CHRONIC VISION LOSS Nathan Wong, RMH 2012 Exams vs Reality Exams – recognising the condition, knowing some of the pathophysiology and tests, memorising.
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CHRONIC VISION LOSS Nathan Wong, RMH 2012 Exams vs Reality Exams – recognising the condition, knowing some of the pathophysiology and tests, memorising the facts Reality – understanding the patient, coming up with a management plan, foreseeing the difficulties Chronic vision loss > 2 weeks Tempo More than just visual acuity Prognosis and impact Prevention *Gradual vision loss will be degeneration or deposition in pathology Vision loss could be neurosurgical The scope of the problem History tips Ask about vision in diabetes, elderly, paediatric developmental cases, etc. Past history, refractive error, contact lens wear Medical conditions – DM, asthma, eczema, immunosuppression, HT, chol Family history for genetic diseases Pain, transient or persistent, one or both eyes, blur/dim/distortion, which part of the field FUNCTION FUNCTION FUNCTION Examination tips Be comprehensive Distance acuity, colour vision Pupils Fields Extra ocular movements (EOM) Lids, orbit, Fundoscopy Corneal sensation, tear film, IOP, etc. etc. Diabetic Retinopathy Know the grades, know what is in each grade Treatments Weight loss, better control of diabetes, HT, chol Glasses (correct refractive error) Laser Injections Surgery Grading Signs of background diabetic retinopathy Microaneurysms usually temporal to fovea Hard exudates Intraretinal dot and blot haemorrhages Retinal oedema Focal diabetic maculopathy • • Circumscribed retinal thickening Associated complete or incomplete circinate hard exudates • • • Focal leakage on FA Focal photocoagulation Good prognosis Diffuse diabetic maculopathy • • • Diffuse retinal thickening Frequent cystoid macular oedema Variable impairment of visual acuity • • • Generalized leakage on FA Grid photocoagulation Guarded prognosis Clinically significant macular oedema Hard exudates within 500 m of centre of fovea with adjacent oedema which may be outside 500 m limit Retinal oedema within 500 m of centre of fovea Retinal oedema one disc area or larger any part of which is within one disc diameter (1500 m) of centre of fovea Treatment of clinically significant macular oedema Grid treatment • • For diffuse retinal thickening located more than 500 m from centre of fovea and 500 m from temporal margin of disc Gentle burns (100-200 m, 0.10 sec), one burn width apart Focal treatment • For microaneurysms in centre of hard exudate rings located 500-3000 m from centre of fovea • Gentle whitening or darkening of microaneurysm (100-200 m, 0.10 sec) Preproliferative diabetic retinopathy Signs • Cotton-wool spots • Venous irregularities • Dark blot haemorrhages • Intraretinal microvascular abnormalities (IRMA) Treatment - not required but watch for proliferative disease Proliferative diabetic retinopathy • • Affects 5-10% of diabetics IDD at increased risk (60% after 30 years) Neovascularization • • Flat or elevated Severity determined by comparing with area of disc Neovascularization of disc = NVD Neovascularization elsewhere = NVE Laser panretinal photocoagulation • • • Initial treatment is 2000-3000 burns Spot size (200-500 m) depends on contact lens magnification Gentle intensity burn (0.10-0.05 sec) • • Area covered by complete PRP Follow-up 4 to 8 weeks Cataract Common, a lot of patients have them Good operation Happy patients Rare but important complications: endophthalmitis, retinal detachment, choroidal haemorrhage Think about the associations Subcapsular cataract Anterior Posterior Nuclear cataract Progression • Exaggeration of normal nuclear ageing change • Increasing nuclear opacification • Causes increasing myopia • Initially yellow then brown Cortical cataract Progression Initially vacuoles and clefts Progressive radial spoke-like opacities Classification according to maturity Immature Hypermature Mature Morgagnian Drugs Systemic or topical steroids Chlorpromazine - initially posterior subcapsular - central, anterior capsular granules Other drugs Long-acting miotics • Amiodarone • Busulphan • Cataract surgery in 3:30 1. Operative complications • Vitreous loss • Posterior loss of lens fragments • Suprachoroidal (expulsive) haemorrhage 2. Early postoperative complications • Iris prolapse • Striate keratopathy • Acute bacterial endophthalmitis 3. Late postoperative complications • Capsular opacification • Implant displacement • Corneal decompensation • Retinal detachment • Chronic bacterial endophthalmitis Acute bacterial endophthalmitis Incidence - about 1:1,000 Common causative organisms • Staph. epidermidis • Staph. aureus • Pseudomonas sp. Source of infection • • • Patient’s own external bacterial flora is most frequent culprit Contaminated solutions and instruments Environmental flora including that of surgeon and operating room personnel Signs of severe endophthalmitis • Pain and marked visual loss • Absent or poor red reflex • Corneal haze, fibrinous exudate and hypopyon • Inability to visualize fundus with indirect ophthalmoscope Signs of mild endophthalmitis • Mild pain and visual loss • Small hypopyon • Anterior chamber cells • Fundus visible with indirect ophthalmoscope Management of Acute Endophthalmitis 1. Preparation of intravitreal injections 2. Identification of causative organisms • Aqueous samples • Vitreous samples 3. Intravitreal injections of antibiotics 4. Vitrectomy - only if VA is PL 5. Subsequent treatment Age related macular degeneration Presentation is loss of central vision Dry versus Wet types FFA and OCT Role of laser, anti VEGF therapy Drusen Histopathology Hard • • Small well-defined spots Usually innocuous Soft • • • Larger, ill-defined spots May enlarge and coalesce Increased risk of AMD Drusen and AMD - progression Atrophic AMD Exudative AMD Atrophic AMD Progression Initially drusen and non-specific RPE changes Late RPE (geographic) atrophy Atrophic AMD Fluorescein angiogram Hyperfluorescence from RPE window defect Management Low-vision aids if appropriate Choroidal neovascularization (CNV) • • • Less common than atrophic AMD but more serious Metamorphopsia is initial symptom Most lesions are not visible clinically Suspicious clinical signs Pinkish-yellow subretinal lesion with fluid Subretinal blood or lipid Angiographic classification of CNV Well-defined (classical) Extrafoveal > 200 m from centre of FAZ • Juxtafoveal < 200 m from centre of FAZ • Subfoveal - involving centre of FAZ • Occult • Poorly defined • Obscured by PED, blood or exudate Possible subsequent course of CNV Haemorrhagic sensory and Subretinal (disciform) scarring RPE detachment Massive subretinal exudationExudative retinal detachment Glaucoma Peripheral field loss Cup to disc ratio, field testing IOP control POAG, closed angle, secondary, congenital Aqueous drainage and the drugs that act on the pathway Aqueous outflow Anatomy a - Uveal meshwork b - Corneoscleral meshwork c - Schwalbe line d - Schlemm canal e - Collector channels f - Longitudinal muscle of ciliary body g - Scleral spur Physiology a - Conventional outflow b - Uveoscleral outflow c - Iris outflow Classification of secondary glaucomas a b Open-angle a. Pre-trabecular - membrane over trabeculum b. Trabecular - ‘clogging up’ of trabeculum c d Angle-closure c. With pupil block - seclusio pupillae and iris bombé d. Without pupil block - peripheral anterior synechiae Tonometers Goldmann Perkins Schiotz Contact applanation Portable contact applanation Contact indentation Air-puff Pulsair 2000 (Keeler) Tono-Pen Non-contact indentation Portable non-contact applanation portable contact applanation Goniolenses Goldmann • • • • • Zeiss Single or triple mirror • Four mirror Contact surface diameter 12 mm • Contact surface diameter 9 mm Coupling substance required • Coupling substance not required Suitable for ALT • Not suitable for ALT Not suitable for indentation gonioscopy• Suitable for indentation gonioscopy Indentation gonioscopy Differentiates ‘appositional’ from ‘synechial’ angle closure Press Zeiss lens posteriorly against cornea Aqueous is forced into periphery of anterior chamber Indentation gonioscopy in iridocorneal contact During indentation • • Before indentation Part of angle is forced open • Complete angle closure Part of angle remains closed by PAS• Apex of corneal wedge not visible Angle structures Schwalbe line Trabeculum Schlemm canal Scleral spur Iris processes Shaffer grading of angle width Grade 4 (35-45 ) • Ciliary body easily visible Grade 3 (25-35 ) • 3 4 2 At least scleral spur visible Grade 2 (20 ) 1 0 • • Only trabeculum visible Angle closure possible but unlikely Grade 1 (10 ) • • Only Schwalbe line and perhaps top of trabeculum visible High risk of angle closure Grade 0 (0 ) • • • Iridocorneal contact present Apex of corneal wedge not visible Use indentation gonioscopy Anatomy of retinal nerve fibres Papillomacular bundle Horizontal raphe Definition and risk factors IOP > 21 mmHg Glaucomatous disc damage Open angle of normal appearance Visual field loss Risk Factors 1. Age - most cases present after age 65 years 2. Race - more common, earlier onset and more severe in blacks 3. Inheritance • Level of IOP, outflow facility and disc size are inherit • Risk is increased by x2 if parent has POAG • Risk is increased x4 if sibling has POAG 4. Myopia Theories of glaucomatous damage Direct damage by pressure Capillary occlusion Interference with axoplasmic flow Optic nerve head Small physiological cup a - Nerve fibre layer a b b - Prelaminar layer c - Laminar layer c Large physiological cup • Normal vertical cup-disc ratio is 0.3 or less • 2% of population have cup-disc ratio > 0.7 • Asymmetry of 0.2 or more is suspicious Total glaucomatous cupping Pallor and cupping Pallor - maximal area of colour contrast Cupping - bending of small blood vessels crossing disc Cupping and pallor correspond Cupping is greater than pallor Progression of glaucomatous cupping a. Normal (c:d ratio 0.2) b. Concentric enlargement (c:d ratio 0.5) c. Inferior expansion with retinal nerve fibre loss d. Superior expansion with retinal nerve fibre loss e. Advanced cupping with nasal displacement of vessels f. Total cupping with loss of all retinal nerve fibres Early visual field defects • Small arcuate scotomas • Tend to elongate circumferentially • Isolated paracentral scotomas • Nasal (Roenne) step Progression of visual field defects • Formation of arcuate defects • Peripheral breakthrough • Enlargement of nasal step • Appearance of fresh arcuate inferior defects • Development of temporal wedge Advanced visual field defects • • Development of ring scotoma Residual central island • Peripheral and central spread • Residual temporal island Technique (1) a b a. Conjunctival incision b. Conjunctival undermining c d c. Clearing of limbus d. Outline of superficial flap e f e. Dissection of superficial flap f. Paracentesis Technique (2) a b a. Cutting of deep block anterior incision b. Posterior incision c d c. Excision of deep block d. Peripheral iridectomy e f e. Suturing of flap and reconstitution of anterior chamber f. Suturing of conjunctiva Filtration blebs Type 1 • • Type 2 • Thin and polycystic Good filtration • • • Type 3 • • • • Flat Engorged surface vessels No microcysts No filtration Flat, thin and diffuse Relatively avascular Microcysts present Good filtration Encapsulated • Localized, firm cyst Engorged surface vessels • No filtration • Pseudoexfoliation glaucoma • Secondary trabecular block open-angle glaucoma • Affects elderly, unilateral in 60% • Prognosis less good than in POAG Pseudoexfoliative material Iris sphincter atrophy Central disc with peripheral band On retroillumination Gonioscopy Trabecular hyperpigmentation - may extend anteriorly (Sampaolesi line) Causes of neovascular glaucoma • Common, secondary angle-closure glaucoma without pupil block • Caused by rubeosis iridis associated with chronic, diffuse retinal ischaemia Ischaemic central retinal vein occlusion (most common) Central retinal artery occlusion (uncommon) Long-standing diabetes (common) Carotid obstructive disease (uncommon) Signs of advanced neovascular glaucoma Severely reduced visual Severe rubeosis iridis acuity, congestion and pain Distortion of pupil and ectropion uveae Synechial angle closure Refractive error Failure to focus light on the retina Myopia – choroidal and retinal degeneration, detachment, staphyloma, glaucoma Hypermetropia Astigmatism Presbyopia Glasses, contacts, surgery Amblyopia Papilloedema Means raised intracranial pressure Needs admission You can only see it if you look for it History of headaches, visual obscurations Circulation of cerebrospinal fluid a (a) Subarachnoid space (b) Lateral ventricle b c d (c) Third ventricle e (d) Aqueduct (e) Fourth ventricle Hydrocephalus Dilated cerebral ventricles Communicating - obstruction to CSF flow in basilar cisterns or cerebral subarachnoid space Non-communicating - obstruction to CSF flow in ventricular system or at exit of foramina of fourth ventricle Early papilloedema • • • • • • VA - normal Mild disc hyperaemia Indistinct disc margins - initially nasal Mild venous engorgement Normal optic cup Spontaneous venous pulsation - absent (also absent in 20% of normals) Established papilloedema (acute) • • • • • • • • VA - usually normal Severe disc elevation and hyperaemia Very indistinct disc margins Obscuration of small vessels on disc Marked venous engorgement Reduced or absent optic cup Haemorrhages + cotton-wool spots Macular star Longstanding papilloedema (chronic) • • • • • VA - variable Marked disc elevation but less hyperaemia Disc margins - indistinct Variable venous engorgement Absent optic cup Atrophic papilloedema (secondary optic atrophy) • • • • • VA - severely decreased Mild disc elevation Indistinct disc margins Disc pallor with few crossing vessels Absent optic cup