Head prof. MUDr. E. Vlková, CSc. MUDr. Karkanová Michala, Oční klinika LF MU a FN Brno Ò3 parts: Øiris (iris) Øciliary body (corpus ciliare) Øchoroid (choroidea) Ò ÒFunction: Øregulating the entry of light into the eye pupil Øacomodation Øproduction of aqueous humor Øfood security of the light-sensitive elements and the retinal pigment epithelium Ò Ò Ò ÒUveitis – inflammation of the uvea Ò ØIntraocular inflammation causes damage of the endothelium of intraocular vessels with the collapse of the blood-barrier. Ò ØThere is a dilation of blood vessels, leakage intravascular content into the intravascular space, migration of leukocytes and other cells. Ò Ò Ò ÒAnatomical: Øfront (iritis, iridocyclitis) Øintermediate (pars planitis, cyclitis, vitritis) Ørear(choroiditis, chorioretinitis) Øall parts (panuveitis) Ø ÒClinical: Øacute - symptoms suddenly, lasting no longer than 6 weeks Øchronical - gradual onset of symptoms, duration of more than 6 weeks Ò Ò Ò Ò Ò ÒPatological: Ò Ønongranulomatous – acute formation, short duration, significant ciliary injection, small precipitates on the corneal endothelium,cells in the anterior chamber, fibrinous exudate, disability choroid rare Ø Øgranulomatous – slow fomation, protracted course, significant ciliary injection, sintered large precipitates on the corneal endothelium, iris nodules, vitritis, often affected choroid Ò Ò Ò Ò Ò Ò Ò Ò ÒAccording to the etiology: ÒExogennous (injury uvea, microorganism invasion from the outside) Ò ÒEndogennous (inner, systemic inflammatory origin) Øuveitis associated with systemic disease Ò (eg. ankylosing spondylitis, sarcoidosis, tuberculosis, Ò multiple sclerosis) Øuveitis associated with parazitic infection (eg. toxokarosis) Øuveitis associated with viral infection (eg. herpes simplex) Øuveitis asscoiated with fungal infection (eg. candida) Øidiopathic uveitis (comprises about 25% of all uveitis) Ø a. Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒSigns and symptoms: Øeye pain, photophobia, epiphora ciliary injection Øsmall precipitates on the corneal endothelium, abundant cells in the anterior chamber, in the course of severe fibrinous exudate in the anterior chamber Øhypopyon Ørear synechiae formation (adhesions between the iris and lens) Ødilation of blood vessels in the iris Øweeks duration of inflammation Øchronic complications (formation of rear synechiae in case of delayed treatment, complicated cataract development) Øtreatment: corticosteroids locally, parabulbar, if necessary, generally, mydriatics, in the case of viral etiology antivirals Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒEtiology: ØHLA B27+ izolation, Ankylozing spondilitis ( M. Bechtěrev), Reiter syndrom, M. Crohn, Colitis ulcerosa, Ò Psoriatic artritis ØM. Behcet – triad: iritis, aphtous stomatitis, ulcers on genital ØGlaukomatocyklic crizis (Posner-Schlossman syndrom) – attacks slight iritis associated with high intraocular pressure elevation ØPhacoanafylaktic uveitis – imunological reaction on free proteins of the lens ØViral diseases – Herpes simplex, zoster in combination with keratitis Ò (maybe nongranulomatous and granulomatous type) Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒSigns and symptoms: Øcreeping course, variable symptoms, usually no pain or only mild pain Ømild ciliary injection, mostly pale bulb, a small amount of precipitates on the corneal endothelium, a small number of cells in the anterior chamber Ølower tendency to the formation of the rear synechiae, chronic complications according to the disease activity (formation of complicated cataract, secondary glaucoma) ØTreatment: corticosteroids and nonsteroidal anti-inflammatory drugs locally, if necessary parabulbar or in total, mydriatics, and according to etiology Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒEtiology: ØJuvenile rheumatoid arthritis ØFuchs heterochromic iridocyclitis (heterochromy – difference in color due to diffuse iris stromal atrophy) ØSarcoidosis (granulomatous inflammation type) ØSyphilis ( roseolae of iris ) ØLyme disease ØTBC ( granulomatous inflammation type, yelow nodules on iris) Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒManifestations, symptoms, etiology: Øcreeping course, without pain, decrease vision- opacities, fog Ømostly pale bulb Øvitritis - vitreous opacities (snowballs, snow benches) Øminimal tendency to form the rear synechiae Øwith increased activity of inflammation macular edema Øchronic complications (development of complicated cataract, macular epiretinal membranes, preretinaland subretinal neovascular membranes) ØTreatment: according to the disease activity monitoring, corticosteroids overall or intravitreal corticosteroids, immunosuppressants (cyclosporine), biological therapy, PPV Øpossible link with MS, Lyme disease or unclear Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒManifestations symptoms: Ò Øbeginning acute and insidious, without pain, decrease vision- vitreous opacities, fog Ømostly pale bulb Øvitritis - vitreous opacities Øill-defined plump yellow inflammatory bearing affecting the retina and choroid (focal or multifocal) Øwith increased activity of inflammation macular edema Øchronic complications (development of chorioretinal scars) ØTreatment: due to etiology, in infectious etiology causally antibiotics, antivirals systemically, in autoimmune etiology systemic corticosteroids or immunosuppressive systemically Øin the differential diagnosis must be ruled malignant disease of intraocular lymphoma Ò Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒEtiology: ØToxoplasmosis (frequently) ØToxocarosis ØCandidosis (in patient with decreased imunity) ØSarcoidosis,TBC (granulomatous inflammation type) ØHerpes simplex, zoster retinitis ØCMV retinitis ( in immunocompromised patients) ØWhite dot syndroms (isolated autoimmune inflammation against retinal structures) ØSympathetic ophthalmia ØVogt-Koyanagi-Harada syndrom (uveoencefalitis) Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒInflammation of the whole uveal tract - the most common etiology: ØToxoplasmosis ØSarkoidosis,TBC ØM. Behcet ØSyphilis ØSympathetic ophthalmia ØVogt-Koyanagi-Harada syndrom (uveoencefalitis) Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒSevere form of intraocular inflammation affecting intraocular tissue structures, but does not go beyond the sclera. ØExogenous - postoperative (acute 1-14 days after surgery, chronic two weeks up to two years after surgery), post-traumatic ØEndogenous - hematogenous transmission of pyogenic bacteria or mold for generalized septicemia Frequently agent: Staphylococcus, Streptococcus, Candida, Propionibacterium, Klebsiella, Haemophilus, Escherichia Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò ÒManifestation, Symptoms: ØAcute endophthalmitis – pain, sudden decrease in vision, conjunctivitis, edema of the eyelids, corneal edema, hypopyon, vitritis ØChronic endophthalmitis – without pain, visual acuity decreased only slightly, hypopyon just sometimes, mild vitritis ÒTreatment: ØATB, antimycotics in infusions, eventuel. intravitreal ØPPV Ø Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò Ò