GLAUCOMA

Defitaria Permatasari
I11109005

 The

glaucomas are a range of disorders with a

characteristic type of optic nerve damage.
damage to the optic nerve is due to increased intraocular
pressure (IOP).
The IOP : the balance between aqueous production inside
the eye and aqueous drainage out of the eye through the
trabecular meshwork. Normal : between 10 and 21 mm
Hg

Major types of glaucoma:

Primary glaucoma
Open-angle glaucoma (chronic, normal-tension / lowtension glaucoma)
Angle-closure glaucoma (acute, subacute, chronic)
Congenital glaucoma
Secondary glaucoma

Mechanism of increased IOP

Open angle glaucoma
Degenerative process in the trabecular
meshworkdeposition of extracellular material within the
meshwork and beneath the endothelial lining of Schlemm's
canalreduction in aqueous drainage IOP

Angle closure glaucoma

Sufficient iris bomb develops to cause occlusion of
the anterior chamber angle by the peripheral
irisblocks aqueous outflowrapidly IOP

PRIMARY GLAUCOMA

Primary open angle glaucoma

The

resistance to outflow through the trabecular

meshwork gradually increases and the pressure in the
eye slowly increases, causing damage to the nerve.
The level of IOP is the major risk factor for visual loss.
There may be other damage mechanisms, particularly
ischaemia of the optic nerve head.

Symptoms
Most people have no
symptoms
Once vision loss occurs,
the damage is already
severe
There is a slow loss of
side (peripheral) vision
(also called tunnel vision)
Advanced glaucoma can
lead to blindness

Groups at risk
The prevalence increases with age from the 40-49 age
group to in those aged over 80.
increased risk include first degree relatives of patients
patients with ocular hypertension (particularly those with
thin corneas, larger cup to disc ratios and higher IOPs)
people with myopia

Signs
the optic disc changes. The cup to disc ratio increases.
Asymmetry of disc cupping
Haemorrhages on the optic disc poor prognostic sign
Visual field loss is difficult to pick up clinically until
considerable damage has occurred

Groups at risk
longsighted people (hypermetropes)
who tend to have shallow anterior chambers and shorter
axial length eyes
With increasing age the lens tends to increase in size and
crowd the anterior segment structures in these eyes.

Examinations
Visual acuity test. measures how well we see at various
distances.
Visual field test. measures peripheral (side vision).
Dilated eye exam. examine retina and optic nerve for
signs of damage and other eye problems
Tonometry. measures pressure inside the eye
Pachymetry is the measurement of the thickness of
cornea

A tonometer
measures
pressure
inside the eye
to detect
glaucoma.

Medical management
Topical-blockers ( timolol, levobunolol, carteolol, betaxolol,
and metipranolol) Reduce the secretion of aqueous.
Given twice a day, or once a day, either alone or in
combination with other drops
Prostaglandin analogues (latanoprost, travoprost, and
bimatoprost) Reduce the IOP by increasing aqueous
outflow from the eye via an alternative drainage route.
Reductions in IOP of up to 3035%. Are used once daily
(at night)

 Parasympathomimetic agents (pilocarpine)

Constrict the pupil and pull on the trabecular

meshwork, increasing the flow of the aqueous out of the
eye.
Should not be used if there is inflammation in the eye
Carbonic anhydrase inhibitors oral (acetazolamide)
reduce the secretion of aqueous, is the most powerful
agent for reducing IOP
Should not be used in patients with sulphonamide allergy.

Normal-Tension Glaucoma (Low-Tension

Glaucoma)
patients with glaucomatous optic disk or visual field

changes
IOP consistently <21 mm Hg
Pathogenesis
An abnormal sensitivity to intraocular pressure because of
vascular
mechanical abnormalities at the optic nerve head
may be a purely vascular disease.
May be an inherited predisposition, disk hemorrhages are
more frequently seen

Must be excluded:
1. Prior episode of raised intraocular pressure, caused by
anterior uveitis, trauma, or topical steroid therapy.
2. Intermittent elevations of intraocular pressure, such as in
subacute angle closure.
3. Underestimation of intraocular pressure due to reduced
corneal thickness.
4. Other causes of optic disk and field changes, including
congenital disk abnormalities, inherited optic neuropathy,
and acquired optic atrophy due to tumors or vascular
disease.

 approximately 60% have progressive visual field loss

Reduction of intraocular pressure is beneficial in patients

with progressive visual field loss

Glaucoma drainage surgery with an antimetabolite may
be required.

Acute angle closure glaucoma

History
The attack comes on quite quickly
the intraocular pressure rises rapidly
Red eye
There is pain in one eye, can be extremely severe
impaired vision and haloes around lights
may have had similar attacks in the past
may be systemically unwell, with severe headache,
nausea, and vomiting

Apposition of the lens to the back of the iris prevents the

flow of aqueous from the posterior chamber to the anterior
chamber.

Risk factors
increasing age
female gender
family history of glaucoma
South-East Asian, Chinese, or Inuit ethnic background.

Examination
The eye is inflamed and tender
The cornea is hazy and the pupil is semidilated and fixed.
Vision is impaired according to the state of the cornea
On gentle palpation the eye feels harder than the other
eye.
The anterior chamber seems shallower than usual, with
the iris being close to the cornea

Differential Diagnosis
Acute iritis
Acute conjunctivitis

Management
Urgent referral to hospital is required.
intravenous acetazolamide 500 mg and pilocarpine 4%
should be instilled in the eye to constrict the pupil
(iridotomy) or surgically (iridectomy) to restore normal
aqueous flow
The other eye should be treated prophylactically in a
similar way.

Subacute Angle Closure Glaucoma

The same etiologic factors operate in subacute as in

acute angle closure

episodes of elevated intraocular pressure are of short
duration and are recurrent.
The episodes of angle closure resolve spontaneously
there is accumulated damage to the anterior chamber
angle formation of peripheral anterior synechiae

 Recurrent short episodes of unilateral pain

Redness
blurring of vision associated with halos around lights
Attacks often occur in the evenings and resolve overnight

Examination
Between attacks may show only a narrow anterior
chamber angle with peripheral anterior synechiae.
The diagnosis can be confirmed by gonioscopy
Treatment
Laser peripheral iridotomy.

Chronic Angle-Closure Glaucoma

Symptoms
Usually asymptomatic, although patients with advanced
disease may present with decreased vision or visual field
loss.

Management
Laser peripheral iridotomy
Intraocular pressure is then controlled medically if
possible; if difficult drainage surgery is often required
Epinephrine and strong miotics must not be used
unless peripheral iridotomy or iridectomy has been
performed because they will accentuate angle closure.

SECONDARY
GLAUCOMA

Secondary glaucoma
is caused by:
Drugs such as corticosteroids
Eye diseases such as uveitis
Systemic diseases
Trauma
Due to lens changes
Post operative
Raised episcleral venous pressure

Due to lens changes

Lens Dislocation anterior (angle closure) & posterior

(open angle)
Intumescence of the Lens acute angle closure
(complication of immature cataract)
Phacolytic Glaucoma open angle (complication of
hypermature cataract)

Due to uveal tract change

Uveitis open angle/acute angle closure
Tumor angle closure
Ciliary Body Swelling angle closure

Glaucoma Secondary to Trauma

Hyphema angle closure

Glaucoma Following Ocular Surgery

Ciliary Block Glaucoma (Malignant Glaucoma)
Peripheral Anterior Synechiae

Steroid-Induced Glaucoma
Open-angle glaucoma

CONGENITAL
GLAUCOMA

 is seen in babies
Often runs in families (is inherited).
It is present at birth.
Primary congenital glaucoma the developmental

abnormalities are restricted to the anterior chamber angle.

It is caused by abnormal eye development ocular and
extraocular

Symptoms
Unusually large eyes of one eye or both eyes
Excessive tearing
Cloudy eyes
Light sensitivity
usually noticed when the child is a few months old
Red eye

ABSOLUTE GLAUCOMA

 The end result of any uncontrolled glaucoma is a hard,

sightless, and often painful eye End-Stage of glaucoma

Treatment
Principe: reducing IOP by decreasing aqueous production
or increasing aqueous outflow
Currently, the effectiveness of a medication in the
treatment of glaucoma is measured by its ability to lower
IOP
Medical, surgical or laser

Medical Treatment
Suppression of Aqueous Production
Topical beta-adrenergic blocking agents, Apraclonidine, Brimonidine,
Dorzolamide hydrochloride and brinzolamide, Carbonic anhydrase
inhibitorsacetazolamide

Facilitation of Aqueous Outflow

The prostaglandin analogsbimatoprost 0.003%, latanoprost
0.005%, and travoprost 0.004% solutions, Parasympathomimetic
agents Pilocarpine, Epinephrine, Dipivefrin
Reduction of Vitreous Volume
Hyperosmotic agents, Oral glycerin (glycerol)

Miotics, Mydriatics, and Cycloplegics

Surgical and laser treatment

Peripheral Iridotomy, Iridectomy, and Iridoplasty
Laser Trabeculoplasty
Glaucoma Drainage Surgery
Trabeculectomy
Viscocanalostomy and deep sclerectomy with collagen implant
Goniotomy

Cyclodestructive Procedures

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