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ORIGINAL ARTICLE
Year : 2018  |  Volume : 5  |  Issue : 1  |  Page : 1-5

Macular thickness in healthy controls and diabetics without diabetic macular edema


Department of Ophthalmology, Sohag Faculty of Medicine, Sohag University, Sohag, Egypt

Date of Web Publication20-Aug-2018

Correspondence Address:
Dr. Mohammed Hussein Elagouz
Department of Ophthalmology, Sohag Faculty of Medicine, Sohag University, 82524 Sohag
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/erj.erj_13_17

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  Abstract 


Aim of the Study: This study aims to evaluate the thickness of the macula in patients with diabetes but without diabetic macular edema (DME) using optical coherence tomography (OCT) and compare these findings with measurements from normal controls which may be useful for early detection of macular thickening. Patients and Methods: Two hundred subjects were included and divided into 4 equal groups: normal controls, diabetics without diabetic retinopathy (DR), diabetics with NPDR and without DME, and diabetics with PDR and without DME. Full ophthalmological evaluation was done and the fast macular OCT scan was done that divides the macula into 9 sectors. The mean ± standard deviation of macular thicknesses by area were analyzed and compared. Results: A central subfield (CS) was statistically significantly thicker in normal controls compared to diabetics with no DR with no significant difference in other sectors. Furthermore, all of the inner sectors (IS, IN, IT, II) and the ON sector were significantly thicker in normal compared to diabetics with nonproliferative DR (NPDR) group with no significant difference in other sectors. Furthermore, between all sectors except IS and IT on comparing normal versus diabetics with PDR, between nasal sectors (IN and ON) but not in other sectors on comparing diabetics with no DR versus diabetics with NPDR, between all sectors except IS on comparing diabetics with no DR versus diabetics with PDR, and between all sectors on comparing diabetics with NPDR versus diabetics with PDR. Conclusion: This study found that the fovea and perifoveal subfields of the ETDRS grid tended to be thinner in diabetics without DR than in healthy controls and still thinner in eyes with DR, but thicker in eyes with PDR than in healthy controls thus confirming that the loss of neural tissue begins in the early stages of diabetes. As diabetes develops, neurodegeneration may be masked by changes in vascular permeability that cause thickening of the retinal layers.

Keywords: Diabetics, healthy controls, macular thickness


How to cite this article:
Shawky SS, Elagouz MH, Ismail AM, Elhawwary AM. Macular thickness in healthy controls and diabetics without diabetic macular edema. Egypt Retina J 2018;5:1-5

How to cite this URL:
Shawky SS, Elagouz MH, Ismail AM, Elhawwary AM. Macular thickness in healthy controls and diabetics without diabetic macular edema. Egypt Retina J [serial online] 2018 [cited 2018 Nov 17];5:1-5. Available from: http://www.egyptretinaj.com/text.asp?2018/5/1/1/239453




  Introduction Top


Diabetic retinopathy (DR) is a severe and widely spread eye disease increasing in incidence as the worldwide number of patients with diabetes grows. Thus, an objective test for the early diagnosis and evaluation of treatment in DR is certainly needed to identify the individuals at great risk for vision-threatening problems.[1]

Several studies [2],[3],[4],[5],[6],[7],[8] showed that retinal neuronal abnormalities are present at the early stages of DM. These abnormalities as retinal ganglion cell (RGC) death and axonal degeneration should increase with increasing DM duration, and this reduces the RNFL thickness. The early detection and intervention to prevent these neuronal abnormalities might prevent neurodegeneration.

Because macular thickness has been found to significantly correlate with visual acuity,[9] knowledge of normal population thickness would be essential for studying and evaluating macular thickening due to various ocular pathologies. Traditional methods of evaluating retinal thickness such as ophthalmoscopy or stereoscopic biomicroscopy are insensitive to detecting small changes in retinal thickness. Optical coherence tomography (OCT) is a noninvasive technology that enables clinicians to detect and monitor subtle changes in macular thickening;[10],[11],[12],[13] it offers the possibility of both high-resolution cross-sectional images of the retina and quantitative measurements of the retinal thickness.[14],[15]

The role of the OCT in the assessment and management of the diabetic retina has become significant in understanding the vitreoretinal relationships and the internal architecture of the retinal structure.[16] OCT images can either be used to qualitatively assess retinal features and pathologies or to objectively make quantitative measurements which is especially important in the early stages of DR when the structural changes are not yet evident with slit-lamp biomicroscopy or angiographically.[17]

Aim of the study

This study aims to evaluate the thickness of the macula in participants with diabetes but without diabetic macular edema (DME) using OCT and compare these findings with measurements from normal controls which may be useful for early detection of macular thickening.


  Patients and Methods Top


This Study was a prospective comparative case-control study.

Inclusion criteria

Two hundred subjects were included in the study and divided into 4 equal groups, each including 50 subjects:

  • Group 1: Normal controls
  • Group 2: Diabetic patients without DR
  • Group 3: Diabetic patients with nonproliferative DR (NPDR) and without DME
  • Group 4: Diabetic Patients with PDR and without DME.


These participants were chosen randomly from patients attending the general Ophthalmology and retina clinics of Sohag University Hospital. Approval of the Faculty Ethics Committee was obtained and written informed consent was obtained from each participant. The study was carried out from March 2015 to February 2016.

The collected data included:

  1. History taking regarding age, duration of diabetes, type of treatment given
  2. Full ophthalmological evaluation including visual acuity (VA), intraocular pressure (IOP), slit-lamp biomicroscopy, examination of the fundus with the slit lamp biomicroscopy and indirect ophthalmoscopy. Fluorescein angiography was done when indicated.


Exclusion criteria

  1. Patients with diabetic macular edema (DME) or other macular diseases
  2. Patients with history of retinal laser treatment
  3. Patients with chronic glaucoma.


We used the Topcon™, 3D OCT-2000 machine to perform the fast macular scan which gives 3 concentric circles: 1, 3, and 5 mm in diameter centered on the fovea. The 3 and 5 circles are each divided into nasal, temporal, superior, and inferior quadrants [Figure 1].
Figure 1: Macular sectors. CS: Central subfield, IS: Inner superior, IN: Inner nasal, II: Inner inferior, IT: Inner temporal, OS: Outer superior, ON: Outer nasal, OI: Outer inferior, OT: Outer temporal.

Click here to view


The mean ± standard deviation (SD) of macular thickness by area in these eyes were analyzed and compared.

The machine was operated by two of the authors (S.S and A.E), and the calculations and revisions of the scans by them and by (M.E and A.I).

Statistical analysis

All analyses were performed using SPSS for windows version 16.0 (SPSS, Inc., Chicago, IL, USA). Data were expressed as mean ± SD. Independent t-test was used to make statistical comparisons. P < 0.05 was considered statistically significant.


  Results Top


This study included 200 eyes divided into 4 groups; group 1 included 50 controls, group 2 included 50 diabetic patients with no DR, group 3 included 50 diabetic patients with NPDR and without DME, and group 4 included 50 diabetic patients with PDR and without DME.

These individuals included 73 male (36.5%) and 127 female (63.5%). The mean age of control, NDR, NPDR, and PDR groups were (53.55 ± 8.34), (57.38 ± 11.29), (57.10 ± 6.94), and (52.96 ± 7.32), respectively.

The clinical data and demographics of all subjects are shown in the table.

OCT was used to examine the 200 eyes. The mean ± SD of macular thickness in the nine sectors in these eyes were recorded and reported in [Table 1]. We compared the thicknesses of each sub-area in the 4 groups against each other: normal against diabetics without DR, normal against diabetics with NPDR, normal against diabetics with PDR, diabetics with no DR against diabetics with NPDR, diabetics with no DR against diabetics with PDR, and diabetics with NPDR against diabetics with PDR [Figure 2] and the results were as follows:
Table 1: Clinical data and demographics of the study groups

Click here to view
Figure 2: A graph showing the thicknesses of the macular sectors in different groups.

Click here to view


The CS sector was statistically significantly thicker in normal controls versus diabetics with no DR but not in other sectors.

A statistically significant difference in thickness was found between inner sectors (IS, IN, IT, II) and the ON sector between normal and diabetics with NPDR groups but not in other sectors, the thickness being less in NPDR group.

A statistically significant difference in thickness was found between all sectors except IS and IT on comparing normal versus diabetics with PDR, being thicker in normal controls.

A statistically significant difference was found between nasal sectors (IN and ON) but not in other sectors on comparing diabetics with no DR versus diabetics with NPDR.

A statistically significant difference was found between all sectors except IS on comparing diabetics with no DR versus diabetics with PDR.

A statistically significant difference was found between all sectors on comparing diabetics with NPDR versus diabetics with PDR.


  Discussion Top


Previous studies have reported changes in the macular retinal thickness and the thicknesses of different layers in diabetic patients with and without DR.[18],[19],[20],[21],[22]

The early diagnosis and early detection of functional changes related to DR that occur before retinal morphology changes are important for preventing DR. Some researchers have found that retinal neurodegeneration may occur in DR before any microcirculatory abnormalities can be detected.

[23],[24] Neural apoptosis and the loss of ganglion cell bodies and glial reactivity are now considered to be the main factors in DR.[25],[26]

Although fluorescein angiography is highly sensitive for the qualitative detection of fluid leakage, which causes macular edema, measurements of retinal thickening may correlate better with areas of retinal dysfunction than does the amount of fluorescein leakage.[9] OCT enables the clinician to show accurately subclinical retinal changes in the absence of CSME or the absence of any signs of DR by detectable fluorescein leakage.[27]

In this study, our OCT findings demonstrated that the central macula in the diabetic patients with no DR group was significantly thinner than that of the control group with mean (233.34 ± 29.15) and (221.38 ± 24.26), respectively.

These results are comparable to Verma et al. who found a reduction in foveal thickness in patients with DM and no retinopathy compared to healthy controls.[28]

These results are not consistent with the past reports.[29],[30],[31] One possible reason for this discrepancy may be the shorter duration of the DM in our NDR group than in the other studies, 5.48 ± 4.39 versus 7.9 ± 7.3 years in the data of Sugimoto.[31]

However, several recent publications have shown that retinal neurodegeneration precedes clinically detectable microvascular damage.[20],[32],[33],[34],[35] The hypothesis referring to the occurrence of neurodegeneration before vascular damage has been confirmed by electrophysiological and psychophysical studies.[36],[37] Recent studies in animals have revealed that diabetes causes the loss of different types of retinal cells including ganglion cells, bipolar cells, amacrine cells, horizontal cells, and eventually photoreceptors.[16],[33],[37],[38] Clinically, different authors have reported a decrease in retinal thickness in diabetic eyes with or without clinical signs of DR compared to normal subjects.[35],[38],[39],[40],[41]

Previous animal and human studies have demonstrated that some RGCs die in diabetes, and some show structural alterations that are likely related to inflammation, excitotoxicity, and oxidative/nitrative stress.[39] Although the molecular mechanism by which RGCs die has not been clarified yet, apoptotic processes have been demonstrated histopathologically in RGCs in diabetes. In particular, it was shown that apoptosis leads to RNFL thinning in rats with streptozotocin (STZ)-induced diabetes and in diabetic patients without or with only minimal DR by using scanning laser polarimetry or SDOCT.[20],[42]

In addition, various signs of retinal neurodegeneration have been found postmortem in the retinas of diabetic donors without any microcirculatory abnormalities during ophthalmoscopic examinations performed the year before death.

[43],[44]

In addition, our findings showed that the central macular thickness with mean (221.38 ± 24.26), (231.30 ± 29.34), and (256.48 ± 39.62) gradually increased with the duration of DM with mean (5.48 ± 4.39), (13.96 ± 4.93), and (14.70 ± 4.17) years in diabetics with no DR, diabetics with NPDR, and diabetics with PDR, respectively, probably because of an increase in vascular permeability in the diabetic retinas. Because of the short duration of DM, early reduction of macular thickness due to neuronal degeneration was not masked by the increase in macular thickness associated with vascular leakage.

Several studies, including ours, showed that retinal neuronal abnormalities are present at the early stage of diabetes.

[2],[3],[4],[5],[6],[7],[8] The neuronal abnormalities may explain the thinner macular thickness if these developed before the increased vascular permeability. Neuronal abnormalities including RGC death and axonal degeneration should increase with an increase in the duration of DM, and in turn, reduce the RNFL thickness. Our findings that macula was thinner at the NDR stage but thicker in the PDR stage would suggest that the neuronal abnormalities may precede the vascular abnormalities.

Furthermore, thicker maculas in the PDR group than that in the normal group is consistent with the earlier reports.[29],[30],[31]

This may be due to increase in serous leakage that probably led to the swelling of the retina.

In this study, comparing normal control group with diabetic patients with NPDR, we found a decrease in macular thickness in eyes with NPDR with statistically significant difference between inner sectors (IS, IT, IN, II) and only outer nasal sector.

This is comparable to Vujosevic and Midena [35] as well as Van Dijk et al.[41],[42] who have shown a reduction in the inner retinal thickness in the macula in diabetics with mild DR. Van Dijk et al. speculates an initial GCL loss in the pericentral areas followed by RNFL thinning in the peripheral macula.[20],[42]

In addition, Vujosevic and Midena found that the outer retina may not be affected at the early stages of DM and concluded that automatic intraretinal layering by SD-OCT may be a useful tool to diagnose and monitor early intraretinal changes in DR.

The drawback of this study is the relatively small number of participants. Further larger-scale studies are needed to study the differential affection of different macular sectors in different stages of DR to detect if there is a preferential affection of these different sectors.


  Conclusion Top


This study detected morphological changes in DM patients using OCT, confirmed that the loss of neural tissue begins in the early stages of diabetes. As diabetes develops, neurodegeneration may be masked by changes in vascular permeability that cause thickening of the retinal layers.

Early thinning of the inner retina occurs in diabetes, even before visible vascular signs of DR. This supports the presence of a neurodegenerative process in eyes of patients with diabetes and warrants neuroprotective intervention to prevent neurodegeneration. The OCT may represent a good tool for identifying early signs of neurodegeneration in diabetic patients.

These results may help in close monitoring of diabetic patients before developing DR.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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