Gout is a form of inflammatory arthritis resulting from the build-up of crystals within a joint, causing sudden and intense pain. While most commonly associated with the joint at the base of the big toe, gout can affect other joints, including the knee. When gout occurs in the knee, it makes walking and bearing weight extremely difficult. This inflammatory response requires accurate diagnosis and prompt management to prevent long-term joint damage and control the frequency of future flare-ups.
The Root Cause of Gout
Gout is caused by hyperuricemia, an elevated concentration of uric acid in the bloodstream. Uric acid is a natural byproduct created when the body metabolizes purines, which are chemical compounds found in cells and many foods. Normally, the kidneys filter out this uric acid, allowing it to be excreted in the urine.
If the body produces too much uric acid or the kidneys excrete too little, blood levels rise. When the concentration exceeds a certain threshold, the uric acid can no longer remain dissolved and begins to form sharp, needle-like crystals. These crystals, known chemically as monosodium urate, deposit in the joints and surrounding tissues. Their presence triggers a powerful inflammatory response from the immune system, which causes the sudden and severe pain characteristic of a gout attack.
Recognizing Gout in the Knee
A gout attack in the knee typically begins with a sudden onset of severe pain, often striking overnight. The pain rapidly reaches maximum intensity within hours, feeling like a sharp, stabbing, or burning sensation deep inside the joint. The knee joint becomes noticeably swollen, and the skin over the affected area often appears red or discolored and feels warm to the touch.
The inflammation makes the joint so tender that even the slightest pressure, such as the weight of a bedsheet, becomes intolerable. This severe swelling and tenderness limits the range of motion, making it challenging to straighten or bend the knee. Since these symptoms can mimic other serious conditions like septic arthritis or pseudogout, a definitive diagnosis is necessary.
To confirm gout, joint aspiration (arthrocentesis) is often performed. This involves using a needle to draw a small sample of synovial fluid from the inflamed joint space. The fluid is then examined under a polarized light microscope to look for the presence of negatively-birefringent, needle-shaped monosodium urate crystals. This microscopic identification of the crystals is the gold standard for diagnosis.
Managing Acute Attacks and Long-Term Health
The immediate goal during an acute gout flare is to quickly reduce pain and inflammation. First-line treatments include nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin or naproxen, which suppress the inflammatory reaction. Colchicine is another common medication that reduces pain and inflammation, particularly if taken within the first 24 hours of an attack. For severe attacks, or for patients who cannot take NSAIDs or colchicine, corticosteroids may be administered orally or injected directly into the affected knee joint. Resting the joint, applying ice packs, and elevating the limb also help reduce local swelling and tenderness.
Long-term management focuses on lowering the serum uric acid level to prevent future attacks and dissolve existing crystal deposits. This is achieved through urate-lowering therapy (ULT), using medications like allopurinol or febuxostat. These drugs work by blocking the enzyme that produces uric acid, reducing its concentration in the blood, ideally to below 6.0 mg/dL.
Lifestyle modifications are also an important part of long-term health. Patients should maintain a healthy weight and increase water intake. They must also limit the consumption of high-purine foods, such as organ meats, certain seafood, and alcoholic beverages, especially beer and liquor. Consistent adherence to both medication and lifestyle changes is necessary to keep uric acid levels low enough to prevent future gout attacks.