Objective To explore the correlation between retinal extracellular edema and vitreous contraction in rabbits. Methods Seventeen pigmented rabbit models with retinal vein occlusion (RVO)was set up by laser photocoagulation. Retinal vascularity area was pathologically examined 1 month later.The vitreous gellength under the gravity condition and the percentage of its weight in the rabbits with extraeellular edema was observed. The mechanisms were investigated by Western immunoblotting of type II collagen.Results Extracellular edema was found in 13 experimental eyes 1 month after the formation of RVO (76.5~) with contracted vitreous gel and released watery liquid, and the a component of type II collagen was cross-linked together to form high-molecular-weight components of 1] and 7, which weakened the stability of collagen net structure.Conclusions Vitreous contraction and retinal extracellular edemawere correlated. The main reason may be the cross-links of vitreous collagen that damages the stability of collagen structure. (Chin J Ocul Fundus Dis，2004，20：2-32)
Diabetic macular edema (DME) is the main cause of visual impairment in diabetic retinopathy patients. It mainly includes focal DME and diffuse DME, while DME of clinical significance needs timely intervention treatment. Optical coherence tomography is currently recognized as the most sensitive method to accurately diagnose DME. Currently, the common treatments of DME include intravitreal injection of anti-vascular endothelial growth factor (VEGF) or glucocorticoid and laser photocoagulation. Among them, anti-VEGF injection is becoming the first-line therapeutic, and corresponding individual treatment or combined treatment strategy should be selected according to the characteristics of DME and the specific conditions of patients. During the diagnosis and treatment of DME, attention should be paid to the systemic treatment of diabetes and the effect of diabetes-related neuroretinopathy on the therapeutic effect of DME. With the appearance of heterogeneity in the efficacy of anti-VEGF drugs, it remains to be further studied how to choose alternative therapeutics and when to replace them.
Objective To evaluate the efficacy and safety of dexamethasone intravitreal implant (Ozurdex) in the treatment of macular edema (ME) secondary to retinal vein occlusion (RVO). Methods Thirty-nine patients (39 eyes) with ME secondary to RVO were enrolles in this study. Of the patients, 27 were male and 12 were female. The mean age was (41.9±16.3) years. The mean course of disease was (5.0±5.3) months. The best corrected visual acuity (BCVA), intraocular pressure and optical coherence tomography (OCT) were performed. BCVA was measured by Early Treatment Diabetic Retinopathy Study charts. Central macular thickness (CMT) was measured by OCT. The mean BCVA was (13.4±15.3) letters. The mean intraocular pressure (IOP) was (14.1±2.8) mmHg (1 mmHg=0.133 kPa). The mean CMT was (876.1±437.9) μm. Of the 39 eyes, 33 were central RVO, 6 were branch RVO. Patients were categorized into ischemic (18 eyes)/non-ischemic (21 eyes) groups and previous treatment (22 eyes)/treatment naïve (17 eyes) groups. All eyes underwent intravitreal 0.7 mg Ozurdex injections. BCVA, IOP and CMT were assessed at 1, 2, 3, 6, 9, 12 months after injection. Three months after injection, intravitreal injections of Ozurdex, triamcinolone acetonide or ranibizumab could be considered for patients with ME recurrence or poor treatment effects. Change of BCVA, IOP and CMT were evaluated with paired t test. The presence of ocular and systemic adverse events were assessed. Results BCVA, IOP significantly increased and CMT significantly decreased at 1 month after injection compared to baseline in all groups (t=3.70, 3.69, 4.32, 3.08, 4.25, 6.09, 6.25, 4.02, 5.49, 8.18, 6.54, 5.73; P＜0.05). Two months after injection, change of BCVA, IOP and CMT was most significant (t=4.93, 6.80, 6.71, 5.53, 4.97, 5.89, 5.13, 7.68, 7.31, 8.67, 8.31, 5.82; P＜0.05). Twelve months after injection, there was no statistical difference regarding BCVA of ischemic RVO group and previous treatment group, compared to baseline (t=1.86, 0.67; P＞0.05); BCVA of non-ischemic RVO group and treatment naïve group significantly increased compared to baseline (t=2.27, 2.30; P＜0.05); there was no statistical difference regarding IOP in all groups (t=0.30, 0.13, 0.64, 1.53; P＞0.05);however, CMT significantly decreased in all groups (t=4.60, 3.26, 3.00, 4.87; P＜0.05). Twenty-seven eyes (69.2%) experiences ME recurrence (4.5±1.5) months after injection. Most common side-effect was secondary glaucoma. 41.0% eyes had IOP more than 25 mmHg, most of which were lowered to normal range with use of topical IOP lowering drugs. Four eyes (10.3%) presented with significant cataract progression and needed surgical treatment, all were central RVO eyes. No serious ocular or systemic adverse events such as vitreous hemorrhage, retinal detachment or endophthalmitis were noted. Conclusions Intravitreal injection of Ozurdex for patients with ME secondary to RVO is effective in increasing BCVA and lowering CMT in the first few months. Significant treatment effect could be seen at 1 month after injection and was most significant at 2 months after injection. The long-term vision of eyes in non-ischemic RVO group and treatment naïve group are better. 69.2% eyes experience ME recurrence at 4 months after injection. Short term adverse events were mostly secondary glaucoma and long term adverse events are mostly cataract progression.
Macular edema is an important cause of visual impairment in many eye diseases such as diabetic retinopathy, retinal vein occlusion and uveitis. Optical coherence tomography (OCT) provides high-resolution image of retinal microstructures in a non-contact and rapid manner, which greatly improves the ability of diagnosis and follow-up to macular edema patients. OCT has been widely used in the clinical detection of patients with macular edema. No matter what the cause of macular edema is, it can be observed in OCT images that there are spot-like deposits with strong reflection signals in the retina, which are mostly distributed discretely or partially convergent, and are called hyperreflective foci. At present, the nature or source of hyperreflective foci is not clear, however, may involve the destruction of the blood retina barrier, retinal inflammatory reaction, neurocellular degeneration, and so on. These mechanisms are also the key physiological mechanisms in the development of macular edema. The clinical research on hyperreflective foci provides a new direction for understanding the pathogenesis of macular edema and predicting the prognosis of macular edema. The distribution and quantity characteristics of hyperreflective foci may be an important biological marker to predict the prognosis of macular edema.nosis of macular edema. foci provides a new direction for understanding the pathogenesis of macular edema and predicting the prognosis of macular edema. The distribution and quantity characteristics of HRF may be an important biological marker to predict the prognosis of macular edema.