Acute Anterior Uveitis

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Article initiated by:

Russell W. Read, MD, PhD

All contributors:

Brad H. Feldman, M.D., Kleonikos A. Tsakiris, MD, MSc, FEBO, Ghazala A. D. O'Keefe, MD, Russell W. Read, MD, PhD, Alex Kozak, Alan Palestine, MD, Jessica Shantha, MD, Marissa Larochelle, MD, Debra A Goldstein, MD, Paulina Liberman

Assigned editor:

Paulina Liberman

Review:

Assigned status Up to Date

 by Paulina Liberman on January 16, 2026.

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Uveitis

DiseasesDB

13676

MedlinePlus

001005

MeSH

D014606

Acute anterior uveitis is the most common form of uveitis.

Disease Entity

Acute Anterior Uveitis

Disease

Uveitis is not a single disease. Similar to arthritis (joint inflammation), uveitis can be a part of many different disease processes. Different types of uveitis often follow characteristic patterns that are distinguished by such factors as the specific affected part of the eye, if the inflammation involves one or both eyes, if the inflammation began suddenly or gradually, and if the inflammation completely resolves with treatment which can be stopped (acute or recurrent acute) or if it recurs off therapy (chronic) disease. The most common presentation for uveitis is acute anterior uveitis (AAU).

Anterior uveitis means that the front (anterior) portion of the uvea, the iris and ciliary body, are primarily affected by the inflammation. The ciliary body synthesizes aqueous humor, the fluid that fills the front of the eye. In anterior uveitis, inflammatory cells may be seen in the anterior chamber (iritis) and sometimes the anterior vitreous (iridocyclitis).

Acute disease is characterized by a sudden onset and limited duration. The symptoms of AAU are pain, redness, and photophobia (sensitivity to light), and typically develop rapidly over a few days. Symptoms usually resolve with appropriate anti-inflammatory therapy. If therapy can be tapered and inflammation does not recur for at least 3 months after cessation of treatment, the disease is said to be of limited duration. The episodes may occur once or may be recurrent (symptoms and signs returning after ≥3 months of absence). This is in contrast to chronic disease, where inflammation (with or without symptoms) recurs when medication is tapered and stopped.

Etiology

Acute anterior uveitis may occur as an isolated problem without any systemic association. It can also arise in the context of a multisystem inflammatory disease, as a manifestation of a localized ocular infection such as herpes simplex or varicella zoster, or rarely as a reaction to a medication. The most common systemic association in adults in the United States is with the HLA-B27 genotype, which is linked to the spondyloarthritides, including ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis. Other systemic diseases that may present with anterior uveitis include juvenile idiopathic arthritis, which produces a chronic, often asymptomatic bilateral anterior uveitis in children; sarcoidosis, which can cause granulomatous anterior uveitis and is frequently associated with pulmonary or cutaneous disease; and Behçet disease, which may manifest as a hypopyon anterior uveitis, particularly in endemic regions. Infectious causes such as herpes simplex virus, varicella zoster virus, cytomegalovirus, and syphilis must also be considered. In addition, Fuchs’ uveitis syndrome represents a distinct, eye-limited chronic anterior uveitis characterized by stellate keratic precipitates, absence of synechiae, and heterochromia.

Risk Factors

As noted above, the HLA-B27 allele, the presence of ankylosing spondylitis and psoriatic arthritis, and certain medications may increase the risk of AAU.

Pathophysiology

Currently, the pathophysiology of AAU is unknown. A leading theory is that a person with a genetic predisposition to AAU is exposed to an infectious agent, resulting in cross-reactivity with ocular-specific antigens (molecular mimicry) and resultant iritis.

Primary Prevention

No information is available on the primary prevention of AAU. There is evidence from animal studies that the gut microbiome may play a role in the development of HLA-B27–related diseases.

Diagnosis

The diagnosis of anterior uveitis is based on careful clinical characterization, considering onset, course, laterality, and ocular findings to narrow the differential. Laboratory testing is applied selectively. All patients should be screened for syphilis because it can mimic any uveitic pattern and requires specific treatment, and Lyme testing is appropriate only in endemic regions or when exposure risk is present. Aqueous humor PCR may confirm viral etiologies such as HSV, VZV, or CMV when clinical features are suggestive. Additional targeted testing may be warranted to identify systemic disease, for example HLA-B27 typing in recurrent acute anterior uveitis or chest imaging and liver function testing when sarcoidosis is suspected. Broad, non-targeted “uveitis survey” testing is discouraged because it has low predictive value and rarely alters management.

Physical Examination

As discussed earlier, the symptoms of AAU include eye redness, pain, and sensitivity to light (photophobia). Sometimes the patient's vision is reduced. Tearing, lid puffiness, and some drooping of the eyelid may also be present. Since inflammation or infection in other parts of the eye may produce similar symptoms, the ophthalmologist must distinguish AAU from diseases of other eye structures, such as conjunctivitis (pink eye), keratitis (inflammation of the cornea), or scleritis (inflammation of the white part of the eye). The slit lamp is the most important tool for conducting a physical examination. In AAU, white blood cells accumulate in the aqueous humor, and these readily detectable by the slit lamp. An AAU diagnosis requires these cells to be present in the anterior chamber. Patients with AAU should initially undergo dilation to permit the examiner to examine the fundus. The possible cause of AAU changes considerably if the inflammation in the anterior segment is accompanied by posterior segment inflammation.

Signs on slit lamp examination are:

• Anterior chamber cell
• Keratic precipitates
• Flare
• Hypopyon
• Iris nodules
• Posterior synechiae
• Fibrin
• Pupillary miosis
• Band keratopathy

Diagnostic Procedures

The basic workup for AAU includes HLA-B27 and syphilis testing. For bilateral granulomatous disease, one should also consider testing for sarcoidosis (a chest x-ray at first); the utility of angiotensin-converting enzyme and lysozyme testing is debated among uveitis specialists. Other laboratory tests can be performed based on clinical suspicion for various diseases. Ocular fluid testing may be warranted in patients who present with hypertensive anterior uveitis to test for herpetic etiology (although many providers treat empirically based on exam findings).

Differential Diagnosis

Infectious

• Syphilis
• Tuberculosis
• HSV
• CMV
• Toxoplasmosis
• Rubella
• VZV

Inflammatory

• HLA-B27–associated inflammatory bowel disease
• Psoriatic arthritis
• Sarcoidosis
• Tubulointerstitial nephritis and uveitis
• Post-infectious

Malignancy

• Lymphoma
• Retinoblastoma

Other

• Idiopathic
• Medication-induced

Management

Medical Therapy

The mainstay of therapy for AAU is topical, including corticosteroid drops such as prednisolone acetate 1% or difluprednate 0.05%, and dilating drops such as cyclopentolate. The corticosteroid drop treats the inflammation, while the dilating drop reduces pain and helps to prevent formation of synechiae (adhesion of the iris to the lens). Dosing frequency depends primarily on the intensity of the inflammation. Forms of AAU that are associated with an infection such as herpes will also require treatment directed at the known infectious cause. On occasion, AAU is severe enough to warrant treatment with a local injection or an oral agent (e.g., prednisone). Any treatment, including eye drops, may result in adverse effects; these must be balanced with potential benefits.

For recurrent or chronic diseases that are vision-threatening despite local therapy, systemic immunosuppression therapy may be indicated. These cases sometimes require the expertise of a rheumatologist or uveitis specialist.

Surgery

There is no specific surgical treatment for AAU. Surgery is reserved for dealing with the complications of uveitis. Typically, intraocular surgery is only performed when there has been no inflammation or other symptoms for at least 3 months.

Complications

Complications include formation of posterior synechiae, band keratopathy, or a rise in intraocular pressure and subsequent glaucoma development. AAU can also cause fluid to accumulate in the macula, this complication is known as cystoid macular edema. Patients may also develop a cataract from inflammation or corticosteroid use. All of these complications may influence the choice of treatment.

Prognosis

Some forms of AAU have a tendency to recur. Prompt initiation of treatment at the time of recurrence may shorten the duration of the attack or improve the prognosis, but treatment should always be guided by a physician who has confirmed the patient's suspected diagnosis at the earliest possible time.

Acknowledgements

This article is based on a patient education monograph originally prepared for the American Uveitis Society in January 2003 by James T. Rosenbaum, MD (Oregon Health Sciences University Portland, Oregon, USA).

Additional Resources

• Boyd K. Uveitis. American Academy of Ophthalmology. Published December 3, 2024. Accessed March 25, 2025. https://www.aao.org/eye-health/diseases/uveitis-list.