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visual loss compressed

  1. 1. Chronic VisualDisturbance and Visual Loss Setareh Ziai April 2nd, 2009
  2. 2. QUICK review
  3. 3. Basic Anatomy
  4. 4. Where is the problem? LMCC Objectives Pre-retinal:  cornea (dystrophy, scarring, edema)  lens (age-related, traumatic, steroid-induced)  glaucoma Retinal:  DM (diabetic retinopathy, macular edema)  vascular insufficiency (arterial or venous occlusion)  tumours  macular degeneration Post-retinal:  anterior to optic chiasm (if optic nerve = monocular) • compressive optic neuropathy (intracranial masses, thyroid eye disease) • toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)  optic chiasm lesions (pituitary adenoma)
  5. 5. Where is the problem? Pre-retinal:  cornea (dystrophy, scarring, edema)  lens (age-related, traumatic, steroid-induced)  glaucoma Retinal:  DM (diabetic retinopathy, macular edema)  vascular insufficiency (arterial or venous occlusion)  tumours  macular degeneration Post-retinal:  anterior to optic chiasm (if optic nerve = monocular) • compressive optic neuropathy (intracranial masses, thyroid eye disease) • toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)  optic chiasm lesions (pituitary adenoma)
  6. 6. Diagnosis based on:- focused ophthalmological history - monocular vs. binocular - acute vs. chronic - painful vs. painless- exam: … start with gross examination - VA - slit lamp biomicroscopy +/- fluorescein - dilated fundus examination- VF testing- fluorescein angiography +/- other tests
  7. 7.  **Remember for exam:  sometimes, chronic visual loss in ONE eye is noted incidentally some time later due to occlusion of normal eye…: CHRONIC LOSS OF VISION CAN PRESENT ACUTELY!!
  8. 8. Corneal Causes - dystrophy - scarring - edema
  9. 9. The Cornea- allows light to enter theeye- provides most of the eye’soptical power- 0.5-0.8 mm thick- transparent due to itsuniformity, avascularityand deturgescence
  10. 10. Epithelium StromaEndothelium
  11. 11. Corneal Dystrophies- rare inherited disorders- progressive, usually bilateral- can affect any of the three layers of the cornea- affect transparency- age at presentation: first to fourth decades
  12. 12. Corneal Dystrophies- divided into: - anterior dystrophies: - epithelium - may present with recurrent corneal erosions - stromal dystrophies: - usually present with visual loss - if very anterior, can cause erosions and pain - posterior dystrophies: - endothelium - vision loss secondary to edema (endothelial dysfx)
  13. 13. Corneal Scarring- multiple causes: - trauma - infectious (eg., herpes) - post-surgical
  14. 14. Corneal Edema- most often caused by dysfunction of the corneal endothelium: - dystrophy - trauma - infectious (eg., herpes) - post-surgical
  15. 15. CornealTransplantation
  16. 16. If the corneal stroma opacifies due to trauma or infection, or if there is swelling or an irregularity of the surface of the cornea, light cannot properly reach the retina.In some cases, a cornea from a deceased donor can be transplanted.
  17. 17. Corneal Transplantation
  18. 18. Lens-Related Causes (cataract) - age-related - traumatic - steroid induced
  19. 19. The Lens Lens- biconvex, avascular,transparent structure- sits inside a thincapsule, attached to theciliary body by thezonules- provides theremainder of the eye’soptical power (alongwith the cornea)
  20. 20.  cataracts are due to the opacification of this normally clear structure
  21. 21. Age-Related Cataract- often affect the nucleus of the lens first: - yellowing, followed by a browning of the lens - eventually, liquefaction- causes myopic changes (increased refractive index of the lens)
  22. 22. Traumatic Cataract- most common cause of unilateral cataract in young individuals- most often caused by direct penetrating injury to the lens- can also be caused by: - concussion - ionizing radiation to ocular tumours - infrared radiation (glassblowers)
  23. 23. Steroid-Induced Cataract- both systemic and topical steroids can be the culprits- posterior part of lens affected first- children may be more susceptible- if lens changes develop, dose should be reduced to the minimum necessary- early opacities may regress with discontinuation of therapy
  24. 24. Glaucoma
  25. 25. Glaucoma disease of the optic nerve, often caused by an increase in intraocular pressure due to poor drainage of aqueous from the trabecular meshwork…
  26. 26. Glaucoma if left untreated, glaucoma can lead to permanent damage to the optic nerve and resultant visual field loss can progress to blindness
  27. 27. Glaucoma by definition, glaucoma is a trimodal disease, characterized by: increased IOP  optic nerve changes  visual field changes
  28. 28. Goldmann Applanation Tonometer
  29. 29. Glaucoma classification:  primary: open-angle, angle-closure  secondary: inflammatory, traumatic, neovascular, steroid-induced etc…  congenital
  30. 30. Risk Factors for Glaucoma age african-american heritage high IOP family history myopia
  31. 31. Symptoms of Glaucoma often asymptomatic with late disease, constriction of peripheral, and later central visual field with very high IOP, can have blurry vision and halos around lights
  32. 32. Glaucoma: Optic Nerve Changes increased cup:disc ratio thinning of neural rim progressive loss of nerve fiber layer flame hemorrhages on disc
  33. 33. Primary Open Angle Glaucoma most common (90%) usually bilateral (can be asymmetric) prevalence increases with age angle is open, eye is quiet increased resistance to aqueous drainage at the level of the trabecular meshwork is thought to be the main pathophysiologic feature
  34. 34. Treatment options goal is to stabilize the IOP to protect the optic nerve against further damage options:  drops  laser  surgery
  35. 35. Glaucoma - Medications mechanism of action:  decrease aqueous production: • beta blockers: timolol • alpha agonists: brimonidine • carbonic anhydrase inhibitors: diamox  increase aqueous outflow: • miotics: pilocarpine • epinephrine • prostaglandin analogs: latanoprost
  36. 36. Glaucoma - Lasers usually when medical management fails  ALT (argon laser trabeculoplasty), SLT (selective laser trabeculoplasty): for open angle glaucomas  peripheral iridotomy: for angle-closure glaucomas high success rate
  37. 37. Glaucoma - Surgery usually when medical management and laser treatments fail  trabeculectomy: sub-conjunctival shunt of aqueous  drainage devices (valves)  cyclodestruction: last resort – destruction of ciliary body
  38. 38. Where is the problem? Pre-retinal:  cornea (dystrophy, scarring, edema)  lens (age-related, traumatic, steroid-induced)  glaucoma Retinal:  DM (diabetic retinopathy, macular edema)  vascular insufficiency (arterial or venous occlusion)  tumours  macular degeneration Post-retinal:  anterior to optic chiasm (if optic nerve = monocular) • compressive optic neuropathy (intracranial masses, thyroid eye disease) • toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)  optic chiasm lesions (pituitary adenoma)
  39. 39. THE RETINA- neural tissue liningthe inside of the eye- converts the visualimage into aneurochemicalmessage and sends itto the brain- is made up of 10anatomic layers
  40. 40. Diabetes - diabetic retinopathy- diabetic macular edema
  41. 41. Diabetic RetinopathyØ microangiopathyØ affects pre-capillary arterioles, capillaries and post-capillary venulesØ features of: l microvascular occlusion l leakage clinically, can be divided into: l background DR (nonproliferative) l preproliferative DR l proliferative DR
  42. 42. Diabetic Retinopathy: Epidemiology 239 million people by 2010 doubling in prevalence since 1994 diabetes will affect: 28 million in western Europe 18.9 million in North America 138.2 million in Asia 1.3 million in Australasia• #1 cause of blindness in patients 20-64 yrs• prevalence increases with duration of diabetes and patient age rare to find DR in children < 10 yrs, regardless of duration risk of developing DR increases after puberty
  43. 43. EpidemiologyWisconsin Epidemiologic Study of Diabetic Retinopathyl Between 1979-1980l 1210 patients with Type 1l 1780 patients with Type 2l predominantly white populationl After 20 yrs, DR present in: • 99% of Type 1 • 60% of Type 2
  44. 44. WESDR: Frequency of retinopathy in subjects with type 1diabetes
  45. 45. WESDR: Frequency of retinopathy in subjects with type 2 diabetes
  46. 46. Diabetic Retinopathy: Risk FactorsØ duration of diabetes: most important risk factorØ poor metabolic controlØ pregnancy: can be associated with rapid progressionØ HTNØ nephropathyØ smokingØ obesityØ hyperlipidemia
  47. 47. Classification of Diabetic RetinopathyØ Classified into 2 stages Nonproliferative Diabetic Retinopathy (NPDR) early stage also known as background DR (BDR) further categorized based upon extent of DR l mild, moderate, severe, very severe l Proliferative Diabetic Retinopathy (PDR) • more advanced stage • ***Macular edema • May be present at any stage of DR
  48. 48. NPDRØ typically asymptomatic l fluctuating visual acuity: • fluctuating blood sugar l decreased visual acuity: CSME macular ischemia review these patients annually
  49. 49. Mild NPDR
  50. 50. Microaneurysm
  51. 51. Moderate NPDR
  52. 52. Severe NPDR
  53. 53. Proliferative Diabetic RetinopathyØ more likely to become symptomatic than early NPDRØ may have decreased vision, sudden vision loss, floaters, cobwebs, flashes, dull eye acheØ PDR can also affect visual function by affecting the macula with resulting macular ischemia and/or edema
  54. 54. Proliferative DRØ affects 5-10% of the diabetic populationØ neovascularization is the hallmark l NVD: neovascularization of the disc l NVE: neovascularization elsewhereØ new vessels are not only extremely fragile (intraretinal or vitreous hemorrhage), but often associated with fibrous proliferation, leading to an increased risk of tractional retinal detachment
  55. 55. Advanced PDR Tractional retinal detachment resulting from contraction of the fibrovascular proliferative tissue on the retina
  56. 56. Panretinal Photocoagulation for High-risk PDR goal is to induce involution (or at least arrest) of new vessels by creating areas of retinal ischemia 1200-3000 burns 4 sessions
  57. 57. Vitrectomy for Vitreous Hemorrhage / TRD
  58. 58. Diabetic Macular Edema (DME)Ø retinal edema threatening or involving the macula diagnosis is made by slit-lamp exam, confirmed by fluorescein angiography and/or OCT important observations include: l location of retinal thickening relative to the fovea l presence and location of exudates
  59. 59. DME and CSME
  60. 60. Treatment of CSME argon laser application intravitreal steroid injection intravitreal anti-VEGF injection pars plana vitrectomy
  61. 61. Ophthalmological Follow-Up Diabetic Screening l Type 1 diabetics: Dilated funduscopic exam (DFE) 5 yrs after diagnosis Newly diagnosed patients with Type 1 diabetes rarely have retinopathy during the first 5 yrs l Type 2 diabetics: Type 2 diabetics typically diagnosed yrs after initial onset DFE at the time of diagnosis Significant portion of newly diagnosed Type 2 diabetics have established DR at the time of diagnosis
  62. 62. Vascular Insufficiency - arterial occlusions (CRAO, BRAO) - venous occlusions (CRVO, BRVO)
  63. 63. CRAO
  64. 64. CRAO most of the retina is supplied by the central retinal artery (branch of the ophthalmic artery, which is the first branch of the ICA) if this supply is interrupted (embolus, thrombosis, inflammation, vasculitis or compression), the retina becomes ischemic irreversible damage occurs after approximately 90 minutes
  65. 65. CRAO presentation is with sudden and profound loss of vision RAPD is present orange reflex from the choroid stands out at the fovea, and contrasts with the surrounding pale retina (cherry-red spot) must r/o temporal arteritis
  66. 66. CRAO most commonly the result of atherosclerosis (thrombosis) but may also be caused by calcific emboli often in older patients, with a hx of arteriosclerosis may have had a hx of amaurosis fugax (transient visual loss)
  67. 67. CRAO OPHTHALMOLOGIC EMERGENCY!! treatment:  decrease IOP  paracentesis  ocular massage goal: to send the embolus distally **remember to r/o giant cell arteritis! (ESR, CRP, plt) poor prognosis: 60% < 20/400
  68. 68. BRAO
  69. 69. BRAO sudden and profound altitudinal or sectoral visual field loss similar causes as CRAO identify and treat associated medical conditions (HTN, DM, hypercholesterolemia, smoking, vasculitis etc…)
  70. 70. BRAO retinal cloudiness in ischemic area +/- visible embolus also has a poor prognosis, unless the obstruction can be dislodged within a few hours
  71. 71. CRVO
  72. 72. CRVO thrombosis of the central retinal vein sudden loss of vision in affected eye severity of symptoms varies…  non-ischemic: 75%  Ischemic most characteristic finding: retinal hemorrhages
  73. 73. CRVO underlying associations  advancing age  systemic conditions: HTN, DM, smoking, obesity, hyperlipidemia  glaucoma  inflammatory diseases: sarcoidosis, Behcet disease  thrombophilic disorders: hyperhomocysteinaemia, antiphospholipid antibody syndrome
  74. 74. CRVO Treatment:  treat associated medical conditions  decrease IOP if elevated  pan-retinal photocoagulation (laser) if: • neovascularization (iris, angle, retina) • …especially if ischemic CRVO
  75. 75. BRVO
  76. 76. BRVO thrombosis of a branch of the central retinal vein visual loss depends on the amount of macular drainage compromised by the occlusion (peripheral occlusions may be asymptomatic) characteristic findings in one sector of the retina:  dilatation and tortuosity of veins  retinal hemorrhages  retinal/macular edema 
  77. 77. BRVO obstruction often at arterio-venous crossings: arteries and veins share adventitial sheath… thickening of the arteriole (arteriosclerosis) compresses the vein, eventually causing an occlusion often associated with:  hypertension (75%)  diabetes (10%)
  78. 78. BRVO prognosis: depends on amt of venous drainage involved by the occlusion and severity of macular ischemia: within 6 mos, about 50% of eyes have a VA of 20/30 or better main complications:  chronic macular edema  neovascularization laser photocoagulation may be helpful in above cases
  79. 79. Retinal Tumours
  80. 80.  ocular tumours:  ciliary body: • melanoma  choroid: • melanoma • hemangioma • metastases  primary ocular lymphoma  retina and optic nerve: • retinoblastoma • astrocytoma • hemangioma
  81. 81. Choroidal Melanoma most common primary intraocular tumour in adults presentation usually in 6th decade:  asymptomatic vs. visual field defect and/or decreased visual acuity signs:  raised, usually pigmented lesion visible at the back of the eye  may be associated with retinal detachment  optic nerve may be involved
  82. 82. Choroidal Melanoma treatment:  consider size, location, activity of tumour, state of fellow eye, general health/age of pt, pt’s wishes/fears • brachytherapy • external radiotherapy • transpupillary thermotherapy • local resection • enucleation • exenteration • palliative (may include chemo)
  83. 83. Choroidal Metastases …with choroidal melanoma, don’t forget general medical investigations!  mets TO the choroid: • most frequently from bronchus in both sexes and the breast in women, rarely kidney or GI  CXR, rectal exam, mammography  mets FROM the choroid: • liver  hepatic u/s, GGT, ALP • lungs (rarely affected before liver)  CXR
  84. 84. Choroidal Metastases usually present with visual impairment only IF tumour is near the macula signs:  fast-growing, creamy coloured lesion  most often in posterior pole  usually not very elevated (infiltrates laterally)
  85. 85. Choroidal Metastases treatment:  observe: if asxic or receiving systemic chemo  radiation: external beam or brachy  transpupillary thermotherapy  systemic therapy for the primary  enucleation: for painful blind eye prognosis is poor…  median survival: 8-12 mos for all pts, 15-17 mos for those with breast ca
  86. 86. Retinoblastoma most common malignant tumour of the eye in childhood (1:20 000) mean age of presentation: 8 mos if inherited, 25 mos if sporadic  60% present with leukocoria (white pupillary reflex)  strabismus (20%)  occasionally: painful, red eye  if inherited: often bilateral
  87. 87. Retinoblastoma malignant transformation of primitive retinal cells before their final differentiation can be caused by germinal mutations (can be passed on to the next generation), or can be sporadic (66% of cases)
  88. 88. Retinoblastoma this is a clinical diagnosis, but CSF and bone marrow should be examined to check for metastatic disease if ON involved or if there is evidence of extraocular extension rx:  small: cryotherapy, photocoagulation  medium: brachytherapy, external beam, chemo  large/advanced cases: chemoreduction + local treatment, enucleation  metastatic disease: chemo (intrathecal if cells in CSF)
  89. 89. Retinoblastoma prognosis:  depends on extent of disease at diagnosis  overall mortality ~ 5-15%  ~ 50% of children with the germinal mutation will eventually develop a second primary tumour (eg., osteosarcoma of the femur or pinealoblastoma)
  90. 90. Macular Degeneration
  91. 91. Macula 1.5 mm in diameter central vision: BEST VISUAL ACUITY colour vision progressive destruction of the macular area: MACULAR DEGENERATION
  92. 92. Macular Degeneration most common cause of irreversible visual loss in the developed world exists in two forms:  non-exudative (dry) macular degeneration  exudative (wet) macular degeneration
  93. 93. Non-exudative Macular Degeneration lipid products arising from photoreceptor outer segments are found under retina  can be seen with ophthalmoscope!  called « drusen »
  94. 94. Exudative Macular Degeneration new vessels from the choroid grow into the sub-retinal space; form a sub- retinal neovascular membrane subsequent hemorrhage into the sub- retinal space or even through the retina into the vitreous is associated with profound loss of vision
  95. 95. Macular Degeneration symptoms:  since fovea is responsible for fine visual resolution, any disruption will cause severe visual impairment • blurry/reduced vision • distorted vision (metamorphopsia) • reduction (micropsia) or enlargement (macropsia) of objects • VF loss (scotoma)
  96. 96. Macular Degeneration rx:  non-exudative (usually slowly progressive): • no actual medical treatment • use low vision aids • high dose antioxidants MAY be beneficial (eg., vitalux)
  97. 97. Macular Degeneration rx:  exudative (can be rapidly progressive and devastating): • intravitreal injections of anti-VEGF factors: bevacizumab, ranibizumab • photodynamic therapy (injection of photosensitizer into systemic circulation followed immediately by laser targeting new vessels in macular area) • combination of above treatments
  98. 98. Where is the problem? Pre-retinal:  cornea (dystrophy, scarring, edema)  lens (age-related, traumatic, steroid-induced)  glaucoma Retinal:  DM (diabetic retinopathy, macular edema)  vascular insufficiency (arterial or venous occlusion)  tumours  macular degeneration Post-retinal:  anterior to optic chiasm (if optic nerve = monocular) • compressive optic neuropathy (intracranial masses, thyroid eye disease) • toxic/nutritional (nutritional deficiencies, alcohol/tobacco amblyopia)  optic chiasm lesions (pituitary adenoma)
  99. 99. OPTIC NERVE 1.2 million cells 80 % visual fibres 20 % pupillary fibres carries visual information from the eye to the brain
  100. 100. OPTIC CHIASMcrossover of nasal fibersabove the pituitaryinternal carotids are justlateralfrom optic chiasm: optic tract to the lateral geniculate body opticradiation to the primary visual cortex
  101. 101. Anterior to Optic Chiasm - compressive optic neuropathies- toxic/nutritional optic neuropathies
  102. 102. Compressive Optic Neuropathies INTRACRANIAL MASSES:  optic nerve glioma • typically affects young women, end of first decade • associated with NF-1  optic nerve sheath meningioma • most frequent in middle-aged women • unilateral, gradual visual impairment  any other orbital or chiasmal tumour compressing any part of the optic nerve THYROID EYE DISEASE
  103. 103. Thyroid Eye Disease may occur in the absence of biochemical evidence of thyroid dysfx autoimmune reaction (IgG Abs) causing:  inflammation of EOMs: pleiomorphic cellular infiltration associated with increased secretion of GAGs and osmotic imbibition of water • muscles can become up to 8 times their original size!! no relation to severity of thyroid dysfx!
  104. 104. Thyroid Eye Disease main findings: (not all are always present!)  soft tissue involvement  lid retraction  proptosis  optic neuropathy  restrictive myopathy
  105. 105. Thyroid Eye Disease vision loss from:  exposure keratopathy • due to severe proptosis resulting in incomplete lid closure → chronically exposed cornea → corneal ulceration & exposure keratopathy  optic neuropathy • affects 5% of pts • compression of ON or its blood supply by congested (enlarged) EOMs • can lead to severe, permanent visual impairment • rx with steroids, surgery if needed
  106. 106. Toxic/Nutritional Optic Neuropathies nutritional deficiencies alcohol-tobacco amblyopia
  107. 107. Nutritional Deficiencies pts with extremely poor diets, often in association with alcohol-tobacco amblyopia usually due to B12 deficiency in combination with cyanide toxicity symmetrical VF loss if early, can be treated with high-dose vitamins and restoration of « well-balanced diet » eventually leads to optic atrophy and permanent vision loss
  108. 108. Alcohol-Tobacco Amblyopia affects heavy drinkers, cigar and pipe smokers: deficient in protein and the B vitamins symptoms: insidious, bilateral, progressive visual impairment + dyschromatopsia signs: symmetrical VF defect, may have pale (or normal) discs rx: 1000 units of hydroxocobalamin qweekly X 10 wks + multivitamins + « well-balanced diet » px:  good in early cases if comply with rx  advanced cases: optic atrophy and permanent visual loss
  109. 109. Optic Chiasm Lesions - pituitary adenoma
  110. 110. Pituitary Adenoma presentation usually in early adult life or middle age symptoms:  h/a  visual symptoms: very gradual onset (often not noticed by pt until very well-established) • VF defect: usually, bitemporal hemianopia, worst in the superior field, and extending inferiorly • colour desaturation across vertical midline • optic atrophy: in 50% of cases with field defects caused by pituitary lesions
  111. 111. Pituitary Adenoma investigations:  MRI: coronal, axial and sagittal sections before and after gadolinium injection  CT: demonstrates enlargement or erosion of the sella  endocrinological investigation: PRL, FSH, TSH, GH
  112. 112. Pituitary Adenoma treatment options:  observation  medical: dopamine agonists (bromocriptine)  surgery  radiotherapy: often used as an adjunct  gamma knife stereotactic radiotherapy
  113. 113. Visual Field Defects
  114. 114. Merci