Gout is monosodium urate crystal-induced inflammatory arthritis associated with hyperuricemia. (1
). Predisposing factors for an acute attack include trauma, surgery, increasing alcohol intake, high levels of intake of meat and fish and medications including diuretics and cyclosporine. Metabolic syndrome and impaired renal function are common co-morbidities in gout patients. Gout is more common in men with a male to female ratio of 4:1 below the age of 65 and 3:1 above the age of 65 (2
Gout classically involves the peripheral joints. In 50% of gout cases, the first joint to be involved is the first metatarsophalangeal joint. There are about 125 cases reported in the English literature describing a variety of gouty lesions in the axial spine(3
In a retrospective review of records of gout patients, approximately 48% of the axial gout patients had involvement of the lumbar vertebrae, 29% the cervical vertebrae and 20% the thoracic vertebrae and 8.7% the sacro-iliac joints (4
). The common symptoms of patients with axial gout are back pain with features suggestive of radiculopathy or weakness(5
It takes years to develop radiographic bony changes secondary to gout. Radiography and CT scan might show paraarticular "punched out" bone erosions often with a thin sclerotic margin which are typical of chronic tophaceous gout. Periosteal new bone formation with classic overhanging edge sign is also seen in tophaceous bone lesions. Bony ankylosis can also occur rarely. Soft-tissue swelling around the involved joints is usually found. Joint space narrowing is not usually seen in gout (3
). In MRI of axial gout, low to intermediate signal intensity may be noted in T1 sequence and intermediate to high signal on T2 sequences (3
). Lesions are usually enhanced with gadolinium (5
). Facet joint erosions in lumbar spine in a patient with gout should raise suspicion for Axial Gouty Arthropathy (3
). It is also important to note that urate crystals are not usually radiologically opaque unless they get calcified (3
Differential diagnosis includes infectious or metastatic process(6
) in the spine. Contrast enhancement occurs in gout as well as epidural or paraspinal abscesses. It is difficult to differentiate spinal gout from infectious pathology like epidural abscess (7
), paraspinal abscess or osteomyelitis based on imaging modality. History of intravenous drug abuse or immuno-compromised state are more common in epidural abscess than gout. Prior history of positivity to PPD, pulmonary tuberculosis or exposure to a TB patient may be present in a case of Tuberculosis of the spine. Also, thoracic spine is more commonly involved than lumbar spine in Tuberculosis. Destructive changes of two contiguous vertebral bodies with collapse of the intervening disc space is a typical finding in vertebral osteomyelitis (8
). CT guided needle biopsy of the lesion with microscopy, gram stain, aerobic, anerobic, mycobacterial and fungal culture of the lesion is needed for final diagnosis.
The medical management of spinal gout is not different from that of acute gout of any other joint. However aggressive lowering of uric acid is essential in the treatment of such patients (9
). In addition, the spinal gout might need surgical intervention especially if cord compression is an issue (9
). Symptoms suggestive of spinal cord compression include radiculopathy, paresthesias, paresis and bladder/bowel dysfunction.
In conclusion, gout should be considered in the differential diagnosis of spine lesions in a patient with risk factors or prior history of gout. This is important clinically, as the treatment and prognosis would obviously be different in gout versus an infectious cause. Early diagnosis would also help avoid unnecessary use of long-term antibiotics.