Acta Ophthalmologica 2014
were cataract progression (12%) and new onset CMO (10%). The proportion of relapses treated with systemic steroids signiﬁcantly reduced from 70% prediabetes to 56% postdiabetes diagnosis. Adding local steroid injection while on systemic steroids increased from 4% to 15% (p = 0.003, chi-square test). No significant diﬀerence was observed in the uveitis relapse treatment success preversus postdiabetes diagnosis (Table 1). Of the 96 eyes with uveitis and DM, one eye developed a clinically signiﬁcant macular oedema after 3 years and required grid laser treatment, while seven eyes of six patients (7.3%) developed non-proliferative diabetic retinopathy, which occurred at a median of six (range, 2–11) years. While one previous study explored the visual outcome of 36 patients with diabetes who later developed uveitis (Oswal et al. 2013), our study further explores the synergistic eﬀect of uveitis and diabetes by examining the eﬀect of newly diagnosed diabetes on the eyes with uveitis and the eﬀect of diabetes on uveitis treatment strategies. In conclusion, the concurrent diagnosis of DM in uveitis patients is associated with a signiﬁcant reduction in visual acuity within the ﬁrst 2 years. More uveitis relapses were treated with local steroid injection rather than increasing systemic corticosteroid dose, without aﬀecting the ability to control uveitis relapses. It is important to optimize treatment protocols for DM and uveitis when occur concurrently.
References Durrani OM, Tehrani NN, Marr JE, Moradi P, Stavrou P & Murray PI (2004): Degree, duration, and causes of visual loss in uveitis. Br J Ophthalmol 88: 1159–1162. Gulliford MC, Charlton J & Latinovic R (2006): Risk of diabetes associated with prescribed glucocorticoids in a large population. Diabetes Care 29: 2728–2729. Lightman S (1991): Uveitis: management. Lancet 338: 1501–1504. Oswal KS, Sivaraj RR, Murray PI & Stavrou P (2013): Clinical course and visual outcome in patients with diabetes mellitus and uveitis. BMC Res Notes 6: 167. Zhang X, Saaddine JB, Chou CF et al. (2010): Prevalence of diabetic retinopathy in the United States, 2005–2008. JAMA 304: 649– 656.
Correspondence: Sue Lightman, PhD, FRCOphth Institute of Ophthalmology, UCL Moorﬁelds Eye Hospital, City Road London EC1V2PD, UK Tel: + 44 20 7566-2266 Fax: + 44 20 7251-9350 Email: [email protected]
Accidental injection of dexamethasone intravitreal implant in the crystalline lens Francesco Fasce, Maurizio Battaglia Parodi, Karl Anders Knutsson, Alessandra Spinelli, Paolo Mauceri, Gianluigi Bolognesi and Francesco Bandello Department of Ophthalmology, San Raﬀaele Scientiﬁc Institute, Milan, Italy doi: 10.1111/aos.12332
Editor, zurdex (Allergan Inc, Irvine, CA, USA), a sustained-release dexamethasone implant, can provide beneﬁcial eﬀects in the management of macular edema (ME) secondary to retinal vein occlusions, diabetic retinopathy and uveitis. (Haller et al. 2010) We describe two cases presenting lens damage after dexamethasone implant for the treatment of ME secondary to central retinal vein occlusion (CRVO). A 67-year-old man, referred to our department for ME secondary to CRVO, underwent dexamethasone implant. Baseline best corrected visual acuity (BCVA) was 20/50 with 1006 lm of central retinal thickness (CRT). Two days after the implant, the patient complained of blurred vision. At slitlamp examination a shiny-yellowish reﬂex, corresponding to the implant, was observed in the inferonasal quadrant of the lens, which was evolving towards cataract. Cataract extraction was performed one week later. After a clear temporal corneal incision, the anterior chamber was ﬁlled with dispersive viscoelastic. Standard capsulorhexis, hydrodelamination, hydrodissection, and phacoemulsiﬁcation were
performed with the aid of a chopper. At the end of nucleus removal, a tear in the posterior capsule was identiﬁed (Fig. 1A). Anterior vitrectomy was performed, the dexamethasone implant was removed through the main incision, and a three-piece intraocular lens (IOL) was implanted in the sulcus (AR40E, AMO, Abbott). Regular follow-up visits were performed, and no further complications were registered. CRT at 30 days was 606 lm, but BCVA was unchanged. A 72-year-old woman was referred to our department to undergo dexamethasone implant for chronic ME following CRVO. BCVA was 20/200 and CRT was 650 lm. The patient received dexamethasone implant and one day later complained of severe vision impairment. At slit-lamp examination the dexamethasone rod turned out to be inserted into the lens (Fig. 1B). BCVA was 20/400. Cataract extraction was performed one week later with the same modality of the previously described case. One month later the patient’s BCVA increased to 20/200, and CRT reduced to 511 lm.
(B) Fig. 1. (A) Case 1. Dexamethasone implant in the anterior vitreous beneath the posterior capsular rent (arrow) during phacoemulsiﬁcation procedures. (B) Case 2. Dexamethasone implant within the lens before initiating surgery.
Acta Ophthalmologica 2014
Few complications involving the anterior segment have been reported after injection of intravitreal dexamethasone implants. Most case reports describe migration of the implant into the anterior chamber in eyes that had previous cataract surgery complicated by posterior capsule rupture. (Cronin et al. 2012; Pardo-L opez et al. 2012; Malcles et al. 2013) Only one article reports a case similar to ours, describing cataract surgery after implant in the crystalline lens. (Koller et al. 2012) Several conclusions can be drawn from this case series. Regarding the intravitreal procedure: the 22-gauge injector has a relatively large diameter compared to 28- or 30-gauge needles used for anti-VEGF treatment, and the injection technique requires a considerable pressure on the globe. In addition, the pain experienced by the patient may provoke inadvertent eye or head movements. Subconjunctival anesthesia can be used in an attempt to minimize this side-eﬀect, even though the presence of ﬂuid under the conjunctiva may interfere with a proper marking procedure. Secondly, when considering cataract extraction, a careful preoperative evaluation in order to identify the site and the extension of posterior capsular tear, is essential. Hydrodelineation procedures with the purpose of separating the nucleus from the epinucleus is mandatory, and when hydrodissection is planned, it must be performed very carefully. During phacoemulsiﬁcation, machine parameters must be lowered and anterior vitrectomy must always be taken into consideration. Implant of a three piece IOL in the sulcus with optic plate in the bag is recommended in order to avoid stress on the already damaged capsular bag and is considered to provide the best stability in these cases. Lens damage can be a complication of dexamethasone implant. A careful cataract surgery can alleviate anatomical and functional damages.
patients with macular edema due to retinal vein occlusion. Ophthalmology 117: 1134– 1146. Koller S, Neuhann T & Neuhann I (2012): Conspicuous crystalline lens foreign body after intravitreal injection. Ophthalmologe 109: 1119–1121. Malcles A, Janin-Maniﬁcat H, Yhuel Y et al. (2013): Anterior chamber migration of intravitreal dexamethasone implant (Ozurdexâ) in pseudophakic eyes: report of three cases. J Fr Ophtalmol 36: 362–367. Pardo-L opez D, Frances-Mu~ noz E, GallegoPinazo R & Dıaz-Llopis M (2012): Anterior chamber migration of dexamethasone intravitreal implant (Ozurdexâ). Graefes Arch Clin Exp Ophthalmol 250: 1703–1704.
Correspondence: Karl Anders Knutsson MD Department of Ophthalmology San Raﬀaele Scientiﬁc Institute Via Olgettina 60 Milan 20132, Italy Tel: + 39 02 2643 2648 Fax: + 39 02 2643 3643 Email: [email protected]
Longitudinal follow-up of siblings with a discordant Stargardt disease phenotype Ravjit Singh,1,2,3 Kaoru Fujinami,2,3,4,5 Li Li Chen,2,3 Michel Michaelides2,3 and Anthony T. Moore2,3 1
Department of Ophthalmology, Prince of Wales Hospital, University of New South Wales, New South Wales, Sydney, Australia; 2UCL Institute of Ophthalmology, London, UK; 3Moorﬁelds Eye Hospital, London, UK; 4Laboratory of Visual Physiology, National Institute of Sensory Organs, National Tokyo Medical Center, Tokyo, Japan; 5 Department of Ophthalmology, Keio University, School of Medicine, Tokyo, Japan doi: 10.1111/aos.12280
References Cronin KM, Govind K & Kurup SK (2012): Late migration of dexamethasone implant into anterior chamber. Arch Ophthalmol 130: 711. Haller JA, Bandello F, Belfort R Jr et al. (2010): Randomized, sham-controlled trial of dexamethasone intravitreal implant in
Editor linical variability in Stargardt disease (STGD)/ABCA4-related disease is well established (Michaelides et al. 2003). Concordance of the phe-
notype within families is well documented, but familial discordance has been reported (Michaelides et al. 2007; Burke et al. 2012). Here, we report longitudinal imaging of two sisters with a discordant STGD phenotype and discuss whether this is related to the underlying ABCA4 mutations. Patient 1 is 44 years old and presented in 1991 aged 23 with deteriorating central vision and visual acuity (VA) of 6/36 in the right eye and 6/60 in the left. Fundus photography in 1994 identiﬁed bilateral numerous yellowish-white ﬂecks at the posterior pole (Fig. 1). In 2003, her VA was 6/60 in each eye, with bilateral macular atrophy surrounded by ﬂecks (Fig. 1). Autoﬂuorescence (AF) imaging in 2005 detected a localized low signal at the macula with numerous foci of abnormal signal (Fig. 1). By 2008, the macular atrophy had enlarged and ﬂecks were less apparent. Patient 2 is the 47-year-old sister of patient 1. At initial examination in 1994, she reported a central scotoma. VA was 6/9 in both eyes with bilateral subtle foveal atrophy and perifoveal yellowish-white ﬂecks (Fig. 1). By 2003, foveal atrophy had progressed with more perifoveal ﬂecks (Fig. 1). In 2012, her VA was 6/12 bilaterally, but fundus ﬁndings remained stable (Fig. 1). AF imaging demonstrated a mottled signal within the central macula, optical coherence tomography showed outer retinal disruption conﬁned to the central macula (Fig. 1). ABCA4 screening detected three variants; two variants p.L541V and p.A1038V – commonly co-inherited in a complex allele in STGD (Maugeri et al. 2000) – and a third novel variant p.R881C (Fig. 1). Patient 1 had all three variants and her sibling (patient 2) harboured the complex allele (p.L541V/p.A1038V). Their mother was found to harbour p.L541V/ p.A1038V, and the father carried the p.R811C mutation; both of whom were asymptomatic with normal retinal examination (Fig. 1). Over a 14 year period, patient 1’s phenotype changed from numerous ﬂecks at the posterior pole (‘fundus ﬂavimaculatus’) to ‘typical’ STGD with macular atrophy surrounded by ﬂecks, which later were absorbed; with corresponding VA reduction. In contrast, her older sibling had a milder phenotype