Anterior uveitis involves inflammation of the iris and ciliary body. Intermediate uveitis involves the posterior ciliary body and pars plana. Posterior uveitis involves the posterior vitreous, retina, choroid, retinal vasculature, and optic nerve. Panuveitis involves inflammation in the anterior, intermediate, and posterior segments of the eye.
All types of uveitis are potentially blinding conditions and should be referred to and managed by an experienced ophthalmologist.
Diagnosis is clinical. Acute anterior uveitis may be idiopathic, or associated with HLA-B27-related disease or viral eye disease. Posterior uveitis is associated with localized infections or systemic infection, or systemic inflammatory disease. Diagnosis of underlying disease may require investigation. In the clinical setting of multiple recurrences or strong suspicion based on history and review of systems, a targeted workup should be undertaken to rule out an underlying infectious cause or coexistent autoimmune disease. Rarely, uveitis can be caused by a previous eye injury or underlying neoplasm.
Even after full laboratory and diagnostic workup and treatment, etiology may not be determined.
Treatment for systemic disease causing uveitis must be given in conjunction with uveitis therapy.
Topical corticosteroids are usually adequate for acute noninfectious anterior uveitis, but intermediate and posterior uveitis usually requires injected local corticosteroids or systemic steroids, or other immunosuppression.
Uveitis is an inflammation of one or all parts of the uvea, or the vascular area between the retina and sclera of the eye. The anterior uvea is composed of the iris and ciliary body; an irritation of this segment, or anterior uveitis, leads to acute painful symptoms and photophobia. Inflammation of the posterior uvea, including the choroid, retina, and retinal vasculature, carries a risk of painless visual loss. Uveitis of all types affects children and adults, and the etiology is most commonly idiopathic.
History and exam
- eye redness without discharge
- constricted or nonreactive pupil
- decreased intraocular pressure
- retinal exudates and edema, optic nerve edema
- retinal vascular sheathing
- macular edema
- optic disk swelling
- retinal hemorrhages
- ciliary flush
- corneal edema
- fluorescent treponemal antibody (FTA-ABS), venereal disease research laboratory (VDRL), and rapid plasma reagin (RPR)
- serum ACE
- antinuclear antibodies
- Lyme titer
- purified protein derivative (PPD) skin test
- cytoplasmic anti-neutrophil cytoplasmic antibodies (c-ANCA)
- perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA)
- C3 and C4
- anti-double-stranded DNA antibody (anti-dsDNA)
- rheumatoid factor
- anti-cyclic citrullinated peptide (anti-CCP) antibodies
- Bartonella henselae titer
- toxoplasma serologic titer
- other HLA antigens
- biochemistry screen
John J. Huang, MD
Connecticut Uveitis Foundation
Associate Clinical Professor
Eye Disease Consultants
JJH declares that he has no competing interests.
Max Elia, MD
Uveitis and Retina Specialist
Medical Eye Center of New Hampshire
ME declares that he has no competing interests.
Dr John J. Huang and Dr Max Elia would like to gratefully acknowledge Dr Richard Gale, Dr Zsolt Varga, Dr Victor L. Perez, and Dr Carlos A. Medina, the previous contributors to this monograph. RG, ZV, VLP, and CAM declare that they have no competing interests.
Jessica Ackert, MD
Mount Sinai Hospital
JA declares that she has no competing interests.
Anthony J. Hall, MD, FRANZCO
Director of Ophthalmology
AJH has been reimbursed by Novartis, the manufacturer of Lucentis, for lecture fees. AJH's employer, the Alfred Hospital, has received research funding from Novartis, the manufacturer of Lucentis, and from Bayer, the manufacturer of Eylea.
Daniel A. Johnson, MD
Department of Ophthalmology
The University of Texas Health Science Center at San Antonio
DAJ declares that he has no competing interests.
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