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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. www. dosonline.org l 47 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