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Br J Ophthalmol 1999;83: LETTERS TO THE EDITOR Indocyanine green angiography in choroidal tuberculomas EDITOR, An 85 year old white woman presented with progressive asthenia, fever, coughing,
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Br J Ophthalmol 1999;83: LETTERS TO THE EDITOR Indocyanine green angiography in choroidal tuberculomas EDITOR, An 85 year old white woman presented with progressive asthenia, fever, coughing, and dyspnoea. Chest roentgenogram showed interstitial pulmonary infiltrates and right pleural evusion. Cultures of the bronchoalveolar lavage fluid subsequently confirmed the presence of Mycobacterium tuberculosis. On admission, best corrected visual acuity was 20/400 in a right amblyopic eye and 20/50 in the left eye. Biomicroscopic examination revealed no sign of anterior or posterior inflammation. Multiple choroidal lesions (Fig 1) were present in both eyes. choroidal lesions were deep, white-yellowish, with indistinct borders. Fluorescence angiography (FA) revealed early nodular hypofluorescence, and Figure 1 Multiple choroidal granulomas in the left posterior pole. Figure 2 (A) Early prolonged blockage and (B) late moderate hyperfluorescence of the choroidal lesions on fluorescein angiography. Figure 3 ICG angiograms reveal early (A) and late (B) phase blockage by the choroidal granulomas. late moderate hyperfluorescence (Fig 2). Indocyanine green (ICG) angiography revealed prolonged hypofluorescence and in the late stage images, moderate delineation of the lesions by a peripheral hyperfluorescent ring (Fig 3). Ocular tuberculosis may occur by haematogenic spread from a pulmonary focus. Choroidal tuberculomas are rare ophthalmic findings even in miliary tuberculosis. 1 Previous reports indicate that these lesions have prolonged hypofluorescence in FA, and late mild hyperfluorescence. 23 Only one description of ICG angiography in a case with presumed ocular tuberculosis has been reported previously in the literature. 4 We found similar angiographic characteristics in our case, which represents, to our knowledge, the first ICG angiography description of multiple choroidal tuberculomas in microbiologically confirmed miliary tuberculosis.hypofluorescence in ICG images may be due to a masking evect of the choroidal vessels by the overlying granulomas. Ophthalmic examination may be contributive when disseminated tuberculosis is suspected. In this case ICG angiography, which was performed to assess the choroidal involvement, showed prolonged hypofluorescence. DAN MILEA CHRISTINE FARDEAU LIVIA LUMBROSO Department of Ophthalmology, Hôpital de la Pitié-Salpêtrière, Paris, France THOMAS SIMILOWSKI Department of Respiratory and Intensive Care Medecine, Hôpital de la Pitié-Salpêtrière, Paris, France PHUC LEHOANG Department of Ophthalmology, Hôpital de la Pitié-Salpêtrière, Paris, France Correspondence to: Phuc Le Hoang, MD, Service d Ophtalmologie, Hôpital de la Pitié-Salpêtrière, Boulevard de l Hôpital, Paris Cedex 13, France. Accepted for publication 3 December Helm C, Holland GN. Ocular tuberculosis. Surv Ophthalmol 1993;38: Espinasse MA, Perrenoud F, Gaudric A, et al. A propos de deux cas de tubercules de Bouchut (étude angiographique). Bull Soc Ophtalmol Fr 1984;5: Grewal A, Kim R, Cunningham ET. Miliary tuberculosis. Arch Ophthalmol 1998;116: Berinstein DM, Gentile RC, McCormick SA, et al. Primary choroidal tuberculoma. Arch Ophthalmol 1997;115: Diagnosis of an atypical case of ocular toxoplasmosis using the demonstration of intraocular antibody production and the polymerase chain reaction EDITOR, Ocular toxoplasmosis is the most frequent infectious cause of chorioretinal inflammation in immunocompetent individuals. 1 Diagnosis is usually made by observing the typical fundus lesion, by detecting the presence of anti-toxoplasma antibodies in the serum, and by excluding other causes of necrotising fundus lesions. 2 In unusual cases, invasive procedures may be required to aid diagnosis. 3 A 17 year old white male presented complaining of floaters and reduced visual acuity in the left eye. Visual acuity was 6/9 in the left eye, 6/6 in the right. Examination revealed moderate anterior chamber activity, marked vitritis, and an active retinochoroiditis adjacent to an area of old chorioretinal scarring inferonasal to the optic disc. A diagnosis of ocular toxoplasmosis was suspected, and topical and oral steroids, and oral clindamycin were commenced. Peripheral blood anti-toxoplasma IgG antibodies, measured using the dye test, were positive (16 IU/ml). Despite treatment, the ocular inflammatory signs increased and 5 weeks following initial presentation he developed a confluent area of retinal necrosis in the peripheral retina leading to a superotemporal retinal detachment. This was distinct from the original area of inflammation. presence of severe vitreous inflammation and peripheral retinal necrosis suggested a unilateral acute retinal necrosis syndrome. 4 Three port trans pars plana vitrectomy with perfluorocarbon liquid and fluid/silicone exchange was performed. At vitrectomy, vitreous humour was taken for anti-toxoplasma and antiviral antibody levels and a retinal biopsy was also obtained. Postoperatively, he was commenced on sulphadiazine, pyrimethamine, and folinic acid and continued on oral steroid medication. Levels of IgG, IgA, and IgM were measured in serum and vitreous aspirate at the same time. Goldmann Witmer coefficient using IgG was greater than 59, using IgA greater than 45, and using IgM greater than 65. This is evidence of intraocular antibody production. Samples were negative for antiviral antibodies. Intraocular Toxoplasma DNA was demonstrated by a polymerase chain reaction (PCR) assay using primers for the P30 gene. PCR testing for viral DNA was negative. InsuYcient material was obtained to attempt to isolate the parasite using tissue culture or animal inoculation. Retinal biopsy demonstrated a mixed inflammatory response without a specific infective agent. patient subsequently responded to treatment and the intraocular inflammatory signs subsided. 754 Letters Ocular toxoplasmosis is a common cause of retinochoroiditis, and can usually be diagnosed clinically. Rarely is it possible to obtain vitreous and retinal biopsies to aid diagnosis, but in doubtful cases, it may be appropriate to perform anterior or posterior chamber aspirate to confirm the diagnosis. assessment of Toxoplasma antibodies in serum is of limited use, unless rising titres can be demonstrated, since the incidence of Toxoplasma infection in the general population is high. demonstration of antibody production within the eye is particularly valuable in the diagnosis of difficult cases. finding of higher anti- Toxoplasma antibody levels in the aqueous humour than in the serum (the Goldmann Witmer coeycient) indicates intraocular antibody production. 5 A further investigation which is extremely useful is the demonstration of parasite DNA within ocular fluid by PCR. 6 With PCR a sequence of DNA is amplified from minuscule amounts of DNA making it amenable to direct analysis. 78 De Boer et al used a combination of the demonstration of intraocular antibody production and PCR analysis in the diagnosis of a variety of infectious uveitis cases. 9 In this case we initially made a diagnosis of ocular toxoplasmosis, but the disease progressed clinically and did not respond to treatment. patient was compliant with prescribed medication, and had no evidence of immunocompromise. Retinal detachment is unusual in ocular toxoplasmosis, 10 but is typical of acute retinal necrosis syndrome, suggesting an alternative diagnosis in this case. We were, however, able to confirm the diagnosis of toxoplasmosis by evidence of intraocular antibody production and by positive PCR amplification. M MINIHAN P E CLEARY Department of Ophthalmology, Cork University Hospital and University College, Cork BCRYAN Department of Medical Microbiology, Cork University Hospital and University College, Cork R HOLLIMAN Toxoplasma Reference Unit, Public Health Laboratory, St George s Hospital, Blackshaw Road, London Correspondence to: Ms Minihan. Accepted for publication 9 December Henderly DE, Gentsler AJ, Smith RE, et al. Changing patterns of uveitis. Am J Ophthalmol 1987;103: Rothova A. Ocular involvement in toxoplasmosis. Br J Ophthalmol 1993;77: Nussenblatt RB, Belfort R. Ocular toxoplasmosis. An old disease revisisited. JAMA 1994;271: Holland GN and the Executive Committee of the American Uveitis Society. Standard diagnostic criteria for the acute retinal necrosis syndrome. Am J Ophthalmol 1994;117: Desmonts G. Definitive serological diagnosis of ocular toxoplasmosis. Arch Ophthalmol 1966;76: Holliman RE, Stevens PJ, DuVy KT,et al. serological investigation of ocular toxoplasmosis. Br J Ophthalmol 1991;75: Kijlstra A, Luyendjik L, Baarsma GS, et al. Aqueous humor analysis as a diagnostic tool in toxoplasma uveitis. Int Ophthalmol 1989;6: Chan C, Palestine AG, Li Q, et al. Diagnosis of ocular toxoplasmosis by the use of immunocytology and the polymerase chain reaction. Am J Ophthalmol 1996;117: De Boer JH, Verhagen C, Bruinenberg M, et al. Serologic and polymerase chain reaction analysis of intraocular fluids in the diagnosis of infectious uveitis. Am J Ophthalmol 1996;121: De Boer JH, Luyendijk L, Rothova A, et al. Detection of intraocular antibody production to herpesviruses in acute retinal necrosis syndrome. Am J Ophthalmol 1994;117: Protein C and protein S deficiency associated with retinal, optic nerve, and cerebral ischaemia EDITOR, Deficiencies in the vitamin K dependent factors protein C and protein S can lead to arterial or venous thrombosis. Branch and central retinal arterial and venous occlusions 1 4 have been associated with deficiencies in these plasma proteins, as have amaurosis fugax 5 and stroke. 6 We report, to the best of our knowledge, the first case of ischaemic optic neuropathy associated with combined protein C and protein S deficiency. A 47 year old woman with non-insulin dependent diabetes mellitus with documented absence of previous retinopathy presented with blurring of vision and bright flashing lights in her right eye for 2 weeks, associated with vague periocular discomfort and left sided facial and leg numbness. Best corrected visual acuity was 20/30 right eye and 20/25 left eye. anterior segment examination was unremarkable and the intraocular pressures were 15 mm Hg right eye and 14 mm Hg left eye. A large cotton wool spot was present inferotemporal to the right optic disc (Fig 1). overlying vitreous was clear. retinal venules appeared moderately tortuous but undilated. Fluorescein angiography revealed normal arterial filling but markedly delayed arteriovenous filling and late disc hyperfluorescence. When she returned 2 weeks later, this cotton wool spot was smaller, but other cotton wool spots superior to the disc had appeared (Fig 2). patient underwent carotid Doppler and cerebral angiography studies which revealed near complete occlusion of the right internal carotid artery. Coumadin therapy was instituted and extensive diagnostic evaluation was pursued. She returned 2 weeks later and all the cotton wool spots were resolving. Three days later she was admitted to the hospital with syncope and left hemiparesis due to an infarct in the territory of the right middle cerebral artery. She also suvered sudden, Figure 1 Initial large cotton wool spot inferotemporal to right optic disc. Figure 2 Initial cotton wool spot along the inferotemporal vessel resolving 2 weeks later with appearance of new cotton wool spots superiorly. Figure 3 Six weeks after initial presentation. Note pale disc with narrowing of the retinal arterioles and an overall reduction in venous calibre and tortuosity. painless loss of vision to the level of hand movements in the right eye. Fundus examination 6 weeks later revealed a pale optic disc with both generalised and focal narrowing of the retinal arterioles, and an overall reduction in venous calibre and tortuosity (Fig 3). Three months later, at which time the visual acuity remained at hand movements, electroretinography (ERG) was performed to distinguish retinal vascular pathology from optic nerve embarrassment. right eye exhibited modest reductions in scotopic b-wave amplitudes in response to dim white flash (33%) and to bright white flash (20%) compared with the left eye. Cone b-wave implicit time on 30 Hz flicker testing was only slightly longer in the right eye compared with the left eye (30.5 ms versus 29.5 ms). Oscillatory potential amplitudes were normal in both eyes. se results were interpreted as showing insuycient evidence for ischaemic retinal damage as an explanation for her profound loss of vision. patient was diagnosed with ischaemic optic neuropathy in the right eye based on clinical findings and the ERG results. Laboratory testing revealed that protein C antigen was 47% and protein S antigen 46% of normal levels. Activated protein C and antithrombin levels were normal, and no lupus anticoagulant activity was detected. This patient, with combined protein C and protein S deficiency, suvered ipsilateral retinal, optic nerve, and cerebral ischaemia within a period of 6 weeks. rapid changes in the appearance of cotton wool spots over a period of several days, which is not consistent with their natural course in diabetic retinopathy, 7 combined with neurological symptoms prompted us to search for systemic causes of ischaemia, including evaluation for hypercoagulable states. We suggest that new cotton wool spots in a patient free of other signs of vascular retinopathy such as microaneurysms or retinal haemorrhages should raise the spectre of a systemic basis for the ischaemia. As the ERG was not compatible with occlusion of the ophthalmic or central retinal arteries, demonstrating only mild retinal ischaemia, we ascribed the sudden visual loss in the face of divuse disc pallor to optic nerve ischaemia, perhaps from occlusion of multiple ciliary vessels. Ischaemic optic neuropathy has, to our knowledge, not previously been associated with protein C or protein S deficiency, and expands the spectrum of ophthalmic manifestations of the hypercoagulable state. Supported, in part, by the Heed Ophthalmic Foundation (Dr Ambati) and an unrestricted grant from Research to Prevent Blindness, Inc, New York, NY (University of Rochester), USA. JAYAKRISHNA AMBATI Letters 755 OMAR E HANUCH GEORGE H BRESNICK Department of Ophthalmology, University of Rochester School of Medicine and Dentistry, Rochester, USA Correspondence to: Dr J Ambati, Retina Service, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114, USA. Accepted for publication 11 December Nelson ME, Talbot JF, Preston FE. Recurrent multiple-branch retinal arteriolar occlusions in a patient with protein C deficiency. Graefes Arch Clin Exp Ophthalmol 1989;227: Greven CM, Weaver RG, Owen J, et al. Protein S deficiency and bilateral branch retinal artery occlusion. Ophthalmology 1991;98: Golub BM, Sibony PA, Coller BS. Protein S deficiency associated with central retinal artery occlusion. Arch Ophthalmol 1990;108: Chung MM, Trese MT, Hong YJ. Protein C levels in retinal vein occlusions. Invest Ophthalmol Vis Sci 1989;30: Smith DB, Ens GE. Protein C deficiency: a cause of amaurosis fugax. J Neurol Neurosurg Psychiatry 1987;50: Martinez HR, Rangel-Guerra RA, Marfil LJ. Ischemic stroke due to deficiency of coagulation inhibitors. Report of 10 young adults. Stroke 1993;24: Kohner EM, Dollery CT, Bulpitt CJ. Cottonwool spots in diabetic retinopathy. Diabetes 1969;18: Macular hole following YAG capsulotomy EDITOR, Since the initial identification of macular holes as pathological entities in the middle of the 19th century, 1 there has been an evolution in the understanding of their aetiology. Tangential macular traction by perifoveal vitreous cortex is now accepted as the causative factor in the development of idiopathic macular holes. 23 With the widespread use of extracapsular cataract extraction procedures, posterior capsule opacification is a frequent complication. YAG laser capsulotomy, although a noninvasive procedure, has been associated with a number of complications, including retinal detachment, cystoid macular oedema, and raised intraocular pressure (IOP). 45 A much rarer complication of YAG capsulotomy herein reported is the formation of a macular hole after YAG capsulotomy. 4 A 71 year old woman underwent an uncomplicated extracapsular cataract extraction with posterior chamber lens implantation in her left eye. Her ocular history was significant for chronic open angle glaucoma. In the immediate postoperative period, there was an acute rise in IOP to 40 mm Hg that responded to Diamox (acetazolamide) orally. Three months postoperatively, best corrected visual acuity was 20/20 in both eyes with IOPs of 17 mm Hg in the right eye and 13 mm Hg in the left. Two years later, the best corrected visual acuity was found to have decreased to 20/80 in the left eye attributable to significant posterior capsule opacification. Posterior capsulotomy was performed with a Nd:YAG laser (4.1 mj/pulse, total energy mj). Postoperatively, there was no increase in IOP and no vitreous prolapse into the anterior chamber. Two weeks after the Nd:YAG laser capsulotomy, the patient noted a decrease in visual acuity, along with a black spot in her central vision. On examination, a stage 3 macular hole was seen with best corrected visual acuity 20/400 left eye. Retinal consultation confirmed the diagnosis and the patient underwent a pars plana vitrectomy, with C 3 F 8 gas instillation and facedown positioning. Evaluation of the patient 4 weeks after surgery revealed an improvement of visual acuity in the left eye to the level of 20/25. Visual acuity 6 months after surgery remained at the level of 20/25 with the macular hole closed. most common complication of extracapsular methods is a late opacification of the posterior capsule. Surgically opening the posterior capsule has been shown in several studies to increase the incidence of both cystoid macular oedema and retinal detachment. 45 With the advent of the Nd:YAG laser, the ease of posterior capsulotomy has been greatly simplified. Retinal complications following YAG laser capsulotomy are well documented. 45 Winslow and Taylor 4 reported one retinal flap, two macular holes, six cases of cystoid macular oedema, and 10 retinal detachments following YAG laser capsulotomy. In this series, macular hole formation occurred 1 and 3 months after capsulotomy while in our case it occurred within 2 weeks. Over the years, several mechanisms have been proposed to explain the increased incidence of retinal complications following posterior capsulotomy including increased vitreous liquefaction, changes in vitreous composition, acoustic transients, and direct retinal damage. Osterlin 6 reported a greater decline in the hyaluronic acid content in vitreous samples from monkey eyes having undergone intracapsular cataract extraction as opposed to extracapsular cataract extraction. He postulated that in the eyes that had undergone intracapsular cataract extraction, hyaluronic acid in the vitreous had divused anteriorly, resulting in the vitreous instability and subsequent retinal complications. Thus, the intact capsule acts as a divusion barrier for hyaluronic acid. This concept of a divusion barrier was again employed by Miyake 7 to theorise a role for the posterior capsule in the development of cystoid macular oedema due to iris synthesised prostaglandins. Significant liquefaction of the vitreous, postulated to be the result of acoustic transients accompanying the laser irradiation, has been documented in monkey and rabbit eyes following Nd:YAG laser irradiation of the posterior capsule. 8 Other more direct injuries to the retina with the formation of macular holes have been reported in industrial accidents involving the Nd:YAG laser. 9 In a case report by Blacharski and Newsome, 10 bilateral macular holes were reported following Nd:YAG laser posterior capsulotomies. In the first eye, a macular hole formed 21 days after capsulotomy in the absence of vitreous pro
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