Makindo Medical Notes

Related Subjects: | Monoarticular Arthritis | Polyarticular Arthritis | Rheumatoid Arthritis | Gout | Pseudogout | Septic Arthritis | Systemic Lupus Erythematosus (SLE) | Enteropathic Spondyloarthritis | Reactive Arthritis

About Monoarticular Arthritis

• Monoarticular arthritis refers to inflammation affecting a single joint. It can be caused by various conditions, but two of the most common causes are gout and pseudogout.
• Gout involves the deposition of sodium urate crystals, while pseudogout involves calcium pyrophosphate crystals in the joints.
• Both conditions lead to acute inflammation, characterized by sudden onset of pain, swelling, and reduced joint mobility.

Aetiology

• Gout: Caused by the deposition of monosodium urate crystals in the joints due to hyperuricemia (high levels of uric acid in the blood).
• Pseudogout: Caused by calcium pyrophosphate dihydrate (CPPD) crystals being deposited in the cartilage and joints.
• In both conditions, neutrophils ingest these crystals, triggering a strong inflammatory response in the joint.

Clinical Features

• Both gout and pseudogout present with sudden onset of joint pain, swelling, and erythema (redness).
• The joint may feel warm and tender to the touch, and the range of motion is usually limited due to pain and swelling.
• Gout: Often affects the first metatarsophalangeal joint (big toe), but can also involve other joints like the ankles, knees, wrists, and fingers.
• Pseudogout: Commonly affects larger joints like the knees, wrists, and shoulders.

Investigations

• Joint aspiration: Synovial fluid analysis is key in diagnosing gout and pseudogout. The fluid is examined under a microscope for the presence of crystals.
• Gout: Negatively birefringent needle-shaped urate crystals are seen under polarized light microscopy.
• Pseudogout: Positively birefringent, rhomboid-shaped calcium pyrophosphate crystals are seen under polarized light microscopy.
• Blood tests: Measure serum uric acid levels (often elevated in gout). However, uric acid levels may not always correlate with an acute gout flare.
• X-rays: May show joint space narrowing, soft tissue swelling, or crystal deposits in chronic cases. Pseudogout can also show calcification in the joint cartilage (chondrocalcinosis).

Pathology

• Gout: Chronic gout can lead to the formation of tophi—hard deposits of urate crystals that may cause deformity and damage to the joints.
• Pseudogout: In chronic pseudogout, long-term inflammation may lead to joint damage and degeneration, similar to osteoarthritis.

Management

• Acute attacks:
  • For both gout and pseudogout, non-steroidal anti-inflammatory drugs (NSAIDs) are first-line treatment options to reduce inflammation and pain.
  • Colchicine may be used for acute gout attacks if NSAIDs are contraindicated.
  • Corticosteroids (oral or intra-articular) can be used when NSAIDs and colchicine are not suitable or ineffective.
• Chronic gout management:
  • Long-term urate-lowering therapy (ULT) with medications like allopurinol or febuxostat can help reduce serum uric acid levels and prevent future gout flares.
  • Lifestyle modifications such as reducing intake of purine-rich foods, alcohol, and managing weight are essential.
• Pseudogout management:
  • There is no specific long-term treatment to lower calcium pyrophosphate levels, but controlling inflammation through NSAIDs, colchicine, and corticosteroids helps manage symptoms.
  • Physical therapy may be beneficial to maintain joint function and mobility.

References

• Gout: Clinical Manifestations, Diagnosis, and Management
• Pseudogout: Clinical Features, Diagnosis, and Management