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GUIDELINE OF

GLAUCOMA
dr. Angela Shinta Dewi Amita, SpM
Current Clinical Practice Guidelines
Komunitas Medik Katolik Indonesia
2015
Glaucoma is an optic neuropathy,
characterized with damage of optic nerve
head and visual field defect, which is
usually due to high intraocular pressure, if
untreated can lead to progressive, permanent
visual loss.
Epidemiology and Burden
of Blindness
Glaucoma is the second leading cause (after cataract) of
blindness worldwide, and is the number one cause of
irreversible vision loss.1
The prevalence of the various types of glaucoma follows racial
and ethnic boundaries.
There may be approximately 409 0002 people with glaucoma
in Canada.
Due to the asymptomatic nature of chronic glaucoma, up to
50% of those with glaucoma in the industrialized world are
unaware of it and are not receiving care.3,4
1. Resnikoff S, et al. 2002. Bull WHO 2004;82:84451.
2. Perruccio AV, et al. Can J Ophthalmol 2007;42:21926.
3. Sommer A, et al. Arch Ophthalmol 1991;109:10905.
4. Mitchell P, et al. Ophthalmology 1996;103:16619.

Canadian Ophthalmological Society evidence-based clinical practice guidelines for the management of glaucoma in the adult eye.
Can J Ophthalmol 2009;44(Suppl 1):S1S93.
Epidemiology (contd)
At the current time there are over 60 million people worldwide with
glaucoma. Most interesting, about half of the people who have
glaucoma don't even know it. Think about that. In the United States,
we have 2.2 million Americans who have glaucoma, and about half
do not even know it.

The longer you live, the more likely you are to have glaucoma. In
2010, it is estimated that 8.4 million individuals worldwide are blind
from primary open-angle glaucoma. By the year 2020, it is estimated
that there will be 11 million individuals who are blind from
glaucoma.

Robert N. Weinreb, MD, Distinguished Professor of Ophthalmology


and Director of the Hamilton Glaucoma Center at the University of
California, San Diego in La Jolla, CA. (2005)
Eye Anatomy
Trabecular Meshwork
Eye with glaucoma
Definition and Classification
The most useful way to classify the glaucoma is according
to anatomy and pathogenesis.

Ocular hypertension
IOP increases when there is obstruction to aqueous outflow. This
occurs when:
the iridocorneal drainage angle is closed due to apposition of the trabecular
meshwork and iris root (closed-angle),
there is obstruction to outflow through the drainage pathways of an open
angle, or
when there is an obstruction to the venous drainage of the eye, but
No optic disc damage or visual field damage

Closed-angle glaucoma
Closed-angle glaucoma develops if the high IOP causes
glaucomatous damage to the optic disc.
Definition and Classification
Open-angle glaucoma
Open-angle glaucoma occurs if damage to the disc is
present in the face of an open angle.
Idiopathic or primary glaucoma
These are open-angle or closed-angle glaucoma with no
identifiable cause.
Secondary angle closure glaucoma
These involve angle closure or elevated IOP with an
identifiable cause.
Who at risk ?
Every one of us !!
Especially :
Age : > 60 y.o
< 60 y.o with glaucoma in family history
Race : Afro American, Hispanic, ASIAN (Japanese & Chinese)
Steroid user (any routes)
High Myope
Systemic Hypertension / Hypotension
Central Corneal Thickness < 0,5 mm
Eye injury
Diabetes Mellitus
Screening for glaucoma

It is recommended that population screening can


be considered for high-risk populations. Screening
should include both structural and functional
measures of the disease. Screening for IOP alone
should be avoided since it has low sensitivity, low
specificity, and poor predictive value for the
detection of glaucoma
Screening (contd)
Screening to identify :
Type of glaucoma
Stage of glaucoma
Mixed and Multiple-mechanism of Glaucoma

Next step :
Treatment strategy
History taking for glaucoma
diagnosis
Why is diagnosis and treatment often delayed?

Glaucoma is painless and the visual symptoms are often very late.
Only half of those who are actually diagnosed with glaucoma
have any symptoms at all.

Vision loss from glaucoma is silent, it is slow, it is progressive, it is


irreversible, but it is treatable. Glaucoma blindness is
preventable.
Examination for glaucoma
diagnosis
Visual acuity and refraction tests
Slit-lamp microscopy
Tonometry : Schiotz Tonometer, Pneumotonometer, Goldman
Tonometer
Gonioscopy
Ophthalmoscopy : Assessment of glaucomatous optic
neuropathy (GON)
Perimetry : Assesment of visual field (VF) damage
Other tests (OCT optic nerve, corneal pachymetry, UBM)
Examination (contd)
Recommendation
Gonioscopy should be performed to determine if an elevated IOP
is associated with an iridocorneal angle that is open, closed or
structurally abnormal. Classification of the glaucoma on the basis
of the appearance of the angle on gonioscopy will guide
appropriate management [Consensus].
Gonioscopy
Visual field exam (Perimetry)
Optic nerve head
Primary open-angle
Glaucoma suspects
An individual who is found on history and clinical
examination to have:
optic disc features suspicious for GON,
suggestive VF defects, with
normal anterior chamber

People with elevated IOP (>21 mm Hg), but with no


evidence of GON or glaucomatous VF damage, would
qualify as POAG suspects on the basis of having ocular
hypertension.
Angle closure glaucoma
5 stages :
Prodromal
Sub-acute
Acute
Chronic
Absolute

Diagnosis:
Subj : Ocular pain, nausea and vomiting, blurring of vision with
haloes,
Obj : IOP > 21 mmHg, conjunctival and ciliary injection, corneal
epithelial oedema, mild-dilated non-reactive pupil, shallow
anterior chamber
Glaucoma Therapies
Preserve visual function.
Maintain or enhance overall health-related
QOL.
Slow or halt progression of the disease.
Achieved through a careful process of:
observing and monitoring visual function,
providing patient education and support,
providing medical, laser, and (or) surgical
intervention
as appropriate, and
observation without treatment in some cases.
Staging of glaucoma damage
(based on highest IOP)

Suspect : 24 mmHg
Early : 20 mmHg
Moderate : 17 mmHg
Advance : 14 mmHg
Follow up
Frequency of follow-up is influenced by a number of
factors.
Patients with stable glaucoma, or ocular hypertension
who are on treatment, need assessment at least once a
year.
Depending on disease severity, other patients will require
more frequent assessments.
Follow up (contd)

Glaucoma suspect : 1-2 years


Early Glaucoma : 12 months
Moderate Glaucoma : 6 months
Advance Glaucoma : 4 months
Therapeutic options
Options for lowering IOP include:
the use of topical or systemic medications,
laser trabeculoplasty,
surgery to improve outflow facility, and
cyclodestructive laser to reduce aqueous production.
Therapeutic (contd)
Set upper limit of initial target IOP range for each eye at
first visit and then re-evaluate at each visit based on
stability/change in structure and function of the optic
nerve (i.e., ONH exam with or without additional imaging
information as well as VF data) [Consensus].
Medical Therapy
Decrease aqueous Increase aqueous outflow
production
Beta adrenergic Alpha-2 adrenergic agonists
antagonists (Timolol, (Brimonidin)
Betaxolol) Parasympathomimetics
Alpha-2 adrenergic /cholinergic agents
agonists (Brimonidin) (Pilocarpine)
Carbonic anhydrase Prostaglandin derivatives
inhibitors systemic (Latanoprost, Travoprost)
and topical
(Asetazolamid,
Dorzolamid )
Medical Therapy
Hyperosmotic agents :

- Reduce IOP by drawing fluid out of the eye


- This drug makes blood plasma hypertonic thus
drawing fluid out of the eye
- Common agents : Glycerin 50%, Manitol 20%
Surgical Therapy

Laser Trabeculoplasty
Trabeculectomy
Trabeculectomy with Tube Shunt
Cyclodestructive
THANK YOU