Table of Contents
Welcome
Table of Contents
Title Page
BENTHAM SCIENCE PUBLISHERS LTD.
End User License Agreement (for non-institutional, personal use)
Usage Rules:
Disclaimer:
Limitation of Liability:
General:
PREFACE
ACKNOWLEDGEMENTS
DEDICATION
CONFLICT OF INTEREST
List of Contributors
Ocular Toxoplasmosis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Ocular Tuberculosis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Cytomegalovirus Retinitis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Necrotizing Herpetic Retinopathies
ACUTE RETINAL NECROSIS: ESSENTIALS OF DIAGNOSIS
MANAGEMENT
PROGRESSIVE OUTER RETINAL NECROSIS: ESSENTIALS OF DIAGNOSIS
MANAGEMENT
DIFFERENTIAL DIAGNOSIS
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Ocular Syphilis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
References
HIV-Related Retinal Microangiopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
References
Neuroretinitis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Endophthalmitis
ESSENTIALS OF DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
References
Acute Posterior Multifocal Placoid Pigment Epitheliopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Multiple Evanescent White Dot Syndrome
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFRENCES
Multifocal Choroiditis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Punctate Inner Choroidopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Birdshot Retinochoroidopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Serpiginous Choroiditis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Diffuse Subretinal Fibrosis Syndrome
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Diffuse Unilateral Subacute Neuroretinitis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Vogt Koyanagi Harada Disease
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Pars Planitis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Sarcoidosis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS (Posterior uveitis)
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Retinoblastoma
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Cavernous Hemangioma of the Retina
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Von Hippel-Lindau Disease
Essentials of Diagnosis
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Astrocytoma Tuberous Sclerosis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Retinal Vasoproliferative Tumor
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Melanocytoma
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
References
Congenital Hypertrophy of the Retinal Pigment Epithelium
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Combined Hamartoma of Retina and Retinal Pigment Epithelium
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Choroidal Nevi
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Choroidal Melanoma
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Choroidal Metastasis
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Leukemic Retinopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Primary Intraocular Lymphoma
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Idiopathic Uveal Effusion
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Hypotony Maculopathy
ESSENTIALS OF DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
REFERENCES
Pregnancy-associated Retinal Diseases
HYPERTENSION: PRE-ECLAMPSIA AND ECLAMPSIA
DIABETIC RETINOPATHY
CENTRAL SEROUS CHORIORETINOPATHY
PRERETINAL OR RETROHYALOID HEMORRHAGES
UVEAL MELANOMA
CHANGES IN BLOOD COAGULATION
OTHER CAUSES FOR BLINDNESS OR SEVERE LOSS OF VISION
CONFLICT OF INTEREST
ACKNOWLEDGEMENTS
Ophthalmology:
Current and Future Developments
(Volume 3)
(Diagnostic Atlas of Retinal Diseases)
Edited by
Mitzy E. Torres Soriano
Unidad Oftalmológica “Dr. Torres López” Centro Médico, Cagua,
Aragua, Venezuela
Gerardo García Aguirre
Asociación para Evitar la Ceguera en Mexico,
Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey,
Mexico City, Mexico
Co-Edited by
Maximiliano Gordon
Centro de la Visión Gordon Manavella,
Rosario, Santa Fe, Argentina
Veronica Kon Graversen
University of North Carolina at Chapel Hill,
Chapel Hill, NC, USA
BENTHAM SCIENCE PUBLISHERS LTD.
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PREFACE
We are honored to contribute to the information and education of ophthalmology stu-dents around the world. We have attempted to distill the current knowledge of medical practice and basic science retina research into a diagnostic atlas of retinal diseases. This is a quick-reference atlas eBook of the retina, edited by specialists in the field, essential to any practicing ophthalmologist or resident who has more than a passing interest in diseases and treatment of the retina.
This e-book includes contributors from Mexico, Venezuela, Argentina, Brazil, United States, Denmark, Spain, Italy, Costa Rica and Peru. It is divided into three volumes: Volume I, retinal vascular diseases, choroidal neovascularization related diseases, vitreomacular interface, and other macular disorders; Volume II, traumatic retinopathies, diseases of vitreous, peripheral degenerations, retinal detachment, pediatric retinal diseases, and retinal dystrophies; and Volume III, posterior uveitis, tumors of the retina, and choroid.
This diagnostic atlas eBook of retinal diseases contains full-color, high quality images of the most frequent retinal pathologies with a brief and comprehensive review of retinal diseases. Each chap-ter includes essentials of diagnosis, differential diagnosis and treatment. The format is concise, well organized, and didactic, without being exhaustive.
We hope and expect that our atlas of retina will facilitate in providing patients with the best pos-sible care.
ACKNOWLEDGEMENTS
We would like to express our gratitude to Judy Soriano, who provided support with english composition and edition.
To our friends and colleagues without whose contribution would not have been possible to real-ize this project.
We also want to thank the staff of Bentham Science for their help and support and give us the opportunity to publish this eBook.
DEDICATION
This e-book is specially dedicated to Guillermo Manuel Gordon, MD. He inspired us to always work hard and try our best. He was a friend and a recognized ophthalmologist of Rosario-Argentina, who died on May 2nd, 2015.
CONFLICT OF INTEREST
The authors confirm that they have no conflict of interest to declare for this publication.
Dr. Mitzy E. Torres Soriano
Unidad Oftalmológica “Dr. Torres López”,
Centro Médico Cagua,
Cagua, Aragua
Venezuela
Retina Department, Ophthalmology Service,
Hospital Provincial del Centenario,
Rosario, Santa Fe,
ArgentinaDr. Gerardo García Aguirre
Retina Department,
Asociación para Evitar la Ceguera en Mexico,
Mexico City,
Mexico
Escuela de Medicina,
Tecnológico de Monterrey,
Mexico City,
MexicoDr. Maximiliano Gordon
Centro de la Visión Gordon Manavella,
Rosario, Santa Fe,
ArgentinaDr. Veronica Kon Graversen
List of Contributors
José Antonio Unzueta MedinaOphthalmology Department, Hospital Angeles Chihuahua, Chihuahua, MexicoEduardo Torres PorrasOphthalmology Department, Hospital Angeles Chihuahua, Chihuahua, MexicoReinaldo Garcia A.Retina & Vitreous Service, Clínica Oftalmológica El Viñedo, Valencia, Venezuela
Ophthalmology Department, Hospital Cristus Muguerza UPAEP, Puebla, Mexico
The Retina Division, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA
The King Khaled Eye Specialist Hospital, Riyadh, Kingdom of, Saudi Arabia
The Neurophthalmology unit “Dr. Rafael Muci Mendoza”, Hospital J. M. Vargas, Caracas, VenezuelaAndrée Henaine BerraHospital General “Dr. Manuel Gea González”, Mexico City, MexicoLourdes ArellanesUveitis Department, Asociación para evitar la Ceguera, Hospital Dr. Luis Sánchez Bulnes IAP, Mexico City, MexicoClaudia RecillasOphthalmology Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, MexicoClaudia RecillasChief of Ophthalmology Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, MexicoGerardo García-AguirreRetina Department, Asociación para Evitar la Ceguera en México, and School of Medicine, Instituto Tecnológico y de Estudios Superiores de Monterrey, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoEzequiel RosendiRetina and Vitreous Department, Hospital de Alta Complejidad El Cruce, Buenos Aires, ArgentinaCecilia MariniCornea and Ocular Surface Department, Hospital de Alta Complejidad El Cruce, Buenos Aires, ArgentinaRicardo BrunziniConsultorio Brunzini, Buenos Aires, ArgentinaMaximiliano GordonCentro de la Visión Gordon-Manavella, Rosario, ArgentinaLuciana GarcíaCentro de la Visión Gordon-Manavella, Rosario, Santa Fe, Argentina
Oftalmofunes, Funes, Santa Fe, ArgentinaAriel SchlaenHospital Universitario Austral, Buenos Aires, ArgentinaAmina L. ChaudhryNorthwestern University, Chicago, IL 60208, USAAmina L. ChaudhryNorthwestern University, Chicago, IL 60208, USAAriel SchlaenHospital Universitario Austral, Buenos Aires, ArgentinaRafael CortezCentro de Cirugía Oftalmológica (CECOF), Caracas, VenezuelaAndrée Henaine BerraHospital General “Dr. Manuel Gea González”, Mexico City, MexicoAntonio Marcelo Barbante CasellaUniversidad Estatal de Londrina, Rodovia Celso Garcia Cid, Km 380, s/n - Campus Universitario, Londrina - PR, 86057-970, BrazilLourdes ArellanesUveitis Department, Asociación para evitar la Ceguera, Hospital Dr. Luis Sánchez Bulnes IAP, Mexico City, MexicoGerardo García-AguirreRetina Department, Asociación para Evitar la Ceguera en México, and School of Medicine, Instituto Tecnológico y de Estudios Superiores de Monterrey, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoVeronica Kon GraversenOphthalmology Department, University of North Carolina at Chapel Hill, NC, USAMaría Ana Martínez-CastellanosRetina Service, Asociación para Evitar la Ceguera en México, Mexico City, Mexico
Hospital Luis Sanchez Bulnes IAP, Mexico City, MexicoGerardo García-AguirreRetina Department, Asociación para Evitar la Ceguera en Mexico, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoGabriela LópezcarasaOphthalmology Department, Hospital Angeles Lomas, Mexico City, MexicoNoel Millán MorenoInstituto de Especialidades Oftalmológicas del Centro (IDEOF), Maracay, Venezuela
Centro Oftalmológico Regional Aragua (CORA), Maracay, VenezuelaGerardo García-AguirreRetina Department, Asociación para Evitar la Ceguera en Mexico, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoGerardo García-AguirreAttending Physician, Retina Department, Asociación para Evitar la Ceguera en Mexico, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoAndrée Henaine-BerraHospital General “Dr. Manuel Gea González”, Mexico City, MexicoRaul Velez MontoyaAssistant Professor. Retina Department, Asociación para Evitar la Ceguera en México, AIP, Mexico City, Mexico
Escuela de Medicina, Tecnológico de Monterrey, Mexico City, MexicoMaximiliano GordonCentro de la Visión Gordon- Manavella, Rosario, Argentina
Hospital Provincial del Centenario, Rosario, ArgentinaMiguel MaterinAssociate Professor of Ophthalmology and Director of Ophthalmic Oncology Program, Smilow Cancer Hospital at Yale, New Haven, USA
Department of Ophthalmology and Visual Science at Yale University, School of Medicine, New Haven, USAMaximiliano GordonRetina Department, Centro de la Visión Gordon-Manavella, Rosario, Argentina
Ophthalmology Department, Hospital Provincial del Centenario, Rosario, ArgentinaDaniel Moreno PáramoOphthalmology Department, Hospital General de Mexico, Mexico City, MexicoJennifer F. WilliamsonDepartment of Ophthalmology, University of North Carolina, Chapel Hill, NC, USADaniel Moreno PáramoOphthalmology Department, Hospital General de Mexico, Mexico City, MexicoAmina L. ChaudhryNorthwestern University, Chicago, IL 60208, USAAlberto ZambranoFundación Zambrano, Buenos Aires, ArgentinaAlberto ZambranoFundación Zambrano, Buenos Aires, ArgentinaNaty C. Torres SorianoCentro Médico Cagua, Unidad Oftalmológica “Dr. Torres López”, Cagua-Aragua, Venezuela
Ophthalmology Department, Hospital Central de Maracay, Maracay, VenezuelaMitzy E. Torres SorianoCentro Médico Cagua, Unidad Oftalmológica “Dr. Torres López”, Cagua-Aragua, Venezuela
Centro de la Visión Gordon-Manavella, Rosario, Argentina
Ocular Toxoplasmosis
Ocular toxoplasmosis is caused by the protozoan parasite Toxoplasma gondii. Infections may be acquired congenitally or through the ingestion of infected raw meat, contaminated vegetables or water. A significant proportion of the world population (approximately the third) is infected by T. gondii which is responsible for the majority of infectious uveitis cases, which in some countries might be up to 50%. It is the main cause of infectious posterior in immunocompetent individuals, and the second most common in patients with HIV/AIDS [1 - 3].
ESSENTIALS OF DIAGNOSIS
Clinical presentation in immunocompetent individuals varies according to the age of the patient and the size, location and severity of the retinochoroidal lesions. Symptoms usually include floaters and decreased visual acuity, which may be secondary to vitreous inflammation or to macular involvement. In immuno-compromised patients, the presentation may vary [4].
The disease may result from congenitally acquired toxoplasmosis or newly acquired infection. Toxoplasmosis usually affects a single eye, causing one or more lesions. Sometimes, lesions in different stages may be observed in the same eye (Fig. 1) [4 - 6].
Typical active lesions appear as yellowish or whitish areas of retinal inflammation (Fig. 2), with adjacent choroiditis, vasculitis, papillitis (Fig. 3), hemorrhage and vitritis. The primary infection occurs in the retina, but other structures such as the choroid, vitreous or anterior chamber may be involved. After the active phase, there is atrophy of the retina and the choroid that leaves a well-circumscribed round punched-out scar (Fig. 4). There is pigment clumping and chorioretinal atrophy that allows the visualization of underlying sclera.
Fig. (1))
The acute lesion is seen often contiguous to an old pigmented scar (Image courtesy of Naty C. Torres Soriano MD, Venezuela).
Toxoplasmosis may present atypically, causing punctate outer retinal toxoplasmosis, retinal vasculitis, retinal vascular occlusions, rhegmatogenous or serous retinal detachments, unilateral pigmentary retinopathy, neuroretinitis and additional forms of optic neuropathy, peripheral retinal necrosis and scleritis. Ocular complications, seen more frequently in children, include choroidal neovascularization, cataract, glaucoma, optic nerve atrophy and retinal detachment [4 - 6].
Fig. (2))
Acute toxoplasmosis presents grayish inflammatory infiltrate within retinal and subretinal tissue.
Fig. (3))
The arrow allows observation of optic disc inflammation (Courtesy of Mitzy E. Torres Soriano, MD).
Fig. (4))
Macular scar secondary to congenital ocular toxoplasmosis (Courtesy of Manuel Torres López MD, Venezuela).
The diagnosis of ocular toxoplasmosis is usually clinical, since presentation is usually typical [7]. There is no reliable diagnostic test to identify toxoplasmic uveitis. Positivity of anti-T gondii IgG antibodies does not confirm the toxoplasmic etiology, but a negative IgG generally discards the possibility. Positivity of these antibodies usually persist for many years after the primary infection. Other diagnostic tool is looking for the presence of T. gondii DNA in the vitreous using polymerase chain reaction, which is especially useful in eyes with atypical presentation [4].
DIFFERENTIAL DIAGNOSIS
Diseases that cause focal retinitis should be considered in the differential diagnosis, such as CMV, herpes simplex virus, herpes zoster virus, fungal retinitis (candidiasis, blastomycosis), septic retinitis, ocular toxocariasis, sarcoidosis, syphilis and tuberculosis. Punctate outer retinal toxoplasmosis should be differentiated from the white dot syndromes [4].
MANAGEMENT
Although ocular toxoplasmosis is usually self-limited, treatment should be initiated as soon as the diagnosis is made in order to avoid scarring, which is the usual cause of long-term visual impairment [8]. The treatment of choice is the combination of systemic antimicrobial drugs and corticosteroids. Antimicrobial agents used most frequently include trimethoprim and sulfamethoxazole, sulfadiazine and pyrimethamine or clindamycin and sulfadiazine [4, 9]. Oral prednisolone (1 mg/kg daily) is started at the third day of treatment and tapered over two to six weeks [7, 10, 11]. Intravitreal clindamycin injection and possibly steroids may be indicated for patients that have contraindication for systemic therapy specific for toxoplasmosis [12]. Treatment with spiramycin should be initiated immediately after diagnosis of recently acquired maternal infection [4].
CONFLICT OF INTEREST
The author confirms that author has no conflict of interest to declare for this publication.
ACKNOWLEDGEMENTS
Declared none.
REFERENCES
[1]Soheilian M., Heidari K., Yazdani S., Shahsavari M., Ahmadieh H., Dehghan M.. Patterns of uveitis in a tertiary eye care center in Iran., Ocul. Immunol. Inflamm..2004; 12(4): 297-310.
[http://dx.doi.org/10.1080/092739490500174] [PMID: 15621869][2]Perkins E.S.. Ocular toxoplasmosis., Br. J. Ophthalmol..1973; 57(1): 1-17.
[http://dx.doi.org/10.1136/bjo.57.1.1] [PMID: 4574554][3]Burnett A.J., Shortt S.G., Isaac-Renton J., King A., Werker D., Bowie W.R.. Multiple cases of acquired toxoplasmosis retinitis presenting in an outbreak., Ophthalmology.1998; 105(6): 1032-1037.
[http://dx.doi.org/10.1016/S0161-6420(98)96004-3] [PMID: 9627653][4]Da Mata A.P., Orifice F.. , ; Toxoplasmosis.. In: Foster C.F., Vitale A.T., editors. Diagnosis and treatment of uveitis.. Philadelphia: Saunders; 2002.[5]Mets M.B., Holfels E., Boyer K.M., Swisher C.N., Roizen N., Stein L., Stein M., Hopkins J., Withers S., Mack D., Luciano R., Patel D., Remington J.S., Meier P., McLeod R.. Eye manifestations of congenital toxoplasmosis., Am. J. Ophthalmol..1996; 122(3): 309-324.
[http://dx.doi.org/10.1016/S0002-9394(14)72057-4] [PMID: 8794703][6]La Hey E., Rothova A., Baarsma G.S., de Vries J., van Knapen F., Kijlstra A.. Fuchs heterochromic iridocyclitis is not associated with ocular toxoplasmosis., Arch. Ophthalmol..1992; 110(6): 806-811.
[http://dx.doi.org/10.1001/archopht.1992.01080180078032] [PMID: 1596229][7]Dodds E.. , . Focal points: Clinical Modules for ophthalmologists.. Vol. XVII. San Francisco: American Academy of Ophthalmology; 1999. Ocular toxoplasmosis: clinical presentation, diagnosis and therapy..[8]Bosch-Driessen L.E., Berendschot T.T., Ongkosuwito J.V., Rothova A.. Ocular toxoplasmosis: clinical features and prognosis of 154 patients., Ophthalmology.2002; 109(5): 869-878.
[http://dx.doi.org/10.1016/S0161-6420(02)00990-9] [PMID: 11986090][9]Nussenbleatt R.B., Whitcup S.M.. , . Uveitis. Fundamentals and Clinical Practice.. 3rd ed. St. Louis: Mosby; 2004.[10]Rothova A., Meenken C., Buitenhuis H.J., Brinkman C.J., Baarsma G.S., Boen-Tan T.N., de Jong P.T., Klaassen-Broekema N., Schweitzer C.M., Timmerman Z., et al. Therapy for ocular toxoplasmosis., Am. J. Ophthalmol..1993; 115(4): 517-523.
[http://dx.doi.org/10.1016/S0002-9394(14)74456-3] [PMID: 8470726][11]Holland G.N., O’Connor R., Belfort R., Remington J.S.. , . Toxoplasmosis.. St. Louis: Mosby Year Book; 1996.[12]Lasave A.F., Díaz-Llopis M., Muccioli C., Belfort R. Jr, Arevalo J.F.. Intravitreal clindamycin and dexamethasone for zone 1 toxoplasmic retinochoroiditis at twenty-four months., Ophthalmology.2010; 117(9): 1831-1838.
[http://dx.doi.org/10.1016/j.ophtha.2010.01.028] [PMID: 20471684]
Ocular Tuberculosis
Tuberculosis (TB) is a clinical disease caused by infection with Mycobacterium tuberculosis and is characterized pathologically by granuloma formation [1]. TB may affect the eye by direct invasion of the tubercle bacillus following hematogenous dissemination, or via a hypersensitivity reaction to the bacillus located elsewhere in the body [2].
Ocular TB is not common; since the 1980’s, it is considered as an etiology of uveitis from 0-4%.
Ocular TB may not be associated with clinical evidence of pulmonary TB; up to 60% of patients with extrapulmonary TB may not have been diagnosed with pulmonary TB [3, 4].
ESSENTIALS OF DIAGNOSIS
Extraocular TB can appear on the external eye as a lid abscess or manifest as chronic blepharitis or atypical chalazia. It can present as a mucopurulent conjunctivitis with regional lymphadenopathy. It can also present as a phlyctenule (an inflammatory nodule at the junction of the cornea and sclera), infectious keratitis, interstitial keratitis, or as an infectious scleritis. Rarely, the orbital disease can also occur [4] (Fig. 1). All of these presentations are rare and are easy to diagnose as material can be obtained for culture and biopsy [2 - 7].
Fig. (1))
(Garcia et al.). A) Right orbital syndrome “frozen orbit” with proptosis and mucopurulent conjunctivitis by direct invasion of the tubercle bacillus following haematogenous dissemination. B) Miliary tuberculosis is uncommon but carries a poor prognosis. It represents haematogeneous dissemination of an uncontrolled tuberculous infection. Miliary deposits appear as 1-3 mm diameter nodules, which are uniform in size and uniformly distributed. C-D) Computed tomographic scan of the head, showing a lesion in the superolateral part of the right orbit with extension into the orbital fissure and soft tissues without bony erosion. E) Histopathology showing chronic granulomatous inflammation with giant cells and caseation necrosis. (H&E).
Intraocular TB often involves delicate structures that are difficult or impossible to biopsy or culture. It may present as unilateral or bilateral granulomatous iritis or iridocyclitis with mutton-fat keratic precipitates and/or granulomatous nodules of the iris (Koeppe or Busacca nodules). Broad-based posterior synechiae and hypopyon may be observed. Intermediate uveitis can also occur. More commonly, intraocular TB presents with involvement of the posterior part of the eye. Vitritis, retinitis and/or choroiditis, and retinal vasculitis would be the presenting clinical scenario. Choroidal lesions including granulomas are probably the most common findings in confirmed cases of ocular TB and can be an early sign of disseminated disease [3, 4]. Choroidal tubercles are solitary, or few in number, yellowish lesions typically elevated centrally with poorly defined borders, and commonly situated in posterior pole (Figs. 2 and 8). Inflammatory cells and subretinal fluid may be present (Fig. 3). Tubercles can be solitary or miliary. Multifocal lesions predominantly present in choroid are also common (Figs. 4 and 5) and sometimes can simulate “Serpiginous-like choroiditis” with two distinct patterns (Fig. 6): one with multifocal discrete choroidal lesions that are initially noncontiguous and later progress to form diffuse lesions with an active edge resembling serpiginous choroiditis, and a solitary, diffuse plaque-like lesion with an amoeboid extension [7]. The retina involvement alone is rare.
Fig. (2))
(Garcia et al.). Choroidal tuberculoma. A-B) Left eye color (A) and red free (B) fundus photograph showing a yellowish-white choroidal mass elevated centrally with poorly defined borders and commonly situated in posterior pole. Inflammatory cells (vitritis), subretinal fluid and a macular star are present. C) Same lesion one month after treatment showing no inflammatory cells, consolidation, and no subretinal fluid. D) Fluorescein angiogram reveals late homogeneous hyperfluorescence with well-defined borders.
Fig. (3))
(Garcia et al.). Choroidal tuberculoma. A) Left eye fundus photograph showing a yellowish-white peripapillary choroidal mass with exudative retinal detachment. B-C) Fluorescein angiogram (FA) reveals early mottled hyperfluorescence and late moderate hyperfluorescence. D) Indocyanine green angiography (ICG-V) shows hypofluorescence in the late phase. (Courtesy of J. Fernando Arevalo and Sulaiman Al-Sulaiman).
Fig. (4))
(Garcia et al.). Presumed tuberculous multifocal choroiditis (MFC). A) Right eye fundus photograph of a 26-year-old male with a strongly positive tuberculin skin test (TST). It shows multiple yellowish choroidal infiltrates of varying sizes. B) Early phase fluorescein angiogram (FA) showing hypofluorescence of these lesions. C) Late phase FA depicting late hyperfluorescence. (Courtesy of J. Fernando Arevalo and Sulaiman Al-Sulaiman).
Fig. (5))
(Garcia et al.). A-B) Indocyanine green angiography (ICG-V) of another patient with presumed tuberculous multifocal choroiditis showing hypofluorescence throughout all phases. (Courtesy of J. Fernando Arevalo and Sulaiman Al-Sulaiman).
The retina is often involved in setting of choroidal TB as retinochoroiditis. Exudative retinal hemorrhagic periphlebitis in a patient with uveitis is highly suggestive of tubercular etiology. The optic nerve may be swollen mimicking an ischemic optic neuropathy. It can also present as an optic neuritis or papillitis [2 - 7] (Fig. 7).
Choroidal tubercles are hypofluorescent in fluorescein angiography (FA), but become hyperfluorescent in late phase (Figs. 2D, 3 B-D, 4 B-C, 5, 6 B-C, 9). OCT scans through the area of suspected granuloma revealed an elevation of the choroid with an area of localized contact between the choriocapillaris-retinal pigment epithelium complex and the overlying neurosensory retina (“contact sign”) despite the presence of subretinal fluid around the lesion (Fig. 10) [8].
Fig. (6))
(Garcia et al.). Serpiginous-like choroiditis A) Right eye fundus photograph of a 28-year-old male with a family history of miliary tuberculosis and a positive tuberculin skin test (TST) showing a serpiginous-like choroiditis. Note the yellowish active edge with amoeboid spread and central atrophy along with some hyperpigmentation. B-C) Fluorescein angiogram (FA) showing early hypofluorescence and late hyperfluorescence. D) Late phase indocyanine green angiography (ICG-V) showing persistent hypofluorescence of the active edge. (Courtesy of J. Fernando Arevalo and Sulaiman Al-Sulaiman).
Fig. (7))
(Garcia et al.). Right eye color fundus photograph of a presumed tuberculous neuroretinitis showing a yellowish-white mass elevated centrally with poorly defined borders over the optic nerve. Inflammatory cells (vitritis), subretinal fluid and a macular star are present.
Fig. (8))
Fundus photograph showing a granuloma next to the fovea with subretinal fluid.
Fig. (9))
FA of the same eye as Fig. (8). (A) FA demonstrates central hypofluorescence with a ring of leaking surrounding the granuloma, choroidal tubercles are hypofluorescent in fluorescein angiography in early stages. (B) FA demonstrates choroidal tubercles are hyperfluorescent in fluorescein angiography in late stages.
Fig. (10))
OCT scan of the same lesion shown in Fig. (9), which shows attachment of the retinal pigment epithelial-choriocapillaris layer and the neurosensory retina over the granuloma (“contact” sign), inflammatory retinal infiltrate in the deeper retinal layers and subretinal fluid.