normal eye with immediately vision loss.pptx

8/13/2019 Normal eye with immediately vision loss.pptx

http://slidepdf.com/reader/full/normal-eye-with-immediately-vision-losspptx 1/44

NORMAL EYE WITH

SUDDENLY VISIONLOSS

Yulisa Handayani



Retinal vein occlusion



Definiton

Vein occlusion occurs as a result of circulatory

dysfunction in the central vein or one of its

branches.



Epidemiology

The second most frequent vascular r etinal

disorder after diabetic retinopathy.

The most frequent underlying systemic

disorders are arterial hypertension anddiabetes mellitus

The most frequent underlying ocular disorder

is glaucoma.



Ethiology

Pressure on the vein by a sclerotic retinal artery

where the two share a common adventitia (e.g.,

just behind the lamina cribrosa and at

arteriovenous crossings). Hyperviscosity of blood as in polycythemia,

hyperlipidemia and macroglobulinemia.

Periphlebitis retinae which can be central or

peripheral.

Raised introcular pressure.

Local causes are orbital cellulitis, facial erysipelas

and cavernous sinus thrombosis.



Classification

Central retinal vein

occlusion

Branch retinal vein

occlusion

Ischaemic CRVO/

haemorrhagic

retinophaty

Non ischaemic

CRVO/ venous statis

retinopathy



Non Ischaemic CRVO

symptom

Fundusexamination: Early

stage

Fundusexamination : late

stage

Mild to moderate

vision loss

Mild venous congestion and tortuosity, a few

superficialflame-shaped haemorrhages more in the

peripheral

than the posterior retina, mild papilloedema and

mild

or no macular oedema.

sheathing around the main veins, and a fewcilioretinal collaterals around the disc. Retinal

haemorrhages are partly absorbed. Macula may

show chronic cystoid oedema in moderate cases

or may be normal in mild cases.



Non-ischaemic CRVO

Treatment

Treatment is not required → The condition

resolves with almost normal vision in about 50

percent cases.

Visual loss → chronic cystoid macular oedema→ no treatment is effective.

Oral steroids for 8-12 weeks may be effective.



Ischaemic CRVO

symptom

Fundus

examination: Early

stage

Fundus examination: late stage

sudden complete occlusion of centralretinalVein→ sudden visual loss →6∕60 –

1/300

massive engorgement, congestion and tortuousityof retinal veins, massive retinal haemorrhages →

‘splashed-tomato’ appearance, numerous soft

exudates, and papilloedema. Macular area is full of

haemorrhages and is severely oedematous.

sheathing around veins and collaterals is seenaround the disc. Neovascularisation may be seen

at the disc (NVD) or in the periphery (NVE).

Macula shows marked pigmentary changes and

chronic cystoid oedema.



Treatment

Panretinal photocoagulation (PRP) or cryo-application → prevent neovascular glaucoma

in patients with widespread capillary occlusion.

Photocoagulation →most of the intraretinalblood is absorbed→ 3-4 months.



Branch Retinal Vein Occlusion

symptom

location

treatment

vision loss →macular

edema, macular

ischemia, or vitreous

hemorrhage

Main branch at the disc margin → hemisphericocclusion

major branch vein away from the disc, at A-Vcrossing → quadrantic occlusion & small macular

or peripheral branch occlusion.

Grid photocoagulation may be required in patientswith chronic macular oedema.

In patients with neovascularisation, scatter

photocoagulation should be carried out.



Retinal Artery Occlusion



Definition

Retinal infarction due to occlusion of an

artery in the lamina cribrosa or a branch

retinal artery occlusion.



Epidemiology

About 1 in 10000 outpatient visits to the

ophthalmologist.

Men are affected than women in the ratio 2:1.

The mean age at onset is about 60years, with

a range of reported ages from the first to the

ninth decade of life.

Right eyes and left eyes appear affected withequal incidence.

Bilateral involvement occurs in 1 –2% of cases.



Ethiology

Atherosclerosis-related thrombosis at the level oflamina cribrosa

Emboli from the carotid artery and those ofcardiac origin

Retinal arteritis with obliteration (associated withgiant cell arteritis) and periarteritis (associatedwith polyarteritis nodosa, systemic lupuserythematosus, Wegner’s granulomatosis andscleroderma)

Angiospasm is a rare cause of retinal arteryocclusion.

Raised intraocular pressure

Thrombo hilic disorders such as inherited defects



Central retinal artery occlusion

symptom

sign

Fundus examination

sudden painless

loss

of vision.

Direct pupillary light reflex is absent.

•retinal arteries are markedly narrowed.•Retina becomes milky white → oedema.

•Central part of the macular area shows cherry-redspot → vascular choroid shining through the thin

retina of this region.

•atrophic changes occur which include grossly

attenuated thread-like arteries and consecutive

optic

atrophy



Treatment

Immediate lowering of intraocular pressure byintravenous mannitol and intermittent ocularmassage →aid the arterial perfusion and alsohelp in dislodging the embolus

Vasodilators and inhalation of a mixture of 5percent carbon dioxide and 95 percent oxygen→ relieving element of angiospasm.

Anticoagulants Intravenous steroids are indicated in patients

with giant cell arteritis



Optic Neuritis



Definition

An inflammation of the optic nerve that may

occur within the globe (papillitis) or posterior to

it (retrobulbar optic neuritis).



Epidemiology

3 –5 per 100,000 per year

prevalence is 115 per 100,000

between the ages of 20 and 50 years.

Women are affected more commonly than

men.



Ethiology

Idiopathic

Hereditary optic neuritis ( Leber’s disease)

Demyelinating disorders

Parainfectious optic neuritis is associated withvarious viral infections → measles, mumps,chickenpox, whooping cough and glandular fever.

Infectious optic neuritis may be sinus related (withacute ethmoiditis) or associated with cat scratch

fever, syphilis (during primary or secondarystage), lyme disease and cryptococcal meningitisin patients with AIDS.

Toxic optic neuritis.



Classification

Papillitis → involvement of the optic disc in

inflammatory and demyelinating disorders.

This condition is usually unilateral but

sometimes may be bilateral. Neuroretinitis → combined involvement of

optic disc and surrounding retina in the

macular area.

Retrobulbar → involvement of optic nerve

behind the eyeball.



Symptom

Visual loss. Sudden, progressive and profoundvisual loss is the hallmark of acute optic neuritis.

Dark adaptation may be lowered.

Visual obscuration in bright light Impairment of colour vision

Movement phosphenes and sound induced phosphenes may be percieved by patients with

optic neuritis. Episodic transient obscuration of vision

Depth perception

Pain



Sign

Visual acuity is usually reduced markedly.

Colour vision is often severely impaired.

Pupil shows ill-sustained constriction to light.

Marcus Gunn pupil which indicates relativeafferent pupillary defect (RAPD) is a diagnosticsign→ swinging flash light test

Ophthalmoscopic features: Papillitis →

hyperaemia of the disc and blurring of themargins. Disc becomes oedematous andphysiological cup is obliterated. Retinal veins arecongested and tortuous. Splinter haemorrhagesand fine exudates may be seen on the disc.



Sign (2)

Slit-lamp examination : inflammatory cells inthe vitreous. Inflammatory signs may also bepresent in the surrounding retina whenpapillitis is associated with macular starformation and the condition is labelled as‘neuroretinitis’

Visual field changes → relative central or

centrocaecal scotoma. Contrast sensitivity is impaired.

Visually evoked response (VER) showsreduced amplitude and delay in the

transmission time.



Differential Diagnose

Papillitis should be differentiated from

papilloedema and pseudo-papilloedema

Acute retrobulbar neuritis must be

differentiated from malingering, hystericalblindness, cortical blindness and indirect optic

neuropathy.



Treatment

Do brain MRI scan. If the brain shows lesionssupportive of multiple sclerosis (MS), regardlessof the severity of visual loss → intravenousmethylprednisolone (1 mg daily) for 3 days

followed by oral prednisolone (1 mg/kg/day) for 11days.

Indications for intravenous methylprednisolone inacute optic neuritis patients with a normal brainMRI scan are:

1. Visual loss in both eyes simultaneously orsubsequently within hours or days of each other.

2. When the only good eye is affected.

3. When the slow progressive visual loss continues

to occur.



posterior uveitis



Definition

Refers to inflammation of the choroid

(choroiditis). Since the outer layers of retina

are in close contact with the choroid and also

depend on it for the nourishment, the choroidalinflammation almost always involves theadjoining retina→ chorioretinitis.



Classification

Suppurative

choroiditis

Non-suppurative

choroiditis

Diffuse choroiditis

Disseminated

choroiditis

Focal choroiditis



Symptom

Defective vision Photopsia→ subjective sensation of flashes of light resulting

due to irritation of rods and cones.

Black spots floating in front of the eyes → large exudativeclumps in the vitreous.

Metamorphopsia→ perceive distorted images of the object →due to alteration in the retinal contour caused by a raisedpatch of choroiditis.

Micropsia → due to separation of visual cells is a commoncomplaint

Macropsia, i.e., perception of the objects larger than they are,may occur due to crowding together of rods and cones.

Positive scotoma, i.e., perception of a fixed large spot in thefield of vision, corresponding to the lesion may be noted bymany patients.



sign

Vitreous opacity

active stage → looks as a pale-yellow or dirty whiteraised area with ill-defined edges → exudation andcellular infiltration of the choroid which hide the

choroidal vessels. The lesion is typically deeper to theretinal vessels. The overlying retina is often cloudyand oedematous.

atrophic stage or healed stage → when active

inflammation subsides, the affected area becomesmore sharply defined and delineated from the rest ofthe normal area. The involved area shows whitesclera below the atrophic choroid and blackpigmented clumps at the periphery of the lesion



complication

complicated cataract, vitreous degeneration,

macular oedema, secondary periphlebitis

retinae and retinal detachment.



Treatment

Non-specific therapy consists of topical and

systemic corticosteroids. Posterior sub-tenon

injections of depot corticosteroids are effective

in checking the acute phase of posterioruveitis.

Specific treatment is required for the causative

disease such as toxoplasmosis, toxocariasis,

tuberculosis, syphilis, etc.

normal eye with immediately vision loss.pptx

Documents