MANAGEMENT OF MACULAR HOLE, Ophthalmology presentation, eye care in the elderly , macular hole as a consequence of trauma, Vitreoretinal surgical cases, ,
MIGS procedures are newer glaucoma surgeries that offer more modest intraocular pressure (IOP) lowering than traditional surgeries, but with a safer risk profile. They are targeted at patients with mild to moderate glaucoma and involve minimally traumatic, ab-interno approaches that preserve the conjunctiva. Common MIGS procedures include implants that bypass the trabecular meshwork (iStent, Hydrus), drain into the suprachoroidal space (CyPass), or excise the trabecular meshwork (Trabectome). Studies show that MIGS procedures lower IOP by 15-20% on average when combined with cataract surgery. Complications are generally mild and
The document discusses diabetic retinopathy (DR) and diabetic macular edema (DME). Some key points:
- DR is a leading cause of vision loss and its prevalence is increasing in India. Effective screening and treatment is needed.
- DR stages include non-proliferative DR and proliferative DR. DME can occur and is a major cause of vision loss.
- Treatments include controlling blood sugar and blood pressure, laser therapy, intravitreal anti-VEGF drugs, and steroids. Anti-VEGF drugs and steroids have largely replaced laser as first-line treatment for DME.
- Optical coherence tomography is important for diagnosing and monitoring DME and treatment response.
This document discusses transpupillary thermotherapy (TTT), a technique that uses low-level heat delivered through the pupil to treat conditions like choroidal neovascularization (CNV), choroidal melanoma, and retinoblastoma. TTT works by inducing tumor necrosis or occlusion of neovascular vessels via localized hyperthermia above 42°C. The document outlines the laser parameters used to treat CNV via TTT, noting that a pilot study found 19% of patients experienced improved vision, 56% had no change, and 25% had declining vision, while 94% saw reduced exudation. TTT is currently being used and studied as a treatment for several ocular diseases.
Scleral buckling for rhegmatogenous retinal detachmentreboca smith
Scleral buckling surgery involves suturing a silicone implant or explant to the outer layer of the eye (sclera) to push the retina back into contact with the retinal pigment epithelium. This is done by creating an inward indentation of the sclera. The implant seals retinal breaks by approximating the retina and RPE over the buckle. Key steps include identifying retinal breaks, treating the breaks with cryotherapy or laser, placing scleral sutures, and sometimes draining subretinal fluid. The goal is to close breaks and reduce traction on the retina to allow it to reattach.
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.
Multifocal IOLs provide both near and distance vision without glasses by utilizing concentric zones of different optical powers (refractive MFIOLs) or diffractive properties to split light between two focal points. While eliminating need for glasses, they can cause visual side effects like glare and reduced contrast sensitivity. Careful patient selection and counseling, accurate biometry and surgical technique are important for successful multifocal IOL implantation outcomes.
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.
The document discusses iridocorneal endothelial (ICE) syndrome, a rare disorder characterized by abnormalities of the corneal endothelium and iris that can cause corneal decompensation and glaucoma. ICE syndrome has three clinical variants (iris nevus/Cogan-Reese syndrome, Chandler syndrome, and essential/progressive iris atrophy) that are characterized by different degrees of iris atrophy. The pathogenesis involves proliferation of abnormal endothelial cells that migrate onto the trabecular meshwork and iris. Investigations include gonioscopy, ultrasound biomicroscopy, and specular microscopy of the corneal endothelium. Treatment involves medications and surgeries to manage glaucoma and corneal edema.
MIGS procedures are newer glaucoma surgeries that offer more modest intraocular pressure (IOP) lowering than traditional surgeries, but with a safer risk profile. They are targeted at patients with mild to moderate glaucoma and involve minimally traumatic, ab-interno approaches that preserve the conjunctiva. Common MIGS procedures include implants that bypass the trabecular meshwork (iStent, Hydrus), drain into the suprachoroidal space (CyPass), or excise the trabecular meshwork (Trabectome). Studies show that MIGS procedures lower IOP by 15-20% on average when combined with cataract surgery. Complications are generally mild and
The document discusses diabetic retinopathy (DR) and diabetic macular edema (DME). Some key points:
- DR is a leading cause of vision loss and its prevalence is increasing in India. Effective screening and treatment is needed.
- DR stages include non-proliferative DR and proliferative DR. DME can occur and is a major cause of vision loss.
- Treatments include controlling blood sugar and blood pressure, laser therapy, intravitreal anti-VEGF drugs, and steroids. Anti-VEGF drugs and steroids have largely replaced laser as first-line treatment for DME.
- Optical coherence tomography is important for diagnosing and monitoring DME and treatment response.
This document discusses transpupillary thermotherapy (TTT), a technique that uses low-level heat delivered through the pupil to treat conditions like choroidal neovascularization (CNV), choroidal melanoma, and retinoblastoma. TTT works by inducing tumor necrosis or occlusion of neovascular vessels via localized hyperthermia above 42°C. The document outlines the laser parameters used to treat CNV via TTT, noting that a pilot study found 19% of patients experienced improved vision, 56% had no change, and 25% had declining vision, while 94% saw reduced exudation. TTT is currently being used and studied as a treatment for several ocular diseases.
Scleral buckling for rhegmatogenous retinal detachmentreboca smith
Scleral buckling surgery involves suturing a silicone implant or explant to the outer layer of the eye (sclera) to push the retina back into contact with the retinal pigment epithelium. This is done by creating an inward indentation of the sclera. The implant seals retinal breaks by approximating the retina and RPE over the buckle. Key steps include identifying retinal breaks, treating the breaks with cryotherapy or laser, placing scleral sutures, and sometimes draining subretinal fluid. The goal is to close breaks and reduce traction on the retina to allow it to reattach.
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.
Multifocal IOLs provide both near and distance vision without glasses by utilizing concentric zones of different optical powers (refractive MFIOLs) or diffractive properties to split light between two focal points. While eliminating need for glasses, they can cause visual side effects like glare and reduced contrast sensitivity. Careful patient selection and counseling, accurate biometry and surgical technique are important for successful multifocal IOL implantation outcomes.
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.
The document discusses iridocorneal endothelial (ICE) syndrome, a rare disorder characterized by abnormalities of the corneal endothelium and iris that can cause corneal decompensation and glaucoma. ICE syndrome has three clinical variants (iris nevus/Cogan-Reese syndrome, Chandler syndrome, and essential/progressive iris atrophy) that are characterized by different degrees of iris atrophy. The pathogenesis involves proliferation of abnormal endothelial cells that migrate onto the trabecular meshwork and iris. Investigations include gonioscopy, ultrasound biomicroscopy, and specular microscopy of the corneal endothelium. Treatment involves medications and surgeries to manage glaucoma and corneal edema.
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.
Pigment dispersion syndrome is characterized by the dispersion of pigment granules from the iris pigment epithelium throughout the anterior segment of the eye. This can lead to elevated intraocular pressure and pigmentary glaucoma. It typically affects young, myopic white males and is caused by rubbing of the iris pigment epithelium against the lens zonules due to posterior bowing of the peripheral iris. Diagnosis is based on finding the classic triad of Krukenberg spindle on the cornea, midperipheral iris transillumination defects, and dense trabecular pigmentation on gonioscopy.
Congenital retinal anomalies can arise from developmental defects, vascular abnormalities, infections, tumors or trauma. Clinical presentation depends on laterality and extent of vision loss. Examination may reveal colobomas, retinal folds, persistent fetal vasculature or lacunae indicative of conditions like Aicardi syndrome. Retinopathy of prematurity is a major cause of vision loss in premature infants and progresses through stages from demarcation lines to retinal detachment. Infectious etiologies can cause chorioretinitis from viruses like cytomegalovirus and parasites including toxoplasmosis. Prompt treatment is aimed at the underlying cause and prevention of complications affecting vision.
This document discusses posterior capsule tears that can occur during cataract surgery. It covers the predisposing factors, mechanisms, identification, and management strategies for posterior capsule tears with or without vitreous loss. Key points include identifying tears early, stabilizing the anterior chamber with viscoelastic, deciding whether to continue phacoemulsification or convert to extracapsular extraction based on the situation, performing anterior vitrectomy when needed with caution to minimize further vitreous disturbance, and properly placing an IOL. The goal is to remove all lens material and prevent further complications while minimizing additional surgery.
Keratoprosthesis is a surgical procedure that replaces a severely damaged or diseased cornea with an artificial cornea to restore vision. The first attempts at keratoprosthesis in humans date back to the mid-19th century, but most implants failed. Modern keratoprosthesis designs like the Boston KPro and AlphaCor KPro sandwich a donor corneal graft between plastic plates. Complications can include melting/extrusion of the implant, infection, glaucoma, retinal detachment, and formation of membranes behind the implant. Close post-operative monitoring is required to manage complications and maintain vision with keratoprosthesis implants.
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, clinical features, complications, investigations, and management. BRVO is caused by obstruction of one of the retinal veins, usually at the arteriovenous crossing point. It can lead to macular edema, neovascularization, vitreous hemorrhage, and retinal detachment. Treatment involves anti-VEGF injections, steroids, laser photocoagulation, and occasionally surgery. Several clinical trials have evaluated therapies for BRVO, finding that anti-VEGF drugs and steroids reduce macular edema but laser provides little additional benefit when combined with anti-VEGF treatment.
This document provides an overview of corneal topography. It begins by defining corneal topography as the study of the shape of the corneal surface. It then describes several techniques for evaluating corneal topography including keratometry, keratoscopy using Placido discs and photokeratoscopy, rasterstereography, and interferometry. Computerized topography systems that provide detailed maps of the corneal surface are also discussed. The document outlines clinical applications of corneal topography and variations in topographic patterns seen in normal and diseased corneas.
This document discusses various vitreous substitutes and intraocular gases used to replace the vitreous humor after surgery. It describes the anatomy and composition of the natural vitreous and ideal properties for substitutes. Common substitutes discussed include gases like air, sulfur hexafluoride and perfluorocarbons; liquids like silicone oil, perfluorocarbon liquids and semi-fluorinated alkanes; and experimental polymers and implants. The document compares different options and provides details on how each works, associated complications, and appropriate uses.
This document discusses peripheral ulcerative keratitis (PUK), a group of inflammatory diseases that cause thinning and ulceration of the peripheral cornea. It describes several types of PUK including Mooren's ulcer, marginal keratitis, Terrien's marginal degeneration, and PUK associated with autoimmune diseases. Mooren's ulcer is a rare autoimmune disease characterized by progressive, peripheral, circumferential ulceration. Marginal keratitis is caused by a hypersensitivity reaction to Staphylococcus exotoxins. Terrien's marginal degeneration causes thinning of the peripheral cornea. PUK associated with autoimmune diseases like rheumatoid arthritis is linked to immune complex deposition in the peripheral cornea. Management involves topical
Posner-Schlossman syndrome is characterized by recurrent unilateral attacks of ocular hypertension accompanied by mild anterior chamber inflammation. It was first described in 1948 and affects people aged 20-50, with males and females equally impacted. The exact pathogenesis is unknown but may involve trabecular meshwork obstruction by mononuclear cells. Symptoms include blurred vision and eye discomfort. Signs include elevated IOP out of proportion to mild inflammation and open iridocorneal angles. While usually self-limiting, long-term damage from recurrent attacks can occur, so treatment focuses on IOP control and inflammation management medically or surgically if needed.
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.
The document discusses evaluation of the optic nerve head and retinal nerve fiber layer. It provides details on the anatomy and characteristics examined, including the intra-papillary and para-papillary regions. Glaucomatous damage results in characteristic signs in these areas like retinal nerve fiber layer defects. Newer imaging techniques like stereo-photogrammetry, scanning laser technologies, and optical coherence tomography (OCT) allow for early diagnosis by focusing on the retinal nerve fiber layer and optic disc. OCT is particularly useful for evaluating pre-perimetric glaucoma and monitoring macular changes.
This document discusses the use of lasers in the treatment of glaucoma. It begins by introducing different types of lasers used, including Nd:YAG lasers. It then covers specific laser procedures for glaucoma such as laser iridotomy to relieve pupillary block, laser iridoplasty to modify the iris, and laser trabeculoplasty to increase outflow. It compares argon laser trabeculoplasty to selective laser trabeculoplasty. The document also discusses laser techniques for angle closure glaucoma, post-operative treatment, and cyclophotocoagulation to reduce aqueous production. Throughout, it provides details on laser parameters and outcomes of these procedures.
The document outlines the anatomy, blood supply, evaluation methods, and appearance of the optic nerve head. It discusses the anatomy in detail, including the components and organization of nerve fibers in the optic nerve head. Evaluation methods covered include clinical examination, structural analysis using slit lamp biomicroscopy, HRT, GDx, OCT, and functional analysis using visual field testing. The normal appearance and variations of structures like the neuroretinal rim, optic cup, and blood vessels are described. Changes in glaucoma like cupping, notching, and rim thinning are also outlined.
UBM and ASOCT provide high-resolution cross-sectional images of the anterior segment including the cornea, anterior chamber, angle, and iris. ASOCT uses optical coherence tomography with a wavelength of 1310nm for improved penetration and reduced retinal damage compared to posterior segment OCT. It allows high-speed imaging of dynamic structures. ASOCT has applications in assessing corneal diseases and procedures, glaucoma (including angle anatomy and iridotomy evaluation), and intraocular lens implantation. Measurements of angle width parameters help evaluate angle closure risk. While valuable for objective angle assessment, ASOCT cannot image all anatomical structures involved in glaucoma.
This document summarizes several studies and clinical trials related to the treatment of diabetic retinopathy and diabetic macular edema. It discusses the Diabetic Retinopathy Study (DRS) and Early Treatment Diabetic Retinopathy Study (ETDRS) which established laser photocoagulation as the standard treatment for proliferative diabetic retinopathy and diabetic macular edema. It also summarizes the Diabetic Retinopathy Clinical Research Network (DRCR.Net) which conducted several clinical trials comparing treatments for diabetic macular edema such as anti-VEGF injections and laser photocoagulation. The document provides high-level overviews of many landmark studies that helped advance the treatment of diabetic eye disease.
Iol power calculation in pediatric patientsAnisha Rathod
- Many factors affect intraocular lens (IOL) power calculation in pediatric patients including age at surgery, laterality, amblyopia, axial length, keratometry, and expected myopic shift due to ongoing eye growth.
- Normal eye development involves rapid growth of the axial length and changes in lens power in the first years of life.
- Target postoperative refraction must account for this myopic shift and generally involves undercorrecting more in younger patients.
- Accurate biometry using immersion ultrasound or optical techniques is important to minimize errors from corneal compression.
- Formulas, IOL type and position can further influence outcomes.
This document provides an overview of macular holes, including:
- Classification into primary (idiopathic) and secondary holes. Primary holes are caused by vitreous traction while secondary have other causes like trauma.
- Stages of macular hole formation based on Gass classification from early detachment to full thickness hole.
- Surgical treatment involves vitrectomy to relieve traction along with internal limiting membrane peeling which has good outcomes in improving vision.
- Differential diagnosis includes epiretinal membranes and pseudoholes which have different presentations and prognoses.
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 retinal artery occlusion, including classifications, epidemiology, clinical features, risk factors, evaluation, treatment, and prognosis for different types. Central retinal artery occlusion typically causes sudden, painless vision loss and has a poor visual prognosis. Branch retinal artery occlusion often causes partial vision loss and has a better prognosis, with vision recovering to 20/40 or better in most cases. Cilioretinal artery occlusion can occur in isolation or with central retinal vein occlusion, and isolated cases typically have a good visual outcome.
This document summarizes macular hole and epiretinal membrane. It discusses the vitreous, macula, OCT imaging, pathogenesis and stages of macular hole. It covers risk factors, signs, differential diagnosis and treatment of macular hole including vitrectomy. It also discusses prevalence, risk factors, pathogenesis and components of epiretinal membrane formation.
- A macular hole is a full-thickness opening in the neurosensory retina at the foveal center that causes metamorphopsia and central vision loss.
- Macular holes form due to vitreomacular traction or cystoid macular edema and are classified into stages based on size and morphology on OCT imaging.
- Surgical repair via pars plana vitrectomy and gas tamponade is effective for most macular holes, especially smaller and newer ones, leading to hole closure and vision improvement in many cases.
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.
Pigment dispersion syndrome is characterized by the dispersion of pigment granules from the iris pigment epithelium throughout the anterior segment of the eye. This can lead to elevated intraocular pressure and pigmentary glaucoma. It typically affects young, myopic white males and is caused by rubbing of the iris pigment epithelium against the lens zonules due to posterior bowing of the peripheral iris. Diagnosis is based on finding the classic triad of Krukenberg spindle on the cornea, midperipheral iris transillumination defects, and dense trabecular pigmentation on gonioscopy.
Congenital retinal anomalies can arise from developmental defects, vascular abnormalities, infections, tumors or trauma. Clinical presentation depends on laterality and extent of vision loss. Examination may reveal colobomas, retinal folds, persistent fetal vasculature or lacunae indicative of conditions like Aicardi syndrome. Retinopathy of prematurity is a major cause of vision loss in premature infants and progresses through stages from demarcation lines to retinal detachment. Infectious etiologies can cause chorioretinitis from viruses like cytomegalovirus and parasites including toxoplasmosis. Prompt treatment is aimed at the underlying cause and prevention of complications affecting vision.
This document discusses posterior capsule tears that can occur during cataract surgery. It covers the predisposing factors, mechanisms, identification, and management strategies for posterior capsule tears with or without vitreous loss. Key points include identifying tears early, stabilizing the anterior chamber with viscoelastic, deciding whether to continue phacoemulsification or convert to extracapsular extraction based on the situation, performing anterior vitrectomy when needed with caution to minimize further vitreous disturbance, and properly placing an IOL. The goal is to remove all lens material and prevent further complications while minimizing additional surgery.
Keratoprosthesis is a surgical procedure that replaces a severely damaged or diseased cornea with an artificial cornea to restore vision. The first attempts at keratoprosthesis in humans date back to the mid-19th century, but most implants failed. Modern keratoprosthesis designs like the Boston KPro and AlphaCor KPro sandwich a donor corneal graft between plastic plates. Complications can include melting/extrusion of the implant, infection, glaucoma, retinal detachment, and formation of membranes behind the implant. Close post-operative monitoring is required to manage complications and maintain vision with keratoprosthesis implants.
This document discusses branch retinal vein occlusion (BRVO), including its pathogenesis, clinical features, complications, investigations, and management. BRVO is caused by obstruction of one of the retinal veins, usually at the arteriovenous crossing point. It can lead to macular edema, neovascularization, vitreous hemorrhage, and retinal detachment. Treatment involves anti-VEGF injections, steroids, laser photocoagulation, and occasionally surgery. Several clinical trials have evaluated therapies for BRVO, finding that anti-VEGF drugs and steroids reduce macular edema but laser provides little additional benefit when combined with anti-VEGF treatment.
This document provides an overview of corneal topography. It begins by defining corneal topography as the study of the shape of the corneal surface. It then describes several techniques for evaluating corneal topography including keratometry, keratoscopy using Placido discs and photokeratoscopy, rasterstereography, and interferometry. Computerized topography systems that provide detailed maps of the corneal surface are also discussed. The document outlines clinical applications of corneal topography and variations in topographic patterns seen in normal and diseased corneas.
This document discusses various vitreous substitutes and intraocular gases used to replace the vitreous humor after surgery. It describes the anatomy and composition of the natural vitreous and ideal properties for substitutes. Common substitutes discussed include gases like air, sulfur hexafluoride and perfluorocarbons; liquids like silicone oil, perfluorocarbon liquids and semi-fluorinated alkanes; and experimental polymers and implants. The document compares different options and provides details on how each works, associated complications, and appropriate uses.
This document discusses peripheral ulcerative keratitis (PUK), a group of inflammatory diseases that cause thinning and ulceration of the peripheral cornea. It describes several types of PUK including Mooren's ulcer, marginal keratitis, Terrien's marginal degeneration, and PUK associated with autoimmune diseases. Mooren's ulcer is a rare autoimmune disease characterized by progressive, peripheral, circumferential ulceration. Marginal keratitis is caused by a hypersensitivity reaction to Staphylococcus exotoxins. Terrien's marginal degeneration causes thinning of the peripheral cornea. PUK associated with autoimmune diseases like rheumatoid arthritis is linked to immune complex deposition in the peripheral cornea. Management involves topical
Posner-Schlossman syndrome is characterized by recurrent unilateral attacks of ocular hypertension accompanied by mild anterior chamber inflammation. It was first described in 1948 and affects people aged 20-50, with males and females equally impacted. The exact pathogenesis is unknown but may involve trabecular meshwork obstruction by mononuclear cells. Symptoms include blurred vision and eye discomfort. Signs include elevated IOP out of proportion to mild inflammation and open iridocorneal angles. While usually self-limiting, long-term damage from recurrent attacks can occur, so treatment focuses on IOP control and inflammation management medically or surgically if needed.
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.
The document discusses evaluation of the optic nerve head and retinal nerve fiber layer. It provides details on the anatomy and characteristics examined, including the intra-papillary and para-papillary regions. Glaucomatous damage results in characteristic signs in these areas like retinal nerve fiber layer defects. Newer imaging techniques like stereo-photogrammetry, scanning laser technologies, and optical coherence tomography (OCT) allow for early diagnosis by focusing on the retinal nerve fiber layer and optic disc. OCT is particularly useful for evaluating pre-perimetric glaucoma and monitoring macular changes.
This document discusses the use of lasers in the treatment of glaucoma. It begins by introducing different types of lasers used, including Nd:YAG lasers. It then covers specific laser procedures for glaucoma such as laser iridotomy to relieve pupillary block, laser iridoplasty to modify the iris, and laser trabeculoplasty to increase outflow. It compares argon laser trabeculoplasty to selective laser trabeculoplasty. The document also discusses laser techniques for angle closure glaucoma, post-operative treatment, and cyclophotocoagulation to reduce aqueous production. Throughout, it provides details on laser parameters and outcomes of these procedures.
The document outlines the anatomy, blood supply, evaluation methods, and appearance of the optic nerve head. It discusses the anatomy in detail, including the components and organization of nerve fibers in the optic nerve head. Evaluation methods covered include clinical examination, structural analysis using slit lamp biomicroscopy, HRT, GDx, OCT, and functional analysis using visual field testing. The normal appearance and variations of structures like the neuroretinal rim, optic cup, and blood vessels are described. Changes in glaucoma like cupping, notching, and rim thinning are also outlined.
UBM and ASOCT provide high-resolution cross-sectional images of the anterior segment including the cornea, anterior chamber, angle, and iris. ASOCT uses optical coherence tomography with a wavelength of 1310nm for improved penetration and reduced retinal damage compared to posterior segment OCT. It allows high-speed imaging of dynamic structures. ASOCT has applications in assessing corneal diseases and procedures, glaucoma (including angle anatomy and iridotomy evaluation), and intraocular lens implantation. Measurements of angle width parameters help evaluate angle closure risk. While valuable for objective angle assessment, ASOCT cannot image all anatomical structures involved in glaucoma.
This document summarizes several studies and clinical trials related to the treatment of diabetic retinopathy and diabetic macular edema. It discusses the Diabetic Retinopathy Study (DRS) and Early Treatment Diabetic Retinopathy Study (ETDRS) which established laser photocoagulation as the standard treatment for proliferative diabetic retinopathy and diabetic macular edema. It also summarizes the Diabetic Retinopathy Clinical Research Network (DRCR.Net) which conducted several clinical trials comparing treatments for diabetic macular edema such as anti-VEGF injections and laser photocoagulation. The document provides high-level overviews of many landmark studies that helped advance the treatment of diabetic eye disease.
Iol power calculation in pediatric patientsAnisha Rathod
- Many factors affect intraocular lens (IOL) power calculation in pediatric patients including age at surgery, laterality, amblyopia, axial length, keratometry, and expected myopic shift due to ongoing eye growth.
- Normal eye development involves rapid growth of the axial length and changes in lens power in the first years of life.
- Target postoperative refraction must account for this myopic shift and generally involves undercorrecting more in younger patients.
- Accurate biometry using immersion ultrasound or optical techniques is important to minimize errors from corneal compression.
- Formulas, IOL type and position can further influence outcomes.
This document provides an overview of macular holes, including:
- Classification into primary (idiopathic) and secondary holes. Primary holes are caused by vitreous traction while secondary have other causes like trauma.
- Stages of macular hole formation based on Gass classification from early detachment to full thickness hole.
- Surgical treatment involves vitrectomy to relieve traction along with internal limiting membrane peeling which has good outcomes in improving vision.
- Differential diagnosis includes epiretinal membranes and pseudoholes which have different presentations and prognoses.
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 retinal artery occlusion, including classifications, epidemiology, clinical features, risk factors, evaluation, treatment, and prognosis for different types. Central retinal artery occlusion typically causes sudden, painless vision loss and has a poor visual prognosis. Branch retinal artery occlusion often causes partial vision loss and has a better prognosis, with vision recovering to 20/40 or better in most cases. Cilioretinal artery occlusion can occur in isolation or with central retinal vein occlusion, and isolated cases typically have a good visual outcome.
This document summarizes macular hole and epiretinal membrane. It discusses the vitreous, macula, OCT imaging, pathogenesis and stages of macular hole. It covers risk factors, signs, differential diagnosis and treatment of macular hole including vitrectomy. It also discusses prevalence, risk factors, pathogenesis and components of epiretinal membrane formation.
- A macular hole is a full-thickness opening in the neurosensory retina at the foveal center that causes metamorphopsia and central vision loss.
- Macular holes form due to vitreomacular traction or cystoid macular edema and are classified into stages based on size and morphology on OCT imaging.
- Surgical repair via pars plana vitrectomy and gas tamponade is effective for most macular holes, especially smaller and newer ones, leading to hole closure and vision improvement in many cases.
This document provides an overview of epiretinal membrane (ERM). Key points include:
- ERMs are cellular sheets that form on the macular surface due to various etiologies. They were first described in 1865.
- Presentation can vary but ERMs often cause mechanical distortion of the macula due to their contractile properties.
- Prevalence increases with age, peaking between 70-79 years old. Studies show a prevalence of 7-11.8% and bilateral involvement in 19.5-31% of cases.
- Classification includes idiopathic ERMs and secondary ERMs associated with other ocular conditions. Formation involves glial cells, extracellular matrix
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.
Disorders of vitreomacular interface by dr navidNavidRahman6
Vitreomacular interface disorders involve abnormal attachments between the vitreous and the macula that can cause vision problems. These include vitreomacular adhesion (VMA), vitreomacular traction (VMT), macular holes, and epiretinal membranes. VMA is an asymptomatic focal adhesion within the macula, while VMT causes macular distortion from traction. Macular holes are full-thickness defects in the macula classified by size. Epiretinal membranes can cause macular wrinkling or distortion. OCT is useful for diagnosing and staging these vitreomacular disorders.
A macular hole is a full-thickness defect in the neurosensory retina located within or just eccentric to the fovea. It is commonly classified based on size and associated findings on exam and OCT imaging. Stage 1 holes show early changes like cysts or pseudocysts at the fovea. Stage 2 holes are full-thickness defects under 400um. Stage 3 holes are larger, over 400um. Stage 4 holes have a complete posterior vitreous detachment. Risk factors include age, female sex, myopia, and trauma. Patients may experience vision distortion or loss.
Urrets-Zavalia Syndrome (UZS) is characterized by a fixed, dilated pupil following penetrating keratoplasty (PKP) for keratoconus. The syndrome was first described in 1963 and is thought to be caused by iris ischemia and acute rise in intraocular pressure during or after surgery. Risk factors include the use of mydriatic agents, elevated IOP, presence of keratoconus, and inflammation. Prevention focuses on maintaining a deep anterior chamber and avoiding iris trauma during PKP. Management includes treatments to lower IOP if elevated, with reconstructive surgery if symptoms from the fixed, dilated pupil are present.
Cscr ( central serous chorioretinopathy )Vinitkumar MJ
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- Eckardt forceps
- Horizontal scissors
- Vertical scissors
Surgeon:
- Membrane pick
- Knobbed spatula
- Scissors
- Gently lift the edge of the membrane with
forceps and cut it with scissors
- Dissect the membrane from the retina using
scissors or pick
- Dissect in a circumferential manner from the
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- Apply endodiathermy to bleeding vessels
- Remove all membranes
- Use scleral depression to flatten the globe and
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- Use bimanual technique for difficult membranes
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- Video recording of this lecture in English language: https://youtu.be/Pt1nA32sdHQ
- Video recording of this lecture in Arabic language: https://youtu.be/uFdc9F0rlP0
- 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
1. EVALUATE AND DISCUSS THE PRINCIPLES OF
MANAGEMENT OF MACULAR HOLE IN A
65YR-OLD RETIRED SCHOOL PRINCIPAL
PRESENTED BY
DR. AVURU CHUKWUNALU JAMES
ON 5TH MAY, 2022
3. INTRODUCTION
• A macular hole is a break in the macular commonly involving the fovea.
• A full thickness macular hole is a defect of the foveal retina involving its full thickness
from the internal limiting membrane (ILM) to the outer segment of the photoreceptor
layer.
• It was first described by Knapp in 1869 in a patient who sustained blunt trauma to the
eye and Subsequent case reports and series in those early days revealed macular
hole to be related to trauma
• However, case series as far back as the 1970s reported that more than 80% of
macular holes are idiopathic and that only less than 10% have associated history of
trauma to the eye
4. INTRODUCTION/BRIEF ANATOMY/PHYSIOLOGY
• Macula is a round area at the
posterior pole temporal to the optic
• 5.5mm in diameter
• Its yellowish color derived from the
presence of xanthophyll pigment
• Comprises of fovea centralis(1.5mm),
foveola(0.35mm) and FAZ(0.4-
0.6mm).
6. SPECIFIC ANATOMIC CONFIGURATION OF THE
FOVEA
• Densest concentration of cones
• A one to one photoreceptor-ganglion cell relationship
• Cones more elongated and slender
• Absence of rods at the foveola
• RPE cells are taller, thinner and deeply pigmented
• Presence of xanthophyll pigment
7. EPIDERMIOLOGY
• Prevalence is approximately 3.3 cases in 1000 in those persons older than 55 year in USA
• Peak incidence of idiopathic macular hole development is in the seventh decade of life,
• Women affected more than men
• Prevalence in India is a reported 0.17%, with a mean age of 67 years.
• Prevalence rate of macular holes is 1.6 out of 1000 elderly Chinese, with a strong female
predilection (Beijing Eye Study)
• It accounts for 4% of retinal diseases in Benin city southern Nigeria, 6.6% in South-South
Nigeria and in Southwestern Nigeria, Macular hole constitutes between 4.2% - 18% of
retinal diseases
8.
9. EPIDERMIOLOGY
• In a study in Ekiti by Iyiade A. Ajayi e’tal, macular hole constituted 0.5% of the number of
new patients with eye disorder and 6.9% of new cases with retinal diseases
• 50% of stage 0 and stage 1 macular holes may resolve spontaneously
• Stage 2 holes progress and worsen in most cases to stage 3 or stage 4
• Incidence of development of an idiopathic full-thickness macular hole in the fellow eye are
approximately 12% in 5yrs
• Rarely, a full-thickness macular hole may spontaneously close with resultant good vision in 0-
10% of cases
• Peak incidence is in the seventh decade of life
10. ETIOLOGY AND RISK FACTORS
• Idiopathic macular hole is the most common presentation
• Risk factors include
• Age
• Female gender
• Myopia : foveal schisis(31% develop FT MH), lamellar holes(4.1% develop FTMH)
• Trauma(6% of contusion eye injuries)
• Ocular inflammation e.g Chronic posterior uveitis
• Ocular surgeries: preceeding Rhegmatogenous RD repair( 1% develop MH
11. PATHOPHYSIOLOGY
• Shrinkage of prefoveal cortical vitreous with persistent adherence of vitreous to the
foveal region results in the causative traction.
• Tangential traction and anterior posterior vitreoretinal traction of the posterior hyaloid
on the parafovea.
• This traction ultimately causes a break or dehiscence to occur at the umbo, the thinnest
and weakest portion of the retina, and subsequent centrifugal movement of the
foveolar tissue
• Trauma-related macular holes have been described to be related to the transmission of
concussive force in a contrecoup manner, which results in the immediate rupture of the
macula at its thinnest point.
12.
13. GASS MACULAR HOLE CLASSIFICATION (CLINICAL
OBSERVATIONS ON EVOLUTION)
• Stage 1(impending Macular hole): loss of the
foveal depression(increased clinical prominence of
xanthophyll pigment)
• Stage 1A: There is foveolar detachment (loss
of the foveal contour and a lipofuscin-colored
spot)
• Stage 1B: foveal detachment (lipofuscin-
colored ring)
14. GASS CLASSIFICATION
• Stage 2: Full thickness break < 400µm in
size (posterior hyaloid still attached to the
fovea)
• Stage 3: Full thickness break ≥400 µm in
size. A grayish macular rim denotes a cuff of
subretinal fluid. Posterior hyaloid is detached
over the fovea with or without an overlying
operculum. The posterior hyaloid remains
attached to the optic disc
15. GASS MACULAR HOLE CLASSIFICATION (CLINICAL
OBSERVATIONS ON EVOLUTION)
• Stage 4: Full thickness break
≥400 µm in size. A grayish
macular rim denotes a cuff of
subretinal fluid. Has complete
posterior vitreous detachment and
Weiss ring.
16. CLASSIFICATION SCHEME OF VITREOMACULAR
TRACTION AND MACULAR HOLES(BASED ON OCT
FINDINGS)
• Vitreomacular adhesion (VMA): No distortion of the foveal contour; size of attachment area
between hyaloid and retina defined as
• focal if </= 1500 microns and
• broad if >1500 microns
• Vitreomacular traction (VMT): Distortion of foveal contour present or intraretinal structural changes
in the absence of a full-thickness macular hole; size of attachment area between hyaloid and retina
defined as
• focal if </= 1500 microns and
• broad if >1500 microns
17. CLASSIFICATION SCHEME OF VITREOMACULAR TRACTION AND
MACULAR HOLES(BASED ON OCT FINDINGS)
• Full-thickness macular hole (FTMH): Full-thickness defect from the internal limiting membrane
to the retinal pigment epithelium.
• Described 3 factors:
• Size -- horizontal diameter at narrowest point:
• small (≤ 250 μm),
• medium (250-400 μm),
• large (> 400 μm); 2)
• Cause -- primary or secondary;
• Presence or absence of VMT
19. HISTORY
• AGE: More >60yrs
• SEX; > females than males
• Onset and Duration of symptoms
20. HISTORY CONTD
• Blurred and distorted vision.
• Straight lines may look wavy or bowed
• Trouble reading small print or driving
• The appearance of a dark spot across the middle of the field of
view
• A decrease in the ability to see fine details when a person is
looking directly at an object
• A break/discontinuity or decrease in calibre at the centre of a
thin object
21. HISTORY CONTD
• Myopia
• Trauma
• Previous eye surgeries
• Ocular inflammation e.g Chronic posterior uveitis
• Hypertension and other cardiovascular diseases
• Previous Hysterectomy
• Treatment sofar
22. PHYSICAL EXAMINATION: VISUAL ACUITY
• Visual acuity: varies according to the size,
location, and the stage of the macular hole.
• Patients with small, eccentric holes may retain
excellent visual acuity in the range of 20/25 to
20/40
• Less than full thickness can have very good
visual acuity in the range of 20/30 to 20/50
• Well developed or full thickness, the usual range
of visual acuity is from 20/80 to 20/400
• STAGE 1:Visual acuity usually
better than 20/50
• STAGE 2: Visual acuity is in the
20/50 - 20/80 range
• STAGE 3: Mean visual acuity :
20/200
23. PHYSICAL EXAMINATION
• VITAL SIGNS
• LID
• ANTERIOR SEGMENT
• VITREOUS
• FUNDUS…….direct and indirect ophthalmoscope
• GRADING OF MACULAR HOLE
24. EXAMINATION: DIRECT OPHTHALMOSCOPY
• A full-thickness macular hole is
characterized by a well-defined round or
oval lesion in the macula with yellow-
white deposits at the base (Yellow dots
probably represent lipofuscin-laden
macrophages or nodular proliferations of
the underlying pigment epithelium with
associated eosinophilic material)
25. EXAMINATION: BIOMICROSCOPIC (SLIT LAMP)
• A round excavation with well-defined
borders interrupting the beam of the slit
lamp
• An overlying semitranslucent tissue,
representing the pseudo-operculum, may
be seen suspended over the hole.
• Surrounding cuff of subretinal fluid
26. MICROPERIMETRY
• Can be done by using Goldmann
III stimuli (10 cd/m2) randomly
presented for a duration of 200
milliseconds on a
1.27 cd/m2 background.
• Central 10° from fixation
accessed.
27. AMSLER GRID TEST
• Not specific for macular hole
• Small central scotomas caused by full-
thickness macular holes
• Difficult to plot because of the poor
fixation in the affected eye
• Bowing of the lines and micropsia could be
seen due to the surrounding area of retinal
edema and intraretinal cysts
28. WATZKE-ALLEN TEST
• Performed at the slit lamp
• Using a macular lens over the eye
• Place a narrow vertical slit beam through the
fovea
• Positive test is elicited when patient detect a
break in the bar of light that is perceived
• Narrowing or distortion of the bar of light is
not diagnostic of full-thickness macular holes
and should be interpreted with caution
29. LASER AIMING BEAM TEST
• Performed at the slit lamp
• Using a macular lens over the eye
• A small 50-µm spot size laser aiming beam is placed within the macular
lesion.
• A positive test is obtained when the patient fails to detect the aiming beam
when it is placed within the lesion but is able to detect it once it is placed
onto normal retina.
30. INVESTIGATIONS-LABORATORY/BODY IMAGING
• No laboratory tests are indicated for diagnosis but may indicated for
uptimization of patient and ensuring general well being
• FBC
• FBS
• E/U/CR
• ABDOMINAL SCAN
• ECG/ECHOCARDIGRAPHY
31. INVESTIGATIONS: FLUORESCEIN ANGIOGRAPHY
• Hyperfluorescence pattern consistent with a
transmission defect due to loss of xanthophyll at base
of the Macular hole.
• A granular hyperfluorescent window associated with
the overlying pigment layer changes
• No leakage or accumulation of dye is observed as
opposed to other lesions
• Study not usually necessary for diagnosis or
management
32. INVESTIGATION: OPTICAL COHERENCE
TOMOGRAPHY(OCT)
• High-resolution OCT image can allow
evaluation of the macula in cross-section
and three-dimensionally.
• Gold standard in the diagnosis and
treatment
• Helpful in detecting subtle macular holes
as well as staging obvious ones
33. B-SCAN ULTRASONOGRAPHY
• Helpful in elucidating the
relationship of the macula to the
vitreous
• May be helpful in staging the
disease
34. MULTIFOCAL ELECTRORETINOGRAPHY
• Multifocal electroretinography is a noninvasive method that objectively
measures visual function by selecting multiple retinal locations around
macular area to provide a topographic map of electrophysiological activity
in the central retina
• mfERG responses show lower amplitudes in the fovea in macular hole
• N1 is generated by photoreceptors in the outer retinal layer and P1 is
generated by Müller and bipolar cells
• Shows loss of retinal function corresponding to the macular hole
35. FUNDUS AUTOFLORESCENCE IN MACULAR HOLE
• There is a strong subfoveal
autofluorescence signal in full-
thickness macular holes
• Punctate autofluorescence for
stage 1
38. FOLLOW UP FOR SPONTANEOUS CLOSURE
• STAGE 0 AND STAGE 1
• Assymptomatic
• No Vitreomacular traction
39. CHEMICAL VITRECTOMY
• Intravitreal ocriplasmin 0.125mg in 0.1ml is used and approved in 2012 by US FDA
• Ocriplasmin is a 27 kilodalton serine protease that demonstrated activity against
fibronectin and laminin and essentially performs pharmacolytic vitreolysis
• Separates the hyaloid from the underlying retina
• MIVI-TRUST clinical trials was a double-blind study, 652 eyes with vitreomacular
adhesion were evaluated this at day 28 post injection, eyes receiving ocriplasmin
exhibited greater release of the vitreoretinal attachment in 26.5% vs. 10.1% p < 0.001
while closure of macular hole (40.6% vs. 10.6%, p < 0.001) in ocriplasmin vs control
respectively .58.3% closure rate for holes of less than 250 µm diameter
40. CHEMICAL VITRECTOMY CONTINUED
• A 2018 study suggests slightly higher closure rates for full-thickness
macular hole following ocriplasmin use.
• 6 patients with vitreomacular traction and a full-thickness macular hole
• By 24 weeks’ of follow-up, four of the six full-thickness macular holes had
closed
• Ocriplasmin has the potential to cause retinal toxicity from its use.
41. SURGICAL TREATMENT-HISTORICAL EVOLUTION
• Once full thicknessmacular holehas developed, the potential for spontaneous resolution
is low.
• Treatment for stage 2 or higher
• In 1982, Gonvers and Machemer were the first to recommend vitrectomy, intravitreal
gas, and prone positioning for retinal detachments secondary to macular holes.
• Kelly and Wendel reported that vision might be stabilized or even improved if it were
possible to surgically relieve tangential traction on the macula, reduce the cystic
changes, and reattach the cuff of detached retina surrounding the macular hole.
42. SURGICAL TREATMENT-HISTORICAL EVOLUTION
CONTD
• In 1991, Kelly and Wendel demonstrated that vitrectomy, removal of cortical
vitreous and epiretinal membranes, and strict face-down gas tamponade could
successfully treat full-thickness macular holes.
• Results of their initial report were a 58% anatomic success rate and visual
improvement of 2 or more lines in 42% of eyes.
• A succeeding report showed a 73% anatomic success rate and 55% of patients
improving 2 or more lines of visual acuity.
• Present anatomic success rates range from 82-100% depending on the series.
43. SURGICAL TREATMENT: VITRECTOMY
• Standard 3-port (light source, vitreous
cutter, irrigation/drainage) pars plana
vitrectomy preferably smaller gauge
vitrectomy systems (ie, 27 gauge, 25
gauge, 23 gauge)…transconjunctival
vitrectomy systems
• The anterior and middle vitreous is
removed
44. SURGICAL TREATMENT: REMOVAL OF
PERIMACULAR TRACTION(INDUCTION OF PVD)
• Removal of the perimacular traction.
• The traction exerted by the posterior hyaloid on the
macula should be relieved by either removing just the
perimacular vitreous or combining it with the induction
of a complete posterior vitreous detachment.
• Use of a soft-tipped silicon cannula or the vitrectomy
cutter with the cutter disengaged
• A "fish-strike sign" or bending of the silicon cannula
shows posterior hyaloid has been engaged
• Released from the underlying retina and removed with
the vitrectomy cutter.
45. SURGICAL TREATMENT: REMOVAL OF INTERNAL
LIMITING MEMBRANE (ILM)
• Removal is also associated with a reduced risk of subsequent reopening
of the macular hole
• ILM peeling can be accomplished via a "rhexis“ using very fine forceps
to peel the ILM from the underlying retina
• Use of vital dyes such as indocyanine green, trypan blue, brilliant blue
G (TissueBlue) to stain the ILM makes it easier to visualize the ILM.
• Triamcinolone acetonide can be used to assist with visualization of the
ILM for peeling.
• Inverted” ILM flap” was first described in 2010 and beneficial for
large macular holes and macular holes in patients with high
myopia ( have a low rate of closure with standard ILM peeling
techniques).
46. SURGICAL TREATMENT: REMOVAL OF INTERNAL
LIMITING MEMBRANE (ILM) CONTD
• The Manchester Large Macular Hole Study showed that the standard ILM peeling was
very effective for macular holes up to 650 microns.
• The closure rate of 90% for holes smaller than 650 microns
• 76% closure rate for holes larger than 650 microns.
• Rizzo et al demonstrated a significant difference in hole closure rates for patients with
axial eye lengths of more than 26mm (39% with ILM peeling vs 88% with ILM flap)
• Rizzo et al also showed that macular holes of more than 400 microns closure rate (79%
with ILM peeling vs 96% with ILM flap).
47. SURGICAL TREATMENT; EPIRETINAL
MEMBRANES REMOVAL
• Epiretinal membranes, if present, also
should be removed. Techniques in
completing this procedure vary from
surgeon to surgeon
• Techniques for this procedure varies
among different surgeons.
48. SURGICAL TREATMENT: AIR-FLUID EXCHANGE
(INTERNAL TAMPONADE)
• Total air-fluid exchange is performed
• Aimed to desiccate the vitreous cavity
• A nonexpansile concentration of a long-acting gas can be used
• Sterile air and varying concentrations of perfluoropropane or sulfur hexafluoride have been used
• Longer period of internal tamponade equated to a higher success rate (duration of the gas
bubble)
• Silicone oil can be used as an internal tamponade for patients with difficulty positioning or
altitude restrictions
49. SURGICAL TREATMENT: AIR-FLUID EXCHANGE
(INTERNAL TAMPONADE)
• Use of silicone oil necessitates a second
subsequent surgery to remove the oil(usually 2-6
months post-op).
• visual results are poorer with silicon oil when
compared to gas tamponade and may be due to
silicone oil toxicity at the level of the
photoreceptors and RPE.
• Rate of single operation macular hole closure
higher in gas tamponade than silicone oil
tamponade
50. SURGICAL TREATMENT: FACE-DOWN
POSITIONING
• Historically, strict face-down
positioning:recommended for patients for up to 4
weeks
• Further study advocated shorter periods of face-
down positioning such as 1 day
• The advent of ILM peeling has encouraged minimal
to no face-down
• Tranos et al showed more rapid progression of
cataract formation with less face-down positioning
• Alberti and Ia Cour compared face-down
positioning with nonsupine positioning and
found equivalent macular hole closure rates
and noninferiority of nonsupine positioning
51. SURGICAL TREATMENT: AUTOLOGOUS
TRANSPLANTATION OF ILM
• Eyes that did not respond to initial surgery with standard ILM
peeling
• Eyes with myopic foveoschisis
• Trauma
• A small piece of the internal limiting membrane was peeled
off to make a free flap
• Then transplanted and placed inside the macular hole under
perfluorocarbon liquids
• Air–fluid exchange was performed and SF6 gas was
injected at a non-expansile concentration.
52. SURGICAL ADJUNCTIVE AGENT-AUTOLOGOUS
SERUM
• An intraoperative adjunctive agent,
• Used to be instilled over the macular hole following an air–fluid exchange to enhance
anatomic success.
• Found to help remove ICG dye used in surgery by significantly shortening the period
of residual retinal ICG staining
• Probably reduce ICG toxicity
• Poor outcome(no difference in anatomic or visual outcome) of treatment on trial
53. COMPLICATIONS
• Retinal detachments: 2-14%(development of iatrogenic retinal breaks
following induction of a posterior vitreous detachment)
• Iatrogenic retinal tears
• Enlargement of the hole
• Macular light toxicity
• Postoperative IOP elevation
• Cataractogenesis.
54. COMPLICATIONS CONTD
• Visual field defects : due to dehydration of the nerve fiber layer.
• Reduced by shorter surgical times
• Lower air flow
• Oblique placement of infusion cannulas caused by beveled incisions of
smaller gauge vitrectomies.
• Failure of hole closure/hole reopening
55. GENERAL CONCERN ON HEALTH AT 65YRS/
OPTIMIZATION
• REFRACTION
• CONCERN FOR COST OF TREATMENT
• COEXISTING CATARACT AT 65YRS OR PSEUDOPHAKIA
• MOBILITY CONCERN
• FREQUENT HOSPITAL VISIT
• FOLLOW UP
56. GENERAL PROGNOSTIC FACTORS FOR
SUCCESSFUL TREATMENT
• Preoperative visual acuity: most important….Better VA correlates with higher rates
of anatomical closure and visual gain.
• Cosure rates higher with shorter duration of symptoms(better visual outcomes).
Hole duration of greater than 9 months(poorer outcome)
• Macular hole size larger than 400 microns(poorer outcome)
• No ILM peeling( poorer outcome)
• Older age of patient(Poorer outcome)
57. CONCLUSION
• Macular hole is one of the retinal problems that causes loss of central
vision
• Early presentation, proper staging and use of appropriate technology and
skills commensurate with the stage of macuar hole will guarantee a better
outcome,
• Counselling of patients that anatomical closure success rate does not
amount to Visual success rate is necessary.
58. REFERENCES
• Kean Theng Oh, Macular Hole Treatment & Management: Medscape.Updated: Jan 02,
2020
• Omesh P. Gupta et’al, Macular Hole. Eyewii:Updatedby Christina Y. Weng, MD, MBA
on August 7, 2021. https://eyewiki.aao.org/Macular_Hole#Figure2
• Macular holes. N Engl J Med. 2012;367(7):606–615.
• Idiopathic Macular Holes, American Academy of ophthalmology: Retna and vitreous,
2016-2017BCSC
• Kanski J. Clinical Ophthalmology: A Systematic Approach. Nineth Ed. Elsevier Health Sciences;
2020.macular hole. p. 592-7.