Cases reported "Scotoma"

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1/12. Conservative management of documented neuroretinitis in cat scratch disease associated with bartonella henselae infection.

    BACKGROUND: bartonella henselae has been identified as the causative agent of the neuroretinitis associated with cat scratch disease (CSD). Immunofluorescent antibody tests with good sensitivity and specificity are available to aid in diagnosis. Despite diagnostic advances, optimal management remains controversial. We present a case of documented B. henselae macular neuroretinitis managed without antibiotics and discuss antibiotic use in this condition. methods: We examined a young woman with macular neuroretinitis and established a diagnosis of CSD. Management consisted of a review of the literature, followed by educating her about the condition and close observation. We documented the course of her disease. RESULTS: We diagnosed neuroretinitis associated with B. henselae infection based on immunofluorescent antibody titres and clinical presentation. Our patient's neuroretinitis resolved promptly without antibiotic therapy. CONCLUSIONS: Macular neuroretinitis in CSD can be satisfactorily diagnosed with the use of fluorescent antibodies in the appropriate clinical setting. Optimal treatment for the disease has not been established and observation combined with patient education remains an appropriate option. The self-limited nature of the disease implies that treatment studies not using controls must be interpreted with great caution. Adverse drug reactions and other iatrogenic complications can be reduced by limiting antibiotic use in settings where a meaningful treatment benefit has not been established.
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2/12. Toxic optic neuropathy after concomitant use of melatonin, zoloft, and a high-protein diet.

    melatonin is a neuromodulating hormone found in the pineal gland and retina. It is involved in light-dark circadian rhythms and mediates retinal processes in a manner antagonistic to that of dopamine. Zoloft (sertraline) is an antidepressant drug that blocks the reuptake of serotonin at the neural synapse. serotonin is the natural precursor of melatonin. A 42-year-old woman sought treatment for visual acuity loss, dyschromatopsia, and altered light adaptation. Neuro-ophthalmologic examination was otherwise normal except for evolving bilateral cecocentral scotomas. She had taken Zoloft for 4 years and began a high-protein diet with melatonin supplementation 2 weeks before onset of visual symptoms. visual acuity and color vision improved within 2 months after melatonin and the high-protein diet were discontinued. Combined use of melatonin, Zoloft, and a high-protein diet may have resulted in melatonin/dopamine imbalance in the retina, manifesting as a toxic optic neuropathy. physicians and patients should be alerted to this potential drug interaction.
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3/12. Incidental retinal phototoxicity associated with ingestion of photosensitizing drugs.

    BACKGROUND: to report on the possible correlation between incident retinal phototoxicity and the use of photosensitizing drugs. methods: four patients were examined because of scotomas and visual loss after an incidental exposure to a strong light source. One patient (two eyes) was exposed to standard camera flash; one patient (one eye) had a brief exposure to welding light; one patient (two eyes) underwent uncomplicated phacoemulsifications with intraocular lens implantation. The fourth patient had a severe retinal phototoxicity following a secondary intraocular lens implantation. All four patients underwent a thorough assessment including history of systemic drug use. These patients had ophthalmologic evaluation including: best corrected visual acuity (ETDRS charts), fundus examination, fluorescein and indocyanine green angiographies and were followed for 1 year. RESULTS: on presentation, the mean visual acuity was 7.5/20 (range: 20/400-20/20). Fundus examination disclosed yellow-gray sub-retinal lesions in all affected eyes. Early phase fluorescein angiography showed one or multiple hypofluorescent spots surrounded by a halo of hyperfluorescent window defect. In the late phase, some of these spots leaked the fluorescein dye. indocyanine green angiography demonstrated hypofluorescent spots throughout with ill-defined borders of hyperfluorescence observed during the late stages. The common finding in these four patients was the fact that they were all taking one or more photosensitizing drugs (hydrochlorothiazide, furosemide, allopurinol, and benzodiazepines). Three of the patients had a full visual recovery a few months after the phototoxicity. The fourth patient remained with a visual acuity of 20/60 12 months after the light exposure. Despite the visual recovery, non-homogeneous retinal pigment epithelial disturbances persisted in all affected eyes. CONCLUSION: phototoxicity following incidental light exposure may occur in patients taking drugs of photosensitizing potential. Therefore, the thorough history of systemic drug ingestion should be obtained if patients have exposure to strong light sources.
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4/12. hydroxychloroquine and chloroquine retinopathy: screening for drug toxicity.

    PURPOSE: To report hydroxychloroquine and chloroquine retinopathy and consider screening for drug toxicity. DESIGN: Retrospective observational case series. methods: review of clinical records, visual fields, fundus photographs, and fluorescein angiography of six patients from a retina referral practice. RESULTS: All cases arose because of failure by physicians to avoid dosing above published safe levels. Five cases developed despite accepted ophthalmologic patterns of screening for toxicity. All cases developed parafoveal retinal pigment epithelial atrophic changes and paracentral scotomas to threshold visual field testing. CONCLUSIONS: New cases of hydroxychloroquine and chloroquine toxicity continue to develop in a screening environment. Increased ophthalmologic attention to dosing, awareness of location and nature of early visual field defects, and traditional attention to presence or absence of maculopathy can reduce the incidence of this avoidable condition.
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5/12. (Hydroxy)-chloroquine retinal toxicity: two case reports and safety guidelines.

    Retinal toxicity as a result of antimalarial therapy has been reported for many years. Retinopathy may be divided into reversible premaculopathy and irreversible true retinopathy. risk factors for the development of toxicity are daily dosage related to body weight, total drug dosage and the specific drug used. The daily dosage of chloroquine should not exceed 4 mg/kg lean body weight a day. Exceeding the total dosage of 300 g increases the risk. The daily dosage of hydroxychloroquine should not exceed 6.5 mg/kg lean body weight a day with increased risk when the duration of treatment exceeds 8 years (1330 g for a patient of 70 kg). Regular dilated fundus examination, visual field testing using Amsler grid test and automated central 10-2 perimetry (to a red test object) is advised to detect reversible premaculopathy. hydroxychloroquine toxicity due to excessive cumulative dosage is discussed in case 1. Chloroquine toxicity due to excessive daily dosage is discussed in case 2.
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6/12. Leber hereditary optic neuropathy associated with use of ephedra alkaloids.

    PURPOSE: We report a case of Leber hereditary optic neuropathy in a patient who was using ephedra alkaloids at the time of onset of his optic neuropathy. DESIGN: Observational case report. methods: Bilateral, painless, progressive loss of vision developed in a 30-year-old man. He reported a one pack-per day, 10-year history of tobacco use and drinking 18 to 24 cans of beer per day as well as the use of a dietary supplement containing ephedra and caffeine before the onset of vision loss. RESULTS: We report the bilateral, progressive, painless loss of vision in a patient with bilateral cecocentral scotomas and optic nerve pallor. Mitochondrial dna testing confirmed a Leber hereditary optic neuropathy mutation site at loci 11778. CONCLUSIONS: We propose that our patient's use of a dietary supplement containing ephedra alkaloids played an additive role to his tobacco and alcohol use in causing stress to the already abnormal mitochondrial function, and thereby contributed to the onset of his optic neuropathy. We recommend that patients and families with known Leber hereditary optic neuropathy should be asked about the use of over-the-counter drugs or supplements, and it may be prudent to advise patients against using such dietary supplements.
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7/12. Disturbance of vision by COX-2 inhibitors.

    In this review, 35 cases of acute, reversible, sometimes severe, disturbances of vision closely associated with the use of celecoxib or rofecoxib are described. These were identified from three different databases using strict selection criteria. The events included temporary blindness, visual field defect, scotoma, teichopsia, blurred vision, decreased vision and abnormal vision. The reactions had a mean onset time of 9.5 days and recovery occurred within 3 days following withdrawal of the drug. The reactions do not appear to be related to age, gender, dose, or indication for use. The incidence of reported cases is estimated to be not less than 5 per 10,000 patients. Possible mechanisms for this type of reaction are described. The most likely appears to be the result of interference with the retinal blood supply through reduced production of prostanoids. Genetic polymorphisms that affect drug metabolism or uptake could be risk factors and are discussed along with suggestions for research.
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8/12. Retrobulbar neuritis as the first sign of the glucagonoma syndrome.

    A 63-year-old man with a metastasising pancreatic glucagonoma is described, who presented with progressive deterioration of vision and bilateral central scotomata as the first symptom. This patient was treated with dacarbazine (DTIC) 250 mg/m2 IV daily for five consecutive days at 4-week intervals. The vision returned completely to normal, in a clinical and biochemical remission. Although there is no wide experience in treatment, the literature seems to indicate that DTIC should be the drug of choice in treating metastatic glucagonoma. Central scotomata may be a new 'paraneoplastic' symptom and a key to the earlier diagnosis of the glucagonoma syndrome by ophthalmologists, just as necrolytic migratory erythema has been for the dermatologists.
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9/12. isoniazid and ethambutol as a cause of optic neuropathy.

    A well-recognized complication of ethambutol use is optic neuropathy, but the potential ocular toxicity of isoniazid is often overlooked. A patient developed optic neuropathy while being treated with isoniazid and ethambutol. The optic neuropathy subsided only when both drugs were discontinued, suggesting an additive toxic effect.
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10/12. Toxic ocular effects of ethambutol.

    ethambutol hydrochloride has been used in the treatment of tuberculosis for 25 years. Its only important adverse effect, retrobulbar neuritis, is thought to be a minor concern with conventional dosages. The author presents four cases of serious visual impairment due to ethambutol therapy. Three of the patients were receiving a maintenance dosage of 15 mg/kg per day. The fourth patient was inadvertently given 25 mg/kg per day for 4 months. After therapy with the drug was stopped, improvement was slow, with complete recovery in two cases and only minor residual changes in a third. The patient who received the higher dosage of ethambutol suffered permanent, marked impairment. ethambutol appears to contribute little to modern short-course antituberculous regimens that include more potent agents such as isoniazid and rifampin. In view of this and the potential for serious visual impairment, alternative antituberculous agents should be considered.
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