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 Table of Contents  
Year : 2023  |  Volume : 3  |  Issue : 1  |  Page : 100-102

Disproportionately large neurosensory retinal detachment in diabetic retinopathy as a sign of diabetic choroidopathy

1 Retina Services, Netralaya Eye Hospital, Kolkata, West Bengal, India
2 Retina Services, Aditya Birla Sankara Nethralaya, Kolkata, West Bengal, India

Date of Submission31-May-2022
Date of Acceptance17-Aug-2022
Date of Web Publication20-Jan-2023

Correspondence Address:
Kumar Saurabh
Netralayam Eye Hospital, 330 Mukundpur Main Road, E. M. Bypass, Kolkata – 700 099, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijo.IJO_1348_22

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Neurosensory retinal detachment (NSD) is a component of diabetic retinopathy. It is associated with other features like diffuse retinal thickening and cystoid macular edema (CME). The present report describes imaging features and the outcome of disproportionately large NSD in the left eye of a 61-year-old lady having proliferative diabetic retinopathy. The NSD was accompanied by minimal intraretinal edema and a choroidal filling defect on fluorescein angiography. There was near complete resolution of NSD with intravitreal ranibizumab. Disproportionately large NSD with minimal intraretinal cystic changes may be considered as a sign of diabetic choroidopathy.

Keywords: Choriocapillaris, diabetic choroidopathy, diabetic retinopathy, neurosensory retinal detachment

How to cite this article:
Saurabh K, Roy R, Paul SS, Das S, Nandi K, Biswas RK, Sinha S. Disproportionately large neurosensory retinal detachment in diabetic retinopathy as a sign of diabetic choroidopathy. Indian J Ophthalmol Case Rep 2023;3:100-2

How to cite this URL:
Saurabh K, Roy R, Paul SS, Das S, Nandi K, Biswas RK, Sinha S. Disproportionately large neurosensory retinal detachment in diabetic retinopathy as a sign of diabetic choroidopathy. Indian J Ophthalmol Case Rep [serial online] 2023 [cited 2023 Feb 7];3:100-2. Available from: https://www.ijoreports.in/text.asp?2023/3/1/100/368135

Optical coherence tomography (OCT) is the primary imaging modality for management of diabetic macular edema (DME). Diffuse retinal thickening, cystoid macular edema (CME), neurosensory retinal detachment (NSD) without posterior hyaloid traction, posterior hyaloid traction without tractional retinal detachment, and posterior hyaloid traction with tractional retinal detachment are the five types of DME distinguished on OCT.[1] NSD is noted in about one third of eyes with DME.[2] Current understanding states that individuals with NSD do not have significantly higher glycosylated hemoglobin or blood pressure than those without NSD.[2] Though presence or absence of NSD does not affect the post-treatment visual outcome, eyes with NSD have reduced retinal sensitivity.[2],[3] These assertions are about NSD as a component of DME alongside other features like CME or diffuse retinal thickening. We hereby report imaging features and the treatment outcome of a patient with disproportionately large NSD with diabetic retinopathy, having minimal OCT features of DME.

  Case Report Top

A 61-year-old lady presented with sudden dimness of vision in her left eye for five days. She was a diabetic and hypertensive and did not have a history of ischemic heart disease, cerebrovascular accident, or chronic renal disease. The best corrected visual acuity was 6/9, N6 in her right eye and counting finger at one meter distance in the left eye. Anterior segment was unremarkable in both eyes. Intraocular pressure (IOP) with applanation tonometer was 12 mmHg in both eyes. Fundus examination of the right eye revealed retinal hemorrhages at macula with drusen. The left eye had retinal hemorrhages at macula and few cotton wool spots. Spectral domain OCT (SDOCT) line scan using Spectralis system (Heidelberg Engineering, Germany) through the macula showed epiretinal membrane with minimal intraretinal cystic spaces in the right eye [Figure 1]a. The left eye showed a large NSD with minimal intraretinal cystic changes [Figure 1]b, [Figure 1]c, [Figure 1]d. Arm-to-retina time was 16 seconds on fluorescein angiography (FA). The right eye showed non-proliferative diabetic retinopathy (NPDR) with microaneurysms and capillary non-perfusion (CNP). The left eye showed proliferative diabetic retinopathy (PDR) with microaneurysms, CNP areas and neovascularization elsewhere [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d. There was an area of hypofluorescence involving the foveal avascular zone and extending superotemporally, which appeared in the early phase and persisted till the late phase in the left eye. There was no pooling of dye or abnormal optic nerve head staining or vascular staining in either eye. A relook at clinical history revealed controlled hypertension with systolic and diastolic blood pressure below 145 and 90 mmHg on multiple occasions. Her current blood pressure was 130/80 mmHg. Complete hemogram revealed anemia with hemoglobin of 11 gm/dl. The total white blood cell count, differential count, and erythrocyte sedimentation rates were normal. The lipid profile was within normal limits, and serum urea and serum creatinine were normal. Blood albumin was 3.76 gm/dl (normal 3.3–5.0 gm/dl) and blood globulin was 3.31 gm/dl (normal 2.0–4.1 gm/dl). Albumin-to-globulin ratio was 1.14 (normal 1.0–2.1). Electrolytes essay was unremarkable with serum sodium at 136.3 mmol/L (normal 137–145 mmol/L) and serum potassium at 3.90 mmol/L (normal 3.5–5.1 mmol/L). Patient received panretinal photocoagulation and intravitreal injection ranibizumab (0.05 ml) in the left eye. One month later, the BCVA in the left eye improved to 6/9, N18. SDOCT scan through the fovea in the left eye revealed restored foveal contour with shallow resolving NSD and hyperreflective dots in the subretinal space [Figure 3]a and [Figure 3]b. There was a hyporeflective double layer sign (DLS) at the fovea. The patient was advised close follow-up and review after three to four weeks.
Figure 1: (a) Spectral domain optical coherence tomography (SDOCT) line scan through the macula in the left eye shows maintained foveal contour with few intraretinal cystic spaces and epiretinal membrane (yellow arrow). (b-d) SDOCT line scan through macula shows large neurosensory retinal detachment (NSD) with minimal intraretinal cystic changes. Note that the NSD is out of proportion of the intraretinal cystic changes. The retinal pigment epithelium appears normal

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Figure 2: (a) Early phase image of fluorescein angiography (FA) shows normal vascular filling with relative hypofluorescence around the fovea (yellow arrows) compared to the surrounding choroidal fluorescence. (b) Early arteriovenous phase shows multiple punctate hyperfluorescence due to microaneurysm. The hypofluorescence at the surrounding fovea (yellow arrows) is well demarcated. (c) Late arteriovenous phase shows continued leakage from microaneurysms. The hypofluorescence around the fovea (yellow arrows) is more demarcated now compared to normal choroidal fluorescence in the adjoining areas. (d) Late phase image shows leaking microaneurysms. The hypofluorescent patch (yellow arrows) around the fovea is persisting

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Figure 3: (a) SDOCT line scan through the macula in the left eye shows shallow-resolving NSD. A shallow hyporeflective double layer sign (yellow arrow) is noted beneath the fovea. (b) Shallow NSD is noted with hyperreflective dots in the subretinal space which are believed to be the result of photoreceptor damage

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  Discussion Top

NSD is a known component of DME wherein it is associated with intraretinal edema. The present case was unique as it had a disproportionately large NSD with minimal intraretinal edema. Such NSD can be a feature of central serous chorioretinopathy which can also be associated with diabetic retinopathy.[4] However, FA did not reveal any central serous chorioretinopathy leak which would suggest it. There was no sign of intraocular inflammation and SDOCT imaging did not reveal any retinal pigment epithelium (RPE) pathology. In the absence of other pathologies, isolated NSD was considered a part of DME and treated on the same line with intravitreal anti-vascular endothelial growth factor (Anti-VEGF). Near-complete resolution of NSD would mean that it was indeed a consequence of VEGF-mediated vascular leakage which is the sine qua non of DME.

The area of hypofluorescence involving the foveal avascular zone, extending superotemporally in the left eye was present in early and late phases and appeared due to choroidal filling defect. It was present in the same area as the NSD. Choriocapillaris drop out and luminal narrowing of small choroidal vessels in diabetic eyes was first termed as diabetic choroidopathy by Hidayat and Fine in 1985.[5] Further, choroidal microaneurysm, dilatation and obstruction of choriocapillaris, increased vascular tortuosity, and vascular non-perfusion have been understood as other choroidal abnormalities in diabetes mellitus.[6],[7] The large NSD, minimal intraretinal edema and concomitant choroidal filling defect on FA may be considered as a manifestation of diabetic choroidopathy. Choriocapillaris are the main source of blood supply to outer retina and choriocapillaris drop out is a precursor of photoreceptor damage.[6] The OCT scan at one month after intravitreal ranibizumab did show hyperreflective dots at the roof of shallow resolving NSD, which are believed to be representation of photoreceptor damage.[6] The shallow hyporeflective DLS at fovea at this visit pointed toward ischemic environment at the level of RPE and choriocapillaris. These imaging features further suggest choriocapillaris ischemia, possibly due to diabetic choroidopathy. In our case, the anemia was not severe and renal parameters were normal which were not suggestive of paraproteinemic maculopathy. FA in paraproteinemic maculopathy is considered angiographically silent.[8] However, the present case had specifically blocked choroidal fluorescence with normal overlying retinal fluorescence. The subretinal fluid as noted on OCT was not turbid to cause blocked choroidal fluorescence. Such turbid fluid is seen in paraproteinemic maculopathy which also have other signs of hyperviscosity like vascular tortuosity and superficial retinal hemorrhage which were not present in this case. The fact that OCT angiography was not obtained in the present case may be considered a drawback of this assertion. However, OCT angiography technique has limited resolution to detect choriocapillaris abnormalities. Indocyanine green angiography (ICGA) would be helpful in identifying choroidal filling defect. ICGA was not indicated clinically and hence not performed. The large NSD in diabetic retinopathy with no intraretinal edema or pooling of dye on FA may be a feature of diabetic choroidopathy. Further examination of this assertion would be needed in a larger case series.

  Conclusion Top

Disproportionately large neurosensory retinal detachment in diabetic retinopathy with minimal or no intraretinal oedema should point towards diabetic choroidopathy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Otani T, Kishi S, Maruyama Y. Patterns of diabetic macular edema with optical coherence tomography. Am J Ophthalmol 1999;127:688-93.  Back to cited text no. 1
Vujosevic S, Torresin T, Berton M, Bini S, Convento E, Midena E. Diabetic macular edema with and without subfoveal neuroretinal detachment: Two different morphologic and functional entities. Am J Ophthalmol 2017;181:149-55.  Back to cited text no. 2
Giocanti-Aurégan A, Hrarat L, Qu LM, Sarda V, Boubaya M, Levy V, et al. Functional and anatomical outcomes in patients with serous retinal detachment in diabetic macular edema treated with ranibizumab. Invest Ophthalmol Vis Sci 2017;58:797-800.  Back to cited text no. 3
Dhurandhar DS, Singh SR, Sahoo NK, Goud A, Lupidi M, Chhablani J. Identifying central serous chorioretinopathy biomarkers in coexisting diabetic retinopathy: A multimodal imaging study. Br J Ophthalmol 2020;104:904-9.  Back to cited text no. 4
Hidayat A, Fine B. Diabetic choroidopathy: Light and electron microscopic observations of seven cases. Ophthalmology 1985; 67:512-22.  Back to cited text no. 5
Borrelli E, Palmieri M, Viggiano P, Ferro G, Mastropasqua R. Photoreceptor damage in diabetic choroidopathy. Retina 2020;40:1062-9.  Back to cited text no. 6
Zhang Y, Qin Y, Wang S, Liu Y, Li X, Sun X. Higher choroidal thickness and lower choriocapillaris blood flow signal density based on optical coherence tomography angiography in diabetics. Sci Rep 2021;11:5799.  Back to cited text no. 7
Ferreira Santos da Cruz N, Milhomens Filho JAP, Ferraro DMN, Polizelli MU, de Moraes Ambrogini NSB. Hyperviscosity retinopathy and immunogammopathy maculopahy as new onset of multiple myeloma. Case Rep Ophthalmol 2021;12:578-84.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]


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