Treatment of traumatic optic neuropathy with corticosteroids--correction.
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Biomedical subjects
Publications and source records attributed to W C Hartel.
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We treated 21 patients (22 eyes) with traumatic optic neuropathy by using intravenous megadose methylprednisolone (13 patients) or high-dose dexamethasone (eight patients). Of 13 patients treated with megadose methylprednisolone, 12 had improved visual function, as did seven of nine eyes treated with intravenous dexamethasone. This difference was not significant (P = .3). Initial total blindness, mechanism of injury, or time from injury to treatment did not correlate with visual improvement.
Serious corneal complications occurred in an otherwise successful experience with continuous-wear soft contact lenses (SCLs) for aphakic correction. One hundred twenty eyes were fit, and 92% attained visual acuity of 20/40 or better. Severe corneal complications were observed in 13 eyes, including bacterial ulcers (six), apical erosions (three), and severe superficial vascularization (four). Corneal ulcers occurred in nondiabetic as well as diabetic subjects. Continuous-wear SCLs are not innocuous; as for any other drug or device, continuous, long-term medical supervision is necessary to minimize potentially severe complications and visual loss.
We report five cases of presumed orbital myositis mimicking extraocular muscle motility disturbances and manifesting clinical signs of active inflammation over the involved muscles. Computed tomographic evidence for extraocular muscle enlargement is helpful in confirming the diagnosis. If not present or atypical, another etiology should be sought. All patients responded rapidly and dramatically to systemic corticosteroids. Anterior inflammation may be accompanied by iritis and respond to topical corticosteroids. We believe the diagnosis of orbital myositis may be made on clinical grounds with confirmation by computed tomographic evidence for extraocular muscle enlargement and clinical response to corticosteroids. Biopsy is unnecessary except in atypical cases.
We describe our experience over the past 2 years with the ocular manifestations in 32 patients with acute and chronic syphilis. We urge that syphilis be considered in evaluating those patients with recurrent iritis, chorioretinitis, papillitis, optic atrophy, or abnormal pupillary findings. Specific serologic testing (FTA-ABS) must be obtained. Screening serologies (VDRL) are inadequate. We suggest that patients with evidence for CSF involvement or active ocular disease be treated by continuous intravenous infusion of 24 million units penicillin G daily for 10 days.
A 35-year-old female without evidence of atherosclerotic vascular disease underwent percutaneous femoral cerebral angiography. Perifoveal retinal infarction by exogenous arteriolar emboli produced a permanent absolute pericentral scotoma. Strict adherence to meticulous angiographic technique may prevent such an angiographic complication.
A case of orbital aspergillosis presenting as a steroid response of optic neuropathy is presented. The invasive and aggressive nature of this infection in the presence of systemic corticosteroids is documented by serial CT scans and necropsy examination. The authors urge inclusion of aspergilloma in the differential diagnosis of a steroid responsive optic neuropathy.