Download Ocular Hypertension

Ocular Trauma
Miscellaneous
Ocular Hypertension
J.P. Chugh
MS
J.P. Chugh2 MS, Prachi Jain2 MS, Harpal Singh Jhagta2 MS,
R.S. Chauhan1 MS, Ashok Rathi1 MS
1. Regional Institute of Ophthalmology, Rohtak, Haryana
2. Riti Eye Care Hospital, Rewari, Haryana
O
cular Hypertension is defined as an IOP > 21 mmHg
without any evidence of glaucomatous optic nerve
damage or visual field defects. There is no underlying
ocular or systemic cause of elevated intraocular pressure.
Individuals with ocular hypertension are 8 times more
susceptible for the development of primary open angle
glaucoma (POAG) as compared to normal subjects.
Therefore, early diagnosis and initiation of ocular
hypotensive medication in high risk group may reduce the
incidence of POAG and subsequent visual disability.
Epidemiology
The prevalence of ocular hypertension varies in different
ethnic groups. Its prevalence increases with age. Highest
prevalence of 12.6% was reported amongst Afro-Caribbean
population in one study1. In the Framingham Eye Study
conducted in Whites, its prevalence was 6.2% amongst
under 65 age group, while 8.7% in individuals above
75 years of age2. In southern India prevalence of 1.1% in
individuals above 40 years of age has been reported3.
Risk Factors for Subsequent Conversion to POAG
Valuable data about significant risk factors contributing to
progression of ocular hypertension to POAG and effect
of ocular hypotensives on the disease course has been
obtained from Ocular Hypertension Treatment Study
(OHTS). OHTS is a long term, multi-centre, randomized
clinical trial started in 1994. It included 1636 participants
aged between 40-80 years and IOP values between 24-32
mm Hg in one eye without any evidence of glaucomatous
damage were randomized to treatment and observation
group. The study determined that the rate of progression
to POAG was reduced to 4.4% in the treatment group in
contrast to 9.4% in observation group in 5 years4. Suggested
risk factors are discussed below.
1. Central Corneal Thickness (CCT) – CCT was found
to be a powerful predictor for the development of
POAG5. IOP assessed by applanation tonometry may
be overestimated or underestimated in thicker and
thinner corneas, respectively. CCT less than 555µ were
found to be at greater risk than eyes with CCT more
than 588µ. The relative risk of POAG increased by
81% for every 40µ decrease in CCT.
2. IOP - Studies have revealed the normal IOP range
of 10-21 mmHg6. Although, IOP readings may show
considerable variations among glaucoma patients, IOP
reading more than 22 mmHg is a positive predictive
factor for the development of POAG.
3. Age – Age is an independent risk factor for the
development of POAG. Individuals with older age had
a greater risk for conversion to glaucoma. OHTS found
an increased risk of POAG with age (per decade),
of 43% in the univariate analysis and 22% in the
multivariate analysis.
4. Pattern Standard Deviation (PSD) - Although the
patients with ocular hypertension may not have visual
field defects on Standard Automated Perimetry (SAP),
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.
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Miscellaneous: Ocular Hypertension
5. Optic Nerve – Although OHT patients have no apparent
glaucomatous disc changes, increased vertical and
horizontal cup-disc ratio is a risk factor for progression
to POAG. Increase in cup-disc ratio by 0.1 leads to
32% and 27% increase in relative risk in vertical and
horizontal cupping, respectively.
2. IOP 22-25 mmHg with central corneal thickness <555
microns.
6. Family history and Black race were not found to be
significant in multivariate analysis in OHTS. However,
other studies have shown them to play significant role
in the development of POAG7,8.
5. High Myopia.
Diagnosis
Ocular hyperstension is a diagnosis of exclusion. Thorough
ocular examination including tonometry, gonioscopy, optic
disc evaluation and visual field testing should be done to
rule out any underlying cause of IOP elevation. History of
ocular trauma and steroid use should be ruled out.
Treatment
Only 1-2% patients progressed to POAG in a yearly followup in OHTS trial. 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 hypotensives. 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. While once in a 2 year follow-up
is recommended for low risk individuals. Suggested risk
crieteria for progression to POAG is described below.
High risk: Requires treatment. Aim for atleast 20% IOP
reduction.
1. Retinal nerve fiber layer defects.
2. Parapapillary changes.
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.
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.
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-onwhite perimetry. Hence, for patients under monitoring, FDP
or SWAP may be beneficial in early initiation of treatment.
References
1.
Nemesure B, Wu SY, Hennis A,et al. Factors related to the 4-year
risk of high intraocular pressure: the Barbados Eye Studies. Arch
Ophthalmol. 2003;121:856-62.
2.
Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye
Study monograph: an ophthalmological and epidemiological study
of cataract, glaucoma, diabetic retinopathy, macular degeneration
and visual acuity in a general population of 2631 adults, 1973-1975.
Surv Ophthalmol. 1980;24:335-610.
3. Ramakrishnan R, Nirmalan PK, Krisnadas R, et al. Glaucoma in
rural population of southern India. The Aravind Comprehensive Eye
Survey. Ophthalmology. 2003;110:1484-90.
4.
Gordon MO, Kass MA. for the Ocular Hypertension Treatment study.
The Ocular Hypertension Treatment Study. Design and baseline
description of the participants. Arch Ophthalmol. 1999;117: 57383.
5.
Gordon MO, Beiser JA, Brandt JD, et al. for the Ocular Hypertension
Treatment study. The Ocular Hypertension Treatment Study.
Baseline factors that predict the onset of primary open angle
glaucoma. Arch Ophthalmol. 2002;120: 714-20.
6.
Armaly MF. On the distribution of applanation pressure. Statistical
features and the effect of age, sex and family history of glaucoma.
Arch Ophthalmol. 1965;73: 11-8.
7.
Hart WM Jr, Yablonski M, Kass MA, et al. Multivariate analysis
of the risk of glaucomatous visual field loss. Arch Ophthalmol.
1979;97:1455-8.
8.
Armaly MF. Ocular pressure and aqueous outflow facility in siblings.
Arch Ophthalmol. 2005;123:1351-60.
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. Treatment initiated at the
earliest documented glaucomatous damage.
1. IOP 24-29 mmHg without retinal nerve fibre layer
damage.
48 l DOS Times - Vol. 20, No. 8 February, 2015