Idiopathic juxtafoveolar retinal telangiectasia: a review and case report

Idiopathic juxtafoveolar retinal telangiectasis is a group of retinal vascular anomalies characterized by retinal vessel dilation and tortuosity, multiple aneurysm formations, varying degrees of vascular leakage and lipid exudate deposition. Idiopathic juxtafoveolar retinal telangiectasis may occur as a primary disorder (either congenital or acquired), or may be caused or accompanied by other systemic or ocular diseases. The visual prognosis and effectiveness of therapy is dependent upon the etiology of the retinal telangiectasis. Included in this review is a case report, as well as the classification system used to identify idiopathic juxtafoveolar retinal telangiectasia.     

Birdshot retinochoroidopathy

Birdshot retinochoroidopathy is a rare bilateral ocular disorder which typically affects healthy, middle-age caucasians. The typical symptoms are recent onset of bilateral floaters with decreased vision in a white and quiet eye. Minimal anterior chamber reaction, vitreous infiltration without snowballs, and multifocal depigmented lesions in the outer retina and choroid are characteristic of birdshot retinochoroidopathy. Other associated findings include retinal vasculitis, paravascular hemorrhage, vitreous hemorrhage, cystoid macular edema, cellophane maculopathy, posterior subcapsular cataract, optic disc edema, vascular attenuation and tortuosity, optic atrophy and retinal or choroidal neovascularization. Management involves Amsler grid self-assessment and routine funduscopic examinations. A recently documented case of treatment with aromatic retinoids showed improvement while many other commonly prescribed medications are equivocal in effect. Laser photoablation or panretinal photocoagulation are recommended for treatable choroidal or retinal neovascularization, respectively.     

mRNA expression of the murine glycoprotein (transmembrane) nmb (Gpnmb) gene is linked to the developing retinal pigment epithelium and iris

The murine homologue of the human glycoprotein (transmembrane) NMB (GPNMB) gene was identified by subtractive cloning from in vitro cultured murine primary osteoblast cells and subsequent RACE-PCR. GPNMB is a highly glycosylated type I transmembrane protein that shares significant sequence homology to several melanosomal proteins. Increasing expression of Gpnmb mRNA was observed during differentiation of murine primary osteoblast cell cultures. To address the potential functions of GPNMB we analysed its mRNA-expression during murine embryonic development. In early development Gpnmb mRNA is detected at high levels in the outer layer of the retina. Later in development expression gets restricted to the retinal pigment epithelium and iris. At the cytoplasmic domain of GPNMB, a conserved di-leucin-based endosomal/melanosomal-sorting signal (ExxPLL) was located, present as well in several known melanosomal proteins. To analyse the subcellular localization we used EGFP-tagged GPNMB transfected in COS7 and HEK293 cells. In both non-pigmented cell lines, the EGFP-GPNMB fusion protein was localized to vesicular, endosomal like structures. Sequence homology to known melanosomal proteins, mRNA expression and subcellular localization are suggestive for GPNMB as an intracellular, endosomal/melanosomal compartment specific protein important for melanin biosynthesis and the development of the retinal pigment epithelium and iris. As the gene coding for human GPNMB was localized to chromosome 7p15, a locus involved in the human inherited disease cystoid macular edema, also known as dominant cystoid macular dystrophy (OMIM 153880) we highly suggest that GPNMB is a candidate gene for this human inherited disease.     

Progression of Diabetic Capillary Occlusion: A Model

An explanatory computational model is developed of the contiguous areas of retinal capillary loss which play a large role in diabetic maculapathy and diabetic retinal neovascularization. Strictly random leukocyte mediated capillary occlusion cannot explain the occurrence of large contiguous areas of retinal ischemia. Therefore occlusion of an individual capillary must increase the probability of occlusion of surrounding capillaries. A retinal perifoveal vascular sector as well as a peripheral retinal capillary network and a deleted hexagonal capillary network are modelled using Compucell3D. The perifoveal modelling produces a pattern of spreading capillary loss with associated macular edema. In the peripheral network, spreading ischemia results from the progressive loss of the ladder capillaries which connect peripheral arterioles and venules. System blood flow was elevated in the macular model before a later reduction in flow in cases with progression of capillary occlusions. Simulations differing only in initial vascular network structures but with identical dynamics for oxygen, growth factors and vascular occlusions, replicate key clinical observations of ischemia and macular edema in the posterior pole and ischemia in the retinal periphery. The simulation results also seem consistent with quantitative data on macular blood flow and qualitative data on venous oxygenation. One computational model applied to distinct capillary networks in different retinal regions yielded results comparable to clinical observations in those regions.     

Macular auto-fluorescence is a follow-up parameter for cystoids macular edema

This study aimed to evaluate if macular autofluorescence(MAF) is a valuable, non-invasive follow-up parameter for cystoid macular edema. A total of 71 eyes(71 cases) with cystoid macular edema(CME) were included in the study. Macular pigment(MP) was evaluated using HRA2(infrared) IF and FA models. The density of MP was graded into three categories: without, partial, and normal amount of MP. A comparison was made between the baseline(before the first administration) level and at the fourth month, following three consecutive intravitreal lucentis injections every month. The morphology and distribution of MAF, and the density and distribution of MP were regarded as the main outcome measures. At the baseline visit, all eyes with CME had petaloid/irregular-shaped MAF in the macular area(100%). No MAF was detected in the control eyes(0). There was significant difference in MAF between the CME and normal groups(P=0.000). At the fourth monthly visit, normal levels of MP density without MAF was detected in 68 eyes(95.8%) with the best corrected spectacular visual acuity increasing to at least 1 line accordingly. We conclude that macular MAF can be used as a follow-up parameter for patients with CME. MP and MAF can indirectly reflect the fovea cone function.     

Maculopathy induced by nicotinic acid

Nicotinic acid is a commonly used oral medication for the treatment of hyperlipidemia. Numerous systemic and ocular adverse effects have been reported. Cystoid macular edema, although uncommon, has been reported and resolves upon cessation of the medication. What makes this maculopathy unusual is the absence of leakage on fluorescein angiography. A 47-year-old white male presented with the complaint of blurred vision OU for several months. The patient had an extensive medical history, including hyperlipidemia, for which he was taking nicotinic acid. Bilateral cystoid macular edema was diagnosed. Nicotinic acid was discontinued and the patient's vision returned to 20/20 after 2 months.     

Retinal Pathology of Pediatric Cerebral Malaria in Malawi

Introduction

The causes of coma and death in cerebral malaria remain unknown. Malarial retinopathy has been identified as an important clinical sign in the diagnosis and prognosis of cerebral malaria. As part of a larger autopsy study to determine causes of death in children with coma presenting to hospital in Blantyre, Malawi, who were fully evaluated clinically prior to death, we examined the histopathology of eyes of patients who died and underwent autopsy.

Methodology/Principal Findings

Children with coma were admitted to the pediatric research ward, classified according to clinical definitions as having cerebral malaria or another cause of coma, evaluated and treated. The eyes were examined by direct and indirect ophthalmoscopy. If a child died and permission was given, a standardized autopsy was carried out. The patient was then assigned an actual cause of death according to the autopsy findings. The eyes were examined pathologically for hemorrhages, cystoid macular edema, parasite sequestration and thrombi. They were stained immunohistochemically for fibrin and CD61 to identify the components of thrombi, β-amyloid precursor protein to detect axonal damage, for fibrinogen to identify vascular leakage and for glial fibrillary acidic protein to detect gliosis. Sixty-four eyes from 64 patients were examined: 35 with cerebral malaria and 29 with comas of other causes. Cerebral malaria was distinguished by sequestration of parasitized erythrocytes, the presence and severity of retinal hemorrhages, the presence of cystoid macular edema, the occurrence and number of fibrin-platelet thrombi, the presence and amount of axonal damage and vascular leakage.

Conclusions/Significance

We found significant differences in retinal histopathology between patients who died of cerebral malaria and those with other diagnoses. These histopathological findings offer insights into the etiology of malarial retinopathy and provide a pathological basis for recently described retinal capillary non-perfusion in children with malarial retinopathy. Because of the similarities between the retina and the brain it also suggests mechanisms that may contribute to coma and death in cerebral malaria.     

Effects of endogenous cyclotronic ionic resonance (ICR) on macular diabetic edema: preliminary results

The intent in this research was to verify the effects of the application of low frequency magnetic fields to cases of macular diabetic edema. We treated six patients afflicted by non-proliferating diabetic retinopathy with macular oedema. Quantitative clinical appraisals of the retinal thickness were obtained for the Optical Coherence Tomography (OCT I). None of the cases affected by non-cystoid macular oedema (non-CMO), or with a relevant ischemic component, evidenced by retinal fluorangiography, had further worsening in their clinical course during the treatment. Only one of the patients, who underwent a long treatment period with ICR demonstrated a significant reduction of the macular edema, with no need of other invasive therapeutic procedures (intravitreous injection of triamcinolone and/or laser therapy).     

Radiation retinopathy

Therapeutic radiation to the eye, or in close proximity to the eye, can result in damage to the retina. Manifestations of radiation retinopathy include: intraretinal hemorrhages, hard exudates, macular edema, cotton wool spots, microaneurysms, telangiectatic vessels, sheathed retinal vessels, retinal capillary non-perfusion, or neovascularization. Factors that influence the development of radiation retinopathy are discussed and a case report which includes radiation retinopathy in the differential diagnosis is presented.     

A Prospective,Observational Study on the Application of Ultra-Wide-Field Angiography in the Evaluation and Management of Patients with Anterior Uveitis

Purpose

Evaluation of peripheral retinal vascular changes in anterior uveitis using ultra-wide-field fluorescein angiography.

Design

A prospective, observational study of a case series of patients diagnosed with anterior uveitis.

Methods

Setting: Clinical observation at an academic medical center. Patient or Study Population: A total of 65 eyes of 33 patients corresponded with the research criteria of anterior uveitis in the opinion of specialists of Peking University First Hospital. Observation Procedures: Patients were diagnosed primarily through clinical examinations and conventional fluorescein angiography. Subsequently, ultra-wide-field fluorescein angiograms were obtained for each patient. Main Outcome Measures: The main outcome was the detection of peripheral retinal changes by ultra-wide-field fluorescein angiography, and how these changes influenced the evaluation and management of the disease.

Results

Peripheral vessel leakage was detected in 27 eyes (42%) with anterior uveitis, of which 15 eyes displayed active inflammation and 12 eyes displayed inactive inflammation. Peripheral vessel leakage was found in seven of eight eyes with cystoid macular edema. Cystoid macular edema was detected in 7 of 27 eyes (26%) with peripheral vessel leakage, whereas 1 of 38 eyes (3%) did not display peripheral vessel leakage (p<0.01). 44.4% of the patients with peripheral vessel leakage had a specific etiology. The relevant treatment strategies were modified based on the results of the ultra-wide-field fluorescein angiography. 12 patients with peripheral vessel leakage and a quiescent anterior segment were added to those receiving topical glucocorticoids, while 3 patients with serious peripheral vessel leakage and an active anterior segment received a sub-Tenon injection of triamcinolone acetonide.

Conclusions

Ultra-wide-field fluorescein angiography was very effective in detecting peripheral retinal vascular pathology in anterior uveitis. The changes found in the periphery were important in the evaluation and management of anterior uveitis.     

Study of 27 Aqueous Humor Cytokines in Type 2 Diabetic Patients with or without Macular Edema

The aim of the present study was to compare the changes in the levels of 27 aqueous humor cytokines between diabetic patients with macular edema (ME) and diabetic patients without ME. Undiluted aqueous humor samples were obtained from 68 consecutive type 2 diabetic patients without ME and 56 consecutive type 2 diabetic patients with ME. The concentrations of 27 cytokines in the aqueous humor samples were measured using a multiplex bead immunoassay. Compared with diabetic patients without ME, diabetic patients with ME had significantly higher concentrations of IL-1β, IL-6, IL-8, IP-10, MCP-1, and VEGF in the aqueous humor. However, the concentrations of IL-10 and IL-12 were significantly lower in the diabetic patients with ME. The aqueous humor levels of IL-1β, IL-6, IL-8, MCP-1, IP-10, and VEGF were closely correlated with retinal macular thickness, retinal macular volume and the severity of ME. In addition, the aqueous humor levels of IL-10 and IL-12 decreased with increasing the severity of ME. A variety of cytokines associated with inflammation and angiogenesis may contribute to the pathogenesis of diabetic macular edema, and both anti-inflammatory and antiangiogenic agents should be included in the treatment of ME simultaneously.     

Extracellular carbonic anhydrase mediates hemorrhagic retinal and cerebral vascular permeability through prekallikrein activation

Excessive retinal vascular permeability contributes to the pathogenesis of proliferative diabetic retinopathy and diabetic macular edema, leading causes of vision loss in working-age adults. Using mass spectroscopy-based proteomics, we detected 117 proteins in human vitreous and elevated levels of extracellular carbonic anhydrase-I (CA-I) in vitreous from individuals with diabetic retinopathy, suggesting that retinal hemorrhage and erythrocyte lysis contribute to the diabetic vitreous proteome. Intravitreous injection of CA-I in rats increased retinal vessel leakage and caused intraretinal edema. CA-I-induced alkalinization of vitreous increased kallikrein activity and its generation of factor XIIa, revealing a new pathway for contact system activation. CA-I-induced retinal edema was decreased by complement 1 inhibitor, neutralizing antibody to prekallikrein and bradykinin receptor antagonism. Subdural infusion of CA-I in rats induced cerebral vascular permeability, suggesting that extracellular CA-I could have broad relevance to neurovascular edema. Inhibition of extracellular CA-I and kallikrein-mediated innate inflammation could provide new therapeutic opportunities for the treatment of hemorrhage-induced retinal and cerebral edema.     

Factors Affecting Reading Speed in Patients with Diabetic Macular Edema Treated with Laser Photocoagulation

Purpose

To study the factors that may affect reading speed in patients with diabetic macular edema previously treated with laser photocoagulation.

Methods

Consecutive patients with type II diabetes treated with laser photocoagulation for diabetic macular edema (DME) at least twelve months previously, with best corrected visual acuity of better than 65 letters (approximately 20/40) measured with Early Treatment Diabetic Retinopathy Study (ETDRS) charts were included in this study. Patients previously treated with pan-retinal photocoagulation, vitrectomy, intravitreal steroid or anti-VEGF therapy were excluded. Any other ocular co-morbidities that may influence reading ability such as cataract, glaucoma or macular degeneration were also excluded. All patients were refracted by a certified examiner, the following measurements were collected: best corrected visual acuity (BCVA), contrast sensitivity with Pelli-Robson chart, reading speed with MNREAD chart, microperimetry with Nidek MP1, and central subfield thickness with Zeiss spectral domain optical coherent topography.

Results

The slow reading group had poorer contrast sensitivity (p = 0.001), reduced retinal sensitivity (p = 0.027) and less stable fixation (p = 0.013). Most interestingly the reduced retinal sensitivity findings were driven by the microperimetry value on the right subfield (p = 0.033), (nasal to the fovea in the right eye and temporal to the fovea in the left eye). Multiple linear regression analysis showed that contrast sensitivity is probably the most important factor that affects reading speed (p = 0.001).

Conclusion

Reduced retinal sensitivity after laser treatment is associated with reduced reading speed in patients with diabetic macular edema.     

玻璃体腔抗VEGF治疗不同光学相干层析成像技术分型下的糖尿病黄斑水肿临床疗效分析

摘要 目的：研究玻璃体腔内抗血管内皮生长因子（VEGF）抗体治疗不同光学相干层析成像技术（OCT）分型下的糖尿病黄斑水肿临床疗效。方法：选取2019年1月到2021年3月在我院进行治疗的糖尿病黄斑水肿患者60例,根据OCT检测分为分弥漫性黄斑水肿（DRT）组、囊样黄斑水肿（CME）组和浆液性视网膜脱离（SRD）组,每组20例。所有患者均接受玻璃体腔内注射抗VEGF抗体治疗,比较三组患者临床治疗疗效、黄斑水肿形态、最佳矫正视力（BCVA）、黄斑中心凹厚度（CMT）以及不良反应发生率。结果：（1）DRT、CME和SRD组患者临床治疗有效率分别为85.0 %、75.0 %和50.0 %,治疗后黄斑水肿消退率分别为55.0 %、25.0 %和10.0 %,且组间比较差异显著（P<0.05）;（2）三组患者治疗前BCVA和CMT均无差异（P>0.05）,治疗后三组患者BCVA和CMT均降低（P<0.05）,并且治疗后DRT和CME组患者BCVA和CMT均低于SRD组（P<0.05）;（3）DRT、CME和SRD组患者治疗期间不良反应发生率分别为10.0 %、10.0 %和25.0 %,但三组患者治疗期间不良反应发生率比较无差异（P>0.05）。结论：不同OCT分型的糖尿病黄斑水肿经玻璃体腔抗VEGF抗体治疗后临床疗效不同,其中DRT患者临床治疗疗效最好,而SRD患者疗效最差。     

糖尿病白内障术后黄斑水肿与房水细胞因子的关系

为了探讨2型糖尿病白内障术后黄斑水肿与房水中细胞因子的关系,本研究选取2016年2月至2017年7月在我院治疗的2型糖尿病白内障患者117例117眼,均行超声乳化白内障摘除术,观察术后4周黄斑水肿发生情况以及房水中多种细胞因子水平。研究结果显示:术后4周,有37眼发生黄斑水肿(观察组),未发生黄斑水肿80眼(对照组);观察组术后4周黄斑区视网膜厚度为(247.28±18.37)μm,明显高于对照组(p<0.05),且明显高于术前水平(p<0.05);观察组术后4周干扰素诱导蛋白-10 (IP-10)、巨噬细胞趋化蛋白(MCP-1)、血管内皮生长因子(VEGF)和细胞因子转化生长因子-β2 (TGF-β2)水平分别为(6.01±0.89) pg/mL、(340.03±45.39) pg/mL、(812.28±40.06) pg/mL和(40.05±10.03) pg/mL,明显高于对照组(p<0.05),且高于术前水平(p<0.05);观察组和对照组手术前后粒细胞-巨噬细胞集落刺激因子(GM-CSF)和碱性成纤维细胞生长因子(b-FGF)比较差异无统计学意义(p>0.05);术后4周IP-10、MCP-1、VEGF和TGF-β2水平与黄斑区视网膜厚度呈正相关(r=0.452, 0.501, 0.466和0.470, p<0.05)。本研究的结果初步说明,房水中IP-10、MCP-1、VEGF和TGF-2水平与2型糖尿病白内障术后黄斑水肿有一定关系,有可能成为黄斑水肿的特异性评价指标,值得进一步研究。     

Betacellulin induces increased retinal vascular permeability in mice

Background

Diabetic maculopathy, the leading cause of vision loss in patients with type 2 diabetes, is characterized by hyper-permeability of retinal blood vessels with subsequent formation of macular edema and hard exudates. The degree of hyperglycemia and duration of diabetes have been suggested to be good predictors of retinal complications. Intervention studies have determined that while intensive treatment of diabetes reduced the development of proliferative diabetic retinopathy it was associated with a two to three-fold increased risk of severe hypoglycemia. Thus we hypothesized the need to identify downstream glycemic targets, which induce retinal vascular permeability that could be targeted therapeutically without the additional risks associated with intensive treatment of the hyperglycemia. Betacellulin is a 32 kD member of the epidermal growth factor family with mitogenic properties for the retinal pigment epithelial cells. This led us to hypothesize a role for betacellulin in the retinal vascular complications associated with diabetes.

Methods and Findings

In this study, using a mouse model of diabetes, we demonstrate that diabetic mice have accentuated retinal vascular permeability with a concomitant increased expression of a cleaved soluble form of betacellulin (s-Btc) in the retina. Intravitreal injection of soluble betacellulin induced retinal vascular permeability in normoglycemic and hyperglycemic mice. Western blot analysis of retinas from patients with diabetic retinopathy showed an increase in the active soluble form of betacellulin. In addition, an increase in the levels of A disintegrin and metalloproteinase (ADAM)-10 which plays a role in the cleavage of betacellulin was seen in the retinas of diabetic mice and humans.

Conclusions

These results suggest that excessive amounts of betacellulin in the retina may contribute to the pathogenesis of diabetic macular edema.     

Structural Modeling of a Novel CAPN5 Mutation that Causes Uveitis and Neovascular Retinal Detachment

CAPN5 mutations have been linked to autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV), a blinding autoimmune eye disease. Here, we link a new CAPN5 mutation to ADNIV and model the three-dimensional structure of the resulting mutant protein. In our study, a kindred with inflammatory vitreoretinopathy was evaluated by clinical eye examinations, DNA sequencing, and protein structural modeling to investigate the disease-causing mutation. Two daughters of an affected mother demonstrated symptoms of stage III ADNIV, with posterior uveitis, cystoid macular edema, intraocular fibrosis, retinal neovascularization, retinal degeneration, and cataract. The women also harbored a novel guanine to thymine (c.750G>T, p.Lys250Asn) missense mutation in exon 6 of CAPN5, a gene that encodes a calcium-activated cysteine protease, calpain-5. Modeling based on the structures of all known calpains revealed the mutation falls within a calcium-sensitive flexible gating loop that controls access to the catalytic groove. Three-dimensional modeling placed the new mutation in a region adjacent to two previously identified disease-causing mutations, all three of which likely disrupt hydrogen bonding within the gating loop, yielding a CAPN5 with altered enzymatic activity. This is the third case of a CAPN5 mutation leading to inherited uveitis and neovascular vitreoretinopathy, suggesting patients with ADNIV features should be tested for CAPN5 mutations. Structural modeling of novel variants can be used to support mechanistic consequences of the disease-causing variants.     

Resolution of pseudophakic cystoid macular edema with combination therapy of topical corticosteroids and nonsteroidal anti-inflammatory drugs

A 69 years old women underwent uneventful cataract surgery of her left eye with phacoemulsification and posterior chamber intraocular lens implantation in topical anesthesia. Patient was postoperatively treated with combination of antibiotic and steroid in decreasing dosages during five weeks: one drop five times a day the first week, three times a day second to forth week and one time a day the fifth week. In each checkup, performed first postoperative day, 7 days, 5 weeks and 12 weeks after the operation, visual acuity with and without correction, tonometry, corneal transparency, biomicroscopy of posterior pole and measure of macular thickness by optical coherence tomography (OCT) were performed. At first day follow-up visit, the patient's visual acuity was 20/25 but 6 weeks after the operation, the patient's vision had worsened to 20/60 after a slow steroid tapper. At that time OCT showed foveal thickening and cystic changes specific for cystoid macular edema (CME). Combination of corticosteroid and non-steroidal anti-inflammatory drug four times daily was included in therapy. The dose was tapered off over the ensuing 8 weeks. The total treatment duration was 12 weeks. At the patient's 2-month follow-up visit, vision has improved to 20/20 and the fovea appeared flat. OCT showed complete resolution of foveal thickening and cystic changes. Combination of corticosteroid and NSAID is effective and safe therapy for treating pseudophakic CME. Patient showed significant improvement in visual acuity and retinal thickness at 2 months post treatment.     

Topical administration of a multi-targeted kinase inhibitor suppresses choroidal neovascularization and retinal edema

Age-related macular degeneration, diabetic retinopathy, and retinal vein occlusions are complicated by neovascularization and macular edema. Multi-targeted kinase inhibitors that inhibit select growth factor receptor tyrosine kinases and/or components of their down-stream signaling cascades (such as Src kinases) are rationale treatment strategies for these disease processes. We describe the discovery and characterization of two such agents. TG100572, which inhibits Src kinases and selected receptor tyrosine kinases, induced apoptosis of proliferating endothelial cells in vitro. Systemic delivery of TG100572 in a murine model of laser-induced choroidal neovascularization (CNV) caused significant suppression of CNV, but with an associated weight loss suggestive of systemic toxicity. To minimize systemic exposure, topical delivery of TG100572 to the cornea was explored, and while substantial levels of TG100572 were achieved in the retina and choroid, superior exposure levels were achieved using TG100801, an inactive prodrug that generates TG100572 by de-esterification. Neither TG100801 nor TG100572 were detectable in plasma following topical delivery of TG100801, and adverse safety signals (such as weight loss) were not observed even with prolonged dosing schedules. Topical TG100801 significantly suppressed laser-induced CNV in mice, and reduced fluorescein leakage from the vasculature and retinal thickening measured by optical coherence tomography in a rat model of retinal vein occlusion. These data suggest that TG100801 may provide a new topically applied treatment approach for ocular neovascularization and retinal edema.     

SDOCT imaging to identify macular pathology in patients diagnosed with diabetic maculopathy by a digital photographic retinal screening programme

Introduction

Diabetic macular edema (DME) is an important cause of vision loss. England has a national systematic photographic retinal screening programme to identify patients with diabetic eye disease. Grading retinal photographs according to this national protocol identifies surrogate markers for DME. We audited a care pathway using a spectral-domain optical coherence tomography (SDOCT) clinic to identify macular pathology in this subset of patients.

Methods

A prospective audit was performed of patients referred from screening with mild to moderate non-proliferative diabetic retinopathy (R1) and surrogate markers for diabetic macular edema (M1) attending an SDOCT clinic. The SDOCT images were graded by an ophthalmologist as SDOCT positive, borderline or negative. SDOCT positive patients were referred to the medical retina clinic. SDOCT negative and borderline patients were further reviewed in the SDOCT clinic in 6 months.

Results

From a registered screening population of 17 551 patients with diabetes mellitus, 311 patients met the inclusion criteria between (March 2008 and September 2009). We analyzed images from 311 patients’ SDOCT clinic episodes. There were 131 SDOCT negative and 12 borderline patients booked for revisit in the OCT clinic. Twenty-four were referred back to photographic screening for a variety of reasons. A total of 144 were referred to ophthalmology with OCT evidence of definite macular pathology requiring review by an ophthalmologist.

Discussion

This analysis shows that patients with diabetes, mild to moderate non-proliferative diabetic retinopathy (R1) and evidence of diabetic maculopathy on non-stereoscopic retinal photographs (M1) have a 42.1% chance of having no macular edema on SDOCT imaging as defined by standard OCT definitions of DME when graded by a retinal specialist. SDOCT imaging is a useful adjunct to colour fundus photography in screening for referable diabetic maculopathy in our screening population.