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The Elastic Properties of the Lens Capsule in Capsulorhexis: Reply
Vol. 112, No.3
Correspondence
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EDITOR:
We thank Drs. Waltz and Rubin for their comments concerning our article. The laboratory measurements of capsulectomy size were indeed direct measurements of lenses of human eyes obtained post mortem and the corneal magnification of 1.15 times was not considered. We agree that this magnification should be taken into consideration during clinical operations when precise sizing of the anterior capsular opening is required. EHUD I. ASS lA, DAVID J. APPLE, JULIE C. TSAI, EDWARD S. LIM,
M.D. M.D. M.D. M.D.
Charleston, South Carolina
Herpes Simplex Dendritic Keratitis After Keratoplasty EDITOR:
In the article, "Herpes simplex dendritic keratitis after keratoplasty" by M. J. Mannis, R. D. Plotnik, I. R. Schwab, and R. D. Newton (Am. J. Ophthalmol. 111:480, April 1991), three patients who had no history of herpetic disease developed herpes simplex viral keratitis between three and 11 months after penetrating keratoplasty. The authors concluded that herpes simplex may cause late-onset epithelial defects after keratoplasty even in the absence of a history of herpes simplex keratitis. Results from our laboratory and clinical studies support their findings. We reported that early-onset, as well as late-onset, epithelial defects after keratoplasty may be caused by a herpes infection; unfortunately, the authors failed to cite our investigations. In our Letter to THE JOURNAL, "Herpes simplex virus and persistent epithelial defects after penetrating keratoplasty," (Am. J. Ophthalmol. 109:95, January 1990), we described a patient with no history of herpes keratitis who developed a persistent paracentral, geographic, epithelial defect involving the donor-recipient interface immediately after keratoplasty. The defect was present on postoperative day 1, re-
355
mained essentially unchanged for two weeks, and did not heal completely until four weeks postoperatively. Ocular herpes cultures were obtained on postoperative days 1, 2, 6, and 15. Two separate cultures obtained on the sixth day were positive for herpes simplex virus. Nearly 40 years ago, Carton and Kilbourne) associated reactivation of latent herpes simplex in humans with surgical trauma. Since the cornea is highly innervated principally by fibers originating in the trigeminal ganglion, we postulated that corneal nerve damage from keratoplasty would similarly reactivate latent virus and result in postkeratoplasty herpes simplex keratitis.v" Using the rabbit we demonstrated that autograft penetrating keratoplasty in conjunction with postoperative corticosteroids significantly increased herpes ocular shedding, epithelial ulceration, and stromal keratitis." In this model, viral shedding and large, geographic, epithelial defects appeared during the first 14 days after keratoplasty. Dendritic lesions and stromal keratitis appeared 26 to 82 days after surgery. We concluded that the surgical trauma from keratoplasty immediately precipitated viral shedding in the tear film, which resulted in early corneal infection and persistent geographic epithelial defects. We further postulated that the herpetic corneal lesions observed weeks to months later may be the result of regenerating corneal nerves that serve as a conduit for the passage of infectious virus from the site of ganglionic latency to the cornea. Therefore, viral reactivation may occur during two periods after keratoplasty: early (days after surgery), as observed in our patient, and late (weeks to months after surgery), as observed by Mannis and colleagues. In the rabbit model, oral acyclovir prophylaxis was effective in reducing herpes simplex virus recurrences after keratoplasty.' In rabbits harboring latent virus, positive cultures coincided with herpetic geographic ulcers only 29% of the time." Multiple cultures, as well as other diagnostic aids such as ELISA, immunofluorescence, and immunoperoxidase studies, may be needed to establish the diagnosis. CRAIG F. BEYER, D.O.
St. Louis, Missouri
JAMES M. HILL, Ph.D. THOMAS J. BYRD, M.D. HERBERT E. KAUFMAN, M.D.
New Orleans, Louisiana
Correspondence
_ _ _ _ _ _ _ Reply
_
EDITOR:
We thank Drs. Waltz and Rubin for their comments concerning our article. The laboratory measurements of capsulectomy size were indeed direct measurements of lenses of human eyes obtained post mortem and the corneal magnification of 1.15 times was not considered. We agree that this magnification should be taken into consideration during clinical operations when precise sizing of the anterior capsular opening is required. EHUD I. ASS lA, DAVID J. APPLE, JULIE C. TSAI, EDWARD S. LIM,
M.D. M.D. M.D. M.D.
Charleston, South Carolina
Herpes Simplex Dendritic Keratitis After Keratoplasty EDITOR:
In the article, "Herpes simplex dendritic keratitis after keratoplasty" by M. J. Mannis, R. D. Plotnik, I. R. Schwab, and R. D. Newton (Am. J. Ophthalmol. 111:480, April 1991), three patients who had no history of herpetic disease developed herpes simplex viral keratitis between three and 11 months after penetrating keratoplasty. The authors concluded that herpes simplex may cause late-onset epithelial defects after keratoplasty even in the absence of a history of herpes simplex keratitis. Results from our laboratory and clinical studies support their findings. We reported that early-onset, as well as late-onset, epithelial defects after keratoplasty may be caused by a herpes infection; unfortunately, the authors failed to cite our investigations. In our Letter to THE JOURNAL, "Herpes simplex virus and persistent epithelial defects after penetrating keratoplasty," (Am. J. Ophthalmol. 109:95, January 1990), we described a patient with no history of herpes keratitis who developed a persistent paracentral, geographic, epithelial defect involving the donor-recipient interface immediately after keratoplasty. The defect was present on postoperative day 1, re-
355
mained essentially unchanged for two weeks, and did not heal completely until four weeks postoperatively. Ocular herpes cultures were obtained on postoperative days 1, 2, 6, and 15. Two separate cultures obtained on the sixth day were positive for herpes simplex virus. Nearly 40 years ago, Carton and Kilbourne) associated reactivation of latent herpes simplex in humans with surgical trauma. Since the cornea is highly innervated principally by fibers originating in the trigeminal ganglion, we postulated that corneal nerve damage from keratoplasty would similarly reactivate latent virus and result in postkeratoplasty herpes simplex keratitis.v" Using the rabbit we demonstrated that autograft penetrating keratoplasty in conjunction with postoperative corticosteroids significantly increased herpes ocular shedding, epithelial ulceration, and stromal keratitis." In this model, viral shedding and large, geographic, epithelial defects appeared during the first 14 days after keratoplasty. Dendritic lesions and stromal keratitis appeared 26 to 82 days after surgery. We concluded that the surgical trauma from keratoplasty immediately precipitated viral shedding in the tear film, which resulted in early corneal infection and persistent geographic epithelial defects. We further postulated that the herpetic corneal lesions observed weeks to months later may be the result of regenerating corneal nerves that serve as a conduit for the passage of infectious virus from the site of ganglionic latency to the cornea. Therefore, viral reactivation may occur during two periods after keratoplasty: early (days after surgery), as observed in our patient, and late (weeks to months after surgery), as observed by Mannis and colleagues. In the rabbit model, oral acyclovir prophylaxis was effective in reducing herpes simplex virus recurrences after keratoplasty.' In rabbits harboring latent virus, positive cultures coincided with herpetic geographic ulcers only 29% of the time." Multiple cultures, as well as other diagnostic aids such as ELISA, immunofluorescence, and immunoperoxidase studies, may be needed to establish the diagnosis. CRAIG F. BEYER, D.O.
St. Louis, Missouri
JAMES M. HILL, Ph.D. THOMAS J. BYRD, M.D. HERBERT E. KAUFMAN, M.D.
New Orleans, Louisiana