A review of the inflammatory chorioretinopathies: the white dot syndromes.

The white dot syndromes are a group of inflammatory chorioretinopathies of unknown etiology which have in common a unique and characteristic appearance of multiple yellow-white lesions affecting multiple layers of the retina, retinal pigment epithelium (RPE), choriocapillaris, and the choroid. They also have overlapping clinical features. We discuss acute retinal pigment epitheliopathy, multiple evanescent white dot syndrome, acute posterior multifocal placoid pigment epitheliopathy, multifocal choroiditis and panuveitis, acute zonal occult outer retinopathy, birdshot chorioretinopathy, and serpiginous choroidopathy. Some of these diseases are associated with a viral prodrome suggesting a possible viral/infectious etiology, while others are associated with a number of systemic processes suggesting an autoimmune etiology. We also review the presentation, evaluation/diagnosis, and treatment of these entities as well as the prognosis. Where applicable we discuss recent advancements in diagnosing and treating the white dot syndromes.

Acute zonal occult outer retinopathy: vision loss in an active duty soldier.

Objective. To describe a case of acute zonal occult outer retinopathy (AZOOR) in an active duty patient. Methods. In this paper we studied fundus photographs, optical coherence tomograph, Humphrey visual field 30-2, fundus autofluorescence images, fluorescein angiograms, and electroretinography. Results. Exam findings on presentation: a 34-year-old American Indian female presented with bilateral photopsias, early RPE irregularity, and an early temporal visual field defect. Progression RPE damage and visual field defect along with ERG findings support final diagnosis of AZOOR. Conclusion. AZOOR may initially be identified as a broader category of disease called the "AZOOR complex of disorders". Specific visual field defects, ERG results, and clinical exam findings will help distinguish AZOOR from other similar disorders.

Pediatric PRK (PhotoRefractive Keratectomy) with Mitomycin C (MCC) for Persistent Anisometropic Amblyopia. A Case Report.

PURPOSE: To evaluate the safety and efficacy of photorefractive keratectomy (PRK) with Mitomycin C (MMC) for the treatment of severe pediatric anisometropia and amblyopia resistant to more conservative treatment modalities. METHODS: A 3 year-old-child, who at 18 months old underwent unilateral diode laser treatment for threshold ROP, developed 11 diopters of anisometropic myopia and secondary dense amblyopia of the Right Eye. Only after all conservative treatment options failed was he treated with PRK and MMC. Principal outcome measures included cycloplegic refraction, the amount of refractive correction, degree of corneal haze and change in visual acuity. RESULTS: On presentation: BCVA: 20/CF OD; 20/30 OS. CRNS: -11.50 diopters sphere OD; -0.50 diopters sphere OS. Unilateral PRK followed by application of MMC (0.2 mg/ml) for 1 min was performed under general anesthesia. Three-month postoperative findings include: VA: 20/30 OD; 20/25 OS. CRNS: +0.25 diopters sphere OD. At one year, the BCVA remained equal at the 20/30 level despite mild myopic regression OD. CRNS OD at one year was -1.25 +050 x 116. No corneal haze was appreciated. CONCLUSION: In this child, treatment with PRK and MMC safely reduced the anisometropia thus facilitating his visual rehabilitation. While encouraging, further study is required to verify the longer term results of this single case. PURPOSE: To evaluate the safety and efficacy of photorefractive keratectomy (PRK) with Mitomycin C (MMC) for the treatment of severe pediatric anisometropia and amblyopia resistant to more conservative treatment modalities. METHODS: A 3 year-old-child, who at 18 months old underwent unilateral diode laser treatment for threshold ROP, developed 11 diopters of anisometropic myopia and secondary dense amblyopia of the Right Eye. Only after all conservative treatment options failed was he treated with PRK and MMC. Principal outcome measures included cycloplegic refraction, the amount of refractive correction, degree of corneal haze and change in visual acuity. RESULTS: On presentation: BCVA: 20/CF OD; 20/30 OS. CRNS: -11.50 diopters sphere OD; -0.50 diopters sphere OS. Unilateral PRK followed by application of MMC (0.2 mg/ml) for 1 min was performed under general anesthesia. Three-month postoperative findings include: VA: 20/30 OD; 20/25 OS. CRNS: +0.25 diopters sphere OD. At one year, the BCVA remained equal at the 20/30 level despite mild myopic regression OD. CRNS OD at one year was -1.25 +050 x 116. No corneal haze was appreciated. CONCLUSION: In this child, treatment with PRK and MMC safely reduced the anisometropia thus facilitating his visual rehabilitation. While encouraging, further study is required to verify the longer term results of this single case.

Optic neuropathy and a reversible splenial lesion after gastric bypass: shared pathophysiology?

A 22-year-old female presented 2months after a laparascopic gastic bypass with 3weeks of progressive painless visual loss. Ophthalmologic exam revealed severely reduced visual acuity, central scotomas, and optic nerve edema bilaterally. She was noted to have a mild encephalopathy. MRI of the brain revealed restricted diffusion in the splenium of the corpus callosum. The patient was treated with 3days of intravenous methylprednisolone, intravenous fluids, and re-institution of vitamin supplementation. Four weeks later, she had significant improvement in her visual acuity and marked reduction in central scotomas. Her encephalopathy resolved and the splenial abnormality disappeared on repeat brain MRI. This is the first reported case of a bilateral optic neuropathy and a reversible splenial lesion syndrome after gastric bypass. The presentation of both conditions in our patient may suggest a shared pathophysiology.