Ocular Hypertension

DEFINITION
• IOP > 21 mm Hg
• No visual field defect
• Normal appearance of the optic disc and
nerve fiber layer
• Open angles on gonioscopy
• No ocular or systemic cause of increased
IOP
 EPIDEMIOLOGY

• 4-10% of the population > 40 year.

• black > White
• More in Women (Barbados Eye Study)
• 7-8% of the population over the age of 40
has an IOP of more than 21 mmHg, only
1% can result in loss of field of view.
 Etiology
• Increasing age
• Glaucoma history in the family
• History of myopia
• Diabetes mellitus
• Cardiovascular disease in the family.
 PATHOPHYSIOLOGY
• The exact pathophysiology of elevated
intraocular pressure (IOP) in ocular
hypertension is not known.
• myocilin (MYOC) gene mutations have
been found and determined to cause
protein misfolding, making trabecular
meshwork cells dysfunctional, with
subsequent decrease in outflow facility
and marked elevation of IOP
Incrase of Aqueous humor outflow
• Obstruction of TM cause of foregin body
• Lost of TM endothel cell
• The reduced density and size of TM pores
on the inner wall of the endothelium
canalis schlemm.The loss of giant
vacuoles on the inner wall of the
endothelium canalis schlemm.
• Loss of normal phagocytic activity.
• Disorders of the mechanism of neurologic
feedback.
Other processes that play a role in
resistance from aqueous outflows include
changes
• corticosteroid metabolism
• adrenergic control
• abnormal immunologic processes
• oxidative damage to TM.
• Oculi hypertension populations should not
be considered as homogeneous
populations. Before classifying patients as
oculi hypertension, the following factors
must be considered there may be errors in
the measurement:
1. Variability of tonometry size per examiner (usually found
to be approximately 10%).

2. Effect of corneal thickness on the accuracy of IOP size.

3. Diurnal variations of IOP. Within 24 hours, normal

individuals have varying IOP 2-6 mmHg. Most people have
diurnal variation of IOP following the pattern of aqueous
reproduction, with maximum pressure in the middle of the
morning (mid-morning hours) and minimum pressure at
midnight or early morning (early in the morning). Most
diurnal pressure variations are caused by fluctuations in the
average aqueous humor formation

4. Repeated reading must be taken and must be seen with

correlative evidence from the field of view and examination
of the optic nerve before diagnosis or therapy.
 Symptoms
• Most people with ocular hypertension do
not feel any symptoms.
 RISK FACTORS
• • Obtained from OHTS
• CCT
- Relative risk of POAG increased by 81%
for every 40µ decrease in CCT.
- CCT less than 555µ were found to be at
greater risk than eyes with CCT more than
588µ.
• IOP
- >22 mmHg is a positive predictive factor for
the development of POAG
• AGE
Individuals with older age hada greater risk
for conversion to glaucoma
PATTERN STANDARD DEVIATION (PSD)
• OHTS found that greater PSD on SAP
correlated with increased risk of
progression to POAG
• With 0.2dB increase in PSD, 22% increase
in relative risk was found in OHTS.
OPTIC NERVE
• increased vertical and horizontal cup-disc
ratio is a risk factor for progression
• Increase in CDR by 0.1 leads to 32% and
27% increase in relative risk in vertical and
horizontal cupping, respectively
 SCREENING AND EARLY
DIAGNOSIS
• Intraocular Pressure and Pachymetry
• Slitlamp Biomicroscopy and Gonioscopy
• Fundus Examination
• Visual Fields
• Imaging of the Optic Nerve and Nerve
Fiber Layer
• Ocular Blood Flow
 Treatment
• 20% reduction in IOP: delay or prevent the
onset of glaucoma.
• Most OHT patients are at low risk. Most
low risk OHT patients can be followed
without medication.
• Some experts recommend strict observation without
treatment because most ocular hypertensive patients are
at low risk of vision loss (only about 1% per year)

• Some experts select and treat individuals at high risk of

developing glaucoma. Although it has been mentioned
before that damage to nerve fibers above 40% can occur
before the field of sight defects, do not do therapy only
on the basis of field vision. The goal of treatment is to
reduce the pressure before the occurrence of vision loss
due to glaucoma.
 Treatment considerations with
regard to risk factors
• High risk factors:
• a. Retinal nerve fiber layer defects.
• b Parapapillary changes (peripapillary atrophy and
bleeding)
• c. IOP> 30 mmHg. When treating patients with high risk
factors, changes in intra oculi pressure are very
important and a decrease in intra oculi pressure to 20%.
Treat the patient and control 1 month later to see if
treatment is effective and there are no adverse effects. If
treatment goals are met, follow-up every 3-4 months.
 Moderete Risk Factor
• a. Intra-ocular pressure 24-29 mmHg without a defect in
the nerve fiber layer.
• b Family history with primary open-angle glaucoma.
• c. High myopia.
• Complete examination follow-up within 2-3 weeks to re-
check the pressure. If the intra ocular pressure is still 3
mmHg above the limit, continue the follow-up
examination every 3-4 weeks with field view and optic
nerve evaluation at least once a year.
 Low risk factor
• Intra-ocular pressure 22-23 mmHg.
Follow-up the examination 2-3 months
later to double-check the pressure at
different times of the day (for example at 8
am, 11 am, 1 pm, 4 pm).
 Drug choices
The conditions
• Very effective in reducing intra oculi pressure.
• There are no adverse effects or systemic exacerbations
of the disease.
• Consider therapy of 1 eye when starting medication,
because another eye's intraocular pressure can be used
as a control
• A difference of more than 4 mmHg between 2 eyes after
treatment shows a clinical effect
• Carbonic anhydrase inhibitors ( CAIs ). Dorzolamide,
Brinzolamide,Acetazolamide, Methazolamide
• Combination beta blockers and carbonic anhydrase inhibitors
 Timolol
• Adrenergics agonists  Brimonidine
• Prostaglandin analog  Latanoprost ( Xalatan 0,0005% ) focus
on outflow TM
• Unoprostone ( Rescula ), Bimatoprost ( Lumigan ), dan
Travoprost ( Travatan )
• Beta-adrenergic blockers Betaxolol 0,25%, Carteolol 1%,
Timolol 0,25% & 0,5%, Levobunolol 0,25% & 0,5%, Metipranolol
0,3%.
• High risk OHT patients may benefit from
more frequent examinations and early
treatment taking into consideration:
• 1. Patient age
• 2. Health status
• 3. Life expectancy
• 4. Personal preference
 Operation
• If drug cannot be achieved with 1-2
treatments consider a diagnosis of ocular
hypertension with the possibility of early
primary open angle glaucoma.
• THANK YOU