Pseudogout is a form of inflammatory arthritis that causes sudden, painful flare-ups in the joints. This condition is known as Calcium Pyrophosphate Deposition (CPPD) disease, caused by the accumulation of Calcium Pyrophosphate Dihydrate crystals within the joint cartilage and fluid. These crystals trigger an intense inflammatory response, leading to symptoms that closely resemble a gout attack. Treatment focuses on a two-pronged approach: quickly resolving the acute inflammation and pain during a flare, and implementing strategies to reduce the frequency of future episodes and prevent joint damage.
Immediate Relief for Acute Flare-Ups
The primary goal during an acute pseudogout attack is to rapidly reduce the severe pain and swelling that immobilize the affected joint. Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are a frequent first-line medication used to combat this inflammation. Options include over-the-counter medications like ibuprofen or naproxen sodium, or prescription NSAIDs such as indomethacin, taken at the onset of symptoms. Healthcare providers must consider the potential for gastrointestinal or kidney side effects, especially since pseudogout often affects older individuals.
Another pharmaceutical option for rapidly addressing an acute flare is oral colchicine, traditionally used for gout. Colchicine works by interfering with the inflammatory response triggered by the crystals, and it is most effective when taken within the first 24 hours of an attack. Modern practice favors a low-dose regimen for acute relief to minimize gastrointestinal side effects. If patients cannot tolerate NSAIDs or colchicine, or when multiple joints are involved, a short course of systemic oral corticosteroids may be prescribed.
Oral corticosteroids, such as prednisone, are powerful anti-inflammatory medications that quickly bring a severe flare under control. They are useful for patients with underlying health concerns, like kidney impairment, that make NSAID use risky.
Supportive care is important for managing the immediate discomfort of a flare-up. Applying ice or a cold pack to the swollen joint helps significantly reduce both inflammation and pain. The affected joint should also be rested, following the R.I.C.E. (Rest, Ice, Compression, Elevation) protocol to help control local swelling.
Physician-Administered Treatment Options
When oral medications do not provide sufficient relief, or when the diagnosis of pseudogout is uncertain, a physician may perform procedures that offer localized and rapid relief. Joint aspiration, also known as arthrocentesis, involves inserting a sterile needle into the affected joint space to withdraw excess fluid. Removing this fluid instantly reduces pressure and pain, and it also removes some of the inflammatory crystal debris from the joint.
This collected joint fluid is then analyzed under a microscope to confirm the presence of the Calcium Pyrophosphate Dihydrate crystals, which is the most definitive way to diagnose pseudogout. Immediately following the fluid removal, the physician can inject a long-acting corticosteroid, such as methylprednisolone, directly into the joint space. This delivers a high concentration of anti-inflammatory medicine right to the source of the flare.
This localized delivery method is highly effective for rapidly resolving inflammation in a single joint, often within 24 to 48 hours. The intra-articular injection of corticosteroids is a preferred treatment for monoarticular (single joint) attacks because it avoids the potential systemic side effects associated with oral steroid use.
Long-Term Management and Prevention
Beyond treating acute attacks, the goal of long-term management is to reduce the frequency and severity of future flare-ups. For individuals who experience recurrent pseudogout episodes, a low-dose daily regimen of colchicine (0.5 to 1 milligram once or twice daily) is often recommended as a prophylactic measure. This helps prevent the inflammatory response from activating, thereby significantly lowering the risk of a new attack.
Management also involves screening for and addressing underlying medical conditions associated with CPPD crystal deposition. Conditions like hyperparathyroidism (high calcium levels) or hemochromatosis (excess iron accumulation) can contribute to crystal formation. Identifying and treating these metabolic disorders is an important step in the overall care plan, though it does not remove existing crystals. Screening for low magnesium levels and thyroid abnormalities is also routinely performed.
Lifestyle measures are a supportive layer in the long-term prevention strategy against inflammation and joint damage. Maintaining a healthy body weight reduces mechanical stress on weight-bearing joints, which can trigger flares. Staying well-hydrated also supports overall joint health. Although no current medication can dissolve existing CPPD crystals, proactively managing associated conditions and implementing these preventive steps minimizes the impact of the chronic disorder.