Gout is a common form of inflammatory arthritis characterized by sudden, severe attacks of pain and swelling, caused by crystal deposition. Bursitis is the inflammation of a bursa, a small, fluid-filled sac that cushions bones, tendons, and muscles near joints. While bursitis is often caused by trauma or repetitive motion, systemic conditions like gout can lead to its development. Gout can directly cause bursitis, a condition often referred to as gouty bursitis.
The Mechanism of Gout Crystal Deposition in the Bursa
Gout begins with hyperuricemia, an abnormally high concentration of uric acid in the bloodstream. Uric acid is the end product of purine metabolism, a natural process involving the breakdown of substances found in food and cells. When the kidneys fail to adequately excrete uric acid or the body produces too much of it, the blood level rises.
At elevated concentrations, uric acid transforms into solid, sharp, needle-like particles called monosodium urate (MSU) crystals. These crystals tend to precipitate in tissues where blood flow is lower and temperatures are cooler, such as the joints and surrounding soft tissues. The bursae, which are fluid sacs located near joints, are a common site for this crystal deposition.
Once MSU crystals settle within the bursa, the body’s immune system recognizes them as foreign invaders. This triggers an aggressive inflammatory response as immune cells attempt to clear the crystals, resulting in the acute onset of pain, redness, and swelling. While gout often affects the big toe joint, the olecranon bursa at the elbow and the prepatellar bursa at the knee are the two most common locations for gouty bursitis.
Differentiating Gouty Bursitis from Other Causes
Bursitis has many potential origins, including trauma, chronic overuse, and infection. Traumatic bursitis usually develops from direct pressure or repetitive motion, such as prolonged kneeling or leaning on elbows. Gouty bursitis, however, displays a specific acute presentation, often involving extreme, rapid-onset pain and intense redness that can mimic an infection.
The definitive diagnostic step involves aspiration, where a sample of fluid is drawn directly from the inflamed bursa. This fluid is then examined under a polarized light microscope to confirm the presence of MSU crystals. Identifying these negatively birefringent, needle-shaped crystals is the gold standard for diagnosing gout, whether it affects a joint or a bursa.
The aspirated fluid is also sent for a cell count and culture to rule out septic bursitis, which is a bacterial infection that requires different management. A gouty flare can sometimes coexist with an infection, making this analysis particularly important for correct treatment.
Treatment Strategies for Gout-Related Inflammation
The management of gouty bursitis requires a dual approach: treating the immediate inflammatory flare and addressing the long-term metabolic cause. For an acute attack, the goal is to quickly reduce the intense pain and swelling caused by the inflammation. Medications commonly used include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids, which can be taken orally or sometimes injected directly into the bursa.
Once the acute episode subsides, the focus shifts to preventing future attacks by lowering the overall uric acid level. This long-term strategy involves uric acid-lowering therapies (ULTs) like allopurinol or febuxostat. These medications decrease the production of uric acid or enhance its excretion by the kidneys, helping dissolve existing MSU crystals and preventing new ones from forming. Maintaining a target uric acid level below the point of crystallization is necessary to avoid the recurrence of gouty bursitis.