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Presentation of cauda equina syndrome due to an intradural extramedullary abscess: a case report
The Spine Journal 14 (2014) e1–e6
Case Report
Presentation of cauda equina syndrome due to an intradural extramedullary abscess: a case report Nitin Agarwal, BS, Janki Shah, BA, David R. Hansberry, PhD, Antonios Mammis, MD, Leroy R. Sharer, MD, Ira M. Goldstein, MD* Department of Neurological Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 90 Bergen St, Suite 8100, PO Box 1709, Newark, NJ 07101-1709, USA Received 12 March 2013; revised 12 August 2013; accepted 19 September 2013
Abstract
BACKGROUND CONTEXT: Cauda equina syndrome is caused by compression or injury to the nerve roots distal to the level of the spinal cord. This syndrome presents as low back pain, motor and sensory deficits in the lower extremities, and bladder as well as bowel dysfunction. Although various etiologies of cauda equina syndrome have been reported, a less common cause is infection. PURPOSE: To report a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus. STUDY DESIGN/SETTING: Case report and review of the literature. METHODS: The literature regarding the infectious causes of cauda equina syndrome was reviewed and a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus was reported. RESULTS: A 37-year-old woman, with history of intravenous drug abuse, hepatitis C, and hepatitis B, presented with low back pain lasting 2 months, lower extremity pain, left greater than right with increasing weakness and difficulty ambulating, and urinary and fecal incontinence. Her presentation was consistent with cauda equina syndrome. The patient underwent a T12–L2 laminectomy, and intradural exploration revealed an abscess. Methicillin-resistant Staphylococcus aureus was found on wound culture. CONCLUSIONS: Cauda equina syndrome, presenting as a result of spinal infection, such as the case reported here, is extremely rare but clinically important. Surgical intervention is generally the recommended therapeutic modality. Ó 2014 Elsevier Inc. All rights reserved.
Keywords:
Cauda equina syndrome; Intradural extramedullary abscess; Infection; Staphylococcus aureus
Introduction Cauda equina syndrome refers to the compression of lumbar and sacral nerve roots within the lower spinal canal FDA device/drug status: Not applicable. Author disclosures: NA: Nothing to disclose. JS: Consultancy: Zimmer Spine (C). DRH: Consultancy: Zimmer Spine (C). AM: Nothing to disclose. LRS: Nothing to disclose. IMG: Consultancy: Zimmer Spine (C). The disclosure key can be found on the Table of Contents and at www. TheSpineJournalOnline.com. Disclosure: The authors have no personal financial or institutional interest in any of the drugs, material, or devices described in this article. * Corresponding author. Department of Neurological Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 90 Bergen St, Suite 8100, PO Box 1709, Newark, NJ 07101-1709, USA. Tel.: (973) 972-8211; fax: (973) 972-8996. E-mail address: [email protected] (I.M. Goldstein) 1529-9430/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.spinee.2013.09.029
distal to the L1 vertebral level. Most commonly associated with acute disc herniation and spinal stenosis, cauda equina syndrome can also be caused by neoplasms, infections, traumatic injury, and iatrogenic causes, such as after surgery [1]. It is characterized by lower back pain, bowel and bladder dysfunction, and sensory deficit in the perineum. Urinary incontinence and loss of rectal tone are observed on physical examination [1–4]. When cauda equina syndrome is suspected, imaging evaluation of the lumbar spinal canal is performed with magnetic resonance imaging (MRI) scan or myelography to evaluate for compressive pathology. On diagnosis with cauda equina syndrome, the treatment is emergent surgical decompression of the spinal canal [2,3]. The authors present the case of a patient with an intradural extramedullary abscess manifesting in cauda equina syndrome.
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Case report History and examination A 37-year-old woman, with history of intravenous drug abuse, HIV, hepatitis C, and hepatitis B, presented with cauda equina syndrome. Her symptoms included low back pain lasting 2 months, lower extremity pain, left greater than right with increasing weakness and difficulty ambulating, and urinary and fecal incontinence. An MRI scan of the lumbar spine demonstrated a large intradural extramedullary mass at T12–L2 (Figs. 1–3). Operation and pathological findings A lumbar decompressive surgery was performed, under general endotracheal anesthesia, with somatosensory evoked potential (SSEP) and electromyographic (EMG) monitoring and bowel and bladder potential monitoring. A laminectomy from T12–L2 was performed, and on evaluation of intradural contents, nerve roots were noted to be plastered dorsally, in the intradural space, which were freed from an underlying mass. A discolored grayish mass could be found beneath the nerve roots and in freeing the roots, a small fenestration was created in this mass. Purulent fluid was then expressed. Several pieces of the mass were sent for frozen pathology and the result was consistent with an inflammatory lesion (Fig. 4). The abscess was evacuated. Postoperative course Postoperatively, the patient was placed on intravenous vancomycin and ceftriaxone for 8 weeks, because of the
Fig. 2. Preoperative T1-weighted sagittal MRI with contrast.
presence of methicillin-resistant Staphylococcus aureus (MRSA) within the wound culture, and was then switched to oral linezolid (Figs. 5–7). At the 2-year follow-up, the patient had seen marked improvement in her lower extremities and her fecal incontinence was largely resolved; however her bladder incontinence persisted and was unchanged. Additionally, there was continued numbness in the perianal region. Discussion Several etiological origins have been proposed for cauda equina syndrome. Although commonly caused by compression of the nerve roots in the lower spinal canal by a lumbar disk herniation and degenerative or congenital spinal stenosis, rare cases of cauda equina syndrome can also be caused by compression of the nerve roots by tumors or spinal infection [5]. Infection Fig. 1. Preoperative T1-weighted sagittal MRI without contrast.
An infectious cause of cauda equina syndrome should be suspected in the patient presenting with the characteristic
N. Agarwal et al. / The Spine Journal 14 (2014) e1–e6
Fig. 3. Preoperative T2-weighted sagittal MRI with contrast.
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symptoms of low back pain, unilateral or bilateral sciatica, and bladder and bowel dysfunction, and, in addition, with positive blood cultures, increased white blood cell count, and elevated erythrocyte sedimentation rate or C reactive protein. Furthermore, the long-term outcomes after surgical decompression in this presentation of cauda equina may be worse because of the increased likelihood of developing postoperative complications, such as arachnoiditis. Cauda equina syndrome caused by spinal infection, as presented in this case, is extremely rare and can have devastating consequences for the patient. Both pyogenic and nonpyogenic organisms can lead to infection of the spinal cord and result in an epidural abscess, leading to cauda equina compression and subsequent neurological damage [6,7]. Pyogenic organisms, particularly S. aureus, as was present within the wound culture of our patient, are the most common cause of spinal epidural abscesses [8–12]. The incidence of pyogenic spinal epidural abscesses is between 0.2 and 1.2 per 10,000 hospital admissions [12–15]. Approximately 35% of people who develop a spinal epidural abscess have a history of intravenous drug abuse, whereas 50% to 60% are immunocompromised due to chronic illness and 10% to 20% have had spinal surgery [12,16]. Furthermore, typically, patients present with low back pain, neurological dysfunction varying from paraplegia to paraparesis, and about one-third of patients experience loss of
Fig. 4. (Upper left) Purulent exudate, with polymorphonuclear leukocytes (PMNs, neutrophils), basophilic (blue-staining) cellular debris, and some fibrin. Hematoxylin and eosin stain, magnification 25. (Upper right) Gram-positive cocci in clusters and individually, with some degeneration of organisms. Tissue Gram stain, magnification 40. (Bottom left) PMNs and plasma cells, with collagen in background, also with some fibroblasts, comprising granulation tissue. Hematoxylin and eosin stain, magnification 10. (Bottom right) PMNs and plasma cells, with collagen in background, also with some fibroblasts, comprising granulation tissue. Masson trichrome stain (collagen is blue), magnification 10.
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Fig. 5. Postoperative 2-year follow-up T1-weighted sagittal MRI without contrast.
bowel or bladder function [12,16–18]. The diagnosis is made with MRI, and the preferred treatment is surgical decompression with drainage of the abscess and longterm antibiotic therapy [9,11,19–23]. Patient outcome with surgery varies based on the clinical history of the patient as well as the degree of neurological dysfunction and the time between the onset of symptoms and surgical treatment of the spinal epidural abscess [6,12,16]. Although spinal infections in the developed world are mostly caused by pyogenic organisms, nonpyogenic organisms are the primary cause of epidural abscesses in immunocompromised populations and populations of underdeveloped countries [6]. Nonpyogenic organisms causing epidural abscesses include Mycobacterium tuberculosis or a fungus, namely Candida or Aspergillus [7,24]. Although very rare, cases of spinal fungal infections have been described in patients receiving immunosuppressants, patients with HIV infection, and intravenous drug users [7,24,25]. Batra et al. [7] reported the first case of spinal epidural abscess caused by Aspergillus fumigatus that manifested as acute cauda equina syndrome. A 45-year-old man presented with a 1- month history of low back pain and weakness of both lower limbs, as well as bladder and bowel dysfunction for 1 day. He experienced diminished sensation below the L5 dermatome on both sides and perianal anesthesia. Cauda equina syndrome was diagnosed. An MRI of the lumbosacral
Fig. 6. Postoperative 2-year follow-up T1-weighted sagittal MRI with contrast.
spine displayed a multilocular extradural collection extending from the L3–S1 vertebra and a laminectomy was performed at the L3–L5 levels. Thick, gray granulation tissue without any pus collection enveloped the cauda equina and dura. Cultures revealed growth of A. fumigatus. The patient was placed on oral itraconazole. Within a week of surgical decompression of the cauda equina, motor and sensory functions were regained and within 3 weeks, sensation and voluntary control of the bladder was established [7]. Intradural extramedullary spinal abscesses are a rare clinical condition with a poor prognosis [26,27]. Unlike a spinal epidural abscess, which most commonly involves the lumbar vertebrae, a spinal intradural abscess can occur anywhere along the spinal cord and most often involves the thoracic region [28,29]. Very rarely, a spinal intradural abscess can lead to symptoms of sciatica or cauda equina syndrome [29,30]. Very few cases have been reported, most of which are due to tuberculosis [31,32]. The most effective treatment for a spinal intradural abscess in patients who present with neurologic deficits is immediate surgical drainage followed by appropriate antimicrobial therapy for 4 to 6 weeks [33–35]. Nonoperative treatment can be considered in patients without neurologic deficits when the risk of
N. Agarwal et al. / The Spine Journal 14 (2014) e1–e6
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It should be considered as part of the differential diagnosis, especially for individuals who are immunocompromised or susceptible to infections. Surgical decompression of the cauda equina, followed by intravenous antibiotics, is the recommended treatment strategy.
References
Fig. 7. Postoperative 2-year follow-up T2-weighted sagittal MRI with contrast.
developing neurologic impairment is low based on the location of the abscess and virulence of the organism [36]. Surgical considerations In cases such as this one, whereby the preoperative imaging may be difficult to discern between a tumor and an abscess, several surgical considerations must be noted for the latter. As mentioned previously, in this case, a number of nerve roots were noted to be plastered dorsally in the intradural space. Given this presentation, neuromonitoring is essential. Moreover, the notion that a total resection will be obtained is not entirely feasible. Still, precautions should be taken to prevent the spillage of infectious materials into the cerebral spinal fluid.
Conclusion Numerous causes of cauda equina syndrome have been reported, with the most common being lumbar disc prolapse or spinal stenosis. However, cauda equina syndrome presenting as a result of an intradural extramedullary abscess caused by S. aureus is rare, but clinically important.
[1] Nascone J, Lauerman WC, Wiesel SW. Cauda equina syndrome: is it a surgical emergency? Univ Pa Orthop J 1999;12:73–6. [2] Gitelman A, Hishmeh S, Morelli BN, et al. Cauda equina syndrome: a comprehensive review. Am J Orthop (Belle Mead NJ) 2008;37:556–62. [3] Spector LR, Madigan L, Rhyne A, et al. Cauda equina syndrome. J Am Acad Orthop Surg 2008;16:471–9. [4] Orendacova J, Cizkova D, Kafka J, et al. Cauda equina syndrome. Prog Neurobiol 2001;64:613–37. [5] Ester D-P. A case study of cauda equina syndrome. Perm J 2003;7:13–7. [6] Cohen DB. Infectious origins of cauda equina syndrome. Neurosurg Focus 2004;16:e2. [7] Batra S, Arora S, Meshram H, et al. A rare etiology of cauda equina syndrome. J Infect Dev Ctries 2011;5:79–82. [8] Sklar EML, Post MJD, Lebwohl NH. Imaging of infection of the lumbosacral spine. Neuroimaging Clin N Am 1993;3:577–90. [9] Danner RL, Hartman BJ. Update on spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis 1987;9:265–74. [10] Nussbaum ES, Rigamonti D, Standiford H, et al. Spinal epidural abscess: a report of 40 cases and review. Surg Neurol 1992;38:225–31. [11] Kaufman DM, Kaplan JG, Litman N. Infectious agents in spinal epidural abscesses. Neurology 1980;30:844–50. [12] Rigamonti D, Liem L, Sampath P, et al. Spinal epidural abscess: contemporary trends in etiology, evaluation, and management. Surg Neurol 1999;52:189–96; discussion 197. [13] Baker AS, Ojemann RG, Swartz MN, Richardson EP Jr. Spinal epidural abscess. N Engl J Med 1975;293:463–8. [14] Schlossberg D, Shulman JA. Spinal epidural abscess. South Med J 1977;70:669–73. [15] Hakin RN, Burt AA, Cook JB. Acute spinal epidural abscess. Paraplegia 1979;17:330–6. [16] Tang HJ, Lin HJ, Liu YC, Li CM. Spinal epidural abscess—experience with 46 patients and evaluation of prognostic factors. J Infect 2002;45:76–81. [17] Hancock DO. A study of 49 patients with acute spinal extradural abscess. Paraplegia 1973;10:285–8. [18] Bouchez B, Arnott G, Delfosse JM. Acute spinal epidural abscess. J Neurol 1985;231:343–4. [19] An HS, Vaccaro AR, Dolinskas CA, et al. Differentiation between spinal tumors and infections with magnetic resonance imaging. Spine 1991;16:S334–8. [20] Post MJ, Sze G, Quencer RM, et al. Gadolinium-enhanced MR in spinal infection. J Comput Assist Tomogr 1990;14:721–9. [21] Numaguchi Y, Rigamonti D, Rothman MI, et al. Spinal epidural abscess: evaluation with gadolinium-enhanced MR imaging. Radiographics 1993;13:545–59; discussion 559–60. [22] Sandhu FS, Dillon WP. Spinal epidural abscess: evaluation with contrast-enhanced MR imaging. AJNR Am J Neuroradiol 1991;12: 1087–93. [23] Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: a metaanalysis of 915 patients. Neurosurg Rev 2000;23:175–204; discussion 205. [24] Ferra C, Doebbeling BN, Hollis RJ, et al. Candida tropicalis vertebral osteomyelitis: a late sequela of fungemia. Clin Infect Dis 1994;19: 697–703. [25] Williams RL, Fukui MB, Meltzer CC, et al. Fungal spinal osteomyelitis in the immunocompromised patient: MR findings in three cases. AJNR Am J Neuroradiol 1999;20:381–5.
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[26] DeSanto J, Ross JS. Spine infection/inflammation. Radiol Clin North Am 2011;49:105–27. [27] Nadkarni T, Shah A, Kansal R, Goel A. An intradural–extramedullary gas-forming spinal abscess in a patient with diabetes mellitus. J Clin Neurosci 2010;17:263–5. [28] Muthukumar N, Sureshkumar V, Ramesh VG. En plaque intradural extramedullary spinal tuberculoma and concurrent intracranial tuberculomas: paradoxical response to antituberculous therapy. J Neurosurg Spine 2007;6:169–73. [29] Ozek E, Iplkcioglu A, Erdal M. Intradural extramedullary tuberculoma mimicking en plaque meningioma. Neurol India 2009;57: 211–2. [30] Achouri M, Hilmani S, Sami A, et al. Intradural extramedullary tuberculous abscess. Apropos of a case. Neurochirurgie 1996;42:306–8.
[31] Kim MS, Kim KJ, Chung CK, Kim HJ. Intradural extramedullary tuberculoma of the spinal cord: a case report. J Korean Med Sci 2000;15:368–70. [32] Tanriverdi T, Kizilkilic O, Hanci M, et al. Atypical intradural spinal tuberculosis: report of three cases. Spinal Cord 2003;41:403–9. [33] Thome C, Krauss JK, Zevgaridis D, Schmiedek P. Pyogenic abscess of the filum terminale. J Neurosurg Spine 2001;95:100–4. [34] Lange M, Tiecks F, Schielke E, et al. Diagnosis and results of different treatment regimes in patients with spinal abscesses. Acta Neurochir 1993;125:105–14. [35] St€abler A, Reiser MF. Imaging of spinal infection. Radiol Clin North Am 2001;39:115–35. [36] Manelfe C. Imaging of the spine and spinal cord. Curr Opin Radiol 1991;3:5–15.
Case Report
Presentation of cauda equina syndrome due to an intradural extramedullary abscess: a case report Nitin Agarwal, BS, Janki Shah, BA, David R. Hansberry, PhD, Antonios Mammis, MD, Leroy R. Sharer, MD, Ira M. Goldstein, MD* Department of Neurological Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 90 Bergen St, Suite 8100, PO Box 1709, Newark, NJ 07101-1709, USA Received 12 March 2013; revised 12 August 2013; accepted 19 September 2013
Abstract
BACKGROUND CONTEXT: Cauda equina syndrome is caused by compression or injury to the nerve roots distal to the level of the spinal cord. This syndrome presents as low back pain, motor and sensory deficits in the lower extremities, and bladder as well as bowel dysfunction. Although various etiologies of cauda equina syndrome have been reported, a less common cause is infection. PURPOSE: To report a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus. STUDY DESIGN/SETTING: Case report and review of the literature. METHODS: The literature regarding the infectious causes of cauda equina syndrome was reviewed and a case of cauda equina syndrome caused by infection of an intradural extramedullary abscess with Staphylococcus aureus was reported. RESULTS: A 37-year-old woman, with history of intravenous drug abuse, hepatitis C, and hepatitis B, presented with low back pain lasting 2 months, lower extremity pain, left greater than right with increasing weakness and difficulty ambulating, and urinary and fecal incontinence. Her presentation was consistent with cauda equina syndrome. The patient underwent a T12–L2 laminectomy, and intradural exploration revealed an abscess. Methicillin-resistant Staphylococcus aureus was found on wound culture. CONCLUSIONS: Cauda equina syndrome, presenting as a result of spinal infection, such as the case reported here, is extremely rare but clinically important. Surgical intervention is generally the recommended therapeutic modality. Ó 2014 Elsevier Inc. All rights reserved.
Keywords:
Cauda equina syndrome; Intradural extramedullary abscess; Infection; Staphylococcus aureus
Introduction Cauda equina syndrome refers to the compression of lumbar and sacral nerve roots within the lower spinal canal FDA device/drug status: Not applicable. Author disclosures: NA: Nothing to disclose. JS: Consultancy: Zimmer Spine (C). DRH: Consultancy: Zimmer Spine (C). AM: Nothing to disclose. LRS: Nothing to disclose. IMG: Consultancy: Zimmer Spine (C). The disclosure key can be found on the Table of Contents and at www. TheSpineJournalOnline.com. Disclosure: The authors have no personal financial or institutional interest in any of the drugs, material, or devices described in this article. * Corresponding author. Department of Neurological Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, 90 Bergen St, Suite 8100, PO Box 1709, Newark, NJ 07101-1709, USA. Tel.: (973) 972-8211; fax: (973) 972-8996. E-mail address: [email protected] (I.M. Goldstein) 1529-9430/$ - see front matter Ó 2014 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.spinee.2013.09.029
distal to the L1 vertebral level. Most commonly associated with acute disc herniation and spinal stenosis, cauda equina syndrome can also be caused by neoplasms, infections, traumatic injury, and iatrogenic causes, such as after surgery [1]. It is characterized by lower back pain, bowel and bladder dysfunction, and sensory deficit in the perineum. Urinary incontinence and loss of rectal tone are observed on physical examination [1–4]. When cauda equina syndrome is suspected, imaging evaluation of the lumbar spinal canal is performed with magnetic resonance imaging (MRI) scan or myelography to evaluate for compressive pathology. On diagnosis with cauda equina syndrome, the treatment is emergent surgical decompression of the spinal canal [2,3]. The authors present the case of a patient with an intradural extramedullary abscess manifesting in cauda equina syndrome.
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Case report History and examination A 37-year-old woman, with history of intravenous drug abuse, HIV, hepatitis C, and hepatitis B, presented with cauda equina syndrome. Her symptoms included low back pain lasting 2 months, lower extremity pain, left greater than right with increasing weakness and difficulty ambulating, and urinary and fecal incontinence. An MRI scan of the lumbar spine demonstrated a large intradural extramedullary mass at T12–L2 (Figs. 1–3). Operation and pathological findings A lumbar decompressive surgery was performed, under general endotracheal anesthesia, with somatosensory evoked potential (SSEP) and electromyographic (EMG) monitoring and bowel and bladder potential monitoring. A laminectomy from T12–L2 was performed, and on evaluation of intradural contents, nerve roots were noted to be plastered dorsally, in the intradural space, which were freed from an underlying mass. A discolored grayish mass could be found beneath the nerve roots and in freeing the roots, a small fenestration was created in this mass. Purulent fluid was then expressed. Several pieces of the mass were sent for frozen pathology and the result was consistent with an inflammatory lesion (Fig. 4). The abscess was evacuated. Postoperative course Postoperatively, the patient was placed on intravenous vancomycin and ceftriaxone for 8 weeks, because of the
Fig. 2. Preoperative T1-weighted sagittal MRI with contrast.
presence of methicillin-resistant Staphylococcus aureus (MRSA) within the wound culture, and was then switched to oral linezolid (Figs. 5–7). At the 2-year follow-up, the patient had seen marked improvement in her lower extremities and her fecal incontinence was largely resolved; however her bladder incontinence persisted and was unchanged. Additionally, there was continued numbness in the perianal region. Discussion Several etiological origins have been proposed for cauda equina syndrome. Although commonly caused by compression of the nerve roots in the lower spinal canal by a lumbar disk herniation and degenerative or congenital spinal stenosis, rare cases of cauda equina syndrome can also be caused by compression of the nerve roots by tumors or spinal infection [5]. Infection Fig. 1. Preoperative T1-weighted sagittal MRI without contrast.
An infectious cause of cauda equina syndrome should be suspected in the patient presenting with the characteristic
N. Agarwal et al. / The Spine Journal 14 (2014) e1–e6
Fig. 3. Preoperative T2-weighted sagittal MRI with contrast.
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symptoms of low back pain, unilateral or bilateral sciatica, and bladder and bowel dysfunction, and, in addition, with positive blood cultures, increased white blood cell count, and elevated erythrocyte sedimentation rate or C reactive protein. Furthermore, the long-term outcomes after surgical decompression in this presentation of cauda equina may be worse because of the increased likelihood of developing postoperative complications, such as arachnoiditis. Cauda equina syndrome caused by spinal infection, as presented in this case, is extremely rare and can have devastating consequences for the patient. Both pyogenic and nonpyogenic organisms can lead to infection of the spinal cord and result in an epidural abscess, leading to cauda equina compression and subsequent neurological damage [6,7]. Pyogenic organisms, particularly S. aureus, as was present within the wound culture of our patient, are the most common cause of spinal epidural abscesses [8–12]. The incidence of pyogenic spinal epidural abscesses is between 0.2 and 1.2 per 10,000 hospital admissions [12–15]. Approximately 35% of people who develop a spinal epidural abscess have a history of intravenous drug abuse, whereas 50% to 60% are immunocompromised due to chronic illness and 10% to 20% have had spinal surgery [12,16]. Furthermore, typically, patients present with low back pain, neurological dysfunction varying from paraplegia to paraparesis, and about one-third of patients experience loss of
Fig. 4. (Upper left) Purulent exudate, with polymorphonuclear leukocytes (PMNs, neutrophils), basophilic (blue-staining) cellular debris, and some fibrin. Hematoxylin and eosin stain, magnification 25. (Upper right) Gram-positive cocci in clusters and individually, with some degeneration of organisms. Tissue Gram stain, magnification 40. (Bottom left) PMNs and plasma cells, with collagen in background, also with some fibroblasts, comprising granulation tissue. Hematoxylin and eosin stain, magnification 10. (Bottom right) PMNs and plasma cells, with collagen in background, also with some fibroblasts, comprising granulation tissue. Masson trichrome stain (collagen is blue), magnification 10.
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Fig. 5. Postoperative 2-year follow-up T1-weighted sagittal MRI without contrast.
bowel or bladder function [12,16–18]. The diagnosis is made with MRI, and the preferred treatment is surgical decompression with drainage of the abscess and longterm antibiotic therapy [9,11,19–23]. Patient outcome with surgery varies based on the clinical history of the patient as well as the degree of neurological dysfunction and the time between the onset of symptoms and surgical treatment of the spinal epidural abscess [6,12,16]. Although spinal infections in the developed world are mostly caused by pyogenic organisms, nonpyogenic organisms are the primary cause of epidural abscesses in immunocompromised populations and populations of underdeveloped countries [6]. Nonpyogenic organisms causing epidural abscesses include Mycobacterium tuberculosis or a fungus, namely Candida or Aspergillus [7,24]. Although very rare, cases of spinal fungal infections have been described in patients receiving immunosuppressants, patients with HIV infection, and intravenous drug users [7,24,25]. Batra et al. [7] reported the first case of spinal epidural abscess caused by Aspergillus fumigatus that manifested as acute cauda equina syndrome. A 45-year-old man presented with a 1- month history of low back pain and weakness of both lower limbs, as well as bladder and bowel dysfunction for 1 day. He experienced diminished sensation below the L5 dermatome on both sides and perianal anesthesia. Cauda equina syndrome was diagnosed. An MRI of the lumbosacral
Fig. 6. Postoperative 2-year follow-up T1-weighted sagittal MRI with contrast.
spine displayed a multilocular extradural collection extending from the L3–S1 vertebra and a laminectomy was performed at the L3–L5 levels. Thick, gray granulation tissue without any pus collection enveloped the cauda equina and dura. Cultures revealed growth of A. fumigatus. The patient was placed on oral itraconazole. Within a week of surgical decompression of the cauda equina, motor and sensory functions were regained and within 3 weeks, sensation and voluntary control of the bladder was established [7]. Intradural extramedullary spinal abscesses are a rare clinical condition with a poor prognosis [26,27]. Unlike a spinal epidural abscess, which most commonly involves the lumbar vertebrae, a spinal intradural abscess can occur anywhere along the spinal cord and most often involves the thoracic region [28,29]. Very rarely, a spinal intradural abscess can lead to symptoms of sciatica or cauda equina syndrome [29,30]. Very few cases have been reported, most of which are due to tuberculosis [31,32]. The most effective treatment for a spinal intradural abscess in patients who present with neurologic deficits is immediate surgical drainage followed by appropriate antimicrobial therapy for 4 to 6 weeks [33–35]. Nonoperative treatment can be considered in patients without neurologic deficits when the risk of
N. Agarwal et al. / The Spine Journal 14 (2014) e1–e6
e5
It should be considered as part of the differential diagnosis, especially for individuals who are immunocompromised or susceptible to infections. Surgical decompression of the cauda equina, followed by intravenous antibiotics, is the recommended treatment strategy.
References
Fig. 7. Postoperative 2-year follow-up T2-weighted sagittal MRI with contrast.
developing neurologic impairment is low based on the location of the abscess and virulence of the organism [36]. Surgical considerations In cases such as this one, whereby the preoperative imaging may be difficult to discern between a tumor and an abscess, several surgical considerations must be noted for the latter. As mentioned previously, in this case, a number of nerve roots were noted to be plastered dorsally in the intradural space. Given this presentation, neuromonitoring is essential. Moreover, the notion that a total resection will be obtained is not entirely feasible. Still, precautions should be taken to prevent the spillage of infectious materials into the cerebral spinal fluid.
Conclusion Numerous causes of cauda equina syndrome have been reported, with the most common being lumbar disc prolapse or spinal stenosis. However, cauda equina syndrome presenting as a result of an intradural extramedullary abscess caused by S. aureus is rare, but clinically important.
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