4. dry eye syndrome - dr. bella

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    DRY-EYE SYNDROMENIKA BELLARINATASARI

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    DEFINITION

    "a multifactorial disease of the tears and ocular surface thatresults in symptoms of discomfort, visual disturbance, andtear-film instability with potential damage to the ocularsurface. It is accompanied by increased osmolarity of thetear film and inflammation of the ocular surface" (DEWS,2007).

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    Dry eye represents a disturbance of the lacrimalfunctional unit (LFU), an integrated system comprisingthe lacrimal glands, ocular surface (cornea, conjunctiva,and meibomian glands), and eyelids, as well as thesensory and motor nerves that connect them

    Its overall functions are

    to preserve tear-film integrity: lubricating, antimicrobial,and nutritional roles

    ocular surface health: maintaining corneal transparency andsurface stem cell population

    quality of image projected onto the retina

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    MECHANISM OF DRY EYE

    The core mechanisms of dry eye are driven by tearhyperosmolarity and tear-film instability

    Tear hyperosmolarity causes damage to the surface

    epithelium by activating a cascade of inflammatoryevents at the ocular surface and release of inflammatorymediators into the tears

    Epithelial damage involves cell death by apoptosis, aloss of goblet cells, and disturbance of mucin expression

    leading to tear-film instability The instability of tear film exacerbates oculer surface

    hyperosmolarity and completes the vicious cycle.

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    Tear-film instability can also be initiated by severaletiologies :

    Xerosing medication

    Xerophthalmia

    Ocular allergy

    Topical preservative use

    Contact lens wear

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    TEAR-FILM EVALUATION

    The best approach

    is to combine information from thehistory and examination with the results of one or moreof the fo llowing diagnostic tests.

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    Inspection Signs of associated systemic disease (rheumatoid arthritis)

    Indications of personal habits (smoking)

    Signs of associated ocular disease (pseudoptosis,blepharospasm)

    Characteristic facial telangiectasia & eyelid marginhyperemia associated with ocular rosacea

    Tear meniscus between the globe and the lower eyelid(normally 1.0 mm in height and convex)

    Tear breakup is a functional measure of tear stability; if

    stability is perturbed (as in lipid or mucin deficiency), thetear breakup time (TBUT) can become more rapid

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    Tear Breakup Time (TBUT)

    The examiner moistens a fluorescein strip with sterile saline

    and applies it to the tarsal conjunctiva (fluorescein-anesthetic combination drops are not suitable for thispurpose).

    After several blinks, the tear film is examined using a broadbeam of the slit lamp with a blue filter.

    The time lapse between the last blink and the appearanceof the first randomly distributed dry spot on the cornea isthe tear breakup time.

    Dry spots appearing in less than 10 seconds are consideredabnormal.

    TBUT should be measured before any eyedrops areinstilled and before the eyelids are man ipulated in any

    way. It is best to wait at least 1 minute after fluorescein

    instillation to evaluate the corneal su rface forfluorescein staining

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    The eye should be carefully

    Tear-film debris

    Conjunctivochalasis (complain of epiphora)

    Floppy eyelid syndrome

    Multiple concretions (chronis blepharitis)

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    TESTS OF TEAR PRODUCTION

    Schirmer testing is performed by placing a thin strip offilter paper in the inferior cul-de-sac. The amount ofwetting can be measured to quanti fy aqueous tearproduction

    The basic secretion test is performed following theinstillation of a topical anesthetic, followed by lightlyblotting residual fluid out of the inferior fornix. A thinfilter-paper strip (5 mm wide, 35 mm long) is placed atthe junction of the middle and lateral thirds of the lowereyelids to minimize ir ritation to the cornea during the

    test. The test can be performed with open or closedeyes, although some recommend the eyes be closed tolimit the effect of blinking.

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    The Schirmer I test, which is si milar to the basicsecretion test but without topical anesthetic, measu resboth basic and reflex tearing combined

    The Schirmer II test, wh ich measures reflex secretion,is performed in a similar manner without topicalanesthetic. However, after the filter-paper strips havebeen inse rted into the in ferior fornices, a cotton-tippedapplicator is used to irritate the nasal mucosa.

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    AQUEOUS TEAR DEFICIENCY

    Definiton : decreased aqueous tear production, asmeasured by Schirmer testing, pattern of conjunctival &/corneal staining with lissamine green or rose bengal,corneal staining by fluorescein, and filamentarykeratopathy

    Symptoms

    Burning, photophobia, dry sensation, blurred vision, foreignbody sensation

    Signs :

    Conjunctival hyperemia, conjunctivochalasis, decreased tearmeniscus, iregular corneal surface, debreis in tear-film

    Epithelial keratopathy

    Filaments & mucous plaques , filamentary keratopathy,marginal or paracentral thinning & perforation corneal(more severe dry eye states)

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    EVAPORATIVE TEARDYSFUNCTION

    Increased tear-film evaporation is most commonlycaused by MGD but may also be caused by disease ofthe meibomian glands, poor apposition of the eyelids tothe ocular surface, increase of the palpebral aperture,

    and contact lens wear.

    Symptoms consist of burning, foreign-body sensation,redness ofthe eyelids and conjunctiva, filmy vision, andrecurrent chalazia.

    Signs of ETD include decreased TBUT, MGD, abnormal

    aqueous tear production, and a characteristic linearpattern of rose bengal/lissamine green staining of theinferior conjunctiva and cornea and eyelid margin.

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    MEIBOM GLAND DYSFUNCTION

    Meibom Gland Dysfunction

    Terjadi akibat obstruksi progresif lubang kelenjar meibom karenakeratinisasi.

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    Sehingga ada penurunan lapisan lipid permukaan mata

    dan peningkatan inflamasi pada kelopak yang ditandai :

    Hiperemia tepi kelopak dan konjungtiva tarsal

    Sekresi meibom bisa jernih, keruh atau kental.

    Lubang kelenjar meibom tertutup plug dan terletak lebih ke

    posterior akibat terbentuk sikatrik pada tepi kelopak dantarsal

    Patogenesis

    Tjd obstr/hiposekresi akibat penyakit blefaritis anterior,rosacea acne, pemfigoid

    Non obstr/ hipersekresi akibat meibomian seborrhea

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    Pasien MGD akan menjadi defisiensi air mata lipid yang

    akan menyebabkan instabil lapisan air mata,peningkatan penguapan tear film, dan peningkatanosmolaritas air mata

    Gejala & tanda

    Terasa terbakar/panas

    Sensasi benda asing, merah kelopak dan konjungtiva

    Filmy vision

    Kalazion rekuren

    Inflamasi tepi posterior kelopak mata, konjungtiva dan

    kornea

    Telangiectasi (brush marks) pada tepi anterior-posterior

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    Plug putih protein keratin menutupi lubang kelenjarmeibom

    Sekresi meibom berubah warna dan viskositasnya

    Bila inflamasi berlangsung th, terjadi atrofi kelenjarmeibom

    Terbentuh buih busa pada tear meniscus

    Rapid TBUT

    Bisa terjadi peradangan pd permukaan mata(konjungtivits, episcleritis, erosi epitel punctat kornea,

    pannus kornea, penipisan kornea)

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    Management

    Eyelid hygiene (1-2x/hari), dengan cara :

    kompres hangat beberapa menit dilanjutkan dg

    Gentle massage dengan menekan sekresimeibom, diikuti dengan membersihkan denganwashcloth, cotton ball, atau pad

    Shampo noniritasi atau pengenceran cairansodium bicarbonat (1 sdt dalam 0,5 liter airmendidih)

    Antibiotika topikal

    Tetrasiklin sistemik 250 mgx4/hari untuk 3-4 minggu

    pertama, bila membaik dosis diturunkan 250-500mg/hari. Atau

    Doxycyclin 100 mg dan minocyclin 50 mg diberikan2x/hari utk 3-4 minggu, ditaper 50-100 mg/hari

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    Eritromisin bila anak2 atau alergi tetrasiklin dandoxycyclin

    Pengobatan ini tujuannya utk mengontrol bukanmenyembuhkan penyakitnya

    Steroid topikal diperlukan bila inflamasinya sedangsmp berat, terutama bila ada infiltrat kornea danvaskularisasi

    Omega 3

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    TERIM K SIH