Uveitis-葡萄膜炎-眼科学-英文分析课件.ppt

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1、UveitisBurning of the eyeRedness of the eyeBlurred visionPhotophobia or sensitivity to lightKeratic precipitatesCASE 1Episodes are considered to be short if they last for less than 3 monthsLong or chronic if they last longer acute or chronicSeverevisual loss is 50% or more of prediseased vision or i

2、f there is 50% or more loss of the electroretinogram amplitudes from normal Mildvisual acuity is less than 50% decreased from baseline or the electroretinogram amplitudes are decreased by less than 50%.severe or mildanterior uveitis includes iritis and iridocyclitisintermediate uveitis includes cycl

3、itis, vitritis, and parsplanitisposterior uveitis includes retinitis and choroiditis.panuveitis -inflammation of all parts of the uveaanterior、intermediate or posteriorunilateraltoxocariasis and Fuchs iridocyclitisunilateralbilateralHLA-B27-associated iridocyclitisbilateralVogt-Koyanagi-Harada (VKH)

4、 syndromeunilateral or bilateralUveitis is considered granulomatous if there are Busacca nodules in the iris stroma, large greasy “mutton-fat” keratic precipitates, large vitreous snowballs, or choroidal granulomasgranulomatous or nongranulomatousciliary spasm. radiate to the periorbital region and

5、to the eye. axon reflex. cycloplegia PAINdistinguished from the photodysphoria or photoaversionprominent symptomcycloplegia may lessen photophobia and painPHOTOPHOBIAfloaters macular edemamicropsia, and metamorphopsia.BLURRED VISIONradiating from the limbus. distinguished from the deeper and more pe

6、ripheral injection of scleritis and from the sectoral or diffuse injection of episcleritis. overlying conjunctival injection neosynephrine CILIARY INJECTIONClusters of inflammatory cells deposited on the endothelial surface of the cornea KERATIC PRECIPITATESslit-lamp beam is seen in the anterior cha

7、mber“flare”represents breakdown of the blood-aqueous barrier with exudation of protein. Flare Description0 Complete absence1+ Faint flare (barely detectable)2+ Moderate flare (iris and lens details clear)3+ Marked flare (iris and lens details hazy)ANTERIOR CHAMBER FLAREactive inflammation of the iri

8、s and ciliary bodylarger cells macrophages or lymphocytessmaller cells may be individual lymphocytesANTERIOR CHAMBER CELLSGrade Cells per Field0 No cellsRare 12Occasional 371+ 7102+ 10203+ 20504+ 50 or morePatients with acute anterior uveitis usually present with low IOPPatients with chronic iridocy

9、clitis frequently develop elevated IOPINTRAOCULAR PRESSUREGrade Description0 No hazeTrace Slight blurring of optic disc margin1+ Slightly blurred optic nerve and vessels2+ Moderately blurred optic nerve and vessels3+ Optic nerve head border blurry but visible4+ Optic nerve head obscuredVITREOUS OPAC

10、ITIES AND HAZEVogtKoyanagiHarada diseasebilateral diffuse uveitispainrednessblurring of vision. auditory (tinnitus,vertigo, and hypoacusis)neurological (meningismus, with malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors;meningitis, C

11、SF pleocytosis, cranial nerve palsies, hemiparesis, transverse myelitis and ciliary ganglionitis)cutaneous manifestations, including poliosis, vitiligo, and alopecia. The vitiligo often is found at the sacral region.may have no symptoms may be fever, headache, nausea, meningismus, tinnitus, and/or v

12、ertigo. orbital pain, photophobia and tearing. skin and hair may be sensitive to touch.cranial nerve palsies and optic neuritis are uncommon.prodromal phase bilateral panuveitis causing blurring of vision if initially unilateralThe process can include bilateral granulomatous anterior uveitis, variab

13、le degree of vitritis, thickening of the posterior choroid with elevation of the peripapillary retinal choroidal layer, optic nerve hyperemia and papillitis, and multiple exudative bullous serous retinal detachments.acute uveitic phasegradual tissue depigmentation of skin with vitiligo and poliosisn

14、ummular depigmented scarsalopecia diffuse fundus depigmentation resulting in a classic orange-red discoloration (sunset glow fundus)retinal pigment epithelium clumping and/or migration.convalescent phaserepeated bouts of uveitisgranulomatous anterior inflammationcataractsglaucomaocular hypertensiond

15、ysacusiachronic recurrent phaseIf tested in the prodromal phase, CSF pleocytosis is found in more than 80%, mainly lymphocytes. This pleocytosis resolves in about 8 weeks even if chronic uveitis persists.diagnosiselectroretinogramvisual field testingretinographyfluorescein indocyanine green angiogra

16、phyoptical coherence tomography ultrasoundocular MRI audiologic testinghistopathology diagnosisthe acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. ocular complications may require an subtenon or intravitreous inje

17、ction of corticosteroids or bevacizumab.in refractory situations, other immunosuppressives such as cyclosporine, or tacrolimus, antimetabolites (azathioprine, mycophenolate mofetil or methotrexate), or biological agents such as intravenous immunoglobulins (IVIG) or infliximab may be needed.cyclopleg

18、ic agentstreatmentVisual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment. Inner ear symptoms usually respond to corticosteroid therapy within weeks to months; hearing usually recovers completely. Chronic eye effects such as cataracts, glaucoma, and optic a

19、trophy can occur. Skin changes usually persist despite therapy.prognosisSympathetic ophthalmiaEye floaters severe uveitis with pain and photophobia. symptoms like VKHseeking a history of eye injuryskin tests with soluble extracts of human or bovine uveal tissue are said to elicit delayed hypersensit

20、ivity responses in these patients.circulating antibodies to uveal antigens have been found in patients with SO and VKH, as well as those with long-standing uveitis, making this a less than specific assay for SO and VKH.diagnosisSympathetic ophthalmia is rare, affecting 0.2% to 0.5% of non-surgical e

21、ye wounds, and less than 0.01% of surgical penetrating eye wounds. There are no gender or racial differences in incidence of SO.EpidemiologyBecause SO is so rarely encountered following eye injury, even when the injured eye is retained, the first choice of treatment may not be enucleation or eviscer

22、ation, especially if there is a chance that the injured eye may regain some function. Additionally, with current advanced surgical techniques, many eyes once considered nonviable now have a fair prognosis.preventionwithin the first 2 weeks of injury.Several retrospective studies involving over 3000

23、eviscerations, however, have failed to identify a single case of SO.preventionImmunosuppressive therapy (mainstay of treatment). it is effective in controlling the inflammation and improving the prognosismild cases may be treated with local application of corticosteroids and pupillary dilators. severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy , may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.treatment