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At least 19 recordsLinked to original sources
PubMedDate not supplied

[Idiopathic macular edema, macular hole, retinal detachment and retinal fibrosis as complications of the involutional vitreoretinal syndrome].

The author suggests calling the involution vitreoretinal syndrome a characteristic symptom complex of vitreoretinal changes occurring in advanced age. He distinguishes three stages in the course of this syndrome an early one, whose signs are, among other things, destruction of the anterior segment of the vitreous body, presence of glial plaques of the retina (coin-shaped and flap reflexes of the fundus oculi), and changes of the posterior lenticular capsule in the lentivitreoretinal form of the syndrome. The mature stage is characterized by total destruction of the vitreous body or its detachment, transformation of a part of glial plaques into individual foci of fibrosis, phacosclerosis of lenticular nucleus. The present communication sums up complications of the syndrome occurring in the third stage of the disease. In 44 of the 109 patients the following complications were observed: macular edema in 6, macular opening in 9, reticular fibrosis in 9, retinal detachment in 8, nuclear cataract in 12. The author explains so high an incidence of complications by the fact that involutional vitreoretinal syndrome cannot be diagnosed at the early stages and that patients come to consult a doctor only when complications are developing as a rule. Physicians' awareness of the early signs of the syndrome may become an essential factor in the prevention of quite a number of intraocular conditions developing in advanced age.

Aged↗
PubMedDate not supplied

Macular edema.

Macular edema is the final common pathway of many intraocular and systemic insults. It may develop in a diffuse pattern where the macula appears generally thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with protean underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory disease. As well as clinical suspicion, a wide range of investigations may lead to the diagnosis of macular edema. Fluorescein angiography and optical coherence tomography provide enhanced visualization of the geometry and distribution of macular edema. A variety of approaches to the treatment of macular edema have been attempted, with a variable degree of success. These options have included topical and systemic steroids, topical and oral non-steroidal anti-inflammatory agents and laser photocoagulation treatment. More recently other therapeutic modalities, including immunomodulators, intravitreal injection of triamcinolone, and pars plana vitrectomy have also been employed. Clinical trials are currently looking into the use of a steroid slow-release intravitreal device for the management of macular edema secondary to uveitis and diabetes. This article reviews the clinical entity of macular edema focusing on the current therapeutic strategies for its management.

Humans↗
PubMed1998

Surgical management of macular edema.

Macular edema, often a component of diabetic retinopathy, can be complicated by many other diseases. It is considered to be multifactorial and difficult to treat. The relation of the vitreous and macular edema is discussed. We examined many eyes of patients with diabetic macular edema that improved after spontaneous posterior vitreous detachment or vitrectomy for proliferative diabetic retinopathy. Recent advances in vitreous surgery have enabled us to treat surgically eyes with good visual acuity. We began surgical treatment for macular edema without the fibrous membrane in 1990. Here we discuss our experience in surgical treatment of macular edema as contrasted to photocoagulation therapy. This review is based on the published and unpublished results of our cases of more than 100 eyes that underwent vitrectomy for diabetic macular edema.

Diabetic Retinopathy↗
PubMed2003

[Vitrectomy in diabetic macular edema].

Macular edema remains one of the important therapeutic issues. Vitero-macular tractions are said, to be the cause of persistent, non responding to laser treatment diabetic macular edema. Surgical removal of these tractions is used in treatment of non resolving macular edema. However, vitrectomy in treatment of diabetic macular edema remains the experimental, method requiring further studying.

Diabetic Retinopathy↗
PubMed1999

When and how to do a grid laser for diabetic macular edema.

Macular edema is a common feature of posterior segment diseases. It is an expression of abnormal permeability in either retinal vessels (inner blood-retinal barrier) or in the retinal pigment epithelium (outer blood-retinal barrier). It occurs in either a diffuse pattern where the macula appears generally thickened or, in more severe cases, as cystoid edema with the typical petaloid appearance. Grid laser treatment may be useful to reduce macular edema. Spots of 100-250 micrometers in diameter are applied to the whole posterior pole, one to two groups apart. The foveal avascular zone remains untouched. In patients treated bilaterally, areas temporal and nasal to the macula must be spared to prevent the development of deep scotomas. The mechanism yielding positive results with the grid technique is still debated. Among the most reliable hypotheses are: Proliferation of pigment epithelial cells, followed by and improved efficiency of the outer blood-retinal barrier; proliferation of endothelial cells in retinal capillaries followed by an improved efficiency of the inner blood-retinal barrier; improvement of the retinochoroidal exchanges, and finally, release by coagulative necrosis of a factor able to improve the efficiency of the blood-retinal barriers. Lasers with long wavelengths, such as krypton red and diode, are the most appropriate ones to perform grid treatment.

Blood-Retinal Barrier↗
PubMed1999

Grid laser treatment of macular edema in macular branch retinal vein occlusion.

AIM: Macular branch retinal vein occlusion (MBRVO) is a subgroup of branch retinal vein occlusion in which the occlusion is limited to a small venous vessel draining a sector of the macular region. The present study aims to evaluate the efficacy of grid laser treatment for macular edema in MBRVO. METHODS: 77 Patients with MBRVO of recent onset were prospectively studied during a 24 month period. Eyes were randomly assigned to a grid laser treatment group and to a control group. Clinical parameters such as visual acuity, presence of macular edema and angiographic features were recorded during the follow-up period. RESULTS: Visual acuity increased significantly in both groups after 3 months of follow-up (p<0.001) and after 1 year of follow-up (p<0.005). No additional improvement was noted at the two year control. There was no statistical difference between the two groups. CONCLUSIONS: The visual prognosis of MBRVO is not improved after grid laser treatment of macular edema. This suggests that sudden ischemic damage to central photoreceptors rather than macular edema is the main factor for permanent visual acuity reduction.

Aged↗
PubMed1981

Macular edema and cystoid macular edema.

We examined the foveomacular regions from three eyes in which fluorescein angiography had demonstrated the characteristic appearance of cystoid macular edema by light and electron microscopy. Cystoid macular edema was present in two eyes (one of which was from a 63-year-old diabetic man) that contained peripheral choroidal melanomas, and in a third eye from a patient with diabetes only. By light microscopy, cystoid macular degeneration was obvious only in the third eye. The electron microscopic findings common to all three eyes were widespread swelling and necrosis of Müller cell cytoplasm. There was no enlargement of intercellular spaces. There was secondary neuronal degeneration. Retinal vascular changes, consisting mainly of endothelial cell abnormalities, were found in all cases but were far more common in the two eyes from diabetic patients. The retinal vascular changes were probably the cause of the cystoid macular edema.

Aged↗
PubMed2002

Experimental macular edema induced by macular venule occlusion in monkey.

PURPOSE: Visual prognosis after retinal vein occlusion varies, because it may be affected by macular edema or an avascular area. The mechanism describing how macular edema and avascular areas occur, however, has not been clearly understood. We induced macular edema in cynomolgus monkeys by occluding macular venules to evaluate the retinal microcirculation. METHODS: We produced venous occlusion by applying dye laser in three cynomolgus monkeys. Macular edema was examined by slit lamp biomicroscopy and optical coherence tomography. Acridine orange leukocyte fluorography (AOLF) and fluorescein angiography were performed to study blood flow and vascular leakage before and after laser application. RESULTS: We observed three types of retinal changes in the macular area: (1) macular edema did not develop; (2) macular edema developed, but improved with avascular area formation; (3) macular edema developed, but disappeared without avascular area formation. Under physiological conditions, observation revealed that leukocytes flowed from arterioles into either superior or inferior venules. When macular edema did not develop, most leukocytes from arterioles escaped into the adjacent non-occluded venules. In contrast, when macular edema occurred, leukocyte flow became stagnated. Macular edema developed when capillary leakage was observed from venules and subsequently arterioles, but disappeared when an avascular area was formed by arteriole occlusion. CONCLUSIONS: We demonstrated that experimental macular edema could be induced by macular venule occlusion in monkeys. According to our observation by AOLF, whether macular edema is induced or not depends on the function of collateral routes of the remaining non-occluded venules. We could consider that a gradual increase in intravascular pressure was associated with the avascular area formation.

Acridine Orange↗
PubMed1993

Classification of aphakic cystoid macular edema with focal macular electroretinograms.

We compared the amplitude and implicit times of the a-waves, b-waves, and oscillatory potentials of the focal macular electroretinograms of 30 eyes with aphakic cystoid macular edema and the healthy fellow eyes. Ten affected eyes were characterized by reduced amplitudes of the oscillatory potentials with normal a-wave and b-wave responses (type 1). Nine affected eyes had both reduced amplitudes of the oscillatory potentials and the b-waves (type 2). Ten affected eyes were characterized by reduced amplitude of the oscillatory potentials, the a-waves, and the b-waves (type 3). One eye could not be classified. Visual acuities were as follows: type 1, 0.55 (20/36.4); type 2, 0.31 (20/64.5); and type 3, 0.12 (20/166.7). The mean time between cataract surgery and the electroretinographic testing was significantly longer for type 2 and 3 eyes than for type 1 eyes. The differences in the electroretinographic responses between the affected eye and the normal fellow eye suggested either an increased severity or the stage of the cystoid macular edema.

Aged↗
PubMed1991

Retinal thickness analysis for quantitative assessment of diabetic macular edema.

Diabetic macular edema is a major cause of vision loss and is evaluated with qualitative or semiquantitative techniques. A new quantitative method for assessment of macular edema using retinal thickness analysis was applied to 19 patients with diabetic macular edema. Foveal thickening was frequently coupled with poor visual acuity. Slit-lamp biomicroscopy and stereophotography detected 80% and 78% of local areas of thickening, respectively, but failed to detect locations with average thicknesses of 1.5 and 1.6 times normal, respectively. Fluorescein leakage on angiography was generally associated with retinal thickening, but locations with similar degrees of leakage had widely varying retinal thickening. Fluorescein leakage in the posterior vitreous correlated poorly with the degree of foveal thickening. These results indicate that quantitative measurement of retinal thickness may become useful in the management of diabetic patients with macular edema.

Aged↗
PubMed1986

Intraocular lens implant exchange and resolution of cystoid macular edema.

Cystoid macular edema is a recognized complication of cataract extraction and intraocular lens implantation with an incidence of 5.2% to 50.0%. We have recently performed lens implant exchange in an eye with cystoid macular edema which suffered recurrent hyphema (UGH syndrome). In addition to resolution of the patient's recurrent hyphema, we observed the resolution of cystoid macular edema in this eye.

Aged↗
PubMed2000

Vitrectomy for refractory diabetic macular edema.

Diabetic macular edema may occur or worsen as a consequence of vitreomacular traction in some eyes. The precise role of the posterior hyaloid in the pathogenesis of diabetic maculopathy remains unclear. The determination of which eyes might benefit from vitrectomy is the most challenging aspect in the treatment of this condition. Fluorescein angiography, B-scan untrasonography, and optical coherence tomography may be helpful in this regard. Most often, vitreous surgery is performed when diabetic macular edema persists despite multiple laser treatments. All reports published to date regarding vitrectomy for diabetic macular edema are uncontrolled and nonrandomized patient series. Visual improvement after vitrectomy is related to the duration of edema, as well as the extent of intraretinal lipid and vascular nonperfusion.

Diabetic Retinopathy↗
PubMed1988

'Very late onset' cystoid macular edema.

Cystoid macular edema typically manifests 4 to 16 weeks after ocular surgery. It has only rarely been documented with an onset more than 2 years postoperatively. We report four patients who developed clinically significant cystoid macular edema between 7 and 16 years after initially successful surgery. Two patients had undergone intracapsular cataract extraction, one extracapsular cataract extraction, and one a scleral buckling procedure. Although such cases of "very late onset" cystoid macular edema are uncommon, it should be considered in patients who suffer visual loss many years after ocular surgery.

Aged↗
PubMed1999

Vitrectomy for traction macular edema.

PURPOSE: Traction macular edema may develop through contraction of macular epiretinal membranes (ERM), or due to persistent vitreomacular traction during the evolution of vitreomacular traction syndrome (VMS). The purpose of this retrospective study was to determine the effect of vitreous surgery and the release of the vitreomacular traction or the removal of epiretinal membranes, on the evolution of traction induced macular edema. MATERIAL AND METHODS: Fourteen eyes from 14 patients presenting with idiopathic or secondary epiretinal membranes, and 11 eyes from 10 patients presenting with vitreomacular traction syndrome, underwent vitrectomy for reduced vision and cystoid macular edema, identified by slit-lamp examination and fluorescein angiography. No coexistent ocular conditions that might have caused macular traction were present. History, preoperative eye examination, operative findings, postoperative course and final examination as well as pre- and postoperative fluorescein angiography were reviewed. RESULTS: In the ERM group, cystoid macular edema disappeared in all cases during the postoperative period and the mean visual acuity (VA) at the end of the follow-up (0.48 +/- 0.23) significantly increased compared to the preoperative one (0.29 +/- 0.2) (p=0.004). In the group of patients suffering from VMS, the posterior vitreous traction on the macula was released and macular edema disappeared in all cases but one. The mean v.a. at the end of the follow-up (0.42 +/- 0.24) significantly increased compared to the preoperative one (0.18 +/- 0.1) (p=0.01). Complications included intraoperative small petechias and postoperative progressive nuclear sclerosis, retinal detachment and retinal pigment epitheliopathy. CONCLUSIONS: Cystoid macular edema may develop secondary to vitreomacular traction syndrome or epiretinal membrane contraction. Vitrectomy is effective in releasing macular traction which, in turn, may induce a decrease of the macular edema with improvement of visual acuity.

Aged↗
PubMedDate not supplied

Pathomechanisms of cystoid macular edema.

Cystoid macular edema (CME) is a well-known endpoint of various ocular diseases, but the relative pathogenic impact of extra- and intracellular fluid accumulation within the retinal tissue still remains uncertain. While most authors favor an extracellular fluid accumulation as the main causative factor of cyst formation, there are indications that Müller cell swelling may also contribute to CME development (particularly in cases without significant angiographic vascular leakage). Vascular leakage occurs after a breakdown of the blood-retinal barrier during traumatic, vascular, and inflammatory ocular diseases, and allows the serum to get into the retinal interstitium. Since intraretinal fluid distribution is restricted by two diffusion barriers, the inner and outer plexiform layers, serum leakage from intraretinal vessels causes cysts mainly in the inner nuclear layer while leakage from choroid/pigment epithelium generates (in addition to subretinal fluid accumulation) cyst formation in the Henle fiber layer. In the normal healthy retina, the transretinal water fluxes are mediated by glial and pigment epithelial cells. These water fluxes are inevitably coupled to fluxes of osmolytes; in the case of glial (Müller) cells, to K(+) clearance currents. For this purpose, the cells express a complex, microtopographically optimized pattern of transporters and channels for osmolytes and water in their plasma membrane. Ischemic/hypoxic alterations of the retinal microvasculature result in gliotic responses which involve down-regulation of K(+) channels in the perivascular Müller cell end-feet. This means a closure of the main pathway which normally generates the osmotic drive for the redistribution of water from the inner retina into the blood. The result is an intracellular K(+) accumulation which, then, osmotically drives water from the blood into the glial cells (i.e., in the opposite direction) and causes glial cell swelling, edema, and cyst formation. While the underlying mechanisms await further research, it is expected that their improved knowledge will stimulate the development of novel therapeutic approaches to resolve edema in retinal tissue.

Blood-Retinal Barrier↗
PubMed1988

Posterior sub-Tenon's injections of corticosteroids in uveitis patients with cystoid macular edema.

Cystoid macular edema (CME) is a major cause of visual impairment and is thought to be due to abnormal perifoveal capillary permeability. Posterior sub-Tenon's corticosteroid injections are used to improve the visual acuity in CME, although their mechanism of action is uncertain. In this study, visual acuity, blood retinal barrier (BRB) permeability, and fluorescein angiograms were recorded immediately before and one and four weeks after the administration of steroid injections. Ten patients (12 treated eyes) with CME secondary to uveitis were studied. Visual improvement, defined as an increase in at least two lines of Snellen visual acuity, was seen in half of the treated eyes. In some patients, these improvements were not directly related to changes in the BRB permeability or the amount of macular fluid. Posterior sub-Tenon's corticosteroid injections do not consistently affect blood retinal barrier permeability.

Adolescent↗
PubMed1996

Cystoid macular edema.

Cystoid macular edema (CME) may develop in association with a wide variety of ocular conditions. It is the result of cystic accumulation of extracellular intraretinal fluid in the outer plexiform and inner nuclear layers of the retina, as a result of breakdown of the blood-retinal barrier. It is most common following intraocular surgery, and in patients with venous occlusive disease, diabetic retinopathy, and posterior segment inflammatory conditions. A variety of approaches to the treatment of CME have been attempted, with a variable degree of success. These options have included topical and oral steroids, nonsteroidal anti-inflammatory agents, and laser photocoagulation treatment. The exact cause of CME and the effective treatment of this condition have remained elusive.

Cataract Extraction↗