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ACUTE VISUAL LOSS
Fadzlina Zabri
082013100006
ACUTE VISUAL LOSS
Central retinal artery
occlusion
Ischaemic central retinal
vein occlusion
Retinal detachment involving
macular area
Massive vitreous hemorrhage
Painless
Acute congestive glaucoma
Acute iridocyclitis
Chemical injuries to the
eyeball
Mechanical injuries to the
eyeball
Painful
PAINLESS
Central retinal artery occlusion
Obstruction at the level of lamina cribrosa
Profound visual loss will become permanent
within hours
Symptoms
Sudden painless
loss of vision over secs
Amaurosis fugax history
in past
Signs
– Visual acuity reduced
– Direct pupillary reflex absent
– Fundus examination shows :
marked narrowing of retinal arteries
retina become milky white due to ischaemic edema
 ‘cherry red spot’ in center of macula
cattle tracking
atrophic changes
Treatment
Immediate lowering of IOP
Ocular massage, IV mannitol
Anterior chamber paracentesis
IV acetazolamide 500mg
Vasodilators and inhalation of a mixture of 5% CO2 and 95% O2
Fibrinolytic therapy
IV Steroids – giant cell arteritis
Laser photodisruption
Work up associated systemic condition
Central retinal vein occlusion
– 10 times more
common than CRAO
– Painless monocular
loss of vision over
hours to days
– Affect elderly patient
– Vision may improve
through the day
– Ischemic vs. non-
ischemic types
Non ischemic CRVO ( venous stasis retinopathy)
– Mild to moderate visual loss
– RAPD absent
– Fewer flamed shape hemorrhage
– May resolve fully or progress to ischemic type
Ischemic CRVO (hemorrhagic)
– Severe visual loss
– RAPD+
– Extensive retinal hemorrhage
and cotton-wool spots
– Reduced amplitude of B-wave
of ERG
– Complication
Rubeosis iridis, neovascular
glaucoma
Treatment
Systemic and ocular associations
Observation and monitoring
Ocular therapy
Intravitreal anti VEGF
Intravitreal triamcinolone
Pars plana vitrectomy
Three –port 20 gauze pars plana vitectomy
Risk Factors
Severe myopia (eg. –12 to –15)
Advanced age
Previous cataract surgery
Blunt trauma
Family history
Separation of
neurosensory retina
proper from pigment
epithelium
Retinal detachment
Prodromal symptom
– Dark spots - floater
– Sensation of flashes of light – Photopsia
Symptoms of detached retina
– Localised relative loss in the field of vision
– Sudden appearance of dark cloud or veil
– Sudden painless loss of vision
DD of Photopsia
scintillating scotoma of migraine, vitreous detachment, retinal tear, and
retinal detachment.
Complication
Proliferative vitreoretinopathy
Complicated cataract
Uveitis
Phtisis bulbi
Treatment
Sealing of retinal breaks
Drainage of SRF
Maintenance of chorioretinal apposition
scleral buckling
pneumatic retinopexy
pars plana vitrectomy, internal tamponade
Prophylactic
– Occur from retinal vessels
– Present as preretinal or intragel hemorrhage
– Symptoms
• Floaters of a sudden onset
in small hemorrhage
• Sudden painless vision loss
in massive
Massive vitreous hemorrhage
Signs
Fate
– Complete absorption within 4-8 weeks
– Organization of hemorhage with yellowish – white
debris
– Complications – liquefaction, degeneration, khaki cell
glaucoma
– Retinitis proliferans
Treatment
– Conservative treatment
– Treatment of the cause
– Vitrectomy by pars plana route
PAINFUL
– Characterized by a sudden rise in IOP in a
susceptible individual with a dilated pupil,
which decompensates the cornea
– Apposition of peripheral iris against the
trabecular meshwork resulting in obstruction
of aqueous outflow by closure of an already
narrow angle of the anterior chamber
Acute congestive glaucoma
Signs
– Corneal haziness
& edema
– Conjunctival hyperemia
– Pupil mid-dilated and
fixed
– Iris bowed (bombe’)
forward
– Swollen lids
– Eyeball firm to palpation
Treatment
Initial treatment
Systemic hyperosmotic agent: IV mannitol or Acetazolamide
Topical antiglaucoma : timolol, betaxolol 0.5%, latanoprost,
pilocarpine 2% QID
Analgesics and antiemetic
Compressive gonioscopy
Topical steroid eye drops
Definitive treatment
Laser peripheral iridotomy
Filtration surgery
Clear lens extraction
Inflammation of uveal tissue from iris and pars
plicata part of ciliary body
Acute iridocyclitis
Symptoms
Pain. Dull aching throbbing
sensation typically worse at night.
Redness.
Photophobia and blepharospasm
Lacrimation
Defective vision.
Signs
By slit lamp biomicroscope
Lid edema
Circumcorneal congestion
Corneal edema, KP’s, posterior corneal
opacity
Anterior chamber signs – cells and flares,
hypopyon
Iris sign – nodules, poterior synechiae
Pupillary signs
Changes in lens
Treatment
Local therapy
Mydriatic-cycloplegia drug
Corticosteroids
Broad spectrum antibiotic
Systemic therapy
Corticosteroids
NSAIDS
Physical measures
Hot fomentation
Dark goggles
Mode of
injury
Domestic accident –
ammonia,
detergent, cosmetic
Agricultural accident
– fertilizer, veg toxin,
insecticide
Chemical laboratory
accident - acid ,
alkali
Deliberate chemical
attack – acid to
disfigure face
Chemical warfare
Self injury -
malingere ,
psycopath
Chemical injuries to the eyeball
Alkali burns
– Most severe chemical
injuries known to the
ophthalmologists.
– Common alkalies
responsible for burns
are: lime, caustic
potash or caustic soda
and liquid ammonia
(most harmful).
Clinical feature in stages
• Conjuntiva – edema, congested, widespread
necrosis, copius discharge
• Cornea – epithelium sloughing, edema
• Iris – violently inflamed, replaced by
granulation tissue
Acute ischemic
attack
• Epithelium regenerates
• Corneal vascularuzation, inflammation
of iris reduced
Reparation
• Symblepharon, recurrent corneal
ulceration, complicated cataract,
secondary glaucoma
Complication
Acid burns
– Less serious than alkali
burns
– Common acids :
sulphuric acid,
hydrochloric acid, nitric
acid
– Causes instant
coagulation of proteins,
act as barrier for deeper
penetrations
Conjunctica will undergo necrosis.
Symblepharon is formed due to
fibrosis
Treatment
Prevent further damage
Immediate irrigation with clean water or normal saline
Removal of contaminated and necrotic tissue
Maintenance
Topical antibiotic drops and Steroid eye drop
Cycloplegic
Ascorbic acid : improve wound healiing, collagen formation
Lubricant eyedrop
Treating Complication
Glaucoma : topical timolol, oral acetazolamide
Poor corneal healing : amniotic membrane transplant
Symblepharon : surgical treatment
– Extraocular foreign
bodies
– Blunt trauma
– Open globe injuries -
Penetrating and
perforating, intraocular
foreign injuries
Mechanical injuries to the eyeball
References
Comprehensive opthalmology , 6th edition by
AK Khurana
Internet

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Acute visual loss

  • 1. ACUTE VISUAL LOSS Fadzlina Zabri 082013100006
  • 2.
  • 3. ACUTE VISUAL LOSS Central retinal artery occlusion Ischaemic central retinal vein occlusion Retinal detachment involving macular area Massive vitreous hemorrhage Painless Acute congestive glaucoma Acute iridocyclitis Chemical injuries to the eyeball Mechanical injuries to the eyeball Painful
  • 5. Central retinal artery occlusion Obstruction at the level of lamina cribrosa Profound visual loss will become permanent within hours Symptoms Sudden painless loss of vision over secs Amaurosis fugax history in past
  • 6. Signs – Visual acuity reduced – Direct pupillary reflex absent – Fundus examination shows : marked narrowing of retinal arteries retina become milky white due to ischaemic edema  ‘cherry red spot’ in center of macula cattle tracking atrophic changes
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  • 8. Treatment Immediate lowering of IOP Ocular massage, IV mannitol Anterior chamber paracentesis IV acetazolamide 500mg Vasodilators and inhalation of a mixture of 5% CO2 and 95% O2 Fibrinolytic therapy IV Steroids – giant cell arteritis Laser photodisruption Work up associated systemic condition
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  • 10. Central retinal vein occlusion – 10 times more common than CRAO – Painless monocular loss of vision over hours to days – Affect elderly patient – Vision may improve through the day – Ischemic vs. non- ischemic types
  • 11. Non ischemic CRVO ( venous stasis retinopathy) – Mild to moderate visual loss – RAPD absent – Fewer flamed shape hemorrhage – May resolve fully or progress to ischemic type
  • 12. Ischemic CRVO (hemorrhagic) – Severe visual loss – RAPD+ – Extensive retinal hemorrhage and cotton-wool spots – Reduced amplitude of B-wave of ERG – Complication Rubeosis iridis, neovascular glaucoma
  • 13. Treatment Systemic and ocular associations Observation and monitoring Ocular therapy Intravitreal anti VEGF Intravitreal triamcinolone Pars plana vitrectomy
  • 14. Three –port 20 gauze pars plana vitectomy
  • 15. Risk Factors Severe myopia (eg. –12 to –15) Advanced age Previous cataract surgery Blunt trauma Family history Separation of neurosensory retina proper from pigment epithelium Retinal detachment
  • 16. Prodromal symptom – Dark spots - floater – Sensation of flashes of light – Photopsia Symptoms of detached retina – Localised relative loss in the field of vision – Sudden appearance of dark cloud or veil – Sudden painless loss of vision DD of Photopsia scintillating scotoma of migraine, vitreous detachment, retinal tear, and retinal detachment.
  • 18. Treatment Sealing of retinal breaks Drainage of SRF Maintenance of chorioretinal apposition scleral buckling pneumatic retinopexy pars plana vitrectomy, internal tamponade Prophylactic
  • 19. – Occur from retinal vessels – Present as preretinal or intragel hemorrhage – Symptoms • Floaters of a sudden onset in small hemorrhage • Sudden painless vision loss in massive Massive vitreous hemorrhage
  • 20. Signs
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  • 23. Fate – Complete absorption within 4-8 weeks – Organization of hemorhage with yellowish – white debris – Complications – liquefaction, degeneration, khaki cell glaucoma – Retinitis proliferans Treatment – Conservative treatment – Treatment of the cause – Vitrectomy by pars plana route
  • 25. – Characterized by a sudden rise in IOP in a susceptible individual with a dilated pupil, which decompensates the cornea – Apposition of peripheral iris against the trabecular meshwork resulting in obstruction of aqueous outflow by closure of an already narrow angle of the anterior chamber Acute congestive glaucoma
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  • 28. Signs – Corneal haziness & edema – Conjunctival hyperemia – Pupil mid-dilated and fixed – Iris bowed (bombe’) forward – Swollen lids – Eyeball firm to palpation
  • 29. Treatment Initial treatment Systemic hyperosmotic agent: IV mannitol or Acetazolamide Topical antiglaucoma : timolol, betaxolol 0.5%, latanoprost, pilocarpine 2% QID Analgesics and antiemetic Compressive gonioscopy Topical steroid eye drops Definitive treatment Laser peripheral iridotomy Filtration surgery Clear lens extraction
  • 30. Inflammation of uveal tissue from iris and pars plicata part of ciliary body Acute iridocyclitis Symptoms Pain. Dull aching throbbing sensation typically worse at night. Redness. Photophobia and blepharospasm Lacrimation Defective vision.
  • 31. Signs By slit lamp biomicroscope Lid edema Circumcorneal congestion Corneal edema, KP’s, posterior corneal opacity Anterior chamber signs – cells and flares, hypopyon Iris sign – nodules, poterior synechiae Pupillary signs Changes in lens
  • 32. Treatment Local therapy Mydriatic-cycloplegia drug Corticosteroids Broad spectrum antibiotic Systemic therapy Corticosteroids NSAIDS Physical measures Hot fomentation Dark goggles
  • 33. Mode of injury Domestic accident – ammonia, detergent, cosmetic Agricultural accident – fertilizer, veg toxin, insecticide Chemical laboratory accident - acid , alkali Deliberate chemical attack – acid to disfigure face Chemical warfare Self injury - malingere , psycopath Chemical injuries to the eyeball
  • 34. Alkali burns – Most severe chemical injuries known to the ophthalmologists. – Common alkalies responsible for burns are: lime, caustic potash or caustic soda and liquid ammonia (most harmful).
  • 35. Clinical feature in stages • Conjuntiva – edema, congested, widespread necrosis, copius discharge • Cornea – epithelium sloughing, edema • Iris – violently inflamed, replaced by granulation tissue Acute ischemic attack • Epithelium regenerates • Corneal vascularuzation, inflammation of iris reduced Reparation • Symblepharon, recurrent corneal ulceration, complicated cataract, secondary glaucoma Complication
  • 36. Acid burns – Less serious than alkali burns – Common acids : sulphuric acid, hydrochloric acid, nitric acid – Causes instant coagulation of proteins, act as barrier for deeper penetrations Conjunctica will undergo necrosis. Symblepharon is formed due to fibrosis
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  • 38. Treatment Prevent further damage Immediate irrigation with clean water or normal saline Removal of contaminated and necrotic tissue Maintenance Topical antibiotic drops and Steroid eye drop Cycloplegic Ascorbic acid : improve wound healiing, collagen formation Lubricant eyedrop Treating Complication Glaucoma : topical timolol, oral acetazolamide Poor corneal healing : amniotic membrane transplant Symblepharon : surgical treatment
  • 39. – Extraocular foreign bodies – Blunt trauma – Open globe injuries - Penetrating and perforating, intraocular foreign injuries Mechanical injuries to the eyeball
  • 40.
  • 41. References Comprehensive opthalmology , 6th edition by AK Khurana Internet

Editor's Notes

  1. Etiology –Emboli, Atherosclerosis-related thrombosis, Retinal arteritis with obliteration, Angiospasm, Raised IOP, Others Amaurosis fugax-  painless temporary loss of vision in one or both eyes.
  2. Retina infarction => pallor, edema, less transparency. Irreversible damage begins at 90 mins Cherry red spot may take 24 h to develop. Visual acuity may be normal if cilioretinal vessel patent
  3. Reduce iop- may aid in aretrial perfusion, help the dislodging embolus Ocular massage (Firm steady pressure x 15 seconds, release, repeat)
  4. Anterior chamber paracentesis Administer local anesthesia Use a 30-gauge needle on a tuberculin syringe Enter the eye at the limbus with bevel up Ensure that the needle does not damage the lens Withdraw fluid until the anterior chamber shallows slightly (0.1-0.2 cc) Administer a topical antibiotic post-procedure
  5. More common than artery occlusion, in elderly
  6. Dd – diabetic retinopathy is bilateral, crvo is unilateral ocular ischemic syndrome . Has dilated veins but not tortous, retinal hemorrhage in periphery
  7. Medical follow-up to screen for atherosclerosis and other risk factors Ophthalmology assessment to follow for late complications (~ 3 mos)
  8. Pars plan is a flat extension of the posterior aspect of the ciliary body 3 port- 3 incision - cutting and aspiration - illumination - infusion
  9. Metamorphopsia , floaters, curtain
  10. Prophylactic- highly indicated for high risk pt- myopia, aphakia, retinal detachment in the fellow eye
  11. RP may be complicated by tractional retinal detachment (PPV) is a surgical procedure that involves removal of vitreous gel from the eye. The procedure derives it name from the fact that vitreous is removed (i.e. vitreous + ectomy = removal of vitreous) and the instruments are introduced into the eye through the pars plana
  12. ** May mimic migraine, heart, or GI disease because of systemic complaints
  13. Defective vision – due to Induced myopia causing ciliary spasm Corneal haze Aqueos turbidity Pupillary block due to exudates Complicated cataract Viterous haze 2ry glaucoma