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See all Premium member Presentation Transcript Slide 1: Prepared By: Dr. Faisal M.B Rehman Slide 2: Glaucoma – Fact File Slide 3: “A group of optical disorders that have in common a characteristic optic neuropathy with associated visual field loss for which elevated IOP is mostly a primary risk factor.” Raised IOP > 24 mmHg Optic Nerve Atrophy Visual Field Loss What is Glaucoma….? Vascular Damage: Raised IOP Mechanical back pressure on optic disk reduced blood supply to optic nerve Ischemia Neural damage. Neural Damage: Atrophy of retinal ganglion cells & nerve fibre bundles cavernous atrophy of optic nerve hyaline degeneration of corneo-scleral trabecular tissue atrophy of entire uveal tract. Slide 4: Aqueous Humor….? “A clear watery fluid present in the ant. & post. chambers of eye.” Composition: pH = Slightly alkaline Volume = about 250 µL. Rate of production = 2.5 µL/min (1% turnover / min) Density = Slightly higher than water Osmotic pressure = Slightly higher than plasma Constituents = Slightly higher ascorbate, pyruvate, & Lactate, but lower protein, urea & glucose Functions: Maintains a healthy eye pressure of 10-24 mmHg. Maintains nutrition of avascular structures like lens & cornea. Slide 5: Aqueous Humor….? “A clear watery fluid present in the ant. & post. chambers of eye.” Formation: Major Source: Ciliary processes of ciliary body Minor Source: Vessels of iris Mechanism: Active secretion, ultra filtration and simple diffusion Flow: Ciliary body Post. Chamber Through Pupil into Ant. Chamber Two pathways of outflow: Trabecular Outflow: TM Schlemm’s Canal Aqueous veins Intra + Episcleral plexus of veins. Uveoscleral Outflow: Supraciliary + suprachroidal spaces sclera Slide 6: Possible Sites to Outflow Obstruction Swelling of ciliary body Pupillary block d/t iris bombe’ Occlusion of pores of TM “An IOP >24 mmHg with Diurnal Variation >10mmHg suggest Glaucoma” What raises the IOP….? Slide 7: Anatomical Classification Slide 8: Etiological Classification Slide 9: Perimetry: Assesses Visual Field defects The tests that work in collaboration for the clinical diagnosis of Glaucoma are: Tonometry: Estimates Intra-Ocular Pressure Gonioscopy: Measures Irido-corneal Angle Opthalmoscopy: Checks Optic-Disk Cupping Clinical Assessment Methods of Examination Slide 10: Clinically IOP is estimated by measuring the force required: To flatten a fixed area of cornea - Applanation Tonometry To indent the cornea - Impression Tonometry The normal range of IOP is 10-24 mmHg. However, Physiological Variations occur: With respiration & pulse beat With day & night The maximum diurnal variation of IOP in a normal eye is 5-8 mmHg. Clinical Assessment 1. Tonometry Slide 11: Here are some types of Tonometers available in the market: Goldmann tonometer: It is a stationary device attached to a slit lamp, that requires anesthesia drops, contact with cornea and a trained Ophthalmologist. Clinical Assessment 1. Tonometry Slide 12: Here are some types of Tonometers available in the market: Tono-Pen: It is a portable electronic, digital pen-like instrument that requires anesthesia drops and contact with cornea. It is especially useful in cases of corneal scar /edema. Clinical Assessment 1. Tonometry Slide 13: Here are some types of Tonometers available in the market: Diaton tono-Pen: It is an advanced digital pen-like instrument that do not require anesthetic drops nor contact with cornea. It measures IOP through eye-lid, so no risk of Infection. Clinical Assessment 1. Tonometry Slide 14: Studies show that the central corneal thickness can affect the measurement of IOP: Thick corneas may give false IOP values & vice versa. Thin corneas may be a risk factor for glaucoma. Pachymetry: It determines the thickness of cornea, which requires anesthetic drops & may (Ultrasonic Pachymeter) or may not (Orbscan Pachymeter) require corneal contact. Clinical Assessment Tonometry with Pachymetry Slide 15: It distinguishes Open-angle Glaucoma from Angle-closure Glaucoma by inspection of Anterior Chamber Angle: Direct Gonioscopy: less distortion & deeper view. Indirect Gonioscopy: better illumination & magnification. Grading of angle width can be done by Shaffer System: Clinical Assessment 2. Gonioscopy Slide 16: Glaucomatous Optic Neuropathy is evident by Optic disk cupping i.e. excavation, due to: Mechanical Compression: Bulging of Lamina Cribrosa Vascular Sclerosis: Ischemic atrophy of Optic Nerve Clinical Assessment 3. Ophthalmoscopy Slide 17: A typical glaucomatous cup has these main features: Characteristic ‘Bean-Spot’ appearance Neuroretinal rim tissue is lost Disc region appears pale Cup is deep with steep sides (C/D ratio >5) Cupping reaches up to margin of disc Pulsation of retinal arteries at the margins Overhanging edges with splinter hemorrhages Clinical Assessment 3. Ophthalmoscopy Slide 18: Aim is to investigate, in correlation with optic disk changes, localized patterns of visual field loss i.e. scotomas, resulting from damage to the conforming retinal nerve fiber bundles: Changes in central field: Mainly central 300 is affected. Starts with baring of blind spot i.e. exclusion of blind spot from the central field. Followed by formation of Bjerrum’s, arcuate, siedel & annular scotomas. Changes in peripheral field: Loss starts in the nasal periphery. Temporal & Central 5-100 are affected late. Only central tubular field is left before blindness. Clinical Assessment 4. Perimetry Slide 19: Primary Glaucoma Slide 20: Primary Glaucoma Slide 21: Risk Factors: IOP: > 24 mmHg Sex: Male > Female Age: > 40yrs & > 70 yrs Race: Predominant in Africans Controversial: Myopia, Diabetes, Migraine etc. Central corneal thickness: <555 µm with IOP Active Screening Program: When patient notices visual loss, it is too late for successful Rx. Screening Programs are hampered d/t unreliability of single IOP measure. Regular ophthalmic assessments of 1st degree relatives ensure success. Primary Glaucoma Slide 22: Clinical features: Painless Often Asymptomatic Bilateral, can be asymmetrical Insidious onset with slow progression IOP(not d/t any ocular/systemic abnormality) Clinical Assessment: Perimetry: Progressive visual field loss Opthalmoscopy: Glaucomatous optic neuropathy Gonioscopy: Open, normal appearing Ant. Chamber angle Tonometry: IOP = 30-40 mmHg, Diurnal Variation >10mmHg Primary Glaucoma Slide 23: Hypothesis: Higher prevalence of Vaso-Spastic disorders such as: Migraine Coagulopathy Raynauds phenomenon Autoimmune diseases Ischemic vascular diseases The Ant. Chamber angle and level of IOP appears normal and there is no contributing ocular or systemic disease, but the typical glaucomatous optic neuropathy exists, esp. splinter haemorrhages at the margins of the disk. Primary Glaucoma Slide 24: Clinical Features: Imbalance b/w optic disk’s arterial perfusion pressure and IOP May follow a transient episode of vascular shock and cease May progress to chronic optic vascular insufficiency & ischemic neuropathy Clinical Assessment: Tonometry: IOP is normal or subnormal Perimetry: Progressive visual field loss Gonioscopy: Open, normal appearing Ant. Chamber angle Opthalmoscopy: Gluc. cup with marginal Splinter haemorrhages Primary Glaucoma Slide 25: Primary Glaucoma Slide 26: Risk Factors: IOP: > 24 mmHg Age: > 50 yrs Sex: Females > Males Race: SE Asians & Japanese Family History: 1st degree relatives Controversial: Hypermetropic Eyes Exciting Factors: Dim-light, stress, mydriatics etc. Ocular Biometrics: shallow ant. chamber, thick lens, ant. lens curvature, short axial length, small corneal radius etc. < May be Acute, Sub-acute, Chronic and Plateau Iris > Primary Glaucoma Slide 27: Clinical feature: Severe pain & photophobia Blurring of vision with haloes Nausea, vomiting, malaise & sweating Mid-dilated pupil with associated Pupillary block Redness with a steamy cornea & ciliary injection Clinical Assessment: Tonometry: IOP >50 mmHg Perimetry: Progressive visual field loss Opthalmoscopy: Glaucomatous optic atrophy Gonioscopy: Closed Ant. Chamber angle, Per. ant. synechiae, Iris bombe, Glaukomﬂecken (ant. sub-capsular lens opacities) Primary Glaucoma Slide 28: Clinical feature: Same as Acute Angle-Closure, but are short & recurrent . Attacks may occur during the evening and resolve overnight. May become Acute or Chronic Angle-Closure Glaucoma. May resolve spontaneously, but with accumulated damage to Anterior Chamber angle with peripheral ant. synechiae. Clinical Assessment: Similar to that of Acute Angle-Closure Glaucoma except that the cornea may be clear rather than cloudy. Primary Glaucoma Slide 29: Clinical feature: Same as of Primary Open-Angle Glaucoma, but with extensive Bilateral visual field loss. Marked by extensive peripheral ant. synechiae accompanied by gradual rise of IOP. May occasionally have attacks of Sub-acute Angle-Closure Glaucoma. Clinical Assessment: Similar to that of acute angle-closure glaucoma except that the cornea may be clear rather than cloudy. The presence of peripheral anterior synechiae distinguishes it from open-angle glaucoma. Primary Glaucoma Slide 30: “An uncommon condition characterized by normal Central Anterior Chamber depth but a narrow Anterior Chamber angle” Mechanism: Congenitally high and anterior insertion of the iris root, thus covering the Trabecular Meshwork. Anterior position of ciliary process pushes peripheral iris forward, thus occluding the Trabecular Meshwork. Plateau Iris Syndrome: When narrow angle (and possible acute closure) is seen, despite of patent Iridectomy, it is called Plateau Iris Syndrome. Primary Glaucoma Slide 31: Clinical feature: Asymptomatic unless acute closure develops Pain, redness & decreased vision Recurrence after peripheral Iridectomy Clinical Assessment: Angle Crowding: Bunching up of the flat peripheral iris, occluding the Anterior Chamber angle. Deep Central Anterior Chamber : This is in contrast to the shallow chamber in Pupillary block with Iris bombe. Double-Hump Sign: Represents elevation of iris due to lens, with more peripheral elevation caused by Ciliary Process indentation. Primary Glaucoma Slide 32: Treatment: Topical hypotensive agents. Peripheral Iridotomy if not done already. Laser Iridoplasty for Plateau Iris Syndrome. Primary Glaucoma Slide 33: Primary Glaucoma Slide 34: Clinical feature: Buphthalmos: Cow’s eye Epiphora & Corneal edema Photophobia & Blepharospasm corneal diameter (>12 mm in 1st year of life) Haab Striae: Tears in Descemet’s Membrane Clinical Assessment: Tonometry: IOP >20 mmHg Perimetry: Aggressive Visual field loss Opthalmoscopy: Glaucomatous optic nephropathy Gonioscopy: Shows Barton’s Membrane, malformed TM etc. Primary Glaucoma Slide 35: Secondary Glaucoma “Deposition of fibrillar material on anterior lens capsule, pupil margin, iris, cornea, zonular fibers, ciliary body and TM”. Mechanism: IOP occurs due to accumulation of pigment & exfoliation material in the TM, reducing conventional outflow. Note: This is in contrast to the ‘True-Exfoliation’ of lens capsule d/t infra-red radiation exposure i.e. Glass Blower’s Cataract. Slide 36: Secondary Glaucoma Gonioscopy reveals dense, dark band at the Trabecular Meshwork 2. Pigmentary Glaucoma: “Degeneration of pigment from posterior iris surface into the ant. Chamber d/t mid-peripheral irido-zonular contact”. Corneal Endothelium: The pigment forms a vertical spindle that can be seen at the slit lamp (Krukenberg Spindle). Trabecular Meshwork: The pigment accumulates into the TM, creating a heavily pigmented band that extends for 3600. Slide 37: Secondary Glaucoma Lens luxation/displacement into the Anterior Chamber above Iris 3. Lens Induced-Ectopia Lentis: “Lens sub-luxation (partial rupture of zonules) or dislocation (complete rupture of zonules) may cause glaucoma” Angle-closure Glaucoma: By Ant. Dislocation into the anterior chamber causing Pupillary-block. Open-angle Glaucoma: By Post. Dislocation into the Vitreous, may remain asymptomatic or cause Phacolytic Glaucoma. Slide 38: Secondary Glaucoma 3. Lens Induced-Phacolytic: “Leakiness of high molecular-weight lens proteins into the ant. chamber by a hyper mature cataract lens ” Mechanism: Inflammatory edema of TM & its occlusion by lens proteins cause acute rise in IOP. Specific Findings: Hyper mature cataract with wrinkles, Plaques & macrophages on ant. lens capsule, Heavy flare in ant. chamber. Phacolytic glaucoma in Morganian cataract-whitish ppt in Lens capsule. Slide 39: Secondary Glaucoma Advance asymmetrical cataract with Lens Intumescence 3. Lens Induced-Phacomorphic: “Lens Intumescence as a result of taking up considerable fluid during cataractous change” Specific Findings: Asymmetrical cataract, with the contra-lateral eye showing a deeper anterior chamber. Mechanism: Enlargement of lens encroaches upon the Anterior Chamber, causing both pupillary block & angle crowding leading to Angle-closure Glaucoma. Slide 40: Secondary Glaucoma Neovascularization of the iris also known as Rubeosis Iridis 4. Neovascular Glaucoma: “Neovascularization of Iris & Ant. Chamber angle in response to retinal ischemia caused by CRVO, diabetic retinopathy etc” Stages: 1: Discrete tufts of new vessels in the pupillary margin 2: Radial extension of vessels toward the ant. angle & TM 3: Crowding of vessels obstruct outflow, but angle is still open 3: Peripheral anterior synechiae lead to angle-closure + IOP Slide 41: Secondary Glaucoma Iris melanoma invading ant. angle, with ed pigmentation in the TM 5. Tumor Induced Glaucoma: “Unilateral chronic glaucoma associated with ocular tumors like Uveal Melanomas, Uveal Metastasis & Retinoblastoma” Angle-closure Glaucoma: Through direct mechanical closure of angle with anterior iris / lens displacement & synechiae formation. Open-angle Glaucoma: Through direct infiltration of the TM & neovascularization at ant. angle blocking the conventional outflow. Slide 42: Secondary Glaucoma Dilated episcleral vessels & chemosis in carotid-cavernous fistula 6. High Episcleral Venous Pressure: “An open-angle glaucoma d/t EVP (>10mmHg), causing outflow resistance, characterized by dilated, tortuous episcleral veins & blood in Schlemm’s canal” Developmental Anomalies: Like carotid-cavernous fistulas and Sturge-Weber syndrome may contribute to a high EVP. Mechanical Compression: Of the venous drainage, by retro-bulbar tumors, vascular thrombosis & sup. vena cava syndrome. Slide 43: Secondary Glaucoma Pigmented iris nodules in Iris Nevus Syndrome 7. Iridocorneoendothelial Syndrome: “Primary abnormality of the corneal endothelium associated with corneal edema, iris atrophy & angle-closure glaucoma.” It is of the following types: Iris Nevus Syndrome: Corectopia & pigmented iris nodules Chandler’s Syndrome: Beaten bronze corneal endothelium Essential iris atrophy: Iris stromal loss, corectopia, ectropion uveae and Hole formation. Slide 44: Secondary Glaucoma Beaten bronze appearance of endothelium in Chandler’s Syndrome 7. Iridocorneoendothelial Syndrome: “Primary abnormality of the corneal endothelium associated with corneal edema, iris atrophy & angle-closure glaucoma.” It is of the following types: Iris Nevus Syndrome: Corectopia & pigmented iris nodules Chandler’s Syndrome: Beaten bronze corneal endothelium Essential iris atrophy: Iris stromal loss, corectopia, ectropion uveae and Hole formation. Slide 45: Secondary Glaucoma Corectopia with Iris stromal loss in Essential Iris Atrophy 7. Iridocorneoendothelial Syndrome: “Primary abnormality of the corneal endothelium associated with corneal edema, iris atrophy & angle-closure glaucoma.” It is of the following types: Iris Nevus Syndrome: Corectopia & pigmented iris nodules Chandler’s Syndrome: Beaten bronze corneal endothelium Essential iris atrophy: Iris stromal loss, corectopia, ectropion uveae and Hole formation. Slide 46: Secondary Glaucoma Hyphema: Blood layering in anterior chamber. 8. Traumatic Glaucoma: “Penetrating & blunt trauma causing equatorial stretching and intraocular lesions that affect the seven ocular rings, leading to Glaucoma.” Pupil tears: At pupillary sphincter. Retinal dialysis: Retinal detachment. Iridodialysis : Separation of iris from ciliary body. Cyclodialysis: Cleft formation b/w ciliary body & sclera. Trabecular dialysis: Creation of a flap in the trabecular meshwork. Angle recession: Tears b/w longitudinal & circular ciliary muscles. Disruption of the zonules: Leading to lens luxation or subluxation. Slide 47: Secondary Glaucoma Extensive peripheral synechiae in a patient with Inflammatory Glaucoma 9. Inflammatory Glaucoma: “Glaucoma secondary to uveitis, herpes simplex trabeculitis, herpes zoster ophthalmicus, syphilis, sarcoidosis etc.” Obstruction of TM by inflammatory cells & protein. Inflammation of the trabecular meshwork itself. Formation of peripheral anterior synechiae. Posterior synechiae leading to pupillary block. Iris neovascularization and neovascular glaucoma. Slide 48: 1 2 3 Facilitation of Aqueous Outflow Suppression of Aqueous Production Reduction of Vitreous Humor Volume 4 Utilization of Miotics, Mydriatics & Cycloplegics “The goal of glaucoma treatment is to preserve the visual field of patients by lowering the IOP, and maintaining a target range which is uniform day & night.” Medical Treatment Slide 49: Bronchospasm, bradycardia, heart block, BP, CNS depression, impotence, allergy, diabetes, punctate-keratitis etc. Inhibiting cAMP production in ciliary epithelium => aqueous secretion 20-50% => decrease IOP 20-30% Non-selective β antagonist: carteolol 1%, levobunolol 0.25%, timolol maleate 0.25% Selective β1 antigonist: betaxolol 0.25% Allergan’s Betagan (Levobunolol Hcl 0.5%) Barrett Hodgson Medical Treatment Slide 50: Lethargy, fatigue, dry mouth, apraclonidine is a clonidine derivative, which cannot cross BBB to cause systemic hypotension Decrease aqueous production Increase uveo-scleral outflow Decrease IOP 20-30% Apraclonidine: aqueous production Brimonidine: Also aqueous outflow Allergan’s Alphagan (Brimonidine Tartarate 0.2%) Barrett Hodgson Drugs that Decrease Aqueous Humor Production Medical Treatment Slide 51: Acidosis, depression, numbness, renal stone, hypokalemia, bone marrow, malaise, depression, punctate keratopathy etc. Blocks CA-II enzyme production of bicarbonate ions, thus production of aqueous humor Systemic Acetazolamide: In acute cases Topical Dorzolamide: Adjunctively with timolol MSD’s Cosopt (Dorzolamide HCl 2% + Timolol Maleate 0.5%) Drugs that Decrease Aqueous Humor Production Medical Treatment Slide 52: Darkening of the iris & periocular skin, conjunctival hyperemia, hypertrichosis, macular edema, uveitis, LFT etc. Uveo-scleral outflow (about 50%) by relaxing ciliary body muscle, thus ing IOP by 25-32% Latanoprost 0.005% Travoprost 0.004% Bimatoprost 0.03% Allergan’s Lumigan (Bimatoprost 0.03%) Barrett Hodgson Medical Treatment Slide 53: Induced miosis, accommodative spasms, retinal detachment, AchE inhibitors potentiate succinylcholine given during anesthesia. Contractile action on longitudinal ciliary muscle => outflow via TM => IOP of about 15-25 % Pilocarpine 0.5-6% Carbachol 0.75-3% Echothiophate 0.03-0.25% Pilocarpine (Pilocarpine HCl 1%) Alcon Laboratories Medical Treatment Slide 54: Headache, BP, tachycardia, arrhythmia, adrenocchrome deposits at the conjunctiva & cornea, pupillary dilation, macular edema in the conventional trabecular and uveo-scleral outflow => thus, IOP of about 15-20 % Epinephrine 0.25-2% Dipivefrin HCl 0.1% C/I in patients with narrow iris-corneal angle Allergan’s Propine (Dipivefrin HCl 0.1%) Barrett Hodgson Medical Treatment Slide 55: Medical Treatment Slide 56: Achieving a uniformly low IOP Protecting neuro-vascular layer Compliance With drug therapy Contemporary Practice Slide 57: Destruction of ciliary body via cryotherpy, diathermy, high-frequency ultrasound and thermal mode neodymium: YAG laser therapy as well as surgically to control IOP. Done in advanced glaucoma after failure of medical and other surgical treatments. Surgical Treatment Laser burns via a goniolens to the TM, to facilitate aqueous outflow. May be used in the initial treatment of open-angle Glaucoma, allowing decrease in medical therapy and postponement of Glaucoma surgery. Trabeculectomy: Creating direct access from ant. chamber to subconjuctival & orbital tissues, in acute angle-closure glaucoma. Goniotomy: Creating openings via goniolens, in the internal portions of TM to allow drainage, in primary congenital Glaucoma. Slide 58: Thank you for your time!! Any Questions?? You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.