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Year : 2016  |  Volume : 8  |  Issue : 1  |  Page : 26-29

Central corneal thickness and severity of visual field loss in primary open-angle glaucoma

Department of Ophthalmology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, Uttar Pradesh, India

Date of Web Publication17-Jun-2016

Correspondence Address:
Syed Wajahat Ali Rizvi
620/7, Rizvi Lodge, Rasalganj, Aligarh - 202 001, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1858-540X.184234

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Purpose: To determine whether central corneal thickness (CCT) is correlated to severity of visual field (VF) loss among patients of primary open-angle glaucoma (POAG) at initial evaluation. Materials and Methods: One hundred and two eyes with POAG were recruited in this cross-sectional study. Humphrey field analysis, applanation tonometry, and CCT measurement were done in all subjects. Based on severity of VF loss, the sample was split into mild (n = 55), moderate (n = 21), and severe VF loss (n = 26) as per Anderson-Patella criteria. For each of the three groups, calculated mean values were compared using analysis of variance (ANOVA). Results: The sample contained 102 eyes of 102 patients which were divided into groups of mild, moderate, and severe VF loss. The mean (±standard deviation [SD]) CCT for Group I was 543.07 μm (±24.60), for Group II was 539.24 μm (±22.30), and for Group III was 536.11 μm (±22.86). The mean (±SD) mean deviation for Group I was –2.78 dB (±1.65), for Group II was −8.91 dB (±2.18), and for Group III was –21.47 dB (±5.98). When analyzed, the mean differences of CCT in patients with mild, moderate, and severe VF involvement were not statistically significant (ANOVA, P = 0.43). Conclusion: We failed to find any significant association between CCT and severity of VF defect in the eyes with POAG.

Keywords: corneal thickness, field defects, optic nerve head

How to cite this article:
Khan AA, Rizvi SW, Adidravid A, Amitava AK, Siddiqui Z. Central corneal thickness and severity of visual field loss in primary open-angle glaucoma. Sudanese J Ophthalmol 2016;8:26-9

How to cite this URL:
Khan AA, Rizvi SW, Adidravid A, Amitava AK, Siddiqui Z. Central corneal thickness and severity of visual field loss in primary open-angle glaucoma. Sudanese J Ophthalmol [serial online] 2016 [cited 2022 Aug 9];8:26-9. Available from: https://www.sjopthal.net/text.asp?2016/8/1/26/184234

  Introduction Top

About one-third of the patients treated for glaucoma keep losing visual field (VF) while maintaining intraocular pressure (IOP) below 21 mmHg, and 27% of the patients with glaucoma may go blind in one eye after 20 years of treatment.[1],[2] These statistics demand an early identification of those patients at high risk of progression to advanced stages to establish a more aggressive control of the IOP and achieve a better preservation of the VF and the quality of life of this population.

Research has been done to measure the “real” or “manometric” IOP using a cannulation method and then to correlate central corneal thickness (CCT) to IOP measurements of Goldmann applanation tonometry (GAT).[3] The IOP value measured with Goldmann tonometer equals the manometric one when CCT value is 520 µm, and variations from this value resulted in overestimation or underestimation of IOP that could be calculated as 7 mmHg for every 100 µm of corneal thickness. Hence, thinner CCT was underestimating the IOP due to which they were associated with greater glaucomatous damage.

In addition, due to the continuity of the cornea, sclera, and optic disc lamina, CCT may represent a factor that reflects the biomechanics of the optic nerve head (ONH). Several researchers have turned to numerical modeling to understand the biomechanical environment within the ONH.[4],[5] The most interesting prediction they made was that the biomechanics of the corneoscleral shell affect cellular deformation in the ONH quite profoundly. Therefore, it seems reasonable that there should be a relationship between the CCT and biomechanical properties of the cornea and those of the sclera and ONH.

  Materials and Methods Top

The patients for this longitudinal, prospective study were recruited from glaucoma and general outpatient clinics. A well-informed written consent was obtained from each patient before enrollment. Institutional board approval was obtained from the ethical committee, and all procedures adhered to the tenets of the Declaration of Helsinki.

The inclusion criteria were (i) diagnosed case of open-angle glaucoma, (ii) characteristic field defects, (iii) best-corrected visual acuity 6/12 or better, and (iv) spherical error within ±5.0 diopters and cylindrical error within ±3.0 diopters.

Patients with corneal edema or opacification, previous cataract surgery, keratoplasty or any other refractive surgery, phthisis bulbi, use of contact lens, history of ocular trauma, neurological disease, stroke, retinopathy, refractive error exceeding 5 diopters equivalent sphere, or 3 diopters of astigmatism were excluded from the study.

We recruited 102 patients diagnosed with primary open-angle glaucoma (POAG) for the study. The right eye of the each patient was chosen for the study. Each patient underwent a biomicroscopic and a VF examination, CCT, and IOP measurements. VF examinations were carried out with static automated perimetry using 30-2 program of the Humphrey field analyzer (Carl Zeiss Meditec, Dublin, CA, USA); CCT was measured with an ultrasound pachymeter (DGH-550 Pachette 2, DGH Technology Inc., Exton, PA, USA); and IOP was measured with GAT.

The eyes were categorized into three VF defect (VFD) groups: Early, moderate, and severe as per the Anderson's classification.[6] An early VFD was defined as follows:

  1. Mean deviation (MD) better than –6 dB,
  2. Fewer than 25% of points (18) are depressed below 5% level and <10 points are depressed below the 1% level of the pattern deviation plot, and
  3. No point in the central 5° with a sensitivity of <15 dB.

A severe field defect was defined as follows:

  1. MD beyond −12 dB,
  2. More than 37 (50%) of the points depressed at the 5% level and more than 20 points depressed at the 1% level, and
  3. A point in the central 5° with 0 dB sensitivity or points closer than 5° of fixation with <15 dB sensitivity in both hemifields.

A moderate VFD was defined as one exceeding one or more of the criteria required to keep it in the early defect category but not meeting the criteria for a severe VFD.

A statistical analysis was conducted to find the association between CCT and severity of VFD. For each of the three VFD groups, a comparison of all calculated mean values was made by one-way analysis of variance (ANOVA).

A statistical analysis was conducted to find the association between CCT and severity of visual field defect. For each of the three visual field defect groups, a comparison of all calculated mean values was made by one-way analysis of variance (ANOVA). A P< 0.05 was considered statistically significant.

  Results Top

[Table 1] shows the demographic details of the patients enrolled in the study.
Table 1: Demographics of patients

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Out of the total 102 patients, 54% had mild, 21% had moderate, and 25% had severe VFD.

[Table 2] shows characteristics of variables based on severity of VFDs. The mean age for Group I was 45.69 (±6.16) years, for Group II was 52.9 (±8.02) years, and for Group III 55.96 (±7.94) years [Table 2]. The mean IOP for Group I was 18.90 (±4.58) mmHg, for Group II was 17.14 (±3.60) mmHg, and for Group III was 16.73 (±6.89) mmHg [Table 2]. The mean CCT for Group I was 543.07 (±24.60) µm, for Group II was 539.24 (±22.30) µm, and for Group III was 536.11 (±22.86) µm [Table 2] and [Figure 1]. The mean MD in VFD for Group I was −2.78 (±1.65) dB, for Group II was −8.91 (±2.18) dB, and for Group III was −21.47 (±5.98) dB [Table 2].
Table 2: Characteristics among visual field defect categories

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Figure 1: Mean differences in central corneal thickness versus visual field defect

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There was no statistically significant difference in mean of CCT in mild, moderate, and severe VF involvement (P = 0.43, ANOVA).

  Discussion Top

In our study, wherein POAG patients were classified into mild, moderate, and severe based on their field defects, we found no statistically significant difference in the mean CCT.

Several studies have shown an association between CCT and VFD and its progression. In ocular hypertensive treatment study,[7] 1636 participants who had ocular hypertension, with an IOP between 24 mmHg and 32 mmHg and no evidence of glaucomatous damage, were randomized to either observation or treatment with commercially available topical ocular hypotensive medications. A thinner central corneal measurement predicted the development of POAG in both univariate and multivariate models. Among participants who developed POAG, the mean ± standard deviation (SD) CCT was 553.1 ± 38.8 µm compared with 574.3 ± 37.8 µm among those who did not develop POAG.

In another study,[8] 88 patients with POAG were followed for an average of 8 years, who had VF loss and progression as defined by modified Anderson criteria. Cases with progression were matched for race, diagnosis, and age at pachymetry with controls who did not have progression. The mean CCT in patients with VF progression was significantly lower than the mean CCT in patients who did not progress (529 ± 36 µm vs. 547 ± 35 µm; P = 0.02). Those with thinner CCT were more likely to progress than those with thicker CCT as identified by cox proportional hazards regression analysis (P = 0.01; hazard ratio, 1.44 for a 40 µm thinner CCT; 95% confidence interval, 1.12-1.80), and CCT was the only risk factor identified to be significantly associated with VF progression.

However, agreement was found with respect to this issue in the studies of Jonas et al.,[9] which included 372 eyes of 215 patients with chronic open-angle glaucoma. Progression of glaucomatous VFDs detected in 119 (21.0%) eyes was statistically independent of CCT in univariate (P = 0.99) and multivariate cox regression analyses (P = 0.19).

Another study was also unable to show an association between CCT and VF progression in POAG.[10] The sample contained 101 eyes of 54 patients (mean [SD] age, 56.5 [9.8] years) with a mean follow-up of 9.2 (0.7) years. Patients were divided into three groups based on corneal thickness with <524 μm, 524-567 μm, and >567 μm. Moreover, comparison with VF indices was performed. The results suggested that VF progression could not be explained in relation to CCT (r = 0.072, P = 0.474 for the total deviation analysis and r = 0.031, P = 0.760 for the pattern deviation analysis).

The reason behind such conflicting results is not quite clear. It may be due to differences in study design (differences in the populations included in every study and the criteria used to define VF loss) or may be due to administration of IOP-lowering drugs for the study population. However, a meta-analysis comprising these similar designed studies is needed to come into more accurate conclusion.

Studies have also shown that measurement of CCT may be a poor correlate of posterior sclera thickness.[11] Indeed, there is even uncertainty regarding an association between CCT and anterior scleral thickness, implying that there is likely to be even greater degree of uncertainty regarding association between CCT and VFD. Evidence from experimental myopia suggests that acquired changes in scleral thickness occur primarily at the posterior pole, and therefore, thickness estimates of the posterior sclera based on measurements of the anterior sclera or cornea may be inaccurate.[12] From a practical perspective, a measurement of CCT can be valuable in the initial assessment of the glaucoma suspect, particularly in ruling out a high risk suggested by an elevated IOP in an eye with high CCT but with normal optic disc and VF findings. However, once glaucomatous damage is present, CCT is unlikely to be useful as a predictor of severity of VFD. We thus conclude that IOP and CCT should best be treated as two independent risks factors or integrated without calculation of “true IOP.”

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Heijl A, Bengtsson B, Hyman L, Leske MC; Early Manifest Glaucoma Trial Group. Natural history of open-angle glaucoma. Ophthalmology 2009;116:2271-6.  Back to cited text no. 1
O'Brien C, Schwartz B, Takamoto T, Wu DC. Intraocular pressure and the rate of visual field loss in chronic open-angle glaucoma. Am J Ophthalmol 1991;111:491-500.  Back to cited text no. 2
Ehlers N, Bramsen T, Sperling S. Applanation tonometry and central corneal thickness. Acta Ophthalmol (Copenh) 1975;53:34-43.  Back to cited text no. 3
Sigal IA, Flanagan JG, Ethier CR. Factors influencing optic nerve head biomechanics. Invest Ophthalmol Vis Sci 2005;46:4189-99.  Back to cited text no. 4
Sigal IA, Flanagan JG, Tertinegg I, Ethier CR. Finite element modeling of optic nerve head biomechanics. Invest Ophthalmol Vis Sci 2004;45:4378-87.  Back to cited text no. 5
Anderson DR, Patella VM. Automated Static Perimetry. St. Louis: Mosby; 1999.  Back to cited text no. 6
Gordon MO, Beiser JA, Brandt JD, Heuer DK, Higginbotham EJ, Johnson CA, et al. The ocular hypertension treatment study: Baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120:714-20.  Back to cited text no. 7
Kim JW, Chen PP. Central corneal pachymetry and visual field progression in patients with open-angle glaucoma. Ophthalmology 2004;111:2126-32.  Back to cited text no. 8
Jonas JB, Stroux A, Velten I, Juenemann A, Martus P, Budde WM. Central corneal thickness correlated with glaucoma damage and rate of progression. Invest Ophthalmol Vis Sci 2005;46:1269-74.  Back to cited text no. 9
Chauhan BC, Hutchison DM, LeBlanc RP, Artes PH, Nicolela MT. Central corneal thickness and progression of the visual field and optic disc in glaucoma. Br J Ophthalmol 2005;89:1008-12.  Back to cited text no. 10
Oliveira C, Tello C, Ritch R, Liebmann JM. Correlation between Central Corneal Thickness, Scleral Thickness and Refractive Error. Annual Meeting of the Association for Research in Vision and Ophthalmology; 2004. p. 963.  Back to cited text no. 11
McBrien NA, Cornell LM, Gentle A. Structural and ultrastructural changes to the sclera in a mammalian model of high myopia. Invest Ophthalmol Vis Sci 2001;42:2179-87.  Back to cited text no. 12


  [Figure 1]

  [Table 1], [Table 2]


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