Uveitis is inflammation of the uvea, the middle vascular layer of the eye. It can involve the iris, ciliary body, choroid, retina, and other ocular structures. Uveitis has many potential causes, including infection or association with systemic disease. It is classified based on the anatomical location of inflammation - anterior uveitis affects the iris and anterior chamber, intermediate uveitis involves the vitreous cavity, and posterior or panuveitis impact the retina and choroid. Determining the type and features of uveitis guides evaluation and treatment selection.
Proliferative diabetic retinopathy affects 5-10% of diabetics and is more common in those with juvenile-onset diabetes. It occurs when hypoxic retinal tissue develops abnormal blood vessels due to angiogenic factors like VEGF. This can lead to neovascularization of the retina or optic disc, vitreous hemorrhage, or tractional retinal detachment. Diabetic macular edema is a leading cause of vision loss and occurs when fluid leaks into the macula due to capillary damage. It is classified by its angiographic appearance and can be focal, diffuse, or ischemic in nature.
The white dot syndromes are a group of diseases characterized by inflammation of the outer retina, retinal pigment epithelium, and choroid. They include birdshot retinochoroidopathy, multifocal choroiditis and panuveitis, punctate inner choroidopathy, subretinal fibrosis and uveitis syndrome, multiple evanescent white dot syndrome, acute posterior multifocal placoid pigment epitheliopathy, and serpiginous choroidopathy. The etiology is unknown but may be autoimmune or infectious. Patients typically present with blurred vision, photopsias, and floaters. Examinations reveal multiple cream-colored lesions throughout the fundus. Treatment involves corticosteroids and immunosuppress
Uveitis refers to inflammation of the uvea, which is the middle layer of the eye that includes the iris, ciliary body, and choroid. Uveitis can be classified based on the location of inflammation as anterior, intermediate, posterior, or panuveitis. Common causes include infection, autoimmune disorders, and malignancy. Symptoms include eye redness, pain, blurred vision, and sensitivity to light. Diagnosis involves examination with a slit lamp and tests to identify underlying causes. Treatment focuses on managing inflammation with corticosteroids and treating any underlying condition. Complications can include cataracts, glaucoma, cystoid macular edema, hypotony, and retinal detachment if uve
This document provides information on choroidal melanoma, including that:
- It is the most common primary malignant intraocular tumor and often affects whites of northern European descent.
- Symptoms can include blurred vision, visual field loss, floaters, and painless progressive vision loss.
- Examination may reveal small nodular masses that can become irregular in shape as they grow.
- Diagnosis involves ultrasonography, angiography, and liver enzyme testing, as choroidal melanoma commonly spreads to the liver.
- Treatment options depend on size and location but include observation, radiation therapy, surgery, and laser treatment.
This document provides an overview of retinal vein occlusion (RVO), including the classification, pathogenesis, risk factors, signs, symptoms, investigations, and management of branch retinal vein occlusion (BRVO), hemiretinal vein occlusion (HRVO), impending retinal vein occlusion, and central retinal vein occlusion (CRVO). It discusses the differences between ischemic and non-ischemic forms of CRVO and highlights their acute and chronic clinical features, progression, complications, and treatment approaches. Funduscopic examination findings, fluorescein angiography patterns, and optical coherence tomography are described for evaluating patients with RVO.
This document provides an overview of high myopia, including its classification, causes, symptoms, complications, and management approaches. High myopia is defined as a refractive error greater than -6.00 diopters or an axial length over 26.5mm. It can be caused by genetic factors or the general growth process. Symptoms include defective vision, closer working distance, and night blindness. Complications involve retinal degeneration and detachment. Management includes high-powered spectacles, contact lenses, and refractive surgeries such as LASIK or clear lens extraction.
Proliferative diabetic retinopathy affects 5-10% of diabetics and is more common in those with juvenile-onset diabetes. It occurs when hypoxic retinal tissue develops abnormal blood vessels due to angiogenic factors like VEGF. This can lead to neovascularization of the retina or optic disc, vitreous hemorrhage, or tractional retinal detachment. Diabetic macular edema is a leading cause of vision loss and occurs when fluid leaks into the macula due to capillary damage. It is classified by its angiographic appearance and can be focal, diffuse, or ischemic in nature.
The white dot syndromes are a group of diseases characterized by inflammation of the outer retina, retinal pigment epithelium, and choroid. They include birdshot retinochoroidopathy, multifocal choroiditis and panuveitis, punctate inner choroidopathy, subretinal fibrosis and uveitis syndrome, multiple evanescent white dot syndrome, acute posterior multifocal placoid pigment epitheliopathy, and serpiginous choroidopathy. The etiology is unknown but may be autoimmune or infectious. Patients typically present with blurred vision, photopsias, and floaters. Examinations reveal multiple cream-colored lesions throughout the fundus. Treatment involves corticosteroids and immunosuppress
Uveitis refers to inflammation of the uvea, which is the middle layer of the eye that includes the iris, ciliary body, and choroid. Uveitis can be classified based on the location of inflammation as anterior, intermediate, posterior, or panuveitis. Common causes include infection, autoimmune disorders, and malignancy. Symptoms include eye redness, pain, blurred vision, and sensitivity to light. Diagnosis involves examination with a slit lamp and tests to identify underlying causes. Treatment focuses on managing inflammation with corticosteroids and treating any underlying condition. Complications can include cataracts, glaucoma, cystoid macular edema, hypotony, and retinal detachment if uve
This document provides information on choroidal melanoma, including that:
- It is the most common primary malignant intraocular tumor and often affects whites of northern European descent.
- Symptoms can include blurred vision, visual field loss, floaters, and painless progressive vision loss.
- Examination may reveal small nodular masses that can become irregular in shape as they grow.
- Diagnosis involves ultrasonography, angiography, and liver enzyme testing, as choroidal melanoma commonly spreads to the liver.
- Treatment options depend on size and location but include observation, radiation therapy, surgery, and laser treatment.
This document provides an overview of retinal vein occlusion (RVO), including the classification, pathogenesis, risk factors, signs, symptoms, investigations, and management of branch retinal vein occlusion (BRVO), hemiretinal vein occlusion (HRVO), impending retinal vein occlusion, and central retinal vein occlusion (CRVO). It discusses the differences between ischemic and non-ischemic forms of CRVO and highlights their acute and chronic clinical features, progression, complications, and treatment approaches. Funduscopic examination findings, fluorescein angiography patterns, and optical coherence tomography are described for evaluating patients with RVO.
This document provides an overview of high myopia, including its classification, causes, symptoms, complications, and management approaches. High myopia is defined as a refractive error greater than -6.00 diopters or an axial length over 26.5mm. It can be caused by genetic factors or the general growth process. Symptoms include defective vision, closer working distance, and night blindness. Complications involve retinal degeneration and detachment. Management includes high-powered spectacles, contact lenses, and refractive surgeries such as LASIK or clear lens extraction.
Choroidal melanomas are the most common primary intraocular malignancies in adults. They arise from melanocytes within the choroid and can be pigmented or amelanotic. Risk factors include light iris color and increased sun exposure. Diagnosis is based on clinical appearance, ultrasound, and fluorescein angiography. Prognosis depends on tumor size, cell type, genetic factors, and presence of extrascleral extension. The liver is the most common site of metastasis.
Keratoconus is a non-inflammatory, progressive thinning and protrusion of the cornea that results in irregular astigmatism and decreased vision. It typically presents after puberty with no gender or racial predilection. Diagnosis is made based on corneal thinning, Fleischer ring, Vogt's striae, and irregular astigmatism seen on keratometry and topography. Mild cases are managed with spectacles while more severe cases require rigid gas permeable contact lenses, Intacs, or corneal transplantation.
This document discusses various types of uveitis including classification, signs, symptoms, complications, investigations, and treatments. It covers infective causes like toxoplasmosis, tuberculosis, syphilis, and fungal infections. It also discusses immune-mediated uveitis associated with conditions like VKH syndrome, Behcet's disease, and sarcoidosis. Intermediate uveitis is characterized by inflammation of the pars plana, peripheral retina, and choroid. Posterior uveitis involves the retina and choroid and can be caused by infections, autoimmune diseases, or unknown etiologies.
This document discusses uveitis, including its classification, description, causes, signs, and treatment. Uveitis can be classified anatomically by the area of the eye affected (anterior, intermediate, posterior, panuveitis) and pathologically (granulomatous vs. non-granulomatous). Common causes include infectious etiologies like toxoplasmosis as well as autoimmune diseases. Clinical examination findings and investigations help determine the underlying cause and guide treatment, which typically involves topical and sometimes systemic corticosteroids.
This document provides information on episcleritis and scleritis. It begins with an overview of scleral anatomy and innervation. It then compares and contrasts episcleritis and scleritis, noting that episcleritis is usually self-limiting and not sight threatening, while scleritis can be vision threatening and is often associated with systemic diseases. The document further details the different types of scleritis, associated risk factors and systemic diseases, clinical presentations, diagnostic testing, complications, and treatment approaches. Infectious scleritis is also briefly discussed.
This document provides information on choroidal effusions and detachment. It defines choroidal effusions as the accumulation of fluid in the suprachoroidal space between the choroid and sclera. The document discusses the anatomy of the choroid, types of effusions (serous and hemorrhagic), causes including inflammation and changes in fluid balance, diagnosis using imaging like B-scan ultrasound, and management including observation, medications, and surgery. Risk factors, presentations, and differential diagnoses of different conditions that can cause choroidal effusions are also covered.
This document discusses retinal artery occlusion, specifically central retinal artery occlusion (CRAO). It provides details on:
- CRAO presentation as acute, painless monocular visual loss in older patients, often with severe final vision loss.
- Anatomy of the retinal blood supply from the ophthalmic artery.
- Risk factors including age, gender, cardiovascular/vascular conditions.
- Examination findings like RAPD and retinal signs of ischemia.
- Differential diagnosis, investigations like fluorescein angiography and treatment involving corticosteroids for CRAO related to temporal arteritis.
1. Several landmark clinical trials have evaluated treatments for diabetic retinopathy and macular edema. The DCCT and UKPDS trials showed that intensive glucose control can significantly reduce the risk of retinopathy progression. The DRS established laser photocoagulation as an effective treatment for proliferative diabetic retinopathy, while the ETDRS defined treatment indications and techniques. The DRVS demonstrated benefits of early vitrectomy for advanced proliferative retinopathy. Recent studies of intravitreal injections showed significant vision gains compared to laser in diabetic macular edema. The DRCR Network continues to evaluate new therapies through multicenter clinical trials.
This document describes diabetic retinopathy (DR), its classification, pathogenesis, risk factors, screening protocols, and treatment. DR is classified as non-proliferative DR (NPDR) or proliferative DR (PDR). NPDR is further divided into mild, moderate, severe, and very severe stages based on lesions seen. PDR is characterized by new blood vessel growth. Clinically significant macular edema (CSME) can occur and cause vision loss. Screening intervals depend on DR severity. Laser treatment is used for CSME, PDR, and sometimes severe NPDR to prevent vision loss complications like vitreous hemorrhage or retinal detachment. Good glucose and blood pressure control can delay DR progression.
This document provides an overview of keratoconus, including its etiology, signs and symptoms, classification, and management. Keratoconus is a non-inflammatory thinning of the cornea that results in a cone-shaped protrusion and irregular astigmatism. It typically onset in teenagers and progresses over time. Management includes rigid gas permeable contact lenses, collagen cross-linking to halt progression, and keratoplasty for advanced cases.
Central serous retinopathy (CSR) is characterized by a serous retinal detachment in the macula due to leakage of fluid from the choroidal vasculature through the retinal pigment epithelium. It typically affects men in their 40s and 50s and can be associated with stress, corticosteroid use, hypertension, and type A personality. While often self-limiting, CSR can become chronic and cause long-lasting visual impairment without treatment. Management options include observation, stress reduction, oral medications like acetazolamide or ketoconazole to lower cortisol levels, and photodynamic therapy for severe or chronic cases.
This document discusses various causes of acute visual loss, categorizing them as ocular or non-ocular. In the ocular category, it describes common causes such as media opacities, retinal issues including vascular occlusions, and optic nerve disorders. It provides details on evaluating and treating specific conditions like acute angle closure glaucoma, retinal detachment, macular diseases, and ischemic optic neuropathies. It emphasizes that many ocular causes of acute visual loss require prompt diagnosis and treatment to prevent permanent vision loss. Non-ocular causes discussed include stroke and functional visual loss.
Glaucoma is the second leading cause of blindness worldwide. It involves damage to the optic nerve due to increased intraocular pressure. While pressure within the eye normally ranges from 11-21 mmHg, pressures above 21 are considered high risk for glaucoma. Damage occurs when pressure is not adequately relieved by drainage from the eye. Early detection through screening and treatment can prevent vision loss, but many patients are asymptomatic in early stages when peripheral vision is lost.
Epiretinal membrane and vitreomacula traction in updates by Panit Cherdchu, MD.Panit Cherdchu
Epiretinal membrane + Vitreomacula traction in focus of PPP from AAO guidelines includes definition, classification, investigation, treatment (Ocriplasmin,vitrectomy,observation)
This document discusses myopia (nearsightedness), including its optics, etiological classifications, clinical varieties, and treatment options. Myopia occurs when light rays focus in front of the retina rather than directly on it. It can be axial, curvatural, or positional. Treatment includes optical correction with glasses or contacts, as well as refractive surgeries like LASIK, PRK, clear lens extraction, phakic IOL implantation, intracorneal ring segments, and orthokeratology. More advanced techniques like LASIK and ICLs can correct higher degrees of myopia over -12 diopters.
This document discusses the embryology and anatomy of the cornea. It describes how the cornea develops from surface ectoderm in the 4th-5th week of gestation, with mesenchymal cells forming the stroma and endothelium. The cornea continues developing through the fetal period, with layers such as Bowman's membrane forming between 12-26 weeks. The document also discusses the cellular components, functions, and common congenital anomalies of the cornea, including microcornea, megalocornea, cornea plana, keratoconus, and others.
This document summarizes ocular manifestations of HIV/AIDS. It discusses how HIV infects CD4+ T cells and establishes latency. Common opportunistic infections affecting the eye include CMV retinitis, which appears as cotton wool spots or granular lesions and can cause vision loss. Treatment involves antiviral drugs like ganciclovir, foscarnet, and cidofovir. Immune reconstitution inflammatory syndrome can also occur after starting HAART therapy. Other infections discussed are VZV retinitis, MAC, histoplasmosis, and toxoplasmosis.
This document discusses several conditions that can mimic anterior or posterior uveitis, including intraocular lymphoma, retinoblastoma, uveal melanoma, leukemias, and juvenile xanthogranuloma. It provides details on the presentation, diagnosis, classification, and treatment of these conditions. Primary intraocular lymphoma often involves infiltration of the retina and optic nerve in patients over 50 years old. Retinoblastoma is the most common primary intraocular malignancy in children and can present as leucocoria, strabismus, or glaucoma. Uveal melanoma, leukemias, and juvenile xanthogranuloma can also involve the eye and be misdiagnosed as uveitis.
This document provides an overview of uveitis, including:
- The anatomy of the uveal tract and classifications of uveitis based on anatomy, clinical course, etiology, and histology.
- The epidemiology, clinical presentation, signs and symptoms, and common causes of the three main types of uveitis - anterior, intermediate, and posterior uveitis.
- Guidelines for taking a thorough history and performing an examination of a uveitis patient.
- A case example is presented of a patient with bilateral uveitis.
This document discusses uveitis, which is inflammation of the uveal tract of the eye. It is classified based on the location of inflammation - anterior (involving the iris and anterior ciliary body), intermediate (primarily involving the vitreous), or posterior (involving the retina and/or choroid). Clinical features vary depending on location but may include eye pain, redness, photophobia, blurred vision, and floaters. Examination findings include cells and flare in the anterior chamber, keratic precipitates, hypopyon, posterior synechiae, vitreous cells/haze, and retinal/choroidal lesions. Investigations are tailored to each individual but aim to identify
Choroidal melanomas are the most common primary intraocular malignancies in adults. They arise from melanocytes within the choroid and can be pigmented or amelanotic. Risk factors include light iris color and increased sun exposure. Diagnosis is based on clinical appearance, ultrasound, and fluorescein angiography. Prognosis depends on tumor size, cell type, genetic factors, and presence of extrascleral extension. The liver is the most common site of metastasis.
Keratoconus is a non-inflammatory, progressive thinning and protrusion of the cornea that results in irregular astigmatism and decreased vision. It typically presents after puberty with no gender or racial predilection. Diagnosis is made based on corneal thinning, Fleischer ring, Vogt's striae, and irregular astigmatism seen on keratometry and topography. Mild cases are managed with spectacles while more severe cases require rigid gas permeable contact lenses, Intacs, or corneal transplantation.
This document discusses various types of uveitis including classification, signs, symptoms, complications, investigations, and treatments. It covers infective causes like toxoplasmosis, tuberculosis, syphilis, and fungal infections. It also discusses immune-mediated uveitis associated with conditions like VKH syndrome, Behcet's disease, and sarcoidosis. Intermediate uveitis is characterized by inflammation of the pars plana, peripheral retina, and choroid. Posterior uveitis involves the retina and choroid and can be caused by infections, autoimmune diseases, or unknown etiologies.
This document discusses uveitis, including its classification, description, causes, signs, and treatment. Uveitis can be classified anatomically by the area of the eye affected (anterior, intermediate, posterior, panuveitis) and pathologically (granulomatous vs. non-granulomatous). Common causes include infectious etiologies like toxoplasmosis as well as autoimmune diseases. Clinical examination findings and investigations help determine the underlying cause and guide treatment, which typically involves topical and sometimes systemic corticosteroids.
This document provides information on episcleritis and scleritis. It begins with an overview of scleral anatomy and innervation. It then compares and contrasts episcleritis and scleritis, noting that episcleritis is usually self-limiting and not sight threatening, while scleritis can be vision threatening and is often associated with systemic diseases. The document further details the different types of scleritis, associated risk factors and systemic diseases, clinical presentations, diagnostic testing, complications, and treatment approaches. Infectious scleritis is also briefly discussed.
This document provides information on choroidal effusions and detachment. It defines choroidal effusions as the accumulation of fluid in the suprachoroidal space between the choroid and sclera. The document discusses the anatomy of the choroid, types of effusions (serous and hemorrhagic), causes including inflammation and changes in fluid balance, diagnosis using imaging like B-scan ultrasound, and management including observation, medications, and surgery. Risk factors, presentations, and differential diagnoses of different conditions that can cause choroidal effusions are also covered.
This document discusses retinal artery occlusion, specifically central retinal artery occlusion (CRAO). It provides details on:
- CRAO presentation as acute, painless monocular visual loss in older patients, often with severe final vision loss.
- Anatomy of the retinal blood supply from the ophthalmic artery.
- Risk factors including age, gender, cardiovascular/vascular conditions.
- Examination findings like RAPD and retinal signs of ischemia.
- Differential diagnosis, investigations like fluorescein angiography and treatment involving corticosteroids for CRAO related to temporal arteritis.
1. Several landmark clinical trials have evaluated treatments for diabetic retinopathy and macular edema. The DCCT and UKPDS trials showed that intensive glucose control can significantly reduce the risk of retinopathy progression. The DRS established laser photocoagulation as an effective treatment for proliferative diabetic retinopathy, while the ETDRS defined treatment indications and techniques. The DRVS demonstrated benefits of early vitrectomy for advanced proliferative retinopathy. Recent studies of intravitreal injections showed significant vision gains compared to laser in diabetic macular edema. The DRCR Network continues to evaluate new therapies through multicenter clinical trials.
This document describes diabetic retinopathy (DR), its classification, pathogenesis, risk factors, screening protocols, and treatment. DR is classified as non-proliferative DR (NPDR) or proliferative DR (PDR). NPDR is further divided into mild, moderate, severe, and very severe stages based on lesions seen. PDR is characterized by new blood vessel growth. Clinically significant macular edema (CSME) can occur and cause vision loss. Screening intervals depend on DR severity. Laser treatment is used for CSME, PDR, and sometimes severe NPDR to prevent vision loss complications like vitreous hemorrhage or retinal detachment. Good glucose and blood pressure control can delay DR progression.
This document provides an overview of keratoconus, including its etiology, signs and symptoms, classification, and management. Keratoconus is a non-inflammatory thinning of the cornea that results in a cone-shaped protrusion and irregular astigmatism. It typically onset in teenagers and progresses over time. Management includes rigid gas permeable contact lenses, collagen cross-linking to halt progression, and keratoplasty for advanced cases.
Central serous retinopathy (CSR) is characterized by a serous retinal detachment in the macula due to leakage of fluid from the choroidal vasculature through the retinal pigment epithelium. It typically affects men in their 40s and 50s and can be associated with stress, corticosteroid use, hypertension, and type A personality. While often self-limiting, CSR can become chronic and cause long-lasting visual impairment without treatment. Management options include observation, stress reduction, oral medications like acetazolamide or ketoconazole to lower cortisol levels, and photodynamic therapy for severe or chronic cases.
This document discusses various causes of acute visual loss, categorizing them as ocular or non-ocular. In the ocular category, it describes common causes such as media opacities, retinal issues including vascular occlusions, and optic nerve disorders. It provides details on evaluating and treating specific conditions like acute angle closure glaucoma, retinal detachment, macular diseases, and ischemic optic neuropathies. It emphasizes that many ocular causes of acute visual loss require prompt diagnosis and treatment to prevent permanent vision loss. Non-ocular causes discussed include stroke and functional visual loss.
Glaucoma is the second leading cause of blindness worldwide. It involves damage to the optic nerve due to increased intraocular pressure. While pressure within the eye normally ranges from 11-21 mmHg, pressures above 21 are considered high risk for glaucoma. Damage occurs when pressure is not adequately relieved by drainage from the eye. Early detection through screening and treatment can prevent vision loss, but many patients are asymptomatic in early stages when peripheral vision is lost.
Epiretinal membrane and vitreomacula traction in updates by Panit Cherdchu, MD.Panit Cherdchu
Epiretinal membrane + Vitreomacula traction in focus of PPP from AAO guidelines includes definition, classification, investigation, treatment (Ocriplasmin,vitrectomy,observation)
This document discusses myopia (nearsightedness), including its optics, etiological classifications, clinical varieties, and treatment options. Myopia occurs when light rays focus in front of the retina rather than directly on it. It can be axial, curvatural, or positional. Treatment includes optical correction with glasses or contacts, as well as refractive surgeries like LASIK, PRK, clear lens extraction, phakic IOL implantation, intracorneal ring segments, and orthokeratology. More advanced techniques like LASIK and ICLs can correct higher degrees of myopia over -12 diopters.
This document discusses the embryology and anatomy of the cornea. It describes how the cornea develops from surface ectoderm in the 4th-5th week of gestation, with mesenchymal cells forming the stroma and endothelium. The cornea continues developing through the fetal period, with layers such as Bowman's membrane forming between 12-26 weeks. The document also discusses the cellular components, functions, and common congenital anomalies of the cornea, including microcornea, megalocornea, cornea plana, keratoconus, and others.
This document summarizes ocular manifestations of HIV/AIDS. It discusses how HIV infects CD4+ T cells and establishes latency. Common opportunistic infections affecting the eye include CMV retinitis, which appears as cotton wool spots or granular lesions and can cause vision loss. Treatment involves antiviral drugs like ganciclovir, foscarnet, and cidofovir. Immune reconstitution inflammatory syndrome can also occur after starting HAART therapy. Other infections discussed are VZV retinitis, MAC, histoplasmosis, and toxoplasmosis.
This document discusses several conditions that can mimic anterior or posterior uveitis, including intraocular lymphoma, retinoblastoma, uveal melanoma, leukemias, and juvenile xanthogranuloma. It provides details on the presentation, diagnosis, classification, and treatment of these conditions. Primary intraocular lymphoma often involves infiltration of the retina and optic nerve in patients over 50 years old. Retinoblastoma is the most common primary intraocular malignancy in children and can present as leucocoria, strabismus, or glaucoma. Uveal melanoma, leukemias, and juvenile xanthogranuloma can also involve the eye and be misdiagnosed as uveitis.
This document provides an overview of uveitis, including:
- The anatomy of the uveal tract and classifications of uveitis based on anatomy, clinical course, etiology, and histology.
- The epidemiology, clinical presentation, signs and symptoms, and common causes of the three main types of uveitis - anterior, intermediate, and posterior uveitis.
- Guidelines for taking a thorough history and performing an examination of a uveitis patient.
- A case example is presented of a patient with bilateral uveitis.
This document discusses uveitis, which is inflammation of the uveal tract of the eye. It is classified based on the location of inflammation - anterior (involving the iris and anterior ciliary body), intermediate (primarily involving the vitreous), or posterior (involving the retina and/or choroid). Clinical features vary depending on location but may include eye pain, redness, photophobia, blurred vision, and floaters. Examination findings include cells and flare in the anterior chamber, keratic precipitates, hypopyon, posterior synechiae, vitreous cells/haze, and retinal/choroidal lesions. Investigations are tailored to each individual but aim to identify
This document discusses uveitis in systemic diseases. It begins with an introduction defining the uvea and uveitis. It then discusses how uveitis can be associated with various systemic diseases and the importance of a thorough history and physical exam. The document outlines various classifications of uveitis and clinical features. It then discusses principles of diagnosis and treatment of uveitis in specific systemic diseases like spondyloarthropathies, juvenile idiopathic arthritis, Behcet's disease, sarcoidosis, and others. It describes characteristics, investigations and management considerations for uveitis related to these systemic conditions.
Uveitis refers to inflammation within the eye and is a leading cause of blindness. It was once considered a single disease but is now known to have various causes, including autoimmune disorders, infections, malignancy, and toxoplasmosis. A thorough evaluation including history, examination, and testing is needed to determine the extent, structures affected, underlying cause, and best treatment. Treatment involves topical steroids as first line but may require periocular injections or oral steroids depending on severity and location of inflammation. Long term management balances control of inflammation with risks of treatment side effects like increased eye pressure.
Classifications of etio pathogenesis of uveitis, anterior uveitis- dr.k.srik...ophthalmgmcri
The document discusses the classification, etiology, pathogenesis, and management of uveitis. Uveitis is categorized based on the location of inflammation within the uvea (anterior, intermediate, posterior, or panuveitis). Treatment involves topical, periocular, or systemic corticosteroids with the addition of immunomodulatory medications for more severe cases.
Classifications of etio pathogenesis of uveitis, anterior uveitis- dr.k.srik...ophthalmgmcri
The document discusses the classification, etiology, pathogenesis, and management of uveitis. Uveitis is categorized based on the location of inflammation within the uvea (anterior, intermediate, posterior, or panuveitis). Treatment involves topical, periocular, or systemic corticosteroids with the addition of immunomodulatory medications for more severe cases.
Uveitis refers to inflammation of the uveal tract of the eye. It can be caused by infections, autoimmune disorders, trauma, medications, or rarely malignancies. It is a leading cause of blindness worldwide. Symptoms and signs depend on the location and severity of inflammation in the eye. Examination findings provide clues to the etiology and classification of uveitis. A thorough history and comprehensive ocular examination are important for diagnosis and management.
Anterior uveitis is an inflammation of the anterior uveal tract including the iris, ciliary body, and choroid. It is classified based on anatomical location and can be idiopathic or associated with other systemic diseases. Common causes include juvenile idiopathic arthritis and tuberculosis. Clinical features include eye pain, redness, photophobia, and cells or flare in the anterior chamber. Treatment involves topical steroids, cycloplegics, and systemic immunosuppression depending on severity and underlying etiology. Complications can include glaucoma, cataracts, and retinal issues if not properly treated.
Uveitis refers to inflammation of the middle layer of the eye called the uvea. There are various types of uveitis classified based on the location of inflammation including anterior uveitis, intermediate uveitis, posterior uveitis, and panuveitis. Signs and symptoms depend on the location and chronicity of inflammation and may include eye pain, blurred vision, and floaters. Treatment involves topical or systemic anti-inflammatory medications such as corticosteroids and immunomodulators to reduce inflammation and prevent vision loss from complications.
Classifications of etio pathogenesis of ueitis, anterior uieitis-dr.k.srikant...ophthalmgmcri
Uveitis refers to inflammation of the middle layer of the eye called the uvea. There are various types of uveitis classified based on the location of inflammation including anterior uveitis, intermediate uveitis, posterior uveitis, and panuveitis. Anterior uveitis involves inflammation in the anterior chamber and can present with pain, photophobia, and blurred vision. Management involves topical cycloplegics, steroids, and potentially systemic immunosuppressants to control inflammation and prevent vision loss from complications.
Classifications of etio pathogenesis of ueitis, anterior uieitis-dr.k.srikant...ophthalmgmcri
Uveitis refers to inflammation of the middle layer of the eye called the uvea. There are various types of uveitis classified based on the location of inflammation including anterior uveitis, intermediate uveitis, posterior uveitis, and panuveitis. Anterior uveitis involves inflammation in the anterior chamber and can present with pain, photophobia, and blurred vision. Management involves topical cycloplegics, steroids, and potentially systemic immunosuppressants to control inflammation and prevent vision loss from complications.
Dr. TP Chhangte discusses anterior uveitis, including its definition, epidemiology, classification, pathology, clinical features, complications, and differential diagnosis. Some key points:
- Anterior uveitis is inflammation of the iris and anterior part of the ciliary body. Its prevalence has been increasing and it commonly affects people aged 20-50.
- Uveitis can be classified anatomically, clinically, etiologically, and pathologically. The anatomical classification divides uveitis into anterior, intermediate, posterior, and panuveitis based on location of inflammation.
- Clinical features of anterior uveitis include eye pain, redness, photophobia, and decreased vision. On examination
Uveitis classification & clinical features 1lijulk
Uveitis is inflammation of the uvea, which includes the iris, ciliary body, and choroid. It is classified based on anatomy, clinical course, etiology, and histology. The Standardization of Uveitis Nomenclature (SUN) Working Group developed standardized classifications including anatomical (anterior, intermediate, posterior, panuveitis), descriptors (onset, duration, course), and grading systems. Clinical features depend on the involved area and can include symptoms like pain, photophobia, blurred vision, and floaters. Signs on examination may reveal cells and flare in the anterior chamber, keratic precipitates, hypopyon, synechiae, and lesions of the iris, retina, or
Uveitis is classified based on the primary site of inflammation in the eye: anterior, intermediate, posterior, or panuveitis. It is also described based on clinical features like onset, duration, and course. A thorough evaluation is needed to categorize uveitis and identify any underlying etiology, as it can be associated with systemic diseases. A standardized system of nomenclature exists to describe uveitis uniformly based on anatomy, activity, and other characteristics. Symptoms depend on the location and severity of inflammation, and may include pain, photophobia, blurred vision, or floaters.
This document discusses various infectious causes of uveitis. It begins by classifying uveitis etiologies as infectious, non-infectious, or masquerade syndromes. Common bacterial causes discussed include tuberculosis, syphilis, leptospirosis, and brucellosis. Viral causes mentioned are cytomegalovirus, herpes simplex, herpes zoster, and others. Fungal causes like candidiasis and aspergillosis as well as parasitic causes such as toxoplasmosis are also reviewed. Diagnosis and treatment approaches for specific infectious etiologies like tuberculosis, syphilis, and brucellosis are provided. The document concludes with sections
This document discusses uveitis, which is inflammation of the uveal tract of the eye. It defines the anatomical locations of uveitis, describes the clinical features and types, and discusses the various etiologies including infectious, immune-related, and idiopathic causes. Specific infectious etiologies covered include tuberculosis, leprosy, syphilis, toxoplasmosis, histoplasmosis, and various viral causes. The clinical presentation, diagnosis, and treatment are described for each condition.
Retinal vasculitis is an inflammatory eye disease affecting the retinal vasculature. It can present as periphlebitis (vein involvement), periarteritis (artery involvement), or angiitis (both). Symptoms include gradual vision loss, floaters, photopsia, and scotomata. Signs include vascular sheathing, attenuation, hemorrhages, cotton-wool spots, and neovascularization. Causes include infectious etiologies like tuberculosis and syphilis, autoimmune diseases like sarcoidosis and Behcet's disease, and primary vasculitis like Eales' disease. Treatment involves managing underlying causes with medications like steroids, immunosuppressants,
1) VKH disease is a multisystem disorder characterized by granulomatous panuveitis with exudative retinal detachments and associated neurologic and cutaneous manifestations.
2) It was first described separately by three doctors (Vogt, Koyanagi, and Harada) in the early 20th century before being recognized as a single disease.
3) It has distinct prodromal, uveitic, chronic, and chronic recurrent stages with characteristic ocular and systemic findings at each stage. International criteria have been developed to classify its complete, incomplete, and probable forms.
Uveitis refers to inflammation of the uveal tract of the eye. It can be caused by infections, autoimmune disorders, or malignancies. Uveitis is classified anatomically by the area of inflammation - anterior, intermediate, posterior, or panuveitis. It is also classified clinically based on duration and course. Anterior uveitis presents with pain, photophobia, redness, and blurred vision. Signs include cells and flare in the anterior chamber, keratic precipitates, and iris lesions. Intermediate uveitis affects the vitreous and peripheral retina. Posterior uveitis causes floaters and fundus lesions. Management involves identifying the etiology, using topical and systemic st
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2. • The uvea consists of the middle, pigmented,
vascular layer of the eye and includes
the iris,
ciliary body, and
choroid.
Uveitis is broadly defined as inflammation (ie, -itis) of the
uvea (from the Latin uva, meaning “grape”).
Inflammation of the uvea can involve other ocular
structures such as the retina, sclera, cornea, vitreous, and
optic nerve.
The etiology of uveitis is infectious or inflammatory and is
variably associated with systemic disease.
OVERVIEW
3. OVERVIEW
Uveitis associated with systemic disease or infection a careful history and review of systems is an
essential first step in diagnosis.
• A comprehensive physical examination of the eye and pertinent organ systems characterize the
type of inflammation present and to identify any associated systemic findings.
• The anatomical location of inflammation combined with results from the history and physical
examination to guide further investigations.
• Multimodal ophthalmic imaging to characterizing certain types of intraocular inflammation.
• Laboratory studies can help determine the etiology of the intraocular inflammation but are never
a substitute for a thorough history and physical examination.
Determining the specific type of uveitis guides the selection of treatment
4. EPIDEMIOLOGY
Uveitis approximately 10% of all blindness in the US and Europe and up to 25% of
blindness worldwide.
In the US --> the prevalence of uveitis is 58–131 per 100,00
Developing world up to 1070 per 100,000
Anterior uveitis is the most common type of uveitis, representing 70%–80% of
cases, followed by panuveitis, posterior uveitis, and intermediate uveitis.
have slightly higher rates of uveitis overall.
Most surveys show that uveitis incidence peaks between 20 and 60 years of age, recent data
suggests that it may also increase over the age of 65.
5. EPIDEMIOLOGY
Prevalence is about five- to tenfold lower in
children than in adults.
Developing countries have higher rates of
infectious uveitis and posterior and
panuveitis compared to industrialized nations.
Certain uveitides have greater distribution by
geographic region, such as :
• Birdshot chorioretinopathy in western Europe,
• Behçet disease in Turkey and China, and
• Tuberculous uveitis in India.
6. CLASSIFICATION OF UVEITIS
SUN system of classification universal method of describing uveitis entities based on :
• Anatomic location of inflammation, and
• Specific descriptors of onset, duration, and course.
This text uses an etiologic division of uveitic entities into :
• noninfectious (autoimmune) and
• infectious conditions
and further describes them using the SUN system’s basic anatomical classification of uveitis into 4
subcategories:
(1) anterior uveitis,
(2) intermediate uveitis,
(3) Posterior uveitis, and
(4) Panuveitis.
When both anterior chamber and vitreous inflammatory cells are present, but the vitritis is more than
expected in an isolated anterior uveitis, the classification should be “anterior and intermediate uveitis”
and not “panuveitis.”
11. ANATOMICAL CLASSIFICATION – ANTERIOR UVEITIS
Anterior uveitis produces inflammatory signs predominantly in the anterior
chamber, as a result of inflammation of the iris and ciliary body.
Iritis : Inflammation confined to the anterior chamber
iridocyclitis : Cells in the retrolental (anterior vitreous) space
keratouveitis : Inflammatory processes that originate in the cornea with
secondary involvement of the anterior chamber
sclerouveitis : An inflammatory reaction that involves the sclera and uveal
tract (iris, ciliary body, and choroid)
When more than one ocular structure is involved, the convention is that the
primary site of inflammation is named first.
Severe or chronic anterior uveitis may produce secondary structural
complications such as uveitic macular edema, optic disc swelling, cataract,
corneal edema, band keratopathy, or iris abnormalities.
These complications are not part of the formal classification system but may
contribute to disease recognition and therapy.
38-old woman with spondyloarthropathy HLA B27 positive, showing severe
anterior uveitis associated with UME. (a): posterior synechiae and fibrinous
deposit in the anterior chamber; (b): horizontal central OCT scan showing UME.
Band
Keratopat
hy
12. ANATOMICAL CLASSIFICATION – INTERMEDIATE UVEITIS
Intermediate Uveitis inflammation is most
prominent in the vitreous cavity
Inflammation occurs in the ciliary body, pars plana
(Pars planitis) and/or peripheral retina.
Clinical signs include :
• Vitreous haze and cellular debris often
associated with peripheral retinal vasculitis.
• Macular edema is the most common structural
complication;
• severe or chronic disease may cause peripheral
exudative or tractional detachments, retinal
neovascularization, cataract, or retrolental membrane
formation.
13. ANATOMICAL CLASSIFICATION – POSTERIOR UVEITIS
Posterior Uveitis is defined as intraocular inflammation primarily involving the retina and/ or choroid.
• Inflammatory cells may be observed diffusely throughout the vitreous cavity,overlying foci of active
inflammation,or on the posterior vitreous face.
• Fundoscopy reveals focal, multifocal, or diffuse areas of retinitis and/or choroiditis, often with retinal vasculitis.
Entities may have a similar clinical appearance, though some clinical patterns of disease are nearly pathognomonic for
diagnosis.
Structural complications such as macular edema, epiretinal membrane,and retinal or choroidal
neovascularization are not sufficient for the anatomical classification of posterior uveitis
In panuveitis, inflammation is present diffusely throughout the eye without a
predominantly affected site.
Inflammation may be associated with an infectious or noninfectious systemic disease.
14. ANATOMICAL CLASSIFICATION – RETINAL VASCULITIS
Retinal vasculitis is defined by the presence of retinal
vascular changes in association with ocular inflammation.
Retinal vasculitis is used in distinction to vasculopathy, in which
there are vessel changes but no visible evidence of
inflammation.
Retinal vasculitis encompasses :
• perivascular sheathing,
• vascular leakage, or
• occlusion shown on fluorescein angiography studies.
Peripheral vascular sheathing can be observed in
intermediate uveitis but is not sufficient for the anatomical
classification of posterior/panuveitis.
Retinal vasculitis is not considered to be a defining feature for the
anatomical classification of uveitis.
Fundus photographs of two patients with extensive vascular sheathing
secondary to intraocular tuberculosis.
Panel A demonstrates vascular sheathing accompanied by intraretinal
hemorrhages.
In Panel B, there are extensive perivascular hemorrhages in all four quadrants.
Fluorescein angiography of
a patient with occlusive
vasculitis. The vessels of
the lower arcade show
inflammation denoted by
leakage of the vessel wall.
There is an extensive area
of capillary non-perfusion
downstream (demarcated
by dotted square)
suggestive of obliteration
of blood flow.
20. CLASSIFICATION BY CLINICAL FEATURES
The severity of the inflammation can influence categorization and
prognosis.
The inflammatory process may occur in one or both eyes, or it may
alternate between them.
The distribution of ocular involvement—focal, multifocal, or diffuse—is
also helpful to note when classifying uveitis.
The classification of uveitis as either granulomatous or nongranulomatous is
still in use.
However, the clinical appearance of uveitis as granulomatous or
nongranulomatous may not necessarily correlate with the histologic description
and can instead be related to the disease stage, the amount of antigen at
21. CLASSIFICATION BY CLINICAL FEATURES
• Nongranulomatous inflammation typically has a lymphocytic
and plasma cell infiltrate; clinically, cellular deposits (keratic
precipitates) tend to be finer and distributed diffusely.
• Granulomatous inflammation also includes epithelioid and
giant cells; clinically, cellular deposits with large, clumped, or
greasy appearance are predominantly located in a gravity-
dependent position on the inferior cornea.
Discrete granulomas are characteristic of sarcoidosis and
tuberculosis;
Diffuse granulomatous inflammation appears in Vogt-
Koyanagi-Harada syndrome and sympathetic ophthalmia.
Zonal granulomatous disease can be observed in lens-
induced uveitis.
22. SYMPTOMS OF UVEITIS
Symptoms produced by uveitis depend on :
• which part of the uveal tract is inflamed,
• the rapidity of onset (sudden or insidious),
• the duration of the disease (limited or persistent),
• the course of the disease (acute, chronic, or recurrent), and
• sometimes the underlying etiology.
Anterior uveitis
• from a quiet asymptomatic white eye to an extremely painful red eye depending on the type of uveitis
and/or severity of inflammation.
• Sudden-onset anterior uveitis usually causes acute pain, photophobia, redness, and blurred vision.
• Pain results from ciliary spasm associated with inflammation in the region of the iris and may
radiate over the larger area served by cranial nerve V (the trigeminal nerve)/ due to ↑ IOP due to
angle closure or trabeculitis
23. SYMPTOMS OF UVEITIS
Chronic anterior uveitis in patients with juvenile idiopathic arthritis (JIA) may not be associated with
any symptoms at all.
However, even if initially asymptomatic, chronic or severe anterior uveitis can cause blurred vision because
of structural complications such as calcific band keratopathy, cataract, or macular edema.
Isolated intermediate uveitis
• a white, quiet eye; and
• produces symptoms of floaters (the shadows cast by vitreous cells and debris on the retina) and
• blurred vision (result from macular edema or vitreous opacities in the visual axis).
Patients with posterior uveitis
• painless blurred vision (primarily by retinitis and/or choroiditis directly affecting macular function, or
secondarily by complications of inflammation),
• floaters,
• photopsias,
• scotomata,
• metamorphopsia,
• nyctalopia, or a combination of these symptoms.
25. SIGN OF UVEITIS
The chemical mediators
involved in inflammation (see
Chapter 1) result in :
• vascular dilation (ciliary
flush),
• increased vascular
permeability (aqueous flare),
and
• chemotaxis of inflammatory
cells into the eye (aqueous
and vitreous cellular reaction)
26. SIGN OF UVEITIS- ANTERIOR SEGMENT
Signs of uveitis in the anterior portion of the
eye include
• inflammatory cells (Fig 5-1)
• flare (Fig 5-2)
• hypopyon
• fibrin in the anterior chamber
• keratic precipitates (Figs 5-3, 5-4)
• iris nodules (Fig 5-5)
• iris atrophy or heterochromia
• pupillary miosis
• synechiae, anterior and posterior (Fig 5-6) •
pigment dispersion
• cataract*
• band keratopathy*
*Observed in long-standing uveitis
27. Signs of uveitis in the anterior portion of the
eye include
• inflammatory cells (Fig 5-1)
• flare (Fig 5-2)
• hypopyon
• fibrin in the anterior chamber
• keratic precipitates (Figs 5-3, 5-4)
• iris nodules (Fig 5-5)
• iris atrophy or heterochromia
• pupillary miosis
• synechiae, anterior and posterior (Fig 5-6) •
pigment dispersion
• cataract*
• band keratopathy*
*Observed in long-standing uveitis
SIGN OF UVEITIS- ANTERIOR SEGMENT
Figure 5-3 Keratic
precipitates (medium and
small).
Figure 5-4 Large “mutton-fat”
keratic precipitates in a patient with
sarcoidosis. Large keratic
precipitates such as these
generally indicate a
granulomatous disease process.
28. Signs of uveitis in the anterior portion of the
eye include
• inflammatory cells (Fig 5-1)
• flare (Fig 5-2)
• hypopyon
• fibrin in the anterior chamber
• keratic precipitates (Figs 5-3, 5-4)
• iris nodules (Fig 5-5)
• iris atrophy or heterochromia
• pupillary miosis
• synechiae, anterior and posterior (Fig 5-6) •
pigment dispersion
• cataract*
• band keratopathy*
*Observed in long-standing uveitis
SIGN OF UVEITIS- ANTERIOR SEGMENT
29. SIGN OF UVEITIS- ANTERIOR SEGMENT
The major finding in anterior uveitis is the
presence of inflammatory cells and flare in
the anterior chamber, but there may be many
additional sequalae.
The SUN system grades the intensity of anterior
chamber cells according to the number of
inflammatory cells observed on slit-lamp
examination in a field defined as a 1 × 1 mm
high-power beam at full intensity at a 45°–60°
angle in a dark room.
Flare is defined by the visibility of the slit-
lamp beam in the anterior chamber.
The SUN system adopted the flare grading method
described previously by Hogan and colleagues (Table
5-8)
The anterior chamber reaction can be described as
• serous (aqueous flare caused by protein influx)
• purulent (polymorphonuclear leukocytes and necrotic
debris causing hypopyon)
• fibrinous (plasmoid, or intense fibrinous exudate)
• sanguinoid (inflammatory cells with erythrocytes, as
manifested by hypopyon mixed with hyphema)
30. SIGN OF UVEITIS- ANTERIOR SEGMENT
• Keratic precipitates (KPs) are collections of inflammatory cells on the corneal endothelium.
Newly formed KPs tend to be white and smoothly rounded, later transitioning to crenated (shrunken),
pigmented, or glassy in nature. Large, yellowish KPs are called mutton- fat KPs and are usually associated
with granulomatous types of inflammation.
• Associated corneal edema may be present.
• Band keratopathy is seen in chronic uveitis (especially JIA associated).
• Iris involvement may manifest as either anterior or posterior synechiae, iris nodules (Koeppe nodules at the
pupillary border, Busacca nodules within the iris stroma and Berlin nodules in the angle, iris granulomas,
heterochromia (eg, Fuchs uveitis syndrome), or stromal atrophy (eg, herpetic uveitis).
• With uveitic involvement of the ciliary body and trabecular meshwork, IOP is often low, secondary to decreased
aqueous production or increased uveoscleral outflow, but IOP may increase precipitously if the meshwork becomes
clogged by inflammatory cells or debris or if the trabecular meshwork itself is the site of inflammation
(trabeculitis). Pupillary block with iris bombé and secondary angle closure may also lead to an acute rise in IOP
31. SIGN OF UVEITIS- INTERMEDIATE SEGMENT
Signs of uveitis in the intermediate portion of the eye include :
• inflammatory cells in vitreous
• vitreous haze (Fig 5-7)
• snowballs (clumped vitreous cells)
• snowbanks (exudate over pars plana)
• ciliary body detachment
• retrolental membrane
• vitreous strands or traction band
• The hallmark of intermediate uveitis is
vitreous cell and haze.
• Cells may be clumped or individual.
• The cells make up vitreous haze when viewed
in combination with protein-aceous vitreous debris.
Uveitis with snowballs,
voluminous white vitreous
condensation, and finer
white-colored linear
inflammatory condensation
of the vitreous associated
with multifocal pigmented
scars in an Ebola survivor.
Snowball (arrow) and a string
of pearls-like vitreous
opacities (circled).
Snowbanks
32. SIGN OF UVEITIS- INTERMEDIATE SEGMENT
The physician typically grades vitreous cells on a 0–4 numeric scale by
observing the retrolental space in a dilated eye using the slit- lamp
biomicroscope and a 1 × 0.5 mm beam.
• The National Institutes of Health grading system for vitreous haze, which the SUN
system adopted, employs a standardized set of fundus photographs that defines
vitreous haze on a 0–4 scale.
• Vitreous haze has been used in inclusion criteria in clinical trials for
uveitis, and a 2- step improvement has been used as a principal outcome
measure.
33. SIGN OF UVEITIS- INTERMEDIATE SEGMENT
Figure 5-7 Grading scale for
vitreous haze: representative
standard images.
Grade 4: Dense opacity
obscuring optic nerve head.
Grade 3: Optic nerve visible,
borders blurred, no retinal
vessels seen.
Grade 2: Significant blurring
of optic nerve and retinal
vessels but still visible.
Grade 1: Few opacities, mild
blurring of optic nerve and
retinal vessels.
Trace (0.5+): Trace.
Grade 0: Clear.
34. SIGN OF UVEITIS- INTERMEDIATE SEGMENT
Additional signs of inflammation in the vitreous include :
• snowball opacities (clumps of inflammatory cells in the vitreous) and
• snowbanks (exudates over the pars plana, especially prominent inferiorly).
Active snowbanks have a fluffy or shaggy appearance.
• As pars planitis becomes inactive, the pars plana appears gliotic or fibrotic and smooth; thus,
these changes are not referred to as snowbanks.
• Vitreal strands and snowballs may vary in clinical appearance by disease type.
• Chronic intermediate uveitis may be associated with cyclitic membrane formation, secondary ciliary
body detachment, and hypotony
35. SIGN OF UVEITIS- POSTERIOR SEGMENT
Signs in the posterior segment of the eye include
• retinal or choroidal inflammatory infiltrates
• inflammatory sheathing of arteries or veins
• exudative, tractional*, or rhegmatogenous* retinal detachment
• retinal pigment epithelial hypertrophy or atrophy*
• atrophy or swelling of the ret ina, choroid, or optic nerve head*
• preretinal or subretinal fibrosis*
• retinal or choroidal neovascularization*
*Indicates structural complications. Retinal and choroidal signs may be unifocal, multifocal, or diffuse.
Posterior segment inflammation is a result of inflammatory or infectious infiltration and resultant
structural damage of the retina and choroid. Retinal and choroidal signs may be unifocal, multifocal, or
diffuse. Lesions are described by size, color, and appearance (eg, well demarcated, geographic), and
anatomical relationship to posterior pole landmarks (see Table 5-7)
36.
37. • infectious agents (viruses, bacteria, fungi, protozoa, and helminths),
• noninfectious entities of presumed immunologic origin, and unknown/ idiopathic causes
(called undifferentiated uveitis).
• Masquerade syndromes such as intraocular lymphoma, retinoblastoma, leukemia,
choroidal metastases, and malignant melanoma can be mistaken for uveitis.
• Other masquerade syndromes include juvenile xanthogranuloma, pigment dispersion
syndrome, retinal detachment, vitreous hemorrhage, retinitis pigmentosa, and ocular
ischemic syndrome.
• One should consider each of these entities in the differential diagnosis of uveitis.
DIFFERENTIAL DIAGNOSIS OF UVEITIS
38. Medical history, review of systems, thorough ophthalmologic and general physical examination,
and formulation of a working differential diagnosis are cornerstones of the workup of a patient with
uveitis.
• Laboratory testing is not a substitute for a thorough, hands-on clinical evaluation.
• Most uveitis specialists do recommend syphilis testing for all uveitis patients, as syphilis
can present as any form of uveitis, and systemic infection is often undiagnosed (treating with
steroid in the presence of untreated occult syphilis infection can be disastrous for patient
outcomes).
• where immunomodulatory therapy (IMT) will be used, most uveitis specialists also recommend
testing for tuberculosis with a purified protein derivative (PPD) skin test or interferon-
gamma release assay.
• A chest radiograph can screen for sarcoidosis, which is a common cause of uveitis with protean
manifestations
ANCILLARY TESTING
39. OPTICAL COHERENCE
TOMOGRAPHY (OCT)
Figure 5-9 Optical coherence tomography image of uveitic macular
edema in a patient with juvenile idiopathic arthritis–associated uveitis
Figure 5-10 Enhanced-depth imaging
optical coherence tomography in a
patient with Vogt- Koyanagi-Harada
syndrome A, During quiescence with
relatively normal choroidal thickness
(arrows). B, During uveitis activity
with diffuse choroidal thickening
(arrows). (
40.
41. Fluorescein angiography is an essential imaging modality for evaluating eyes with chorioretinal
disease and structural complications caused by posterior uveitis.
Fluorescein angiography can detect :
• macular edema (Fig 5-11),
• retinal vasculitis, secondary choroidal or retinal neovascularization, and
• areas of optic nerve, retinal, and
• choroidal inflammation.
Several of the retinochoroidopathies, or white dot syndromes, have characteristic appearances on
FA. Wide and ultrawidefield FA can identify retinal vascular pathology not noted on clinical examination
FLUORESCEIN ANGIOGRAPHY
Figure 5-11 Late transit phase fluorescein angiogram of the left eye
of a patient with sarcoid-associated anterior uveitis showing a
petalloid pattern typical of uveitic macular edema.
42. Anterior segment ultrasound biomicroscopy can be useful in diagnosing pathology of the ciliary
body, iris, and iridocorneal angle in uveitis.
Posterior segment ultrasound, or B-scan ultrasound, can be useful in demonstrating vitreous
opacities, choroidal thickening or elevation, retinal detachment, and cyclitic membrane
formation, as well as in ruling out occult foreign bodies, particularly if media opacities preclude a
view of the posterior segment.
Retained IOL fragments may be visualized in the anterior or posterior segment.
Ultrasonographic imaging may be diagnostic for posterior scleritis.
ULTRASONOGRAPHY
43. • Paracentesis involves using sterile technique at the slit lamp or with the patient supine on a
treatment gurney or chair.
• Topical anesthetic drops are instilled;
• the eye is prepared with topical povidone- iodine solution; and
• a lid speculum can be placed.
• A tuberculin (1- mL) syringe is attached to a sterile 30- gauge needle.
• The syringe is then advanced under direct or slit-lamp visualization into the anterior chamber
through the temporal limbus or clear cornea parallel to the iris plane.
• As much aqueous is aspirated as is safely possible (usually 0.1–0.2 mL), avoiding contact with
the iris and lens.
• Possible complications include :
• anterior chamber bleeding,
• infection, and
• damage to the iris or lens
ANTERIOR CHAMBER PARACENTESIS TECHNIQUE
44. Vitreous specimens can be obtained either by needle tap or by using a vitrectomy instrument.
If a small sample is desired, a needle tap of the vitreous is typically performed with the patient partially
reclining in an examination room chair.
Topical and subconjunctival anesthesia are administered;
the eye is prepared with topical povidone- iodine solution, and
a lid speculum is placed.
Typically, a 25- gauge, 1-inch needle on a 3mL syringe (to provide greater vacuum) is introduced through the
pars plana, directed toward the mid-vitreous cavity, and used to aspirate the vitreous sample.
A diagnostic vitrectomy is performed via a standard 3- port pars plana.
The most common indications for vitreous biopsy include:
• suspected infection,
• primary intraocular lymphoma or
• other intraocular malignancy, and
• infectious etiologies of posterior uveitis or
• panuveitis.
VITREOUS BIOPSY TECHNIQUE
45. chronic uveitis that has an atypical presentation or an inadequate response to
conventional therapy may warrant diagnostic vitrectomy.
Testing typically requires undiluted vitreous specimens.
It is possible to obtain 0.5–1.0 mL of undiluted vitreous for evaluation using standard
vitrectomy techniques.
VITREOUS BIOPSY TECHNIQUE
46. Complications of diagnostic vitrectomy in uveitic eyes can include :
• retinal tears or detachment,
• suprachoroidal or vitreous hemorrhage,
• worsening of cataract or inflammation, and,
• rarely, sympathetic ophthalmia.
Although vitreous surgery can be therapeutic and diagnostic in cases of uveitis, the
pharmacokinetics of delivered intravitreal drugs are markedly altered in eyes that have
undergone pars plana vitrectomy; the half-life of intravitreal corticosteroids, for example, is
significantly reduced in vitrectomized eyes.
VITREOUS BIOPSY TECHNIQUE