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
7.
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
9.
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
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
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
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.
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).
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
37.
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
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.
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
Reduce iop- may aid in aretrial perfusion, help the dislodging embolus
Ocular massage (Firm steady pressure x 15 seconds, release, repeat)
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
More common than artery occlusion, in elderly
Dd – diabetic retinopathy is bilateral, crvo is unilateral
ocular ischemic syndrome . Has dilated veins but not tortous, retinal hemorrhage in periphery
Medical follow-up to screen for atherosclerosis and other risk factors
Ophthalmology assessment to follow for late complications (~ 3 mos)
Pars plan is a flat extension of the posterior aspect of the ciliary body
3 port- 3 incision
- cutting and aspiration
- illumination
- infusion
Metamorphopsia , floaters, curtain
Prophylactic- highly indicated for high risk pt- myopia, aphakia, retinal detachment in the fellow eye
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
** May mimic migraine, heart, or GI disease because of systemic complaints
Defective vision – due to
Induced myopia causing ciliary spasm
Corneal haze
Aqueos turbidity
Pupillary block due to exudates
Complicated cataract
Viterous haze
2ry glaucoma