E048 Spinal gout: an unusual cause of paraplegia
Authors: Zollinger-Read Caroline A , Cox Miriam , Kumari Rakesh 
Published: April 2024

Abstract

Background/Aims
Gout is a common inflammatory arthritis caused by the deposition of monosodium urate crystals. Gout usually causes peripheral joint arthritis. Axial involvement is likely under-recognised, affecting an estimated 10-20% of gout patients. Spinal gout is an established phenomenon in patients with chronic tophaceous gout and sustained hyperuricaemia. Gout can affect any segment of the spine. Clinical presentation of spinal gout is variable including back pain, radiculopathy and cord compression. Due to its nonspecific presentation, it can be confused for other spinal pathologies such as epidural abscess, malignancy, spondylodiscitis and vertebral osteomyelitis.

Methods
We present a case report of a young male with tophaceous gout of the thoracic spine.

Results
A 37 year old man presented with 4 day history of acute thoracic back pain followed by flaccid lower limb paralysis. He was morbidly obese (BMI 60) and had a 13-year history of poorly controlled gout with most recent uric acid being 627. He had previously declined urate lowering therapy but commenced allopurinol treatment one month prior to admission.
On examination power was 0/5 in both lower limbs with absent reflexes and a T12 sensory level. MRI showed multi-level facet joint arthropathy. An epidural collection was present at T8-10, causing complete occlusion of the vertebral artery. He underwent an urgent posterior thoracic decompression. ‘White cheese like epidural pus’ was removed and he was initially treated as facet joint infection. He had ongoing fevers [&gt;38.5C], despite empirical antibiotics, and C-reactive-protein was persistently elevated [highest at 360mg/L]. Uric acid was 423. Enrichment culture of the epidural collection and serial blood cultures were negative. Repeat MRI of spine did not demonstrate any reoccurrence of collection.
Subsequently the histology of the epidural collection was reported as characteristic of gout with ‘amorphous material and giant cells’. No urate crystals were identified as the sample was prepared with formalin, which would have dissolved any crystals present. He was referred to rheumatology who identified synovitis in his hands, wrist and elbows, consistent with active polyarticular gout. There were small tophi present on his heels and pinna. The patient was commenced on oral prednisolone and allopurinol was rapidly up-titrated. Unfortunately, the patient did not recover neurological function.

Conclusion
We present a unique case of acutely presenting tophaceous thoracic spinal gout causing irreversible paraplegia in a young patient, mimicking an epidural abscess. Our patient had hyperuricaemia for over 10 years without treatment, raising his risk of axial complications. A high index of suspicion for spinal gout is needed for patients presenting with acute back pain and neurological symptoms with a history of chronic gout. This case highlights diagnostic challenges in identifying spinal gout and the importance of treating tophaceous gout early to prevent devastating long-term complications.

Disclosure
C.A. Zollinger-Read: None. M. Cox: None. R. Kumari: None.