Uveitis 葡萄膜炎 眼科学 英文分析课件.ppt

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1、Uveitis,Burning of the eyeRedness of the eyeBlurred visionPhotophobia or sensitivity to lightKeratic precipitates,CASE 1,Episodes are considered to be short if they last for less than 3 monthsLong or chronic if they last longer,acute or chronic,Severevisual loss is 50% or more of prediseased vision

2、or if 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 mild,anterior uveitis includes iritis and iridocyclitisintermediate uveitis include

3、s cyclitis, vitritis, and parsplanitisposterior uveitis includes retinitis and choroiditis.panuveitis -inflammation of all parts of the uvea,anterior、intermediate or posterior,unilateraltoxocariasis and Fuchs iridocyclitisunilateralbilateralHLA-B27-associated iridocyclitisbilateralVogt-Koyanagi-Hara

4、da (VKH) syndrome,unilateral or bilateral,Uveitis is considered granulomatous if there are Busacca nodules in the iris stroma, large greasy “mutton-fat” keratic precipitates, large vitreous snowballs, or choroidal granulomas,granulomatous or nongranulomatous,ciliary spasm. radiate to the periorbital

5、 region and to the eye. axon reflex. cycloplegia,PAIN,distinguished from the photodysphoria or photoaversionprominent symptomcycloplegia may lessen photophobia and pain,PHOTOPHOBIA,floaters macular edemamicropsia, and metamorphopsia.,BLURRED VISION,radiating from the limbus. distinguished from the d

6、eeper and more peripheral injection of scleritis and from the sectoral or diffuse injection of episcleritis. overlying conjunctival injection neosynephrine,CILIARY INJECTION,Clusters of inflammatory cells deposited on the endothelial surface of the cornea,KERATIC PRECIPITATES,slit-lamp beam is seen

7、in the anterior chamber“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 FLARE,active in

8、flammation of the iris and ciliary bodylarger cells macrophages or lymphocytessmaller cells may be individual lymphocytes,ANTERIOR CHAMBER CELLS,Grade Cells per Field0 No cellsRare 12Occasional 371+ 7102+ 10203+ 20504+ 50 or more,Patients with acute anterior uveitis usually present with low IOPPatie

9、nts with chronic iridocyclitis frequently develop elevated IOP,INTRAOCULAR PRESSURE,Grade 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

10、head obscured,VITREOUS OPACITIES AND HAZE,VogtKoyanagiHarada disease,bilateral 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 o

11、f these factors;meningitis, CSF 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, m

12、eningismus, tinnitus, and/or vertigo. 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 granulo

13、matous anterior uveitis, variable 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 phase,gradual tissue depigmentation of

14、 skin with vitiligo and poliosisnummular depigmented scarsalopecia diffuse fundus depigmentation resulting in a classic orange-red discoloration (sunset glow fundus)retinal pigment epithelium clumping and/or migration.,convalescent phase,repeated bouts of uveitisgranulomatous anterior inflammationca

15、taractsglaucomaocular hypertensiondysacusia,chronic recurrent phase,If 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.,diagnosis,electroretinogramvisual field testingretinograph

16、yfluorescein indocyanine green angiographyoptical coherence tomography ultrasoundocular MRI audiologic testinghistopathology,diagnosis,the acute uveitis phase of VKH is usually responsive to high-dose oral corticosteroids; parenteral administration is usually not required. ocular complications may r

17、equire an subtenon or intravitreous injection 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 (IVI

18、G) or infliximab may be needed.cycloplegic agents,treatment,Visual 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 effect

19、s such as cataracts, glaucoma, and optic atrophy can occur. Skin changes usually persist despite therapy.,prognosis,Sympathetic ophthalmia,Eye floaters severe uveitis with pain and photophobia. symptoms like VKH,seeking a history of eye injuryskin tests with soluble extracts of human or bovine uveal

20、 tissue are said to elicit delayed hypersensitivity 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.,diagnosis,Sympathetic ophthalmia i

21、s rare, affecting 0.2% to 0.5% of non-surgical eye wounds, and less than 0.01% of surgical penetrating eye wounds. There are no gender or racial differences in incidence of SO.,Epidemiology,Because SO is so rarely encountered following eye injury, even when the injured eye is retained, the first cho

22、ice of treatment may not be enucleation or evisceration, 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.,prevention,within the first 2 weeks of injur

23、y.Several retrospective studies involving over 3000 eviscerations, however, have failed to identify a single case of SO.,prevention,Immunosuppressive therapy (mainstay of treatment). it is effective in controlling the inflammation and improving the prognosismild cases may be treated with local appli

24、cation 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,