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 D. O'Keefe, MD, Russell W. Read, MD, PhD, Alex Kozak, Alan Palestine, MD, Jessica Shantha, MD, Marissa Larochelle, MD, Debra A Goldstein, MD

Assigned editor:

Review:

Assigned status Update Pending

 by Marissa Larochelle, MD on December 22, 2022.

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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

AAU may occur as an isolated medical problem without any association with illness or inflammation elsewhere in the body. It might also arise as part of an illness affecting multiple parts of the body, in tandem with a localized infection (e.g., cold sores, herpes simplex), or as an adverse reaction to a medication, though the latter cause is rare. The most common illnesses associated with AAU are also associated with a genotype known as HLA-B27. A detailed explanation of HLA-B27 and those diseases associated with HLA-B27 is found elsewhere on this website, but the most common that is linked directly with AAU is ankylosing spondylitis, an inflammatory arthritis. Other diseases linked with AAU are apparent from associated symptoms; for example, a patient with bowel inflammation or colitis associated with AAU would usually have abdominal problems such as cramps, weight loss, and/or diarrhea. Sarcoidosis, interstitial nephritis (a rare kidney inflammation), relapsing polychondritis (a rare autoimmune disease), and vasculitis (an inflammation of the blood vessel wall) may also occur in tandem with AAI.

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 AAI 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

If the patient shows characteristic disease in the setting of known risk factors (HLA-B27), with exclusion of other possible causes, a complete workup with syphilis titers should be ordered. Depending on patient presentation and workup results, other diagnostic tests may be warranted, including ocular fluid testing for the herpes simplex virus (HSV), cytomegalovirus (CMV), and varicella zoster virus (VZV).

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 fluid-filled space in the front of the eye, and these readily detectable by the slit lamp. An AAU diagnosis requires that these cells to be present in the anterior chamber. Patients with AAU should initially undergo dilation to permit the examiner to see toward the back of the eye. The possible cause of AAU changes considerably if the inflammation in the front of the eye is accompanied by marked inflammation in the back of the eye.

• 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, as many factors impact the level. 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 drops, including corticosteroid drops such as prednisolone acetate 1% and dilating drops such as cyclopentolate. The corticosteroid drop treats the underlying inflammation, while the dilating drop reduces pain and helps to prevent the pupil sticking to the adjacent 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 of corticosteroid near the eye itself 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 disease and flares 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 macular, the portion of the retina responsible for central vision; 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.