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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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Sudden Painless Loss Of Vision

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Sudden painless loss of vision l.jpg

Sudden Painless Loss Of Vision

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Minal G. Birambole.


G.A.M &R.C,


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  • 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.

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Causes of sudden loss of vision

  • Central Retinal artery occlusion

  • Vitreous hemorrhage

  • Retinal detachment

  • Central Retinal vein occlusion

  • Optic neuritis

  • Methyl alcohol amblypia

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Retinal artery occlusion


  • more common in patients suffering from hypertension.

  • Thrombosis

  • Embolism

  • Retinal artritis

  • Angiospasm

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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.

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Symptom –

Painless sudden loss of vision

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  • 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.

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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.

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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

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

    relive angiospasm

  • Anticoagulant

  • IV steroids

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

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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)

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  • Raised intraocular pressure,more common in primary open angle glaucoma

  • Local cause-

    orbital cellulitis

    facial erysipelas

    cavernous sinus thrombosis

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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.

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  • 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.

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  • 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.

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  • Ischemic-

    Refers to acute complete occlusion of central retinal vein

    Characterised by marked Sudden loss of vision

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Fundus examination-

in early stage-

  • Massive engorgement

  • Congestion

  • Tortusity of veins

  • Massive retinal haemorrhage

  • Papilloedema

  • Macular area oedematous

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in later stage-

  • Sheathing around vein & collatrals seen around disc

  • Neovascularisation at disc

  • Macula-marked pigmentary change

  • Chronic cystoid oedema

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Difference between ischemic from non ischemic

  • Presence of relative afferent pupillary defect

  • Visual field defect

  • Reduced amplitude of b-wave of ERG.

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  • Rubiosis iridis

  • Neovascular glaucoma in more than 50% cases within 3 months

  • Few develops vitreous hemorrhage

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  • Panretinal photocoagulation

  • Cryo-application

  • Photocoagulation

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

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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

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  • Occlusion oedema & haemorrhge are limited to area drain by affected vein.

  • Vision is affected when macular area is involve.

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  • Grid photocoagulations-

    in chronic macular odema

  • Scatterphotocoagulations-

    in neovascularisation

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Vitreous haemorrhage

Usually occur from retinal vessels

Pre retinal intrageal

haemorrhage haemorrhage

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  • Associated with PVD

  • Trauma to eye

  • Inflamatory disease like chorioretinitis,periphlebitis retinae

  • Vascular disoders like HTN retinopathy

  • Metabolic disease like DM retinopathy

  • Neoplasm

  • idiopathic

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Clinical features-


  • 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.

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  • In less haemorrhage-

    sudden development of floaters.

  • In more haemorrhage-

    sudden painless loss of vision

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  • Conservative treatment-

    bed rest

    elevation of patients head

    bilateral eye patches

  • Treatment of cause-

    management of retinal break, phlebitis, proliferative retinopathy.

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  • Vitrectomy-

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

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Retinal detachment

Separation of neurosensory retina proper from the pigment epithelium.


  • Primary retinal detachment

  • Secondary retinal detachment

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Primary retinal detachment

Usually associated with retinal break

Sub retinal fluid seeps

Separate the sensory retina from pigmentary epithelium

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  • Most common in 40-60 yrs.

  • More in males

  • 40% cases are myopic

  • More common in aphakes

  • Retinal degenaration

  • Trauma

  • Senile post.vitreous detachment

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Senile acute predisposing

Post.vitreous retinal

Detachment degenaration aphakia

Retinal break trauma

Degenarated fluid seeps through retinal breaks

Retinal detachment

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Clinical features-

Prodromal symptom-

dark spot in front of the eye



  • loss in field of vision which progress total loss when detachment progress to macular area.

  • Sudden painless loss of vision

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A view from person having retinal detachment.

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  • External examination-

    eye is usually normal

  • Intraoccular pressure is low

  • Plain mirror examination-

    an altered red reflex in pupilary area.

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  • 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.

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  • Electroretinography-

    subnormal or absent

  • Ultrasonography-

    confirm the diagnosis

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proliferative vitreoretinopathy

complicated cataract


phthisis bulbi

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Proliferative vitreoretinopathy

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Pthisis bulbi

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  • Sealing of retinal breaks-

    by producing aseptic chorioretinitis,



  • Scleral buckling-

    To bring the sclrochoroid & retina near to each other

  • Drainage of SRF

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  • Internal tamponade by SF6 gas or silicon oil

  • Pars plana vitrectomy

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Solid retinal detachment

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


  • Systemic disease-

    toxaemia in pregnancy

    renal HTN

    blood dyscrasias

    polyarthritis nodosa

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  • 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

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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

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  • Absorption of fluid

  • Treatment of causative factor

  • If tumour-enucleation

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Optic neuritis

Includes inflammatory & demyelinating disorder of optic nerve


  • Idiopathic

  • Hereditary optic neuritis

  • Demyelinating disorders-

    multiple sclerosis

    neuromyelitis optica

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Clinical features-

Classified in to three-

  • Papilitis

  • Neuroretinitis

  • Retrobulber neuritis

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  • Papilitis-

    It is inflammation of optic disc.

    Usually unilateral


    • 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.

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  • 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.

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  • 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.

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Methyl alcohol amblyopia

Acute onset

Resulting in optic atrophy & permanent blindness


  • Intake of wood alcohol spirit in cheap adulterated beverages

  • Inhalation of fumes in industries

  • Absorbed from skin following prolonged daily use of linments

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Methyl alcohol metabolized very slowly,

stay longer period

Oxidised in to formic acid & formaldehyde


Degenaration of ganglion cell of retina

Complete blindness

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Clinical features-

  • Headache

  • Dizziness

  • Nausea

  • Vomiting

  • Abdominal pain

  • Delirium

  • Stupor

  • Even death

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Diagnostic sign-

Presence of charecteristic odour due to excretion of formaldehyde

Occular features-

mild disc oedema

markedly narrowed blood vessels

bilatral optic atrophy

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  • 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.

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The eye is the lamp of the body

If your eyes are good,

Your whole body will be full of light,


Take care of your eyes.

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Thank you

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