This document discusses various refractive surgery procedures used to correct refractive errors of the eye, including incisional keratotomy techniques, lamellar procedures, laser ablation procedures, corneal implants, and lens-based procedures. It provides details on common procedures like radial keratotomy, LASIK, PRK, and LASEK. It covers patient evaluation, surgical techniques, potential complications, and advantages of different approaches. Wavefront-guided customized excimer laser surgery is also introduced to correct higher-order aberrations in addition to spherical and cylindrical errors.
Most retinal surgeons are trained to create formal retinal drawings of the fundus.
Retinal drawings are useful to document pathology, although more and more people now prefer fundus photographs.
Can be used for serial follow up of patients to document changes in the pathology.
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.
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.
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.
Binocular single vision refers to simultaneous vision with two eyes that occurs when an individual fixates on an object. There are three grades of binocular vision: simultaneous perception, fusion, and stereopsis. Fusion is the ability to see a composite picture from two similar images, while stereopsis provides the impression of depth by superimposing images from slightly different angles. Tests for binocular vision include those for simultaneous perception, fusion, and stereopsis using instruments like the synaptophore. Binocular vision develops through infancy and childhood as the visual axes become coordinated to direct each fovea at the object of regard.
Gonioscopy refers to techniques for examining the anterior chamber angle of the eye to evaluate and classify normal and abnormal angle structures. It involves using specialized lenses and lights to view the iridocorneal angle. There are two main methods: direct gonioscopy uses large contact lenses requiring saline, while indirect uses smaller lenses with mirrors or prisms that utilize tear film. Gonioscopy is used to diagnose angle-closure glaucoma and other conditions by allowing visualization of the trabecular meshwork, scleral spur, and other angle structures. Indentation gonioscopy, where the lens is pressed against the cornea, can differentiate appositional from synechial angle closure. Proper technique and
This document discusses various refractive surgery procedures used to correct refractive errors of the eye, including incisional keratotomy techniques, lamellar procedures, laser ablation procedures, corneal implants, and lens-based procedures. It provides details on common procedures like radial keratotomy, LASIK, PRK, and LASEK. It covers patient evaluation, surgical techniques, potential complications, and advantages of different approaches. Wavefront-guided customized excimer laser surgery is also introduced to correct higher-order aberrations in addition to spherical and cylindrical errors.
Most retinal surgeons are trained to create formal retinal drawings of the fundus.
Retinal drawings are useful to document pathology, although more and more people now prefer fundus photographs.
Can be used for serial follow up of patients to document changes in the pathology.
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.
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.
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.
Binocular single vision refers to simultaneous vision with two eyes that occurs when an individual fixates on an object. There are three grades of binocular vision: simultaneous perception, fusion, and stereopsis. Fusion is the ability to see a composite picture from two similar images, while stereopsis provides the impression of depth by superimposing images from slightly different angles. Tests for binocular vision include those for simultaneous perception, fusion, and stereopsis using instruments like the synaptophore. Binocular vision develops through infancy and childhood as the visual axes become coordinated to direct each fovea at the object of regard.
Gonioscopy refers to techniques for examining the anterior chamber angle of the eye to evaluate and classify normal and abnormal angle structures. It involves using specialized lenses and lights to view the iridocorneal angle. There are two main methods: direct gonioscopy uses large contact lenses requiring saline, while indirect uses smaller lenses with mirrors or prisms that utilize tear film. Gonioscopy is used to diagnose angle-closure glaucoma and other conditions by allowing visualization of the trabecular meshwork, scleral spur, and other angle structures. Indentation gonioscopy, where the lens is pressed against the cornea, can differentiate appositional from synechial angle closure. Proper technique and
This document discusses target intraocular pressure (IOP) for treating glaucoma. It defines target IOP as the upper limit of IOP that prevents further glaucoma damage. Establishing an individualized target IOP is important to slow retinal ganglion cell loss and glaucoma progression over a patient's lifetime with minimal effects on quality of life. The target IOP should be based on factors like the amount of existing eye damage, maximum past IOP levels, life expectancy, and risk factors. The target is dynamic and must be reevaluated periodically, lowering it if damage progresses or raising it if side effects occur from low IOP. Clinical studies show that greater IOP reductions correlate with less glaucoma progression
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.
Specular microscopy is used to examine the corneal endothelium and analyze pathological changes. There are contact and non-contact types, with contact providing higher resolution but potential discomfort. The procedure involves placing the patient comfortably and using fixation to keep the eye still while obtaining images. Images are then analyzed to study normal endothelium morphology, diagnose corneal endothelial diseases, and monitor conditions like aging, diabetes, surgery, trauma, and compare surgical techniques. Specular microscopy can detect disorders like Fuchs' endothelial dystrophy and help with decisions like eye banking and surgery.
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.
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.
This document summarizes neurotrophic keratitis, a degenerative disease of the cornea characterized by impaired healing due to loss of corneal sensation. It discusses the causes including infections, medications, trauma and systemic diseases. Three stages of the condition are described from early punctate keratitis and epithelial defects to stromal ulceration and potential perforation. The role of sensory innervation in maintaining the corneal epithelium is explained through animal studies. Diagnosis involves rose Bengal staining and fluorescein evaluation, while treatment aims to promote re-epithelialization in early stages to prevent progression to stromal melting and perforation.
This document discusses the evaluation of the nasolacrimal system. It covers the history and anatomy of the system, classification of epiphora, diagnostic tests used to evaluate the system including anatomical tests like syringing and probing, functional tests like dye disappearance tests, and secretory tests like Schirmer's test. The document also discusses differentiating anatomical obstruction from functional/physiological causes of excessive tearing and localization of blockages in the system.
Optical coherence tomography in glaucoma - Dr Shylesh DabkeShylesh Dabke
This document discusses optical coherence tomography (OCT) in evaluating glaucoma. It begins by outlining the importance of early glaucoma detection to prevent vision loss. OCT is described as the most appropriate technology for detecting glaucoma as it can assess retinal nerve fiber layer (RNFL) thickness before visual field or optic disc changes occur. RNFL thinning is an early sign of glaucoma. The document then provides details on OCT technology and analysis of RNFL thickness, optic nerve head, and macula to diagnose and monitor glaucoma. RNFL analysis, especially of the inferior quadrant, is highlighted as the most useful OCT assessment for detecting early glaucoma.
The optic nerve receives its blood supply from multiple sources along its path from the eye to the brain. In the eye, it is supplied by retinal arterioles and occasionally the ciliary artery. In the prelaminar region, it receives blood from ciliary region vessels and peripapillary choroidal or short posterior ciliary vessels. Deeper regions receive supply from ciliary and retinal circulations, including recurrent pial vessels and branches of the central artery of the retina. In the orbit, it has periaxial vessels from the ophthalmic artery and axial vessels from the central retinal artery. Within the cranium, it is supplied by the pial plexus fed by branches from the ophthalmic artery.
This document discusses intravitreal injections for drug delivery to the posterior segment of the eye. It begins by explaining the challenges of drug delivery due to the blood-ocular barrier and how sustained release systems and nano-particles were developed. It then provides details on the procedure of intravitreal injection, including indications, agents used, aseptic technique, complications, and anti-VEGF agents like bevacizumab, ranibizumab, pegaptanib, and aflibercept.
This document provides information on anterior ischemic optic neuropathy (AION), which is the most common cause of acute optic neuropathy in older age groups. It can be divided into two types: arteritic AION, which is due to giant cell arteritis; and non-arteritic AION, which makes up most cases. Both types present with sudden painless vision loss and optic disc swelling. Arteritic AION carries a worse prognosis and requires high-dose steroid treatment to prevent loss of vision in the fellow eye. Non-arteritic AION has a variable course but generally a poor rate of recovery without any proven effective treatments.
Interpretation of visual fields with special reference to octopusHaitham Al Mahrouqi
The document provides an overview of visual field interpretation using the Octopus perimeter. It discusses what a visual field is, why they are important, and types of perimetry including static and kinetic. It describes advantages of different test strategies like TOP and SITA fast that can reduce test time. Key aspects of the Octopus 7-in-1 printout are outlined including demographic data, reliability indices, threshold values compared to norms, and mean deviation and pattern deviation plots.
This document discusses the use of bandage contact lenses after refractive surgery procedures like LASIK and PRK. It describes how bandage contact lenses can help reduce pain, promote healing of the epithelium, and prevent complications like striae or epithelial in-growth after surgery. Different types of bandage contact lens materials are reviewed, including hydrogels, silicone hydrogels, collagen shields, and scleral lenses. Factors like oxygen transmissibility, diameter, and disposable versus reusable lenses are discussed when selecting a bandage contact lens. Potential complications are also mentioned.
- Squint, or strabismus, is a misalignment of the visual axes that leads to loss of binocular single vision. It can be caused by issues in the orbit, eye muscles, motor nerves, or brainstem.
- Strabismus is classified as apparent, latent, or manifest. Manifest strabismus is further divided into concomitant, where the deviation is the same in all gazes, and incomitant, where the deviation varies with gaze.
- Evaluation of strabismus involves assessing history, visual acuity, refractive error, eye alignment tests, and binocular vision. Accurately measuring any refractive errors and prescribing corrections as needed is important for diagnosis and treatment of
This document discusses glaucoma and how it is characterized by progressive optic neuropathy and loss of retinal ganglion cells, resulting in visual field loss. It can now be detected earlier through evaluation of optic nerve head changes and retinal nerve fiber layer defects, before visual field loss occurs. Specific morphological changes are seen in the optic nerve head in glaucoma, including loss of neuroretinal rim tissue, notching of the rim, hemorrhages across the rim, cupping of the disc, and defects in the retinal nerve fiber layer. Features like cup-to-disc ratio, location of blood vessels, and peripapillary changes can provide clues to detecting glaucomatous damage.
LIMBUS… • The limbus forms the border between the transparent cornea and opaque sclera, contains the pathways of aqueous humour outflow, and is the site of surgical incisions for cataract and glaucoma
2. Anatomical Limbus: Circumcorneal transitional zone of the conjunctivocorneal & corneoscleral junction Conjunctivo-corneal junction: • Bulbar conjunctiva is firmly adherent to underlying structures • Substantia propria of the conjunctiva stops here but its epithelium continues with that of the cornea. Sclero-corneal junction: • Transparent corneal lamellae become continuous • With the oblique, circular and opaque fibres of sclera
3. CONTINUE…. • In the area near limbus, the conjunctiva, tenon’s capsule & the episcleral tissue are fused into a dense tissue which is strongly adherent to corneo scleral junction.It is preferred site for obtaining a firm hold of the eyeball during ocular surgery. • The limbus is a common site for the occurrence of corneal epithelial neoplasm. • The Limbus contains radially oriented fibrovascular ridge known as the palisades of Vogt that may harbour a stem cell population. The palisades of Vogt are more common in the superior and inferior quadrants around the eye
This document provides a history of the development of the ophthalmoscope and techniques for indirect ophthalmoscopy. It discusses key developments such as Mery making the first ophthalmoscopic observations in 1704, Cumming and Brucke explaining the principles in 1846, and Helmholtz describing the basic principles in 1852. Later sections cover the design of monocular and binocular indirect ophthalmoscopes, use of scleral depressors, techniques for peripheral examination, and diagnostic uses of indentation. The document presents information on indirect ophthalmoscopy in a detailed but structured manner.
This document discusses choroidal coloboma, beginning with definitions and epidemiology. It describes the embryonic development of the eye and how failure of fusion of the embryonic fissure can result in coloboma. Types of coloboma are classified based on location and presence of other anomalies. Complications like retinal detachment are discussed. Management of cataracts and other ocular issues in the context of coloboma are covered. The prognosis depends on factors like presence of microphthalmos, corneal diameter, and type and timing of surgery.
This document provides an overview of approaches to orbital surgery. It discusses the different surgical spaces in the orbit and various instrumentation used. It describes techniques for superior, inferior, medial, lateral, and transcranial approaches. Key steps are outlined for each approach. The document also discusses orbital decompression procedure and postoperative care. Potential complications of orbital surgery are noted. References for further reading are provided.
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 discusses corneal ulcers, including their definition, causes, microbiology, pathogenesis, stages, grading, symptoms, clinical examination, investigations, treatment, and complications. Key points include:
- Corneal ulcers are tissue excavations associated with epithelial defects, edema, infiltration and necrosis. They are usually caused by injury or foreign materials that allow microbial infection.
- Common microbes include bacteria (e.g. streptococcus, pseudomonas), fungi (e.g. candida, fusarium), protozoa (e.g. acanthamoeba), and viruses (e.g. herpes).
- Treatment involves local and systemic antibiotics, antifungals, or antiv
This document discusses target intraocular pressure (IOP) for treating glaucoma. It defines target IOP as the upper limit of IOP that prevents further glaucoma damage. Establishing an individualized target IOP is important to slow retinal ganglion cell loss and glaucoma progression over a patient's lifetime with minimal effects on quality of life. The target IOP should be based on factors like the amount of existing eye damage, maximum past IOP levels, life expectancy, and risk factors. The target is dynamic and must be reevaluated periodically, lowering it if damage progresses or raising it if side effects occur from low IOP. Clinical studies show that greater IOP reductions correlate with less glaucoma progression
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.
Specular microscopy is used to examine the corneal endothelium and analyze pathological changes. There are contact and non-contact types, with contact providing higher resolution but potential discomfort. The procedure involves placing the patient comfortably and using fixation to keep the eye still while obtaining images. Images are then analyzed to study normal endothelium morphology, diagnose corneal endothelial diseases, and monitor conditions like aging, diabetes, surgery, trauma, and compare surgical techniques. Specular microscopy can detect disorders like Fuchs' endothelial dystrophy and help with decisions like eye banking and surgery.
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.
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.
This document summarizes neurotrophic keratitis, a degenerative disease of the cornea characterized by impaired healing due to loss of corneal sensation. It discusses the causes including infections, medications, trauma and systemic diseases. Three stages of the condition are described from early punctate keratitis and epithelial defects to stromal ulceration and potential perforation. The role of sensory innervation in maintaining the corneal epithelium is explained through animal studies. Diagnosis involves rose Bengal staining and fluorescein evaluation, while treatment aims to promote re-epithelialization in early stages to prevent progression to stromal melting and perforation.
This document discusses the evaluation of the nasolacrimal system. It covers the history and anatomy of the system, classification of epiphora, diagnostic tests used to evaluate the system including anatomical tests like syringing and probing, functional tests like dye disappearance tests, and secretory tests like Schirmer's test. The document also discusses differentiating anatomical obstruction from functional/physiological causes of excessive tearing and localization of blockages in the system.
Optical coherence tomography in glaucoma - Dr Shylesh DabkeShylesh Dabke
This document discusses optical coherence tomography (OCT) in evaluating glaucoma. It begins by outlining the importance of early glaucoma detection to prevent vision loss. OCT is described as the most appropriate technology for detecting glaucoma as it can assess retinal nerve fiber layer (RNFL) thickness before visual field or optic disc changes occur. RNFL thinning is an early sign of glaucoma. The document then provides details on OCT technology and analysis of RNFL thickness, optic nerve head, and macula to diagnose and monitor glaucoma. RNFL analysis, especially of the inferior quadrant, is highlighted as the most useful OCT assessment for detecting early glaucoma.
The optic nerve receives its blood supply from multiple sources along its path from the eye to the brain. In the eye, it is supplied by retinal arterioles and occasionally the ciliary artery. In the prelaminar region, it receives blood from ciliary region vessels and peripapillary choroidal or short posterior ciliary vessels. Deeper regions receive supply from ciliary and retinal circulations, including recurrent pial vessels and branches of the central artery of the retina. In the orbit, it has periaxial vessels from the ophthalmic artery and axial vessels from the central retinal artery. Within the cranium, it is supplied by the pial plexus fed by branches from the ophthalmic artery.
This document discusses intravitreal injections for drug delivery to the posterior segment of the eye. It begins by explaining the challenges of drug delivery due to the blood-ocular barrier and how sustained release systems and nano-particles were developed. It then provides details on the procedure of intravitreal injection, including indications, agents used, aseptic technique, complications, and anti-VEGF agents like bevacizumab, ranibizumab, pegaptanib, and aflibercept.
This document provides information on anterior ischemic optic neuropathy (AION), which is the most common cause of acute optic neuropathy in older age groups. It can be divided into two types: arteritic AION, which is due to giant cell arteritis; and non-arteritic AION, which makes up most cases. Both types present with sudden painless vision loss and optic disc swelling. Arteritic AION carries a worse prognosis and requires high-dose steroid treatment to prevent loss of vision in the fellow eye. Non-arteritic AION has a variable course but generally a poor rate of recovery without any proven effective treatments.
Interpretation of visual fields with special reference to octopusHaitham Al Mahrouqi
The document provides an overview of visual field interpretation using the Octopus perimeter. It discusses what a visual field is, why they are important, and types of perimetry including static and kinetic. It describes advantages of different test strategies like TOP and SITA fast that can reduce test time. Key aspects of the Octopus 7-in-1 printout are outlined including demographic data, reliability indices, threshold values compared to norms, and mean deviation and pattern deviation plots.
This document discusses the use of bandage contact lenses after refractive surgery procedures like LASIK and PRK. It describes how bandage contact lenses can help reduce pain, promote healing of the epithelium, and prevent complications like striae or epithelial in-growth after surgery. Different types of bandage contact lens materials are reviewed, including hydrogels, silicone hydrogels, collagen shields, and scleral lenses. Factors like oxygen transmissibility, diameter, and disposable versus reusable lenses are discussed when selecting a bandage contact lens. Potential complications are also mentioned.
- Squint, or strabismus, is a misalignment of the visual axes that leads to loss of binocular single vision. It can be caused by issues in the orbit, eye muscles, motor nerves, or brainstem.
- Strabismus is classified as apparent, latent, or manifest. Manifest strabismus is further divided into concomitant, where the deviation is the same in all gazes, and incomitant, where the deviation varies with gaze.
- Evaluation of strabismus involves assessing history, visual acuity, refractive error, eye alignment tests, and binocular vision. Accurately measuring any refractive errors and prescribing corrections as needed is important for diagnosis and treatment of
This document discusses glaucoma and how it is characterized by progressive optic neuropathy and loss of retinal ganglion cells, resulting in visual field loss. It can now be detected earlier through evaluation of optic nerve head changes and retinal nerve fiber layer defects, before visual field loss occurs. Specific morphological changes are seen in the optic nerve head in glaucoma, including loss of neuroretinal rim tissue, notching of the rim, hemorrhages across the rim, cupping of the disc, and defects in the retinal nerve fiber layer. Features like cup-to-disc ratio, location of blood vessels, and peripapillary changes can provide clues to detecting glaucomatous damage.
LIMBUS… • The limbus forms the border between the transparent cornea and opaque sclera, contains the pathways of aqueous humour outflow, and is the site of surgical incisions for cataract and glaucoma
2. Anatomical Limbus: Circumcorneal transitional zone of the conjunctivocorneal & corneoscleral junction Conjunctivo-corneal junction: • Bulbar conjunctiva is firmly adherent to underlying structures • Substantia propria of the conjunctiva stops here but its epithelium continues with that of the cornea. Sclero-corneal junction: • Transparent corneal lamellae become continuous • With the oblique, circular and opaque fibres of sclera
3. CONTINUE…. • In the area near limbus, the conjunctiva, tenon’s capsule & the episcleral tissue are fused into a dense tissue which is strongly adherent to corneo scleral junction.It is preferred site for obtaining a firm hold of the eyeball during ocular surgery. • The limbus is a common site for the occurrence of corneal epithelial neoplasm. • The Limbus contains radially oriented fibrovascular ridge known as the palisades of Vogt that may harbour a stem cell population. The palisades of Vogt are more common in the superior and inferior quadrants around the eye
This document provides a history of the development of the ophthalmoscope and techniques for indirect ophthalmoscopy. It discusses key developments such as Mery making the first ophthalmoscopic observations in 1704, Cumming and Brucke explaining the principles in 1846, and Helmholtz describing the basic principles in 1852. Later sections cover the design of monocular and binocular indirect ophthalmoscopes, use of scleral depressors, techniques for peripheral examination, and diagnostic uses of indentation. The document presents information on indirect ophthalmoscopy in a detailed but structured manner.
This document discusses choroidal coloboma, beginning with definitions and epidemiology. It describes the embryonic development of the eye and how failure of fusion of the embryonic fissure can result in coloboma. Types of coloboma are classified based on location and presence of other anomalies. Complications like retinal detachment are discussed. Management of cataracts and other ocular issues in the context of coloboma are covered. The prognosis depends on factors like presence of microphthalmos, corneal diameter, and type and timing of surgery.
This document provides an overview of approaches to orbital surgery. It discusses the different surgical spaces in the orbit and various instrumentation used. It describes techniques for superior, inferior, medial, lateral, and transcranial approaches. Key steps are outlined for each approach. The document also discusses orbital decompression procedure and postoperative care. Potential complications of orbital surgery are noted. References for further reading are provided.
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 discusses corneal ulcers, including their definition, causes, microbiology, pathogenesis, stages, grading, symptoms, clinical examination, investigations, treatment, and complications. Key points include:
- Corneal ulcers are tissue excavations associated with epithelial defects, edema, infiltration and necrosis. They are usually caused by injury or foreign materials that allow microbial infection.
- Common microbes include bacteria (e.g. streptococcus, pseudomonas), fungi (e.g. candida, fusarium), protozoa (e.g. acanthamoeba), and viruses (e.g. herpes).
- Treatment involves local and systemic antibiotics, antifungals, or antiv
Fungal keratitis is a serious ocular infection that can lead to blindness. It is most common in tropical climates and developing nations. Common causative organisms include Aspergillus, Fusarium, and Candida. Risk factors include ocular trauma, contact lens use, and pre-existing ocular surface disease. Symptoms are mild but signs include dry-looking ulcers with feathery margins. Diagnosis involves KOH microscopy and culture of corneal scrapings. Treatment requires prolonged topical antifungals like natamycin or voriconazole alongside debridement. Surgery may be needed for severe or non-resolving cases to prevent blindness.
Bacterial and fungal corneal ulcers are common causes of blindness that result from loss of corneal epithelium and inflammation due to invading microorganisms. The lecture covered the classification, causative organisms, clinical presentation, diagnostic evaluation, medical and surgical management, as well as complications of corneal ulcers. Timely treatment with topical antibiotics for bacteria or antifungals for fungi can resolve the infection and prevent vision loss.
Lecture on Uveitis For 4th Year MBBS Undergraduate Students By Prof. Dr. Huss...DrHussainAhmadKhaqan
This document provides information about uveitis, including:
- Uveitis represents inflammation within the eye that can involve the uveal tract, retina, vitreous, optic nerve, cornea, and sclera.
- Uveitis is classified anatomically based on the primary site of inflammation - anterior, intermediate, posterior or panuveitis. It is also classified clinically based on infectious vs non-infectious causes.
- Anterior uveitis is inflammation in the anterior chamber and causes pain, redness, photophobia, tearing and decreased vision. Workup and treatment depends on identified cause but may include topical steroids, cycloplegics, and systemic immunos
This document discusses fungal keratitis, including its pathogenesis, classification, predisposing factors, clinical features, investigations, treatment, and recent advances. Some key points:
- Fungal keratitis is a major cause of corneal blindness in tropical areas and has a worse prognosis than bacterial keratitis due to delayed diagnosis and lack of effective antifungal agents.
- It is commonly caused by trauma with plant materials and can lead to corneal perforation. Classification includes yeasts like Candida and filamentous fungi.
- Clinical features include pain, discharge, ulcers with feathery edges, and satellite lesions. Diagnosis involves staining, cultures, and PCR of corneal scrapes.
- Treatment
Trachoma is a chronic eye disease caused by Chlamydia trachomatis infection. It is a major cause of preventable blindness worldwide. The infection is transmitted through contact with infected eye or nasal secretions or flies. Recurrent infections during childhood can lead to scarring of the conjunctiva and inwards turning of the eyelashes (trichiasis) in adulthood, causing corneal opacification and blindness. The WHO-led SAFE strategy (surgery, antibiotics, facial cleanliness, and environmental improvement) aims to eliminate trachoma as a public health problem by 2020.
Drug delivery to the posterior segment of the eye for pharmacologic therapyMeenank Bheeshva
This document summarizes various methods for drug delivery to the posterior segment of the eye. It discusses challenges with topical, systemic, and intravitreal delivery and explores sustained release options including implants, microparticles, nanoparticles, and liposomes. Biodegradable implants made of polymers like PLGA are presented as a way to provide controlled drug release over weeks or months while avoiding complications of non-biodegradable implants. Encapsulating drugs in microspheres, nanospheres, or liposomes can also provide sustained release when injected intravitreally.
Dr. Tushar Kumar discusses the profiling, examination, diagnostic testing, and management of various types of corneal ulcers. Key points include:
1. A thorough history and physical exam is important to categorize ulcers as infectious, non-infectious, and determine etiology. Signs and symptoms provide clues to common infectious causes.
2. Examination includes visual acuity, slit lamp evaluation of the eyelids, conjunctiva, cornea and anterior chamber. Features of the ulcer like size, depth and borders are noted.
3. Diagnostic testing depends on severity and response to initial treatment, and may include cultures, smears, biopsy or imaging to identify organism or guide management
Fungal corneal ulcers are common, caused mainly by Aspergillus in India. Risk factors include ocular trauma, contact lens use, pre-existing eye conditions, and systemic immunosuppression. Diagnosis involves corneal scrapings, cultures, and stains showing fungal hyphae or spores. Treatment consists of topical natamycin or amphotericin B, sometimes with adjunctive debridement, intracameral/intracorneal injections, or therapeutic keratoplasty for severe cases. Systemic antifungals may also be used for extensive infections.
fungal / mycotic corneal ulcer power point presentation for O.A 2nd year stud...Vinitkumar MJ
Belong suborder Acanthopodina and the genus Acanthamoeba
• Family of free-living cyst-forming protozoans that are ubiquitous in air, soil, dust and water.
• 11 species of which A. Castellanii and A. polyphaga are the most common in keratitis
• Life cycle consist of motile trophozoite and cyst dormant stage
This document summarizes various fungal eye diseases including blepharitis, keratitis, panophthalmitis, endophthalmitis, and orbital disease. It describes the most common fungal causes such as Fusarium, Candida, Aspergillus, and Mucor. Symptoms and signs vary depending on location and type of fungus. Management involves identifying the causative fungus through cultures or biopsies and using antifungal medications topically or systemically in combination with procedures like debridement, vitrectomy, or surgery as needed. Visual outcomes depend on factors like type of fungus, location, and how quickly treatment is initiated.
This document discusses endophthalmitis, including its definition, classification, etiology, clinical presentation, diagnosis, and treatment approaches. It classifies endophthalmitis as infective or non-infective, exogenous or endogenous, and describes the most common causative agents. It provides details on clinical evaluation, diagnostic testing, medical and surgical management strategies, and prevention. It also summarizes key findings from the Endophthalmitis Vitrectomy Study regarding the role of vitrectomy and intravenous antibiotics in post-operative endophthalmitis.
1. Endophthalmitis is an intraocular inflammation that predominantly affects the inner spaces of the eye.
2. It can be classified as infectious (exogenous or endogenous) or non-infectious. The most common type is exogenous endophthalmitis, which accounts for over 85% of cases.
3. Treatment depends on the type and severity of endophthalmitis. For acute postoperative endophthalmitis with vision of light perception or worse, immediate pars plana vitrectomy and intravitreal antibiotics is recommended. For vision of hand motions or better, a tap and inject of intravitreal antibiotics is recommended initially.
This document provides information on diagnosing and treating various types of infective keratitis. It begins by emphasizing the importance of systematically describing any corneal lesion and differentiating infectious keratitis based on history and examination. The main types of infective keratitis discussed are bacterial, viral, fungal, amoebic, and non-infectious keratitis. For each type, the document describes distinguishing examination findings, investigations, and treatment approaches. It provides details on herpes simplex virus keratitis, including its various clinical manifestations and recommendations for long-term antiviral prophylaxis. The document also compares treatment for bacterial versus fungal versus amoebic keratitis. Throughout, it emphasizes the significance of early diagnosis
This document defines and classifies conjunctivitis, discussing its various causes including viral, bacterial, allergic, and other non-infectious origins. It describes the signs and symptoms, treatment, and when referral is necessary for different types of conjunctivitis such as viral, bacterial, hyperacute, chronic, and allergic conjunctivitis. It also briefly discusses other eye lesions including keratitis, uveitis, episcleritis, scleritis, hordeolum, chalazion, and pterygium.
Early complications of intraocular lens (IOL) surgery include corneal edema, wound leak, shallow anterior chamber, hyphaema, retained lens matter, and uveitis. Late complications include posterior capsular opacification, cystoid macular edema, endophthalmitis, and retinal detachment. Post-operative endophthalmitis is a vision-threatening complication that is treated with topical, systemic, and intravitreal antibiotics along with steroids. Posterior capsular opacification occurs in 10-50% of cases due to proliferation of lens epithelial cells.
1. Vitrectomy is an important treatment for endophthalmitis as it removes infected vitreous material to reduce the bacterial load and toxins in the eye.
2. The Endophthalmitis Vitrectomy Study showed that for acute post-operative endophthalmitis presenting with light perception vision or worse, immediate vitrectomy provided significant benefits over antibiotics alone. For better vision, vitreous tap with intravitreal antibiotics was equally effective.
3. Traumatic and chronic endophthalmitis often require vitrectomy due to severity of infection and inflammation, and difficulty sterilizing the vitreous cavity with antibiotics alone. Vitrectomy allows removal of infected material
This document provides an overview of infectious keratitis. Keratitis is an infection of the cornea that is usually caused by contact lens use or trauma. Bacterial keratitis is the most common type and can progress rapidly, threatening vision. Diagnosis involves fluorescein staining and corneal scrapings for analysis. Treatment involves topical antibiotics like fluoroquinolones every hour along with cycloplegics for pain. Other types include fungal, viral like herpes simplex, and rare parasitic infections like acanthamoeba. Early diagnosis and aggressive treatment are important to prevent vision loss and perforation of the cornea.
1. The document discusses the anatomy, physiology, and pharmacology of the autonomic nervous system as it relates to pupil function and abnormalities.
2. Key topics covered include the causes, features, and approaches to evaluating anisocoria, Horner's syndrome, Adie's tonic pupil, and other pupil abnormalities.
3. Tests involving pharmacological agents are described that can help localize lesions in various parts of the autonomic nervous system pathways controlling the pupil.
Ocular motility disorders: the Approach
Supra- vs infra- nuclear disorders and its related basic science
Other: synkinesis/aberrant regeneration, nystagmus
This document summarizes ocular motility and eye movements. It discusses the anatomy and physiology of the supranuclear and infranuclear control of eye movements, including the cranial nerves, brainstem structures, and eye muscle actions involved in different types of eye movements like saccades, smooth pursuit, vestibulo-ocular reflex, and vergence. It also outlines various eye movement systems and laws of ocular motility.
Classification Staging Grading in OphthalmologyMeng Hsien Yong
This document discusses various classification and staging systems used in ophthalmology. It covers classifications for corneal and external eye diseases, glaucoma, uveitis, vitreo-retinal diseases, and others. For each condition, it provides details on the classifications used to describe risk factors, pathogenesis, clinical features, severity, investigations, and management approaches. The classifications discussed include international standardized systems as well as other commonly used staging methods.
Vascular events in the eye can be ischemic or hemorrhagic in nature and can occur suddenly or gradually. Ischemic events include central retinal artery occlusion, branch retinal artery occlusion, central retinal vein occlusion, and anterior ischemic optic neuropathy. Hemorrhagic events include subconjunctival, vitreous, retinal, subretinal, and retroorbital hemorrhages. Risk factors include atherosclerosis, hypercoagulability, inflammation, vasculitis, and underlying medical conditions. Presenting symptoms often involve changes in vision. Management depends on the specific condition and may involve observation, medical therapy, laser treatment, or surgery.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
8. CU: Specific Signs
Ring Infiltrate
• Pseudomonas
• Herpes
• Fungal
• Acanthamoeba
Wessely ring
pseudomonas
HSV/HZV
Intact EpiT
• LHDN
Evidence of healing
• symptoms
(pain/discharge/VA)
• infiltrate (density)
• corneal edema
• AC cell/hypopyon
• Ocular surface/tear
9.
10. Rx- Principles
• Control infection (sterilization phase)
• Corneal scraping/stain/C&S +- PCR
• Antimicrobial (topical +- systemic)
• Sterilization phase (48-72H) VS healing phase
• Control inflammation (healing phase)
• steroid
• Promote re epithelialization (healing phase)
• Doxycycline, Vit A, topical AT/NAC/terramycin
• Symptoms relief
• Cycloplegic/pain killer
• Common pitfall
• delay in Dx, inappropriate sample collection, inadequate therapy, drug
toxicity, and delayed follow- up
11. Corneal Scraping- Details
• before AB/12H stop AB
• Perservative free LA/b4 fluorescein
• No 15 blade/25G needle/Kimura spatula
• Edge (area of uninvolved to involved)
• Avoid thin area
• Gram stain/KOH/C&S (blood/chocolate/Mc
Conkey/Sabouraud)
• Extra:
– conj swab
– epithelium for virology C&S/PCR
– non nutrient agar with E.Coli for Acanthamoeba (CL case), transport
with page’s saline
– Propionibacterium need 2wk C&S
– confocal microscope for hyphae/acanthamoeba cyst
– AC tap
– corneal biopsy (2-3mm trephine/base & edge) for HPE & C&S
– Giemsa stain instant result and equal sensitivity for fungal (vs Gram)
12.
13. Antimicrobial
• Bacteria
– Dual: ceftazidime 5%/cefuroxime 5% + gentamicin 0.9% or quinolone
– Mono: quinolone
• 2nd gen (cipro-/o-floxacin): less spectrum
• 3rd/4th gen (levo/ganti/moxi-floxacin): less pseudomonas activity
• Fungal (3/12 Rx/NO steroid! +- epiT debridement))
– Dual: amphotericin B 0.15-0.5% + fluconazole 0.2% or oral 200mg BD
– Mono: natamycin 5% (>filamentous/fusarium), voriconazole 1% (both)
• Viral (+- prophylaxis)
– aciclovir occ, oral 400mg 5x (HSV) or 800mg 5x (HZV), or famcidar
– need epiT debridement (penetration)
• Acathamoeba (1-2H x 2wk taper QID x 6/12 Rx)
– Biguanide (for cyst/trophozoite)- PHMB or chlorhexidine 0.02%
– Diamidine- Propamidine/Brolene 0.1% or hexamidine
– need epithelial debridement (remove nidus + penetration)
– CXL (riboflavin x 30min UV)
14. Acanthamoeba
• First-line therapy is biguanides, chlorhexidine gluconate 0.02% to 0.2%,
or polyhexamethylene biguanide (PHMB) 0.02% to 0.06%, with
monotherapy a consideration for early cases. Δ
• For chronic or later stages, dual therapy with propamidine isetionate
0.1% (Brolene, Sanofi-Aventis), or oral or topical voriconazole 1% may be
needed to reduce resistance to therapy. Δ
• Dosing is hourly for a continuous 48 hours, followed by hourly while
awake for the next 72 hours, then q2h to q3h for 3 to 4 weeks. Dosing for
the oral anti-fungal agent is 200 mg twice a day. Response to therapy may
not be apparent for up to 2 weeks.
• For refractory cases lasting 3 to 4 months, miltefosine (Impavido,
Profounda, Inc.) is an FDA-approved oral medication for Acanthamoeba
keratitis dosed at 50 mg t.i.d. and continued until resolution of the
keratitis.
• Early amoebic keratitis is mainly intraepithelial, and debridement
reduces the microbial burden while facilitating antibiotic penetration
15.
16. ACSIKS 2018
• 6626 eyes (>male in general + w trauma, >female w CL)
• Bacterial38% vs fungal 33% vs viral 13%
• Major risk (trauma 35% > CL 11% > prior ocular surgery
7% > ocular surface dz 4%))
• Fusarium 18% > Pseudomonas aeruginosa 11% >
Aspergillus flavus 8% > Strep pneumoniae 6%
• Cornea transplantation 46% failed
• Moderate visual impairment (<20/60) 54%
• ACSIKS Clinical Protocol
• ACSIKS Microbiological Protocol
• Study did not standardize the treatment
17. Mycotic Ulcer Treatment Trial (MUTT)
There are two MUTT:-
MUTT I (2013): for filamentous fungal ulcer especially Fusarium species,
topical natamycin 5% was associated with significantly better outcomes
compared to topical voriconazole 1%.
MUTT II (2016): for filamentous fungal ulcer that being treated with topical
natamycin 5% and topical voriconazole 1%, the addition of oral voriconazole
does not appear to be beneficial.
smear-positive ulcers presenting in eyes that have vision between 20/40 and
20/400, topical natamycin 5% (Natacyn, Alcon) was found effective. For more
severe mycotic ulcers presenting with 20/400 visual acuity or worse, the
management of topical natamycin 5% (Natacyn, Alcon) was combined with
voriconazole 1%.
18.
19. Antibiotic Precipitates
• Ciprofloxacin @pH of 4.5
• Moxifloxacin @pH of 6.8
• Normal ocular surface pH @7.5, but can
increase during infection.
• As the pH rises, antibiotics can become less
soluble and precipitate onto the cornea
• Moxifloxacin is more soluble than
ciprofloxacin at tear-film pH and is thus less
likely to form corneal precipitates.
20.
21. Antifungal
• topical natamycin 5% is limited by its poor penetration into the
corneal stroma
• Topical amphotericin B 0.3% to 0.5% is an alternative, but its use
requires access to a compounding pharmacy and is limited by
toxicity.
• Voriconazole, a newer-generation triazole, has gained popularity
in the treatment of fungal keratitis because of its excellent ocular
penetration
• intracameral injection of amphotericin with or without hypopyon
drainage
• intrastromal injection of voriconazole
• at this time, topical natamycin remains the most evidence-based
treatment for filamentous fungal keratitis, and adjuvant oral
voriconazole should be considered if the organism is Fusarium
22.
23.
24.
25. Intrastromal Injection
• Peribulbar, sterile/OT/microscope
• Needle bevel down, inserted obliquely from the
uninvolved clear area to just reach the abscess at
mid-stromal level
• Inject till amount of hydration of the cornea is
used as a guide to assess the area covered, then
plunger is withdrawn slightly to ensure
discontinuation of the capillary column and thus
prevent back-leakage
• At least 2 (2-5) deposit surrounding the lesion
(circumferential/barricade)
26. CU: Supportive Rx
Doxycycline/tetracycline
• Antibiotic: esp for
blephalitis/meibomianitis (lid flora)
• Collagenease (matirx
metalloproteinase) inhibitor →
reduce breakdown/melting of
corneal tissue
• Altering meibomian gland function
to lower free fatty acid production
• Systemic Ab (Cipro 750mg BD): if
+endopth, limbal involved,
impending perforation
• Vit C: corneal thin/melt
Steroid
• controversial/SCUT showed no
difference
• never used alone/b4 antimicrobial +
low dose if ED + monitor melt
• Pros: reduce inflam/scar, for ED
• Cons: promote ifx, reduce collagen
synthesis
Admission: severe ifx, non-compliance
Tectonic graft: perforation/failed glue,
at least 2d intensive Rx
Therapeutic graft: non response,
large, infiltrate near limbus esp fungal,
melting
27. Corneal matrix metalloproteinases (MMPs)
• MMPs are a family of Zn2+-dependent enzymes responsible for
degradation of the components of the extracellular matrix
(including proteoglycans and various types of collagens) during
normal development as well as in disease processes.
• only MMP-2 proenzyme has been found in the normal healthy
cornea.
• However, after corneal injury, additional MMPs (including MMP-
1, MMP-3, and MMP-9) are synthesized.
• The proteinase inhibitors of the cornea play a key role in corneal
protection by restricting damage during corneal inflammation,
ulceration, and wound healing.
• Many of these inhibitors are synthesized by resident cells of the
cornea; some are derived from tears, aqueous humor, and limbal
blood vessels.
28. Steroid for infectious keratitis
• benefit of limiting corneal melt and
neovascularization versus the risk of potentiating
the infection and further complications from
delayed epithelial healing
• clinically significant benefit in visual outcomes
using steroids when: 1) used early, 2 to 3 days,
after antibiotic pretreatment; 2) severe ulcers
presented with acuity of counting fingers
regardless of depth of involvement or thinning;
and 3) there were invasive rather than cytotoxic
strains of P. aeruginosa. Δ Δ
29. Keratitis: Key studies & result
• Steroids for Corneal Ulcers Trial found that although steroids provided
no significant improvement overall, they did seem beneficial for ulcers
that were central, deep or large, non-Nocardia, or classically invasive
Pseudomonas aeruginosa; for patients with low baseline vision; and when
started early after the initiation of antibiotics.
• Mycotic Ulcer Treatment Trial (MUTT) I showed a benefit of topical
natamycin over topical voriconazole for fungal ulcers, particularly among
those caused by Fusarium.
• MUTT II showed that oral voriconazole did not improve outcomes
overall, although there may have been some effect among Fusarium
ulcers. Given an increase in nonserious adverse events, the authors
concluded that they could not recommend oral voriconazole.
• The Herpetic Eye Disease Study (HEDS) I showed a significant benefit of
topical corticosteroids and oral acyclovir for stromal keratitis.
• HEDS II showed that oral acyclovir decreased the recurrence of any
type of herpes simplex virus keratitis by approximately half
• New: ZEDS
30. SCUT
• 500 pt/multicenter-region
• topical prednisolone sodium phosphate
1.0% or topical placebo starting after a 48-
hour course of topical moxifloxacin 0.5%
• culture-positive bacterial ulcers
• overall data showing no difference in
outcomes such as 3-month visual acuity, 3-
month scar size, or rate of perforation
31. SCUT
• subgroup analyses suggested that corticosteroids are beneficial in certain
subgroups. Patients with low vision (counting fingers or worse) at baseline had 1.7
lines better vision at 3 months in the corticosteroid group compared with the
placebo group (P ¼ 0.03). Central ulcers, covering the central 4-mm pupil, that
were treated with corticosteroids also had better 3-month best spectacle-
corrected visual acuity (BSCVA) compared with placebo (w2 lines better; P ¼ 0.02).
Likewise, patients with deep ulcers at baseline fared better with topical steroids
(1.5 lines better; P ¼ 0.07). Timing of steroid administration also proved to be a
significant factor, with patients randomized to corticosteroids after only 2 to 3
days of antibiotics having better BSCVA at 3 months than those randomized to
placebo (w 1 line better BSCVA; P ¼ 0.01).
• Nocardia ulcers randomized to corticosteroids had 0.40 mm larger infiltrate or
scar size at 3 months compared with placebo (P ¼ 0.03), although this did not
result in worse 3-month BSCVA (P ¼ 0.21) (Fig 2).63 This trend continued at 12
months, with nonNocardia ulcers faring better with corticosteroids (1 line
improvement of BSCVA; P ¼ 0.02) and Nocardia ulcers faring worse (average scar
size increased by 0.47 mm; P ¼ 0.02; no difference in BSCVA).64 Overall,
Pseudomonas aeruginosa ulcers did not benefit from the addition of
corticosteroids; however, the classically invasive subtype of P. aeruginosa
demonstrated 2.5 lines of visual acuity improvement at 3-month BSCVA when
randomized to steroids versus placebo
43. Question of Corneal Transplant
Short notes
1) Indications of corneal grafting
2) Storage of donor tissue
3) Prognostic factors of PK
4) Post-operative complications of PK
5) Graft Rejection VS failure
6) Paediatric corneal transplant
7) Lamellar keratoplasty
8) Keratoprothesis
Long Question
1) Donor selection
2) Causes of graft failure , clinical feature, Mx & immunological basis of
transplant rejection?
3) Indication of grafting and prognostic factor
44. Storage of Corneal Graft
1. Short term (days)
• Moist chamber (humidity 100%/4°C/for 48H)
• McCarey-Kaufman medium (standard tissue culture medium-
TC199/D5%/Ab/4°C/for 2–4D)
2. Intermediate term (weeks)
• Dexsol/Optisol GS/Ksol/Procell
– standard tissue culture medium- TC 199
– chondroitin sulphate 2.5%
– HCO3 buffer/amino acid/Vit C & B12/D1%/gentamicin
– 4°C/for 2 weeks
• Organ culture (low rejection but high infection rate/37°C/for 4 weeks)
– >complex >cost >opaque cornea on op, but can keep longer)
3. Long term (months)
• Cryopreservation (liquid nitrogen/-196°C/for 1 year/expensive and unpredictable
results; usually not suitable for optical grafts)
45. Keratoplasty: Prognostic Factors
The big 4
• Ocular inflammation
• Glaucoma
• Corneal vascularization
• Ocular surface abnormalities (lid/tear/neurotrophic)
Others
• Underlying eye disease
– (Brightbill’s classification I → V, KC/CD > FED/PBK > keratitis >
glaucoma/paeds cases > SJS/OCP/chemical/burn)
• AC problem (PAS/rubeosis/cataract)
• Post segment (retinal/CMO/Optic atrophy)
• Visual potential (amblyopia)
Management
• Preop assessment (Visual potential, IOP/AC cell/dry eye/blepharitis)
• Preop topical antibiotics / steroids / cyclosporin A if necessary
47. Donor graft assessment
Systemic diseases
• extreme age: < 2yo ( difficult to handle/to small/friable/steep K 50D), >
65 years
• death to preservation time <12-18H
• Death/CNS dz from unknown cause
• Infections (rubella, rabies, hepatitis, AIDS, syphilis,
encephalitis/septicemia/IE)
• Malignancies (leukemias, lymphomas, disseminated cancer)
• severe hemodilution: Affects accuracy of serological testing
Ocular factors
• +- Intraocular surgery
• glaucoma/uveitis/tumors
• low endothelial cell count <2K
• +- prev refractive surgery
48. • Lions Eye Donation Service,
• Melbourne, Australia. The standards and guidelines of the
• Eye Bank Association of Australia and New Zealand[2] and
• the Therapeutic Goods Administration of Australia[3,4] were
• employed and followed. Donor history was obtained from
• hospital medical records and from medical records of the
• donor family physician. Further history was obtained from
• a knowledgeable historian during a donor risk assessment
• interview, which included explicit questions regarding
• previous ocular surgery, pathology, refractive procedures,
• or therapies. All corneoscleral discs underwent routine
• screening, which included in situ penlight examination, slit
• lamp biomicroscopy examination of the excised corneoscleral
• disc, specular microscopy of the endothelium, placement into
• organ culture preservation media with repeat microbiological
• testing, and light microscopy examination at the end of the
• storage period. Reported demographic and clinical data were
• taken from clinic and eye bank medical records.
49. • may not be able to detect pathologies such
• corneal scars or previous corneal laser
refractive surgery scars.
• previous laser-assisted in situ
keratomileusis (LASIK) surgery
• o incorporate AS-OCT imaging of donor
corneal tissue into
• routine eye bank screening procedures
50. PK- Procedure
• Recipient size: 7.5-8.0mm
• If more +reject/PAS/glaucoma, if less high astig
• Donor size: 0.25-0.5mm larger
• >watertight/AC depth/flattening (less astig), <PAS/glaucoma/wound gap
• Prepare cornea surface
• mark center +- radial keratotomy marker (suture placement)
• Flieringa scleral fixation ring with silk 7/0 (esp pseudo/aphakia/post tppv/low sclera rigidity)
• Prepare AC
• paracentesis and fill AC with OVD
• Donor button
• cut from endothelial side using a trephine (hand-held, gravity, vacuum-driven- Barron).
• Host button
• trephine (Katena/blade) stopped at the DM/first release of aqueous slower decompression
with the blade or corneal scissors.
• Suture
• cardinal sutures: use 4 to 8 10–0 nylon
• Complete suturing: interrupted sutures (often 16 in total) or a continuous running suture
• Key: 90% depth, watertight with mild eversion, buried
• Adjust suture tension to minimize astigmatism (handheld karatometer)
• Refill AC with BSS/sunconj dexa&genta/pad with occ maxitrol/+-BCL
• Post op: topical steroid/Ab/mydriatic, +- systemic steroid/aciclovir (HSV)/diamox (avoid
topical antiglaucoma
• TCA & cornea topo/ref STO PK 12mth (adjust continuous suture aft 1/12), DALK
6/12, stat if loose
51. PK + cataract extraction
• better intraoperative visibility
• prompt visual rehabilitation
• avoids later cataract extraction and graft endothelial loss.
• inability to accurately estimate IOL power (unpredictable postoperative
keratometry and suture-induced astigmatism)
• Cataract extraction- open-sky when view is poor
• Closed-chamber phaco followed by a penetrating keratoplasty (if good
view):
– decrease open sky time
– allow a rhexis and in-the-bag IOL placement.
– Phaco incisions should be scleral or limbal and short
• For active corneal ulcers, if performing a therapeutic keratoplasty, the
crystalline lens should be retained as a barrier to pathogen entry into the
posterior segment
52. EK- DSEK/DSAEK/DMEK
• 3-6mm limbal/scleral incision (varies)
• DM stripping: descemetorrhexis (reverse Sinski hook) + air in AC/vision blue
(increase contrast)/OVD/BSS irrigation
• Graft insert: glide/Busin/push-through (centration/gentle)
• Adhesion: air bubble full x 10min
– +- venting incision, peripheral bed scrapping, roller sweeping
– Optional PI (inferior)
• Post op: gutt steroid/AB/position IOP/air/graft check
• Cx intraop: donor/host cornea injury/centration
• Early post op: graft decenter/double AC/detach vs pupillary block
• Late post op: epiT ingrowth, interface problem, Ref change, cataract, graft
failure/rejection, endoC loss 50% in 5yr
• Air bubble pupillary block- prevention:
– Dilate pupil
– Lying position
– Inf PI
• DMEK- better VA outcome/less rejection, more difficult
• New theories: endoT migration, endoT transplant (DMET)
53. • pre-Descemet’s EK (PDEK), utilising three techniques that
I have described to increase success and repeatability –
endoilluminator-assisted PDEK, air pump-assisted PDEK and
host Descemetic scaffolding.
• remove a non-cataractous crystalline lens too as the risk
of cataract developing secondary to air tamponade,
prolonged steroid usage, inflammation, natural ageing etc.
is high and can result in the need for surgery, which can in
turn cause loss of precious graft endothelial cells
• air pump-assisted PDEK technique allows synechiolysis
under air tamponade and prevents bleeding from the iris,
hyphema and a fibrinous atmosphere. It helps achieve
effective intraoperative graft attachment
54. • DSAEKStd- 150um
• thin- 135um
• ultrathin- 100um
• nanothin-50um
• DMEK- 25um
• PDEK-35um
• thinner faster visual rehab/recovery, less
rejection
• thinner more challenging in handling, >detach
esp in higher risk (ACIOL, aphakia, post PPV)
55. DALK
• Ant lamellar down to DM
• IndiC: stromal dz w normal endoT
– Esp corneal ectasia, stromal scar, corneal ulcer/impending perforation
– Less rejection/astig, stronger wound, non penetrating, less donor criteria
– +interface opacity
• Partial corneal trephine till target level, depth around 90%
– Trephine complete turn 250um, quarter 62.5um
• Melles with manual lamellar dissection
– Stepwise: remove 70% ant lamellar with crescent blade/Devers dissector
– Paracentesis and separate stroma-DM: w Healon or cyclodialysis spatula
– Remove/resect with curved corneal scissor
• Big bubble Anwar technique (pneumodissection)
– 27/30G needle or Fogla dissector w 25G cannula
• +- air bubble in AC- to confirm DM detachement
• Oversize graft 0.25mm only
• Convert to PK if DM rupture
• Early STO 4-6mth
• Dia-DALK techniques
56. DMEK/DSO
● relatively small area of abnormal Descemet membrane
and endothelium
● (descemetorhexis) resulted in mitosis of normal
endothelial cells from the periphery, leading to
● resolution of the edema and improvement in vision. In
the future, more traditional keratoplasty
● may be replaced with descemetorhexis combined with
topical and/or intracameral Rho kinase
● (ROCK) inhibitor to stimulate endothelial proliferation.
Another future treatment may be
● injection of the patient’s own cultured endothelial cells.
57. Post PK- Cx
• Intraop
– Trephine/handling of host/donor related
– Open sky related/intraocular content injury
• Post op (TRO ifx/inflam-rejection/failure without rejection)
– Primary/early failure <72H>
• Cornea graft (PED >2wk/leak/rupture/ifx/endoph)
• Suture (loose/tight/ifx/jetting)
• AS (flat/glaucoma/uveitis)
• Fixed dilated pupil @ Urrets-Zavalia)
– Secondary/late failure
• Graft rejection (>2wk)
– causes: HLA/ABO (collaborative corneal transplant study- >ABO), sensitization of
recipient by donor cell (afferent arm), immune reaction/rejection (efferent arm)
– SSx: circumcorneal injection, epiT (line/elevation/Krachmer), stroma (haze), endoT
(KPs/Khodadoust line), uveitis
– Mx: early aggressive topical/systemic steroid
• Suture (astig/break), wound (epiT ingrowth/membrane),
glaucoma/uveitis/CMO/recur dz
58.
59. Post op steroid
• PK: Topical prednisolone acetate 1% or dexamethasone
sodium phosphate 0.1% every 2, 3, or 4 h initially is then
slowly reduced over a period of 6–12 months but
maintained once daily indefinitely
• Immediate postoperative subconjunctival injections of
methylprednisolone acetate 40 mg/mL or dexamethasone
disodium phosphate 0.1%
• if the eye is not phakic or experiencing steroid-
responsive glaucoma, once-daily steroid drops should be
continued indefinitely after DSAEK
• DMEK weak topical steroid once daily indefinitely,
especially in pseudophakic and controlled patients with IOP
• maintain DALK patients on topical corticosteroids at least
once daily for the first 12 postoperative months.
60. Corneal Graft Rejection RX
• Systemic:
– Oral Pred 1mg/kg (max 80mg) 1-2wk then taper
• Paeds:
– IVMP 500mg-1g, 1-3days
• Paeds: IVMP 10-30mg/kg/day x 3-5d (max 250mg tds or 10mg/kg tds)
– CSA
• Local:
– Subconjunctival: betamethasone 2-3mg , dexamethasone
phosphate 2-4mg, 0.5-1.0ml
– Topical (a must): maxidex/pred forte as frequent as hourly &
RTC/maxitrol ointment ON taper slow
• Need >4wk for Rx response/considered failed
• Others:
– collagen shield soaked in corticosteroids
61. • topical prednisolone acetate 1% every hour
and systemic oral prednisone 1 mg/kg usually
tapered over 6–8 weeks
• subconjunctival betamethasone 2 mg
injection and dexamethasone 0.1% drops in
the affected eye every hour for 24 h.
• subconjunctival injection of triamcinolone
acetonide 20 mg, in combination with the
topical application of prednisolone acetate
1%,
62. Post PK high astig- Mx
• Usually -4 to -5
• Suture removal-glasses-CL
• Relaxing incision/compression suture/coupling
• IOL exchange/piggyback/toric IOL
• PRK/LASIK
– At least 1yr post PK, 4/12 post all STO, if continuous
suture adjust aft 1/12
• Maloney intraoperative keratometer
• postoperative suture adjustment: selective
suture removal or suture replacement
63. Keratoprosthesis
• =artificial corneal implant
• IndiC:
– Unsuitable for keratoplasty
– Severe LSCD (SJS/chemical)
– Multiple failed PK/AMT/LSC Tx
– BL poor vision (normal ON/retina Fx)
• Types:
– OOKP- osteo-odonto-Kpro (tooth root/alveolar bone + center
optical cylinder, 2 stages 2-4mth apart)
– Boston Kpro (aphakic or pseudophakic)
– LVP KPro
• Pre op assessment
• Cx:
– Corneal/Kpro- retroprothesis membrane, cylinder tilt/extrusion
– Others: glaucoma (difficult monitor), RD, endoph
64. Temporary KPro TKP
• Landers 3rd-gen wide-field TKP-
– PMMA
– 1mm cylinder protruding to the anterior chamber (diameters: 6.2/7.2/8.2
mm). New trunkless fix size up to 8.5mm corneal opening.
– mushroom-shape corneal surface: diameter 15.5mm
– 6 suture holes in the periphery- sutured to the limbus using Vicryl 6.0 or 8.0
• Corneal trephine size: 0.2mm less than TKP
• If combine PKP: donor corneal 0.25-0.5mm oversized
• Others: endoscopy-assisted PPV, open sky PPV, stage surg (PK then
PPV)
65. Bowman Layer Transplantation
• Indications: keratoconus, postrefractive scarring/persistent
subepithelial haze, Salzmann nodular degeneration
– reestablish the physiologic barrier between the epithelium and anterior
stroma
• Preparation: manual stripping and femtosecond laser ablation
– Manual: epithelium debrided trypan blue dripped cornea lightly
scored just inside limbus 360 w 30-gauge needle nontoothed forceps to
grasp BL cut edge & peel from stroma roll thinner (11mm) w shaggy
stromal remnants
– Femtosecond: thicker (37mm) but displayed smooth-cut posterior surfaces
• Transplantation: inlay or onlay (sutureless)
– Inlay: mid stromal pocket (manual/femtosecond), insert via glide
– Onlay: epi debridement, BL on top with AMT/BCL
66.
67.
68. Number @ Corneal Transplant
• Graft survival rate: 95% at 5yr (low risk case)
• Graft failure rate: 35% at 3yr (high risk case)
• Mean keratoplasty to rejection time: 19.8 ±
20.4 mth (majority within 1 ½ year)
• Rejection to failure rate: 50%
• Rejection site: endoT 50%/mixed 40%/epiT
2%/subepiT 1%
• EndoT cell loss post op: 60% at 3yr
69. Corneal Immuno-privilege
• 6 points
• 3 absent/low (afferent blockage)
– No vessels
– No lymphatic system
– Low expression of MHC Ag
• 3 present/high (efferent blockage)
– ACAID/immune-tolerance
– FAS-ligand/TNF/CRP (T cells apoptosis)
– Immunomodulator e.g. TGF-B, a-MSH (inhibit T
cells/complement)
70. Combine or stage surgery
• anterior chamber depth
• corneal surface keratometer
• type of lens implant to use
• desired refractive outcome
71. • DMEK in pediatric patients, however, may
be more challenging attributable to difficulty
stripping the host endothelium, more
aggressive intraocular inflammation (including
a predisposition to generate fibrin) and
challenges with postoperative compliance
72. GDD in corneal transplant
• Cornea Glaucoma Implant Study Group
demonstrated that in patients requiring a
corneal transplant and a glaucoma tube
shunt, the incidence of graft failure and
immunologic rejection was decreased with
pars plana insertion of the tube
73. Corneal Transplant Registry
• European Cornea and Cell Transplantation
Registry (ECCTR)
• information on the recipient, donor and eye
bank processing
• transplant procedure and two year follow-up
including graft survival and failure
• patient-reported outcome measures (PROMs)
• addition of a limbal stem cell transplant
component to the registry
75. Keratoconus
• Def: progressive/triad:-
– Central/paracentral stromal thinning + Apical protrusion +
Irregular astigmatism
• Aetio (6C):
– Primary: idiopathic/AD w FHx (10%)
– Secondary (ocular): VKC/eye rubbing/CL/aniridia/blue
sclera/Leber/RP/floppy eyelid
– Secondary (systemic): Ehlers Danlos/Marfan/OI/Down
– Aggravated by refractive surgery
• Class:
– Mild/mod/severe: K 48-54 OR forme fruste/early/late OR
Amsler Krumeich stage I-IV
• Histology:
– epiT scar/iron, fragmentation of Bowman’s, thin stroma, DM
fold/break (only in hydrops)
76. Key Questions
• KC vs other ectatic diseases
• KC all about
• Corneal topography VS tomography
• Staging & Progression
• Management
77. Global Consensus on Keratoconus
and Ectatic Diseases 2015
• Currently, there is no consistent or clear
definition of ectasia progression
• Currently there is no clinically adequate
classification system for keratoconus and that
the historical Amsler–Krumeich classification
fails to address current information and
technological advances
78. Keratoconus- SSx/Ix
• SSX: onset puberty → BL/asym (50% within 16yr)- BOV with
unstable ref +- hydrops attack
– Inspect: Munson
– Torch: Rizzuti for cone (nipple/oval/globus)
– Direct: Oil droplet (Charleaux)
– Retinoscope: scissoring
– Placido disc
– Slit lamp: Vogt striae (vertical/stroma), prominent nerve, Fleischer
ring (iron @basal epiT, in blue)
+ stromal thin/cone protrusion/hydrop (DM rupture)/scar
(epiT/Bowman)
+ evidence of atopic eye dz + syndrome + CL/Rx related problem
– Keratometer/corneal topo: sym bow-tie → irreg astig (inf temporal
steep) + 2eyes mirror image/enantiomorphism
• Rabinovite-McDonell criteria: K >48/astig >1.5D/I-S asym >1.7D/CCT <450um @
thinnest/skewed radial axis >21degree/centra-thinnest cornea difference >20um
– Orbscan/pentacam – post corneal curvature (forme fruste)
• Berlin-ambrosio index
– Pachymeter- in case for CXL (450um)
– Ant seg OCT- scar level in case for PK/DALK
80. Belin ABCD KC Staging
• Ant & Back radius of
curvature (3mm),
• Corneal thickness
(minimal)
• Distance VA
(DCVA)
81. Pentacam for KC
• Topo + Ref + Astig + Km + CCT AK classification
• K Max & ABCD & Thinnest pachy progression
– Ant & Back radius of curvature (3mm), Corneal thickness
(minimal), Distance VA (BCVA)
• Indices colour code, KISA (60-100), IS (1.4-1.9)
• BAD D (enhanced ectasia) screening & colour code
(change/different: ant 5-7 & post 12-16 )
• Covis biomechanical: CBI & TBI
• Asphericity/Q value: normal -0.01 to -0.8
– Q-val <0/-ve/oblate = normal or KC or post hyperop LVC
– Q-val >0/+ve/prolate = post myopic LVC
– Q-val=0/sphere
82. Keratoconus- Mx
• Acute MX + Visual Rehab + Progression prevention
• Hydrops (heal with scar in 6-10wk)
– Hypertonic saline/cycloplegic/BCL +- topical steroid
– Intracameral gas (DM tear)
• Visual rehab (conservative)
– Glasses/CL (soft → rigid/hybrid/piggyback → sclera)
• Visual rehab (surgical)
– DALK/PK (if h/o hydrops)
• Indications: scar/hydrops, intolerance to CL, failed others with poor VA
• Principle: large graft slight eccentric (more than base of cone/Fleischer ring)
– Phakic IOL
– Intrastromal corneal ring segment (laser/manual)- for CL tolerance/VA
– Nodulectomy (central subepithelial scar)
• Progression prevention
– progress fast within 3yr, stable by 35yo (f/up + topo q3m stable 6m)
– Progression= BCVA 1line or astig 0.75D in 18mth, or 12mth astig 1D/sphere -
0.5D/10um loss at thinnest part
– Treat atopic/VKC/avoid rubbing
– CXL (Dresden protocol or Averdo Accelerated CXL)
• Contraindicated in refractive surgery
83. Corneal Hydrops
• Prevalence 3%
• break in the Descemet’s layer aq penetrate stroma bullous
keratopathy
• Resolved spontaneously 2-6 mth
• Rx aims to reduce pain and reduce inflammation to prevent
further complications
• Topical cycloplegic, hypertonic saline and steroid & antibiotic
• intracameral air/gas injection or compression corneal sutures
PK (60% need PK, higher risk of rejection)
• Longer duration > complications (infection, perforation, and
corneal neovascularization)
• +- improvement in UCVA due to drastic corneal flattening
following corneal healing or secondary scarring +- improve contact
lens fitting endpoints and even vision
84. CL for KC
• Mild KC- toric soft CL
• Mod KC- RGB
– Flat with apex contact- swelling/stain/scar risk
– 3-point touch- less apical contact, min peripheral touch
– Customisable e.g. Rose K/K2/K2 XL (for cornea with
graft)
• Combination lenses: piggyback RGB on soft base,
hybrid single piece
• Scleral CL: vault higher, more comfort, need saline to
insert
• Principle: repeat fitting for best fit,
85. CXL (or CCL/C3R)
• Intro: photochemical process for biomechanical stiffening & fibril stabilization
• Indications
– Progressive ectasia e.g keratoconus, PMD (to stabilize/slow progression/ +- reverse/reshape)
– microbial keratitis
– post surgery/LASIK ectasia
• MOA: photosensitizing agent/riboflavin + photochemical induction UVA (365-375um) +
O2 lysyl oxidase enzyme free radical O2 covalent bond/polymerization of
collagen strengthen bond 300%
• Procedure: CXL (Dresden protocol or Avedro Accelerated CXL)
1. CCT check (>400um) + recheck post epiT off + b4 UV/aft 30min riboflavin
2. Topical anest/clean (providone)
3. With or W/out epiT removal- alcohol loosening/crescent or beaver blade (8-9mm zone)
– Epi on: less effective (50%), but X pain X BCL, allow thinner cornea
4. Riboflavin/Vit B2
– Standard: 0.1% (in 20% dextran)- q2min for 30min b4 UVA + during UVA
– Epi-on: TE-CXL solution
– Thin cornea: hypotonic solution, add topical H2O,+- use of well (trephine/LASIK) to maintain hypo solution longer
5. UV-A light 370nm (270nm for keratitis): distance 5.5-6cm (guided by treatment area within
cornea)
6. Irradiance/power 3mW/cm2 (30min, total 5.45 J/cm2)- other option: 9mW (10min)
7. Rinse off with BSS BCL topical antibiotic/steroid
86. CXL
• Post op care:
– BCL for epi defect + topical AB (Cravit/Vigamox TDS/QID)- off aft ED healed
– Topical steroid: either post op or after epi defect healed- QID or lower (taper &
complete 1 mth)
– KIV pain relief (ED): cycloplegic, NSAIDs, pain killer
– Re-start CL after ED healed
– Wait at least 6/12 (up to 5yr) for stabilization for other surgery/CL fitting
• SE/Cx:
– Cytotoxic/keratocyte/limbus/endothelium (esp thin cornea) depopulation
– CXL haze- transient
– ED related Cx/ifx
– Corneal melting/scar
– X for pregnancy (+progression during pregnancy, to do b4 pregnant)
– X for RA/severe stromal scar
- Other (new):
- - CXL-plus: + PRK, + ICRS
- - LASIK-Xtra
- - Topography guided, variable fluence/pattern CXL
- - Maillard reaction in young DM (reducing sugar with natural CXL → no KC progression)
87. • The standard treatment protocol, called the Dresden
protocol[2], was formulated by Wollensak et al. for corneas
with minimal thickness of 400µm, and is as follows:
• Instill topical anesthetic drops in the eye
• Debride the central 7-9mm of corneal epithelium
• Instill 0.1% riboflavin 5-phosphate drops and 20%
dextran solution every 5 minutes for 30 minutes
• Exposure to UVA (370nm, 3mw/cm2) for 30 minutes
while continuing instilling the above drops every 5minutes.
• At the end of the procedure, apply topical antibiotics and
soft BCL with good oxygen permeability.
88. CXL
• epithelial-off standard (SCXL) VS accelerated
corneal collagen cross-linking (ACXL)
–Metanalysis IOVS 2018
–ACXL less decrease in: central corneal thickness
(CCT), and endothelial cell density (ECD),
–ACXL less reduction in: maximum keratometry
(Kmax)
–Same mean keratometry (mean K). VA
89. CXL: Standard Vs Accelerated Protocol
• ultraviolet-A (UVA) protocol of 3 mW/cm2
intensity at 370 nm over an exposure time of 30
minutes (now termed the ‘‘Dresden protocol’’).
• ACXL protocols are carried out in a shorter
period such as 3, 5, or 10 minutes by using 30,
18, or 9 mW/cm2 irradiance, respectively,
• with a cumulative irradiation dose of 5.4 J/cm2
• ACXL- potential advantages of reducing the rate
of complications such as corneal thinning, haze,
infection, and melting. However, it may affect
efficacy
90. Thin cornea for CXL
• Dresden protocol: minimal corneal thickness required is 400
µm.
• Modification: thickness 320-400µm hypo-osmolar riboflavin
solution
– increase in thickness of up to about 25% of the original value
– Effective? Not compromised as the anterior stroma remains the same
while it is the posterior corneal stroma that swells + protect endothelium.
• Modification: higher concentration riboflavin of 0.2%
– increase the UV absorption in the anterior stroma and hence protect the
endothelium
• Modification: dextran-free riboflavin
– allow corneal thickness to increase
• Rescue: BSS saline onto well
91. CXL: Criteria & Progression
• Good candidates: mild to moderate disease
demonstrating Kmax > 47.0, inferior-to-
superior K ratio > 1.5, corneal thickness after
deepithelialization > 400 um, best corrected
visual acuity (BCVA) < 20/20, and evidence of
disease progression.
• Progression: no global consensus
92.
93.
94.
95. Scleral CL
• Boston scleral CL
• Difficult fitting- need expert, expensive
• Ind: advanced KC
97. • Corneal Allogenic Intrastromal Ring Segments
(CAIRS). This utilises thin segments of de-
epithelialised and de-endothelialised donor
corneal stroma that is implanted into mid-
peripheral intra-stromal channels similar to
synthetic intra-stromal corneal ring segments
• flatten and regularise the cornea, centralise the
cone, decrease refractive error and improve
uncorrected and best-corrected visual acuity
while avoiding synthetic-related complications.
98. Keratoglobus
• Intro: Progressive/BL globular thinning/protrusion
(whole cornea)
• PathoP: collagen synthesis defect, non
inflam/hereditary (=KC/PMD)
• Primary (at birth) vs Acquired
– At birth DDX cong glaucoma, megalocornea/high
myope/deep AC/K 50-60D
– +-hydrops/rupture, no K ring/Vogt line
– a/w: Leber, blue sclera, Ehlers Danlos VI
• Rx: avoid trauma (rupture), same as KC
102. PUK
• Peripheral corneal stromal degradation.
• progress both centrally and circumferentially
• unresponsive to topical or conservative local
therapy
• collagenolytic and proteolytic enzymes
released from neutrophils and/or
macrophages
103. PUK- Rx
• liaise with renal physician/ rheumatologist if necessary
• Corticosteroids (pulsed IVMP 6-9 pulses or high- dose oral pred)
(NB >60y: bone density scans; calcium/ vitamin D supplements,
alendronic acid, gastric protection).
• 2nd line: methotrexate, ciclosporin, mycophenolate, azathioprine,
or continuous oral cyclophosphamide.
• Resistant cases = failed on two immunosuppressants, unable to
reduce oral steroid to <10mg daily anti- TNF (adalimumab) or
anti- CD20 (rituximab)
• Topical: lubricant + antibiotic + steroid (caution thinning)
• Systemic: doxycycline, vitamin c
• Surgery: conjunctival recession, AMG, lamellar patch graft
• Other: CL, glue
104. Differences between
peripheral & central cornea
• Anatomic, physiology/immunologic
• proximity and contiguity with the sclera, episclera and conjunctiva
• Vascular: avascular central, peripheral- anterior conjunctival and deep episclera
vessels (0.5 mm into the clear cornea) allow limited diffusion of Ig and
complement components into the cornea
• Lymphatic: subconjunctival lymphatics (afferent arm of immunologic reactions)
• Antibody: [IgA and IgG] peripheral = central cornea, [IgM] > periphery (larger
size restricts diffusion into the centre)
• Langerhans cells, the dendritic antigen presenting cells >periphery
• Mediator/complement/inflame cell: > antigen-antibody complexes, > effective
complement activation, >inflammatory cells/mediator attraction, > release
proteolytic and collagenolytic (destruction)
• Histologically, the peripheral cornea also contains a reservoir of inflammatory
cells including neutrophils, eosinophils, lymphocytes, plasma cells and mast cells .
• Clinical: prone to infections, hypersensitivity disorders, mass lesions and
degenerations may secondarily spread to involve the limbus and peripheral cornea
• more susceptible to alteration in a wide variety of infectious and non-infectious
systemic and local diseases, leading to a clinical entity termed Peripheral
Ulcerative Keratitis (PUK).
105. PUK: Activity vs Resolution
• Active: ED + stromal melting +
conj/sclera/episcleral inflam
• Conj: resolution of inflammation
• Epithelium: Epithelialization of the corneal
• Thickness: residual stable thinning
• Scar: residual stable vascularized scar
106. PUK Vs Mooren
• PUK without systemic association is known
as Mooren's ulcer and contributes to 31.5% of
PUK causes
• Mooren's ulcer occurs in the absence of
scleritis and is a diagnosis of exclusion, with a
distinctive overhanging edge.
• PUK Females are more likely to be affected
generally, although this is reversed for
Mooren ulcers.
108. IC3D 2015 (International
Classification of Corneal
Dystrophies)
- Genetic (chromosomal/gene)
- Clinical (pattern/anatomical layer)
- Pathology (histo/biochem/confocal)
109. Staining- Others
-Macular CD (MPS/GAG):
colloidal blue (+ Alcian blue)
- Iron: Prussian blue
- Myelin: Lusol fast blue
110. FED
• medical management in the form of Rho
kinase inhibitors for endothelial regeneration,
hypertonic saline to deturgesce the cornea
and anti-glaucoma medications to decrease
endothelial stress.
111. ● Endothelial cell counts less than 1000/mm2,
morning increase in corneal thickness, or the
presence of epithelial edema suggests that the
cornea may decompensate following
intraocular surgery
117. Band Keratopathy
• Calcification/Ca plaque@ superficial/Bowman +-subepi/ant stroma @
interpalpebral fissure
• Chronic: mths to years, +- lucent hole (= nerve end)
• Ca & phosphate imbalance +- alkalosis
• Causes
– a/w chornic eye inflam/uveitis/surface dz or systemic high Ca
– Inflam: chronic uveitis (JIA/herpetic/IK/sarcoid)
– Systemic: hyperPTH/high vit D, renal dz/lupus/gout
– Surface: dry eyes, ocular injury (chemical), eye drops
• Others contributing factors
– SO with aphakia
– Intracameral rtPA
– Endothelial compromise
• Ix
– Ca/PO4, uric acid/PTH, RP/urine analysis, uveitis workup
• Management
– EDTA chelation/removal
– Superficial keratectomy: manual/PTK
118. retrocorneal fibrous membrane
(RCFM)
• Infiltration of polymorphonuclear leukocytes in
response to severe corneal injury can induce
endothelial cells to become fibroblastic and to
synthesize a retrocorneal fibrous membrane
(RCFM). RCFM forms between the Descemet
membrane and the corneal endothelium and
causes a significant decrease in visual acuity.
Unlike normal corneal endothelial cells, which
accumulate a limited amount of type I collagen
protein, the fibroblastic cells isolated from the
RCFM predominantly express type I collagen.
119. Medication & cornea
• Drug-Induced Deposition and Pigmentation
–Corneal Epithelial Deposits
–Stromal and Descemet Membrane Pigmentation
–Endothelial Manifestations
• Toxic Keratoconjunctivitis From Medications
125. Descemet’s Detachment
• rhegmatogenous (tear), tractional, bullous and complex
detachments based on pathophysiology, clinical, ASOCT findings
and treatment required.
• Rhegmatogenous: a/w tear, free float undulating membrane,
instrument injury (phaco probe/IOL injector
• Bullous: a/w hydroseparation, intraop fluid wave/well defined
plana or convex detachment, stromal hydration/vision blue/OVD inj
(cannula too posterior)/
• Spontaneously resolve
• Intervention if: visual axis, pain/bullae, non resolve
• Pneumo-descemeto-pexy
• Relaxing descemetomy (keratome, bent 26G needle) + air
bubble/pneunodescemetopexy- more for bullous DD
• Venting incision- more for tear associated
126. AdenoV eye dz
• four distinct syndromes: pharyngoconjunctival fever
(PCF); epidemic keratoconjunctivitis (EKC); acute
nonspecific follicular conjunctivitis (NCF) and chronic
keratoconjunctivitis
• redness and keratitis, up to 20 uniform, subepithelial
corneal infiltrates (the hallmark of EKC) develop on day
11 and are most prevalent during the third and fourth
weeks of infection. Approximately 30 to 50 percent of
patients with EKC will de-velop these infiltrates, which
may contribute to persistent visual loss and light
sensitivity and necessitate long-term steroid therapy
127. • 4 times a day of topical 0.05% CsA
(Restasis®), in addition to the topical
corticosteroids they were using for the first 15
days, and then 2 times a day of topical 0.05%
CsA (Restasis®) after topical corticosteroids
were discontinued.
134. Epithelial In-/Down-growth
• Epithelial migration (fr conj/cornea) to
– intraocular structure/s (after penetrating ocular surgery/trauma)
– or corneal flap/stromal bed (after LASIK)
• Cells fibrosis
– Melting (collagenase release fr necrotic epiT)
– Inflam
– Astig/cover axis
• Probst/Machat EI classifications (>post LASIK)
– 1: 2cells thick/2mm fr flap (thin transparent, well delineated white line edge)
– 2: thicker/>/=2mm (rolled or grey edge)
– 3: >thick/>/=2mm (opaque-white-rolled edge-progress-flap melt)
• Fluorescein staining (epiT fistula)
• Mx (intraocular):
– En bloc excision + full thickness corneo-scleral graft
– Devitalised with cryoT or photocoagulation
– Intracameral 5FU or MMC
• Mx (LASIK flap):
– Grade 1- monitor weekly for 1mth stable vs progression
– Lift & scrape +- ethanol/MMC/PTK with closure /tight suture/glue +- Nd-YAG
135. • Fibrovascular Downgrowth vs. Epithelial Downgrowth
• The term retrocorneal membrane can encompass both epithelial downgrowth and fibrous downgrowth. Both can be a result of trauma or
intraocular surgery; for example, fibrous downgrowth has been reported after cataract surgery[38], rigid Schreck anterior chamber lens
implantation[39], intraocular telescope implantation[40], and traumatic corneoscleral wound dehiscence.[41] Risk factors appear to be similar,
including prolonged inflammation, wound dehiscence, and delayed wound closure. Symptoms in each are nonspecific, and both appear as a
translucent retrocorneal membrane. Complications of fibrous downgrowth are like that of epithelial downgrowth, including glaucoma.[42] However,
there are a few distinctions. The membrane in fibrous downgrowth may be vascular and is predominately fibrous instead of cellular.[19][14] Fibrous
downgrowth is also more common than epithelial downgrowth and tends to progress more slowly. There are few adjunctive tests to confirm the
presence of fibrous downgrowth, although there are reports that immunohistochemical positive staining for α-smooth muscle actin can help sway
the diagnosis towards fibrous downgrowth.[43] However, management mainly appears to be similar between epithelial and fibrous downgrowth
with the use of photocoagulation, surgical excision, and intracameral metabolites. Bevacizumab has been suggested as a unique treatment for
fibrous downgrowth. Mansour reports using combined intracorneal (0.05 mL; 1.25 mg) and subconjunctival (0.1 mL; 2.5 mg) injections of
bevacizumab in a patient to halt vascularization within the fibrous membrane to reduce intraocular bleeding.[14] Intracorneal and subconjunctival
routes of injection were chosen instead of intracameral due to the presence of glaucoma and intravitreal silicone oil.
• Pseudophakic Bullous Keratopathy vs. Epithelial Downgrowth
• Pseudophakic bullous keratopathy (PBK) is the development of irreversible corneal edema after cataract surgery and postoperative
inflammation. This corneal edema occurs due to the loss of corneal endothelium secondary to surgical trauma. PBK can clinically resemble epithelial
downgrowth with a reduction in visual acuity, tearing, and pain. However, signs of PBK include stromal edema and sub-epithelial bullae. Epithelial
downgrowth should be considered in patients undergoing penetrating keratoplasty for presumed diagnoses of PBK, and these may be distinguished
immunohistochemically with the presence of anti-cytokeratin antibodies in epithelial downgrowth.[20]
• Epithelial Downgrowth vs. Secondary Endothelial Proliferation
• Secondary endothelization usually arises from ischemia and can also present after multiple intraocular surgeries. The endothelial cells can
proliferate in the angle and anterior surface of the iris. This can be considered a precursor to rubeosis iridis (neovascularization of the iris), which can
lead to neovascular glaucoma, a form of secondary glaucoma. Clinically, this can appear as neovascularization of the iris. Histologically, this can be
differentiated from epithelial downgrowth by a lack of stratification.[16]
137. Dx
• Clinical: advancing edge, sheet like, scalloped border,
connection to wound
• sometimes appears as a cyst or as cells floating in the
anterior chamber.
• spot of argon laser photocoagulation is applied to
the area overlying the iris. If a membrane is present,
the laser spot will cause the tissue to blanch and
whiten, while laser applied to normal iris will result in a
sharp, darkened burn
• Aqueous aspiration and cytologic examination can
also be performed to assess for the presence of free
epithelial cells.
138.
139. Intrastomal Blue-dye Injection
• Iatrogenic/inadvertent
• Toxic keratopathy w intraop edema, bluish
discolouration
• Resolved by 6wk (start 3/7 and near
resolved fully 2wk)
• DDx: DM detachment (deep stromal
separation) need ASOCT to confirm
• Mx: postpone op in no view + ASOCT + gutt
steroid/Ab
141. AMT
• Intro: single epiT cell layer w BM, from human embryo sac (post
partum/ifx screen)
• Properties:
– Inert/no Ag-rejection/+substrate for cell growth/healing
(laminin/bioactin/GF)
– reduce scar/anti-inflam/anti angiogenesis/anti microbial
• Types: air-dry, glycerol preserved, fresh frozen
• IndiC: ocular (cornea & conj reconstruction), systemic
(wound/burn)
• Preop/postop
• Op: epithelial side up (for cell migration), side down (for anti
inflam), +- multilayer, inlay (cover defect area only, e side up),
overlay (cover large area as patch, e side up or down)
• Cx: disintegrate/necrosis/melt, ifx/contamination
• Limit: need normal stem cell/keratocyte to heal, need resolved
inflam/ifx
• Fresh frozen: price RM 1000+ (incl delivery fr HUSM, store -20,
expired 6/12), 097674039 (HUSM tissue bank)
142. AMT expanded IndiC
• corneal surface reconstruction
– PED
– Shield ulcer VKC
– total limbal stem cell deficiency (+limbal stem cell
transplantation)
• conjunctival substitute
– removal of pterygia, conjunctival lesions and
symblephara.
• substrate for ex vivo cultivation of limbal,
corneal and conjunctival epithelial cells
143. AMT Types
• cryopreserved (Cryo-AM) versus air-dried is
– cryo-AM >substrate for cultivating human limbal
epithelial cells increases release of wound-healing
mediators
• PROKERA®: Corneal Bandage
– PROKERA Slim: thinner ring to contour to the ocular
surface
– PROKERA Clear: retain visual acuity in the affected eye.
– PROKERA Plus: double layer for intense, sustained tissue
coverage
144. Omnigen AMT
• modified human amnion
• gamma-radiated and decellularised with
sodium dodecyl sulfate
• low heat vacuum dried amniotic membrane
without spongy layer
• efficient substates for the ex-vivo expansion
of limbal stem cells, and have certain
advantages but also some limitations such as
limited flexibility and early dissolution
147. EDTA chelation
• Indication: symptomatic band K (vision or chronic surface d/o)
• Procedure:
– LA/topical
– Epithelial debridement: crescent/beaver blade, +- 20% alcohol in
well (40s)
– EDTA 0.5-3%: gutt/soaked in Weck-cel sponge (2-3min)
– Debride
– +-BCL/gutt Ab/steroid
• Other option: +-sup keratectomy +- AMT
• Causes of bank K:
– primary vs secondary (ocular vs systemic)
– esp preservative eyedrops, chronic ifx/inflam/ulcer, chemical, SO,
– CKD/Ca/phosphate level
148. How to order EDTA
(ethylenediaminetetracetic)
• EDTA 3% (in syringe/patient)
• For band keratopathy chelation
• Call pharmacist in charge Mr Ian 1/7 prior &
before 12noon (ext 5860 or 6701)
• Write a manual prescription slip to send
down to ward supply pharmacy (basement)
149. Superficial Keratectomy &
Diamond Burr
• The corneal epithelium around the pterygium remnant was
removed down to Bowman’s layer and residual pterygium tissue
was scraped by a crescent knife. Diamond burr polishing was then
performed to smooth the entire corneal surface. A handheld
battery-driven ophthalmic burr with a 3.3 mm diameter diamond-
dusted sphere was used to polish the corneal surface for
approximately 10–15 seconds. To avoid haze, mitomycin C (0.2
mg/mL) was applied for one minute with a Weck-Cel® sponge
(Beaver-Visitec International, Waltham, MA, USA) and the eye was
thoroughly irrigated with balanced salt solution. A soft bandage
contact lens was placed on the eye at the end of the procedure.
Postoperatively, the patient was instructed to instill a topical
steroid, a topical antibiotic, and artificial tears, each four times
daily, for one month after surgery. The contact lens was removed
five days after the procedure.
150. • multiple, even, circular movements, taking
care not to induce irregular topography by
pushing too hard or tarrying in one region too
long.
158. New in cornea/ant seg
• Corneal tomography
– Pentacam (oculus)
– Orbscan (B&L)
– Sirius (CSO)
– Galilei (Zeimer)
• ICRS
• CAIRS (corneal allogenic
intrastomal RS)
• epiT mapping for KC
– OCT RTvue (Optovue)
– VHF U/S Artemis
(ArcScan)
• Aberration
– higher/lower
–Lenticular/cornea
–Ref surgery WF guided
LASIK, KC/ectasia
• Tear imaging: OCT, fringe
interferometry
• Meibography:
fx/density/anatomy
• Mydriasert (conj insert
for dilatation)
• Intracameral moxifloxacin
0.5mg/0.1ml)
159. Corneal Imaging- New
• Biomechanical properties
• Corneal ectasia
• Scheimpflug
• Ocular response analyser ORA Reichert
• Corvis ST (corneal visualization Scheimpflug tech)
• VHF US Artemis ArcScan
• BAD D value
• Corvis Biomechanical Index (CBI)
• Tomographic Biomechanical Index (TBI)
• Amsler-Krumeich
• CLEK (collaborative Longitudinal Evaluation of keratoconus
• Brillouin microscopy imaging (longitudinal modulus/mechanical compressibility of tissue-
cornea/lens/sclera)
• Pre-Descemet endothelial keratoplasty (PDEK)
• Endoilluminator-assisted, S or F stamp, Moutsouris sign for DMEK
• Dysphotopsia- positive (glare/halo/starbursts) vs negative (dark shadow at periphery)
160. OCT for ant seg/cornea
• N cornea
• Pathological cornea
• Corneal transplant
– level of scar/pathology
– esp lamellar K
• Refractive surgery
• Phakic IOL
• IOL calculation
• Post op DM
detachment
• VS optical system/UBM-
longer time, difficult,
corneal clarity, behind iris
penetration
• Multimodal imaging:
UBM, AS-photo, confocal
microscopy,
topo/tomography
• Intraop OCT
• OCT A
• Ultra-high-resolution
OCT
161. Corneal Imaging- New
• Corneal ectasia: early changes @post cornea & thickness
• BFS/ enhanced
• CTSP
• Deviation of front, back, thickness...5Deviation
• Tomo vs topo of cornea
• Biomechanical profile
• Corvis CBI Pentacam BAD
• Topo -- tomo -- tomo + biomechanic
• Scheimpflug based tomo
• AUC in ophthal study
• Vinciguerra screening report