A biodegradable intravitreal dexamethasone implant (Ozurdex; Allergan Inc., Irvine, CA) has shown effec- tiveness for resolution of macularoedema, including cystoidmacularoedema, associated with other aetio- logies.  Herein, we report a case of SLE complicated with CMO, for which intravitreal dexamethasone the- rapy was performed and resulted in complete resolution of CMO without any significant ocular complication. We also summarize the previous reports on the treat- ment of CMO in eyes with HCQ retinopathy, to
We report a case of fingolimod-associated bilateral cystoidmacularoedema in a patient with multiple sclerosis (MS). A 34- year-old female, diagnosed with MS at age of 30, developed bilateral blurred vision 5 days after initiation of fingolimod. She was misdiagnosed as optic neuritis initially and fingolimod was only discontinued 3 weeks after onset of her visual symptoms when OCT showed prominent bilateral cystoidmacularoedema and subretinal fluid. Although her left corrected vision returned to 6/6, she had persistently decreased right visual acuity of 6/12 after 5 months. This paper aims to raise awareness among ophthalmologists and neurologists of the importance of early recognition of macularoedema associated with fingolimod.
What is already known about this subject? Cystoidmacularoedema (CMO), a vision-threatening condition, is one of the most frequent complications in retinitis pigmentosa (RP). Although various treatment approaches using carbonic anhydrase inhibitors (CAIs) or steroids have been reported, and intravitreal or subtenon’s corticosteroids have shown efficacy in managing CMO, a less invasive topical steroid therapy has been studied in only one case report. The present study hence retrospectively investigated the efficacy of additional topical betamethasone in persistent CMO after CAI therapy in RP, representing specific treatments that have not been previously reported.
We believe our rate of detecting CMO was much higher as a consequence of using SD-OCT. Typically, percentages of angiographic and tomographic CMO are much higher than clinical CMO. In one study using FA, the rate of angiographic CMO at 6 weeks after uncom- plicated cataract surgery was 18.7%, although the rate of clinical CMO was only 2.1% . More specifically, in the subgroup with intraoperative complications, the rate of angiographic CMO and clinical CMO was 11% and 4.8%, respectively. Previously, Ching et al. used OCT to detect CMO following uneventful phacoemulsification . They found 4 out of 131 patients (3%) developed CMO. Unfortu- nately, these patients were excluded from the analysis and the serial macular thickness was not given. Minnella et al. gave OCT details of 15 patients with Irvine-Gass syndrome . However they did not mention whether these patients had intraoperative complication during surgery.
The following case of a 67-year-old lady highlights some interesting and important learning points that would be of value to both trainee and practising ophthalmologists involved in the management of post-operative cataract patients and of patients presenting to eye casualty. The case details the im- portant sequelae that can occur following the inadvertent implantation of a single-piece intraocular lens into the ciliary sulcus during cataract surgery; secondary pigment dispersion glaucoma, recurrent an- terior uveitis and macularoedema. A timeline detail- ing the patient’s management can be seen in Fig. 1.
Over the years a number of diagnostic criteria have been proposed. The original description by Ryan and Maume- nee listed: (1) White, painless eye; (2) minimal, if any, anterior segment inflammation; (3) diffuse vitritis with- out snowballs or snowbanking; (4) retinal vascular leak- age, particularly in the posterior pole, which may be associated with macularoedema and optic disc oedema; (5) distinctive, discrete, cream coloured or depigmented spots throughout the fundus . Later, Priem and Oosterhuis suggested an abridged version of these cri- teria based on their observation of 102 cases of BCR. They suggested minimal criteria as being: (1) Bilateral typical birdshot lesions with (2) two or more of (i) vitritis, (ii) cystoidmacularoedema, (iii) arteriolar narrowing and irregularity of the veins, (iv) retinal vasculitis, (v) disc oedema, (vi) cellophane-like macu- lopathy, (vii) retinal neovascularization, (viii) choroidal (‘subretinal’) neovascularization and macular scar, and (ix) optic atrophy .
Results: A total of 36 patients (M/F: 18/18, 58 eyes) were included, Of the 36 patients, 35 had Type 2 DM and one had Type 1 DM. Mean age of onset of DM was 49 years and uveitis 55 years. The uveitis was bilateral in 22 (61%) patients. There were 19 patients with anterior uveitis, 12 with panuveitis and 5 with intermediate uveitis. Mean follow up was 4.4 years (range 1-18). Mean number of uveitis recurrences was 3 (range 1-7). Causes of vision of 6/18 or worse appeared related to the uveitis in 9 eyes and diabetes in 4 eyes. Cataract occurred in 22 eyes, glaucoma in 17 eyes, and cystoidmacularoedema in 10 eyes. Diabetic retinopathy was detected in 38 (65.5%) eyes (29 non-proliferative including 6 with clinically significant macularoedema, and 9 proliferative). Progression of diabetic retinopathy to proliferative stage occurred in 7 eyes of 4 patients over a mean duration of 4.4 years. In 10 patients with active uveitis the mean HbA1c was 80 mmol/mol [9.5%], (range 49-137 [6.6-14.7]), and 67 mmol/mol [8.3%] (range 46-105 [6.4-11.8]) when the uveitis was quiescent, p = 0.01. Better glycaemic control was required in 10 patients during episodes of uveitis.
Conclusion: More results from randomized controlled trials with long follow-up periods are needed for interventions for uveitic macular edema to assist in determining the overall long-term benefit of different treatments. The only intervention with sufficiently robust randomized con- trolled trials for a meta-analysis was acetazolamide, which was shown to be ineffective in improv- ing vision in eyes with uveitic macular edema, and is clinically now rarely used. Interventions showing promise in this disease include dexamethasone implants, immunomodulatory drugs and anti-vascular endothelial growth-factor agents. When macular edema has become refractory after multiple interventions, pars plana vitrectomy could be considered. The disease pathophysiology is uncertain and the course of disease unpredictable. As there are no clear guidelines from the literature, interventions should be tailored to the individual patient.
Purpose: To describe the use of nepafenac 0.1% for cystoidmacular edema (CME). Methods: This was a multicenter retrospective review of 22 CME cases (20 patients) treated with nepafenac 0.1% (six with concomitant prednisolone acetate 1%) from December 2005 to April 2008: three acute pseudophakic CME cases, 13 chronic/recalcitrant pseudophakic CME cases, and six cases of uveitic CME. Pre- and post-treatment retinal thickness and visual acuity were reported.
Fig. 6 Right eye of a 48-year old male patient with longstanding inferior major BRVO. a. Color fundus photo showing the pathological arterio-venous crossing (black arrow). Note the collateral vessels that have developed on the optic nerve head (white arrow) reminiscent of chronic course. b. Corresponding SS-OCT radial scan shows multiple hyporeflective cystic space in the inferior para-foveal area. The outer retinal layers are preserved. c, f. Corresponding en-face SS-OCTA images in a 6 × 6 mm field of the SCP and the DCP, respectively. The SCP demonstrates mild ischemic changes in the form of flow-voids mainly located in the inferior quadrants Q3 and Q4. The inferior portion of the perifoveal capillary arcade is rarified (white arrow). The DCP shows flow-voids (asterisk) and compensatory telangiectasia (white arrow) in the inferior quadrants Q3 and Q4. The perifoveal capillary arcade shows pruning, and capillary loss. The FAZ is enlarged and cystoid changes are seen in the fovea. Note that the ischemic changes are more pronounced than those appreciated by examining the SCP image. d, g. En-face SS-OCTA images of the SCP and the DCP displayed in 3 × 3 mm field for higher definition. e, h. En-face SS- OCT images at the planes of the SCP and the DCP respectively, in a 3 × 3 mm field. Note that the entire extent of cystoid spaces is best revealed at the DCP plane
The patient returned to clinic on July 25th, 2005, with stable, decreased vision OS. The patient had no discomfort OS. He reported compliance to the treatment regimen. Pertinent findings included best corrected VA of 20/50 OS. Stable central distortion was seen on the Amsler grid OS. Slit lamp findings were normal OD. Conjunctiva/sclera showed no injection OS. The cornea OS still had fine keratic precipitates corneal endothelium OS. Anterior chamber angle was deep with trace cells and flare OS. IOP was 15 mmHg OD and OS with applanation tonometry. Dilated fundus exam was stable OU with the macula showing thickening with cystoid
at 12 months. Landré et al (23) reported a significant improvemed in term of macular edema treatment in which the mean central foveal thickness decreased from 598 μm. to 286 μm at month 1, 338 μm at month 3, and was 441 μm at month 12 with Ozurdex injection. They reported that some of their patients needed another dexamethasone implant injections. Klamann et al. (24) reported that 66% of their patient out of 12 patients needed more than one injection and recurring macular edema had been completely reduced by re-injection
In order to safely replace a face-to-face slit-lamp clinic review, incorporating retinal imaging with a virtual review using retinal imaging data only for new and follow-up patient appointments, the data collected during a virtual assessment should ideally be as sensitive as clinical evalua- tion with a slit lamp alongside the appropriate imaging. 36 To improve sensitivity an OCT scan accompanied by a colour photo of the macula is helpful for nAMD/DMO macular assessments to detect retinal haemorrhage. UWF is often used to assess peripheral DR status. 30 Although pathways with only virtual clinic follow-up assessments struggle to deliver holistic care, supplementing a predominantly virtual pathway with occasional slit-lamp clinics is a good com- promise. Regular routine MR consultant arbitration of images and decision-making within the virtual pathway for services with non-consultant level HCPs making deci- sions ensures ongoing safety levels.
A 53-year-old male noted progressive pericentral blurring in the right eye for 4 days associated with pain in the right eye. Uncorrected visual acuity (UCVA) measured 20/25 in the right eye and 20/20 in the left eye with an IOP of 11 mmHg in both eyes. Fundoscopic exam revealed macular edema and retinal hemorrhages associated with a branch retinal vein occlusion in the right eye. OCT studies revealed CME with CMT of 356 µ m (Figure 6A). FA studies were performed and confirmed branch retinal vein occlusion with CME. He was started on difluprednate, nepafenac, and brinzolamide,
Our study has several strengths and weaknesses. To the best of our knowledge, this is the first prospective study to evaluate the safety and efficacy of ziv-aflibercept for macular edema due to RVOs. The study reports data gathered from more than one site but the small cohort prevents us from detecting statistically significant visual acuity changes. Because of the small cohort, we elected to analyze eyes with central RVO and branch RVO together, even though these conditions often have different baseline characteristics and responses to treatment. The mixed composition of the cohort – patients who were actively being treated for RVO and others whose last injections were at
Abstract: Macular edema (ME) represents the most common cause for visual loss among uveitis patients. The management of uveitic macular edema (UME) may be challenging, due to its often recalcitrant nature. Corticosteroids remain the mainstay of treatment, through their capability of effectively controlling inflammation and the associated ME. Topical steroids may be effective in milder cases of UME, particularly in edema associated with anterior uveitis. Posterior sub-Tenon and orbital floor steroids, as well as intravitreal steroids often induce rapid regression of UME, although this may be followed by recurrence of the pathology. Intra- vitreal corticosteroid implants provide sustained release of steroids facilitating regression of ME with less frequent injections. Topical nonsteroidal anti-inflammatory drugs may provide a safe alternative or adjuvant therapy to topical steroids in mild UME, predominantly in cases with underlying anterior uveitis. Immunomodulators including methotrexate, mycophenolate mofetil, tacrolimus, azathioprine, and cyclosporine, as well as biologic agents, notably the anti- tumor necrosis factor-α monoclonal antibodies adalimumab and infliximab, may accomplish the control of inflammation and associated ME in refractory cases, or enable the tapering of steroids. Newer biotherapies have demonstrated promising outcomes and may be considered in persisting cases of UME.
A cross sectional and retrospective study of 582 patients, 203 (35%) exhibited blindness or visual impairment, bilateral legal blindness developed in 22 (4%) patients, 26 (4.5%) had one blind eye with visual impairment of the other and nine (1.5%) had bilateral visual impairment. Unilateral blindness developed in 82 (14%) patients, whereas 64 (11%) exhibited unilateral visual impairment. The most important causes of both blindness and visual impairment was cystoidmacular edema (29% and 41% respectively). Complications of uveitis were encountered in more than half of the patients and 23% underwent one or more surgical procedures. Patients with panuveitis had worst visual prognosis.