Title: Glaucoma
1Glaucoma
2Intraocular 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
3Types of Glaucoma
- Narrow/closed angle glaucoma
- Attributable to restricted outflow of aqueous
humor through the eyes 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
4Narrow/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)
5History 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
6Examination in Cases of Narrow/Closed Angle
Glaucoma
- Anterior segment
- Macroscopic
- hard, red eye
- cloudy cornea
- fixed, mid-dilated pupil
- Microscopic
- raised IOP (typically gt 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
7Angle closure glaucoma
- Note red eye, hazy cornea and semi-dilated pupil
8Management of Narrow/Closed Angle Glaucoma
- The management of narrow/closed angle glaucoma is
urgent, and involves 3 steps - Step 1 Normalise IOP in the acute phase
- 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)
- 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
9Management of Narrow/Closed Angle Glaucoma
- Step 2 Manage the other eye
- 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 - 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 - Anti-glaucoma drops
- Sometimes, glaucoma filtration surgery will be
required
10YAG 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
11Open Angle Glaucoma
- Congenital/infantile/paediatric
- 40 congenital, 55 within first 2 years of life
- congenital and infantile forms are attributable
to developmental abnormality of trabecular
meshwork - Acquired
- primary
- secondary
- To ocular abnormalities
- pseodoexfoliation
- pigment dispersion
- aniridia
- To ocular disease
- lens capsule perforation (lens-induced) link
- phacomorphic link
- trauma
- uveitis
- To drugs
- Steroids, especially topical steroids
12Congenital Glaucoma
- History
- There may be a family history of congenital
glaucoma - Examination
- Macroscopic
- Photophobia
- Lacrimation
- Blepharospasm
- Buphthalmos (large cornea, gt 12 mm in diameter)
- Microscopic
- Raised IOP
- Cupped discs (see below)
13Picture of buphthalmos
14Management 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
15Primary 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)
16POAG
- 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
17History, Examination and Investigations
- History
- In non-advanced disease, the patient is typically
asymptomatic - There may be a family history of glaucoma
- History of ocular trauma?
- Examination
- IOP
- 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) - Look for ocular disease or abnormalities that can
cause secondary glaucoma - Pseuodexfoliation
- Pigment dispersion
- Swollen or perforated lens
- Signs of trauma
- Uveitis
- Gonioscopy
- This involves the use of a special lens to grade
the degree to which the drainage angle is open - Investigations
- Visual field analysis (see below)
- Neuro-imaging
- 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
18Goldman 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
19Diagram of view through slit lamp of tonometry
- Undercorrected
- Overcorrected
- Correct pressure
20Visual 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
21Humphrey visual fields
- Normal visual field right eye
- Superior arcuate field loss in the left eye due
to glaucoma
22Humphrey 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
23Diagnosis of Primary Open Angle Glaucoma (POAG)
- The diagnosis of POAG is made on a case-by-case
basis, based on the following - 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
24Normal disc on left and cupped disc on rightnote
increased area of pallour and the bending of the
blood vessels at the disc margin in the cupped
disc.
25Management of Primary Open Angle Glaucoma
- The aim of management is to lower the IOP
- 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
- 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) - Surgical management
- Trabeculectomy
- Reserved for a minority of cases where the
condition progresses in spite of maximal
tolerable therapy
26Trabeculectomy
- Note
- cystic drainage bleb
- peripheral iridectomy
27POAG
- 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
28Normal 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,
neuro-imaging of the optic chiasm should be
undertaken - The management is precisely the same as that of
POAG, but aiming for a lower target IOP
29Ocular 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
30Secondary 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
31Pseudoexfoliation
- Note white deposit on anterior lens capsule at
periiphery and also just outside the margin of
the pupil before it was dilated.
32Pigment Dispersion Syndrome
- Characterised by dispersion of pigment throughout
the anterior segment - Pigment on the corneal endothelium (known as
Krukenbergs spindle) - Pigment on the anterior lens surface (known as
Scheies 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
33Pigment Dispersion Syndrome
- Note pigment on corneal endothelium
34Aniridia
- 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
35Glaucoma secondary to ocular disease
- 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