Glaucoma

Medical student teaching

December 2007

Poornima Rai
Specialist Registrar
Western Eye Hospital
 Glaucoma –Over view
 Anatomy and physiology
 Epidemiology
 Types
 Primary open angle glaucoma (POAG)
 Investigations and treatment
 Angle closure glaucoma (ACG)
 Presentation and treatment
 Secondary glaucoma
 Further reading
Anatomy of aqueous flow
 Epidemiology of glaucoma
 New statistics gathered by the World Health Organization
(WHO) in 2002 show that glaucoma is now the second leading
cause of blindness worldwide, after cataracts
 Glaucoma is the second most frequent cause of blindness in
industrialized countries.
 Estimated 9.25 million glaucoma patients in Europe.
(Michelson G, Groh MJ. Curr Opin Ophthalmol 2001).
 UK- 5% over 80 years of age.
 RCO: 570,000 suspected cases and 15,000 definite cases of
POAG.
 POAG to increase by a third by 2021.(Tuck MW and Crick
Ophthalmic Physiol Opt 2003).
 What is glaucoma
 Raised intraocular pressure secondary to blockage of
the aqueous drainage pathway or the trabecular
meshwork (drainage angle)

 Damage to optic nerve

 Reduced blood flow to the optic nerve

 Visual field defect

 Symptoms
 Painless loss of visual fields over time

 Mainly affects peripheral visual fields

 Risk factors
 a family history of glaucoma
 diabetes
 migraine
 short sightedness (myopia)
 eye injuries
 hypertension
 past or present use of cortisone drugs
(steroids)
 Method of clinical examination
 Intraocular pressure check (tonometry)- Normal
range 11- 21 mm HG
 Gonioscopy
 Central Corneal Thickness
 optic nerve assessment with an ophthalmoscope/ Slit
lamp examination
 visual field assessment if needed - this tests the
sensitivity of the side vision, where glaucoma strikes
first
 Optic disc analysis -HRT
 Examination
Topical anaesthesia & fluorescien
Goldmann’s applanation tonometry

Tonopen
Gonioscopy
 Optic disc assessment

Optic disc cupping

with disc haemorrhage

Progression of glaucomatous optic disc cupping

Normal optic disc Early glaucomatous Advanced glaucomatous

Optic disc cupping Optic disc cupping
Humphrey’s visual field analyser
Optic disc analysis with Heidelberg
Retinal Tomography
Central Corneal Thickness-CCT
 Corneal pachymetry is a
measurement of the thickness
of the cornea.

 the normal human cornea

measures approximately 550
pm thick centrally and a full
millimeter thick peripherally.

 The thinner the CCT higher

the risk of intraocular pressure
causing glaucomatous damage
 Ocular hypertension
 An intraocular pressure greater than 21 mm Hg in one
or both eyes as measured by applanation tonometry
on 2 or more occasions
 No glaucomatous defects on visual field testing
 Normal appearance of the optic disc and nerve fiber
layer
 Open angles on gonioscopy, with no history of angle
closure
 Absence of any ocular disease contributing to the
elevation of pressure
 Treatment
 Eyedrops - these are the most common form of
treatment and must be used regularly. The drops can be
varied to best suit the patient and the type of glaucoma.
 Laser (laser trabeculoplasty) - this is performed when
eye drops do not stop deterioration in the field of vision.
In many cases eye drops will need to be continued after
laser.
 Surgery (trabeculectomy) - this is performed usually
after eye drops and laser have failed to control the eye
pressure. A new channel for the fluid to leave the eye is
created.
 Medical treatment
 Miotics - Increase the outflow of aqueous humor from the eye

 Epinephrine compounds - Increase the outflow of aqueous humor from the eye

 Beta-blockers - Reduce the amount of aqueous humor produced in the eye

 Carbonic anhydrase inhibitors and alpha-adrenergic agonists - Reduce the

amount of aqueous humor produced in the eye

 Prostaglandin analogs - Work near the drainage area of the eye to increase the
secondary route ( uveoscleral outflow) of aqueous humor outflow to lower IOP

 Oral Carbonic anhydrase inhibitors -which slow the production of aqueous

humor in the eye

 Intravenous Mannitol & oral glecerol -rapidly reduces intraocular pressure by

reducing the volume of vitreous
 LASER Treatment
 Trabeculoplasty - A laser is applied to stimulate the trabecular
endothelial cells to pump more efficiently to transport aqueous
humor out of the eye. Furthermore, contraction of the burns
induced by the laser increases the spaces in the adjacent
(untreated) tissue, resulting in increased outflow in the drainage
area of the eye (the trabecular meshwork).

 Iridotomy-The laser makes a small hole in the iris to allow the

aqueous humor to flow more freely within the eye. The iris
does not plug up the trabecular meshwork.

 Cyclophotocoagulation (CPC)- a laser is used to destroy

selected areas of the ciliary body (the part of the eye that
produces the aqueous humor) to reduce fluid production.
Trabeculectomy surgery
 Types of glaucoma
 Chronic (primary open-angle) glaucoma is the most common form of this disease. However,
other forms occur:
 Ocular hypertension ****
 Low-tension or normal tension glaucoma . Occasionally optic nerve damage can occur in
people with so-called normal eye pressure. This form of glaucoma is treated in the same
manner as open-angle glaucoma.
 Acute (angle-closure) glaucoma. Acute glaucoma is when the pressure inside the eye rapidly
increases due to the iris blocking the drain. An attack of acute glaucoma is often severe.
People suffer pain, nausea, blurred vision and redness of the eye. Immediate medical help
should be sought. If treatment is delayed there can be permanent visual damage in a very short
time. Usually, laser surgery performed promptly can clear the blockage and protect against
visual impairment.
 Congenital glaucoma. This is a rare form of glaucoma caused by an abnormal drainage
system. It can exist at birth or develop later. Parents may note that the child is sensitive to
light, has enlarged and cloudy eyes, and excessive watering. Surgery is usually needed.
 Secondary glaucomas. These glaucomas can develop as a result of other disorders of the eye
such as injuries, cataracts, eye inflammation. The use of steroids (cortisone) has a tendency to
raise eye pressure and therefore pressures should be checked frequently when steroids are
used.
 Angle closure
 Individuals predisposed to
developing pupil block
angle closure glaucoma tend
to have anatomically small
anterior chamber volumes
relative to the lens size.
Known risk factors include:
 hyperopia
 females have a 3 - 4 times
higher prevalence
 increased age
 first degree relatives with an
angle closure glaucoma
history
 higher prevalence in Inuit and
Chinese
 Acute angle closure
 Symptoms are usually
sudden in onset and
patients present with:
 pain in and around the
eye
 redness of the eye
 nausea and vomiting
 blurred vision
 a prodrome of rainbow
coloured halos around
lights may be reported
 Signs in acute angle closure
 Examination of the eye usually
reveals several of the following
signs:
 elevated IOP (usually over 40 mm
Hg, may be off the scale at 79
mm Hg)
 conjunctival injection
 cloudy cornea (edema)
 shallow anterior chamber
 mid-dilated, sluggishly reactive or
nonreactive pupil
 flare and cells in the anterior
chamber
 closed angle on gonioscopy (use
contralateral eye if necessary)
 Treatment of AAC
 Refer to Ophthalmologist
 Intravenous cannula- IV Carbonic anhydrase
inhibitor
 instill topical antiglaucoma medications
 miotic (pilocarpine alone may be sufficient in
mild attacks)
 give aqueous suppressants (topical beta
blockers and oral carbonic anhydrase inhibitors
 give intravenous or oral hyperosmotic agents
 Treatment of Angle closure
glaucoma
 YAG peripheral
iridotomy in both eyes
to relieve the pupil
block

 Assess patency of the

peripheral iridotomy

 Repeat gonioscopy to
assess the angle width
 Secondary glaucoma
 Uveitic glaucoma
 Rubeotic glaucoma
 Traumatic glaucoma
 Lens induced glaucoma
 Steroid induced glaucoma
 Psuedoexfoliation glaucoma
 Pigmentary glaucoma
 Uveitic glaucoma
 Uveitis can cause secondary
angle closure if the inflamed
iris becomes entirely stuck to
the lens - if extensive, these
posterior synechiae (PS) can
prevent aqueous from
draining through the pupil - a
secondary pupil block
 The iris is displaced
anteriorly by aqueous
trapped behind it - prevent
by using mydriatics to
reduce PS formation
 Rubeotic glaucoma- NVG
 Abnormal blood vessels developing on the
surface of the iris (rubeosis) and over the
trabecular meshwork
 Initially the angle is open but, as the
fibrovascular tissue consolidates, permanent
adhesions form and angle closure glaucoma
develops
 NVG is commonly due to underlying retinal
ischemia with proliferative diabetic retinopathy
and central retinal vein occlusions the most
common causes
 Prophylactic retinal laser photocoagulation is
the treatment of choice in early presentation
 Regular checkups for diabetics are extremely
important.
 Laser therapy to the ischemic retina may cause
vessels to regress
 NVG has a very poor visual prognosis; if useful
vision remains, surgical filtration procedures are
possible
 If the eye is blind and painful, ciliary body
destructive procedures with cyclodiode laser is
performed
 Traumatic hyphaema
 A hyphaema can induce elevation of IOP
due to blood blocking trabecular
meshwork

 Angle recession glaucoma occurs with

blunt, nonpenetrating trauma to globe and
orbit

 the force of the injury causes tears in the

trabecular meshwork and ciliary body with
secondary scarring. Angle recession
glaucoma may present years after the
inciting injury.

 Treatment is with topical medication

 Sickle cell disease patients should be

treated with great caution and carbonic
anhydrase inhibitor should be avoided
 Lens induced glaucoma
 Phacolytic glaucoma -the
reminant lens fragments result in
inflammation and cause
secondary glaucoma

 Treatment is to reduce
inflammation with topical steroids
and removal of the lens fragments

 Phacomorphic glaucoma- Lens

blocks the pupil due to increase in
size results in raised intraocular
pressure

 Treatment option is to remove the

lens by phacoemulsification
 Steroid induced glaucoma
 Topical or systemic corticosteroid (glucocorticoid) use can
induce secondary glaucoma

 25% of the general population will develop steroid‑induced

increases in IOP after 4 weeks of qid topical steroid drugs

 5% of the population are "super-responders" - these patients

develop pressure elevations greater than 10 to 15 mm Hg with
topical steroid use and may develop a pressure rise within 2
weeks

 Topical steroids should not be prescribed unless patient can be

monitored by an ophthalmologist for IOP changes
 Pseudoexfoliation Syndrome
 An abnormal basement
membrane-like material produced
in the eye and clogs the
trabecular meshwork

 This causes a secondary OAG

typically in the elderly

 The zonules tend to be weak and

need to be taken into
consideration in these patients
when performing cataract surgery
 Pigment Dispersion Syndrome

 Iris pigment clogs trabecular

meshwork
 This causes a secondary
OAG typically in younger
myopes
 Trabecular meshwork is
heavily pigmented with iris
pigment
 Treatment is with topical
medication
 Glaucoma-Further reading
 Moorfields Manual of Ophthalmology.
Jackson et al.

 Ophthalmology: An Illustrated Colour Text.

Batterbury and Bowling.

 Clinical Ophthalmology: A Systematic

approach. Kanski