Gout Foot Pain
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Gout is among the oldest of disease, written about by the ancient Egyptians. (1)
This material comes from the American College of Rheumatology and the Arthritis Foundation
Gout is a metabolic condition characterized by excessive levels of serum urate. The consensus is that a serum urate level above 6.8 mg/dL, the saturation point of urate in biological fluids, is the cause of gout.
Elevated levels of serum urate over time leads to the deposition of monosodium urate crystals within joints. Attacks of gout are due to the sudden release of these crystals into the joint where they causer an acute inflammatory response characterized by warmth, redness, swelling, and excruciating pain.
The pain often starts at night or early in the morning. Patients will state that they are awakened by foot pain so severe that they can’t “bear the weight of the sheet” on the foot. Walking is next to impossible.
In addition to these symptoms, fatigue, malaise, and low grade fever may be present.
Most attacks resolve, at least early on, within three to fourteen days, even without treatment. However, with time, the attacks become more frequent, last longer, and spread to involve other joints.
Ninety per cent of first attacks affect one joint, usually the first metatarsophalangeal joint. This condition is called “podagra.”
However, other types of arthritis such as calcium pyrophosphate arthropathy (CPPD), Reiter’s disease, septic arthritis, and psoriatic arthritis can produce a similar picture. The instep of the foot may also be a target for a first attack and a patient may think they’ve “turned their ankle”. Also, because osteoarthritis also affects the first metatarsophalangeal joint, leading to a bunion, this condition may often be mistaken for gout. A quick note: in cases where septic (infectious) arthritis is a possibility, joint aspiration is mandatory.
Finally, cellulitis is another condition that can be confused with acute gout.
The American College of Rheumatology criteria for the classification of acute arthritis of primary gout includes (2):
1. More than 1 attack of acute arthritis
2. Maximum inflammation develops within a day
3. Monoarthritis attack
4. Redness over joints
5. First metatarsophalangeal joint painful or swollen
6. Unilateral first metatarsophalangeal joint attack
7. Unilateral tarsal joint attack
10. Asymmetric swelling within a joint on radiography
11. Subcortical cysts without erosions on radiography
12. Monosodium urate crystals in joint fluid during an attack
13. Joint fluid culture negative for organisms during an attack
A diagnosis of gout is highly likely if:
• Monosodium urate crystals are detected in joint fluid
• A tophus containing urate crystals is identified
• Six or more of the above criteria are present
Measurement of serum uric acid during an attack may be helpful in that a highly elevated level supports the diagnosis; however, a normal level does not exclude the diagnosis.
Serum urate levels, though, do tend to be elevated two weeks after an attack.
One study demonstrated that measurement of serum urate during an attack and then two weeks later yields two serum urate levels that can be compared to help with the diagnosis. The authors concluded that patients with low serum urate levels (<4 mg/dL) 2 weeks following an inflammatory arthritis attack were unlikely to have gout.(3)
The patient history may also provide clues. These clues include a family history of documented gout, cold exposure, history of excessive alcohol ingestion, overindulgence in high purine containing foods such as shellfish or red meat immediately preceding the attack, and a history of hyperuricemia. Patients treated with thiazide diuretics and cyclosporine are also at risk for hyperuricemia and gout.
In our clinic, we feel that in a patient presenting with monoarticular arthritis, a firm diagnosis is important and tend to perform an arthrocentesis in order to make a solid diagnosis in most patients.
Acute gout can be treated effectively with any number of non-steroidal-anti-inflammatory drugs (NSAIDS). These drugs should be used cautiously in patients who have significant renal, cardiovascular, or gastrointestinal diseases. NSAIDS are contraindicated in patients who have an aspirin allergy. The concomitant use of a proton pump inhibitor may be helpful for gastric prophylaxis. Of all the NSAIDS, indomethacin is the one which should be avoided the most in elderly patients because of the high incidence of potential side effects including dizziness, headaches, and confusion.
NSAIDS also should not be used in patients on anticoagulation therapy with warfarin.
Alternatively, colchicine in a dose of 0.6 mgs twice a day can be used. It should be avoided in patients who have underlying liver or kidney disease and it is contraindicated in patients undergoing dialysis. Colchicine should also be avoided in patients taking statin drugs, macrolide antibiotics, and cyclosporine because of drug interaction.
When NSAIDS or colchicines cannot be used, oral corticosteroids can be used instead. A prednisone burst starting at 30 mgs and reducing by 5 mgs daily is effective. Also, direct injection of glucocorticoid into the joint using ultrasound needle guidance is very effective for aborting attacks in a single joint. Patients with diabetes mellitus should be counseled about blood sugar elevation. Patients with brittle diabetes probably should not receive high dose oral steroids.
If there is any concern regarding infection, steroids should not be used.
Treating acute attacks does not treat the underlying disease. Dealing with the metabolic condition requires lowering serum urate levels below 6.0 mg/dL for an extended period of time in order to reduce the crystal burden and prevent further uric acid crystal deposition.
This is more than an academic exercise since extended high levels of hyperuricemia has been associated not only with chronic gouty arthritis but also with chronic kidney disease, hypertension, and cardiovascular disease.(4)
Comorbid conditions such as hyperlipidemia, diabetes, hypertension, chronic renal disease, and cardiovascular disease are collectively referred to as the “metabolic syndrome” and are associated with the development of gout. (5)
Over tim,e tendons can also be come inflamed along with joints. Chronic gout, which involves multiple joints may look like rheumatoid arthritis. This becomes a confounding problem in the older patient who may also develop rheumatoid factor positivity as a result of the aging process. The development of tophaceous deposits can be mistaken for rheumatoid nodules. Plus gout and rheumatoid arthritis can co-exist.
The decision to treat a patient with chronic uric acid lowering therapy is one that should be individualized and should take into consideration the patient’s lifestyle, co-morbid conditions, concomitant medications, and willingness to take chronic medicine.
Younger patients with normal renal function who excrete less than 800 mg/dL per 24 hour urine collection are usually treated with uricosuric drugs such as probenecid. Uricosuric drugs cause patients to eliminate uric acid in the urine. There is a risk for the development of kidney stones in patients who overproduce uric acid. In addition, the drugs need to be taken twice daily and fluid intake needs to be increased.
Since abrupt changes in serum uric acid can trigger flares, concomitant colchicine in a dose of 0.6 mg daily for prophylaxis against acute attacks during the first six months is recommended. The aim is to keep the serum uric acid level at or below 6.0 mg/dL.
Patients on chronic colchicine should be monitored carefully for neuromuscular symptoms. These problems occur more often in patients with renal insufficiency, or who are also taking statin or macrolide drugs.
Another uricosuric agent which can be used is sulfinpyrazone (Anturane). This drug has the added benefit of reducing platelet adhesiveness. Losartan (Cozaar), an anti-hypertensive drug also is a mild uricosuric drug.
Patients who excrete more than 800 mg/dL per 24 hour urine collection should receive a xanthine oxidase inhibitor such as allopurinol or febuxostat (Uloric). These drugs inhibit the conversion of purines to uric acid. They are effective in patients who are underexcreters and overproducers of urate. Patients with compromised renal function require adjustment in dosing. Drug interaction may present a problem.
For instance, the dose of allopurinol should be reduced in patients who require azathioprine. Achieving the target of 6.0 mgs/dL is not always easy.
Allopurinol also has multiple severe toxicities, including death, the ultimate side effect. Uloric appears to be safer.
Another drug is PEG-ricase (Krystexxa). This medicine must be administered intravenously and is reserved for patients with severe chronic gout. It works by converting urate to a soluble and easily excreted compound called allantoin. There are concerns related to infusion reactions.
1. Pillinger, MH; Rosenthal P, Abeles AM. Hyperuricemia and gout: new insights into pathogenesis and treatment. Bulletin of the NYU Hospital for Joint Diseases 65: 215–221.
2. Wallace SL, et al. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum 1977; 20: 895-900.
3. Rigby AS, Wood PH. Serum uric acid levels and gout: what does this herald for the population? Clin Exp Rheumatol 1994; 12: 395-400.
4. Krishnan E, Baker JF, Furst DE, Schumaker HR Jr. Gout and the risk of acute myocardial infarction. Arthritis Rheum 2006; 54: 2688-2696.
5. Choi HIK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med 2005; 143: 499-516
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