OCULAR HYPERTENSIONSIVATEJA CHALLA

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

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

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

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

EPIDEMIOLOGY• 4-10% population over 40 yrs18.4% 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

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

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

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 

Eye EYE EXAMINATION AAO PPP

SLBCORNEA• 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

•  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.

• 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

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

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

• 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

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.

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.

LOW RISK: Follow-up every 2 years1. 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.

• 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

• 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

• 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.

THANK YOU