Spinal epidural abscess due to acute pyelonephritis.

Background: Spinal epidural abscesses are rare and are misdiagnosed in up to 75% of cases. Fever, back pain, and neurological deficits are part of the classical triad. Here, the authors report a patient with a L2-L5 spinal epidural abscess with the left paravertebral extension attributed to acute pyelonephritis. Case Description: A 54-year-old female presented with persistent low back pain and lower extremity weakness accompanied by paresthesias. Previously, she had been hospitalized with the left acute pyelonephritis. The lumbosacral MRI documented a T12/L5 anterior epidural abscess with ring enhancement on the contrast study; the maximum diameter of the abscess at the L2-L3 level contributed to severe cauda equina compression. She underwent a L2/L4 decompressive laminectomy with drainage of the intraspinal/extradural and paravertebral components. Intraoperative microbiological sampling grew Staphylococcus aureus for which she then received targeted antibiotic therapy. Fifteen days later, she was walking adequately when discharged.
Conclusion: Thoracolumbar epidural abscesses are rare. They must be considered among the differential diagnoses when patients present with acute back pain, fever, and new neurological deficits following prior treatment for acute pyelonephritis. Copyright:

INTRODUCTION

Spinal epidural abscesses (SEAs) are rare and are misdiagnosed in up to 75% of cases.[2,7] They are typically hematogenous in origin.[4,5] The typical presenting triad for SEA includes fever, pain, and the onset of new neurological dysfunction.[1,13] Most SEA originate anteriorly from inflammatory changes in the vertebral bodies and disks that then extend into the spinal canal. Pyelonephritis may contribute to SEA, as organisms can spread hematogenously through the major venous epidural network connected with Batson’s plexus.[3,8] Here, the authors report a 54-year-old female who, following acute pyelonephritis, developed a intraspinal/epidural L2–L5 SEA with the left paravertebral extension.

CASE REPORT

Clinical history

A 54-year-old female was previously hospitalized with acute pyelonephritis for 3 weeks. She was now admitted after about 1 week with persistent lumbar pain (visual analog scale score of 8 / 10) and the onset of a spastic paraparesis (4 / 5 BMRC) without sphincter dysfunction. The lumbar CT scan showed left paravertebral and epidural collections extending from T12 to L5. The lumbosacral MRI documented a T12/L5 anterior epidural hypointense lesion with ring enhancement; the maximum AP diameter was 1.2 cm at the L2–L3 where it caused severe cauda equina compression [Figure 1].

Figure 1:

Preoperative sagittal T1-WI with contrast enhancement (a), sagittal T2-WI (b), and axial T2-WI (c) MRI showed a T12/L5 anterior epidural hypointensity with ring enhancement on T1-WI sequences after gadolinium administration, with a maximum diameter of 1.2 cm at L2–L3 causing severe cauda equina compression.

Surgery and postoperative course

The patient underwent a L2/L4 decompressive laminectomy with drainage of the intraspinal/extradural and paravertebral SEA; at surgery, a ventral extradural frankly purulent collection identified. After drainage, local vancomycin powder was applied. Postoperatively, within 15 days, she was pain free, had no residual neurological deficits, and was discharged home. One week postoperative, lumbar MRI documented adequate canal decompression with complete abscess drainage [Figure 2].

Figure 2:

Postoperative sagittal T1-WI with gadolinium administration (a) and sagittal T2-WI (b) MRI documented an adequate decompression with complete abscess drainage.

Pathogen

Staphylococcus aureus was the organism isolated from surgery. The patient, therefore, underwent targeted antibiotic therapy with daptomycin, meropenem, and teicoplanin until serum inflammatory values returned to normal.

DISCUSSION

There are a few select reports attributing SEA to pyelonephritis.[6,9,10,11] Several studies discussed a lumbar SEA occurring in patients following episodes of severe pyelonephritis [Table 1].[6] Kim and Noh, additionally, highlighted the occurrence of SEA due to acute pyelonephritis caused by S. aureus.[9] Ogoshi et al. discussed coexisting cervical (C1–C2: with extension into the oropharyngeal region) and lumbar (L4–L5: muscle structures-iliopsoas- piriformis) SEA due to pyelonephritis attributed to methicillin-resistant S. aureus.[12] Liu et al. described a cervical SEA spondylitis after acute pyelonephritis due to Escherichia coli bacteremia following interferon treatment.[11]

Table 1:

Patient’s demographics regarding literature review on lumbar spinal epidural abscess secondary to acute pyelonephritis.

CONCLUSION

SEA may occur due to hematogenous extension of bacteria attributed to prior pyelonephritis. Here, a 54-year-old female, following pyelonephritis 4 weeks ago, presented with low back pain and a paraparesis attribute to a CT/MR documented T12/L5 anterior SEA successfully treated with an L2–L4 laminectomy.