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Case Report

All that glitters is not gold: A spinal epidural empyema following epidural steroid injection

Department of Biomedicine Neurosciences and Advanced Diagnostic, University of Palermo, School of Medicine, Palermo, Sicily, Italy,
Department of Neurosurgery, ARNAS Garibaldi, P.O. Garibaldi Nesima, Via Palermo, 636, Catania, Italy,
Division of Neurosurgery, Villa Sofia Hospital, Palermo, Sicily, Italy.
Corresponding author: Lara Brunasso, Department of Biomedicine Neurosciences and Advanced Diagnostic, University of Palermo, School of Medicine, Palermo, Sicily, Italy.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Brunasso L, Basile L, Iacopino DG, Gulì C, Graziano F, Pino MA, et al. All that glitters is not gold: A spinal epidural empyema following epidural steroid injection. Surg Neurol Int 2020;11:240.



Therapeutic epidural spinal injections (ESIs) of steroids are one of the most common nonsurgical management modalities employed for alleviating pain due to chronic persistent lumbar spinal disease. However, it is well documented that they have significant risks and complications without any long-term efficacy. ESI may result in epidural empyema which may be difficult to diagnose with delays resulting in significant permanent neurological sequelae.

Case Description:

A 45-year-old female presented with a lumbar spinal epidural empyema after receiving ESI for low back and right leg pain due to a lumbar disc herniation. Laboratory studies showed elevations of multiple inflammatory markers, and the MR documented a significant lumbar epidural empyema contributing to significant thecal sac compression. Clinically, the patient had an acute cauda equina syndrome warranting emergency surgery consisting of a laminectomy for debridement/decompression followed by long-term antibiotic treatment.


Epidural empyema is a major potential complication of lumbar ESI. Multiple markedly elevated inflammatory markers (WBC, ESR, CRP, and procalcitonin) and MRI evidence of an epidural empyema necessitates emergent surgical intervention to limit morbidity, neurological sequelae, and mortality.


Lumbar degenerative disease
Pain management
Spinal epidural abscess
Spinal infection
Spinal procedure


Spinal epidural empyema (SEE), also called spinal epidural abscesses (SEA), posts a significant risk of neurological morbidity and mortality (e.g., rates of 4–31% worldwide).[16,31] Several risk factors for SEE/SEA include diabetes, intravenous drug abuse, and recent spinal surgery (most frequent cause).[22,30,31,33-35] Fever, spinal tenderness/back pain, and progressive neurological deficits are the triad of symptoms/signs classically seen with SEE/SEA.[8,16,17,33,34,39]

Here, we present a patient with an acute cauda equina syndrome due to an MR-documented L4- L5 SEE/SEA following a spinal epidural spinal injection (ESI).


A 45-year-old female with a symptomatic lumbar disc herniation had an ESI. Over the next few weeks, she complained constipation with increasing leg pain and the progressive inability to walk; she finally developed in acute urinary retention. On examination, she had a cauda equina syndrome; 3/5 motor function in both lower extremities, with perineal hypoesthesia. Laboratory studies showed a high white blood cell count of 19.79 × 103/ml, while the emergent lumbar MRI without gadolinium showed an anterior epidural L4-L5-S1 empyema/abscess (e.g., low signal on T1- and a high signal in T2-weighted images) with marked thecal sac/root compression [Figure 1]. With the diagnosis of a SEE/SEA, an emergent laminectomy/decompression was performed that revealed thick, purulent, grayish fluid compressing the thecal sac anteriorly. Several samples were obtained for culture.

Figure 1:: Preoperative emergency MRI without gadolinium. In (a), the sagittal T1-weighted image provides suboptimal visualization of epidural abscess. In (b), the sagittal T2-weighted image demonstrates a longitudinally oriented mass-like lesion in the anterior epidural space spreading between the posterior wall of L4 and L5. In (c), the axial T2-weighted image demonstrates right side epidural abscess compressing both the cauda equina and right L5 and S1 emergent nerve roots.

The presumptive initial vancomycin and ceftazidime were changed to clindamycin and gentamicin to address the methicillin-resistant Staphylococcus aureus and Streptococcus parasanguinis. The 3-day postoperative lumbar MRI documented adequate decompression of the cauda equina [Figure 2], and the remainder of the postoperative course was uneventful; 1 month postoperatively, she had residual 4/5 motor function in the right lower extremity without any residual sphincter dysfunction [Figure 3].

Figure 2:: Three days postoperative MRI without gadolinium. In (a), the sagittal T1-weighted image, in (b), the sagittal T2-weighted image, in (c), the axial T2-weighted image demonstrate marked reduction of the preoperative empyema mass at L4 and L5 level in the anterior epidural space with consensual reduction of the compression on the adjoining meningeal and neural structures.
Figure 3:: One month postoperative MRI. In (a), the sagittal T2-weighted image and in (b), the axial T2-weighted image demonstrates the complete resolution of the infectious process.


Despite the lack of documented safety and efficacy[37,41] and without approval of the Food and Drug Administration, ESIs are still being performed.[1,4,5,13,19,29] Nevertheless, as noted here, there are serious complications of ESIs that include spinal epidural and subdural hematomas, brain/cord infarctions (cervical ESI), and spinal epidural/subdural abscesses.[3,11,24,37,42]

The classical triad of SEE/SEA includes fever, back pain, and neurological deficits which may rapidly progress to quadriplegia/paraplegia. Laboratory studies usually show elevated WBC counts and increased ESR, CRP, and procalcitonin levels.[6,7,9,10,21,25,32,34]

Enhanced MRI remains the study of choice for documenting SEE/SEA that is most frequently found in the thoracic (48%), lumbar (31%), and cervical regions.[2] A definitive diagnosis of the offending organism is critical to choosing appropriate antibiotic therapy. Where inflammatory markers continue to rise, MR studies show worsening, and neurological deficits progress, operative decompression/drainage is warranted in a timely fashion.[12,18,38] Notably, the majority of SEE/SEA are due to a S. aureus species.[15,28,36]

[Table 1] summarizes reported reviewed cases of extradural abscess following extradural analgesic injection for low back and radiculopathies to our knowledge.[4,14,20,23,27,40,42]

Table 1:: Summary of case reports on spinal epidural abscess following spinal epidural steroid injection.

Following spinal ESI, patients generally present within few weeks with back pain, fever, radiculopathies, and/or myelopathy. Enhanced MRI studies are the examinations of choice as they will demonstrate show epidural infections within 2–4 weeks; X-rays and CT studies will take up to 6–10 weeks to show abnormalities.[26]

Here, the patient presented with pain, fever, and a neurological deficit (3/5 motor function of RLE), perineal hypoesthesia, and urinary retention. Once abnormally elevated laboratory inflammatory markers and an MR confirming an anterior L4-S1 epidural empyema were obtained, an emergent decompressive hemilaminectomy was performed that largely resolved the patient’s preoperative deficits. Sample biopsy was crucial to maximize efficacy, tailored antibiotic therapy, and limit resistance.


SEE diagnosis should be suspected in a patient presenting with the classic triad of back pain, fever, and a neurological deficit, associated with elevated laboratory inflammatory markers and MRI findings of significant epidural spinal compression. This clinical picture should prompt early neurosurgical intervention/decompression to minimize long-term neurological sequelae.

Declaration of patient consent

Patient’s consent not required as patients identity is not disclosed or compromised.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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