kuliah mata 1 - keratitis

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    Dr. RITA HENDRAWATI,SpM

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    1. INFECTIONBACTERIALVIRALF N AL

    ACANTHAOMEBA

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    Common causative agents :

    (affecting corneal epithelial integrity)

    Staph. epidermidis

    Staph. AureusStrept. PneumoniaH.infleunza

    P.aeruginosaN.gonorrhea

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    Predisposing factors:contact lens userskeratoconjunctivitis sicca (dry eye)prolonged use of topical steroids

    Trauma (breach in a corneal epithelium)use of contaminated ocular medicationsRecent corneal disease (herpetic keratitis,neurotrophic keratopathy)

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    Symptoms:Reduced visionPain in the eye (often sudden)Purulent dischargeExcessive tearingIncreased light sensitivity

    gns:Hypopyon ( a mass white cells collected in antchamber)White corneal opacityConjuctival injection (redness of eyes)

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    Complications:Corneal ulcerCorneal perforation 2ndary endopthalmitisVision lossIrregular astigmatism (uneven healing of stroma)Corneal leukoma (scar tss formation w cornealvascularization)

    Beware:Sight-threatening process

    Rapid progression infection; corneal destruction maybe complete in 24-48 hours

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    Treatment:Initiate topical broad-spectrum antibiotics :

    tobramycin (aminoglycoside gram -ve) alternating with

    fortified cefazolin (cephalosporin).If the corneal ulcer is small, peripheral and noimpending perforation is present, intensivemonotherapy with fluoroquinolones is an

    alternative treatment.Corneal graft ( in severe cases) .

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    HERPES SIMPLEX KERATITISHERPES ZOSTER OPTHALMICUS

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    HSV 1 : common viral cause of ocular diseases

    HSV 2: genital dis. Rarely can cause ocularmanifestations (rarely) such as keratitis & infantilechorioretinitis.HSV

    Primary infx is usually early in lifeEnters a latent period in the trigeminal ganglion,When activated it moves along the sensory partof the N. toward the target epith. causingdamage & ulceration.Factors leading to activation :psychiatric dis. ,systemic illnesses, immunocompromised pt.

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    Symptoms:

    -Typically unilateral red eye-Variable degree of pain-Occular irritation

    -Tearing-Vision may or may not be affected-Vesicular skin rash and follicular conjunctivitis

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    Signs:A dendritic corneal ulcer (hallmark sign of HSV

    infection)Ulcer may heal without scar but may progressedto stromal keratitis

    edemaLoss of corneal transparency in more severepresentations.

    Uveitis and glaucoma may accompany disease

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    Because the virus invades and compromises theepithelial cells surrounding the ulcer, the leadingedges (the so-called "terminal end-bulbs") will stainwith rose bengal or lissamine green.

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    Diagnosed with a slit lamp examinationTreatment :

    topical antivirals acyclovir ointment

    DONT USE TOPICAL STEROIDS as theyworsen the ulcer to geographic ulcerIf recur more than twice a year give oral acyclovir

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    Varicela zoster virus -affect the ophthalmicdivision of the trigeminal N. (15% )Increases with age (6 th-7 th decades).

    nasocillary N is involved >>lid swelling (maybebilateral), keratitis ,iritis, secondary glaucoma.Other ocular manifest. :ptosis, mucus secreting

    conjunctivitis, neuralgia& scleritis which may leadto scleral atrophy.

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    Symptoms:Have prodromal period, typically presents withnondescript facial pain, fever and generalmalaise .About four days after onset, a unilateral vesicularskin rash over forehead, upper eyelid, nose (1 stdiv of 5 th CN) , characteristically respecting the

    .begin to scab over after about one week. The pain isextreme during the inflammatory stage, and patientsare tremendously symptomatic.

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    Signs:Cornea : Punctate epithelial keratitis (swollenepithelium, 1-2 d); dendritic keratitis (treebranchlike epithelial defects, 4-6 d); stromal keratitis(fine infiltrates beneath the surface, 1-2 wk); deepstromal keratitis (lipid infiltrates and cornealneovascularization, 1 month to years); neurotrophickeratopathy (erosions, persistent defects, cornealulcers, months to years)Ocular involvement ma include follicular

    conjunctivitis, epithelial and/or interstitialkeratitis, dendritic keratitis, ant chamber uveitis,scleritis or episcleritis, chorioretinitis, opticneuropathy, and even neurogenic motilitydisorders (especially fourth cranial nerve palsy).

    Prognostic indicator: Hutchinsons Sign

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    Hutchinsons Sign

    Lesions at tip, side, root ofnoseInnervated by ant ethmoidal

    branch of nasociliary N.Nasociliary N. also innervatescornea n ciliary body

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    Treatment:

    Oral and topical antiviral : acyclovir , valcycloviror famcyclovir ( prevent post-infective neuralgia-severe chronic pain over the rash)

    - .

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    Infxs r rare , but they very severe & devastatingas they cause stromal necrosis.They r capable of penetrating the descemetsmembrane reaching the ant. chamber where wecannot do anything because of the poorpenetration of antimycotic agents to the ant.

    Chamber.Most common causative pathogens :

    Filamentous (aspergillus & fusarium) fungi

    Candida albicansProgression is much slower & less painful than inbacterial.

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    Keratomycosis in consideration when we findlack of response to antibacterial therapy ofcorneal ulceration.

    Signs include :Filamentous infx: grayish infiltrate with indistinct margins

    Candidal infx: yellow to white ulcer with suppuration

    similar to bacterial keratitis.Treatment : topical antifungals pimaricin 5%

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