Glaucoma Lecture 2024 PDF
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2024
Dr Nermeen Zaied, MBCHB, MD
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This document is a presentation on glaucoma, covering various aspects of the disease.
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GLUCOMA DR NERMEEN ZAIED MBCHB , MD 2024 ILOS Define glaucoma and why it is a Leading cause for irreversible blindness. Determine the frequency of glaucoma globally and appreciate the variation in frequency between populat...
GLUCOMA DR NERMEEN ZAIED MBCHB , MD 2024 ILOS Define glaucoma and why it is a Leading cause for irreversible blindness. Determine the frequency of glaucoma globally and appreciate the variation in frequency between populations. List the major risk factors for glaucoma. Explain anatomy and physiology of the anterior chamber Classify of glaucoma Pathogenesis of open angle and closed angle glaucoma Outline the cardinal clinical features List the essential Investigations and management Up date in glaucoma mangment DEFINITION Is a progressive optic neuropathy with characteristic cupping of the optic disc with a corresponding visual field defects that is associated with irreversible visual loss EPIDEMIOLOGY It is the second leading cause of blindness worldwide after cataract It is the first leading cause of irreversible blindness worldwide The global prevalence of glaucoma to be 3.54%, with the highest prevalence in Africa. The number will increase from 64.3 million in 2013 to 111.8 million in 2040, affecting people residing in Asia and Africa -High IOP RISK FACTORS -Age -Gender -Race - Myopia - Family history Hypermetrope -DM Steroid in take ANATOMY OF THE ANTERIOR CHAMBER Aqueous humour : it is a transparent intra-ocular fluid that fills the anterior &post. Function : 1- maintenance of the normal IOP. 2- Nutrition to avascular structure 3- one of the refractive media ( RI = 1.33). PRODUCTION OF AQUEOUS HUMOR Aqueous humor is secreted by the non pigmented epithelium lining the ciliary processes paras plicata Production is influenced by sympathetic nervous system beta-2 receptors and alpha-2 receptors. active secretion 60% of aqueous formation. Passive diffusion 40% of aqueous formation DRAINAGE OF AQUEOUS HUMOR CLASSIFICATION OF GLAUCOMA Primary vs Secondary ( in terms of etiology) Open or closed ( in terms of angle anatomy) Adult, juvenile or infantile ( in terms of onset) CLASSIFICATION OF GLAUCOMA ACCORDING TO ANATOMY PRIMARY OPEN ANGLE GLAUCOMA (POAG) is defined by an open, normal appearing anterior chamber angle and raised intraocular pressure (IOP) There is characteristic cupping of the optic disc with corresponding visual field defects, due to retinal ganglion cell loss GENERAL PATHOLOGY narrowed intertrabecular spaces reduction in trabecular endothelial cells Loss of trabecular endothelial cell phagocytic activity narrowing of collector channels closure of Schlemm’s canal. scleral spur thickening SYMPTOMS The majority are asymptomatic. Typically are only symptomatic in late disease More frequently, patients are usually diagnosed as part of a routine eye test Patient may complain of eye ache ,headache ,delayed dark adaptation time ,frequent changing of reading glasses DIAGNOSIS Increase in Intraocular pressure Open- normal appearing anterior chamber angle Characteristics signs of optic disc damage Visual function loss on perimetry IOP MEASUREMENT EXAMINATION OF AC ANGLE Goniolens Structures seen: 1-Schwalbe's line 2- Trabecular meshwork 3-Sclera spure 4-base of cilliary body 5-Root of the iris EVALUATION OF OPTIC DISC CUPPING High cup : disc ratio Cup : disc ratio asymmetry between Splinter hemorrhage. Increased visibility of the pores of the lamina cribrosa VISUAL FLIED DEFECTS four major patterns: isolated scotoma arcuate scotoma nasal step generalized depression DISTRIBUTION OF RETINAL NERVE FIBERS: Fibers from nasal half of the retina come directly to the optic disc as superior and inferior radiating fibers Fibers from the macular area come horizontally as papillomacular bundle Fibers from the temporal superior and inferior arcuate fibers with a horizontal raphe in between ARRANGEMENT OF NERVE FIBERS WITHIN OPTIC NERVE HEAD Deeper fibers from peripheral retina occupy peripheral or superficial location in ONH Superficial fibers from central retina occupy central or deep location in ONH SECONDARY OPEN-ANGLE GLAUCOMA Trabecular Pigment particles (pigmentary glaucoma). Red blood cells (red cell glaucoma Degenerate red cells (ghost cell glaucoma). Macrophages and lens proteins (phacolytic glaucoma). Proteins (uveitis). Pseudoexfoliative material (pseudoexfoliation glaucoma). the trabecular fibres oedema (uveitis) or scarring (e.g. post-traumatic angle recession). Post-trabecular Carotid-cavernous fistula. Sturge–Weber syndrome. Obstruction of the superior vena cava. MEDICAL TREATMENT TOPICAL Prostaglandin analogues (Latanoprost, Travoprost , biamtoprost) Beta blockers (Timolol) Carbonic anhydrase inhibitors (Brinzolamide , Dorzolamide) Alpha – adrenergic agonists (Brimonidine) Systemic therapy Acetazolamide (carbonic anhydrase inhibitor ) Hyperosmotic agents (glycerin, mannitol) Acetazolamide is available as 250 mg tablets (250–1000 mg daily in divided doses and 500 mg powder vials for injection Osmotic agents lower IOP by creating an osmotic gradient so that water is ‘drawn out’ from the vitreous into the blood SIDE EFFECT OF DRUGS Xaltan Conjunctival hyperaemia Eyelash lengthening macular oedema following cataract surgery. Anterior uveitis Beta blockers Bronchospasm, heart block , bradycardia SURGICAL TREATMENT laser trabeculoplasty (SLT) Trabeculectomy Trablotomy Shunt procedures ahmad valve Cyclodestructive Phacoemulsification frequently associated with a significant fall in IOP, it can be combined with a filtration procedure (phacotrablotomyomy) PCAG The incidence of blindness is higher in angle-closure glaucoma despite it being less common than open-angle glaucoma PACG is not as prevalent as POAG and only affects 0.17% of individuals younger than 40 years, particularly East Asians. RISK FACTORS Age : Average at presentation 50 -60 yrs. Gender : more in females 4 : 1 Race : seen commonly in South-East Asian population and black Africans Heredity : first degree relatives are at increased risk Refractive error : - more common in hypermetropes PATHOLOGY Angle closure occurs when the peripheral iris is in contact with the trabecular meshwork (TM) Specific mechanisms leading to angle closure can be divided into 2 categories: push and pull 1)Mechanisms that push the iris from behind relative pupillary block, enlarged or anteriorly displaced lens 2) Mechanisms that pull the iris into contact with the Tm due to inflammatory membrane as in uveitis, fibrovascular tissue as in iris neovascularization. Chronic intermittent friction between the iris and the TM With time, adhesions (synechiae) form between the iris and parts of the TM. Eventually the TM is so dysfunctional or obstructed that aqueous outflow from the eye is impaired and IOP rises. CLINICAL FEATURES OF AACG Halos around elevated IOP lights Corneal edema Aching eye or Engorged brow pain conjunctival Headache vessels Nausea, vomiting Fixed dilated Reduced acuity pupil Eye redness Closed angle on gonioscopy DIAGNOSTIC TESTS Slit-lamp examination Gonioscopy examination of anterior chamber angle Evaluation of the optic nerve head by fundoscopy Anterior segment optical coherence tomography (OCT) of angle Automatic static perimetry Ultrasound biomicroscopy Retinal OCT PROVOCATIVE TESTS maneuvers are used in an attempt to induce pupillary block A test is considered positive if the IOP increases by 8 or more mmHg. In the dark room test, patients are placed in a dark room for 1-2 hours The prone test involves placing the patient in the prone position for 1-2 hours Combining anterior chamber imaging mydriatic eye drops to increase pupillary TREATMENT OPTIONS Acute—Initial Presentation Chronic Topical prostaglandin analog and/or Oral carbonic anhydrase inhibitors topical beta-blocker and/or topical and/or topical beta-blocker and/or alpha-2 agonist topical alpha-2 agonist Carbonic anhydrase inhibitors Topical cholinergic agonists Lens extraction surgery Hyperosmotic agents Trabeculectomy and/or tube shunt Laser peripheral iridotomy after acute attack resolved (once corneal edema resolves lens extraction after acute attack resolved URGENT MANAGEMENT OF PCAG Intravenous acetazolamide 500 mg state to block the production of aqueous humor. Intravenous mannitol 1 to 2 grams/kg can be given Topical beta-blocker (timolol 0.5%) one drop twice to block the production of aqueous humor. Topical alpha 2-agonist (apraclonidine 1%) one drop three times to block the production of aqueous humor. Topical pilocarpine 1% to 2% one drop every 15 minutes for two doses once intraocular pressure is below 40 mm Hg to increase the outflow of aqueous humor. This is not effective at higher pressures due to pressure- induced ischemic paralysis of the iris. Intraocular pressure needs to be checked every hour. MEDICAL TREATMENT PAACG COMPLICATION OF GLAUCOMA SURGERY Cyclodestructive surgery Filtering Hypotony Hyphema Over or under filtration Retinal detachment Shallow AC Blebitis Phthisis Cataract Scleral flap leak Choroidal detachment Tube lens touch Retinal detachment Endothelial tube Phthisis bulbi touch Endophthalmitis VOGT’S TRIAD is seen in postcongestive primary angle closure It is characterised by: * Glaucomflecken (anterior subcapsular lenticular opacity) * Patches of iris atrophy * Slightly dilated non reacting pupil (due to sphincter atrophy). SECONDARY ANGLE CLOSURE GLAUCOMA NVG is a devastating severe ocular disease that cause blindness and is directly linked to fibrovascular proliferation of the eye newly formed vessels on the iris and angle. End result will lead to painfull blind eye which can be treated by cyclocryo or diod Phacomorphic glaucoma anterior displacement of the lens causes angle blakge Vagots triad Phacomorphic glaucoma CONGENITAL GLAUCOMA BUPHTHALMUS rise of intraocular pressure due to congenital anomalies of the angle Incidence:- bilateral in 70% of cases, asymmetric more common in boys 65 %. present before of 6 month 80%. family history & Inherited A.R. PATHOGENESIS Mal-development of the angle of AC associted with other major ocular anomalies isolated trabeculodysgenesis CLASSIFICATION True in which IOP becomes elevated during intrauterine life Infantile which manifests prior to the third birthday Juvenile which develops after third birthday but before 16yr CLINICAL FEATURE symptoms early : lacrimation , photophobia , Blepharospasm late : large eye due to elasticity of outer coat hazy cornea SIGNS Horizontal corneal diameter increased up to (13-14mm) Haab,s stria (horizontal stria )duo to descement membrane breaks Haze cornea duo to corneal edema High iop Fundus examination: optic disc asymmetry or cupping Gonioscopy :-to see congenital anomalies TREATMENT Goniotomty At time of examination and diagnosis is confirmed If cornea is clear and good visualization of the angle Trabeculotomy If cornea is cloudy In failed goniotomy Last not least trabeculectomy Trabeculotomy. conjunctival flap is made partial thickness scleral flap. A scleral incision is made and the Schlemm canal is exposed. The Harm’s trabeculotome is passed along the Schlemm’s canal The trabeculotome is then rotated towards the anterior chamber to break the inner wall of the canal. UP DATE IN GLAUCOMA Investigations Anterior segment OCT (AS-OCT) uses a diode light source instead of sound to produce highly detailed images of the cornea, angle region, and anterior ciliary body Ultrasound Biomicroscopy anterior champer Hood report OPERATIONS micro invasive glaucoma surgery (MIGS) High safety profile MIGS carry a much lower risk of serious complications Minimal disruption of normal anatomy Ab interno approach MIGS should offer meaningful IOP lowering effect. rapid recovery with minimal additional downtime for patients Example Gonioscopy Assisted Transluminal Trabeculotomy (GATT) Deepsclerotomy YOU TUBE https://youtu.be/1laohyDLi2A gatt https://www.youtube.com/watch?v=StoTD0oGPu4 deepsclerotomy https://www.youtube.com/watch?v=mXvOWH0D_qI SLT https://www.youtube.com/watch?v=rVicnPkZ6WA LASER PI https://www.youtube.com/watch?v=Ir9OYWgmWwQ YAG CAPSULECTOMY https://www.youtube.com/watch?v=gxOz0EfkVU8 trabolotomy TAKE HOME MESSAGE Glaucoma it is the second leading cause of irreversible silent blindness worldwide after cataracts. Make it a habit to check IOP and checking optic disc. Acute angle closure is an emergency needs proper diagnosis and mangment. Diagnosis of buphthalmus as early as possible for early surgical intervention has better prognosis than late. REFERENCES http://www.nei.nih.gov/eyedata/glaucoma.asp https://bjo.bmj.com/ https://eyewiki.org/Main_Page https://bjo.bmj.com/ https://www.aaojournal.org/