Egyptian Retina Journal

: 2018  |  Volume : 5  |  Issue : 2  |  Page : 25--31

Optical coherence tomography characteristics of active and regressed retinal neovessels secondary to proliferative diabetic retinopathy before and after panretinal photocoagulation

Islam Shereen Hamdy Ahmed 
 Department of Ophthalmology, Faculty of Medicine, Alexandria University, Alexandria, Egypt

Correspondence Address:
Dr. Islam Shereen Hamdy Ahmed
Department of Ophthalmology, Faculty of Medicine, Alexandria University, Champilion Square, Azarita, Alexandria


Aim: To describe the changes in the appearance of diabetic neovascularization and vitreoretinal interface before and after panretinal photocoagulation (PRP) using high-resolution spectral-domain optical coherence tomography (SD-OCT). Design: A prospective noncomparative observational case series study was performed on 15 eyes with proliferative diabetic retinopathy (PDR). Patients and Methods: Patients with PDR were scanned using SD-OCT scans directly over the region of the neovessels before and after PRP treatment. Results: The study included 15 treatment-naive eyes with PDR of 11 patients, 8 females and 3 males with a mean age of 54.18 ± 10.9 years (range 29–65 years). The mean best-corrected logarithm of the minimum angle of resolution visual acuity was 0.68 ± 0.19 (range 0.4–1). One (9.1%) case had insulin-dependent diabetes mellitus (type 1) and 10 (9.1%) cases had noninsulin-dependent diabetes (type 2). Posterior hyaloid was detached and identifiable in pretreatment SD-OCT scans in 11 (73.33% of studied eyes) eyes and not identifiable in 4 (36.67%) eyes. Changes in SD-OCT scan appearance after PRP included progression of posterior hyaloid separation with possible progressive retinal traction and retinoschisis, consolidation of the neovessels, regression of neovessels, or occurrence of preretinal hemorrhage. One case showed no visible change at the vitreoretinal interface. Conclusion: There are changes in the appearance of the diabetic neovessels and the vitreoretinal interface after PRP treatment that could be detected by SD-OCT.

How to cite this article:
Ahmed IS. Optical coherence tomography characteristics of active and regressed retinal neovessels secondary to proliferative diabetic retinopathy before and after panretinal photocoagulation.Egypt Retina J 2018;5:25-31

How to cite this URL:
Ahmed IS. Optical coherence tomography characteristics of active and regressed retinal neovessels secondary to proliferative diabetic retinopathy before and after panretinal photocoagulation. Egypt Retina J [serial online] 2018 [cited 2019 Mar 20 ];5:25-31
Available from:

Full Text


Diabetic retinopathy (DR) is one of the major blinding diseases.[1] The risk of blindness in diabetics is 25 times higher than in the general population.[2] Within 15 years of the diabetes diagnosis, proliferative DR (PDR) is estimated to develop in 33% of type 1 and 17% of type 2 diabetics.[3]

DR is classified into nonproliferative or proliferative retinopathy according to the degree of retinal vascular changes.

Nonproliferative diabetic retinopathy (NPDR) is the less severe form of the disease which can progress to proliferative retinopathy.

PDR is a more advanced form of the disease characterized by the presence of extra-retinal neovascularization, which may be neovascularization of the optic disc (NVD) and/or neovascularization elsewhere (NVE). This stage may become complicated by retinal detachment and vitreous or preretinal hemorrhage causing severe visual loss if left untreated.

In diabetics, the neovessels are known to develop from the venous side of the retinal circulation in the outer plexiform layer. They emerge as a bud of new vessels which penetrates the internal limiting membrane (ILM). They lie flat on the retinal surface in the earlier stages of the disease. Later, they show more progressive extra-retinal growth invading the cortical vitreous.[4],[5]

High-risk PDR is characterized by one of the following: (a) NVD approximately >1/4–1/3 disc area, with or without vitreous or preretinal hemorrhage; (b) vitreous and/or preretinal hemorrhage with NVD <1/4 disc area; and (c) NVE ≥1/2 disc area.[6]

Proliferative activity was found to be greater in mid-peripheral than posterior retina; this could be attributed to the worse degree of capillary nonperfusion in the mid-peripheral retina.[7]

The DR study (DRS) gave strong evidence that the panretinal photocoagulation (PRP) is safe and effective to treat PDR. Since then, PRP has been remaining the gold standard treatment for patients with PDR as well as severe NPDR under certain circumstances such as poor compliance with follow-up, pregnancy, impending cataract extraction, or a history of vision loss in the contralateral eye due to diabetic complications. The DRS demonstrated that the strongest benefit of PRP treatment occurs in eyes with high-risk PDR. In addition, the risk of visual loss at 2 years in severe NVD without hemorrhage was estimated to decrease from 26% to 9% with PRP.[8],[9],[10],[11],[12]

Optical coherence tomography (OCT) is a modern noninvasive method for ocular imaging; it is essential in the management of diabetic macular edema by helping not only in diagnosis, quantification, and monitoring the condition but also in diagnosing potentially associated vitreomacular traction (VMT) or associated changes in retinal layer morphology.[13],[14],[15]

Vitreoretinal interface changes in PDR were previously described in some histopathological studies; some suggested that the neovessels attach to the posterior vitreous surface or become incorporated into the cortical vitreous and become elevated during involutional vitreous changes such as vitreous synchysis.[16],[17]

Some previous studies reported OCT appearance of PDR; NVD was identified as a hyperreflective line protruding from the optic disc cup and connected to the cortical vitreous when detached or as a hyperreflective tissue over the optic disc when the vitreous was still attached. On the other hand, NVE appeared as homogenous hyperreflective loops that arise from the outer plexiform layer of the retina and penetrate the inner nuclear, inner plexiform, ganglion cell, and nerve fiber layers with loss of demarcation between these layers; the neovessels then penetrate through the ILM over the retina and become incorporated in the posterior hyaloid. This may lead to progressive retinal traction with or without retinal detachment or retinoschisis when the posterior hyaloids detach.[18]

To the best of our knowledge, no previous study made use of the commercially available spectral-domain OCT (SD-OCT) machine to describe the changes of the neovessels and the vitreoretinal interface by scanning the exact same location of the fundus before and after PRP treatment; we hope that this study will help better understanding the pattern of regression of the neovessels after control of proliferative activity by PRP treatment.

 Patients and Methods

A cohort of patients with PDR was studied in a prospective noncomparative observational case series. We included 15 treatment-naive eyes with PDR between January and October 2017. The study was conducted in Alexandria Main University Hospital – one of the largest tertiary referral centers in Northern Egypt.

The protocol of this study was approved by the Research Ethics Committee, Faculty of Medicine, Alexandria University, Egypt. The study was adhered to the tenets of the Declaration of Helsinki. Informed consent was taken from all participants before enrolment in the study.

The patient inclusion criteria included diabetic patients older than 18 years of age; evidence of PDR by clinical examination; no previous intraocular drug therapy or laser treatment to the study eye; clear ocular media and satisfactory pupil dilation allowing good-quality SD-OCT scans and PRP treatment; and posteriorly located neovessels (within central 30°) allowing capturing an OCT image using a commercially available SD-OCT machine.

After confirmation of eligibility for enrolment, the purpose and procedure of the study were explained to every patient and informed consent was signed. All patients underwent logarithm of the minimum angle of resolution best-corrected visual acuity testing, comprehensive ophthalmic examination including dilated fundus examination using slit-lamp biomicroscopy and a noncontact 90D fundus lens done by a medical retina consultant.

On the same day, before PRP treatment, SD-OCT scans (Spectralis, Heidelberg Engineering, Heidelberg, Germany) were obtained on the area of NVD or NVE using a macular cube or line raster. The location of the NVD or NVE to be scanned was determined guided by the near-infrared fundus image of the OCT machine after pupillary dilation.

At least 6 weeks after completion of PRP, dilated fundus examination was done by the same medical retina consultant using slit-lamp biomicroscopy and a noncontact 90D fundus lens; follow-up SD-OCT scans were captured.

The “follow-up” SD-OCT acquisition software (Spectralis, Heidelberg Engineering, Heidelberg, Germany) uses fundus landmarks to precisely center the OCT scans exactly on the same location of the reference image. It was used in the current study to make sure that the postlaser scans were centered exactly at the same location where the neovessels were scanned before the laser treatment. The SD-OCT scans before and after laser treatment were reviewed and analyzed.

To maximize the signal-to-noise ratio and improve image quality, we used the automatic real-time averaging and eye-tracking features and each scan comprised 100 averaged scans.


We conducted this case series study on 15 treatment-naive eyes with PDR of 11 patients. Data analysis was done using IBM SPSS software package version 20.0 (SPSS, Inc., Chicago, IL, USA).

Baseline characteristics of the patients and eyes included in the current study are summarized in [Table 1] and [Table 2], respectively.{Table 1}{Table 2}

On presentation, SD-OCT scans of the NVD or NVE were obtained using a commercially available SD-OCT machine (Spectralis, Heidelberg Engineering, Heidelberg, Germany). This was repeated at least 6 weeks after PRP treatment using the “follow-up” software with setting reference to the area of NVD or NVE in the pretreatment scans to enable accurate comparison of the changes in the appearance of OCT scans of the exact location.

On the SD-OCT scans, the NVD showed as hyperreflective tissue arising from the optic cup and lying on the disc if posterior hyaloid was not detached or extending to it if detached. On the other hand, NVE appeared as hyperreflective tissue arising from the inner retinal layers and penetrating the ILM to attach to the posterior hyaloid which may or may not be detached. We noticed the loss of demarcation between the inner retinal layers. Pegs of adhesions between retina and posterior hyaloid with possible retinoschisis or tractional retinal detachment could be seen in some cases.

The posterior hyaloid face could be identified in the SD-OCT scans in 11 (73.3% of studied eyes) eyes. While in 4 (26.7% of studied eyes) eyes, it was not identifiable.

For facilitation of description of the findings and statistical analysis, we divided the studied eyes according to the appearance of posterior hyaloid in the SD-OCT scans before the PRP treatment into the following categories as shown in [Figure 1].{Figure 1}

Changes in SD-OCT scans in eyes with detectable posterior hyaloid face in the pretreatment SD-OCT scans (11 eyes representing 73.3% of studied eyes) included:

Progression of posterior vitreous detachment was observed in 9 eyes representing 60% of a total number of studied eyes with:

Progressive worsening of the retinal traction. This was observed in 5 (33.33% of studied eyes) eyes as shown in [Figure 2], [Figure 3], [Figure 4], [Figure 5]. Increased traction was complicated with retinoschisis in 4 (26.67% of studied eyes) eyes as shown in [Figure 2], [Figure 3], [Figure 4], or with the occurrence of a new preretinal hemorrhage due to increased traction over the preexisting neovessels which was noticed in 1 (6.67% of studied eyes) eye as shown in [Figure 4]Relief of preexisting retinal traction due to the separation of pegs of adhesion between the posterior hyaloid and the inner retinal surface was observed in 1 (6.67% of studied eyes) eye as shown in [Figure 6]Stable retinal traction was observed in 3 (20% of studied eyes) eyes as shown in [Figure 5]{Figure 2}{Figure 3}{Figure 4}{Figure 5}{Figure 6}

No visible change at the vitreoretinal interface was detected in 2 (6.67% of studied eyes) eyes [Figure 7]{Figure 7}

SD-OCT changes in eyes with no visible posterior hyaloid face in the pretreatment SD-OCT scans (4 eyes representing 26.67% of studied eyes) included:

Regression of neovessels was noted in 3 (20% of the studied eyes) eyes as demonstrated in [Figure 8] and [Figure 9]Postlaser detachment of previously attached posterior hyaloid was noted in one eye (6.67% of studied eyes)Thickening and consolidation of the neovessels were detected in 3 eyes (20% of studied eyes), one of which showed identifiable posterior hyaloid face on the SD-OCT scans as demonstrated in [Figure 10]. Two eyes did not show detectable posterior hyaloid on the SD-OCT scans as shown in [Figure 11] and [Figure 12].{Figure 8}{Figure 9}{Figure 10}{Figure 11}{Figure 12}


PRP is the current gold standard treatment for PDR. It works by destructing the ischemic areas of the retina leading to a decrease in the production of the mediators responsible for the growth of the neovessels, which eventually leads to regression of the neovessels with subsequent decline in the risk of complications including hemorrhage and fibrovascular proliferation leading to progressive retinal traction.

SD-OCT is an important tool in the evaluation of several macular conditions. It enables both studying the morphology of retinal layers and vitreoretinal interface in vivo and quantification of macular edema.

Few previous studies made use of the SD-OCT machine to describe the appearance of NVE, NVD, or IRMA in eyes suffering DR – first of which was published in 2013 by Cho et al.,[18] which described the SD-OCT appearance active or regressed neovessels.[18],[19] Other published studies focused on differentiating SD-OCT characteristics of intraretinal microvascular abnormality and NVE[20] or comparing SD-OCT scan appearance of active versus regressed diabetic neovessels.[21]

To the best of our knowledge, this is the first study to evaluate the PRP-induced changes in the appearance of the neovessels and the vitreoretinal interface at the same exact location before and after laser treatment using one of the commercially available SD-OCT, which is still more widely used in everyday clinical practice than the OCT angiography.

We noticed that the posterior vitreous acts as a scaffold for the growth of the neovessels which was reported in previous works.[4],[5] In addition, there was an agreement between the description of the SD-OCT appearance of the NVE and NVD in the current study and previous ones.[18],[19],[20],[21]

We noticed in the current study that in most of the studied eyes, after PRP treatment, there was a progressive separation of the posterior hyaloid in all cases with detached hyaloid face in the pretreatment SD-OCT scans. In addition, in most of the cases this was associated with progressive traction on the retina at the epicenters possibly with subsequent retinoschisis. In few cases, the progressive detachment of the posterior hyaloid led to released traction at neovascular pegs with subsequent relief of traction on the inner retina; this was noticed when there were only focal pegs of vitreoretinal adhesion, rather than diffuse adhesions.

On the other hand, cases with attached posterior hyaloid face in the pretreatment SD-OCT scans showed either progressive detachment of posterior hyaloid or regression in the size of neovascular tufts without vitreous detachment after PRP treatment.

Regression of the neovessels was identified as diminution in size, complete disappearance of neovessels, or consolidation of previously patent neovessels detected before PRP treatment; this was observed in our series only in eyes with attached posterior hyaloid face in the SD-OCT.

The progressive detachment of the posterior hyaloid is thought to have some important implications. First, during diabetic vitrectomy for delamination of the posterior hyaloid finding, a plane for safe delamination is expected to be easier in the areas between epicenters in eyes previously treated with PRP because the posterior hyaloid is expected to be more detached at these sites.

Second, vitreous or preretinal hemorrhages that may complicate PRP treatment can be explained by the fact that the progression of vitreous detachment may cause traction on the neovessels with subsequent bleeding.

Limitations of the current study include the following: first, we were capable of capturing only the SD-OCT scans of the NVD and posteriorly located NVE due to the limited field of the machine we used, Neovessels elsewhere are known to develop more commonly in the mid-peripheral retina which is better to be studied with the swept source OCT. In addition, it was reported that the mid-vitreous is usually detached diabetic vitrectomy and it will be interesting to study the vitreoretinal interface changes in that area.

Second, we depended only on the clinical examination to diagnose PDR; this may cause missing of cases with very early PDR in which neovessels could not be detected clinically; however, we need to conduct the study only on cases with evident neovascularization because we were not sure whether there would be detectable changes on the SD-OCT scans or not; we thought that detecting those changes would be more challenging on cases with very early neovascularization. In addition, confirmation of complete regression of PDR with postlaser fundus fluorescein angiography was not a must in the study protocol for capturing posttreatment SD-OCT scans, although almost all cases showed clinical signs of regression.

Finally, the evidence provided by the current study would be stronger if we included a control group of diabetic eyes with PDR to be followed up with SD-OCT scans without laser treatment to detect if there will be any changes on the neovessels or the vitreoretinal interface. However, in addition to the ethical issue of putting the patient to additional risk if left untreated, previous studies demonstrated that vitreoretinal interface changes in diabetic eyes are gradual and cannot progress over the period of few weeks.[4],[5]

There is growing evidence about the safety and efficacy of intravitreal antivascular endothelial growth factor (anti-VEGF) injections as a treatment of PDR[21],[22] and it will be very interesting to conduct another similar study about the SD-OCT changes of the neovessels and the vitreoretinal interface before and after PDR treatment by intravitreal anti-VEGF and compare them to the changes noticed in the current study.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Moss SE, Klein R, Klein BE. The 14-year incidence of visual loss in a diabetic population. Ophthalmology 1998;105:998-1003.
2Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974;78:58-67.
3Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. The Wisconsin epidemiologic study of diabetic retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years. Arch Ophthalmol 1984;102:520-6.
4Yassur Y, Pickle LW, Fine SL, Singerman L, Orth DH, Patz A, et al. Optic disc neovascularisation in diabetic retinopathy: II. Natural history and results of photocoagulation treatment. Br J Ophthalmol 1980;64:77-86.
5Dobree JH. Proliferative diabetic retinopathy: Evolution of the retinal lesions. Br J Ophthalmol 1964;48:637-49.
6Four risk factors for severe visual loss in diabetic retinopathy. The third report from the diabetic retinopathy study. The diabetic retinopathy study research group. Arch Ophthalmol 1979;97:654-5.
7Shimizu K, Kobayashi Y, Muraoka K. Mid-peripheral fundus involvement in diabetic retinopathy. Ophthalmology 1981;88:601-12.
8Indications for photocoagulation treatment of diabetic retinopathy: Diabetic retinopathy study report no 14. The diabetic retinopathy study research group. Int Ophthalmol Clin 1987;27:239-53.
9Photocoagulation treatment of proliferative diabetic retinopathy: The second report of diabetic retinopathy study findings. Ophthalmology 1978;85:82-106.
10Photocoagulation for diabetic macular oedema. Early treatment diabetic retinopathy study report number 1. Early treatment diabetic retinopathy study research group. Arch Ophthalmol 1985;103:1796-806.
11Treatment techniques and clinical guidelines for photocoagulation of diabetic macular oedema. Early treatment diabetic retinopathy study report number 2. Early treatment diabetic retinopathy study research group. Ophthalmology 1987;94:761-74.
12Techniques for scatter and local photocoagulation treatment of diabetic retinopathy: Early treatment diabetic retinopathy study report no 3. The early treatment diabetic retinopathy study research group. Int Ophthalmol Clin 1987;27:254-64.
13Davis MD, Bressler SB, Aiello LP, Bressler NM, Browning DJ, Flaxel CJ, et al. Comparison of time-domain OCT and fundus photographic assessments of retinal thickening in eyes with diabetic macular oedema. Invest Ophthalmol Vis Sci 2008;49:1745-52.
14Yeung L, Lima VC, Garcia P, Landa G, Rosen RB. Correlation between spectral domain optical coherence tomography findings and fluorescein angiography patterns in diabetic macular oedema. Ophthalmology 2009;116:1158-67.
15Virgili G, Menchini F, Dimastrogiovanni AF, Rapizzi E, Menchini U, Bandello F, et al. Optical coherence tomography versus stereoscopic fundus photography or biomicroscopy for diagnosing diabetic macular oedema: A systematic review. Invest Ophthalmol Vis Sci 2007;48:4963-73.
16Hamilton CW, Chandler D, Klintworth GK, Machemer R. A transmission and scanning electron microscopic study of surgically excised preretinal membrane proliferations in diabetes mellitus. Am J Ophthalmol 1982;94:473-88.
17Faulborn J, Bowald S. Microproliferations in proliferative diabetic retinopathy and their relationship to the vitreous: Corresponding light and electron microscopic studies. Graefes Arch Clin Exp Ophthalmol 1985;223:130-8.
18Cho H, Alwassia AA, Regiatieri CV, Zhang JY, Baumal C, Waheed N, et al. Retinal neovascularization secondary to proliferative diabetic retinopathy characterized by spectral domain optical coherence tomography. Retina 2013;33:542-7.
19Muqit MM, Stanga PE. Fourier-domain optical coherence tomography evaluation of retinal and optic nerve head neovascularisation in proliferative diabetic retinopathy. Br J Ophthalmol 2014;98:65-72.
20Lee CS, Lee AY, Sim DA, Keane PA, Mehta H, Zarranz-Ventura J, et al. Reevaluating the definition of intraretinal microvascular abnormalities and neovascularization elsewhere in diabetic retinopathy using optical coherence tomography and fluorescein angiography. Am J Ophthalmol 2015;159:101-10.
21Sivaprasad S, Prevost AT, Vasconcelos JC, Riddell A, Murphy C, Kelly J, et al. Clinical efficacy of intravitreal aflibercept versus panretinal photocoagulation for best corrected visual acuity in patients with proliferative diabetic retinopathy at 52 weeks (CLARITY): A multicentre, single-blinded, randomised, controlled, phase 2b, non-inferiority trial. Lancet 2017;389:2193-203.
22Writing Committee for the Diabetic Retinopathy Clinical Research Network, Gross JG, Glassman AR, Jampol LM, Inusah S, Aiello LP, et al. Panretinal photocoagulation vs. intravitreous ranibizumab for proliferative diabetic retinopathy: A randomized clinical trial. JAMA 2015;314:2137-46.