Radiation Retinopathy and Benign Lymphoproliferative Orbital Tumor Presenting 47 Years Following Treatment of Hereditary Retinoblastoma.

PURPOSE: To better understand onset of radiation retinopathy and secondary orbital tumors in the setting of retinoblastoma treated with radiation and chemotherapy. METHODS: Case report. RESULTS: Here we present a 48-year-old female with a history of bilateral hereditary retinoblastoma status-post enucleation of the left eye and radiation therapy to the right eye, along with systemic chemotherapy. She underwent bladder leiomyosarcoma resection at age 24. In 2020, she presented with significantly delayed radiation retinopathy complicated by cystoid macular edema, and bevacizumab injections were initiated. An incidental benign lymphoproliferative tumor in the right lacrimal gland was found on B-scan ultrasound and was successfully excised. CONCLUSION: It is rare for radiation retinopathy to present with significant delay after local radiation treatment, with only 2 other cases found in the literature describing a similar late onset. In addition, there have been no other published cases of a secondary benign lymphoproliferative tumor in the setting of retinoblastoma treated with radiation and chemotherapy.

EIGHTY-TWO-YEAR-OLD MONOCULAR FEMALE WITH ACUTE DECREASED CENTRAL VISION.

PURPOSE: To present a case of suspected sympathetic ophthalmia in an 82-year-old monocular woman. METHODS: Case report. RESULTS: Here, we present an 82-year-old woman, status postcataract extraction with lens subluxation followed by a complicated course ultimately requiring enucleation because of a blind and painful eye in 2020, who developed contralateral choroidal lesions 6 months postenucleation along with vitritis and anterior uveitis. The lesions were suspicious for an infectious versus autoimmune etiology. Thorough systemic work-up and multimodal imaging suggest an autoimmune case. The findings in this patient suggest early identified sympathetic ophthalmia with multifocal choroiditis. This patient responded well to treatment of the acute episode with systemic corticosteroids and ultimately required steroid-sparing immunosuppression. CONCLUSION: Sympathetic ophthalmia is a rare entity classically observed after intraocular surgery and trauma. It may mimic many infectious and noninfectious uveitis entities. In this patient, sympathetic is a primary concern given her history and age of presentation with consideration for other uveitic entities.

Causes of Horner Syndrome: A Study of 318 Patients.

BACKGROUND: Some reports have indicated that when a cause for Horner syndrome can be determined, it is most often chest and neck tumors and stroke. Others have suggested that Horner syndrome is more frequently caused by surgical procedures in the neck and chest. These differences may be explained by disparate accrual methods. Therefore, we decided to compare the cause of Horner syndrome in cases where the diagnosis was confirmed by apraclonidine testing conducted by ophthalmologists to cases in which the diagnosis was made entirely on clinical grounds mostly by nonophthalmologists. METHODS: We applied a new search engine to the inpatient and outpatient electronic medical records text at the University of Michigan Medical Center from 1996 to 2018 for Horner syndrome with and without pharmacologic confirmation through ocular instillation of apraclonidine 0.5%. Among apraclonidine-confirmed cases, 159 met inclusion criteria. Among apraclonidine-unconfirmed cases, more than 2,000 cases were identified, so that we included only the first 159 cases that met inclusion criteria. In these 318 cases, we documented patient demographics, ophthalmologic features, imaging, underlying cause, and whether the cause was discovered before or after the diagnosis of Horner syndrome. RESULTS: In the cohort of 159 apraclonidine-confirmed cases of Horner syndrome, a cause was identified in 97 (61%). Procedures in the neck, chest, skull base, and paraspinal region accounted for most of the identified causes, with cervical carotid dissection the next most common cause. In a cohort of 159 cases of Horner syndrome not tested with apraclonidine because the clinical diagnosis appeared firm, procedures again accounted for the largest percentage, but tumor was the next most common cause. In both groups, when a cause for Horner syndrome could be identified, that cause was nearly always known before Horner syndrome was identified. However, in an important minority of cases, mostly involving carotid dissection or tumor, the identification of Horner syndrome was critical to the discovery of those conditions. CONCLUSIONS: The prevalence of causes of Horner syndrome depends on the accrual method. Among pharmacologically-confirmed cases, the cause was often undetermined or due to a preceding neck or chest procedure. Among pharmacologically-unconfirmed cases, a substantial proportion had also been caused by neck and chest procedures, but tumors in that region were also common. When a cause of Horner syndrome was found in both cohorts, it was usually known before Horner syndrome was discovered, making Horner syndrome an afterthought. However, in an important minority of cases where the cause was not yet known, the identification of Horner syndrome was valuable in leading to important diagnoses such as carotid dissection and tumor.