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NORMAL EYE WITH SUDDEN DECREASED VISION YENI ANGGRAINI I11107014 ANGGI PATRANITA I11107022

Mata Tenang Visus Turun Mendadak

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Page 1: Mata Tenang Visus Turun Mendadak

NORMAL EYE WITH SUDDEN

DECREASED VISION

YENI ANGGRAINI

I11107014

ANGGI PATRANITA

I11107022

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RETINAL DETACHMENToccurs when subretinal fluid

accumulates in the potential space between the neurosensory retina

and the underlying retinal pigment epithelium (RPE)

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Retinal detachment occurs when subretinal fluid accumulates in the potential space between the neurosensory retina and the underlying retinal pigment epithelium (RPE).

Depending on the mechanism of subretinal fluid accumulation, retinal detachments traditionally have been classified into rhegmatogenous, tractional, and exudative.

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EPIDEMIOLOGY

A retinal detachment can occur at any age

more common in people over age 40 It affects men more than women, and

Whites more than African Americans.

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Rhegmatogenous

A tear or break in the retina allows fluid to get under the retina and separate it from the retinal pigment epithelium (RPE), the pigmented cell layer that nourishes the retina. These types of retinal detachments are the most common.

Most RRDs occur in persons aged 40-70 years. It is at this time that the syneretic vitreous undergoes separation from the retina.

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Pathophysiology Vitreoretinal traction is responsible for the

occurrence of most RRD. As the vitreous becomes more syneretic (liquefied) with age, a posterior vitreous detachment (PVD) occurs. In most eyes, the vitreous gel separates from the retina without any sequelae. However, in certain eyes, strong vitreoretinal adhesions are present and the occurrence of a PVD can lead to a retinal tear formation; then, fluid from the liquefied vitreous can seep under the tear, leading to a retinal detachment.

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Risk factors include: Increasing age Short-sightedness Some abnormalities of the peripheral part

of the retina A history of retinal detachment A family history of retinal detachment,

inherited retinal weakness Previous cataract surgery Trauma

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Tractional In this type of

detachment, scar tissue on the retina’s surface contracts and causes the retina to separate from the RPE. This type of detachment is less common.

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Exudative

Frequently caused by retinal diseases, including inflammatory disorders and injury/trauma to the eye. In this type, fluid leaks into the area underneath the retina, but there are no tears or breaks in the retina.

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SIGNS AND SYMPTOMS

Light Flashes Wavy or watery vision Veil or curtain obstructing vision Shower of floaters that resemble spots,

bugs, or spider webs Sudden decrease of vision

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Floaters are opacities in the vitreous that cast a dark shadow according to their form and shape in the patient's visual field as they float in the vitreous cavity.

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• When the macula becomes detached (ie, extension of subretinal fluid into the macula), the patient experiences a drop in visual acuity.

Loss of Side Vision Caused by Retinal Detachment

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Physical assesment Slit Lamp

Cell and flare may be seen in the anterior chamber of eyes with a rhegmatogenous retinal detachment (RRD)

Examining the retina with ophthalmoscopy to determine whether the macula .

Ultrasound imaging of the eye is also very useful to see additional detail of the condition of the retina from several angles.

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Retinal detachment. A 60" view of the

fundus reveals folds of retina extending into the macula inferotemporal to the disc. In this photograph, the focus is on the elevated retina, which renders the disc slightly out of focus.

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Clinical picture of a rhegmatogenous retinal detachment. Notice that the macula is involved and that the retina is corrugated and has a slightly opaque color.

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Retinal Detachment Surgery1. Laser therapy

For Small holes and tears, by using a laser beam, which burns the tears in the retina, which leads to fibrosis and the fibrous tissue to meet the parties to these holes, cracks or ruptures and thus prevent leakage of fluid

2 - Treatment freeze (cryopexy) freezes the area around the hole and helps reattach the retina using (Nitrous oxide),

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3. Pneumatic Retinopexy is a technique in which a temporary gas bubble is inserted into the vitreous cavity and used to close the retinal tear and push the detached retina back into position.

After the retina is back in position, laser or freezing therapy is used to seal the retina to the eye wall.

The patient’s head position must be strictly maintained for about seven days to keep the bubble in contact with the area of detachment.

The gas bubble is slowly absorbed, and the space it occupied in the vitreous cavity is filled by fluid normally produced by the eye.

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4. Scleral Buckling is a technique in which a piece of soft silicone material is sewn against the outside wall of the eye.

This creates an indentation that closes the retinal defect that caused the retinal detachment.

The surgeon may also drain the fluid which has accumulated behind the retina.

Laser or freezing therapy is used to seal the retina back in place once it is reattached.

The scleral buckle stays in place permanently and does not harm the eye.

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In a scleral buckling procedure, one of the eye's rectus muscles are severed to gain access to the sclera (A). The sclera is cut open (B), and an electrode is applied to the area of retinal detachment (C). A silicone buckle is threaded into place beneath the rectus muscles (D), and the severed muscle is repaired

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5. Vitrectomy Surgery is a technique in which microscopic cutting instruments are used to remove the vitreous gel and any scar tissue which may be present inside the eye.

The fluid which created the retinal detachment is then drained through the existing retinal tear, which reattaches the retina.

A temporary gas bubble holds the retina in position as laser or freezing treatment seals the retina to the eye wall.

Removing the vitreous does not affect the function of the eye. The gas bubble is slowly absorbed and the vitreous cavity is filled by fluid normally produced by the eye.

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Prognosis over 90 percent of those with a retinal detachment

can be successfully treated the visual outcome is not always predictable. The

final visual result may not be known for up to several months following surgery.

Even under the best of circumstances, and even after multiple attempts at repair, treatment sometimes fails and vision may eventually be lost.

Visual results are best if the retinal detachment is repaired before the macula detaches

in about 10 to 20% of cases, repeat surgery is needed.

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COMPLICATION

Complications retinal detachment surgery: - Infections of the eye. - Bleeding in the eye.

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Prophylaxis Indirect Ophthalmoscope (IDO) Laser Cerclage treating visible areas of retinal pathology (focal

prophylaxis laser photocoagulation) in high risk eyes. 

Laser Cerclage nearly eliminates future tear occurrence in the areas of treatment. Treatment to the peripheral area of the retina is advantageous for the patient subjectively because visual function in the peripheral retina is low, rarely noticed.

Focal laser prophylaxis does prevent retinal detachment from the specific area treated but has been disappointing in preventing retinal detachment.  Because new tears can develop in the untreated peripheral areas of focally treated high risk eyes and often lead to retinal detachment.

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OPTIC NEURITIS

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Optic Neuritis Is an inflamation of optic

nerve that is usually idiopathic

Reduce visual acuity and relative afferent pupillary defect are regular feature

The optic disc appear hyperemic and swollen

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This most commonly occurs in association with a plaque of demyelination in the optic nerve in patients with multiple sclerosis.

The prognosis for the return of vision of single attack is good

Certai patiens may benefit from high dose intravenous corticosteroid

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Causes

Optic neuritis is associated with various diseases and conditions, such as:

mumps; measles; influenza; multiple sclerosis; Leber’s optic neuropathy (a rare eye condition

that runs in families); vascular occlusions of the optic nerve. In most cases, however, optic neuritis occurs with

noknown cause.

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Signs and Symptoms Pain with eye movement (more than 90% of patients) Tender, sore eye Mild to severe decrease in central vision Dull, dim vision Reduced color perception Decreased peripheral vision Central blind spot Fever Headache Nausea Decreased vision following exercise, hot bath or

shower (activities that e levate body temperature)

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Retrobulbar Optic Neuritis A young adult who is experiencing a

monocular loss of vision that has developed over hours to days and that is often accompanied by pain on movement of the eye who shows NO abnormalities in eye examination probably has retrobulbar optic neuritis

Vision is poor and afferent pupillary defect is present.

In severe cases, the sight of the affected eye can be lost completely

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On examination, a relative afferent pupil defect on the affected side might be the only objective evidence of disease.

The fundus is often normal initially (retrobulbar neuritis), although there can be slight swelling of the optic disc (optic neuritis).

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In retrobulbar optic neuritis, the inflammation and demyelination occur behind the globe of the eye. The optic disc appears normal with no signs of swelling or pallor.

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The attack is unilateral in 90% of cases, although there is a risk that the other eye can be affected at a later date and recurrent attacks in one or both eyes can cause permanent damage to the vision.

Fortunately, it is extremely rare for a patient to be made blind by multiple sclerosis.

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Papilitis

is an inflammation of the optic disc or papilla

Vision is usually (but not always) significantly decreased and examination of the pupils will reveal a relative afferent pupillary defect.

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PapillitisThe margin of the optic disk is slightly obscured by edema and hyperemia of the head of the optic nerve. The optic cup is obscured.

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assesment The diagnosis at the time of the acute attack relies

on the history and noting the pupil reaction. It is often advisable to make the diagnosis in

retrospect. The patient might give a history of visual loss in

one eye, which has recovered, and at a later date, presents with other nonocular signs and symptoms of demyelinating disease.

If it can be confirmed that the patient has had a previous attack of optic neuritis, this can help in the confirmation of the diagnosis of disseminated sclerosis.

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Under these circumstances, the pallor of the disc can be helpful, but careful assessment of the colour vision, visual acuity and measurement of the visually evoked potential can provide conclusive evidence.

At the time of the acute attack, testing the visual field might reveal a central scotoma.

The size of this defect diminishes as healing occurs, often leaving a small residual defect between blind spot and central area.

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Treatment

Intravenous steroid medication (but not oral steroids) reduces the risk of developing MS later on.

May be important to recognize those patients at higher risk to start earlier treatment. This is best determined by MRI.

There is no treatment that will absolutely prevent ON

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Prognosis In most cases, vision will either improve

significantly or return to normal over a period of days to weeks.

For some, a complete recovery may take months.

Some patients, however, may not recover their normal vision, particularly if they have a pre-existing condition such as multiple sclerosis.

The visual prognosis is generally good. Most patients make a complete or nearly complete recovery after 6–12 weeks.

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Resolution of left optic disc swellingin the same patient 2 weeks later

Resolution of right optic disc swellingin the same patient 2 weeks later

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THANK’S FOR YOUR ATTENTION

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Vitreous Haemorrhage

Haemorrhage into the vitreous cavity can result in sudden pain-

less loss of vision.The extent of visual loss will depend on the de-

gree of haemorrhage.

•A large haemorrhage will cause total visual loss

•A small haemorrhage will present as floaters and normal or only slightly reduced visual acuity

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Aetiology:

Proliferative retinopathy—spontaneous rupture of abnormal fragile new vessels that grow on the retinal surface cause bleeding into the vitreous cavity. Most common is proliferative diabetic retinopathy

Retinal detachment—a small retinal blood vessel may rupture when the retinal break occurs,bleeding into the vitreous cavity

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Trauma Posterior vitreous detachment can result

in vitreous haemorrhage if,as the vitreous separates from the retina,it pulls and ruptures a small blood vessel

Age-related macula degeneration (AMD)—haemorrhage may occur into the vitreous from the abnormally weak vessels forming a subretinal neovascular membrane

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The patient complains of a sudden onset of floaters, or “blobs,” in the vision.

The visual acuity may be normal or, if the haemorrhage is dense, it may be reduced.

Flashing lights indicate retinal traction and are a dangerous symptom.

Haemorrhage may occur from spontaneous rupture of vessels, avulsion of vessels during retinal traction, or bleeding from abnormal new vessels.

If the patient is shortsighted, retinal detachment is more likely.

If there is associated diabetesmellitus the patient may have bled from new vessels and the vitreous haemorrhage may herald potentially sight threatening diabetic retinopathy.

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The visual acuity depends on the extent of the haemorrhage.

Projection of light is accurate unless the haemorrhage is extremely dense.

Ophthalmoscopy shows the red reflex to be reduced; there may be clots of blood that move with the vitreous

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The patient should be referred to an ophthalmologist to exclude a retinal detachment.

Underlying causes such as diabetes must also be excluded.

If a vitreous haemorrhage fails to clear spontaneously the patient may benefit from having the vitreous removed (vitrectomy)

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Scleral Buckling, operasi untuk memperbaiki lepasnya retina dengan pemasangan pita silicon yang dijahitkan pada sclera.

Lensectomy, operasi untuk mengangkat lensa dari mata.

Laser photocoagulation, pengobatan menggunakan sinar laser dengan panjang gelombang tertentu di dalam mata.

Silicone oil, pengisian minyak silikon untuk menggantikan vitreus pada beberapa kasus lepasnya retina. Minyak ini akan dikeluarkan dari mata dengan operasi beberapa bulan kemudian.

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Central Retina Vein Occlusion

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The patient presents with painless loss of vision, often mixed with sparkles, that may be sudden or evolve over hours to days. Systemic hypertension is the most common cause; hyperviscous and hypercoagulable states must also be considered.

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Patients may otherwise complain only of a vague visual disturbance or of field loss

The arteries and veins share a common sheath in the eye, and venous occlusion most commonly occurs where arteries and veins cross, and in the head of the nerve

Thus raised arterial pressure can give rise to venous occlusion

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Visual acuity will not be affected unless the macula is damaged

Ophthalmoscopy shows characteristic flame haemorrhages in the affected areas, with a swollen disc if there is occlusion of the central vein

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Branch Retinal Vein Occlusion (BRVO)

BRVO is a retinal vascular disease most often related to hypertension, elevated lipids/triglyceride/cholesterol, diabetes, carotid artery disease, cardiac disease, or hematologic (blood) disorders. In BRVO there is an occlusion of a branch retinal vein by a compressing, sclerotic retinal artery. This often leads to hemorrhage (bleeding), edema (swelling), or ischemia (poor circulation) of the retina and macula with resultant visual loss.

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Central Retinal Vein Occlusion (CRVO)

CRVO is also a retinal vascular disease but involves occlusion of the main central retinal vein. Vascular, hematologic, and cardiac disease may predispose individuals to develop CRVO which leads to leakage of blood and fluid into the retina. In many cases the resultant poor circulation (ischemia) can lead to abnormal blood vessel formation in the iris (rubeosis) with painful increases in eye pressure (neovascular glaucoma).

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Hypertension, diabetes mellitus, hyperviscosity syndromes, and chronic glaucoma must be identified and treated if present

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Central Retina Artery the CRA supplies the

superficial nerve fibre layer and inner two-thirds of the retina

The choriocapillaris sup-plies the outer retina

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Central Retina Artery Occlusion

The patient complains of a sudden onset of visual disturbance, often described as a “greyout” of the vision or as a “curtain” descending over the vision, in one or both eyes.

This may be temporary (amaurosis fugax) if the obstruction dislodges or permanent if tissue infarction occurs

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Causes of retinal arterial occlusion

Emboli Thrombosis ±atherosclerosis Congenital thrombophilic states Acquired thrombophilic states Vasculitis Infection Trauma Vasospasm Raised intraocular pressure

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Signs

Perform a dilated fundal examination to detect:

• Cherry red spot at macula.

• Embolus occasionally visible at optic disc.

• Attenuation of arterioles.

• Retinal pallor.

• Mild disc swelling

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Central Retina Artery Occlusion

When the retina infarcts it becomes oedematous and pale and masks the choroidal circulation except at the macula, which is extremely thin—hence the “cherry red spot” appearance.

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TreatmentThe aim is to re-establish circulation within the CRA.This is

at-

tempted by:

• Lowering the intraocular pressure (IOP) using:

—acetazolamide 500mg i.v.;

—ocular massage;

—anterior chamber paracentesis (1ml aqueous withdrawn).

• Start cholesterol lowering statins,e.g.Simvastatin,Atorvastatin.

• Start antiplatelets,e.g.aspirin 300mg stat then 75mg daily or

clopidogrel 75mg daily,within 48hrs.

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Prognosis

The prognosis is poor because irreparable damage to the inner layers of the retina occurs within one hour.

The prognosis is better where only a branch of the artery is occluded unless a macular branch is affected.

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THANK YOU