Also known as gouty arthritis, gout is a metabolic disease marked by urate deposits in the joints, which cause painfully arthritic joints. It can strike any joint but favors those in the feet and legs. Primary gout usually occurs in men older than age 30 and in postmenopausal women. Secondary gout occurs in older people.
Gout follows an intermittent course and commonly leaves patients free from symptoms for years between attacks. Gout can lead to chronic disability or incapacitation and, rarely, severe hypertension and progressive renal disease. The prognosis is good with treatment.
Although the exact cause of primary gout remains unknown, it seems linked to a genetic defect in purine metabolism, which causes overproduction of uric acid (hyperuricemia), retention of uric acid, or both.
In secondary gout, which develops during the course of another disease (such as obesity, diabetes mellitus, hypertension, sickle cell anemia, and renal disease), hyperuricemia results from the breakdown of nucleic acid.
Secondary gout can also follow drug therapy, especially the use of hydrochlorothiazide or pyrazinamide, which interferes with urate excretion. An increased concentration of uric acid leads to urate deposits, called tophi, in joints or tissues, causing local necrosis or fibrosis.
Another condition — pseudogout — results when calcium pyrophosphate crystals collect in the periarticular joint structures. (See Pseudogout, page 348.)
Gout develops in four stages: asymptomatic, acute, intercritical, and chronic.
In asymptomatic gout, serum urate levels rise but produce no symptoms.
As the disease progresses, it may cause hypertension or nephrolithiasis, with severe back pain. The first acute attack strikes suddenly and peaks quickly. Although it generally involves only one or a few joints, this initial attack is extremely painful. Affected joints appear hot, tender, inflamed, dusky red, or cyanotic.
The metatarsophalangeal joint of the great toe usually becomes inflamed first (podagra), followed by the instep, ankle, heel, knee, or wrist joints. A low-grade fever is sometimes present. Mild acute attacks commonly subside quickly but recur at irregular intervals. Severe attacks may persist for days or weeks.
Symptom-free intervals between gout attacks are called intercritical periods. Most patients have a second attack within 6 months to 2 years, but in some, the second attack is delayed for 5 to 10 years. Delayed attacks are more common in those who are untreated, and they last longer and are more severe than initial attacks.
Such attacks are also polyarticular, invariably affecting joints in the feet and legs, and are sometimes accompanied by fever. A migratory attack sequentially strikes various joints and the Achilles tendon and is associated with either subdeltoid or olecranon bursitis.
Eventually, chronic polyarticular gout sets in. This final, unremitting stage of the disease (chronic or tophaceous gout) is marked by persistent painful polyarthritis with large, subcutaneous tophi in cartilage, synovial membranes, tendons, and soft tissue.
Tophi form in the fingers, hands, knees, feet, ulnar sides of the forearms, helix of the ear, Achilles tendons and, rarely, internal organs, such as the kidneys and myocardium.
The skin over the tophus may ulcerate and release a chalky, white exudate or pus. Chronic inflammation and tophaceous deposits precipitate secondary joint degeneration, with eventual erosions, deformity, and disability. Kidney involvement with associated tubular damage leads to chronic renal dysfunction. Hypertension and albuminuria occur in some patients; urolithiasis is common.
The presence of monosodium urate monohydrate crystals in synovial fluid taken from an inflamed joint or a tophus establishes the diagnosis. Aspiration of synovial fluid (arthrocentesis) or tophaceous material reveals needlelike intracellular crystals of sodium urate.
Although hyperuricemia isn’t specifically diagnostic of gout, the serum uric acid level is above normal. The urine uric acid level is usually higher in secondary gout than in primary gout.
Initially, X-ray examinations are normal. However, in chronic gout, X-rays show damage of the articular cartilage and subchondral bone. Outward displacement of the overhanging margin from the bone contour characterizes gout.
Correct management seeks to terminate an acute attack, reduce hyperuricemia, and prevent recurrence, complications, and the formation of renal calculi.
Treatment for the patient with acute gout consists of bed rest, local application of heat or cold, and immobilization and protection of the inflamed, painful joints.
Analgesics, such as acetaminophen, relieve the pain associated with mild attacks, but acute inflammation requires concomitant treatment with colchicine (by mouth or I.V.) every hour for 8 hours until the pain subsides or until nausea, vomiting, cramping, or diarrhea develops.
Phenylbutazone or indomethacin in therapeutic doses may be used instead, but each is less specific. Resistant inflammation may require corticosteroids or corticotropin (I.V. drip or I.M.) or joint aspiration and an intra-articular corticosteroid injection.
Treatment of chronic gout consists of the following measures:
❑ A continuing maintenance dosage of allopurinol is given in many cases to suppress uric acid formation or control uric acid levels, preventing further attacks. This powerful drug should be used cautiously in patients with renal failure.
❑ Colchicine prevents recurrent acute attacks until uric acid returns to its normal level, but it doesn’t affect the uric acid level. Uricosuric agents (probenecid and sulfinpyrazone) promote uric acid excretion and inhibit its accumulation, but their value is limited in patients with renal impairment. These drugs shouldn’t be given to patients with renal calculi.
❑ Other therapeutic measures include a few dietary restrictions, primarily the avoidance of alcohol and purine-rich foods. Obese patients should try to lose weight because obesity puts additional stress on painful joints.
❑ In some cases, surgery may be necessary to improve joint function or correct deformities. Tophi must be excised and drained if they become infected or ulcerated. They can also be excised to prevent ulceration, improve the patient’s appearance, or make it easier for him to wear shoes or gloves.
❑ Encourage bed rest, but use a bed cradle to keep bedcovers off extremely sensitive, inflamed joints.
❑ Give pain medication as needed, especially during acute attacks. Apply hot or cold packs to inflamed joints. Administer anti-inflammatory medication and other drugs, and watch for adverse effects. Be alert for GI disturbances with colchicine.
❑ Urge the patient to drink plenty of fluids (up to 2 qt [2 L]/day) to prevent formation of renal calculi.
❑ When forcing fluids, record intake and output accurately. Be sure to monitor serum uric acid levels regularly. Alkalinize urine with sodium bicarbonate or another agent as needed.
Clinical tip Watch for acute gout attacks 24 to 96 hours after surgery. Even minor surgery can precipitate an attack. Before and after surgery, administer colchicine to help prevent gout attacks as needed.
❑ Make sure the patient understands the importance of having serum uric acid levels checked periodically. Tell him to avoid high-purine foods, such as anchovies, liver, sardines, kidneys, sweetbreads, lentils, and alcoholic beverages (especially beer and wine), all of which raise the urate level.
❑ Explain the principles of a gradual weight reduction diet to obese patients. Such a diet features foods that contain moderate amounts of protein and little fat.
❑ Advise the patient who is receiving allopurinol, probenecid, or other drugs to report adverse effects, such as drowsiness, dizziness, nausea, vomiting, urinary frequency, and dermatitis, immediately.
❑ Warn the patient taking probenecid or sulfinpyrazone to avoid aspirin and other salicylates. Their combined effect causes urate retention.
❑ Inform the patient that long-term colchicine therapy is essential during the first 3 to 6 months of treatment with uricosuric drugs or allopurinol.
Review other book chapters online related to Gout:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
|
More About This Book:
Title: Handbook of Diseases Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2003 ISBN: 1-58255-266-5 
|
|
What do you think about the features of this website? Take our user survey and have your say:
Next articles:
Tools & Services:
Medical Articles:
Search Specialists by State and City
By using this site you agree to our Terms of Use. Information provided on this site is for informational purposes only; it is not intended as a substitute for advice from your own medical team. The information on this site is not to be used for diagnosing or treating any health concerns you may have - please contact your physician or health care professional for all your medical needs. Please see our Terms of Use.
Copyright © 2009 Health Grades Inc. All rights reserved.
