Gout is a type of inflammatory arthritis resulting from persistently elevated levels of uric acid in the blood (hyperuricemia). When uric acid levels exceed solubility, the substance crystallizes into sharp, needle-like crystals that deposit within tissues throughout the body. While most commonly associated with the joint at the base of the big toe, gout can affect virtually any joint or soft tissue structure. Gout can affect the Achilles tendon, a manifestation classified as extra-articular gout. This involvement is a significant concern because the symptoms can easily be mistaken for more common conditions, such as Achilles tendinitis.
Gout and Tendon Involvement
Gout affects the Achilles tendon when uric acid crystallizes into monosodium urate (MSU) crystals within the tissue. The Achilles tendon, like other tendons and ligaments, is a site where these crystals frequently deposit, often at the tendon’s insertion site.
The presence of MSU crystals within the tendon or surrounding bursae triggers a potent inflammatory response, which is the mechanism behind a gout flare. The crystals activate a specific inflammatory pathway, leading to the recruitment of immune cells like neutrophils. This localized inflammatory reaction in the tendon is referred to as gouty tendinopathy.
With chronic, untreated hyperuricemia, these crystal deposits can accumulate into larger, visible lumps called tophi. Tophi are collections of MSU crystals encased by inflammatory cells and connective tissue, and they can form directly within the Achilles tendon sheath or adjacent soft tissue. The presence of tophi indicates advanced gout and can lead to structural changes, including a reduction in tendon stiffness, which may affect the tendon’s ability to transmit muscle force.
Recognizing Achilles Gout
An acute gout flare in the Achilles tendon typically presents with sudden, intense pain that reaches its maximum severity in under 12 hours. The area near the heel becomes markedly tender, warm, and visibly swollen and red. This extreme sensitivity can make even light contact, such as the weight of a bedsheet, intolerable.
Achilles gout differs significantly from Achilles tendinitis, which usually causes pain that lessens as the tendon warms up with activity. Gout pain, by contrast, is often severe even at rest and frequently wakes the patient during the night. The inflammatory signs of redness and warmth strongly indicate inflammatory gout rather than a mechanical injury.
In cases of chronic or advanced Achilles gout, the presentation may involve the formation of tophi, which can be felt as firm, non-mobile lumps under the skin near the tendon. These chronic deposits cause persistent stiffness and tenderness, making movement difficult. The appearance of this extra-articular inflammation can sometimes mimic a severe soft tissue infection, which can lead to misdiagnosis.
Diagnosis and Treatment Approaches
Confirming a diagnosis of Achilles gout involves clinical assessment and specific testing. A physical examination revealing intense, localized inflammation strongly suggests a gout flare. Blood tests measuring serum uric acid levels are routinely performed, but these levels may be within the normal range during an acute flare, as the uric acid has deposited into the tissue.
Imaging techniques are used to visualize crystal deposits within the tendon. Musculoskeletal ultrasound is effective at detecting urate crystals and tophi. Dual-energy CT (DECT) scanning is an advanced method that identifies the chemical composition of uric acid in the tissue, even when no inflammation is present. The gold standard for definitive diagnosis remains aspiration of fluid or tissue to identify MSU crystals under a polarized light microscope.
Treatment addresses both the acute flare and the underlying cause of high uric acid levels. Acute attacks are managed with anti-inflammatory medications to rapidly reduce pain and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) like indomethacin or naproxen, colchicine, or corticosteroids suppress the immune response.
Long-term management focuses on lowering the uric acid concentration in the blood to prevent future flares and dissolve existing crystal deposits. This is achieved through urate-lowering therapies (ULTs), such as allopurinol or febuxostat. These medications reduce the body’s production of uric acid, preventing new crystal formation and allowing the body to clear existing deposits. Lifestyle adjustments, including reducing purine-rich foods and alcohol, also support maintaining healthy uric acid levels.