PubMed Health⌕ Search

Biomedical subjects

Lucy H Young

Publications and source records attributed to Lucy H Young.

10 recordsLinked to original sources
PubMed2006

Predictors of visual outcome and choroidal neovascular membrane formation after traumatic choroidal rupture.

OBJECTIVE: To determine predictors of choroidal neovascularization (CNV) and visual outcome after traumatic choroidal rupture. METHODS: A retrospective review of patients with traumatic choroidal rupture diagnosed in the Retina Service, Massachusetts Eye and Ear Infirmary, Boston, between January 1993 and August 2001 was performed. Parametric and nonparametric statistical methods were used to evaluate visual prognosis, CNV, and retinal detachment after traumatic choroidal rupture. RESULTS: One hundred eleven cases were identified and reviewed. Visual acuity (VA) changes were recorded in all of the cases. Thirty-eight (34%) of the 111 patients recovered driving vision (VA > or =20/40). Rupture location was recorded in 107 cases. Recovery of driving vision was seen in 20 (59%) of 34 eyes with peripheral choroidal ruptures, 17 (22%) of 73 eyes with macular choroidal ruptures, 38 (38%) of 99 eyes without CNV, 1 (8%) of 12 eyes with CNV, 38 (40%) of 96 eyes without retinal detachment, and 1 (7%) of 15 eyes with retinal detachment. Older age and location of rupture within the arcades were positively associated with CNV formation (P = .04 and .03, respectively). Foveal location of rupture, multiple ruptures, and poor baseline VA were associated with failure to recover driving vision in univariate regression analyses. In multivariate analysis, rupture location and baseline VA were independently associated with visual outcome. Of 12 patients diagnosed with CNV, 5 were not treated, 4 were treated with argon laser photocoagulation, 1 was treated with surgery, 1 was treated with argon laser photocoagulation followed by surgery, and 1 was treated with verteporfin photodynamic therapy. CONCLUSIONS: Most patients with traumatic choroidal rupture do not achieve final VA of 20/40 or better. Poor visual outcome was most highly associated with a macular rupture and baseline VA of less than 20/40. The formation of CNV was most strongly associated with older age and macular choroidal rupture.

Adolescent↗
PubMedDate not supplied

Ocular manifestations and treatment of syphilis.

Syphilis is a sexually transmitted, chronic, systemic infection caused by the spirochete Treponema pallidum. If left untreated, the disease progresses through four stages, with the potential to cause significant morbidity to any major organ of the body. Frequent syphilitic ocular manifestations, which can occur at any stage of the disease, include interstitial keratitis, anterior, intermediate, and posterior uveitis, chorioretinitis, retinitis, retinal vasculitis and cranial nerve and optic neuropathies. Diagnosis is centered around a high level of clinical suspicion and includes treponemal specific and non-treponemal serologic tests. All patients with newly diagnosed syphilis should be tested for co-infection with human immunodeficiency virus, as the risk factors are similar for both diseases. Additionally, all patients with ocular syphilis should be tested for neurosyphilis. The preferred treatment for all stages of syphilis remains parenteral penicillin G. With proper diagnosis and prompt antibiotic treatment, the majority of cases of syphilis can result in a cure.

Anti-Bacterial Agents↗
PubMedDate not supplied

Sympathetic ophthalmia.

Sympathetic ophthalmia is a rare, bilateral granulomatous uveitis that occurs after either surgical or accidental trauma to one eye. The ocular inflammation in the fellow eye becomes apparent usually within 3 months after injury. Clinical presentation is an insidious or acute anterior uveitis with mutton-fat keratic precipitates. The posterior segment manifests moderate to severe vitritis, usually accompanied by multiple yellowish-white choroidal lesions. Evidence suggests that sympathetic ophthalmia represents an autoimmune inflammatory response against choroidal melanocytes mediated by T cells. Diagnosis is based on clinical findings and a history of previous ocular trauma or surgery. Other causes of granulomatous uveitis, such as Vogt-Koyanagi-Harada disease, sarcoidosis, tuberculosis, and syphilis should be considered. Treatment of sympathetic ophthalmia consists of systemic anti-inflammatory agents with high dose oral corticosteroid as the drug of choice. However, if the inflammation cannot be controlled, cyclosporine is then used. Other immunosuppressive agents, such as chlorambucil, cyclophosphamide or azathioprine, may be necessary for the control of inflammation. The role of enucleation after the diagnosis of sympathetic ophthalmia remains controversial. Visual prognosis is reasonably good with prompt wound repair and appropriate immunomodulatory therapy.

Diagnosis, Differential↗
PubMedDate not supplied

Vogt-Koyanagi-Harada disease.

Vogt-Koyanagi-Harada disease (VKH) is a multisystem autoimmune disorder principally affecting pigmented tissues in the ocular, auditory, integumentary and central nervous systems. Patients are typically 20 to 50 years old and have no history of either surgical or accidental ocular trauma. Pigmented races are more commonly affected. Depending on revised diagnostic criteria, the disease is classified as complete, incomplete or probable based on the presence of extraocular findings (neurological, auditory and integumentary). The clinical course of VKH is divided into four phases: prodromal (mimics a viral infection), uveitic (bilateral diffuse uveitis with papillitis and exudative retinal detachment), convalescent (tissue depigmentation), and chronic recurrent (recurrent uveitis and ocular complications). The pathogenesis of VKH is thought to be related to an aberrant T cell-mediated immune response directed against self-antigens found on melanocytes. VKH has been linked to human leukocyte antigen DR4 (HLA-DR4) and HLA-Dw53, with strongest associated risk for HLA-DRB1*0405 haplotype. The diagnosis of VKH is clinical, and differential includes sympathetic ophthalmia, sarcoidosis, primary intraocular B-cell lymphoma, posterior scleritis, and uveal effusion syndrome. Treatment is typically initiated with high-dose oral corticosteroids, but other immunomondulatory agents (most oftentimes cyclosporine) may be needed for non-responsive patients or when corticosteroid side-effects are not tolerated. Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment.

Diagnosis, Differential↗
PubMedDate not supplied

Treatment options for metastatic tumors to the choroid.

Metastatic tumors are generally considered to be the most common intraocular tumors. These tumors may metastasize from a variety of different primary sites with breast carcinoma being the most common primary malignancy in women and lung cancer being the most common primary malignancy in men. Treatment options for these patients include systemic therapy, conventional external beam radiation, plaque brachytherapy, proton beam irradiation, photodynamic therapy, transpupillary thermotherapy, and laser photocoagulation. Overall, treatment of patients with metastatic tumors to the choroid has proven to be effective in both improving the patient's visual acuity and quality of life.

Antineoplastic Agents↗
PubMedDate not supplied

Retinal toxicity of intravitreal triamcinolone acetonide: a morphological study.

PURPOSE: To evaluate the morphologic effects of intravitreal triamcinolone acetonide (TA) on rabbit retina. METHODS: Intravitreal injections of 0.5 mg, 1 mg, 4 mg, 8 mg, and 20 mg of TA (Kenalog-40; Bristol-Myers Squibb, Princeton, NJ) in 0.1 mL were given to pigmented rabbits. For control, 0.1 mL of TA vehicle and saline were injected. Animals were killed on day 14, and retinas were analyzed by light as well as electron microscopy. RESULTS: No ophthalmoscopic change was found. Eyes injected with 0.5 mg and 1 mg of TA did not have morphologic abnormality. Eyes injected with 4 mg, 8 mg, and 20 mg showed destruction of photoreceptor outer segments and migration of macrophage-like cells in the subretinal space. Eyes injected with 20 mg showed more extensive damage and increased pigment granules in the retinal pigment epithelium cells with large oil droplets in the cytoplasm. Electron microscopy also showed loss of photoreceptor/retinal pigment epithelium interdigitations. Eyes injected with vehicle or saline did not show morphologic changes. CONCLUSION: Single intravitreal injection of 0.5 mg or 1 mg of TA did not produce morphologic retinal changes in pigmented rabbits. However, injections of 4 mg, 8 mg, and 20 mg of TA produced outer retina toxic effects. These findings suggest that long-term retinal toxicity studies should be carried out, using single and repeated injections before this therapy becomes more widely used.

Animals↗