738
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men. One month postoperatively the lesion again recurred, and was 1.5 x 1.5 x 1.5 mm. The lesion grew to 4 x 4 x 4 mm in one week. Gonioscopy disclosed intraocular invasion with involvement of the angle. After discussing various treatment options, we enucleated the eye. Examination of the enucleated eye showed intraocular invasion of the epibulbar tumor (Fig. 2). The tumor was cohesive and had histopathologic features similar to those of the initial lesion and first recurrence, namely epithelial cells with waxy, eosinophilic cytoplasm surrounding a central, keratin-filled core. The clinical history, craterform histologic architecture, and cytologic features in our patient are consistent with a diagnosis of keratoacanthoma, although the invasiveness suggests squamous cell carcinoma. The intraocular, well-demarcated mass is unlike the diffuse infiltrative involvement of squamous cell carcinoma of the conjunctiva.' Keratoacanthoma has been shown to have dermal invasion in some instances." Although some pathologists argue that squamous cell carcinoma can originate from keratoacanthoma, it is likely that these neoplasms are squamous cell carcinoma, which closely mimics the histologic features of keratoacanthoma rather than carcinoma ex keratoacanthorna." The pathogenesis of intraocular invasion in our patient is unknown. Possibly mechanical trauma introduced the epibulbar neoplasm into the eye or the tumor invaded through an emissary canal. Perineural invasion has been reported in association with keratoacanthoma, and perhaps perineural invasion through an emissary canal occurred in our patient.
References 1. Bellamy, E. D., Allen, J. H., and Hart, N. L.: Keratoacanthoma bulbar conjunctiva. Arch. Ophthalmol. 70:512, 1963. 2. Roth, A. M.: Solitary keratoacanthoma of the conjunctiva. Am. J. Ophthalmol. 85:647, 1978. 3. Freeman, R. G., Cloud, T. M., and Knox, J. M.: Keratoacanthoma of the conjunctiva. A case report. Arch. Ophthalmol. 65:817, 1961. 4. Wexler, S. A., and Wallow, I. H. L.: Squamous cell carcinoma of the conjunctiva presenting with intraocular extension. Arch. Ophthalmol. 103:1175, 1985.
5. Lever, W. F., and Schaumburg-Lever, G.: Histopathology of the Skin, ed. 6. Philadelphia, J. B. Lippincott, 1983, p. 506.
June, 1990
Infectious Crystalline Keratopathy Caused by Mycobacterium fortuitum and Pseudomonas aeruginosa Fung-Rong Hu, M.D. Department of Ophthalmology, National Taiwan University Hospital. Inquiries to Fung-Rong Hu, M.D., Department of Ophthalmology, National Taiwan University Hospital, 1 Chang-Te St., Taipei, Taiwan, Republic of China. Infectious crystalline keratopathy is characterized by a slowly progressive, white refractile anterior stromal infiltrate found in patients receiving long-term corticosteroid therapy. Streptococcus viridans has been identified as the cause in most of the reported cases.' We treated a patient with infectious crystalline keratopathy caused by Mycobacterium fortuitum and
Pseudomonas aeruginosa.
A 3D-year-old woman had a bacterial corneal ulceration of the right eye 14 years previously that resulted in a dense, central corneal scar. She underwent penetrating keratoplasty with 16 interrupted sutures in December 1988. Postoperative medications included betamethasone and antibiotic eyedrops. All sutures were removed in August 1989, except for two broken stitches at the 7 o'clock and 8 o'clock meridians. The patient had mild pain without redness in October 1989. Betamethasone was used without improvement. The patient returned to our clinic one week after the episode. A white, refractile stromal infiltrate with anterior onesixth stromal loss was found at the graft-host junction surrounding the broken stitch at the 8 0' clock meridian (Fig. 1). A scraping of the ulcer showed numerous acid-fast bacilli and a few gram-negative bacilli. Corneal cultures grew M. fortuitum and P. aeruginosa. Betamethasone was discontinued and topical amikacin and carbenicillin were instituted. The infiltrate became confluent with progressive stromal melting and endothelial plaque formation despite treatment (Fig. 2). Systemic amikacin and carbenicillin were added two weeks later because of impending scleral involvement. The corneal infiltrate, endothelial plaque, and anterior chamber reaction slowly resolved. Repeated bacteriologic studies were negative. There was no sign of reepithelialization because of the necrotic stromal bed. Six weeks later, lamellar keratectomy of the involved area was performed to remove the necrotic stroma. The specimen showed acute inflammatory cell infiltration, but no bacterium or other abnormality was found. Epithe-
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Letters to the Journal
this infection. This is supported by our patient who developed suppurative inflammation upon cessation of corticosteroid therapy. Pseudomonas species had been reported to be the causal agents of infectious crystalline keratopathy," although not the species of P. aeruginasa. Because many microorganisms besides S. viridans are found to cause infectious crystalline keratopathy."" thorough microbiologic study and proper antibiotic treatment are mandatory in the management of this disease.
References
Fig. 1 (Hu). Crystalline anterior stromal infiltrate with exposed stitch at the 8 o'clock meridian and lack of surrounding inflammation.
lialization was complete two weeks after the operation and has remained stable. Gorovoy and associates" reported that longterm corticosteroid therapy inhibited inflammatory response to the bacterial colonization in
1. Reiss, G. R., Campbell, J., and Bourne, W. M.: Infectious crystalline keratopathy. Surv. Ophthalmol. 31:69,1986. 2. Corovoy, M. S., Stern, G. A, Hood, e. I., and Allen, e.: Intrastromal noninflammatory bacterial colonization of a corneal graft. Arch. Ophthalmol. 101:1749, 1983. 3. Rabinowitz, S. M., Alfonso, E., Culbertson, W. W., Holland, S. P., Roussel, T. j.. Kattan, H., and Foster, R. K.: Infectious crystalline keratopathy. A report of ten cases and presentation of new clinical observation. ARVO abstracts. Supplement to Invest. Ophthalmol. Vis. Sci. Philadelphia, ]. B. Lippincott, 1989, p. 276. 4. Groden, L. R., Pascucci, S. E., and Brinser,]. H.: Haemophilus aphraphilus as a cause of crystalline keratopathy. Am. J. Ophthalmol. 104:89, 1987. 5. Weisenthal, R. W., Krachmer, ]. H., Folberg, R., Dunn, S. P., and Whitson, W. E.: Postkeratoplasty crystalline deposits mimicking bacterial infectious crystalline keratopathy. Am. J. Ophthalmol. 105:70, 1988.
Penetrating Scleral Patch
Keratoplasty Graft
After
Woodford S. Van Meter, M.D., Joseph R. Gussler, M.D., Ekktet Chansue, M.D., Winai Chaidaroon, M.D., and Surapong Duangratana, M.D. Fig. 2 (Hu). The same eye as seen in Figure 1, two weeks after cessation of corticosteroid therapy and initiation of fortified topical antibiotic treatment, showing suppurative process with marked conjunctival congestion.
Department of Ophthalmology, University of Kentucky (W.S.V., J.R.G.), and Chiang Mai University rs.c.. w.c.. S.D.).
Inquiries to Woodford S. Van Meter, M.D., Department of Ophthalmology, University of Kentucky, 800 Rose St., Lexington, KY 40536-0084.
AMERICAN JOURNAL OF OPHTHALMOLOGY
men. One month postoperatively the lesion again recurred, and was 1.5 x 1.5 x 1.5 mm. The lesion grew to 4 x 4 x 4 mm in one week. Gonioscopy disclosed intraocular invasion with involvement of the angle. After discussing various treatment options, we enucleated the eye. Examination of the enucleated eye showed intraocular invasion of the epibulbar tumor (Fig. 2). The tumor was cohesive and had histopathologic features similar to those of the initial lesion and first recurrence, namely epithelial cells with waxy, eosinophilic cytoplasm surrounding a central, keratin-filled core. The clinical history, craterform histologic architecture, and cytologic features in our patient are consistent with a diagnosis of keratoacanthoma, although the invasiveness suggests squamous cell carcinoma. The intraocular, well-demarcated mass is unlike the diffuse infiltrative involvement of squamous cell carcinoma of the conjunctiva.' Keratoacanthoma has been shown to have dermal invasion in some instances." Although some pathologists argue that squamous cell carcinoma can originate from keratoacanthoma, it is likely that these neoplasms are squamous cell carcinoma, which closely mimics the histologic features of keratoacanthoma rather than carcinoma ex keratoacanthorna." The pathogenesis of intraocular invasion in our patient is unknown. Possibly mechanical trauma introduced the epibulbar neoplasm into the eye or the tumor invaded through an emissary canal. Perineural invasion has been reported in association with keratoacanthoma, and perhaps perineural invasion through an emissary canal occurred in our patient.
References 1. Bellamy, E. D., Allen, J. H., and Hart, N. L.: Keratoacanthoma bulbar conjunctiva. Arch. Ophthalmol. 70:512, 1963. 2. Roth, A. M.: Solitary keratoacanthoma of the conjunctiva. Am. J. Ophthalmol. 85:647, 1978. 3. Freeman, R. G., Cloud, T. M., and Knox, J. M.: Keratoacanthoma of the conjunctiva. A case report. Arch. Ophthalmol. 65:817, 1961. 4. Wexler, S. A., and Wallow, I. H. L.: Squamous cell carcinoma of the conjunctiva presenting with intraocular extension. Arch. Ophthalmol. 103:1175, 1985.
5. Lever, W. F., and Schaumburg-Lever, G.: Histopathology of the Skin, ed. 6. Philadelphia, J. B. Lippincott, 1983, p. 506.
June, 1990
Infectious Crystalline Keratopathy Caused by Mycobacterium fortuitum and Pseudomonas aeruginosa Fung-Rong Hu, M.D. Department of Ophthalmology, National Taiwan University Hospital. Inquiries to Fung-Rong Hu, M.D., Department of Ophthalmology, National Taiwan University Hospital, 1 Chang-Te St., Taipei, Taiwan, Republic of China. Infectious crystalline keratopathy is characterized by a slowly progressive, white refractile anterior stromal infiltrate found in patients receiving long-term corticosteroid therapy. Streptococcus viridans has been identified as the cause in most of the reported cases.' We treated a patient with infectious crystalline keratopathy caused by Mycobacterium fortuitum and
Pseudomonas aeruginosa.
A 3D-year-old woman had a bacterial corneal ulceration of the right eye 14 years previously that resulted in a dense, central corneal scar. She underwent penetrating keratoplasty with 16 interrupted sutures in December 1988. Postoperative medications included betamethasone and antibiotic eyedrops. All sutures were removed in August 1989, except for two broken stitches at the 7 o'clock and 8 o'clock meridians. The patient had mild pain without redness in October 1989. Betamethasone was used without improvement. The patient returned to our clinic one week after the episode. A white, refractile stromal infiltrate with anterior onesixth stromal loss was found at the graft-host junction surrounding the broken stitch at the 8 0' clock meridian (Fig. 1). A scraping of the ulcer showed numerous acid-fast bacilli and a few gram-negative bacilli. Corneal cultures grew M. fortuitum and P. aeruginosa. Betamethasone was discontinued and topical amikacin and carbenicillin were instituted. The infiltrate became confluent with progressive stromal melting and endothelial plaque formation despite treatment (Fig. 2). Systemic amikacin and carbenicillin were added two weeks later because of impending scleral involvement. The corneal infiltrate, endothelial plaque, and anterior chamber reaction slowly resolved. Repeated bacteriologic studies were negative. There was no sign of reepithelialization because of the necrotic stromal bed. Six weeks later, lamellar keratectomy of the involved area was performed to remove the necrotic stroma. The specimen showed acute inflammatory cell infiltration, but no bacterium or other abnormality was found. Epithe-
Vol. 109, No.6
739
Letters to the Journal
this infection. This is supported by our patient who developed suppurative inflammation upon cessation of corticosteroid therapy. Pseudomonas species had been reported to be the causal agents of infectious crystalline keratopathy," although not the species of P. aeruginasa. Because many microorganisms besides S. viridans are found to cause infectious crystalline keratopathy."" thorough microbiologic study and proper antibiotic treatment are mandatory in the management of this disease.
References
Fig. 1 (Hu). Crystalline anterior stromal infiltrate with exposed stitch at the 8 o'clock meridian and lack of surrounding inflammation.
lialization was complete two weeks after the operation and has remained stable. Gorovoy and associates" reported that longterm corticosteroid therapy inhibited inflammatory response to the bacterial colonization in
1. Reiss, G. R., Campbell, J., and Bourne, W. M.: Infectious crystalline keratopathy. Surv. Ophthalmol. 31:69,1986. 2. Corovoy, M. S., Stern, G. A, Hood, e. I., and Allen, e.: Intrastromal noninflammatory bacterial colonization of a corneal graft. Arch. Ophthalmol. 101:1749, 1983. 3. Rabinowitz, S. M., Alfonso, E., Culbertson, W. W., Holland, S. P., Roussel, T. j.. Kattan, H., and Foster, R. K.: Infectious crystalline keratopathy. A report of ten cases and presentation of new clinical observation. ARVO abstracts. Supplement to Invest. Ophthalmol. Vis. Sci. Philadelphia, ]. B. Lippincott, 1989, p. 276. 4. Groden, L. R., Pascucci, S. E., and Brinser,]. H.: Haemophilus aphraphilus as a cause of crystalline keratopathy. Am. J. Ophthalmol. 104:89, 1987. 5. Weisenthal, R. W., Krachmer, ]. H., Folberg, R., Dunn, S. P., and Whitson, W. E.: Postkeratoplasty crystalline deposits mimicking bacterial infectious crystalline keratopathy. Am. J. Ophthalmol. 105:70, 1988.
Penetrating Scleral Patch
Keratoplasty Graft
After
Woodford S. Van Meter, M.D., Joseph R. Gussler, M.D., Ekktet Chansue, M.D., Winai Chaidaroon, M.D., and Surapong Duangratana, M.D. Fig. 2 (Hu). The same eye as seen in Figure 1, two weeks after cessation of corticosteroid therapy and initiation of fortified topical antibiotic treatment, showing suppurative process with marked conjunctival congestion.
Department of Ophthalmology, University of Kentucky (W.S.V., J.R.G.), and Chiang Mai University rs.c.. w.c.. S.D.).
Inquiries to Woodford S. Van Meter, M.D., Department of Ophthalmology, University of Kentucky, 800 Rose St., Lexington, KY 40536-0084.
