Volcano like pattern in optical coherence tomography in chronic diabetic macular edema

In this article we herein report an interesting vitreo-macular interface abnormality associated with chronic diabetic cystoid macular edema. It is an observational case study of three diabetic patients examined in the diabetic clinic. All the patients had proliferative diabetic retinopathy with chronic macular edema. A serial cross sectional OCT examination and tracking of both the longitudinal progression of macular thickening and vitreo-macular interface revealed cystoid macular edema with a characteristic hyperreflective vitreous shadow emerging from the vitreofoveal interface. All the patients had dehiscence of inner retinal layers.This particular morphological feature at the vitreo-foveolar interface, which we name as “volcano sign”, has not been described earlier. The probable mechanism of such a finding probably could be due to slow progressive leakage of chronic cytoid fluid into the vitreous with condensation of the overlying vitreous. Vitreo-macular traction followed by posterior vitreous detachment probably would have contributed to such a morphological event.     

Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease

Posterior vitreous detachment (PVD) is the consequence of changes in the macromolecular structure of gel vitreous that result in liquefaction, concurrent with alterations in the extracellular matrix at the vitro-retinal interface that allow the posterior vitreous cortex to detach from the internal limiting lamina of the retina. Gel liquefaction that exceeds the degree of vitro-retinal dehiscence results in anomalous PVD (APVD). APVD varies in its clinical manifestations depending upon where in the fundus vitreo-retinal adhesion is strongest. At the periphery, APVD results in retinal tears and detachments. In the macula, APVD causes vitreo-macular traction syndrome, results in vitreoeschisis with macular pucker or macular holes, or contributes to some cases of diabetic macular edema. At the optic disc and retina, APVD causes vitreo-papillary traction and promotes retinal and optic disc neovascularization. Unifying the spectrum of vitreo-retinal diseases into the conceptual frame-work of APVD underscores that to more effectively treat, and ultimately prevent, these disorders it is necessary to replicate the two components of an innocuous PVD, i.e., gel liquefaction and vitreo-retinal dehiscence. Pharmacologic vitreolysis is designed to mitigate against APVD by chemically breaking down vitreous macromolecules and weakening vitro-retinal adhesion to safely detach the posterior vitreous cortex. This would not only facilitate surgery, but if performed early in the natural history of disease, it should prevent progressive disease.     

Vitreomacular traction and age-related macular degeneration

The interaction between the vitreous and the internal limiting membrane of the retina is important in the pathoetiology of numerous ocular disease processes. Recent studies have focused on the vitreo-retinal interface in the context of age-related macular degeneration (AMD), linking vitreo-retinal adhesion to exudative AMD in particular. This review summarizes our knowledge of vitreous anatomy and recent investigations regarding vitreomacular adhesion and AMD.     

Optical coherence tomography use in evaluation of the vitreoretinal interface: a review

Optical coherence tomography (OCT) is a valuable tool for assessment of the vitreoretinal interface. This article reviews the normal process of age-related posterior vitreous detachment as viewed by OCT. Abnormalities of the vitreoretinal interface as imaged by OCT are described including vitreomacular traction syndrome, cystoid macular edema/ diabetic macular edema, epiretinal membranes, full thickness macular holes, lamellar holes, pseudoholes, microholes, and schisis from myopia or optic pits/colobomas. This tool has given us new insights into the pathogenesis of these retinal abnormalities.     

醋酸去炎松在玻璃体切割术和黄斑水肿的临床应用研究进展

去炎松是一种非水溶性的长效糖皮质激素，能强力抑制炎症。已被用作抗炎药防治实验性增生性玻璃体视网膜病变和眼内新生血管形成。新近在玻璃体切割术中将去炎松注入玻璃体内，能增加玻璃体的可见度，提高手术操作的安全性，并抑制术后血—眼屏障的破坏。玻璃体内注射醋酸去炎松还用于治疗难治性糖尿病黄斑水肿，由于视网膜中央静脉阻塞或炎症引起的慢性黄斑水肿，以及渗出性年龄相关性黄斑变性。这是一种有希望的疗法，目前尚未发现不能控制的并发症。其长期效果和安全性还有待评价。     

The influence of spontaneous posterior vitreous detachment in resolution of diabetic macular edema in NIDDM

PURPOSE: To establish the influence of posterior vitreous detachment on development and resolution of diabetic macular edema in NIDDM. To asses the posterior vitreous detachment role in argon laser treatment of diabetic macular edema. MATERIAL AND METHODS: Retrospective study. RESULTS: 68 eyes of 36 patients were involved into the study, 52 eyes (76.5%) with macular edema and 16 eyes (23.5%) without macular edema. Posterior vitreous detachment (PVD) was present in 62.5% of cases without macular edema, and only 30.77% of cases had macular edema. Laser treatment applied in accordance to general standards cased resolution of macular edema in all cases with posterior vitreous detachment. In group with no spontaneous posterior vitreous detachment, macular edema resolved only in 19.23% of cases. CONCLUSIONS: Diabetic macular edema is less common in eyes with spontaneous posterior vitreous detachment. This observation shows, that not only vascular factor but also vitreo-macular tractions are responsible for macular pathology in diabetic macular edema. The efficacy of standard argon laser treatment depends also on vitreo-macular relation--presence of PVD, and is more sufficient in eyes with posterior vitreous detachment.     

Intravitreal dexamethasone implant for a vitrectomized eye with diabetic macular edema

A 71-year-old man suffered from diabetic vitreous hemorrhage in his left pseudophakic eye. He received 20-gauge pars plana vitrectomy and removal of taut posterior hyaloid traction in June 2011. Spectral-domain optical coherence tomography demonstrated cystoid macular edema 1 month after the operation. The macular edema did not respond to macular grid laser. Intravitreal bevacizumab (1.25 mg) was injected, which was effective for managing diabetic macular edema initially. The edema recurred 3 months following the bevacizumab injection. Subsequent intravitreal triamcinolone 1 mg also failed to treat the macular edema. Ozurdex, a dexamethasone implant, was injected intravitreally in January 2012. The central foveal thickness decreased, and visual acuity improved. The effect persisted for 6 months. There was no systemic or ocular adverse event during the follow-up period. This intravitreal dexamethasone implant could be helpful for diabetic macular edema in vitrectomized eyes.     

糖尿病性黄斑水肿抗VEGF治疗对视网膜毛细血管影响的研究进展

抗血管内皮生长因子(vascular endothelial growth factor,VEGF)药物对于治疗视网膜疾病,比如渗出性年龄相关性黄斑变性、糖尿病视网膜病变(diabetic retinopathy,DR)、视网膜静脉阻塞具有革命性意义。玻璃体腔内注射抗VEGF药物后能明显减轻黄斑水肿,但同时是否也会破坏视网膜微循环、加快视网膜毛细血管闭塞？本文通过相干光断层扫描血流成像(optical coherence tomography angiography,OCTA)和超广角眼底血管造影(ultra-widefield fluorescein angiography,UWFA)技术观察糖尿病性黄斑水肿(diabetic macular edema,DME)患者抗VEGF治疗对视网膜毛细血管的影响,从黄斑无血管区面积、无灌注区大小及血流密度三方面进行综述。     

Interfaces

There are important similarities in molecular composition and structural organization of the interface between the vitreous and retina and that between the retina and retinal pigment epithelium. It is striking that the two most common causes of severe vision loss in the western world involve neovascularization at these interfaces; i.e., proliferative diabetic vitreo-retinopathy at the vitreo-retinal interface and exudative age-related macular degeneration at the retina-retinal pigment epithelium interface. Improved knowledge of the physiology of these interfaces will lead to a better understanding of the effects of aging and diseases, especially those that involve neovascularization. Such advances will no doubt result in new treatment strategies offering more effective therapy, and, even more importantly, perhaps providing prevention from these devastating causes of blindness.     

Subjective evaluation of visual acuity is not reliable to detect disease activity in different exudative maculopathies

Graefe's Archive for Clinical and Experimental Ophthalmology - Patients with exudative maculopathies (neovascular age-related macular degeneration (nAMD), diabetic macular edema (DME), and...     

Erythropoietin levels in aqueous humour in eyes with exudative age-related macular degeneration and diabetic retinopathy

The purpose of this study was to evaluate whether the concentration of erythropoietin as another potent ischemia-induced angiogenic factor is elevated in eyes with neovascular (age-related macular degeneration [AMD]) or oedematous (diabetic retinopathy) maculopathies. The clinical comparative study included 28 patients with diabetic macular oedema, 59 patients with exudative AMD, and 49 patients with cataract. For all patients, aqueous humour was collected during cataract surgery or during an intravitreal injection of triamcinolone acetonide. Erythropoietin levels were measured using a solid-phase chemiluminescence immunoassay. The mean concentration of erythropoietin was significantly higher in the diabetic group (60.1 +/- 46.7 mUnits/mL; P < 0.001) than in the age-related macular degeneration group (22.9 +/- 23.2 mUnits/mL) and in the control group (22.0 +/- 21.0 mUnits/mL; P < 0.001). The two latter groups did not vary significantly (P = 0.41). The results indicate that erythropoietin may be present in considerably higher concentrations in eyes with diabetic macular oedema than in eyes with exudative AMD or normal eyes.     

Lamellar macular hole following intravitreal pegaptanib sodium (Macugen) injection for diabetic macular edema

To report on a patient who developed a lamellar macular hole 1 month after an intravitreal pegaptanib sodium injection. Interventional case report. A 66 year old patient developed a lamellar macular hole 1 month after an intravitreal pegaptanib sodium injection for diabetic macular edema (DME). The pathogenesis of the lamellar macular hole in our case can be attributed to the intravitreal injection that may have induced vitreous incarceration, causing vitreoretinal traction at the macula and development of a lamellar macular hole. Alternatively or in association, pegaptanib itself may have caused the lamellar macular hole by inducing sudden reduction of the DME and exacerbation of tangential traction of the posterior vitreous on the overlying macular retina. Lamellar macular hole seems to be a potential complication of pegaptanib injection even in patients without pretreatment clinically detectable vitreomacular traction.     

曲安奈德眼内注射的并发症不容忽视

眼内注射曲安奈德治疗由糖尿病视网膜病变、葡萄膜炎、渗出型老年黄斑变性或视网膜静脉阻塞等引起的黄斑水肿、慢性低眼压等疾病的有效性已得到公认，其临床应用日趋普遍，在充分肯定其治疗作用的同时，曲安奈德的副作用及并发症——继发性青光眼、并发性白内障、眼内炎、视网膜脱离及玻璃体积血等这些已经报道的及尚未认识到的并发症必须引起临床医师的高度警惕及重视。     

非外伤非增生性糖尿病视网膜病变玻璃体积血原因分析

目的：探讨非外伤非增生性糖尿病视网膜病变玻璃体积血的原因。

方法：对2009-07/2013-06在我科住院的46例46眼玻璃体积血病例资料进行回顾性病因分析。

结果：本组中视网膜静脉阻塞(RVO)所致玻璃体积血最多,为16眼(34.8%),其次为视网膜裂孔及孔源性视网膜脱离(RH/RD)8眼(17.4%),渗出型年龄相关性黄斑变性(EAMD)8眼(17.4%),再次为玻璃体后脱离(PVD)4眼(8.7%),其它少见原因为视网膜大动脉瘤3眼(6.5%)、高血压视网膜病变及视网膜静脉周围炎各2眼(4.3%),特发性息肉样脉络膜血管病变、脉络膜上腔出血、葡萄膜炎各1眼(2.2%)。

结论：视网膜静脉阻塞、视网膜裂孔及孔源性视网膜脱离、年龄相关性黄斑变性是非外伤非增生性糖尿病视网膜病变玻璃体积血的主要原因。     

Role of the vitreous in age-related macular degeneration

PURPOSE: To investigate the relationship between posterior vitreous detachment (PVD) and age-related macular degeneration (AMD). METHODS: The condition of the vitreous was examined by slit-lamp funduscopy and ultrasonography in 93 eyes of 50 patients with AMD (exudative or dry) and 100 eyes of 50 controls. RESULTS: There was complete PVD in 31 of the 93 eyes (33.3%) of 50 patients with AMD and the posterior vitreous was attached in 62 of these eyes (66.6%). In the control group, in 50 eyes (50%) of 50 subjects there was posterior vitreous detachment. The prevalence of PVD in eyes with macular degeneration was significantly lower (P < .05). There was no statistically significant difference between the exudative and the nonexudative groups in respect to PVD. CONCLUSIONS: PVD may have a protective role against the development of AMD. Chronic vitreomacular traction and/or continuous exposure to free radicals and cytokines may possibly be one of the causes of AMD in eyes with attached vitreous.     

Macular hole formation in diabetic retinopathy: the role of coexisting macular edema

The aim of this study was to characterise different etiologies for the development of macular holes in diabetic retinopathy. We examined 8 eyes of 8 patients with known diabetic retinopathy who had developed a macular hole. These were classified as follows: related to macular edema (4 eyes), non-related to macular edema (2 eyes), intraoperative (1 eye) or postoperative (1 eye) after pars plana vitrectomy for proliferative diabetic retinopathy. In three patients the macular holes were treated with pars plana vitrectomy and fluid air exchange. In diabetic eyes with macular edema, macular holes may develop because of intraretinal exudation combined with increased vitreomacular attachments and tractions. The mechanism of macular hole formation in diabetic eyes without macular edema probably results from the same increased tangential vitreous traction which is seen in idiopathic age-related macular holes. Iatrogenically induced macular holes during pars plana vitrectomy for proliferative diabetic retinopathy may be also due to intraoperative vitreoretinal tugging. Finally, macular holes developing after vitrectomy may have an etiology not related to vitreous tractions or attachments. This revised version was published online in July 2006 with corrections to the Cover Date.     

Mechanisms of maculopathy

This article will review the cellular constituents of the macula and speculate on their contribution to the pathogenesis of macular disease. The retinal pigment epithelium (RPE) has been implicated in senile macular degeneration (SMD). Over time, RPE dysfunction and death may result from the cumulative effect of light and free radical damage. Inherited metabolic abnormalities or the degree of uveal pigmentation could increase the RPE's susceptibility to environmental stress. In exudative SMD, the excessive production of extracellular matrix material by the RPE may contribute to sub-RPE neovascularization and disciform scar formation. Macular edema reflects a breakdown in the blood-retinal barrier. Inflammatory mediators produced in the anterior segment may cause aphakic cystoid macular edema (CME). Recent observations suggest that Müller cell dysfunction is important in CME. Vascular incompetence, as well as capillary occlusion characterize diabetic retinopathy. Angiogenic factors elaborated by ischemic retina are thought to be the stimulus for neovascularization. Diabetic tractional macular detachment results from neovascular proliferation on the partially detached vitreous. Posterior vitreous detachment predisposes to epiretinal gliosis. Endogenous infections and metastatic neoplasms have a predilection for the macula, reflecting the region's high blood flow.     

玻璃体腔注射康柏西普治疗渗出性年龄相关性黄斑变性

目的：观察玻璃体腔注射康柏西普治疗渗出性年龄相关性黄斑变性(age-related macular degeneration,ARMD)的临床疗效。

方法：回顾性研究我院2015-07/2016-01确诊的渗出性ARMD患者45例45眼,采取每月1次玻璃体腔注射康柏西普(0.5mg/0.05mL),连续治疗3mo,之后按需给药(3+PRN),随访2a。分别观察治疗前和治疗后最佳矫正视力(best corrected visual acuity,BCVA)、黄斑中心凹厚度(central macular thickness,CMT)变化情况。

结果：治疗后第1、2、3mo,1、2a后的BCVA较治疗前显著提高,差异有统计学意义(t=5.208、5.111、4.323、4.701、5.156,P<0.05),CMT较治疗前显著减低,差异有统计学意义(t=3.807、4.556、2.841、2.707、3.145,P<0.05)。

结论：康柏西普眼用注射液3+PRN方案治疗渗出性ARMD可以有效提高视力、减轻黄斑水肿。     

玻璃体腔内注射贝伐单抗后视网膜电图明视负向反应改变

目的研究玻璃体腔内注射贝伐单抗后渗出性年龄相关性黄斑变性（AMD）、增生性糖尿视网膜病变（PDR）患者视力、闪光视网膜电图（ERG）明视负向反应（PhNR）和黄斑神经上皮层厚度（CRT）变化。设计回顾性、自身对照研究。研究对象8例渗出性AMD患者（9眼）和3例PDR患者（3眼）。方法患者于表面麻醉下给予1．25mg（0．05ml）贝伐单抗玻璃体腔内注射。患者治疗前及治疗后1个月检查EDTR视力、眼压、视野、荧光素眼底血管造影、相干光断层扫描和闪光ERG。主要指标PhNR振幅、视力和CRT。结果治疗前后CRT显著下降（n=12,P=0．008）,但PhNR振幅和视力变化不显著（n=12,P=0．153）。CRT与PHNR振幅（r=0．294,P=0．145）、CRT与视力无显著相关性（r=0．358,P=0．073）。结论玻璃体腔内单次注射贝伐单抗可减轻渗出性AMD和PDR患者的黄斑水肿,但对视功能的改善需要进一步的观察。（跟科,2009,18：243—246）     

Frequency of cataract surgery after intravitreal injection of high-dosage triamcinolone acetonide

PURPOSE: To evaluate the frequency of cataract surgery after intravitreal injection of high-dosage triamcinolone acetonide in elderly patients. METHODS: This clinical interventional case series study included 144 phakic eyes that consecutively received an intravitreal injection of about 20 mg triamcinolone acetonide for diffuse diabetic macular edema (n=42 eyes), exudative age-related macular degeneration (n=98), and branch retinal vein occlusion (n=4). Mean age was 72.3-/+8.9 years. Mean follow-up was 11.0-/+6.8 months (median, 8.8 months; range, 3 to 35.5 months). Reinjections were carried out in 12 (8.3%) eyes. RESULTS: Cataract surgery was performed in 20 (13.9%) eyes 17.4-/+9.1 months (median, 12.7 months; range, 8.0 to 35.5 months) after the first intravitreal injection. Out of the 20 eyes undergoing cataract surgery, 19 (95%) eyes had received one intravitreal injection, and 1 (5%) eye had received two previous injections. CONCLUSIONS: In the elderly population of patients with exudative age-related macular degeneration, diffuse diabetic macular edema, or branch retinal vein occlusion, intravitreal high-dosage injection of triamcinolone acetonide leads to clinically significant cataract with eventual cataract surgery in about 15% to 20% of eyes within about 1 year after the intravitreal injection.