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Toxic granulomatous anterior uveitis in live intracameral cysticercosis masquerading as leukocoria
Correspondence
Toxic granulomatous anterior uveitis in live intracameral cysticercosis masquerading as leukocoria A 6-year-old female child was referred to us with a diagnosis of cataract in the left eye. Examination under anaesthesia revealed a large, translucent, white cyst with a live mobile evaginating scolex extending from iris to the back of the cornea (about 6 mm in diameter) freely floating in the anterior chamber (Fig. 1). Fresh nonpigmented granulomatous keratic precipitates were scattered diffusely over the entire endothelium (Fig. 1) without corneal edema or fibrinous anterior chamber reaction. Pupillary dilation was slow and difficult in the affected eye, but lens appeared to be clear. Right eye was within normal limits. Sonography ruled out posterior segment cysts, whereas computerized tomography scan of the brain ruled out intracranial cysts. A diagnosis of free-floating live anterior chamber cysticercosis cyst with toxic granulomatous anterior uveitis was hence made.
Fig. 1 — Clinical photograph demonstrating the cyst with evaginating scolex in the anterior chamber along with keratic precipitates present diffusely over the corneal endothelium.
The patient was prescribed topical steroid therapy with prednisolone acetate (1%) eye drops at 2 hourly intervals, and the keratic precipitates resolved within 3 days. After a week, surgical removal of the cyst was done successfully with viscoexpression technique (Fig. 2), and histopathological evaluation confirmed the diagnoses. Visual acuity had improved to at least 6/60, and there was no ocular inflammation until a follow-up of 4 months in the left eye. Intense inflammation, fibrinous reactions, and glaucoma are known to occur in children with anterior segment cysticercosis (ASC),1–4 which is partially responsive or nonresponsive to topical steroids. It was interesting that ASC was mistaken initially for cataract by the referring physician, but the size and location of the cyst in the pupillary axis could have been misdiagnosed in an uncooperative child because of the anterior uveitis on torch light examination. In fact, ASC has previously been confused with anterior dislocation of lens.5 Anterior segment optical coherence tomography was helpful in actual localization of the cyst in this case and has been previously published.6 Usually the degenerative stage of dead scolex results in release of large amounts of toxins causing a significant fibrinous reaction at the site of the cyst. However, in this case, there was absence of severe inflammatory reaction because the cyst was live (exhibiting a mobile scolex). The anterior uveitis presentation may be explained because of the toxin and heterologous protein leakage through the vesicle wall of the cysticercosis in the vesicular stage of its development.7 Posterior segment cysticercosis is far more common than ASC.8,9 Apart from the presentations of ASC in children discussed earlier, pupillary block glaucoma has been reported in adults.10 Because antihelminthic therapy can lead to severe inflammation in the event of a live cyst degenerating, surgical removal is the modality of choice in live intraocular cysticercosis.11 Viscoexpression is perhaps the best technique for surgical management of ASC.12,13 Systemic cysticercosis
Fig. 2 — A and B, Intraoperative photographs demonstrating cyst removal with viscoexpression technique.
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CAN J OPHTHALMOL — VOL. 49, NO. 6, DECEMBER 2014
Correspondence should be ruled out because it would require antihelminthic therapy with steroid cover after ocular surgery.14 Live ASC, a rare occurrence in children, can be associated with anterior uveitis and may even masquerade as leukocoria. Timely diagnoses and surgical management result in good outcomes. Brijesh Takkar, * Parijat Chandra, * Kiran Kumar, † Murugesan Vanathi † *
Vitreo Retina Services and †Cornea & Ocular Surface Services, Dr R P Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India Correspondence to: Murugesan Vanathi, MD: [email protected] REFERENCES 1. Mahendradas P, Biswas J, Khetan V. Fibrinous anterior uveitis due to cysticercus cellulosae. Ocul Immunol Inflamm. 2007;15:451-4. 2. Cortez MA, Giuliari GP, Escaf L, et al. Ocular cysticercosis of the anterior segment. J AAPOS. 2007;11:628-9. 3. Schmidt U, Klauss V, Stefani FH. Unilateral iritis by cysticercal larva in the anterior chamber. Ophthalmologica. 1990;200:210-5. 4. Swastika K, Dewiyani CI, Yanagida T, et al. An ocular cysticercosis in Bali, Indonesia caused by Taenia solium Asian genotype. Parasitol Int. 2012;61:378-80. 5. Kapoor S, Sood GC, Aurora AL, et al. Ocular cysticercosis. Report of a free floating cysticersus in the anterior chamber. Acta Ophthalmol (Copenh). 1977;55:927-30.
6. Takkar B, Mehdi MU, Ahmed NR, Chandra P, Vanathi M. Anterior segment optical coherence tomography of live ocular cysticercosis. Clin Experiment Ophthalmol. doi:10.1111/ceo.12339. [Epub ahead of print]. 7. Juan-Juan Li, Li-Wei Zhang, Hua Li, Zhu-Lin Hu. Clinical and pathological characteristics of intraocular cysticercosis. Korean J Parasitol. 2013;51:223-9. 8. Madigubba S, Vishwanath K, Reddy G, et al. Changing trends in ocular cysticercosis over two decades: an analysis of 118 surgically excised cysts. Indian J Med Microbiol. 2007;25:214-9. 9. Wender JD, Rathinam SR, Shaw RE, et al. Intraocular cysticercosis: case series and comprehensive review of the literature. Ocul Immunol Inflamm. 2011;19:240-5. 10. Chandra A, Singh MK, Singh VP, et al. A live cysticercosis in anterior chamber leading to glaucoma secondary to pupillary block. J Glaucoma. 2007;16:271-3. 11. Kai S, Vanathi M, Vengayil S, et al. Viscoexpression of large free floating Cysticercus cyst from the anterior chamber of the eye by double incision technique. Indian J Med Microbiol. 2008;26: 277-9. 12. Das JC, Chaudhuri Z, Bansal RL. Viscoexpression of anterior chamber cysticercus cellulosae. Indian J Ophthalmol. 2002;50: 133-5. 13. Beri S, Vajpayee RB, Dhingra N. Managing anterior chamber cysticercosis by viscoexpression: a new surgical technique. Arch Ophthalmol. 1994;112:1279-80. 14. García HH, Gonzalez AE, Evans CA, et al. Taenia solium cysticercosis. Lancet. 2003;362:547-56. Can J Ophthalmol 2014;49:e140–e141 0008-4182/14/$-see front matter & 2014 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2014.08.011
Bilateral posterior scleritis as a presenting manifestation of giant cell arteritis: A case report
appeared in the literature.3–5 We report a case of bilateral posterior scleritis that was diagnosed in association with GCA.
Posterior scleritis is a rare and frequently misdiagnosed form of ocular inflammation that may be either idiopathic or associated with various systemic diseases. The systemic associations1 are similar to those observed in anterior scleritis and include rheumatoid arthritis, Wegener granulomatosis, systemic lupus erythematosus, systemic vasculitis, relapsing polychondritis, sarcoidosis, and other autoimmune diseases. Moreover, it may occur in isolation or associated with either anterior scleritis or anterior uveitis. Giant cell arteritis (GCA) is a systemic immune-mediated vasculitis that affects medium-sized and large arteries. GCA has a wide spectrum of clinical features related to both systemic inflammation and ischemia. The most common symptoms are headache, scalp tenderness, jaw claudication, and systemic manifestations (fever, weight loss, anorexia, and malaise). Ophthalmologic symptoms are common manifestations of GCA and may occur alone, without other symptoms of GCA. Arteritic anterior ischemic optic neuropathy (AAION) is the most common ophthalmologic manifestation. Other ocular manifestations are central or branch retinal artery occlusion and diplopia that results from ischemia of extraocular muscles or ocular motor nerves.2 A few other reports about the association of GCA with scleritis have
CASE REPORT A 93-year-old female with progressive bilateral visual loss and a 1-month history of constant headache was referred to our hospital. She had a history of systemic hypertension and coronary heart disease. At the first examination, best-corrected decimal visual acuity was 0.1 (20/200) in the right eye and 0.3 (20/63) in the left eye. Anterior segment examination and intraocular pressure were unremarkable (the patient was pseudophakic). Posterior segment examination evidenced bilateral disc swelling and bilateral serous retinal detachment involving the macular region as well as the peripheral inferior retina of the right eye. Fundus fluorescein angiography (FFA) found bilateral optic nerve leakage and vascular tortuosity (Fig. 1). B-scan ultrasonography found bilateral scleral and choroid thickening and serous retinal detachment, more evident in the right eye (Fig. 2). According to optical coherence tomography (OCT) examination, the macular region of both eyes and the right eye inferior retina were affected with serous detachment (OD4OS) (Fig. 3). Based on these findings, bilateral posterior scleritis was diagnosed.
CAN J OPHTHALMOL — VOL. 49, NO. 6, DECEMBER 2014
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Toxic granulomatous anterior uveitis in live intracameral cysticercosis masquerading as leukocoria A 6-year-old female child was referred to us with a diagnosis of cataract in the left eye. Examination under anaesthesia revealed a large, translucent, white cyst with a live mobile evaginating scolex extending from iris to the back of the cornea (about 6 mm in diameter) freely floating in the anterior chamber (Fig. 1). Fresh nonpigmented granulomatous keratic precipitates were scattered diffusely over the entire endothelium (Fig. 1) without corneal edema or fibrinous anterior chamber reaction. Pupillary dilation was slow and difficult in the affected eye, but lens appeared to be clear. Right eye was within normal limits. Sonography ruled out posterior segment cysts, whereas computerized tomography scan of the brain ruled out intracranial cysts. A diagnosis of free-floating live anterior chamber cysticercosis cyst with toxic granulomatous anterior uveitis was hence made.
Fig. 1 — Clinical photograph demonstrating the cyst with evaginating scolex in the anterior chamber along with keratic precipitates present diffusely over the corneal endothelium.
The patient was prescribed topical steroid therapy with prednisolone acetate (1%) eye drops at 2 hourly intervals, and the keratic precipitates resolved within 3 days. After a week, surgical removal of the cyst was done successfully with viscoexpression technique (Fig. 2), and histopathological evaluation confirmed the diagnoses. Visual acuity had improved to at least 6/60, and there was no ocular inflammation until a follow-up of 4 months in the left eye. Intense inflammation, fibrinous reactions, and glaucoma are known to occur in children with anterior segment cysticercosis (ASC),1–4 which is partially responsive or nonresponsive to topical steroids. It was interesting that ASC was mistaken initially for cataract by the referring physician, but the size and location of the cyst in the pupillary axis could have been misdiagnosed in an uncooperative child because of the anterior uveitis on torch light examination. In fact, ASC has previously been confused with anterior dislocation of lens.5 Anterior segment optical coherence tomography was helpful in actual localization of the cyst in this case and has been previously published.6 Usually the degenerative stage of dead scolex results in release of large amounts of toxins causing a significant fibrinous reaction at the site of the cyst. However, in this case, there was absence of severe inflammatory reaction because the cyst was live (exhibiting a mobile scolex). The anterior uveitis presentation may be explained because of the toxin and heterologous protein leakage through the vesicle wall of the cysticercosis in the vesicular stage of its development.7 Posterior segment cysticercosis is far more common than ASC.8,9 Apart from the presentations of ASC in children discussed earlier, pupillary block glaucoma has been reported in adults.10 Because antihelminthic therapy can lead to severe inflammation in the event of a live cyst degenerating, surgical removal is the modality of choice in live intraocular cysticercosis.11 Viscoexpression is perhaps the best technique for surgical management of ASC.12,13 Systemic cysticercosis
Fig. 2 — A and B, Intraoperative photographs demonstrating cyst removal with viscoexpression technique.
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CAN J OPHTHALMOL — VOL. 49, NO. 6, DECEMBER 2014
Correspondence should be ruled out because it would require antihelminthic therapy with steroid cover after ocular surgery.14 Live ASC, a rare occurrence in children, can be associated with anterior uveitis and may even masquerade as leukocoria. Timely diagnoses and surgical management result in good outcomes. Brijesh Takkar, * Parijat Chandra, * Kiran Kumar, † Murugesan Vanathi † *
Vitreo Retina Services and †Cornea & Ocular Surface Services, Dr R P Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India Correspondence to: Murugesan Vanathi, MD: [email protected] REFERENCES 1. Mahendradas P, Biswas J, Khetan V. Fibrinous anterior uveitis due to cysticercus cellulosae. Ocul Immunol Inflamm. 2007;15:451-4. 2. Cortez MA, Giuliari GP, Escaf L, et al. Ocular cysticercosis of the anterior segment. J AAPOS. 2007;11:628-9. 3. Schmidt U, Klauss V, Stefani FH. Unilateral iritis by cysticercal larva in the anterior chamber. Ophthalmologica. 1990;200:210-5. 4. Swastika K, Dewiyani CI, Yanagida T, et al. An ocular cysticercosis in Bali, Indonesia caused by Taenia solium Asian genotype. Parasitol Int. 2012;61:378-80. 5. Kapoor S, Sood GC, Aurora AL, et al. Ocular cysticercosis. Report of a free floating cysticersus in the anterior chamber. Acta Ophthalmol (Copenh). 1977;55:927-30.
6. Takkar B, Mehdi MU, Ahmed NR, Chandra P, Vanathi M. Anterior segment optical coherence tomography of live ocular cysticercosis. Clin Experiment Ophthalmol. doi:10.1111/ceo.12339. [Epub ahead of print]. 7. Juan-Juan Li, Li-Wei Zhang, Hua Li, Zhu-Lin Hu. Clinical and pathological characteristics of intraocular cysticercosis. Korean J Parasitol. 2013;51:223-9. 8. Madigubba S, Vishwanath K, Reddy G, et al. Changing trends in ocular cysticercosis over two decades: an analysis of 118 surgically excised cysts. Indian J Med Microbiol. 2007;25:214-9. 9. Wender JD, Rathinam SR, Shaw RE, et al. Intraocular cysticercosis: case series and comprehensive review of the literature. Ocul Immunol Inflamm. 2011;19:240-5. 10. Chandra A, Singh MK, Singh VP, et al. A live cysticercosis in anterior chamber leading to glaucoma secondary to pupillary block. J Glaucoma. 2007;16:271-3. 11. Kai S, Vanathi M, Vengayil S, et al. Viscoexpression of large free floating Cysticercus cyst from the anterior chamber of the eye by double incision technique. Indian J Med Microbiol. 2008;26: 277-9. 12. Das JC, Chaudhuri Z, Bansal RL. Viscoexpression of anterior chamber cysticercus cellulosae. Indian J Ophthalmol. 2002;50: 133-5. 13. Beri S, Vajpayee RB, Dhingra N. Managing anterior chamber cysticercosis by viscoexpression: a new surgical technique. Arch Ophthalmol. 1994;112:1279-80. 14. García HH, Gonzalez AE, Evans CA, et al. Taenia solium cysticercosis. Lancet. 2003;362:547-56. Can J Ophthalmol 2014;49:e140–e141 0008-4182/14/$-see front matter & 2014 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jcjo.2014.08.011
Bilateral posterior scleritis as a presenting manifestation of giant cell arteritis: A case report
appeared in the literature.3–5 We report a case of bilateral posterior scleritis that was diagnosed in association with GCA.
Posterior scleritis is a rare and frequently misdiagnosed form of ocular inflammation that may be either idiopathic or associated with various systemic diseases. The systemic associations1 are similar to those observed in anterior scleritis and include rheumatoid arthritis, Wegener granulomatosis, systemic lupus erythematosus, systemic vasculitis, relapsing polychondritis, sarcoidosis, and other autoimmune diseases. Moreover, it may occur in isolation or associated with either anterior scleritis or anterior uveitis. Giant cell arteritis (GCA) is a systemic immune-mediated vasculitis that affects medium-sized and large arteries. GCA has a wide spectrum of clinical features related to both systemic inflammation and ischemia. The most common symptoms are headache, scalp tenderness, jaw claudication, and systemic manifestations (fever, weight loss, anorexia, and malaise). Ophthalmologic symptoms are common manifestations of GCA and may occur alone, without other symptoms of GCA. Arteritic anterior ischemic optic neuropathy (AAION) is the most common ophthalmologic manifestation. Other ocular manifestations are central or branch retinal artery occlusion and diplopia that results from ischemia of extraocular muscles or ocular motor nerves.2 A few other reports about the association of GCA with scleritis have
CASE REPORT A 93-year-old female with progressive bilateral visual loss and a 1-month history of constant headache was referred to our hospital. She had a history of systemic hypertension and coronary heart disease. At the first examination, best-corrected decimal visual acuity was 0.1 (20/200) in the right eye and 0.3 (20/63) in the left eye. Anterior segment examination and intraocular pressure were unremarkable (the patient was pseudophakic). Posterior segment examination evidenced bilateral disc swelling and bilateral serous retinal detachment involving the macular region as well as the peripheral inferior retina of the right eye. Fundus fluorescein angiography (FFA) found bilateral optic nerve leakage and vascular tortuosity (Fig. 1). B-scan ultrasonography found bilateral scleral and choroid thickening and serous retinal detachment, more evident in the right eye (Fig. 2). According to optical coherence tomography (OCT) examination, the macular region of both eyes and the right eye inferior retina were affected with serous detachment (OD4OS) (Fig. 3). Based on these findings, bilateral posterior scleritis was diagnosed.
CAN J OPHTHALMOL — VOL. 49, NO. 6, DECEMBER 2014
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