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Pearls of ophthalmology

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lecture notes of Sir Idrees
addition of pictures for comprehensive understanding

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Pearls of ophthalmology

  1. 1. Instructor Dr. Idrees sb Prep by: Abdul Wasay Baloch abdulwasay789@gmail.com OPHTALMOLOGY
  2. 2. Vision System Units “Curiosity is gluttony. To see is to devour.” ― Victor Hugo, Les Misérables
  3. 3.  Unit 1 - Protection :  Orbital Rim  Eye lids  Lacrimal glands  Unit 2 – Transmission of Light  Media  Cornea  Iris  Sclera  Pupil  Lens  Unit 3 – transformation of light  Macula – have only cones, fine vision  Rods – periphery of reitna , crude vision
  4. 4.  Unit 4 – axons or nerve fibers  1 million axons in one retina  Optic pathway  Unit 5 – transformation  Takes place in visual cortex, Temporal region
  5. 5. Basic Concept
  6. 6. Refraction
  7. 7. Convergence  FACTORS:  80% - Cornea  20% - lens taking constant  Length of eye ball  Refraction Errors: 1) Myopia 2) Hypermetropia 3) Astigmatism 4) Presbyopia
  8. 8. Myopia  Rays fall short of Retina  Cornea more convex  Length of eyeball increase  Big eye  Disadvantages:  More chances of Retinal Detachment  Treatment:  Concave lens
  9. 9. Hypermetropia  Small eyeball  Converging beyond the retina  Eye ball length may be decreased  Cornea less convex  Convex lens used for treatment  More chances of Acute Narrow Angle Glaucoma
  10. 10. Astigmatism  Irregularity of eyeball  Cornea is irregularly irregular  Spherical lens may be used  Cylinderical no applied having Axis
  11. 11. Presbyopia  Loss of accommodation with age  Usually above 40  Accommodation + convergence problems  Ciliary body contracts and lens relaxed  Ciliary body relaxes, zonules contracts – lens become convex  Degeneration of ciliary body, zonules cause loss of accommodation  Need of convex lens  Treatment:  Glasses  Contact Lens  Laser Treatment
  12. 12.  Excimer Laser  Applied on Stroma  LASIK:  Cornea slicing  IOL implantation VISION  Uncorrected  Corrected  Pin hole
  13. 13. Lacrimal Apparatus
  14. 14.  Lacrimal gland – 90 %  Accessory glands – 10 %  Secretions may increase – wet eye  Secretions may decrease – dry eye  Causes  Congenital – underdeveloped drainage system. Self corrected  Old age  Any cause of irritation of eye – rubbing, infection, allergy
  15. 15. Congenital Causes  Appears during first 6 months of life  Under developed  Massaging the duct 2-3 times  Treatment:  Recurrent infection of sack obstruction flow hinders. In case of bacterial infection, Mucoprulent discharge. Regurgitation test is positive  Treat actively  Treat the cause
  16. 16. Old Age  Stenosis  Hardening of walls, Puncta and canalculi  Entropian – lids inward, Puncta is displaced  Clinical Feature  Blurring of vision  Chances of infection  Discomfort  Treatment:  Massage  Regurgitation for minor block  Puncta dilating  Dacryocystogram – dye injecting – x ray
  17. 17.  Treatment:  DCR (Dacrycysto Renotomy)  Artificial passage at sac level, fluid is direct to middle meatus
  18. 18. Dry Eye  Congential problems  Age related – secretion decrease  More common in females  Con tissue disorders Rheumatic dis, SLE  Chemical injuries  Dry eye – infection –  Bells phenomenon  Eye ball rubbing against upper eyelid – corneal ulcer – refraction problems – pain – irritation  Treatment:  Artificial tears  Blockage of Puncta
  19. 19.  Conjectival grafting  Avoiding dry atmosphere  Humidifier  Avoiding direct under fan
  20. 20. Dacryocystitis  Blockage of Lacrimal sac  Old age  Medial canthus swelling  Pain redness and tenderness  Regurgitation tes is positive  Complication  Infection  Cellulitis  Osteomyelitis  Treatment  Antibiotics  Removal of sac
  21. 21. Cataract
  22. 22.  Age related changes  Opacificaition of Lens  Congenital  Maternal disease  Trauma  Presentation:  Gradual decrease of vision  In children, white Pupillary Reflex (also RETINOBLASTOMA, Squint)  Pathogenesis:  Lens dehydration  Normally avascular  Media opacified due to metabolic disorders •Young cataract •Trauma •Steriods •Diabettes •Hypoparathyroidism
  23. 23.  Treatment  Phacoemulsification with lens implant  Complication may be  Hydration due to rupture of endothelium  Rupture of post capsule with nucleus drop  Infection  Extracapsular Lens extraction  Manual compression and aspiration  Incision large  Heal time 2-6 months  Delayed recovery  Astigmatism  Trauma to Iris  LASER
  24. 24. LIDS
  25. 25. Diseases  Ptosis  Entropian  Ectropian  Swelling of lids  Stye  Chalazion  Tumor – BCC , SCC  Blephritis
  26. 26. Swelling of Lids
  27. 27. Stye  Inflammation on the margin of lid  Inflammation of hair follicle and Zeils Glands  Staph, strep, Pneumococci are responsible  Painful swelling  May press cornea – Astigmatism  Palpebral part of conjunctiva is red  Treatment  Medical – pain killer, anti inflammatory, antibiotics, warm compression, Hot Spoon or towel • Excision after local anesthesia
  28. 28. Chalazion  Inflammation of Mobean gland  Swelling is usually not on lid margin  Non tender  Treatment:  Localized sterilized injection  Incision is vertical, half thickness after everting lid  Not extending upto lid margin  Scooping out
  29. 29. Tumors  BCC  Sun exposed areas  Abnormal growth - ulcer , non healing – bleeding  Localized or may be spread  Treatment surgically  Excision  Radiation
  30. 30. Entropian  Usually of lower lid  Cause :  Congenital  Trachoma  Old age  Trauma  Space occupying lesion  Adhesion of palperbral and Bulbar conjunctiva  Chemical injury  Mechanism  Imbalance between orbicularis occuli
  31. 31. PTOSIS
  32. 32.  Drooping of upper eye lid  Due to orbicularis occuli (closure of eye)  Or Levator Palpebral (open the eyelid)  Balance disturbed – Ptosis occur  Cause  Weakness of muscle  Nerve supply disturb  Old age  Trauma  Sympathetic problems – Horner syndrome  3rd nerve Palsy  Myasthenia Gravis  Squint •Features •In children •Vision problem •Cosmetic defect
  33. 33.  Treatment:  Treat the cause  Medical – Botox injection(3-6 months)  Surgical – treated with replacement of fascia lata  Moderate resection – shortening of muscle •Test : •Ruler test above 6mm normal •Finger on frontalis muscle
  34. 34.  Problems:  Exposure of conjunctiva – exposure Keratitis, ulceration, infection  Cosmetic disfigurement  Watery eyes  Treatment :  Essentially surgical  Cauterizing on palperbral Conjuvtiva of mild Entropian
  35. 35. Blephritis  Dandruff cause  Mobean gland dysfunction MGD  Skin abonrmality – dryess – scales  Redness  Deposits onscales  Droping of scales into eyelids  Irritation of eye  Treatment:  Lid hygiene - clean with Na2CO3  Antibiotics oinment  Warm compression  Doxycycline for 3-6 months
  36. 36. RED EYE
  37. 37. Conjunctivitis  Conjuvtiva is red  Causes  Viral - adenovirus  Bacterial – staph , strep  Allergic  Adenovirus  No defect in epithelium (flouroscent stain)  Opacities on cornea ( Sick Epi – Rose bangol stain) •Features •No pain •No vision loss •Redness more on palperbral part •Discomfort due to chemosis
  38. 38. Keratitis (Bacterial & Fungal)  Cause:  Trauma – epithelium breach – entry – infection  Fungal – vegetative injury  Features  Sensory nerve endings below epithelium – painful  Cicumcorneal congestion – limbal area  Treatment  Scrapping after local anaesthesia  Complication :  Infection – abscess  Corneal scarring  Perforation of cornea  Spread of infection to ant chamber – hypopean  Endophthalmitis •Hyphema : •Blood in anterior chamber •Blunt trauma •Bleeding disorders •Anticoagulants •Trauma •INR monitoring •Rest for five days – heal •Always examine the FUNDUS •Check IOP •Dialtion of pupil – rest •Steriods •Reexamine
  39. 39. Herpes simplex H. Zoster  Big dendritic patterns  Cold sore of eye  Attack nerve  Red eye  Opacity on cornea  Fluorescent takes  Episcleritic scleritis may be caused  Treat by Acylovior  Loss of sensation of cornea  Small dendritic patterns  Hemi headache, hemi forehead  Vesicles – rash – papule – ulcer  Shingles  Numbness  Pain  Can involve any part of eye
  40. 40.  Sterile Corneal Ulcer:  No involvement of org  Breach of epithelium  Treatment:  Antibiotic drops – prophylactic  Lubricants  Pain killers  Interstitial Keratitis  Notorious syphillis  Classical scaring  Saddle shape nose
  41. 41. Keratoconus  Cone shaped cornea  10 -30 year  Cause:  Cogential weakness of cornea at that place  Aqous pressure rise  Asthama or allergy association  Consequences  Astigmatism  Perforation  Treatment  Glasses  Hard contact lens  Corneal ring with laser  Corneal graft •Complications •Acute hydrops •Perforation •Prevention •Avoid contact sports
  42. 42. Trachoma
  43. 43.  Leading cause of death  In between bacterial and viral  Due to unhygienic conditions  Pathology :  New blood vessel formation  And scarring  Limited to upper part of palpebral part of conjunctiva and cornea  Also cause Entropian of upper eyelid – eyelids rub and cause corneal ulcer  Also cause pits called HERBET PITS  Treatment :  Self limited  Erythomycin 1g state, repeat after six months  Tetracycline  3rg generation antibiotics  Entropian – surgical treatment  Scarring – corneal graft
  44. 44. PTERIGIUM
  45. 45.  Abnormal growth of fibrovascular tissue  Growth towards cornea  Commonly from Nose side  Hot climate  Dust climate  Sandy climate  Disadvantages:  Corneal pull – astigmatism  Pupillary area – vision problem  Treatment :  Surgical treatment  Excision with Mitomycin on limbal area  Excision with conjunvtival grafting
  46. 46. Corneal graft  Removal of cornea and replaced with donor • Full thickness graft • Partial thickness graft • Test for donor: • Jacob test • Blood sample • Indication : • Scarring • Trachoma • Trauma • Abscess • Pterigium • Massive endothelial damage • Post cataract surgery
  47. 47. UVEITIS
  48. 48.  Uveal tissue  Most vascular part of eye  Nutrition  Systemic diseases effects  Common inflammation  Infection  Non infective – ankylsing spondyloisosis, HLA  Features  Red eye (congestion more Bulbar part of conjunctiva), Painful, Vision disturbed  Causes:  Corneal problems  Uveitis  Acute glaucomma Cicumcorneal Congestion
  49. 49.  Examination  Vision  Redness  Corneal clarity  Pupil may be irregular or small, stick to lens POST Psynechia  Anterior chamber contain Iris cells that mat stick to endothelium of cornea – Keratopreicipitates  Cells visible on slit lamp – Flares  White grayish patches on retina along with blood vessels – Periphlebitis  Fluid oozes out from choroid into macula – Macular edema  Optic nerve inflammation  Retina may also have patches  Vitrous turbid
  50. 50.  Causes  Any systemic infection, MS, T.B, Sarcoidosis, septecemia  Treated acc to cause  NON infective – steriods, cytotoxic drugs  INFECTIVE – treat the infection  Complication  Long standing – cataract  Glaucoma  Retinal detachment  Macular edema  Optic nerve dysfunction
  51. 51. Iritis / Uveitis  In acute glaucoma  Perforation of gloe  Corneal propalsion  Penetrating injury  History  Viral (adenovirus)– watery discharge, glands usually involed
  52. 52. Scleritis and Episclretis  Localized and diffused infection  Clinical Feature  Pain  Vision affected  May have systemic assosiation , Autoimmune disorders, Con tissue disorders ( ESR and CRP tests)  Hemiheadache  Nausea vomitting  DD – migraine
  53. 53. Glaucoma
  54. 54.  Types 1. Congenital 2. Closed angle glaucoma 3. Chronic open angle glaucoma 4. Secondary glaucoma  Pathogenesis  Ciliary body – lens – pupil – ant chamber – meshwork – canals of Shemn – episcleral vein  Angle between Iris and Cornea  Normal pressure is 10 – 20 mmHg, varies with age  Above 40 considered high
  55. 55. Congenital Glaucoma  Trabecular meshwork or canals of shlemn not developed  Agenesis , disgenesis, fluid drain problem – pressure – BUPHTHALMOS  Due to elasticity – Big eye  Corneal fluid – hazy cornea  Refraction problem  Squint  Diagnosis  EUA  Check IOP  Refraction  Complete examination of eye including Optic Disc
  56. 56.  Treatment  Medical  Antiglaucoma drops Dimox and Acetazolamide  Surgical  Modified trabeculectomy – placement of tube in ant chamber  Prognosis  Not very good
  57. 57. Narrow Angle Glaucoma  Angle narrow or closed  Fluid obstruct  Back pressure buily  Precipitating factor is CATARACT  Small hypermetric eye  Middle to lat age presentation  Subacute attacks when pupil is Dilated  Hallows around the vision in Evening  Colorful vision  Hydration of cornea  Goneoscopy – examining lens of ant chamber , Gonolens
  58. 58.  Treatment  Peripheral iriodotomy  Methods  Yag Laser  Making hole at limbal region  Clinical features at extreme conditons  Red  Pain assosiated with nausea vomitting  Pupil semidialted fixed  Cataract may be present  In acute attack, Nerve fibers may damage causing blindness in a day
  59. 59. Treatment of Acute Attack  Maxillon inj for nusea  Acetazolamide 500 mg iv  Antiglaucoma drops Pilocarpine 4%  Beta blockerrs  Steriod drops – reducing swelling and congestion  Ultimate peripheral Iridotomy  And cataract surger ( precipitating factor)
  60. 60. Chronic Open Angle Glaucoma  Resistance at trabeculated meshwork  Slowly progress,  Age 20 30 and old age  Pressure increase  Increase Blood Supply of axon  Pressure on axon  patient does not complaint unless get worsen in 60’s  Peripheral patchy field defect  Tunnel vision at end stage (also in Retina pigmentosum  Quality of vision loss  Screening program detection ususally •White Pupillary reflex •Cataract •Retinoblastoma •Retinopathy
  61. 61. diagnosis  Screening program  IOP pilination Tononmeter  Examination of optic nerve  Check the field of vision  Perimetery  OCT of optic nerve  Nerve fiber analysis NFA  Family history of Diabettes  Diabetes  Hypertension  Glaucoma  Cholesterol increase Normal Tension Glaucoma •Pressure is normal •Any pressure damaging nerve of eye •Occular hyper discc
  62. 62. SQUINT
  63. 63.  Misalignment of two eye  Types  Paralytic ( CN 3 , 4, 6)  4th nerve damage – diagnosed by Head Tilt, Head Trauma  6th nerve – lateral rectus paralysed – inward eye  3rd and 6th are caused by old age, Diabetes, Hypertension and increase Cholestremia  Non paralytic  Investigations  Assessment  Causes  Clinical Feature  Ptosis  Outward or inward eye  Disfigurement  Double Vision due non fusion of both images in visual cortex •Aneurysm of PCA •Ptosis •3rd CN paralysis •Dilatation of pupil •painful
  64. 64.  Treatment  Blockage of bad eye  Counseling to the patient  Recovery is 6 weeks to 3 months  Prolong one vision cause supression of bad eye  Field of vision loss  Diagnosis  2 feet examination  Eye movements  Botulin toxin in antagonist eye  Accommodating and Non accommodating squint  Squint goes away when covering the bad eye  Partial – half eye corrected •Monocular and Binocular •Steropsis •Depth of perception •3D imaging
  65. 65. Non Accommodating Squint  Eye movements are not restricted  Common in children  Inward turning of eye – ESO  Tropia – when squint is always there  Phoria – when squint is sometime present  Causes  Refractive errors  Ptosis  Cataract  Clinical features  Focus problem  Vision reduced
  66. 66.  Amblyopic eye – eye sight is normal but eye is tilt  Squint  In children – hypermetropia and ESO deviation  Examination  Preferential looking test  100 and 1000 test  Refraction  K test  Complete examination of eye including fundus  Torch corneal reflex  Two feet examination  Cover uncover test  Alternate test  Prism Cover Test  synaptophore
  67. 67. Summary – Check List Examination  Refraction  Visual acquity  Check vision  Two feet examination and eye movements  Pupillary reflex  Coves uncover test  Prism cover test  Synatophore  Stereopsis •Ptosis complete •Corneal examination •Pupil reflex •Refraction •Cataract •Media for opacification •Retina examination •EUA for kids
  68. 68. Management  Cosmetic and vision problem  Treat the cause  Refractive error  Ptosis  Corneal scarring  Cataract  Any congenital problem  Use glasses  Treat cataract  Corneal grafting  Emblopic Therapy : for certain day of time, Patch the good eye dilate the good eye Surgical treatment Recession of eye – weakening of muscle Resection – strongthe muscle
  69. 69. Retinal Detachment
  70. 70.  Retina is separated from Choroid  Pigment epithelium remain attached  Due to Fluid Push or Myopia  Types  Rigmatogenous – tear or hole, common in myopes  Non Rigmatogenous – in acute glaucoma, common in Hypermetropes
  71. 71. Rigmatogenous RD  In myopes – BIG EYE - retina thin – more chances  Trauma  Vitrous degeneration  Problems (3F)  Field defect of that area  Retina dead due to low nourishment  Loss of central vision  Vitrous degenerated into pieces – FLOATERS  Retina pull – FLASHES  Bleeding via pulling of vessel  Decreased vision  Treatment –  seal hole or tear, (CRYO and LASER)  Approximate the retina – drainage of fluid OR ( Plomb Or BUCCAL) •CRYOBUCCAL PROCEDURE •Freezing -200 probe •Scar •Approximate •Plomb and buccal •VITRECTOMY •ENDOLASER •GAS OR SILICON OIL
  72. 72. Non RG RD  Choroidal melanoma  Growth – pigmentation – ulceration – pain  Diabetic retinopathy  Usually upper temporal side defect and upper nasal  Treat the cause
  73. 73. Vascular Problems
  74. 74.  Retinal artery occlusion  Systemic  Diabetic retinopathy – ischemia – weak wall- pale – dead axon (cotton wool spots)  Retinal Vein occlusion – back pressure increase – fluid – edema  Hypertiension Retinopathy - pressure increased  New Blood vessel formation  Enothelial growth factors  New blood vessel formation  Fragile – tendency to bleed  Causes (inside wall – lumen reduced, Outside – mass occupying lesion)  Diabetes  Hypertension  Age factor  hypercholestrol
  75. 75. Sudden Artery Occlusion  Sudden loss of vision  Afferent Pupillary pathway defect  Clinical Features:  Pupil – Blue in centre  Vision loss depends on area affected  HM +ve – because cilioretinal branch of ophthalmic division is spared  Retina – Pale ischemic Retina, thin arteries  Cherry Red Spots  Macular thin, choroidal blood vessels glow  After sometime, disc becomes pale  See the clots in blood vessels  Investigation  Carotid Bruit  Scan pulse feeble  Heart murmur •Treatment •Lower the IOP •No treatment satisfactory •Aspirin •Treat cause •Prognosis poor
  76. 76. Hypertensive Retinopathy  Hyperemic swellen disc  Macular edema  Treatment  Treat the cause BP  Young hypertensive patien die due to Renal problems  Look for Renal problems
  77. 77. Diabetic Retinopathy  Treat the cause  Argon Laser ( Never do it on Macula and Disc)  Macular edema  New b.v formation  Intravitreal injection of endothelial growth factor inhibitor  Vitrectomy with endolaser  Vein Occlusion  Back pressure – bleeding – SECTORIAL FIELD DEFEC  Central field defect  Treat the occlusion
  78. 78.  Macular edema  Argon laser  Endothelial growth factor inhinitor  Antiplatelets  Screening of Diabetes  Macular edema  Heamorrhage  Vitrous bleed
  79. 79. Age Related Macular Degeneration  Types  Dry ARMD  Wear and tear, Choroidal macula  Wet ARMD  Exudation – fluid – bleeding –  Clinical Feature  Distorsion of vision  O pain or rednes  AMSLER CHART  Complete examination  Investigation  Optic Coherence Tomography (OCT)  Layaer by layer examination  Macular fluid – push – macular detachment  Fundus Flourosent Angiography FFA  Leading cause of blindness •BLINDING CAUSES macular detachemnt •COAG ARMD •DRP •Myopic degenration •Trachoma
  80. 80.  Treatment  Dry ARMD – no satisfactory treatment  Wet  Intravitreal growth factor inhibitor  Laser treatment  Prevention  Fresh green leafy vegetebles  Antioxidants  Multivitamin  UV light precuation
  81. 81. DISC
  82. 82.  Raise ICP – pupil edema  CSF incr  Head injury  Tumor  Cyst  Optic nerve pressure  Space occupying lesion  Choroditis  Uveitis  Optic nerve inflammation  Diabetes  DRUSEN – bolloid bodies  Venous occlusion Swelling of Disc
  83. 83. Retina pigmentosa  Night blindness  Genetic disease  Rod Cones decreased  Retina destruction  Features ( Classic Triad)  Waxy pale disc  Thin attenuated blood vessels  Bony specules (black pigment around retina)  Macular edema  Cataract  Tunnel vision ( also in COAG)  no satisfactory treatment  Marriage counseling  Steropic glasses
  84. 84. Retinoblastoma  Nerve tissue tumore  2-5 years age comon  White pupillary reflex  Squint , absent red reflex  Treatment  Complete removal of eyeball along with optic nerve  radiation and laser treatment at early stages  May spread to neural tissue  Optica chiasma
  85. 85. Orbital Cellulitis  Inflammation of cellular tissue  Souces  Chalazion clamp  Sinuses  An infection  Clinical features  Sweeling, tenderness and apin  Redness of eye ball  Painful eye movements  Treatment  Local oral antibiotics if eye ball not involved otherwise IV
  86. 86. Optic Nerve Function tests 1. Decreased vision 2. Decreased intensity of light 3. Decreased color vision 4. Field vision defects 5. Pupillary defect 1. Relative Afferent Pupil Defect
  87. 87. Thyrotoxis – squint  Exophthalmus  Inflammatory tissue in retro orbital space  Eye movements restricted LID LAG PHENOMENON  Inflammatory tissue may compress optic nerve - Blindness  IOP raised  Treatment  Treat the cause  Routine management  In emergency – iv steroids and Acetazolamide  Surgery – ORBITAL DECOMPRESSION 1. Lateral canthectomy 2. Medial floor canthotomy 3. Tear drops 4. Treat squint
  88. 88. Temporal Arteritis  Inflammatory cells affect medium and small sized arteries  Unknown etiology  Common in old age  Clinical feature  Jaw claudication  Tendeness on scalp  Retinal arteries blockage  Complication  Retinal artery occlusion  CN Palsy •ESR •TA •TB •MM •Autoimmune dis
  89. 89.  Diagnosis  CRP  ESR v. high  Temporal artery biopsy  Slide – lumen blac  Treatment  Steroids high doses
  90. 90. Melanoma  Pigment tumor  Iris may be involeved  Not Normal  Increase in size  Incr in growth  Incr in pain  Incr in ulceration  Accidental finding  Loss of vision  Complication  Locally invasive  Metastatise to liver
  91. 91.  Treatment  Local resection  Radiation – palque attack of laser  Cryo Laser
  92. 92. Central Serous Retinopathy  Usual age 30 to 40 years  Vision defect  Tense type personality  Blood vessels around macula – leak – fluid – blur vision – retina deachment – field defect  Self restoring about three months  Scarring  Recurrent conditions  Treatment not successful  Laser  IVGHI  Complication
  93. 93.  Complication  Scarring  Reoccurrence  Fundus fluorescent angiography
  94. 94. Sudden Loss of Vision  Vitrous haemorrhage  Diabetic retinopathy  Retinal detachment  Bitemporal hemianopia  Pituitary tumor  Nasal fibers representing temporal side after decussation
  95. 95. Headache  Temporal arteritis  PCA aneurysm  Occipital headache in young  Disc swelling – ICP rise – headache  Tumors  Binign –  Intracranial hypertension  Morning sickness  Management  MRI scan  acetazolamide
  96. 96. Nystagmus  Jerky movements of eyes  Constant vision  Visual pathway defect  Cataract may be one of cause
  97. 97. Investigation of eye
  98. 98.  Excimer Laser  Cornea refractive surgery  Argon Laser  Retinal problems – sealing  Glaucoma  Laser trabeculoplasty  YAG laser  For narrow angle glaucoma  Periperal ididectomy  Capluletomy – post  RUBIOSIS – blood vessels on Iris  Fundus Flurosent Angiography  Cornel topography for uneven cornea
  99. 99.  OCT  Diabetes  ARMD  Corneal ulcer  Fluorescent dye  Rosebangol for sick epithelium  Pupillary reaction  ERG electroretinography  EOG – electro occular gram  Field defect test  Nerve Fiber analysis  Ophtalmoscope  Direct  Indirect – using lens
  100. 100.  Refraction  Comp auto ref  Retinoscope  Scans  Alpha scan – length of eye ball  B scans – retina state observe  Cataract power of Lens  Keratometer  A scan

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