Gout and pseudogout

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Pathophysiology

  • Primarily an illness of middle-aged males and elderly adults
    • Gout in females usually occurs only after menopause
  • Gout is most common form of inflammatory joint disease in men >40yr
  • Presence of crystals does not exclude septic arthritis

Precipitants

Clinical Features

Acute gout affecting the first MP joint (podagra)
Tophaceous gout affecting the right great toe and finger interphalangeal joints. Note the asymmetrical swelling and yellow-white discoloration
Distribution of joints typically affected by gout
  • Joint pain may develop over period of hours
  • Primarily involves first MTP, knee, ankle

Differential Diagnosis

Monoarticular arthritis

Algorithm for Monoarticular arthralgia

Evaluation

  • Synovial fluid aspiration
    • Gout = Negatively birefringent, needle-shaped monosodium urate crystals
    • Pseudogout = Positively birefringent, rhomboid-shaped, calcium pyrophosphate crystals
  • Serum uric acid levels are not helpful (30% of patients with gout attack have normal levels)
    • Uric acid during attacks can be low due to the precipitation of gout crystals
    • High uric acid is >6.8
  • ESR may be elevated
  • No bacteria on Gram Stain
  • Pseudogout: X-ray of joint space may show radiolucent calcium pyrophosphate crystals

Arthrocentesis of synoval fluid

Synovium Normal Noninflammatory Inflammatory Septic
Clarity Transparent Transparent Cloudy Cloudy
Color Clear Yellow Yellow Yellow
WBC <200 <200-2000 200-50,000

>1,100 (prosthetic joint)

>25,000; LR=2.9

>50,000; LR=7.7

>100,000; LR=28

PMN <25% <25% >50%

>64% (prosthetic joint)

>90%

Culture Neg Neg Neg >50% positive
Lactate <5.6 mmol/L <5.6 mmol/L <5.6 mmol/L >5.6 mmol/L
LDH <250 <250 <250 >250
Crystals None None Multiple or none None
  • Viscosity of synovial fluid may actually be decreased in inflammatory or infectious etiologies, as hyaluronic acid concentrations decrease
  • The presence of crystals does not rule out septic arthritis; however, the diagnosis is highly unlikely with synovial WBC < 50,000[1]

Management

Patients usually only require opioid and NSAID treatment in the ED with continued NSAID treatment as an oupatient. However any combination of the following treatments are acceptable[2]

All patients

  • Hold diuretics
  • Consider starting losartan to replace diuretic (has modest uricosuric effect)
  • Alcohol and dietary counseling
  • Continue uric acid-lowering agents if already on prophylactic regimen (do not start)
  • Follow up with Primary Doctor or Rheumatology if having continued flares

NSAIDs

  • Do not give to patients with renal insufficiency (use opioids instead)
  • Substantial pain relief should occur within 2hr
  • Options:

Other options

Colchicine

  • Can be used as alternative agent to NSAIDs in patient with normal renal/hepatic function
  • 1.2mg PO (load), followed by 0.6mg one hour later x 1 [3]
  • May use to maximum of x3 doses, with more aggressive regimens totaling max dose up to 6mg[4]
  • Wait at least x3 days before starting another round of colchicine therapy
  • Renal impairment not absolute contraindication for acute flare but may consider dose reduction.
  • Dose adjustments for CYP3A4 inhibitors (HARRT, Calcium Channel Blockers, fluconazole, erythromycin, clarithromycin)
  • Colchicine should not be administered intravenously

Initial: 0.6-1.2mg, followed by 0.6 every 1-2 hours; some clinicians recommend a maximum of 3 doses; more aggressive approaches have recommended a maximum dose of up to 6mg. Wait at least 3 days before initiating another course of therapy

Steroids

  • Prednisone 30 to 50mg initially, and gradually tapered over 10 days, results in clinical resolution without rebound pain or complications[5][6]

Glucocorticoid injection

  • Even if gout has been diagnosed in the past, be cautious with glucocorticoid joint injection if the current clinical picture is uncertain since a septic joint can coexist with gout and a steroid injection would then worsen the patient's clinical status.


Other Therapies

  • Anakinra
    • Disease-modifying agent; Interleukin-1 Receptor Antagonist
    • Reserve use for patients who have frequent flares and in whom first-line therapies are ineffective, contraindicated, or not tolerated
    • 100 mg subq once daily until symptom improvement; usual duration: 3 to 5 days
    • NOT routinely used in the ED.

Disposition

  • Generally outpatient treatment

See Also

References

  1. ↑ Shah K, Spear J, Nathanson LA, Mccauley J, Edlow JA. Does the presence of crystal arthritis rule out septic arthritis?. J Emerg Med. 2007;32(1):23-6.
  2. ↑ Khanna D. et al. 2012 American College of Rheumatology guidelines for management of gout. Part 2: Therapy and antiinflammatory prophylaxis of acute gouty arthritis. Arthritis Care Res. Oct 2012;64(10):1447-61
  3. ↑ Terkeltaub RA et al. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62(4):1060.
  4. ↑ GlobalRPH. http://www.globalrph.com/gout.htm*colchicine
  5. ↑ Groff GD et al. Systemic steroid therapy for acute gout: a clinical trial and review of the literature. Semin Arthritis Rheum. 1990;19(6):329
  6. ↑ Janssens H. et al. Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. Lancet. 2008;371(9627):1854.
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