Aphakic Cystoid Macular Edema Research Articles

Abnormal focal macular electroretinograms in eyes with idiopathic epimacular membrane

PURPOSE: To study the functional state of the retina beneath an epimacular membrane by means of focal macular electroretinography. METHODS: Focal macular electroretinograms of 30 consecutive patients (age 25 to 75 years) with unilateral idiopathic epimacular membrane were recorded prospectively. The amplitudes and implicit times of the a and b waves and the oscillatory potentials (O1, O2, O3) recorded from the eye with idiopathic epimacular membrane were compared with those of the normal fellow eye. RESULTS: There was a statistically significant reduction in the amplitude of the a wave ( P < .001), the b wave ( P < .001), and the oscillatory potentials (O1 + O2 + O3; P < .001) of the affected eyes. The reduction of the b-wave amplitude was significantly greater than that of the a wave, resulting in a lower b/a wave ratio ( P = .003) in the affected eyes. The reduction in the amplitude of the oscillatory potentials was significantly greater than that of the other two components ( P < .001). The implicit times were significantly prolonged for the a wave ( P < .001), the b wave ( P = .004), and O3 ( P < .001). There was a significant correlation between relative b-wave amplitude (affected/normal fellow eye) and the visual acuity (r = −0.50, P = .007). These findings were similar to those we reported for eyes with aphakic cystoid macular edema. CONCLUSIONS: The focal macular electroretinograms in eyes with epimacular membrane disclosed abnormalities that were similar to those of eyes with cystoid macular edema. This suggests that the epimacular membrane probably induced damage to the neurons in the inner retinal layers. Dysfunction of these neurons is one possible cause of visual impairment in this disease.

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.

Classification of Aphakic Cystoid Macular Edema with Focal Macular Electroretinograms

Classification of Aphakic Cystoid Macular Edema with Focal Macular Electroretinograms

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.

Management of aphakic and pseudophakic cystoid macular edema

Management of aphakic and pseudophakic cystoid macular edema

Prophylaxis of Aphakic Cystoid Macular Edema without Corticosteroids: A Paired-comparison, Placebo-controlled Double-masked Study

Prior investigations have reported that topical nonsteroidal anti-inflammatory drug (NSAID) therapy prevents the development of postoperative angiographic signs of angiographic cystoid macular edema (CME). However, these studies include concurrent use of corticosteroids. The current study reports therapeutic efficacy for ketorolac ophthalmic solution (an NSAID) in the prophylaxis of angiographic aphakic CME (ACME) after cataract surgery without concurrent corticosteroids for the first time. Fifty patients with bilateral cataracts were enrolled in this placebo-controlled, paired-comparison, double-masked study. Eleven patients had evidence of angiographic ACME on postoperative day 40. Two of these patients demonstrated bilateral ACME, one patient had ACME in the NSAID-treated eye, and eight patients demonstrated ACME in the placebo-treated eye. This is a statistically significant difference favoring drug treatment. The signs of anterior ocular inflammation were greater in the eyes with ACME. This study suggests prophylactic treatment of ACME may be possible without the risks of concurrent corticosteroid toxicity. In addition, a higher incidence of ACME in black patients (22%) is observed in this study than has been recognized previously.

Aphakic Cystoid Macular Edema Secondary to Betaxolol Therapy

Since the approval of timolol for the treatment of open-angle glaucoma, beta-adrenergic blocking drugs have replaced epinephrine, a pure alpha and beta agonist, as the treatment of choice for glaucoma in aphakic patients. To date, there have been no reports of cystoid macular edema secondary to timolol, a non-selective beta-adrenergic blocker that apparently has little intrinsic sympathomimetic activity. Betaxolol is a new beta-adrenergic receptor blocker that preferentially blocks beta 1 receptors. We report a case of angiographically proven cystoid macular edema secondary to betaxolol therapy that resolved after discontinuation and recurred after a monocular therapeutic trial.

Vitreous Incarceration Complicating Cataract Surgery: A Light and Electron Microscopic Study

Vitreous incarceration in the cataract wound may contribute to development of aphakic cystoid macular edema, vitreoretinal traction and retinal detachment, and corneal decompensation. Thirty-one eyes in which vitreous was incarcerated in the cataract wound were examined postmortem and the corneal, anterior segment, and vitreoretinal changes were reported. Light and electron microscopy specimens demonstrated migration of corneal endothelium onto the adherent vitreous with production of basement membrane (descemetization). Fibrous ingrowth was present in 84% of the eyes. Iridovitreal synechiae were seen in 87% of the eyes. Cystoid macular edema, present in six eyes (19%), was usually accompanied by retinal phlebitis and often by distortion of the pars plicata. Vitreoretinal traction was seen in four eyes (13%), retinal tears were seen in two eyes (6%), and one eye had a total retinal detachment. Preretinal membranes were present in five eyes (16%) without other macular pathology. Persistent cystoid macular edema appears to occur in a minority of eyes with vitreous incarcerated in the cataract wound. If a vitrectomy is to be performed, the surgeon should excise vitreous adherent to the iris and in the anterior vitreous cavity in addition to the vitreous in the region of the wound.

Vitrectomy for Chronic Aphakic Cystoid Macular Edema: Results of a National, Collaborative, Prospective, Randomized Investigation

A five-year (1979–1984) prospective, randomized, controlled, collaborative study was performed by 27 experienced vitrectomy surgeons in 15 medical centers on 136 surgically aphakic eyes without lens implants but with vitreous adherent to the corneoscleral wound and with chronic aphakic cystoid macular edema (ACME). One hundred fifteen eyes completed the entire course of investigation. The purpose of the study was twofold: to determine the effectiveness of vitrectomy in eliminating established ACME and to determine the natural history of this condition. Following criteria contained within the study protocol, 68 eyes were randomized to surgery (RAN-S) or control (RAN-C), and 47 eyes were observed in the long-term observation group (LTO). Twenty-one eyes were eliminated from the investigation for reasons stated in the text. The RAN-S group proved to have a significantly better visual course than the RAN-C group (P = <0.01). An analysis of the LTO group revealed that if central vision did not decline to a level of 20/80 or worse, 27% of the eyes had a chance of spontaneously improving to a level of 20/50 or better. However, if central vision declines to or beyond this point, spontaneous visual improvement to 20/50 or better only occurred in 8% of eyes. Also reported are other important clinical findings such as the role of systemic diseases in ACME, the incidence of vitreous traction on the macula, prognostic value of pre-surgical medical therapy, a comparison of limbal versus pars plana surgical approach, the timing of surgery, and the effectiveness of fluorescein angiography as an objective monitor of visual function.

Pharmacologic Therapy of Aphakic and Pseudophakic Cystoid Macular Edema: 1985 Update

Major advances in the pharmacologic therapy of aphakic cystoid macular edema (ACME) have not occurred since 1982. Topical nonsteroidal anti-inflammatory agents are still not commercially available for ocular therapy. Topical indomethacin remains the one agent which has been proven to be of prophylactic value for angiographic aphakic cystoid macular edema although other non-steroidal agents may also work. The therapeutic value of these compounds for established ACME remains uncertain. No prospective randomized prophylactic or therapeutic trials of either topical or systemic corticosteroids have been performed.

Pars plana vitrectomy for aphakic cystoid macular edema.

The authors used a combined limbal and pars plana vitrectomy approach to treat 17 consecutive eyes (16 patients) with chronic aphakic cystoid macular edema associated with vitreous incarceration in the cataract wound. Criteria for surgery included: decreased visual acuity to 20/50 or worse; cystoid macular edema confirmed by fluorescein angiography; persistent edema of 6 months or longer; and visible vitreous incarceration in the limbal wound. The vitreous was successfully removed from the limbal wound in 16 of 17 eyes. Postoperatively, vision improved by two lines or more in 11 eyes (65%). The surgical technique is described.

Ocular blood flow in phakic and aphakic monkey eyes

Alterations in regional ocular blood flow produced by topical epinephrine were studied in phakic and aphakic eyes of Macaca arctoides using the radioactive microsphere technique. Three isotopes were used to make sequential blood flow measurements just prior to topical epinephrine administration, 1 hr later and 3 hr later. Significant reductions of flow were found in the iris, ciliary body, and optic nerve head of both phakic and aphakic groups. Choroidal and posterior optic nerve flow decreased significantly in aphakic eyes only. Decreases in flow were maximal at 3 hr. Significant changes in retinal flow were not detected. The implications of these findings regarding epinephrine-induced aphakic cystoid macular edema and the suitability of epinephrine or its derivatives in the treatment of glaucoma are discussed.

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 imcompetence, 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.

Prophylaxis and therapy of aphakic cystoid macular edema

Aphakic cystoid macular edema (ACME) can be a visually significant complication of modern cataract surgery. Prophylaxis of ACME is preferable to therapy of established ACME. Selection of the appropriate cataract operation, control of systemic factors, avoidance of topical catecholamines, control of intraocular inflammation and use of topical or systemic pharmacologic agents may play a role in the prevention of ACME. If it is proven that light toxicity influences the development of ACME, filters in operating microscopes or in intraocular lenses, cataract glasses, or contact lenses may be helpful. Once ACME is present, antiinflammatory therapy has been the main intervention, although its longterm value remains uncertain. Surgical approaches of unproven value have included photocoagulation, vitrectomy, and removal of an intraocular lens.

A perspective on the treatment of aphakic cystoid macular edema

Concepts related to the pathogenesis of aphakic cystoid macular edema (ACME) are presented with reference to possible management considerations. The role of certain aspects of cataract surgical technique, laser photocoagulation, vitreoretinal surgery and medical therapy utilizing corticosteroids and antiprostaglandins are discussed. The difficulties encountered in the evaluation of the efficacy of any treatment modality advocated for ACME are reviewed. Preliminary results of studies on the medical treatment of ACME currently under investigation by the author are also presented.

Pathogenesis of cystoid macular edema: An anatomic consideration of vitreoretinal adhesions

Although it had been widely accepted that vitreous traction plays a key role in the pathogenesis of aphakic cystoid macular edema, vitreoretinal traction is not observable in many patients and other hypotheses have also been investigated. The authors review the present knowledge of the anatomy of the vitreoretinal interface and the pathologic findings in cystoid macular edema. A new hypothesis combining the effects of both traction and inflammation is proposed.

The national, prospective, randomized vitrectomy study for chronic aphakic cystoid macular edema. Progress report and comparison between the control and nonrandomized groups

Three years ago, a prospective, randomized, collaborative study investigating the effectiveness of vitrectomy for chronic aphakic cystoid macular edema in eyes with vitreous adherent to the cataract wound but without an intraocular lens was started. To date, the study consists of 130 eyes which have been assigned to three different groups. Without disturbing the data related to the question of the effectiveness of surgery, an analysis of patient histories and eye findings reveal interesting facts. The time between cataract surgery and onset of visual decrease was three months. Most of the eyes have a detached posterior vitreous face, and only 4% had evidence of vitreous traction on the macula. All eyes demonstrated some degree of flare and cells in the aqueous or vitreous, and the presence of systemic vascular disease in the patient does not seem to determine the eye's long term visual performance.

Aphakic Cystoid Macular Edema in Children After Vitrectomy for Anterior Segment Injuries

Twenty-four children had surgery utilizing vitrectomy instrumentation for anterior segment trauma. Lensectomy was performed in 23 of 24 eyes. In each child a pars plicata approach was used. Fluorescein angiography or angioscopy performed two months to seven years after surgery failed to document aphakic cystoid macular edema.

An Anterior Surgical Approach To Aphakic Cystoid Macular Edema

Fifteen consecutive eyes in 14 patients (six men and eight women, ranging in age from 43 to 75 years) underwent anterior vitrectomy for chronic cystoid macular edema documented by fluorescein angiography. All eyes had either vitreous adhesions to the cataract incision with pupillary distortion, or adherence of vitreous strands to the iris. Anterior vitrectomy via the corneoscleral limbus was performed in each case to remove vitreous from anterior segment structures. Thirteen of the 15 eyes showed visual improvement, with 12 of the 15 showing improvement of two Snellen lines or more. There was no direct correlation between the duration of aphakic cystoid macular edema and final visual acuity.

Double-Masked Trial of Fenoprofen Sodium: Treatment of Chronic Aphakic Cystoid Macular Edema

Aphakic cystoid macular edema is a serious eye disease. Its etiology is unknown, but a widely held theory attributes it to an inflammatory response to surgical trauma. In a double-masked study, a 1% solution of fenoprofen sodium, a topically applied antiprostaglandin agent, was evaluated against placebo in determining the effectiveness of fenoprofen in the treatment of chronic aphakic cystoid macular edema. Fourteen patients, five women and nine men, participated in the study. Fenoprofen sodium was found to have no effect on the course of chronic aphakic cystoid macular edema. We believe that the lack of effect may have been due to the duration of edema at the time of treatment or to the small sample size. Larger studies in the immediate postoperative period are suggested. The importance of iris angiography as a possible predicting technique of macular leakage is emphasized.