LETTERS
TO THE
Severe Ocular Anterior Segment Ischemia After Long-Term Trifluridine Treatment for Presumed Herpetic Keratitis
JOURNAL of the left anterior bulbar and inferior palpebral conjunctiva with nonperfused conjunctival arteries and peri phlebitic subconjunctival hemorrhages (Fig. 1). The entire left corneal and inferonasal conjunctival epithelium was disrupted as evidenced by fluorescein staining. There was diffuse corneal haze. The corneal thickness measured 0.61 mm by ultrasonic pachymetry. The left anterior chamber had a moderate cellular reaction with diffuse fine keratic precipitates and a small hypopyon. Intraocular pressure by Mackay-Marg tonometry was R.E.: 14 mm Hg and L.E.: 52 mm Hg. Examination of the posterior segment was normal in each eye. Fluorescein angiography of the anterior segment (Fig. 2) showed an absence of inferior palpebral and anterior bulbar conjunctival and episcleral perfusion with large areas of iris nonperfusion. Laboratory evaluation including a complete blood cell count with differential, serum glucose level, sedimentation rate, antinuclear antibody level, and rheumatoid factor was within normal limits. Both herpes simplex and varicella zoster titers were positive at 1:40 for IgG. IgM levels were not measurable. The trifluridine and prednisolone were discontinued, and acetazolamide and timolol were given with lowering of the intraocular pressure to 35 mm Hg. Over the ensuing five months, conjunctival neovascularization, cataract, band keratopathy, and iris atrophy have developed. Anterior segment ischemia has resulted from temporal arteritis, hyperviscosity syndromes, disseminated intravascular coagulopathy, vascular disease, and ophthalmic surgical procedures.! None of these associated factors were apparent in this case. The ischemia may have been secondary to zoster ophthalmicus without
Douglas R. Shearer, M.D., and William M. Bourne, M.D. Department of Ophthalmology, Mayo Clinic and Mayo Foundation.
Inquiries to William M. Bourne, M.D., Mayo Foundation, 200 First St. S. W., Rochester, MN 55905.
Falcon and associates! reported a case of conjunctival ischemia after chronic topical trifluridine treatment. We treated a patient with severe anterior segment ischemia that occurred after four months of topical trifluridine treatment for presumed herpetic keratitis. A 61-year-old woman developed injection and irritation in her left eye. The patient previously had recurrent keratitis that was symptomatically similar to the current episode. Her ophthalmologist diagnosed herpes simplex keratitis and initiated treatment with trifluridine and prednisolone acetate. Trifluridine six to seven times daily and prednisolone four times daily were continued for over four months until the patient developed left supraorbital boring pain that prompted her referral to our institution. She had no history of significant medical problems or cardiovascular disease and was not taking any other medications. She had no previous ocular surgery or trauma. Visual acuity was R.E.: 20/20 and L.E.: 20/ 400. The left pupil was mid-dilated and nonreactive, but no afferent pupillary defect was apparent. Visual fields by confrontation were full in each eye. There were pallor and chemosis
THE JOURNAL welcomes letters that describe unusual clinical or pathologic findings, experimental results, and new instruments or techniques. The title and the names of all authors appear in the Table of Contents and are retrievable through the Index Medicus and other standard indexing services. Letters must not duplicate data previously published or submitted for publication. Each letter must be accompanied by a signed disclosure statement and copyright transfer agreement published in each issue of THE JOURNAL. Letters must be typewritten, double-spaced, on 81/2 x l l-inch bond paper with 1 I/2-inch margins on all four sides. (See Instructions to Authors.) An original and two copies of the typescript and figures must be sent. The letters should not exceed 500 words of text. A maximum of two black-and-white figures may be used; they should be cropped to a width of 3 inches (one column). Color figures cannot be used. References should be limited to five. Letters may be referred to outside editorial referees for evaluation or may be reviewed by members of the Editorial Board. All letters are published promptly after acceptance. Authors do not receive galley proofs but if the editorial changes are extensive, the corrected typescript is submitted to them for approval. These instructions markedly limit the opportunity for an extended discussion or review. Therefore, THE JOURNAL does not publish correspondence concerning previously published letters.
346
Vol. 109, No.3
Letters to the Journal
347
infectious vasculitis cannot be ruled out, we believe that a toxic effect of long-term topical trifluridine therapy is the most likely cause in this case.
References
Fig. 1 (Shearer and Bourne). Bulbar subconjunctival hemorrhages, conjunctival pallor, disrupted corneal epithelium, and hypopyon.
an accompanying dermatologic manifestation, but the history of numerous similar recurrent episodes beginning at an early age makes this cause unlikely." Although not previously reported, a virulent herpes simplex strain may have been responsible. The previous episodes were relatively mild, however, and the ischemic event occurred four months after this episode's initial onset. The toxic effects of trifluridine are similar to those of other topical antiviral agents, and include punctate epithelial keratopathy, follicular conjunctival hypertrophy, punctaI occlusion, contact hypersensitivity, conjunctival cicatrization, and inhibition of corneal epithelial wound healing.' Additionally, a case of conjunctival ischemia from topical trifluridine has been reported.' Although an
1. Falcon, M. G., Jones, B. R., Williams, H. P., Wilhelmus, K., and Coster, D. J.: Adverse reactions in the eye from topical therapy with idoxuridine, adenine arabinoside and trifluorothymidine. In Sundmacher, R. (ed.): Herpetische Augenerkrankungen. Munchen. J. F. Bergmann Verlag, 1981, pp. 263-268. 2. Crock, G.: Clinical syndromes of anterior segment ischemia. Trans. Ophthalmol. Soc. U.K. 87:513, 1967.
3. Naumann, G., Cass, J. D. M., and Font, R. L.: Histopathology of herpes zoster ophthalmicus. Am. J. Ophthalmol. 65:533, 1968. 4. Stern, G. A., and Killingsworth, D. W.: Complications of topical antimicrobial agents. Int. Ophthalmol. Clin. 29:137,1989.
Combined Superior and Brown's Syndrome Blepharoplasty
Oblique Paresis After
Kimberly A. Neely, M.D.,
J. Terry Ernest, M.D.,
and Marianne Mottier,
c.o.
Department of Ophthalmology and Visual Science, University of Chicago. This study was supported in part by an unrestricted grant to the Department of Ophthalmology and Visual Science from Research to Prevent Blindness, Inc. Inquiries to J. Terry Ernest, M.D., 939 E. 57th Chicago, IL 60637.
Fig. 2 (Shearer and Bourne). Anterior segment fluorescein angiogram demonstrating non perfusion of the palpebral and bulbar conjunctiva and iris.
si..
Complications of blepharoplasty include blepharoptosis, ectropion, and blindness.' Diplopia occurs less often and usually after injury to the inferior rectus or inferior oblique muscle.! We treated a patient who developed superior oblique muscle paresis later combined with Brown's syndrome after blepharoplasty. A 59-year-old woman underwent bilateral upper eyelid blepharoplasty with fat removal under general anesthesia. An injection of lidocaine hydrochloride with epinephrine hydrochloride was given in the superonasal orbit bilaterally for hemostasis. Immediately after the operation, the patient noted double vision
TO THE
Severe Ocular Anterior Segment Ischemia After Long-Term Trifluridine Treatment for Presumed Herpetic Keratitis
JOURNAL of the left anterior bulbar and inferior palpebral conjunctiva with nonperfused conjunctival arteries and peri phlebitic subconjunctival hemorrhages (Fig. 1). The entire left corneal and inferonasal conjunctival epithelium was disrupted as evidenced by fluorescein staining. There was diffuse corneal haze. The corneal thickness measured 0.61 mm by ultrasonic pachymetry. The left anterior chamber had a moderate cellular reaction with diffuse fine keratic precipitates and a small hypopyon. Intraocular pressure by Mackay-Marg tonometry was R.E.: 14 mm Hg and L.E.: 52 mm Hg. Examination of the posterior segment was normal in each eye. Fluorescein angiography of the anterior segment (Fig. 2) showed an absence of inferior palpebral and anterior bulbar conjunctival and episcleral perfusion with large areas of iris nonperfusion. Laboratory evaluation including a complete blood cell count with differential, serum glucose level, sedimentation rate, antinuclear antibody level, and rheumatoid factor was within normal limits. Both herpes simplex and varicella zoster titers were positive at 1:40 for IgG. IgM levels were not measurable. The trifluridine and prednisolone were discontinued, and acetazolamide and timolol were given with lowering of the intraocular pressure to 35 mm Hg. Over the ensuing five months, conjunctival neovascularization, cataract, band keratopathy, and iris atrophy have developed. Anterior segment ischemia has resulted from temporal arteritis, hyperviscosity syndromes, disseminated intravascular coagulopathy, vascular disease, and ophthalmic surgical procedures.! None of these associated factors were apparent in this case. The ischemia may have been secondary to zoster ophthalmicus without
Douglas R. Shearer, M.D., and William M. Bourne, M.D. Department of Ophthalmology, Mayo Clinic and Mayo Foundation.
Inquiries to William M. Bourne, M.D., Mayo Foundation, 200 First St. S. W., Rochester, MN 55905.
Falcon and associates! reported a case of conjunctival ischemia after chronic topical trifluridine treatment. We treated a patient with severe anterior segment ischemia that occurred after four months of topical trifluridine treatment for presumed herpetic keratitis. A 61-year-old woman developed injection and irritation in her left eye. The patient previously had recurrent keratitis that was symptomatically similar to the current episode. Her ophthalmologist diagnosed herpes simplex keratitis and initiated treatment with trifluridine and prednisolone acetate. Trifluridine six to seven times daily and prednisolone four times daily were continued for over four months until the patient developed left supraorbital boring pain that prompted her referral to our institution. She had no history of significant medical problems or cardiovascular disease and was not taking any other medications. She had no previous ocular surgery or trauma. Visual acuity was R.E.: 20/20 and L.E.: 20/ 400. The left pupil was mid-dilated and nonreactive, but no afferent pupillary defect was apparent. Visual fields by confrontation were full in each eye. There were pallor and chemosis
THE JOURNAL welcomes letters that describe unusual clinical or pathologic findings, experimental results, and new instruments or techniques. The title and the names of all authors appear in the Table of Contents and are retrievable through the Index Medicus and other standard indexing services. Letters must not duplicate data previously published or submitted for publication. Each letter must be accompanied by a signed disclosure statement and copyright transfer agreement published in each issue of THE JOURNAL. Letters must be typewritten, double-spaced, on 81/2 x l l-inch bond paper with 1 I/2-inch margins on all four sides. (See Instructions to Authors.) An original and two copies of the typescript and figures must be sent. The letters should not exceed 500 words of text. A maximum of two black-and-white figures may be used; they should be cropped to a width of 3 inches (one column). Color figures cannot be used. References should be limited to five. Letters may be referred to outside editorial referees for evaluation or may be reviewed by members of the Editorial Board. All letters are published promptly after acceptance. Authors do not receive galley proofs but if the editorial changes are extensive, the corrected typescript is submitted to them for approval. These instructions markedly limit the opportunity for an extended discussion or review. Therefore, THE JOURNAL does not publish correspondence concerning previously published letters.
346
Vol. 109, No.3
Letters to the Journal
347
infectious vasculitis cannot be ruled out, we believe that a toxic effect of long-term topical trifluridine therapy is the most likely cause in this case.
References
Fig. 1 (Shearer and Bourne). Bulbar subconjunctival hemorrhages, conjunctival pallor, disrupted corneal epithelium, and hypopyon.
an accompanying dermatologic manifestation, but the history of numerous similar recurrent episodes beginning at an early age makes this cause unlikely." Although not previously reported, a virulent herpes simplex strain may have been responsible. The previous episodes were relatively mild, however, and the ischemic event occurred four months after this episode's initial onset. The toxic effects of trifluridine are similar to those of other topical antiviral agents, and include punctate epithelial keratopathy, follicular conjunctival hypertrophy, punctaI occlusion, contact hypersensitivity, conjunctival cicatrization, and inhibition of corneal epithelial wound healing.' Additionally, a case of conjunctival ischemia from topical trifluridine has been reported.' Although an
1. Falcon, M. G., Jones, B. R., Williams, H. P., Wilhelmus, K., and Coster, D. J.: Adverse reactions in the eye from topical therapy with idoxuridine, adenine arabinoside and trifluorothymidine. In Sundmacher, R. (ed.): Herpetische Augenerkrankungen. Munchen. J. F. Bergmann Verlag, 1981, pp. 263-268. 2. Crock, G.: Clinical syndromes of anterior segment ischemia. Trans. Ophthalmol. Soc. U.K. 87:513, 1967.
3. Naumann, G., Cass, J. D. M., and Font, R. L.: Histopathology of herpes zoster ophthalmicus. Am. J. Ophthalmol. 65:533, 1968. 4. Stern, G. A., and Killingsworth, D. W.: Complications of topical antimicrobial agents. Int. Ophthalmol. Clin. 29:137,1989.
Combined Superior and Brown's Syndrome Blepharoplasty
Oblique Paresis After
Kimberly A. Neely, M.D.,
J. Terry Ernest, M.D.,
and Marianne Mottier,
c.o.
Department of Ophthalmology and Visual Science, University of Chicago. This study was supported in part by an unrestricted grant to the Department of Ophthalmology and Visual Science from Research to Prevent Blindness, Inc. Inquiries to J. Terry Ernest, M.D., 939 E. 57th Chicago, IL 60637.
Fig. 2 (Shearer and Bourne). Anterior segment fluorescein angiogram demonstrating non perfusion of the palpebral and bulbar conjunctiva and iris.
si..
Complications of blepharoplasty include blepharoptosis, ectropion, and blindness.' Diplopia occurs less often and usually after injury to the inferior rectus or inferior oblique muscle.! We treated a patient who developed superior oblique muscle paresis later combined with Brown's syndrome after blepharoplasty. A 59-year-old woman underwent bilateral upper eyelid blepharoplasty with fat removal under general anesthesia. An injection of lidocaine hydrochloride with epinephrine hydrochloride was given in the superonasal orbit bilaterally for hemostasis. Immediately after the operation, the patient noted double vision
