Crystalline Arthropathy of the Hand

Crystalline Arthropathy is joint inflammation from crystal deposition: monosodium urate (gout) or calcium pyrophosphate (CPPD/pseudogout).

Hand Involvement:

• Gout: 10-15% present with hand involvement (wrist, MCP, PIP, DIP)
• CPPD: Wrist most common hand site (TFCC calcification)

Gout (Monosodium Urate) Pathophysiology:

1. Hyperuricemia: Uric acid greater than 7 mg/dL (overproduction or underexcretion)
2. Crystal Formation: Urate crystals precipitate in synovial fluid/tissue (lower temperature in extremities)
3. Acute Attack: Crystals trigger inflammatory response (neutrophil activation, IL-1β release)
4. Chronic Tophaceous Phase: Persistent hyperuricemia → tophus formation (aggregates of urate crystals with granulomatous reaction)
5. Joint/Tendon Damage: Tophi erode bone, weaken tendons, compress nerves, ulcerate skin

Tophus Composition: Chalky white monosodium urate deposits surrounded by foreign body giant cells

CPPD (Calcium Pyrophosphate Deposition) Pathophysiology:

1. Pyrophosphate Accumulation: Abnormal cartilage metabolism (age-related, genetic, metabolic)
2. Crystal Deposition: Calcium pyrophosphate crystals deposit in cartilage (chondrocalcinosis)
3. Acute Pseudogout: Crystal shedding into joint → acute inflammatory attack
4. Chronic CPPD Arthropathy: Progressive cartilage/bone damage (OA-like pattern)

TFCC calcification in wrist is classic for CPPD.

Hand Sites:

Key to Success: Perioperative and long-term uric acid control with ULT (allopurinol/febuxostat). Target less than 6 mg/dL.

Global Epidemiology:

• Gout is the most common inflammatory arthritis worldwide; prevalence is rising with ageing populations and metabolic syndrome
• Age-standardised prevalence in adults 65+ was ~3,100 per 100,000 (GBD 2021), with burden in older men nearly double that of women and projected to keep rising to 2050
• Marked ethnic variation: highest prevalence in Māori and Pacific Island populations of Oceania (genetic urate transporter variants); lower rates historically reported in parts of Africa and East Asia
• Hand/wrist involvement complicates roughly 10-15% of established gout; CPPD prevalence rises steeply with age

Side-by-Side Guidelines:

Unresolved questions:

• No disease-modifying therapy exists for CPPD - management remains symptomatic, and no agent reliably dissolves calcium pyrophosphate deposits.
• Optimal reconstruction after tophus-related tendon rupture (primary repair vs graft vs transfer) is not standardised.
• Whether to treat asymptomatic hyperuricaemia to prevent crystal arthropathy is not supported by current guidelines.

The mnemonic, complication tables and the "unresolved questions" above all flag tendon rupture as a surgical driver, yet the pattern and its reconstruction deserve fuller treatment because it is a distinct hand problem. Urate does not simply compress tendons from outside - tophaceous material infiltrates the tendon substance and tenosynovium, so failure is attritional and infiltrative rather than a clean traumatic laceration.

The Doscher hand series (see Evidence Base) is directly relevant: en masse excision and curettage in urate-controlled patients restored tendon excursion and joint mobility with no recurrence over follow-up to fifteen years - reinforcing that meticulous excision plus sustained urate-lowering therapy, not excision alone, salvages tendon function. There is no standardised reconstruction algorithm, so the choice is individualised to the defect, tendon bed, and the patient's demands.

The topic repeatedly warns that tophaceous gout can produce ulnar drift and swan-neck deformity that "mimics rheumatoid" and can "mimic OA or SLAC wrist," but never sets out how to tell them apart - a very common hand exam question. The underlying diseases are covered in the rheumatoid hand and wrist and CPPD topics; what follows are the this-topic discriminators.

Radiographic discriminators (gout vs rheumatoid):

Clinical and laboratory discriminators:

• Tophi vs rheumatoid nodules: both are firm, but a tophus may ulcerate and discharge chalky white material; aspiration or histology showing MSU crystals is definitive. Rheumatoid nodules favour extensor surfaces and are associated with seropositive erosive disease.
• Serology: RA is associated with RF and anti-CCP; gout is associated with hyperuricaemia (which can be normal during a flare) and negatively birefringent MSU crystals on aspiration.
• Osteoarthritis / nodal OA: Heberden (DIP) and Bouchard (PIP) nodes with osteophytes and subchondral sclerosis, not overhanging erosions.
• CPPD: look for chondrocalcinosis (TFCC, cartilage), hook-like osteophytes at the second and third MCP joints, and a radiocarpal/SLAC-type pattern - detailed in the pseudogout/CPPD topic.

The trap to avoid: a deforming asymmetric hand arthropathy with subcutaneous nodules is not automatically rheumatoid - "pseudo-rheumatoid" tophaceous gout is a classic mimic, and joint aspiration for crystals settles it.