9.10 Acute Gouty Arthritis
Usually a male patient over 50 years old with an established diagnosis of gout or
hyperuricemia rapidly develops an intensely painful monarticular
arthritis, often in the middle of the night, but sometimes a few hours following a minor trauma. Any joint may be affected, but most common is the
metatarsophalangeal joint of the great toe (podagra). The joint is red,
hot, swollen, and intensely tender to touch or movement. There is usually no
fever, rash, or other sign of systemic illness. The patient may have predisposing factors that increase his risk of developing gout, like obesity, moderate to heavy alcohol intake, high blood pressure, diabetes and abnormal kidney function, or he may be taking certan drugs including thiazide diuretics, low-dose aspirin, and tuberculosis medications (pyrazinamide and ethambutol).
What to do:
- If the patient has not been previously diagnosed by arthocentesis that showed crystals, then tap the involved joint as described in acute monarticular arthritis. In addition to ruling out infection, look under the microscope for crystals in the joint fluid. Urate crystals look like needles, and may be in white cells. Polarizing filters above and below the sample can help disclose and differentiate crystals.
- Provide rapid pain relief with loading doses of non-steroidal anti-inflammatory drugs (NSAIDs) such as ketorolac (Toradol) 60mg im, indomethicin (Indocin) 50mg po,
ibuprofen (Motrin) 800mg po or naproxin (Anaprox) 550mg po, then tapering, once pain is relieved, to maintenance doses for the next few days (Indocin 25mg tid or Motrin 600mg qid). Excruciating pain may require one dose of narcotics while the anti-inflammatory drugs take effect.
- If the patient has a medical problem (e.g., peptic ulcer or gastritis, liver or kidnney disease) which might contraindicate use of the non-steroidal anti-inflammatory medications or colchicine, but no infection or uncontrolled diabetes or hypertension, use parenteral, oral or intra-articular corticosteroids, like triamcinolone 60mg im or prednisone 40-50mg qd. Delay injecting corticosteroids into the joint until the possibility of infection is eliminated, then use an aqueous suspension of methylprednisolone, about 40mg in 0.5ml. Adrenocorticotropic hormone (ACTH) 80 USP Units IM is also effective in about three hours.
- Instruct the patient to elevate and rest the painful extremity, apply ice packs, and arrange for followup.
What not to do:
- Do not depend on serum uric acid to diagnose acute gouty
arthritis--it may or may not be elevated (> 8mg/ dl) at the
time of an acute arthritis.
- Do not use NSAIDs when a patient has a history of active peptic ulcer disease with bleeding. Relative contraindications include renal insufficiency, volume depletion, gastritis, inflammatory bowel disease, asthma and congestive heart disease.
- Do not start maintenance NSAID doses for an acute inflammation. It will take a day or more to reach therapeutic levels and pain relief.
- Do not insist upon re-confirming a diagnosis of gout in the ED by ordering serum uric acid levels (which are often normal during the acute attack) or tapping an exquisitely painful joint in a patient with known gout.
- Do not, during an acute attack of gouty arthritis, attempt to reduce the serum uric acid level with probenecid, allopurinol, or sulfinpyrazone. This will not help the arthritis, and may even be counterproductive. Leave it for follow up.
DiscussionGout is almost exclusively a disease of adult men and is rare in premenopausal women and prepubertal children. While hyperuricemia may indicate an increased risk of gout, the relationship between serum uric acid and arthritis is unclear. Many patients with hyperuricemia do not develop gout, while some patients with repeated gout attacks have normal or low uric acid levels. In addition to the first metatarsophalahgeal joint involved in podagra, gout can strike ankles, knees, wrists, fingers and elbows. These painful attacks usually subside in hours to days with or without treatment. Most patients with gout experience repeated attacks of arthritis over the years. Conditions other than septic arthritis that can mimic gout include psoriatic arthritis, rheumatoid arthritis and pseudogout (in which crystals of calcium oxalate replace uric acid).
Uric-acid-lowering medications like allopurinol, probenecid or sulfinpyrazone are useful for prophylaxis but can actually worsen an attack when used acutely. If patients are already taking maintenance doses, they may be continued and need not be held during an acute attack. An alternative treatment for acute gouty arthritis is colchicine po 1-2mg qh until pain is relieved, the patient develops nausea, vomiting or diarrhea, or a maximum dose of 6mg is reached. Colchicine can also be given iv 2mg q6h to a maximum of 4mg. After these maximum doses, no more colchicine should be prescribed for a week to avoid toxicity. Relief is faster with intravenous administration and gastric toxicity is lower, but heptic toxicity is greater and extravasation can cause tissue necrosis. These doses should be halved in renal insufficiency and elderly patients. Colchicine may also be used for prophylaxis in the smaller dose of 0.6mg po qd, especially in the first few months of treatment with allopurinol, probenecid or sulfinpyrazone, which lower uric acid but can initially precipitate attacks.
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Craig Feied, MD
Mark Smith, MD
Jon Handler, MD
Michael Gillam, MD