Gout is a term used to describe a group of conditions all related to various defects in purine metabolism leading to hyperuricemia and episodes of severe joint pain. One to 3 percent of the U.S. population are affected by gout, with the prevalence and impact of gout increasing over the last few decades.1 Ninety percent of those afflicted are male.2
Pathophysiology of Gout
Primary gout is characterized by an overproduction of uric acid or a decreased urate excretion in the kidney.3 It is often caused by an inherited disorder in purine metabolism.
Secondary gout is caused by any of a wide number of diseases or drugs that decrease the kidney's ability to excrete uric acid, increase the production of uric acid that exceeds the excretion capability of the kidneys, or a combination of both.4 Conditions associated with secondary gout include diabetic ketoacidosis, chronic alcoholism, severe dieting, metabolic syndrome, dyslipidemia, hypertension, and those diseases associated with a rapid cell turnover and cell breakdown, such as leukemia, multiple myeloma, psoriasis, hemolytic anemia and polycythemia.5 Medications associated with gout include diuretics, aspirin, ergotamine, pyrazinamide and anti-leukemic agents.
The patient presenting with an attack, or "flare" of acute gouty arthritis typically complains of sudden, severe pain in a single joint, most often the metatarsophalangeal joint of the big toes. This pain may be accompanied by complaints of burning, tingling and numbness. Joints in the heels, ankles, wrists, fingers, knees or elbows also may be affected.
The affected joint(s) may be reddened, warm, swollen and tender to palpation. Attacks usually have a sudden onset and often occur at night. Many attacks appear to be related to changes in serum uric acid levels; therefore, ask the patient regarding any recent ingestion of alcohol, surgery, dehydration, injury to the joint, or illness. Patients experiencing an episode of acute gouty arthritis also may have systemic signs of inflammation, including an elevated temperature and complaints of malaise, headache and chills.6
In the patient with chronic tophaceous gout, inspect the skin for small white nodules, called tophi, most often found on the outer ear, ulnar surface of the forearms and skin overlying joints, especially the elbows and knees.7 These nodules are firm on palpation, irregular and painless.8 Assess any enlarged joint for deformities, palpable nodules and limitations in the range of motion.
The diagnosis of a classic case of acute gouty arthritis is generally straightforward and can be made with a thorough history and physical. Gout should be considered in the differential diagnosis of any patient who presents with extreme pain limited to one joint, particularly in the big toe.
Laboratory results should be evaluated for hyperuricemia, and elevations in the erythrocyte sedimentation rate and the white blood cell count. BUN, creatinine levels and a 24-hour urine analysis also should be performed to determine if there is any renal involvement. A radiograph of the kidneys may confirm the presence of any suspected calculi. To confirm a diagnosis of gout, a synovial fluid analysis of an involved joint needs to be performed to evaluate for the presence of uric acid crystals.
Management of Acute Gout
Acute gout is one of the easiest diseases to treat in its early phases. The goal of short-term therapy is to provide the patient symptomatic relief. NSAIDs are the drugs of choice for treating the intense pain and inflammation that accompany acute attacks.4 The NSAIDs most commonly used are indomethacin (Indocin, Novomethacin), ibuprofen (Motrin) and naproxen (Naprosyn), taken as scheduled oral doses.9
Most patients will see marked relief within 24 hours, with the pain associated with the attack subsiding over the next few days. Persons should be advised to rest the joint as much as possible in a position of comfort. Ice and the use of bed cradles may help with reducing discomfort.10
Once considered a mainstay of therapy, the use of colchicine in combination therapy with analgesics is now reserved for those who are not responsive to, or cannot tolerate, analgesic medications alone.9 The risk of serious dose-related side effects is the major limitation to therapy. Colchicine is most effective when taken within the first 12 hours of an acute attack. The patient should take 1.2 mg of oral colchicine every 6 hours until joint symptoms begin to improve, up to a maximum dose of 2.5 mg in 24 hours.11 If intravenous dosing is used, a single 2 mg dose may produce relief for many patients.
Glucocorticoids are useful for the short-term therapy of acute gout, particularly when the symptoms are in a single joint, and the medication is delivered intra-articularly.4 Glucocorticoids also can be used orally for those who have many involved joints or who are sensitive to NSAIDS and cannot use NSAIDS for analgesia. The most commonly used corticosteroid is prednisone. When used orally, prescribe a dosage of 20 mg daily, for 4-5 days.12
The most important need in the management of chronic gout is for the patient to be compliant with the prescribed medication regimen, as recurring attacks can result in significant long-term effects.14 Counseling also must be given regarding a variety of other factors that can precipitate an attack, including the avoidance of all forms of alcohol, aspirin, niacin and diuretics.15 If patients need to be on a restricted diet, they should be taught to avoid certain high-purine foods including red meats and seafoods. If the patient is obese, dietary restrictions and a moderate exercise program that result in weight loss will lead to a reduction in gout symptoms.12 The client should be encouraged to drink at least 2 liters of fluid each day.