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Central Retinal Artery Occlusion After Varicella
Vol. 113, No. 5
Letters to The Journal
suit in unwanted vertical traction in the lower eyelid. This is especially true in a patient with underlying senescent facial and eyelid chang es.1 The redundant folds of skin on the face provide a platform for the spectacle frame, which can cause vertical traction on the eyelid with previous significant laxity and then uncov er an incipient latent ectropion. Thus, we can potentially discover valuable information by looking through our patients' glasses.
591
Inquiries to Nam-chun Cho, M.D., Department of Oph thalmology, Chonbuk National University Medical School, San 2-20 Keum Am Dong Chon Ju City Chon Buk, Republic of Korea, South. Visual disturbances resulting from chickenpox have focused on the optic nerve and macular abnormalities. Patients usually recover good vision or have but a partial visual field defect.
We treated a patient who developed permanent visual loss after chickenpox. An 8-year-old girl who developed the typical rash of chickenpox five days previously com plained of sudden loss of vision in her right eye. The pupil reacted consensually but not directly to light. Applanation tension was 14 mm Hg in each eye. Ophthalmoscopy disclosed marked retinal edema and a cherry-red spot in the right eye (Fig. 1). Fluorescein angiography demon strated a central retinal artery occlusion with delayed arteriolar filling at 182 seconds (Fig. 2). Treatment with intravenous acetazolamide and anterior chamber paracentesis was not success ful. Results of general examination were unre markable except for the rash. Results of com plete blood cell and platelet counts, plasma viscosity, electrophoresis, fasting blood glu cose and lipids, and urinalysis were normal. Serologic studies for syphilis were negative. The erythrocyte sedimentation rate and the immunoglobulins for chickenpox were marked ly increased. The retinal edema decreased over the subsequent six months, and the appearance of the arterioles remained the same. The optic disk became atrophic. Her visual acuity was unchanged. Three cases of permanent visual field defect caused by optic neuritis and retinal branch artery occlusion have been described. Valerie, Nicholas, and David 1 described a 14-year-old girl who developed chickenpox and a visual field defect one week after the onset of chickenpox. Visual acuity remained poor in the right eye and color vision was lost in both eyes. Watt2 described a 19-year-old man who developed a visual field defect three days after the onset of the rash; the author suggested a focal optic
Fig. 1 (Cho and Han). Marked retinal edema and cherry-red spot in the right eye.
Fig. 2 (Cho and Han). Fluorescein angiogram show ing the characteristic delayed arteriolar filling.
Reference 1. Shore, J. W.: Changes in lower eyelid resting position, movement, and tone with age. Am. J. Ophthalmol. 99:415, 1985.
Central Retinal Artery Occlusion After Varicella N a m - c h u n Cho, M.D., and Hong-joo Han, M.D. Department of Ophthalmology, Chonbuk National University Medical School, Republic of Korea.
592
AMERICAN JOURNAL OF OPHTHALMOLOGY
neuritis as the cause. David3 described a 16year-old girl with a persistent unilateral visual field defect that occurred four days after the onset of chickenpox. Although central retinal artery occlusion does not seem to be associated with the varicel la-zoster virus, many complications of varicel la-zoster infections in adults may have an ischemic basis 4 —a retinal vasculitis or perivasculitis, or a granulomatous angiitis af fecting the brain. 5 We believed vasculitis caused the central retinal artery occlusion in our pa tient, although a more widespread vasculitis was not evident. The exact cause of the central retinal artery occlusion in our patient is not known, but its coincidence with chickenpox is interesting.
References 1. Valerie, P., Nicholas, H., and David, D.: Varicel la optic neuritis. Neurology 38:501, 1988. 2. Watt, L. L.: Branch retinal arteriolar occlusion with chicken-pox. Br. J. Ophthalmol. 72:78, 1988. 3. David, S. I. T.: Optic disc pigmentation associ ated with a field defect following chickenpox. J. Pediatr. Ophthalmol. 13:80, 1976. 4. Liesegang, T. J.: The varicella zoster virus. Sys temic and ocular features. J. Am. Acad. Dermatol. 11:165, 1984. 5. Blue, M. C, and Rosenblum, W. I.: Granuloma tous angiitis of the brain with herpes zoster and varicella encephalitis. Arch. Pathol. Lab. Med. 107:126, 1983.
May, 1992
and mild papillitis in the setting of an acute primary varicella infection (chickenpox). 14 We recently encountered a patient with similar findings, yet unique with regard to age at mani festation, onset of ocular symptoms before the dermatologic exanthem, and ensuing profound loss of vision. A 2-year-old boy manifested an intermittent left exotropia approximately two days before developing the characteristic cutaneous mani festations of primary varicella infection (chic kenpox). His two siblings had acute chickenpox concurrently. The exotropia became constant over the ensuing two weeks, when the parents sought ophthalmic consultation. Vision was central, steady, and maintained in both eyes, with a frank right fixation prefer ence. No afferent pupillary defect was seen. There was an intermittent left exotropia of 40 diopters. Ophthalmoscopy disclosed papillitis, phlebitis, scattered intraretinal hemorrhages, and a macular lipid star, with scattered lipid superior and nasal to the disk. An arcuate area of retinal opacification was present just outside the inferotemporal retinal vascular arcade, with smaller white foci of retinitis in the superotemporal quadrant. Perivascular sheathing, primarily venous, was apparent superotemporally and inferotemporally. Dot and blot in traretinal hemorrhages were scattered in all quadrants. The right fundus was normal. At tempts to photograph the left fundus were unsuccessful because of poor cooperation.
The presumptive diagnosis was varicella reti nitis. Confirmatory IgM titers were not drawn. After two days, against medical advice, the parents insisted on leaving the hospital. Ar rangements were made to complete the oneweek course of intravenous acyclovir therapy at Central Visual Loss Caused by home. One month later fixation was no longer Chickenpox Retinitis in a 2-Year-Old steady or maintained, and there was a frank left Child afferent pupillary defect. A left exotropia of 45 diopters at distance was present. A localized A n t o n i o Capone, Jr., M.D., vitreous hemorrhage occurred over the infero and Travis A. Meredith, M.D. temporal arcade. The most densely sheathed Retina Service, Department of Ophthalmology, peripheral vessels became sclerotic. Mottling of Emory University. Supported in part by an unre the macular retinal pigment epithelium ensued stricted departmental grant from Research to Prevent Blindness, Inc., New York, New York. Dr. Capone upon resolution of macular lipid. was a Heed Foundation Fellow (1989-1990). The onset of retinitis and papillitis coincident with the characteristic eruption of primary vari Inquiries to Antonio Capone, jr., M.D., Emory Eye Center, 1327 Clifton Rd. N.E., Fourth Floor, Atlanta, GA cella infection strongly implicate varicella zos 30033. ter as the causal agent in this child. Varicella zoster is at least one cause of the acute retinal Reports in the ophthalmic literature have necrosis syndrome, characterized by anterior documented a clinical syndrome characterized segment inflammation, retinal vasculitis, vitby focal retinitis, negligible vitreitis, phlebitis,
Letters to The Journal
suit in unwanted vertical traction in the lower eyelid. This is especially true in a patient with underlying senescent facial and eyelid chang es.1 The redundant folds of skin on the face provide a platform for the spectacle frame, which can cause vertical traction on the eyelid with previous significant laxity and then uncov er an incipient latent ectropion. Thus, we can potentially discover valuable information by looking through our patients' glasses.
591
Inquiries to Nam-chun Cho, M.D., Department of Oph thalmology, Chonbuk National University Medical School, San 2-20 Keum Am Dong Chon Ju City Chon Buk, Republic of Korea, South. Visual disturbances resulting from chickenpox have focused on the optic nerve and macular abnormalities. Patients usually recover good vision or have but a partial visual field defect.
We treated a patient who developed permanent visual loss after chickenpox. An 8-year-old girl who developed the typical rash of chickenpox five days previously com plained of sudden loss of vision in her right eye. The pupil reacted consensually but not directly to light. Applanation tension was 14 mm Hg in each eye. Ophthalmoscopy disclosed marked retinal edema and a cherry-red spot in the right eye (Fig. 1). Fluorescein angiography demon strated a central retinal artery occlusion with delayed arteriolar filling at 182 seconds (Fig. 2). Treatment with intravenous acetazolamide and anterior chamber paracentesis was not success ful. Results of general examination were unre markable except for the rash. Results of com plete blood cell and platelet counts, plasma viscosity, electrophoresis, fasting blood glu cose and lipids, and urinalysis were normal. Serologic studies for syphilis were negative. The erythrocyte sedimentation rate and the immunoglobulins for chickenpox were marked ly increased. The retinal edema decreased over the subsequent six months, and the appearance of the arterioles remained the same. The optic disk became atrophic. Her visual acuity was unchanged. Three cases of permanent visual field defect caused by optic neuritis and retinal branch artery occlusion have been described. Valerie, Nicholas, and David 1 described a 14-year-old girl who developed chickenpox and a visual field defect one week after the onset of chickenpox. Visual acuity remained poor in the right eye and color vision was lost in both eyes. Watt2 described a 19-year-old man who developed a visual field defect three days after the onset of the rash; the author suggested a focal optic
Fig. 1 (Cho and Han). Marked retinal edema and cherry-red spot in the right eye.
Fig. 2 (Cho and Han). Fluorescein angiogram show ing the characteristic delayed arteriolar filling.
Reference 1. Shore, J. W.: Changes in lower eyelid resting position, movement, and tone with age. Am. J. Ophthalmol. 99:415, 1985.
Central Retinal Artery Occlusion After Varicella N a m - c h u n Cho, M.D., and Hong-joo Han, M.D. Department of Ophthalmology, Chonbuk National University Medical School, Republic of Korea.
592
AMERICAN JOURNAL OF OPHTHALMOLOGY
neuritis as the cause. David3 described a 16year-old girl with a persistent unilateral visual field defect that occurred four days after the onset of chickenpox. Although central retinal artery occlusion does not seem to be associated with the varicel la-zoster virus, many complications of varicel la-zoster infections in adults may have an ischemic basis 4 —a retinal vasculitis or perivasculitis, or a granulomatous angiitis af fecting the brain. 5 We believed vasculitis caused the central retinal artery occlusion in our pa tient, although a more widespread vasculitis was not evident. The exact cause of the central retinal artery occlusion in our patient is not known, but its coincidence with chickenpox is interesting.
References 1. Valerie, P., Nicholas, H., and David, D.: Varicel la optic neuritis. Neurology 38:501, 1988. 2. Watt, L. L.: Branch retinal arteriolar occlusion with chicken-pox. Br. J. Ophthalmol. 72:78, 1988. 3. David, S. I. T.: Optic disc pigmentation associ ated with a field defect following chickenpox. J. Pediatr. Ophthalmol. 13:80, 1976. 4. Liesegang, T. J.: The varicella zoster virus. Sys temic and ocular features. J. Am. Acad. Dermatol. 11:165, 1984. 5. Blue, M. C, and Rosenblum, W. I.: Granuloma tous angiitis of the brain with herpes zoster and varicella encephalitis. Arch. Pathol. Lab. Med. 107:126, 1983.
May, 1992
and mild papillitis in the setting of an acute primary varicella infection (chickenpox). 14 We recently encountered a patient with similar findings, yet unique with regard to age at mani festation, onset of ocular symptoms before the dermatologic exanthem, and ensuing profound loss of vision. A 2-year-old boy manifested an intermittent left exotropia approximately two days before developing the characteristic cutaneous mani festations of primary varicella infection (chic kenpox). His two siblings had acute chickenpox concurrently. The exotropia became constant over the ensuing two weeks, when the parents sought ophthalmic consultation. Vision was central, steady, and maintained in both eyes, with a frank right fixation prefer ence. No afferent pupillary defect was seen. There was an intermittent left exotropia of 40 diopters. Ophthalmoscopy disclosed papillitis, phlebitis, scattered intraretinal hemorrhages, and a macular lipid star, with scattered lipid superior and nasal to the disk. An arcuate area of retinal opacification was present just outside the inferotemporal retinal vascular arcade, with smaller white foci of retinitis in the superotemporal quadrant. Perivascular sheathing, primarily venous, was apparent superotemporally and inferotemporally. Dot and blot in traretinal hemorrhages were scattered in all quadrants. The right fundus was normal. At tempts to photograph the left fundus were unsuccessful because of poor cooperation.
The presumptive diagnosis was varicella reti nitis. Confirmatory IgM titers were not drawn. After two days, against medical advice, the parents insisted on leaving the hospital. Ar rangements were made to complete the oneweek course of intravenous acyclovir therapy at Central Visual Loss Caused by home. One month later fixation was no longer Chickenpox Retinitis in a 2-Year-Old steady or maintained, and there was a frank left Child afferent pupillary defect. A left exotropia of 45 diopters at distance was present. A localized A n t o n i o Capone, Jr., M.D., vitreous hemorrhage occurred over the infero and Travis A. Meredith, M.D. temporal arcade. The most densely sheathed Retina Service, Department of Ophthalmology, peripheral vessels became sclerotic. Mottling of Emory University. Supported in part by an unre the macular retinal pigment epithelium ensued stricted departmental grant from Research to Prevent Blindness, Inc., New York, New York. Dr. Capone upon resolution of macular lipid. was a Heed Foundation Fellow (1989-1990). The onset of retinitis and papillitis coincident with the characteristic eruption of primary vari Inquiries to Antonio Capone, jr., M.D., Emory Eye Center, 1327 Clifton Rd. N.E., Fourth Floor, Atlanta, GA cella infection strongly implicate varicella zos 30033. ter as the causal agent in this child. Varicella zoster is at least one cause of the acute retinal Reports in the ophthalmic literature have necrosis syndrome, characterized by anterior documented a clinical syndrome characterized segment inflammation, retinal vasculitis, vitby focal retinitis, negligible vitreitis, phlebitis,