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Sterile spondylodiscitis
Case Report
Sterile spondylodiscitis Janine Rufener, Christina Claudia Schulze, Kristina Tänzler, Daniel Aeberli, Parham Sendi Lancet 2012; 379: 1850 Department of General Internal Medicine (J Rufener MD, K Tänzler MD), Department of Rheumatology and Clinical Immunology/Allergology (D Aeberli MD), and University Clinic for Infectious Diseases (C C Schulze MD, P Sendi MD), University Hospital Bern and University of Bern, Switzerland Correspondence to: Dr Parham Sendi, University Clinic for Infectious Diseases, University Hospital Bern and University of Bern, 3010 Bern, Switzerland [email protected]
In April, 2011, an 85-year-old man was referred to our hospital with suspected septic spondylodiscitis; he had acute immobilising back pain, raised body temperature, and high C-reactive protein (CRP) concentration. His medical history included chronic back pain because of advanced spinal degeneration, chronic renal insufficiency, and gouty arthritis. On physical examination, his lumbar spine and right flank were very tender. The distal interphalangeal joint of the right index finger was painful, warm, and swollen. He was clinically stable. Blood tests showed the following raised values: white blood cell count 25∙3×10⁹/L (without a left shift of the neutrophils), CRP 349 mg/L, creatinine 162 μmol/L, and uric acid 513 μmol/L. MRI of the lumbar spine was consistent with spondylodiscitis at L1–L2, and showed an abscess-like formation in the right psoas muscle (figure). Debridement was done and biopsy samples were taken from the psoas muscle and lumbar discs. Surprisingly, no pus was seen during surgery. In the psoas muscle, an encapsulated structure with hardened tissue was found. After surgery, intravenous antimicrobial treatment (amoxicillin/clavulanate) was initiated. The samples showed no growth of microorganisms and eubacterial PCR analyses (16S-RNA) of specimens revealed no pathogens. However, examination of the specimens from the psoas muscle by polarised light microscopy showed needle-shaped uric acid crystals. A diagnosis of tophaceous gout mimicking psoas abscess and lumbar spondylodiscitis was made, on the basis of the history of gout, the findings at the index finger, and the uric acid
crystals seen in the biopsy samples. Antibiotic treatment was stopped and non-steroidal anti-inflammatory drugs (NSAIDs) given. The further clinical course was favourable. When last seen in October, 2011, the patient reported no signs of acute gouty flare-ups. Acute gouty arthritis includes severe pain, redness, swelling, and disability. Most attacks involve a single joint of the foot (eg, first metatarsophalangeal joint). Involvement of other joints, such as shoulders, sternoclavicular joints, spine, or sacroiliac joints, is rare, and hence, often causes diagnostic confusion.1 In our case, infection was ruled out by exhaustive analysis of the samples. In reports of gouty arthritis involving the spine, most patients were male, had a history of gout, presented with neurological deficits and localised pain, and had high concentrations of urate and inflammatory markers in the serum.1–3 The latter finding is probably a result of the release of interleukins by monocytes and synoviocytes reacting to crystals. Spinal gout is predominantly located in the lumbar region.3,4 Radiological findings include vertebral erosions predominantly at the discovertebral junction and epidural space.4 On MRI, these erosions are commonly isointense or hypointense and show homogeneous contrast enhancement.2,3 Several risk factors have been proposed to trigger, or to be associated with, acute attacks of gouty arthritis.5 High urate concentrations in conjunction with previous degenerative change may have predisposed our patient to gouty inflammation. Treatment of spinal gout is the same as at other sites, and includes the use of colchicine, glucocorticoids, or NSAIDs. Gouty arthritis is a frequently occurring autoinflammatory disease, and an important differential diagnosis of septic arthritis. Our case illustrates that spinal gout is a differential diagnosis of septic spondylodiscitis and should be considered in patients with a history of gout and when specimens yield no growth of microorganisms despite correct sampling. Contributors All authors were involved in patient management and in writing the report. Written consent to publish was obtained.
Figure: MRI of the lumbar spine Homogeneous contrast enhancement mimicking psoas abscess (arrow).
1850
References 1 Suk KS, Kim KT, Lee SH, Park SW, Park YK. Tophaceous gout of the lumbar spine mimicking pyogenic discitis. Spine J 2007; 7: 94–99. 2 Hou LC, Hsu AR, Veeravagu A, Boakye M. Spinal gout in a renal transplant patient: a case report and literature review. Surg Neurol 2007; 67: 65–73. 3 Barrett K, Miller ML, Wilson JT. Tophaceous gout of the spine mimicking epidural infection: case report and review of the literature. Neurosurgery 2001; 48: 1170–72. 4 Konatalapalli RM, Demarco PJ, Jelinek JS, et al. Gout in the axial skeleton. J Rheumatol 2009; 36: 609–13. 5 Agudelo CA, Wise CM. Gout: diagnosis, pathogenesis, and clinical manifestations. Curr Opin Rheumatol 2001; 13: 234–39.
www.thelancet.com Vol 379 May 12, 2012
Sterile spondylodiscitis Janine Rufener, Christina Claudia Schulze, Kristina Tänzler, Daniel Aeberli, Parham Sendi Lancet 2012; 379: 1850 Department of General Internal Medicine (J Rufener MD, K Tänzler MD), Department of Rheumatology and Clinical Immunology/Allergology (D Aeberli MD), and University Clinic for Infectious Diseases (C C Schulze MD, P Sendi MD), University Hospital Bern and University of Bern, Switzerland Correspondence to: Dr Parham Sendi, University Clinic for Infectious Diseases, University Hospital Bern and University of Bern, 3010 Bern, Switzerland [email protected]
In April, 2011, an 85-year-old man was referred to our hospital with suspected septic spondylodiscitis; he had acute immobilising back pain, raised body temperature, and high C-reactive protein (CRP) concentration. His medical history included chronic back pain because of advanced spinal degeneration, chronic renal insufficiency, and gouty arthritis. On physical examination, his lumbar spine and right flank were very tender. The distal interphalangeal joint of the right index finger was painful, warm, and swollen. He was clinically stable. Blood tests showed the following raised values: white blood cell count 25∙3×10⁹/L (without a left shift of the neutrophils), CRP 349 mg/L, creatinine 162 μmol/L, and uric acid 513 μmol/L. MRI of the lumbar spine was consistent with spondylodiscitis at L1–L2, and showed an abscess-like formation in the right psoas muscle (figure). Debridement was done and biopsy samples were taken from the psoas muscle and lumbar discs. Surprisingly, no pus was seen during surgery. In the psoas muscle, an encapsulated structure with hardened tissue was found. After surgery, intravenous antimicrobial treatment (amoxicillin/clavulanate) was initiated. The samples showed no growth of microorganisms and eubacterial PCR analyses (16S-RNA) of specimens revealed no pathogens. However, examination of the specimens from the psoas muscle by polarised light microscopy showed needle-shaped uric acid crystals. A diagnosis of tophaceous gout mimicking psoas abscess and lumbar spondylodiscitis was made, on the basis of the history of gout, the findings at the index finger, and the uric acid
crystals seen in the biopsy samples. Antibiotic treatment was stopped and non-steroidal anti-inflammatory drugs (NSAIDs) given. The further clinical course was favourable. When last seen in October, 2011, the patient reported no signs of acute gouty flare-ups. Acute gouty arthritis includes severe pain, redness, swelling, and disability. Most attacks involve a single joint of the foot (eg, first metatarsophalangeal joint). Involvement of other joints, such as shoulders, sternoclavicular joints, spine, or sacroiliac joints, is rare, and hence, often causes diagnostic confusion.1 In our case, infection was ruled out by exhaustive analysis of the samples. In reports of gouty arthritis involving the spine, most patients were male, had a history of gout, presented with neurological deficits and localised pain, and had high concentrations of urate and inflammatory markers in the serum.1–3 The latter finding is probably a result of the release of interleukins by monocytes and synoviocytes reacting to crystals. Spinal gout is predominantly located in the lumbar region.3,4 Radiological findings include vertebral erosions predominantly at the discovertebral junction and epidural space.4 On MRI, these erosions are commonly isointense or hypointense and show homogeneous contrast enhancement.2,3 Several risk factors have been proposed to trigger, or to be associated with, acute attacks of gouty arthritis.5 High urate concentrations in conjunction with previous degenerative change may have predisposed our patient to gouty inflammation. Treatment of spinal gout is the same as at other sites, and includes the use of colchicine, glucocorticoids, or NSAIDs. Gouty arthritis is a frequently occurring autoinflammatory disease, and an important differential diagnosis of septic arthritis. Our case illustrates that spinal gout is a differential diagnosis of septic spondylodiscitis and should be considered in patients with a history of gout and when specimens yield no growth of microorganisms despite correct sampling. Contributors All authors were involved in patient management and in writing the report. Written consent to publish was obtained.
Figure: MRI of the lumbar spine Homogeneous contrast enhancement mimicking psoas abscess (arrow).
1850
References 1 Suk KS, Kim KT, Lee SH, Park SW, Park YK. Tophaceous gout of the lumbar spine mimicking pyogenic discitis. Spine J 2007; 7: 94–99. 2 Hou LC, Hsu AR, Veeravagu A, Boakye M. Spinal gout in a renal transplant patient: a case report and literature review. Surg Neurol 2007; 67: 65–73. 3 Barrett K, Miller ML, Wilson JT. Tophaceous gout of the spine mimicking epidural infection: case report and review of the literature. Neurosurgery 2001; 48: 1170–72. 4 Konatalapalli RM, Demarco PJ, Jelinek JS, et al. Gout in the axial skeleton. J Rheumatol 2009; 36: 609–13. 5 Agudelo CA, Wise CM. Gout: diagnosis, pathogenesis, and clinical manifestations. Curr Opin Rheumatol 2001; 13: 234–39.
www.thelancet.com Vol 379 May 12, 2012