Anda di halaman 1dari 9

BAB I PENDAHULUAN Bola Mata terdiri atas dinding bola mata dan isi bola mata,dimana dinding bola

mata terdiri atas sclera dan kornea sedangkan isi bola mata terdiri atas lensa,uvea,badan kaca dan retina.Uvea merupakan lapisan dinding kedua dari bola mata setelah sclera dan tenon.Uvea merupakan jaringan lunak,terdiri dari iris,badan siliar dan koroid.7 Uveitis adalah inflamasi traktus uvea (iris,korpus siliaris,dan koroid) dengan berbagai penyebabnya.Struktur yang berdekatan dengan jaringan uvea yang mengalami inflamasi biasanya juga ikut mengalami inflamasi.Peradangan pada uvea dapat hanya mengenai bagian depan jaringan uvea atau iris yang disebut iritis. Bila mengenai badan tengah disebut siklitis.Iritis dengan siklitis disebut iridosiklitis atau disebut juga dengan uveitis anterior dan merupakan bentuk uveitis tersering. Dan bila mengenai lapisan koroid disebut uveitis posterior atau koroiditis.1,2 Uveitis umumnya unilateral,biasanya terjadi pada dewasa muda dan usia pertengahan. Ditandai adanya riwayat sakit,fotofobia,dan penglihatan yang kabur,mata merah (merah sirkumneal) tanpa tahi mata purulen dan pupil kecil atau ireguler.Berdasarkan reaksi radang, uveitis anterior dibedakan tipe granulomatosa dan non granulomatosa. Penyebab uveitis anterior dapat bersifat eksogen dan endogen. Penyebab uveitis anterior meliputi: infeksi, proses autoimun, yang berhubungan dengan penyakit sistemik, neoplastik dan idiopatik.1 Pola penyebab uveitis anterior terus berkembang sesuai dengan perkembangan teknik pemeriksaan laboratorium sebagai sarana penunjang diagnostik. Lebih dari 75% uveitis endogen tidak diketahui penyebabnya, namun 37% kasus di antaranya ternyata merupakan reaksi imunologik yang berkaitan dengan penyakit sistemik. Penyakit sistemik yang berhubungan dengan uveitis anterior meliputi: spondilitis ankilosa, sindroma Reiter, artritis psoriatika, penyakit Crohn, kolitis ulserativa, dan penyakit Whipple. Keterkaitan antara uveitis anterior dengan spondilitis ankilosa pada pasien

dengan predisposisi genetik HLA-B27 positif pertama kali dilaporkan oleh Brewerton et al.1,2 Insidensi uveitis sekitar 15 per 100.000 orang.Sekitar 75% merupakan uveitis anterior.Sekitar 50% pasien dengan uveitis menderita penyakit sistemik terkait.Di Amerika Serikat,uveitis merupakan penyebab kebutaan nomor tiga setelah Retinopati Diabetik dan Degenerasi Macular.Umur penderita biasanya bervariasi antara usia prepubertal sampai 50 tahun. 1,3 Variasi gejala sering dijumpai, hal ini berhubungan dengan faktor penyebabnya dan dimana kelainan itu terjadi,biasanya pasien datang mengeluh nyeri ocular,Fotofobia,penglihatan kabur, dan mata merah.Pada pemeriksaan didapatkan tajam penglihatan menurun,terdapat injeksi siliar,KP,flare,hipopion,sinekia posterior,tekanan intra okuler bisa meningkat hingga sampai edema macular.1,2,3 Tujuan penulisan referat ini adalah untuk mengetahui secara umum mengenai definisi, etiologi dan fisiologi anatomi, patofisiologi dan patogenesis, manifestasi klinis, penegakan diagnosis, penatalaksanaan serta prognosis dari uveitis anterior.

BAB II TINJAUAN PUSTAKA DEFINISI Uveitis adalah inflamasi traktus uvea (iris,korpus siliaris,dan koroid) dengan berbagai penyebabnya.Struktur yang berdekatan dengan jaringan uvea yang mengalami inflamasi biasanya juga ikut mengalami inflamasi. ETIOLOGI

Uveitis anterior merupakan peradangan iris dan badan siliar yang dapat berjalan akut maupun kronis. Penyebab dari iritis tidak dapat diketahui dengan melihat gambaran klinisnya saja. Iritis dan iridisiklitis dapat merupakan suatu manifestasi klinik reaksi imunologik terlambat, dini atau sel mediated terhadap jaringan uvea anterior. Uveitis anterior dapat disebabkan oleh gangguan sistemik di tempat lain, yang secara hematogen dapat menjalar ke mata atau timbul reaksi alergi mata.5 Penyebab uveitis anterior diantaranya yaitu: idiopatik; penyakit sistemik yang berhubungan dengan HLA-B27 seperti; ankylosing spondilitis, sindrom Reiter, penyakit crohns, Psoriasis, herpes zoster/ herpes simpleks, sifilis, penyakit lyme, inflammatory bowel disease; Juvenile idiopathic arthritis; Sarcoidosis, trauma dan infeksi. 1,3, 4,5,6 ANATOMI FISIOLOGI Uvea terdiri dari : iris, badan siliaris (corpus siliaria) dan koroid. Bagian ini adalah lapisan vascular tengah mata dan dilindungi oleh kornea dan sklera. Bagian ini juga ikut memasok darah ke retina. Iris dan badan siliaris disebut juga uvea anterior sedangkan koroid disebut uvea posterior. 6,7 Iris adalah lanjutan dari badan siliar ke anterior dan merupakan diafragma yang membagi bola mata menjadi 2 segmen, yaitu segmen anterior dan segmen posterior, di tengah-tengahnya berlubang yang disebut pupil. Iris membagi bilik mata depan (camera oculi anterior) dan bilik mata posterior (camera oculi posterior). Iris mempunyai kemampuan mengatur secara otomatis masuknya sinar ke dalam bola mata. 5,6 Secara histologis iris terdiri dari stroma yang jarang diantaranya terdapat lekukanlekukan dipermukaan anterior yang berjalan radier yang dinamakan kripa. Didalam stroma terdapat sel-sel pigmen yang bercabang, banyak pembuluh darah dan saraf.

Uveitis
URL of this page: http://www.nlm.nih.gov/medlineplus/ency/article/001005.htm

Uveitis is swelling and irritation of the uvea, the middle layer of the eye. The uvea provides most of the blood supply to the retina.

Causes
Uveitis can be caused by autoimmune disorders such as rheumatoid arthritis or ankylosing spondylitis, infection, or exposure to toxins. However, in many cases the cause is unknown. The most common form of uveitis is anterior uveitis, which involves inflammation in the front part of the eye. It is often called iritis because it usually only affects the iris, the colored part of the eye. The inflammation may be associated with autoimmune diseases, but most cases occur in healthy people. The disorder may affect only one eye. It is most common in young and middle-aged people. Posterior uveitis affects the back part of the uvea, and involves primarily the choroid, a layer of blood vessels and connective tissue in the middle part of the eye. This type of uveitis is called choroiditis. If the retina is also involved, it is called chorioretinitis. You may develop this condition if you have had a body-wide (systemic) infection or if you have an autoimmune disease. Another form of uveitis is pars planitis. This inflammation affects the narrowed area (pars plana) between the colored part of the eye (iris) and the choroid. Pars planitis usually occurs in young men and is generally not associated with any other disease. However, some evidence suggests it may be linked to Crohn's disease and possibly multiple sclerosis. Uveitis can be associated with any of the following:

AIDS Ankylosing spondylitis Behcet syndrome CMV retinitis Herpes zoster infection Histoplasmosis Injury Kawasaki disease Psoriasis

Reactive arthritis Rheumatoid arthritis Sarcoidosis Syphilis Toxoplasmosis Tuberculosis Ulcerative colitis

Symptoms
Uveitis can affect one or both eyes. Symptoms may develop rapidly and can include:

Blurred vision Dark, floating spots in the vision Eye pain Redness of the eye Sensitivity to light

Exams and Tests


A complete medical history and eye examination should be performed. Laboratory tests may be done to rule out infection or an autoimmune disorder. Persons over age 25 with pars planitis should have an MRI of their brain and spine to rule out multiple sclerosis.

Treatment
Iritis is usually mild. Treatment may involve:

Dark glasses Eye drops that dilate the pupil to relieve pain Steroid eye drops

Pars planitis is often treated with steroid eye drops. Other medicines, including steroids taken by mouth, may be prescribed to help suppress the immune system. Posterior uveitis treatment depends on the underlying cause but almost always includes steroids taken by mouth. Additional specialists in infectious disease or autoimmunity may be needed for such diseases as syphilis, tuberculosis, AIDS, sarcoidosis, or Behcet syndrome. If the uveitis is caused by a body-wide infection, treatment may involve antibiotics and powerful anti-inflammatory medicines called corticosteroids. See autoimmune disorders for information on treating such diseases.

Outlook (Prognosis)
With proper treatment, most attacks of anterior uveitis go away in a few days to weeks. However, relapses are common. Inflammation related to posterior uveitis may last from months to years and may cause permanent vision damage, even with treatment.

Possible Complications

Cataracts Fluid within the retina Glaucoma Retinal detachment Vision loss

When to Contact a Medical Professional


Call for an appointment with your health care provider if you have symptoms of uveitis. Eye pain or reduced vision are urgent symptoms that require prompt medical attention.

Prevention
Treatment of an underlying disorder may help to prevent uveitis in persons with a bodywide (systemic) infection or disease

ANTERIOR UVEITIS
SIGNS AND SYMPTOMS
The typical presentation of anterior uveitis involves pain, photophobia and excessive tearing. Patients report a deep, dull aching of the involved eye and surrounding orbit. Associated sensitivity to lights may be severe; often, these patients will present wearing dark sunglasses. The excessive tearing occurs secondary to increased neural stimulation of the lacrimal gland, and is not associated with a foreign body sensation. Visual acuity is not usually impaired to any great extent (20/40 or better is common), although patients may report some haziness. Accommodative tasks, however, may prove more difficult and uncomfortable. Inspection may reveal mild to moderate congestion of the lids, resulting in pseudoptosis. You'll typically see a deep perilimbal injection of the conjunctiva and episclera, although the palpebral conjunctiva is characteristically normal. The cornea may display mild edema upon biomicroscopy. In more severe reactions, you may observe grayish brown endothelial deposits, known as keratic precipitates.

The hallmark signs of anterior uveitis are "cells and flare." Cells are leukocytes (white blood cells) floating in the convection currents of the aqueous; flare refers to liberated protein from the inflamed iris or ciliary body which gives the aqueous a particulate, or smoky, appearance. The iris may adhere to the lens capsule (posterior synechia) or, less commonly, to the peripheral cornea (anterior synechia). Additionally, you may see granulomatous nodules within the iris stroma. Intraocular pressure in the affected eye is initially reduced due to secretory hypotony of the ciliary body. However, as the reaction persists, inflammatory by-products may accumulate in the trabeculum. If this debris builds significantly, and if the ciliary body resumes its normal secretory output, the pressure may rise sharply, resulting in a secondary uveitic glaucoma.

PATHOPHYSIOLOGY
Uveitis, as the name implies, represents an inflammation of the uveal tissues, chiefly the iris and ciliary body. Inflammation may be associated with underlying systemic disease, or it may occur as a direct result of ocular trauma. Occasionally, inflammatory reactions in adjacent tissues (e.g., keratitis), can induce a secondary uveitis. Uveitis can be either acute or chronic. The chronic form is more often associated with systemic disorders including, but not limited to, ankylosing spondylitis, Behet's syndrome, inflammatory bowel disease, juvenile rheumatoid arthritis, Reiter's syndrome, sarcoidosis, syphilis, tuberculosis, and Lyme disease. Chronic uveitis most likely occurs due to an immunopathological mechanism which is not fully understood.

MANAGEMENT
There are two primary goals when managing anterior uveitis. First, immobilize the iris and ciliary body to decrease pain and prevent exacerbation of the condition. Second, quell the inflammatory response. Begin by cyclopleging the patient with homatropine 5% TID/QID, scopolamine 0.25% BID/QID or atropine 1% BID, depending upon the severity of the reaction. Next, prescribe a topical steroid Q2-3H, or more often if the reaction is severe. If there's a posterior synechia present, attempt to break the adhesion in the office using atropine 1% and phenylephrine 10%. Treat secondary elevations in IOP using standard anti-glaucoma agents, such as timolol 0.5% BID or dorzolamide 2% TID. Avoid pilocarpine in uveitic glaucoma, as it will only serve to worsen the inflammatory response by mobilizing the uveal tissues. After beginning treatment, re-evaluate the patient every one to seven days depending on the severity of the reaction. As the uveitis resolves, discontinue the cycloplegics and taper the steroids to QID or TID. Generally, it is better to taper slowly rather than abruptly, and patients may need to remain on steroid drops daily or every other day for several weeks. In recalcitrant uveitis which is unresponsive to conventional therapy, consider injectible steroids such as methylprednisolone 60mg or even oral steroids such as prednisone 60 to 80mg.

CLINICAL PEARLS
Acute anterior uveitis results most commonly as a result of blunt ocular trauma. In most instances, these cases resolve without incident and do not recur when properly managed. Consider any cases of recurrent uveitis, defined as three or more unexplained incidents, to be representative of underlying systemic inflammatory disease until proven otherwise. Hematologic testing is indicated for any recurrent, chronic or bilateral presentation. A standard battery of laboratory tests should include: complete blood count (CBC) with differential, antinuclear antibody (ANA), HLA-B27, rheumatoid factor (RF), angiotensin-converting enzyme (ACE), purified protein derivative (PPD), fluorescent treponemal antibody absorption (FTA-ABS) and rapid plasma reagin (RPR). A chest X-ray is also important in identifying both sarcoidosis and tuberculosis. A Lyme titer is also recommended if you suspect that the patient may have been bitten by a deer tick.

Always perform a comprehensive, dilated fundus evaluation in these cases. Anterior uveitis may actually constitute a "spillover" of posterior ocular inflammation.