Blood cultures remained negative, and transesophageal echocardiogram (TEE) did not show any valvular vegetations. During the hospitalization, the patient’s pain worsened to the point where he was unable to move his right leg and left wrist, despite antibiotic therapy. Knee and ankle X-rays did not show erosions, bony changes, fractures or soft tissue inflammation (see Figures 1–4).
You Might Also Like
Explore This IssueApril 2017
Although plain radiographs play a minor a role in the diagnosis of septic arthritis, their ease and low cost make X-rays useful tools. The earliest changes seen with septic arthritis include soft tissue swelling, and joint space widening or narrowing. Evidence of superimposed osteomyelitis can be seen in the form of periosteal bone reaction and bone destruction.1 Erosions are a feature common to infectious, as well as inflammatory, joints in the setting of both gout and rheumatoid arthritis.
Next, the patient underwent arthroscopic lavage of the left elbow, which showed 30,000 cells with 82% neutrophils, negative cultures, 154,000 red blood cells and positive intracellular monosodium urate crystals.
Left wrist and right knee synovial biopsies revealed mild to moderate acute inflammatory changes consistent with gouty arthritis. No crystals were visualized, possibly due to specimen fixation in formalin solution. Antibiotic therapy was continued despite the lack of positive cultures, and colchicine was started for polyarticular gout. Corticosteroids were not given because of persistent fevers and concern for systemic infection.
The patient’s leukocytosis and inflammatory markers improved, and the patient was eventually discharged after 40 days of hospitalization.
Which of the following is the most commonly used treatment modality for acute gout?
Gout is the most common form of inflammatory arthritis, with a prevalence of 5% in the U.S., and is characterized by swollen, erythematous and tender joint(s). Risk factors include alcohol use, obesity, kidney disease and any disease causing high cellular turnover, such as malignancy.
Depending on the clinical situation, acute attacks are generally treated with corticosteroids, colchicine or non-steroidal anti-inflammatory drugs (NSAIDs). Recurrent attacks can be prevented with colchicine, NSAIDs, urate-lowering agents, such as xanthine oxidase inhibitors (allopurinol or febuxostat) or uricase, or by increasing secretion in a functioning kidney with probenecid or sulfinpyrazone. Urate-lowering agents are indicated in patients with tophaceous gout, frequent attacks despite prophylactic colchicine or NSAID use, urolithiasis and multiple comorbidities.2 When primary measures are ineffective or contraindicated, therapies targeted at cytokines IL-1, such as anakinra, can help treat gouty attacks.