Other ocular changes may involve the cornea, lens, and uvea. RESULTS: A 14-year-old girl with no significant medical history developed bilateral Bull's eye maculopathy after taking sertraline for 1 year. Acute Idiopathic Maculopathy classically presents as an abrupt, severe loss in vision (visual acuity 20/200 or worse) in one or both eyes in young, otherwise health individuals. Medications linked to maculopathy have been found to disrupt metabolic functions of the RPE and photoreceptors. Thioridazine toxicity at dosages less than 800 mg/day is rare, though cases have been reported with lower doses over several years. cone dystrophy, Laurence-Moon-Bardet-Biedl syndrome). The Ophthalmic News and Education Network, American Academy of Ophthalmology. Medications in this drug class include sulfa antibiotics, acetazolamide, chlorthalidone, disothiazide, ethoxyzolamide, hydrochlorothiazide, metronidazole, sulphonamide, topiramate, and triamterene. Venkat AG, Arepalli S, Sharma S, et al. Image License and Citation Guidelines. FA is often normal until the advanced stage of the disease. 3). [3], Unilateral Acute Idiopathic Maculopathy (UIAM) was first described as a syndrome by Yannuzzi, et al in 1991. Xu C, Zhu L, Chan T, et al. These yellow-white punctate crystals are found in the posterior pole and periarterially. The earliest signs of toxicity involve loss of the foveal light reflex with subtle macular stippling. In most cases, the CME will resolve with discontinuation of the medication. It may result from drug toxicity or hereditary conditions (e.g. In the advanced stages of toxicity, the pigment abnormalities can involve the peripheral retina with a clinical picture that resembles primary tapetoretinal degeneration with optic disc pallor, retinal vessel attenuation, ⦠Hisvision was 6/9 right, 6/6 left with paracentral scotomata. SD-OCT is extremely helpful in detailing the extent and location of the serous detachments. [24] The exact mechanism of toxicity is unknown but thought to involve impaired retinal microcirculation. AtLee WE. List of authors. [29] Treatment of inflammation includes topical, local, or systemic corticosteroids. PATIENT: A 14-year-old girl. These features can be helpful in distinguishing the MEK inhibitor associated serous detachments from central serous chorioretinopathy (CSR). Patients can also report a history of a flulike illness preceding the onset of vision loss. Pathology shows granulocyte clogging of retinal vasculature. Partial, and sometimes complete, resolution of injury is possible after drug abuse cessation. Initially an irregular neurosensory retinal detachment overlying a smaller, grayish thickening at the level of the retinal pigment epithelium is seen. Hadad A, Helmy O, Leeman S, Schaal S. A Novel Multimethod Image Analysis to Quantify Pentosan Polysulfate Sodium Retinal Toxicity. In the acute phase of maculopathy spectral-domain OCT (SD-OCT) and STRATUSOCT show abnormal heterogeneous hyperreflective thickening at the level of the outer retina and RPE in the foveal region. This page will review the toxicities most likely to be encountered in common clinical practice. In cases where the CME is refractory or the inciting agent cannot be discontinued, various treatments can be trialed for CME including topical anti-inflammatory agents, sub-Tenon or intravitreal corticosteroids, and topical or oral carbonic anhydrase inhibitors. This table presents a brief overview of drug-induced retinal toxicities and the pattern of injury typically associated with each drug. Bull's-eye maculopathy - American Academy of Ophthalmology Forty-seven year-old male patient with medical history of psoriatic arthritis treated with chloroquine. Intravitreal injection of aminoglycoside antibiotics is extremely toxic to the posterior segment. Courtesy of Joana Portelinha, MD File Size: 360 KB. Local therapy for cancer therapy-associated uveitis: a case series and review of the literature. Kwak EL, Bang YJ, Camidge DR, et al. Chlorpromazine binds strongly to melanin and can also cause hyperpigmentation in the skin, conjunctiva, cornea, and lens. Human immunodeficiency virus has also been implicated. Congenital ptosis, optic atrophy, and ectopia lentis have also been reported. Today, they are more commonly used to treat autoimmune conditions such as rheumatoid arthritis or systemic lupus erythematosus. Witkin AJ, Chang DF, Jumper JM, et al. Miller FS, Bunt-Milam AH, Kalina RE. This page was last edited on May 12, 2021, at 13:19. Kim HA, Lee S, Eah KS, Yoon YH. Talk:Drug induced maculopathy. [23] Clinical examination will show intraretinal hemorrhage, vascular occlusion, and retinal ischemia. ⦠Unilateral Acute Idiopathic Maculopathy patients present with a profound painless, central vision loss that is acute in nature. The mechanism is thought to be related to a rare type IV hypersensitivity reaction causing damage to the vascular endothelium approximately a week after administration. , search. Ramsey MS, Fine BS. [34] Retinal folds are typically seen in young patients. Enroll in the Residents and Fellows contest, Enroll in the International Ophthalmologists contest, "Unilateral Acute Idopathic Maculopathy. Clinical use of intravitreal antibiotics to treat bacterial endophthalmitis. "Unilateral Acute Idiopathic Maculopathy. Yasha S. Modi, M.D., and Rishi P. Singh, M.D. Prolonged use of the chloroquine derivatives typically results in a pigmentary maculopathy. The overall prognosis for this disease is favorable as most patients achieve full visual recovery upon resolution of the maculopathy. Stargardtâs disease. Initially, the it was reported to present unilaterally and associated with a viral prodromal illness. They include crizotinib, ceritinib, alectinib, brigatinib, lorlatinib. Ocular involvement in hereditary hemochromatosis is relatively rare. The patient should be managed closely with an oncologist. Adapted from Zhu I, Andreoli MT, Mittra RA, et al. Wang L, Damji KF, Chialant D, Hodge WG. Cerletti A, Taeschler M, Weidmann H. Pharmacologic studies on the structure-activity relationship of hydroxyindole alkylamines. Gentamicin is the most toxic aminoglycoside followed by tobramycin and amikacin. Three months after onset, a slight pigmentary granularity appeared at the macula in the right eye, and the bullâs eye maculopathy became gradually more apparent (Fig 1B). ", "The Founder of VRMNY, Dr. Yanuzzi Has Made Numerous Innovative.". Overall prevalence has been calculated around 7.5%, according to one study, though this varies with duration of use and daily dose. Onset can occur days to weeks after initiation of therapy. Diagnosis may depend on characteristic ERG changes, including a depressed full-field photopic ERG. It could happen that patients donât notice any vision problem, because the healthy eye compensates. Fields: unchanged. Herein we report the case of an individual who developed a bull's-eye maculopathy after ingesting uva ursi, a known inhibitor of melanin synthesis. Olivopontocerebellar atrophy. maculopathy, bull's eye An ocular condition in which degeneration of the retinal pigment epithelium in the macular area causes alternating ring-like light and dark zones of pigmentation, as in a target. [19] The mechanism is thought to be due to RPE induced dysfunction with subsequent accumulation of subretinal fluid. No medical therapy is indicated as the maculopathy resolves on its own over the course of several days to weeks. The fundus may appear normal or have mild changes early in the disease process that can progress to bull's-eye maculopathy and central RPE atrophy later. Hyporeflective exudation and subretinal fluid with detachment and disruption of photoreceptor outer segment can also be seen. Hypotony may be defined both statistically and clinically. Visual acuity is affected when the pigmentary abnormalities involve the center of the fovea. DOI: 10.1056/NEJMicm0708021. Links to Coxsackie virus ha⦠"Acute Idiopathic Maculopathy. The classic presentation is a bull's eye-maculopathy appearance where the fovea is surrounded by a ring of depigmentation followed by a ring of hyperpigmentation. After surgery, they should be placed in an upright position to prevent gravity from directing remaining drug molecules to the posterior segment. Systemic Features: Affected individuals have a characteristic facial ⦠Aggio FB, Farah ME, Meirelles RL, Souza EC. [3][12] Also, the various macular dystrophies should be considered, however, the progressive loss of vision and pigmentary changes associated with SRF can help distinguish them from AIM. Arch Ophthalmol. Hugo Mesquita Nogueira, M.D., and Rita Dinis Gama, M.D. Rosenthal AR, Kolb H, Bergsma D, Huxsoll D, Hopkins JL. hydroxychloroquine or chloroquine toxicity, Stargardt disease, cone dystrophy, cone-rod dystrophy, Cone dystrophy may present as an autosomal ⦠[28] They currently include ipilimumab, pembrolizumab, nivolumab, cemiplimab, atezolizumab, avelumab, durvalumab. Phenotypic Spectrum of Pentosan Polysulfate Sodium-Associated Maculopathy: A Multicenter Study. Possible Causes. Ehrenfeld M, Nesher R, Merin S. Delayed-onset chloroquine retinopathy. The ⦠N Engl J Med 2009; 360:2224. The majority of ocular side effects are related to induced autoimmune reactions. The imaging changes induced by chloroquine derivatives are nonspecific and often a multimodal imaging approach is utilized with the results interpreted in the appropriate clinical context. Signs include parafoveal pigmented deposits at the level of the RPE, vitelliform deposits, and patchy paracentral RPE atrophy similar in appearance to pattern dystrophy.
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