Case Presentation: A 51 year old male with history of obesity, spinal stenosis, and gout presented with 1 week of worsening low back pain with bilateral radiculopathy. He had no bladder or bowel incontinence, or other neurologic compromise. He was afebrile, with normal vital signs. Lab data was significant for WBC 25 x 10^9/L, hemoglobin 13.1g/dL, platelets 481,000, normal comprehensive metabolic panel and elevated ESR 98 mm/h and CRP 399mg/dL. MRI of the spine revealed endplate irregularity with edema at L5-S1 suspicious for discitis/osteomyelitis, for which vancomycin/ceftriaxone was started. Given lack of improvement, he underwent L5-S1 laminectomy, irrigation and debridement. He continued to show no clinical improvement. He did complain of migratory joint pains: bilateral shoulders, knees, ankles, great toes; and was noted to have significant warmth, erythema, and tenderness of these joints. He was also noted to have tophi on his right elbow. Polyarticular septic arthritis vs acute gout flare was suspected. No evidence of infection was identified from blood cultures, operative cultures, synovial fluid analysis, chest xray or echocardiogram. Corticosteroids were eventually started for acute gout flare with marked improvement in his symptoms and normalization of his bloodwork. His presentation was ultimately attributed to spinal gout.

Discussion: Gout is a common inflammatory arthritis in response to monosodium urate crystal deposition, classically affecting the peripheral joints. Spinal gout is an unusual manifestation. Diagnosis is challenging with presentation ranging from back pain alone, to various neurologic syndromes to mimicking spinal infections (vertebral osteomyelitis, discitis, and epidural abscess). Fever, leukocytosis, elevated ESR and CRP are common, but nonspecific. Uric acid levels are often normal. MRI detects spinal gout with a sensitivity of only 21% and findings can be indistinguishable from osteomyelitis/discitis. CT imaging can better detect characteristic articular erosions and sclerotic margins, but is not the imaging modality chosen for patients in which spinal infection must be ruled out. Treatment for spinal gout is the same as gout of the peripheral joints: nonsteroidal anti-inflammatory medications, colchicine, corticosteroids, and long-term treatment with allopurinol to dissolve tophaceous deposits. In cases of diagnostic uncertainty, surgical intervention is warranted. Sampling of spinal gout reveals a white, chalky material, rather than the purulence seen with infection. Because urate crystals dissolve in formalin, a separate sample must be sent at the time of biopsy, preserved in 100% alcohol.

Conclusions: Spinal gout is an underrecognized manifestation of gout. In patients with a known history of tophaceous gout, who present with back pain and no obvious infection, spinal gout should be suspected. CT is the preferred imaging modality over MRI. In the absence of concern for infection, spinal gout can be managed medically with nonsteroidal anti-inflammatory medications, colchicine, corticosteroids, and long-term treatment with allopurinol. For patients in whom infection is suspected, spinal gout should remain on the differential diagnosis, particularly for patients with a history of tophaceous gout. While undergoing workup for infection, a high index of suspicion for spinal gout pre-operatively can lead to appropriate sampling at the time of biopsy, and can aid in distinguishing between spinal gout and spinal infection.