The coincidence of HSV-1 ocular cultures with HSV-1 corneal epithelial defects in rabbits after experimental penetrating keratoplasty.

Penetrating keratoplasty (PKP) in conjunction with postoperative corticosteroids may reactivate latent herpes simplex virus type 1 (HSV-1) to cause persistent postoperative epithelial defects. The clinical diagnosis of HSV keratitis after penetrating keratoplasty is difficult because the postoperative appearance may be nondendritic and, therefore, not characteristic of HSV-1 infection. Presently, the most reliable method to diagnose HSV-1 under these conditions is to culture eyes for the presence of HSV-1. To determine the coincidence of positive HSV-1 ocular cultures with HSV-1 epithelial defects, 15 rabbits (20 eyes) latently infected with HSV-1 underwent autograft PKP with postoperative corticosteroids. Daily ocular cultures and slit-lamp examinations were performed on postoperative days 1-8 and 10. Viral shedding occurred in 15 of 19 (79.0%) of the eyes postoperatively. Superficial punctate keratopathy (SPK) was observed in 19 of 19 (100%) of the eyes and coincided with positive HSV-1 cultures 24% of the time. Dendritic lesions were observed in three of 19 (15.8%) of the eyes; the dendrites coincided with positive HSV-1 cultures 60% of the time. Finally, epithelial ulcers were seen in eleven of 19 (57.9%) of the eyes, thus coinciding with HSV-1 positive cultures 29% of the time. The greatest coincidence of positive HSV-1 cultures with nondendritic epithelial lesions occurred on postoperative day number 4. The results suggest that an epithelial lesion following PKP and postoperative corticosteroids could represent HSV infection, even if a single HSV ocular culture is negative.

Surgical management of corneal ulceration and perforation.

Corneal ulceration leading to perforation can occur secondary to a number of conditions, including infection, trauma, corneal dryness, and exposure keratitis. Because the ocular morbidity of corneal perforations is high, prompt diagnosis and treatment is critical. When persistent corneal ulceration does not respond to medical treatment, including antibiotics, therapeutic soft contact lenses, or tarsorrhaphy, surgical intervention is indicated. In this review, the evaluation of patients with recalcitrant ulceration or perforation is summarized, and indications and techniques for surgical treatment (epithelial transplantation, conjunctival flaps, lamellar and penetrating keratoplasty, tissue adhesives, periosteal grafts) are described.

Embolic anterior ischemic optic neuropathy.

The presumed cause of anterior ischemic optic neuropathy is atherosclerotic vascular changes. Small-vessel occlusive vascular disease most likely causes occlusion of one or more posterior ciliary arteries, compromising blood flow to the optic nerve head and choroid. We present the case of a 59-year-old black man with cholesterol emboli within the retinal vasculature combined with a clinical picture of anterior ischemic optic neuropathy and choroidal nonperfusion demonstrated by i.v. fluorescein angiography. We believe this is evidence that, in a rare case, embolic phenomena may be the cause of anterior ischemic optic neuropathy.

Idiopathic spontaneous deep venous thrombophlebitis in an adolescent: a case report.

A rare case of spontaneous deep venous thrombophlebitis in a 15-year-old adolescent is presented. This case is remarkable as it lacks any associated conditions and predisposing factors, as well as an etiologic diagnosis.