Management of Pseudogout (CPPD) in Older Adults with Significant Joint Pain
For acute pseudogout in older adults, intra-articular glucocorticosteroid injection combined with joint aspiration is the optimal first-line treatment, followed by a short course of oral prednisone 0.5 mg/kg/day for 5-10 days if systemic therapy is needed. 1, 2
Acute Attack Management Algorithm
First-Line Treatment: Intra-articular Approach
- Perform joint aspiration first to confirm CPP crystals under polarized light microscopy (positively birefringent) and exclude septic arthritis—this is critical as injecting steroids into an infected joint can be catastrophic 1, 3
- Inject triamcinolone acetonide 60 mg (or equivalent long-acting corticosteroid) directly into the affected joint after aspiration 1, 2
- This approach has the highest strength of evidence from EULAR guidelines and provides rapid symptom relief with minimal systemic effects 1
- Combine with ice application and temporary rest of the joint 4
Second-Line: Systemic Steroids (When Intra-articular Not Feasible)
- Oral prednisone/prednisolone 0.5 mg/kg/day for 5-10 days, then discontinue without tapering if course is short 2
- Alternative: Full dose for 2-5 days, then taper over 7-10 days 2
- Intramuscular triamcinolone acetonide 60 mg as single dose showed ≥50% clinical improvement in all patients within 14 days 2
- Prednisone likely provides the best benefit-risk ratio in older adults compared to NSAIDs or colchicine 5
Critical Pitfall to Avoid
Never use prolonged corticosteroid courses without a clear tapering plan—this increases adverse effects (hyperglycemia, hypertension, osteoporosis) without additional benefit in this elderly population 1, 2
Alternative Acute Treatments (When Steroids Contraindicated)
NSAIDs
- Use with extreme caution in older adults due to cardiovascular, renal, and gastrointestinal risks 4
- Always assess cardiovascular, renal, and metabolic comorbidities before prescribing NSAIDs in patients over 60 1
- Evidence is extrapolated from gout studies, not specific CPPD trials 4
Colchicine
- Less effective for acute attacks than steroids but can be considered 5
- Risk of diarrhea and drug interactions in elderly patients with polypharmacy 4
Chronic CPPD Management with Concurrent Osteoarthritis
Prophylaxis for Recurrent Attacks
- Low-dose colchicine 0.5 mg twice daily has an NNT of 2 for >30% pain reduction in chronic CPPD with knee OA 4, 1
- This was demonstrated in a double-blind RCT with minimal side effects (mild dyspepsia, no severe diarrhea) 4
- Continue for 8 weeks initially, then as needed 4
Refractory Chronic Disease
- Hydroxychloroquine showed NNT of 2 for clinical response (>30% reduction in swollen/tender joint count) in a 6-month RCT 4
- Low-dose methotrexate 5-10 mg weekly showed excellent response in refractory cases with marked improvement within 7.4 weeks, though evidence is limited to small case series 4
- Consider for patients failing conventional treatments 4
Emerging Biologics (Severe Refractory Cases)
- IL-1 inhibitors (anakinra) and IL-6 inhibitors (tocilizumab) show promise for refractory disease 6, 5
- Evidence remains limited but these target the NLRP3 inflammasome pathway central to CPP crystal inflammation 4, 7
Screening for Metabolic Comorbidities
Screen all patients with early-onset CPPD (age <60) or severe disease for:
- Primary hyperparathyroidism (OR 3.03 for CPPD association) 4
- Hemochromatosis 4, 3
- Hypomagnesemia 4, 3
- Hypophosphatasia 5
Treat identified metabolic conditions per their respective guidelines, though whether this affects CPPD outcomes remains unclear 4
What NOT to Do
- Avoid high molecular weight hyaluronan intra-articular injections—these may induce acute CPPD attacks 1
- Do not treat asymptomatic chondrocalcinosis—it is age-related and requires no intervention 4
- Never assume infection is excluded without joint aspiration in monoarticular presentations before steroid injection 2
Key Distinction from Gout
Unlike gout, there is currently no treatment to dissolve or prevent CPP crystal formation—all therapy is directed at controlling inflammation and symptoms 4, 5. This fundamentally different pathophysiology means urate-lowering strategies are irrelevant in CPPD 7.