Sudden painless loss of vision
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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


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.

  • 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

  • Central Retinal artery occlusion

  • Vitreous hemorrhage

  • Retinal detachment

  • Central Retinal vein occlusion

  • Optic neuritis

  • Methyl alcohol amblypia


Retinal artery occlusion

Etiology-

  • more common in patients suffering from hypertension.

  • Thrombosis

  • Embolism

  • Retinal artritis

  • Angiospasm


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.


Symptom –

Painless sudden loss of vision


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.


ERGs of CRAO


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.


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


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

    relive angiospasm

  • Anticoagulant

  • IV steroids


Complication-

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


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)


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

  • Local cause-

    orbital cellulitis

    facial erysipelas

    cavernous sinus thrombosis


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.


  • 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.


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.


  • Ischemic-

    Refers to acute complete occlusion of central retinal vein

    Characterised by marked Sudden loss of vision


Fundus examination-

in early stage-

  • Massive engorgement

  • Congestion

  • Tortusity of veins

  • Massive retinal haemorrhage

  • Papilloedema

  • Macular area oedematous


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

  • Presence of relative afferent pupillary defect

  • Visual field defect

  • Reduced amplitude of b-wave of ERG.


Complication-

  • Rubiosis iridis

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

  • Few develops vitreous hemorrhage


Treatment-

  • Panretinal photocoagulation

  • Cryo-application

  • Photocoagulation

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


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


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

  • Vision is affected when macular area is involve.


Treatment-

  • Grid photocoagulations-

    in chronic macular odema

  • Scatterphotocoagulations-

    in neovascularisation


Vitreous haemorrhage

Usually occur from retinal vessels

Pre retinal intrageal

haemorrhage haemorrhage


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


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.


Symptoms-

  • In less haemorrhage-

    sudden development of floaters.

  • In more haemorrhage-

    sudden painless loss of vision


Treatment-

  • Conservative treatment-

    bed rest

    elevation of patients head

    bilateral eye patches

  • Treatment of cause-

    management of retinal break, phlebitis, proliferative retinopathy.


  • Vitrectomy-

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


Retinal detachment

Separation of neurosensory retina proper from the pigment epithelium.

Classification-

  • Primary retinal detachment

  • Secondary retinal detachment


Primary retinal detachment

Usually associated with retinal break

Sub retinal fluid seeps

Separate the sensory retina from pigmentary epithelium


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


Pathogenesis-

Senile acute predisposing

Post.vitreous retinal

Detachment degenaration aphakia

Retinal break trauma

Degenarated fluid seeps through retinal breaks

Retinal detachment


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


A view from person having retinal detachment.


Sign-

  • External examination-

    eye is usually normal

  • Intraoccular pressure is low

  • Plain mirror examination-

    an altered red reflex in pupilary area.


  • 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.


  • Electroretinography-

    subnormal or absent

  • Ultrasonography-

    confirm the diagnosis


Complication-

proliferative vitreoretinopathy

complicated cataract

uvelitis

phthisis bulbi


Proliferative vitreoretinopathy


Uveitis


Pthisis bulbi


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


chororetinitis


  • Internal tamponade by SF6 gas or silicon oil

  • Pars plana vitrectomy


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


  • 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


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


Treatment-

  • Absorption of fluid

  • Treatment of causative factor

  • If tumour-enucleation


Optic neuritis

Includes inflammatory & demyelinating disorder of optic nerve

Etiology-

  • Idiopathic

  • Hereditary optic neuritis

  • Demyelinating disorders-

    multiple sclerosis

    neuromyelitis optica


Clinical features-

Classified in to three-

  • Papilitis

  • Neuroretinitis

  • Retrobulber neuritis


  • 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.


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.


  • 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

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


Pathogenesis-

Methyl alcohol metabolized very slowly,

stay longer period

Oxidised in to formic acid & formaldehyde

oedema

Degenaration of ganglion cell of retina

Complete blindness


Clinical features-

  • Headache

  • Dizziness

  • Nausea

  • Vomiting

  • Abdominal pain

  • Delirium

  • Stupor

  • Even death


Diagnostic sign-

Presence of charecteristic odour due to excretion of formaldehyde

Occular features-

mild disc oedema

markedly narrowed blood vessels

bilatral optic atrophy


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.


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.


Thank you


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