Gout is a form of inflammatory arthritis resulting from a buildup of uric acid in the body, known as hyperuricemia. While most commonly recognized for causing sudden, severe pain in the joints, particularly the big toe, gout is a systemic metabolic disorder. Uric acid is a waste product formed during the breakdown of purines, found naturally in the body and in many foods. If the body produces too much uric acid or fails to excrete enough through the kidneys, the excess can crystallize and deposit in various tissues. Although rare, this deposition can extend to affect the delicate structures of the eye, sometimes leading to painful inflammation and vision problems.
How Uric Acid Damages Ocular Tissue
The damage to ocular tissue from hyperuricemia occurs through physical crystal deposition and a generalized inflammatory response. When uric acid levels become high, it supersaturates the blood and body fluids, leading to the formation of monosodium urate (MSU) crystals. These crystals tend to precipitate in less vascularized, cooler areas of the eye, such as the cornea and sclera, forming microscopic deposits or larger chalky nodules called tophi.
The presence of MSU crystals physically irritates and obstructs ocular structures. The crystals also activate the innate immune system, triggering an intense inflammatory cascade. This process involves the release of inflammatory mediators, such as interleukin-1β, which recruit immune cells to the eye. This localized inflammation causes redness, swelling, and pain.
Systemic hyperuricemia promotes a chronic, low-grade inflammatory state. Elevated uric acid levels are linked to oxidative stress and endothelial cell dysfunction, which can affect the eye’s microvasculature. This generalized inflammation can contribute to various ocular surface abnormalities and internal eye issues.
Specific Eye Conditions Linked to Gout
Hyperuricemia can manifest in the eye as several distinct conditions, often mimicking other common eye diseases. One severe manifestation is uveitis, which is inflammation of the uveal tract (the middle layer of the eye). Uveitis symptoms include eye pain, sensitivity to light (photophobia), blurred vision, and floaters. If left untreated, this inflammation can lead to permanent vision damage.
The deposition of urate crystals on the eye’s clear front surface can cause keratopathy. These crystalline deposits appear within the corneal layers, causing opacification that may impair visual acuity. Patients may also experience chronic irritation or a foreign body sensation.
Another common presentation is inflammation of the white part of the eye, known as scleritis or episcleritis. Episcleritis involves the superficial layer of the sclera and presents as transient, localized redness. Scleritis is a more profound inflammation of the deeper scleral layer, causing intense, stabbing eye pain and deep, dark red discoloration. Gout is also associated with conjunctivitis, inflammation of the thin membrane covering the sclera and lining the eyelids.
Acute Diagnosis and Ophthalmic Treatment
Diagnosing an ocular manifestation of gout requires focusing on both the eye and the patient’s systemic health history. When a patient presents with suspicious eye inflammation, an ophthalmologist performs a detailed examination using a slit-lamp microscope. This instrument allows for a magnified view of the anterior eye structures, enabling the visualization of monosodium urate crystals deposited in the cornea or conjunctiva.
Diagnosis is supported by coordinating with a general practitioner or rheumatologist to confirm underlying hyperuricemia. This involves a blood test to measure serum uric acid levels, which are often elevated during a flare. If gout-related eye inflammation is confirmed, immediate treatment focuses on managing the acute flare and reducing localized inflammation. Acute ophthalmic treatment often involves topical corticosteroid eye drops, such as prednisolone acetate 1%, to suppress the immune response and alleviate pain.
Non-steroidal anti-inflammatory drugs (NSAIDs) may also be prescribed in eye drop form to control pain and inflammation in the short term. The goal of this immediate therapy is to gain control over the inflammation and prevent long-term damage. However, this ocular treatment is only a temporary measure and must be paired with comprehensive management of the underlying systemic condition.
Systemic Management for Eye Health
The only way to prevent recurring ocular flares and progressive eye damage is by achieving long-term control over hyperuricemia. This is primarily accomplished through Urate-Lowering Therapy (ULT), which aims to reduce the overall uric acid burden. The most commonly prescribed ULT medications are xanthine oxidase inhibitors, such as allopurinol and febuxostat, which block the enzyme responsible for uric acid production.
Consistency in taking these medications is important to ensure that serum uric acid levels remain below the target threshold, typically 6.0 mg/dL. Maintaining levels below this point allows for the gradual dissolution of MSU crystals deposited throughout the body, including those in the eye. For patients who cannot tolerate allopurinol or do not achieve the target level, febuxostat provides an effective alternative.
Systemic management also incorporates lifestyle adjustments. Increasing daily fluid intake helps the kidneys excrete uric acid more efficiently. Dietary modifications include reducing the consumption of high-purine foods and limiting alcohol and sugary drinks, as these can trigger uric acid production. Comprehensive care requires close collaboration between the eye specialist and the rheumatologist or primary care physician to manage both localized eye symptoms and the systemic root cause.