Case 47

A 63-Year-Old Male With Acute Polyarticular Arthritis

Dawn Piarulli, R. Michelle Koolaee

A 63-year-old male with a past medical history significant for obesity, type 2 diabetes, hypertension, hyperlipidemia, chronic kidney disease (CKD), and heart failure is admitted with an episode of acute decompensated systolic heart failure. His home medications include lisinopril, carvedilol, aspirin, atorvastatin, hydrochlorothiazide, and sitagliptin. He is treated with aggressive intravenous (IV) diuresis with furosemide. Three days into his admission he begins to complain of severe bilateral wrist, elbow, and right knee pain. On exam, he is febrile to 38.22 °C (100.8 °F). His cardiopulmonary exam is significant for an S3 heart sound, bibasilar crackles, and pitting pedal edema of the lower extremities bilaterally. Musculoskeletal exam reveals tenderness and swelling of the wrists and elbows; there is a moderate effusion in the right knee with associated warmth and tenderness. There are nodules on the extensor surface of the right 3rd and 5th metacarpophalangeal (MCP) joints, as well as both olecranon bursae.

What is the differential diagnosis for this patient’s joint pain?

This is a patient presenting with an acute polyarticular inflammatory arthritis. The causes of polyarticular arthritis include but are not limited to:

• Viral infection (especially parvovirus B19 but also hepatitis B/C and human immunodeficiency virus [HIV] among others)

• Reactive arthritis (i.e., Chlamydia trachomatis, Yersinia, Salmonella, Shigella, Campylobacter, Escherichia coli, Clostridium difficile, and Chlamydia pneumonia)

• Bacterial arthritis (i.e., Neisseria gonorrhoeae [gonorrhea], poststreptococcal arthritis, Staphylococcus aureus)

• Other infections (i.e., tubercular and fungal organisms, Borrelia burgdorferi [Lyme disease])

• Crystal-induced arthritis (i.e., gout, pseudogout, calcium oxalate, hydroxyapatite)

• Systemic rheumatic disease (i.e., rheumatoid arthritis [RA], systemic lupus erythematosus [SLE], Sjögren’s syndrome, inflammatory myositis)

• Systemic vasculitis

• Spondyloarthropathies (i.e., psoriatic arthritis, ankylosing spondylitis, inflammatory bowel disease–related arthritis, reactive arthritis)

• Endocrinopathies (i.e., hyperparathyroidism, hyperthyroidism, hypothyroidism)

• Malignancy (metastatic cancer, multiple myeloma)

The acuity of his symptoms makes causes such as crystal-induced arthritis very likely (especially gout, given his comorbidities, along with use of diuretics; calcium oxalate crystals is less common but is seen exclusively in patients with CKD). An infectious arthritis is also possible, given the acuity of the symptom. A systemic rheumatic illness is unlikely; these tend to present with chronic inflammatory arthritis.

How does the physical exam in this case help to narrow the differential diagnosis?

This patient has multiple nodules of the extensor surfaces of his joints. The differential diagnosis of nodules includes xanthoma (history of hyperlipidemia), rheumatoid nodules (multiple joints involved), sarcoidosis (usually located on the lower rather than upper extremities), tumors (less likely to be present in multiple locations superficially), and tophi (which are due to deposition of monosodium urate crystals in and about the joints of a gout patient). Given the location of the nodules, along with the acuity of his arthritic symptoms, his nodules likely represent tophi (nodules in RA and sarcoidosis would be associated with a chronic inflammatory arthritis). Figure 47.1 represents examples of gouty tophi.

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Clinical Pearl

It is far more common to see tophi in the olecranon bursae than on the ears.

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Clinical Pearl

Fevers are not specific for an infectious arthritis; in fact, it is not common for patients with crystal-induced arthritis to also present with fevers.

Figure 47.1 A, Ulcerating tophus of the right index finger. B, Tophi along the fourth distal interphalangeal joint of the left hand. C, Tophus along the interphalangeal joint of the right hallux. (From van der Klooster JM, Peters R, Burgmans JPJ, Grootendorst AF. Chronic tophaceous gout in the elderly. Netherlands J Med. 1998;53[2]:69-75.)

Furthermore, based on his comorbidities (obesity, type 2 diabetes, CKD, and hypertension; all of which are associated with gout), likely tophi in the elbows, and the onset of symptoms during hospitalization for diuretic therapy, the most likely diagnosis is acute polyarticular gout. Table 47.1 highlights the common risk factors for gout flares.

What is the single best test to help determine the diagnosis?

The best way to determine the etiology of any arthritis with effusion is arthrocentesis. Synovial fluid analysis is a valuable tool to help in the diagnostic workup.

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Clinical Pearl

A diagnosis of gout can never be made based on the uric acid level alone. Furthermore, the uric acid level does not correlate with the severity of the gout flare (some patients have severe polyarticular flares with only modest elevation in the serum uric acid).

Laboratory tests reveal a serum creatinine of 1.5 mg/dL (at baseline) and uric acid level of 9.6 mg/dL. 15 mL of straw-colored synovial fluid is aspirated from the patient’s right knee. Synovial fluid leukocyte count is 42,000/µL ([42 × 10⁹/L], 82% polymorphonuclear cells). Polarized light microscopy reveals several needle-shaped, negatively birefringent crystals. Gram stain and cultures are negative.

Diagnosis: Acute polyarticular gout flare

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Clinical Pearl

You should be able to read newspaper print if it is placed behind a sample of normal synovial fluid. The more inflammatory the fluid becomes, the cloudier it will be, and the more difficult it will be to read the print.

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Clinical Pearl

Only one drop of fluid is need for crystal analysis using polarized light microscopy (more fluid is necessary for cell count and fluid culture).

How do you interpret the synovial fluid analysis results?

The leukocyte count above 2,000/mm³ confirms the presence of inflammatory fluid.

Figure 47.2 demonstrates monosodium urate (MSU) crystals, which have the characteristic needle-shaped appearance and are negatively birefringent on polarized light microscopy; this is the definitive way to diagnose gout. Septic arthritis can rarely occur simultaneously as an acute gout flare, but the leukocyte count is usually over 50,000/mm³. Table 47.2 compares synovial fluid findings in patients with inflammatory versus noninflammatory arthritis.