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Sudden Painless Loss Of Vision. By Minal G. Birambole. (internee) G.A.M &R.C, Shiroda,Goa. Sudden loss of vision is alarming to both the patient and the clinician alike.

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slide2
By

Minal G. Birambole.

(internee)

G.A.M &R.C,

Shiroda,Goa

slide4
Sudden loss of vision is alarming to both the patient and the clinician alike.
  • sudden & transient visual loss or obstruction may simply be a symptom of dry eye or may herald the onset of irreversible visual loss or stroke.
causes of sudden loss of vision
Causes of sudden loss of vision
  • Central Retinal artery occlusion
  • Vitreous hemorrhage
  • Retinal detachment
  • Central Retinal vein occlusion
  • Optic neuritis
  • Methyl alcohol amblypia
retinal artery occlusion
Retinal artery occlusion

Etiology-

  • more common in patients suffering from hypertension.
  • Thrombosis
  • Embolism
  • Retinal artritis
  • Angiospasm
central retinal artery occlusion
Central retinal artery occlusion

Clinical Features -

  • More common in male
  • Usually unilatral,rarely bilateral
  • It is due to obstruction at the level of lamina cribriosa.
slide8
Symptom –

Painless sudden loss of vision

slide9
Signs-
  • Direct pupilary reflex is absent.
  • Retinal artery markly narrow.
  • Retinal vein look normal.
  • Retina become milky white.
  • Chery red spot (central part of macular area)
  • Blood coloum is segmented.
branch retinal artery occlusion
branch retinal artery occlusion
  • Usually occurs following lodgment of embolus at bifercation.
  • Retina distal to occlusion become odematous.
  • Later on permanent sectorial visual field defect.
slide12
Management–

treatment is unsatisfactory as retinal tissue can’t survive ischemia more than few hours.

Emergency treatment-

  • Immediate lowering of intraocular pressure

by IV Mannitol

intermittent occular massage

paracentesis of anterior chamber

slide13
Vasodilator & inhalation of mixture of 5% carbon-di-oxide & 95% of water.

relive angiospasm

  • Anticoagulant
  • IV steroids
slide14
Complication-

neovascular glaucoma with incidence varying from 1% to 5%.

retinal vein occlusion
Retinal vein occlusion

Etiology -

  • More common than artery occlusion
  • Typically affects elderly patients in 6th or 7th decade in life
  • Pressure on the vein by sclerotic retinal artery
  • Hyperviscocity of blood as in polycythemia
  • Periphlebitis retinae(central or peripheral)
slide16
Raised intraocular pressure,more common in primary open angle glaucoma
  • Local cause-

orbital cellulitis

facial erysipelas

cavernous sinus thrombosis

central retinal vein occlusion
Central retinal vein occlusion
  • Non ischemic
  • most common clinical variety
  • Characterised by mild to moderate visual loss.

Fundus examination-

In early stage-

  • mild venous congesion
  • Tortusity
  • Few superficial flame shaped haemorrhage more in periphery than posterior.
slide18
Mild papillodema
  • Mild macular odema

In later stage-

  • Sheathing arround main vein
  • Few cilioretinal collatrals around disc
  • Retinal haemorrhage partly absorbed
  • Macula shows chronic cystoid odema.
slide19
Treatment-
  • Usually not required
  • Condition resolve with almost normal vision in about 50% cases.
  • No treatment is effective for chronic cystoid macular odema
  • Course of oral steroids 8-12 weeks may be effective.
slide20
Ischemic-

Refers to acute complete occlusion of central retinal vein

Characterised by marked Sudden loss of vision

slide21
Fundus examination-

in early stage-

  • Massive engorgement
  • Congestion
  • Tortusity of veins
  • Massive retinal haemorrhage
  • Papilloedema
  • Macular area oedematous
slide22
in later stage-
  • Sheathing around vein & collatrals seen around disc
  • Neovascularisation at disc
  • Macula-marked pigmentary change
  • Chronic cystoid oedema
difference between ischemic from non ischemic
Difference between ischemic from non ischemic
  • Presence of relative afferent pupillary defect
  • Visual field defect
  • Reduced amplitude of b-wave of ERG.
slide24
Complication-
  • Rubiosis iridis
  • Neovascular glaucoma in more than 50% cases within 3 months
  • Few develops vitreous hemorrhage
slide25
Treatment-
  • Panretinal photocoagulation
  • Cryo-application
  • Photocoagulation

Above is carried out when most of interretinal blood is absorbed.

branch retinal vein occlusion
Branch retinal vein occlusion
  • More common than central retinal vein occlusion
  • Occur at following site
  • main branch at disc margin
  • Major branch vein away from disc
  • At A-V crossing causing quadratic occlusion
  • Small macular occlusion
slide27
Occlusion oedema & haemorrhge are limited to area drain by affected vein.
  • Vision is affected when macular area is involve.
slide28
Treatment-
  • Grid photocoagulations-

in chronic macular odema

  • Scatterphotocoagulations-

in neovascularisation

vitreous haemorrhage
Vitreous haemorrhage

Usually occur from retinal vessels

Pre retinal intrageal

haemorrhage haemorrhage

slide30
Etiology-
  • Associated with PVD
  • Trauma to eye
  • Inflamatory disease like chorioretinitis,periphlebitis retinae
  • Vascular disoders like HTN retinopathy
  • Metabolic disease like DM retinopathy
  • Neoplasm
  • idiopathic
slide31
Clinical features-

Sign-

  • Distant direct opthalmoscopy-

black shadow against the red glow in small haemorrhage.

  • Direct & indirect opthalmoscopy-

presence of blood in vitreous cavity

  • Ultrasonography with B-scan-

it help in diagnosis.

slide32
Symptoms-
  • In less haemorrhage-

sudden development of floaters.

  • In more haemorrhage-

sudden painless loss of vision

slide33
Treatment-
  • Conservative treatment-

bed rest

elevation of patients head

bilateral eye patches

  • Treatment of cause-

management of retinal break, phlebitis, proliferative retinopathy.

slide34
Vitrectomy-

by pars plana route, if haemorrhage is not absorb after 3 months.

retinal detachment
Retinal detachment

Separation of neurosensory retina proper from the pigment epithelium.

Classification-

  • Primary retinal detachment
  • Secondary retinal detachment
primary retinal detachment
Primary retinal detachment

Usually associated with retinal break

Sub retinal fluid seeps

Separate the sensory retina from pigmentary epithelium

slide37
Etiology-
  • Most common in 40-60 yrs.
  • More in males
  • 40% cases are myopic
  • More common in aphakes
  • Retinal degenaration
  • Trauma
  • Senile post.vitreous detachment
slide38
Pathogenesis-

Senile acute predisposing

Post.vitreous retinal

Detachment degenaration aphakia

Retinal break trauma

Degenarated fluid seeps through retinal breaks

Retinal detachment

slide39
Clinical features-

Prodromal symptom-

dark spot in front of the eye

photopsia

Symptoms-

  • loss in field of vision which progress total loss when detachment progress to macular area.
  • Sudden painless loss of vision
slide41
Sign-
  • External examination-

eye is usually normal

  • Intraoccular pressure is low
  • Plain mirror examination-

an altered red reflex in pupilary area.

slide42
Opthlmoscopy-
        • Detach retina gives grey reflex & raised anteriorly.
        • it thrown in to folds which oscilate with the movement of eye
        • Total detachment of retina funnel shaped, being attached only at disc & ora serrata
        • Retinal vessels appear dark tortuous.
slide43
Electroretinography-

subnormal or absent

  • Ultrasonography-

confirm the diagnosis

slide44
Complication-

proliferative vitreoretinopathy

complicated cataract

uvelitis

phthisis bulbi

slide48
Treatment-
  • Sealing of retinal breaks-

by producing aseptic chorioretinitis,

cyocoagulation,

photocoagulation

  • Scleral buckling-

To bring the sclrochoroid & retina near to each other

  • Drainage of SRF
solid retinal detachment
Solid retinal detachment

Occurs due to retina being pushed sway by neoplasm or accumulation of fluid beneath the retina.

Etiology-

  • Systemic disease-

toxaemia in pregnancy

renal HTN

blood dyscrasias

polyarthritis nodosa

slide52
Occular disease-
        • Inflammation like the Harada’s disease, posterior scleritis,orbital cellulitis
        • Vascular disease like central serous retinopathy & exudative retinopathy
        • Neoplasm like malignant melanoma of choroids
slide53
Clinical features-

Can be differentiate from simple

  • Absence of photopsia
  • Holes or tears
  • Folds
  • Undulation
  • Smooth & convex detachment
  • At summit of tumour,it usually rounded & fixed
  • Pattern of retinal vessel is disturbed
slide54
Treatment-
  • Absorption of fluid
  • Treatment of causative factor
  • If tumour-enucleation
optic neuritis
Optic neuritis

Includes inflammatory & demyelinating disorder of optic nerve

Etiology-

  • Idiopathic
  • Hereditary optic neuritis
  • Demyelinating disorders-

multiple sclerosis

neuromyelitis optica

slide56
Clinical features-

Classified in to three-

  • Papilitis
  • Neuroretinitis
  • Retrobulber neuritis
slide57
Papilitis-

It is inflammation of optic disc.

Usually unilateral

Symptom-

      • Sudden profusal visual loss is hallmark of papilitis
      • Dark adaptation is depressed
      • Light brightness is depressed
      • Colour object may look wash away
      • Depth perception percularly for moving object may be impaird.
slide58
Signs-
  • Visual acuty reduced markly
  • colour vision often severly impaired
  • Pupil-ill-stained constriction to light
  • Ophthalmoscope-
      • Hyperemia of disc
      • Bluring of margin
      • Disc become oedematous & physiological cup is obliterated
      • Retinal veins are congested
      • Splinter haemorrhage is seen.
slide59
Visual field change-

central or centroceacal scotoma.

the field defect are more marked to red colour than white

  • Visually evoked response (VER)shows reduced amplitude & delayed in the transmission time.
methyl alcohol amblyopia
Methyl alcohol amblyopia

Acute onset

Resulting in optic atrophy & permanent blindness

Etiology-

  • Intake of wood alcohol spirit in cheap adulterated beverages
  • Inhalation of fumes in industries
  • Absorbed from skin following prolonged daily use of linments
slide61

Pathogenesis-

Methyl alcohol metabolized very slowly,

stay longer period

Oxidised in to formic acid & formaldehyde

oedema

Degenaration of ganglion cell of retina

Complete blindness

slide62
Clinical features-
  • Headache
  • Dizziness
  • Nausea
  • Vomiting
  • Abdominal pain
  • Delirium
  • Stupor
  • Even death
slide63
Diagnostic sign-

Presence of charecteristic odour due to excretion of formaldehyde

Occular features-

mild disc oedema

markedly narrowed blood vessels

bilatral optic atrophy

slide64
Treatment-
  • Gastric lavage
  • Admission of alkali to overcame acidosis.sodabicarb may be given orally or IV
  • Eliminative treatment by diaphoresis in the form of peritoneal dialysis
  • Prognosis is usually poor, death may occur.
slide65
The eye is the lamp of the body

If your eyes are good,

Your whole body will be full of light,

so

Take care of your eyes.

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