Glaucoma and Inactive Syphilitic Interstitial Keratitis.

THE concept of an association between congenital syphilitic interstitial keratitis and the development of late glaucoma is not new. Hutchinson (1863) reported the case of a man aged 24 with congenital syphilis who had suffered bilateral interstitial keratitis at the age of 6; both eyes had deeply cupped and atrophic optic discs and iridectomy failed to control the glaucoma. Hutchinson believed that the glaucoma was due to the interstitial keratitis. Fuchs (1899) said that "an increase of tension is but rarely observed, and, when it is, sometimes occurs years after the inflammation has run its course". de Schweinitz (1916) stated that "secondary glaucoma may develop, with deep cupping of the disc", but gave no interval. Kraupa (1934) reported three cases of late glaucoma following interstitial keratitis. Schulmann (1934) described glaucoma 4 years after bilateral interstitial keratitis. Duke-Elder (1938a) recognized that secondary glaucoma might follow the uveitis of interstitial keratitis. Knox (1961) recorded fourteen instances of delayed glaucoma occurring in 88 patients with inactive interstitial keratitis found in the diagnostic files of the Johns Hopkins Hospital for the years 1936 to 1952. In addition, he described nine other cases of delayed glaucoma undergoing treatment. From this total of 23 patients, he recognized two dissimilar modes of onset: in fifteen patients the onset was insidious and resembled that of chronic simple glaucoma, and in eight it was relatively acute. The age at onset of glaucoma varied between 23 and 70 years, the peak occurring between 33 and 35 years. There was a marked variation in the interval between active keratitis and the onset of glaucoma. In six of Knox's patients gonioscopy was done and showed similar findings. There were open angles with small finger-like peripheral anterior synechiae; the trabecular area was noted to be a dense grey to white in colour, Schwalbe's line being poorly defined. Knox suggested that there was an increased density or hyalinization of the trabecular area. He made two suggestions as to pathogenesis: