Glaucoma 1 PDF

 2 Glaucoma 1 Why is this important? 3 Glaucoma is the second leading cause of blindness in the world. It has a relatively high prevalence: affecting 2-3% of individuals > 40 years old. Objectives...

 2 Glaucoma 1 Why is this important? 3 Glaucoma is the second leading cause of blindness in the world. It has a relatively high prevalence: affecting 2-3% of individuals > 40 years old. Objectives 4 By the end of this lecture you should: Recall the relevant anatomy and physiology of the anterior chamber and optic nerve, as it relates to Glaucoma. Differentiate between the different types of glaucoma. Outline the aetiology, pathogenesis, presentation, and management of Primary Open Angle Glaucoma. Critically analyse an optic disc and fundus for glaucomatous related changes. Overview 5 Pre-requisite Anatomy Definitions Aetiology and pathogenesis Classification Risk factors Ocular Hypertension Primary Open Angle Glaucoma (POAG) Normal Tension Glaucoma Primary Closed Angle Glaucoma  6 Anatomy & Physiology Recap  7 Anterior chamber & aqueous production recap  The Anterior Chamber 8 Corneal Endothelium Cornea Anterior chamber Iris Pupil Anterior Chamber Angle  Anterior Chamber Angle Trabecular Meshwork 9 Trabecular meshwork (TM) 1. Uveal TM: Inner most region, has largest pores thus least resistance to aqueous humour. 2. Corneo-scleral TM: Middle portion, thickest, smaller pores than Uveal TM, thus increased resistance to aqueous humour. 3. Juxtacanalicular TM: innermost portion, smallest pores thus most resistance to aqueous humour. This part of the TM links to the endothelium of the inner wall of the Schlemm canal. Schlemm canal: This channel runs around the limbus and empties into the episcleral veins. Aqueous Humour: Production and Outflow 10 https://www.youtube.com/w atch?v=K69zsRG_T3U Aqueous is constantly being Aqueous is produced 11 produced and drained out in the ciliary body. It passes in front of the lens Through the pupil. It then takes 2 routes to exit the eye Trabecular pathway (90% of aqueous exits via this route) Uveoscleral pathway (10% of aqueous exits via this route).  Trabecular Pathway (~90% of outflow) Trabecular Meshwork 12 Aqueous enters the anterior chamber. Drains through the Trabecular Meshwork Drains through the Schlemm canal. Into collector channels Into the episcleral venous system.  Uveo-scleral Pathway (~10% of outflow) 13 Aqueous enters the anterior chamber. Fluid drains into the space between the ciliary body and sclera Exits via veins in the ciliary muscle and anterior choroid Drains into Vortex veins  14 Optic Nerve Recap 15 https://jaypeedigital.com/eReader/chapter/9789352702947/ch1 16 https://www.pnas.org/doi/full/10.1073/pnas.0801621105  17 Retinal Ganglion cell Axons https://www.google.com/search?q=distribution%20of%20retinal%20nerve%20fibres%20along%20optic%20nerve%20head&tbm=isch&tbs=rimg:CaC- lTbfqk_1CYUmA2IaWUVHRsgIRCgIIABAAOgQIARAAVQSmAD_1AAgDYAgDgAgA&rlz=1C1GCEA_enGB1082GB1082&hl=en&sa=X&ved=0CBoQuIIBahcKEwiAhaLvra2EAxUAAAAAHQAAAAAQKA&biw=151 9&bih=738#imgrc=d9HUoDb-4yt3pM  Optic Nerve Head 18 The optic nerve head is the intra-ocular segment of the optic nerve. Consists of 3 segments: 1. Surface nerve fibre layer: convergence of the retinal nerve fibre layer (RGC Axons) onto the optic nerve head. 2. Pre-laminar region: This is the region above the lamina cribrosa. Here the nerve fibres form into bundles so that they are able to pass through the pores of the lamina cribrosa. 3. Lamina cribrosa: This is a connective tissue with multiple openings. The lamina cribrosa provides nutrition to the nerve fibre bundles. The pores are larger in the superior and inferior lamina cribrosa as there are larger nerve fibre bundles here.. https://link.springer.com/chapter/10.1007/978-3-031-27327-8_5  19 https://link.springer.co m/chapter/10.1007/97 8-3-031-27327-8_5 Optic disc 20 Optic Disc: Optic cup + NRR Small disc 2.2mm Neuro-retinal Rim Optic cup  ISNT RULE 21 Expected thickness: Inferior > Superior > Nasal > Temporal High sensitivity in picking out glaucomatous changes (81%). However optic nerves that are not glaucomatous often do not follow this rule.  22 Glaucoma https://www.youtube.com/watch?v=XlI_JXYMzbs What is Glaucoma 24 Group of conditions that result in chronic progressive optic neuropathy. It is often (but not always) associated with raised intraocular pressure. This is a key modifiable factor. Characterized by: Retinal ganglion cell death Visual field defects Classification 25 Primary Aetiology Secondary Congenital Pathogenesis Acquired Acute Rate of onset Subacute Chronic Anterior chamber Open angle Closed angle angle: Infantile Age of onset Juvenile Adult  Classification Terminology Congenital: Born with it Acquired: Not present at birth, acquired over time. Open angle: Anterior chamber angle is open, the blockage is at the level of the trabecular meshwork. Closed angle: The anterior chamber is closed and aqueous cannot reach the trabecular meshwork. Primary open angle glaucoma Pre-trabecular Open angle (POAG) Primary: not associated with another ocular or Secondary open Trabecular systemic condition. angle glaucoma Acquired Secondary: This is a sequela or complication Glaucoma Primary Post-trabecular of another ocular or systemic condition. Congenital Closed angle Secondary  27 Primary Open Angle Glaucoma  28 Ocular Hypertension Overview 29 Ocular hypertension refers to the state of consistently raised intraocular pressure (>21 mmHg) without the associated optic nerve damage. Epidemiology 4.5-9.4% of those >40 years old (COO, 2022) 10% of patients with untreated ocular hypertension go onto develop primary open angle glaucoma within 5 years. (COO, 2022) The Ocular Hypertension Treatment Study found that 45.5% of individuals with ocular hypertension went on to develop chronic open angle glaucoma within 20 years. (COO, 2022). Presentation 30 Symptoms: Asymptomatic Signs: Elevated IOP (>21mmHg) using Goldmann Applanation Tonometry (GAT) Note: Anterior chamber angle is open in these patients and there is no associated neuropathy (if there was then this would class as glaucoma). Investigation 31 Central visual field assessment Standard automated perimetry (sita 24-2) Slit lamp examination: Optic nerve head assessment Anterior chamber assessment (Van Hericks, Gonioscopy) Goldmann Applanation Tonometry/ Perkins Fundus imaging OCT (Anterior OCT and Optic Nerve Head OCT) Management 32 If IOP 40 years old in the UK. Note that this prevalence increases with age Affecting ~1% of individuals around 40 years old ~3% individuals aged 60 years old ~8% of individuals 80 The Global Burden of Glaucoma: Findings from the years old). Global Burden of Disease 2019 Study and Predictions by Bayesian Age–Period–Cohort Analysis Risk factors 36 Raised IOP Main modifiable risk factor Increasing age Family history of POAG Ethnicity Corticosteroid use Type 2 Diabetes Myopia Vascular disease Ocular perfusion pressure (difference between arterial blood pressure and intraocular pressure) Aetiology & Pathogenesis 37 Aetiology Increased resistance to drainage through the trabecular meshwork (despite the fact that the drainage angle is open). This blockage results in progressive optic neuropathy. Pathogenesis: Mechanical damage to retinal nerve fibres at ONH as they pass through the lamina cribrosa. Ischaemic damage: compression of blood vessels supplying the optic nerve head. Note: it is likely that the pathogenesis is a combination of both Work up 38 Central visual field assessment using standard automated perimetry (full or suprathreshold). Optic nerve head assessment and fundus examination Slit lamp OCT IOP measurement using Goldmann-type applanation (Perkins will also work here) IOP threshold value of ≥24mmHg Pachymetry Peripheral anterior chamber depth and configuration Van Herick, OCT, or Gonioscopy Glaucomatous visual field defects 39 Paracentral scotoma (Figure A) Nasal step scotoma (Figure B) Arcuate scotoma (Figure C) Ring scotoma (Figure D) OCT 40 (Salmon, 2021) Optic Disc changes in Glaucoma Overview (we will 41 cover each of these in detail on the following slides) Notching (focal and diffuse) Asymmetry in the C:D ratio between the two eyes NRR thinning RNFL defects Lamina dot sign: grey dot like fenestrations in the lamina cribrosa become visible Peri-papillary atrophy (particularly of B-zone) Loss of nasal NRR Vascular changes Splinter haemorrhages near disc Baring of circumlunar blood vessels Bayoneting of blood vessels Collateral disc vessels Optic disc assessment 42 It is important to note the disc size in deciding whether a C:D ratio is normal. To determine disc size, a narrow slit beam is focused on the lens. The height of the beam is adjusted to match the distance between the superior and inferior limits of the Neuroretinal rim. This reading is taken and multiplied by a correction factor(see chart below). Small. disc 2.2mm Large discs are more likely to be damaged, particularly in the case of Normal Tension Glaucoma. Note: A large disc has a large cup and this can be healthy, however smaller discs with large cups is abnormal and should be investigated. Optic disc 43 Optic Disc: Optic cup + NRR Neuro-retinal Rim Optic cup Remember the donut analogy? 44 What is the difference between these two donuts? Optic Disc changes in glaucoma 45 Retinal Nerve Fibre layer defects Notching Focal Diffuse Inferior Notching https://www.sciencedirect.com/science/ article/abs/pii/S0002939498000026 C:D ratio asymmetry 46 https://www.researchgate.net/figure/A-Asymmetry-in-disk-size-leading-to-asymmetry-in-CD-ratio-Left-disk-is-larger_fig2_261141258 Retinal Nerve fibre layer defects 47 These are subtle defects that usually precede the development of optic nerve head changes and visual field loss. These can be observed as localized wedge shaped defects or diffuse defects. It is often easier to see this in red-free illumination. https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC4741153&blobtype=pdf Laminar dot sign 48 Laminar dot sign Visible lamina cribrosa pores/ increased lamina cribrosa pore size as a result of loss of RGC axons. Observed in 70% of patients with Primary Open Angle Glaucoma (Saba et al., 2019).  Alpha and Beta zones 49 White dotted line: Alpha Source: https://www.sciencedirect.com/science/article/pii/S1350946220301051 zone. Yellow dotted line: Beta zone. Peripapillary atrophy 50 Early sign of glaucomatous damage in patient’s with ocular hypertension Alpha-zone: superficial RPE changes ‘Outer zone’ This is larger and more common in glaucomatous eyes Beta zone: Inner zone Chorioretinal atrophy Larger and more common in glaucoma It’s presence indicates a risk factor for glaucomatous progression The location of peripapillary B zone is indicative of likely location of visual field loss. Disc haemorrhages 51 Splinter or flame-shaped haemorrhage (feathered margins) From NRR to retina. Note that this can also occur in individuals with systemic vascular disease (ie/ Hypertensive retinopathy, Diabetic retinopathy, BRVO, CRVO, or papillitis). When you observe a disc haemorrhage, note the location as these are often transient and can point to the region of glaucomatous visual field damage. https://www.aao.org/eyenet/article/disc-hemorrhages-in-eyes-with-glaucoma  Vascular changes Glaucoma 52 Baring of circumlinear blood vessels: Early sign (thinning of NRR). Gap between the NRR and superficial blood vessels Bayoneting: Double angulation of a blood vessel The vessels entering the optic disc sharply bends into the disc and then again it will turn towards its original direction to run through the lamina cribrosa. Collaterals: This occurs between 2 veins at the disc. This is uncommon When to refer? 53 If any of the following conditions are present: Optic nerve head damage Visual field defect consistent with glaucomatous damage (consider repeat measurements before referring) IOP is ≥24mmHg using Goldmann-type applanation tonometry. (NG 81; 11.14-11.15). Routine referral to Ophthalmology (After repeating measures) Once referred…. 54 Tests that need to be performed to provide diagnosis: Visual field assessment (using standard automated perimetry- central threshold test). Dilated slit lamp exam: Optic nerve head examination and fundus examination Obtain a baseline image of the Optic Nerve head. IOP measurement using Goldmann application Peripheral anterior chamber configuration and depth using gonioscopy [If unable to do this then Van Herick can be perfumed]. Central corneal thickness measurement Management 55 Note this will be covered in depth in next week’s lecture. 1st line treatment: Selective Laser Trabeculoplasty (SLT) For those who have IOP > 24mmHg and chose not to have SLT/ SLT is not suitable: Prostaglandin analogue eye drops (First choice) Topical beta blocker (second choice) Carbonic anhydrase inhibitors Or a combination of treatments.  56 Normal Tension Glaucoma Overview 57 Variant of Primary Open Angle Glaucoma whereby IOP is within normal range Characterised by: Glaucomatous optic neuropathy Characteristic Glaucomatous visual field loss IOP is consistently ≤ 21mmHg Anterior chamber angle is open No signs of secondary glaucoma Risk factors 58 Age (Patients tend to be older than those who develop primary open angle glaucoma) Race Family history of NTG Thin central corneal thickness Systemic hypotension (including dips in blood pressure at night) Abnormal Vaso regulation (ie/ in patients who suffer from migraine, or Raynaud's syndrome) Low cerebrospinal fluid pressure Work up (Salient points) 59 History & symptoms: Specifically ask about the following: migraine history, Raynaud phenomenon, previous episodes of hypovolaemic shock (sudden drop in fluid/blood volume in the body), headache/other neurological symptoms, intermittent steroid use, systemic beta blockers. Examination: Check IOP (this may have been higher in teenage years) Glaucomatous optic disc changes similar to those seen in POAG Focal neuroretinal rim notches more likely here than in POAG Disc splinter haemorrhages more common than in POAG Peripapillary atrophy more common here than in POAG Visual Fields Visual Field defects are closer to fixation and more localized. Management 60 Routine referral to HES  61 Thank you herts.ac.uk