This document provides information on central retinal vein occlusion (CRVO), including its prevalence, risk factors, pathogenesis, clinical presentation, investigations, complications, and differences between ischemic and non-ischemic CRVO. Some key points are: CRVO affects around 0.8 in 1000 people over 30 years old and is more common in older patients and those with hypertension, diabetes, or cardiovascular disease. It occurs when a thrombus forms in the central retinal vein, often at the level of the lamina cribrosa. Presentation includes sudden unilateral vision loss. Fundus findings include dilated, tortuous veins and retinal hemorrhages. Classification as ischemic or non-ischemic determines risk of neovascularization and visual prognosis.
Central retinal vein occlusion (CRVO) is the second most common retinal vascular disease after diabetic retinopathy. It is multifactorial in origin, involving abnormalities in blood flow, vessel walls, and blood coagulability. The most common risk factors for CRVO include older age, hypertension, diabetes, obesity, and cardiovascular diseases. CRVO typically presents as sudden unilateral decreased vision without pain. Examination may reveal retinal hemorrhages, dilated tortuous veins, optic disc swelling, and macular edema. Treatment aims to prevent complications like neovascular glaucoma, but has not been shown to reliably reverse the occlusion or improve vision in ischemic CRVO. Management of macular edema includes intravitreal corticost
DR WANI'S TALK ON CRVO FOR RESIDENTS KLE 14 JAN 2023.pptxvbwani
This detailed talk about central retinal vein occlusion deals with all aspects of the disease
It deals with incidence and prevalence, risk factors and clinical features
It also deals with classification, importance of recognizing the ischemic type and the means to recognize it .
It deals with historical studies that gave nformation abour natural course and treatment options
sEveral studies that were conducted to treat CRVO are dealt with in which emphasis is given to anti VEGF drugs
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.
Central retinal vein occlusion (CRVO) occurs when there is a thrombus in the central retinal vein, blocking blood flow and oxygen to the retina. It is a leading cause of vision loss in older adults. CRVO can be non-ischemic or ischemic depending on the extent of blood flow reduction. Risk factors include hypertension, diabetes, hyperlipidemia, and certain blood disorders. Current treatments focus on managing complications like macular edema with anti-VEGF drugs and neovascularization with laser therapy or surgery. Prognosis is generally poor for ischemic CRVO without treatment. Close monitoring is needed to detect complications and guide further management.
This document discusses central retinal vein occlusion (CRVO), including distinguishing between ischemic and non-ischemic types. Ischemic CRVO carries a poorer prognosis due to increased risk of neovascularization and vision loss. Features like extensive hemorrhaging and cotton wool spots indicate ischemic occlusion. Non-ischemic CRVO has a milder appearance and course. The document also outlines evaluation, management considerations, and complications like neovascular glaucoma for CRVO.
This document discusses central retinal vein occlusion (CRVO), including distinguishing between ischemic and non-ischemic types. Ischemic CRVO carries a poorer prognosis due to increased risk of neovascularization and vision loss. Features like extensive hemorrhaging and cotton wool spots indicate ischemic occlusion. Non-ischemic CRVO has a milder appearance and course. The document also outlines evaluation, management considerations, and complications like neovascular glaucoma for CRVO.
This document provides an overview of branched retinal vein occlusion (BRVO). It discusses the classification, epidemiology, risk factors, pathogenesis, signs and symptoms, diagnostic evaluation, and management of BRVO. Key points include that BRVO is the most common type of retinal vein occlusion and risk factors include hypertension, glaucoma, hyperlipidemia, and advancing age. Diagnostic testing includes fluorescein angiography and OCT to evaluate for macular edema, capillary nonperfusion, and neovascularization. Laser photocoagulation and anti-VEGF injections are common treatment approaches for complications such as macular edema.
This document discusses central retinal vein occlusion (CRVO), a retinal vascular disorder where the central retinal vein becomes blocked. It has a prevalence of 0.4% and can be caused by compression of the vein, intraluminal thrombosis, or inflammation. CRVO is classified as perfused or non-perfused based on fluorescein angiography and the degree of retinal capillary non-perfusion. Treatment focuses on managing macular edema and neovascularization, common complications. While no treatment reverses CRVO itself, risk factor modification and therapies targeting edema and neovascularization can help preserve vision.
Central retinal vein occlusion (CRVO) is the second most common retinal vascular disease after diabetic retinopathy. It is multifactorial in origin, involving abnormalities in blood flow, vessel walls, and blood coagulability. The most common risk factors for CRVO include older age, hypertension, diabetes, obesity, and cardiovascular diseases. CRVO typically presents as sudden unilateral decreased vision without pain. Examination may reveal retinal hemorrhages, dilated tortuous veins, optic disc swelling, and macular edema. Treatment aims to prevent complications like neovascular glaucoma, but has not been shown to reliably reverse the occlusion or improve vision in ischemic CRVO. Management of macular edema includes intravitreal corticost
DR WANI'S TALK ON CRVO FOR RESIDENTS KLE 14 JAN 2023.pptxvbwani
This detailed talk about central retinal vein occlusion deals with all aspects of the disease
It deals with incidence and prevalence, risk factors and clinical features
It also deals with classification, importance of recognizing the ischemic type and the means to recognize it .
It deals with historical studies that gave nformation abour natural course and treatment options
sEveral studies that were conducted to treat CRVO are dealt with in which emphasis is given to anti VEGF drugs
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.
Central retinal vein occlusion (CRVO) occurs when there is a thrombus in the central retinal vein, blocking blood flow and oxygen to the retina. It is a leading cause of vision loss in older adults. CRVO can be non-ischemic or ischemic depending on the extent of blood flow reduction. Risk factors include hypertension, diabetes, hyperlipidemia, and certain blood disorders. Current treatments focus on managing complications like macular edema with anti-VEGF drugs and neovascularization with laser therapy or surgery. Prognosis is generally poor for ischemic CRVO without treatment. Close monitoring is needed to detect complications and guide further management.
This document discusses central retinal vein occlusion (CRVO), including distinguishing between ischemic and non-ischemic types. Ischemic CRVO carries a poorer prognosis due to increased risk of neovascularization and vision loss. Features like extensive hemorrhaging and cotton wool spots indicate ischemic occlusion. Non-ischemic CRVO has a milder appearance and course. The document also outlines evaluation, management considerations, and complications like neovascular glaucoma for CRVO.
This document discusses central retinal vein occlusion (CRVO), including distinguishing between ischemic and non-ischemic types. Ischemic CRVO carries a poorer prognosis due to increased risk of neovascularization and vision loss. Features like extensive hemorrhaging and cotton wool spots indicate ischemic occlusion. Non-ischemic CRVO has a milder appearance and course. The document also outlines evaluation, management considerations, and complications like neovascular glaucoma for CRVO.
This document provides an overview of branched retinal vein occlusion (BRVO). It discusses the classification, epidemiology, risk factors, pathogenesis, signs and symptoms, diagnostic evaluation, and management of BRVO. Key points include that BRVO is the most common type of retinal vein occlusion and risk factors include hypertension, glaucoma, hyperlipidemia, and advancing age. Diagnostic testing includes fluorescein angiography and OCT to evaluate for macular edema, capillary nonperfusion, and neovascularization. Laser photocoagulation and anti-VEGF injections are common treatment approaches for complications such as macular edema.
This document discusses central retinal vein occlusion (CRVO), a retinal vascular disorder where the central retinal vein becomes blocked. It has a prevalence of 0.4% and can be caused by compression of the vein, intraluminal thrombosis, or inflammation. CRVO is classified as perfused or non-perfused based on fluorescein angiography and the degree of retinal capillary non-perfusion. Treatment focuses on managing macular edema and neovascularization, common complications. While no treatment reverses CRVO itself, risk factor modification and therapies targeting edema and neovascularization can help preserve vision.
This document discusses retinal venous occlusive disease, which is the second most prevalent retinal vascular disorder following diabetic retinopathy. It can cause partial or complete obstruction of retinal veins, leading to macular edema and vision loss. The document covers the definition, prevalence, risk factors, pathogenesis, classification into central and branch retinal vein occlusions, associated signs and symptoms, investigations, complications, and treatment options. It also presents a clinical case of a patient with a branch retinal vein occlusion who presented with reduced vision and was found to have hypertension.
This document summarizes retinal vein occlusion, including branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). It discusses risk factors, pathogenesis, clinical features, evaluation, and treatment approaches. For BRVO, laser photocoagulation and anti-VEGF injections are used to treat macular edema. For CRVO, outcomes depend on initial visual acuity and perfusion status, with neovascularization and macular edema treated similarly to BRVO.
This document discusses various retinal vascular diseases and associated findings. It covers central retinal vein occlusion and the associated findings except for neovascular glaucoma. It notes that the most common cause of neovascular glaucoma is ischemic central retinal vein occlusion. The document also discusses ophthalmic artery occlusion findings compared to central retinal artery occlusion. Additional topics covered include hypertensive retinopathy, sickle cell retinopathy, Coats disease, retinal artery macroaneurysms, and other retinal conditions like radiation retinopathy. Treatment options are provided for several of the conditions.
This document discusses various topics related to pachychoroid disease including:
1. Key findings on imaging include a thickened choroid, dilated choroidal vessels, and choroidal hyperpermeability. Common symptoms include blurred vision and metamorphopsia.
2. Potential causes include hypertension, tobacco use, corticosteroid use, and emotional stress. Treatment depends on severity but may include stopping exacerbating factors, observation, laser treatment, photodynamic therapy, or anti-VEGF injections.
3. The document describes several subtypes of pachychoroid disease including central serous chorioretinopathy (CSCR), pachychoroid pigment epitheliopathy, poly
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system by thrombus formation and may involve the central, hemi-central or branch retinal vein.
The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, risk factors, clinical features, investigations, and management approaches. Some key points:
- BRVO is the second most common cause of vision loss due to retinal vascular disease, after diabetic retinopathy. It occurs most often in patients in their 50s-60s and is caused by obstruction of a branch retinal vein.
- Risk factors include hypertension, diabetes, hyperlipidemia, glaucoma, smoking, and age-related atherosclerosis. Laser treatment can help manage macular edema and neovascularization complications.
- Treatment aims to address modifiable risk factors and manage sight-threatening complications like macular edema,
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, risk factors, clinical features, investigations, and management approaches. Some key points:
- BRVO is the second most common cause of vision loss due to retinal vascular disease, after diabetic retinopathy. It occurs most often in patients in their 50s-60s and is caused by obstruction of a branch retinal vein.
- Risk factors include hypertension, diabetes, hyperlipidemia, glaucoma, smoking, and age-related atherosclerosis. Laser treatment can help manage macular edema and neovascularization complications.
- Treatment aims to manage modifiable risk factors and sight-threatening complications like macular edema, non
This document provides information on various types of corneal degeneration. It discusses age-related degenerations like arcus senilis and Vogt's white limbal girdle. Pathological degenerations described include fatty degeneration, hyaline degeneration, amyloidosis, and calcific degeneration (band keratopathy). Specific conditions like Salzmann's nodular degeneration, furrow degeneration, pellucid marginal degeneration, and Terrien's marginal degeneration are also summarized. The classifications, clinical features, etiology, and treatment approaches for different corneal degenerations are concisely outlined.
The document describes various retinal conditions and findings. It discusses hypertensive retinopathy, diabetic retinopathy, sickle cell retinopathy, retinopathy of prematurity, central retinal artery occlusion, ocular ischemic syndrome, Coats disease, lattice degeneration, retinal detachment, retinoschisis, hereditary hyaloidoretinopathies including Stickler syndrome and familial exudative vitreoretinopathy. It provides details on clinical findings, risk factors, treatments, and prognosis for each condition.
This document discusses retinal vein occlusion (RVO), including the classification, pathogenesis, risk factors, clinical presentation, management, and prognosis of central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). It summarizes key studies on the management of CRVO and BRVO with anti-VEGF agents, steroids, laser photocoagulation, and extended follow up protocols. Prognosis is generally poor for CRVO and depends on factors like chronic macular edema or ischemia for BRVO.
1) Age-related macular degeneration (ARMD) is caused by the degeneration of retinal pigment epithelium cells, which leads to the accumulation of metabolic waste known as drusen. Large or numerous drusen are risk factors for future vision loss.
2) Optical coherence tomography angiography (OCTA) can detect changes in blood flow associated with drusen and differentiate between dry and wet ARMD. It can also characterize the abnormal new blood vessel growth associated with wet ARMD.
3) Anti-VEGF therapies are an established treatment for wet ARMD by inhibiting vascular endothelial growth factor A (VEGF-A), which drives the abnormal blood vessel proliferation. OCTA is useful
- Diabetic retinopathy is a leading cause of blindness in people aged 20-74 and affects individuals in their most productive years. The risk and severity of retinopathy increases with longer duration of diabetes and poorer blood glucose control.
- The disease involves microvascular changes including microaneurysms, hemorrhages, hard exudates, and new abnormal blood vessel growth. Without treatment, this can lead to vision loss from macular edema, retinal detachment, or vitreous hemorrhage.
- Treatment involves managing blood sugar and blood pressure, as well as laser photocoagulation surgery or intravitreal injections to prevent vision loss from proliferative retinopathy or macular edema.
This document discusses retinal vascular occlusions, including their classification, presentation, investigations, and management. It begins by introducing retinal arterial and venous occlusions as significant causes of blindness. It then covers the anatomy of retinal blood supply and classifies occlusions by anatomical site. The remainder of the document details the characteristics, risk factors, clinical features, investigations, and treatment approaches for various types of retinal arterial occlusions (central retinal artery occlusion, branch retinal artery occlusion, cilioretinal artery occlusion) and venous occlusions (central retinal vein occlusion, branch retinal vein occlusion, hemiretinal vein occlusion).
1. Branch retinal vein occlusion (BRVO) is a common cause of retinal vascular disease that affects the retinal veins, usually occurring at arteriovenous crossings where a retinal artery crosses over a vein.
2. BRVO can lead to vision loss through macular ischemia, macular edema, or complications from neovascularization. Fluorescein angiography and optical coherence tomography are important for evaluating macular perfusion status and edema.
3. Treatment of macular edema from BRVO includes intravitreal anti-VEGF injections or laser photocoagulation, while prophylactic panretinal photocoagulation can reduce risks of neovascularization in eyes with large areas of capillary non
Choroidal neovascular membranes (CNVM)Md Riyaj Ali
Choroidal neovascularization (CNV) involves the abnormal growth of new blood vessels from the choroid layer of the eye through Bruch's membrane. This can cause vision loss and is a common cause of wet macular degeneration. CNV occurs due to alterations in Bruch's membrane and high levels of vascular endothelial growth factor. It is classified based on its location relative to the retinal pigment epithelium and fovea. Symptoms include sudden vision loss and visual distortions. CNV is diagnosed through imaging like optical coherence tomography and fluorescein angiography and treated with injections of anti-VEGF drugs to inhibit blood vessel growth.
Retinal vascular diseases can cause vision loss. This document discusses retinal vein occlusion (RVO) and retinal artery occlusion (RAO). For RVO, it covers risk factors like age and hypertension. It also describes treatments for complications like neovascularization and macular edema using anti-VEGF injections or steroids. For RAO, it notes the cherry red spot sign and discusses potentially treating the underlying cause to prevent further vision loss in the fellow eye. Systemic workup aims to identify conditions like giant cell arteritis that require treatment to prevent bilateral involvement.
Angioid streaks are cracks in Bruch's membrane that were first described in 1889. They are typically bilateral and radiate out from the optic disc in a cruciate pattern. The cracks are caused by calcification and degradation of Bruch's membrane. The most common complication is choroidal neovascularization, which can cause vision loss if untreated. Modern treatments with anti-VEGF agents have shown promise in preventing scarring and vision loss from neovascularization in angioid streaks.
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.[1] The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
It's an indepth presentation by Dr. Shah-Noor Hassan.
Medical imaging practice, diagnosis, symptoms and treatment for Cerebral Cavernous Malformation, written, edited and reviewed by Dr Walif Chbeir. Images can be found on WalifChbeir.net.
This document provides information on superior vena cava syndrome (SVCS), including its anatomy, pathophysiology, clinical features, grading, etiology, diagnosis, and management. SVCS is caused by obstruction of the superior vena cava, most commonly due to malignancy involving compression or invasion of the vessel. Diagnosis involves imaging such as CT or MR venography to identify the site and cause of obstruction. Treatment depends on symptom severity and underlying cause, but may include endovascular stenting, radiation therapy, or chemotherapy.
Retinal dystrophies are a group of degenerative retinal disorders with genetic and clinical heterogeneity. They can affect rods, cones, or both photoreceptors. Retinitis pigmentosa is the most common form of inherited retinal dystrophy and is characterized by rod degeneration followed by cone loss. It presents with night blindness, progressive peripheral vision loss, attenuation of retinal vessels, waxy pallor of the optic disc, and bone spicule pigmentation. Electroretinography shows a rod-cone pattern of dysfunction. Genetic testing can identify mutations in over 270 associated genes.
This document discusses retinal venous occlusive disease, which is the second most prevalent retinal vascular disorder following diabetic retinopathy. It can cause partial or complete obstruction of retinal veins, leading to macular edema and vision loss. The document covers the definition, prevalence, risk factors, pathogenesis, classification into central and branch retinal vein occlusions, associated signs and symptoms, investigations, complications, and treatment options. It also presents a clinical case of a patient with a branch retinal vein occlusion who presented with reduced vision and was found to have hypertension.
This document summarizes retinal vein occlusion, including branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO). It discusses risk factors, pathogenesis, clinical features, evaluation, and treatment approaches. For BRVO, laser photocoagulation and anti-VEGF injections are used to treat macular edema. For CRVO, outcomes depend on initial visual acuity and perfusion status, with neovascularization and macular edema treated similarly to BRVO.
This document discusses various retinal vascular diseases and associated findings. It covers central retinal vein occlusion and the associated findings except for neovascular glaucoma. It notes that the most common cause of neovascular glaucoma is ischemic central retinal vein occlusion. The document also discusses ophthalmic artery occlusion findings compared to central retinal artery occlusion. Additional topics covered include hypertensive retinopathy, sickle cell retinopathy, Coats disease, retinal artery macroaneurysms, and other retinal conditions like radiation retinopathy. Treatment options are provided for several of the conditions.
This document discusses various topics related to pachychoroid disease including:
1. Key findings on imaging include a thickened choroid, dilated choroidal vessels, and choroidal hyperpermeability. Common symptoms include blurred vision and metamorphopsia.
2. Potential causes include hypertension, tobacco use, corticosteroid use, and emotional stress. Treatment depends on severity but may include stopping exacerbating factors, observation, laser treatment, photodynamic therapy, or anti-VEGF injections.
3. The document describes several subtypes of pachychoroid disease including central serous chorioretinopathy (CSCR), pachychoroid pigment epitheliopathy, poly
Retinal vein occlusion (RVO) is an obstruction of the retinal venous system by thrombus formation and may involve the central, hemi-central or branch retinal vein.
The most common aetiological factor is compression by adjacent atherosclerotic retinal arteries.
Other possible causes are external compression or disease of the vein wall e.g. vasculitis.
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, risk factors, clinical features, investigations, and management approaches. Some key points:
- BRVO is the second most common cause of vision loss due to retinal vascular disease, after diabetic retinopathy. It occurs most often in patients in their 50s-60s and is caused by obstruction of a branch retinal vein.
- Risk factors include hypertension, diabetes, hyperlipidemia, glaucoma, smoking, and age-related atherosclerosis. Laser treatment can help manage macular edema and neovascularization complications.
- Treatment aims to address modifiable risk factors and manage sight-threatening complications like macular edema,
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, risk factors, clinical features, investigations, and management approaches. Some key points:
- BRVO is the second most common cause of vision loss due to retinal vascular disease, after diabetic retinopathy. It occurs most often in patients in their 50s-60s and is caused by obstruction of a branch retinal vein.
- Risk factors include hypertension, diabetes, hyperlipidemia, glaucoma, smoking, and age-related atherosclerosis. Laser treatment can help manage macular edema and neovascularization complications.
- Treatment aims to manage modifiable risk factors and sight-threatening complications like macular edema, non
This document provides information on various types of corneal degeneration. It discusses age-related degenerations like arcus senilis and Vogt's white limbal girdle. Pathological degenerations described include fatty degeneration, hyaline degeneration, amyloidosis, and calcific degeneration (band keratopathy). Specific conditions like Salzmann's nodular degeneration, furrow degeneration, pellucid marginal degeneration, and Terrien's marginal degeneration are also summarized. The classifications, clinical features, etiology, and treatment approaches for different corneal degenerations are concisely outlined.
The document describes various retinal conditions and findings. It discusses hypertensive retinopathy, diabetic retinopathy, sickle cell retinopathy, retinopathy of prematurity, central retinal artery occlusion, ocular ischemic syndrome, Coats disease, lattice degeneration, retinal detachment, retinoschisis, hereditary hyaloidoretinopathies including Stickler syndrome and familial exudative vitreoretinopathy. It provides details on clinical findings, risk factors, treatments, and prognosis for each condition.
This document discusses retinal vein occlusion (RVO), including the classification, pathogenesis, risk factors, clinical presentation, management, and prognosis of central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO). It summarizes key studies on the management of CRVO and BRVO with anti-VEGF agents, steroids, laser photocoagulation, and extended follow up protocols. Prognosis is generally poor for CRVO and depends on factors like chronic macular edema or ischemia for BRVO.
1) Age-related macular degeneration (ARMD) is caused by the degeneration of retinal pigment epithelium cells, which leads to the accumulation of metabolic waste known as drusen. Large or numerous drusen are risk factors for future vision loss.
2) Optical coherence tomography angiography (OCTA) can detect changes in blood flow associated with drusen and differentiate between dry and wet ARMD. It can also characterize the abnormal new blood vessel growth associated with wet ARMD.
3) Anti-VEGF therapies are an established treatment for wet ARMD by inhibiting vascular endothelial growth factor A (VEGF-A), which drives the abnormal blood vessel proliferation. OCTA is useful
- Diabetic retinopathy is a leading cause of blindness in people aged 20-74 and affects individuals in their most productive years. The risk and severity of retinopathy increases with longer duration of diabetes and poorer blood glucose control.
- The disease involves microvascular changes including microaneurysms, hemorrhages, hard exudates, and new abnormal blood vessel growth. Without treatment, this can lead to vision loss from macular edema, retinal detachment, or vitreous hemorrhage.
- Treatment involves managing blood sugar and blood pressure, as well as laser photocoagulation surgery or intravitreal injections to prevent vision loss from proliferative retinopathy or macular edema.
This document discusses retinal vascular occlusions, including their classification, presentation, investigations, and management. It begins by introducing retinal arterial and venous occlusions as significant causes of blindness. It then covers the anatomy of retinal blood supply and classifies occlusions by anatomical site. The remainder of the document details the characteristics, risk factors, clinical features, investigations, and treatment approaches for various types of retinal arterial occlusions (central retinal artery occlusion, branch retinal artery occlusion, cilioretinal artery occlusion) and venous occlusions (central retinal vein occlusion, branch retinal vein occlusion, hemiretinal vein occlusion).
1. Branch retinal vein occlusion (BRVO) is a common cause of retinal vascular disease that affects the retinal veins, usually occurring at arteriovenous crossings where a retinal artery crosses over a vein.
2. BRVO can lead to vision loss through macular ischemia, macular edema, or complications from neovascularization. Fluorescein angiography and optical coherence tomography are important for evaluating macular perfusion status and edema.
3. Treatment of macular edema from BRVO includes intravitreal anti-VEGF injections or laser photocoagulation, while prophylactic panretinal photocoagulation can reduce risks of neovascularization in eyes with large areas of capillary non
Choroidal neovascular membranes (CNVM)Md Riyaj Ali
Choroidal neovascularization (CNV) involves the abnormal growth of new blood vessels from the choroid layer of the eye through Bruch's membrane. This can cause vision loss and is a common cause of wet macular degeneration. CNV occurs due to alterations in Bruch's membrane and high levels of vascular endothelial growth factor. It is classified based on its location relative to the retinal pigment epithelium and fovea. Symptoms include sudden vision loss and visual distortions. CNV is diagnosed through imaging like optical coherence tomography and fluorescein angiography and treated with injections of anti-VEGF drugs to inhibit blood vessel growth.
Retinal vascular diseases can cause vision loss. This document discusses retinal vein occlusion (RVO) and retinal artery occlusion (RAO). For RVO, it covers risk factors like age and hypertension. It also describes treatments for complications like neovascularization and macular edema using anti-VEGF injections or steroids. For RAO, it notes the cherry red spot sign and discusses potentially treating the underlying cause to prevent further vision loss in the fellow eye. Systemic workup aims to identify conditions like giant cell arteritis that require treatment to prevent bilateral involvement.
Angioid streaks are cracks in Bruch's membrane that were first described in 1889. They are typically bilateral and radiate out from the optic disc in a cruciate pattern. The cracks are caused by calcification and degradation of Bruch's membrane. The most common complication is choroidal neovascularization, which can cause vision loss if untreated. Modern treatments with anti-VEGF agents have shown promise in preventing scarring and vision loss from neovascularization in angioid streaks.
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.[1] The vitreous humor is the clear gel that fills the space between the lens and the retina of the eye. A variety of conditions can result in blood leaking into the vitreous humor, which can cause impaired vision, floaters, and photopsia.
It's an indepth presentation by Dr. Shah-Noor Hassan.
Medical imaging practice, diagnosis, symptoms and treatment for Cerebral Cavernous Malformation, written, edited and reviewed by Dr Walif Chbeir. Images can be found on WalifChbeir.net.
This document provides information on superior vena cava syndrome (SVCS), including its anatomy, pathophysiology, clinical features, grading, etiology, diagnosis, and management. SVCS is caused by obstruction of the superior vena cava, most commonly due to malignancy involving compression or invasion of the vessel. Diagnosis involves imaging such as CT or MR venography to identify the site and cause of obstruction. Treatment depends on symptom severity and underlying cause, but may include endovascular stenting, radiation therapy, or chemotherapy.
Similar to zzzCENTRAL RETINAL VEIN OCCLUSION.pptx (20)
Retinal dystrophies are a group of degenerative retinal disorders with genetic and clinical heterogeneity. They can affect rods, cones, or both photoreceptors. Retinitis pigmentosa is the most common form of inherited retinal dystrophy and is characterized by rod degeneration followed by cone loss. It presents with night blindness, progressive peripheral vision loss, attenuation of retinal vessels, waxy pallor of the optic disc, and bone spicule pigmentation. Electroretinography shows a rod-cone pattern of dysfunction. Genetic testing can identify mutations in over 270 associated genes.
ECTROPION^JENTROPION AND THEIR MANAGEMENT 2.pptxHarshika Malik
This document discusses ectropion and entropion of the eyelids, including their causes, types, clinical evaluation, and management. Ectropion is the outward turning of the eyelid margin, while entropion is the inward turning. Involutional ectropion most commonly affects the lower eyelids in elderly patients due to gravitational changes. Management depends on the type but may include procedures to shorten the eyelid or correct underlying issues like laxity of the medial or lateral canthal tendons. Prompt treatment is important to prevent complications such as dry eye or corneal damage.
This document discusses episcleritis and scleritis. Episcleritis involves inflammation of the episclera and is typically benign and self-limiting. Scleritis involves inflammation of the sclera and can be more serious, potentially causing vision loss if untreated. Scleritis is classified as anterior (non-necrotizing or necrotizing) or posterior. Treatment involves topical steroids and NSAIDs for mild cases and systemic steroids and immunosuppressants for more severe or necrotizing forms. Both conditions require treatment of any underlying systemic diseases.
The document discusses the history and evolution of corneal transplantation (keratoplasty) from early experiments in the 18th-19th centuries to modern techniques. Some key events include the first successful human corneal transplant being performed by Eduard Zirm in 1906, the introduction of antibiotics and steroids improving outcomes in the 1940s, and recent advances with femtosecond lasers and other technologies. The document also reviews the various surgical techniques used for corneal transplantation and postoperative care considerations.
The document discusses lamellar keratoplasty, which involves replacing diseased corneal tissue while retaining normal tissue. It describes anterior lamellar keratoplasty (ALKP) and posterior lamellar keratoplasty (PLKP). ALKP replaces varying amounts of anterior corneal tissue, while PLKP replaces the Descemet's membrane and endothelium. The document also discusses indications, surgical techniques like the Anwar bubble technique, and complications for anterior lamellar keratoplasty. Posterior lamellar keratoplasty techniques like DSAEK are described to replace dysfunctional endothelium.
This document provides an overview of retinopathy of prematurity (ROP), including:
1) ROP is a disorder of the developing retina in premature infants that can lead to blindness if left untreated. It occurs when the retina is incompletely developed and blood vessels grow abnormally.
2) Risk factors include prematurity, low birth weight, excess oxygen exposure, and other medical complications. The pathogenesis involves abnormal vasoproliferation and retinal neovascularization due to disrupted retinal vascular development.
3) ROP is classified based on location within zones of the retina, stage of disease progression from mild to severe, and presence of "plus disease" indicating worse prognosis. Timely screening and treatment can
This document provides an overview of thyroid ophthalmopathy (TED), also known as Graves' ophthalmopathy. It discusses the epidemiology, etiology, risk factors, pathogenesis, clinical signs and symptoms, diagnosis, and management of the autoimmune disease. TED is caused by inflammation and accumulation of fluids in the orbit, raising pressure and causing enlargement of the extraocular muscles and adipose tissue. Symptoms include eye bulging, double vision, and dryness. Management involves treating any thyroid abnormalities, using corticosteroids, radiation, or surgery to address eye involvement and symptoms.
The orbit is a pyramidal space located between the anterior cranial fossa and the maxillary sinuses. It is formed by seven bones and contains the eyeball as well as nerves, blood vessels and extraocular muscles. Proptosis refers to forward displacement of the eyeball. It can be caused by infections, inflammation, vascular abnormalities, tumors or trauma based on characteristics like age of onset and laterality. Evaluation involves inspection of periorbital region and eye examination along with imaging studies and biopsy as needed to identify the cause which guides treatment.
Mechanical ocular trauma can cause a wide range of eye injuries from relatively minor to vision threatening. The document defines standard terminology for different types of eye injuries using the Birmingham Eye Trauma Terminology (BETT) system. It describes closed globe injuries which involve no penetration of the eyewall, open globe injuries which involve penetration of the eyewall, and different types of open globe injuries including globe rupture, penetrating injuries, and perforating injuries. It provides details on mechanisms of injury, clinical findings, examination techniques, and treatment approaches for different injury types.
Retinal detachment is defined as the separation of the neurosensory retina from the retinal pigment epithelium. There are three main types: rhegmatogenous retinal detachment caused by a retinal break, tractional retinal detachment caused by vitreous traction, and exudative retinal detachment caused by fluid accumulation beneath the retina. Rhegmatogenous retinal detachment is usually associated with a retinal break and treated surgically by sealing the break with photocoagulation or cryotherapy and using scleral buckling or vitrectomy to reattach the retina. Tractional and exudative retinal detachments are generally treated with vitrectomy but may also be treated medically or with laser in some cases
The document discusses the anatomy and physiology of ocular muscles. It describes:
1. The intrinsic and extrinsic muscles that control eye movement and pupil size/lens shape.
2. The origins, insertions, innervation and actions of individual muscles.
3. Principles of binocular vision including fusion, stereopsis, prerequisites for development and anomalies like suppression and amblyopia.
4. Types of strabismus like tropia, phoria, pseudostrabismus and their characteristics. Heterophoria is defined and compensated vs decompensated types discussed.
Diabetic retinopathy is a progressive dysfunction of the retinal blood vessels caused by chronic hyperglycemia. It can cause vision loss and blindness if not treated. The risk and severity of retinopathy increases with the duration of diabetes and poor blood sugar control. Early stages are characterized by microaneurysms and hemorrhages, while proliferative stages involve new blood vessel growth. Macular edema can occur at any stage and is a leading cause of vision loss. Treatment includes laser photocoagulation, anti-VEGF injections, and vitrectomy surgery depending on the severity of retinopathy and presence of macular edema. Strict blood sugar and blood pressure control can help prevent and slow the progression of diabetic ret
Optic Neuritis, Papilledema document discusses optic nerve conditions. It defines optic neuritis as inflammation of the optic nerve impairing nerve conduction that can be caused by demyelination, infection, or autoimmunity. Papilledema is defined as bilateral, non-inflammatory swelling of the optic disc due to increased intracranial pressure. The document covers causes, signs, symptoms, diagnostic tests, treatment, and prognosis for both conditions.
The retina is the innermost layer of the eye that contains photoreceptor cells. Retinoblastoma is a malignant tumor that arises from these photoreceptor cells in the retina, most commonly affecting young children under 5 years old. It can be hereditary if caused by a mutation in the RB1 gene, resulting in bilateral and multifocal tumors, or non-hereditary if caused by somatic mutations, usually presenting as a unilateral tumor. Treatment depends on tumor size and extent but may include chemotherapy, local therapies like cryotherapy or brachytherapy, and enucleation of the eye for advanced cases. Early diagnosis and treatment can help preserve vision and life.
Secondary glaucoma is caused by an underlying ocular or systemic disease that leads to increased intraocular pressure and potential vision loss. It can be classified based on the mechanism of pressure rise into open-angle or angle-closure glaucoma. Common causes include lens-induced glaucoma, pigmentary glaucoma, neovascular glaucoma due to retinal ischemia, inflammatory glaucoma, traumatic glaucoma, steroid-induced glaucoma, pseudoexfoliative glaucoma, and glaucoma following cataract surgery. Treatment depends on the underlying cause but may include medications, laser treatment, or surgery to lower pressure and prevent further optic nerve damage.
This document discusses approaches to treating paediatric cataracts. It notes that paediatric cataract accounts for 7.4-15.3% of paediatric blindness worldwide. Etiologies include genetic factors, intrauterine infections, metabolic disorders, trauma, and prematurity. A thorough history, ocular exam, and laboratory tests are required to evaluate the cataract and check for associated ocular or systemic abnormalities. Surgical removal is indicated for visually significant cataracts. Challenges of paediatric cataract surgery include performing accurate biometry and intraocular lens power calculations due to the developing eye, achieving a stable anterior chamber, and addressing post-operative aphakia or amblyopia management.
This document discusses various types of ischemic optic neuropathies including anterior ischemic optic neuropathy (AION) and posterior ischemic optic neuropathy (PION). It describes the differences between arteritic AION (caused by giant cell arteritis) and non-arteritic AION, with the former affecting older patients and often causing bilateral simultaneous vision loss. Risk factors for NAION include hypertension, diabetes, and sleep apnea. The document provides details on clinical evaluation, imaging, and management of these vision-threatening conditions.
This document provides information on diseases of the lacrimal apparatus. It describes the anatomy of the lacrimal gland and drainage system. It discusses conditions such as dacryocystitis, which is inflammation of the lacrimal sac. Dacryocystitis can be congenital in infants due to blockage, or adult onset due to infection. Chronic dacryocystitis is more common and can lead to a lacrimal mucocele or pyocoele if left untreated. Surgical treatments like dacryocystorhinostomy are described to repair blockages and restore tear drainage.
The document discusses diseases of the lens, including its anatomy, transparency mechanisms, and types of cataracts. It describes the lens's structure and functions. For cataracts, it covers the differential diagnosis, etiological classification including congenital vs acquired cataracts, and morphological classification. Evaluation, indications for surgery, timing of surgery, intraocular lens power calculation and material selection, surgical techniques, and post-operative rehabilitation are summarized.
Spontaneous Bacterial Peritonitis - Pathogenesis , Clinical Features & Manage...Jim Jacob Roy
In this presentation , SBP ( spontaneous bacterial peritonitis ) , which is a common complication in patients with cirrhosis and ascites is described in detail.
The reference for this presentation is Sleisenger and Fordtran's Gastrointestinal and Liver Disease Textbook ( 11th edition ).
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7shruti jagirdar
Unit 4: MRA 103T Regulatory affairs
This guideline is directed principally toward new Molecular Entities that are
likely to have significant use in the elderly, either because the disease intended
to be treated is characteristically a disease of aging ( e.g., Alzheimer's disease) or
because the population to be treated is known to include substantial numbers of
geriatric patients (e.g., hypertension).
Congestive Heart failure is caused by low cardiac output and high sympathetic discharge. Diuretics reduce preload, ACE inhibitors lower afterload, beta blockers reduce sympathetic activity, and digitalis has inotropic effects. Newer medications target vasodilation and myosin activation to improve heart efficiency while lowering energy requirements. Combination therapy, following an assessment of cardiac function and volume status, is the most effective strategy to heart failure care.
Travel Clinic Cardiff: Health Advice for International TravelersNX Healthcare
Travel Clinic Cardiff offers comprehensive travel health services, including vaccinations, travel advice, and preventive care for international travelers. Our expert team ensures you are well-prepared and protected for your journey, providing personalized consultations tailored to your destination. Conveniently located in Cardiff, we help you travel with confidence and peace of mind. Visit us: www.nxhealthcare.co.uk
Giloy in Ayurveda - Classical Categorization and SynonymsPlanet Ayurveda
Giloy, also known as Guduchi or Amrita in classical Ayurvedic texts, is a revered herb renowned for its myriad health benefits. It is categorized as a Rasayana, meaning it has rejuvenating properties that enhance vitality and longevity. Giloy is celebrated for its ability to boost the immune system, detoxify the body, and promote overall wellness. Its anti-inflammatory, antipyretic, and antioxidant properties make it a staple in managing conditions like fever, diabetes, and stress. The versatility and efficacy of Giloy in supporting health naturally highlight its importance in Ayurveda. At Planet Ayurveda, we provide a comprehensive range of health services and 100% herbal supplements that harness the power of natural ingredients like Giloy. Our products are globally available and affordable, ensuring that everyone can benefit from the ancient wisdom of Ayurveda. If you or your loved ones are dealing with health issues, contact Planet Ayurveda at 01725214040 to book an online video consultation with our professional doctors. Let us help you achieve optimal health and wellness naturally.
PGx Analysis in VarSeq: A User’s PerspectiveGolden Helix
Since our release of the PGx capabilities in VarSeq, we’ve had a few months to gather some insights from various use cases. Some users approach PGx workflows by means of array genotyping or what seems to be a growing trend of adding the star allele calling to the existing NGS pipeline for whole genome data. Luckily, both approaches are supported with the VarSeq software platform. The genotyping method being used will also dictate what the scope of the tertiary analysis will be. For example, are your PGx reports a standalone pipeline or would your lab’s goal be to handle a dual-purpose workflow and report on PGx + Diagnostic findings.
The purpose of this webcast is to:
Discuss and demonstrate the approaches with array and NGS genotyping methods for star allele calling to prep for downstream analysis.
Following genotyping, explore alternative tertiary workflow concepts in VarSeq to handle PGx reporting.
Moreover, we will include insights users will need to consider when validating their PGx workflow for all possible star alleles and options you have for automating your PGx analysis for large number of samples. Please join us for a session dedicated to the application of star allele genotyping and subsequent PGx workflows in our VarSeq software.
“Psychiatry and the Humanities”: An Innovative Course at the University of Mo...Université de Montréal
“Psychiatry and the Humanities”: An Innovative Course at the University of Montreal Expanding the medical model to embrace the humanities. Link: https://www.psychiatrictimes.com/view/-psychiatry-and-the-humanities-an-innovative-course-at-the-university-of-montreal
Breast cancer: Post menopausal endocrine therapyDr. Sumit KUMAR
Breast cancer in postmenopausal women with hormone receptor-positive (HR+) status is a common and complex condition that necessitates a multifaceted approach to management. HR+ breast cancer means that the cancer cells grow in response to hormones such as estrogen and progesterone. This subtype is prevalent among postmenopausal women and typically exhibits a more indolent course compared to other forms of breast cancer, which allows for a variety of treatment options.
Diagnosis and Staging
The diagnosis of HR+ breast cancer begins with clinical evaluation, imaging, and biopsy. Imaging modalities such as mammography, ultrasound, and MRI help in assessing the extent of the disease. Histopathological examination and immunohistochemical staining of the biopsy sample confirm the diagnosis and hormone receptor status by identifying the presence of estrogen receptors (ER) and progesterone receptors (PR) on the tumor cells.
Staging involves determining the size of the tumor (T), the involvement of regional lymph nodes (N), and the presence of distant metastasis (M). The American Joint Committee on Cancer (AJCC) staging system is commonly used. Accurate staging is critical as it guides treatment decisions.
Treatment Options
Endocrine Therapy
Endocrine therapy is the cornerstone of treatment for HR+ breast cancer in postmenopausal women. The primary goal is to reduce the levels of estrogen or block its effects on cancer cells. Commonly used agents include:
Selective Estrogen Receptor Modulators (SERMs): Tamoxifen is a SERM that binds to estrogen receptors, blocking estrogen from stimulating breast cancer cells. It is effective but may have side effects such as increased risk of endometrial cancer and thromboembolic events.
Aromatase Inhibitors (AIs): These drugs, including anastrozole, letrozole, and exemestane, lower estrogen levels by inhibiting the aromatase enzyme, which converts androgens to estrogen in peripheral tissues. AIs are generally preferred in postmenopausal women due to their efficacy and safety profile compared to tamoxifen.
Selective Estrogen Receptor Downregulators (SERDs): Fulvestrant is a SERD that degrades estrogen receptors and is used in cases where resistance to other endocrine therapies develops.
Combination Therapies
Combining endocrine therapy with other treatments enhances efficacy. Examples include:
Endocrine Therapy with CDK4/6 Inhibitors: Palbociclib, ribociclib, and abemaciclib are CDK4/6 inhibitors that, when combined with endocrine therapy, significantly improve progression-free survival in advanced HR+ breast cancer.
Endocrine Therapy with mTOR Inhibitors: Everolimus, an mTOR inhibitor, can be added to endocrine therapy for patients who have developed resistance to aromatase inhibitors.
Chemotherapy
Chemotherapy is generally reserved for patients with high-risk features, such as large tumor size, high-grade histology, or extensive lymph node involvement. Regimens often include anthracyclines and taxanes.
5-hydroxytryptamine or 5-HT or Serotonin is a neurotransmitter that serves a range of roles in the human body. It is sometimes referred to as the happy chemical since it promotes overall well-being and happiness.
It is mostly found in the brain, intestines, and blood platelets.
5-HT is utilised to transport messages between nerve cells, is known to be involved in smooth muscle contraction, and adds to overall well-being and pleasure, among other benefits. 5-HT regulates the body's sleep-wake cycles and internal clock by acting as a precursor to melatonin.
It is hypothesised to regulate hunger, emotions, motor, cognitive, and autonomic processes.
- Video recording of this lecture in English language: https://youtu.be/RvdYsTzgQq8
- Video recording of this lecture in Arabic language: https://youtu.be/ECILGWtgZko
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. INTRODUCTION
Retinal vein occlusions RVOs (
BRVO+CRVO+HEMI-CRVO) are 2nd most
common retinal vascular diseases ( 1st is
Diabetic Retinopathy )
Branch retinal vein occlusions(BRVO) >
CRVOs
BRVO-80%, CRVO-20%
3. CRVO PREVALENCE & INCIDENCE
Prevalence- CRVO was 0.8/1000 and BRVO was 4.4/1000 population aged 30 years and above
(5.2/1000)
Incidence- RVO 16 per 10,000/year in persons aged 50 years and above – CRVO is
3/10000,BRVO is 13/10000 per year
4. CRVO RISK FACTORS
CRVO is multifactorial in origin,in which
Virchow’s traid of abnormalities of
blood flow
vessel walls
blood coagulability
all play a role
5. CRVO SYSTEMIC RISK FACTORS
a) Age- Higher age. 90% of CRVOS are > 50 years old
b) Hypertension- present in 64% of patients with RVO
c) Diabetes Mellitus- present in 10-25% of RVO cases
d) Obesity
e) Cardiovascular diseases
f) Hyperlipidemia -35% cases – cholesterol >6.5 mmol/l
6. g) Inflammatory Diseases- they cause retinal vasculitis (pts aged < 45 yrs)
ENDOTHELIAL DAMAGE
Sarcoidosis
Behcet’s disease
Wegener’s granulomatosis
Goodpastures syndrome
Other diseases with retinal vasculitis
7. H) Myeloproliferative disorders ( to be considered in pts < 45 yrs )-
STASIS OF BLOOD FLOW
Polycythemia
Abnormal plasma proteins ( myeloma,waldenstrom macroglobuinaemia )
Leukiamias
i) Thrombophilic disorders ( to be considered in pts < 45 yrs)-
HYPERCOAGULABILITY
Hyperhomocysteinaemia
Anti-phospholipid antibodies ( lupus anticoagulant & anti-cardiolipin )
8. J) Inherited disorders of hypercoagulability
Factor V Leidin deficiency
Protein C deficiency
Protein S deficiency
k) More unusual associations
Oral contraceptives
Chronic renal failure
Other secondary causes of HTN and DM (e.g.- CUSHINGs SYNDROME)
Secondary causes of hyperlipidaemia (e.g.- hypothyroidism)
9. CRVO OCULAR RISK FACTORS
a) Glaucoma – CRVO>BRVO ( 5times more likely to have CRVO if glaucoma is present )
b) Retinal vasculitis – Eales disease
c) Carotid cavernous fistula
d) Orbital tumors
e) Disc drusens
13. PATHOGENESIS
The occlusion of the CRV occurs at the level of lamina cribrosa or just behind
The occlusion occurs due to formation of a thrombus in the vein
14. Why at lamina cribrosa?-conditions that
favor occlusion at this place
Narrow lumen of CRV and CRA
in lamina cribrosa-tunnel in LC is
narrow
Common adventitial sheath
envelopes CRA and CRV in lamina
cribrosa. So an atherosclerotic
CRA can compress CRV and cause
turbulence of flow-thrombus
formation if other risk factors
play a part too
15. Green et al Pathogenesis
Blood flow is turbulent in crv in lc
If atherosclerosis + CRA hardens and presses on CRV-lumen of CRV further narrows-turbulence
increases
Turbulence and pressure by CRA causes endothelial damage of CRV
Exposure of the collagen of vessel wall-platelets aggregate and thrombus formation takes place
16.
17.
18. Damage to retina and vision depend upon
1. Rapidity of development of CRVO
2. Degree of occlusion-mild,moderate or severe
3. Availability of collateral pathways
19. PATHOLOGY
Ischaemic CRVO-haemorrhagic infarction of the retina-the inner retinal layers
Neovascularization of the iris and angle
Less frequently – NVD NVE rare
Later changes include thickening of the retina and reactive gliosis
20. HISTOPATHOLOGY
Note the intraretinal haemorrhages in various layers of the retina(arrows) and the eosinophilic
proteinaceous exudates in the outer plexiform layer (asterisk) and subretinal space (S)
21. CLINICAL FEATURES-PRESENTATION
Sudden UNILATERAL painless DECREASE of vision
Fairly sudden decrease but not as much as CRAO
Decrease of vision varies from just blurring of vision to severe loss of vision
No redness,pain or watering in fresh cases in most cases
Very few patients may have mild redness and photophobia on the initial few days or few weeks
If a patient presents with pain and severe redness it is due to NVG a complication of CRVO-LATE
Asymptomatic –routine examination may reveal old CRVO
22. SIGNS
Decreased V/A, RAPD,Fundus findings
Degree/severity of the clinical features depend upon the type of CRVO
Two types are recognized-ischaemic and non-ischaemic
23. Classification of CRVO
Ischaemic (non-perfused or haemorrhagic )-20%
Non-ischaemic (perfused)-80%
Indeterminate group where the definite classification in to ischaemic or non-ischaemic is not
possible
24. Why classification is important?
Prediction of the risk of neovascularization and risk of NVG
To give visual prognosis
Decision as to appropriate follow-up intervals
Treatment to initiate in cases of CRVO with macular oedema
25. CLINICAL EXAMINATION
V/A-HM to 20/30 depending upon ischaemic or non-ischaemic
Extremely important to record the presenting BCVA
RAPD+,strongly positive in ischaemic cases
SLE Biomicroscopy-rarely circumciliary congestion,AC clear or few cells,iris-look for NVI in
undilated eye
Gonioscopy to rule out NVA
IOP-usually low in initial phase in non-glaucoma patients,important to rule out glaucoma in
both eyes
26. CRVO-FUNDUS
Findings vary according to ,whether it is ischaemic or non-ischaemic
Fundus findings like haemorrhages,cotton-wool spots are less marked in non-ischaemic
Media –usually clear – rarely there may be vitreous haemorrhage in fresh cases of CRVO
Disc – may be normal or hyperemic,swollen,covered and surrounded by haemorrhages and
cotton-wool spots
Disc cup may or may not be obliterated
Venous pulsations are absent
28. Retinal findings in CRVO
VEINS-markedly dilated,tortuous and dark colored-blood flow is slow
RETINAL HAEMORRHAGES- most important and obvious sign
All shapes of haemorrhages seen
Superficial haemorrhages +++,confluent,some large haemorrhages covering the underlying
retina,dot and blot haemorrhages
Haemorrhages more in the posterior pole covering macula
Sometimes haemorrhages break in to subhyaloid space and vitreous
BLOOD AND THUNDER APPEARANCE OR TOMATO KETCHUP APPEARANCE
COTTON-WOOL SPOTS are common and are scattered
34. FUNDUS
Microaneuryms are not seen in acute stage
MACULA
May appear normal in non-ischaemic or few haemorrhages
Haemorrhages +++ in ischaemic
Edema –diffuse or cystoid
Subretinal fluid may be +
Visual loss occurs because of macular edema ,ischaemia,capillary non-perfusion,overlying
haemorrhages(either retinal or vitreal) or a combination of all these
37. Course of CRVO
Haemorrhages ,cotton-wool spots,venous dilatation and tortuousity- gradually disappear over
many months
Few flame-shaped haemorrhages and dot haemorrhages ,cotton wool spots- may remain for
years
Optico ciliary shunt vessels may develop in about 50% of patients on the disc surface- 3 to 14
months
These are collateral vessels between the obstructed disc capillaries and the unobstructed
choroidal or pial capillaries
Blood flows from high pressure retinal circulation to low pressure choroidal circulation
38. Opticociliary shunt vessels
They are differentiated from NVD by
Not discrete vessels,they are like bag of worms,larger
FFA-no leak
These retinochoroidal collateral veins,may protect against anterior segment neovascularization
but may not be associated with a better visual prognosis
39. CRVO-late changes
Sheathing of veins around the disc
The disc-nearly normal/some blurring of the
margins/sometimes optic atrophy is present
Rarely NVD
40. Chronic changes-MACULA
Macular cysts and macular edema
Macular hole- PTMH or full thickness
Pigment clumping or stippling or atrophy in macula
Persistent macular haemorrhages,even years after the occlusion may +
Hard exudates with irregular circinate configuration around the macula and become more
prominent months later
Occasionally an epiretinal membrane
41. INVESTIGATIONS
Systemic –BP and systemic evaluation
Lab – CBC,ESR,peripheral smear,BS,lipid profile
OCT
FFA
ERG
Visual field – perimetry
In most patients who are older with known risk factors OCT,FFA,BP,CBC,ESR,BS are enough
42. However in younger patients(<50 years) with no systemic known risk
factors more extensive investigations are needed to assess the possible
etiology
Rule out sarcoidosis,Behcet’s disease and other collagen vascular disorders ( x-ray
chest,ACE,HLA typing,systemic work up)
Plasma homocystein levels
Anti phospholipid levels
Protein C, PROTEIN S levels,Factor V Leiden factor levels
Rule out hyperviscosity syndromes-leukemias,macroglobulinemia etc.
Rule out oral contraceptives in females
43. FFA in Ischaemic CRVO
Dye fills up delayed in venous tree and
capillary networks
Blockage of fluorescence due to retinal
haemorrhages
Extensive leaking of fluorescein into the
retina – in macular area
FAZ may be enlarged
Capillary non-perfusion in mid-periphery >10
DD may be masked by haemorrhages
Late-phase photographs show patchy
extravascular areas of fluorescence and
staining of the retinal veins
44. FFA in Non-ischaemic CRVO
A prolonged venous transit time
Mild staining og the walls of veins,and
varying degrees macular leakage may be
present(including cystoid macular edema)
Capillary nonperfusionis not a prominent
feature
If present<10DD areas in mid-periphery
45. FFA in ischaemic VS non-ischaemic CRVO
The amount of non-perfusion or ischaemia is determined by inspecting the fluorescein
angiogram-MIDPERIPHERY
In ischaemic cases drop out areas measure >10 DD or more and in non-ischaemic they measure
<10 DD.
Also it is difficult to interpret FFA in fresh cases because of blocking of fluroscein by
haemorrhages
47. Further course
Some eyes with non-ischamic CRVO convert to ischaemic type upto 34%-----half of them within
4 months rest upto 3 years
?progression of the vein occlusion or ? Progressive retinal capillary nonperfusion is unknown
Conversion is higher for older patients
Macular edema is most important cause of DOV in those who are not converting into ischaemic
type
Pigmentary changes in macula can be late changes
48. OCT
Extremely useful non-invasive technique to
examine the macula
Useful in initial assessment and for follow-up
during treatment
May be normal in non-ischaemic
Macular edema – spongy,cystoid,SRF
Late cases may show atrophy of
retina,RPE,PTMH,FTMH OR ERM
49. Other investigations
ERG-reduced b wave amplitudes in ischaemic
cases
ERG- B/A ratio 60% of the normal both
scotopic and photopic
Perimetry-in ischaemic cases contracted
visual fields and central field defects
51. OCULAR RISK FACTORS FOR NVI/NVA
Poor initial visual acuity(P<0.001)
Amount of non-perfusion seen by fluorescein angiogram(P<0.001)
VENOUS TORTUOSITY(P=0.02)
Extensive retinal haemorrhages(P=0.07)
Duration less than 1 month(P=0.08)
CVOS STUDY 726 EYES
52. Neovascularization in CRVO
Iris (NVI) and angle- NVA
NVD rare,NVE is extremely uncommon
NVA can develop from 2 weeks to years after
CRVO-so follow up every 2 weeks initially
Most occur within 3-6 months
NVI/NVA seen in 35% (61/176) of
ischaemic/indeterminate CRVO and
10%(56/538) in non-ischaemic CRVO
Not all cases of NVI/NVA are NVG
CVOS STUDY-726 EYES
53. Incidence of NVG
Incidence varies
2% in CRVO study and 23% in some other studies
Do gonioscopy every 2 weeks in ischaemic cases
CVOS STUDY-726 EYES
54. Ischaemic VS Non-ischaemic CRVO
Factor Ischaemic CRVO Non-Ischaemic CRVO
Age Older age (68 yrs) Younger by 5 yrs (63 yrs)
V/A Poor initial vision
90% have VA<3/60
Better initial vision
>60% have VA>6/60
RAPD Strong RAPD Absent or mild
Disc Swollen Not swollen or mild
Retinal haemorrhages,CWS ++++ ++
Macula Haemorrhages,edema++ Less marked or normal
55. Factor Ischaemic CRVO Non-Ischaemic CRVO
Visual Field Reduced VF with central scotoma Normal or less reduced
ERG Reduced B wave Noraml or borderline
FFA Drop out areas >10DD,leakage in
macular areas,staining of veins
Less drop out areas <10DD,less
marked leakage
NVI/NVA More common Less common
NVG Common upto 25% Less common <10%
Prognosis for VA Not good Good
56. Which signs and tests best detect/predict
ischaemic CRVO ?
RAPD
ERG
RAPD+ERG-predicted ischemic in 97% of cases
Perimetry – next most reliable
Visual acuity
FFA
Fundus appearance –least reliable
57. Few odd facts
Fellow eye in a patient with CRVO has 5% risk of developing CRVO in 3 years
Bilateral simultaneous CRVO is known to occur mainly in patients with systemic illnesses with
predisposition to CRVO
CRVO can occur with cilioretinal artery occlusion or with CRAO
58. TREATMENT OF CRVO
AIMS OF TREATMENT:
Reverse the obstruction in the CRVO
Establish collaterals to by pass the obstruction
Prevent the complications-NVG
Treat the complications-macular edema and NVG
60. 4.) SURGICAL THERAPY-
Pars plana vitrectomy (PPV) with R-TPA injection in to the vein
PPV with removal of posterior hyaloid and/or internal limiting membrane
PPV with radial optic neurotomy/laminar puncture
PPV with retinal endovascular surgery
PPV with chorioretinal venous anastomosis
61. Treatment of CRVO
None of the studies have been shown to be effective in
REVERSING THE OBSTRUCTION
IMPROVING VISION IN ISCHAEMIC CRVO
62. A. Reverse the CRVO
Thrombolysis by recombinant tissue
plasminogen activator r-TPA given iv and
intavitreally
r-TPA was also injected into the CRV itself
after PPV
Haemodilution (heparin,erythrocytopherisis)
Anticoagulants-aspirin and antiplatelet drugs
PPV with optic radial neurotomy
DON’T STOP ANTI-COAGULANTS IF THEY ARE
ALREADY ON IT
ANTI-COAGULANTS CAN BE HARMFUL FOR
CRVO
63. B. Establish collaterals to relieve the
obstruction
By LASER- use argon laser to cause a break in the Bruch’smembrane and then cause a small
hole in the vein near the area of Bruch’s membrane break. Anastomoses develop-thus retinal
circulation by passes the CRV. However,it is recommended for non-ischaemic type only.
64. C. Prevent complications
The most important complication is NVG
CVO study showed that to prevent NVG- apply PRPC only if any NVA or two clock hours of NVI
develop and not before
65. D. Treat Complications
1.Treatment of NVG-
PRPC
Anti-glaucoma medications
Atropine, steroid drops
Anti-VEGF injection
Shunt surgery
Cyclo-destructive procedures
66. 2. Macular oedema-
It is an important cause of reduction in VA in CRVO and BRVO
Macular oedema in ischaemic cases is not amenable to treatment
But there are many options to treat in non-ischaemic cases
Role of macular grid photocoagulation in CVO related macuar oedema
Not effective- proved by randomized study of 155 cases of CVO
CVO STUDY
67. Treatment modalities for macular edema
1.) INTRAVITREAL STERIOD INJECTION
Triamcinolone (SCORE STUDY)
Dexamethasone depot-Ozurdex implant (GENEVA TRIAL)
Fluocinolone implant-ILUVIEN implant
2.) INTRAVITREAL ANTI-VEGF INJECTION
Bevacizumab
Ranimizumab -CRUISE STUDY
Afibercept -COPERNICUS STUDY
3.)PPV with ILM PEELING FOR RESISTANT EDEMA
68. Intravitreal TA steroid injection
Cheap,lasts for 3 months
The SCORE (Standard care vs Corticosteroid for Retinal vein occlusion)study showed that
Intravitreal injection of 1 mg or 4 mg
Gain of 15 letters or more of vision occurred in 27% in injection group against 7% only in
observation
It is better to use 1 mg dose than 4 mg for its safety profile
69. ADVANTAGES –
Cheap
Easy treatment
DISADVANTAGES are side effects-
Effect lasts for 3 months so repeat injections are needed
Raised IOP in 35% needing medications and surgery
Cataract (90%)
Endophthalmitis
Are sparingly used now after the availability of anti-VEGF drugs
70. Intravitreal steroids-depot injections
New intravitreal slow release biodegradable device with dexamethasone-ozurdex-0.7mg
Advantage-effect lasts for 3-6 months
IOP,cataract concerns remain however but are less marked than triamcinolone injection
73. BEVACIZUMAB (Epstein et al)
Monthly injections for 6 months ,increased VA by 16 letters-3 lines
Delayed treatment especially in older individuals yielded poorer results
74. RANIBIZUMAB (CRUISE TRIAL)
Ranibizumab 0.3mg and 0.6mg or sham injections were used in 3 groups of patients (130
patients in each group)
All CRVO were perfused
Gain of>15 letters 47-50% in ranibizumab vs 33% in sham group at the end of 12 months
Mean change in VA was 13-14 letters in lucentis group vs 7 letters in sham group
75.
76.
77. AFLIBERCEPT OR EYELEA
A new drug that traps VEGF
VEGF receptor fusion protein-DECOY-that binds all forms of VEGF-A,along with placental
growth factor(PIGF),another member of the VEGF family was also believed to be implicated in
the development of wet age related macular degeneration(AMD)
It is supposed to have more affinity for VEGF than the natural receptors of VEGF
78.
79.
80. Which anti-VEGF is better?
Avastin,ranibizumab and aflibercept were shown to be equally effective in ME associated with
non-ischaemic CRVO
81. Anti-VEGF
DISADVANTAGES-
Need to be given every month for 3 months—
then sos
First year as many as 10 injections
Recurrence of edema is common
Regular follow-ups are needed
Systemic side-effects are a concern
Cost of ranibizumab and aflibercept are
prohibitive
Endophthalmitis and RD are rare but do occur
ADVANTAGES-
Improves VA
Decreases ME
Reduce chances of NVA and NVI
Easy treatment
Whether is prevents conversion to ischaemic
type is not known
82. Anti-VEGF V/S Intravitreal steroid implant
Both are effective for macular edema associated with CRVO
Steroid implant-effect lasts for 3 months so cost effective and systemic side effects are not
known but IOP and cataract are concern
Anti-VEGF- no cataract or IOP spikes and very effective in improvement of VA but more
repeated injections and cost are concern
A meta analysis favored –anti-VEGF’s over steroid implants