Few studies have investigated the effect of PRP laser in proliferativediabeticretinopathypatients on visualevoked potential parameters. Shenoy et al 19 assessed PRVEP para- meters prior to and 4 weeks after PRP in patients with uncontrolled diabetes mellitus and reported a signi ﬁ cant decrease in VEP amplitudes in 48% and increase in latency in 75% of eyes. Consistent with Shenoy ’ s 19 study, reduction in P100 amplitude and delay in P100 latency was observed in the patients with proliferativediabeticretinopathy in the current study. However, the relative recovery of P100 amplitude and latency were observed after 1.5 months of ﬁ nal laser therapy. Perhaps the reason for the differences in the results of these two studies is related to the number of patients, the method of measuring VEP parameters, the laser treatment method and the duration of the evaluation after the PRP. In fact, most studies have assessed the changes of visualevoked potential components in diabetes without any medical intervention in eye structures or even prior to the onset of vascular abnormalities. The results of various studies about changes in visualevoked potential components due to diabetes pointed to a delay in latency, especially P100 wave, in patients with different types of diabetes, as well as with or without retinopathy. 20 – 25 In fact, the high varia- bility of P100 latency changes ranging from 9% to 77% were found in these studies. However, in the present study, changes in PRVEP parameters after laser therapy were evaluated and, contrary to the mentioned studies, changes were not only considered in diabetes but in all of the patient ’ s therapeutic procedures including three laser ther- apy sessions.
Objective To evaluate the occurrence of vitreous haemorrhage (VH) secondary to proliferativediabeticretinopathy (PDR) and the efficacy of intravitreal bevacizumab (IVB) for VH in 5- year real- life data. Methods and analysis 850 adult patients with type 1 (T1D) or type 2 diabetes (T2D) with PDR were screened for VH. The effect of IVB was evaluated by the clearage of VH and the change in best corrected visual acuity (BCVA). The rates of VHs, reinjections, macular oedema, complications, additional treatments and outcomes of spontaneous resorption, panretinalphotocoagulation or pars plana vitrectomy (PPV) for VH were also investigated. results VH occurred in 16% of patients with T1D and 9% of patients with T2D with PDR. 336 VHs in 140 eyes of 103 patients were documented. VH was cleared in 92% of cases in less than 3 months by the initial IVB. IVB was superior to other treatment methods in shortening the time for clearance of VH (Kaplan- Meier, p<0.0001). The average rate of IVB reinjections was 1.7±1.1 and the reinjection interval was 7.2±3.9 weeks. BCVA increased 0.73±0.04 logarithm of the minimum angle of resolution units after IVB (generalised estimating equations, p=0.0004). In 5 years, the patients had 2.2±2.7 recurrence of VHs. A simultaneous 72% decrease in the rate of PPVs was documented (p<0.0001).
This prospective cohort study was conducted after attain- ing Institutional Review Board approval from the Farabi Eye Hospital, Tehran University of Medical Sciences. The study adhered to the Declaration of Helsinki. Written informed consent was obtained from all the patients. Patients with a history of unilateral high-risk PDR demon- strated on ﬂ uorescein angiography, were included. Eyes with PDR had a diabeticretinopathy severity scale (DRSS) of 61 − 71 and a DRSS of 47 – 53 in the fellow eye. Patients with greater severity scores that might require additional interventions and patients with signi ﬁ cant symmetry in DRSS between their two eyes were excluded from the analysis. Furthermore, patients with a prior history of intravitreal injections, retinal lasers, signi ﬁ cant media opa- city, ocular abnormality that might impact ERG measure- ments (including more than 3 diopters of myopia), prior history of retinal detachment, center involving diabetic macular edema (that may require imminent treatment), or prior history of vitrectomy were excluded from this study. The purpose of the study was to attempt to isolate the effect of PRP on ERG measures. The fellow, non-PDR, eye was used as a control since diabeticretinopathy can impact ERG measures and there can be a high degree intra-subject variability.
Examination included assessment of visual acuity using a Snellen chart, anterior segment examination by slit-lamp biomicroscopy, intraocular pressure measurement with applanation tonometry, and fundus examination by slit- lamp biomicroscopy and indirect ophthalmoscopy. Vision was recorded using the Snellen chart and converted to the logarithm of the minimum angle of resolution (logMAR) for data analysis. Fundus photography was done for documenta- tion and follow-up whenever necessary. Fundus fluorescein angiography and OCT were carried out for all patients before PRP. Fluorescein angiography was done to rule out macular ischemia and to confirm early PDR. Patients with macular ischemia were excluded from the study at baseline because this could have had a bearing on the visual outcome and be a confounding variable during analysis. OCT was done before and one week, one month, and 3 months after PRP. Line scan and fast macular scans were done to study the macula on the Stratus OCT (Carl Zeiss Meditec, Dublin, CA, USA), and a 5-line raster scan and cube 512 × 200 scan was done on the Cirrus OCT (Carl Zeiss Meditec, Dublin, CA, USA). The line scan/5-line raster protocol were used to study the morphological features of macular edema, ie, spongy edema/ spongy retinal thickening, epiretinal membrane, vitreomacu- lar traction, subretinal fluid, and cystoid macular edema. Spongy edema/retinal thickening was defined as increased retinal thickness with reduced intraretinal reflectivity and expanded areas of lower reflectivity on OCT. Fast macular protocol/cube data were used to study central foveal thick- ness. PRP was done with standard parameters using green laser in 3–4 sittings, with a one-week interval between each sitting. After completion of PRP, patients were followed up at one week, one month, and 3 months. At each visit, visual acuity was assessed by Snellen chart, and a qualitative and quantitative study of the macula was done with OCT and clinical examination. Comparison of visual acuity and macular changes with regard to morphological and macular thickness was made at each post treatment visit. The Chi- square test, paired t-test, and Pearson’s correlation were used in the statistical analysis, which was performed using the Statistical Package for the Social Sciences version 19.0 (SPSS Inc, Chicago, IL).
Purpose: Evaluation of the neuroprotective effect of weekly glatiramer acetate (GA) on retinal structure and function in diabeticpatients who underwent panretinalphotocoagulation (PRP). Patients and methods: Patients with severe nonproliferative or early proliferativediabeticretinopathy and no previous laser treatment were randomly divided into two groups: (1) those who received four GA treatments and (2) those who received placebo treatment. The sub- cutaneous injections were administered 1 week prior to laser and weekly in the subsequent three sessions of PRP in both groups. All patients underwent a full ophthalmic examination (best-corrected logMAR visual acuity, slit lamp examination, applanation tonometry, fundus biomicroscopy and indirect fundus examination); functional examination (standard automated perimetry, electroretinography and frequency-doubling technology C-20 visual field) and ana- tomic examination (color photography, optical coherence tomography (OCT) and Heidelberg retinal tomography). The examinations were performed before the photocoagulation and repeated 1,3,6, and 12 months after treatment (in a double-masked manner). To compare the two groups, generalized estimating equation models were performed to account for the dependence between eyes of the same patient.
Interestingly, in the proliferative DRP group we found a statistically significant higher capillary blood flow as compared to the non-DRP group and controls. This group had previously been treated with panretinalphotocoagulation. Studies investigating VEGF levels and blood flow in major retinal vessels suggest a decrease in blood flow afterpanretinalphotocoagulation compared to pre-treatment [21–24]. Blood flow, measured in the larger retinal arteries, was found to decrease after retinal photocoagulation in these studies. To investigate whether panretinalphotocoagulation changes retinal blood flow, we measured blood flow in a group of type 1 and type 2 diabetes patients with proliferativediabeticretinopathy before and afterpanretinalphotocoagulation. In partial support of our findings, Cuypers et al. , using the same method, reported capillary blood flow to be increased in proliferativeretinopathy as measured in the papillo- macular area and unchanged in other parts of the retina . In pDRP two important hemodynamic changes are present. Firstly, this group has a more compromised vascular system with a more decreased autoregulatory function . Secondly, panretinalphotocoagulation destroys a significant part of the retinal microcirculation, but larger vessels are left intact. Blood from larger vessels then enters a damaged microcirculation with a diminished number of capillaries. This changed distribution of blood and decreased autoregulation function of the retinal vessels might lead to a higher flow in these capillaries. Capillary drop-out and peripheral areas of non-perfusion are present in proliferativediabeticretinopathy . As we did not find extremely low blood flow values in the pDRP group, it can be assumed that capillary drop-out was modest in the measured areas. The peripheral retina could not be measured using our technique and therefore, and because our measurements were limited to the peri- papillary area, we are not able to extrapolate our findings to the entire retina. Hemodynamic changes are thought to parallel diabeticretinopathy progression and possibly even precede visible fundus changes. Studies have found differences in retinal and choroidal blood flow in relation to retinopathy severity [7, 8]. One study found changes in retinal blood flow in diabeticpatients without retinopathy . We found a significant positive linear trend for blood
Patients undergoing argon laser panretinalphotocoagulation (PRP) for proliferativediabeticretinopathy (PDR) developed temporary losses in high spatial frequency CS during the closely spaced PRP treatments. Since Snellen’s visual acuity remained stable at the pre-laser level, these results indicate the need for more sensitive measures of visual resolution to monitor foveal integrity in patients undergoing PRP. 7 Hellstedt et al. 8 suggested that contrast sensitivity is a sensitive indicator of changes in diabeticretinopathy and macular edema, especially at low- to mid- range spatial frequencies. Isolated losses of CS exist in certain diseases, and in many others, loss of contrast sensitivity is more prominent and disturbing to the patient than the loss of visual acuity .9
reported the bene ﬁ t of IVB as an additive treatment to PRP in reducing DME and ME secondary to PRP. 20 In the present study, eyes in group A received IVB injection 1 week prior to the ﬁ rst session of PRP, while eyes in group B received IVB injection 1 week after the last session of PRP. CMT was evaluated before and 1 month after injec- tion. CMT reduction of eyes in group A was consistent with previous studies. 21 Bevacizumab prevented ME sec- ondary to PRP in these patients. However, eyes in group B also had decreased CMT. There was no signi ﬁ cant differ- ence in the change of macular thickness between groups. Reduction of VEGF activity was still able to catch up to PRP, stabilizing secondary ME. The visual acuity pre- and post-treatment between the two groups were signi ﬁ cantly signi ﬁ cant; however, these ﬁ ndings were suggested due to the different staging and severity of the DR.
When the retinal angiogenesis occurs, the NPDR enters the PDR stage, and it can cause fibroplasia and even lead to retinal detachment, resulting in a dramatic decline in vision and even blindness. Many angiogenesis factors are involved in the formation of NPDR. HIF-1 is hypoxic signaling protein, and high blood glucose environment can induce HIF-1 expression and promote DR progress  . VEGF is the signature molecule of DR, which can directly promote the vascular endothelial cell proliferation and angiogenesis, and its serum content is positively correlated with the severity of the disease [14,15] . Ang-2 is also a factor that promotes angiogenesis, highly expressed VEGF can regulate the expression of Ang-2 and other downstream genes, and they participate in the retinal angiogenesis of DR together  . In this study, it was found that compared with those before treatment, serum HIF-1, VEGF and Ang-2 contents of both groups decreased after treatment, indicating that both treatments could reduce the degree of retinal angiogenesis; further compared with those of control group, serum HIF-1, VEGF and Ang-2 contents of probucol group were lower after treatment, confirming that adjuvant probucol therapy on the basis of retinal photocoagulation can further inhibit the retinal angiogenesis, and this is one of the fundamental mechanisms for it to implement treatment effect.
He was recommended intravitreal bevacizumab injec- tion, however he refused again. Instead, another round of PRP was attempted in both eyes. He presented 2 days later with bilateral extensive serous RDs involving the macula (Fig. 2 upper panel). His unaided visual acuity was 1/200 in his right eye and 5/200 in his left eye, with no improvement with pinhole correction. At this point, he accepted a single off-label injection of 1.25 mg beva- cizumab (Avastin; Genentech, South San Francisco, CA, USA) in each eye. Eleven days after the bilateral injection, the serous RD had regressed completely in his left eye, and there was a substantial regression in his right eye (Fig. 2 lower panel), which subsequently regressed completely over the following 2 weeks. During
blood vessels can become permeable and cause swelling of the center of the retina, called diabetic macular oedema. Clinically significant macular oedema is a leading cause of moderate visual loss in diabetes. Proliferativeretinopathy, severe non-proliferativeretinopathy and clinically significant macular oedema can be considered as sight threatening retinopathy . At these stages, un- less it is treated, DR will almost inevitably evolve to irre- versible blindness . In facts, patients with untreated proliferative DR have over 50% chance of becoming blind within 5 years . Prevention of retinopathy is the best approach in reducing the risk of blindness in diabeticpatients. Laser photocoagulation for sight threatening diabeticretinopathy is not widely available in sub-Saharan Africa.
Experimental models suggest that neovascularization is mediated in part by the interaction between insulin‐like growth factor (IGF‐1) and vascular endothelial growth factor (VEGF).Animal study showed IGF-1 antagonist reduced the incident of neovascularization.this is clinically evident by worsening of diabeticretinopathyafter insulin therapy. Insulin increases serum IGF-1 while Pituitary injury decreases IGF-1 which reverse the condition.Recently, studies more focused on VEGF role in neovascularization. It has been demonstrated that VEGF more concentrated in vitreous in case of PDR than those with NPDR, and intensity of immunostaining for VEGF is proportional to the severity of retinopathy. This theory become more evident because VEGF inhibitors have been successful in controlling hypoxia‐induced neovascularization in certain animal models.
a few cases were of less than one year duration (n=05) while all the rest had the disease since many years. Recruitment of the cases was done by using the exclusion criteria patients on lipid lowering medications/glitazones, female patients on Oral Contraceptive Pills (OCP) or Hormone Replacement Therapy (HRT), hypothyroid cases, familial hypercholesterolaemia, Chronic Kidney Disease (CKD), chronic liver disease, pregnant females and known cases of haemoglobinopathies. A total of 228 patients were initially identified and 135 of them were selected on the basis of the exclusion criteria. Informed written consent was taken from the individual patients. The sample size was based on Creative Research System Survey Software with a confidence level of 95%. The data was maintained by the principal investigator with the clinical component filled up in the OPD when the patients were evaluated for their diabeticretinopathy status. Fasting blood samples for serum (lipid profile & apolipoproteins) and plasma with sodium Ethylene Diamine Tetraacetic Acid (EDTA) as anticoagulant samples for HbA1c estimation were collected. Following fundoscopic examination, the patients were classified as per International Clinical DiabeticRetinopathy Disease Severity Scale , which is based on the Early Treatment DiabeticRetinopathy Study (ETDRS) classification as NPDR and PDR. The patients in the NPDR category were further sub-classified as mild, moderate and severe. Apart from these cases, diabetic with no retinopathypatients were also selected. A total of 100 healthy controls (age and sex matched) were selected from patients attending the daily OPD who did not have diabetes mellitus or CKD and had reported to the hospital for routine annual examination.
and VA impairment despite previous anti-VEGF treatment, had modest improvement in visual gain despite signi ﬁ cant reductions in retinal thickness on OCT. 137 In phakic eyes receiving continuous anti-VEGF therapy for DME, the addition of intravitreous corticosteroids did not result in signi ﬁ cant visual improvements. 138,139 Recent reports sum- marizing observational studies investigating dexametha- sone implants in DME have reported similar ﬁ nal VA outcomes when compared to anti-VEGF monotherapy, but superior visual gains in real-life practice. 140–142 There appears to be a predictive correlation between the early response to anti-VEGF therapy with the visual and anato- mical outcomes following a switch to intravitreal corticos- teroids. Those with poor responses to anti-VEGF demonstrated a more robust increase in BCVA. 143 Side effects of cataract in phakic eyes and intraocular pressure elevation without regard to lens status have accompanied all steroids studied, although to varying degrees. 144–149 However, there may be a role for long-acting intraocular corticosteroids in reducing overall treatment burden in DME as early data from both the TYBEE and PALADIN studies have recently demonstrated. 150–152 Likewise, intra- vitreal triamcinolone 4 mg injections for DME reduced 2 step progression in severity of diabeticretinopathy com- pared to focal/grid laser at 3 years. 110 Similar data obtained from the DR-Pro-DEX Study and others demonstrated that the dexamethasone and ﬂ uocinolone implants signi ﬁ cantly delayed the progression and reduced the severity of DR over a 24-month study period. 153,154
which is usually confirmed with fluorescence fundus angiography imaging. PDR is the more advanced stage of DR. In PDR, proliferating neovasculature contributes to severe complications, eg, vitreous hemorrhage, retinal scars, and tractional retinal detachment, all of which often need vitreoretinal surgery. However, the endpoint of PDR is variable, and irreversible vision loss is attributed to retinal structure damage and layer thinning. Thus, the Early Treat- ment of Diabetes Retinopathy Study (ETDRS) has staged NPDR with mild, moderate, and severe grades, aimed to screen risk factors and to detect the earlier stages of DR for nonsurgical treatment, eg, retinal photocoagulation or antiangiogenic therapy. 10,11
Physicians were asked to fill out the characteristics of retinopathy and maculopathy findings on drop down menus. Each retina evaluation screen showed the standard ETDRS 8a 4 and 2a 4 photos for IRMA and DBH, respectively. The following non-proliferative features were included: IRMA (choices of none, <8a in 1-4 quadrants, >8a in 1 quadrant, >8a in 2 quadrants, >8a in 3 quadrants, >8a in 4 quadrants), venous beading (none, 1 quadrant, 2 or more quadrants), venous loops/reduplication (yes or no), hemorrhages (none, MA only, hemorrhages <next level, >=4 blot hemorrhages in any quadrant and >=8 in total, >=2a in any quadrant, >2a in all quadrant), cotton wool spots (none, <=5, >5). The fields that were required to define ETDRS grade were compulsory.
I hereby declare that this dissertation titled “A STUDY TO ANALYZE PATTERNS OF STRUCTURAL CHANGES IN CLINICALLY SIGNIFICANT DIABETIC MACULAR EDEMA ON OPTICAL COHERENCE TOMOGRAPHY” is a bonfide and genuine research work carried out by me under the guidance of Prof. Dr, R . Ravikumar M.S.,D.O, Professor Department of Uvea and Retina services , Regional institiute of ophthalmology. Government Ophthalmic hospital. Chennai -600008.
This study included only patients with type 2 diabetes to reduce the possible variability in pathogenesis. Although the mechanism of diabeticretinopathy is likely to be iden- tical in both type 1 and type 2 diabetes, previous studies such as the Early Treatment DiabeticRetinopathy Study and DiabeticRetinopathy Study have investigated each type of diabetes separately. Laser photocoagulation was an exclusion criterion as it affects tritan colour vision . Cataract and pseudophakia were not excluded as both are more common in diabetics and exclusion would have limited the usefulness of the Chromatest in screening. It is understood that lens-yellowing effects due to cataract may cause pre-retinal absorption of short-wavelength light resulting in tritan deficits. This may have influenced the overall sensitivity and specificity of the study, but it was a representation of the realistic setting clinicians experience in their practice.
vision was most obvious 3 months after treatment; the vision of some patients declined 6 months after treatment compared with 3 months after treatment, but there was still a significant difference in vision before treatment (P,0.05). The vision variation tendency was consistent with CMT. Three months after treatment, the CMT was the lowest, and vision improvement was the most obvious in the observation group. Vision was worsened 6 months after treatment and strongly correlated with the retention time of ranibizumab in the vitreous body. The control group showed no significant improvement in vision, a finding that was considered to be correlated with the slow relief of macular edema. All of the findings suggest that macular edema is the direct cause of the vision decline in DME patients, and vision can be improved as edema is gradually relieved. This conclusion is similar to the research results of a previous study. 16
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