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PubMed1996

Detection of diabetic macular edema: Nidek 3Dx stereophotography compared with fundus biomicroscopy.

PURPOSE: To assess the use of the Nidek 3Dx simultaneous stereophotography camera in diabetic patients, comparing the detection of clinically significant macular edema by fundus biomicroscopy to detection by the Nidek 3Dx simultaneous fundus stereophotograph. METHODS: Two hundred eight eyes of 123 diabetic patients at the Wilmer Retinal Vascular Center were examined for this prospective study between August 1993 and October 1993. Each patient was examined by one of three retina specialists by contact lens biomicroscopy for clinically significant macular edema and foveal center thickening. Nidek 3Dx fundus stereophotographs were obtained and graded independently for clinically significant macular edema and foveal center thickening by a fourth ophthalmologist masked from the clinical examination findings. Percent agreement, kappa statistic, and weighted kappa statistic were determined for the two diagnostic methods. RESULTS: One hundred eighty-four (88%) of the 208 stereophotographs were of sufficient quality to detect clinically significant macular edema; 175 (84%) of the 208 stereophotographs detected foveal center thickening. The agreement between the clinician and the photographic grading, measured by weighted kappa, was 0.52 for clinically significant macular edema and 0.58 for foveal center thickening, representing fair to good agreement beyond chance. Agreement was improved when normal fundus Nidek stereophotographs were available as standards for comparison. CONCLUSIONS: The Nidek 3Dx camera is suitable for photographic detection of clinically significant macular edema and may have a potential advantage over conventional cameras by achieving good-quality, gradable stereophotographs in a large proportion of photographed eyes.

Adult↗
PubMed1998

Cystoid macular edema associated with latanoprost in aphakic and pseudophakic eyes.

PURPOSE: To describe four patients who developed cystoid macular edema shortly after onset of treatment with latanoprost. METHOD: Retrospective review of medical records of patients with open-angle glaucoma who developed cystoid macular edema shortly after starting latanoprost. RESULTS: The use of topical latanoprost was temporally related to the development of cystoid macular edema in four patients (six eyes; two aphakic eyes and four pseudophakic eyes). Cystoid macular edema resolved in all patients after latanoprost was discontinued. CONCLUSIONS: Cystoid macular edema is a potential complication of latanoprost therapy. Further observations are needed to determine if the risk of cystoid macular edema is limited to or greatest in patients who are pseudophakic or aphakic.

Aged↗
PubMed1999

Attached posterior hyaloid membrane and the pathogenesis of honeycombed cystoid macular edema in patients with diabetes.

PURPOSE: To investigate the pathogenesis of honeycombed cystoid macular edema in patients with diabetes. METHODS: The relationship between the posterior hyaloid membrane and honeycombed cystoid macular edema was examined in 24 eyes of 20 patients with diabetes who underwent vitrectomy for cystoid macular edema. RESULTS: In 19 eyes of 15 patients with diabetes, the posterior hyaloid membrane was attached to the macula, and in five eyes of five patients, the posterior hyaloid membrane was separated from the macula. In 14 (74%) of the 19 eyes with an attached posterior hyaloid membrane, honeycombed cystoid macular edema was detected. Conversely, honeycombed cystoid edema was not detected in any of the five eyes with posterior hyaloid detachment (P = .0059). CONCLUSIONS: These observations demonstrate a strong correlation between an attached posterior hyaloid membrane and the presence of honeycombed cystoid macular edema. We suggest that retinal traction by the posterior hyaloid membrane is involved in the pathogenesis of honeycombed cystoid changes in diabetic patients.

Adult↗
PubMed1999

Vitrectomy for chronic pseudophakic cystoid macular edema.

PURPOSE: We report the results of pars plana vitrectomy for chronic pseudophakic cystoid macular edema unresponsive to medical treatment. METHODS: Retrospective analysis of 23 consecutive eyes of 23 patients with chronic pseudophakic cystoid macular edema was performed. Eyes with vitreous incarceration into the cataract wound or vitreous-cornea contact were excluded from the study. Preoperatively, all eyes had cystoid macular edema confirmed on fluorescein angiography and were unresponsive to medical treatment. Pars plana vitrectomy was performed using standard techniques and vitreous adhesions to the iris, intraocular lens, or both were lysed if present. RESULTS: The mean interval between cataract surgery and vitrectomy was 32.3+/-30.9 months (median, 20 months; range, 3 to 110 months). The vitreous was adherent to the iris or intraocular lens in 12 eyes (52.2%) and was present in the anterior chamber with no evidence of adhesions in seven eyes (30.4%). In four eyes (17.4%) the vitreous was posterior to the iris plane with no adhesions to anterior segment structures. The median preoperative best-corrected visual acuity was 20/200, and the median final postoperative best-corrected visual acuity was 20/60 (P<.0001) after a mean follow-up of 30.2+/-31.2 months (median, 14 months; range, 2 to 109 months). Final best-corrected visual acuity improved by a mean of 3.3+/-2.6 Snellen lines, with a median percent change of 70% (mean, 57.3%; range, 0% to 99%). In all 23 eyes the cystoid macular edema resolved postoperatively by biomicroscopic examination in a mean period of 3.3 months (median, 2 months; range, 1 to 12 months). CONCLUSIONS: In pseudophakic eyes with chronic cystoid macular edema unresponsive to medical treatment, vitrectomy resulted in resolution of the cystoid macular edema with improved visual acuity in some cases. Clinical improvement may occur in eyes with no apparent vitreous disturbance.

Aged↗
PubMed2000

Tomographic assessment of vitreous surgery for diabetic macular edema.

PURPOSE: To evaluate the retinal structure before and after vitrectomy for diabetic macular edema and to assess the correlation between thickness of neurosensory retina and best-corrected visual acuity. METHODS: Tomographic features of 13 eyes (nine patients) with diabetic macular edema were prospectively evaluated with optical coherence tomography before and after vitrectomy. The foveal thickness (the distance between the inner retinal surface and the retinal pigment epithelium) and the retinal thickness (thickness of neurosensory retina) were measured by optical coherence tomography preoperatively and postoperatively. The correlation of the best-corrected visual acuity with foveal and retinal thickness was determined. RESULTS: All 13 eyes had retinal swelling with low intraretinal reflectivity. In addition to retinal swelling, there were cystoid spaces in five (38%) of 13 eyes, a serous retinal detachment in three (23%), and both cystoid spaces and serous detachment in three (23%). Six months postoperatively, the mean foveal thickness significantly decreased from 630 +/- 170 to 350 +/- 120 microm (P <.01, paired t test) and the mean thickness of neurosensory retina decreased from 540 +/- 160 to 320 +/- 140 microm (P <.01, paired t test). A serous retinal detachment occurred transiently in 3 eyes. Compared with the preoperative level, the postoperative best-corrected visual acuity level improved by more than 2 lines in five of the 13 eyes (38%), remained the same in seven eyes (54%), and decreased in one eye (8%). The postoperative thickness of neurosensory retina at the fovea and best-corrected visual acuity level at the sixth postoperative month had a strong negative correlation (correlation coefficient, -0.76; P <.01, Spearmans rank test). CONCLUSIONS: Vitrectomy was generally effective in treatment of diabetic macular edema. Optical coherence tomography demonstrated the intraretinal changes of macular edema and the process of edema absorption. During the process of macular edema absorption, intraretinal fluid appeared to move into the subretinal space in some cases. Best-corrected visual acuity improvement was greater in eyes with less preoperative increase in thickness of neurosensory retina.

Aged↗
PubMed1996

Iatrogenic myocardial edema: increased diastolic compliance and time course of resolution in vivo.

BACKGROUND: Perfusion-induced edema reduces diastolic compliance in isolated hearts, but this effect and the time for edema to resolve after blood reperfusion have not been defined in large animals. METHODS: Edema was induced by coronary perfusion with Plegisol (750 mL, 289 mOsm/L) during a 1-minute aortic occlusion in 6 pigs. This was followed by whole blood reperfusion, inotropic support, and circulatory assistance until sinus rhythm and contractile function were restored. A control group (n = 6) was treated similarly, with 1 minute of electrically induced ventricular fibrillation and no coronary perfusion. Recorded data included electrocardiogram, left ventricular pressure and conductance, aortic flow, and two-dimensional echocardiography. Preload reduction by vena caval occlusion was used to define systolic and diastolic properties. Data were recorded at baseline and at 15-minute intervals for 90 minutes after reperfusion. RESULTS: In the edema group, average left ventricular mass (132 +/- 7 [standard error of the mean] versus 106 +/- 4 g) and ventricular stiffness constant (0.15 +/- 0.02 versus 0.05 +/- 0.01) increased after Plegisol versus baseline (p < 0.05), returning to normal after 45 minutes of reperfusion. In controls, mass (118 +/- 6 versus 116 +/- 4 g) and ventricular stiffness (0.06 +/- 0.01 versus 0.05 +/- 0.01) did not change significantly. There was no significant change in systolic function. Myocardial water content at the end of the study was not different for the two groups. CONCLUSIONS: Crystalloid-induced edema and diastolic stiffness resolve after 45 minutes in pigs. This suggests that edema caused solely by cardioplegia during cardiac operations should not cause significant perioperative ventricular dysfunction.

Animals↗
PubMed2002

Noninvasive measurement of cerebral bioimpedance for detection of cerebral edema in the neonatal piglet.

The association of sustained cerebral edema with poor neurological outcome following hypoxia-ischaemia in the neonate suggests that measurement of cerebral edema may allow early prediction of outcome in these infants. Direct measurements of cerebral impedance have been widely used in animal studies to monitor cerebral edema, but such invasive measurements are not possible in the human neonate. This study investigated the ability of noninvasive cerebral impedance measurements to detect cerebral edema following hypoxia-ischaemia. One-day-old piglets were anaesthetized, intubated and ventilated. Hypoxia was induced by reducing the inspired oxygen concentration to 4-6% O(2). Noninvasive cerebral bioimpedance was measured using gel electrodes attached to the scalp. Cerebral bioimpedance was also measured directly by insertion of two silver-silver chloride electrodes subdurally. Noninvasive and invasive measurements were made before, during and after hypoxia. Whole body impedance was measured to assess overall fluid movements. Intracranial pressure was measured continuously via a catheter inserted subdurally, as an index of cerebral edema. There was good agreement between noninvasive and invasive measurements of cerebral impedance although externally obtained responses were attenuated. Noninvasive measurements were also well correlated with intracranial pressure. Whole body impedance changes did not account for increases in noninvasively measured cerebral impedance. Results suggest that noninvasive cerebral impedance measurements do reflect intracranial events, and are able to detect cerebral edema following hypoxia-ischaemia in the neonate.

Animals↗
PubMed1999

Mild hypothermia modifies ammonia-induced brain edema in rats after portacaval anastomosis.

BACKGROUND & AIMS: The pathogenesis of brain edema in fulminant hepatic failure is still unresolved. Mild hypothermia (33 degrees-35 degreesC) can ameliorate brain edema after traumatic brain injury. We evaluated mild hypothermia in a model of ammonia-induced brain edema in which accumulation of brain glutamine has been proposed as a key pathogenic factor. METHODS: After portacaval anastomosis, anesthetized rats were infused with ammonium acetate at 33 degrees, 35 degrees, and 37 degreesC or vehicle at 37 degreesC. Water and glutamine levels in the brain, cardiac output, and regional and cerebral hemodynamics were measured when intracranial pressure increased 3-4-fold (ammonia infusion at 37 degrees) and matched times (other groups). RESULTS: Mild hypothermia reduced ammonia-induced brain swelling and increased intracranial pressure. Brain glutamine level was not decreased by hypothermia. Brain edema was accompanied by a specific increase in cerebral blood flow and oxygen consumption, which were normal in both hypothermic groups. When the ammonia infusion was continued in hypothermic rats, plasma ammonia levels continued to increase and brain swelling eventually developed. CONCLUSIONS: Mild hypothermia delays ammonia-induced brain edema. In this model, an increase in cerebral perfusion is required for brain edema to become manifest. Mild hypothermia could be tested for treatment of intracranial hypertension in fulminant hepatic failure.

Acetates↗
PubMed2002

Melatonin reduces cerebral edema formation caused by transient forebrain ischemia in rats.

Reduction of cerebral edema, an early symptom of ischemia, is one of the most important remedies for reducing subsequent chronic neural damage in stroke. Melatonin, a metabolite of tryptophan released from the pineal gland, has been found to be effective against neurotoxicity in vitro. The present study was aimed to demonstrate the effectiveness of melatonin in vivo in reducing ischemia-induced edema using magnetic resonance imaging (MRI). Rats were subjected to middle cerebral artery (MCA) occlusion/reperfusion surgery. Melatonin was administered twice (6.0 mg/kg, p.o.): just prior to 1 h MCA occlusion and 1 day after the surgery. T2-weighted multislice spin-echo images were acquired 1 day after the surgery. Increases in T2-weighted signals in ischemic sites of the brain were clearly observed after MCA occlusion. The signal increase was found mainly in the striatum and in the cerebral cortex in saline-treated control rats. In the melatonin-treated group, the total volume of cerebral edema was reduced by 45.3% compared to control group (P < 0.01). The protective effect of melatonin against cerebral edema was more clearly observed in the cerebral cortex (reduced by 56.1%, P < 0.01), while the reduction of edema volume in the striatum was weak (reduced by 23.0%). The present MRI study clearly demonstrated that melatonin is effective in reducing edema formation in ischemic animals in vivo, especially in the cerebral cortex. Melatonin may be highly useful in preventing cortical dysfunctions such as motor, sensory, memory, and psychological impairments.

Acute Disease↗
PubMed2002

Physician-reported management of edema and destabilized blood pressure in cyclooxygenase-2-specific inhibitor users with osteoarthritis and treated hypertension.

BACKGROUND: The addition of a nonsteroidal anti-inflammatory drug to the regimen of a patient with treated hypertension can cause a destabilization of blood pressure. OBJECTIVE: The aim of this study was to describe physician-reported management of clinically significant edema and/or destabilized blood pressure in patients with osteoarthritis (OA) and hypertension when initiating therapy with rofecoxib or celecoxib. METHODS: A cross-sectional survey was administered to physicians who attended one of several arthritis consultant programs sponsored by Pharmacia Corporation, with attendees selected by local sales representatives. Each program included a clinical presentation by a physician concerning the cardiorenal safety of celecoxib, followed by a consultative presentation and session led by a Pharmacia Clinical Education Manager. RESULTS: A total of 828 physicians in the following specialties completed the survey: family practice (33.0%), internal medicine (25.0%), orthopedics (15.2%), and rheumatology (11.4%). Responding physicians expected that the majority of patients who experienced edema would contact them (68.4%). They reported that they schedule follow-up visits for blood pressure monitoring 65.6% of the time after initiating a cyclooxygenase-2 (COX-2)-specific inhibitor, with family practitioners and internists most likely to indicate that they would do so and orthopedists least likely. Responding physicians indicated that the presence of edema and destabilized blood pressure generally led to discontinuation of the COX-2-specific inhibitor (58%-82% of the time). Internists and family practitioners were most likely to report that they treat edema by initiating or modifying diuretic therapy (33%-51% of the time). For destabilized blood pressure, an antihypertensive drug was reported to be initiated or modified 40% to 55% of the time by family practitioners and internists, whereas orthopedists indicated that they referred patients to the primary care provider. The COX-2-specific inhibitor prescribed resulted in management differences: physicians indicated that they were more likely to switch from rofecoxib to celecoxib in the event of edema or destabilized blood pressure, whereas they were more likely to adjust the celecoxib dose than the rofecoxib dose. Because the data were captured from convenience samples of physicians attending sponsored meetings, it is possible that respondents provided the answers they thought the sponsor would want. Because this was a cross-sectional survey, reported behavior was not compared with actual behavior. CONCLUSIONS: A significant percentage of physicians reported that they monitor patients with OA and hypertension for the occurrence of destabilized blood pressure and edema after initiation of a COX-2-specific inhibitor. Physicians indicated that they would nearly always intervene when either event is identified.

Celecoxib↗
PubMed2001

Pars plana vitrectomy for cystoid macular edema secondary to sarcoid uveitis.

OBJECTIVE: To examine the results of pars plana vitrectomy for cystoid macular edema secondary to sarcoid uveitis resistant to medical treatment. DESIGN: Retrospective, interventional, noncomparative case series. SUBJECTS: Fourteen consecutive subjects (18 eyes) with cystoid macular edema associated with sarcoid uveitis resistant to medical treatment. INTERVENTION: All eyes underwent pars plana vitrectomy. Nine eyes also underwent peeling of the epiretinal membrane or removal of the posterior vitreous cortex. MAIN OUTCOME MEASURES: Status of macular edema, visual acuity, and complications. RESULTS: Ten eyes (56%) improved 2 or more lines of Snellen visual acuity within 12 months. Six eyes (33%) remained unchanged, within a line of preoperative Snellen visual acuity, and two eyes (11%) worsened by 2 or more lines of Snellen visual acuity. Slit-lamp biomicroscopy showed that cystoid macular edema had resolved in 14 eyes (78%) within 9 months postoperatively. One eye (6%) had minimal edema, whereas three eyes (17%) remained unchanged biomicroscopically at the final visit. Postoperative complications included cataract formation, glaucoma, optic nerve atrophy, epiretinal membrane formation, and tractional retinal detachment. No severe postoperative inflammation was noted. CONCLUSIONS: Pars plana vitrectomy seems to have a beneficial effect on cystoid macular edema caused by sarcoidosis resistant to medical treatment.

Adult↗
PubMed2003

Proposed international clinical diabetic retinopathy and diabetic macular edema disease severity scales.

PURPOSE: To develop consensus regarding clinical disease severity classification systems for diabetic retinopathy and diabetic macular edema that can be used around the world, and to improve communication and coordination of care among physicians who care for patients with diabetes. DESIGN: Report regarding the development of clinical diabetic retinopathy disease severity scales. PARTICIPANTS: A group of 31 individuals from 16 countries, representing comprehensive ophthalmology, retina subspecialties, endocrinology, and epidemiology. METHODS: An initial clinical classification system, based on the Early Treatment Diabetic Retinopathy Study and the Wisconsin Epidemiologic Study of Diabetic Retinopathy publications, was circulated to the group in advance of a workshop. Each member reviewed this using e-mail, and a modified Delphi system was used to stratify responses. At a later workshop, separate systems for diabetic retinopathy and macular edema were developed. These were then reevaluated by group members, and the modified Delphi system was again used to measure degrees of agreement. MAIN OUTCOME MEASURES: Consensus regarding specific classification systems was achieved. RESULTS: A five-stage disease severity classification for diabetic retinopathy includes three stages of low risk, a fourth stage of severe nonproliferative retinopathy, and a fifth stage of proliferative retinopathy. Diabetic macular edema is classified as apparently present or apparently absent. If training and equipment allow the screener to make a valid decision, macular edema is further categorized as a function of its distance from the central macula. CONCLUSIONS: There seems to be a genuine need for consistent international clinical classification systems for diabetic retinopathy and diabetic macular edema that are supported with solid evidence. The proposed clinical classification systems provide a means of appropriately categorizing diabetic retinopathy and macular edema. It is hoped that these systems will be valuable in improving both screening of individuals with diabetes and communication and discussion among individuals caring for these patients.

Diabetic Retinopathy↗
PubMed1983

Diabetic maculopathy. A critical review highlighting diffuse macular edema.

Retinal ischemia and edema are the two major intraretinal components of diabetic maculopathy. Focal macular edema is caused by focal leakage from retinal microaneurysms and dilated capillary segments; diffuse edema is caused by leakage from diffusely dilated retinal capillaries throughout the posterior pole. Diffuse macular edema may be exacerbated by systemic factors such as cardiac or renal failure, and hypertension. It is postulated that dysfunction of the retinal pigment epithelial barrier and transport functions might contribute to the problem of diffuse macular edema. Newer techniques of laser grid photocoagulation for diffuse edema have been proposed. It is postulated that photocoagulative debridement of a disordered retinal pigment epithelium could be a mechanism of action of this treatment.

Adolescent↗
PubMed1984

The Wisconsin epidemiologic study of diabetic retinopathy. IV. Diabetic macular edema.

The prevalence of macular edema and its relationship to a number of risk factors were examined in a population-based study in southern Wisconsin. Macular edema was determined from its presence on stereoscopic fundus photographs or from past history as recorded and documented in clinic records and photographs. For participants whose age at diagnosis of diabetes was less than 30 years and who were taking insulin (n = 919), prevalence rates of macular edema varied from 0% in those who had diabetes less than 5 years to 29% in those whose duration of diabetes was 20 or more years. In these persons, macular edema was associated with longer duration of diabetes, presence of proteinuria, diuretic use, male gender and higher glycosylated hemoglobin. For those whose age at diagnosis was 30 years or older (n = 1121), prevalence rates of macular edema varied from 3% in those who had diabetes less than 5 years to 28% in those whose duration of diabetes was 20 or more years. In these persons, presence of macular edema was associated with longer duration of diabetes, higher systolic blood pressure, insulin use, higher glycosylated hemoglobin, and presence of proteinuria.

Adolescent↗
PubMed1989

The Wisconsin epidemiologic study of diabetic retinopathy. XI. The incidence of macular edema.

As part of a population-based study of diabetes mellitus, the 4-year incidence of macular edema and its relationship to various risk factors was examined in a group of younger onset insulin-taking persons (n = 610) and older onset persons (n = 652). The presence of macular edema at the baseline and follow-up examinations was determined from gradings of stereoscopic fundus photographs. The overall incidence of macular edema in the younger onset group was 8.2% (50/610); in the group of older onset persons using insulin, 8.4% (23/273) and in the group of those not using insulin, 2.9% (11/379). The incidence of macular edema was associated with higher level of glycosylated hemoglobin, longer duration of diabetes, and more severe retinopathy at the baseline examination in both younger and older onset groups. These data provide accurate population-based estimates of incidence of macular edema, and suggest that the level of glycemia is a significant risk factor for the development of macular edema.

Adolescent↗
PubMed1995

The Wisconsin Epidemiologic Study of Diabetic Retinopathy. XV. The long-term incidence of macular edema.

BACKGROUND: As part of a population-based study of diabetes mellitus, the incidence of macular edema over a 10-year period and its relation to various risk factors are examined. METHODS: There were 891 younger-onset people with a diagnosis of having had diabetes before 30 years of age who were taking insulin at baseline examination and 987 older-onset people with a diagnosis of having had diabetes at 30 years of age or older who participated in baseline and 4-year examinations. Of these, 765 younger-onset and 533 older-onset people also participated in a 10-year examination. The presence of macular edema at baseline and follow-up examinations was determined from gradings of stereoscopic fundus photographs. RESULTS: The incidence of macular edema over the 10-year period was 20.1% in the younger-onset group, 25.4% in the older-onset group taking insulin, and 13.9% in the older-onset group not taking insulin. The incidence of macular edema over the 10-year period was associated with higher levels of glycosylated hemoglobin and more severe retinopathy in both younger- and older-onset groups, and with being female and increased diastolic blood pressure in the older-onset group. CONCLUSIONS: These data suggest a relatively high incidence of macular edema. The authors' data also suggest that a reduction in hyperglycemia may result in a beneficial decrease in the incidence of macular edema.

Adult↗
PubMed1996

A randomized, masked, cross-over trial of acetazolamide for cystoid macular edema in patients with uveitis.

PURPOSE: To study the effect of acetazolamide on cystoid macular edema in patients with uveitis. METHODS: Forty patients with chronic intermediate, posterior, or panuveitis associated cystoid macular edema were randomized into a masked, cross-over trial comparing acetazolamide versus placebo. Patients received an initial 4-week course of either acetazolamide or placebo (course A) followed by a 4-week washout period. They then received a 4-week course of the opposite study medication (course B). Primary endpoints included area of cystoid macular edema measured on late-phase views of fluorescein angiography and visual acuity. RESULTS: Thirty-seven patients completed the trial and were available for analysis; 17 (46%) were randomized to receive acetazolamide and 20 (54%) to receive placebo during course A. Acetazolamide resulted in a 0.5-disc area (25%) decrease in cystoid macular edema over that of placebo (P = 0.01; estimated treatment effect = -0.5 disc areas; 95% confidence interval, -0.9 to -0.1). However, there was no statistically significant effect of acetazolamide on visual acuity (P = 0.61; estimated treatment effect = 0.6 letters; 95% confidence interval, -2 to 3). CONCLUSIONS: A 4-week course of acetazolamide therapy results in a statistically significant but small decrease in cystoid macular edema in patients with chronic uveitis, and does not improve visual acuity. In contrast to previous studies in the literature, acetazolamide may have a more limited clinical benefit in patients with long-standing cystoid macular edema associated with chronic uveitis.

Acetazolamide↗
PubMed1999

Ketorolac treatment of pseudophakic cystoid macular edema identified more than 24 months after cataract extraction.

OBJECTIVE: To evaluate whether ketorolac ophthalmic drops prescribed four times a day can be associated with improved visual acuity and prompt resolution of edema for patients with pseudophakic cystoid macular edema identified more than 24 months after cataract surgery. DESIGN: Prospective, nonrandomized, comparative (subject self-controlled) trial. PARTICIPANTS: The records of nine patients who had pseudophakic cystoid macular edema more than 24 months after cataract surgery at the time treatment commenced were identified at the Wilmer Retinal Vascular Center from September 1, 1996, through March 1, 1997. MAIN OUTCOME MEASURES: Best-corrected visual acuities measured on a retroilluminated Bailey-Lovie chart approximately every 3 months, contact lens biomicroscopy, and fluorescein angiography following ketorolac. INTERVENTION: Commercially available ketorolac ophthalmic drops 0.5% were prescribed for the affected eye four times a day for at least 3 months and continued until edema resolved. RESULTS: Ten eyes of nine patients were identified more than 24 months after cataract extraction (median, 59 months). Seven eyes (70%) improved (mean, +3.2 lines; range, +1 to +13 lines), including six by 2 or more lines 3 months after treatment initiation. Two eyes (20%) were unchanged, and one eye (10%) was 1 line worse. All seven eyes that improved 1 line or more had some or complete angiographic resolution of fluorescein dye leakage. In these seven eyes, ketorolac was discontinued when dye leakage completely resolved or failed to continue to improve on periodic 3-month follow-up examinations. In all seven eyes, recurrence of edema was noted within 3 months after ketorolac was stopped. CONCLUSIONS: Chronic pseudophakic cystoid macular edema identified more than 24 months after cataract surgery can improve with topical ketorolac but probably requires persistent use.

Aged↗