it is secondary
to uveitis) and management of IOP as for POAG