oc htn

1. OCULAR HYPERTENSION
SIVATEJA CHALLA

2. • DEFINITION
• EPIDEMIOLOGY
• PATHOPHYSIOLOGY
• RISK FACTORS
• DIAGONOSIS
• DIFFERENTIAL DIAGONOSIS
• TREATMENT

3. DEFINITION
• Ocular Hypertension is defined as
1.IOP > 21 mmHg
2.No evidence of optic nerve damage
3. No visual field defects.
4.open angles
5. no systemic or ocular cause for raised IOP

4. SYNONYMS
• Glaucoma suspect
• Open angle with out damage
• Early glaucoma

5. What to do with these patients?
 How often should they be examined?
 Is preventative treatment effective?
 Who should be treated?

6. EPIDEMIOLOGY
• 4-10% population over 40 yrs
18.4% in black african descent
13% in mixed race
4.6% in whites
• In southern India prevalence of 1.1% in
individuals above 40 years of age has been reported

7. 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

8. RISK FACTORS
• Obtained from OHTS

10. 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

12. 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

14. DIAGONOSIS of exclusion !!
• HISTORY- to R/O any sec causes for elvated IOP like
trauma/steroid usage
• Usage of antihypertensives as they cause IOP
fluctuations
• advanced age (>50 y), African American descent,
myopia, and positive family history/severity of
glaucoma in a first-degree relative

15. Eye
EYE EXAMINATION AAO PPP

16. SLB
CORNEA
• microcystic edema can be found with a sudden
elevation of IOP.
• KP’S, pigment on the endothelium (Krukenberg
spindle), and congenital and other anomalies
suggest a secondary cause of elevated IOP

17. • ANTERIOR CHAMBER, assess for an absence of
cell or flare, hyphema, foreign bodies, and angle
closure.
• IRIS atrophy, synechiae, rubeosis, ectropion uveae,
iris bombé, difference in iris coloration bilaterally
(eg, Fuchs heterochromic iridocyclitis),
or pseudoexfoliation (PXF) material.
• LENS assess for an absence of phacomorphic, PXF,
Morgagnian, or phacolytic cataract.

18. • OPTHALMOSCOPY –normal optic disc with no E/O
cupping or RNFL loss
• GONIOSCOPY-open angles
• IOP- >21 mm Hg
• PACHYMETRY
• VF/AUTOMATED PERIMETRY TESTING
• OTHER TESTS : OCT HRT GDX

19. • Medeioros and colleagues developed a risk
calculator for OHT that may progress to glaucoma

22. TREATMENT
• Considering the low
rate of progression to
POAG, cost of ocular
hypotensive
medications, long
term compliance
issues and side effect
of drugs, not every
case of ocular
hypertension is
subjected to
treatment with ocular
hypo tensiveS

23. • Therefore, treatment is recommended only in high
risk group
• Lowering of IOP by atleast 20% is recommened.
• Topical beta blockers or prostaglandin analogues are
usually the preferred agents
• Patients with moderate risk of progression should
be monitored closely and treatment is initiated with
the earliest sign of glaucomatous damage

24. HIGH RISK- NEED RX
1. Retinal nerve fiber layer defects.
2. Parapapillary changes.
3. IOP > 30 mmHg
4. IOP > 26 mmHg with central corneal thickness
<555 microns.
5. Vertical cup-disc ratio 0.4:1 or more with central
corneal thickness <555 microns.

25. MODERATE RISK: annual follow-up
1. IOP 24-29 mmHg without retinal nerve fibre layer
damage.
2. IOP 22-25 mmHg with central corneal thickness
<555
microns.
3. Vertical cup-disc ratio 0.4:1 or more with central
corneal thickness between 555-588 microns.
4. Family history of POAG in first degree relative.
5. High Myopia.

26. LOW RISK: Follow-up every 2 years
1. IOP 22-23 mmHg with central corneal thickness
more than 588 microns.
2. Vertical cup-disc ratio 0.4 or more with central
corneal thickness more than 588 microns.

27. • Other possible indications for treatment
1.One eyed patient
2.Young patient,will be exposed to high pressures for
many years
3.Unreliable visual or optic disc assesment
4.Patient who is in content with treatment initiated by
another physician and tolerating medicaton well
5.An ocular htn pt who desires treatment
6. OHTN pt who has developed vascular occlusion in
either eye

28. • Monotherapy is preferred with a max of 2
medications at a time
• If not reducing SLT can be used
• Aggressive therapy should never be tried

29. • Hence, early recognition and treatment of high risk
patients can limit the visual disability due to POAG.
• Frequency doubling perimetry (FDP) or short
wavelength automated perimetry (SWAP) detects
glaucomatous damage at a very early stage, 4 years
before the changes appear in white-on white
perimetry.
• Hence, for patients under monitoring, FDP or SWAP
may be beneficial in early initiation of treatment.

30. THANK YOU