Background
Uveitis is defined as inflammation of the uveal tract of which the anatomy includes the iris, ciliary body, and choroid.
Anatomy of the eye. The iris regulates the amount of light that enters the eye, the ciliary body produces aqueous humor and supports the lens, and the choroid provides oxygen and nourishment for the retina.
A classification scheme for uveitis exists based upon anatomic location.[1]
Table 1. Classification of Uveitis (Open Table in a new window)
| Type | Primary Site of Inflammation | Includes |
| Anterior uveitis | Anterior chamber | Iritis/iridocyclitis/anterior cyclitis |
| Intermediate uveitis | Vitreous | Pars planitis/posterior cyclitis/hyalitis |
| Posterior uveitis | Choroid | Focal, multifocal, or diffuse choroiditis/chorioretinitis/retinochoroiditis/retinitis/Neuroretinitis |
| Panuveitis | Anterior chamber, vitreous, and/or choroid |
Anterior uveitis is the form most likely to present to the emergency department. When the inflammation is limited to the iris it is termed iritis. If the ciliary body is also involved, then it is called iridocyclitis.
After anatomical classification, uveitis is further described by the following[2] :
- Onset (sudden vs insidious)
- Duration (limited — less than 3 months in duration, or persistent — greater than 3 months in duration)
- Course (acute, recurrent, or chronic)
- Laterality (unilateral vs bilateral)
The distribution of general uveitis cases by anatomic site of disease has been found to differ significantly between community-based practice (anterior, 90.6%; intermediate, 1.4%; posterior 4.7%; panuveitis, 1.4%) and university referral practice (anterior, 60.6%; intermediate, 12.2%; posterior, 14.6%; panuveitis, 9.4%; P< 0.00005).[3]
Pathophysiology
The etiology of uveitis is often idiopathic,[2] However, genetic, traumatic, or infectious mechanisms are known to promote or trigger uveitis. Diseases that predispose a patient to uveitis and are likely to present to the emergency department include inflammatory bowel disease, rheumatoid arthritis, systemic lupus erythematosus (SLE), sarcoidosis, tuberculosis, syphilis, and AIDS.
The mechanism for trauma is believed to be a combination of microbial contamination and accumulation of necrotic products at the site of injury, thereby stimulating proinflammatory processes.[2]
For infectious etiologies of uveitis, it is postulated that the immune reaction directed against foreign molecules or antigens may injure the uveal tract vessels and cells.
When uveitis is found in association with autoimmune disorders, the mechanism may be a hypersensitivity reaction involving immune complex deposition within the uveal tract.
In one study at a tertiary referral center by Rodriguez et al,[4] the distribution in etiology among all anatomic forms of uveitis, anterior, intermediate, and posterior were as follows:
- Idiopathic (34%)
- Seronegative spondyloarthropathies (10.4%)
- Sarcoidosis (9.6%)
- Juvenile rheumatoid arthritis (JRA) (5.6%)
- SLE (4.8%)
- Beh ç et's disease (2.5%)
- AIDS (2.4%)
Seronegative arthropathies include nonspecific, ankylosing spondylitis, Reiter's syndrome, psoriatic arthropathy, and inflammatory bowel disease.
In the same Rodriguez et al study,[4] anterior uveitis was the most common form at 51.6% and the etiologic distribution was as follows:
- Idiopathic (37.8%)
- Seronegative arthropathies (21.6%)
- JRA (10.8%)
- Herpes virus (9.7%)
- Sarcoidosis (5.8%)
- SLE (3.3%)
- Rheumatoid arthritis (0.9%)
Posterior uveitis was next most common with 19.4% of cases, with the most common etiologies being Toxoplasma (24.6%), idiopathic (13.3%), cytomegalovirus (CMV) (11.6%), SLE (7.9%), and sarcoidosis (7.5%).
Epidemiology
Frequency
United States
The estimated annual incidence is approximately 12 cases per 100,000 persons.[5]
International
Uveitis is more common in Finland, where the annual incidence is approximately 23 cases per 100,000 persons. This is probably because of high frequency of the gene HLA-B27 in the population.[5]
Mortality/Morbidity
No deaths due to iritis or uveitis have been reported.
Morbidity results from posterior synechiae formation (adhesions between the iris and the lens) that may lead to high intraocular pressure and subsequent optic nerve loss.
Additional morbidity may include cataract formation, an adverse effect of topical steroid use.
Race
Racial predisposition to uveitis is related to the patient's underlying systemic disease.[6]
- Caucasian: HLA-B27, multiple sclerosis
- African American: Sarcoidosis, SLE
- Mediterranean/Middle Eastern: Beh ç et's disease
- Asian: Beh ç et's disease
Sex
In general, uveitis does not have a gender predisposition except in cases secondary to systemic disease, such as JRA and SLE.[6]
Age
The majority of patients are aged 20-50 years.
Jabs DA, Nussenblatt RB, Rosenbaum JT; Standardization of Uveitis Nomenclature (SUN) Working Group. Standardization of uveitis nomenclature for reporting clinical data. Results of the First International Workshop. Am J Ophthalmol. Sept 2005;140:509-16. [Medline].
Yanoff and Duker. Uveitis and other intraocular inflammations. In: Ophthalmology. 3rd ed. Mosby; 2008.
McCannel CA, Holland GN, Helm CJ, Cornell PJ, Winston JV, Rimmer TG. Causes of uveitis in the general practice of ophthalmology. UCLA Community-Based Uveitis Study Group. Am J Ophthalmol. Jan 1996;121(1):35-46. [Medline].
Rodriguez A, Calonge M, Pedroza-Seres M, Akova YA, Messmer EM, D'Amico DJ, et al. Referral patterns of uveitis in a tertiary eye care center. Arch Ophthalmol. May 1996;114(5):593-9. [Medline].
[Best Evidence] Islam N, Pavesio C. Uveitis (acute anterior). Clin Evid (Online). November 2009;04:705.
Wills Eye Hospital. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease. 5th ed. Philadelphia, Pa: Lippincott; 2008.
Abad S, Seve P, Dhote R, Brezin AP. [Guidelines for the management of uveitis in internal medicine]. Rev Med Interne. Jun 2009;30(6):492-500. [Medline].
Lyon F, Gale RP, Lightman S. Recent developments in the treatment of uveitis: an update. Expert Opin Investig Drugs. May 2009;18(5):609-16. [Medline].
Lim LL, Smith JR, Rosenbaum JT. Retisert (Bausch & Lomb/Control Delivery Systems). Curr Opin Investig Drugs. Nov 2005;6(11):1159-67. [Medline].
Mohammad DA, Sweet BV, Elner SG. Retisert: is the new advance in treatment of uveitis a good one?. Ann Pharmacother. Mar 2007;41(3):449-54. [Medline].
Wirbelauer C. Management of the red eye for the primary care physician. Am J Med. Apr 2006;119(4):302-6. [Medline].
Dunne JA, Travers JP. Topical steroids in anterior uveitis. Trans Opthalmol soc UK. 1979;99(4):481-4. [Medline].
Foster CS, Alter G, DeBarge LR, Raizman MB, Crabb JL, Santos CI, et al. Efficacy and safety of rimexolone 1% ophthalmic suspension vs 1% prednisolone acetate in the treatment of uveitis. Am J Ophthalmol. Aug 1996;122(2):171-82. [Medline].
Merck Manuals: Uveitis. Available at http://www.merck.com/mmhe/sec20/ch232/ch232a.html.
Nishimoto JY. Iritis. How to recognize and manage a potentially sight-threatening disease. Postgrad Med. Feb 1996;99(2):255-7, 261-2. [Medline].
Nussenblatt R, Whitcup S, Palestine A. Uveitis: Fundamentals and Clinical Practice. 2nd ed. St. Louis, Mo: Mosby; 1996.
Tessler H. Classification and symptoms and signs of uveitis. In: Duane T, ed. Clinical Ophthalmology. New York, NY: Harper and Row; 1987:1-10.
| Type | Primary Site of Inflammation | Includes |
| Anterior uveitis | Anterior chamber | Iritis/iridocyclitis/anterior cyclitis |
| Intermediate uveitis | Vitreous | Pars planitis/posterior cyclitis/hyalitis |
| Posterior uveitis | Choroid | Focal, multifocal, or diffuse choroiditis/chorioretinitis/retinochoroiditis/retinitis/Neuroretinitis |
| Panuveitis | Anterior chamber, vitreous, and/or choroid |
Print
