Man With Sharp Ankle Pain of Sudden Onset

Author:
Ronald N. Rubin, MD—Series Editor
Professor of medicine at Temple University School of Medicine and chief of clinical hematology in the department of medicine at Temple University Hospital in Philadelphia.

Citation:
Rubin RN. Man with sharp ankle pain of sudden onset. Consultant. 2011;51(5):279-280.

A 57-year-old man presents with pain in his left ankle. He denies trauma to the ankle or foot. His symptoms began 2 nights earlier when he was awakened from sleep by the sudden onset of pain in the medial ankle area. He felt feverish and diaphoretic that night, but these symptoms have subsided. The pain in the ankle area is sharp and occurs with ankle motion as well as when a shoe compresses the area. No other joints are involved, and he feels otherwise well.

HISTORY

The patient works as a mechanic in a tire shop. He consumes 1 or 2 alcoholic drinks per day during the week and probably more on the weekends. He also has a history of significant allergy to sulfa drugs and penicillin. Five years earlier, essential hypertension was diagnosed and treated with an angiotensin-converting enzyme inhibitor to which a thiazide diuretic was recently added.

PHYSICAL EXAMINATION

This well-appearing man is about 30 lb over his ideal body weight. Blood pressure is 115/78 mm Hg, and he is afebrile. There are no tophi evident on the ears, elbows, or elsewhere on his body. The left ankle has decreased range of motion because of pain. The medial area below the malleolus is red, warm, and exquisitely tender to palpation.

LABORATORY RESULTS

Hemogram is normal. Electrolyte levels are normal. The blood urea nitrogen level is 28 mg/dL, and the creatinine level is 2.2 mg/dL. Uric acid level is 7.2 mg/dL.

Answer on next page

CORRECT ANSWER: D

This patient has acute gouty arthritis. His age, male sex, and monoarticular presentation are highly characteristic of the disease. Although definitive diagnosis requires the direct identification of uric acid crystals and the exclusion of infection, this is not always practical in an office setting. This patient’s very typical epidemiology, lack of systemic toxicity suggestive of infection, presence of a monoarticular arthritis in the foot or ankle area, and strong clinical clues of obesity, high alcohol intake, and recent initiation of a thiazide diuretic all make this diagnosis likely—and most clinicians would find it reasonable to treat accordingly.^1,2

Management of gout involves addressing 2 issues: treatment of the acute gouty arthritis and evaluation to determine whether long-term suppressive and/or hypouricemic therapy is warranted. In a hospital setting or in a rheumatologist’s office, joint aspiration of fluid for diagnosis (and exclusion of infection) and intra-articular injection of corticosteroids would likely be optimal. However, this treatment choice was not offered; thus, other therapeutic modalities need to be considered.

Oral colchicine (A) is a reasonable choice and is an accepted first-line therapy in many uncomplicated cases.³ The story of how this century-old, effective treatment only recently underwent a small trial that resulted in patent protection and a marked price escalation has recently been reviewed and makes interesting reading indeed.⁴ However, in many trials the therapeutic ratio to adverse effects has been found to be higher for oral colchicine than for other treatments.³ Further, this patient’s symptoms started 2 nights earlier, and colchicine is most effective when administered at the first sign of arthritis and certainly within 24 hours of onset. In addition, he has renal insufficiency, which is a relative contraindication when other agents are available.

Choice B, initiation of allopurinol, addresses the more long-term management of gout; this drug inhibits xanthine oxidase and thereby reduces uric acid synthesis and lowers uric acid levels. Allopurinol is thus effective whether elevated levels result from overproduction or undersecretion. However, several clues in the presentation point away from allopurinol therapy for now. First, none of the principal indications for long-term uric acid–lowering therapy are present. These include presence of tophi, frequent attacks (more than 3 per year), and documented state of uric acid overproduction.⁴ Second, this is an acute attack and it has been suggested that uric acid–lowering maneuvers can worsen an acute flare.

Finally, several reversible conditions that predispose to elevated uric acid values and acute arthritis are present (obesity, alcohol use, and thiazide use); if these can be addressed, long-term therapy may not be necessary. Thus, allopurinol therapy is premature at best and perhaps not indicated at all in this case. Use of an NSAID for 5 days (choice C) is an effective therapy for many patients.

Symptomatic relief is usually obtained within 24 hours, the treatment is relatively inexpensive, and the toxicity profile is acceptable in most patients. However, this patient has renal insufficiency, which is a contraindication to most NSAIDs. Thus, a short course of corticosteroids (choice D) seems optimal here. Under ideal conditions, a monoarthritic attack can be addressed with an intra-articular injection. In most office settings, oral corticosteroids in a dosage of 30 mg/d for 5 days are effective. In good randomized trials, oral corticosteroids were equivalent to both naproxen and indomethacin.³ Outcome of this case. The patient experienced significant relief within 24 hours and was pain free by day 4. He was told to limit his alcohol intake and lose weight. His antihypertensive agent was changed, with effective blood pressure control and no change in the creatinine level. At 6 months, he has not had a recurrence of acute gouty arthritis.

The Take-Home Message

In an office setting, a short course of oral corticosteroids is a reasonable choice for treatment of acute gouty arthritis in a patient with renal insufficiency.

REFERENCES

1. Choi HK, Atkinson K, Karlson EW, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093-1103.
2. Zhang W, Doherty M, Pascual E, et al. EULAR evidence based recommendations for gout. Part 1: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65:1301-1311.
3. Neogi T. Clinical practice. Gout. N Engl J Med. 2011;364:443-452.
4. Kesselheim AS, Solomon DH. Incentives for drug development—the curious case of colchicine. N Engl J Med. 2010;362:2045-2047.