|Year : 2017 | Volume
| Issue : 2 | Page : 61-66
Central proliferative diabetic retinopathy: evaluation and management
Mohamed I Elkasaby1, Hazem Mohamed Azab2, Maged Adly Naguib2, Ali Hendy El Ghamdi3, Mostafa Mahmoud Darwish1
1 Department of Ophthalmology, Al-Azhar University, Cairo, Egypt
2 Giza Memorial Institute, Ophthalmology Hospital, Giza, Egypt
3 Faculty of Medicine, Al Baha University, Saudi Arabia
|Date of Submission||19-May-2016|
|Date of Acceptance||06-Apr-2017|
|Date of Web Publication||21-Nov-2017|
Mohamed I Elkasaby
Assistant Professor, Department of Ophthalmology, Al-Azhar University, Cairo
Source of Support: None, Conflict of Interest: None
Aims The aim of this study was to evaluate the outcome of central proliferative diabetic retinopathy (PDR) after pars planavitrectomy.
Patients and methods This prospective, observation, randomized study included 90 eyes of 64 patients with central PDR who underwent pars planavitrectomy by a single vitreoretinal surgeon. Patients were followed up on the second postoperative day, at 1 week, 2 weeks, and at 1, 3, 6, and 12 months after surgery. Clinical outcomes were recorded at every visit.
Results Ninety eyes of 64 patients with severe PDR that involved the macula and central retina were studied. Of 36 patients 16 (44.4%) patients were female, whereas 20 (55.5%) patients out of 36 were male. Their ages ranged from 20 to 70 years. Out of 36 patients 12 (33.3%)had bilateral PDR. 20 of 36 (55.5%) patients had type І diabetes mellitus and 16 (44.4%) of 36 patients had type ІІ.
Keywords: diabetes, retinopathy, vitrectomy
|How to cite this article:|
Elkasaby MI, Azab HM, Naguib MA, El Ghamdi AH, Darwish MM. Central proliferative diabetic retinopathy: evaluation and management. Al-Azhar Assiut Med J 2017;15:61-6
|How to cite this URL:|
Elkasaby MI, Azab HM, Naguib MA, El Ghamdi AH, Darwish MM. Central proliferative diabetic retinopathy: evaluation and management. Al-Azhar Assiut Med J [serial online] 2017 [cited 2020 Apr 3];15:61-6. Available from: http://www.azmj.eg.net/text.asp?2017/15/2/61/218853
| Introduction|| |
Diabetic retinopathy (DR) is one of the most common complications of diabetes affecting millions of working adults worldwide, in which the retina becomes progressively damaged, leading to vision loss and blindness . Proliferative diabetic retinopathy (PDR) commonly develops in the central and peripheral retina or both. Central PDR is secondary to ischemic proliferative processes and neovascularization of disc and is commonly seen in type-I diabetic patients, whereas peripheral PDR is seen in neglected vitreous hemorrhage and with neovascularization elsewhere and is commonly seen in patients with type II diabetes. Tractional retinal detachment (TRD) involving or threatening the macula is one of the primary indications for vitrectomy in DR .
| Patients and methods|| |
Overall, 90 eyes of 64 patients underwent preoperative evaluation. All patients were subjected to full preoperative ophthalmologic assessment including history taking, clinical examination, and some investigations. The current study included 64 patients, 32 (50%) male and 32 (50%) female, with a duration of diabetes ranging from up to 10 to 21 years (mean: 17.41%).
Full patient history taking was carried out with special emphasis on age of the patients, onset of diabetes (discovery) and duration of diabetes from discovery until time of inclusion, positive family history, type of diabetic patients (type I and type II), associated systemic disease, and associated systemic complication to diabetes mellitus (DM).
Best-corrected visual acuity (VA) was measured using landolts chart (broken rings), and hand motion and counting fingers were used if the patients could not see the chart. Best-corrected VA was recorded. It was measured using Snellen’s VA charts and it was converted to the decimal system to allow statistical analysis. Slit lamp examination was carried out with special focus on the presence of any corneal opacities that may affect vision or prevent laser delivery and presence of early rubeosis before pupillary dilatation, and gonioscopy was recommended to exclude neovascular glaucoma. Presence of any lens opacity was determined, and intraocular tension was measured using application tonometry after application of surface anesthetic eye drops. Fundus examination was carried out after maximum pupillary dilatation with a combination of tropicamide 1% eye drops and phenylephrine 2.5% drops. Both slit lamp biomicroscopy with noncontact lens +90D Volk (American Bifocal Co., Cleveland, Ohio, USA) or wide filed lens +160D lens and indirect opthalmoscopy using a +20D a biconvex spheric lens were used to examine the vitreous for the presence of hemorrhage, membranes, and the extent of posterior detachment. The retina was evaluated for the presence and extent of neovascularization, preretinal and epiretinal fibrovascular membranes, retinal and macular traction or detachment, and extent of laser photocoagulation if present. B-scan ultrasound was performed for patients with severe vitreous hemorrhage; extension with tractional proliferative tissues and fundus details could not be evaluated. Fundus fluorescein angiography and ocular coherence tomography were performed for anatomical and functional evaluation. Medical and laboratory examinations such as complete general examination, fasting and 2 h postprandial blood sugar, renal and hepatic functional tests, and ECG were carried out. Preoperative topical cycloplegic and a combination of antibiotic/steroid preparation were used. Preoperative data included age, general medical condition, affected eye, ocular diagnosis, VA, type and severity of pre-existing lens changes, and status of the fellow eye. Intraoperative data recorded included inadvertent lens damage, iatrogenic breaks, hemorrhage, and other operative complications.
Vitrectomy (20 and 23 G) was performed in all cases using a wide-angle vitrectomy system (BIOM lens) in a standardized procedure. Ringer lactate solution and balance salt solution were used as the infusion fluid. Phacovitrectomy was performed in cases of dense cataract; anterior vitrectomy was performed behind the lens, meticulously removing the central vitreous gel in phakic eyes. Taut posterior hyaloid extending from the posterior pole to the vitreous base was circumcised. Removal of epipapillary neovascular proliferations was avoided. A triamcinolone aqueous suspension (Kenacort-A; SmithKline Beecham Egypt L.L.C, Misr, Al-Harm, Giza; an affiliated co. to GlaxoSmithKline) was left standing for 30 s and the vehicle of triamcinolone acetonide was discarded. The remaining triamcinolone acetonide (40 mg) suspension was mixed with 5 ml of balanced salt solution and then was used for the following procedure as a triamcinolone suspension.
Posterior hyaloid separation
A core vitrectomy was performed using Accurus and constellation (Alcon Laboratories Inc., Fort Worth, Texas, USA). Vitrectomy machine with the following parameters and accessories: a light source (built in accurus vitrectomy machine) connected to endoillumination probe, which may be panoramic or focal type; cutting rate ranging from 1000 to 2500 cycles/s using disposable cutter; aspiration pressure ranging from 100 to 300 mmHg; and infusion bottle of BSS at a height of 75±10 cm. Removal of clotted blood, release of epiretinal membranes, and tangential traction was carried out by sectioning preretinal membranes with vitreous scissors. Perfluorocarbone liquid was used in most cases to flatten an retinal detachment (RD) that developed when a tight vitreoretinal adhesion was loosened to facilitate effective endolaser. Retinal tamponade was achieved by injecting silicone oil (5000 cs) controlled by intraocular pressure (IOP), which measured digitally during operation. Endodiathermy was necessary to control bleeding. Diode laser panretinal endophotocoagulation was performed with wave length 810 nm diode laser. The 23 G cannula with compression was removed and massaged for 15 s to prevent escape of fluid, and then eye patching was carried out after instilling topical corticosteroids and antibiotics.
All patients were discharged within the first postoperative day and the following medications were given: hypoglycemic drugs according to the previous schedule, systemic antibiotics and combined steroid–antibiotic eye drops that were gradually tapered over the first postoperative 1.5 months, and topical cycloplegic eye drops three times for 1 week.
All patients were followed up after 1 day, 1 week, 2 weeks, 1 month, 3 months, 6 months, and yearly. In every follow-up visit patients were subjected to the following: best-corrected VA; slit lamp examination for corneal edema abrasion ulcer, presence of lens complications such as cataract, and development or regression of rubeosisiridis; IOP measurement digitally or using applanation tonometer; fundus examination; and presence of complications.
All data were collected retrospectively, and preoperative diagnosis, intraoperative data, and postoperative data were recorded. The follow-up interval ranged from 1 day up to year. All data were collected and entered into a database for Statistical analysis. International Business Machines Statistical Package for the Social Sciences (version 19.0; IBM Corporation, USA) was used for data analysis. Data were expressed as mean±SD for quantitative parametric measures in addition to median percentiles for quantitative nonparametric measures, and both number and percentage were used for categorized data. A P value of less than 0.05 was considered significant. The datagraph 2.90h for MS Office XP Prof. was used for analysis of refractive and other visual outcome data and to generate standard graphs.
| Results|| |
The current study included 64 patients (90 eyes), 32 (50%) male and 32 (50%) female patients with duration of diabetes from up to 10 to 21 years (mean: 17.41%). All patients suffered from DM with duration of diabetes between 10 years or less and 21 years with a mean±SD of 17.41±4.9.
Complications such as lens touch cataract, postoperative hemorrhage, increased IOP, and progressive ischemia were observed. VA diminished in six (28.6%) eyes, improved in 11 (52.4%) eyes, and was constant in four (19.0%) eyes with previous complications.
| Discussion|| |
Retinopathy is the most feared complication of diabetes, compromising the quality of life in most sufferers. Almost all patients with type 1 diabetes will develop retinopathy over a 15-year to 20-year period, and ∼20–30% will advance to the blinding stage of the disease. Greater than 60% of patients with type-II diabetes will have retinopathy. With the global epidemic of type-II diabetes, this predicament is set to worsen as over 360 million people are estimated to suffer from diabetes and its complications by 2030. Vision loss from diabetes is due to a number of factors, including hemorrhage from new and poorly formed blood vessels, RD due to contraction of deposited fibrous tissue, and neovascular glaucoma resulting in increased IOP. Diabetic macular edema is now the principal cause of vision loss in diabetes and involves leakage from a disrupted blood–retinal barrier . Progressive macular traction is characterized by partial vitreous detachment with vitreoretinal traction along the temporal arcades and the optic nerve head. It causes retinal traction extending through the fovea and, if progression occurs, it will lead to macular heterotopia or tractional RD of the macula. Several authors have suggested that these changes are features of proliferative diabetic retinopathy . The indications for surgical intervention in patients with diabetic retinopathy are broad; the diabetic vitrectomy study established the role of early surgery for patients with type I diabetes and vitreous hemorrhage ,. TRD involving or threatening the macula is one of the primary indications for vitrectomy in DR; the visual benefit surgery for TRD is variable and depends on the degree of the macular function. Severe active fibrovascular proliferation (FVP) despite maximum PDR is also an indication for operative intervention . In our study, we focused on anatomical and functional results after vitreoretinal surgery in advanced PDR invaded macula and central retina following activation of fibrovascular arcades ended with formation of membranes tend obscured macular area ([Figure 1] and [Figure 2]). The goal of surgery consists in the shaving and elimination of proliferative and fibrovascular proliferative membranes as much as possible to open the visual pathway in front of the macular area, relieve tractional force on the retinal surface with reattachment of the retina, and stabilization with heavy internal tamponade such as silicone oil. One of the goals was to wash and lavage the internal vitreal media from the proliferative factors to inhibit the activation of proliferative cycle. The main goal of surgery in these cases was to increase the lifespan of vision for a longer time, because most cases usually lost vision within short time secondary to activation of proliferative cycle and progression of ischemic changes.
|Figure 1 Preoperative central proliferative diabetic retinopathy with tractional retinal detachment.|
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|Figure 2 Postoperative fundus fluorescein angiography and color photography.|
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In our study, preoperative best-corrected VA ranged from 0.005 to 0.5 because we had a variety of preoperative indications for surgery ranging from cases of dense vitreous hemorrhage (vision from hand motion to counting fingers) to cases with mild vitreous hemorrhage and FVP and cases of tractional macular edema with a relatively good vision up to 0.5 (20/40). All too often, final VA is limited despite successful achievement of the surgical and anatomic objectives. This outcome is usually attributable to generalized retinal ischemia, which may be evident as attenuated arterioles, capillary nonperfusion, and retinal thinning (featureless) .
In this study the total number of eyes of patients with type-I diabetes was 15 (16.6%) and that of type-II was 75 (83.3%).
Of concern, there is epidemiological evidence that retinopathy begins to develop at least 7 years before the clinical diagnosis of noninsulin dependent DM is made. Usually, central PDR develops in type-I DM. In our study, recurrent activation of proliferative cycle and progression of ischemic changes were statistically high in type-I DM than in type-II DM.
The mean duration of diabetes was 17.41±4.9 (3.0–30.0) years (ranging from ≤10 to +21 years) since discovery of the disease.
The strongest predictor for the prevalence of retinopathy in individuals with type-I and type-II diabetes is the duration of diabetes. In the younger-onset group in the Wisconsin Epidemiologic Study of Diabetic Retinopathy, the prevalence of any retinopathy was 8% among participants with diabetes duration of 3 years, 25% for patients with duration of 5 years, 60% for patients with duration of 10 years, and 80% for patients with duration of 15 years. The prevalence of PDR was 0% for those with diabetes duration of 3 years, increasing to 25% for diabetes duration of 15 years . In our study, the average duration of diabetes is relatively long ranging from up to 10 to more than 21 years because all patients in the study had been diagnosed with PDR and then all patients had panretinal photocoagulation. We followed up the patients to diagnose progression despite retinal laser photocoagulation; 9.8 (60-<13.5>) at 6 months shows average change in VA at 1 and 6 months. Overall, 22 (24.4%) eyes showed recession of anatomical and functional results secondary to progression of ischemic changes and diabetic blood insufficiency or activation of proliferative cycle and recurrent proliferative and fibrovascular tissue formation with recurrent TRD. In all, 68 (75%) eyes had preserved vision due to established vascular supply secondary control of DM, hypertension, and other factors, which included 13 (14.4%) patients with type I and 63 (70.0%) patients with type II. Systemic blood sugar, hypertension, and lipid control should be optimized before surgical intervention. In this study, follow-up period extended up to 1 year. Vitreoretinal surgery is difficult to perform, with a high rate of anatomical reduction but a poor functional recovery rate for late PDR with macular area or central PDR . In case of severe PDR with TRD not involving the macula, it is best to defer vitrectomy unless definite progression that threatens the vascular center is documented . This study was coincide with the study done by Smiddy et al., who reported that improvement of vision in 68 (32%) patients. Initial management with PP lensectomy and vitrectomy with silicone oil tamponade can achieve favorable anatomic and visual outcomes in selected patients with cataract and TRD involving macula associated with severe PDR. The number of study eyes with best-corrected vision of 6 over 60 or better increased from 52 (57.7%) at 1 month to 53 (58.8%) eyes at 6 months up to 1 year .
Glaucoma was described by many authors in varying percentages (from 1.7 to 8%) after vitrectomy ,. Transient increase in IOP was observed in nine (10.8%) eyes. In five eyes it was secondary to escape of silicone oil to the anterior chamber. Medical treatment in the form of IOP-lowering drops was successful in managing those cases without the need for glaucoma-filtering surgery.
The number of eyes of patients with associated systemic diseases such as diabetic nephropathy, hypertension, and liver impairment was 23 (25.5%) eyes. Hypertension has long been hypothesized to be a risk factor for retinopathy in patients with diabetes . Data from epidemiological studies and clinical trials support clinical guidelines to control elevated blood pressure in patients with type II diabetes to reduce visual loss from retinopathy, as well as morbidity and mortality from cardiovascular diseases .
The most common postoperative complication after vitrectomy was cataract formation, which occurred in 24 (63.2%) of the 38 phakic eyes . In our study, cataract occurred in two of 57 eyes with clear lens preoperatively and became cataractous at 6-month postoperative follow-up with silicone oil internal tamponade. The incidence of postoperative cataract formation in our study is comparable to the previous results of other researchers.
Postoperative vitreous hemorrhage occurred to some degree in seven (7.7) cases  and postoperative vitreous hemorrhage developed in one (10%) of 10 eyes after vitrectomy and surgical removal of the posterior hyaloid but resolved spontaneously over a 2-month period. In the study by Yamamoto and colleagues, postoperative vitreous hemorrhage occurred only in one of 65 (1.5%) eyes. In our study, all intraoperative hemorrhage was controllable and all surgeries had been completed successfully. Recurrent vitreous hemorrhage developed in patients under renal dialysis with anticoagulant and therapy and uncontrolled hypertension and D.M.
In our study, intraoperative retinal breaks occurred in 18 (20%) cases during removal of epiretinal FVPs.
Our percentage is close to the percentage of intraoperative retinal tears discovered in a series of patients operated by Yamamoto et al. . In his series, intraoperative retinal tears have been encountered in 21% of cases. This is due to the fact that the retina in diabetic patients is ischemic. Moreover, the vitreoretinal relationship in patients with diabetic retinopathy is abnormal and thus overly aggressive stripping of the posterior cortical vitreous should be avoided in diabetic patients with an attached hyaloid. Intraoperative incomplete removal of proliferative tractional membrane over main vascular arcades with still detached retina away from the macular area is recommended. This complication was recorded in our study in three cases without threat to VA and preserved vision to 6/60 or better.
Other complications related to vitrectomy, such as choroidal hemorrhage and endophthalmitis were not detected in the follow-up period among the patients of this study. Cataract extraction (phacoemulsification) with intraocular lens implantation was performed during silicone oil removal at least 6 months after surgery.
| Conclusion|| |
Overall 90 eyes showed improved anatomically, but poor vision due to severe ischaemia, the blood vessels ended with fibrous tissue and recurrent fibrovascular tissue proliferation. Failed anatomical and functional success, secondary to severe diabetic blood insufficiently until ended with fibrosed blood vessels or recurrent fibrovascular tissue proliferation secondary to activation of proliferative cycle, so that the goal of vitreoretinal surgery in central PDR, just prolonged life spane of vision longe time as possible as in such cases.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Ismail-Beigi F, Craven T, Banerji MA, Basile J, Calles J, Cohen RM et al.
Accord trial group. Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the accord randomised trial. Lancet 2010; 376:419–430.
Wilkinson-Berka JL, Miller AG. Update on the treatment of diabetic retinopathy. ScientificWorldJournal 2008; 8:98–120.
Pastor JC. Vitrectomy for diabetic retinopathy (Chapter 8). In: Cunha-Vaz J, editor, Diabetic retinopathy. Singapore: Published by World Scientific Publishing Co. Pte. Ltd.; 2011. pp. 237–256.
Dauglas MJ, Scott IU, Flynn HW. Pars plana lensectomy, pars plana vitrectomy and silicone oil tamponade as initial management of cataract and combind tractional/rhegmatogenous retinal detachement involving the macular associated with sever proliferative diabetic retinopathy. Ophthalmic Surg Lasers Imaging 2003; 34:270–278.
Imamura Y, Minami M, Ueki M, Satoh B, Ikeda T. Use of perfluorocarbon liquid during vitrectomy for severe proliferative diabetic retinopathy. Br J Ophthalmol 2003; 87:563–566.
Smiddy WE, Flynn HW. Vitrectomy for diabetic retinopathy. In: Scott IU, Flynn HW Jr, Smiddy WE, editors. Diabetes and ocular disease; past, present, and future therapies. San Francisco, CA: Published by Oxford University Press. In cooperation with the American Academy of Ophthalmology; 2010. pp. 207–234.
Klein R, Klein BE, Moss SE, DeMets DL, Kaufman I, Voss PS. Prevalence of diabetes mellitus in southern Wisconsin. Am J Epidemiol 1984; 119:54–61.
Avitabile T, Bonifiglio V, Castigilione F, Castaing M, Contarino F, Mistretta A. Severe proliferative diabetic retinopathy treated with vitrectomy or panretinal photocoagulation: a monocenter randomized controlled clinical trial. Can J Ophthalmol 2011; 46:345–351.
Tachi N, Ogino N. Vitrectomy for diffuse macular edema in cases of diabetic retinopathy. Am J Ophthalmol 1996; 122:258–260.
Yang CM. Surgical treatment for sever diabetic macular edema with massive hard exudates. Retina 2000; 20:121–125.
Rassam SM, Patel V, Kohner EM. The effect of experimental hypertension on retinal vascular autoregulation in humans: a mechanism for the progression of diabetic retinopathy. Exp Physiol 1995; 80:53–68.
Wong TY, Klein R, Klein BE. Epidemiology and risk factors of diabetic retinopathy. In: Scott IU, Flynn HW Jr, Smiddy WE, editors. Diabetes and ocular disease; past, present, and future therapies. San Francisco, CA: Published by Oxford University Press. In cooperation with the American Academy of Ophthalmology; 2010. pp. 71–99.
Pendergast SD, Hassan TS, Williams GA, Cox MS, Margherio RR, Ferrone PJ et al.
Vitrectomy for diffuse diabetic macular edema associated with a taut premacular posterior hyaloid. Am J Ophthalmol 2000; 130:178–186.
Harbour JW, Smiddy WE, Flynn HW Jr, Rubsamen PE. Vitrectomy for diabetic macular edema associated with a thickened and taut posterior hyaloid membrane. Am J Ophthalmol 1996; 121(4):405–413.
Pendergast SD. Vitrectomy for diabetic macular edema associated with a taut premacular posterior hyaloid. Curr Opin Ophthalmol 1998; 9(3): 71–75.
Williams DF, Williams GA, Hartz A, Mieler WF, Abrams GW, Aaberg TM. Result of vitrectomy for diabetic traction retinal detachement of the macula. Arch Ophthalmol 1987; 105:479–502.
Smiddy WE, Fever W, Irvine D, Flynn HW, George W, Kenship B. Vitrectomy for complication of proliferative diabetic retinopathy: functional outcome. Ophthalmology 1995; 102:1688–1696.
Yamamoto T, Akabane N, Takeuchi S. Vitrectomy for diabetic macular edema: the role of posterior vitreous detachment and epimacular membrane. Am J Ophthalmol 2001; 132: 369–377.
[Figure 1], [Figure 2]