IOL power calculation is challenging in eyes with prior refractive surgery or other special situations. In eyes with prior radial keratotomy, standard keratometry overestimates corneal power due to flattening outside the central optical zone. Multiple methods of IOL power calculation should be used, including topography to measure the flattest central corneal power. A study comparing methods in eyes with prior RK found IOL power calculation using topographic keratometry was least accurate compared to formulas from the ESCRS calculator. No single method provided reliable results, highlighting the difficulty in IOL power calculation for eyes with prior refractive surgery.
An epiretinal membrane is an avascular fibrocellular membrane that grows on the inner surface of the retina, causing macular dysfunction. It consists of various cell types and collagen. Symptoms include blurry vision and metamorphopsia. Observation is usually sufficient for mild cases, but surgery is recommended for significant vision loss or distortion. Peeling the membrane improves vision in most cases, though cataracts are a common complication. Prognosis is better when pre-op vision is good and the duration of symptoms is short.
This document provides an overview of congenital optic disc anomalies. It describes the normal optic disc morphology and discusses various anomalies including colobomas, hypoplasia, megalopapilla, tilted discs, morning glory discs, myelinated nerve fibers, and optic pits. For each anomaly, it covers pathogenesis, clinical features, associations, and in some cases, treatment approaches. The key information provided includes a detailed description of the anatomy and histology of the normal optic disc and explanations for how abnormalities during embryonic development can result in different congenital optic disc anomalies.
Posterior vitreous detachment (PVD) occurs when the vitreous gel in the eye separates from the retina. It is a natural aging process that usually happens in people's 60s and 70s. PVDs are often asymptomatic, but can sometimes cause floaters, flashes of light, or a cobweb-like visual effect. While PVD itself does not affect vision, on rare occasions it can cause retinal tears or detachments, which require prompt treatment to prevent vision loss if left untreated. PVD is typically diagnosed via dilated eye exam but may also require tests like OCT or ultrasound. No treatment is needed for most PVDs but follow up exams are recommended to check for complications.
The document discusses the anatomy and physiology of the retina. It begins by describing the embryological origin and topography of the retina. It then describes the major anatomical structures in detail, including the optic disc, macula lutea, fovea, and layers of the retina. The microscopic architecture contains 10 layers arranged from the sclerad to the vitread side. The physiology section briefly outlines the process of phototransduction and visual signal transmission through the retina and visual pathways.
This document provides an overview of central serous chorioretinopathy (CSC), including its pathogenesis, clinical presentation, diagnosis, course and treatment. CSC is characterized by a localized serous retinal detachment in the macula due to leakage of fluid from the choroid. It typically affects men ages 30-50 and can be associated with stress, corticosteroid use, hypertension and type A personality. Diagnosis is usually clinical but can be confirmed with fluorescein angiography showing characteristic leakage patterns or optical coherence tomography identifying subretinal fluid. While most cases resolve spontaneously, laser photocoagulation or photodynamic therapy may be used in persistent or recurrent cases to seal leaking sites and accelerate resolution.
This document discusses non-penetrating glaucoma surgery techniques that facilitate the drainage of aqueous humor through the trabecular meshwork and Schlemm's canal without opening the anterior chamber. It describes several procedures including deep sclerectomy, viscocanalostomy, canaloplasty, ab-externo trabeculectomy, and laser trabecular ablation. The goal is to bypass the highest resistance point to outflow in the juxtacanalicular meshwork. Advantages include lower risks of complications like hypotony compared to penetrating surgeries. Indications and contraindications are provided for various non-penetrating glaucoma procedures.
The document discusses the anatomy, embryology, and function tests of the macula lutea. It describes the macula lutea as a 5.5mm circular area at the posterior pole of the retina that subserves central vision. It notes the macula's delayed development until 8 months gestation and specialization of the fovea which contains the highest concentration of cones. The document outlines various macular function tests used to evaluate macular diseases, including visual acuity, Amsler grid, microperimetry, and electroretinography. It provides details on the anatomy and cell layers of the fovea centralis and techniques for assessing macular integrity with tests like the Maddox rod.
IOL power calculation is challenging in eyes with prior refractive surgery or other special situations. In eyes with prior radial keratotomy, standard keratometry overestimates corneal power due to flattening outside the central optical zone. Multiple methods of IOL power calculation should be used, including topography to measure the flattest central corneal power. A study comparing methods in eyes with prior RK found IOL power calculation using topographic keratometry was least accurate compared to formulas from the ESCRS calculator. No single method provided reliable results, highlighting the difficulty in IOL power calculation for eyes with prior refractive surgery.
An epiretinal membrane is an avascular fibrocellular membrane that grows on the inner surface of the retina, causing macular dysfunction. It consists of various cell types and collagen. Symptoms include blurry vision and metamorphopsia. Observation is usually sufficient for mild cases, but surgery is recommended for significant vision loss or distortion. Peeling the membrane improves vision in most cases, though cataracts are a common complication. Prognosis is better when pre-op vision is good and the duration of symptoms is short.
This document provides an overview of congenital optic disc anomalies. It describes the normal optic disc morphology and discusses various anomalies including colobomas, hypoplasia, megalopapilla, tilted discs, morning glory discs, myelinated nerve fibers, and optic pits. For each anomaly, it covers pathogenesis, clinical features, associations, and in some cases, treatment approaches. The key information provided includes a detailed description of the anatomy and histology of the normal optic disc and explanations for how abnormalities during embryonic development can result in different congenital optic disc anomalies.
Posterior vitreous detachment (PVD) occurs when the vitreous gel in the eye separates from the retina. It is a natural aging process that usually happens in people's 60s and 70s. PVDs are often asymptomatic, but can sometimes cause floaters, flashes of light, or a cobweb-like visual effect. While PVD itself does not affect vision, on rare occasions it can cause retinal tears or detachments, which require prompt treatment to prevent vision loss if left untreated. PVD is typically diagnosed via dilated eye exam but may also require tests like OCT or ultrasound. No treatment is needed for most PVDs but follow up exams are recommended to check for complications.
The document discusses the anatomy and physiology of the retina. It begins by describing the embryological origin and topography of the retina. It then describes the major anatomical structures in detail, including the optic disc, macula lutea, fovea, and layers of the retina. The microscopic architecture contains 10 layers arranged from the sclerad to the vitread side. The physiology section briefly outlines the process of phototransduction and visual signal transmission through the retina and visual pathways.
This document provides an overview of central serous chorioretinopathy (CSC), including its pathogenesis, clinical presentation, diagnosis, course and treatment. CSC is characterized by a localized serous retinal detachment in the macula due to leakage of fluid from the choroid. It typically affects men ages 30-50 and can be associated with stress, corticosteroid use, hypertension and type A personality. Diagnosis is usually clinical but can be confirmed with fluorescein angiography showing characteristic leakage patterns or optical coherence tomography identifying subretinal fluid. While most cases resolve spontaneously, laser photocoagulation or photodynamic therapy may be used in persistent or recurrent cases to seal leaking sites and accelerate resolution.
This document discusses non-penetrating glaucoma surgery techniques that facilitate the drainage of aqueous humor through the trabecular meshwork and Schlemm's canal without opening the anterior chamber. It describes several procedures including deep sclerectomy, viscocanalostomy, canaloplasty, ab-externo trabeculectomy, and laser trabecular ablation. The goal is to bypass the highest resistance point to outflow in the juxtacanalicular meshwork. Advantages include lower risks of complications like hypotony compared to penetrating surgeries. Indications and contraindications are provided for various non-penetrating glaucoma procedures.
The document discusses the anatomy, embryology, and function tests of the macula lutea. It describes the macula lutea as a 5.5mm circular area at the posterior pole of the retina that subserves central vision. It notes the macula's delayed development until 8 months gestation and specialization of the fovea which contains the highest concentration of cones. The document outlines various macular function tests used to evaluate macular diseases, including visual acuity, Amsler grid, microperimetry, and electroretinography. It provides details on the anatomy and cell layers of the fovea centralis and techniques for assessing macular integrity with tests like the Maddox rod.
This document summarizes the development and structure of the vitreous humor in the eye. It discusses how the vitreous develops in three stages - primitive, secondary, and tertiary vitreous - beginning in the first month of gestation. It describes the layers and parts of the vitreous, including the hyaloid layer, cortical vitreous, and central vitreous. It also outlines the attachments and zones of the vitreous within the eye.
This document provides an overview of the anatomy of the uveal tract, which includes the iris, ciliary body, and choroid. It begins with an introduction and overview of the embryology and development of the uveal tract. It then discusses the anatomy and microstructure of each part of the uveal tract in detail, including their nerve and blood supply. It also briefly discusses some congenital anomalies that can affect the uveal tract.
Macular hole is a defect in the macula involving its full thickness. It was first described in 1869. Idiopathic macular holes are the most common type and affect people over age 55. Staging of macular holes ranges from stage 1 to 4 based on size and pathology. Symptoms include decreased vision and metamorphopsia. Diagnosis involves examination, OCT, and sometimes FA. Treatment is usually vitrectomy surgery for stages 2-4 to relieve traction on the macula. Prognosis depends on pre-op vision and hole size/duration, with most patients gaining vision after surgery.
This document discusses the surgical management of Pellucid marginal degeneration (PMD), a non-inflammatory thinning of the cornea. It describes various surgical techniques used to treat PMD including INTACS inserts, eccentric penetrating keratoplasty, large diameter epikeratoplasty, lamellar crescentic keratoplasty, lamellar crescentic resection, and wedge resection. The goal of these surgeries is to reshape the cornea and reduce high astigmatism caused by PMD through techniques like inserting inserts, excising the thinned area, or using donor tissue grafts. Complications can include increased risk of rejection, vascularization, and long-term astigmatism changes.
Retinoschisis is a splitting within the neurosensory layer of the retina that frequently occurs in the inferotemporal quadrant. It is usually asymptomatic but can potentially cause visual field defects. On examination, it appears as a well-circumscribed, dome-shaped elevation of the inner retina. OCT shows a break between the retinal layers. While often stable, it can occasionally lead to retinal detachment or holes. Treatment may be needed if complications occur.
The retina is the innermost layer of the eye. It is attached to the back of the eyeball and detects light and sends signals to the brain. The document describes the detailed anatomy of the retina including its layers, blood supply, nerves and relationship to surrounding structures like the vitreous, choroid and extraocular muscles. Special attention is given to anatomical structures that are important to consider during retinal surgery like the vortex veins and long posterior ciliary arteries.
The document discusses the anatomy and surgical applications of the limbus. It defines the limbus as the transitional zone between the cornea and sclera, containing the pathways for aqueous humor outflow. Histologically, it describes how the layers of the cornea and conjunctiva become continuous at the limbus. Surgically, it notes the anterior limbal border, blue limbal zone, mid-limbal line, posterior limbal border, and white limbal zone. The best site for cataract incisions is the mid-limbal line, while anterior or posterior incisions risk damage to underlying structures. The limbus contains stem cells that renew the corneal epithelium.
Anatomy and embryology of crystalline lens DrBPdrbhushan17
This document provides an overview of the embryology and anatomy of the crystalline lens. It discusses how the lens forms from the lens vesicle which sinks from the surface ectoderm. The lens vesicle then develops into the lens as lens fibers elongate from the posterior wall. The lens fibers form the embryonic, fetal, and adult nuclei over time. The document also describes the detailed anatomy of the adult lens, including its capsule, epithelium, fibers organized into the nucleus and cortex. It notes the lens' role in the eye's optical system and ability to accommodate.
This document discusses the diagnosis of pre-perimetric glaucoma. It begins by defining pre-perimetric glaucoma as optic nerve abnormalities seen on structural tests with normal visual fields. It then discusses the need for early diagnosis before functional changes occur. Various functional tests are described like standard automated perimetry, short wavelength automated perimetry, frequency doubling technology, and others. Structural tests like confocal scanning laser ophthalmoscopy, optical coherence tomography, and their principles are summarized.
This document discusses the anatomy and development of the vitreous humor in the eye. It begins by describing the embryological origin of vitreous cells from surface ectoderm, neuroectoderm, and mesodermal tissues. During the primary vitreous stage, the vitreous body begins forming before closure of the choroidal fissure and appears as a fibrillated secretion filling the vitreous space. The document then covers the general features, structure including hyaloid layers, cortical and medullary regions, attachments, composition and transport processes of the mature vitreous humor. It concludes by describing the physicochemical properties and factors affecting expansion and contraction of the vitreous gel.
Anophthalmia is the absence of the eyeball and can be congenital or acquired. The optimal management of an anophthalmic socket involves maintaining adequate volume with a well-positioned implant, healthy conjunctiva, and symmetric eyelids. Complications after enucleation like enophthalmos, eyelid deformities, and socket contracture can be addressed through procedures like dermis fat grafts, fornix deepening sutures, and implant replacement. Proper prosthesis fitting and care is also important for optimal cosmetic and functional results.
The document summarizes the structure and function of the tear film. It consists of three layers - an outer lipid layer, middle aqueous layer, and inner mucin layer. The lipid layer prevents evaporation and overflow of tears. The aqueous layer hydrates the cornea and contains nutrients. The mucin layer lubricates the eye surface. Tears are produced through basal and reflex secretion and drain through the lacrimal system into the nose. Blinking spreads and replenishes the layers, while evaporation and lipid migration cause the film to thin and rupture between blinks.
Peripheral fundus & its disorders
Presented by Dr Rohit Rao
This document summarizes the key anatomical structures and pathologies of the peripheral retina. It describes the ora serrata, pars plana, vitreous base, dentate processes, meridional folds, and other peripheral features. It then discusses various degenerative conditions like lattice degeneration, retinoschisis, and pavingstone degeneration. Treatment options for retinal breaks including cryopexy and laser photocoagulation are also summarized.
Anatomy and embryology of anterior chamber angle ppt newanupama manoharan
This document discusses the anatomy and embryology of the angle of the anterior chamber. It begins by defining the angle of the anterior chamber as the recess formed between the posterior surface of the cornea and anterior surface of the iris, which is the main pathway for drainage of aqueous humor. It then covers the embryology of eye development from the formation of the optic vesicle and stalk to the optic cup. The document also discusses conditions that affect the angle such as congenital glaucoma and posterior embryotoxon. Assessment techniques for the anterior chamber angle including gonioscopy, torchlight examination, and imaging modalities like UBM and OCT are provided.
The document provides an overview of clinical evaluation of optic disc changes. It discusses examining the papillary changes including size, shape, neuroretinal rim, cupping and color. It also discusses vascular changes like nasalization of vessels and bayoneting of vessels. Peripapillary changes like RNFL defects, hemorrhages and gray crescent are also covered. The document outlines different staging systems to classify optic disc changes including the Disc Damage Likelihood Scale which quantifies glaucomatous damage based on rim width and disc size.
Angle recession glaucoma is a type of secondary glaucoma that can develop years after blunt ocular trauma causes tearing of the ciliary body and recession of the iris root. It is often underdiagnosed due to delayed onset and forgotten injury history. Management involves topical glaucoma medications, with filtering surgeries used if medication fails to control pressure. Early diagnosis and aggressive treatment are important to prevent glaucoma-related vision loss from this condition.
This document discusses the morphological changes that occur in the optic nerve head and retinal nerve fiber layer in glaucoma. It describes the various patterns of glaucomatous optic nerve damage including focal notching, concentric cupping, saucerization, and advanced cupping. Features that indicate glaucomatous damage include neuroretinal rim thinning, disc hemorrhages, and changes in the retinal vasculature around the optic disc. Evaluation of the optic nerve head is important for early detection of glaucoma before visual field loss occurs.
The retina has multiple layers that process light and transmit visual signals. The outermost layer is the retinal pigment epithelium, followed inwardly by the layers of photoreceptors, bipolar and ganglion cells. The innermost layer is the nerve fiber layer containing ganglion cell axons. Specialized structures include the macula for high acuity vision and optic disc where ganglion cell axons exit as the optic nerve. Blood supply comes from the choroid circulated by the ciliary arteries. The retina converts light to electrical signals that travel through the optic nerve to the brain for visual processing.
Pseudoexfoliation syndrome is a systemic condition characterized by grey-white fibrillar deposits that can lead to open-angle glaucoma. It involves the trabecular meshwork, lens, ciliary body and other ocular tissues, and is a major risk factor for glaucoma. Treatment involves managing elevated intraocular pressure through medications, laser trabeculoplasty, trabeculectomy or cataract surgery due to the increased risk of complications from zonular weakness.
Limbal Stem Cell Deficiency & its managementKaran Bhatia
1) Limbal stem cells are located in the palisades of Vogt region of the limbus and are responsible for maintaining the normal corneal epithelium. Limbal stem cell deficiency occurs when the source of these cells is damaged, causing severe problems to the ocular surface.
2) Limbal stem cell deficiency can be partial or total, and is classified based on extent and etiology. Common causes include chemical/thermal burns, Stevens-Johnson syndrome, and multiple ocular surgeries.
3) Management is based on the extent and severity of deficiency, and involves steps from conservative treatment to more invasive procedures like limbal stem cell transplantation or keratoprosthesis. The goal is to replace
Retinitis pigmentosa is a group of hereditary retinal diseases characterized by progressive degeneration of photoreceptors. It begins with night blindness and peripheral vision loss and can progress to tunnel vision or legal blindness. Genetic mutations affecting photoreceptor structure and function or RNA splicing are responsible. On examination, bone spicule pigmentation, vascular attenuation, optic nerve pallor and RPE changes are seen. Diagnosis is confirmed by electroretinography showing photoreceptor dysfunction. There is currently no cure but management focuses on low vision aids, vitamins, and gene or stem cell therapies which are under investigation.
This document summarizes the development and structure of the vitreous humor in the eye. It discusses how the vitreous develops in three stages - primitive, secondary, and tertiary vitreous - beginning in the first month of gestation. It describes the layers and parts of the vitreous, including the hyaloid layer, cortical vitreous, and central vitreous. It also outlines the attachments and zones of the vitreous within the eye.
This document provides an overview of the anatomy of the uveal tract, which includes the iris, ciliary body, and choroid. It begins with an introduction and overview of the embryology and development of the uveal tract. It then discusses the anatomy and microstructure of each part of the uveal tract in detail, including their nerve and blood supply. It also briefly discusses some congenital anomalies that can affect the uveal tract.
Macular hole is a defect in the macula involving its full thickness. It was first described in 1869. Idiopathic macular holes are the most common type and affect people over age 55. Staging of macular holes ranges from stage 1 to 4 based on size and pathology. Symptoms include decreased vision and metamorphopsia. Diagnosis involves examination, OCT, and sometimes FA. Treatment is usually vitrectomy surgery for stages 2-4 to relieve traction on the macula. Prognosis depends on pre-op vision and hole size/duration, with most patients gaining vision after surgery.
This document discusses the surgical management of Pellucid marginal degeneration (PMD), a non-inflammatory thinning of the cornea. It describes various surgical techniques used to treat PMD including INTACS inserts, eccentric penetrating keratoplasty, large diameter epikeratoplasty, lamellar crescentic keratoplasty, lamellar crescentic resection, and wedge resection. The goal of these surgeries is to reshape the cornea and reduce high astigmatism caused by PMD through techniques like inserting inserts, excising the thinned area, or using donor tissue grafts. Complications can include increased risk of rejection, vascularization, and long-term astigmatism changes.
Retinoschisis is a splitting within the neurosensory layer of the retina that frequently occurs in the inferotemporal quadrant. It is usually asymptomatic but can potentially cause visual field defects. On examination, it appears as a well-circumscribed, dome-shaped elevation of the inner retina. OCT shows a break between the retinal layers. While often stable, it can occasionally lead to retinal detachment or holes. Treatment may be needed if complications occur.
The retina is the innermost layer of the eye. It is attached to the back of the eyeball and detects light and sends signals to the brain. The document describes the detailed anatomy of the retina including its layers, blood supply, nerves and relationship to surrounding structures like the vitreous, choroid and extraocular muscles. Special attention is given to anatomical structures that are important to consider during retinal surgery like the vortex veins and long posterior ciliary arteries.
The document discusses the anatomy and surgical applications of the limbus. It defines the limbus as the transitional zone between the cornea and sclera, containing the pathways for aqueous humor outflow. Histologically, it describes how the layers of the cornea and conjunctiva become continuous at the limbus. Surgically, it notes the anterior limbal border, blue limbal zone, mid-limbal line, posterior limbal border, and white limbal zone. The best site for cataract incisions is the mid-limbal line, while anterior or posterior incisions risk damage to underlying structures. The limbus contains stem cells that renew the corneal epithelium.
Anatomy and embryology of crystalline lens DrBPdrbhushan17
This document provides an overview of the embryology and anatomy of the crystalline lens. It discusses how the lens forms from the lens vesicle which sinks from the surface ectoderm. The lens vesicle then develops into the lens as lens fibers elongate from the posterior wall. The lens fibers form the embryonic, fetal, and adult nuclei over time. The document also describes the detailed anatomy of the adult lens, including its capsule, epithelium, fibers organized into the nucleus and cortex. It notes the lens' role in the eye's optical system and ability to accommodate.
This document discusses the diagnosis of pre-perimetric glaucoma. It begins by defining pre-perimetric glaucoma as optic nerve abnormalities seen on structural tests with normal visual fields. It then discusses the need for early diagnosis before functional changes occur. Various functional tests are described like standard automated perimetry, short wavelength automated perimetry, frequency doubling technology, and others. Structural tests like confocal scanning laser ophthalmoscopy, optical coherence tomography, and their principles are summarized.
This document discusses the anatomy and development of the vitreous humor in the eye. It begins by describing the embryological origin of vitreous cells from surface ectoderm, neuroectoderm, and mesodermal tissues. During the primary vitreous stage, the vitreous body begins forming before closure of the choroidal fissure and appears as a fibrillated secretion filling the vitreous space. The document then covers the general features, structure including hyaloid layers, cortical and medullary regions, attachments, composition and transport processes of the mature vitreous humor. It concludes by describing the physicochemical properties and factors affecting expansion and contraction of the vitreous gel.
Anophthalmia is the absence of the eyeball and can be congenital or acquired. The optimal management of an anophthalmic socket involves maintaining adequate volume with a well-positioned implant, healthy conjunctiva, and symmetric eyelids. Complications after enucleation like enophthalmos, eyelid deformities, and socket contracture can be addressed through procedures like dermis fat grafts, fornix deepening sutures, and implant replacement. Proper prosthesis fitting and care is also important for optimal cosmetic and functional results.
The document summarizes the structure and function of the tear film. It consists of three layers - an outer lipid layer, middle aqueous layer, and inner mucin layer. The lipid layer prevents evaporation and overflow of tears. The aqueous layer hydrates the cornea and contains nutrients. The mucin layer lubricates the eye surface. Tears are produced through basal and reflex secretion and drain through the lacrimal system into the nose. Blinking spreads and replenishes the layers, while evaporation and lipid migration cause the film to thin and rupture between blinks.
Peripheral fundus & its disorders
Presented by Dr Rohit Rao
This document summarizes the key anatomical structures and pathologies of the peripheral retina. It describes the ora serrata, pars plana, vitreous base, dentate processes, meridional folds, and other peripheral features. It then discusses various degenerative conditions like lattice degeneration, retinoschisis, and pavingstone degeneration. Treatment options for retinal breaks including cryopexy and laser photocoagulation are also summarized.
Anatomy and embryology of anterior chamber angle ppt newanupama manoharan
This document discusses the anatomy and embryology of the angle of the anterior chamber. It begins by defining the angle of the anterior chamber as the recess formed between the posterior surface of the cornea and anterior surface of the iris, which is the main pathway for drainage of aqueous humor. It then covers the embryology of eye development from the formation of the optic vesicle and stalk to the optic cup. The document also discusses conditions that affect the angle such as congenital glaucoma and posterior embryotoxon. Assessment techniques for the anterior chamber angle including gonioscopy, torchlight examination, and imaging modalities like UBM and OCT are provided.
The document provides an overview of clinical evaluation of optic disc changes. It discusses examining the papillary changes including size, shape, neuroretinal rim, cupping and color. It also discusses vascular changes like nasalization of vessels and bayoneting of vessels. Peripapillary changes like RNFL defects, hemorrhages and gray crescent are also covered. The document outlines different staging systems to classify optic disc changes including the Disc Damage Likelihood Scale which quantifies glaucomatous damage based on rim width and disc size.
Angle recession glaucoma is a type of secondary glaucoma that can develop years after blunt ocular trauma causes tearing of the ciliary body and recession of the iris root. It is often underdiagnosed due to delayed onset and forgotten injury history. Management involves topical glaucoma medications, with filtering surgeries used if medication fails to control pressure. Early diagnosis and aggressive treatment are important to prevent glaucoma-related vision loss from this condition.
This document discusses the morphological changes that occur in the optic nerve head and retinal nerve fiber layer in glaucoma. It describes the various patterns of glaucomatous optic nerve damage including focal notching, concentric cupping, saucerization, and advanced cupping. Features that indicate glaucomatous damage include neuroretinal rim thinning, disc hemorrhages, and changes in the retinal vasculature around the optic disc. Evaluation of the optic nerve head is important for early detection of glaucoma before visual field loss occurs.
The retina has multiple layers that process light and transmit visual signals. The outermost layer is the retinal pigment epithelium, followed inwardly by the layers of photoreceptors, bipolar and ganglion cells. The innermost layer is the nerve fiber layer containing ganglion cell axons. Specialized structures include the macula for high acuity vision and optic disc where ganglion cell axons exit as the optic nerve. Blood supply comes from the choroid circulated by the ciliary arteries. The retina converts light to electrical signals that travel through the optic nerve to the brain for visual processing.
Pseudoexfoliation syndrome is a systemic condition characterized by grey-white fibrillar deposits that can lead to open-angle glaucoma. It involves the trabecular meshwork, lens, ciliary body and other ocular tissues, and is a major risk factor for glaucoma. Treatment involves managing elevated intraocular pressure through medications, laser trabeculoplasty, trabeculectomy or cataract surgery due to the increased risk of complications from zonular weakness.
Limbal Stem Cell Deficiency & its managementKaran Bhatia
1) Limbal stem cells are located in the palisades of Vogt region of the limbus and are responsible for maintaining the normal corneal epithelium. Limbal stem cell deficiency occurs when the source of these cells is damaged, causing severe problems to the ocular surface.
2) Limbal stem cell deficiency can be partial or total, and is classified based on extent and etiology. Common causes include chemical/thermal burns, Stevens-Johnson syndrome, and multiple ocular surgeries.
3) Management is based on the extent and severity of deficiency, and involves steps from conservative treatment to more invasive procedures like limbal stem cell transplantation or keratoprosthesis. The goal is to replace
Retinitis pigmentosa is a group of hereditary retinal diseases characterized by progressive degeneration of photoreceptors. It begins with night blindness and peripheral vision loss and can progress to tunnel vision or legal blindness. Genetic mutations affecting photoreceptor structure and function or RNA splicing are responsible. On examination, bone spicule pigmentation, vascular attenuation, optic nerve pallor and RPE changes are seen. Diagnosis is confirmed by electroretinography showing photoreceptor dysfunction. There is currently no cure but management focuses on low vision aids, vitamins, and gene or stem cell therapies which are under investigation.
This document discusses various retinal dystrophies including:
1) Generalized photoreceptor dystrophies such as retinitis pigmentosa, which affects rod photoreceptors and later cones, causing progressive vision loss.
2) Macular dystrophies that primarily affect the macula.
3) Generalized choroidal dystrophies affecting the choroid layer.
4) Vitreoretinopathies involving the vitreous or retina.
Retinitis pigmentosa is described in detail, outlining its genetics, symptoms, fundus findings, investigations and treatment options. Atypical forms of retinal pigmentosa associated with other systemic disorders are also mentioned.
The document discusses various diagnostic imaging modalities used in ophthalmology including fluorescein angiography, indocyanine green angiography, optical coherence tomography, autofluorescence, near-infrared imaging, adaptive optics, B-scan ultrasound, and their applications and indications. The goal of these modalities is to non-invasively evaluate ocular structures, identify pathological lesions, and distinguish between normal and abnormal physiological responses through different imaging techniques. Newer spectral domain OCT provides higher resolution images compared to older time domain OCT.
This document summarizes various inherited retinal dystrophies, including:
1. Diffuse photoreceptor dystrophies like retinitis pigmentosa and Leber's congenital amaurosis, and macular dystrophies like Stargardt's disease, vitelliform macular dystrophy, and pattern dystrophy.
2. It then describes choroidal dystrophies like choroideremia, gyrate atrophy, and Sorsby fundus dystrophy.
3. Key features, pathogenesis, genetic causes, clinical findings, investigations, and management are outlined for each condition. Differential diagnoses are also provided to help distinguish between similar appearing dystrophies.
Retinitis pigmentosa is a genetically heterogeneous group of retinal disorders characterized by progressive loss of photoreceptors and retinal pigment epithelium. It is a common cause of visual impairment, affecting around 1 in 3000-5000 people. The disease typically begins with night blindness in adolescence or early adulthood due to rod photoreceptor degeneration, eventually progressing to include cone cell death and visual field constriction. Genetic testing can help determine the inheritance pattern and risk of transmission to family members. Further research aims to identify all disease-causing genes and mutations to improve molecular diagnosis and understanding of retinitis pigmentosa.
This document provides information about cone and rod dystrophy (CORD), including its genetics, clinical presentation, classification, and mechanisms. It discusses how CORD is a genetically heterogeneous group of inherited retinal dystrophies involving both cone and rod photoreceptors. The document outlines the typical stages and symptoms of CORD and compares it to other conditions like achromatopsia. It also describes syndromic forms of CORD and provides a classification system for CORD based on genetics.
Cataract surgery is the most common surgery that we perform on a outpatient basis. Evaluation of the patient is critical and essential for a desirable visual outcome.
PRE-OPERATIVE EVALUATION IN CATARACT SURGERYAlexLino17
This document summarizes the key points in assessing a patient for cataract surgery. It discusses obtaining a thorough history including vision symptoms, medical history, medications and allergies. A comprehensive eye exam evaluates visual acuity, refraction, external exam, slit lamp exam of the anterior segment and dilated fundus exam. Additional tests may include biometry to calculate IOL power, corneal topography and lab tests. Special considerations are discussed for conditions like uveitis, glaucoma, retinal disease and prior refractive surgery. A complete pre-op evaluation is important to identify risks and ensure the best surgical outcome and post-op visual rehabilitation.
Optical Coherence Tomography(OCT) in posterior segment diseasesShagil Khan
Optical coherence tomography (OCT) is a non-invasive imaging technique that uses light to generate high-resolution cross-sectional images of the retina and optic nerve. It provides detailed visualization of retinal structures on a microscopic scale. OCT is useful for diagnosing and monitoring various posterior segment diseases. It allows differentiation between stages of macular hole, detection of epiretinal membranes, and identification of fluid associated with neovascular age-related macular degeneration. Advances in spectral domain OCT technology have improved imaging speed and resolution, enabling clearer visualization of small retinal structures and layers.
This document provides information on macular dystrophies. It begins with the anatomical landmarks of the macula including the fovea and foveola. It then discusses various hereditary macular dystrophies including X-linked juvenile retinoschisis, Stargardt's disease, Best's disease, dominant familial drusen, and pattern dystrophy. For each condition, it provides information on genetics, symptoms, signs, imaging findings, and management. The document uses images to illustrate many of the clinical features described.
Pigmentary glaucoma - Dr Shylesh B DabkeShylesh Dabke
Pigment Dispersion Syndrome (PDS) involves abnormal amounts of pigment released from the iris that deposit throughout the eye. It can sometimes progress to Pigmentary Glaucoma (PG). PDS is more common in young, white, myopic males and has genetic links. Theories for its pathogenesis include mechanical abrasion between the iris and lens zonules or abnormal iris cell degeneration. Over time, PDS can cause increased eye pressure and vision loss from PG if not properly treated with medications, laser procedures, or surgery.
Optical coherence tomography (OCT) is a non-invasive imaging technique that uses light to capture high-resolution, cross-sectional images of the retina and anterior segment of the eye. OCT provides depth resolution on the scale of 10 microns, allowing it to visualize and measure individual layers of the retina. OCT can detect various retinal pathologies through qualitative and quantitative analysis of the pre-retinal, overall retinal, foveal, and macular profiles. It is useful for diagnosing conditions like macular edema, retinal detachments, and glaucoma.
Optical Coherence Tomography - principle and uses in ophthalmologytapan_jakkal
Optical coherence tomography (OCT) is a non-invasive imaging technique that uses light to capture high-resolution, cross-sectional images of the retina and anterior segment of the eye. OCT provides depth resolution on the scale of 10 microns, allowing it to visualize detailed layers and structures within the retina. OCT can be used to qualitatively and quantitatively analyze the retina, detecting various pathological features and measuring retinal thickness. Anterior segment OCT also allows high-resolution imaging of the cornea, iris, angle, and anterior chamber.
Optical coherence tomography (OCT) is a non-invasive imaging technique that uses light to capture high-resolution, cross-sectional images of the retina and anterior segment of the eye. OCT provides depth resolution on the scale of 10 microns, allowing it to visualize and measure individual layers of the retina. OCT can detect various retinal pathologies and abnormalities through qualitative and quantitative analysis of the pre-retinal, overall retinal, foveal, and macular profiles.
Electrophysiological techniques allow clinical investigations to include a ‘dissection’ of the visual system. Using suitable electrophysiological techniques, the ‘dissection’ allows function to be ascribed to the different photoreceptors (rod and cone photoreceptors), retinal layers, retinal location or the visual pathway up to the visual cortex. Combined with advances in genetics, retinal biochemistry, visual fields and ocular imaging, it is now possible to obtain a better understanding of diseases affecting the retina and visual pathways.
Electrophysiology of the eye includes tests like ERG, EOG, and VEP that objectively measure visual system function. ERG records the retinal response, EOG assesses the retinal pigment epithelium, and VEP measures the brain response. ERG is the most commonly used test and involves stimulating the retina with flashes of light of varying intensities while the eye is dark or light adapted to evaluate rod, cone, and retinal ganglion cell function based on the waveform produced. Pattern ERG and multifocal ERG provide more localized assessment of the macula. Electrophysiology complements structural imaging to evaluate visual function.
Optic atrophy is the permanent loss of retinal ganglion cell axons and death of these cells, resulting in changes to the optic disc such as pallor. It has many potential causes, including diseases that damage the optic nerve or retina. On examination, patients with optic atrophy typically have reduced visual acuity and color vision, as well as an afferent pupillary defect. The optic disc appears pale on ophthalmoscopy.
Electrophysiological assessment of optic neuritis: is there still a roleClare Fraser
Visual evoked potentials were once in the diagnostic criteria for Multiple Sclerosis, but have been left off the most recent criteria. However, there are newer techniques available which are still invaluable in the diagnosis of optic neuritis and its common mimics.
Birdshot choroidopathy is a rare autoimmune uveitis characterized by yellow-white choroidal lesions clustered around the optic nerve and radiating towards the periphery, nearly always involving the inferior and nasal areas. It causes symptoms like nyctalopia, floaters, flashes of light, and dyschromatopsia. Diagnosis requires bilateral disease, ≥3 peripapillary lesions, vitreous cells and haze, and may include HLA-A29 positivity and retinal vasculitis. Investigations include fluorescein angiography, indocyanine green angiography, visual field testing, electroretinography, and optical coherence tomography. Acute flares are treated with oral or intravitreal st
Central serous chorioretinopathy (CSR) is characterized by localized serous detachment of the neurosensory retina in the macular region. It is idiopathic and multifactorial in nature. CSR typically affects young-to-middle aged males and is associated with stress, steroid use, and sleep apnea. Common symptoms include blurry vision, micropsia, and para central scotoma. Diagnosis is confirmed via imaging like fundus fluorescein angiography and optical coherence tomography. While CSR often resolves spontaneously, recurrence is common and persistent cases can lead to permanent vision loss from complications like retinal pigment epithelium atrophy. Treatment aims to speed recovery and prevent recurrence using
This document provides information on the management of intermittent exotropia. It defines intermittent exotropia as an abnormal outward deviation of one eye that is intermittent and has a constant angle of deviation. The causes include loss of concentration and fatigue. Intermittent exotropia is classified into basic type, divergence excess, and convergence insufficiency. Treatment involves glasses, occlusion therapy if needed, orthoptic exercises, and surgery if non-surgical methods fail or the deviation progresses to constant exotropia. The goal of treatment is to prevent amblyopia, which is commonly associated with intermittent exotropia. Regular follow up is important as intermittent exotropia is a progressive condition.
1) Strabismic amblyopia is caused by abnormal alignment of the eyes that disrupts normal visual development. It can be treated by correcting refractive errors, patching the non-amblyopic eye, and sometimes using penalization methods to blur vision in the strong eye.
2) Patching protocols depend on the child's age and severity of amblyopia, usually following the "one week per year of age" rule. Patching is most effective when started before age 5.
3) If patching fails to improve vision after 3 months, more active treatments like pleoptic exercises may be tried, but most active methods still require more research before being widely adopted. Early diagnosis and strict compliance with patching
This document discusses various positional eyelid disorders including ptosis, entropion, ectropion, and lagophthalmos. It defines each condition, describes the structural layers of the eyelid, and provides normal measurements. Evaluation of ptosis includes measuring marginal reflex distance, vertical fissure height, and levator function. Causes, types, and treatments are outlined for each disorder. Surgical treatments aim to correct underlying structural issues like shortening or lengthening tissues.
This document discusses investigations for lacrimal system disorders like epiphora. It describes probing and irrigation, Jones dye tests, and regurgitation tests to diagnose epiphora. Causes of epiphora include eyelid abnormalities, lacrimal pump failure, and obstruction of the lacrimal drainage system. Dry eye is classified based on symptoms and signs. Tests for dry eye include tear film break up time, rose bengal and lissamine green staining, schirmer tests, and osmolality. Schirmer 1 and 2 differentiate basic versus reflex tearing. Precautions are outlined for accurate schirmer test administration.
This document provides an overview of fundus fluorescein angiography (FFA). It describes what FFA is, its indications, contraindications, procedure, interpretation, limitations, and comparisons to indocyanine green angiography. FFA involves injecting fluorescein dye intravenously and taking photographs of the retina over time to study the retinal and choroidal vasculature. It can help diagnose and monitor various retinal conditions by revealing vascular abnormalities, leaks, pooling, and staining patterns not visible on regular exam. Potential side effects are generally mild but can include nausea, vomiting, or allergic reactions in rare cases.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
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Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
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2. Def.
It is a clinically and genetically heterogeneous group of inherited
retinal disorders ch.ch by :-
a) diffuse progressive dysfunction of predominantly rods.
b) subsequent degeneration of cones & (RPE).
What is the etiology ?
Since RP is a collection of many different genetic disorders, the
etiology is quite variable.
the final common pathway appears to be (photoreceptor cell death
by apoptosis ).
What we mean by ( apoptosis ) ?
It is a Greek word means drooping / falling off used to describe
normal death of cells in sequence.
3. Pathology : ( in order )
a) Degeneration of rods 1st
b) Start @ equator
c) Peripheral extension
d) Degeneration of cones
NB :-
Pathologic findings of an enucleated eye in a patient with autosomal
recessive RP showed that:-
1. the rod and cone outer segments were shortened and
disorganized in the patient’s best field of vision.
2. while in the area of visual loss there was a total loss of outer
segments and a decrease in photoreceptors number.
4. What is most common inheritance of RP ?
AR
What is the best inheritance prognosis in RP ?
AD
What is the worst inheritance prognosis in RP ?
XLR ( X LINKED RECESSIVE )
What is the most common gene involved in RP ?
RDS ( peripherin gene)
5. symptoms ( bilateral )
1. Night blindness ( Rods)
2. Loss of peripheral vision 1st .
3. Later on , Loss of central vision (cones)
10. Others :-
1. Keratoconus .
2. PSCC
3. Vitreous cells
4. RPE atrophy
5. CME
What are the commonest refractive errors in RP ?why?
1. Myopia ??
2. Hyperopia ??
3. Non of above ??
11. What are investigations needed?
VF ( findings) /
1) Peripheral scotoma
2) Ring scotoma
3) Progressive constricted field
4) Tubular vision .
What is scotoma ?
It is the area of obscurity of VF surrounded by normal VF
( normal retinal sensitivity)
12.
13. ERG (electroretinogram)
it measures the electrical potential generated by rods and
cones after a light stimulus.
Findings :-
1) Subnormal a wave ( photoreceptors) = negative
2) Subnormal b wave ( bipolar & mullers cells) = positive.
Electrooculogram (EOG) :-
It is a measurement of the function of the RPE and
photoreceptors by measuring the standing potential
between the cornea and the retina
14.
15. Is there any roles of OCT , FFA in RP? Discuss in brief.
Yes ,
It is mainly to diagnose other associations of RP such as ;-
1. CME ( OCT , FFA ).
2. Early deterioration in RPE ( FFA ).
Is there any role of lab. tests in RP diagnosis ?
Yes ,
Genetic test is important in diagnosis of atypical cases of RP.
Ornithine-lysine ratio (for gyrate atrophy of the retina)
16. From previous mentioned tests , what is the main
diagnostic test & main prognostic test ?
----------------------------------------------------
17. What is DD of RP ?
1. gyrate atrophy.
2. Chorideremia ( rare , X-linked recessive form of hereditary retinal
degeneration)
3. cone-rod dystrophy.
4. cone dystrophy.
5. Lebers congenital amaurosis.
6. Drug toxicity from thioridazine hydrochloride (Mellaril) (can lead
to diffuse pigmentary and RPE atrophy).
7. diffuse unilateral subacute neuroretinitis (DUSN) can cause
similar pigmentary retinopathy seen in patients with RP.
18. How to DD between DUSEN & RP ?
DUSEN Ch. Ch. by /
1. Unilateral.
2. Caused by parasite.
3. The worm can be seen by fundus examination.
19. What are the causes of pseudo-RP ?
1. Trauma
2. Congenital Syphilis (leopard skin retinopathy).
3. Congenital rubella.
4. Drug induced: Thioridazine streaks, chloroquine, quinine
5. Laser scars
6. Chronic RD.
7. Chronic uveitis
8. Cancer-associated retinopathy
20. What are the criteria of Atypical RP ?
1) Cone –rod dystrophy ( starts @ cones)
2) Sectorial RP ( affect one sectors of the retina)
3) Peri-centric RP ( around the macula)
4) Punctate RP (scattered white spots without
pigmentation)
21. Can we prevent RP ?
Since RP is a genetic disorder, there is currently no intervention that
would prevent manifestations of RP.
Treatment
Usually ,, No treatment but new trials Can be done /
1) Sub retinal injection of RPE 65 ( gene therapy)
2) Retinal implant .
3) Retinal transplantation
4) Stem cells
5) Vitamin therapy ( Vit. A)
6) Psychological and visual rehabilitation
NB : DON’T FORGET Examination of other family members of the
affected person is recommended
26. Can a pt. with RP be legally blind in spite of having good central
vision?
----------------------------------------------------------------------------------
What are the Types of Sunglasses preferred in RP ?
-----------------------------------------------------------------------------------
27. Can an RP patient be legally blind in spite of having good central
vision?
Yes, visual field of less than 10 degrees even with VA of 6/6.
What are the Types of Sunglasses preferred in RP ?
Some clinicians prefer :-
1. orange photochromic sunglasses with tinted side shields.
2. dark amber sunglasses with tinted side shields.
NB :-
Sunglasses should be selected for outdoor use that provide maximal
comfort to the vision without compromising vision.
28. What is the Mechanism of glaucoma in RP. ?
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29. What is the Mechanism of glaucoma in RP. ?
RP can be associated with both angle closure and open angle
glaucoma.
Angle closure glaucoma:-
There is increased zonular instability with anterior shifting of iris lens
diaphragm resulting in angle narrowing and angle closure
glaucoma.
POAG, NTG :-
a) attributed to the mutation of gene for retinitis pigmentosa
b) GTPase regulator-interacting protein 1 (RPGRIP1) on
chromosome 14q11.
c) ++ IOP
30. What is the difference ( ) Amsler grid chart &
Amsler Dubois chart ?
31.
32.
33.
34.
35.
36. What is DD of night blindness ?
1. ------------
2. ----------------
3. ------------------
4. -----------------------
37. What is DD of night blindness ?
1. Idiopathic
2. RP
3. Gyrate disease
4. Vit. A deficiency
38. Which of the following not associated with RP ?
1. CME
2. PSCC
3. ERM
4. Endophthalmitis